Category: Murderers


Ebo-Lie: Man Living In Ghana Confirms Ebola Is A Hoax!


Ebo-Lie: Man Living In Ghana

Confirms Ebola Is A Hoax!

Saturday, November 1, 2014 12:05

(Before It’s News)

  By Steven Bancarz October 16, 2014 Health and Wellness, Medicine

By Steven Bancarz| A statement made by a man in Ghana named Nana Kwame has rocked the internet in the last few days.   The following information needs to reach people.  We need to see Ebola for what it really is.  It’s time that the world wakes up to the agenda behind all of this hysteria. Here is what this man has to say about what is happening in his home country:

“People in the Western World need to know what’s happening here in West Africa. THEY ARE LYING!!! “Ebola” as a virus does NOT Exist and is NOT “Spread”. The Red Cross has brought a disease to 4 specific countries for 4 specific reasons and it is only contracted by those who receive treatments and injections from the Red Cross. That is why Liberians and Nigerians have begun kicking the Red Cross out of their countries and reporting in the news the truth. Now bear with me:

REASONS:

Most people jump to “depopulation” which is no doubt always on the mind of the West when it comes to Africa. But I assure you Africa can NEVER be depopulated by killing 160 people a day when thousands are born per day. So the real reasons are much more tangible.

Reason 1:

This vaccine implemented sickness being “called” Ebola was introduced into West Africa for the end goal of getting troops on the ground in Nigeria, Liberia, and Sierra Leone. If you remember America was just trying to get into Nigeria for “Boko Haram”. BULLSHIT.  But that fell apart when Nigerians started telling the truth. There ARE NO GIRLS MISSING. Global support fell through the floor, and a new reason was needed to get troops into Nigeria and steal the new oil reserves they have discovered.

Reason 2:

Sierra Leone is the World’s Largest Supplier of Diamonds. For the past 4 months they have been on strike, refusing to provide diamonds due to horrible working conditions and slave pay. The West will not pay a fair wage for the resources because the idea is to keep these people surviving on rice bags and foreign aid so that they remain a source of cheap slave labor forever. A reason was also needed to get troops on the ground in Sierra Leone to force an end to the diamond miners strikes. This is not the first time this has been done. When miners refuse to work troops are sent in and even if they have to kill and replace them all, the only desire is to get diamonds back flowing out of the country.
Of course to launch multiple campaigns to invade these countries separately would be way too fishy. But something like “Ebola” allows access to an entire area simultaneously…

Reason 3:

In addition to stealing Nigerian oil, and forcing Sierra Leone back to mining, troops have also been sent in to FORCE vaccinations (Deadly “Ebola” Poison) onto those Africans who are not foolish enough to take them willingly.

3000 troops are being sent in to make sure that this “poison” continues to spread, because again it is only spread through vaccination. As more and more news articles are released as they have been in Liberia, informing the populous of the US lies and manipulation, more and more Africans are refusing to visit the Red Cross. Troops will force these vaccinations upon the people to ensure the visible appearance of an Ebola pandemic. In addition to this they will protect the Red Cross from the Liberians and Nigerians who have been rightfully ejecting them from their countries.

Reason 4:

Last but not least, the APPEARANCE of this Ebola “pandemic” (should Americans not catch on) will be used to scare the countless millions into taking an “Ebola vaccine” which in reality is the pandemic. Already they have started with stories of how it has been brought to the U.S. and has appeared in Dallas, how white doctors were cured but black infected are not being allowed to be treated, etc.

ALL that will do is make blacks STRIVE to get the vaccine, because it appears that the “cure” is being held back from blacks. They will run out in droves to get it and then there will be serious problems. With all we have seen revealed about vaccines this year you would think we learned our lesson. All I can do is hope so, Because they rely on our ignorance to complete their agendas.

Ask yourself: If Ebola really was spread from person to person, instead of controlled spread through vaccination – then WHY would the CDC and the US Government continue to allow flights in and out of these countries with absolutely no regulation, Or At All? We have got to start thinking and sharing information globally because they do not give the true perspective of the people who live here in West Africa. They are lying for their own benefit and there aren’t enough voices out there with a platform to help share our reality. Hundreds of thousands have been killed, paralyzed and disabled by these and other “new” vaccines all over the world and we are finally becoming aware of it. Now what will we do with all this information?”

The original piece written by him can be found here.

A Liberian-born faculty member of a US university wrote an article on Liberian newspaper, the Daily Observer, claiming that Ebola is the result of bioterrorism experiments conducted by the US.

Dr. Cyril Broderick claimed, among other things, that “sites around Africa, and in west Africa, have over the years been set up for testing emerging diseases, especially Ebola.

“WHO and several other UN Agencies have been implicated in selecting and enticing Africancountries to participate in the testing events, promoting vaccinations, but pursuing various testing regiments,” he continued.

“Reports narrate stories of the US Department of Defense (DoD) funding Ebola trials on humans, trials which started just weeks before the Ebola outbreak in Guinea and Sierra Leone” Claims a report from International Business Times.

It also happens that the Ebola breakout coincides with UN vaccine campaigns.  Pharmaceutical and biotech industries will have profited handsomely from the ebola crisis when biodefense-research generals, high civil servants and UN bureaucrats sheepishly sign multimillion-euro R&D contracts.  It’s quite the coincidence that the earliest breakout in Guinea happened along side three major vaccine campaigns conducted by the World Health Organization (WHO) and the UN children’s agency UNICEF. At least two of the vaccination programs were implemented by Medicins Sans Frontieres (MSF, or Doctors Without Borders), while some of those vaccines were produced by Sanofi Pasteur, a French pharmaceutical whose major shareholder is the Rothschild Group.  Of course, the Rothschilds run nearly all of the worlds central banks and have a family network of around 500 trillion dollars.  They are the ones pulling strings on this planet, and they will only profit from this outbreak.

Now, I am personally no expert on Ebola, but history has a funny way of repeating itself.  Here is my prediction.  Expect a false flag attack in the US as a way to further contain/control the population and kill them off in the process.  The are going to announce an outbreak (which may actually the release of a chemical bioweapon, and not Ebola) and then they will start administering the Ebola vaccine to the population.  They may even try to make it mandatory.  DON’T TAKE THE VACCINE.  This is how Ebola will spread, and this is how the will justify occupying other foreign countries and establishing military bases there.  This is part of their globalist agenda.

Don’t think this is a conspiracy yet? Check this out:

 

Oops. Guess they forgot the cameras were rolling.  Now here is where it gets weird.  Did you know that the CDC has a patent on the Ebola virus?  That’s right.  The US government owns it.  As reported on NaturalNews, The U.S. Centers for Disease Control owns a patent on a particular strain of Ebola known as “EboBun.” It’s patent No. is CA2741523A1 and it was awarded in 2010. You can view it here.

Patent applicants are clearly described on the patent as including:

The Government Of The United States Of America As Represented By The Secretary, Department Of Health & Human Services, Center For Disease Control.

The patent summary says, “The invention provides the isolated human Ebola (hEbola) viruses denoted as Bundibugyo (EboBun) deposited with the Centers for Disease Control and Prevention (“CDC”; Atlanta, Georgia, United States of America) on November 26, 2007 and accorded an accession number 200706291.”

Why the patent? Patenting Ebola seems as odd as trying to patent cancer or diabetes. Why would a government organization claim to have “invented” this infectious disease and then claim a monopoly over its exploitation for commercial use?

Does the CDC hope to collect a royalty on Ebola vaccines? Is it looking to “invent” more variants and patent those too?

They think we’re stupid or something. 911 and Sandy Hook weren’t enough I guess. “Let’s patent a virus and test it out in Africa so we can occupy their land, secure oil supplies, and create hysteria back home so they all think they need a vaccination containing a live virus.” says the global elitists.  The Ebola story has all of the ingredients of a classic false flag operation.  If Ebola is real, why the “Ebola is real campaign”?  What’s up with that anyways?

Please spread this information.  Enough with the propaganda fed to us by mainstream news.  We have testimony coming directly from Ghana telling us that the outbreak is being created by Red Cross vaccinations.  This is a massive lie and manipulative effort by the US government for ulterior motives.  Here is a video I recently made containing all of the evidence you could ever hope to see proving that Ebola is a conspiracy:

Sources: Listed within the article

About the author:  My name is Steven Bancarz, and I am the creator of Spirit Science and Metaphysics.  Thanks for reading this article! Please share it with your friends and family.  The world needs to wake up. If you wish to subscribe to my newsletter, you can do so HERE

http://www.spiritscienceandmetaphysics.com/ebo-lie-man-living-in-ghana-confirms-ebola-is-a-hoax/


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.

High security laboratory

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

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.

bird_flu

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.”

F2.medium

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.

H5N1virus

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.”

h5n1

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.

bird-flu-0002

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.”

Influenza A Pandemics

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.

The-Difference-bird-flu-avian-influenza-a-h5n1-30089904-754-552

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.

11951_12034_3

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.

Figure 5_MACKAY

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.”

h5n1_online_630px

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.

Marburg 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.

1a02f12

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.

bw24b

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.

Arenaviridae-Schema

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.

824-112474

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.

Manchupo

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.

NAmerican viruses

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.

KFD-Distribution-In-India

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.

kyasanur-virus-ecology

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.

Kyasanur Forest Disease Host

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.

pathogens-02-00402-g001-1024

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.

kyasanur_forest_disease

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.

flaviviridae

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.

800px-Symptoms_of_AIDS.svg

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.

1024px-Symptoms_of_acute_HIV_infection.svg

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.

940px-HIV-AIDS_world_map_-_DALY_-_WHO2004.svg

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.

AIDS_Clinic,_McLeod_Ganj,_2010

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.

HBV_replication

The virus is transmitted by exposure to infectious blood or body fluidsInfection 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 hepadnavirushepa 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.

HBV_prevalence_2005

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).

Hepatitis-B_virions

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.

425px-HBV_Genome.svg

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.

HBV_serum_markers

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).

HBV

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.

All-about-hepatitis-C

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.

hepatitis-c-the-ticking-time-bomb

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.

Hepatitis_C_Virus_Hcv-3

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_liver_pic

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.

hepatitis-clivers fucked

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.

Hepatitis-CPam

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.

Hepatitis-skeleton-iStock4406779

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.

hepatitis-c-treatment

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.

Natural-Cure-For-Hepatitis-C

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.

Causes of hep C(4)

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.

Cover-image-Hepatitis-C-purple-brochure

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.

yellowfever

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.

https://i0.wp.com/mentalfloss.com/sites/default/files/styles/insert_main_wide_image/public/rabies.jpg

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.

Anthrax

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.

Malaria

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.

cholera

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

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

Mers-CoV666

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.

SuperBug-Virus

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.

MERS-CoV

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.

virusmers

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.

Carrying away the victims of plague

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.

the plague bacterium

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.

human-papillomavirus

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.

human_papilloma_virus-17356

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.

Human_Papillomavirus_Hpv-2

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.

Human-Papillomavirus-294x300

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).

11238_11320_2

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.

Human-Papilloma-Virus-4-150x150

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%.

th

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.

7159-22457-1-PB

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.pathogens-02-00264-g002-1024

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.)

bonobo

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.

giesbers-edwin-madagascar-fruit-bat-flying-fox-berenty-reserve-madagascar

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.

CSIRO_ScienceImage_24_The_Nipah_virus

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.

ncomms1796-f3

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.

sn-virus

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.3273481_pone.0027918.g003

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.
 
featured-image-2
 
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.

 3246969817

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.

photo1

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.

MyMedia16820130802193258

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).83980497

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?

tuberculosis1

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.

Tuberculosis550_ab

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.

tuberculosis_incidence_global_2011

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.

Mycobacterium_tuberculosis

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.

22-08a_Tuberculosis_1

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.

MTMxOTc5MDgwMzMxOTBfMQ

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.

encephalitis-viral-5049_3
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.

viral-encephalitis-15997_0

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.

F1.large

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
west-nile-viruszaq

Other symptoms include:
• Clumsiness, unsteady gait
• Confusion, disorientation
• Drowsiness
• Irritability or poor temper control
• Light sensitivity
• Stiff neck and back (occasionally)
• Vomiting
800px-Tick-Borne_Encephalitis_Virus

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
Encephalitis

• 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

fig54_6

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.

chicken-pox-virus-cell-543

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.

chicken-pox-virus-cell-5414

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."

Chickenpox

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.

chickenpox1

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.

chicken-pox-virus-cell-5410

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.

chicken-pox-virus-cell-5415

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.

herpes-zoster-shingles

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.

hzostophth11

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.

poxvirus-2012-i7

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.

