Ebola, Obama and Oil

Obama’s “War on Ebola” or War for Oil?

Sending 3000 Troops to African “Ebola”

Areas that Happen to Export Oil to China

 

The most vague and unsubstantiated basis lies behind President Obama’s new War on Ebola

Image Credits: Eric Kounce, Wikimedia Commons

by F. William Engdahl | New Eastern Outlook | October 4, 2014

For a Nobel Peace Prize President, Barack Obama seems destined to go down in history books as the President who presided over one of the most aggressive series of wars ever waged by a bellicose Washington Administration. Not even George Bush and Dick Cheney came close.

First, before the ink was even dry on his Nobel Prize certificate, Obama announced the Afghanistan “surge”, pouring another 30,000 US military into that destroyed part of the world. Then came Obama’s war against Libya’s Qaddafi, followed rapidly by his war to try to topple Syria’s Bashar al Assad. Soon after came Obama’s “war for democracy in Ukraine,” otherwise better called Obama’s attempt to provoke Russia into a new war confrontation with NATO by backing a gaggle of Ukrainian oligarchs, criminals and outright neo-nazis in Kiev. In July of this year, Obama’s Administration was pushing the President to launch a second try at bombing Syria back to the Stone Age, allegedly to destroy ISIS, a looney Jihadist Sunni sect that was said to be a joint venture of the CIA and Israeli intelligence.

Now Obama’s advisers, no doubt led by the blood-thirsty National Security Adviser, Susan Rice, have come up with a new war. This is the War Against Ebola. On September 16, President Obama solemnly declared the war. He announced, to the surprise of most sane citizens, that he had ordered 3,000 American troops, the so-called “boots on the ground” that the Pentagon refuses to agree to in Syria, to wage a war against….a virus?

In a carefully stage-managed appearance at the US Centers for Disease Control (CDC), Obama read a bone-chilling speech. He called the alleged Ebola outbreaks in west Africa, “a global threat, and it demands a truly global response. This is an epidemic that is not just a threat to regional security. It’s a potential threat to global security, if these countries break down, if their economies break down, if people panic,” Obama continued, conjuring images that would have made Andromeda Strain novelist Michael Chrichton drool with envy. Obama added, “That has profound effects on all of us, even if we are not directly contracting the disease. This outbreak is already spiraling out of control.”

With that hair-raising introduction, the President of the world’s greatest Superpower announced his response. In his role as Commander-in-Chief of the United States of America announced he has ordered 3,000 US troops to west Africa in what he called, “the largest international response in the history of the CDC.” He didn’t make clear if their job would be to shoot the virus wherever it reared its ugly head, or to shoot any poor hapless African suspected of having Ebola. Little does it matter that the US military doesn’t have anywhere near 3,000 troops with the slightest training in public health.

Before we all panic and line up to receive the millions of doses of untested and reportedly highly dangerous “Ebola vaccines” the major drug-makers are preparing to dump on the market, some peculiarities of this Ebola outbreak in Africa are worth noting.

Certified Ebola Deaths?

The World Health Organization, under the Director, Dr Margaret Chan, in a press conference on September 13, sounded the alarm, warning that Ebola in west Africa was surging out of control. “In the three hardest hit countries, Guinea, Liberia and Sierra Leone, the number of new patients is moving far faster than the capacity to manage them,” Chan claimed. WHO claims that almost half of 301 health-care workers dealing with alleged Ebola patients have themselves died, and that 2,400 people out of 4,784 cases in Africa have died of Ebola. On August 8, Chan declared the African Ebola situation a “Public Health Emergency of International Concern,” whatever that is supposed to mean.

A major problem for Chan and her backers, however, is that her Ebola statistics are very, very dubious. For those whose memory is short, this is the same Dr Margaret Chan at WHO in Geneva who was guilty in 2009 of trying to panic the world into taking unproven vaccines for “Swine Flu” influenza, by declaring a Global Pandemic with statistics calling every case of symptoms that of the common cold to be “Swine Flu,” whether it was runny nose, coughing, sneezing, sore throat. That changed WHO definition of Swine Flu allowed the statistics of the disease to be declared Pandemic. It was an utter fraud, a criminal fraud Chan carried out, wittingly or unwittingly (she could be simply stupid but evidence suggests otherwise), on behalf of the major US and EU pharmaceutical cartel.

In a recent Washington Post article it was admitted that sixty-nine percent of all the Ebola cases in Liberia registered by WHO have not been laboratory confirmed through blood tests. Liberia is the epicenter of the Ebola alarm in west Africa. More than half of the alleged Ebola deaths, 1,224, and nearly half of all cases, 2,046, have been in Liberia says WHO. And the US FDA diagnostic test used for the lab confirmation of Ebola is so flawed that the FDA has prohibited anyone from claiming they are safe or effective. That means, a significant proportion of the remaining 31 % of the Ebola cases lab confirmed through blood tests could be false cases.

In short, no one knows what 1,224 Liberians in recent weeks have died from. But WHO claims it to be Ebola. Note that the countries affected by the Ebola alarm are among the poorest and most war-torn regions in the world. Wars over blood diamonds and colonial genocidal tribal wars have left a devastated, mal-nourished population in its wake.

WHO’s official fact sheet on Ebola, which now they renamed EVD for Ebola Virus Disease, claims, “The first EVD outbreaks occurred in remote villages in Central Africa, near tropical rainforests, but the most recent outbreak in west Africa has involved major urban as well as rural areas…” WHO further notes that, “It is thought that fruit bats of the Pteropodidae family are natural Ebola virus hosts. Ebola is introduced into the human population through close contact with the blood, secretions, organs or other bodily fluids of infected animals such as chimpanzees, gorillas, fruit bats, monkeys, forest antelope and porcupines found ill or dead or in the rainforest.”

Then the official WHO Ebola Fact Sheet dated September, 2014, states, “It can be difficult to distinguish EVD from other infectious diseases such as malaria, typhoid fever and meningitis.”

Excuse me, Dr Margaret Chan, can you say that slowly? It can be difficult to distinguish EVD from other infectious diseases such as malaria, typhoid fever and meningitis? And you admit that 69% of the declared cases have never been adequately tested? And you state that the Ebola symptoms include “sudden onset of fever fatigue, muscle pain, headache and sore throat. This is followed by vomiting, diarrhea, rash, symptoms of impaired kidney and liver function, and in some cases, both internal and external bleeding”?

In short it is all the most vague and unsubstantiated basis that lies behind President Obama’s new War on Ebola.

War on Ebola or War for Oil?

One striking aspect of this new concern of the US President for the situation in Liberia and other west African states where alleged surges of Ebola are being claimed is the presence of oil, huge volumes of untapped oil.

The offshore coast of Liberia and east African ‘Ebola zones’ conveniently map with the presence of vast untapped oil and gas resources shown here

The issue of oil in west Africa, notably in the waters of the Gulf of Guinea have become increasingly strategic both to China who is roaming the world in search of future secure oil import sources, and the United States, whose oil geo-politics was summed up in a quip by then Secretary of State Henry Kissinger in the 1970’s: ‘If you control the oil, you control entire nations.’

The Obama Administration and Pentagon policy has continued that of George W. Bush who in 2008 created the US military Africa Command or AFRICOM, to battle the rapidly-growing Chinese economic presence in Africa’s potential oil-rich countries. West Africa is a rapidly-emerging oil treasure, barely tapped to date. A US Department of Energy study projected that African oil production would rise 91 percent between 2002 and 2025, much from the region of the present Ebola alarm.

Chinese oil companies are all over Africa and increasingly active in west Africa, especially Angola, Sudan and Guinea, the later in the epicenter of Obama’s new War on Ebola troop deployment.

If the US President were genuine about his concern to contain a public health emergency, he could look at the example of that US-declared pariah Caribbean nation, Cuba. Reuters reports that the Cuban government, a small financially distressed, economically sanctioned island nation of 11 million people, with a national budget of $50 billion, Gross Domestic Product of 121 billion and per capita GDP of just over $10,000, is dispatching 165 medical personnel to Africa to regions where there are Ebola outbreaks. Washington sends 3,000 combat troops. Something smells very rotten around the entire Ebola scare.

F. William Engdahl is strategic risk consultant and lecturer, he holds a degree in politics from Princeton University and is a best-selling author on oil and geopolitics, exclusively for the online magazine “New Eastern Outlook”

35 of the Most Dangerous Viruses and Bacteria’s in the World Today

The Black Plague, Marburg, Ebola, Influenza, Enterovirus virus may all sound terrifying, but it’s not the most dangerous virus in the world. It isn’t HIV either. Here is a list of the most dangerous viruses and Bacteria’s on the Planet Earth.

1. Marburg Virus The most dangerous virus is the Marburg virus. It is named after a small and idyllic town on the river Lahn – but that has nothing to do with the disease itself. The Marburg virus is a hemorrhagic fever virus. As with Ebola, the Marburg virus causes convulsions and bleeding of mucous membranes, skin and organs. It has a fatality rate of 90 percent.  The Marburg virus causes a rare, but severe hemorrhagic fever that has a fatality rate of 88%. It was first identified in 1967 when outbreaks of hemorrhagic fever cropped up simultaneously in Marburg, where the disease got its name, Frankfurt in Germany and Belgrade, Serbia.

Marburg and Ebola came from the Filoviridae family of viruses. They both have the capacity to cause dramatic outbreaks with the greatest fatality rates. It is transmitted to humans from fruit bats and spreads to humans through direct contact with the blood, secretions and other bodily fluids of infected humans. No anti-viral treatment or vaccine exists against the Marburg virus. In 1967, a group of lab workers in Germany (Marburg and Frankfurt) and Serbia (then Yugoslavia) contracted a new type of hemorrhagic fever from some virus-carrying African green monkeys that had been imported for research and development of polio vaccines. The Marburg virus is also BSL-4, and Marburg hemorrhagic fever has a 23 to 90 percent fatality rate. Spread through close human-to-human contact, symptoms start with a headache, fever, and a rash on the trunk, and progress to multiple organ failure and massive internal bleeding.

There is no cure, and the latest cases were reported out of Uganda at the end of 2012. An American tourist who had explored a Ugandan cave full of fruit bats known to be reservoirs of the virus contracted it and survived in 2008. (But not before bringing his sick self back to the U.S.)

2. Ebola Virus  There are five strains of the Ebola virus, each named after countries and regions in Africa: Zaire, Sudan, Tai Forest, Bundibugyo and Reston. The Zaire Ebola virus is the deadliest, with a mortality rate of 90 percent. It is the strain currently spreading through Guinea, Sierra Leone and Liberia, and beyond. Scientists say flying foxes probably brought the Zaire Ebola virus into cities.

Typically less than 100 lives a year. UPDATE: A severe Ebola outbreak was detected in West Africa in March 2014. The number of deaths in this latest outbreak has outnumbered all other known cases from previous outbreaks combined. The World Health Organization is reporting nearly 2,000 deaths in this latest outbreak.
Once a person is infected with the virus, the disease has an incubation period of 2-21 days; however, some infected persons are asymptomatic. Initial symptoms are sudden malaise, headache, and muscle pain, progressing to high fever, vomiting, severe hemorrhaging (internally and out of the eyes and mouth) and in 50%-90% of patients, death, usually within days. The likelihood of death is governed by the virulence of the particular Ebola strain involved. Ebola virus is transmitted in body fluids and secretions; there is no evidence of transmission by casual contact. There is no vaccine and no cure.

Its melodic moniker may roll off the tongue, but if you contract the virus (above), that’s not the only thing that will roll off one of your body parts (a disturbing amount of blood coming out of your eyes, for instance). Four of the five known Ebola viral strains cause Ebola hemorrhagic fever (EHF), which has killed thousands of people in sub-Saharan African nations since its discovery in 1976.

The deadly virus is named after the Ebola River in the Democratic Republic of the Congo where it was first reported, and is classified as a CDC Biosafety Level 4, a.k.a. BSL-4, making it one of the most dangerous pathogens on the planet. It is thought to spread through close contact with bodily secretions. EHF has a 50 to 90 percent mortality rate, with a rapid onset of symptoms that start with a headache and sore throat and progress to major internal and external bleeding and multiple organ failure. There’s no known cure, and the most recent cases were reported at the end of 2012 in Uganda.

3. The Hantavirus describes several types of viruses. It is named after a river where American soldiers were first thought to have been infected with the Hantavirus, during the Korean War in 1950. Symptoms include lung disease, fever and kidney failure.

70,000 Deaths a Year
Hantavirus pulmonary syndrome (HPS) is a deadly disease transmitted by infected rodents through urine, droppings, or saliva. Humans can contract the disease when they breathe in aerosolized virus. HPS was first recognized in 1993 and has since been identified throughout the United States. Although rare, HPS is potentially deadly. Rodent control in and around the home remains the primary strategy for preventing hantavirus infection. Also known as House Mouse Flu. The symptoms, which are very similar to HFRS, include tachycardia and tachypnea. Such conditions can lead to a cardiopulmonary phase, where cardiovascular shock can occur, and hospitalization of the patient is required.

There are many strains of hantavirus floating around (yep, it’s airborne) in the wake of rodents that carry the virus. Different strains, carried by different rodent species, are known to cause different types of illnesses in humans, most notably hemorrhagic fever with renal syndrome (HFRS)—first discovered during the Korean War—and hantavirus pulmonary syndrome (HPS), which reared its ugly head with a 1993 outbreak in the Southwestern United States. Severe HFRS causes acute kidney failure, while HPS gets you by filling your lungs with fluid (edema). HFRS has a mortality rate of 1 to 15 percent, while HPS is 38 percent. The U.S. saw its most recent outbreak of hantavirus—of the HPS variety—at Yosemite National Park in late 2012.

4. Avian Influenza Bird Flu The various strains of bird flu regularly cause panic – which is perhaps justified because the mortality rate is 70 percent. But in fact the risk of contracting the H5N1 strain – one of the best known – is quite low. You can only be infected through direct contact with poultry. It is said this explains why most cases appear in Asia, where people often live close to chickens.

This form of the flu is common among birds (usually poultry) and infects humans through contact with secretions of an infected bird.

Although rare, those infected have a high incidence of death. Symptoms are like those of the more common human form of influenza.

Bird flu (H5N1) has receded from international headlines for the moment, as few human cases of the deadly virus have been reported this year. But when Dutch researchers recently created an even more transmissible strain of the virus in a laboratory for research purposes, they stirred grave concerns about what would happen if it escaped into the outside world. “Part of what makes H5N1 so deadly is that most people lack an immunity to it,” explains Marc Lipsitch, a professor of epidemiology at Harvard School of Public Health (HSPH) who studies the spread of infectious diseases. “If you make a strain that’s highly transmissible between humans, as the Dutch team did, it could be disastrous if it ever escaped the lab.”

H5N1 first made global news in early 1997 after claiming two dozen victims in Hong Kong. The virus normally occurs only in wild birds and farm-raised fowl, but in those isolated early cases, it made the leap from birds to humans. It then swept unimpeded through the bodies of its initial human victims, causing massive hemorrhages in the lungs and death in a matter of days. Fortunately, during the past 15 years, the virus has claimed only 400 victims worldwide—although the strain can jump species, it hasn’t had the ability to move easily from human to human, a critical limit to its spread.

That’s no longer the case, however. In late 2011, the Dutch researchers announced the creation of an H5N1 virus transmissible through the air between ferrets (the best animal model for studying the impact of disease on humans). The news caused a storm of controversy in the popular press and heated debate among scientists over the ethics of the work. For Lipsitch and many others, the creation of the new strain was cause for alarm. “H5N1 influenza is already one of the most deadly viruses in existence,” he says. “If you make [the virus] transmissible [between humans], you have to be very concerned about what the resulting strain could do.”

To put this danger in context, the 1918 “Spanish” flu—one of the most deadly influenza epidemics on record—killed between 50 million and 100 million people worldwide, or roughly 3 to 6 percent of those infected. The more lethal SARS virus (see “The SARS Scare,” March-April 2007, page 47) killed almost 10 percent of infected patients during a 2003 outbreak that reached 25 countries worldwide. H5N1 is much more dangerous, killing almost 60 percent of those who contract the illness.

If a transmissible strain of H5N1 escapes the lab, says Lipsitch, it could spark a global health catastrophe. “It could infect millions of people in the United States, and very likely more than a billion people globally, like most successful flu strains do,” he says. “This might be one of the worst viruses—perhaps the worst virus—in existence right now because it has both transmissibility and high virulence.”

Ironically, this is why Ron Fouchier, the Dutch virologist whose lab created the new H5N1 strain, argues that studying it in more depth is crucial. If the virus can be made transmissible in the lab, he reasons, it can also occur in nature—and researchers should have an opportunity to understand as much as possible about the strain before that happens.

Lipsitch, who directs the Center for Communicable Disease Dynamics at HSPH, thinks the risks far outweigh the rewards. Even in labs with the most stringent safety requirements, such as enclosed rubber “space suits” to isolate researchers, accidents do happen. A single unprotected breath could infect a researcher, who might unknowingly spread the virus beyond the confines of the lab.

In an effort to avoid this scenario, Lipsitch has been pushing for changes in research policy in the United States and abroad. (A yearlong, voluntary global ban on H5N1 research was lifted in many countries in January, and new rules governing such research in the United States were expected in February.) Lipsitch says that none of the current research proposals he has seen “would significantly improve our preparational response to a national pandemic of H5N1. The small risk of a very large public health disaster…is not worth taking [for] scientific knowledge without an immediate public health application.” His recent op-eds in scientific journals and the popular press have stressed the importance of regulating the transmissible strain and limiting work with the virus to only a handful of qualified labs. In addition, he argues, only technicians who have the right training and experience—and have been inoculated against the virus—should be allowed to handle it.

These are simple limitations that could drastically reduce the danger of the virus spreading, he asserts, yet they’re still not popular with some researchers. He acknowledges that limiting research is an unusual practice scientifically but argues, “These are unusual circumstances.”

Lipsitch thinks a great deal of useful research can still be done on the non-transmissible strain of the virus, which would provide valuable data without the risk of accidental release. In the meantime, he hopes to make more stringent H5N1 policies a priority for U.S. and foreign laboratories. Although it’s not a perfect solution, he says, it’s far better than a nightmare scenario.

5. Lassa Virus  A nurse in Nigeria was the first person to be infected with the Lassa virus. The virus is transmitted by rodents. Cases can be endemic – which means the virus occurs in a specific region, such as in western Africa, and can reoccur there at any time. Scientists assume that 15 percent of rodents in western Africa carry the virus.

The Marburg virus under a microscope

This BSL-4 virus gives us yet another reason to avoid rodents. Lassa is carried by a species of rat in West Africa called Mastomys. It’s airborne…at least when you’re hanging around the rat’s fecal matter. Humans, however, can only spread it through direct contact with bodily secretions. Lassa fever, which has a 15 to 20 percent mortality rate, causes about 5000 deaths a year in West Africa, particularly in Sierra Leone and Liberia.

It starts with a fever and some retrosternal pain (behind the chest) and can progress to facial swelling, encephalitis, mucosal bleeding and deafness. Fortunately, researchers and medical professionals have found some success in treating Lassa fever with an antiviral drug in the early stages of the disease.

6. The Junin Virus is associated with Argentine hemorrhagic fever. People infected with the virus suffer from tissue inflammation, sepsis and skin bleeding. The problem is that the symptoms can appear to be so common that the disease is rarely detected or identified in the first instance.

A member of the genus Arenavirus, Junin virus characteristically causes Argentine hemorrhagic fever (AHF). AHF leads to major alterations within the vascular, neurological and immune systems and has a mortality rate of between 20 and 30%.  Symptoms of the disease are conjunctivitis, purpura, petechia and occasional sepsis. The symptoms of the disease are relatively indistinct and may therefore be mistaken for a different condition.

Since the discovery of the Junin virus in 1958, the geographical distribution of the pathogen, although still confined to Argentina, has risen. At the time of discovery, Junin virus was confined to an area of around 15,000 km². At the beginning of 2000, the distribution had risen to around 150,000 km². The natural hosts of Junin virus are rodents, particularly Mus musculus, Calomys spp. and Akodon azarae.

Direct rodent to human transmission only transpires when contact is made with excrement of an infected rodent. This commonly occurs via ingestion of contaminated food or water, inhalation of particles within urine or via direct contact of broken skin with rodent excrement.

7. The Crimea-Congo Fever Virus is transmitted by ticks. It is similar to the Ebola and Marburg viruses in the way it progresses. During the first days of infection, sufferers present with pin-sized bleedings in the face, mouth and the pharynx.

Transmitted through tick bites this disease is endemic (consistently present)  in most countries of West Africa and the Middle East. Although rare, CCHF has a 30% mortality rate. The most recent outbreak of the disease was in 2005 in Turkey. The Crimean-Congo hemorrhagic fever is a common disease transmitted by a tick-Bourne virus. The virus causes major hemorrhagic fever outbreaks with a fatality rate of up to 30%. It is chiefly transmitted to people through tick and livestock. Person-to-person transmission occurs through direct contact with the blood, secretions and other bodily fluids of an infected person. No vaccination exists for both humans and animals against CCHF.

8. The Machupo Virus is associated with Bolivian hemorrhagic fever, also known as black typhus. The infection causes high fever, accompanied by heavy bleedings. It progresses similar to the Junin virus. The virus can be transmitted from human to human, and rodents often the carry it.

Bolivian hemorrhagic fever (BHF), also known as black typhus or Ordog Fever, is a hemorrhagic fever and zoonotic infectious disease originating in Bolivia after infection by Machupo virus.BHF was first identified in 1963 as an ambisense RNA virus of the Arenaviridae family,by a research group led by Karl Johnson. The mortality rate is estimated at 5 to 30 percent.

Due to its pathogenicity, Machupo virus requires Biosafety Level Four conditions, the highest level.In February and March 2007, some 20 suspected BHF cases (3 fatal) were reported to the El Servicio Departmental de Salud (SEDES) in Beni Department, Bolivia, and in February 2008, at least 200 suspected new cases (12 fatal) were reported to SEDES.In November 2011, a SEDES expert involved in a serosurvey to determine the extent of Machupo virus infections in the Department after the discovery of a second confirmed case near the departmental capital of Trinidad in November, 2011, expressed concern about expansion of the virus’ distribution outside the endemic zone in Mamoré and Iténez provinces.

Bolivian hemorrhagic fever was one of three hemorrhagic fevers and one of more than a dozen agents that the United States researched as potential biological weapons before the nation suspended its biological weapons program. It was also under research by the Soviet Union, under the Biopreparat bureau.

9. Kyasanur Forest Virus  Scientists discovered the Kyasanur Forest Virus (KFD) virus in woodlands on the southwestern coast of India in 1955. It is transmitted by ticks, but scientists say it is difficult to determine any carriers. It is assumed that rats, birds and boars could be hosts. People infected with the virus suffer from high fever, strong headaches and muscle pain which can cause bleedings.

The disease has a morbidity rate of 2-10%, and affects 100-500 people annually.The symptoms of the disease include a high fever with frontal headaches, followed by hemorrhagic symptoms, such as bleeding from the nasal cavity, throat, and gums, as well as gastrointestinal bleeding.An affected person may recover in two weeks time, but the convalescent period is typically very long, lasting for several months. There will be muscle aches and weakness during this period and the affected person is unable to engage in physical activities.

There are a variety of animals thought to be reservoir hosts for the disease, including porcupines, rats, squirrels, mice and shrews. The vector for disease transmission is Haemaphysalis spinigera, a forest tick. Humans contract infection from the bite of nymphs of the tick.

The disease was first reported from Kyasanur Forest of Karnataka in India in March 1957. The disease first manifested as an epizootic outbreak among monkeys killing several of them in the year 1957. Hence the disease is also locally known as Monkey Disease or Monkey Fever. The similarity with Russian Spring-summer encephalitis was noted and the possibility of migratory birds carrying the disease was raised. Studies began to look for the possible species that acted as reservoirs for the virus and the agents responsible for transmission. Subsequent studies failed to find any involvement of migratory birds although the possibility of their role in initial establishment was not ruled out. The virus was found to be quite distinctive and not closely related to the Russian virus strains.

Antigenic relatedness is however close to many other strains including the Omsk hemorrhagic fever (OHF) and birds from Siberia have been found to show an antigenic response to KFD virus. Sequence based studies however note the distinctiveness of OHF.Early studies in India were conducted in collaboration with the US Army Medical Research Unit and this led to controversy and conspiracy theories.

Subsequent studies based on sequencing found that the Alkhurma virus, found in Saudi Arabia is closely related. In 1989 a patient in Nanjianin, China was found with fever symptoms and in 2009 its viral gene sequence was found to exactly match with that of the KFD reference virus of 1957. This has however been questioned since the Indian virus shows variations in sequence over time and the exact match with the virus sequence of 1957 and the Chinese virus of 1989 is not expected.

This study also found using immune response tests that birds and humans in the region appeared to have been exposed to the virus.Another study has suggested that the virus is recent in origin dating the nearest common ancestor of it and related viruses to around 1942, based on the estimated rate of sequence substitutions. The study also raises the possibility of bird involvement in long-distance transfer. It appears that these viruses diverged 700 years ago.

10. Dengue Fever is a constant threat. If you’re planning a holiday in the tropics, get informed about dengue. Transmitted by mosquitoes, dengue affects between 50 and 100 million people a year in popular holiday destinations such as Thailand and India. But it’s more of a problem for the 2 billion people who live in areas that are threatened by dengue fever.

25,000 Deaths a year Also known as ‘breakbone fever’ due to the extreme pain felt during fever, is an relatively new disease caused by one of four closely-related viruses. WHO estimates that a whopping 2.5 billion people (two fifths of the World’s population) are at risk from dengue. It puts the total number of infections at around 50 million per year, and is now epidemic in more than 100 countries.

Dengue viruses are transferred to humans through the bites of infective female Aedes mosquitoes. The dengue virus circulates in the blood of a human for two to seven days, during the same time they have the fever. It usually appears first on the lower limbs and the chest; in some patients, it spreads to cover most of the body. There may also be severe retro-orbital pain, (a pain from behind the eyes that is distinctive to Dengue infections), and gastritis with some combination of associated abdominal pain, nausea, vomiting coffee-grounds-like congealed blood, or severe diarrhea.

The leading cause of death in the tropics and subtropics is the infection brought on by the dengue virus, which causes a high fever, severe headache, and, in the worst cases, hemorrhaging. The good news is that it’s treatable and not contagious. The bad news is there’s no vaccine, and you can get it easily from the bite of an infected mosquito—which puts at least a third of the world’s human population at risk. The CDC estimates that there are over 100 million cases of dengue fever each year. It’s a great marketing tool for bug spray.

11. HIV 3.1 Million Lives a Year Human Immunodeficiency Virus has claimed the lives of more than 25 million people since 1981. HIV gets to the immune system by infecting important cells, including helper cells called CD4+ T cells, plus macrophanges and dendritic cells. Once the virus has taken hold, it systematically kills these cells, damaging the infected person’s immunity and leaving them more at risk from infections.

The majority of people infected with HIV go on to develop AIDS. Once a patient has AIDS common infections and tumours normally controlled by the CD4+ T cells start to affect the person.  
In the latter stages of the disease, pneumonia and various types of herpes can infect the patient and cause death.

Human immunodeficiency virus infection / acquired immunodeficiency syndrome (HIV/AIDS) is a disease of the human immune system caused by infection with human immunodeficiency virus (HIV). The term HIV/AIDS represents the entire range of disease caused by the human immunodeficiency virus from early infection to late stage symptoms. During the initial infection, a person may experience a brief period of influenza-like illness. This is typically followed by a prolonged period without symptoms. As the illness progresses, it interferes more and more with the immune system, making the person much more likely to get infections, including opportunistic infections and tumors that do not usually affect people who have working immune systems.

HIV is transmitted primarily via unprotected sexual intercourse (including anal and oral sex), contaminated blood transfusions, hypodermic needles, and from mother to child during pregnancy, delivery, or breastfeeding. Some bodily fluids, such as saliva and tears, do not transmit HIV. Prevention of HIV infection, primarily through safe sex and needle-exchange programs, is a key strategy to control the spread of the disease. There is no cure or vaccine; however, antiretroviral treatment can slow the course of the disease and may lead to a near-normal life expectancy. While antiretroviral treatment reduces the risk of death and complications from the disease, these medications are expensive and have side effects. Without treatment, the average survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype.

Genetic research indicates that HIV originated in west-central Africa during the late nineteenth or early twentieth century. AIDS was first recognized by the United States Centers for Disease Control and Prevention (CDC) in 1981 and its cause—HIV infection—was identified in the early part of the decade. Since its discovery, AIDS has caused an estimated 36 million deaths worldwide (as of 2012). As of 2012, approximately 35.3 million people are living with HIV globally. HIV/AIDS is considered a pandemic—a disease outbreak which is present over a large area and is actively spreading.

HIV/AIDS has had a great impact on society, both as an illness and as a source of discrimination. The disease also has significant economic impacts. There are many misconceptions about HIV/AIDS such as the belief that it can be transmitted by casual non-sexual contact. The disease has also become subject to many controversies involving religion. It has attracted international medical and political attention as well as large-scale funding since it was identified in the 1980s

 

12. Rotavirus 61,000 Lives a Year  According to the WHO, this merciless virus causes the deaths of more than half a million children every year. In fact, by the age of five, virtually every child on the planet has been infected with the virus at least once. Immunity builds up with each infection, so subsequent infections are milder. However, in areas where adequate healthcare is limited the disease is often fatal. Rotavirus infection usually occurs through ingestion of contaminated stool.

Because the virus is able to live a long time outside of the host, transmission can occur through ingestion of contaminated food or water, or by coming into direct contact with contaminated surfaces, then putting hands in the mouth.
Once it’s made its way in, the rotavirus infects the cells that line the small intestine and multiplies. It emits an enterotoxin, which gives rise to gastroenteritis.

13. Smallpox   Officially eradicated – Due to it’s long history, it impossible to estimate the carnage over the millennia Smallpox localizes in small blood vessels of the skin and in the mouth and throat. In the skin, this results in a characteristic maculopapular rash, and later, raised fluid-filled blisters. It has an overall mortality rate of 30–35%. Smallpox is believed to have emerged in human populations about 10,000 BC. The disease killed an estimated 400,000 Europeans per year during the closing years of the 18th century (including five reigning monarchs), and was responsible for a third of all blindness. Of all those infected, 20–60%—and over 80% of infected children—died from the disease.
Smallpox was responsible for an estimated 300–500 million deaths during the 20th century alone. In the early 1950s an estimated 50 million cases of smallpox occurred in the world each year.

As recently as 1967, the World Health Organization (WHO) estimated that 15 million people contracted the disease and that two million died in that year. After successful vaccination campaigns throughout the 19th and 20th centuries, the WHO certified the eradication of smallpox in December 1979.
Smallpox is one of only two infectious diseases to have been eradicated by humans, the other being Rinderpest, which was unofficially declared eradicated in October 2010.

The virus that causes smallpox wiped out hundreds of millions of people worldwide over thousands of years. We can’t even blame it on animals either, as the virus is only carried by and contagious for humans. There are several different types of smallpox disease that result from an infection ranging from mild to fatal, but it is generally marked by a fever, rash, and blistering, oozing pustules that develop on the skin. Fortunately, smallpox was declared eradicated in 1979, as the result of successful worldwide implementation of the vaccine.

14. Hepatitis B  521,000 Deaths a Year A third of the World’s population (over 2 billion people) has come in contact with this virus, including 350 million chronic carriers. In China and other parts of Asia, up to 10% of the adult population is chronically infected. The symptoms of acute hepatitis B include yellowing of the skin of eyes, dark urine, vomiting, nausea, extreme fatigue, and abdominal pain.

Luckily, more than 95% of people who contract the virus as adults or older children will make a full recovery and develop immunity to the disease. In other people, however, hepatitis B can bring on chronic liver failure due to cirrhosis or cancer.

Hepatitis B is an infectious illness of the liver caused by the hepatitis B virus (HBV) that affects hominoidea, including humans. It was originally known as "serum hepatitis". Many people have no symptoms during the initial infected. Some develop an acute illness with vomiting, yellow skin, dark urine and abdominal pain. Often these symptoms last a few weeks and rarely result in death. It may take 30 to 180 days for symptoms to begin. Less than 10% of those infected develop chronic hepatitis B. In those with chronic disease cirrhosis and liver cancer may eventually develop.

The virus is transmitted by exposure to infectious blood or body fluids.  Infection around the time of birth is the most common way the disease is acquired in areas of the world where is common. In areas where the disease is uncommon intravenous drug use and sex are the most common routes of infection. Other risk factors include working in a healthcare setting, blood transfusions, dialysis, sharing razors or toothbrushes with an infected person, travel in countries where it is common, and living in an institution.

Tattooing and acupuncture led to a significant number of cases in the 1980s; however, this has become less common with improved sterility. The hepatitis B viruses cannot be spread by holding hands, sharing eating utensils or drinking glasses, kissing, hugging, coughing, sneezing, or breastfeeding.  The hepatitis B virus is a hepadnavirus—hepa from hepatotropic (attracted to the liver) and dna because it is a DNA virus. The viruses replicate through an RNA intermediate form by reverse transcription, which in practice relates them to retroviruses.It is 50 to 100 times more infectious than HIV.

The infection has been preventable by vaccination since 1982. During the initial infected care is based on the symptoms present. In those who developed chronic disease antiviral medication such as tenofovir or interferon maybe useful, however are expensive.

About a third of the world population has been infected at one point in their lives, including 350 million who are chronic carriers. Over 750,000 people die of hepatitis B a year. The disease has caused outbreaks in parts of Asia and Africa, and it is now only common in China. Between 5 and 10% of adults in sub-Saharan Africa and East Asia have chronic disease. Research is in progress to create edible HBV vaccines in foods such as potatoes, carrots, and bananas.In 2004, an estimated 350 million individuals were infected worldwide. National and regional prevalence ranges from over 10% in Asia to under 0.5% in the United States and northern Europe. Routes of infection include vertical transmission (such as through childbirth), early life horizontal transmission (bites, lesions, and sanitary habits), and adult horizontal transmission (sexual contact, intravenous drug use).

The primary method of transmission reflects the prevalence of chronic HBV infection in a given area. In low prevalence areas such as the continental United States and Western Europe, injection drug abuse and unprotected sex are the primary methods, although other factors may also be important. In moderate prevalence areas, which include Eastern Europe, Russia, and Japan, where 2–7% of the population is chronically infected, the disease is predominantly spread among children. In high-prevalence areas such as China and South East Asia, transmission during childbirth is most common, although in other areas of high endemicity such as Africa, transmission during childhood is a significant factor. The prevalence of chronic HBV infection in areas of high endemicity is at least 8% with 10-15% prevalence in Africa/Far East. As of 2010, China has 120 million infected people, followed by India and Indonesia with 40 million and 12 million, respectively. According to World Health Organization (WHO), an estimated 600,000 people die every year related to the infection. In the United States about 19,000 new cases occurred in 2011 down nearly 90% from 1990.

Acute infection with hepatitis B virus is associated with acute viral hepatitis – an illness that begins with general ill-health, loss of appetite, nausea, vomiting, body aches, mild fever, and dark urine, and then progresses to development of jaundice. It has been noted that itchy skin has been an indication as a possible symptom of all hepatitis virus types. The illness lasts for a few weeks and then gradually improves in most affected people. A few people may have more severe liver disease (fulminant hepatic failure), and may die as a result. The infection may be entirely asymptomatic and may go unrecognized.

Chronic infection with hepatitis B virus either may be asymptomatic or may be associated with a chronic inflammation of the liver (chronic hepatitis), leading to cirrhosis over a period of several years. This type of infection dramatically increases the incidence of hepatocellular carcinoma (liver cancer). Across Europe hepatitis B and C cause approximately 50% of hepatocellular carcinomas. Chronic carriers are encouraged to avoid consuming alcohol as it increases their risk for cirrhosis and liver cancer. Hepatitis B virus has been linked to the development of membranous glomerulonephritis (MGN).

Symptoms outside of the liver are present in 1–10% of HBV-infected people and include serum-sickness–like syndrome, acute necrotizing vasculitis (polyarteritis nodosa), membranous glomerulonephritis, and papular acrodermatitis of childhood (Gianotti–Crosti syndrome). The serum-sickness–like syndrome occurs in the setting of acute hepatitis B, often preceding the onset of jaundice. The clinical features are fever, skin rash, and polyarteritis. The symptoms often subside shortly after the onset of jaundice, but can persist throughout the duration of acute hepatitis B.  About 30–50% of people with acute necrotizing vasculitis (polyarteritis nodosa) are HBV carriers. HBV-associated nephropathy has been described in adults but is more common in children.Membranous glomerulonephritis is the most common form. Other immune-mediated hematological disorders, such as essential mixed cryoglobulinemia and aplastic anemia.

15. Influenza 500,000 Deaths a Year Influenza has been a prolific killer for centuries. The symptoms of influenza were first described more than 2,400 years ago by Hippocrates. Pandemics generally occur three times a century, and can cause millions of deaths. The most fatal pandemic on record was the Spanish flu outbreak in 1918, which caused between 20 million and 100 million deaths. In order to invade a host, the virus shell includes proteins that bind themselves to receptors on the outside of cells in the lungs and air passages of the victim. Once the virus has latched itself onto the cell it takes over so much of its machinery that the cell dies. Dead cells in the airways cause a runny nose and sore throat. Too many dead cells in the lungs causes death.

 
Vaccinations against the flu are common in developed countries. However, a vaccination that is effective one year may not necessarily work the next year, due to the way the rate at which a flu virus evolves and the fact that new strains will soon replace older ones. No virus can claim credit for more worldwide pandemics and scares than influenza.

The outbreak of the Spanish flu in 1918 is generally considered to be one of the worst pandemics in human history, infecting 20 to 40 percent of the world’s population and killing 50 million in the span of just two years. (A reconstruction of that virus is above.) The swine flu was its most recent newsmaker, when a 2009 pandemic may have seen as many as 89 million people infected worldwide.

Effective influenza vaccines exist, and most people easily survive infections. But the highly infectious respiratory illness is cunning—the virus is constantly mutating and creating new strains. Thousands of strains exist at any given time, many of them harmless, and vaccines available in the U.S. cover only about 40 percent of the strains at large each year.

16. Hepatitis C  56,000 Deaths a Year An estimated 200-300 million people worldwide are infected with hepatitis C.

 

Most people infected with hepatitis C don’t have any symptoms and feel fine for years. However, liver damage invariably rears its ugly head over time, often decades after first infection. In fact, 70% of those infected develop chronic liver disease, 15% are struck with cirrhosis and 5% can die from liver cancer or cirrhosis. In the USA, hepatitis C is the primary reason for liver transplants.

Hepatitis C is an infectious disease affecting primarily the liver, caused by the hepatitis C virus (HCV). The infection is often asymptomatic, but chronic infection can lead to scarring of the liver and ultimately to cirrhosis, which is generally apparent after many years. In some cases, those with cirrhosis will go on to develop liver failure, liver cancer, or life-threatening esophageal and gastric varices.

HCV is spread primarily by blood-to-blood contact associated with intravenous drug use, poorly sterilized medical equipment, and transfusions. An estimated 150–200 million people worldwide are infected with hepatitis C. The existence of hepatitis C (originally identifiable only as a type of non-A non-B hepatitis) was suggested in the 1970s and proven in 1989. Hepatitis C infects only humans and chimpanzees.

The virus persists in the liver in about 85% of those infected. This chronic infection can be treated with medication: the standard therapy is a combination of peginterferon and ribavirin, with either boceprevir or telaprevir added in some cases. Overall, 50–80% of people treated are cured. Those who develop cirrhosis or liver cancer may require a liver transplant. Hepatitis C is the leading reason for liver transplantation, though the virus usually recurs after transplantation. No vaccine against hepatitis C is available.

Hepatitis C infection causes acute symptoms in 15% of cases. Symptoms are generally mild and vague, including a decreased appetite, fatigue, nausea, muscle or joint pains, and weight loss and rarely does acute liver failure result. Most cases of acute infection are not associated with jaundice. The infection resolves spontaneously in 10–50% of cases, which occurs more frequently in individuals who are young and female.

About 80% of those exposed to the virus develop a chronic infection.  This is defined as the presence of detectable viral replication for at least six months. Most experience minimal or no symptoms during the initial few decades of the infection.Chronic hepatitis C can be associated with fatigue and mild cognitive problems. Chronic infection after several years may cause cirrhosis or liver cancer. The liver enzymes are normal in 7–53%.  Late relapses after apparent cure have been reported, but these can be difficult to distinguish from reinfection.

Fatty changes to the liver occur in about half of those infected and are usually present before cirrhosis develops.  Usually (80% of the time) this change affects less than a third of the liver. Worldwide hepatitis C is the cause of 27% of cirrhosis cases and 25% of hepatocellular carcinoma.  About 10–30% of those infected develop cirrhosis over 30 years. Cirrhosis is more common in those also infected with hepatitis B, schistosoma, or HIV, in alcoholics and in those of male gender. In those with hepatitis C, excess alcohol increases the risk of developing cirrhosis 100-fold.Those who develop cirrhosis have a 20-fold greater risk of hepatocellular carcinoma. This transformation occurs at a rate of 1–3% per year.  Being infected with hepatitis B in additional to hepatitis C increases this risk further.

Liver cirrhosis may lead to portal hypertension, ascites (accumulation of fluid in the abdomen), easy bruising or bleeding, varices (enlarged veins, especially in the stomach and esophagus), jaundice, and a syndrome of cognitive impairment known as hepatic encephalopathy. Ascites occurs at some stage in more than half of those who have a chronic infection.

The most common problem due to hepatitis C but not involving the liver is mixed cryoglobulinemia (usually the type II form) — an inflammation of small and medium-sized blood vessels. Hepatitis C is also associated with Sjögren’s syndrome (an autoimmune disorder); thrombocytopenia; lichen planus; porphyria cutanea tarda; necrolytic acral erythema; insulin resistance; diabetes mellitus; diabetic nephropathy; autoimmune thyroiditis and B-cell lymphoproliferative disorders.  Thrombocytopenia is estimated to occur in 0.16% to 45.4% of people with chronic hepatitis C. 20–30% of people infected have rheumatoid factor — a type of antibody. Possible associations include Hyde’s prurigo nodularis and membranoproliferative glomerulonephritis. Cardiomyopathy with associated arrhythmias has also been reported. A variety of central nervous system disorders have been reported.  Chronic infection seems to be associated with an increased risk of pancreatic cancer.

Persons who have been infected with hepatitis C may appear to clear the virus but remain infected. The virus is not detectable with conventional testing but can be found with ultra-sensitive tests.The original method of detection was by demonstrating the viral genome within liver biopsies, but newer methods include an antibody test for the virus’ core protein and the detection of the viral genome after first concentrating the viral particles by ultracentrifugation. A form of infection with persistently moderately elevated serum liver enzymes but without antibodies to hepatitis C has also been reported. This form is known as cryptogenic occult infection.

Several clinical pictures have been associated with this type of infection. It may be found in people with anti-hepatitis-C antibodies but with normal serum levels of liver enzymes; in antibody-negative people with ongoing elevated liver enzymes of unknown cause; in healthy populations without evidence of liver disease; and in groups at risk for HCV infection including those on haemodialysis or family members of people with occult HCV. The clinical relevance of this form of infection is under investigation. The consequences of occult infection appear to be less severe than with chronic infection but can vary from minimal to hepatocellular carcinoma.

The rate of occult infection in those apparently cured is controversial but appears to be low 40% of those with hepatitis but with both negative hepatitis C serology and the absence of detectable viral genome in the serum have hepatitis C virus in the liver on biopsy.How commonly this occurs in children is unknown.
There is no cure, no vaccine.

17. Measle  197,000 Deaths a Year Measles, also known as Rubeola, has done a pretty good job of killing people throughout the ages. Over the last 150 years, the virus has been responsible for the deaths of around 200 million people. The fatality rate from measles for otherwise healthy people in developed countries is 3 deaths per thousand cases, or 0.3%. In underdeveloped nations with high rates of malnutrition and poor healthcare, fatality rates have been as high as 28%. In immunocompromised patients (e.g. people with AIDS) the fatality rate is approximately 30%.

During the 1850s, measles killed a fifth of Hawaii’s people. In 1875, measles killed over 40,000 Fijians, approximately one-third of the population. In the 19th century, the disease decimated the Andamanese population. In 1954, the virus causing the disease was isolated from an 11-year old boy from the United States, David Edmonston, and adapted and propagated on chick embryo tissue culture.

To date, 21 strains of the measles virus have been identified.

18. Yellow Fever  30,000 Deaths a Year. Yellow fever is an acute viral hemorrhagic disease transmitted by the bite of female mosquitoes and is found in tropical and subtropical areas in South America and Africa. The only known hosts of the virus are primates and several species of mosquito. The origin of the disease is most likely to be Africa, from where it was introduced to South America through the slave trade in the 16th century. Since the 17th century, several major epidemics of the disease have been recorded in the Americas, Africa and Europe. In the 19th century, yellow fever was deemed one of the most dangerous infectious diseases.

Yellow fever presents in most cases with fever, nausea, and pain and it generally subsides after several days. In some patients, a toxic phase follows, in which liver damage with jaundice (giving the name of the disease) can occur and lead to death. Because of the increased bleeding tendency (bleeding diathesis), yellow fever belongs to the group of hemorrhagic fevers.

Since the 1980s, the number of cases of yellow fever has been increasing, making it a reemerging disease Transmitted through infected mosquitoes, Yellow Fever is still a serious problem in countries all over the world and a serious health risk for travelers to Africa, South America and some areas in the Caribbean.  Fatality rates range from 15 to over 50%. Symptoms include high fever, headache, abdominal pain, fatigue, vomiting and nausea.

Yellow fever is a hemorrhagic fever transmitted by infected mosquitoes. The yellow is in reference to the yellow color (jaundice) that affects some patients. The virus is endemic in tropical areas in Africa and South America.

The disease typically occurs in two phases. The first phase typically causes fever, headache, muscle pain and back pain, chills and nausea. Most patients recover from these symptoms while 15% progresses to the toxic second phase. High fever returns, jaundice becomes apparent, patient complains of abdominal pain with vomiting, and bleeding in the mouth, eyes, nose or stomach occurs. Blood appears in the stool or vomit and kidney function deteriorates. 50% of the patients that enter the toxic phase die within 10 to 14 days.

There is no treatment for yellow fever. Patients are only given supportive care for fever, dehydration and respiratory failure. Yellow fever is preventable through vaccination.

19. Rabies  55,000 Deaths a Year Rabies is almost invariably fatal if post-exposure prophylaxis is not administered prior to the onset of severe symptoms. If there wasn’t a vaccine, this would be the most deadly virus on the list.

It is a zoonotic virus transmitted through the bite of an animal. The virus worms its way into the brain along the peripheral nerves. The incubation phase of the rabies disease can take up to several months, depending on how far it has to go to reach the central nervous system. It provokes acute pain, violent movements, depression, uncontrollable excitement, and inability to swallow water (rabies is often known as ‘hydrophobia’). After these symptoms subside the fun really starts as the infected person experiences periods of mania followed by coma then death, usually caused by respiratory insufficiency.

Rabies has a long and storied history dating back to 2300 B.C., with records of Babylonians who went mad and died after being bitten by dogs. While this virus itself is a beast, the sickness it causes is now is wholly preventable if treated immediately with a series of vaccinations (sometimes delivered with a terrifyingly huge needle in the abdomen). We have vaccine inventor Louis Pasteur to thank for that.

Exposure to rabies these days, while rare in the U.S., still occurs as it did thousands of years ago—through bites from infected animals. If left untreated after exposure, the virus attacks the central nervous system and death usually results. The symptoms of an advanced infection include delirium, hallucinations and raging, violent behavior in some cases, which some have argued makes rabies eerily similar to zombification. If rabies ever became airborne, we might actually have to prepare for that zombie apocalypse after all.

21. Common Cold  No known cure The common cold is the most frequent infectious disease in humans with on average two to four infections a year in adults and up to 6–12 in children. Collectively, colds, influenza, and other infections with similar symptoms are included in the diagnosis of influenza-like illness.

They may also be termed upper respiratory tract infections (URTI). Influenza involves the lungs while the common cold does not.
It’s annoying as hell, but there’s nothing to do but wave the white flag on this one.
Virus: Infinity. People: 0

22. Anthrax  Anthrax is a diseased caused by a bacterium called Bacillus Anthracis. There are three types of anthrax, skin, lung, and digestive. Anthrax has lately become a major world issue for its ability to become an epidemic and spread quickly and easily among people through contact with spores.

It is important to know that  Anthrax is not spread from person to person, but is through contact/handling of products containing spores. Flu like symptoms, nausea, and blisters are common symptoms of exposure. Inhalational anthrax and gastrointestinal anthrax are serious issue because of their high mortality rates ranging from 50 to 100%.

Anthrax is a severe infectious disease caused by the bacteria Bacillus anthracis. This type of bacteria produces spores that can live for years in the soil. Anthrax is more common in farm animals, though humans can get infected as well. Anthrax is not contagious. A person can get infected only when the bacteria gets into the skin, lungs or  digestive tract.

There are three types of anthrax: skin anthrax, inhalation anthrax and gastrointestinal anthrax. Skin anthrax symptoms include fever, muscle aches, headache, nausea and vomiting. Inhalation anthrax begins with flu-like symptoms, which progresses  with severe respiratory distress. Shock, coma and then death follows. Most patients do not recover even if given appropriate antibiotics due to the toxins released by the anthrax bacteria. Gastrointestinal anthrax symptoms include fever, nausea, abdominal pain and bloody diarrhea.

Anthrax is treated with antibiotics.

23. Malaria  Malaria is a mosquito-borne illness caused by parasite. Although malaria can be prevented and treated, it is often fatal.

Each year about 1 million people die from Malaria.  Common symptoms include fever, chills, headache. Sweats, and fatigue. Malaria is a serious disease caused by Plasmodium parasites that infects Anopheles mosquitoes which feeds on humans. Initial symptoms include high fever, shaking chills, headache and vomiting – symptoms that may be too  mild to be identified as malaria. If not treated within 24 hours, it can progress to severe illnesses that could lead to death.

The WHO estimates that malaria caused 207,000,000 clinical episodes and 627,000 deaths, mostly among African children,  in 2012. About 3.5 billion people from 167 countries live in areas at risk of malaria transmission.

24. Cholera  Due to the severe dehydration it causes, if left untreated Cholera can cause death within hours. In 1991 a major outbreak occurred in South America though currently few cases are known outside of Sub-Saharan Africa.

Symptoms include severe diarrhea, vomiting and leg cramping. Cholera is usually contracted through ingestion of contaminated water or food. Cholera is an acute intestinal infection caused by a bacterium called Vibrio cholera. It has an incubation period of less than a day to five days and causes painless, watery diarrhea that quickly leads to severe dehydration and death if treatment is not promptly given.

Cholera remains a global problem and continues to be a challenge for countries where access to safe drinking water and sanitation is a problem.

25.  Typhoid Fever  Patients with typhoid fever sometimes demonstrate a rash of flat, rose-colored spots and a sustained fever of 103 to 104.

Typhoid is contracted through contact with the S. Typhi bacteria, which is carried by humans in both their blood stream and stool. Over 400 cases occur in the US, 20% of those who contract it die. Typhoid fever is a serious and potentially fatal disease caused by the bacterium Salmonella Typhi. This type of bacteria lives only in humans. People sick with typhoid fever carry the bacteria in their bloodstream and intestinal tract and transmit the bacteria through their stool.

A person can get typhoid fever by drinking or eating food contaminated with Salmonella Typhi or if contaminated sewage gets into the water used for drinking or washing dishes.

Typhoid fever symptoms include high fever, weakness, headache, stomach pains or loss of appetite. Typhoid fever is determined by testing the presence of Salmonella Typhi in the stool or blood of an infected person. Typhoid fever is treated with antibiotics.

26. SARS (Severe Acute Respiratory Syndrome) and the MERS VIRUS A new Pneumonia disease that emerged in China in 2003. After news of the outbreak of SARS China tried to silence news about it both internal and international news , SARS spread rapidly, reaching neighboring countries Hong Kong and Vietnam in late February 2003, and then to other countries via international travelers.Canada Had a outbreak that was fairly well covered and cost Canada quite a bit financially

The last case of this epidemic occurred in June 2003. In that outbreak, 8069 cases arise that killed 775 people. There is speculation that this disease is Man-Made SARS, SARS has symptoms of flu and may include: fever, cough, sore throat and other non-specific symptoms.

The only symptom that is common to all patients was fever above 38 degrees Celsius. Shortness of breath may occur later. There is currently no vaccine for the disease so that countermeasures can only assist the breathing apparatus. The virus was said to be the Virus of the End Times

27.  MERS(Middle Eastern Respiratory Syndrome) The Middle East respiratory syndrome coronavirus (MERS-CoV), also termed EMC/2012 (HCoV-EMC/2012), is positive-sense, single-stranded RNA novel species of the genus Betacoronavirus.

First called novel coronavirus 2012 or simply novel coronavirus, it was first reported in 2012 after genome sequencing of a virus isolated from sputum samples from patients who fell ill in a 2012 outbreak of a new flu.

As of June 2014, MERS-CoV cases have been reported in 22 countries, including Saudi Arabia, Malaysia, Jordan, Qatar, Egypt, the United Arab Emirates, Kuwait, Oman, Algeria, Bangladesh, the Philippines (still MERS-free), Indonesia (none was confirmed), the United Kingdom, and the United States. Almost all cases are somehow linked to Saudi Arabia. In the same article it was reported that Saudi authorities’ errors in response to MERS-CoV were a contributing factor to the spread of this deadly virus.

27. Enterovirus (Brain Inflammation) Entero virus is a disease of the hands, feet and mouth, and we can not ignored occasional Brain Inflammation. Enterovirus attack symptoms are very similar to regular flu symptoms so its difficult to detect it, such as fever, sometimes accompanied by dizziness and weakness and pain.

Next will come the little red watery bumps on the palms and feet following oral thrush. In severe conditions, Enterovirus can attack the nerves and brain tissue to result in death.

The virus is easily spread through direct contact with patients. Children are the main victims of the spread of enterovirus in China. Since the first victim was found but reporting was delayed until several weeks later.

24 thousand people have contracted the enterovirus. More than 30 of them died mostly children. The virus is reported to have entered Indonesia and infecting three people in Sumatra.  2014Enterovirus 68 is presently spreading across North America mainly and started in the USA has probably spread to Canada and Mexico by now. Enterovirus 68’s spread is unprecedented up till now

28.  The Black Plague  The 1918 flu virus and HIV are the biggest killers of modern times. But back in the 14th century, the bacterium that causes bubonic plague, or the Black Death as it was also known, was the baddest bug of all. In just a few years, from 1347 to 1351, the plague killed off about 75,000,000 people worldwide, including one-third of the entire population of Europe at that time.

It spread through Asia, Italy, North Africa, Spain, Normandy, Switzerland, and eastward into Hungary. After a brief break, it crossed into England, Scotland, and then to Norway, Sweden, Denmark, Iceland and Greenland.

Yersinia pestis, the plague bacteria
Courtesy of Neal Chamberlain

The plague bacterium is called Yersinia <yer-sin-ee-uh> pestis. There are two main forms of the disease. In the bubonic <boo-bah-nick> form, the bacteria cause painful swellings as large as an orange to form in the armpits, neck and groin. These swellings, or buboes, often burst open, oozing blood and pus. Blood vessels leak blood that puddles under the skin, giving the skin a blackened look. That’s why the disease became known as the Black Death. At least half of its victims die within a week.

The pneumonic <new-mon-ick> form of plague causes victims to sweat heavily and cough up blood that starts filling their lungs. Almost no one survived it during the plague years. Yersinia pestis is the deadliest microbe we’ve ever known, although HIV might catch up to it. Yersinia pestis is still around in the world. Fortunately, with bacteria-killing antibiotics and measures to control the pests—rats and mice—that spread the bacteria, we’ve managed to conquer this killer.

29. Human Papillomavirus  Human papillomavirus (HPV) is a DNA virus from the papillomavirus family that is capable of infecting humans. Like all papillomaviruses, HPVs establish productive infections only in keratinocytes of the skin or mucous membranes.

Most HPV infections are subclinical and will cause no physical symptoms; however, in some people subclinical infections will become clinical and may cause benign papillomas (such as warts [verrucae] or squamous cell papilloma), or cancers of the cervix, vulva, vagina, penis, oropharynx and anus.HPV has been linked with an increased risk of cardiovascular disease. In addition, HPV 16 and 18 infections are a cause of a unique type of oropharyngeal (throat) cancer and are believed to cause 70% of cervical cancer, which have available vaccines, see HPV vaccine.

More than 30 to 40 types of HPV are typically transmitted through sexual contact and infect the anogenital region. Some sexually transmitted HPV types may cause genital warts. Persistent infection with "high-risk" HPV types—different from the ones that cause skin warts—may progress to precancerous lesions and invasive cancer. High-risk HPV infection is a cause of nearly all cases of cervical cancer.However, most infections do not cause disease.

Seventy percent of clinical HPV infections, in young men and women, may regress to subclinical in one year and ninety percent in two years. However, when the subclinical infection persists—in 5% to 10% of infected women—there is high risk of developing precancerous lesions of the vulva and cervix, which can progress to invasive cancer. Progression from subclinical to clinical infection may take years; providing opportunities for detection and treatment of pre-cancerous lesions.

In more developed countries, cervical screening using a Papanicolaou (Pap) test or liquid-based cytology is used to detect abnormal cells that may develop into cancer. If abnormal cells are found, women are invited to have a colposcopy. During a colposcopic inspection, biopsies can be taken and abnormal areas can be removed with a simple procedure, typically with a cauterizing loop or, more commonly in the developing world—by freezing (cryotherapy).

Treating abnormal cells in this way can prevent them from developing into cervical cancer. Pap smears have reduced the incidence and fatalities of cervical cancer in the developed world, but even so there were 11,000 cases and 3,900 deaths in the U.S. in 2008. Cervical cancer has substantial mortality worldwide, there are an estimated 490,000 cases and 270,000 deaths each year.

It is true that infections caused by human papillomavirus (HPV) are not fatal, but chronic infection may result in cervical cancer. Apparently, HPV is responsible for almost all cervical cancers (approx. 99%). HPV results in 275,000 deaths per year.

30. Henipaviruses The genus Henipavirus comprises of 3 members which are Hendra virus (HeV), Nipah virus (NiV), and Cedar virus (CedPV). The second one was introduced in the middle of 2012, although affected no human, and is therefore considered harmless. The rest of the two viruses, however, are lethal with mortality rate up to 50-100%.

Hendra virus (originally Equine morbillivirus) was discovered in September 1994 when it caused the deaths of thirteen horses, and a trainer at a training complex in Hendra, a suburb of Brisbane in Queensland, Australia.

The index case, a mare, was housed with 19 other horses after falling ill, and died two days later. Subsequently, all of the horses became ill, with 13 dying. The remaining 6 animals were subsequently euthanized as a way of preventing relapsing infection and possible further transmission.The trainer, Victory (‘Vic’) Rail, and a stable hand were involved in nursing the index case, and both fell ill with an influenza-like illness within one week of the first horse’s death. The stable hand recovered while Mr Rail died of respiratory and renal failure. The source of the virus was most likely frothy nasal discharge from the index case.

A second outbreak occurred in August 1994 (chronologically preceding the first outbreak) in Mackay 1,000 km north of Brisbane resulting in the deaths of two horses and their owner. The owner, Mark Preston, assisted in necropsies of the horses and within three weeks was admitted to hospital suffering from meningitis. Mr Preston recovered, but 14 months later developed neurologic signs and died. This outbreak was diagnosed retrospectively by the presence of Hendra virus in the brain of the patient.

A survey of wildlife in the outbreak areas was conducted, and identified pteropid fruit bats as the most likely source of Hendra virus, with a seroprevalence of 47%. All of the other 46 species sampled were negative. Virus isolations from the reproductive tract and urine of wild bats indicated that transmission to horses may have occurred via exposure to bat urine or birthing fluids.  However, the only attempt at experimental infection reported in the literature, conducted at CSIRO Geelong, did not result in infection of a horse from infected flying foxes. This study looked at potential infection between bats, horses and cats, in various combinations. The only species that was able to infect horses was the cat (Felix spp.)

Nipah virus was identified in April 1999, when it caused an outbreak of neurological and respiratory disease on pig farms in peninsular Malaysia, resulting in 257 human cases, including 105 human deaths and the culling of one million pigs.  In Singapore, 11 cases, including one death, occurred in abattoir workers exposed to pigs imported from the affected Malaysian farms. The Nipah virus has been classified by the Centers for Disease Control and Prevention as a Category C agent. The name "Nipah" refers to the place, Kampung Baru Sungai Nipah in Negeri Sembilan State, Malaysia, the source of the human case from which Nipah virus was first isolated.

The outbreak was originally mistaken for Japanese encephalitis (JE), however, physicians in the area noted that persons who had been vaccinated against JE were not protected, and the number of cases among adults was unusual Despite the fact that these observations were recorded in the first month of the outbreak, the Ministry of Health failed to react accordingly, and instead launched a nationwide campaign to educate people on the dangers of JE and its vector, Culex mosquitoes.

Symptoms of infection from the Malaysian outbreak were primarily encephalitic in humans and respiratory in pigs. Later outbreaks have caused respiratory illness in humans, increasing the likelihood of human-to-human transmission and indicating the existence of more dangerous strains of the virus. Based on seroprevalence data and virus isolations, the primary reservoir for Nipah virus was identified as Pteropid fruit bats, including Pteropus vampyrus (Large Flying Fox), and Pteropus hypomelanus (Small flying fox), both of which occur in Malaysia.

The transmission of Nipah virus from flying foxes to pigs is thought to be due to an increasing overlap between bat habitats and piggeries in peninsular Malaysia. At the index farm, fruit orchards were in close proximity to the piggery, allowing the spillage of urine, feces and partially eaten fruit onto the pigs. Retrospective studies demonstrate that viral spillover into pigs may have been occurring in Malaysia since 1996 without detection. During 1998, viral spread was aided by the transfer of infected pigs to other farms, where new outbreaks occurred.

Cedar Virus (CedPV) was first identified in pteropid urine during work on Hendra virus undertaken in Queensland in 2009. Although the virus is reported to be very similar to both Hendra and Nipah, it does not cause illness in laboratory animals usually susceptible to paramyxoviruses. Animals were able to mount an effective response and create effective antibodies.

The scientists who identified the virus report:

Hendra and Nipah viruses are 2 highly pathogenic paramyxoviruses that have emerged from bats within the last two decades. Both are capable of causing fatal disease in both humans and many mammal species. Serological and molecular evidence for henipa-like viruses have been reported from numerous locations including Asia and Africa, however, until now no successful isolation of these viruses have been reported. This paper reports the isolation of a novel paramyxovirus, named Cedar virus, from fruit bats in Australia. Full genome sequencing of this virus suggests a close relationship with the henipaviruses.

 

 

Antibodies to Cedar virus were shown to cross react with, but not cross neutralize Hendra or Nipah virus. Despite this close relationship, when Cedar virus was tested in experimental challenge models in ferrets and guinea pigs, we identified virus replication and generation of neutralizing antibodies, but no clinical disease was observed. As such, this virus provides a useful reference for future reverse genetics experiments to determine the molecular basis of the pathogenicity of the henipaviruses.

30. Lyssaviruses  This genus comprises of not only rabies virus (causing death of almost everyone who is infected) but certain other viruses such as Duvenhage virus, Mokola virus, and Australian bat lyssavirus. Although small number of cases are reported, but the ones reported have always been fatal. Bats are vectors for all of these types except for Mokola virus.

 

Lyssavirus (from Lyssa, the Greek goddess of madness, rage, and frenzy) is a genus of viruses belonging to the family Rhabdoviridae, in the order Mononegavirales. This group of RNA viruses includes the rabies virus traditionally associated with the disease. Viruses typically have either helical or cubic symmetry. Lyssaviruses have helical symmetry, so their infectious particles are approximately cylindrical in shape. This is typical of plant-infecting viruses. Human-infecting viruses more commonly have cubic symmetry and take shapes approximating regular polyhedra. The structure consists of a spiked outer envelope, a middle region consisting of matrix protein M, and an inner ribonucleocapsid complex region, consisting of the genome associated with other proteins.

Lyssavirus genome consists of a negative-sense, single-stranded RNA molecule that encodes five viral proteins: polymerase L, matrix protein M, phosphoprotein P, nucleoprotein N, and glycoprotein G.

Based on recent phylogenetic evidence, lyssa viruses are categorized into seven major species. In addition, five species recently have been discovered: West Caucasian bat virus, Aravan virus, Khuj and virus, Irkut virus and Shimoni bat virus. The major species include rabies virus (species 1), Lagos bat virus (species 2), Mokola virus (species 3), Duvenhage virus (species 4), European Bat lyssaviruses type 1 and 2 (species 5 and 6), and Australian bat lyssavirus (species 7).

Based on biological properties of the viruses, these species are further subdivided into phylogroups 1 and 2. Phylogroup 1 includes genotypes 1, 4, 5, 6, and 7, while phylogroup 2 includes genotypes 2 and 3. The nucleocapsid region of lyssavirus is fairly highly conserved from genotype to genotype across both phylogroups; however, experimental data have shown the lyssavirus strains used in vaccinations are only from the first species(i.e. classic rabies).

31. Tuberculosis  Mucous, fever, fatigue, excessive sweating and weight loss. What do they all have in common?

They are symptoms of pulmonary tuberculosis, or TB. TB is a contagious bacterial infection that involves the lungs, but it may spread to other organs. The symptoms of this disease can remain stagnant for years or affect the person right away. People at higher risk for contracting TB include the elderly, infants and those with weakened immune systems due to other diseases, such as AIDS or diabetes, or even individuals who have undergone chemotherapy.

Being around others who may have TB, maintaining a poor diet or living in unsanitary conditions are all risk factors for contracting TB. In the United States, there are approximately 10 cases of TB per 100,000 people. Tuberculosis, MTB, or TB (short for tubercle bacillus), in the past also called phthisis, phthisis pulmonalis, or consumption, is a widespread, and in many cases fatal, infectious disease caused by various strains of mycobacteria, usually Mycobacterium tuberculosis.

Tuberculosis typically attacks the lungs, but can also affect other parts of the body. It is spread through the air when people who have an active TB infection cough, sneeze, or otherwise transmit respiratory fluids through the air. Most infections do not have symptoms, known as latent tuberculosis. About one in ten latent infections eventually progresses to active disease which, if left untreated, kills more than 50% of those so infected.

The classic symptoms of active TB infection are a chronic cough with blood-tinged sputum, fever, night sweats, and weight loss (the latter giving rise to the formerly common term for the disease, "consumption"). Infection of other organs causes a wide range of symptoms. Diagnosis of active TB relies on radiology (commonly chest X-rays), as well as microscopic examination and microbiological culture of body fluids.

Diagnosis of latent TB relies on the tuberculin skin test (TST) and/or blood tests. Treatment is difficult and requires administration of multiple antibiotics over a long period of time. Social contacts are also screened and treated if necessary. Antibiotic resistance is a growing problem in multiple drug-resistant tuberculosis (MDR-TB) infections. Prevention relies on screening programs and vaccination with the bacillus Calmette-Guérin vaccine.

One-third of the world’s population is thought to have been infected with M. tuberculosis, with new infections occurring in about 1% of the population each year.In 2007, an estimated 13.7 million chronic cases were active globally, while in 2010, an estimated 8.8 million new cases and 1.5 million associated deaths occurred, mostly in developing countries. The absolute number of tuberculosis cases has been decreasing since 2006, and new cases have decreased since 2002.

The rate of tuberculosis in different areas varies across the globe; about 80% of the population in many Asian and African countries tests positive in tuberculin tests, while only 5–10% of the United States population tests positive. More people in the developing world contract tuberculosis because of a poor immune system, largely due to high rates of HIV infection and the corresponding development of AIDS.

32. Encephalitis Virus Encephalitis is an acute inflammation of the brain, commonly caused by a viral infection. Victims are usually exposed to viruses resulting in encephalitis by insect bites or food and drink. The most frequently encountered agents are arboviruses (carried by mosquitoes or ticks) and enteroviruses ( coxsackievirus, poliovirus and echovirus ). Some of the less frequent agents are measles, rabies, mumps, varicella and herpes simplex viruses.

Patients with encephalitis suffer from fever, headache, vomiting, confusion, drowsiness and photophobia. The symptoms of encephalitis are caused by brain’s defense mechanisms being activated to get rid of infection (brain swelling, small bleedings and cell death). Neurologic examination usually reveals a stiff neck due to the irritation of the meninges covering the brain. Examination of the cerebrospinal fluidCerebrospinal fluid CSF in short, is the clear fluid that occupies the subarachnoid space (the space between the skull and cortex of the brain). It acts as a "cushion" or buffer for the cortex.

Also, CSF occupies the ventricular system of the brain and the obtained by a lumbar puncture In medicine, a lumbar puncture (colloquially known as a spinal tap is a diagnostic procedure that is done to collect a sample of cerebrospinal fluid (CSF) for biochemical, microbiological and cytological analysis. Indications The most common indication for procedure reveals increased amounts of proteins and white blood cells with normal glucose. A CT scan examination is performed to reveal possible complications of brain swelling, brain abscess Brain abscess (or cerebral abscess) is an abscess caused by inflammation and collection of infected material coming from local (ear infection, infection of paranasal sinuses, infection of the mastoid air cells of the temporal bone, epidural abscess) or re or bleeding. Lumbar puncture procedure is performed only after the possibility of a prominent brain swelling is excluded by a CT scan examination.

What are the main Symptoms?
Some patients may have symptoms of a cold or stomach infection before encephalitis symptoms begin.
When a case of encephalitis is not very severe, the symptoms may be similar to those of other illnesses, including:
• Fever that is not very high
• Mild headache
• Low energy and a poor appetite

Other symptoms include:
• Clumsiness, unsteady gait
• Confusion, disorientation
• Drowsiness
• Irritability or poor temper control
• Light sensitivity
• Stiff neck and back (occasionally)
• Vomiting

Symptoms in newborns and younger infants may not be as easy to recognize:
• Body stiffness
• Irritability and crying more often (these symptoms may get worse when the baby is picked up)
• Poor feeding
• Soft spot on the top of the head may bulge out more
• Vomiting

• Loss of consciousness, poor responsiveness, stupor, coma
• Muscle weakness or paralysis
• Seizures
• Severe headache
• Sudden change in mental functions:
• "Flat" mood, lack of mood, or mood that is inappropriate for the situation
• Impaired judgment
• Inflexibility, extreme self-centeredness, inability to make a decision, or withdrawal from social interaction
• Less interest in daily activities
• Memory loss (amnesia), impaired short-term or long-term memory

Children and adults should avoid contact with anyone who has encephalitis.
Controlling mosquitoes (a mosquito bite can transmit some viruses) may reduce the chance of some infections that can lead to encephalitis.
• Apply an insect repellant containing the chemical, DEET when you go outside (but never use DEET products on infants younger than 2 months).
• Remove any sources of standing water (such as old tires, cans, gutters, and wading pools).
• Wear long-sleeved shirts and pants when outside, particularly at dusk.
Vaccinate animals to prevent encephalitis caused by the rabies virus.

 

33. Chicken Pox Virus Chickenpox is a highly contagious disease caused by primary infection with varicella zoster virus (VZV).It usually starts with a vesicular skin rash mainly on the body and head rather than on the limbs. The rash develops into itchy, raw pockmarks, which mostly heal without scarring. On examination, the observer typically finds skin lesions at various stages of healing and also ulcers in the oral cavity and tonsil areas. The disease is most commonly observed in children.

Chickenpox is an airborne disease which spreads easily through coughing or sneezing by ill individuals or through direct contact with secretions from the rash. A person with chickenpox is infectious one to two days before the rash appears. They remain contagious until all lesions have crusted over (this takes approximately six days). Immunocompromised patients are contagious during the entire period as new lesions keep appearing. Crusted lesions are not contagious.Chickenpox has been observed in other primates, including chimpanzees and gorillas.

The origin of the term chicken pox, which is recorded as being used since 1684,is not reliably known. It has been said to be a derived from chickpeas, based on resemblance of the vesicles to chickpeas, or to come from the rash resembling chicken pecks. Other suggestions include the designation chicken for a child (i.e., literally ‘child pox’), a corruption of itching-pox, or the idea that the disease may have originated in chickens. Samuel Johnson explained the designation as "from its being of no very great danger."

The early (prodromal) symptoms in adolescents and adults are nausea, loss of appetite, aching muscles, and headache. This is followed by the characteristic rash or oral sores, malaise, and a low-grade fever that signal the presence of the disease. Oral manifestations of the disease (enanthem) not uncommonly may precede the external rash (exanthem). In children the illness is not usually preceded by prodromal symptoms, and the first sign is the rash or the spots in the oral cavity. The rash begins as small red dots on the face, scalp, torso, upper arms and legs; progressing over 10–12 hours to small bumps, blisters and pustules; followed by umbilication and the formation of scabs.

At the blister stage, intense itching is usually present. Blisters may also occur on the palms, soles, and genital area. Commonly, visible evidence of the disease develops in the oral cavity & tonsil areas in the form of small ulcers which can be painful or itchy or both; this enanthem (internal rash) can precede the exanthem (external rash) by 1 to 3 days or can be concurrent. These symptoms of chickenpox appear 10 to 21 days after exposure to a contagious person. Adults may have a more widespread rash and longer fever, and they are more likely to experience complications, such as varicella pneumonia.Because watery nasal discharge containing live virus usually precedes both exanthem (external rash) and enanthem (oral ulcers) by 1 to 2 days, the infected person actually becomes contagious one to two days prior to recognition of the disease. Contagiousness persists until all vesicular lesions have become dry crusts (scabs), which usually entails four or five days, by which time nasal shedding of live virus also ceases.

Chickenpox is rarely fatal, although it is generally more severe in adult men than in women or children. Non-immune pregnant women and those with a suppressed immune system are at highest risk of serious complications. Arterial ischemic stroke (AIS) associated with chickenpox in the previous year accounts for nearly one third of childhood AIS. The most common late complication of chickenpox is shingles (herpes zoster), caused by reactivation of the varicella zoster virus decades after the initial, often childhood, chickenpox infection.

Shingles  Herpes zoster After a chickenpox infection, the virus remains dormant in the body’s nerve tissues. The immune system keeps the virus at bay, but later in life, usually as an adult, it can be reactivated and cause a different form of the viral infection called shingles (scientifically known as herpes zoster). The United States Advisory Committee on Immunization Practices (ACIP) suggests that any adult over the age of 60 years gets the herpes zoster vaccine as a part of their normal medical check ups.

Many adults who have had chickenpox as children are susceptible to shingles as adults, often with the accompanying condition postherpetic neuralgia, a painful condition that makes it difficult to sleep. Even after the shingles rash has gone away, there can be night pain in the area affected by the rash.Shingles affects one in five adults infected with chickenpox as children, especially those who are immune suppressed, particularly from cancer, HIV, or other conditions.

However, stress can bring on shingles as well, although scientists are still researching the connection.Shingles are most commonly found in adults over the age of 60 who were diagnosed with chickenpox when they were under the age of 1.A shingles vaccine is available for adults over 50 who have had childhood chickenpox or who have previously had shingles.

34. POXVIRUS  Poxviruses (members of the family Poxviridae) are viruses that can, as a family, infect both vertebrate and invertebrate animals.

Four genera of poxviruses may infect humans: orthopox, parapox, yatapox, molluscipox. Orthopox: smallpox virus (variola), vaccinia virus, cowpox virus, monkeypox virus; Parapox: orf virus, pseudocowpox, bovine papular stomatitis virus; Yatapox: tanapox virus, yaba monkey tumor virus; Molluscipox: molluscum contagiosum virus (MCV).The most common are vaccinia (seen on Indian subcontinent) and molluscum contagiousum, but monkeypox infections are rising (seen in west and central African rainforest countries). Camelpox is a disease of camels caused by a virus of the family Poxviridae, subfamily Chordopoxvirinae, and the genus Orthopoxvirus. It causes skin lesions and a generalized infection. Approximately 25% of young camels that become infected will die from the disease, while infection in older camels is generally more mild.

The ancestor of the poxviruses is not known but structural studies suggest it may have been an adenovirus or a species related to both the poxviruses and the adenoviruses. Based on the genome organization and DNA replication mechanism it seems that phylogenetic relationships may exist between the rudiviruses (Rudiviridae) and the large eukaryal DNA viruses: the African swine fever virus (Asfarviridae), Chlorella viruses (Phycodnaviridae) and poxviruses (Poxviridae).The mutation rate in these genomes has been estimated to be 0.9-1.2 x 10⁻⁶ substitutions per site per year.A second estimate puts this rate at 0.5-7 × 10⁻⁶ nucleotide substitutions per site per year.  A third estimate places the rate at 4-6 × 10⁻⁶.

The last common ancestor of the extant poxviruses that infect vertebrates existed 0.5 million years ago. The genus Avipoxvirus diverged from the ancestor 249 ± 69 thousand years ago. The ancestor of the genus Orthopoxvirus was next to diverge from the other clades at 0.3 million years ago. A second estimate of this divergence time places this event at 166,000 ± 43,000 years ago. The division of the Orthopox into the extant genera occurred ~14,000 years ago. The genus Leporipoxvirus diverged ~137,000 ± 35,000 years ago. This was followed by the ancestor of the genus Yatapoxvirus. The last common ancestor of the Capripoxvirus and Suipoxvirus diverged 111,000 ± 29,000 years ago.

A model of a poxvirus cut-away in
cross-section to show the internal
structures. Poxviruses are shaped like
flattened capsules/barrels or are lens or
pill-shaped.

Their structure is complex,
neither icosahedral nor helical. This
model is based on Vaccinia, the smallpox
virus. The structures are also highly
variable and often incompletely studied.

 

35. West Nile Virus  West Nile virus (WNV) is a mosquito-borne zoonotic arbovirus belonging to the genus Flavivirus in the family Flaviviridae.

This flavivirus is found in temperate and tropical regions of the world. It was first identified in the West Nile subregion in the East African nation of Uganda in 1937. Prior to the mid-1990s, WNV disease occurred only sporadically and was considered a minor risk for humans, until an outbreak in Algeria in 1994, with cases of WNV-caused encephalitis, and the first large outbreak in Romania in 1996, with a high number of cases with neuroinvasive disease. WNV has now spread globally, with the first case in the Western Hemisphere being identified in New York City in 1999; over the next five years, the virus spread across the continental United States, north into Canada, and southward into the Caribbean islands and Latin America. WNV also spread to Europe, beyond the Mediterranean Basin, and a new strain of the virus was identified in Italy in 2012. WNV is now considered to be an endemic pathogen in Africa, Asia, Australia, the Middle East, Europe and in the United States, which in 2012 has experienced one of its worst epidemics. In 2012, WNV killed 286 people in the United States, with the state of Texas being hard hit by this virus, making the year the deadliest on record for the United States.

The main mode of WNV transmission is via various species of mosquitoes, which are the prime vector, with birds being the most commonly infected animal and serving as the prime reservoir host—especially passerines, which are of the largest order of birds, Passeriformes. WNV has been found in various species of ticks, but current research suggests they are not important vectors of the virus. WNV also infects various mammal species, including humans, and has been identified in reptilian species, including alligators and crocodiles, and also in amphibians. Not all animal species that are susceptible to WNV infection, including humans, and not all bird species develop sufficient viral levels to transmit the disease to uninfected mosquitoes, and are thus not considered major factors in WNV transmission.

Approximately 80% of West Nile virus infections in humans are subclinical, which cause no symptoms. In the cases where symptoms do occur—termed West Nile fever in cases without neurological disease—the time from infection to the appearance of symptoms (incubation period) is typically between 2 and 15 days. Symptoms may include fever, headaches, fatigue, muscle pain or aches, malaise, nausea, anorexia, vomiting, myalgias and rash. Less than 1% of the cases are severe and result in neurological disease when the central nervous system is affected. People of advanced age, the very young, or those with immunosuppression, either medically induced, such as those taking immunosupressive drugs, or due to a pre-existing medical condition such as HIV infection, are most susceptible. The specific neurological diseases that may occur are West Nile encephalitis, which causes inflammation of the brain, West Nile meningitis, which causes inflammation of the meninges, which are the protective membranes that cover the brain and spinal cord, West Nile meningoencephalitis, which causes inflammation of the brain and also the meninges surrounding it, and West Nile poliomyelitis—spinal cord inflammation, which results in a syndrome similar to polio, which may cause acute flaccid paralysis.

Currently, no vaccine against WNV infection is available. The best method to reduce the rates of WNV infection is mosquito control on the part of municipalities, businesses and individual citizens to reduce breeding populations of mosquitoes in public, commercial and private areas via various means including eliminating standing pools of water where mosquitoes breed, such as in old tires, buckets, unused swimming pools, etc. On an individual basis, the use of personal protective measures to avoid being bitten by an infected mosquito, via the use of mosquito repellent, window screens, avoiding areas where mosquitoes are more prone to congregate, such as near marshes, areas with heavy vegetation etc., and being more vigilant from dusk to dawn when mosquitoes are most active offers the best defense. In the event of being bitten by an infected mosquito, familiarity of the symptoms of WNV on the part of laypersons, physicians and allied health professions affords the best chance of receiving timely medical treatment, which may aid in reducing associated possible complications and also appropriate palliative care.

The incubation period for WNV—the amount of time from infection to symptom onset—is typically from between 2 and 15 days. Headache can be a prominent symptom of WNV fever, meningitis, encephalitis, meningoencephalitis, and it may or may not be present in poliomyelytis-like syndrome. Thus, headache is not a useful indicator of neuroinvasive disease.(CDC)

• West Nile fever (WNF), which occurs in 20 percent of cases, is a febrile syndrome that causes flu-like symptoms. Most characterizations of WNF generally describe it as a mild, acute syndrome lasting 3 to 6 days after symptom onset. Systematic follow-up studies of patients with WNF have not been done, so this information is largely anecdotal. In addition to a high fever, headache, chills, excessive sweating, weakness, fatigue, swollen lymph nodes, drowsiness, pain in the joints and flu-like symptoms. Gastrointestinal symptoms that may occur include nausea, vomiting, loss of appetite, and diarrhea. Fewer than one-third of patients develop a rash.

• West Nile neuroinvasive disease (WNND), which occurs in less than 1 percent of cases, is when the virus infects the central nervous system resulting in meningitis, encephalitis, meningoencephalitis or a poliomyelitis-like syndrome.  Many patients with WNND have normal neuroimaging studies, although abnormalities may be present in various cerebral areas including the basal ganglia, thalamus, cerebellum, and brainstem.

• West Nile virus encephalitis (WNE) is the most common neuroinvasive manifestation of WNND. WNE presents with similar symptoms to other viral encephalitis with fever, headaches, and altered mental status. A prominent finding in WNE is muscular weakness (30 to 50 percent of patients with encephalitis), often with lower motor neuron symptoms, flaccid paralysis, and hyporeflexia with no sensory abnormalities.

• West Nile meningitis (WNM) usually involves fever, headache, and stiff neck. Pleocytosis, an increase of white blood cells in cerebrospinal fluid, is also present. Changes in consciousness are not usually seen and are mild when present.

• West Nile meningoencephalitis is inflammation of both the brain (encephalitis) and meninges (meningitis).

• West Nile poliomyelitis (WNP), an acute flaccid paralysis syndrome associated with WNV infection, is less common than WNM or WNE. This syndrome is generally characterized by the acute onset of asymmetric limb weakness or paralysis in the absence of sensory loss. Pain sometimes precedes the paralysis. The paralysis can occur in the absence of fever, headache, or other common symptoms associated with WNV infection. Involvement of respiratory muscles, leading to acute respiratory failure, can sometimes occur.

• West-Nile reversible paralysis,. Like WNP, the weakness or paralysis is asymmetric. Reported cases have been noted to have an initial preservation of deep tendon reflexes, which is not expected for a pure anterior horn involvement.Disconnect of upper motor neuron influences on the anterior horn cells possibly by myelitis or glutamate excitotoxicity have been suggested as mechanisms.The prognosis for recovery is excellent.

• Nonneurologic complications of WNV infection that may rarely occur include fulminant hepatitis, pancreatitis,  myocarditis, rhabdomyolysis, orchitis, nephritis, optic neuritis and cardiac dysrhythmias and hemorrhagic fever with coagulopathy.^[15] Chorioretinitis may also be more common than previously thought.

• Cutaneous manifestations specifically rashes, are not uncommon in WNV-infected patients; however, there is a paucity of detailed descriptions in case reports and there are few clinical images widely available. Punctate erythematous (?), macular, and papular eruptions, most pronounced on the extremities have been observed in WNV cases and in some cases histopathologic findings have shown a sparse superficial perivascular lymphocytic infiltrate, a manifestation commonly seen in viral exanthems (?). A literature review provides support that this punctate rash is a common cutaneous presentation of WNV infection. (Anderson RC et al.)

West Nile virus life cycle. After binding and uptake, the virion envelope fuses with cellular membranes, followed by uncoating of the nucleocapsid and release of the RNA genome into the cytoplasm. The viral genome serves as messenger RNA (mRNA) for translation of all viral proteins and as template during RNA replication. Copies are subsequently packaged within new virus particles that are transported in vesicles to the cell membrane.

WNV is one of the Japanese encephalitis antigenic serocomplex of viruses. Image reconstructions and cryoelectron microscopy reveal a 45–50 nm virion covered with a relatively smooth protein surface. This structure is similar to the dengue fever virus; both belong to the genus Flavivirus within the family Flaviviridae.

The genetic material of WNV is a positive-sense, single strand of RNA, which is between 11,000 and 12,000 nucleotides long; these genes encode seven nonstructural proteins and three structural proteins. The RNA strand is held within a nucleocapsid formed from 12-kDa protein blocks; the capsid is contained within a host-derived membrane altered by two viral glycoproteins. Phylogenetic tree of West Nile viruses based on sequencing of the envelope gene during complete genome sequencing of the virus

Studies of phylogenetic lineages determined WNV emerged as a distinct virus around 1000 years ago. This initial virus developed into two distinct lineages, lineage 1 and its multiple profiles is the source of the epidemic transmission in Africa and throughout the world. Lineage 2 was considered an Africa zoonosis. However, in 2008, lineage 2, previously only seen in horses in sub-Saharan Africa and Madagascar, began to appear in horses in Europe, where the first known outbreak affected 18 animals in Hungary in 2008. Lineage 1 West Nile virus was detected in South Africa in 2010 in a mare and her aborted fetus; previously, only lineage 2 West Nile virus had been detected in horses and humans in South Africa. A 2007 fatal case in a killer whale in Texas broadened the known host range of West Nile virus to include cetaceans.

The United States virus was very closely related to a lineage 1 strain found in Israel in 1998. Since the first North American cases in 1999, the virus has been reported throughout the United States, Canada, Mexico, the Caribbean, and Central America. There have been human cases and equine cases, and many birds are infected. The Barbary macaque, Macaca sylvanus, was the first nonhuman primate to contract WNV.  Both the United States and Israeli strains are marked by high mortality rates in infected avian populations; the presence of dead birds—especially Corvidae—can be an early indicator of the arrival of the virus.

The West Nile virus maintains itself in nature by cycling between mosquitoes and certain species of birds. A mosquito (the vector) bites an uninfected bird (the host), the virus amplifies within the bird, an uninfected mosquito bites the bird and is in turn infected. Other species such as humans and horses are incidental infections, as they are not the mosquitoes’ preferred blood meal source. The virus does not amplify within these species and they are known as dead-end hosts.

The West Nile virus (WNV) is transmitted through female mosquitoes, which are the prime vectors of the virus. Only females feed on blood, and different species have evolved to take a blood meal on preferred types of vertebrate hosts. The infected mosquito species vary according to geographical area; in the United States, Culex pipiens (Eastern United States), Culex tarsalis (Midwest and West), and Culex quinquefasciatus (Southeast) are the main sources.The various species that transmit the WNV prefer birds of the Passeriformes order, the largest order of birds. Within that order there is further selectivity with various mosquito species exhibiting preference for different species. In the United States WNV mosquito vectors have shown definitive preference for members of the Corvidae and Thrush family of birds. Amongst the preferred species within these families are the American crow, a corvid, and the American robin (Turdus migratorius), a thrush.

The proboscis of a female mosquito—here a Southern House Mosquito (Culex quinquefasciatus)—pierces the epidermis and dermis to allow it to feed on human blood from a capillary: this one is almost fully tumescent. The mosquito injects saliva, which contains an anesthetic, and an anticoagulant into the puncture wound; and in infected mosquitoes, the West Nile virus.

The birds develop sufficient viral levels after being infected, to transmit the infection to other biting mosquitoes that in turn go on to infect other birds. In crows and robins, the infection is fatal in 4–5 days. This epizootic viral amplification cycle has been shown to peak 15–16 days before humans become ill. This may be due to the high mortality, and thus depletion of the preferred hosts, i.e., the specific bird species. The mosquitoes become less selective and begin feeding more readily on other animal types such as humans and horses which are considered incidental hosts.

In mammals, the virus does not multiply as readily (i.e., does not develop high viremia during infection), and mosquitoes biting infected mammals are not believed to ingest sufficient virus to become infected,making mammals so-called dead-end hosts.

Direct human-to-human transmission initially was believed to be caused only by occupational exposure, or conjunctive exposure to infected blood. The US outbreak identified additional transmission methods through blood transfusion,organ transplant intrauterine exposure, and breast feeding. Since 2003, blood banks in the United States routinely screen for the virus among their donors. As a precautionary measure, the UK’s National Blood Service initially ran a test for this disease in donors who donate within 28 days of a visit to the United States, Canada or the northeastern provinces of Italy and the Scottish National Blood Transfusion Service asks prospective donors to wait 28 days after returning from North America or the northeastern provinces of Italy before donating.

Recently, the potential for mosquito saliva to impact the course of WNV disease was demonstrated. Mosquitoes inoculate their saliva into the skin while obtaining blood. Mosquito saliva is a pharmacological cocktail of secreted molecules, principally proteins, that can affect vascular constriction, blood coagulation, platelet aggregation, inflammation, and immunity. It clearly alters the immune response in a manner that may be advantageous to a virus. Studies have shown it can specifically modulate the immune response during early virus infection, and mosquito feeding can exacerbate WNV infection, leading to higher viremia and more severe forms of disease.

Vertical transmission, the transmission of a viral or bacterial disease from the female of the species to her offspring, has been observed in various West Nile virus studies, amongst different species of mosquitoes in both the laboratory and in nature.Mosquito progeny infected vertically in autumn, may potentially serve as a mechanism for WNV to overwinter and initiate enzootic horizontal transmission the following spring.

35 of the Most Dangerous Viruses and Bacteria’s in the World Today

The Black Plague, Marburg, Ebola, Influenza, Enterovirus virus may all sound terrifying, but it’s not the most dangerous virus in the world. It isn’t HIV either. Here is a list of the most dangerous viruses and Bacteria’s on the Planet Earth.

1. Marburg Virus The most dangerous virus is the Marburg virus. It is named after a small and idyllic town on the river Lahn – but that has nothing to do with the disease itself. The Marburg virus is a hemorrhagic fever virus. As with Ebola, the Marburg virus causes convulsions and bleeding of mucous membranes, skin and organs. It has a fatality rate of 90 percent.  The Marburg virus causes a rare, but severe hemorrhagic fever that has a fatality rate of 88%. It was first identified in 1967 when outbreaks of hemorrhagic fever cropped up simultaneously in Marburg, where the disease got its name, Frankfurt in Germany and Belgrade, Serbia.