Poxvirus model in section (Pov_Ray)

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.

20409_S_poxvirus-replication-m

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.

Poxvirus Pov-Ray model 2

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.

Poxvirus Pov-Ray model 3

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.

west-nile-virus-ny

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.

West_Nile_virus_transmission_cycle

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.

Culex_sp_larvae

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.

WestNileGraphic_thumb

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.

westnilevirus

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-virus 2

  • 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.
  • 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.)

USA WEST NILE VIRUS

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_life_cycle

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.

Em wnvirus j7908i.jpg

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

Phylogenetic_tree_of_West_Nile_viruses

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.

west_nile_virus

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.

FightTheBite_en-300x292

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.

94263909-west-nile-virus

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.

Print

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.

1280px-Mosquito_Netting

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.

West-Nile-Virus-rash-300x243

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.

West Nile Virus Replication

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.

41

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.

High security laboratory

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

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.

bird_flu

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.”

F2.medium

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.

H5N1virus

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.”

h5n1

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.

bird-flu-0002

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.”

Influenza A Pandemics

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.

The-Difference-bird-flu-avian-influenza-a-h5n1-30089904-754-552

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.

11951_12034_3

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.

Figure 5_MACKAY

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.”

h5n1_online_630px

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.

Marburg 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.

1a02f12

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.

bw24b

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.

Arenaviridae-Schema

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.

824-112474

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.

Manchupo

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.

NAmerican viruses

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.

KFD-Distribution-In-India

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.

kyasanur-virus-ecology

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.

Kyasanur Forest Disease Host

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.

pathogens-02-00402-g001-1024

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.

kyasanur_forest_disease

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.

flaviviridae

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.

800px-Symptoms_of_AIDS.svg

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.

1024px-Symptoms_of_acute_HIV_infection.svg

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.

940px-HIV-AIDS_world_map_-_DALY_-_WHO2004.svg

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.

AIDS_Clinic,_McLeod_Ganj,_2010

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.

HBV_replication

The virus is transmitted by exposure to infectious blood or body fluidsInfection 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 hepadnavirushepa 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.

HBV_prevalence_2005

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).

Hepatitis-B_virions

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.

425px-HBV_Genome.svg

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.

HBV_serum_markers

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).

HBV

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.

All-about-hepatitis-C

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.

hepatitis-c-the-ticking-time-bomb

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.

Hepatitis_C_Virus_Hcv-3

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_liver_pic

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.

hepatitis-clivers fucked

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.

Hepatitis-CPam

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.

Hepatitis-skeleton-iStock4406779

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.

hepatitis-c-treatment

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.

Natural-Cure-For-Hepatitis-C

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.

Causes of hep C(4)

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.

Cover-image-Hepatitis-C-purple-brochure

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.

yellowfever

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.

https://i0.wp.com/mentalfloss.com/sites/default/files/styles/insert_main_wide_image/public/rabies.jpg

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.

Anthrax

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.

Malaria

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.

cholera

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

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

Mers-CoV666

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.

SuperBug-Virus

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.

MERS-CoV

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.

virusmers

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.

Carrying away the victims of plague

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.

the plague bacterium

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.

human-papillomavirus

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.

human_papilloma_virus-17356

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.

Human_Papillomavirus_Hpv-2

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.

Human-Papillomavirus-294x300

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).

11238_11320_2

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.

Human-Papilloma-Virus-4-150x150

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%.

th

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.

7159-22457-1-PB

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.pathogens-02-00264-g002-1024

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.)

bonobo

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.

giesbers-edwin-madagascar-fruit-bat-flying-fox-berenty-reserve-madagascar

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.

CSIRO_ScienceImage_24_The_Nipah_virus

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.

ncomms1796-f3

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.

sn-virus

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.3273481_pone.0027918.g003

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.
 
featured-image-2
 
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.

 3246969817

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.

photo1

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.

MyMedia16820130802193258

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).83980497

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?

tuberculosis1

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.

Tuberculosis550_ab

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.

tuberculosis_incidence_global_2011

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.

Mycobacterium_tuberculosis

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.

22-08a_Tuberculosis_1

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.

MTMxOTc5MDgwMzMxOTBfMQ

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.

encephalitis-viral-5049_3
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.

viral-encephalitis-15997_0

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.

F1.large

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
west-nile-viruszaq

Other symptoms include:
• Clumsiness, unsteady gait
• Confusion, disorientation
• Drowsiness
• Irritability or poor temper control
• Light sensitivity
• Stiff neck and back (occasionally)
• Vomiting
800px-Tick-Borne_Encephalitis_Virus

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
Encephalitis

• 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

fig54_6

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.

chicken-pox-virus-cell-543

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.

chicken-pox-virus-cell-5414

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."

Chickenpox

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.

chickenpox1

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.

chicken-pox-virus-cell-5410

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.

chicken-pox-virus-cell-5415

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.

herpes-zoster-shingles

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.

hzostophth11

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.

poxvirus-2012-i7

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.

Poxvirus model in section (Pov_Ray)

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.

20409_S_poxvirus-replication-m

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.

Poxvirus Pov-Ray model 2

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.

Poxvirus Pov-Ray model 3

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.

west-nile-virus-ny

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.

West_Nile_virus_transmission_cycle

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.

Culex_sp_larvae

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.

WestNileGraphic_thumb

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.

westnilevirus

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-virus 2

  • 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.
  • 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.)

USA WEST NILE VIRUS

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_life_cycle

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.

Em wnvirus j7908i.jpg

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

Phylogenetic_tree_of_West_Nile_viruses

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.

west_nile_virus

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.

FightTheBite_en-300x292

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.

94263909-west-nile-virus

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.

Print

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.

1280px-Mosquito_Netting

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.

West-Nile-Virus-rash-300x243

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.

West Nile Virus Replication

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.

41

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.

High security laboratory

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

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.

bird_flu

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.”

F2.medium

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.

H5N1virus

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.”

h5n1

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.

bird-flu-0002

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.”

Influenza A Pandemics

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.

The-Difference-bird-flu-avian-influenza-a-h5n1-30089904-754-552

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.

11951_12034_3

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.

Figure 5_MACKAY

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.”

h5n1_online_630px

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.

Marburg 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.

1a02f12

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.

bw24b

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.

Arenaviridae-Schema

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.

824-112474

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.

Manchupo

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.

NAmerican viruses

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.

KFD-Distribution-In-India

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.

kyasanur-virus-ecology

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.

Kyasanur Forest Disease Host

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.

pathogens-02-00402-g001-1024

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.

kyasanur_forest_disease

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.

flaviviridae

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.

800px-Symptoms_of_AIDS.svg

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.

1024px-Symptoms_of_acute_HIV_infection.svg

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.

940px-HIV-AIDS_world_map_-_DALY_-_WHO2004.svg

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.

AIDS_Clinic,_McLeod_Ganj,_2010

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.

HBV_replication

The virus is transmitted by exposure to infectious blood or body fluidsInfection 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 hepadnavirushepa 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.

HBV_prevalence_2005

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).

Hepatitis-B_virions

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.

425px-HBV_Genome.svg

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.

HBV_serum_markers

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).

HBV

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.

All-about-hepatitis-C

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.

hepatitis-c-the-ticking-time-bomb

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.

Hepatitis_C_Virus_Hcv-3

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_liver_pic

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.

hepatitis-clivers fucked

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.

Hepatitis-CPam

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.

Hepatitis-skeleton-iStock4406779

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.

hepatitis-c-treatment

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.

Natural-Cure-For-Hepatitis-C

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.

Causes of hep C(4)

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.

Cover-image-Hepatitis-C-purple-brochure

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.

yellowfever

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.

https://i0.wp.com/mentalfloss.com/sites/default/files/styles/insert_main_wide_image/public/rabies.jpg

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.

Anthrax

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.

Malaria

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.

cholera

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

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

Mers-CoV666

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.

SuperBug-Virus

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.

MERS-CoV

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.

virusmers

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.

Carrying away the victims of plague

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.

the plague bacterium

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.

human-papillomavirus

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.

human_papilloma_virus-17356

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.

Human_Papillomavirus_Hpv-2

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.

Human-Papillomavirus-294x300

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).

11238_11320_2

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.

Human-Papilloma-Virus-4-150x150

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%.

th

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.

7159-22457-1-PB

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.pathogens-02-00264-g002-1024

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.)

bonobo

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.

giesbers-edwin-madagascar-fruit-bat-flying-fox-berenty-reserve-madagascar

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.

CSIRO_ScienceImage_24_The_Nipah_virus

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.

ncomms1796-f3

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.

sn-virus

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.3273481_pone.0027918.g003

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.
 
featured-image-2
 
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.

 3246969817

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.

photo1

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.

MyMedia16820130802193258

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).83980497

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?

tuberculosis1

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.

Tuberculosis550_ab

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.

tuberculosis_incidence_global_2011

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.

Mycobacterium_tuberculosis

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.

22-08a_Tuberculosis_1

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.

MTMxOTc5MDgwMzMxOTBfMQ

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.

encephalitis-viral-5049_3
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.

viral-encephalitis-15997_0

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.

F1.large

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
west-nile-viruszaq

Other symptoms include:
• Clumsiness, unsteady gait
• Confusion, disorientation
• Drowsiness
• Irritability or poor temper control
• Light sensitivity
• Stiff neck and back (occasionally)
• Vomiting
800px-Tick-Borne_Encephalitis_Virus

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
Encephalitis

• 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

fig54_6

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.

chicken-pox-virus-cell-543

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.

chicken-pox-virus-cell-5414

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."

Chickenpox

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.

chickenpox1

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.

chicken-pox-virus-cell-5410

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.

chicken-pox-virus-cell-5415

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.

herpes-zoster-shingles

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.

hzostophth11

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.

poxvirus-2012-i7

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.

Poxvirus model in section (Pov_Ray)

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.

20409_S_poxvirus-replication-m

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.

Poxvirus Pov-Ray model 2

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.

Poxvirus Pov-Ray model 3

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.

west-nile-virus-ny

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.

West_Nile_virus_transmission_cycle

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.

Culex_sp_larvae

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.

WestNileGraphic_thumb

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.

westnilevirus

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-virus 2

  • 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.
  • 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.)

USA WEST NILE VIRUS

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_life_cycle

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.

Em wnvirus j7908i.jpg

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

Phylogenetic_tree_of_West_Nile_viruses

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.

west_nile_virus

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.

FightTheBite_en-300x292

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.

94263909-west-nile-virus

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.

Print

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.

1280px-Mosquito_Netting

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.

West-Nile-Virus-rash-300x243

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.

West Nile Virus Replication

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.

41

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.


Ebola Biological Hazard Pandemic in Africa

 

Updated:
Sunday, 14 September, 2014 at 14:29 UTC

Description

Sierra Leone has lost a fourth doctor to Ebola after a failed effort to transfer her abroad for medical treatment, a government official said Sunday, a huge setback to the impoverished country that is battling the virulent disease amid a shortage of health care workers. Dr. Olivet Buck died late Saturday, hours after the World Health Organization said it could not help medically evacuate her to Germany, Chief Medical Officer Dr. Brima Kargbo confirmed to The Associated Press. Sierra Leone had requested funds from WHO to transport Buck to Europe, saying the country could not afford to lose another doctor. WHO had said that it could not meet the request but instead would work to give Buck "the best care possible" in Sierra Leone, including possible access to experimental drugs. Ebola is spread through direct contact with the bodily fluids of sick patients, making doctors and nurses especially vulnerable to contracting the virus that has no vaccine or approved treatment. More than 300 health workers have become infected with Ebola in Guinea, Liberia and Sierra Leone. Nearly half of them have died, according to WHO. The infections have exacerbated shortages of doctors and nurses in West African countries that were already low on skilled health personnel. So far, only foreign health and aid workers have been evacuated abroad from Sierra Leone and Liberia for treatment. Dr. Sheik Humarr Khan, Sierra Leone’s top Ebola doctor, was being considered for evacuation to a European country when he died of the disease in late July.

 

Updated:
Tuesday, 02 September, 2014 at 18:14 UTC

Description

A second American doctor working in Liberia has tested positive for Ebola, missionary group Serving in Mission USA is confirming, as per the AP. It’s not clear how the doctor, who was not named, contracted the virus: He was working in an obstetrics unit in a Monrovia hospital, and not in the isolation unit. He immediately isolated himself and is said to be doing well, reports NBC. SIM USA’s president, Bruce Johnson, said in a statement: "My heart was deeply saddened, but my faith was not shaken, when I learned another of our missionary doctors contracted Ebola. As a global mission, we are surrounding our missionary with prayer, as well as our Liberian SIM/ELWA colleagues, who continue fighting the Ebola epidemic in Liberia."

 

Updated:
Wednesday, 27 August, 2014 at 14:12 UTC

Description

A senior adviser to Sierra Leone’s president says a third doctor has died from Ebola, marking a setback in the country’s fight against the virulent disease. Presidential adviser Ibrahim Ben Kargbo said Wednesday that Dr. Sahr Rogers had been working in a clinic in the eastern town of Kenema when he contracted the virus. News of his death came as a Senegalese epidemiologist working in Sierra Leone was evacuated to Germany for medical treatment. He had been doing surveillance work for the World Health Organization. Ebola is spread by direct contact with the bodily fluids of people sick with the virus. Health workers have been the most vulnerable because of their proximity to patients. The WHO says more than 120 health workers have died in the four affected countries.

 

Updated:
Monday, 18 August, 2014 at 08:22 UTC

Description

Liberian officials fear Ebola could soon spread through the capital’s largest slum after residents raided a quarantine center for suspected patients and took items including bloody sheets and mattresses. The violence in the West Point slum occurred late Saturday and was led by residents angry that patients were brought to the holding center from other parts of Monrovia, Tolbert Nyenswah, a$sistant health minister, said Sunday. Local witnesses told Agence France Presse that there were armed men among the group that attacked the clinic. "They broke down the doors and looted the place. The patients all fled," said Rebecca Wesseh, who witnessed the attack and whose report was confirmed by residents and the head of Health Workers a$sociation of Liberian, George Williams. Up to 30 patients were staying at the center and many of them fled at the time of the raid, said Nyenswah. Once they are located they will be transferred to the Ebola center at Monrovia’s largest hospital, he said. The attack comes just one day after a report of a crowd of several hundred local residents, chanting, ‘No Ebola in West Point,’ drove away a burial team and their police escort that had come to collect the bodies of suspected Ebola victims in the slum in the capital, Reuters reports. West Point residents went on a "looting spree," stealing items from the clinic that were likely infected, said a senior police official, who insisted on anonymity because he was not authorized to brief the press. The residents took medical equipment and mattresses and sheets that had bloodstains, he said. Ebola is spread through bodily fluids including blood, vomit, feces and sweat. "All between the houses you could see people fleeing with items looted from the patients," the official said, adding that he now feared "the whole of West Point will be infected." Some of the looted items were visibly stained with blood, vomit and excrement, said Richard Kieh, who lives in the area.
The incident creates a new challenge for Liberian health officials who were already struggling to contain the outbreak. Liberian police restored order to the West Point neighborhood Sunday. Sitting on land between the Montserrado River and the Atlantic Ocean, West Point is home to at least 50,000 people, according to a 2012 survey. Distrust of government runs high in West Point, with rumors regularly circulating that the government plans to clear the slum out entirely. Though there had been talk of putting West Point under quarantine should Ebola break out there, a$sistant health minister Nyenswah said Sunday no such step has been taken. "West Point is not yet quarantined as being reported," he said. While the armed attack is likely the most brazen attack on health workers trying to contain the deadly outbreak, it is far from the first in the region worst-hit by it. There have been numerous reports of locals attacking those trying to stop the disease by throwing stones at aid workers, blocking aid convoys and forcibly removing patients from clinics. Many locals blame foreigners for bringing the disease, saying it had never been there before they arrived. The mistrust of central government and help from outside runs deep in this part of West Africa. All three countries worst-hit by the outbreak — Liberia, Sierra Leone, and Guinea — are relatively fresh off decades of either brutal civil war or iron-fisted dictatorships. The Ebola outbreak that has k!lled more than 1,100 people in West Africa could last another six months, the Doctors Without Borders charity group said Friday. One aid worker acknowledged that the true de@th toll is still unknown. New figures released by the World Health Organization showed that Liberia has recorded more Ebola de@ths – 413 – than any of the other affected countries. Tarnue Karbbar, who works for the aid group Plan International in northern Liberia, said response teams simply aren’t able to document all the erupting Ebola cases. Many of the sick are still being hidden at home by their relatives, who are too fearful of going to an Ebola treatment center.
Others are being buried before the teams can get to remote areas, he said. In the last several days, about 75 cases have emerged in Voinjama, a single Liberian district. "Our challenge now is to quarantine the area (in Voinjama) to successfully break the transmission," he said. There is no cure or licensed treatment for Ebola and patients often die gruesome de@ths with external bleeding from their mouths, eyes or ears. The k!ller virus is transmitted through bodily fluids like blood, sweat, urine and diarrhea. A handful of people have received an experimental drug whose effectiveness is unknown. Liberia’s a$sistant health minister, Tolbert Nyenswah, said three people in Liberia were receiving the ZMapp on Friday. Previously, only two Americans and a Spaniard had gotten it. The Americans are improving, but it is not known what role ZMapp played. The Spaniard died. The American doctor infected with Ebola while working in Liberia said Friday he is "recovering in every way" and holding onto the hope of a reunion with his family. Dr. Kent Brantly remained hospitalized Friday at Emory University Hospital in Atlanta. His comments came in a statement issued through the Christian aid group Samaritan’s Purse. The World Health Organization has approved the use of such untested drugs but their supply is extremely limited. The U.N. health agency has said the focus on containing the outbreak should be on practicing good hygiene and quickly identifying the sick and isolating them. That task is made harder, however, by the shortage of treatment facilities. Beds in such centers are filling up faster than they can be provided, evidence that the outbreak in West Africa is far more severe than the numbers show, said Gregory Hartl, a spokesman for World Health Organization in Geneva.
There are 40 beds at one treatment center that Doctors Without Borders recently took over in one quarantined county in Liberia. But 137 people have flocked there, packing the hallways until they can be sorted into those who are infected and those are not, said Joanne Liu, the group’s international president. Nyenswah described a similar situation in a treatment center in Liberia’s capital of Monrovia: In one ward meant to accommodate up to 25 people, 80 are now crowded in. Another treatment center with 120 beds is expected to open Saturday outside Monrovia. "It’s absolutely dangerous," said Liu, who recently returned from Guinea, Liberia and Sierra Leone. "With the massive influx of patients that we had over the last few days, we’re not able to keep zones of patients anymore. Everybody is mixed." Liu likened the situation to a state of war because the "frontline" was always moving and unpredictable. She said the outbreak could last six more months. The de@th toll is now 1,145 people in four countries across West Africa, according to figures released Friday by the World Health Organization. At least 2,127 cases have been reported in Liberia, Sierra Leone, Guinea and Nigeria, WHO said. Sierra Leone’s president, Ernest Bai Koroma, told journalists Friday that the country has lost two doctors and 32 nurses to Ebola. "We need specialized clinicians and expertise and that is why we are appealing to the international community for an enhanced response to our f!ght" against Ebola, he said. The Ebola crisis is also disrupting food supplies and transportation. Some 1 million people in isolated areas could need food a$sistance in the coming months, according to the U.N. World Food Program, which is preparing a regional emergency operation. Amid a growing number of airline cancellations, the U.N. will start flights for humanitarian workers on Saturday to ensure that aid operations aren’t interrupted. In the coming weeks, they will also ferry staff to remote areas by helicopter.

 

Updated:
Thursday, 14 August, 2014 at 03:27 UTC

Description

Guinean President Alpha Conde on Wednesday declared a deadly Ebola outbreak that has killed 377 in the west African nation a "health emergency". "The World Health Organisation has declared a global health emergency over Ebola. Considering that Guinea is a signatory to the WHO constitution I declare Ebola a national health emergency in Guinea," Conde said in a statement read on state television. He announced a series of nine measures including strict controls at border points, travel restrictions and a ban on moving bodies "from one town to another until the end of the epidemic." In addition all suspected victims will automatically be hospitalised until laboratory results are obtained, Conde said. He said all people who had been in contact with Ebola victims were "formally banned from leaving their homes until the end of their surveillance period." Anyone found in contravention of the measures would be considered "a threat to public health and will face the might of the law," the statement said, without elaborating. The current outbreak of Ebola — the worst since the disease was discovered in then-Zaire four decades ago — was first detected in Guinea at the start of the year. It has claimed 1,069 lives and infected nearly 2,000 people as it has spread to Liberia, Sierra Leone and Nigeria.

 

Updated:
Tuesday, 12 August, 2014 at 14:38 UTC

Description

Eight Chinese medical workers who treated Ebola patients have been quarantined in Sierra Leone, as health experts grapple with ethical questions over the use of experimental drugs to combat the killer virus. China’s ambassador to Sierra Leone, Zhao Yanbo, said seven doctors and one nurse who treated Ebola patients had been placed under quarantine, but would not be drawn on whether they were displaying symptoms of the disease. In addition, 24 nurses in Sierra Leone, most from the military hospital in the capital, have also been quarantined, according to Yanbo and hospital director Sahr Foday. Gripped by panic, west African nations battling the tropical disease ramped up drastic containment measures that have caused transport chaos, price hikes and food shortages. The World Health Organisation has scrambled to draft guidelines for the use of experimental medicines at a meeting in Geneva as the death toll from the worst Ebola outbreak in history neared 1,000. It is to present its conclusions on Tuesday.

 

Updated:
Friday, 08 August, 2014 at 03:48 UTC

Description

The army blockaded on Thursday rural areas in Sierra Leone that have been hit by the deadly Ebola virus, a senior officer said, after neighbouring Liberia declared a state of emergency to tackle the worst outbreak of the disease on record.

 

Updated:
Friday, 08 August, 2014 at 03:49 UTC

Description

President Ellen Johnson Sirleaf has declared a 90-day State of Emergency throughout Liberia as government steps up its fight to restrain the spread of the lethal Ebola virus disease which has now spread to eight of the country’s 15 counties. "By the virtue of the powers vested in me as President of the Republic of Liberia, I, Ellen Johnson Sirleaf, President of the Republic of Liberia, and in keeping with Article 86(a) (b) of the Constitution of the Republic of Liberia, hereby declare a State of Emergency throughout the Republic of Liberia effective as of August 6, 2014 for a period of 90 days," the Liberian leader, who is also Commander-in-Chief of the Armed Forces of Liberia announced, adding further, "Under this State of Emergency, the Government will institute extraordinary measures, including, if need be, the suspensions of certain rights and privileges." According to an Executive Mansion release, President Sirleaf made this rare Declaration when she addressed the Nation late Wednesday evening, August 6, 2014, from the studios of the state broadcaster, the Liberia Broadcasting System, and the Renaissance Communications Incorporated, both in Paynesville City. As mandated by the Constitution, the Liberian leader is expected to immediately forward this Declaration of the State of Emergency to the National Legislature, accompanied by an explanation of the facts and circumstances leading to the Declaration.
President Sirleaf, who is also chair of the National Task Force on Ebola, addressing the Nation said the deadly Ebola virus now poses serious risks to the health, safety, security and welfare of the nation and beyond the public health risk, the disease is now undermining the economic stability of the country to the tone of millions of dollars in lost revenue, productivity and economic activity. Liberia is among three countries in the Mano River Union experiencing an unprecedented outbreak of the virus, the larger ever since this virus was first discovered. "The heath care system in the county is now under immense strain and the Ebola epidemic is having a chilling effect on the overall health care delivery," the Liberian leader emphasized, explaining further, "Out of fear of being infected with the disease, health care practitioners are afraid to accept new patients, especially in community clinics all across the country. Consequently, many common diseases which are especially prevalent during the rainy season, such as malaria, typhoid and common cold, are going untreated and may lead to unnecessary and preventable deaths." She pointed out that the aggregate number of cases confirmed, probable and suspected in Liberia has now exceeded 500 with about 271 cumulative deaths with 32 deaths among health care workers; noting that the death rate among citizens, especially among health workers is alarming. On measures the Government has taken so far to respond to the crisis, President Sirleaf instructed all non-essential government staff to stay home for 30 days, ordered the closure of schools, and authorized the fumigation of all public buildings, shut down markets in affected areas and have restricted movement in others, improved response time and contact tracking as well as begun coordinating with regional and international partners.
"Despite these and other continuing efforts, the threat continues to grow," she pointed out, adding that ignorance, poverty, as well as entrenched religious and cultural practices continue to exacerbate the spread of the disease especially in the counties. "The actions allowed by statues under the Public Health Law are no longer adequate to deal with the Ebola epidemic in as comprehensive and holistic as the outbreak requires," she noted. "The scope and scale of the epidemic, the virulence and deadliness of the virus now exceed the capacity and statutory responsibility of any one government agency or ministry," President Sirleaf informed the nation, stressing that the Ebola virus disease, the ramifications and consequences thereof, now constitute an unrest affecting the existence, security, and well-being of the Republic amounting to a clear and present danger. "The Government and people of Liberia require extraordinary measures for the very survival of our state and for the protection of the lives of our people."