Marburg and Ebola came from the Filoviridae family of viruses. They both have the capacity to cause dramatic outbreaks with the greatest fatality rates. It is transmitted to humans from fruit bats and spreads to humans through direct contact with the blood, secretions and other bodily fluids of infected humans. No anti-viral treatment or vaccine exists against the Marburg virus. In 1967, a group of lab workers in Germany (Marburg and Frankfurt) and Serbia (then Yugoslavia) contracted a new type of hemorrhagic fever from some virus-carrying African green monkeys that had been imported for research and development of polio vaccines. The Marburg virus is also BSL-4, and Marburg hemorrhagic fever has a 23 to 90 percent fatality rate. Spread through close human-to-human contact, symptoms start with a headache, fever, and a rash on the trunk, and progress to multiple organ failure and massive internal bleeding.

There is no cure, and the latest cases were reported out of Uganda at the end of 2012. An American tourist who had explored a Ugandan cave full of fruit bats known to be reservoirs of the virus contracted it and survived in 2008. (But not before bringing his sick self back to the U.S.)

2. Ebola Virus  There are five strains of the Ebola virus, each named after countries and regions in Africa: Zaire, Sudan, Tai Forest, Bundibugyo and Reston. The Zaire Ebola virus is the deadliest, with a mortality rate of 90 percent. It is the strain currently spreading through Guinea, Sierra Leone and Liberia, and beyond. Scientists say flying foxes probably brought the Zaire Ebola virus into cities.

Typically less than 100 lives a year. UPDATE: A severe Ebola outbreak was detected in West Africa in March 2014. The number of deaths in this latest outbreak has outnumbered all other known cases from previous outbreaks combined. The World Health Organization is reporting nearly 2,000 deaths in this latest outbreak.
Once a person is infected with the virus, the disease has an incubation period of 2-21 days; however, some infected persons are asymptomatic. Initial symptoms are sudden malaise, headache, and muscle pain, progressing to high fever, vomiting, severe hemorrhaging (internally and out of the eyes and mouth) and in 50%-90% of patients, death, usually within days. The likelihood of death is governed by the virulence of the particular Ebola strain involved. Ebola virus is transmitted in body fluids and secretions; there is no evidence of transmission by casual contact. There is no vaccine and no cure.

Its melodic moniker may roll off the tongue, but if you contract the virus (above), that’s not the only thing that will roll off one of your body parts (a disturbing amount of blood coming out of your eyes, for instance). Four of the five known Ebola viral strains cause Ebola hemorrhagic fever (EHF), which has killed thousands of people in sub-Saharan African nations since its discovery in 1976.

The deadly virus is named after the Ebola River in the Democratic Republic of the Congo where it was first reported, and is classified as a CDC Biosafety Level 4, a.k.a. BSL-4, making it one of the most dangerous pathogens on the planet. It is thought to spread through close contact with bodily secretions. EHF has a 50 to 90 percent mortality rate, with a rapid onset of symptoms that start with a headache and sore throat and progress to major internal and external bleeding and multiple organ failure. There’s no known cure, and the most recent cases were reported at the end of 2012 in Uganda.

3. The Hantavirus describes several types of viruses. It is named after a river where American soldiers were first thought to have been infected with the Hantavirus, during the Korean War in 1950. Symptoms include lung disease, fever and kidney failure.

70,000 Deaths a Year
Hantavirus pulmonary syndrome (HPS) is a deadly disease transmitted by infected rodents through urine, droppings, or saliva. Humans can contract the disease when they breathe in aerosolized virus. HPS was first recognized in 1993 and has since been identified throughout the United States. Although rare, HPS is potentially deadly. Rodent control in and around the home remains the primary strategy for preventing hantavirus infection. Also known as House Mouse Flu. The symptoms, which are very similar to HFRS, include tachycardia and tachypnea. Such conditions can lead to a cardiopulmonary phase, where cardiovascular shock can occur, and hospitalization of the patient is required.

There are many strains of hantavirus floating around (yep, it’s airborne) in the wake of rodents that carry the virus. Different strains, carried by different rodent species, are known to cause different types of illnesses in humans, most notably hemorrhagic fever with renal syndrome (HFRS)—first discovered during the Korean War—and hantavirus pulmonary syndrome (HPS), which reared its ugly head with a 1993 outbreak in the Southwestern United States. Severe HFRS causes acute kidney failure, while HPS gets you by filling your lungs with fluid (edema). HFRS has a mortality rate of 1 to 15 percent, while HPS is 38 percent. The U.S. saw its most recent outbreak of hantavirus—of the HPS variety—at Yosemite National Park in late 2012.

4. Avian Influenza Bird Flu The various strains of bird flu regularly cause panic – which is perhaps justified because the mortality rate is 70 percent. But in fact the risk of contracting the H5N1 strain – one of the best known – is quite low. You can only be infected through direct contact with poultry. It is said this explains why most cases appear in Asia, where people often live close to chickens.

This form of the flu is common among birds (usually poultry) and infects humans through contact with secretions of an infected bird.

Although rare, those infected have a high incidence of death. Symptoms are like those of the more common human form of influenza.

Bird flu (H5N1) has receded from international headlines for the moment, as few human cases of the deadly virus have been reported this year. But when Dutch researchers recently created an even more transmissible strain of the virus in a laboratory for research purposes, they stirred grave concerns about what would happen if it escaped into the outside world. “Part of what makes H5N1 so deadly is that most people lack an immunity to it,” explains Marc Lipsitch, a professor of epidemiology at Harvard School of Public Health (HSPH) who studies the spread of infectious diseases. “If you make a strain that’s highly transmissible between humans, as the Dutch team did, it could be disastrous if it ever escaped the lab.”

H5N1 first made global news in early 1997 after claiming two dozen victims in Hong Kong. The virus normally occurs only in wild birds and farm-raised fowl, but in those isolated early cases, it made the leap from birds to humans. It then swept unimpeded through the bodies of its initial human victims, causing massive hemorrhages in the lungs and death in a matter of days. Fortunately, during the past 15 years, the virus has claimed only 400 victims worldwide—although the strain can jump species, it hasn’t had the ability to move easily from human to human, a critical limit to its spread.

That’s no longer the case, however. In late 2011, the Dutch researchers announced the creation of an H5N1 virus transmissible through the air between ferrets (the best animal model for studying the impact of disease on humans). The news caused a storm of controversy in the popular press and heated debate among scientists over the ethics of the work. For Lipsitch and many others, the creation of the new strain was cause for alarm. “H5N1 influenza is already one of the most deadly viruses in existence,” he says. “If you make [the virus] transmissible [between humans], you have to be very concerned about what the resulting strain could do.”

To put this danger in context, the 1918 “Spanish” flu—one of the most deadly influenza epidemics on record—killed between 50 million and 100 million people worldwide, or roughly 3 to 6 percent of those infected. The more lethal SARS virus (see “The SARS Scare,” March-April 2007, page 47) killed almost 10 percent of infected patients during a 2003 outbreak that reached 25 countries worldwide. H5N1 is much more dangerous, killing almost 60 percent of those who contract the illness.

If a transmissible strain of H5N1 escapes the lab, says Lipsitch, it could spark a global health catastrophe. “It could infect millions of people in the United States, and very likely more than a billion people globally, like most successful flu strains do,” he says. “This might be one of the worst viruses—perhaps the worst virus—in existence right now because it has both transmissibility and high virulence.”

Ironically, this is why Ron Fouchier, the Dutch virologist whose lab created the new H5N1 strain, argues that studying it in more depth is crucial. If the virus can be made transmissible in the lab, he reasons, it can also occur in nature—and researchers should have an opportunity to understand as much as possible about the strain before that happens.

Lipsitch, who directs the Center for Communicable Disease Dynamics at HSPH, thinks the risks far outweigh the rewards. Even in labs with the most stringent safety requirements, such as enclosed rubber “space suits” to isolate researchers, accidents do happen. A single unprotected breath could infect a researcher, who might unknowingly spread the virus beyond the confines of the lab.

In an effort to avoid this scenario, Lipsitch has been pushing for changes in research policy in the United States and abroad. (A yearlong, voluntary global ban on H5N1 research was lifted in many countries in January, and new rules governing such research in the United States were expected in February.) Lipsitch says that none of the current research proposals he has seen “would significantly improve our preparational response to a national pandemic of H5N1. The small risk of a very large public health disaster…is not worth taking [for] scientific knowledge without an immediate public health application.” His recent op-eds in scientific journals and the popular press have stressed the importance of regulating the transmissible strain and limiting work with the virus to only a handful of qualified labs. In addition, he argues, only technicians who have the right training and experience—and have been inoculated against the virus—should be allowed to handle it.

These are simple limitations that could drastically reduce the danger of the virus spreading, he asserts, yet they’re still not popular with some researchers. He acknowledges that limiting research is an unusual practice scientifically but argues, “These are unusual circumstances.”

Lipsitch thinks a great deal of useful research can still be done on the non-transmissible strain of the virus, which would provide valuable data without the risk of accidental release. In the meantime, he hopes to make more stringent H5N1 policies a priority for U.S. and foreign laboratories. Although it’s not a perfect solution, he says, it’s far better than a nightmare scenario.

5. Lassa Virus  A nurse in Nigeria was the first person to be infected with the Lassa virus. The virus is transmitted by rodents. Cases can be endemic – which means the virus occurs in a specific region, such as in western Africa, and can reoccur there at any time. Scientists assume that 15 percent of rodents in western Africa carry the virus.

The Marburg virus under a microscope

This BSL-4 virus gives us yet another reason to avoid rodents. Lassa is carried by a species of rat in West Africa called Mastomys. It’s airborne…at least when you’re hanging around the rat’s fecal matter. Humans, however, can only spread it through direct contact with bodily secretions. Lassa fever, which has a 15 to 20 percent mortality rate, causes about 5000 deaths a year in West Africa, particularly in Sierra Leone and Liberia.

It starts with a fever and some retrosternal pain (behind the chest) and can progress to facial swelling, encephalitis, mucosal bleeding and deafness. Fortunately, researchers and medical professionals have found some success in treating Lassa fever with an antiviral drug in the early stages of the disease.

6. The Junin Virus is associated with Argentine hemorrhagic fever. People infected with the virus suffer from tissue inflammation, sepsis and skin bleeding. The problem is that the symptoms can appear to be so common that the disease is rarely detected or identified in the first instance.

A member of the genus Arenavirus, Junin virus characteristically causes Argentine hemorrhagic fever (AHF). AHF leads to major alterations within the vascular, neurological and immune systems and has a mortality rate of between 20 and 30%.  Symptoms of the disease are conjunctivitis, purpura, petechia and occasional sepsis. The symptoms of the disease are relatively indistinct and may therefore be mistaken for a different condition.

Since the discovery of the Junin virus in 1958, the geographical distribution of the pathogen, although still confined to Argentina, has risen. At the time of discovery, Junin virus was confined to an area of around 15,000 km². At the beginning of 2000, the distribution had risen to around 150,000 km². The natural hosts of Junin virus are rodents, particularly Mus musculus, Calomys spp. and Akodon azarae.

Direct rodent to human transmission only transpires when contact is made with excrement of an infected rodent. This commonly occurs via ingestion of contaminated food or water, inhalation of particles within urine or via direct contact of broken skin with rodent excrement.

7. The Crimea-Congo Fever Virus is transmitted by ticks. It is similar to the Ebola and Marburg viruses in the way it progresses. During the first days of infection, sufferers present with pin-sized bleedings in the face, mouth and the pharynx.

Transmitted through tick bites this disease is endemic (consistently present)  in most countries of West Africa and the Middle East. Although rare, CCHF has a 30% mortality rate. The most recent outbreak of the disease was in 2005 in Turkey. The Crimean-Congo hemorrhagic fever is a common disease transmitted by a tick-Bourne virus. The virus causes major hemorrhagic fever outbreaks with a fatality rate of up to 30%. It is chiefly transmitted to people through tick and livestock. Person-to-person transmission occurs through direct contact with the blood, secretions and other bodily fluids of an infected person. No vaccination exists for both humans and animals against CCHF.

8. The Machupo Virus is associated with Bolivian hemorrhagic fever, also known as black typhus. The infection causes high fever, accompanied by heavy bleedings. It progresses similar to the Junin virus. The virus can be transmitted from human to human, and rodents often the carry it.

Bolivian hemorrhagic fever (BHF), also known as black typhus or Ordog Fever, is a hemorrhagic fever and zoonotic infectious disease originating in Bolivia after infection by Machupo virus.BHF was first identified in 1963 as an ambisense RNA virus of the Arenaviridae family,by a research group led by Karl Johnson. The mortality rate is estimated at 5 to 30 percent.

Due to its pathogenicity, Machupo virus requires Biosafety Level Four conditions, the highest level.In February and March 2007, some 20 suspected BHF cases (3 fatal) were reported to the El Servicio Departmental de Salud (SEDES) in Beni Department, Bolivia, and in February 2008, at least 200 suspected new cases (12 fatal) were reported to SEDES.In November 2011, a SEDES expert involved in a serosurvey to determine the extent of Machupo virus infections in the Department after the discovery of a second confirmed case near the departmental capital of Trinidad in November, 2011, expressed concern about expansion of the virus’ distribution outside the endemic zone in Mamoré and Iténez provinces.

Bolivian hemorrhagic fever was one of three hemorrhagic fevers and one of more than a dozen agents that the United States researched as potential biological weapons before the nation suspended its biological weapons program. It was also under research by the Soviet Union, under the Biopreparat bureau.

9. Kyasanur Forest Virus  Scientists discovered the Kyasanur Forest Virus (KFD) virus in woodlands on the southwestern coast of India in 1955. It is transmitted by ticks, but scientists say it is difficult to determine any carriers. It is assumed that rats, birds and boars could be hosts. People infected with the virus suffer from high fever, strong headaches and muscle pain which can cause bleedings.

The disease has a morbidity rate of 2-10%, and affects 100-500 people annually.The symptoms of the disease include a high fever with frontal headaches, followed by hemorrhagic symptoms, such as bleeding from the nasal cavity, throat, and gums, as well as gastrointestinal bleeding.An affected person may recover in two weeks time, but the convalescent period is typically very long, lasting for several months. There will be muscle aches and weakness during this period and the affected person is unable to engage in physical activities.

There are a variety of animals thought to be reservoir hosts for the disease, including porcupines, rats, squirrels, mice and shrews. The vector for disease transmission is Haemaphysalis spinigera, a forest tick. Humans contract infection from the bite of nymphs of the tick.

The disease was first reported from Kyasanur Forest of Karnataka in India in March 1957. The disease first manifested as an epizootic outbreak among monkeys killing several of them in the year 1957. Hence the disease is also locally known as Monkey Disease or Monkey Fever. The similarity with Russian Spring-summer encephalitis was noted and the possibility of migratory birds carrying the disease was raised. Studies began to look for the possible species that acted as reservoirs for the virus and the agents responsible for transmission. Subsequent studies failed to find any involvement of migratory birds although the possibility of their role in initial establishment was not ruled out. The virus was found to be quite distinctive and not closely related to the Russian virus strains.

Antigenic relatedness is however close to many other strains including the Omsk hemorrhagic fever (OHF) and birds from Siberia have been found to show an antigenic response to KFD virus. Sequence based studies however note the distinctiveness of OHF.Early studies in India were conducted in collaboration with the US Army Medical Research Unit and this led to controversy and conspiracy theories.

Subsequent studies based on sequencing found that the Alkhurma virus, found in Saudi Arabia is closely related. In 1989 a patient in Nanjianin, China was found with fever symptoms and in 2009 its viral gene sequence was found to exactly match with that of the KFD reference virus of 1957. This has however been questioned since the Indian virus shows variations in sequence over time and the exact match with the virus sequence of 1957 and the Chinese virus of 1989 is not expected.

This study also found using immune response tests that birds and humans in the region appeared to have been exposed to the virus.Another study has suggested that the virus is recent in origin dating the nearest common ancestor of it and related viruses to around 1942, based on the estimated rate of sequence substitutions. The study also raises the possibility of bird involvement in long-distance transfer. It appears that these viruses diverged 700 years ago.

10. Dengue Fever is a constant threat. If you’re planning a holiday in the tropics, get informed about dengue. Transmitted by mosquitoes, dengue affects between 50 and 100 million people a year in popular holiday destinations such as Thailand and India. But it’s more of a problem for the 2 billion people who live in areas that are threatened by dengue fever.

25,000 Deaths a year Also known as ‘breakbone fever’ due to the extreme pain felt during fever, is an relatively new disease caused by one of four closely-related viruses. WHO estimates that a whopping 2.5 billion people (two fifths of the World’s population) are at risk from dengue. It puts the total number of infections at around 50 million per year, and is now epidemic in more than 100 countries.

Dengue viruses are transferred to humans through the bites of infective female Aedes mosquitoes. The dengue virus circulates in the blood of a human for two to seven days, during the same time they have the fever. It usually appears first on the lower limbs and the chest; in some patients, it spreads to cover most of the body. There may also be severe retro-orbital pain, (a pain from behind the eyes that is distinctive to Dengue infections), and gastritis with some combination of associated abdominal pain, nausea, vomiting coffee-grounds-like congealed blood, or severe diarrhea.

The leading cause of death in the tropics and subtropics is the infection brought on by the dengue virus, which causes a high fever, severe headache, and, in the worst cases, hemorrhaging. The good news is that it’s treatable and not contagious. The bad news is there’s no vaccine, and you can get it easily from the bite of an infected mosquito—which puts at least a third of the world’s human population at risk. The CDC estimates that there are over 100 million cases of dengue fever each year. It’s a great marketing tool for bug spray.

11. HIV 3.1 Million Lives a Year Human Immunodeficiency Virus has claimed the lives of more than 25 million people since 1981. HIV gets to the immune system by infecting important cells, including helper cells called CD4+ T cells, plus macrophanges and dendritic cells. Once the virus has taken hold, it systematically kills these cells, damaging the infected person’s immunity and leaving them more at risk from infections.

The majority of people infected with HIV go on to develop AIDS. Once a patient has AIDS common infections and tumours normally controlled by the CD4+ T cells start to affect the person.  
In the latter stages of the disease, pneumonia and various types of herpes can infect the patient and cause death.

Human immunodeficiency virus infection / acquired immunodeficiency syndrome (HIV/AIDS) is a disease of the human immune system caused by infection with human immunodeficiency virus (HIV). The term HIV/AIDS represents the entire range of disease caused by the human immunodeficiency virus from early infection to late stage symptoms. During the initial infection, a person may experience a brief period of influenza-like illness. This is typically followed by a prolonged period without symptoms. As the illness progresses, it interferes more and more with the immune system, making the person much more likely to get infections, including opportunistic infections and tumors that do not usually affect people who have working immune systems.

HIV is transmitted primarily via unprotected sexual intercourse (including anal and oral sex), contaminated blood transfusions, hypodermic needles, and from mother to child during pregnancy, delivery, or breastfeeding. Some bodily fluids, such as saliva and tears, do not transmit HIV. Prevention of HIV infection, primarily through safe sex and needle-exchange programs, is a key strategy to control the spread of the disease. There is no cure or vaccine; however, antiretroviral treatment can slow the course of the disease and may lead to a near-normal life expectancy. While antiretroviral treatment reduces the risk of death and complications from the disease, these medications are expensive and have side effects. Without treatment, the average survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype.

Genetic research indicates that HIV originated in west-central Africa during the late nineteenth or early twentieth century. AIDS was first recognized by the United States Centers for Disease Control and Prevention (CDC) in 1981 and its cause—HIV infection—was identified in the early part of the decade. Since its discovery, AIDS has caused an estimated 36 million deaths worldwide (as of 2012). As of 2012, approximately 35.3 million people are living with HIV globally. HIV/AIDS is considered a pandemic—a disease outbreak which is present over a large area and is actively spreading.

HIV/AIDS has had a great impact on society, both as an illness and as a source of discrimination. The disease also has significant economic impacts. There are many misconceptions about HIV/AIDS such as the belief that it can be transmitted by casual non-sexual contact. The disease has also become subject to many controversies involving religion. It has attracted international medical and political attention as well as large-scale funding since it was identified in the 1980s

 

12. Rotavirus 61,000 Lives a Year  According to the WHO, this merciless virus causes the deaths of more than half a million children every year. In fact, by the age of five, virtually every child on the planet has been infected with the virus at least once. Immunity builds up with each infection, so subsequent infections are milder. However, in areas where adequate healthcare is limited the disease is often fatal. Rotavirus infection usually occurs through ingestion of contaminated stool.

Because the virus is able to live a long time outside of the host, transmission can occur through ingestion of contaminated food or water, or by coming into direct contact with contaminated surfaces, then putting hands in the mouth.
Once it’s made its way in, the rotavirus infects the cells that line the small intestine and multiplies. It emits an enterotoxin, which gives rise to gastroenteritis.

13. Smallpox   Officially eradicated – Due to it’s long history, it impossible to estimate the carnage over the millennia Smallpox localizes in small blood vessels of the skin and in the mouth and throat. In the skin, this results in a characteristic maculopapular rash, and later, raised fluid-filled blisters. It has an overall mortality rate of 30–35%. Smallpox is believed to have emerged in human populations about 10,000 BC. The disease killed an estimated 400,000 Europeans per year during the closing years of the 18th century (including five reigning monarchs), and was responsible for a third of all blindness. Of all those infected, 20–60%—and over 80% of infected children—died from the disease.
Smallpox was responsible for an estimated 300–500 million deaths during the 20th century alone. In the early 1950s an estimated 50 million cases of smallpox occurred in the world each year.

As recently as 1967, the World Health Organization (WHO) estimated that 15 million people contracted the disease and that two million died in that year. After successful vaccination campaigns throughout the 19th and 20th centuries, the WHO certified the eradication of smallpox in December 1979.
Smallpox is one of only two infectious diseases to have been eradicated by humans, the other being Rinderpest, which was unofficially declared eradicated in October 2010.

The virus that causes smallpox wiped out hundreds of millions of people worldwide over thousands of years. We can’t even blame it on animals either, as the virus is only carried by and contagious for humans. There are several different types of smallpox disease that result from an infection ranging from mild to fatal, but it is generally marked by a fever, rash, and blistering, oozing pustules that develop on the skin. Fortunately, smallpox was declared eradicated in 1979, as the result of successful worldwide implementation of the vaccine.

14. Hepatitis B  521,000 Deaths a Year A third of the World’s population (over 2 billion people) has come in contact with this virus, including 350 million chronic carriers. In China and other parts of Asia, up to 10% of the adult population is chronically infected. The symptoms of acute hepatitis B include yellowing of the skin of eyes, dark urine, vomiting, nausea, extreme fatigue, and abdominal pain.

Luckily, more than 95% of people who contract the virus as adults or older children will make a full recovery and develop immunity to the disease. In other people, however, hepatitis B can bring on chronic liver failure due to cirrhosis or cancer.

Hepatitis B is an infectious illness of the liver caused by the hepatitis B virus (HBV) that affects hominoidea, including humans. It was originally known as "serum hepatitis". Many people have no symptoms during the initial infected. Some develop an acute illness with vomiting, yellow skin, dark urine and abdominal pain. Often these symptoms last a few weeks and rarely result in death. It may take 30 to 180 days for symptoms to begin. Less than 10% of those infected develop chronic hepatitis B. In those with chronic disease cirrhosis and liver cancer may eventually develop.

The virus is transmitted by exposure to infectious blood or body fluids.  Infection around the time of birth is the most common way the disease is acquired in areas of the world where is common. In areas where the disease is uncommon intravenous drug use and sex are the most common routes of infection. Other risk factors include working in a healthcare setting, blood transfusions, dialysis, sharing razors or toothbrushes with an infected person, travel in countries where it is common, and living in an institution.

Tattooing and acupuncture led to a significant number of cases in the 1980s; however, this has become less common with improved sterility. The hepatitis B viruses cannot be spread by holding hands, sharing eating utensils or drinking glasses, kissing, hugging, coughing, sneezing, or breastfeeding.  The hepatitis B virus is a hepadnavirus—hepa from hepatotropic (attracted to the liver) and dna because it is a DNA virus. The viruses replicate through an RNA intermediate form by reverse transcription, which in practice relates them to retroviruses.It is 50 to 100 times more infectious than HIV.

The infection has been preventable by vaccination since 1982. During the initial infected care is based on the symptoms present. In those who developed chronic disease antiviral medication such as tenofovir or interferon maybe useful, however are expensive.

About a third of the world population has been infected at one point in their lives, including 350 million who are chronic carriers. Over 750,000 people die of hepatitis B a year. The disease has caused outbreaks in parts of Asia and Africa, and it is now only common in China. Between 5 and 10% of adults in sub-Saharan Africa and East Asia have chronic disease. Research is in progress to create edible HBV vaccines in foods such as potatoes, carrots, and bananas.In 2004, an estimated 350 million individuals were infected worldwide. National and regional prevalence ranges from over 10% in Asia to under 0.5% in the United States and northern Europe. Routes of infection include vertical transmission (such as through childbirth), early life horizontal transmission (bites, lesions, and sanitary habits), and adult horizontal transmission (sexual contact, intravenous drug use).

The primary method of transmission reflects the prevalence of chronic HBV infection in a given area. In low prevalence areas such as the continental United States and Western Europe, injection drug abuse and unprotected sex are the primary methods, although other factors may also be important. In moderate prevalence areas, which include Eastern Europe, Russia, and Japan, where 2–7% of the population is chronically infected, the disease is predominantly spread among children. In high-prevalence areas such as China and South East Asia, transmission during childbirth is most common, although in other areas of high endemicity such as Africa, transmission during childhood is a significant factor. The prevalence of chronic HBV infection in areas of high endemicity is at least 8% with 10-15% prevalence in Africa/Far East. As of 2010, China has 120 million infected people, followed by India and Indonesia with 40 million and 12 million, respectively. According to World Health Organization (WHO), an estimated 600,000 people die every year related to the infection. In the United States about 19,000 new cases occurred in 2011 down nearly 90% from 1990.

Acute infection with hepatitis B virus is associated with acute viral hepatitis – an illness that begins with general ill-health, loss of appetite, nausea, vomiting, body aches, mild fever, and dark urine, and then progresses to development of jaundice. It has been noted that itchy skin has been an indication as a possible symptom of all hepatitis virus types. The illness lasts for a few weeks and then gradually improves in most affected people. A few people may have more severe liver disease (fulminant hepatic failure), and may die as a result. The infection may be entirely asymptomatic and may go unrecognized.

Chronic infection with hepatitis B virus either may be asymptomatic or may be associated with a chronic inflammation of the liver (chronic hepatitis), leading to cirrhosis over a period of several years. This type of infection dramatically increases the incidence of hepatocellular carcinoma (liver cancer). Across Europe hepatitis B and C cause approximately 50% of hepatocellular carcinomas. Chronic carriers are encouraged to avoid consuming alcohol as it increases their risk for cirrhosis and liver cancer. Hepatitis B virus has been linked to the development of membranous glomerulonephritis (MGN).

Symptoms outside of the liver are present in 1–10% of HBV-infected people and include serum-sickness–like syndrome, acute necrotizing vasculitis (polyarteritis nodosa), membranous glomerulonephritis, and papular acrodermatitis of childhood (Gianotti–Crosti syndrome). The serum-sickness–like syndrome occurs in the setting of acute hepatitis B, often preceding the onset of jaundice. The clinical features are fever, skin rash, and polyarteritis. The symptoms often subside shortly after the onset of jaundice, but can persist throughout the duration of acute hepatitis B.  About 30–50% of people with acute necrotizing vasculitis (polyarteritis nodosa) are HBV carriers. HBV-associated nephropathy has been described in adults but is more common in children.Membranous glomerulonephritis is the most common form. Other immune-mediated hematological disorders, such as essential mixed cryoglobulinemia and aplastic anemia.

15. Influenza 500,000 Deaths a Year Influenza has been a prolific killer for centuries. The symptoms of influenza were first described more than 2,400 years ago by Hippocrates. Pandemics generally occur three times a century, and can cause millions of deaths. The most fatal pandemic on record was the Spanish flu outbreak in 1918, which caused between 20 million and 100 million deaths. In order to invade a host, the virus shell includes proteins that bind themselves to receptors on the outside of cells in the lungs and air passages of the victim. Once the virus has latched itself onto the cell it takes over so much of its machinery that the cell dies. Dead cells in the airways cause a runny nose and sore throat. Too many dead cells in the lungs causes death.

 
Vaccinations against the flu are common in developed countries. However, a vaccination that is effective one year may not necessarily work the next year, due to the way the rate at which a flu virus evolves and the fact that new strains will soon replace older ones. No virus can claim credit for more worldwide pandemics and scares than influenza.

The outbreak of the Spanish flu in 1918 is generally considered to be one of the worst pandemics in human history, infecting 20 to 40 percent of the world’s population and killing 50 million in the span of just two years. (A reconstruction of that virus is above.) The swine flu was its most recent newsmaker, when a 2009 pandemic may have seen as many as 89 million people infected worldwide.

Effective influenza vaccines exist, and most people easily survive infections. But the highly infectious respiratory illness is cunning—the virus is constantly mutating and creating new strains. Thousands of strains exist at any given time, many of them harmless, and vaccines available in the U.S. cover only about 40 percent of the strains at large each year.

16. Hepatitis C  56,000 Deaths a Year An estimated 200-300 million people worldwide are infected with hepatitis C.

 

Most people infected with hepatitis C don’t have any symptoms and feel fine for years. However, liver damage invariably rears its ugly head over time, often decades after first infection. In fact, 70% of those infected develop chronic liver disease, 15% are struck with cirrhosis and 5% can die from liver cancer or cirrhosis. In the USA, hepatitis C is the primary reason for liver transplants.

Hepatitis C is an infectious disease affecting primarily the liver, caused by the hepatitis C virus (HCV). The infection is often asymptomatic, but chronic infection can lead to scarring of the liver and ultimately to cirrhosis, which is generally apparent after many years. In some cases, those with cirrhosis will go on to develop liver failure, liver cancer, or life-threatening esophageal and gastric varices.

HCV is spread primarily by blood-to-blood contact associated with intravenous drug use, poorly sterilized medical equipment, and transfusions. An estimated 150–200 million people worldwide are infected with hepatitis C. The existence of hepatitis C (originally identifiable only as a type of non-A non-B hepatitis) was suggested in the 1970s and proven in 1989. Hepatitis C infects only humans and chimpanzees.

The virus persists in the liver in about 85% of those infected. This chronic infection can be treated with medication: the standard therapy is a combination of peginterferon and ribavirin, with either boceprevir or telaprevir added in some cases. Overall, 50–80% of people treated are cured. Those who develop cirrhosis or liver cancer may require a liver transplant. Hepatitis C is the leading reason for liver transplantation, though the virus usually recurs after transplantation. No vaccine against hepatitis C is available.

Hepatitis C infection causes acute symptoms in 15% of cases. Symptoms are generally mild and vague, including a decreased appetite, fatigue, nausea, muscle or joint pains, and weight loss and rarely does acute liver failure result. Most cases of acute infection are not associated with jaundice. The infection resolves spontaneously in 10–50% of cases, which occurs more frequently in individuals who are young and female.

About 80% of those exposed to the virus develop a chronic infection.  This is defined as the presence of detectable viral replication for at least six months. Most experience minimal or no symptoms during the initial few decades of the infection.Chronic hepatitis C can be associated with fatigue and mild cognitive problems. Chronic infection after several years may cause cirrhosis or liver cancer. The liver enzymes are normal in 7–53%.  Late relapses after apparent cure have been reported, but these can be difficult to distinguish from reinfection.

Fatty changes to the liver occur in about half of those infected and are usually present before cirrhosis develops.  Usually (80% of the time) this change affects less than a third of the liver. Worldwide hepatitis C is the cause of 27% of cirrhosis cases and 25% of hepatocellular carcinoma.  About 10–30% of those infected develop cirrhosis over 30 years. Cirrhosis is more common in those also infected with hepatitis B, schistosoma, or HIV, in alcoholics and in those of male gender. In those with hepatitis C, excess alcohol increases the risk of developing cirrhosis 100-fold.Those who develop cirrhosis have a 20-fold greater risk of hepatocellular carcinoma. This transformation occurs at a rate of 1–3% per year.  Being infected with hepatitis B in additional to hepatitis C increases this risk further.

Liver cirrhosis may lead to portal hypertension, ascites (accumulation of fluid in the abdomen), easy bruising or bleeding, varices (enlarged veins, especially in the stomach and esophagus), jaundice, and a syndrome of cognitive impairment known as hepatic encephalopathy. Ascites occurs at some stage in more than half of those who have a chronic infection.

The most common problem due to hepatitis C but not involving the liver is mixed cryoglobulinemia (usually the type II form) — an inflammation of small and medium-sized blood vessels. Hepatitis C is also associated with Sjögren’s syndrome (an autoimmune disorder); thrombocytopenia; lichen planus; porphyria cutanea tarda; necrolytic acral erythema; insulin resistance; diabetes mellitus; diabetic nephropathy; autoimmune thyroiditis and B-cell lymphoproliferative disorders.  Thrombocytopenia is estimated to occur in 0.16% to 45.4% of people with chronic hepatitis C. 20–30% of people infected have rheumatoid factor — a type of antibody. Possible associations include Hyde’s prurigo nodularis and membranoproliferative glomerulonephritis. Cardiomyopathy with associated arrhythmias has also been reported. A variety of central nervous system disorders have been reported.  Chronic infection seems to be associated with an increased risk of pancreatic cancer.

Persons who have been infected with hepatitis C may appear to clear the virus but remain infected. The virus is not detectable with conventional testing but can be found with ultra-sensitive tests.The original method of detection was by demonstrating the viral genome within liver biopsies, but newer methods include an antibody test for the virus’ core protein and the detection of the viral genome after first concentrating the viral particles by ultracentrifugation. A form of infection with persistently moderately elevated serum liver enzymes but without antibodies to hepatitis C has also been reported. This form is known as cryptogenic occult infection.

Several clinical pictures have been associated with this type of infection. It may be found in people with anti-hepatitis-C antibodies but with normal serum levels of liver enzymes; in antibody-negative people with ongoing elevated liver enzymes of unknown cause; in healthy populations without evidence of liver disease; and in groups at risk for HCV infection including those on haemodialysis or family members of people with occult HCV. The clinical relevance of this form of infection is under investigation. The consequences of occult infection appear to be less severe than with chronic infection but can vary from minimal to hepatocellular carcinoma.

The rate of occult infection in those apparently cured is controversial but appears to be low 40% of those with hepatitis but with both negative hepatitis C serology and the absence of detectable viral genome in the serum have hepatitis C virus in the liver on biopsy.How commonly this occurs in children is unknown.
There is no cure, no vaccine.

17. Measle  197,000 Deaths a Year Measles, also known as Rubeola, has done a pretty good job of killing people throughout the ages. Over the last 150 years, the virus has been responsible for the deaths of around 200 million people. The fatality rate from measles for otherwise healthy people in developed countries is 3 deaths per thousand cases, or 0.3%. In underdeveloped nations with high rates of malnutrition and poor healthcare, fatality rates have been as high as 28%. In immunocompromised patients (e.g. people with AIDS) the fatality rate is approximately 30%.

During the 1850s, measles killed a fifth of Hawaii’s people. In 1875, measles killed over 40,000 Fijians, approximately one-third of the population. In the 19th century, the disease decimated the Andamanese population. In 1954, the virus causing the disease was isolated from an 11-year old boy from the United States, David Edmonston, and adapted and propagated on chick embryo tissue culture.

To date, 21 strains of the measles virus have been identified.

18. Yellow Fever  30,000 Deaths a Year. Yellow fever is an acute viral hemorrhagic disease transmitted by the bite of female mosquitoes and is found in tropical and subtropical areas in South America and Africa. The only known hosts of the virus are primates and several species of mosquito. The origin of the disease is most likely to be Africa, from where it was introduced to South America through the slave trade in the 16th century. Since the 17th century, several major epidemics of the disease have been recorded in the Americas, Africa and Europe. In the 19th century, yellow fever was deemed one of the most dangerous infectious diseases.

Yellow fever presents in most cases with fever, nausea, and pain and it generally subsides after several days. In some patients, a toxic phase follows, in which liver damage with jaundice (giving the name of the disease) can occur and lead to death. Because of the increased bleeding tendency (bleeding diathesis), yellow fever belongs to the group of hemorrhagic fevers.

Since the 1980s, the number of cases of yellow fever has been increasing, making it a reemerging disease Transmitted through infected mosquitoes, Yellow Fever is still a serious problem in countries all over the world and a serious health risk for travelers to Africa, South America and some areas in the Caribbean.  Fatality rates range from 15 to over 50%. Symptoms include high fever, headache, abdominal pain, fatigue, vomiting and nausea.

Yellow fever is a hemorrhagic fever transmitted by infected mosquitoes. The yellow is in reference to the yellow color (jaundice) that affects some patients. The virus is endemic in tropical areas in Africa and South America.

The disease typically occurs in two phases. The first phase typically causes fever, headache, muscle pain and back pain, chills and nausea. Most patients recover from these symptoms while 15% progresses to the toxic second phase. High fever returns, jaundice becomes apparent, patient complains of abdominal pain with vomiting, and bleeding in the mouth, eyes, nose or stomach occurs. Blood appears in the stool or vomit and kidney function deteriorates. 50% of the patients that enter the toxic phase die within 10 to 14 days.

There is no treatment for yellow fever. Patients are only given supportive care for fever, dehydration and respiratory failure. Yellow fever is preventable through vaccination.

19. Rabies  55,000 Deaths a Year Rabies is almost invariably fatal if post-exposure prophylaxis is not administered prior to the onset of severe symptoms. If there wasn’t a vaccine, this would be the most deadly virus on the list.

It is a zoonotic virus transmitted through the bite of an animal. The virus worms its way into the brain along the peripheral nerves. The incubation phase of the rabies disease can take up to several months, depending on how far it has to go to reach the central nervous system. It provokes acute pain, violent movements, depression, uncontrollable excitement, and inability to swallow water (rabies is often known as ‘hydrophobia’). After these symptoms subside the fun really starts as the infected person experiences periods of mania followed by coma then death, usually caused by respiratory insufficiency.

Rabies has a long and storied history dating back to 2300 B.C., with records of Babylonians who went mad and died after being bitten by dogs. While this virus itself is a beast, the sickness it causes is now is wholly preventable if treated immediately with a series of vaccinations (sometimes delivered with a terrifyingly huge needle in the abdomen). We have vaccine inventor Louis Pasteur to thank for that.

Exposure to rabies these days, while rare in the U.S., still occurs as it did thousands of years ago—through bites from infected animals. If left untreated after exposure, the virus attacks the central nervous system and death usually results. The symptoms of an advanced infection include delirium, hallucinations and raging, violent behavior in some cases, which some have argued makes rabies eerily similar to zombification. If rabies ever became airborne, we might actually have to prepare for that zombie apocalypse after all.

21. Common Cold  No known cure The common cold is the most frequent infectious disease in humans with on average two to four infections a year in adults and up to 6–12 in children. Collectively, colds, influenza, and other infections with similar symptoms are included in the diagnosis of influenza-like illness.

They may also be termed upper respiratory tract infections (URTI). Influenza involves the lungs while the common cold does not.
It’s annoying as hell, but there’s nothing to do but wave the white flag on this one.
Virus: Infinity. People: 0

22. Anthrax  Anthrax is a diseased caused by a bacterium called Bacillus Anthracis. There are three types of anthrax, skin, lung, and digestive. Anthrax has lately become a major world issue for its ability to become an epidemic and spread quickly and easily among people through contact with spores.

It is important to know that  Anthrax is not spread from person to person, but is through contact/handling of products containing spores. Flu like symptoms, nausea, and blisters are common symptoms of exposure. Inhalational anthrax and gastrointestinal anthrax are serious issue because of their high mortality rates ranging from 50 to 100%.

Anthrax is a severe infectious disease caused by the bacteria Bacillus anthracis. This type of bacteria produces spores that can live for years in the soil. Anthrax is more common in farm animals, though humans can get infected as well. Anthrax is not contagious. A person can get infected only when the bacteria gets into the skin, lungs or  digestive tract.

There are three types of anthrax: skin anthrax, inhalation anthrax and gastrointestinal anthrax. Skin anthrax symptoms include fever, muscle aches, headache, nausea and vomiting. Inhalation anthrax begins with flu-like symptoms, which progresses  with severe respiratory distress. Shock, coma and then death follows. Most patients do not recover even if given appropriate antibiotics due to the toxins released by the anthrax bacteria. Gastrointestinal anthrax symptoms include fever, nausea, abdominal pain and bloody diarrhea.

Anthrax is treated with antibiotics.

23. Malaria  Malaria is a mosquito-borne illness caused by parasite. Although malaria can be prevented and treated, it is often fatal.

Each year about 1 million people die from Malaria.  Common symptoms include fever, chills, headache. Sweats, and fatigue. Malaria is a serious disease caused by Plasmodium parasites that infects Anopheles mosquitoes which feeds on humans. Initial symptoms include high fever, shaking chills, headache and vomiting – symptoms that may be too  mild to be identified as malaria. If not treated within 24 hours, it can progress to severe illnesses that could lead to death.

The WHO estimates that malaria caused 207,000,000 clinical episodes and 627,000 deaths, mostly among African children,  in 2012. About 3.5 billion people from 167 countries live in areas at risk of malaria transmission.

24. Cholera  Due to the severe dehydration it causes, if left untreated Cholera can cause death within hours. In 1991 a major outbreak occurred in South America though currently few cases are known outside of Sub-Saharan Africa.

Symptoms include severe diarrhea, vomiting and leg cramping. Cholera is usually contracted through ingestion of contaminated water or food. Cholera is an acute intestinal infection caused by a bacterium called Vibrio cholera. It has an incubation period of less than a day to five days and causes painless, watery diarrhea that quickly leads to severe dehydration and death if treatment is not promptly given.

Cholera remains a global problem and continues to be a challenge for countries where access to safe drinking water and sanitation is a problem.

25.  Typhoid Fever  Patients with typhoid fever sometimes demonstrate a rash of flat, rose-colored spots and a sustained fever of 103 to 104.

Typhoid is contracted through contact with the S. Typhi bacteria, which is carried by humans in both their blood stream and stool. Over 400 cases occur in the US, 20% of those who contract it die. Typhoid fever is a serious and potentially fatal disease caused by the bacterium Salmonella Typhi. This type of bacteria lives only in humans. People sick with typhoid fever carry the bacteria in their bloodstream and intestinal tract and transmit the bacteria through their stool.

A person can get typhoid fever by drinking or eating food contaminated with Salmonella Typhi or if contaminated sewage gets into the water used for drinking or washing dishes.

Typhoid fever symptoms include high fever, weakness, headache, stomach pains or loss of appetite. Typhoid fever is determined by testing the presence of Salmonella Typhi in the stool or blood of an infected person. Typhoid fever is treated with antibiotics.

26. SARS (Severe Acute Respiratory Syndrome) and the MERS VIRUS A new Pneumonia disease that emerged in China in 2003. After news of the outbreak of SARS China tried to silence news about it both internal and international news , SARS spread rapidly, reaching neighboring countries Hong Kong and Vietnam in late February 2003, and then to other countries via international travelers.Canada Had a outbreak that was fairly well covered and cost Canada quite a bit financially

The last case of this epidemic occurred in June 2003. In that outbreak, 8069 cases arise that killed 775 people. There is speculation that this disease is Man-Made SARS, SARS has symptoms of flu and may include: fever, cough, sore throat and other non-specific symptoms.

The only symptom that is common to all patients was fever above 38 degrees Celsius. Shortness of breath may occur later. There is currently no vaccine for the disease so that countermeasures can only assist the breathing apparatus. The virus was said to be the Virus of the End Times

27.  MERS(Middle Eastern Respiratory Syndrome) The Middle East respiratory syndrome coronavirus (MERS-CoV), also termed EMC/2012 (HCoV-EMC/2012), is positive-sense, single-stranded RNA novel species of the genus Betacoronavirus.

First called novel coronavirus 2012 or simply novel coronavirus, it was first reported in 2012 after genome sequencing of a virus isolated from sputum samples from patients who fell ill in a 2012 outbreak of a new flu.

As of June 2014, MERS-CoV cases have been reported in 22 countries, including Saudi Arabia, Malaysia, Jordan, Qatar, Egypt, the United Arab Emirates, Kuwait, Oman, Algeria, Bangladesh, the Philippines (still MERS-free), Indonesia (none was confirmed), the United Kingdom, and the United States. Almost all cases are somehow linked to Saudi Arabia. In the same article it was reported that Saudi authorities’ errors in response to MERS-CoV were a contributing factor to the spread of this deadly virus.

27. Enterovirus (Brain Inflammation) Entero virus is a disease of the hands, feet and mouth, and we can not ignored occasional Brain Inflammation. Enterovirus attack symptoms are very similar to regular flu symptoms so its difficult to detect it, such as fever, sometimes accompanied by dizziness and weakness and pain.

Next will come the little red watery bumps on the palms and feet following oral thrush. In severe conditions, Enterovirus can attack the nerves and brain tissue to result in death.

The virus is easily spread through direct contact with patients. Children are the main victims of the spread of enterovirus in China. Since the first victim was found but reporting was delayed until several weeks later.

24 thousand people have contracted the enterovirus. More than 30 of them died mostly children. The virus is reported to have entered Indonesia and infecting three people in Sumatra.  2014Enterovirus 68 is presently spreading across North America mainly and started in the USA has probably spread to Canada and Mexico by now. Enterovirus 68’s spread is unprecedented up till now

28.  The Black Plague  The 1918 flu virus and HIV are the biggest killers of modern times. But back in the 14th century, the bacterium that causes bubonic plague, or the Black Death as it was also known, was the baddest bug of all. In just a few years, from 1347 to 1351, the plague killed off about 75,000,000 people worldwide, including one-third of the entire population of Europe at that time.

It spread through Asia, Italy, North Africa, Spain, Normandy, Switzerland, and eastward into Hungary. After a brief break, it crossed into England, Scotland, and then to Norway, Sweden, Denmark, Iceland and Greenland.

Yersinia pestis, the plague bacteria
Courtesy of Neal Chamberlain

The plague bacterium is called Yersinia <yer-sin-ee-uh> pestis. There are two main forms of the disease. In the bubonic <boo-bah-nick> form, the bacteria cause painful swellings as large as an orange to form in the armpits, neck and groin. These swellings, or buboes, often burst open, oozing blood and pus. Blood vessels leak blood that puddles under the skin, giving the skin a blackened look. That’s why the disease became known as the Black Death. At least half of its victims die within a week.

The pneumonic <new-mon-ick> form of plague causes victims to sweat heavily and cough up blood that starts filling their lungs. Almost no one survived it during the plague years. Yersinia pestis is the deadliest microbe we’ve ever known, although HIV might catch up to it. Yersinia pestis is still around in the world. Fortunately, with bacteria-killing antibiotics and measures to control the pests—rats and mice—that spread the bacteria, we’ve managed to conquer this killer.

29. Human Papillomavirus  Human papillomavirus (HPV) is a DNA virus from the papillomavirus family that is capable of infecting humans. Like all papillomaviruses, HPVs establish productive infections only in keratinocytes of the skin or mucous membranes.

Most HPV infections are subclinical and will cause no physical symptoms; however, in some people subclinical infections will become clinical and may cause benign papillomas (such as warts [verrucae] or squamous cell papilloma), or cancers of the cervix, vulva, vagina, penis, oropharynx and anus.HPV has been linked with an increased risk of cardiovascular disease. In addition, HPV 16 and 18 infections are a cause of a unique type of oropharyngeal (throat) cancer and are believed to cause 70% of cervical cancer, which have available vaccines, see HPV vaccine.

More than 30 to 40 types of HPV are typically transmitted through sexual contact and infect the anogenital region. Some sexually transmitted HPV types may cause genital warts. Persistent infection with "high-risk" HPV types—different from the ones that cause skin warts—may progress to precancerous lesions and invasive cancer. High-risk HPV infection is a cause of nearly all cases of cervical cancer.However, most infections do not cause disease.

Seventy percent of clinical HPV infections, in young men and women, may regress to subclinical in one year and ninety percent in two years. However, when the subclinical infection persists—in 5% to 10% of infected women—there is high risk of developing precancerous lesions of the vulva and cervix, which can progress to invasive cancer. Progression from subclinical to clinical infection may take years; providing opportunities for detection and treatment of pre-cancerous lesions.

In more developed countries, cervical screening using a Papanicolaou (Pap) test or liquid-based cytology is used to detect abnormal cells that may develop into cancer. If abnormal cells are found, women are invited to have a colposcopy. During a colposcopic inspection, biopsies can be taken and abnormal areas can be removed with a simple procedure, typically with a cauterizing loop or, more commonly in the developing world—by freezing (cryotherapy).

Treating abnormal cells in this way can prevent them from developing into cervical cancer. Pap smears have reduced the incidence and fatalities of cervical cancer in the developed world, but even so there were 11,000 cases and 3,900 deaths in the U.S. in 2008. Cervical cancer has substantial mortality worldwide, there are an estimated 490,000 cases and 270,000 deaths each year.

It is true that infections caused by human papillomavirus (HPV) are not fatal, but chronic infection may result in cervical cancer. Apparently, HPV is responsible for almost all cervical cancers (approx. 99%). HPV results in 275,000 deaths per year.

30. Henipaviruses The genus Henipavirus comprises of 3 members which are Hendra virus (HeV), Nipah virus (NiV), and Cedar virus (CedPV). The second one was introduced in the middle of 2012, although affected no human, and is therefore considered harmless. The rest of the two viruses, however, are lethal with mortality rate up to 50-100%.

Hendra virus (originally Equine morbillivirus) was discovered in September 1994 when it caused the deaths of thirteen horses, and a trainer at a training complex in Hendra, a suburb of Brisbane in Queensland, Australia.

The index case, a mare, was housed with 19 other horses after falling ill, and died two days later. Subsequently, all of the horses became ill, with 13 dying. The remaining 6 animals were subsequently euthanized as a way of preventing relapsing infection and possible further transmission.The trainer, Victory (‘Vic’) Rail, and a stable hand were involved in nursing the index case, and both fell ill with an influenza-like illness within one week of the first horse’s death. The stable hand recovered while Mr Rail died of respiratory and renal failure. The source of the virus was most likely frothy nasal discharge from the index case.

A second outbreak occurred in August 1994 (chronologically preceding the first outbreak) in Mackay 1,000 km north of Brisbane resulting in the deaths of two horses and their owner. The owner, Mark Preston, assisted in necropsies of the horses and within three weeks was admitted to hospital suffering from meningitis. Mr Preston recovered, but 14 months later developed neurologic signs and died. This outbreak was diagnosed retrospectively by the presence of Hendra virus in the brain of the patient.

A survey of wildlife in the outbreak areas was conducted, and identified pteropid fruit bats as the most likely source of Hendra virus, with a seroprevalence of 47%. All of the other 46 species sampled were negative. Virus isolations from the reproductive tract and urine of wild bats indicated that transmission to horses may have occurred via exposure to bat urine or birthing fluids.  However, the only attempt at experimental infection reported in the literature, conducted at CSIRO Geelong, did not result in infection of a horse from infected flying foxes. This study looked at potential infection between bats, horses and cats, in various combinations. The only species that was able to infect horses was the cat (Felix spp.)

Nipah virus was identified in April 1999, when it caused an outbreak of neurological and respiratory disease on pig farms in peninsular Malaysia, resulting in 257 human cases, including 105 human deaths and the culling of one million pigs.  In Singapore, 11 cases, including one death, occurred in abattoir workers exposed to pigs imported from the affected Malaysian farms. The Nipah virus has been classified by the Centers for Disease Control and Prevention as a Category C agent. The name "Nipah" refers to the place, Kampung Baru Sungai Nipah in Negeri Sembilan State, Malaysia, the source of the human case from which Nipah virus was first isolated.

The outbreak was originally mistaken for Japanese encephalitis (JE), however, physicians in the area noted that persons who had been vaccinated against JE were not protected, and the number of cases among adults was unusual Despite the fact that these observations were recorded in the first month of the outbreak, the Ministry of Health failed to react accordingly, and instead launched a nationwide campaign to educate people on the dangers of JE and its vector, Culex mosquitoes.

Symptoms of infection from the Malaysian outbreak were primarily encephalitic in humans and respiratory in pigs. Later outbreaks have caused respiratory illness in humans, increasing the likelihood of human-to-human transmission and indicating the existence of more dangerous strains of the virus. Based on seroprevalence data and virus isolations, the primary reservoir for Nipah virus was identified as Pteropid fruit bats, including Pteropus vampyrus (Large Flying Fox), and Pteropus hypomelanus (Small flying fox), both of which occur in Malaysia.

The transmission of Nipah virus from flying foxes to pigs is thought to be due to an increasing overlap between bat habitats and piggeries in peninsular Malaysia. At the index farm, fruit orchards were in close proximity to the piggery, allowing the spillage of urine, feces and partially eaten fruit onto the pigs. Retrospective studies demonstrate that viral spillover into pigs may have been occurring in Malaysia since 1996 without detection. During 1998, viral spread was aided by the transfer of infected pigs to other farms, where new outbreaks occurred.

Cedar Virus (CedPV) was first identified in pteropid urine during work on Hendra virus undertaken in Queensland in 2009. Although the virus is reported to be very similar to both Hendra and Nipah, it does not cause illness in laboratory animals usually susceptible to paramyxoviruses. Animals were able to mount an effective response and create effective antibodies.

The scientists who identified the virus report:

Hendra and Nipah viruses are 2 highly pathogenic paramyxoviruses that have emerged from bats within the last two decades. Both are capable of causing fatal disease in both humans and many mammal species. Serological and molecular evidence for henipa-like viruses have been reported from numerous locations including Asia and Africa, however, until now no successful isolation of these viruses have been reported. This paper reports the isolation of a novel paramyxovirus, named Cedar virus, from fruit bats in Australia. Full genome sequencing of this virus suggests a close relationship with the henipaviruses.

 

 

Antibodies to Cedar virus were shown to cross react with, but not cross neutralize Hendra or Nipah virus. Despite this close relationship, when Cedar virus was tested in experimental challenge models in ferrets and guinea pigs, we identified virus replication and generation of neutralizing antibodies, but no clinical disease was observed. As such, this virus provides a useful reference for future reverse genetics experiments to determine the molecular basis of the pathogenicity of the henipaviruses.

30. Lyssaviruses  This genus comprises of not only rabies virus (causing death of almost everyone who is infected) but certain other viruses such as Duvenhage virus, Mokola virus, and Australian bat lyssavirus. Although small number of cases are reported, but the ones reported have always been fatal. Bats are vectors for all of these types except for Mokola virus.

 

Lyssavirus (from Lyssa, the Greek goddess of madness, rage, and frenzy) is a genus of viruses belonging to the family Rhabdoviridae, in the order Mononegavirales. This group of RNA viruses includes the rabies virus traditionally associated with the disease. Viruses typically have either helical or cubic symmetry. Lyssaviruses have helical symmetry, so their infectious particles are approximately cylindrical in shape. This is typical of plant-infecting viruses. Human-infecting viruses more commonly have cubic symmetry and take shapes approximating regular polyhedra. The structure consists of a spiked outer envelope, a middle region consisting of matrix protein M, and an inner ribonucleocapsid complex region, consisting of the genome associated with other proteins.

Lyssavirus genome consists of a negative-sense, single-stranded RNA molecule that encodes five viral proteins: polymerase L, matrix protein M, phosphoprotein P, nucleoprotein N, and glycoprotein G.

Based on recent phylogenetic evidence, lyssa viruses are categorized into seven major species. In addition, five species recently have been discovered: West Caucasian bat virus, Aravan virus, Khuj and virus, Irkut virus and Shimoni bat virus. The major species include rabies virus (species 1), Lagos bat virus (species 2), Mokola virus (species 3), Duvenhage virus (species 4), European Bat lyssaviruses type 1 and 2 (species 5 and 6), and Australian bat lyssavirus (species 7).

Based on biological properties of the viruses, these species are further subdivided into phylogroups 1 and 2. Phylogroup 1 includes genotypes 1, 4, 5, 6, and 7, while phylogroup 2 includes genotypes 2 and 3. The nucleocapsid region of lyssavirus is fairly highly conserved from genotype to genotype across both phylogroups; however, experimental data have shown the lyssavirus strains used in vaccinations are only from the first species(i.e. classic rabies).

31. Tuberculosis  Mucous, fever, fatigue, excessive sweating and weight loss. What do they all have in common?

They are symptoms of pulmonary tuberculosis, or TB. TB is a contagious bacterial infection that involves the lungs, but it may spread to other organs. The symptoms of this disease can remain stagnant for years or affect the person right away. People at higher risk for contracting TB include the elderly, infants and those with weakened immune systems due to other diseases, such as AIDS or diabetes, or even individuals who have undergone chemotherapy.

Being around others who may have TB, maintaining a poor diet or living in unsanitary conditions are all risk factors for contracting TB. In the United States, there are approximately 10 cases of TB per 100,000 people. Tuberculosis, MTB, or TB (short for tubercle bacillus), in the past also called phthisis, phthisis pulmonalis, or consumption, is a widespread, and in many cases fatal, infectious disease caused by various strains of mycobacteria, usually Mycobacterium tuberculosis.

Tuberculosis typically attacks the lungs, but can also affect other parts of the body. It is spread through the air when people who have an active TB infection cough, sneeze, or otherwise transmit respiratory fluids through the air. Most infections do not have symptoms, known as latent tuberculosis. About one in ten latent infections eventually progresses to active disease which, if left untreated, kills more than 50% of those so infected.

The classic symptoms of active TB infection are a chronic cough with blood-tinged sputum, fever, night sweats, and weight loss (the latter giving rise to the formerly common term for the disease, "consumption"). Infection of other organs causes a wide range of symptoms. Diagnosis of active TB relies on radiology (commonly chest X-rays), as well as microscopic examination and microbiological culture of body fluids.

Diagnosis of latent TB relies on the tuberculin skin test (TST) and/or blood tests. Treatment is difficult and requires administration of multiple antibiotics over a long period of time. Social contacts are also screened and treated if necessary. Antibiotic resistance is a growing problem in multiple drug-resistant tuberculosis (MDR-TB) infections. Prevention relies on screening programs and vaccination with the bacillus Calmette-Guérin vaccine.

One-third of the world’s population is thought to have been infected with M. tuberculosis, with new infections occurring in about 1% of the population each year.In 2007, an estimated 13.7 million chronic cases were active globally, while in 2010, an estimated 8.8 million new cases and 1.5 million associated deaths occurred, mostly in developing countries. The absolute number of tuberculosis cases has been decreasing since 2006, and new cases have decreased since 2002.

The rate of tuberculosis in different areas varies across the globe; about 80% of the population in many Asian and African countries tests positive in tuberculin tests, while only 5–10% of the United States population tests positive. More people in the developing world contract tuberculosis because of a poor immune system, largely due to high rates of HIV infection and the corresponding development of AIDS.

32. Encephalitis Virus Encephalitis is an acute inflammation of the brain, commonly caused by a viral infection. Victims are usually exposed to viruses resulting in encephalitis by insect bites or food and drink. The most frequently encountered agents are arboviruses (carried by mosquitoes or ticks) and enteroviruses ( coxsackievirus, poliovirus and echovirus ). Some of the less frequent agents are measles, rabies, mumps, varicella and herpes simplex viruses.

Patients with encephalitis suffer from fever, headache, vomiting, confusion, drowsiness and photophobia. The symptoms of encephalitis are caused by brain’s defense mechanisms being activated to get rid of infection (brain swelling, small bleedings and cell death). Neurologic examination usually reveals a stiff neck due to the irritation of the meninges covering the brain. Examination of the cerebrospinal fluidCerebrospinal fluid CSF in short, is the clear fluid that occupies the subarachnoid space (the space between the skull and cortex of the brain). It acts as a "cushion" or buffer for the cortex.

Also, CSF occupies the ventricular system of the brain and the obtained by a lumbar puncture In medicine, a lumbar puncture (colloquially known as a spinal tap is a diagnostic procedure that is done to collect a sample of cerebrospinal fluid (CSF) for biochemical, microbiological and cytological analysis. Indications The most common indication for procedure reveals increased amounts of proteins and white blood cells with normal glucose. A CT scan examination is performed to reveal possible complications of brain swelling, brain abscess Brain abscess (or cerebral abscess) is an abscess caused by inflammation and collection of infected material coming from local (ear infection, infection of paranasal sinuses, infection of the mastoid air cells of the temporal bone, epidural abscess) or re or bleeding. Lumbar puncture procedure is performed only after the possibility of a prominent brain swelling is excluded by a CT scan examination.

What are the main Symptoms?
Some patients may have symptoms of a cold or stomach infection before encephalitis symptoms begin.
When a case of encephalitis is not very severe, the symptoms may be similar to those of other illnesses, including:
• Fever that is not very high
• Mild headache
• Low energy and a poor appetite

Other symptoms include:
• Clumsiness, unsteady gait
• Confusion, disorientation
• Drowsiness
• Irritability or poor temper control
• Light sensitivity
• Stiff neck and back (occasionally)
• Vomiting

Symptoms in newborns and younger infants may not be as easy to recognize:
• Body stiffness
• Irritability and crying more often (these symptoms may get worse when the baby is picked up)
• Poor feeding
• Soft spot on the top of the head may bulge out more
• Vomiting

• Loss of consciousness, poor responsiveness, stupor, coma
• Muscle weakness or paralysis
• Seizures
• Severe headache
• Sudden change in mental functions:
• "Flat" mood, lack of mood, or mood that is inappropriate for the situation
• Impaired judgment
• Inflexibility, extreme self-centeredness, inability to make a decision, or withdrawal from social interaction
• Less interest in daily activities
• Memory loss (amnesia), impaired short-term or long-term memory

Children and adults should avoid contact with anyone who has encephalitis.
Controlling mosquitoes (a mosquito bite can transmit some viruses) may reduce the chance of some infections that can lead to encephalitis.
• Apply an insect repellant containing the chemical, DEET when you go outside (but never use DEET products on infants younger than 2 months).
• Remove any sources of standing water (such as old tires, cans, gutters, and wading pools).
• Wear long-sleeved shirts and pants when outside, particularly at dusk.
Vaccinate animals to prevent encephalitis caused by the rabies virus.

 

33. Chicken Pox Virus Chickenpox is a highly contagious disease caused by primary infection with varicella zoster virus (VZV).It usually starts with a vesicular skin rash mainly on the body and head rather than on the limbs. The rash develops into itchy, raw pockmarks, which mostly heal without scarring. On examination, the observer typically finds skin lesions at various stages of healing and also ulcers in the oral cavity and tonsil areas. The disease is most commonly observed in children.

Chickenpox is an airborne disease which spreads easily through coughing or sneezing by ill individuals or through direct contact with secretions from the rash. A person with chickenpox is infectious one to two days before the rash appears. They remain contagious until all lesions have crusted over (this takes approximately six days). Immunocompromised patients are contagious during the entire period as new lesions keep appearing. Crusted lesions are not contagious.Chickenpox has been observed in other primates, including chimpanzees and gorillas.

The origin of the term chicken pox, which is recorded as being used since 1684,is not reliably known. It has been said to be a derived from chickpeas, based on resemblance of the vesicles to chickpeas, or to come from the rash resembling chicken pecks. Other suggestions include the designation chicken for a child (i.e., literally ‘child pox’), a corruption of itching-pox, or the idea that the disease may have originated in chickens. Samuel Johnson explained the designation as "from its being of no very great danger."

The early (prodromal) symptoms in adolescents and adults are nausea, loss of appetite, aching muscles, and headache. This is followed by the characteristic rash or oral sores, malaise, and a low-grade fever that signal the presence of the disease. Oral manifestations of the disease (enanthem) not uncommonly may precede the external rash (exanthem). In children the illness is not usually preceded by prodromal symptoms, and the first sign is the rash or the spots in the oral cavity. The rash begins as small red dots on the face, scalp, torso, upper arms and legs; progressing over 10–12 hours to small bumps, blisters and pustules; followed by umbilication and the formation of scabs.

At the blister stage, intense itching is usually present. Blisters may also occur on the palms, soles, and genital area. Commonly, visible evidence of the disease develops in the oral cavity & tonsil areas in the form of small ulcers which can be painful or itchy or both; this enanthem (internal rash) can precede the exanthem (external rash) by 1 to 3 days or can be concurrent. These symptoms of chickenpox appear 10 to 21 days after exposure to a contagious person. Adults may have a more widespread rash and longer fever, and they are more likely to experience complications, such as varicella pneumonia.Because watery nasal discharge containing live virus usually precedes both exanthem (external rash) and enanthem (oral ulcers) by 1 to 2 days, the infected person actually becomes contagious one to two days prior to recognition of the disease. Contagiousness persists until all vesicular lesions have become dry crusts (scabs), which usually entails four or five days, by which time nasal shedding of live virus also ceases.

Chickenpox is rarely fatal, although it is generally more severe in adult men than in women or children. Non-immune pregnant women and those with a suppressed immune system are at highest risk of serious complications. Arterial ischemic stroke (AIS) associated with chickenpox in the previous year accounts for nearly one third of childhood AIS. The most common late complication of chickenpox is shingles (herpes zoster), caused by reactivation of the varicella zoster virus decades after the initial, often childhood, chickenpox infection.

Shingles  Herpes zoster After a chickenpox infection, the virus remains dormant in the body’s nerve tissues. The immune system keeps the virus at bay, but later in life, usually as an adult, it can be reactivated and cause a different form of the viral infection called shingles (scientifically known as herpes zoster). The United States Advisory Committee on Immunization Practices (ACIP) suggests that any adult over the age of 60 years gets the herpes zoster vaccine as a part of their normal medical check ups.

Many adults who have had chickenpox as children are susceptible to shingles as adults, often with the accompanying condition postherpetic neuralgia, a painful condition that makes it difficult to sleep. Even after the shingles rash has gone away, there can be night pain in the area affected by the rash.Shingles affects one in five adults infected with chickenpox as children, especially those who are immune suppressed, particularly from cancer, HIV, or other conditions.

However, stress can bring on shingles as well, although scientists are still researching the connection.Shingles are most commonly found in adults over the age of 60 who were diagnosed with chickenpox when they were under the age of 1.A shingles vaccine is available for adults over 50 who have had childhood chickenpox or who have previously had shingles.

34. POXVIRUS  Poxviruses (members of the family Poxviridae) are viruses that can, as a family, infect both vertebrate and invertebrate animals.

Four genera of poxviruses may infect humans: orthopox, parapox, yatapox, molluscipox. Orthopox: smallpox virus (variola), vaccinia virus, cowpox virus, monkeypox virus; Parapox: orf virus, pseudocowpox, bovine papular stomatitis virus; Yatapox: tanapox virus, yaba monkey tumor virus; Molluscipox: molluscum contagiosum virus (MCV).The most common are vaccinia (seen on Indian subcontinent) and molluscum contagiousum, but monkeypox infections are rising (seen in west and central African rainforest countries). Camelpox is a disease of camels caused by a virus of the family Poxviridae, subfamily Chordopoxvirinae, and the genus Orthopoxvirus. It causes skin lesions and a generalized infection. Approximately 25% of young camels that become infected will die from the disease, while infection in older camels is generally more mild.

The ancestor of the poxviruses is not known but structural studies suggest it may have been an adenovirus or a species related to both the poxviruses and the adenoviruses. Based on the genome organization and DNA replication mechanism it seems that phylogenetic relationships may exist between the rudiviruses (Rudiviridae) and the large eukaryal DNA viruses: the African swine fever virus (Asfarviridae), Chlorella viruses (Phycodnaviridae) and poxviruses (Poxviridae).The mutation rate in these genomes has been estimated to be 0.9-1.2 x 10⁻⁶ substitutions per site per year.A second estimate puts this rate at 0.5-7 × 10⁻⁶ nucleotide substitutions per site per year.  A third estimate places the rate at 4-6 × 10⁻⁶.

The last common ancestor of the extant poxviruses that infect vertebrates existed 0.5 million years ago. The genus Avipoxvirus diverged from the ancestor 249 ± 69 thousand years ago. The ancestor of the genus Orthopoxvirus was next to diverge from the other clades at 0.3 million years ago. A second estimate of this divergence time places this event at 166,000 ± 43,000 years ago. The division of the Orthopox into the extant genera occurred ~14,000 years ago. The genus Leporipoxvirus diverged ~137,000 ± 35,000 years ago. This was followed by the ancestor of the genus Yatapoxvirus. The last common ancestor of the Capripoxvirus and Suipoxvirus diverged 111,000 ± 29,000 years ago.

A model of a poxvirus cut-away in
cross-section to show the internal
structures. Poxviruses are shaped like
flattened capsules/barrels or are lens or
pill-shaped.

Their structure is complex,
neither icosahedral nor helical. This
model is based on Vaccinia, the smallpox
virus. The structures are also highly
variable and often incompletely studied.

 

35. West Nile Virus  West Nile virus (WNV) is a mosquito-borne zoonotic arbovirus belonging to the genus Flavivirus in the family Flaviviridae.

This flavivirus is found in temperate and tropical regions of the world. It was first identified in the West Nile subregion in the East African nation of Uganda in 1937. Prior to the mid-1990s, WNV disease occurred only sporadically and was considered a minor risk for humans, until an outbreak in Algeria in 1994, with cases of WNV-caused encephalitis, and the first large outbreak in Romania in 1996, with a high number of cases with neuroinvasive disease. WNV has now spread globally, with the first case in the Western Hemisphere being identified in New York City in 1999; over the next five years, the virus spread across the continental United States, north into Canada, and southward into the Caribbean islands and Latin America. WNV also spread to Europe, beyond the Mediterranean Basin, and a new strain of the virus was identified in Italy in 2012. WNV is now considered to be an endemic pathogen in Africa, Asia, Australia, the Middle East, Europe and in the United States, which in 2012 has experienced one of its worst epidemics. In 2012, WNV killed 286 people in the United States, with the state of Texas being hard hit by this virus, making the year the deadliest on record for the United States.

The main mode of WNV transmission is via various species of mosquitoes, which are the prime vector, with birds being the most commonly infected animal and serving as the prime reservoir host—especially passerines, which are of the largest order of birds, Passeriformes. WNV has been found in various species of ticks, but current research suggests they are not important vectors of the virus. WNV also infects various mammal species, including humans, and has been identified in reptilian species, including alligators and crocodiles, and also in amphibians. Not all animal species that are susceptible to WNV infection, including humans, and not all bird species develop sufficient viral levels to transmit the disease to uninfected mosquitoes, and are thus not considered major factors in WNV transmission.

Approximately 80% of West Nile virus infections in humans are subclinical, which cause no symptoms. In the cases where symptoms do occur—termed West Nile fever in cases without neurological disease—the time from infection to the appearance of symptoms (incubation period) is typically between 2 and 15 days. Symptoms may include fever, headaches, fatigue, muscle pain or aches, malaise, nausea, anorexia, vomiting, myalgias and rash. Less than 1% of the cases are severe and result in neurological disease when the central nervous system is affected. People of advanced age, the very young, or those with immunosuppression, either medically induced, such as those taking immunosupressive drugs, or due to a pre-existing medical condition such as HIV infection, are most susceptible. The specific neurological diseases that may occur are West Nile encephalitis, which causes inflammation of the brain, West Nile meningitis, which causes inflammation of the meninges, which are the protective membranes that cover the brain and spinal cord, West Nile meningoencephalitis, which causes inflammation of the brain and also the meninges surrounding it, and West Nile poliomyelitis—spinal cord inflammation, which results in a syndrome similar to polio, which may cause acute flaccid paralysis.

Currently, no vaccine against WNV infection is available. The best method to reduce the rates of WNV infection is mosquito control on the part of municipalities, businesses and individual citizens to reduce breeding populations of mosquitoes in public, commercial and private areas via various means including eliminating standing pools of water where mosquitoes breed, such as in old tires, buckets, unused swimming pools, etc. On an individual basis, the use of personal protective measures to avoid being bitten by an infected mosquito, via the use of mosquito repellent, window screens, avoiding areas where mosquitoes are more prone to congregate, such as near marshes, areas with heavy vegetation etc., and being more vigilant from dusk to dawn when mosquitoes are most active offers the best defense. In the event of being bitten by an infected mosquito, familiarity of the symptoms of WNV on the part of laypersons, physicians and allied health professions affords the best chance of receiving timely medical treatment, which may aid in reducing associated possible complications and also appropriate palliative care.

The incubation period for WNV—the amount of time from infection to symptom onset—is typically from between 2 and 15 days. Headache can be a prominent symptom of WNV fever, meningitis, encephalitis, meningoencephalitis, and it may or may not be present in poliomyelytis-like syndrome. Thus, headache is not a useful indicator of neuroinvasive disease.(CDC)

• West Nile fever (WNF), which occurs in 20 percent of cases, is a febrile syndrome that causes flu-like symptoms. Most characterizations of WNF generally describe it as a mild, acute syndrome lasting 3 to 6 days after symptom onset. Systematic follow-up studies of patients with WNF have not been done, so this information is largely anecdotal. In addition to a high fever, headache, chills, excessive sweating, weakness, fatigue, swollen lymph nodes, drowsiness, pain in the joints and flu-like symptoms. Gastrointestinal symptoms that may occur include nausea, vomiting, loss of appetite, and diarrhea. Fewer than one-third of patients develop a rash.

• West Nile neuroinvasive disease (WNND), which occurs in less than 1 percent of cases, is when the virus infects the central nervous system resulting in meningitis, encephalitis, meningoencephalitis or a poliomyelitis-like syndrome.  Many patients with WNND have normal neuroimaging studies, although abnormalities may be present in various cerebral areas including the basal ganglia, thalamus, cerebellum, and brainstem.

• West Nile virus encephalitis (WNE) is the most common neuroinvasive manifestation of WNND. WNE presents with similar symptoms to other viral encephalitis with fever, headaches, and altered mental status. A prominent finding in WNE is muscular weakness (30 to 50 percent of patients with encephalitis), often with lower motor neuron symptoms, flaccid paralysis, and hyporeflexia with no sensory abnormalities.

• West Nile meningitis (WNM) usually involves fever, headache, and stiff neck. Pleocytosis, an increase of white blood cells in cerebrospinal fluid, is also present. Changes in consciousness are not usually seen and are mild when present.

• West Nile meningoencephalitis is inflammation of both the brain (encephalitis) and meninges (meningitis).

• West Nile poliomyelitis (WNP), an acute flaccid paralysis syndrome associated with WNV infection, is less common than WNM or WNE. This syndrome is generally characterized by the acute onset of asymmetric limb weakness or paralysis in the absence of sensory loss. Pain sometimes precedes the paralysis. The paralysis can occur in the absence of fever, headache, or other common symptoms associated with WNV infection. Involvement of respiratory muscles, leading to acute respiratory failure, can sometimes occur.

• West-Nile reversible paralysis,. Like WNP, the weakness or paralysis is asymmetric. Reported cases have been noted to have an initial preservation of deep tendon reflexes, which is not expected for a pure anterior horn involvement.Disconnect of upper motor neuron influences on the anterior horn cells possibly by myelitis or glutamate excitotoxicity have been suggested as mechanisms.The prognosis for recovery is excellent.

• Nonneurologic complications of WNV infection that may rarely occur include fulminant hepatitis, pancreatitis,  myocarditis, rhabdomyolysis, orchitis, nephritis, optic neuritis and cardiac dysrhythmias and hemorrhagic fever with coagulopathy.^[15] Chorioretinitis may also be more common than previously thought.

• Cutaneous manifestations specifically rashes, are not uncommon in WNV-infected patients; however, there is a paucity of detailed descriptions in case reports and there are few clinical images widely available. Punctate erythematous (?), macular, and papular eruptions, most pronounced on the extremities have been observed in WNV cases and in some cases histopathologic findings have shown a sparse superficial perivascular lymphocytic infiltrate, a manifestation commonly seen in viral exanthems (?). A literature review provides support that this punctate rash is a common cutaneous presentation of WNV infection. (Anderson RC et al.)

West Nile virus life cycle. After binding and uptake, the virion envelope fuses with cellular membranes, followed by uncoating of the nucleocapsid and release of the RNA genome into the cytoplasm. The viral genome serves as messenger RNA (mRNA) for translation of all viral proteins and as template during RNA replication. Copies are subsequently packaged within new virus particles that are transported in vesicles to the cell membrane.

WNV is one of the Japanese encephalitis antigenic serocomplex of viruses. Image reconstructions and cryoelectron microscopy reveal a 45–50 nm virion covered with a relatively smooth protein surface. This structure is similar to the dengue fever virus; both belong to the genus Flavivirus within the family Flaviviridae.

The genetic material of WNV is a positive-sense, single strand of RNA, which is between 11,000 and 12,000 nucleotides long; these genes encode seven nonstructural proteins and three structural proteins. The RNA strand is held within a nucleocapsid formed from 12-kDa protein blocks; the capsid is contained within a host-derived membrane altered by two viral glycoproteins. Phylogenetic tree of West Nile viruses based on sequencing of the envelope gene during complete genome sequencing of the virus

Studies of phylogenetic lineages determined WNV emerged as a distinct virus around 1000 years ago. This initial virus developed into two distinct lineages, lineage 1 and its multiple profiles is the source of the epidemic transmission in Africa and throughout the world. Lineage 2 was considered an Africa zoonosis. However, in 2008, lineage 2, previously only seen in horses in sub-Saharan Africa and Madagascar, began to appear in horses in Europe, where the first known outbreak affected 18 animals in Hungary in 2008. Lineage 1 West Nile virus was detected in South Africa in 2010 in a mare and her aborted fetus; previously, only lineage 2 West Nile virus had been detected in horses and humans in South Africa. A 2007 fatal case in a killer whale in Texas broadened the known host range of West Nile virus to include cetaceans.

The United States virus was very closely related to a lineage 1 strain found in Israel in 1998. Since the first North American cases in 1999, the virus has been reported throughout the United States, Canada, Mexico, the Caribbean, and Central America. There have been human cases and equine cases, and many birds are infected. The Barbary macaque, Macaca sylvanus, was the first nonhuman primate to contract WNV.  Both the United States and Israeli strains are marked by high mortality rates in infected avian populations; the presence of dead birds—especially Corvidae—can be an early indicator of the arrival of the virus.

The West Nile virus maintains itself in nature by cycling between mosquitoes and certain species of birds. A mosquito (the vector) bites an uninfected bird (the host), the virus amplifies within the bird, an uninfected mosquito bites the bird and is in turn infected. Other species such as humans and horses are incidental infections, as they are not the mosquitoes’ preferred blood meal source. The virus does not amplify within these species and they are known as dead-end hosts.

The West Nile virus (WNV) is transmitted through female mosquitoes, which are the prime vectors of the virus. Only females feed on blood, and different species have evolved to take a blood meal on preferred types of vertebrate hosts. The infected mosquito species vary according to geographical area; in the United States, Culex pipiens (Eastern United States), Culex tarsalis (Midwest and West), and Culex quinquefasciatus (Southeast) are the main sources.The various species that transmit the WNV prefer birds of the Passeriformes order, the largest order of birds. Within that order there is further selectivity with various mosquito species exhibiting preference for different species. In the United States WNV mosquito vectors have shown definitive preference for members of the Corvidae and Thrush family of birds. Amongst the preferred species within these families are the American crow, a corvid, and the American robin (Turdus migratorius), a thrush.

The proboscis of a female mosquito—here a Southern House Mosquito (Culex quinquefasciatus)—pierces the epidermis and dermis to allow it to feed on human blood from a capillary: this one is almost fully tumescent. The mosquito injects saliva, which contains an anesthetic, and an anticoagulant into the puncture wound; and in infected mosquitoes, the West Nile virus.

The birds develop sufficient viral levels after being infected, to transmit the infection to other biting mosquitoes that in turn go on to infect other birds. In crows and robins, the infection is fatal in 4–5 days. This epizootic viral amplification cycle has been shown to peak 15–16 days before humans become ill. This may be due to the high mortality, and thus depletion of the preferred hosts, i.e., the specific bird species. The mosquitoes become less selective and begin feeding more readily on other animal types such as humans and horses which are considered incidental hosts.

In mammals, the virus does not multiply as readily (i.e., does not develop high viremia during infection), and mosquitoes biting infected mammals are not believed to ingest sufficient virus to become infected,making mammals so-called dead-end hosts.

Direct human-to-human transmission initially was believed to be caused only by occupational exposure, or conjunctive exposure to infected blood. The US outbreak identified additional transmission methods through blood transfusion,organ transplant intrauterine exposure, and breast feeding. Since 2003, blood banks in the United States routinely screen for the virus among their donors. As a precautionary measure, the UK’s National Blood Service initially ran a test for this disease in donors who donate within 28 days of a visit to the United States, Canada or the northeastern provinces of Italy and the Scottish National Blood Transfusion Service asks prospective donors to wait 28 days after returning from North America or the northeastern provinces of Italy before donating.

Recently, the potential for mosquito saliva to impact the course of WNV disease was demonstrated. Mosquitoes inoculate their saliva into the skin while obtaining blood. Mosquito saliva is a pharmacological cocktail of secreted molecules, principally proteins, that can affect vascular constriction, blood coagulation, platelet aggregation, inflammation, and immunity. It clearly alters the immune response in a manner that may be advantageous to a virus. Studies have shown it can specifically modulate the immune response during early virus infection, and mosquito feeding can exacerbate WNV infection, leading to higher viremia and more severe forms of disease.

Vertical transmission, the transmission of a viral or bacterial disease from the female of the species to her offspring, has been observed in various West Nile virus studies, amongst different species of mosquitoes in both the laboratory and in nature.Mosquito progeny infected vertically in autumn, may potentially serve as a mechanism for WNV to overwinter and initiate enzootic horizontal transmission the following spring.

35 of the Most Dangerous Viruses and Bacteria’s in the World Today

The Black Plague, Marburg, Ebola, Influenza, Enterovirus virus may all sound terrifying, but it’s not the most dangerous virus in the world. It isn’t HIV either. Here is a list of the most dangerous viruses and Bacteria’s on the Planet Earth.

1. Marburg Virus The most dangerous virus is the Marburg virus. It is named after a small and idyllic town on the river Lahn – but that has nothing to do with the disease itself. The Marburg virus is a hemorrhagic fever virus. As with Ebola, the Marburg virus causes convulsions and bleeding of mucous membranes, skin and organs. It has a fatality rate of 90 percent.  The Marburg virus causes a rare, but severe hemorrhagic fever that has a fatality rate of 88%. It was first identified in 1967 when outbreaks of hemorrhagic fever cropped up simultaneously in Marburg, where the disease got its name, Frankfurt in Germany and Belgrade, Serbia.

Marburg and Ebola came from the Filoviridae family of viruses. They both have the capacity to cause dramatic outbreaks with the greatest fatality rates. It is transmitted to humans from fruit bats and spreads to humans through direct contact with the blood, secretions and other bodily fluids of infected humans. No anti-viral treatment or vaccine exists against the Marburg virus. In 1967, a group of lab workers in Germany (Marburg and Frankfurt) and Serbia (then Yugoslavia) contracted a new type of hemorrhagic fever from some virus-carrying African green monkeys that had been imported for research and development of polio vaccines. The Marburg virus is also BSL-4, and Marburg hemorrhagic fever has a 23 to 90 percent fatality rate. Spread through close human-to-human contact, symptoms start with a headache, fever, and a rash on the trunk, and progress to multiple organ failure and massive internal bleeding.

There is no cure, and the latest cases were reported out of Uganda at the end of 2012. An American tourist who had explored a Ugandan cave full of fruit bats known to be reservoirs of the virus contracted it and survived in 2008. (But not before bringing his sick self back to the U.S.)

2. Ebola Virus  There are five strains of the Ebola virus, each named after countries and regions in Africa: Zaire, Sudan, Tai Forest, Bundibugyo and Reston. The Zaire Ebola virus is the deadliest, with a mortality rate of 90 percent. It is the strain currently spreading through Guinea, Sierra Leone and Liberia, and beyond. Scientists say flying foxes probably brought the Zaire Ebola virus into cities.

Typically less than 100 lives a year. UPDATE: A severe Ebola outbreak was detected in West Africa in March 2014. The number of deaths in this latest outbreak has outnumbered all other known cases from previous outbreaks combined. The World Health Organization is reporting nearly 2,000 deaths in this latest outbreak.
Once a person is infected with the virus, the disease has an incubation period of 2-21 days; however, some infected persons are asymptomatic. Initial symptoms are sudden malaise, headache, and muscle pain, progressing to high fever, vomiting, severe hemorrhaging (internally and out of the eyes and mouth) and in 50%-90% of patients, death, usually within days. The likelihood of death is governed by the virulence of the particular Ebola strain involved. Ebola virus is transmitted in body fluids and secretions; there is no evidence of transmission by casual contact. There is no vaccine and no cure.

Its melodic moniker may roll off the tongue, but if you contract the virus (above), that’s not the only thing that will roll off one of your body parts (a disturbing amount of blood coming out of your eyes, for instance). Four of the five known Ebola viral strains cause Ebola hemorrhagic fever (EHF), which has killed thousands of people in sub-Saharan African nations since its discovery in 1976.

The deadly virus is named after the Ebola River in the Democratic Republic of the Congo where it was first reported, and is classified as a CDC Biosafety Level 4, a.k.a. BSL-4, making it one of the most dangerous pathogens on the planet. It is thought to spread through close contact with bodily secretions. EHF has a 50 to 90 percent mortality rate, with a rapid onset of symptoms that start with a headache and sore throat and progress to major internal and external bleeding and multiple organ failure. There’s no known cure, and the most recent cases were reported at the end of 2012 in Uganda.

3. The Hantavirus describes several types of viruses. It is named after a river where American soldiers were first thought to have been infected with the Hantavirus, during the Korean War in 1950. Symptoms include lung disease, fever and kidney failure.

70,000 Deaths a Year
Hantavirus pulmonary syndrome (HPS) is a deadly disease transmitted by infected rodents through urine, droppings, or saliva. Humans can contract the disease when they breathe in aerosolized virus. HPS was first recognized in 1993 and has since been identified throughout the United States. Although rare, HPS is potentially deadly. Rodent control in and around the home remains the primary strategy for preventing hantavirus infection. Also known as House Mouse Flu. The symptoms, which are very similar to HFRS, include tachycardia and tachypnea. Such conditions can lead to a cardiopulmonary phase, where cardiovascular shock can occur, and hospitalization of the patient is required.

There are many strains of hantavirus floating around (yep, it’s airborne) in the wake of rodents that carry the virus. Different strains, carried by different rodent species, are known to cause different types of illnesses in humans, most notably hemorrhagic fever with renal syndrome (HFRS)—first discovered during the Korean War—and hantavirus pulmonary syndrome (HPS), which reared its ugly head with a 1993 outbreak in the Southwestern United States. Severe HFRS causes acute kidney failure, while HPS gets you by filling your lungs with fluid (edema). HFRS has a mortality rate of 1 to 15 percent, while HPS is 38 percent. The U.S. saw its most recent outbreak of hantavirus—of the HPS variety—at Yosemite National Park in late 2012.

4. Avian Influenza Bird Flu The various strains of bird flu regularly cause panic – which is perhaps justified because the mortality rate is 70 percent. But in fact the risk of contracting the H5N1 strain – one of the best known – is quite low. You can only be infected through direct contact with poultry. It is said this explains why most cases appear in Asia, where people often live close to chickens.

This form of the flu is common among birds (usually poultry) and infects humans through contact with secretions of an infected bird.

Although rare, those infected have a high incidence of death. Symptoms are like those of the more common human form of influenza.

Bird flu (H5N1) has receded from international headlines for the moment, as few human cases of the deadly virus have been reported this year. But when Dutch researchers recently created an even more transmissible strain of the virus in a laboratory for research purposes, they stirred grave concerns about what would happen if it escaped into the outside world. “Part of what makes H5N1 so deadly is that most people lack an immunity to it,” explains Marc Lipsitch, a professor of epidemiology at Harvard School of Public Health (HSPH) who studies the spread of infectious diseases. “If you make a strain that’s highly transmissible between humans, as the Dutch team did, it could be disastrous if it ever escaped the lab.”

H5N1 first made global news in early 1997 after claiming two dozen victims in Hong Kong. The virus normally occurs only in wild birds and farm-raised fowl, but in those isolated early cases, it made the leap from birds to humans. It then swept unimpeded through the bodies of its initial human victims, causing massive hemorrhages in the lungs and death in a matter of days. Fortunately, during the past 15 years, the virus has claimed only 400 victims worldwide—although the strain can jump species, it hasn’t had the ability to move easily from human to human, a critical limit to its spread.

That’s no longer the case, however. In late 2011, the Dutch researchers announced the creation of an H5N1 virus transmissible through the air between ferrets (the best animal model for studying the impact of disease on humans). The news caused a storm of controversy in the popular press and heated debate among scientists over the ethics of the work. For Lipsitch and many others, the creation of the new strain was cause for alarm. “H5N1 influenza is already one of the most deadly viruses in existence,” he says. “If you make [the virus] transmissible [between humans], you have to be very concerned about what the resulting strain could do.”

To put this danger in context, the 1918 “Spanish” flu—one of the most deadly influenza epidemics on record—killed between 50 million and 100 million people worldwide, or roughly 3 to 6 percent of those infected. The more lethal SARS virus (see “The SARS Scare,” March-April 2007, page 47) killed almost 10 percent of infected patients during a 2003 outbreak that reached 25 countries worldwide. H5N1 is much more dangerous, killing almost 60 percent of those who contract the illness.

If a transmissible strain of H5N1 escapes the lab, says Lipsitch, it could spark a global health catastrophe. “It could infect millions of people in the United States, and very likely more than a billion people globally, like most successful flu strains do,” he says. “This might be one of the worst viruses—perhaps the worst virus—in existence right now because it has both transmissibility and high virulence.”

Ironically, this is why Ron Fouchier, the Dutch virologist whose lab created the new H5N1 strain, argues that studying it in more depth is crucial. If the virus can be made transmissible in the lab, he reasons, it can also occur in nature—and researchers should have an opportunity to understand as much as possible about the strain before that happens.

Lipsitch, who directs the Center for Communicable Disease Dynamics at HSPH, thinks the risks far outweigh the rewards. Even in labs with the most stringent safety requirements, such as enclosed rubber “space suits” to isolate researchers, accidents do happen. A single unprotected breath could infect a researcher, who might unknowingly spread the virus beyond the confines of the lab.

In an effort to avoid this scenario, Lipsitch has been pushing for changes in research policy in the United States and abroad. (A yearlong, voluntary global ban on H5N1 research was lifted in many countries in January, and new rules governing such research in the United States were expected in February.) Lipsitch says that none of the current research proposals he has seen “would significantly improve our preparational response to a national pandemic of H5N1. The small risk of a very large public health disaster…is not worth taking [for] scientific knowledge without an immediate public health application.” His recent op-eds in scientific journals and the popular press have stressed the importance of regulating the transmissible strain and limiting work with the virus to only a handful of qualified labs. In addition, he argues, only technicians who have the right training and experience—and have been inoculated against the virus—should be allowed to handle it.

These are simple limitations that could drastically reduce the danger of the virus spreading, he asserts, yet they’re still not popular with some researchers. He acknowledges that limiting research is an unusual practice scientifically but argues, “These are unusual circumstances.”

Lipsitch thinks a great deal of useful research can still be done on the non-transmissible strain of the virus, which would provide valuable data without the risk of accidental release. In the meantime, he hopes to make more stringent H5N1 policies a priority for U.S. and foreign laboratories. Although it’s not a perfect solution, he says, it’s far better than a nightmare scenario.

5. Lassa Virus  A nurse in Nigeria was the first person to be infected with the Lassa virus. The virus is transmitted by rodents. Cases can be endemic – which means the virus occurs in a specific region, such as in western Africa, and can reoccur there at any time. Scientists assume that 15 percent of rodents in western Africa carry the virus.