Ebola Biological Hazard Pandemic in Africa

 

Updated:
Sunday, 14 September, 2014 at 14:29 UTC

Description

Sierra Leone has lost a fourth doctor to Ebola after a failed effort to transfer her abroad for medical treatment, a government official said Sunday, a huge setback to the impoverished country that is battling the virulent disease amid a shortage of health care workers. Dr. Olivet Buck died late Saturday, hours after the World Health Organization said it could not help medically evacuate her to Germany, Chief Medical Officer Dr. Brima Kargbo confirmed to The Associated Press. Sierra Leone had requested funds from WHO to transport Buck to Europe, saying the country could not afford to lose another doctor. WHO had said that it could not meet the request but instead would work to give Buck "the best care possible" in Sierra Leone, including possible access to experimental drugs. Ebola is spread through direct contact with the bodily fluids of sick patients, making doctors and nurses especially vulnerable to contracting the virus that has no vaccine or approved treatment. More than 300 health workers have become infected with Ebola in Guinea, Liberia and Sierra Leone. Nearly half of them have died, according to WHO. The infections have exacerbated shortages of doctors and nurses in West African countries that were already low on skilled health personnel. So far, only foreign health and aid workers have been evacuated abroad from Sierra Leone and Liberia for treatment. Dr. Sheik Humarr Khan, Sierra Leone’s top Ebola doctor, was being considered for evacuation to a European country when he died of the disease in late July.

 

Updated:
Tuesday, 02 September, 2014 at 18:14 UTC

Description

A second American doctor working in Liberia has tested positive for Ebola, missionary group Serving in Mission USA is confirming, as per the AP. It’s not clear how the doctor, who was not named, contracted the virus: He was working in an obstetrics unit in a Monrovia hospital, and not in the isolation unit. He immediately isolated himself and is said to be doing well, reports NBC. SIM USA’s president, Bruce Johnson, said in a statement: "My heart was deeply saddened, but my faith was not shaken, when I learned another of our missionary doctors contracted Ebola. As a global mission, we are surrounding our missionary with prayer, as well as our Liberian SIM/ELWA colleagues, who continue fighting the Ebola epidemic in Liberia."

 

Updated:
Wednesday, 27 August, 2014 at 14:12 UTC

Description

A senior adviser to Sierra Leone’s president says a third doctor has died from Ebola, marking a setback in the country’s fight against the virulent disease. Presidential adviser Ibrahim Ben Kargbo said Wednesday that Dr. Sahr Rogers had been working in a clinic in the eastern town of Kenema when he contracted the virus. News of his death came as a Senegalese epidemiologist working in Sierra Leone was evacuated to Germany for medical treatment. He had been doing surveillance work for the World Health Organization. Ebola is spread by direct contact with the bodily fluids of people sick with the virus. Health workers have been the most vulnerable because of their proximity to patients. The WHO says more than 120 health workers have died in the four affected countries.

 

Updated:
Monday, 18 August, 2014 at 08:22 UTC

Description

Liberian officials fear Ebola could soon spread through the capital’s largest slum after residents raided a quarantine center for suspected patients and took items including bloody sheets and mattresses. The violence in the West Point slum occurred late Saturday and was led by residents angry that patients were brought to the holding center from other parts of Monrovia, Tolbert Nyenswah, a$sistant health minister, said Sunday. Local witnesses told Agence France Presse that there were armed men among the group that attacked the clinic. "They broke down the doors and looted the place. The patients all fled," said Rebecca Wesseh, who witnessed the attack and whose report was confirmed by residents and the head of Health Workers a$sociation of Liberian, George Williams. Up to 30 patients were staying at the center and many of them fled at the time of the raid, said Nyenswah. Once they are located they will be transferred to the Ebola center at Monrovia’s largest hospital, he said. The attack comes just one day after a report of a crowd of several hundred local residents, chanting, ‘No Ebola in West Point,’ drove away a burial team and their police escort that had come to collect the bodies of suspected Ebola victims in the slum in the capital, Reuters reports. West Point residents went on a "looting spree," stealing items from the clinic that were likely infected, said a senior police official, who insisted on anonymity because he was not authorized to brief the press. The residents took medical equipment and mattresses and sheets that had bloodstains, he said. Ebola is spread through bodily fluids including blood, vomit, feces and sweat. "All between the houses you could see people fleeing with items looted from the patients," the official said, adding that he now feared "the whole of West Point will be infected." Some of the looted items were visibly stained with blood, vomit and excrement, said Richard Kieh, who lives in the area.
The incident creates a new challenge for Liberian health officials who were already struggling to contain the outbreak. Liberian police restored order to the West Point neighborhood Sunday. Sitting on land between the Montserrado River and the Atlantic Ocean, West Point is home to at least 50,000 people, according to a 2012 survey. Distrust of government runs high in West Point, with rumors regularly circulating that the government plans to clear the slum out entirely. Though there had been talk of putting West Point under quarantine should Ebola break out there, a$sistant health minister Nyenswah said Sunday no such step has been taken. "West Point is not yet quarantined as being reported," he said. While the armed attack is likely the most brazen attack on health workers trying to contain the deadly outbreak, it is far from the first in the region worst-hit by it. There have been numerous reports of locals attacking those trying to stop the disease by throwing stones at aid workers, blocking aid convoys and forcibly removing patients from clinics. Many locals blame foreigners for bringing the disease, saying it had never been there before they arrived. The mistrust of central government and help from outside runs deep in this part of West Africa. All three countries worst-hit by the outbreak — Liberia, Sierra Leone, and Guinea — are relatively fresh off decades of either brutal civil war or iron-fisted dictatorships. The Ebola outbreak that has k!lled more than 1,100 people in West Africa could last another six months, the Doctors Without Borders charity group said Friday. One aid worker acknowledged that the true de@th toll is still unknown. New figures released by the World Health Organization showed that Liberia has recorded more Ebola de@ths – 413 – than any of the other affected countries. Tarnue Karbbar, who works for the aid group Plan International in northern Liberia, said response teams simply aren’t able to document all the erupting Ebola cases. Many of the sick are still being hidden at home by their relatives, who are too fearful of going to an Ebola treatment center.
Others are being buried before the teams can get to remote areas, he said. In the last several days, about 75 cases have emerged in Voinjama, a single Liberian district. "Our challenge now is to quarantine the area (in Voinjama) to successfully break the transmission," he said. There is no cure or licensed treatment for Ebola and patients often die gruesome de@ths with external bleeding from their mouths, eyes or ears. The k!ller virus is transmitted through bodily fluids like blood, sweat, urine and diarrhea. A handful of people have received an experimental drug whose effectiveness is unknown. Liberia’s a$sistant health minister, Tolbert Nyenswah, said three people in Liberia were receiving the ZMapp on Friday. Previously, only two Americans and a Spaniard had gotten it. The Americans are improving, but it is not known what role ZMapp played. The Spaniard died. The American doctor infected with Ebola while working in Liberia said Friday he is "recovering in every way" and holding onto the hope of a reunion with his family. Dr. Kent Brantly remained hospitalized Friday at Emory University Hospital in Atlanta. His comments came in a statement issued through the Christian aid group Samaritan’s Purse. The World Health Organization has approved the use of such untested drugs but their supply is extremely limited. The U.N. health agency has said the focus on containing the outbreak should be on practicing good hygiene and quickly identifying the sick and isolating them. That task is made harder, however, by the shortage of treatment facilities. Beds in such centers are filling up faster than they can be provided, evidence that the outbreak in West Africa is far more severe than the numbers show, said Gregory Hartl, a spokesman for World Health Organization in Geneva.
There are 40 beds at one treatment center that Doctors Without Borders recently took over in one quarantined county in Liberia. But 137 people have flocked there, packing the hallways until they can be sorted into those who are infected and those are not, said Joanne Liu, the group’s international president. Nyenswah described a similar situation in a treatment center in Liberia’s capital of Monrovia: In one ward meant to accommodate up to 25 people, 80 are now crowded in. Another treatment center with 120 beds is expected to open Saturday outside Monrovia. "It’s absolutely dangerous," said Liu, who recently returned from Guinea, Liberia and Sierra Leone. "With the massive influx of patients that we had over the last few days, we’re not able to keep zones of patients anymore. Everybody is mixed." Liu likened the situation to a state of war because the "frontline" was always moving and unpredictable. She said the outbreak could last six more months. The de@th toll is now 1,145 people in four countries across West Africa, according to figures released Friday by the World Health Organization. At least 2,127 cases have been reported in Liberia, Sierra Leone, Guinea and Nigeria, WHO said. Sierra Leone’s president, Ernest Bai Koroma, told journalists Friday that the country has lost two doctors and 32 nurses to Ebola. "We need specialized clinicians and expertise and that is why we are appealing to the international community for an enhanced response to our f!ght" against Ebola, he said. The Ebola crisis is also disrupting food supplies and transportation. Some 1 million people in isolated areas could need food a$sistance in the coming months, according to the U.N. World Food Program, which is preparing a regional emergency operation. Amid a growing number of airline cancellations, the U.N. will start flights for humanitarian workers on Saturday to ensure that aid operations aren’t interrupted. In the coming weeks, they will also ferry staff to remote areas by helicopter.

 

Updated:
Thursday, 14 August, 2014 at 03:27 UTC

Description

Guinean President Alpha Conde on Wednesday declared a deadly Ebola outbreak that has killed 377 in the west African nation a "health emergency". "The World Health Organisation has declared a global health emergency over Ebola. Considering that Guinea is a signatory to the WHO constitution I declare Ebola a national health emergency in Guinea," Conde said in a statement read on state television. He announced a series of nine measures including strict controls at border points, travel restrictions and a ban on moving bodies "from one town to another until the end of the epidemic." In addition all suspected victims will automatically be hospitalised until laboratory results are obtained, Conde said. He said all people who had been in contact with Ebola victims were "formally banned from leaving their homes until the end of their surveillance period." Anyone found in contravention of the measures would be considered "a threat to public health and will face the might of the law," the statement said, without elaborating. The current outbreak of Ebola — the worst since the disease was discovered in then-Zaire four decades ago — was first detected in Guinea at the start of the year. It has claimed 1,069 lives and infected nearly 2,000 people as it has spread to Liberia, Sierra Leone and Nigeria.

 

Updated:
Tuesday, 12 August, 2014 at 14:38 UTC

Description

Eight Chinese medical workers who treated Ebola patients have been quarantined in Sierra Leone, as health experts grapple with ethical questions over the use of experimental drugs to combat the killer virus. China’s ambassador to Sierra Leone, Zhao Yanbo, said seven doctors and one nurse who treated Ebola patients had been placed under quarantine, but would not be drawn on whether they were displaying symptoms of the disease. In addition, 24 nurses in Sierra Leone, most from the military hospital in the capital, have also been quarantined, according to Yanbo and hospital director Sahr Foday. Gripped by panic, west African nations battling the tropical disease ramped up drastic containment measures that have caused transport chaos, price hikes and food shortages. The World Health Organisation has scrambled to draft guidelines for the use of experimental medicines at a meeting in Geneva as the death toll from the worst Ebola outbreak in history neared 1,000. It is to present its conclusions on Tuesday.

 

Updated:
Friday, 08 August, 2014 at 03:48 UTC

Description

The army blockaded on Thursday rural areas in Sierra Leone that have been hit by the deadly Ebola virus, a senior officer said, after neighbouring Liberia declared a state of emergency to tackle the worst outbreak of the disease on record.