The Marburg virus under a microscope

This BSL-4 virus gives us yet another reason to avoid rodents. Lassa is carried by a species of rat in West Africa called Mastomys. It’s airborne…at least when you’re hanging around the rat’s fecal matter. Humans, however, can only spread it through direct contact with bodily secretions. Lassa fever, which has a 15 to 20 percent mortality rate, causes about 5000 deaths a year in West Africa, particularly in Sierra Leone and Liberia.

It starts with a fever and some retrosternal pain (behind the chest) and can progress to facial swelling, encephalitis, mucosal bleeding and deafness. Fortunately, researchers and medical professionals have found some success in treating Lassa fever with an antiviral drug in the early stages of the disease.

6. The Junin Virus is associated with Argentine hemorrhagic fever. People infected with the virus suffer from tissue inflammation, sepsis and skin bleeding. The problem is that the symptoms can appear to be so common that the disease is rarely detected or identified in the first instance.

A member of the genus Arenavirus, Junin virus characteristically causes Argentine hemorrhagic fever (AHF). AHF leads to major alterations within the vascular, neurological and immune systems and has a mortality rate of between 20 and 30%.  Symptoms of the disease are conjunctivitis, purpura, petechia and occasional sepsis. The symptoms of the disease are relatively indistinct and may therefore be mistaken for a different condition.

Since the discovery of the Junin virus in 1958, the geographical distribution of the pathogen, although still confined to Argentina, has risen. At the time of discovery, Junin virus was confined to an area of around 15,000 km². At the beginning of 2000, the distribution had risen to around 150,000 km². The natural hosts of Junin virus are rodents, particularly Mus musculus, Calomys spp. and Akodon azarae.

Direct rodent to human transmission only transpires when contact is made with excrement of an infected rodent. This commonly occurs via ingestion of contaminated food or water, inhalation of particles within urine or via direct contact of broken skin with rodent excrement.

7. The Crimea-Congo Fever Virus is transmitted by ticks. It is similar to the Ebola and Marburg viruses in the way it progresses. During the first days of infection, sufferers present with pin-sized bleedings in the face, mouth and the pharynx.

Transmitted through tick bites this disease is endemic (consistently present)  in most countries of West Africa and the Middle East. Although rare, CCHF has a 30% mortality rate. The most recent outbreak of the disease was in 2005 in Turkey. The Crimean-Congo hemorrhagic fever is a common disease transmitted by a tick-Bourne virus. The virus causes major hemorrhagic fever outbreaks with a fatality rate of up to 30%. It is chiefly transmitted to people through tick and livestock. Person-to-person transmission occurs through direct contact with the blood, secretions and other bodily fluids of an infected person. No vaccination exists for both humans and animals against CCHF.

8. The Machupo Virus is associated with Bolivian hemorrhagic fever, also known as black typhus. The infection causes high fever, accompanied by heavy bleedings. It progresses similar to the Junin virus. The virus can be transmitted from human to human, and rodents often the carry it.

Bolivian hemorrhagic fever (BHF), also known as black typhus or Ordog Fever, is a hemorrhagic fever and zoonotic infectious disease originating in Bolivia after infection by Machupo virus.BHF was first identified in 1963 as an ambisense RNA virus of the Arenaviridae family,by a research group led by Karl Johnson. The mortality rate is estimated at 5 to 30 percent.

Due to its pathogenicity, Machupo virus requires Biosafety Level Four conditions, the highest level.In February and March 2007, some 20 suspected BHF cases (3 fatal) were reported to the El Servicio Departmental de Salud (SEDES) in Beni Department, Bolivia, and in February 2008, at least 200 suspected new cases (12 fatal) were reported to SEDES.In November 2011, a SEDES expert involved in a serosurvey to determine the extent of Machupo virus infections in the Department after the discovery of a second confirmed case near the departmental capital of Trinidad in November, 2011, expressed concern about expansion of the virus’ distribution outside the endemic zone in Mamoré and Iténez provinces.

Bolivian hemorrhagic fever was one of three hemorrhagic fevers and one of more than a dozen agents that the United States researched as potential biological weapons before the nation suspended its biological weapons program. It was also under research by the Soviet Union, under the Biopreparat bureau.

9. Kyasanur Forest Virus  Scientists discovered the Kyasanur Forest Virus (KFD) virus in woodlands on the southwestern coast of India in 1955. It is transmitted by ticks, but scientists say it is difficult to determine any carriers. It is assumed that rats, birds and boars could be hosts. People infected with the virus suffer from high fever, strong headaches and muscle pain which can cause bleedings.

The disease has a morbidity rate of 2-10%, and affects 100-500 people annually.The symptoms of the disease include a high fever with frontal headaches, followed by hemorrhagic symptoms, such as bleeding from the nasal cavity, throat, and gums, as well as gastrointestinal bleeding.An affected person may recover in two weeks time, but the convalescent period is typically very long, lasting for several months. There will be muscle aches and weakness during this period and the affected person is unable to engage in physical activities.

There are a variety of animals thought to be reservoir hosts for the disease, including porcupines, rats, squirrels, mice and shrews. The vector for disease transmission is Haemaphysalis spinigera, a forest tick. Humans contract infection from the bite of nymphs of the tick.

The disease was first reported from Kyasanur Forest of Karnataka in India in March 1957. The disease first manifested as an epizootic outbreak among monkeys killing several of them in the year 1957. Hence the disease is also locally known as Monkey Disease or Monkey Fever. The similarity with Russian Spring-summer encephalitis was noted and the possibility of migratory birds carrying the disease was raised. Studies began to look for the possible species that acted as reservoirs for the virus and the agents responsible for transmission. Subsequent studies failed to find any involvement of migratory birds although the possibility of their role in initial establishment was not ruled out. The virus was found to be quite distinctive and not closely related to the Russian virus strains.

Antigenic relatedness is however close to many other strains including the Omsk hemorrhagic fever (OHF) and birds from Siberia have been found to show an antigenic response to KFD virus. Sequence based studies however note the distinctiveness of OHF.Early studies in India were conducted in collaboration with the US Army Medical Research Unit and this led to controversy and conspiracy theories.

Subsequent studies based on sequencing found that the Alkhurma virus, found in Saudi Arabia is closely related. In 1989 a patient in Nanjianin, China was found with fever symptoms and in 2009 its viral gene sequence was found to exactly match with that of the KFD reference virus of 1957. This has however been questioned since the Indian virus shows variations in sequence over time and the exact match with the virus sequence of 1957 and the Chinese virus of 1989 is not expected.

This study also found using immune response tests that birds and humans in the region appeared to have been exposed to the virus.Another study has suggested that the virus is recent in origin dating the nearest common ancestor of it and related viruses to around 1942, based on the estimated rate of sequence substitutions. The study also raises the possibility of bird involvement in long-distance transfer. It appears that these viruses diverged 700 years ago.

10. Dengue Fever is a constant threat. If you’re planning a holiday in the tropics, get informed about dengue. Transmitted by mosquitoes, dengue affects between 50 and 100 million people a year in popular holiday destinations such as Thailand and India. But it’s more of a problem for the 2 billion people who live in areas that are threatened by dengue fever.

25,000 Deaths a year Also known as ‘breakbone fever’ due to the extreme pain felt during fever, is an relatively new disease caused by one of four closely-related viruses. WHO estimates that a whopping 2.5 billion people (two fifths of the World’s population) are at risk from dengue. It puts the total number of infections at around 50 million per year, and is now epidemic in more than 100 countries.

Dengue viruses are transferred to humans through the bites of infective female Aedes mosquitoes. The dengue virus circulates in the blood of a human for two to seven days, during the same time they have the fever. It usually appears first on the lower limbs and the chest; in some patients, it spreads to cover most of the body. There may also be severe retro-orbital pain, (a pain from behind the eyes that is distinctive to Dengue infections), and gastritis with some combination of associated abdominal pain, nausea, vomiting coffee-grounds-like congealed blood, or severe diarrhea.

The leading cause of death in the tropics and subtropics is the infection brought on by the dengue virus, which causes a high fever, severe headache, and, in the worst cases, hemorrhaging. The good news is that it’s treatable and not contagious. The bad news is there’s no vaccine, and you can get it easily from the bite of an infected mosquito—which puts at least a third of the world’s human population at risk. The CDC estimates that there are over 100 million cases of dengue fever each year. It’s a great marketing tool for bug spray.

11. HIV 3.1 Million Lives a Year Human Immunodeficiency Virus has claimed the lives of more than 25 million people since 1981. HIV gets to the immune system by infecting important cells, including helper cells called CD4+ T cells, plus macrophanges and dendritic cells. Once the virus has taken hold, it systematically kills these cells, damaging the infected person’s immunity and leaving them more at risk from infections.

The majority of people infected with HIV go on to develop AIDS. Once a patient has AIDS common infections and tumours normally controlled by the CD4+ T cells start to affect the person.  
In the latter stages of the disease, pneumonia and various types of herpes can infect the patient and cause death.

Human immunodeficiency virus infection / acquired immunodeficiency syndrome (HIV/AIDS) is a disease of the human immune system caused by infection with human immunodeficiency virus (HIV). The term HIV/AIDS represents the entire range of disease caused by the human immunodeficiency virus from early infection to late stage symptoms. During the initial infection, a person may experience a brief period of influenza-like illness. This is typically followed by a prolonged period without symptoms. As the illness progresses, it interferes more and more with the immune system, making the person much more likely to get infections, including opportunistic infections and tumors that do not usually affect people who have working immune systems.

HIV is transmitted primarily via unprotected sexual intercourse (including anal and oral sex), contaminated blood transfusions, hypodermic needles, and from mother to child during pregnancy, delivery, or breastfeeding. Some bodily fluids, such as saliva and tears, do not transmit HIV. Prevention of HIV infection, primarily through safe sex and needle-exchange programs, is a key strategy to control the spread of the disease. There is no cure or vaccine; however, antiretroviral treatment can slow the course of the disease and may lead to a near-normal life expectancy. While antiretroviral treatment reduces the risk of death and complications from the disease, these medications are expensive and have side effects. Without treatment, the average survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype.

Genetic research indicates that HIV originated in west-central Africa during the late nineteenth or early twentieth century. AIDS was first recognized by the United States Centers for Disease Control and Prevention (CDC) in 1981 and its cause—HIV infection—was identified in the early part of the decade. Since its discovery, AIDS has caused an estimated 36 million deaths worldwide (as of 2012). As of 2012, approximately 35.3 million people are living with HIV globally. HIV/AIDS is considered a pandemic—a disease outbreak which is present over a large area and is actively spreading.

HIV/AIDS has had a great impact on society, both as an illness and as a source of discrimination. The disease also has significant economic impacts. There are many misconceptions about HIV/AIDS such as the belief that it can be transmitted by casual non-sexual contact. The disease has also become subject to many controversies involving religion. It has attracted international medical and political attention as well as large-scale funding since it was identified in the 1980s

 

12. Rotavirus 61,000 Lives a Year  According to the WHO, this merciless virus causes the deaths of more than half a million children every year. In fact, by the age of five, virtually every child on the planet has been infected with the virus at least once. Immunity builds up with each infection, so subsequent infections are milder. However, in areas where adequate healthcare is limited the disease is often fatal. Rotavirus infection usually occurs through ingestion of contaminated stool.

Because the virus is able to live a long time outside of the host, transmission can occur through ingestion of contaminated food or water, or by coming into direct contact with contaminated surfaces, then putting hands in the mouth.
Once it’s made its way in, the rotavirus infects the cells that line the small intestine and multiplies. It emits an enterotoxin, which gives rise to gastroenteritis.

13. Smallpox   Officially eradicated – Due to it’s long history, it impossible to estimate the carnage over the millennia Smallpox localizes in small blood vessels of the skin and in the mouth and throat. In the skin, this results in a characteristic maculopapular rash, and later, raised fluid-filled blisters. It has an overall mortality rate of 30–35%. Smallpox is believed to have emerged in human populations about 10,000 BC. The disease killed an estimated 400,000 Europeans per year during the closing years of the 18th century (including five reigning monarchs), and was responsible for a third of all blindness. Of all those infected, 20–60%—and over 80% of infected children—died from the disease.
Smallpox was responsible for an estimated 300–500 million deaths during the 20th century alone. In the early 1950s an estimated 50 million cases of smallpox occurred in the world each year.

As recently as 1967, the World Health Organization (WHO) estimated that 15 million people contracted the disease and that two million died in that year. After successful vaccination campaigns throughout the 19th and 20th centuries, the WHO certified the eradication of smallpox in December 1979.
Smallpox is one of only two infectious diseases to have been eradicated by humans, the other being Rinderpest, which was unofficially declared eradicated in October 2010.

The virus that causes smallpox wiped out hundreds of millions of people worldwide over thousands of years. We can’t even blame it on animals either, as the virus is only carried by and contagious for humans. There are several different types of smallpox disease that result from an infection ranging from mild to fatal, but it is generally marked by a fever, rash, and blistering, oozing pustules that develop on the skin. Fortunately, smallpox was declared eradicated in 1979, as the result of successful worldwide implementation of the vaccine.

14. Hepatitis B  521,000 Deaths a Year A third of the World’s population (over 2 billion people) has come in contact with this virus, including 350 million chronic carriers. In China and other parts of Asia, up to 10% of the adult population is chronically infected. The symptoms of acute hepatitis B include yellowing of the skin of eyes, dark urine, vomiting, nausea, extreme fatigue, and abdominal pain.

Luckily, more than 95% of people who contract the virus as adults or older children will make a full recovery and develop immunity to the disease. In other people, however, hepatitis B can bring on chronic liver failure due to cirrhosis or cancer.

Hepatitis B is an infectious illness of the liver caused by the hepatitis B virus (HBV) that affects hominoidea, including humans. It was originally known as "serum hepatitis". Many people have no symptoms during the initial infected. Some develop an acute illness with vomiting, yellow skin, dark urine and abdominal pain. Often these symptoms last a few weeks and rarely result in death. It may take 30 to 180 days for symptoms to begin. Less than 10% of those infected develop chronic hepatitis B. In those with chronic disease cirrhosis and liver cancer may eventually develop.

The virus is transmitted by exposure to infectious blood or body fluids.  Infection around the time of birth is the most common way the disease is acquired in areas of the world where is common. In areas where the disease is uncommon intravenous drug use and sex are the most common routes of infection. Other risk factors include working in a healthcare setting, blood transfusions, dialysis, sharing razors or toothbrushes with an infected person, travel in countries where it is common, and living in an institution.

Tattooing and acupuncture led to a significant number of cases in the 1980s; however, this has become less common with improved sterility. The hepatitis B viruses cannot be spread by holding hands, sharing eating utensils or drinking glasses, kissing, hugging, coughing, sneezing, or breastfeeding.  The hepatitis B virus is a hepadnavirus—hepa from hepatotropic (attracted to the liver) and dna because it is a DNA virus. The viruses replicate through an RNA intermediate form by reverse transcription, which in practice relates them to retroviruses.It is 50 to 100 times more infectious than HIV.

The infection has been preventable by vaccination since 1982. During the initial infected care is based on the symptoms present. In those who developed chronic disease antiviral medication such as tenofovir or interferon maybe useful, however are expensive.

About a third of the world population has been infected at one point in their lives, including 350 million who are chronic carriers. Over 750,000 people die of hepatitis B a year. The disease has caused outbreaks in parts of Asia and Africa, and it is now only common in China. Between 5 and 10% of adults in sub-Saharan Africa and East Asia have chronic disease. Research is in progress to create edible HBV vaccines in foods such as potatoes, carrots, and bananas.In 2004, an estimated 350 million individuals were infected worldwide. National and regional prevalence ranges from over 10% in Asia to under 0.5% in the United States and northern Europe. Routes of infection include vertical transmission (such as through childbirth), early life horizontal transmission (bites, lesions, and sanitary habits), and adult horizontal transmission (sexual contact, intravenous drug use).

The primary method of transmission reflects the prevalence of chronic HBV infection in a given area. In low prevalence areas such as the continental United States and Western Europe, injection drug abuse and unprotected sex are the primary methods, although other factors may also be important. In moderate prevalence areas, which include Eastern Europe, Russia, and Japan, where 2–7% of the population is chronically infected, the disease is predominantly spread among children. In high-prevalence areas such as China and South East Asia, transmission during childbirth is most common, although in other areas of high endemicity such as Africa, transmission during childhood is a significant factor. The prevalence of chronic HBV infection in areas of high endemicity is at least 8% with 10-15% prevalence in Africa/Far East. As of 2010, China has 120 million infected people, followed by India and Indonesia with 40 million and 12 million, respectively. According to World Health Organization (WHO), an estimated 600,000 people die every year related to the infection. In the United States about 19,000 new cases occurred in 2011 down nearly 90% from 1990.

Acute infection with hepatitis B virus is associated with acute viral hepatitis – an illness that begins with general ill-health, loss of appetite, nausea, vomiting, body aches, mild fever, and dark urine, and then progresses to development of jaundice. It has been noted that itchy skin has been an indication as a possible symptom of all hepatitis virus types. The illness lasts for a few weeks and then gradually improves in most affected people. A few people may have more severe liver disease (fulminant hepatic failure), and may die as a result. The infection may be entirely asymptomatic and may go unrecognized.

Chronic infection with hepatitis B virus either may be asymptomatic or may be associated with a chronic inflammation of the liver (chronic hepatitis), leading to cirrhosis over a period of several years. This type of infection dramatically increases the incidence of hepatocellular carcinoma (liver cancer). Across Europe hepatitis B and C cause approximately 50% of hepatocellular carcinomas. Chronic carriers are encouraged to avoid consuming alcohol as it increases their risk for cirrhosis and liver cancer. Hepatitis B virus has been linked to the development of membranous glomerulonephritis (MGN).

Symptoms outside of the liver are present in 1–10% of HBV-infected people and include serum-sickness–like syndrome, acute necrotizing vasculitis (polyarteritis nodosa), membranous glomerulonephritis, and papular acrodermatitis of childhood (Gianotti–Crosti syndrome). The serum-sickness–like syndrome occurs in the setting of acute hepatitis B, often preceding the onset of jaundice. The clinical features are fever, skin rash, and polyarteritis. The symptoms often subside shortly after the onset of jaundice, but can persist throughout the duration of acute hepatitis B.  About 30–50% of people with acute necrotizing vasculitis (polyarteritis nodosa) are HBV carriers. HBV-associated nephropathy has been described in adults but is more common in children.Membranous glomerulonephritis is the most common form. Other immune-mediated hematological disorders, such as essential mixed cryoglobulinemia and aplastic anemia.

15. Influenza 500,000 Deaths a Year Influenza has been a prolific killer for centuries. The symptoms of influenza were first described more than 2,400 years ago by Hippocrates. Pandemics generally occur three times a century, and can cause millions of deaths. The most fatal pandemic on record was the Spanish flu outbreak in 1918, which caused between 20 million and 100 million deaths. In order to invade a host, the virus shell includes proteins that bind themselves to receptors on the outside of cells in the lungs and air passages of the victim. Once the virus has latched itself onto the cell it takes over so much of its machinery that the cell dies. Dead cells in the airways cause a runny nose and sore throat. Too many dead cells in the lungs causes death.

 
Vaccinations against the flu are common in developed countries. However, a vaccination that is effective one year may not necessarily work the next year, due to the way the rate at which a flu virus evolves and the fact that new strains will soon replace older ones. No virus can claim credit for more worldwide pandemics and scares than influenza.

The outbreak of the Spanish flu in 1918 is generally considered to be one of the worst pandemics in human history, infecting 20 to 40 percent of the world’s population and killing 50 million in the span of just two years. (A reconstruction of that virus is above.) The swine flu was its most recent newsmaker, when a 2009 pandemic may have seen as many as 89 million people infected worldwide.

Effective influenza vaccines exist, and most people easily survive infections. But the highly infectious respiratory illness is cunning—the virus is constantly mutating and creating new strains. Thousands of strains exist at any given time, many of them harmless, and vaccines available in the U.S. cover only about 40 percent of the strains at large each year.

16. Hepatitis C  56,000 Deaths a Year An estimated 200-300 million people worldwide are infected with hepatitis C.

 

Most people infected with hepatitis C don’t have any symptoms and feel fine for years. However, liver damage invariably rears its ugly head over time, often decades after first infection. In fact, 70% of those infected develop chronic liver disease, 15% are struck with cirrhosis and 5% can die from liver cancer or cirrhosis. In the USA, hepatitis C is the primary reason for liver transplants.

Hepatitis C is an infectious disease affecting primarily the liver, caused by the hepatitis C virus (HCV). The infection is often asymptomatic, but chronic infection can lead to scarring of the liver and ultimately to cirrhosis, which is generally apparent after many years. In some cases, those with cirrhosis will go on to develop liver failure, liver cancer, or life-threatening esophageal and gastric varices.

HCV is spread primarily by blood-to-blood contact associated with intravenous drug use, poorly sterilized medical equipment, and transfusions. An estimated 150–200 million people worldwide are infected with hepatitis C. The existence of hepatitis C (originally identifiable only as a type of non-A non-B hepatitis) was suggested in the 1970s and proven in 1989. Hepatitis C infects only humans and chimpanzees.

The virus persists in the liver in about 85% of those infected. This chronic infection can be treated with medication: the standard therapy is a combination of peginterferon and ribavirin, with either boceprevir or telaprevir added in some cases. Overall, 50–80% of people treated are cured. Those who develop cirrhosis or liver cancer may require a liver transplant. Hepatitis C is the leading reason for liver transplantation, though the virus usually recurs after transplantation. No vaccine against hepatitis C is available.

Hepatitis C infection causes acute symptoms in 15% of cases. Symptoms are generally mild and vague, including a decreased appetite, fatigue, nausea, muscle or joint pains, and weight loss and rarely does acute liver failure result. Most cases of acute infection are not associated with jaundice. The infection resolves spontaneously in 10–50% of cases, which occurs more frequently in individuals who are young and female.

About 80% of those exposed to the virus develop a chronic infection.  This is defined as the presence of detectable viral replication for at least six months. Most experience minimal or no symptoms during the initial few decades of the infection.Chronic hepatitis C can be associated with fatigue and mild cognitive problems. Chronic infection after several years may cause cirrhosis or liver cancer. The liver enzymes are normal in 7–53%.  Late relapses after apparent cure have been reported, but these can be difficult to distinguish from reinfection.

Fatty changes to the liver occur in about half of those infected and are usually present before cirrhosis develops.  Usually (80% of the time) this change affects less than a third of the liver. Worldwide hepatitis C is the cause of 27% of cirrhosis cases and 25% of hepatocellular carcinoma.  About 10–30% of those infected develop cirrhosis over 30 years. Cirrhosis is more common in those also infected with hepatitis B, schistosoma, or HIV, in alcoholics and in those of male gender. In those with hepatitis C, excess alcohol increases the risk of developing cirrhosis 100-fold.Those who develop cirrhosis have a 20-fold greater risk of hepatocellular carcinoma. This transformation occurs at a rate of 1–3% per year.  Being infected with hepatitis B in additional to hepatitis C increases this risk further.

Liver cirrhosis may lead to portal hypertension, ascites (accumulation of fluid in the abdomen), easy bruising or bleeding, varices (enlarged veins, especially in the stomach and esophagus), jaundice, and a syndrome of cognitive impairment known as hepatic encephalopathy. Ascites occurs at some stage in more than half of those who have a chronic infection.

The most common problem due to hepatitis C but not involving the liver is mixed cryoglobulinemia (usually the type II form) — an inflammation of small and medium-sized blood vessels. Hepatitis C is also associated with Sjögren’s syndrome (an autoimmune disorder); thrombocytopenia; lichen planus; porphyria cutanea tarda; necrolytic acral erythema; insulin resistance; diabetes mellitus; diabetic nephropathy; autoimmune thyroiditis and B-cell lymphoproliferative disorders.  Thrombocytopenia is estimated to occur in 0.16% to 45.4% of people with chronic hepatitis C. 20–30% of people infected have rheumatoid factor — a type of antibody. Possible associations include Hyde’s prurigo nodularis and membranoproliferative glomerulonephritis. Cardiomyopathy with associated arrhythmias has also been reported. A variety of central nervous system disorders have been reported.  Chronic infection seems to be associated with an increased risk of pancreatic cancer.

Persons who have been infected with hepatitis C may appear to clear the virus but remain infected. The virus is not detectable with conventional testing but can be found with ultra-sensitive tests.The original method of detection was by demonstrating the viral genome within liver biopsies, but newer methods include an antibody test for the virus’ core protein and the detection of the viral genome after first concentrating the viral particles by ultracentrifugation. A form of infection with persistently moderately elevated serum liver enzymes but without antibodies to hepatitis C has also been reported. This form is known as cryptogenic occult infection.

Several clinical pictures have been associated with this type of infection. It may be found in people with anti-hepatitis-C antibodies but with normal serum levels of liver enzymes; in antibody-negative people with ongoing elevated liver enzymes of unknown cause; in healthy populations without evidence of liver disease; and in groups at risk for HCV infection including those on haemodialysis or family members of people with occult HCV. The clinical relevance of this form of infection is under investigation. The consequences of occult infection appear to be less severe than with chronic infection but can vary from minimal to hepatocellular carcinoma.

The rate of occult infection in those apparently cured is controversial but appears to be low 40% of those with hepatitis but with both negative hepatitis C serology and the absence of detectable viral genome in the serum have hepatitis C virus in the liver on biopsy.How commonly this occurs in children is unknown.
There is no cure, no vaccine.

17. Measle  197,000 Deaths a Year Measles, also known as Rubeola, has done a pretty good job of killing people throughout the ages. Over the last 150 years, the virus has been responsible for the deaths of around 200 million people. The fatality rate from measles for otherwise healthy people in developed countries is 3 deaths per thousand cases, or 0.3%. In underdeveloped nations with high rates of malnutrition and poor healthcare, fatality rates have been as high as 28%. In immunocompromised patients (e.g. people with AIDS) the fatality rate is approximately 30%.

During the 1850s, measles killed a fifth of Hawaii’s people. In 1875, measles killed over 40,000 Fijians, approximately one-third of the population. In the 19th century, the disease decimated the Andamanese population. In 1954, the virus causing the disease was isolated from an 11-year old boy from the United States, David Edmonston, and adapted and propagated on chick embryo tissue culture.

To date, 21 strains of the measles virus have been identified.

18. Yellow Fever  30,000 Deaths a Year. Yellow fever is an acute viral hemorrhagic disease transmitted by the bite of female mosquitoes and is found in tropical and subtropical areas in South America and Africa. The only known hosts of the virus are primates and several species of mosquito. The origin of the disease is most likely to be Africa, from where it was introduced to South America through the slave trade in the 16th century. Since the 17th century, several major epidemics of the disease have been recorded in the Americas, Africa and Europe. In the 19th century, yellow fever was deemed one of the most dangerous infectious diseases.

Yellow fever presents in most cases with fever, nausea, and pain and it generally subsides after several days. In some patients, a toxic phase follows, in which liver damage with jaundice (giving the name of the disease) can occur and lead to death. Because of the increased bleeding tendency (bleeding diathesis), yellow fever belongs to the group of hemorrhagic fevers.

Since the 1980s, the number of cases of yellow fever has been increasing, making it a reemerging disease Transmitted through infected mosquitoes, Yellow Fever is still a serious problem in countries all over the world and a serious health risk for travelers to Africa, South America and some areas in the Caribbean.  Fatality rates range from 15 to over 50%. Symptoms include high fever, headache, abdominal pain, fatigue, vomiting and nausea.

Yellow fever is a hemorrhagic fever transmitted by infected mosquitoes. The yellow is in reference to the yellow color (jaundice) that affects some patients. The virus is endemic in tropical areas in Africa and South America.

The disease typically occurs in two phases. The first phase typically causes fever, headache, muscle pain and back pain, chills and nausea. Most patients recover from these symptoms while 15% progresses to the toxic second phase. High fever returns, jaundice becomes apparent, patient complains of abdominal pain with vomiting, and bleeding in the mouth, eyes, nose or stomach occurs. Blood appears in the stool or vomit and kidney function deteriorates. 50% of the patients that enter the toxic phase die within 10 to 14 days.

There is no treatment for yellow fever. Patients are only given supportive care for fever, dehydration and respiratory failure. Yellow fever is preventable through vaccination.

19. Rabies  55,000 Deaths a Year Rabies is almost invariably fatal if post-exposure prophylaxis is not administered prior to the onset of severe symptoms. If there wasn’t a vaccine, this would be the most deadly virus on the list.

It is a zoonotic virus transmitted through the bite of an animal. The virus worms its way into the brain along the peripheral nerves. The incubation phase of the rabies disease can take up to several months, depending on how far it has to go to reach the central nervous system. It provokes acute pain, violent movements, depression, uncontrollable excitement, and inability to swallow water (rabies is often known as ‘hydrophobia’). After these symptoms subside the fun really starts as the infected person experiences periods of mania followed by coma then death, usually caused by respiratory insufficiency.

Rabies has a long and storied history dating back to 2300 B.C., with records of Babylonians who went mad and died after being bitten by dogs. While this virus itself is a beast, the sickness it causes is now is wholly preventable if treated immediately with a series of vaccinations (sometimes delivered with a terrifyingly huge needle in the abdomen). We have vaccine inventor Louis Pasteur to thank for that.

Exposure to rabies these days, while rare in the U.S., still occurs as it did thousands of years ago—through bites from infected animals. If left untreated after exposure, the virus attacks the central nervous system and death usually results. The symptoms of an advanced infection include delirium, hallucinations and raging, violent behavior in some cases, which some have argued makes rabies eerily similar to zombification. If rabies ever became airborne, we might actually have to prepare for that zombie apocalypse after all.

21. Common Cold  No known cure The common cold is the most frequent infectious disease in humans with on average two to four infections a year in adults and up to 6–12 in children. Collectively, colds, influenza, and other infections with similar symptoms are included in the diagnosis of influenza-like illness.

They may also be termed upper respiratory tract infections (URTI). Influenza involves the lungs while the common cold does not.
It’s annoying as hell, but there’s nothing to do but wave the white flag on this one.
Virus: Infinity. People: 0

22. Anthrax  Anthrax is a diseased caused by a bacterium called Bacillus Anthracis. There are three types of anthrax, skin, lung, and digestive. Anthrax has lately become a major world issue for its ability to become an epidemic and spread quickly and easily among people through contact with spores.

It is important to know that  Anthrax is not spread from person to person, but is through contact/handling of products containing spores. Flu like symptoms, nausea, and blisters are common symptoms of exposure. Inhalational anthrax and gastrointestinal anthrax are serious issue because of their high mortality rates ranging from 50 to 100%.

Anthrax is a severe infectious disease caused by the bacteria Bacillus anthracis. This type of bacteria produces spores that can live for years in the soil. Anthrax is more common in farm animals, though humans can get infected as well. Anthrax is not contagious. A person can get infected only when the bacteria gets into the skin, lungs or  digestive tract.

There are three types of anthrax: skin anthrax, inhalation anthrax and gastrointestinal anthrax. Skin anthrax symptoms include fever, muscle aches, headache, nausea and vomiting. Inhalation anthrax begins with flu-like symptoms, which progresses  with severe respiratory distress. Shock, coma and then death follows. Most patients do not recover even if given appropriate antibiotics due to the toxins released by the anthrax bacteria. Gastrointestinal anthrax symptoms include fever, nausea, abdominal pain and bloody diarrhea.

Anthrax is treated with antibiotics.

23. Malaria  Malaria is a mosquito-borne illness caused by parasite. Although malaria can be prevented and treated, it is often fatal.

Each year about 1 million people die from Malaria.  Common symptoms include fever, chills, headache. Sweats, and fatigue. Malaria is a serious disease caused by Plasmodium parasites that infects Anopheles mosquitoes which feeds on humans. Initial symptoms include high fever, shaking chills, headache and vomiting – symptoms that may be too  mild to be identified as malaria. If not treated within 24 hours, it can progress to severe illnesses that could lead to death.

The WHO estimates that malaria caused 207,000,000 clinical episodes and 627,000 deaths, mostly among African children,  in 2012. About 3.5 billion people from 167 countries live in areas at risk of malaria transmission.

24. Cholera  Due to the severe dehydration it causes, if left untreated Cholera can cause death within hours. In 1991 a major outbreak occurred in South America though currently few cases are known outside of Sub-Saharan Africa.

Symptoms include severe diarrhea, vomiting and leg cramping. Cholera is usually contracted through ingestion of contaminated water or food. Cholera is an acute intestinal infection caused by a bacterium called Vibrio cholera. It has an incubation period of less than a day to five days and causes painless, watery diarrhea that quickly leads to severe dehydration and death if treatment is not promptly given.

Cholera remains a global problem and continues to be a challenge for countries where access to safe drinking water and sanitation is a problem.

25.  Typhoid Fever  Patients with typhoid fever sometimes demonstrate a rash of flat, rose-colored spots and a sustained fever of 103 to 104.

Typhoid is contracted through contact with the S. Typhi bacteria, which is carried by humans in both their blood stream and stool. Over 400 cases occur in the US, 20% of those who contract it die. Typhoid fever is a serious and potentially fatal disease caused by the bacterium Salmonella Typhi. This type of bacteria lives only in humans. People sick with typhoid fever carry the bacteria in their bloodstream and intestinal tract and transmit the bacteria through their stool.

A person can get typhoid fever by drinking or eating food contaminated with Salmonella Typhi or if contaminated sewage gets into the water used for drinking or washing dishes.

Typhoid fever symptoms include high fever, weakness, headache, stomach pains or loss of appetite. Typhoid fever is determined by testing the presence of Salmonella Typhi in the stool or blood of an infected person. Typhoid fever is treated with antibiotics.

26. SARS (Severe Acute Respiratory Syndrome) and the MERS VIRUS A new Pneumonia disease that emerged in China in 2003. After news of the outbreak of SARS China tried to silence news about it both internal and international news , SARS spread rapidly, reaching neighboring countries Hong Kong and Vietnam in late February 2003, and then to other countries via international travelers.Canada Had a outbreak that was fairly well covered and cost Canada quite a bit financially

The last case of this epidemic occurred in June 2003. In that outbreak, 8069 cases arise that killed 775 people. There is speculation that this disease is Man-Made SARS, SARS has symptoms of flu and may include: fever, cough, sore throat and other non-specific symptoms.

The only symptom that is common to all patients was fever above 38 degrees Celsius. Shortness of breath may occur later. There is currently no vaccine for the disease so that countermeasures can only assist the breathing apparatus. The virus was said to be the Virus of the End Times

27.  MERS(Middle Eastern Respiratory Syndrome) The Middle East respiratory syndrome coronavirus (MERS-CoV), also termed EMC/2012 (HCoV-EMC/2012), is positive-sense, single-stranded RNA novel species of the genus Betacoronavirus.

First called novel coronavirus 2012 or simply novel coronavirus, it was first reported in 2012 after genome sequencing of a virus isolated from sputum samples from patients who fell ill in a 2012 outbreak of a new flu.

As of June 2014, MERS-CoV cases have been reported in 22 countries, including Saudi Arabia, Malaysia, Jordan, Qatar, Egypt, the United Arab Emirates, Kuwait, Oman, Algeria, Bangladesh, the Philippines (still MERS-free), Indonesia (none was confirmed), the United Kingdom, and the United States. Almost all cases are somehow linked to Saudi Arabia. In the same article it was reported that Saudi authorities’ errors in response to MERS-CoV were a contributing factor to the spread of this deadly virus.

27. Enterovirus (Brain Inflammation) Entero virus is a disease of the hands, feet and mouth, and we can not ignored occasional Brain Inflammation. Enterovirus attack symptoms are very similar to regular flu symptoms so its difficult to detect it, such as fever, sometimes accompanied by dizziness and weakness and pain.

Next will come the little red watery bumps on the palms and feet following oral thrush. In severe conditions, Enterovirus can attack the nerves and brain tissue to result in death.

The virus is easily spread through direct contact with patients. Children are the main victims of the spread of enterovirus in China. Since the first victim was found but reporting was delayed until several weeks later.

24 thousand people have contracted the enterovirus. More than 30 of them died mostly children. The virus is reported to have entered Indonesia and infecting three people in Sumatra.  2014Enterovirus 68 is presently spreading across North America mainly and started in the USA has probably spread to Canada and Mexico by now. Enterovirus 68’s spread is unprecedented up till now

28.  The Black Plague  The 1918 flu virus and HIV are the biggest killers of modern times. But back in the 14th century, the bacterium that causes bubonic plague, or the Black Death as it was also known, was the baddest bug of all. In just a few years, from 1347 to 1351, the plague killed off about 75,000,000 people worldwide, including one-third of the entire population of Europe at that time.

It spread through Asia, Italy, North Africa, Spain, Normandy, Switzerland, and eastward into Hungary. After a brief break, it crossed into England, Scotland, and then to Norway, Sweden, Denmark, Iceland and Greenland.

Yersinia pestis, the plague bacteria
Courtesy of Neal Chamberlain

The plague bacterium is called Yersinia <yer-sin-ee-uh> pestis. There are two main forms of the disease. In the bubonic <boo-bah-nick> form, the bacteria cause painful swellings as large as an orange to form in the armpits, neck and groin. These swellings, or buboes, often burst open, oozing blood and pus. Blood vessels leak blood that puddles under the skin, giving the skin a blackened look. That’s why the disease became known as the Black Death. At least half of its victims die within a week.

The pneumonic <new-mon-ick> form of plague causes victims to sweat heavily and cough up blood that starts filling their lungs. Almost no one survived it during the plague years. Yersinia pestis is the deadliest microbe we’ve ever known, although HIV might catch up to it. Yersinia pestis is still around in the world. Fortunately, with bacteria-killing antibiotics and measures to control the pests—rats and mice—that spread the bacteria, we’ve managed to conquer this killer.

29. Human Papillomavirus  Human papillomavirus (HPV) is a DNA virus from the papillomavirus family that is capable of infecting humans. Like all papillomaviruses, HPVs establish productive infections only in keratinocytes of the skin or mucous membranes.

Most HPV infections are subclinical and will cause no physical symptoms; however, in some people subclinical infections will become clinical and may cause benign papillomas (such as warts [verrucae] or squamous cell papilloma), or cancers of the cervix, vulva, vagina, penis, oropharynx and anus.HPV has been linked with an increased risk of cardiovascular disease. In addition, HPV 16 and 18 infections are a cause of a unique type of oropharyngeal (throat) cancer and are believed to cause 70% of cervical cancer, which have available vaccines, see HPV vaccine.

More than 30 to 40 types of HPV are typically transmitted through sexual contact and infect the anogenital region. Some sexually transmitted HPV types may cause genital warts. Persistent infection with "high-risk" HPV types—different from the ones that cause skin warts—may progress to precancerous lesions and invasive cancer. High-risk HPV infection is a cause of nearly all cases of cervical cancer.However, most infections do not cause disease.

Seventy percent of clinical HPV infections, in young men and women, may regress to subclinical in one year and ninety percent in two years. However, when the subclinical infection persists—in 5% to 10% of infected women—there is high risk of developing precancerous lesions of the vulva and cervix, which can progress to invasive cancer. Progression from subclinical to clinical infection may take years; providing opportunities for detection and treatment of pre-cancerous lesions.

In more developed countries, cervical screening using a Papanicolaou (Pap) test or liquid-based cytology is used to detect abnormal cells that may develop into cancer. If abnormal cells are found, women are invited to have a colposcopy. During a colposcopic inspection, biopsies can be taken and abnormal areas can be removed with a simple procedure, typically with a cauterizing loop or, more commonly in the developing world—by freezing (cryotherapy).

Treating abnormal cells in this way can prevent them from developing into cervical cancer. Pap smears have reduced the incidence and fatalities of cervical cancer in the developed world, but even so there were 11,000 cases and 3,900 deaths in the U.S. in 2008. Cervical cancer has substantial mortality worldwide, there are an estimated 490,000 cases and 270,000 deaths each year.

It is true that infections caused by human papillomavirus (HPV) are not fatal, but chronic infection may result in cervical cancer. Apparently, HPV is responsible for almost all cervical cancers (approx. 99%). HPV results in 275,000 deaths per year.

30. Henipaviruses The genus Henipavirus comprises of 3 members which are Hendra virus (HeV), Nipah virus (NiV), and Cedar virus (CedPV). The second one was introduced in the middle of 2012, although affected no human, and is therefore considered harmless. The rest of the two viruses, however, are lethal with mortality rate up to 50-100%.

Hendra virus (originally Equine morbillivirus) was discovered in September 1994 when it caused the deaths of thirteen horses, and a trainer at a training complex in Hendra, a suburb of Brisbane in Queensland, Australia.

The index case, a mare, was housed with 19 other horses after falling ill, and died two days later. Subsequently, all of the horses became ill, with 13 dying. The remaining 6 animals were subsequently euthanized as a way of preventing relapsing infection and possible further transmission.The trainer, Victory (‘Vic’) Rail, and a stable hand were involved in nursing the index case, and both fell ill with an influenza-like illness within one week of the first horse’s death. The stable hand recovered while Mr Rail died of respiratory and renal failure. The source of the virus was most likely frothy nasal discharge from the index case.

A second outbreak occurred in August 1994 (chronologically preceding the first outbreak) in Mackay 1,000 km north of Brisbane resulting in the deaths of two horses and their owner. The owner, Mark Preston, assisted in necropsies of the horses and within three weeks was admitted to hospital suffering from meningitis. Mr Preston recovered, but 14 months later developed neurologic signs and died. This outbreak was diagnosed retrospectively by the presence of Hendra virus in the brain of the patient.

A survey of wildlife in the outbreak areas was conducted, and identified pteropid fruit bats as the most likely source of Hendra virus, with a seroprevalence of 47%. All of the other 46 species sampled were negative. Virus isolations from the reproductive tract and urine of wild bats indicated that transmission to horses may have occurred via exposure to bat urine or birthing fluids.  However, the only attempt at experimental infection reported in the literature, conducted at CSIRO Geelong, did not result in infection of a horse from infected flying foxes. This study looked at potential infection between bats, horses and cats, in various combinations. The only species that was able to infect horses was the cat (Felix spp.)

Nipah virus was identified in April 1999, when it caused an outbreak of neurological and respiratory disease on pig farms in peninsular Malaysia, resulting in 257 human cases, including 105 human deaths and the culling of one million pigs.  In Singapore, 11 cases, including one death, occurred in abattoir workers exposed to pigs imported from the affected Malaysian farms. The Nipah virus has been classified by the Centers for Disease Control and Prevention as a Category C agent. The name "Nipah" refers to the place, Kampung Baru Sungai Nipah in Negeri Sembilan State, Malaysia, the source of the human case from which Nipah virus was first isolated.

The outbreak was originally mistaken for Japanese encephalitis (JE), however, physicians in the area noted that persons who had been vaccinated against JE were not protected, and the number of cases among adults was unusual Despite the fact that these observations were recorded in the first month of the outbreak, the Ministry of Health failed to react accordingly, and instead launched a nationwide campaign to educate people on the dangers of JE and its vector, Culex mosquitoes.

Symptoms of infection from the Malaysian outbreak were primarily encephalitic in humans and respiratory in pigs. Later outbreaks have caused respiratory illness in humans, increasing the likelihood of human-to-human transmission and indicating the existence of more dangerous strains of the virus. Based on seroprevalence data and virus isolations, the primary reservoir for Nipah virus was identified as Pteropid fruit bats, including Pteropus vampyrus (Large Flying Fox), and Pteropus hypomelanus (Small flying fox), both of which occur in Malaysia.

The transmission of Nipah virus from flying foxes to pigs is thought to be due to an increasing overlap between bat habitats and piggeries in peninsular Malaysia. At the index farm, fruit orchards were in close proximity to the piggery, allowing the spillage of urine, feces and partially eaten fruit onto the pigs. Retrospective studies demonstrate that viral spillover into pigs may have been occurring in Malaysia since 1996 without detection. During 1998, viral spread was aided by the transfer of infected pigs to other farms, where new outbreaks occurred.

Cedar Virus (CedPV) was first identified in pteropid urine during work on Hendra virus undertaken in Queensland in 2009. Although the virus is reported to be very similar to both Hendra and Nipah, it does not cause illness in laboratory animals usually susceptible to paramyxoviruses. Animals were able to mount an effective response and create effective antibodies.

The scientists who identified the virus report:

Hendra and Nipah viruses are 2 highly pathogenic paramyxoviruses that have emerged from bats within the last two decades. Both are capable of causing fatal disease in both humans and many mammal species. Serological and molecular evidence for henipa-like viruses have been reported from numerous locations including Asia and Africa, however, until now no successful isolation of these viruses have been reported. This paper reports the isolation of a novel paramyxovirus, named Cedar virus, from fruit bats in Australia. Full genome sequencing of this virus suggests a close relationship with the henipaviruses.

 

 

Antibodies to Cedar virus were shown to cross react with, but not cross neutralize Hendra or Nipah virus. Despite this close relationship, when Cedar virus was tested in experimental challenge models in ferrets and guinea pigs, we identified virus replication and generation of neutralizing antibodies, but no clinical disease was observed. As such, this virus provides a useful reference for future reverse genetics experiments to determine the molecular basis of the pathogenicity of the henipaviruses.

30. Lyssaviruses  This genus comprises of not only rabies virus (causing death of almost everyone who is infected) but certain other viruses such as Duvenhage virus, Mokola virus, and Australian bat lyssavirus. Although small number of cases are reported, but the ones reported have always been fatal. Bats are vectors for all of these types except for Mokola virus.

 

Lyssavirus (from Lyssa, the Greek goddess of madness, rage, and frenzy) is a genus of viruses belonging to the family Rhabdoviridae, in the order Mononegavirales. This group of RNA viruses includes the rabies virus traditionally associated with the disease. Viruses typically have either helical or cubic symmetry. Lyssaviruses have helical symmetry, so their infectious particles are approximately cylindrical in shape. This is typical of plant-infecting viruses. Human-infecting viruses more commonly have cubic symmetry and take shapes approximating regular polyhedra. The structure consists of a spiked outer envelope, a middle region consisting of matrix protein M, and an inner ribonucleocapsid complex region, consisting of the genome associated with other proteins.