 

Updated:
Friday, 08 August, 2014 at 03:49 UTC

Description

President Ellen Johnson Sirleaf has declared a 90-day State of Emergency throughout Liberia as government steps up its fight to restrain the spread of the lethal Ebola virus disease which has now spread to eight of the country’s 15 counties. "By the virtue of the powers vested in me as President of the Republic of Liberia, I, Ellen Johnson Sirleaf, President of the Republic of Liberia, and in keeping with Article 86(a) (b) of the Constitution of the Republic of Liberia, hereby declare a State of Emergency throughout the Republic of Liberia effective as of August 6, 2014 for a period of 90 days," the Liberian leader, who is also Commander-in-Chief of the Armed Forces of Liberia announced, adding further, "Under this State of Emergency, the Government will institute extraordinary measures, including, if need be, the suspensions of certain rights and privileges." According to an Executive Mansion release, President Sirleaf made this rare Declaration when she addressed the Nation late Wednesday evening, August 6, 2014, from the studios of the state broadcaster, the Liberia Broadcasting System, and the Renaissance Communications Incorporated, both in Paynesville City. As mandated by the Constitution, the Liberian leader is expected to immediately forward this Declaration of the State of Emergency to the National Legislature, accompanied by an explanation of the facts and circumstances leading to the Declaration.
President Sirleaf, who is also chair of the National Task Force on Ebola, addressing the Nation said the deadly Ebola virus now poses serious risks to the health, safety, security and welfare of the nation and beyond the public health risk, the disease is now undermining the economic stability of the country to the tone of millions of dollars in lost revenue, productivity and economic activity. Liberia is among three countries in the Mano River Union experiencing an unprecedented outbreak of the virus, the larger ever since this virus was first discovered. "The heath care system in the county is now under immense strain and the Ebola epidemic is having a chilling effect on the overall health care delivery," the Liberian leader emphasized, explaining further, "Out of fear of being infected with the disease, health care practitioners are afraid to accept new patients, especially in community clinics all across the country. Consequently, many common diseases which are especially prevalent during the rainy season, such as malaria, typhoid and common cold, are going untreated and may lead to unnecessary and preventable deaths." She pointed out that the aggregate number of cases confirmed, probable and suspected in Liberia has now exceeded 500 with about 271 cumulative deaths with 32 deaths among health care workers; noting that the death rate among citizens, especially among health workers is alarming. On measures the Government has taken so far to respond to the crisis, President Sirleaf instructed all non-essential government staff to stay home for 30 days, ordered the closure of schools, and authorized the fumigation of all public buildings, shut down markets in affected areas and have restricted movement in others, improved response time and contact tracking as well as begun coordinating with regional and international partners.
"Despite these and other continuing efforts, the threat continues to grow," she pointed out, adding that ignorance, poverty, as well as entrenched religious and cultural practices continue to exacerbate the spread of the disease especially in the counties. "The actions allowed by statues under the Public Health Law are no longer adequate to deal with the Ebola epidemic in as comprehensive and holistic as the outbreak requires," she noted. "The scope and scale of the epidemic, the virulence and deadliness of the virus now exceed the capacity and statutory responsibility of any one government agency or ministry," President Sirleaf informed the nation, stressing that the Ebola virus disease, the ramifications and consequences thereof, now constitute an unrest affecting the existence, security, and well-being of the Republic amounting to a clear and present danger. "The Government and people of Liberia require extraordinary measures for the very survival of our state and for the protection of the lives of our people."


Henry Kissinger on the Assembly of a

New World Order

http://online.wsj.com/articles/henry-kissinger-on-the-assembly-of-a-new-world-order-1409328075?tesla=y

The concept that has underpinned the modern geopolitical era is in crisis

The concept of order that has underpinned the modern era is in crisis, writes Henry Kissinger. Above, a pro-Russian fighter stands guard at a checkpoint close to Donetsk, Ukraine in July. European Pressphoto Agency

Libya is in civil war, fundamentalist armies are building a self-declared caliphate across Syria and Iraq and Afghanistan’s young democracy is on the verge of paralysis. To these troubles are added a resurgence of tensions with Russia and a relationship with China divided between pledges of cooperation and public recrimination. The concept of order that has underpinned the modern era is in crisis.

The search for world order has long been defined almost exclusively by the concepts of Western societies. In the decades following World War II, the U.S.—strengthened in its economy and national confidence—began to take up the torch of international leadership and added a new dimension. A nation founded explicitly on an idea of free and representative governance, the U.S. identified its own rise with the spread of liberty and democracy and credited these forces with an ability to achieve just and lasting peace. The traditional European approach to order had viewed peoples and states as inherently competitive; to constrain the effects of their clashing ambitions, it relied on a balance of power and a concert of enlightened statesmen. The prevalent American view considered people inherently reasonable and inclined toward peaceful compromise and common sense; the spread of democracy was therefore the overarching goal for international order. Free markets would uplift individuals, enrich societies and substitute economic interdependence for traditional international rivalries.

In the Middle East, religious militias violate borders at will. Getty Images

This effort to establish world order has in many ways come to fruition. A plethora of independent sovereign states govern most of the world’s territory. The spread of democracy and participatory governance has become a shared aspiration if not a universal reality; global communications and financial networks operate in real time.

The years from perhaps 1948 to the turn of the century marked a brief moment in human history when one could speak of an incipient global world order composed of an amalgam of American idealism and traditional European concepts of statehood and balance of power. But vast regions of the world have never shared and only acquiesced in the Western concept of order. These reservations are now becoming explicit, for example, in the Ukraine crisis and the South China Sea. The order established and proclaimed by the West stands at a turning point.

First, the nature of the state itself—the basic formal unit of international life—has been subjected to a multitude of pressures. Europe has set out to transcend the state and craft a foreign policy based primarily on the principles of soft power. But it is doubtful that claims to legitimacy separated from a concept of strategy can sustain a world order. And Europe has not yet given itself attributes of statehood, tempting a vacuum of authority internally and an imbalance of power along its borders. At the same time, parts of the Middle East have dissolved into sectarian and ethnic components in conflict with each other; religious militias and the powers backing them violate borders and sovereignty at will, producing the phenomenon of failed states not controlling their own territory.

The challenge in Asia is the opposite of Europe’s: Balance-of-power principles prevail unrelated to an agreed concept of legitimacy, driving some disagreements to the edge of confrontation.

The clash between the international economy and the political institutions that ostensibly govern it also weakens the sense of common purpose necessary for world order. The economic system has become global, while the political structure of the world remains based on the nation-state. Economic globalization, in its essence, ignores national frontiers. Foreign policy affirms them, even as it seeks to reconcile conflicting national aims or ideals of world order.

This dynamic has produced decades of sustained economic growth punctuated by periodic financial crises of seemingly escalating intensity: in Latin America in the 1980s; in Asia in 1997; in Russia in 1998; in the U.S. in 2001 and again starting in 2007; in Europe after 2010. The winners have few reservations about the system. But the losers—such as those stuck in structural misdesigns, as has been the case with the European Union’s southern tier—seek their remedies by solutions that negate, or at least obstruct, the functioning of the global economic system.

The international order thus faces a paradox: Its prosperity is dependent on the success of globalization, but the process produces a political reaction that often works counter to its aspirations.

A third failing of the current world order, such as it exists, is the absence of an effective mechanism for the great powers to consult and possibly cooperate on the most consequential issues. This may seem an odd criticism in light of the many multilateral forums that exist—more by far than at any other time in history. Yet the nature and frequency of these meetings work against the elaboration of long-range strategy. This process permits little beyond, at best, a discussion of pending tactical issues and, at worst, a new form of summitry as “social media” event. A contemporary structure of international rules and norms, if it is to prove relevant, cannot merely be affirmed by joint declarations; it must be fostered as a matter of common conviction.

The penalty for failing will be not so much a major war between states (though in some regions this remains possible) as an evolution into spheres of influence identified with particular domestic structures and forms of governance. At its edges, each sphere would be tempted to test its strength against other entities deemed illegitimate. A struggle between regions could be even more debilitating than the struggle between nations has been.

The contemporary quest for world order will require a coherent strategy to establish a concept of order within the various regions and to relate these regional orders to one another. These goals are not necessarily self-reconciling: The triumph of a radical movement might bring order to one region while setting the stage for turmoil in and with all others. The domination of a region by one country militarily, even if it brings the appearance of order, could produce a crisis for the rest of the world.

A world order of states affirming individual dignity and participatory governance, and cooperating internationally in accordance with agreed-upon rules, can be our hope and should be our inspiration. But progress toward it will need to be sustained through a series of intermediary stages.

To play a responsible role in the evolution of a 21st-century world order, the U.S. must be prepared to answer a number of questions for itself: What do we seek to prevent, no matter how it happens, and if necessary alone? What do we seek to achieve, even if not supported by any multilateral effort? What do we seek to achieve, or prevent, only if supported by an alliance? What should we not engage in, even if urged on by a multilateral group or an alliance? What is the nature of the values that we seek to advance? And how much does the application of these values depend on circumstance?

For the U.S., this will require thinking on two seemingly contradictory levels. The celebration of universal principles needs to be paired with recognition of the reality of other regions’ histories, cultures and views of their security. Even as the lessons of challenging decades are examined, the affirmation of America’s exceptional nature must be sustained. History offers no respite to countries that set aside their sense of identity in favor of a seemingly less arduous course. But nor does it assure success for the most elevated convictions in the absence of a comprehensive geopolitical strategy.

—Dr. Kissinger served as national security adviser and secretary of state under Presidents Nixon and Ford. Adapted from his book “World Order,” to be published Sept. 9 by the Penguin Press.

http://online.wsj.com/articles/henry-kissinger-on-the-assembly-of-a-new-world-order-1409328075?tesla=y

Why isn’t this Piece of Shit Kissinger not in jail awaiting his execution for crimes against Humanity? Answer: Because he’s a ZIONIST ELITE

MERS “Middle Eastern Respiratory Syndrome”


A NEW VIRUS IS A "THREAT TO THE WORLD"

https://truthtalk13.files.wordpress.com/2014/08/3d828-mers-transmission-modelv2-1.jpg

Published June 24, 2013 | by Sentinel

Virus from the Middle East began to claim lives

https://i2.wp.com/www.cdph.ca.gov/programs/cder/PublishingImages/MERS-CoV%20Map.jpg

By Callum Wood – June 4, 2013 –

A potentially deadly from the Middle East virus made his way to Europe, highlighting the increased potential pandemics facing us. The virus, respiratory syndrome coronavirus in the Middle East (MERS-CoV), formerly known as the new coronavirus was confirmed in 44 people worldwide since its initial detection. The majority of cases came from the Middle East. Scientists are puzzled as to how the virus could reach into humans, and where it has spread. The strain of the larger family of coronaviruses, which covers many illnesses from the common cold to severe acute respiratory syndrome (SARS), which does not help to identify the origin of the virus.

There is still a lot that scientists do not know about MERS-CoV. Margaret Chan, Director General of the World Health Organization, gave a speech at the 66th World Health Assembly in Geneva on May 27, the deadly new strain of coronavirus. She said, "We will understand only too little about this virus when compared to the magnitude of the potential threat. Any new disease that is growing faster than our understanding is never under control. "

When a high-ranking member of one of the most prestigious health organizations in the world bluntly states that experts do not yet understand this deadly virus, people have to sit and listen.

Chan’s speech was full of warnings. She described the virus as "a threat to the entire world." Keep in mind that this statement was made ​​by someone who deals with health issues around the world on a daily basis. She sees this new strain as a major cause for concern, even more than the recent outbreak of H7N9 influenza in Asia.

https://i2.wp.com/media-cache-ak0.pinimg.com/736x/16/65/be/1665becf658ef46c8aa1ec00012a8647.jpg

His warning comes at a time when the MERS-CoV has traveled the Middle East to Europe. A man traveled from Saudi Arabia to France while carrying the virus without knowing it. When he fell ill and was taken to hospital, he then infected at least one other person before succumbing to the disease. The second infected man left the hospital before doctors realize what had happened. The incubation period of the virus is more than 12 days, which makes it difficult to detect. The man was then taken back to the hospital in critical condition.

Of the 44 cases reported worldwide, 23 people died, fixing the mortality rate at about 50 percent. With so many outstanding questions about the disease, Chan said: "We need more information, and we need it quickly, urgently."

https://i0.wp.com/www.tg1news.com/wp-content/uploads/2014/04/946085_10152864656115596_1139851763_n.jpg

But what kind of information do they need? Science can come up with something to try and eliminate this new disease, but how many deaths will it take to get there? There are several strains of influenza and other emerging diseases, but there is rarely another virus similar to penicillin from laboratories. As mentioned above, the H7N9 is resistant to drugs that have been used in the past.

The information that humanity needs is why these plagues fall on us in the first place. While the pharmaceutical industry has been effective in the fight against many diseases, new diseases continue to grow.

https://i0.wp.com/a.abcnews.com/images/Health/mers_coronavirus_world_map_140502_v12x5_12x5_992.jpg

As we explained in our article titled, "The coming pandemic diseases," the four horsemen of the Apocalypse are biblical figures that many can identify, but few can really understand the meaning. One of those riders, the pale horse, means the spread of disease and pestilence in this period of the End Times. MERS-CoV may not be the beginning of a major pandemic, but it is connected to the most tragic time that have yet to befall mankind.

Do you understand the weather where you live? Are you ready for unprecedented devastation by diseases such as the world has ever known? For those who faithfully obey God, He promises;

https://i1.wp.com/www.thehindu.com/multimedia/dynamic/01649/12bgscreening_eps_1649419f.jpg

"You will not fear the terror of night, nor the arrow that flies by day, nor the pestilence that stalks in darkness, nor the plague that destroys at midday. A thousand shall fall at thy side, and ten thousand at your right, you will not be achieved. "(Psalm 91: 5-7)

This is a great hope that we can have, knowing the difficult times ahead.

https://truthtalk13.files.wordpress.com/2014/08/f3974-mers-cov.jpg

"And there will be great earthquakes in various places, and famines and pestilences; and it will seem terrible things and great signs from heaven. "(Luke 21: 11)

http://www.thetrumpet.com/article/10669.18.0.0/society/health/new-virus-a-threat-to-the-entire-world

Happy 1st birthday Middle East respiratory syndrome coronavirus (MERS-CoV)

A coronavirus schematic. The spiky bits give the virus
its name(corona=crown) and represent the
receptor binding, antigenic Spike protein.

…I can remember when you were just a novel little thing.
How you have grown young prince and how clever of you to emerge in a Kingdom of all places (corona=crown, named for it’s spikey appearance). You’ve certainly garnered attention worthy of a King given the relatively few cases of disease you gave been associated with in the first year we’ve known of you.
It was September 20th when Dr Zaki 1st alerted the world to the death of a Saudi man due to what looked to be a new coronavirus (CoV). Today we have over 135 cases 58 deaths (43%).
I’ve previously covered Zaki’s disocvery and the problems posed for the Kingdom of Saudi Arabia (KSA) by the way in which he announced that discovery, apparently without the Ministry of Health’s (MOH) foreknowledge. The way in which the sample was exported from the KSA without their prior consent was also problematic for them.

https://i1.wp.com/cdn.24.co.za/files/Cms/General/d/2396/5aef8eaae1b94d88b71468f6ff7d1714.jpg
Soon after we heard of it, we had virus-detection assays with which we could seek out new cases. Were they used as they might have been in the days of the SARS-CoV? Nope. And there still seems to be only a single laboratory in KSA testing for MERS-CoV (despite reports of 3), with Dr Abdullah Al-Aeeri (a director of hospital infection control) claiming a 72-hour reporting turnaround time.
Is there an antibody detection assay that has been validated using a panel of known positive sera? Nope. There are some innovative antibody-detection methods around but why do they only include a single positive control? Is there no collaboration at all? Why is the KSA not leading the charge to develop these diagnostics and to hunt for an animal host? Why wait on advice from external organizations to screen samples?

https://i2.wp.com/d.ibtimes.co.uk/en/full/1361348/camel.jpg

Why has the necessary testing capacity not been built well before now? Is it to do with that pesky material transfer agreement? I hope not because there is little evidence for that being a real block to anything from a public health standpoint.
At least we have some new MERS-CoV sequences to celebrate the birthday with. Although they and the 9 preceding them represent less than half of the relatively small number of cases described to date. Why can’t the typing region sequences be released? That should really be part of the diagnostic process. Okay, those may not inform us about the evolution of key regions of the virus but they do confirm it is the strain we know. Why not focus on full or subgenomic Spike gene sequences? They might be a better sentinel for keeping tabs on MERS-CoV change over time.

https://i1.wp.com/assets.rappler.com/93A3FB8965334123A482F055E7873C10/img/BFE8489A971B4AA5AF126FF26754F4A0/infographic-mers-symptoms-prevention-20140427.jpg
Most of the detail about MERS-CoV and cases of MERS has come through the peer-reviewed scientific literature. That is pretty normal for respiratory viruses that are not notifiable. But it’s generally a slow medium. Is MERS infection a notifiable disease? It is in some countries (e.g. the US and New Zealand), but is it at the epicenter of the outbreak, the KSA? I’m not sure. It’s not obviously stated as such anywhere I looked on the KSA MOH website.
The World Health Organization politely notes:

WHO encourages all Member States to enhance their surveillance for severe acute respiratory infections (SARI) and to carefully review any unusual patterns of SARI or pneumonia cases. WHO urges Member States to notify or verify to WHO any probable or confirmed case of infection with MERS-CoV.

https://i0.wp.com/www.bulletin.us.com/media/uploads/2/MERS_CoV_map_web.jpg

How’s that been working out? In a nice summary of the lack of communication, Helen Branswell and Declan Butler highlight that, as usual, everyone who was asked agreed that it’s not working out well at all. In fact it’s pretty woeful. And to add to matters, the latest WHO Disease Outbreak News (DON) takes the form of a summary of 18 "new" cases; no extra or confirmatory detail to be had from it. SO the KSA MOH is now the source for detail.

If we were talking about wanting more data on the monthly proportion of rhinovirus infections, the KSA would be justified in saying that the world doesn’t need to know (I’d like to but that’s my thing).

If we were talking about influenza, then there are plenty of international public health sites publishing these notifiable data on the internet; here’s Queensland, Australia’s for example.

https://i0.wp.com/l3.yimg.com/bt/api/res/1.2/eyt6Dq_tPVtxTsy.mRLj7Q--/YXBwaWQ9eW5ld3M7cT04NTt3PTYwMA--/http://l.yimg.com/os/publish-images/news/2014-04-24/98f7a3f0-cba7-11e3-a0bb-25537a06410c_infographic_mers_corona_virus.jpg

But we’re talking about an emerging disease which kills half of the people it infects, is caused by a novel virus for which no host is known, which transmits between people in a way we don’t yet understand, which is shed from ill (or well) people for an undefined period of time (if at all), which remains infectious in the environment for who knows how long, which jumps to other countries, which may only cause severe disease in those who are already ill with another disease, which may be endemically spreading within the community as mild or asymptomatic infections, for which there is no vaccine or proven antiviral therapy available..I’d say it’s a no-brainer that at the very least the WHO deserves regular and detailed updates of what’s going on. Reading between the lines, that does not seem to be happening even behind closed doors.
The mass gathering of pilgrims known as the Hajj is fast approaching. This may trigger a large increase in MERS cases or, in the worst case, a pandemic. I personally believe it won’t go that far. We shouldn’t forget is the 2nd Hajj for MERS. But perhaps the virus is much more widespread than it was in October 2012. But without testing data, we can only guess.
So, it’s your 1st birthday MERS-CoV. But instead of wishing you a happy birthday you opportunistic, spiky little killer, I’m wishing Dr Zaki well and congratulating him on co-parenting the birth of this novel coronavirus. Going by what we’ve seen to date, his actions may have been the only way we would have ever heard of this virus otherwise.
And, as noted previously, but not given much air to in the above rant (thanks to @MicorbeLover for straightening me out)…

https://i0.wp.com/s2.wheninmanila.com/wp-content/uploads/2014/04/Health-Tips-2.jpg

It’s very sad that there are real people in these numbers who have died from MERS. You may have noticed that I try and stick with the cold number-crunching aspect of these outbreaks. It’s not because I’m a heartless b&^$# but because that is not what this blog is about. That and my editorialisation and expositionary writing consume what little time I have spare. But I don’t feel that I have enough information to make any other comments about these or any other lives lost to infectious disease. I personally feel that any unexpected and acute loss of life (if I had to scale loss of life) is the worst kind of loss; it’s a waste of potential, a source of great sorrow for all involved and it’s something we should all strive to prevent, if we can. I know that’s not much to convey, but it’s all I can offer from my kinda comfy chair in Brisbane.

The Saudi MOH says it better in anyway; May Allah have mercy upon the deceased.

virusmers


glyphosate

Urgent action alert: EPA about to raise allowable concentrations of glyphosate on food crops, edible oils and animal feed   

Tuesday, June 18, 2013
by Mike Adams, the Health Ranger
Editor of NaturalNews.com (See all articles…)

(NaturalNews) This is an urgent action alert from Natural News and the Health Ranger. Public comments are due by July 1 to object to new EPA regulations which are already in place, allowing glyphosate contamination of food crops, edible oils and waterways at concentrations which are thousands of times higher than the amount needed to cause cancer.
The new regulation, which can be viewed HERE, sets the following regulations regarding glyphosate residues on crops:
• It allows forage and hay teff to contain up to 100 ppm glyphosate (that’s over one million times the concentration needed to cause cancer according to a recent study). See PubMed source here:
http://www.ncbi.nlm.nih.gov/pubmed/23756170
• Allows oilseed crops (flax oil, canola oil, soybean oil, olive oil, etc.) to contain up to 40 ppm glyphosate (which is over 100,000 times the concentration needed to cause cancer)
• RAISES the allowable glyphosate contamination level of root crops (such as potatoes) from 200 ppb to 6000 ppb.
• Allows glyphosate contamination of fruits at anywhere from 200 ppb to 500 ppb.
Importantly, the EPA says no one even commented on all this when it was initially filed! "There were no comments received in response to the notice of filing." Since then, a total of just 396 people have posted a public comment at the time of this story being published.
You can post your comments with the EPA at this page:
http://www.regulations.gov/#!documentDetail;D=EPA-HQ-OPP-2012-0132-00…

EPA declares glyphosate to be perfectly safe

Borrowing a page right out of Monsanto’s quack science playbook, the EPA says:
A chronic feeding/carcinogenicity study in rats found no systemic effects in any of the parameters examined (body weight, food consumption, clinical signs, mortality, clinical pathology, organ weights, and histopathology).
The EPA even offers this utterly absurd, false statement as justification for its allowable contamination levels of glyphosate: "EPA has concluded that glyphosate does not pose a cancer risk to humans. Therefore, a dietary exposure assessment for the purpose of assessing cancer risk is unnecessary." (SOURCE)
Huh? Do you understand this? The EPA is saying glyphosate is so incredibly safe that it is not even necessary to study its possible carcinogenic effects in humans. No science needed! The EPA simply waves a magic (Monsanto) wand and says, "Shazam! Glyphosate is safe enough to EAT!"
The EPA, of course, is sadly mistaken. It is apparently not aware of two crucial facts to consider in all this:
1) The Seralini study released last year showed an alarming increase in cancer tumors in rats that were fed glyphosate in their drinking water.
2) Monsanto has already been found guilty of committing scientific fraud by altering the results of "scientific" studies in order to trick regulators.
The "scientific" data proving glyphosate to be "safe" has been fabricated! And the EPA is basing its conclusions on fabricated, corporate-quackified junk science that has one purpose: trick regulators into thinking the deadly poison is safe, thereby vastly increasing the usage of the chemical by farmers.

ACTION ITEM: Post your comments to protest the EPA’s glyphosate poisoning of the American people

It is crucial that We the People let the EPA know that raising the allowable levels of glyphosate in foods is unacceptable. This is especially true given the recent studies linking glyphosate to breast cancer, a disease that is ravaging women across America and has reached epidemic levels.
Post your comments in the following ways:
METHOD #1 – POSTING ONLINE
1) Go to this page:
http://www.regulations.gov/#!documentDetail;D=EPA-HQ-OPP-2012-0132-00…
2) Click the "Comment Now!" button on the top right.
3) Enter your information and comment, then click "Submit." Be sure to include reasons WHY you believe the EPA should not allow such high levels of glyphosate in foods, edible oils and animal feed. You can quote pages like GMOevidence.com:
http://gmoevidence.com/location/roundup-evidence/
You can also quote this excellent article from GM Watch which explains why the corporate-controlled media (and industry) so viciously attacked the Seralini rat study, trying to discredit it:
http://gmwatch.org/latest-listing/51-2012/14514
METHOD #2 – MAIL IT IN
1) Write your letter of protest. To ensure proper receipt by EPA, you must identify docket ID number EPA-HQ-OPP-2012-0132 on the first page of your letter.
2) Mail it to: (all mail must be received by July 1st)
OPP Docket
Environmental Protection Agency Docket Center (EPA/DC), (28221T)
1200 Pennsylvania Ave. NW.
Washington, DC 20460–0001
METHOD #3 – EMAIL ANDREW ERTMAN
Please use Method #1 or #2 if you want your comments to actually count. But if you also wish to email or phone the EPA person from the Office of Pesticide Programs, you may contact:
Andrew Ertman, Registration Division, Office of Pesticide Programs, Environmental Protection Agency
Telephone number: (703) 308-9367
Email address: ertman.andrew@epa.gov
Note: If you choose to email Andrew Ertman, please be polite in your email. Do NOT send stupid things like death threats or emails full of profanity. Make your case clearly and politely, and ask him to review the full breadth of the scientific evidence now available instead of just the selected subset Monsanto wants EPA scientists to be aware of.