Lyssavirus genome consists of a negative-sense, single-stranded RNA molecule that encodes five viral proteins: polymerase L, matrix protein M, phosphoprotein P, nucleoprotein N, and glycoprotein G.

Based on recent phylogenetic evidence, lyssa viruses are categorized into seven major species. In addition, five species recently have been discovered: West Caucasian bat virus, Aravan virus, Khuj and virus, Irkut virus and Shimoni bat virus. The major species include rabies virus (species 1), Lagos bat virus (species 2), Mokola virus (species 3), Duvenhage virus (species 4), European Bat lyssaviruses type 1 and 2 (species 5 and 6), and Australian bat lyssavirus (species 7).

Based on biological properties of the viruses, these species are further subdivided into phylogroups 1 and 2. Phylogroup 1 includes genotypes 1, 4, 5, 6, and 7, while phylogroup 2 includes genotypes 2 and 3. The nucleocapsid region of lyssavirus is fairly highly conserved from genotype to genotype across both phylogroups; however, experimental data have shown the lyssavirus strains used in vaccinations are only from the first species(i.e. classic rabies).

31. Tuberculosis  Mucous, fever, fatigue, excessive sweating and weight loss. What do they all have in common?

They are symptoms of pulmonary tuberculosis, or TB. TB is a contagious bacterial infection that involves the lungs, but it may spread to other organs. The symptoms of this disease can remain stagnant for years or affect the person right away. People at higher risk for contracting TB include the elderly, infants and those with weakened immune systems due to other diseases, such as AIDS or diabetes, or even individuals who have undergone chemotherapy.

Being around others who may have TB, maintaining a poor diet or living in unsanitary conditions are all risk factors for contracting TB. In the United States, there are approximately 10 cases of TB per 100,000 people. Tuberculosis, MTB, or TB (short for tubercle bacillus), in the past also called phthisis, phthisis pulmonalis, or consumption, is a widespread, and in many cases fatal, infectious disease caused by various strains of mycobacteria, usually Mycobacterium tuberculosis.

Tuberculosis typically attacks the lungs, but can also affect other parts of the body. It is spread through the air when people who have an active TB infection cough, sneeze, or otherwise transmit respiratory fluids through the air. Most infections do not have symptoms, known as latent tuberculosis. About one in ten latent infections eventually progresses to active disease which, if left untreated, kills more than 50% of those so infected.

The classic symptoms of active TB infection are a chronic cough with blood-tinged sputum, fever, night sweats, and weight loss (the latter giving rise to the formerly common term for the disease, "consumption"). Infection of other organs causes a wide range of symptoms. Diagnosis of active TB relies on radiology (commonly chest X-rays), as well as microscopic examination and microbiological culture of body fluids.

Diagnosis of latent TB relies on the tuberculin skin test (TST) and/or blood tests. Treatment is difficult and requires administration of multiple antibiotics over a long period of time. Social contacts are also screened and treated if necessary. Antibiotic resistance is a growing problem in multiple drug-resistant tuberculosis (MDR-TB) infections. Prevention relies on screening programs and vaccination with the bacillus Calmette-Guérin vaccine.

One-third of the world’s population is thought to have been infected with M. tuberculosis, with new infections occurring in about 1% of the population each year.In 2007, an estimated 13.7 million chronic cases were active globally, while in 2010, an estimated 8.8 million new cases and 1.5 million associated deaths occurred, mostly in developing countries. The absolute number of tuberculosis cases has been decreasing since 2006, and new cases have decreased since 2002.

The rate of tuberculosis in different areas varies across the globe; about 80% of the population in many Asian and African countries tests positive in tuberculin tests, while only 5–10% of the United States population tests positive. More people in the developing world contract tuberculosis because of a poor immune system, largely due to high rates of HIV infection and the corresponding development of AIDS.

32. Encephalitis Virus Encephalitis is an acute inflammation of the brain, commonly caused by a viral infection. Victims are usually exposed to viruses resulting in encephalitis by insect bites or food and drink. The most frequently encountered agents are arboviruses (carried by mosquitoes or ticks) and enteroviruses ( coxsackievirus, poliovirus and echovirus ). Some of the less frequent agents are measles, rabies, mumps, varicella and herpes simplex viruses.

Patients with encephalitis suffer from fever, headache, vomiting, confusion, drowsiness and photophobia. The symptoms of encephalitis are caused by brain’s defense mechanisms being activated to get rid of infection (brain swelling, small bleedings and cell death). Neurologic examination usually reveals a stiff neck due to the irritation of the meninges covering the brain. Examination of the cerebrospinal fluidCerebrospinal fluid CSF in short, is the clear fluid that occupies the subarachnoid space (the space between the skull and cortex of the brain). It acts as a "cushion" or buffer for the cortex.

Also, CSF occupies the ventricular system of the brain and the obtained by a lumbar puncture In medicine, a lumbar puncture (colloquially known as a spinal tap is a diagnostic procedure that is done to collect a sample of cerebrospinal fluid (CSF) for biochemical, microbiological and cytological analysis. Indications The most common indication for procedure reveals increased amounts of proteins and white blood cells with normal glucose. A CT scan examination is performed to reveal possible complications of brain swelling, brain abscess Brain abscess (or cerebral abscess) is an abscess caused by inflammation and collection of infected material coming from local (ear infection, infection of paranasal sinuses, infection of the mastoid air cells of the temporal bone, epidural abscess) or re or bleeding. Lumbar puncture procedure is performed only after the possibility of a prominent brain swelling is excluded by a CT scan examination.

What are the main Symptoms?
Some patients may have symptoms of a cold or stomach infection before encephalitis symptoms begin.
When a case of encephalitis is not very severe, the symptoms may be similar to those of other illnesses, including:
• Fever that is not very high
• Mild headache
• Low energy and a poor appetite

Other symptoms include:
• Clumsiness, unsteady gait
• Confusion, disorientation
• Drowsiness
• Irritability or poor temper control
• Light sensitivity
• Stiff neck and back (occasionally)
• Vomiting

Symptoms in newborns and younger infants may not be as easy to recognize:
• Body stiffness
• Irritability and crying more often (these symptoms may get worse when the baby is picked up)
• Poor feeding
• Soft spot on the top of the head may bulge out more
• Vomiting

• Loss of consciousness, poor responsiveness, stupor, coma
• Muscle weakness or paralysis
• Seizures
• Severe headache
• Sudden change in mental functions:
• "Flat" mood, lack of mood, or mood that is inappropriate for the situation
• Impaired judgment
• Inflexibility, extreme self-centeredness, inability to make a decision, or withdrawal from social interaction
• Less interest in daily activities
• Memory loss (amnesia), impaired short-term or long-term memory

Children and adults should avoid contact with anyone who has encephalitis.
Controlling mosquitoes (a mosquito bite can transmit some viruses) may reduce the chance of some infections that can lead to encephalitis.
• Apply an insect repellant containing the chemical, DEET when you go outside (but never use DEET products on infants younger than 2 months).
• Remove any sources of standing water (such as old tires, cans, gutters, and wading pools).
• Wear long-sleeved shirts and pants when outside, particularly at dusk.
Vaccinate animals to prevent encephalitis caused by the rabies virus.

 

33. Chicken Pox Virus Chickenpox is a highly contagious disease caused by primary infection with varicella zoster virus (VZV).It usually starts with a vesicular skin rash mainly on the body and head rather than on the limbs. The rash develops into itchy, raw pockmarks, which mostly heal without scarring. On examination, the observer typically finds skin lesions at various stages of healing and also ulcers in the oral cavity and tonsil areas. The disease is most commonly observed in children.

Chickenpox is an airborne disease which spreads easily through coughing or sneezing by ill individuals or through direct contact with secretions from the rash. A person with chickenpox is infectious one to two days before the rash appears. They remain contagious until all lesions have crusted over (this takes approximately six days). Immunocompromised patients are contagious during the entire period as new lesions keep appearing. Crusted lesions are not contagious.Chickenpox has been observed in other primates, including chimpanzees and gorillas.

The origin of the term chicken pox, which is recorded as being used since 1684,is not reliably known. It has been said to be a derived from chickpeas, based on resemblance of the vesicles to chickpeas, or to come from the rash resembling chicken pecks. Other suggestions include the designation chicken for a child (i.e., literally ‘child pox’), a corruption of itching-pox, or the idea that the disease may have originated in chickens. Samuel Johnson explained the designation as "from its being of no very great danger."

The early (prodromal) symptoms in adolescents and adults are nausea, loss of appetite, aching muscles, and headache. This is followed by the characteristic rash or oral sores, malaise, and a low-grade fever that signal the presence of the disease. Oral manifestations of the disease (enanthem) not uncommonly may precede the external rash (exanthem). In children the illness is not usually preceded by prodromal symptoms, and the first sign is the rash or the spots in the oral cavity. The rash begins as small red dots on the face, scalp, torso, upper arms and legs; progressing over 10–12 hours to small bumps, blisters and pustules; followed by umbilication and the formation of scabs.

At the blister stage, intense itching is usually present. Blisters may also occur on the palms, soles, and genital area. Commonly, visible evidence of the disease develops in the oral cavity & tonsil areas in the form of small ulcers which can be painful or itchy or both; this enanthem (internal rash) can precede the exanthem (external rash) by 1 to 3 days or can be concurrent. These symptoms of chickenpox appear 10 to 21 days after exposure to a contagious person. Adults may have a more widespread rash and longer fever, and they are more likely to experience complications, such as varicella pneumonia.Because watery nasal discharge containing live virus usually precedes both exanthem (external rash) and enanthem (oral ulcers) by 1 to 2 days, the infected person actually becomes contagious one to two days prior to recognition of the disease. Contagiousness persists until all vesicular lesions have become dry crusts (scabs), which usually entails four or five days, by which time nasal shedding of live virus also ceases.

Chickenpox is rarely fatal, although it is generally more severe in adult men than in women or children. Non-immune pregnant women and those with a suppressed immune system are at highest risk of serious complications. Arterial ischemic stroke (AIS) associated with chickenpox in the previous year accounts for nearly one third of childhood AIS. The most common late complication of chickenpox is shingles (herpes zoster), caused by reactivation of the varicella zoster virus decades after the initial, often childhood, chickenpox infection.

Shingles  Herpes zoster After a chickenpox infection, the virus remains dormant in the body’s nerve tissues. The immune system keeps the virus at bay, but later in life, usually as an adult, it can be reactivated and cause a different form of the viral infection called shingles (scientifically known as herpes zoster). The United States Advisory Committee on Immunization Practices (ACIP) suggests that any adult over the age of 60 years gets the herpes zoster vaccine as a part of their normal medical check ups.

Many adults who have had chickenpox as children are susceptible to shingles as adults, often with the accompanying condition postherpetic neuralgia, a painful condition that makes it difficult to sleep. Even after the shingles rash has gone away, there can be night pain in the area affected by the rash.Shingles affects one in five adults infected with chickenpox as children, especially those who are immune suppressed, particularly from cancer, HIV, or other conditions.

However, stress can bring on shingles as well, although scientists are still researching the connection.Shingles are most commonly found in adults over the age of 60 who were diagnosed with chickenpox when they were under the age of 1.A shingles vaccine is available for adults over 50 who have had childhood chickenpox or who have previously had shingles.

34. POXVIRUS  Poxviruses (members of the family Poxviridae) are viruses that can, as a family, infect both vertebrate and invertebrate animals.

Four genera of poxviruses may infect humans: orthopox, parapox, yatapox, molluscipox. Orthopox: smallpox virus (variola), vaccinia virus, cowpox virus, monkeypox virus; Parapox: orf virus, pseudocowpox, bovine papular stomatitis virus; Yatapox: tanapox virus, yaba monkey tumor virus; Molluscipox: molluscum contagiosum virus (MCV).The most common are vaccinia (seen on Indian subcontinent) and molluscum contagiousum, but monkeypox infections are rising (seen in west and central African rainforest countries). Camelpox is a disease of camels caused by a virus of the family Poxviridae, subfamily Chordopoxvirinae, and the genus Orthopoxvirus. It causes skin lesions and a generalized infection. Approximately 25% of young camels that become infected will die from the disease, while infection in older camels is generally more mild.

The ancestor of the poxviruses is not known but structural studies suggest it may have been an adenovirus or a species related to both the poxviruses and the adenoviruses. Based on the genome organization and DNA replication mechanism it seems that phylogenetic relationships may exist between the rudiviruses (Rudiviridae) and the large eukaryal DNA viruses: the African swine fever virus (Asfarviridae), Chlorella viruses (Phycodnaviridae) and poxviruses (Poxviridae).The mutation rate in these genomes has been estimated to be 0.9-1.2 x 10⁻⁶ substitutions per site per year.A second estimate puts this rate at 0.5-7 × 10⁻⁶ nucleotide substitutions per site per year.  A third estimate places the rate at 4-6 × 10⁻⁶.

The last common ancestor of the extant poxviruses that infect vertebrates existed 0.5 million years ago. The genus Avipoxvirus diverged from the ancestor 249 ± 69 thousand years ago. The ancestor of the genus Orthopoxvirus was next to diverge from the other clades at 0.3 million years ago. A second estimate of this divergence time places this event at 166,000 ± 43,000 years ago. The division of the Orthopox into the extant genera occurred ~14,000 years ago. The genus Leporipoxvirus diverged ~137,000 ± 35,000 years ago. This was followed by the ancestor of the genus Yatapoxvirus. The last common ancestor of the Capripoxvirus and Suipoxvirus diverged 111,000 ± 29,000 years ago.

A model of a poxvirus cut-away in
cross-section to show the internal
structures. Poxviruses are shaped like
flattened capsules/barrels or are lens or
pill-shaped.

Their structure is complex,
neither icosahedral nor helical. This
model is based on Vaccinia, the smallpox
virus. The structures are also highly
variable and often incompletely studied.

 

35. West Nile Virus  West Nile virus (WNV) is a mosquito-borne zoonotic arbovirus belonging to the genus Flavivirus in the family Flaviviridae.

This flavivirus is found in temperate and tropical regions of the world. It was first identified in the West Nile subregion in the East African nation of Uganda in 1937. Prior to the mid-1990s, WNV disease occurred only sporadically and was considered a minor risk for humans, until an outbreak in Algeria in 1994, with cases of WNV-caused encephalitis, and the first large outbreak in Romania in 1996, with a high number of cases with neuroinvasive disease. WNV has now spread globally, with the first case in the Western Hemisphere being identified in New York City in 1999; over the next five years, the virus spread across the continental United States, north into Canada, and southward into the Caribbean islands and Latin America. WNV also spread to Europe, beyond the Mediterranean Basin, and a new strain of the virus was identified in Italy in 2012. WNV is now considered to be an endemic pathogen in Africa, Asia, Australia, the Middle East, Europe and in the United States, which in 2012 has experienced one of its worst epidemics. In 2012, WNV killed 286 people in the United States, with the state of Texas being hard hit by this virus, making the year the deadliest on record for the United States.

The main mode of WNV transmission is via various species of mosquitoes, which are the prime vector, with birds being the most commonly infected animal and serving as the prime reservoir host—especially passerines, which are of the largest order of birds, Passeriformes. WNV has been found in various species of ticks, but current research suggests they are not important vectors of the virus. WNV also infects various mammal species, including humans, and has been identified in reptilian species, including alligators and crocodiles, and also in amphibians. Not all animal species that are susceptible to WNV infection, including humans, and not all bird species develop sufficient viral levels to transmit the disease to uninfected mosquitoes, and are thus not considered major factors in WNV transmission.

Approximately 80% of West Nile virus infections in humans are subclinical, which cause no symptoms. In the cases where symptoms do occur—termed West Nile fever in cases without neurological disease—the time from infection to the appearance of symptoms (incubation period) is typically between 2 and 15 days. Symptoms may include fever, headaches, fatigue, muscle pain or aches, malaise, nausea, anorexia, vomiting, myalgias and rash. Less than 1% of the cases are severe and result in neurological disease when the central nervous system is affected. People of advanced age, the very young, or those with immunosuppression, either medically induced, such as those taking immunosupressive drugs, or due to a pre-existing medical condition such as HIV infection, are most susceptible. The specific neurological diseases that may occur are West Nile encephalitis, which causes inflammation of the brain, West Nile meningitis, which causes inflammation of the meninges, which are the protective membranes that cover the brain and spinal cord, West Nile meningoencephalitis, which causes inflammation of the brain and also the meninges surrounding it, and West Nile poliomyelitis—spinal cord inflammation, which results in a syndrome similar to polio, which may cause acute flaccid paralysis.

Currently, no vaccine against WNV infection is available. The best method to reduce the rates of WNV infection is mosquito control on the part of municipalities, businesses and individual citizens to reduce breeding populations of mosquitoes in public, commercial and private areas via various means including eliminating standing pools of water where mosquitoes breed, such as in old tires, buckets, unused swimming pools, etc. On an individual basis, the use of personal protective measures to avoid being bitten by an infected mosquito, via the use of mosquito repellent, window screens, avoiding areas where mosquitoes are more prone to congregate, such as near marshes, areas with heavy vegetation etc., and being more vigilant from dusk to dawn when mosquitoes are most active offers the best defense. In the event of being bitten by an infected mosquito, familiarity of the symptoms of WNV on the part of laypersons, physicians and allied health professions affords the best chance of receiving timely medical treatment, which may aid in reducing associated possible complications and also appropriate palliative care.

The incubation period for WNV—the amount of time from infection to symptom onset—is typically from between 2 and 15 days. Headache can be a prominent symptom of WNV fever, meningitis, encephalitis, meningoencephalitis, and it may or may not be present in poliomyelytis-like syndrome. Thus, headache is not a useful indicator of neuroinvasive disease.(CDC)

• West Nile fever (WNF), which occurs in 20 percent of cases, is a febrile syndrome that causes flu-like symptoms. Most characterizations of WNF generally describe it as a mild, acute syndrome lasting 3 to 6 days after symptom onset. Systematic follow-up studies of patients with WNF have not been done, so this information is largely anecdotal. In addition to a high fever, headache, chills, excessive sweating, weakness, fatigue, swollen lymph nodes, drowsiness, pain in the joints and flu-like symptoms. Gastrointestinal symptoms that may occur include nausea, vomiting, loss of appetite, and diarrhea. Fewer than one-third of patients develop a rash.

• West Nile neuroinvasive disease (WNND), which occurs in less than 1 percent of cases, is when the virus infects the central nervous system resulting in meningitis, encephalitis, meningoencephalitis or a poliomyelitis-like syndrome.  Many patients with WNND have normal neuroimaging studies, although abnormalities may be present in various cerebral areas including the basal ganglia, thalamus, cerebellum, and brainstem.

• West Nile virus encephalitis (WNE) is the most common neuroinvasive manifestation of WNND. WNE presents with similar symptoms to other viral encephalitis with fever, headaches, and altered mental status. A prominent finding in WNE is muscular weakness (30 to 50 percent of patients with encephalitis), often with lower motor neuron symptoms, flaccid paralysis, and hyporeflexia with no sensory abnormalities.

• West Nile meningitis (WNM) usually involves fever, headache, and stiff neck. Pleocytosis, an increase of white blood cells in cerebrospinal fluid, is also present. Changes in consciousness are not usually seen and are mild when present.

• West Nile meningoencephalitis is inflammation of both the brain (encephalitis) and meninges (meningitis).

• West Nile poliomyelitis (WNP), an acute flaccid paralysis syndrome associated with WNV infection, is less common than WNM or WNE. This syndrome is generally characterized by the acute onset of asymmetric limb weakness or paralysis in the absence of sensory loss. Pain sometimes precedes the paralysis. The paralysis can occur in the absence of fever, headache, or other common symptoms associated with WNV infection. Involvement of respiratory muscles, leading to acute respiratory failure, can sometimes occur.

• West-Nile reversible paralysis,. Like WNP, the weakness or paralysis is asymmetric. Reported cases have been noted to have an initial preservation of deep tendon reflexes, which is not expected for a pure anterior horn involvement.Disconnect of upper motor neuron influences on the anterior horn cells possibly by myelitis or glutamate excitotoxicity have been suggested as mechanisms.The prognosis for recovery is excellent.

• Nonneurologic complications of WNV infection that may rarely occur include fulminant hepatitis, pancreatitis,  myocarditis, rhabdomyolysis, orchitis, nephritis, optic neuritis and cardiac dysrhythmias and hemorrhagic fever with coagulopathy.^[15] Chorioretinitis may also be more common than previously thought.

• Cutaneous manifestations specifically rashes, are not uncommon in WNV-infected patients; however, there is a paucity of detailed descriptions in case reports and there are few clinical images widely available. Punctate erythematous (?), macular, and papular eruptions, most pronounced on the extremities have been observed in WNV cases and in some cases histopathologic findings have shown a sparse superficial perivascular lymphocytic infiltrate, a manifestation commonly seen in viral exanthems (?). A literature review provides support that this punctate rash is a common cutaneous presentation of WNV infection. (Anderson RC et al.)

West Nile virus life cycle. After binding and uptake, the virion envelope fuses with cellular membranes, followed by uncoating of the nucleocapsid and release of the RNA genome into the cytoplasm. The viral genome serves as messenger RNA (mRNA) for translation of all viral proteins and as template during RNA replication. Copies are subsequently packaged within new virus particles that are transported in vesicles to the cell membrane.

WNV is one of the Japanese encephalitis antigenic serocomplex of viruses. Image reconstructions and cryoelectron microscopy reveal a 45–50 nm virion covered with a relatively smooth protein surface. This structure is similar to the dengue fever virus; both belong to the genus Flavivirus within the family Flaviviridae.

The genetic material of WNV is a positive-sense, single strand of RNA, which is between 11,000 and 12,000 nucleotides long; these genes encode seven nonstructural proteins and three structural proteins. The RNA strand is held within a nucleocapsid formed from 12-kDa protein blocks; the capsid is contained within a host-derived membrane altered by two viral glycoproteins. Phylogenetic tree of West Nile viruses based on sequencing of the envelope gene during complete genome sequencing of the virus

Studies of phylogenetic lineages determined WNV emerged as a distinct virus around 1000 years ago. This initial virus developed into two distinct lineages, lineage 1 and its multiple profiles is the source of the epidemic transmission in Africa and throughout the world. Lineage 2 was considered an Africa zoonosis. However, in 2008, lineage 2, previously only seen in horses in sub-Saharan Africa and Madagascar, began to appear in horses in Europe, where the first known outbreak affected 18 animals in Hungary in 2008. Lineage 1 West Nile virus was detected in South Africa in 2010 in a mare and her aborted fetus; previously, only lineage 2 West Nile virus had been detected in horses and humans in South Africa. A 2007 fatal case in a killer whale in Texas broadened the known host range of West Nile virus to include cetaceans.

The United States virus was very closely related to a lineage 1 strain found in Israel in 1998. Since the first North American cases in 1999, the virus has been reported throughout the United States, Canada, Mexico, the Caribbean, and Central America. There have been human cases and equine cases, and many birds are infected. The Barbary macaque, Macaca sylvanus, was the first nonhuman primate to contract WNV.  Both the United States and Israeli strains are marked by high mortality rates in infected avian populations; the presence of dead birds—especially Corvidae—can be an early indicator of the arrival of the virus.

The West Nile virus maintains itself in nature by cycling between mosquitoes and certain species of birds. A mosquito (the vector) bites an uninfected bird (the host), the virus amplifies within the bird, an uninfected mosquito bites the bird and is in turn infected. Other species such as humans and horses are incidental infections, as they are not the mosquitoes’ preferred blood meal source. The virus does not amplify within these species and they are known as dead-end hosts.

The West Nile virus (WNV) is transmitted through female mosquitoes, which are the prime vectors of the virus. Only females feed on blood, and different species have evolved to take a blood meal on preferred types of vertebrate hosts. The infected mosquito species vary according to geographical area; in the United States, Culex pipiens (Eastern United States), Culex tarsalis (Midwest and West), and Culex quinquefasciatus (Southeast) are the main sources.The various species that transmit the WNV prefer birds of the Passeriformes order, the largest order of birds. Within that order there is further selectivity with various mosquito species exhibiting preference for different species. In the United States WNV mosquito vectors have shown definitive preference for members of the Corvidae and Thrush family of birds. Amongst the preferred species within these families are the American crow, a corvid, and the American robin (Turdus migratorius), a thrush.

The proboscis of a female mosquito—here a Southern House Mosquito (Culex quinquefasciatus)—pierces the epidermis and dermis to allow it to feed on human blood from a capillary: this one is almost fully tumescent. The mosquito injects saliva, which contains an anesthetic, and an anticoagulant into the puncture wound; and in infected mosquitoes, the West Nile virus.

The birds develop sufficient viral levels after being infected, to transmit the infection to other biting mosquitoes that in turn go on to infect other birds. In crows and robins, the infection is fatal in 4–5 days. This epizootic viral amplification cycle has been shown to peak 15–16 days before humans become ill. This may be due to the high mortality, and thus depletion of the preferred hosts, i.e., the specific bird species. The mosquitoes become less selective and begin feeding more readily on other animal types such as humans and horses which are considered incidental hosts.

In mammals, the virus does not multiply as readily (i.e., does not develop high viremia during infection), and mosquitoes biting infected mammals are not believed to ingest sufficient virus to become infected,making mammals so-called dead-end hosts.

Direct human-to-human transmission initially was believed to be caused only by occupational exposure, or conjunctive exposure to infected blood. The US outbreak identified additional transmission methods through blood transfusion,organ transplant intrauterine exposure, and breast feeding. Since 2003, blood banks in the United States routinely screen for the virus among their donors. As a precautionary measure, the UK’s National Blood Service initially ran a test for this disease in donors who donate within 28 days of a visit to the United States, Canada or the northeastern provinces of Italy and the Scottish National Blood Transfusion Service asks prospective donors to wait 28 days after returning from North America or the northeastern provinces of Italy before donating.

Recently, the potential for mosquito saliva to impact the course of WNV disease was demonstrated. Mosquitoes inoculate their saliva into the skin while obtaining blood. Mosquito saliva is a pharmacological cocktail of secreted molecules, principally proteins, that can affect vascular constriction, blood coagulation, platelet aggregation, inflammation, and immunity. It clearly alters the immune response in a manner that may be advantageous to a virus. Studies have shown it can specifically modulate the immune response during early virus infection, and mosquito feeding can exacerbate WNV infection, leading to higher viremia and more severe forms of disease.

Vertical transmission, the transmission of a viral or bacterial disease from the female of the species to her offspring, has been observed in various West Nile virus studies, amongst different species of mosquitoes in both the laboratory and in nature.Mosquito progeny infected vertically in autumn, may potentially serve as a mechanism for WNV to overwinter and initiate enzootic horizontal transmission the following spring.

Computer Models Tell Us That This Ebola Pandemic Could Soon Kill Millions

Computer Models Tell Us That This Ebola Pandemic Could Soon Kill Millions

We could potentially be on the verge of the greatest health crisis that any of us have ever seen

Image Credits: Sebástian Freire / Flickr (Medical workers)

by Michael Snyder | Economic Collapse | September 16, 2014

We could potentially be on the verge of the greatest health crisis that any of us have ever seen.  The number of Ebola cases in Africa has approximately doubled over the past three weeks, and scientific computer models tell us that this Ebola pandemic could ultimately end up killing millions of us – especially if it starts spreading on other continents.  At first, many assumed that this Ebola outbreak would be just like all the others – that it would flare up for a little while and then it would completely fade away.  But that has not happened this time.  Instead, this epidemic has seemed to pick up momentum with each passing week.  Despite extraordinary precautions,hundreds of health workers have gotten the virus, and the head of the CDC says that the spread of Ebola is “spiraling out of control” and that it is “going to get worse in the very near future.”  For those that have thought that all of this talk about Ebola was just “fearmongering”, it is time for you to wake up.

Right now, the World Health Organization says that we could see the total number of Ebola cases reach 20,000 nine months from now.  But computer models created for the National Institutes of Health and the Department of Defense are projecting that Ebola could soon be growing at a rate of 20,000 cases per month…

The Ebola epidemic affecting West Africa is predicted to last a further 12 to 18 months, according to U.S. scientists.

Epidemiologists have been creating computer models of the Ebola epidemic for the National Institutes of Health and the Defense Department.

The model they have created is a far less optimistic estimate than that of the World Health Organization (WHO), which last month said it hoped to contain the outbreak within nine months and 20,000 total cases.

The New York Times reports that various researchers have said the virus could grow at a rate that could be closer to 20,000 per month.

The WHO is sticking to its estimates, a spokesman said Friday.

Other scientists are even more pessimistic.

For example, a model created jointly by a researcher at the University of Tokyo and a researcher at Arizona State University has produced a “worst-case scenario” of 277,124 Ebola cases by the end of this year…

The Eurosurveillance paper, by two researchers from the University of Tokyo and Arizona State University, attempts to derive what the reproductive rate has been in Guinea, Liberia and Sierra Leone. (Note for actual epidemiology geeks: The calculation is for the effective reproductive number, pegged to a point in time, hence actually R_t.) They come up with an R of at least 1, and in some cases 2; that is, at certain points, sick persons have caused disease in two others.

You can see how that could quickly get out of hand, and in fact, that is what the researchers predict. Here is their stop-you-in-your-tracks assessment:

In a worst-case hypothetical scenario, should the outbreak continue with recent trends, the case burden could gain an additional 77,181 to 277,124 cases by the end of 2014.

That is a jaw-dropping number.

If we do see an explosion like that, how many millions of cases will we see by the time 2015 is through?

A different model has produced an even more jaw-dropping number.

An “econometric simulation model” created by Francis Smart at Michigan State University is predicting that a whopping 1.2 million people will die from Ebola in the next six months…

An econometric simulation model based on the assumption the World Health Organization and others will be unable to control the Ebola outbreak in West Africa predicts 1.2 million people will die from the disease in the next six months.

Six months is the minimum time the WHO projects will be necessary to contain the epidemic.

In his analysis, econometrics research assistantFrancis Smart at Michigan State University took seriously the conclusions of Canadian researchers who proved the strain of Ebola in the current West African epidemic could go airborne.

The Ebola virus could be transmitted between humans through breathing, Smart says.

In developing the model, Smart began with WHO’s Aug. 28 statement that the Ebola epidemic in West Africa could afflict more than 20,000 people before it is brought under control.

That has got to be the worst possible number, right?

Wrong.

The other day a prominent German virologist came forward and declared that “it is too late” to stop Ebola and that five million people will die in Sierra Leone and Liberia alone…

A top German virologist has caused shockwaves by asserting that it’s too late to halt the spread of Ebola in Sierra Leone and Liberia and that five million people will die, noting that efforts should now be focused on stopping the transmission of the virus to other countries.

Jonas Schmidt-Chanasit of the Bernhard Nocht Institute for Tropical Medicine in Hamburg told Germany’s Deutsche Welle that hope is all but lost for the inhabitants of Sierra Leone and Liberia and that the virus will only “burn itself out” when it has infected the entire population and killed five million people.

“The right time to get this epidemic under control in these countries has been missed,” said Schmidt-Chanasit. “That time was May and June. “Now it is too late.”

So which of the numbers discussed above are accurate?

Only time will tell.

Meanwhile, the U.S. federal government is feverishly preparing for the worst.

This week we learned that Barack Obama is going to ask Congress for 88 million dollars for the purpose of conducting “a major Ebola offensive” in Africa.

Granted, Obama will ask Congress for money at the drop of a hat these days.  He wants 500 million dollars to arm the allies of ISIS and his reckless spending has been one of the primary factors why the U.S. national debt has risen by more than a trillion dollars over the past 12 months.

But it is still noteworthy.

Even more noteworthy is the fact that the U.S. State Department has just ordered 160,000 Hazmat suits…

The U.S. State Department has ordered 160,000 Hazmat suits for Ebola, prompting concerns that the federal government is anticipating the rapid spread of a virus that has already claimed an unprecedented number of lives.

In a press release posted by Market Watch, Lakeland Industries, a manufacturer of industrial protective clothing for first responders, announced that it had signaled its intention “to join the fight against the spread of Ebola” by encouraging other suppliers to meet the huge demand created by the U.S. State Department’s order of 160,000 hazmat suits.

“With the U.S. State Department alone putting out a bid for 160,000 suits, we encourage all protective apparel companies to increase their manufacturing capacity for sealed seam garments so that our industry can do its part in addressing this threat to global health,” states the press release.

The huge bulk order of hazmat suits for Ebola has stoked concerns that the U.S. government expects the virus to continue to ravage countries in west Africa and may also be concerned about an outbreak inside the United States.

You don’t order that many Hazmat suits unless you are anticipating an outbreak of apocalyptic proportions.

And the CDC has just issued a six page Ebola checklist to hospitals to help them spot potential Ebola patients in America…

The Centers for Disease Control and Prevention, warning hospitals and doctors that “now is the time to prepare,” has issued a six-page Ebola “checklist” to help healthcare workers quickly determine if patients are infected.

While the CDC does not believe that there are new cases of Ebola in the United States, the assumption in the checklist is that it is only a matter of time before the virus hits home.

Let us hope and pray that these precautions do not become necessary.

Because if Ebola starts spreading like wildfire in this country, we are going to see pain and suffering beyond anything that most of us have ever imagined.

Just consider what a health worker on the front lines is seeing on a day to day basis…

I wake up each morning – if I have managed to sleep – wondering if this is really happening, or if it is a horror movie. In decades of humanitarian work I have never witnessed such relentless suffering of fellow human beings or felt so completely paralysed and utterly overwhelmed at our inability to provide anything but the most basic, and sometimes less than adequate, care.

I am supervising the suspect tent, which has room for 25 patients who are likely to have Ebola – 80-90% of those we test have the virus. We administer treatment for malaria, start patients on antibiotics, paracetamol, multivitamins, rehydration supplements, food, water and juice while they wait for their results. Sometimes people have arrived too late and die shortly after arriving.

In one afternoon last week I watched five seemingly fit, healthy, young men die. I gave the first a bottle of oral rehydration solution and came back with another for the second. In the half a minute or so in which I had been away the first man died, his bottle of water spilt across the floor. The four others followed in quick succession.

Ebola is truly a terrible, terrible disease.

The moment that cases start popping up in the United States, all of our lives will instantly change.

I hope that you are getting prepared for that.

Is the Deadly Kissing Bug Disease the New HIV/AIDS?

 

photo credit: Wikipedia

Chagas, a disease caused by a parasite transmitted via the Triatoma bug (aka, the kissing bug), is claiming thousands of lives in Central and South America.  Some experts are even calling it the “new HIV/AIDS of the Americas”.  But is this comparison accurate, and how big a threat is the disease to the US?

Chagas is not a new disease. It’s named after Carlos Chagas (circa 1909), a Brazilian doctor who discovered that Triatoma carry a potentially lethal parasite called Trypanosoma cruzi. After several of his patients developed a strange infection that he couldn’t identify, Chagas set out to investigate how humans come in contact with the pathogen and its effects on the body of its host.  He probably didn’t realize at the time that his work would prove to be groundbreaking in the history of epidemiology (Chagas later went on to identify the parasitic fungal genus Pneumocystis, another major discovery).

Kissing bugs, named because they bite the face and lips of humans (they’re also called assassin bugs),  live in tropical climates near warm-blooded vertebrates to gain easy access to their blood.  They stay hidden for much of the day, living in concealed places such as the cracks in a piece of wood and thatched roofs, and usually strike their victims as they sleep.  The bugs defecate as they feed, allowing the parasite they carry to infect a new host.

According to the Centers for Disease Control and Prevention (CDC), the early stage of Chagas occurs immediately after infection and may have mild or no symptoms at all.  Symptoms generally include fever, malaise, and a swelling of one eye. If left untreated, the infection can continue for years, often with no further symptoms, and over time it damages the heart, intestines and esophagus.  There are two known treatments for the disease but they only work when administered in the early stages of infection. Once organ tissue has been damaged, it’s usually too late.

According to an editorial in the online journal PLoS, about 10 million people are currently living with Chagas, making it one of the most common neglected tropical diseases in Latin America and the Caribbean. It kills roughly 20,000 people worldwide every year. Lead author Dr. Peter Hotez, dean of the National School of Tropical Medicine at Baylor College of Medicine inHouston, warns that the disease is spreading globally and there may be between 300,000 and 1 million cases in the US.

While the infection is triggered by contact with a kissing bug, the disease appears to spread most rapidly via blood transfusions, organ transplants, and from mother to child during pregnancy — hence the comparison with HIV/AIDS.

There are, however, major differences between Chagas and HIV/AIDS, including that the parasite is not transmitted via sexual contact. And unlike HIV, which evaded detection in the blood supply for years, Chagas can be identified through blood screening and eliminated before it spreads.  The problem is that screening requirements differ from country to country, and too often screening procedures are poorly administered or simply ignored.

Also unlike HIV/AIDS–at least in the early days of the disease–we know proven ways to prevent Chagas infection.  Insect nets that prevent kissing bugs from biting humans are effective. Proper screening of the blood supply and reporting the disease are critical steps, as well as screening for the disease during pregnancy.

Is the disease a threat to the US? That depends on where you live. Texans, in particular, may have cause for concern because blood-donation screening is not mandatory in the state and physicians are not required to report the disease’s occurrence to health authorities, according to Wired.

What we do know is that Chagas is a major problem throughout Central and South America, and will continue to be until measures are taken to prevent its transmission.  Unfortunately, those measures require adequate funding, and the countries most afflicted by the disease are also among the poorest.  And since people can remain infected for up to 30 years before succumbing, we may have only started to see the true extent of the damage.

You can find me on Twitter @neuronarrative and at my website, The Daily Brain.

Chagas Disease: New AIDS Of The Americas Tropical Disease Brought By The Kissing Bug

image credit: trialx.com

Public Library of Science’s Neglected Tropical Diseases published an editorial in a medical journal
called the “The new AIDS of the Americas,” a tropical disease spread by insects called “chagas” similar to HIV/AIDS epidemic.

“There are a number of striking similarities between people living with Chagas disease and people living with HIV/AIDS,” the authors wrote, “particularly for those with HIV/AIDS who contracted the disease in the first two decades of the HIV/AIDS epidemic.”

Unlike HIV, Chagas is not a s-e-x-u-a-l-l-y transmitted disease: it’s “caused by parasites
transmitted to humans by blood-s-u-c-k-i-n-g insects.” It’s called the kissing bug. When it ingests your blood, it excretes the parasite at the same time. When you wake up and scratch the itch, the parasite moves into the wound and you’re infected.”

According to Dr. Peter Hotez, a researcher at Baylor College of Medicine and one of the
editorial’s authors, there are two problems:

First, once the heart symptoms start, which is the most dreaded complication—the Chagas
cardiomyopathy—the medicines no longer work very well and second the medicines are extremely toxic.

Apparently, more than 8 million people have been infected by Chagas, most of them in Latin and Central America. But more than 300,000 live in the United States.

Chagas, also known as American trypanosomiasis, k-i-l-l-s about 20,000 people per year, the journal said. Chagas disease is caused by blood s-u-c-k-i-n-g insects who transmit trypanosomes. watch the video.

The ‘new AIDS of the Americas’: Experts warn of deadly insect-borne disease that can cause victims’ hearts to explode

By Daily Mail Reporter

PUBLISHED: 20:13 GMT, 29 May 2012 | UPDATED: 08:49 GMT, 30 May 2012

A little-known life-threatening illness caused by blood sucking insects has been labelled the ‘new AIDS of the Americas’ by experts.

The parasitic illness called Chagas Disease has similarities to the early spread of HIV, according to a new study.

Similar to AIDS, Chagas is difficult to detect and it can take years for symptoms to emerge, according to experts writing in the journal PLOS Neglected Tropical Diseases.

The new AIDS? A parasitic illness called Chagas disease has been dubbed the ‘new AIDS of the Americas’ by experts. It is usually transmitted from the bite of blood-sucking insect species called Triatome bugs, which include ‘Kissing bugs’ (Triatomids)

An estimated 10 million people worldwide are infected with most sufferers in Bolivia, Mexico, Columbia and Central America, as well as approximately 30,000 people in the U.S., reported the New York Times.

The disease – once largely contained to Latin America – has spread into the U.S due to increases in travel and immigration.

THE DANGEROUS SPREAD OF CHAGAS DISEASE

Named after the Brazilian doctor who discovered it in 1909, Chagas disease is a potentially deadly illness spread by blood-sucking insects including Triatomids most commonly known as ‘kissing bugs.’

Like AIDS, the illness is difficult to detect and has a long remission period.

It spreads easily through blood transfusions and from mother to child.

Approximately a quarter of victims who contract the disease develop enlarged heart or intestines that can burst causing sudden death.

An estimated 10 million people worldwide are infected, including 30,000 people in the U.S.

Chagas is considered one of the Neglected Parasitic Infections, a group of five parasitic diseases that have been targeted by CDC for public health action.

It is estimated that in 2008 Chagas disease killed more than 10,000 people.

Due to the severity of the illness, the amount of people infected and the ability of prevention, Chagas is considered one of the Neglected Parasitic Infections, a group of five parasitic diseases that have been targeted by CDC for public health action.

Chagas commonly affects people in poverty-stricken areas and most U.S. cases are found in immigrants.

If caught early enough, the disease can be prevented with an intense 3-month drug treatment.

However, because of the lengthy incubation period and costly medication, Chagas is often left untreated.

Also known as the American trypanosomiasis, the disease spreads easily either through blood transfusions or, less commonly, from mother to child.

All blood banks in the U.S. and Latin America screen for traces of the disease.

Most blood banks in the U.S began screening for it in 2007.

Chagas is usually transmitted from the bite of blood-sucking insect species called Triatome bugs which release a parasite called Trypanosoma cruzi into the victim’s bloodstream.

The species includes Triatomids – black wingless beetles about 20mm in length commonly known as ‘kissing bugs’. Their closest relative is the Tsetse fly, found in Africa, which spread Sleeping Sickness (where the victim’s brain swells).

Chagas disease comes in two phases – acute and severe.

The acute phase may have no symptoms but can present a fever, general feeling of being unwell and swelling in one eye.

Victim: Charles Darwin may have contracted the disease as he travelled the globe on HMS Beagle in his 20s

After the acute phase the disease goes into remission and it can take years before symptoms, such as constipation, abdomen pain and digestive problems, emerge again in the severe stage.

The parasite can eventually make its way to the heart, where it can live and multiply.

About a quarter of the people who contract Chagas, develop enlarged heart or intestines that can burst causing sudden death.

Although the drugs available are not as expensive as those for AIDS, there are shortages of the medication in poorer countries and little money is being spent on discovering new treatments.

Chagas disease is named after Carlos Ribeiro Justiniano Chagas, a Brazilian doctor who first discovered the disease in 1909.

Researchers from the University of Maryland School of Medicine said last year that they believed Charles Darwin suffered from three different illnesses, including a Chagas infection.

The experts believe he contracted the disease during a five-year trip around the globe on the HMS Beagle in his 20s – and attributed it to his death of heart failure 47 years later.

The father of modern life scientists wrote in his journal that he had been bitten by a ‘wingless black bug’ during the expedition, where he visited South America.

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SOME OTHER BAD BUGS

Arthropod Vectors

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Soft Ticks

Class:     Arachnida
    Subclass:     Acari
Order:         Ixodida
Family:     Argasidae
Genus:      Ornithodorous

Image 12-1. Ornithodoros – Soft Tick(SOURCE: CDC)

Image 12-2. Ornithodorus moubata, the most important soft tick disease vector found throughout the world (SOURCE: CDC)

General Characteristics

Soft Ticks are characterized by a tough leathery integument and a flattened oval shape when examined dorsally.  The Argasidae lack the dorsal shield present in the Hard Ticks (Ixodidae), and need to be examined ventrally to observe their capitulum or mouthparts. Soft ticks generally have a world-wide distribution, with the most important disease vector Ornithodoros populatingEurope, Africa, Asia and the Americas.

Life Cycles

Illustration 12-1.  Life Cycle of  Soft Ticks. (SOURCE: Unknown)

Soft ticks have a hemimetabolous life cycle, with eggs hatching six legged larvae, which molt to eight legged nymphs. There are five to seven larval instars depending on the species, with each stage requiring a blood meal to proceed. Larvae of Ornithodoros moubata do not require a blood meal to molt to the nymph stage. Adult females lay small egg batches following each blood meal. The duration of the life cycle depends on the temperature, host availability, and inherently the particular species in question.

The adults are flat and oval in outline and have tough, leathery, wrinkled bodies. The mouthparts are situated underneath the body and are not visible from above.  The eggs are laid in the places where the adults rest, such as cracks and crevices in the walls and floors of houses and in furniture. The larva, the five nymphal stages and the adults all actively search for hosts from which to take blood-meals. After feeding, which lasts about 30 minutes, they drop to the ground. Most species can survive for more than a year between blood-meals, and some for more than 10 years.

The soft ticks live apart from their hosts and are most common in the nests and resting places of the animals on which they feed. Some species, such as the chicken tick and the pigeon tick (Argasspecies) may feed on humans when the preferred hosts are not available.

Species that commonly feed on humans are found around villages and inside houses. Their habits are comparable to those of bedbugs: ticks often emerge from hiding places at night to suck the blood of humans and animals. Some species are common on travel routes, in rest houses and camping sites, and in caves and crevices.

Disease

Soft Ticks are vectors for serious disease including tick borne relapsing fever (Borrelia duttoni), rickettsial disease (Coxiella burneti), and some arboviruses. The most important disease spread by soft ticks is tick borne relapsing fever which occurs world-wide and is spread by spirochete infected Ornithodoros. Q-fever and arboviruses can be spreadfollowing a blood meal, but are both primarily introduced into the population by the Hard Ticks.

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Tick-borne Relapsing Fever

This disease is caused by a microorganism of the genus Borrelia. It is transmitted by biting soft ticks of the genus Ornithodoros in many countries in the tropics and subtropics and also in Europe and North America. The ticks usually feed quickly at night in or near houses, and then leave the host.