Over 200 million pounds of glyphosate poison is a chemical attack on America

The following map, compiled by the USDA, shows the use of glyphosate across America:

This is also a map of the mass poisoning of America with a chemical that has been scientifically linked to an increased risk of cancer.
Compare it to this map showing the rates of cancer by state:

By the way, Monsanto has already been caught committing scientific fraud in attempting to fake safety studies on glyphosate. The company also engaged in wildly false advertising, claiming RoundUp was "safer than table salt" (implying that it’s safe to eat in high doses).
Now the EPA is about to allow glyphosate in animal feed at concentrations that are one million times the concentration needed to cause cancer.
At the same time, the EPA continues to allow glyphosate at 700 ppb in public drinking water, too.
We are all being mass poisoned by this deadly chemical, and the EPA is actively conspiring with the chemical industry to downplay the real dangers of glyphosate, pretending it’s safe enough to eat in quantities that are orders of magnitude larger than should be allowed.
Allowing 100 ppm of glyphosate in animal feed is equivalent to allowing 1000 ppm of lead in children’s candy. It’s a deadly poison that inundates our food supply at such high concentrations that it’s guaranteed to cause deadly diseases in huge numbers of people.

EPA document is a blueprint for the mass euthanasia of Americans

This EPA regulation document is a blueprint for billions of dollars in profits for the cancer industry. It’s also a death sentence for America’s soils, farmers and food consumers. And it is insane policies like this that will ultimately lead to the downfall and collapse of modern human civilization… a civilization so stupid that it poisons its own food, water, soils and even its own children… all to make a quarterly profit on the selling of a deadly poison.
Humanity is being mass-euthanized by GMOs and glyphosate, and the EPA is standing by and openly allowing it to happen. This is an agency that did tremendous good back in the 1970’s but has since become nothing more than a corporate sellout and a purveyor of poison.
The EPA wants you to eat glyphosate. There’s no harm, they say. Lick it up!

What concentration of glyphosate should be allowed in foods? No more than 10 ppt

There is no safe level of exposure to glyphosate. The chemical has now been shown to promote cancer cell proliferation at ppt concentrations. This demands that glyphosate be eliminated from being sold in the USA — BANNED for life.
Remember: Glyphosate is the new DDT. But it’s much worse than DDT because its toxic effects kick in at far lower concentrations. If a "safe" level of glyphosate exposure were based on legitimate scientific studies that weren’t faked by Monsanto, it would have to be set no higher than 10 ppt.
In other words, it would need to be virtually undetectable even by the most precise laboratory equipment available today.
Glyphosate has no place in a civilized nation. I call it "Satan’s Molecule" because it is a destroyer of life and a destroyer of worlds.
No wonder it was invented by a scientist working for — guess who? — MonSatan.

Take action today. Comments are due by July 1, and if the EPA doesn’t hear from the People, it’s going to do whatever Monsanto tells it to do. Heck, it will probably do that anyway, but at least if you post a comment, when all of us die from cancer you will know that you did not willfully participate in the mass murder of Americans.

************

California allows up to 1000 times more glyphosate in drinking water than needed

…to cause breast cancer in women

Mike Adams
Natural News
June 17, 2013

Late last week, a story broke that revealed glyphosate — the chemical name of Roundup herbicide — multiplies the proliferation of breast cancer cells by 500% to 1300%… even at exposures of just a few parts per trillion (ppt).

The study, published in Food and Chemical Toxicology, is entitled, “Glyphosate induces human breast cancer cells growth via estrogen receptors.” You can read the abstract here.

There’s a whole lot more to this story, however, but to follow it, you need to understand these terms:

ppm = parts per million = 10 (-6) = number of parts out of a million

ppb = parts per billion = 10 (-9), which is 1,000 times smaller than ppm

ppt = parts per trillion = 10 (-12), which is 1,000 times smaller than ppb and 1,000,000 times smaller than ppm

The study found that breast cancer cell proliferation is accelerated by glyphosate in extremely low concentrations: ppt to ppb. The greatest effect was observed in the ppb range, including single-digit ppb such as 1 ppb.

This news, all by itself, sent shockwaves across the ‘net all weekend. Women were asking things like: “You mean to tell me that glyphosate residues on crops in just ppt or ppb concentrations can give me breast cancer?” It doesn’t exactly translate like that. It depends on how much you eat vs. your body mass (nanograms of glyphosate per kilogram of body weight). But with ridiculously small amounts of this chemical now being correlated to cancer cell proliferation, you don’t have to eat much at all in order to put yourself at risk.

But it’s not just eating glyphosate that’s the problem. You’re also DRINKING it.

California allows 1,000 ppb of glyphosate in drinking water

In December of 1997, California released its Glyphosate in Drinking Water California Public Health Goal (PHG) document. You can view the document yourself at:
http://oehha.ca.gov/water/phg/pdf/glypho_c.pdf

The document openly admits:

Glyphosate is a non-selective systemic herbicide used in agriculture, rights-of-way and aquatic systems. Exposure to glyphosate may occur from its normal use due to drift, residues in food crops and from runoff into potential drinking water sources.

It then goes on to state something borrowed straight from Monsanto’s quack science team: “Glyphosate is not mutagenic or teratogenic and there is no evidence for reproductive toxicity in multigeneration studies in rats.”

Based on this blatant lie, California set an upper limit of “1.0 mg/L (1,000 ppb) for glyphosate in drinking water.”

Yes, that’s 1,000 times higher than the amount now shown to cause a 500% to 1300% increase in cancer cell proliferation.

What’s even more shocking is that California’s allowable exposure level was nearly 50% HIGHER than the federal (EPA) level — 700 ppb.

Yes, California — the state where more people are concerned about GMOs than seemingly anywhere else — actually used Monsanto-sounding language in its “official” report that set a higher water contamination level than the federal government!

Glyphosate carcinotoxicity was documented years earlier

Even though California released this document in 1997, the state was already willfully ignoring a growing body of scientific evidence documenting glyphosate toxicity. For example, a study published two years earlier — in 1995 — in the Journal of Pesticide Reform (Volume 15, Number 3, Fall 1995) written by Caroline Cox concluded:

Glyphosate-containing products are acutely toxic to animals, including humans. …In animal studies, feeding of glyphosate for three months caused reduced weight gain, diarrhea, and salivary gland lesions. Lifetime feeding of glyphosate caused excess growth and death of liver cells, cataracts and lens degeneration, and increases in the frequency of thyroid, pancreas, and liver tumors.

Glyphosate-containing products have caused genetic damage in human blood cells… reduced sperm counts in male rats… an increase in fetal loss…

In other words, California knew — or should have known — that glyphosate was harmful to humans. But the California government willfully ignored this evidence and seemingly went out of its way to incorporate deceptive Monsanto spin into its “Public Health Goal” documents, thereby allowing 1,000 times higher levels of glyphosate in drinking water than we now know to cause cancer cell proliferation.

Ten years later, California lowers its level by just 10%

Fast forward to 2007. After a public comment period which was no doubt dominated by disinfo-spewing Monsanto trolls, the state of California issued an updated Public Health Goal (PHG) document.

You can view that document here:
http://oehha.ca.gov/water/phg/pdf/080406dglyphosate.pdf

It concludes that the allowable glyphosate exposure for all Californians should be lowered to 900 ppb — still nine hundred times higher than the amount needed to accelerate cancer cell growth as we see in the study released last week.

This 2007 document from the California government also borrows language that sounds like it’s right out of Monsanto’s P.R. department: “Based on the genotoxicity and carcinogenicity study results, glyphosate is not likely to pose a cancer hazard to humans,” it says.

Now the evidence is becoming clear: Monsanto’s chemicals are killing women

Now it’s 2013. We’ve seen the horrific results of the GMO rat study revealing the growth of massive tumors in rats exposed to GMOs and Roundup (glyphosate). We’ve also now seen the “parts per trillion” studyshowing cancer cell proliferation being caused by ultra-low concentrations of glyphosate.

We also know the biotech industry has gone to ridiculous lengths to spread disinfo on all this — to try to discredit scientists who speak out against GMOs and glyphosate, to get scientists blackballed from the industry, and to buy off politicians and members of the press to make sure there is no coverage granted to any scientific studies reporting the dangers of genetically modified crops (and their related chemical herbicides).

Glyphosate is the new DDT

Based on what we’re seeing now, I believe glyphosate is the most toxic chemical that has ever been widely deployed across our food supply. Glyphosate is the new DDT, and it’s contaminating our waterways, soils, food and bodies.

Furthermore, the California government has clearly been complicit in allowing extremely high levels of glyphosate to contaminate the public drink water, thereby causing tens of millions of Californians to be poisoned with concentrations of glyphosate that promote cancer cell growth.

And what will the California government tell you now that the truth has come out? Now that they’ve allowed their own population to be exposed to a thousand times the concentration needed to accelerate the growth of cancer tumors?

“Run for the cure!” And don’t label GMOs, either, because you don’t have a right to know whether you’re eating deadly poison in your food.

Join the Monsanto Video Revolt, July 24, 2013

Take part in the global video revolt against Monsanto. Learn more at:
www.MonsantoVideoRevolt.com

 

Glyphosate – GlyphoSatan

Glyphosate, Part 1: Toxicology.

Caroline Cox. Journal of Pesticide Reform, Volume 15, Number 3, Fall 1995. Northwest Coalition for Alternatives to Pesticides, Eugene, OR.

Glyphosate, Part 1: Toxicology

by Caroline Cox

Introduction

Glyphosate is a broad-spectrum herbicide widely used to kill unwanted plants both in agriculture and in nonagricultural landscapes. Estimated use in the U.S. is between 19 and 26 million pounds per year.

Most glyphosate-containing products are either made or used with a surfactant, chemicals that help glyphosate to penetrate plant cells.

Glyphosate-containing products are acutely toxic to animals, including humans. Symptoms include eye and skin irritation, cardiac depression, gastrointestinal pain, vomiting, and accumulation of excess fluid in the lungs. The surfactant used in a common glyphosate product (Roundup) is more acutely toxic than glyphosate itself; the combination of the two is yet more toxic.

In animal studies, feeding of glyphosate for three months caused reduced weight gain, diarrhea, and salivary gland lesions. Lifetime feeding of glyphosate caused excess growth and death of liver cells, cataracts and lens degeneration, and increases in the frequency of thyroid, pancreas, and liver tumors.

Glyphosate-containing products have caused genetic damage in human blood cells, fruit flies, and onion cells.

Glyphosate causes reduced sperm counts in male rats, a lengthened estrous cycle in female rats, and an increase in fetal loss together with a decrease in birth weights in their offspring.

It is striking that laboratory studies have identified adverse effects of glyphosate or glyphosate-containing products in all standard categories of toxicological testing.

Two serious cases of fraud have occurred in laboratories conducting toxicology and residue testing for glyphosate and glyphosate-containing products.

————————————————

Advertised as herbicides that can "eradicate weeds and unwanted grasses effectively with a high level of environmental safety,"1 glyphosate-based herbicides can seem like a silver bullet to those dealing with unwanted vegetation. However, an independent, accurate evaluation of their health and environmental hazards can draw conclusions very different than those presented by these advertisements. The following summary of glyphosate’s hazards is intended to serve that purpose. It will appear in two parts: Part 1 discusses the toxicology of glyphosate, its metabolites, and the other ingredients of glyphosate products and Part 2 will discuss human exposure to glyphosate and its ecological effects.