The disease causes bouts of fever alternating with periods without fever. Death occurs in about 2-10% of persons who are untreated.

Treatment

Treatment is possible with tetracycline or its derivatives.

Prevention

Prevention requires measures to control soft ticks and to avoid their bites.

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Hard Ticks

Class:     Arachnida
Subclass:     Acari
Order:         Ixodida
Family:     Ixodidae
Species:Ixodes, Amblyomma, Rhipicephalus, Dermacentor

General Characteristics

Hard ticks appear flattened when examined dorsally and can be primarily characterized by the presence of a dorsal plate or scutum, and a capitulum that projects beyond the body outline. The scutum regularly covers the entire dorsal area, although females may have a reduced plate present directly behind the capitulum. Ixodes spp. inhabit in Canada, Europe, Asiatic Russia, China, Japan, and Australia.

Image 12-3. Ixodes scapularis – male – showing the scutum covering the whole length of the body (left); Ixodes scapularis – female, showing the scutum covering half the length of the body (right)

Image 12-4. Amblyomma variegatum – male – showing the scutum covering the whole length of the body (left); Amblyomma variegatum – female – showing the scutum covering half the length of the body (right)

Image 12-5. Rhipicephalus sanguineus – female – showing the scutum covering half the length of the body (left); Rhipicephalus sanguineus – male – showing the scutum covering the whole length of the body (right).(AFPMB – used with permission)

Image 12-6. Dermacentor variabilis – male – showing the scutum covering the whole length of the body (left); Dermacentor variabilis – female – showing the scutum covering half the length of the body (right) (Image courtesy of: Iowa State University)

Life Cycle

 

Hard Ticks have a hemimetabolous life cycle similar to that of the Soft Ticks. Hard tick larvae search for suitable hosts, feed for several days, and drop off engorged to the ground below. Molting to the nymph stage follows several days later and the tick again searches for a suitable blood source. There is only one nymphal stage in Ixodes, and following several weeks of stasis the nymph will molt into an adult. Females lay one large mass of eggs, which forms a cellular mass on the scutum of the ovipositing female.

Disease

Hard ticks transmit a variety of diseases including Lyme Disease, Tick Paralysis, Rickettsia, arboviruses that are responsible for encephalitis and hemorrhagic fevers, tularemia and Babesia microtiinfection.  Tick paralysis is caused by the toxins present in the saliva of the tick, and is introduced during feeding.

Lyme disease is a serious ailment caused by the spirochete Borrelia burgdorferi.  Lyme disease results in acute erythema, systematic lesions and eventually chronic involvement of multiple organs.

Rickettsiae diseases spread by Ixodes include Q-fever (Coxiella burneti) and arboviruses that cause serious encephalitis.

Babesia microti infection primarily involves animals, with Man as an accidental host. The parasite is present in the tick salivary glands and is passed to Man via tick bite. Once in the bloodstream, the parasites enter the erythrocytes. Infection with B. microti ranges from asymptomatic to severe illness. Symptoms generally resemble those of malaria with fever, rigors, myalgia, and malaise. Occasionally there is mild or moderate hemolytic anemia and jaundice (renal failure). Parasitemia can be up to 25% in the immunocompetent individual, and up to 80% in patients who have been splenectomized.

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Other Medically Important Hard Ticks

General Characteristics

Several other species of ticks are also responsible for the spread of disease throughout the world. Wood ticks (Dermacentor andersoni) are found in the mountainous west of North America; dog ticks (Rhipicephalus) are found in coastal areas. Lone Star ticks (Amblyomma americanum) are found in forests in SE USA where deer are found. The females of these species are known to cause a condition known as tick paralysis.

Image 12-7. Amblyomma, hard tick. The scutum is so-called ‘enameled’ colored areas, and is described as being an ornate species.  (SOURCE:  PHIL 5981 – CDC)

Image 12-8. Dermacentor variabilis, ticks of this species show very ornate scutums, covering the length of the body (left – male). When blood engorged it is harder to see the scutum (right – female). (SOURCE:  PHIL 5977 – CDC)

Life Cycle

 

Illustration 12-2.  One-host tick life cycle.  (SOURCE: CDC)

Illustration 12-3.  Two-host tick life cycle. (SOURCE: CDC)

Illustration 12-4.  Three-host tick life cycle. (SOURCE: CDC)

Hard Ticks have a hemimetabolous life cycle similar to that of the soft ticks. Hard tick larvae search for suitable hosts feed for several days, and drop off engorged to the ground below. Molting to the nymph stage follows several days later and the tick again searches for a suitable blood source. There is only one nymphal stage in Ixodes, and following several weeks of stasis the nymph will molt into an adult. Females lay one large mass of eggs, which forms a cellular mass on the scutum of the ovipositing female.

Image 12-9. Female tick with egg mass. (SOURCE:  PHIL 5968 – CDC)

Diseases

Both Dermacentor and Amblyomma transmit Rocky Mountain Spotted Fever (Rickettsia rickettsia). The different strains transmitted by these species vary in their virulence and subsequent manifestation of the disease. Dermacentor are known to transmit serious arboviruses responsible for encephalitis and hemorrhagic fevers. D. variabilis are also responsible for spreading tularemia (Francisella tularensis) and human granulocytic erlichiosis (Ehrlichia chaffeensis). Rhipicephalus sanguineus transmits Mediterranean Spotted Fever and African Tick Typhus.

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Tick Paralysis

Hard ticks inject into the body with their saliva certain toxins that can cause a condition in people and animals called tick paralysis. It appears 5-7 days after a tick begins feeding, paralyzing the legs and affecting speaking ability, swallowing and breathing. It occurs worldwide and is most common and severe in children aged up to two years. Treatment involves removing the tick.

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Tick-borne Rickettsial Fevers

This group of diseases is caused by closely related Rickettsia microorganisms transmitted by tick bites or contamination of the skin with crushed tissues or feces of the tick.

· Spotted fever due to Rickettsia rickettsii occurs in Brazil, Canada, Colombia, Mexico, Panama and the USA.

· Spotted fever due to R. sibirica occurs in Japan, the Russian Federation and the Pacific.

· Spotted fever due to R. conori is found in the Mediterranean region, Africa and southern Asia.

· Spotted fever due to R. australis occurs in Queensland, Australia.

· Q fever, caused by Coxiella burneti, has a worldwide distribution and is commonly present in abattoirs, meat-packing and meat-rendering plants, diagnostic laboratories, stockyards and poultry farms. It is transmitted to humans mainly by the consumption of milk and meat from contaminated cattle or the inhalation of dried infected tick feces by people working with cattle.

Symptoms in humans are sudden fever persisting for several weeks, malaise, muscle and joint pains, severe headache and chills. A rash sometimes spreads over the entire body. Death may result in about 15-20% of persons if the disease is misdiagnosed or left untreated.

Treatment

Antibiotics such as tetracycline or chloramphenicol can be used.

Prevention

Tick bites should be avoided and attached ticks should be removed rapidly and carefully. Several hours of attachment are needed before the Rickettsia organisms can infect humans.

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Lyme Disease

Lyme disease (erythema chronicum migrans) is a severe and often debilitating condition caused by a spirochete, Borrelia burgdorferi. Acute Lyme disease is a flu-like illness, characterized by an expanding red rash in about 50% of patients, accompanied by fever, fatigue, and muscle and joint pain. Weeks or even months after the infecting tick bite, patients may experience swelling and pain in large joints (knee, elbow), encephalitis, facial palsy, ocular lesions and carditis, irrespective of whether a rash occurred in the acute phase. Later, perhaps years after the bite, there may be cartilage erosion (arthritis) and neuromuscular dysfunction (Fig. 4.29). Lyme disease occurs principally in northern temperate regions of the world, including China, Europe, the USA and the former USSR.

Illustration 12-5.  A typical symptom of Lyme disease is swelling and pain in the large joints, such as the knees, and chronic arthritis. (SOURCE: Unknown)

Transmission

 

The disease is transmitted mostly by Ixodes ticks, commonly in the summer when the nymphs are abundant. Small rodents, especially mice, serve as reservoirs of infection while large mammals serve principally as hosts maintaining tick populations. The larvae acquire infection while feeding on mice, and nymphs or adults can transmit spirochetes during subsequent blood-meals. In the northern temperate zone, where it occurs most intensely, Lyme disease has become more common as deer populations have increased and as this critical host has adapted to living in closer proximity to people.  In many areas, Lyme disease is acquired in the suburban residential environment.

Treatment

Further development of the disease in adults may be reduced or prevented by treatment with tetracycline or its derivatives for 2-4 weeks, and in children by treatment with penicillin.

Prevention

Prevention requires avoidance of tick habitats and bites, and vector control. Personal protection may be possible by the use of repellents on the skin and clothing in tick-infested areas. The removal of attached ticks within 24 hours may prevent spirochete transmission. Prophylactic antibiotic therapy may be desirable following the bite of an infected tick. New molecular assays are commercially available for detecting the spirochetes in tick samples.

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Tularemia

Tularemia, also known as rabbit fever, deerfly fever and O’Hara disease, is caused by the infectious agent Francisella tularensis. The symptoms, which vary according to how the agent enters the body, include headache, chills, fever and the swelling of lymph nodes. The disease occurs in Europe, Japan, North America and the former USSR.

Transmission

Transmission takes place through the bites of ticks and deerflies (see Chapter 1) or as a result of handling infected animals such as rabbits and other game. Hunters and forest workers are at the highest risk of infection.

Treatment

Antibiotics such as streptomycin can be used to treat the disease.

Prevention

Tick bites and tick habitats should be avoided, impermeable gloves should be worn when skinning and dressing game animals, wild game meat should be thoroughly cooked, and untreated drinking-water should be avoided in areas where the disease occurs.

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Tick-borne Viral Encephalitides

This is a group of viral diseases causing acute inflammation of the brain, spinal cord and meninges. The symptoms vary in severity with the type of disease. Many infections do not result in disease. Severe infections may cause violent headaches, high fever, nausea, coma and death.

· Far Eastern tick-borne encephalitis is found in the far east of the former USSR.

· Central European tick-borne encephalitis occurs in Europe from the Urals to France.

· Louping ill is a disease of sheep in the United Kingdom which sometimes affects people.

Transmission and Prevention

These diseases are transmitted by biting ticks and by the consumption of milk from infected animals. No specific treatment is available but vaccines have been developed against some of the diseases. Prevention requires avoidance or rapid removal of ticks.

Principal Hard Tick Vectors

Usually various tick species act as vectors for any one disease and their importance varies from region to region.

Disease

Vector

Lyme disease

Deer tick (Ixodes scapularis)

Spotted fever due to:

•

Rickettsia rickettsii

American dog tick (Dermacentor variabilis)

•

Rickettsia sibirica

Asiatic wood tick (Dermacentor silvarum)

•

Rickettsia conori

Brown dog tick (Rhipicephalus sanguineus)

•

Rickettsia australis

Wattle tick (Ixodes holocyclus)

Q fever

Lone star tick (Amblyomma americanum)

Tularemia

American rabbit tick (Haemaphysalis leporispalustris)

Far Eastern tick-borne encephalitis

Taiga tick (Ixodes persulcatus)

Central European tick-borne encephalitis

Castor bean ticks (Ixodes ricinus)

Kyasanur Forest disease

A tick of birds and monkeys (Haemaphysalis spinigera)

Colorado tick fever

American wood tick (Dermacentor andersoni)

Crimean-Congo hemorrhagic fever

A tick of birds and mammals (Hyalomma marginatum)

Table 12-1.  Principle Hard Tick Vectors

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Other Viral Diseases

Kyasanur Forest disease occurs in parts of India.

Omsk hemorrhagic fever is found in south-western Siberia; it causes severe disease and death in muskrat handlers; it is mainly waterborne, although it is found in hard ticks.

Colorado tick fever is a moderately severe disease that occurs in western North America.

Crimean-Congo hemorrhagic fever is an acute, often severe and fatal disease found in parts of Africa, Asia and Europe.

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Mites

Class:     Arachnida
    Subclass:     Acari
Order:         Astigmata
Family:     Pyroglyphidae
Genus:  Dermatophagoides (Dust mites)
Family:     Sarcoptidae
Genus:Sarcoptes (Scabies mites)
Order:         Prostigmata
Family:     Democidae
Genus:Demodex (Hair follicle mite)
Order:         Mesostigmata
Genus: Leptotrombidium (Other Mites)

General Characteristics

Dermatophagoides, the common dust mite, commonly inhabit beds, mattresses, carpets and house dust. They are motile and feed on residual organic debris and are typically 0.3 µm in length. They characteristically have four long legs with suckers and pincer chelicerae.

Image 12-10.  A Dust Mite (Dermatophagoides). They commonly inhabit mattresses, carpets and house dust.

Demodex folliculorum mites are 300 microns in length, live in the follicle for 5-6 days and migrate onto contiguous skin at night.  Classically, they appear as 1 µm “sleeves” around the base of the eyelashes.

Image 12-11. Demodex folliculorum (SOURCE: CDC)

The mite, Sarcoptes scabiei, lives exclusively on human skin and causes scabies.  It is small (the larger female is 0.3-0.4µm), colorless and oval with 8 short legs.

Image 12-12. Picture of the human parasite scabies (Sarcoptes scabiei).  They live exclusively on human skin causing the condition known as scabies.  (SOURCE:  PHIL 3810 – CDC/Joe Miller/Reed and Crnrick pharmaceuticals.)

Leptotrombidium

adultsare normally reddish and covered with velvet like hair.  It is the larvae that are parasitic and they too regularly appear reddish, but only have three pairs of legs. The palps are segmented, and the mouthparts are large and easily identifiable. Leptotrombidium larvae are distinguished by large eyes, two feathered sensillae and five feathered setae that are present on the scutum.

Image 12-13. Leptotrombidium (SOURCE: CDC of Taiwan)

Disease and Control

Dermatophagoides are antigenic, even when dead (fecal pellets are also allergenic), and are associated with complex allergies with symptoms such as asthma, perennial rhinitis, conjunctivitis and atopic dermatitis.  A diagnosis can be made using reactive skin tests and treatment involves removal of accumulated antigens from mattresses and pillows.

Demodex have been implicatedin dermatitis, acne and should be considered in chronic, therapy-resistant cases of blepharitis. The role of this mite in ocular disease is uncertain. Washing with soap and water is the most effective method of prevention.

Symptoms of Sarcoptes infection arise after 4-6 weeks and comprise a papular pruritic eruption at a site often unrelated to the site of infestation; symptoms of secondary infestations arise almost immediately.  Zoonotic scabies have shorter incubation periods but are also self-limiting.  Persistent nodular scabies comprises itchy erythematous or scabbed nodules, often on the penis.  When the immune system is impaired, Norwegian (crusted) scabies may develop: this presents with erythema and hyperkeratosis but little itching.

Diagnosis demands discovery of the mites, scybala or eggs by epidermal shave biopsy or superficial scraping.  Burrows are best seen on wrists and interdigital spaces. They fluoresce under a Wood’s lamp after application of liquid tetracycline and, later, alcohol; alternatively ink may be used.  Lindane (Quellada) lotion is the treatment of choice in the USA; permethrin or crotamiton are alternatives.  Ivermectin has been recommended for Norwegian scabies.  Malathion (Derbac-M) liquid or permethrin are recommended in the UK (benzyl benzoate is also active).  Malathion should be avoided in infants and lindane should be avoided in pregnancy, breast-feeding and young children.  Treatment is applied over the whole body except the head and neck and washed off after 24 hours.  Normal laundering of bed linen and clothes is recommended.  Household and sexual contacts should also be treated.  Symptoms may continue after treatment because of persisting antigens, Calamine or Eurax lotion may be used; other problems include reinfestation and secondary bacterial infection.

Feeding by Leptotrobidium causes cellular damage and initially results in intense itching and irritation for the host.  The agent of scrub typhus, Rickettsia tsutsugamuchi, is often transmitted by the larval trombiculid mite. Scrub typhus results in infection in those living or working near ‘mite islands’ which are usually found in transitional vegetation and provide a stable environment for mite proliferation. Prevention has generally been with chemical repellents or herbicides to remove the scrub habitat.

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Mosquitoes

 

Class:     Insecta
Order:      Diptera
Family:     Culicidae
Subfamily:     Anophelinae
Genus:         Anopheline
Subfamily:     Culicinae
Genus:         Culicine

Anopheles
(SOURCE:  PHIL 7949 – CDC)

Aedes
(SOURCE:  PHIL 9261 – CDC/ Prof. Frank Hadley Collins, Dir., Cntr. for Global Health and Infectious Diseases, Univ. of Notre Dame)

Culex
(SOURCE:  PHIL 7957 – CDC)

Image 12-14. Anopheline and Culicine mosquitoes.

Introduction

 

Mosquitoes are small with a clearly demarcated body and very long slender legs. The head contains a large pair of kidney shaped compound eyes, a pair of antennae, and a single long proboscis for feeding. The thorax, abdomen and wings are often covered with scales. Differential coloration and pattern of these scales provides a means of visually distinguishing species. The large wings are folded over the segmented abdomen, which generally appears brown-black and slender but turns a bright red and swells following feeding.

Image 12-15.

Image of a typical Culicine mosquito. Adults are generally brown – black, at rest they place their abdomens parallel to the ground. (SOURCE:  PHIL 4487 – CDC)

Mosquitoes may be classified as Anopheline (Anopheles) or Culicine (Aedes, Culex). The antennae of male mosquitoes are plumose (many feathery hairs); females are pilose (few spidery hairs).  The male Anopheline palps are long and clubbed; those of the male Culicine are long but not clubbed.  The female Anopheline palps are long; the female Culicine are short. If a mosquito is incorrectly sexed, a female Anopheline may be confused with a male Culicine.

Illustration 12-6. Image of typical male Anopheline mosquito showing the characteristic features of the mosquitoes head; the palps are as long as the proboscis with clubbed like ends and the antennae are plumose. The female Culicine mosquito shows the short palps and the pilose antennae. (SOURCE: CDC)

At rest, Anophelines usually position their abdomens at an angle to the surface; Culicines maintain their abdomen in a parallel position.

Illustration 12-7. Typical Anopheline and Culicine at rest, showing the abdomen at an angle to the surface. (SOURCE: CDC)

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Anopheline (Anopheles) Mosquitoes

Class:     Insecta
Order:          Dipthera
Family:     Culicidae
Subfamily:     Anophelinae
Genus:         Anopheline
Species: Anopheles

Image 12-16. Typical Anophelesmosquitoes (SOURCE:  PHIL 7862 – CDC)

General Characteristics

Anopheles mosquitoes are characterized by dark and pale scale blocks arranged on their wings. They have palps that are of equal length to the proboscis, which appear terminally clubbed in males. Anopheles always rest at an angle when standing on surfaces and preferring to feed at twilight or night. Breeding sites are varied but Anopheles prefer unpolluted fresh or saltwater.

Life Cycle

Anopheles lay 50 to 200 dark color eggs in aquatic environments, and hatch in several days to several weeks depending on the external temperature. Anopheles larvae have a dark brown head and 6-7 anterior segments covered with dorsal palmate hairs. Accessory tegral plates are present on the dorsal side of segments 1-10 and two sets of anal papillae emerge from the last abdominal segment.

There are four larval instars that survive by filter feeding and breathing oxygen through their spiracles. Anopheles larvae occur throughout many different habitats including both permanent marshes and swamps, and temporary locations such as pots filled with water. In general Anopheles prefer to inhabit clean habitats. The larval period lasts about a week, but may be extended depending on the environmental conditions. The pupa is comma shaped with a set of trumpet shaped breathing tubes. The abdomen is covered with setae, and segments 2-7 have distinct spines.  The pupal period may last a few days to weeks depending on the temperature.

Disease – Malaria

Anopheles are vectors of malaria, Bancroftian and Brugian filariasis and of multiple arboviruses (dengue fever; yellow fever; encephalitides and hemorrhagic fevers). Malaria is caused by Plasmodium falciparum, P. vivax, P. malariae and P. ovale. Transmission of the disease occurs in virtually all of tropical Africa, Central and South America, and the Middle and Far East.  South East Asia is a particular problem due to multiple drug resistance.  P. falciparum is found in Africa and other tropical countries as well as in subtropics.  P. malariae has a low prevalence in both tropics and subtropics. P .vivax is the most widespread in temperate regions and subtropics but may also be found in the tropics.  P. ovale has a low prevalence in West Africa.  In Africa alone, 370 million people live in endemic areas.

Illustration 12-8. World map showing the distribution of malaria. (CDC)

P .vivax causes benign tertian malaria (43% of cases) and P. falciparum results in malignant tertian or sub-tertian malaria and pernicious malaria (50% of cases). P .ovale (mild tertian malaria, 1% of cases) and P. malariae (quartan malaria, 7% of cases) contribute a small percentage of malarial cases.

Clinical features including fever and chills are due to the host inflammatory response and are associated with rupture of erythrocytic schizonts. Fever presents in three stages – a) Cold: rigors and fever lasting 15 minutes to 1 hour; b) Hot: the patient is flushed with tachycardia and is pyrexial (40C) for 2-6 hours; c) Sweating: the temperature falls (over 2-4 hours).  Each paroxysm lasts 8-12 hours in total.  All erythrocytes containing a trophozoite will be destroyed within 48-72 hours.  Periodic fever often takes more than seven days to develop, and anemia can be hemolytic or due to toxic marrow suppression.  Splenomegaly occurs in all malaria: it may be acute or chronic (+/- hypersplenism).  Jaundice may be hemolytic and/or hepatic (only P. falciparum).  In addition, there may be headache, myalgia, arthralgia, diarrhea and vomiting.

Plasmodium falciparum is the most virulent form (invades mature and immature RBCs) and is often fatal if untreated.  Blood schizogony takes place in deep capillaries and micro-circulatory failure can occur in individuals with little immunity to malaria.  It does not relapse but recrudescence may occur. The time between paroxysms is 48 hours but fever may last for 24-36 hours.  Very rapid progression and complications include diarrhea and vomiting; delirium; coma; convulsions; renal failure, including hemoglobinuria (blackwater fever); jaundice; pulmonary edema; hypoglycemia and abortion. Cerebral malaria often results in delirium, disorientation, stupor, coma, convulsions and death.

P. vivax / ovale exhibit 48 hours between paroxysms; relapses may occur up to 8 years after primary infection and only infects immature RBCs of those with Duffy blood group. Plasmodium malariaegenerally results in 72 hours between paroxysms, only infects older RBCs, and recrudescence may occur decades after primary infection.

The global malaria situation is serious and becoming worse: 300-500 million clinical cases occur annually. 1.5-2.7 million people die of malaria each year with approximately one million deaths among children under five years of age are attributed to malaria alone or in combination with other diseases. Countries in tropical Africa account for more than 90% of the total malaria incidence and the great majority of malaria deaths (WHO data). The death toll of African children with malaria is expected to double by 2010, conceivably reaching four million deaths per year. Many factors influence the epidemiology of this disease including: breeding habits of the various mosquito vectors; agricultural practices; economic conditions; industrialization and pesticide use.  Increasing air-traffic from malaria endemic areas has led to the possibility of malaria developing in non-endemic areas where the mosquito vector has been imported onboard aircraft.

Treatments and Control – Malaria

If the infective species is not known, or the infection is known to be mixed, initial treatment should be with quinine, mefloquine or rarely halofantrine.  Falciparum (malignant) malaria is often resistant to chloroquine and should be treated with quinine, mefloquine, halofantrine, quinidine or pyrimethamine-sulphadoxine.  Benign malaria (P. vivax) should be treated with chloroquine although resistance has been reported from New Guinea.  Malarial prophylaxis is relative and not absolute.

The UK Consensus Group on Malaria Prophylaxis (1997) recommend mefloquine for UK travelers to West, Central and East Africa for periods of greater than two weeks and for travelers to specific areas within south-east Asia: prophylaxis should be commenced two weeks before departure.  Doxycycline can be used in older children and adults who cannot tolerate mefloquine.

Prevention is most dependent upon coverage of exposed skin and the use of insect repellent, mosquito nets impregnated with permethrin and correct prophylaxis.  The vector may be controlled by water clearance programs, house spraying (DDT) and destruction of breeding areas.  Drug resistance to DDT and ethical resistance to its use have limited its effectiveness. Natural immunity involves both antibody and cell-mediated systems and appears to require frequent boosting; antigens from different stages of the parasite’s life cycle will be important in vaccine development.

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Disease – Filariasis

Anopheline mosquitoes also transmit the filarial worms Wuchereria bancrofti, Brugia malayi and Brugia timori. Wuchereria bancrofti is the main cause of “elephantiasis” (Bancroftian filariasis) and the most widely distributed filarial parasite of man. The adults live in the lymphatic system, and can survive for 30 years or more.  Once they have mated they produce a pre-larval form, the microfilaria.  Both the adults and the microfilaria may play a role in generating the symptoms and signs.  Microfilaria measure 240-300mm in length by 7-10mm in width.  They are sheathed (derived from ovum membrane) and nuclei terminate 15-20mm proximal to the pointed tail.  There are fewer, more distinct nuclei than in other species and there are less body curves.  Adult worms are slender and white (males 4cm; females stout and 10cm in length)

Initial infection with Wuchereria is usually asymptomatic.  There may be recurrence of attacks of “cellulitis” affecting the limbs, breast, scrotum or elsewhere. Infection is associated with fever, lymphangitis, lymphadenopathy and occasionally abscess formation.  These initially settle but later on the tissues eventually become edematous and hypertrophied. Further effects may include scrotal involvement and hydrocoele, which can lead to scrotal enlargement and lymph scrotum.  This is “elephantiasis” and is associated with dermal hypertrophy, verrucous changes and the rupture of lymph varices into various sites.

Brugian (Malayan) filariasis is less widespread, less common and less serious than its Bancroftian counterpart. The life cycle is identical to that of Wuchereria bancrofti with Brugia malayi limited to Asia and B. timori restricted to Indonesia. Infection results in lymphadenopathy involving most frequently the inguinal area, lymphoedema normally below the knee, eosinophilia, and in rare cases chyluria.

Treatments and Control – Filariasis

Diethylcarbamazine (DEC) kills microfilaria. Ivermectin suppresses microfilaria production but its overall effectiveness remains untried and elephantiasis can be treated surgically.  Control measures comprise draining of mosquito breeding sites and killing larvae.  Many mosquitoes are resistant to insecticides but mosquito repellents and nets are effective.  The infective pool may be reduced by periodic mass treatment with DEC. Brugia malayi is more susceptible to diethylcarbamazine (DEC) than is Wuchereria bancrofti.  Anopheline larvae may be suffocated in their breeding sites but Culicine larvae (Mansonia sp.) derive oxygen from plants and are not vulnerable to such measures.  Control depends upon the use of mosquito nets and periodic mass treatment.

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Culicine(Aedes) Mosquitoes

Class:     Insecta
Order:    Dipthera
Family:    Culicidae
Subfamily:    Culicinae
Genus:        Culicine
Species:Aedes

General Characteristics

Aedes can generally be distinguished by patterns of black and silvery scales present on the abdomen and thorax. The legs appear to have black and white rings along their length. The wings are generally covered with black scales. Aedes breed in marshes and other wetland areas and have a worldwide distribution.

Image 12-17. Typical Aedesmosquito. They are clearly distinguished from Anopheline mosquitoes due to the presence of black and slivery scales on the abdomen and thorax.  (SOURCE:  PHIL 9252 – CDC/ Prof. Frank Hadley Collins, Dir., Cntr. for Global Health and Infectious Diseases, Univ. of Notre Dame)

Life Cycle

Female Aedes lay eggs on damp areas such mud, detritus, clay and rock.  The eggs are very robust and can survive desiccation and other environmental pressures. The eggs hatch in waves depending on the environmental cues. Aedes larvae have a stout barrel shaped siphon with one pair of subventral tufts. There are three pairs of setae on the ventral brush, and large setae are not present on the abdominal segments.

Disease

Aedes are vectors of Bancroftian filariasis and arboviruses such as yellow fever and dengue. Wuchereria bancrofti is the main cause of “elephantiasis” (Bancroftian filariasis) and the most widely distributed filarial parasite of Man. The adults live in the lymphatic system, and can survive for 30 years or more.  They copulate and generate a pre-larval form, the microfilaria.  Both the adults and the microfilaria may play a role in generating the symptoms and signs.  Microfilaria measure 240-300mm in length by 7-10mm in width.  They are sheathed (derived from ovum membrane) and nuclei terminate 15-20mm proximal to the pointed tail.  There are fewer, more distinct nuclei than in other species and there are less body curves.  Adult worms are slender and white (males 4cm; females, stout and 10cm in length).

Initial infection with Wuchereria is usually asymptomatic.  There may be recurrence of attacks of “cellulitis” affecting the limbs, breast, scrotum or elsewhere. Infection is associated with fever, lymphangitis, lymphadenopathy and occasionally abscess formation.  These initially settle but later on the tissues eventually become edematous and hypertrophied. Further effects may include scrotal involvement and hydrocoele, which can lead to scrotal enlargement and lymph scrotum.  This is “elephantiasis” and is associated with dermal hypertrophy, verrucous changes and the rupture of lymph varices into various sites.

Yellow fever and dengue hemorrhagic fever are serious viral infections spread by the Aedes mosquito. Dengue is now the most important mosquito borne virus, with global infection increasing.

Control and Treatment

In general the most effective control for Culicine mosquitoes are repellents and fine screening or netting. Treatment with insecticides will also serve to reduce the vector population, but increased problems are encountered with Culicines because they also feed during the daytime. If filarial infection occurs, treatment with Diethylcarbamazine (DEC) will kill microfilaria. Ivermectin suppresses microfilaria production but its overall effectiveness remains untried and elephantiasis can be treated surgically.

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Culicine (Culex) Mosquitoes

Class:     Insecta
Order:    Dipthera
Family:    Culicidae
Subfamily:    Culicinae
Genus:        Culicine
Species:    Culex

General Characteristics

Culex are distinguished by their lack of coloration and feature. The thorax, abdomen, legs and wings are often covered with brown-black scales giving a generally dark appearance. The abdomen may occasionally also have white scales arranged in segments. Culex breeds mainly in aquatic habitats, often in areas containing large quantities of organic waste.

Illustration 12-8. Typical illustration of a Culexmosquito, showing the characteristic brown-black scales on the thorax, abdomen, legs and wings giving it a general dark appearance. (Illustration: Trustees of the British Museum)

Image 12-18. ACulexmosquitotaking a blood meal from a human host. The abdomen becomes distended and blood red in color.  (SOURCE:  PHIL 4464 – CDC/Jim Gathany)

Life Cycle

 

Female Culex lay dark brown eggs in characteristic clumps of approximately 300 eggs. As mentioned these eggs are often found in organic waste deposits or polluted waters. Culex larvae have a long and narrow siphon with more than one pair of subventral tufts.

Disease

Culex mosquitoes are vectors of Bancroftian filariasis throughout Africa, but most importantly arboviruses such as Japanese encephalitis. Encephalitis occurs throughout the world, with Culex acting as an important vector for spread and infection. Culex mosquitoes are similar to Culicine mosquitoes, but prefer to bite at night and breed in organic refuse.

Control and Treatment

Culex mosquitoes are most easily controlled by improving sanitation and removing static water sources from the affected area. In general the most effective control for Culex mosquitoes are also repellents and fine screening or netting. Treatment with insecticides will also serve to reduce the vector population, but increased problems are encountered with Culicine mosquitoes because they also feed during the daytime. If filarial infection occurs treatment with Diethylcarbamazine (DEC) will kill microfilaria. Ivermectin suppresses microfilaria production but its overall effectiveness remains untried and elephantiasis can be treated surgically.

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Tsetse Flies

Class:     Insecta
Order:     Diptera
Family:     Glossinidae
            Genus:    Glossina

General Characteristics

Tsetse flies are large, yellow-brown or brown-black and measure 6-15µm in length. They are distinguished by a rigid projecting proboscis and a long pair of accompanying palps.  There is a characteristic axe-shaped venation of the wings when viewed dorsally resembling an inverted hatchet in the central cell. The antennae appear short and feathery, and the abdomen is segmented and often striped or patched. Both males and females suck blood every 4-5 days, outside in open spaces.

Image 12-19. Typical illustration of a Tsetse Fly. They are yellow-brown in Colour and usually measure 6 – 15µm in length.  Their characteristic feature is the hatchet shaped cell in the centre of the wing venation. (IMAGE SOURCE: Trustees of the British Museum)

Life Cycle

Female Tsetse flies are unique in the sense that they deposit larvae and do not lay eggs. The eggs mature within the female and are supplied with essential nourishment to complete larval development. This cycle requires a large number of blood meals to maintain and thus the female requires regular feeding. The larvae are normally deposited in shaded areas. There are three larval instars with the mature larva appearing white, visibly segmented with a pair of lobes at the posterior end. Pupation of the third instar results in a dark colored puparium with posterior lobes. The pupal period is extended (3-7 weeks) depending on the surrounding environmental conditions.

Disease

Tsetse flies are vectors for African sleeping sickness (Trypanosoma brucei sp. The two subspecies of T. brucei that infect Man are morphologically identical.  T. b. gambiense causes Gambian sleeping sickness in Western Africa and T. b. rhodesiense causes Rhodesian sleeping sickness in East Africa.  Another subspecies, T. b. brucei, causes nagana in cattle.

Illustration 12-9.

Distribution of African Trypanosomiasis throughout Africa (WHO, 1991)

Initially the patient has a headache, fever, chills and loss of appetite but specific clinical signs are absent.  Parasitaemia comes in characteristic waves. Later, the spleen, liver and lymph nodes enlarge (Winterbottom’s sign). Finally, there may be CNS involvement leading to coma and death within several years.  Trypanosoma brucei rhodesiense (rural East Africa): this is so acute that the patient invariably dies before classical symptoms develop.  Without appropriate treatment, both forms are fatal.

Human African trypanosomiasis is rural and focal, with humans as the principal reservoir of infection of T. b. gambiense, and domestic cattle and wild animals as important reservoirs of T. b. rhodesiense.  By the 1960s, it had been brought under control, but since 1970 the situation has deteriorated and the disease has reappeared, with major flare-ups in countries which have not maintained surveillance activities.  It is estimated that 55-60 million people are exposed to the risk of becoming infected with trypanosomiasis, but only four million of them are under active surveillance or have access to health centers where reliable diagnosis is available: the estimated number of infected persons is over 300,000 (WHO data).

Treatment and Control

Anemia and other infections should be treated first.  If given before the parasite has invaded the brain (hemolymphatic stage), suramin (Rhodesian disease) or pentamidine (Gambian disease) appear to be effective.  For late disease (CNS involvement), drugs of choice are melarsoprol or eflornithine, with tryparsamide plus suramin as an alternative.  Tsetse-infested areas should be avoided.  Protective, light-colored clothing and repellents should be used.  Tsetse flies are difficult to treat with insecticide (DDT has been tried) as their larvae live in burrows in the ground; protective vegetation must first be removed.  Pentamidine prophylaxis is no longer advocated.  Reservoir hosts should be identified and removed.  It is possible to breed resistant or tolerant cattle (West Africa).  Trypanosomes other thanT. brucei are also transmissible by Tabanid flies or by sexual contact.

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Sand Flies

Class:     Insecta
Order:     Dipthera
Family:     Psychodidae
Genera:     Phlebotomus, Lutzomyia

Introduction

 

Sandflies are small (1.5-5µm) with a hairy head, thorax, antennae and wings. The antennae are long, may appear beaded, and protrude near a large set of black compound eyes. The wings are upwardly pointing at rest, and are a distinctive feature of Phlebotomine sandflies. Only the females are blood feeders, the males feed on plant nectar. Biting predominates nocturnally and they rest in moist and dark walls, cracks and tree trunks during the day.

Illustration 12-10. Typical illustration of a Sand Fly. The head, thorax, abdomen, legs and antennae are hairy, they are small usually measuring 1.5-5µm long.  (Phlebotomus) (Illustration Source: Trustees of the British Museum)

Life Cycle

 

Female Phlebotomine sandflies deposit 30-70 minute eggs at each oviposition. The eggs are laid in dry areas, but require humidity to avoid desiccating.  There are four instars and the mature larva is characterized by a distinct black head, 12 segments, thick bristles covering the body, and two pairs of caudal setae on their posterior end. As with other fly vectors the length of the larval stage depends on the ambient temperature, species in question, and food availability. The larval skin and caudal bristles remain attached at the posterior end during the pupal stage which lasts 5-10 days.

Disease

Sandflies are the only vectors for several species and subspecies of obligate intracellular protozoa responsible for leishmaniasis (Leishmania sp.) Cutaneous, mucocutaneous and visceral leishmaniasis are caused by different species of Leishmania contentiously linked to temperature preferences.  Geographic location and host immune response also play a role in determining the form of disease.Leishmania tropica and L. major cause dermal cutaneous leishmaniasis; visceral leishmaniasis (kala-azar) is caused by L. donovani and mucocutaneous leishmaniasis is caused by L. braziliensis andL. mexicana.  Visceral leishmaniasis in Europe is caused by L.infantum with dogs as the main reservoir. Leishmania tropica is found in the Middle East, North Africa, India and the Mediterranean. Leishmania donovani is found in the old and new worlds: South America, the Mediterranean, North and East Africa, India and China.  Leishmania braziliensis is found in Central and South America. Leishmania mexicana is found in North and Central America, Texas and Mexico.

Dermal cutaneous leishmaniasis or Old World leishmaniasis is also known as “Tropical or Oriental Sore” or “Delhi Boil” and is generally localized to the skin surrounding the bite of the Phlebotomussandfly.  The ulcers (volcano sign) are “draining” but produce “dry” ulcers that crust over.  They usually resolve within one year but superinfection (yaws or myiasis) may occur and immunity develops. Cutaneous leishmaniasis affects over 300,000 people. The mucosal form affects the mucosa of the nose, pharynx, palate, larynx and upper lip causing ulcers that often become secondarily infected.  Scarring can lead to death from pneumonia.

Visceral leishmaniasis, or “Kala-azar” is transmitted by Phlebotomus sandflies and is spread via the lymphatics from an often minor cutaneous lesion.  They multiply in macrophages to form Leishman-Donovan bodies.  Symptoms are usually chronic and comprise malaise, lymphadenopathy, cough, diarrhea, wasting and anemia, bleeding, and low-grade fever (3/day); liver and spleen enlarge and visibly distend the abdomen.  Untreated, death ensues within three years, usually from secondary infection.

Leishmaniasis currently affects some 12 million people in 88 countries, all but 16 of which are in the developing world.  It is estimated that 350 million people are exposed to the risk of infection by the different species of Leishmania parasite. The annual incidence of new cases is about two million (1.5 million of cutaneous leishmaniasis, and 0.5 million of visceral leishmaniasis).  Recently, the WHO has reported an increase in overlapping of visceral leishmaniasis (VL) and HIV infection due to the spread of the AIDS pandemic.  Leishmania / HIV co-infection is considered to be a real “emerging disease”, especially in southern Europe, where 25-70% of adult VL cases are related to HIV infection, and 1.5-9.5% of AIDS cases suffer from newly acquired or reactivated VL.  Intravenous drug users have been identified as the main population at risk.

Treatment and Control

Dermal leishmaniasis usually resolves spontaneously.  Visceral leishmaniasis is treated with extended courses of antimonial compounds (e.g. sodium stibogluconate or meglumine antimonate) and dietary supplementation (pentamidine isethionate has been used in antimony-resistant cases).  WHO regimes are changing and pentamidine may be used.  Mucocutaneous leishmaniasis is also treated with antimonial compounds.  However, only around 50% of patients respond to antimonial compounds and relapses are seen.  Pentamidine isethionate, paromomycin (aminosidine), allopurinol, ketoconazole, itraconazole, interferon gamma and liposomal amphotericin B have all been used; amphotericin B appears the most effective.  Control of sandflies is difficult although buildings may be sprayed with insecticide.  Sandflies cannot bite through clothing.  Repellents are effective although mosquito nets are of limited value (sandflies are 3 µm).  Sandflies are nocturnal and can be avoided.  Rodent and dog control is a possibility.  Vaccines (killed or live attenuated promastigotes) have been tried but effectiveness has not been assessed.

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Black Flies

Class:     Insecta
Order:     Diptera
Family:     Simuliidae
Genus:    Simulium

Introduction

Black Flies are small (1.5-4µm in length) and normally black with short hairless legs and antennae. They have large compound eyes and a characteristically hairy humped thorax.  Flies of the genusSimulium are generally found near free-flowing well-oxygenated water and bite during the day, tearing the skin to reach blood vessels.

Illustration 12-11. Typical illustration of a Black Fly(Simulium). They are usually small (1.4–4µm in length), black with short hairless legs and antennae.(SOURCE:  PHIL 4639 – CDC)

Image 12-20.  Image of a Black fly receiving a blood meal. (SOURCE: Unknown)

Life Cycle

Simuliidae eggs are laid in flowing or turbid waters in clusters of 200-800 eggs depending on the species. Hatching is mediated by the external environment, generally occurring several days following oviposition. There are 6-9 larval instars, with the larvae remaining essentially sedentary for the period and feeding through filtration. Movement is possible if necessary with some larval species acting as predators. The mature larvae can be recognized by a characteristic black “gill spot” on the thorax. The pupa is enclosed in a dark colored cocoon, identifiable by a series of filamentous respiratory gills protruding from the anterior end. In most cases the adult fly emerges from the pupal stage following one week of incubation.

Disease

Simulium are vectors for the filarial parasitic nematode responsible for Onchocerciasis (Onchocerca volvulus). It is distributed throughout Africa, Arabia, Central America, northern South America and Mexico with 30 million people infected in Africa alone; it is one of the most important causes of blindness in the world.  Adult worms (up to 50cm) live in the subcutaneous tissue of man (the only known host) and release microfilariae into the skin. These are taken up by Simulium (S. damnosum and S. naevei in Africa; S. ochraceum and S. metallicum in Central America).  Microfilariae penetrate the gut wall, migrate to the thoracic muscles, molt to L₂ stages and molt again to filariform L₃ stages which are passed to the next host during a blood meal.  Larvae mature to adults in one year and may live for up to 20 years.  Microfilariae can live for up to two years but are often trapped, in fibrous nodules, by the host’s cellular response and are responsible for the pathology.  Microfilariae are highly motile, unsheathed and measure 300 by 7 microns; there are no nuclei in the end of the tail, which is long and pointed; the head is slightly enlarged.  Microfilariae are not found in blood.

  Skin problems include nodules (2cm to 5cm in diameter) containing adult worms. Onchodermatitis is caused by death of microfilariae in the skin and is associated with severe pruritis (adopts different forms in different geographical localities e.g. “erysipelas de la costa” in Central America, “leopard skin” in parts of Africa), skin depigmentation and premature ageing.  There may be minor elephantiasis of the inguinal area (“hanging groin”) or of the genitals (including hydrocoele).  Eye involvement is due to microfilariae entering the eye and dying and may eventually lead to blindness through sclerosing keratitis and retinal damage (microfilaria can be seen in the anterior chamber of the eye).  There may be competition between parasite and host for vitamin A.

Treatments and Control

Ivermectin destroys microfilariae and renders adult female worms infertile; the manufacturer provides this drug without charge.  Nodules may be surgically removed to reduce the worm-load and decrease the chances of ocular involvement.  In areas of East Africa, S. naevei has been eradicated with insecticide (the larvae of this parasite attach to freshwater crabs).  S. damnosum inhabit areas far distant to its breeding sites and control is much more difficult.  However, the WHO larvicide program in concert with mass Ivermectin treatment has the potential to control the problem.  Vegetation should be cleared around villages and irrigation should be devised to avoid fast-flowing water currents.

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Tabanid Flies

Class:     Insecta
Order:     Diptera
Family:     Tabanidae
Subfamily:     Chrysopsinae (Deer flies)
Genus:         Chrysops
Subfamily:     Tabaninae (Horse flies)
Genus:         Tabanus

Introduction

Chrysops are 9-10µm in length with broad wings and large iridescent eyes. The abdomen is yellow or orange and can be patterned with black markings. The antennae consist of three segments, lacking a projection from the second segment and with the third segment subdivided into four smaller sections.  Female Chrysops are attracted by smoke and normally bite in the morning or late afternoon.  They breed in shaded muddy areas and have a worldwide distribution.

Image 12-21.  Image of a Deer fly receiving a blood meal. They have large iridescent eyes and broad wings. Generally measure between 9–10µm in length. (SOURCE: University of Florida)

Life Cycle

Female Tabanids generally lay 100 -1000 large creamy white eggs on the undersides of plants and rocks surrounding aquatic areas. The eggs hatch following several weeks of incubation. Larvae live and feed in wet rotting vegetation but survive breathing oxygen. The larval stage can be quite prolonged (1-3 years) with 6-13 larval instars depending on the species. The mature larvae migrate to dry areas and undergo pupation. The pupa often gets buried in the soil and can often be large. The pupal stage lasts several weeks, and the adults emerge to feed.

Disease

Tabanids are vectors for the parasitic nematode Loa loa. TheirMicrofilariae are large and sheathed and contain nuclei extending to the end of the rounded tail.  Adult worms are thin and white (females 2cm-7cm long, 425µm in diameter and males 2cm-3.4cm long, 350µm in diameter). Clinical features of Loa loa infections include considerable pruritis and transient painful subcutaneous swellings termed Calabar swellings. Migrating adult worms can cross the conjunctiva or the bridge of the nose and ectopic worms cause problems such as hydrocoele, orchitis, colonic lesions, encephalitis.

Treatment and Control

Worms traversing the conjunctiva may be removed surgically.  Diethyl-carbamazine (DEC) is a proven treatment; prevention comprises the use of prophylactic DEC.  However, DEC may have fatal side effects including encephalitis and the current drug of choice is Ivermectin. Drugs kill microfilariae but not adult worms. Antihistamines and corticosteroids may prevent allergic reactions brought about by rapid destruction of microfilariae in heavy infections.  Insect control is not practical.

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Biting Midges

Class:    Insecta
Order:    Dipthera
Family:     Ceratopogonidae
Genus:     Culicoides

Introduction
Biting midges are 1µm-2µm long with a small head, long antennae and segmented palps. The thorax is often black spotted and contains a distinctive set of small depressions called the “humeral pits” just posterior of the head on the upper thorax. Biting midges have long legs and wings that fold over the thorax when at rest. Only the females take blood meals and normally swarm and bite in the early morning or late evening, especially during overcast weather.

Illustration 12-12: Typical Illustration of a Biting Midge(Culicoides). The thorax is often black spotted and contains a distinctive set of small depressions called the “humeral pits” just posterior of the head (SOURCE:  PHIL 3822 – CDC/Dr. Richard Darsie)

Life Cycle

Female culicoides lay 30-250 dark, cylindrical eggs on the surface of wet soil or organic debris. Larvae emerge from the eggs soon thereafter depending on the environmental conditions. There are four larval instars, and the mature larvae resemble that of a nematode worm. They have a small dark head, 12 segments, and terminal papillae. The larvae feed on detritus and may development for extended periods of time depending on the species and conditions. The pupal period lasts 3-10 days, with the adult females emerging to feed and breed.

Disease

Culicoides species possess the ability to transmit various filarial parasites to humans (Mansonella perstans, M. streptocerca and M. ozzardi). Adult Mansonella streptocerca reach 3 cm in length and live in the skin.  Microfilariae are small and thin (200µm in length), unsheathed and nuclei extend to the end of a hooked tail.  The major symptoms of infection are pruritis, papular eruptions and pigment changes.

Mansonella ozzardi is found in South and Central America and the adult worms live in the peritoneal cavity.  Microfilariae are small, thin (150-200 by 4.5 microns) and unsheathed with indistinct nuclei that do not extend to the end of the pointed tail.  They are found in the skin and blood and are non-periodic.  Most infected persons are asymptomatic but may be associated with arthralgias, headaches, fever, pruritis, hepatomegaly, pulmonary symptoms and adenopathy: there is no proven therapy.

Mansonella perstans is found in tropical Africa and coastal South America with adult worms measuring 4cm-8cm. They inhabit the peritoneal and, rarely, pleural cavities.  Infections are usually asymptomatic but can be associated with pruritis, fever, arthralgias and neurological changes.

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Head and Body Lice

Class:     Insecta
Order:     Phthiraptera
Genus:Pediculus

Introduction

 

Pediculus humanus capitis (the head louse) and Pediculus humanus humanus (the body louse) are 2µm-4µm long and flattened dorsoventrally. They are wingless with distinct head, thorax (bearing three pairs of clawed legs) and abdomen (seven segments).  The fore legs are well developed to grasp clothing and hair, with terminal claws to aid grip on the host. Pediculus feed using two stylets which suck blood whilst a third directs saliva into the skin; meanwhile feces are continually passed onto the skin.

Image 12-22.  DorsalImage of a typical body louse (Pediculus humanus humanus). They are wingless and dorsoventrally flattened, bearing a distinct head, thorax and abdomen. They measure approximately 2–4µm in length.  (SOURCE:  PHIL 9205 – CDC/ Frank Collins, Ph.D.)

Life Cycle

 

The head and body louse share very similar life cycles only differing in the placement of their eggs; the body louse cements eggs to clothing and the head louse cements single eggs at the base of hairs. Females can lay upwards of 300 eggs during a lifetime. Lice have a hemimetabolous lifecycle. The nymph hatches from the egg and appears very structurally similar to the adult louse. There are three nymphal instars that require blood meals to proceed.  It only takes 7-12 days to proceed to the adult stage if blood meals are readily available, but conversely lice will perish if not fed for several days.

Image 12-23.  DorsalImage of a typical head louse (Pediculus humanus capitis)(SOURCE:  PHIL 377 – CDC/ Dr. Dennis D. Juranek)

Disease

 

Colonization by lice may result in serious infection and disease. Lice can potentially pass Rickettsia prowazeki resulting in epidemic typhus and other pathogens such as Rochalimaea quintana andBorrelia recurrentis that result in potentially serious fever. The mode of transmission for all infectious agents is through physically crushing and spreading feces or waste into the wound created through feeding.

Control

The most effective control is to remain clean, but insecticides are often necessary during epidemics to avoid reinfestation.

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Pubic Lice

Class: Insecta
Order:          Phithiraptera
Genus: Phthirus

Introduction

The crab louse is 1µm-2µm long and distinguished by a square, undifferentiated body and massive claws on the two posterior sets of forelegs. These claws are able to grasp both pubic and facial hair (including eyelashes), and allow the louse to remain tightly bound to the host. They are spread mostly by sexual contact, but may also be transmitted through fomites.

Life Cycle

The life cycle of Phthirus is very similar to Pediculus. Females lay bundles of eggs on the coarse pubic hairs and dense facial hairs of humans. The crab lice proceed through a cycle similar to the head and body lice, with the nymphal stage proceeding several days longer. Phthirus are less active than Pediculus, but similarly can not survive for very long without a host and blood meals.

Image 12-24.  VentralImage of a typical Crab louse (Phthirus). They hold onto pubic hair with the large claws found on the posterior legs.(SOURCE:  PHIL 4077 – CDC)

Disease

 

There appears to be very little evidence of disease transmission by Phthirus, but have the ability to cause severe localized allergic reactions during infestations.

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Fleas

Class:    Insecta
Order:      Siphonaptera
Genus:     Pulex, Xenopsylla, Ctenocephalides, Tunga

Introduction

Fleas are laterally compressed and wingless (1µm-4µm) with powerful legs. The entire body is generally covered with bristles, and the mouthparts point downwards. Pulex irritans (the human flea) andXenopsylla cheopsis (the tropical rat flea) are combless.  Nosopsyllus fasciatus (the rat flea) has a pronotal comb (behind its head).  Ctenocephalides felis (the cat flea) and C. canis have two combs – a pronotal comb and a genal comb (under the head).

Image 12-25.  Image of the cat flea Ctenocephalides felis. Fleas are laterally compressed and wingless (1-4 µm) with powerful legs. (SOURCE: CDC)

Tunga penetrans (the Chigoe or jigger flea) demonstrates compressed thoracic segments and attacks man in the Americas, Africa and India, commonly penetrating the stratum corneum between the toes or in the toenail margins

Image 12-26.  Image of the Chigoe flea Tunga penetrans. They commonly penetrate between the toes or under the toenail. (SOURCE: Unknown)

Life Cycle

Flea larvae hatch from eggs generally following a week incubation. The larvae are legless, segmented, and covered with setae. The larvae feed on organic material, and proceed through two or three larval instars depending on the environment. The larva spins a cocoon and pupates and emerges when the conditions appear favorable for survival. The life cycle can be as short as several weeks or up to several years depending on the stimuli surrounding the pupa. Both sexes take blood meals can live for long periods of time allowing females to lay an enormous number of eggs over their lifetime.

Disease

Fleas are a general nuisance, often biting humans on exposed surfaces resulting in discomfort. Flea-bites induce pruritic papular urticaria commonly on the unprotected lower leg of women and all over the body of children who have intimate animal contact; a generalized allergic response may occur.

Certain fleas, notably the rat fleas, spread plague (Yersinia pestis) and murine typhus (Rickettsia typhi), and serve as intermediate hosts for species of tapeworm (Hymenolepis sp.).  Cat and dog fleas serve as intermediate hosts for another common tapeworm (Dipylidium caninum), which can be spread to humans, especially children with exposure to pet animals. Pulex irritans is not a major vector of disease but may play a minor role in the transmission of plague. Infection is often spread by the bite alone, but can also potential be transmitted through fecal abrasion. Tunga penetrans does not transmit disease to humans, but females will burrow into host skin. The pinpoint lesion enlarges to pea-size within two weeks necessitating removal of the gravid female using a pin, a needle or a sliver of bamboo. This may potentially lead to a secondary bacterial infection.

Control and Treatment

Control of fleas is generally mediated through insecticidal powders and aerosols. If outbreaks of murine typhus or plague occur steps to control the rodent populations in the affected area may be employed.

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Bedbugs

Class:    Insecta
Order:      Siphonaptera
Genus: Cimex

Introduction

 

Common bedbugs (Cimex lectularius) are 3µm-7µm long, wingless, and flattened dorsoventrally. They have long legs, clearly segmented antennae and abdomen, and a distinctive set of compound eyes.Bedbugs are characteristically pale brown but swell and turn to black-red when engorged with blood. Both sexes infest clothing, beds and laundry and pierce the skin with an elongated proboscis to feed.

Image 12-27.  Image of the common Bedbug Cimex lectularius. Bed bugs are usually pale brown in color but swell and turn black-red after a blood meal.  (SOURCE:  PHIL 6283 – CDC/ Donated by the World Health Organization, Geneva, Switzerland.)

Life Cycle

Cimex nymphs appear yellow and very similar structurally to the adults. The life cycle is hemimetabolous with five nymphal instars that require blood meals to proceed. The adults primarily feed nocturnally, and females may lay upwards of 500 eggs during their lifetime. Life cycle duration and the number of offspring produced are primarily determined by the humidity and temperature of the surrounding environment.

Disease

Cimex blood meals result in inflammation, irritation and intense itching. These are the most common results of an infestation, but Cimex have also been found to carry Hepatitis B in India.

Treatment and Control

A female lays around 200 adherent eggs at the rate of 3 or 4 per day: eggs are white and 1mm in length. Control is by application of insecticide to mattresses and crevices where they hide during the daytime (to a height of several feet from the floor).

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Triatomine bugs

Class:     Insecta
Order:     Hemiptera
Family:     Reduviidae
            Genus:     Triatoma

General Characteristics

Triatomine bugs (a.k.a., Assassin bugs, Kissing bugs, Cone-nosed beetles, Walapai Tiger, or Reduviid bugs) are of variable size but are often large (10mm-30mm). They typically appear brown-black, but can have bright coloration. They are distinguished by a large snout with dark compound eyes, a thin and straight proboscis, and a triangular pronotum. They have long slender legs with terminal claws and segmented antennae. A set of large wings covers the oval abdomen. They live in the mud-walls of housing and woodpiles and come out to feed at night when the host is asleep: they are voracious biters, often on the face around the eyes.

Image 12-28.  Image of the Triatomine Bugs Triatoma infestans. Reduviid bugs are of variable size but are often large (10-30 mm). They typically appear brown-black, but can have bright coloration.  (SOURCE:  PHIL 2538 – CDC/World Health Organization.)

Life Cycle

The life cycle of Triatoma is hemimetabolous. The emergence of nymphs from eggs is primarily determined by the environment, and blood meals are required to proceed through the five nymphal instars. The nymphs and adults feed nocturnally and generally lay 50 to 1000 eggs depending on life term and the quantity of blood meals taken.

Disease

The primary disease transmitted by Triatoma is Chaga’s Disease caused by Trypanosoma cruzi. Chagas disease is endemic in 21 countries; around 100 million people in Central and South America could be exposed to reduviid bugs; the prevalence of Chaga’s disease is about 16-18 million. Rural migrations to urban areas during the 1970s and 1980s changed the traditional epidemiological pattern of Chaga’s disease: it became an urban disease, as unscreened blood transfusion created a second way of transmission.  Between 1960 and 1989, the prevalence of infected blood in blood banks in selected cities of South America ranged from 1.7% in Sao Paulo, Brazil to 53% in Santa Cruz, Bolivia, a percentage far higher than that of hepatitis or HIV infection (WHO data).

Illustration 12-13.

Worldwide distribution of Chagas Disease (Trypanosoma cruzi) (SOURCE: WHO)

Triatomids are blood feeders and deposit infected feces (containing metacyclic trypanomastigotes) on the host’s skin during feeding.  The host rubs the feces into the wound; alternatively trypanosomes enter through the mucous membranes or conjunctivae.  Once in the bloodstream, trypanomastigotes penetrate the spleen, liver, lymph nodes and muscle by an unknown mechanism (possibly via receptor-ligand binding proteins).  The parasite transforms to the amastigote form that divides by binary fission and forms a pseudocyst.  This ruptures and released amastigotes transform to flagellated trypanomastigotes via promastigotes and epimastigotes and enter the bloodstream.  Unlike African bloodstream trypomastigotes, these do not replicate.  If a Reduviid bug eats trypanomastigotes, they transform to epimastigotes, replicate by binary fission, and are passed as trypanomastigotes two weeks later.  Trypanosoma cruzi does not exhibit antigenic variation but can persist for the life of the host.  T. cruzi may also be transmitted in blood products or transplacentally.  Humans and a large number of species of domestic and wild animals constitute the reservoir, and the vector bugs infest poor housing and thatched roofs.

In the acute phase (generally seen in children) a small red nodule (Chagoma) may form at the site of the bite.  Romana’s signs comprise fever, unilateral bipalpebral edema and ophthalmia. Most acute phases are asymptomatic and resolve to an asymptomatic chronic stage in 2-3 months.  However, the patient may present with myalgia, bone pain, fever and chills, lymphadenopathy, hepatosplenomegaly and anorexia.  Young children may develop meningoencephalitis.  Pseudocysts form in heart muscle and fatal heart failure arises within one month.  Neurological disorders, gastrointestinal disease and chronic myocarditis are features of chronic disease (mainly seen in adults) which arises 10-20 years after the initial infection and is untreatable.  Congenital infection may lead to abortion, still birth or acute disease.  Reactivation occurs in HIV-infected patients. Diagnosis is by detection of trypanosomes in peripheral anti-coagulated blood, CSF or node aspirate using wet film or Giemsa stain (acute disease) or by serology (Chaga’s IgG ELISA in chronic disease). Trypanosoma cruzi is usually C-shaped, 12-30µm in length with a narrow membrane and a flagellum.  The posterior kinetoplast is characteristically large and the nucleus is central.

Control

There is no satisfactory treatment.  Extended therapy with the toxic agents, benznidazole or nifurtimox, only kills extra-cellular parasites and optimum efficacy (60%) is achieved during the acute phase.  Chronic disease is treated symptomatically.  Control is by improvements in housing, health education and insecticidal treatment of dwellings.  Vaccines and chemoprophylaxis are ineffective (associated with autoimmune disease).  For the control of blood-transmitted infections the aim is to screen all blood donors from endemic countries for T. cruzi antibodies, and to strengthen health service infrastructures for multiple blood screening (HIV, Hepatitis B and T. cruzi).

TRYPANOSOMA CRUZI (克氏锥虫)
Trypanosoma cruzi causes Chagas disease (恰加斯病), a zoonotic disease that can be transmitted to humans by blood-sucking reduviid bugs (锥蝽). Chagas disease (South American trypansomiasis) is commonly seen in the countries of South America.

MORPHOLOGY AND LIFE CYCLE
Three forms exist in T. cruzi life cycle. In man and other vertebrate host, T. cruzi exists amastigotes and non-multiplying trypomastigotes; the insect form includes epimastigotes and multiplying trypomastigotes.
Amastigote (无鞭毛体): It is the non-flagellated, intracellular parasite found in man and other vertebrate host. Amastigote is a round or oval body measuring 2 to 4µm in diameter. It has a nucleus, kinetoplast and an axoneme. Morphologically it resembles the amastigote of Leishmania species; hence it is frequently called as leishmanial form. It multiplies in man in this stage only.
Trypanomastigote (锥鞭毛体)（Fig Ⅱ-Ⅴ-2）: It is the flagellated form and has two types. The multiplying forms are found in the stomach of reduviid bug and in the culture, and non-multiplying forms are found in the blood in man and other mammalian hosts.

Fig Ⅴ-Ⅴ-2 Trypanomastigote of T. cruzi

Trypanomastigotes are usually C-shaped and slender, 11.7-30.4µm in lengths and 0.7-5.9µm in breadth. The posterior end is wedge-shaped. At the anterior end, a free flagellum originates and traverses on surface of the parasite as a narrow undulating membrane. They have a centrally placed prominent nucleus and a large round to oval kinetoplast at the posterior end.
T. cruzi need two hosts to complete its life cycle. The vertebrate hosts are man and other reservoir hosts, the insect host Reduviid bug (kissing bug, so named because they often feed around the lips of sleeping people).
When an infected triatomine (锥猎蝽亚科) insect vector (or kissing bug) takes a blood meal and releases trypomastigotes in its feces near the site of the bite wound, Trypomastigotes enter the host through the wound or through intact mucosal membranes, such as the conjunctiva (结膜). Common triatomine vector species for trypanosomiasis belong to the genera Triatoma, Rhodinius, and Panstrongylus. Inside the host, the trypomastigotes invade cells, where they differentiate into intracellular amastigotes. The amastigotes multiply by binary fission and differentiate into trypomastigotes, and then are released into the circulation as bloodstream trypomastigotes. Trypomastigotes infect cells from a variety of tissues and transform into intracellular amastigotes in new infection sites. Clinical manifestations can result from this infective cycle. The bloodstream trypomastigotes do not replicate (different from the African trypanosomes). Replication resumes only when the parasites enter another cell or are ingested by another vector. Feeding on human or animal blood that contains circulating parasites infects the “kissing” bug. The ingested trypomastigotes transform into epimastigotes in the vector’s midgut. The parasites multiply and differentiate in the midgut and differentiate into infective metacyclic trypomastigotes in the hindgut. Within 8-10 days, these trypanomastigotes are excreted in the faeces of the bug, as the bug takes the blood meal from a host and the cycle is continued. Trypanosoma cruzi can also be transmitted through blood transfusions, organ transplantation, transplacentally, and in laboratory accidents.

FigⅤ-Ⅴ-3  Life cycle of Trypanosoma cruzi

PATHOGENESIS AND SYMPTOMS
The pathogenesis of acute Chagas’ disease depends upon the destruction of parasitised and non-parasitised host cells. Destruction of host cells is responsible for the clinical symptoms of the disease at the early stage. Chagas’ disease is a chronic condition. Infected persons may show few, if any, signs of disease and may survive for decades, even though still infected.
Acute Chagas’ disease
It occurs most commonly in infants and children. The first sign of illness occurs at least 1 week after invasion by the parasites.
A local lesion (chagoma, palpebral edema) can appear at the site of inoculation. Chagoma (恰加氏肿) is localized swelling of the skin and contains intracellular amastigotes in leucocytes and subcutaneous. When the parasite is inoculated in the conjunctiva, a unilateral painless oedema of the palpebral and perioccular tissue develops in the eye. It is called Romana’s sign and is the classical finding in the acute Chagas’ disease. The acute phase is usually asymptomatic, but presents with manifestations that include fever, anorexia, lymphadenopathy, and mild hepatosplenomegaly; in severe infection, myocarditis may develop. Most deaths in acute Chagas’ disease are due to heart failure or meningoencephalitis. The acute stage lasts for 20-30 days. Symptoms resolve in most of the patients, who then enter into asymptomatic or indeterminate stage of T. cruzi.
Chronic Chagas’ disease
It is seen in older children and adults between 20-40 years of age. The symptomatic chronic stage may not occur for years or even decades after initial infection; it may also be seen in persons without any previous episode of acute disease. Its manifestations include cardiomyopathy (心肌症) (the most serious manifestation), pathologies of the digestive tract such as megaesophagus and megacolon, and weight loss. Chronic Chagas’ disease and its complications can be fatal.
During the chronic phase, although signs may not be apparent, the repeated cycle of intracellular multiplication are continually destroying cells, not only those in which the amastigotes multiply, but also neighbouring cells. An autoimmune mechanism is probably involved. Neurons are particularly vulnerable to destruction. If the intracellular groups of parasite (pseudocysts) are concentrated in parts of gastrointes

tinal tract, especially in oesophagus or colon, peristalsis may be interfered and the organ may become hugely distended. This condition is indicated by the prefix mega, for example megaoesophagus (巨食管) or megacolon (巨结肠). The unfortunate patient may be unable to swallow and die of starvation. Megacolon may become so gross leading to rupture of colon and death..
If the pseudocysts congregate in the heart muscle, and some strains are more prone to do this than others, the ensuing neuronal and muscle destruction may gravely weaken the heart wall, causing irreversible damage and leading to an early death from heart attack.

DIAGNOSIS
The diagnostic procedure in acute Chagas’ disease is to demonstrate the causal agent. It can be achieved by:
Microscopic examinations: a) of fresh anticoagulated blood, or its buffy coat, for motile parasites; and b) of thin and thick blood smears stained with Giemsa, for visualization of parasites.
Isolation of the agent by: a) inoculation into mice; b) culture in specialized media (e.g. NNN, LIT); and c) xenodiagnosis (病媒接种诊断法), where uninfected reduviid bugs are fed on the patient’s blood, and their gut contents examined for parasites 4 weeks later.
Immunological diagnosis: During the chronic stage of infection, parasites are rare or absent from the circulation; immunodiagnosis is the method of choice for determining whether the patient is infected. Although IFA is very sensitive, cross-reactivity occurs with sera from patients with leishmaniasis, a protozoan disease that occurs in the same geographical areas as T. cruzi. Sensitivity and specificity of EIA tests that use crude antigens are similar to those of the IFA test. Although differentiating between acute and chronic infection is very important in determining therapy, serology cannot be used to do so. A positive titer indicates only infection at some unknown time, and not acute infection.

EPIDEMOLOGY
Chagas’ disease is a zoonoses. The infection is transmitted from animals to man. It is distributed in the Americas from the southern United States to southern Argentina, mostly in poor, rural areas of Central and South America. Chronic Chagas’ disease is a major health problem in many Latin American countries. With increased population movements, the possibility of transmission by blood transfusion has become more substantial in the United States.
Two major cycles of transmission of infection take place: domestic cycle and sylvatic (栖息于森林的) cycle. In domestic cycle, the infection is transmitted between man and domestic animals by the bite of blood sucking reduviid bugs. Naturally infected dog, bug and rabbit are the reservoir hosts. They are the sources of infection of man. This type of infection is common in rural areas with low socio-economic condition and poor sanitation.
In sylvatic cycle, the infection is transmitted between sylvatic reduviid bugs and small mammals including rodents and marsupials. These are the reservoirs and source of infection for man. Chagas’ disease is transmitted commonly by kissing bugs. Less frequently, the disease may be transmitted by blood transfusion or congenital infection, and laboratory infection.

PREVENTION AND CONTROL
1) Treatment: Medication for Chagas’ disease is usually effective when given during the acute stage of infection. The drugs of choice are benznidazole or nifurtimox (under an investigational New Drug Protocol from the CDC Drug Service). Once the disease has progressed to later stages, no medication has been proven to be effective. In the chronic stage, the treatment involves managing symptoms associated with the disease.
Acute Chagas disease must be treated early. The decision for initiating therapy must not be swayed by negative findings or delayed while waiting for results of isolation attempts, if the clinical and epidemiologic suspicion of the disease is strong.
2) The preventive measures include: a) application of insecticides to kill the vector bugs in human dwellings and improvement of rural housing environment to eliminate the breeding places of kissing bug, b) Personal protection by using mosquito nets and insect repellants, and c) Serological screening of blood donors for T. cruzi to prevent transmission by blood transfusion.

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Poisonous snakes, spiders & bugs whilst on vacation in Mexico and the Caribbean.

Mexico, home to venomous killer caterpillars, poisonous spiders, fatal tsetse fly, blood sucking deer ticks and the ancient Aztecs. Mexico is an adorable place, absolutely beautiful, with world class hotels and superb beaches providing fantastic cheap vacations.

But Mexico is full of poisonous insects and snakes in virtually every place you could go to, killing hundreds of people every year, and infecting thousands more, including tourists. When in Mexico, or any other foreign country, please remember to pack anit-histamine tablets, these will help if you are ever bitten, and if someone you know has been bitten by a snake, never suck out the poison.

Very Small Brown Recluse Spider

The Brown Recluse Spider

The Brown Recluse Spider, or the Violin Spider, are very small and grow between 6-20mm in size, but they can pack a huge punch. They like undisturbed placed like garages, and wood or rock piles, but are frequently found in the house behind wardrobes, in clothes or linen piles, cupboards and under beds. They are nocturnal creatures and if the male goes hunting at night, it can often be found in temporary cover, like footwear or drawers.

Venomous Brown Recluse Spiders are not aggressive, but when they feel threatened, they will attack. Most of the bites from these spiders go by unnoticed, which is where the danger lies. Many of these bites will come to nothing more than a bit of itching and swelling, whereas some, as you can see by the picture above, are a bit more serious. Once a Brown Recluse Spider bites someone, the venom will be throughout their blood system in minutes, but still giving them time to seek medical attention before serious internal injuries can happen.

Most fatalities occur in younger children up to the age of seven, or the elderly or anyone with an insufficient immune system, even a cold or illness can cause these bites to turn into something deadly. If bitten, symptoms may include vomiting, rashes, fever and joint pain, which may lead to coma and death. Seek medical attention immediately if anybody has been bitten.

This is Mexico’s most venomous spider. Whilst on vacation or on holiday to Mexico, ensure to check clothes before they are worn.

Brown Recluse Spider

Brown Recluse Spider

The 700 islands of the Bahamas and Jamaica are a tropical paradise. The venomous spider named the Brown Recluse Spider is a vicious yet still shy creature. The above picture shows a venomous bite from this spider which has been left untreated.

The Caribbean Brown Recluse Spider is shy, but packs a powerful punch. They are found in cupboards, under beds, and within towels on shelves. They usually bite when someone inadvertently puts on their clothes with the spider nestled inside. The venom is more toxic that a rattle snakes bite. Cheap vacations in the Bahamas can turn into a deadly battle for life with tropical spider bites.

This venomous spider can be found throughout the Bahamas and Jamaica. Also known as the Violin Spider, this creature is only approximately 1cm – 2.5cm in size. The initial bite may not be noticed by the victim as the bite is so small. Not all bites will be poisonous, but you never can tell.

The poison is hemotoxin, which actually destroys soft tissue. The bites become itchy within 1 – 8 hours, then after 12 hours pain will begin to develop along with redness and possible swelling of the bitten area. Over the next few days skin lesions will develop and can grow to over 25 cm in diameter. The wound can become gangrenous with the possibility of a limb being amputated. These wounds are painful and may take over a year to heal.

If at any time you think you may of been bitten by a spider, seek medical attention. Do not take chances not only can your Jamaican vacation be ruined, but your life could change completely.

Very, Very Dangerous Caterpillars

Puss Caterpillar

The adorable puss caterpillar goes by many different names, such as the Tree Asp, Southern Flannel Moth, Pussy Moth, and the Asp Caterpillar. And this moth, is only dangerous in its caterpillar stage. The caterpillar is covered in tiny reddish hairs, and all these are attached to venom glands, and once anything comes into contact with the very sharp hairs, they are injected with venom.

Symptoms of caterpillar hair poisoning are nausea, rashes, blisters, abdominal pains, swelling, burning sensations, numbness, chest pains, difficulty in breathing and death. If injected by these furry critters, get help immediately, stop for nothing, your life may depend on it.

Many vacations to Mexico have been ruined when children pick up these caterpillars to play with.

• Poisonous Processional Caterpillars in Portugal

Tiny Tick, Big Bite

The Deer Tick

The Deer Tick, sounds like a normal little animal tick which obviously is attracted to animals, and you would be right, BUT……..it does bite humans. If a tic bites a person, 99% of the time, they do not notice the initial bite, and the tic can stay on the body, drinking your blood, for nearly four days, before it falls off, full.

The Deer Tic can give its host Lyme Disease, and the initial symptoms of this are headache and fevers, and as time goes by, stiff joints and heart problems, possibly leading to death. If bitten, or even if you suspect a bite, see a doctor, if not treated quickly, the bitten person can suffer with these medical problems for years.

Assassin Bug Bite

Assassin Bug

Assasin Bug

The Assassin Bug has over thirty different names, but the disease they carry, Chagas Disease, is still the same. It is estimated the nearly eleven million people in Mexico have this potentially fatal disease, but do not yet know it, similar to Mesothelioma ( Asbestos Poisoning ) this disease will stay with you for life, and it may only show itself after twenty to thirty years after the initial bite. Vacations to Mexico are fantastic, but not worth thirty years of pain.

There are several species of this bug, some with bites that you will feel instantly, and some with bites that you will never notice. One of the names of this bug is the Kissing Bug, because they will bite their victims at night around the nose and mouth area, many people who have felt the bite in the dark have mistook it for a mosquito bite.

Initial bites can be cured with medicines, with a 90% cure rate, if the bite goes untreated, after four weeks then you will be 80% likely to have Chagas Disease for the rest of your life. 40% of these people will develop heart and digestive problems later on in life, with the cause being constantly misdiagnosed. If bitten by anything whilst on holidays to Mexico, seek medical advice, no matter how trivial it may seem.

Coral Snake

Snakes

Mexico is home to over 60 different species of Coral Snakes, all venomous, all bite, some can kill.Coral snakes are regarded as one of the top five most poisonous snakes in the world, killing many people annually, especially in South America and Mexico. Their colors vary, but many have a distinct three colour pattern.

In Mexico, they are called the twenty minute snake, because after you have been bitten, you will be dead within twenty minutes.

Most of these snakes are very small, some about 20cm, but some can grow to 150 cm ( 5 feet ), the venom from the Coral Snake is a neurotoxin, and will immediately begin to attack your breathing systems, and medical attention needs to be given very quickly. Anti venom is available but artificial respiration may be required to save the life. If a person is bitten whilst on vacation to Mexico and becomes unconscious, continue with artificial respiration until medical help arrives, do not stop, their life depends on it.

Free Link: WARNING: The Screw Worm Fly is a deadly and dangerous tissue eating maggot. It kills herds of cattle, sheep and people. It is now known to be in Mexico, Jamaica, and Panama. It is on Americas most wanted list for deadly insects. Follow the free link to our sister site for more information.

There are many vacation packages and holiday deals to Mexico online. Prior to leaving, ensure about inoculations for everyone.

Caribbean vacations and holidays may never be the same again. There are many venomous spiders and poisonous snakes in and around the beautiful Bahamas islands. Deadly biting insects await the careless traveller, whose vacation could transform into a nightmare. The tropical weather of Jamaica and the Bahamas make these places an ideal breeding ground for some of the worlds deadliest creatures.

Venomous snakes and venomous poisonous can kill. Here are some of the scary and potentially dangerous creatures that await you on your Bahamas vacations.

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Banana Spider

The Caribbean poisonous spiders known as the Banana Spiders or the Brazilian Wandering Spiders are lethal. The Guinness book of records has them listed as the most venomous spider in the world. They are nocturnal spiders whom forage through the undergrowth at night for food. They reside is moist places such as under logs, in rock piles or cellars, and are usually found close to human habitats. This is the spider which has ruined many vacations in the Caribbean.

The neurotoxin from the Banana Spider can cause pain during an erection and can lead to impotency. The initial bite will be painful, and swelling and reddening around the bite mark will happen in minutes. Muscle spasms will follow shortly afterwards, intense pain will rack the body as the venom begins to flow through the blood system. Paralysis will begin to take hold as the venom attacks the respiratory system. This leads to asphyxiation then a painful and slow death.

This all only takes from as little as two hours. If anyone has been bitten by this beautiful yet very deadly creature, run like the wind to the nearest medical station, your life depends on it. Caribbean vacations are out of this world and can blow your mind, just take care with any insect bite that you may recive.

Fer-de-lance Snakes

Poisonous snakes have never really been a problem in the Caribbean. Occasionally a tourist on vacation may be bitten by a non-venomous snake. The sighting of the odd Fer-de-lance or Lance Head snake may be a bit worrying though.

The fer-de-lance snake has hemotoxin venom, which can cause nausea, loss of weight, black outs, loss of memory and even temporary paralysis. Treatments for this snake bite are readily available, although there have been no reports of a person being bitten by one of these in the Caribbean for years.

There are only a few islands which do have land snakes on them, St. Lucia, Martinque, Guadaloupe, and Trinidad are the reportedly the only islands. The snakes on these islands are not meant to pose a threat to tourists at all. Do not believe what you see in the movies, not all snakes hunt humans on vacation as a quick snack,

Poison Dart Frogs

Poison Dart Frog

There are many species of brightly colored poisonous frogs in the Caribbean and Jamaica areas. The Poison Dart Frog, or Poison Arrow Frog, only measures approximately 1.5 cm, but carries enough toxin on its’ skin to kill twenty men, or at least 10,000 mice. Poisonous frogs present no immediate threat to humans, unless they are touched, which whilst on vacation in the Caribbean, some tourists have been known to stroke these deadly creatures, not realizing the potential danger.

Venomous frogs secrete poisons onto their skin to deter predators. It is said that the poisons are taken from the millipedes and other insects that they eat, as the frogs cannot produce their own poisons. Medically, one of the toxins they produce can be used as a painkiller and is said to be more than 200 times more potent than morphine.

The Poison Dart Frog was used by natives on their spear heads to poison and kill their quarry. If you touch one of these frogs accidentally, quickly hop to the nearest medical centre for help. These frogs can kill, so do not take it lightly. Be careful if on vacation with young children, the bright coloring often temps children to pick up these frogs.

Scolopendra Gigantea

This is a very big, scary, and dangerous centipede. This massive centipede reaches an amazing 29 cm in length, that is nearly 1 foot long. This meat eating monster eats tarantula spiders, birds, lizards and even bats. The fast moving centipede is able to outrun a small child and is found more usually in Jamaica.

The venom of this impressive beast is delivered through two modified claws from around the head. The young of this poisonous animal are black with red heads. The extremely potent venom will cause severe itching, redness and extreme swelling. Chills and sweating will follow soon afterwards and a weakness will overcome the victim. Fatalities are rare from this over sized insect, but they are scary and will deliver a vacation wrecking bite. People on vacation in the Caribbean often leave their brains at home and become careless, it is at this time that most bites happen.

Giant African Land Snail

This is a deadly snail which can kill humans. The chances of being hunted down and killed by this timid beast are very rare. But it has been known to kill through infections. The snail is described as a pest as it devastates crops and the USA has began exterminating it where ever it shows up in America. Just one of these snails in an area will produce a total colony of thousands within a year.

The Giant African Land Snail carries at least eight different parasites which can infect animals and humans. The major known disease they carry is rabies, which is carried in the snails dung. Dogs have died from eating a sing snail. The dung left behind if touched by human hands can transmit rabies.

The land snails can grow up to 7cm tall and over 20cm in length and the shell is conical shaped. Some nations keep them as pets whilst others use them as a food source. This slimey creature should not ruin a fantastic vacation to the Caribben, but steer clear of them just in case.

Screw Worm

The Screw Worm

This may be the devil re-incarnated. This little demon is neither venomous nor poisonous. There are five types of screw worm, and only one type flies. The maggots from this flying insect are the actual screw worm, and they eat living flesh, not like normal maggots which only eat the dead flesh.

The female Screwworm will lay 3000 eggs within her life cycle, which is only 20 days. These maggots are usually laid in an open wound, no matter how small, in the navel of new born animals and humans. The maggots hatch within hours and begin to burrow into the soft flesh as they eat their way into the body. If a person scratches the wound, the maggots ‘screw’ deeper. These maggots cause many deaths.

In 1998, a woman came back from a vacation in Trinidad and complained to her doctor within days about vomiting and headaches. After an x ray, 94 of these maggots were taken from inside the back of her neck. They had apparently entered through a mosquito bite. If they were not removed, they would have killed the woman by eating into her brain.

If you have been to the Caribbean on vacation and suffer from abnormal headaches or pain in areas where a wound ( even the smallest bite form a mosquito ) has occurred, go to the hospital for an ex-ray.

Screw Worm Larvae Puncture Hole

Screw Worm Eradication Measures

South America used to be infested with the screw worm, it killed herds of cattle, sheep, and many people. An idea was launched to infiltrate the screw worm population with specially bred infertile screw worm adult flies. This would reduce the number of pregnant screw worms whislt they mate, which is between 4 -5 times in their 20 day life. Billions of these infertile adult screw worms were bred and released into the air. It worked.

South America is now free from this pest, Mexico, Jamaica and other places are not. Factories in South America produce billions of these adult screw worm flies every year to eradicate this demon of a pest. They are exported to other parts of the world as the eradication process of a very dangerous creature progresses.

Do not underestimate this creature. The screw worm is on Americas most wanted list. If this insect is suspected of being alive or infecting animals or humans on American soil. the authorities at the highest levels are notified and actions are implemented within hours. Be warned, it is dangerous and will kill without mercy.

The maggots are only under the skin for five days, if they do not leave the skin as they should do within five days, there is little hope for a person with a minimum of 250 flesh eating maggots crawling under the skin. Even cheap vacations in the Caribbean can resort in death if a person is not careful.

Follow this free link to a sister presentation to discover the insect that kills over 3000 people each day, and is rife around the Caribbean. The killer mosquito.

 

VaxTruth Fights Vaccine Damages

 

New Organization VaxTruth Fights Vaccine Damages

A.M. Freyed
Infowars.com
August 7, 2012

A new national organization called VaxTruth is dedicated to telling people about their rights to legally refuse vaccines for themselves and their children.

As an article by Russell L. Blaylock, M.D. posted at the alternative health website Mercola.com points out that in the early 1980s, autism presented itself in 1 of 10,000 births. By 2005, that was 1 in 250 births, and as of 2008, it was 1 in 150 births and still rising.

While the medical establishment refuses to consider it as a cause, the biggest change during this time had to do with a radical rise in vaccines being given at a very early age. It is this rise that an increasing amount of parents with autistic children hold responsible.

In fact, the problem may be considerably larger than autism. There is apparently virtual worldwide genocide going on thanks to vaccines. In the US it’s been noticed because of the startlingly high rates of autism … but commentators such as Guylaine Lanctot, M.D. have noted that vaccines may have wiped out whole populations in Africa where vaccines are provided aggressively.

While naturopaths and some others hold that vaccines’ efficacy is entirely the result of elitist propaganda, a less radical view that circulates within the alternative media accepts that vaccines are utile but that they are over-used and under-analyzed.

It is quite likely, according to this view, that a proportion of children are either sensitive to vaccines or become prone to injury because of the amount of vaccines they are receiving. Children in the US for instance are now scheduled for nearly 20 vaccines, and the number keeps rising.

It is likely that a portion of the population has an increasingly attenuated immune response because of vaccines and this makes them susceptible to conditions such as AIDS (whatever it actually is).

The pharmaceutical industry serves at the pleasure of globalists who have long made population reduction their goal. As part of their secretive goal to formally run the world, they use famine, war and vaccine injury to injure and ultimately reduce human populations.

Thanks mainly to the Internet, both the elite agenda and problems with vaccines have been uncovered and shared worldwide. As with many issues pertaining to elite neo-authoritarianism, the United States has led the way because of a cultural exceptionalism that encourages citizen activism.

VaxTruth is a good example of this sort of citizen activism. The vaccine information group has placed billboards in four states over the last year: Indiana, Texas, Colorado and California. The billboards proclaim: “No Shots, No School… NOT TRUE!!” Austin, Texas and Kansas are scheduled to receive such billboards next.

The group has received attention via articles on vaccine-education websites such as Age of Autism. It is run in part by Marcella Piper-Terry who explains on the website VaxTruth.com that she finally decided she’d “had enough of the one-sided reporting” regarding parents’ legal rights to accept or reject vaccine regimes for themselves and, especially, their children. Piper-Terry writes that she has a child injured by vaccines.

Her bio also notes that she has a master’s degree in psychology and has worked as a therapist and as a neuropsychological evaluator of children and adults. She founded VaxTruth with two others, Megan and Spencer Pond in the fall of 2011.

Piper-Terry who lives in Southwestern Indiana, acted after the Evansville Courier and Press newspaper printed a front page story telling parents their kids couldn’t go to school unless their vaccines were “up-to-date.” She asked for a retraction and was told it would not take place.

She quotes the Metro Editor as saying he would not “print anything that would cause parents to question the safety of vaccines.” Piper-Terry then decided to act on her own to inform people of their rights. “That’s how VaxTruth and the Billboard Campaign came into existence,” she explains.

VaxTruth encourages fundraisers that can generate cash to buy billboards. Most states have various kinds of exemptions that allow concerned parents to remove their children from vaccine programs if they are concerned with the ramifications.

To make the point about the importance of vaccine non-compliance, VaxTruth publishes and republishes articles about parents’ interactions with the medical community. One article recently posted to the website is a first person account by Alisha Lynn Ramsey on a “a horrible experience with a doctor” within the context of vaccine demands.

She writes that she took her son Adam in for his two year “well visit” and that during the check up, it became apparent to both the senior doctor (pediatrician) and the student doctor that she was “selectively” vaccinating. The article continues as follows:

We wait 30 minutes and the student doctor and the pediatrician finally walk in the exam room and the pediatrician doesn’t even look at me or speak to me. Instead they go to his chart and are talking back and forth and the student doctor is nodding and writing things down. That’s when the pediatrician turns to me and asks “Has he had any vaccinations at all?” I respond, “He’s had a few at birth but none since.” He turns back to the student and tells him something and he writes it down. Then the student doctor tries to take my son from my arms, and as he is reaching for him the pediatrician tells me “Your son will be receiving 14 vaccinations today, Mrs. Ramsey.”

… I instinctively pull my son back to me and tell him, “No. We do not want any vaccines.” The pediatrician goes on to tell me that everything I’ve read online about autism isn’t true. I respond, telling him that’s not why we aren’t vaccinating. He says to me, “You are going to kill your son. You don’t want to be responsible for killing this little boy, do you Mrs. Ramsey?”

Before I could respond he nods to the student doctor, who steps forward to try to take Adam out of my arms AGAIN. I pull back and am backed literally into a corner at this point and I’m shaking. The pediatrician goes on about how I am not thinking of the best interest of my child and how I’m going to kill him and that he WILL be getting the vaccines today and more every month until he is up-to-date in full.

His voice is beginning to raise by now and the look on his face stern. “This is for the best, Mrs. Ramsey so be compliant.” As he says this to me, for a 3rd time the student doctor tries to take Adam from my arms; this time a little more assertively. The student doctor looked as white as a sheet but also looked like he was doing what he HAD to do because of what his boss was telling him. He looked young enough to be wet behind the ears.

I’m standing in a corner, in a room the size of a box with these 2 men trying to take my child and vaccinate him against my will. I hold onto Adam as the student doctor is trying to take him from my arms and Adam begins to cry and cling to me. I’m shaking; I’m afraid and Adam can sense this. I put both arms around Adam and bring his head towards my bosom to protect him and I pull bravery from somewhere.

“He will NOT be vaccinated. You will NOT be putting poison in my son.” I stammered, shaking like a leaf but I held strong.

The pediatrician GLARED at me. “Well,” he says clearly irritated.” If you aren’t going to comply, then you leave me no choice. Not only will you not be allowed back at this clinic but I will be reporting you to Child Protective Services. You are endangering your child.”

I didn’t wait for him to say anything more, I pushed past them and walked out. As I’m walking downthe hall as fast as possible, with Adam screaming scared to death and me shaking like mad, he hollers after me, “You’re going to be sorry for letting Google be your doctor!”

I walked faster and got out of there as fast as I could.

The website is www.VaxTruth.org

And RIGHTFULLY SO Mrs. Ramsey 14 vaccines in one day is complete medical malpractice in my books. FKN NAZI DOCTORS HOW DARE THAT PEDIATRICIAN MURDERING BASTARDS they should be in jail… These kind of doctors are complicit in the complete crime As first off they know they can’t vaccinate a child without parental consent yet they still use extortion,intimidate and threatening on her, many parents at this point would comply out of fear of many things but of loosing there kids most of all as threatened by the doc. How can they not know the reality about vaccines there supposedly intelligent DOCTORS. I’m no doctor but I’ve read enough proof over the last 5 years to conclusively say there DANGEROUS. Its all over the internet almost a ton of direct evidence showing vaccines to be injectable poison cocktails… So they know but the kickbacks are just too good so lot of doctors ignore the truth and murder and meme innocent baby children with vaccines for  profit and greed never mind the Hippocratic Oath of do NO HARM that they supposedly take on becoming a doctor????????? That’s nothing compared to dollar bills

And of course Big Pharma never lies right…

Pfizer settles foreign bribery charges

By James O’Toole @CNNMoney August 7, 2012: 1:50 PM ET

Pfizer reached settlements with the SEC and the Department of Justice.

NEW YORK (CNNMoney) — Pharmaceutical giant Pfizer will pay $60 million to settle charges that it paid millions in bribes to foreign officials, federal authorities announced Tuesday.

Pfizer will pay roughly $45 million to the Securities and Exchange Commission to settle charges that the company, along with fellow pharmaceutical firm Wyeth, which Pfizer acquired a few years ago, violated the Foreign Corrupt Practices Act.

The SEC says staff from the companies’ subsidiaries paid bribes to foreign government officials to boost sales and obtain regulatory approvals. The violations occurred in Bulgaria, China, Croatia, the Czech Republic, Italy, Kazakhstan, Russia and Serbia, the SEC said.

Pfizer also entered into a deferred prosecution agreement with the Department of Justice, agreeing to pay a $15 million penalty.

“Corrupt pay-offs to foreign officials in order to secure lucrative contracts creates an inherently uneven marketplace and puts honest companies at a disadvantage,” James McJunkin of the FBI’s Washington field office said in a statement.

In China, for example, Pfizer employees rewarded government doctors who prescribed large amounts of the company’s drugs by inviting them to meetings with “extensive recreational and entertainment activities,” the SEC said. In Croatia, the agency said, government doctors received a portion of the proceeds from Pfizer’s drug sales to the doctors’ own institutions.

Pfizer noted that there is no allegation that anyone at the company’s corporate headquarters knew of the conduct in question, which it voluntarily reported to the government.

“The actions which led to this resolution were disappointing, but the openness and speed with which Pfizer voluntarily disclosed and addressed them reflects our true culture and the real value we place on integrity and meeting commitments,” Amy Schulman, executive vice president and general counsel at Pfizer (PFE, Fortune 500), said in a statement.

The SEC said the violations date as far back as 2001, and that Pfizer initially reported them in 2004.

Shares of Pfizer were down 1.5% in mid-day trading Tuesday.