Glyphosate, N-(phosphonomethyl) glycine (Figure 1), is a post-emergent, systemic, and non-selective herbicide used to kill broad-leaved, grass, and sedge species.2 It has been registered as a broad spectrum herbicide in the U.S. since 1974 and is used to control weeds in a wide variety of agricultural, lawn and garden, aquatic, and forestry situations.3

Most glyphosate herbicides contain the isopropylamine salt of glyphosate. A related chemical, the sodium salt of glyphosate, acts as a growth regulator in sugar cane and peanuts and is marketed for that purpose. The monoammonium salt of glyphosate is also marketed as an herbicide and growth regulator.4

Glyphosate products are manufactured by Monsanto Company worldwide. The herbicide is marketed under a variety of trade names: Roundup (including Roundup D-Pak, Roundup Lawn and Garden Concentrate, and Roundup Ready-to-Use) and Rodeo are the most common U.S. trade names.2 The sodium salt is sold as Quotamaster. The monoammonium salt is sold as Deploy Dry.2 Other brand names used for the isopropylamine salt are Accord,5 Vision, Ranger, and Sting.2

As an herbicidal compound, glyphosate is unusual in that essentially no structurally related compounds show any herbicidal activity.6

Use

Glyphosate is the eighth most commonly used herbicide in U.S. agriculture and the second most commonly used herbicide in nonagricultural situations. Estimated annual use according to the U.S. Environmental Protection Agency (EPA) is between 15 and 20 million pounds in agriculture and between 4 and 6 million pounds elsewhere.7 The largest agricultural uses are in the production of soybeans, hay and pasture, corn, and oranges.4

About 25 million applications per year are made in U.S. households; most of these are made on lawns or outdoor areas where a total vegetation kill is wanted.8

In California, where pesticide use reporting is more comprehensive than in other states, about 3.4 million pounds were used in 1992; about 25 percent of this was used along rights-of-way, while 15 percent was used on almonds and 10 percent was used on grapes.9

Mode of Action

The mode of action of glyphosate is "not known at this time,"4 according to EPA. However, "herbicidal action probably arises from the inhibition of the biosynthesis of aromatic amino acids."10 These amino acids (phenylalanine, tyrosine, and tryptophan) are used in the synthesis of proteins and are the essential for growth and survival of most plants. One particular enzyme important in aromatic amino acid synthesis, called 5-enolpyruvylshikimate-3- phosphate synthase, is inhibited by glyphosate.10 Glyphosate also "may inhibit or repress"4 two other enzymes, chlorismate mutase and prephrenate hydratase, involved in other steps of the synthesis of the same amino acids. These enzymes are all part of what is called the shikimic acid pathway, present in higher plants and microorganisms but not in animals.11

Two of the three aromatic amino acids (tryptophan and phenylalanine) are essential amino acids in the human diet because humans, like all higher animals, lack the shikimic acid pathway, cannot synthesize these amino acids, and rely on their foods to provide these compounds. Tyrosine is synthesized in animals through another pathway.12

Glyphosate can affect enzymes not connected with the shikimic acid pathway. In sugar cane, it reduces the activity of one of the enzymes involved in sugar metabolism, acid invertase. This reduction appears to be mediated by auxins, plant hormones.13

Glyphosate also affects enzyme systems found in animals and humans. In rats, injection into the abdomen decreases the activity of two detoxification enzymes, cytochrome P-450 and a monooxygenase, and decreases the intestinal activity of the enzyme aryl hydrocarbon hydroxylase (another detoxification enzyme).14

"Inert" Ingredients in Glyphosate-containing Products

Virtually every pesticide product contains ingredients other than what is called the "active" ingredient(s), those designed to provide killing action. Their purpose is to make the product easier to use or more efficient. These ingredients are called "inert," although they are often not biologically, chemically, or toxicologically inert. In general, they are not identified on the label of the pesticide product.

In the case of glyphosate products, many "inerts" have been identified. Roundup contains a polyethoxylated tallowamine surfactant (usually abbreviated POEA), related organic acids of glyphosate, isopropylamine, and water. Both Rodeo and Accord contain glyphosate and water.15 (However, label instructions usually require adding a surfactant during use.15) See "Toxicology of ‘Inert’ Ingredients of Glyphosate- containing Products," p. 17, for basic information about these "inert" ingredients.

Many of the toxicology studies that will be summarized in this factsheet have been conducted using glyphosate, the active ingredient, alone. Some have been conducted with commercial products containing glyphosate and "inert" ingredients. When toxicology testing is not done with the product as it is actually used, it is impossible to accurately assess its hazards.

We will discuss both types of studies, and will identify insofar as is possible exactly what material was used to conduct each study.

Acute Toxicity to Laboratory Animals

Glyphosate’s acute oral median lethal dose (the dose that causes death in 50 percent of a population of test animals; LD50) in rats is greater than 4,320 milligrams per kilogram (mg/kg) of body weight. This places the herbicide in Toxicity Category III (Caution).4 Its acute dermal toxicity (dermal LD50) in rabbits is greater than 2,000 mg/kg of body weight, also Toxicity Category III.4

If animals are given glyphosate in other ways, it is much more acutely toxic. When given intraperitoneally (the dose applied by injection into the abdomen), glyphosate is between 10 and 20 times more toxic to rats (with an LD50 between 192- 467 mg/kg)2,16 than it is when given orally. Intraperitoneal injection also caused fever, cessation of breathing, and convulsions.17 While this kind of exposure is not one that would be encountered under conditions of normal use, these studies indicate the kinds of effects glyphosate can potentially cause in mammals.

Commercial glyphosate-containing products are more acutely toxic than glyphosate alone. Two recent (1990 and 1991) studies compared the amount of Roundup required to cause death in rats with the amount of either glyphosate alone or POEA alone that would cause death. The studies found that in combination, the amount of glyphosate and POEA required to kill was about 1/3 of a lethal dose of either compound separately. The Roundup formulation tested was also more toxic than POEA alone.18,19

As with glyphosate alone, glyphosate-containing products are more toxic when administered other ways than orally. Inhalation of Roundup by rats caused "signs of toxicity in all test groups,"20 even at the lowest concentration tested. These signs included a dark nasal discharge, gasping, congested eyes, reduced activity, hair standing erect,21 and body weight loss following exposure.20 Lungs were red or blood-congested.21 The dose required to cause lung damage and mortality following pulmonary administration of Roundup Lawn and Garden Concentrate or Roundup-Ready-to-Use (the glyphosate product is directly forced into the trachea, the tube carrying air into the lungs) was only 1/10 the dose causing damage through oral administration.18

Effects on the Circulatory System: When dogs were given intravenous injections of glyphosate, POEA, or Roundup so that blood concentrations were approximately those found in humans who ingested glyphosate, a variety of circulatory effects were found. Glyphosate increased the ability of the heart muscle to contract. POEA reduced the output of the heart and the pressure in the arteries. Together (Roundup), the result was cardiac depression.22

Eye Irritation: Glyphosate is classified as a mild eye irritant by EPA, with effects lasting up to seven days4 although more serious effects were found by the World Health Organization. In two of the four studies they reviewed, glyphosate was "strongly irritating"2 to rabbits’ eyes and a third test found it "irritating."2 In tests of glyphosate- containing products, all eight products tested were irritating to rabbit eyes, and four of the products were "strongly" or "extremely" irritating.2

Skin Irritation: Glyphosate is classified as a slightly irritating to skin. Roundup is a "moderate skin irritant" and causes redness and swelling on both intact and abraded rabbit skin. Recovery can take more than two weeks.20

Acute Toxicity to Humans

The acute toxicity of glyphosate products to humans was first widely publicized by physicians in Japan who studied 56 cases of Roundup poisoning. Most of the cases were suicides or attempted suicides; nine cases were fatal. Symptoms of acute poisoning in humans included gastrointestinal pain, vomiting, excess fluid in the lungs, pneumonia, clouding of consciousness, and destruction of red blood cells.23 They calculated that the mean amount ingested in the fatal cases was slightly more than 200 milliliters (about 3/4 of a cup). They believed that POEA was the cause of Roundup’s toxicity.23 More recent reviews of glyphosate poisoning incidents have found similar symptoms, as well as lung congestion or dysfunction,24-26, erosion of the gastrointestinal tract,24,26 abnormal electrocardiograms,26 massive gastrointestinal fluid loss,27 low blood pressure,23,26 and kidney damage or failure.24,25,27

Smaller amounts of Roundup also cause adverse effects. In general these include the skin or eye irritation documented in animal studies, as well as some of the symptoms seen in humans following ingestion. For example, rubbing of Roundup in an eye caused swelling of the eye and lid, rapid heartbeat, palpitations, and elevated blood pressure. Wiping the face with a hand that had contacted leaky Roundup spray equipment caused a swollen face and tingling of the skin. Accidental drenching with Roundup (horticultural strength) caused recurrent eczema of the hands and feet lasting two months.25

Different symptoms have been observed when a different type of exposure has occurred. In Great Britain, a study compared the effects of breathing dust from a flax milling operation that used flax treated with Roundup with the effects of dust from untreated flax. Treated flax dust caused a decrease in lung function and an increase in throat irritation, coughing, and breathlessness.28

Subchronic Toxicity

Experiments in which glyphosate was fed to laboratory animals for 13 weeks showed a variety of effects. In experiments conducted by the National Toxicology Program (NTP), microscopic salivary gland lesions were found in all doses tested in rats (200 – 3400 mg/kg per day) and in all but the lowest dose tested in mice (1,000-12,000 mg/kg per day). Both the parotid and submandibular salivary glands were affected in rats; in mice the lesions were confined to the parotid gland. Based on further experiments, NTP concluded the lesions were mediated by the adrenal hormone adrenalin.29

The NTP study also found evidence of effects on the liver: increases in bile acids as well as two liver enzymes were found in both males and females. Other effects found in this study were reduced weight gain in male and female rats and mice; diarrhea in male and female rats; and changes in the relative weights of kidney, liver and thymus in male rats and mice.29

Other subchronic laboratory tests found decreased weight gains (using doses of 2500 mg/kg per day)30 along with an increase in the weights of brain, hearts, kidney, and livers in mice.2 In rats, blood levels of potassium and phosphorus increased at all doses tested (60-1600 mg/kg/day) in both sexes. There was also an increase in pancreatic lesions in males.4

As in acute toxicity tests, glyphosate-containing products are more toxic than glyphosate alone in subchronic tests. In a 7 day study with calves, 790 mg/kg of Roundup caused labored breathing, pneumonia, and death of 1/3 of the animals tested. At lower doses decreased food intake and diarrhea were observed.2

Chronic Toxicity

Glyphosate is also toxic in long-term studies. The following effects were found in lifetime glyphosate feeding studies using mice: decreased body weight, excessive growth of particular liver cells, death of the same liver cells, and chronic inflammation of the kidney. Effects were significant only in males and at the highest dose tested (about 4800 mg/kg of body weight per day). In females, excessive growth of some kidney cells occurred.31 At a lower dose (814 mg/kg of body weight per day) excessive cell division in the urinary bladder occurred.2

Lifetime feeding studies with rats found the following effects: decreased body weight in females; an increased incidence of cataracts and lens degeneration in males; and increased liver weight in males. These effects were significant at the highest dose tested (900-1200 mg/kg of body weight per day).4 At a lower dose (400 mg/kg of body weight per day) inflammation of the stomach’s mucous membrane occurred in both sexes.2

Carcinogenicity

The potential of glyphosate to cause cancer has been a controversial subject since the first lifetime feeding studies were analyzed in the early 1980s. The first study (1979-1981) found an increase in testicular interstitial tumors in male rats at the highest dose tested (30 mg/kg of body weight per day).32 as well as an increase in the frequency of a thyroid cancer in females.33 The second study (completed in 1983) found dose-related increases in the frequency of a rare kidney tumor in male mice.34 The most recent study (1988-1990) found an increase in the number of pancreas and liver tumors in male rats together with an increase of the same thyroid cancer found in the 1983 study in females.35

All of these increases in tumor incidence are "not considered compound-related"35 according to EPA. In each case, different reasons are given for this conclusion. For the testicular tumors, EPA accepted the interpretation of an industry pathologist who said that the incidence in treated groups (12 percent) was similar to those observed in other control (not glyphosate-fed) rat feeding studies (4.5 percent).36 For the thyroid cancer, EPA stated that it was not possible to consistently distinguish between cancers and tumors of this type, so that the incidences of the two should be considered together. The combined data are not statistically significant.33 For the kidney tumors, the registrants reexamined slides of kidney tissue, finding an additional tumor in untreated mice so that statistical significance was lost. This was despite a memo from EPA’s pathologist stating that the lesion in question was not really a tumor.34 For the pancreatic tumors, EPA stated that there was no dose-related trend and no progression to malignancy. For the liver tumors and the thyroid tumors, EPA stated that pairwise comparisons between treated and untreated animals were not statistically significant and there was no progression to malignancy.35

EPA concluded that glyphosate should be classified as Group E, "evidence of non-carcinogenicity for humans."35 They added that this classification "is based on the available evidence at the time of evaluation and should not be interpreted as a definitive conclusion that the agent will not be a carcinogen under any circumstances." 35 From a public health perspective, the results of the laboratory tests leave many questions unanswered. An EPA statistician wrote in a memo concerning one of the carcinogenicity studies, "Viewpoint is a key issue. Our viewpoint is one of protecting the public health when we see suspicious data."36 Unfortunately, EPA has not taken that conservative viewpoint in its assessment of glyphosate’s cancer-causing potential.

There are no studies available to NCAP evaluating the carcinogenicity of Roundup or other glyphosate-containing products. Without such tests, the carcinogenicity of glyphosate-containing products is unknown.

Mutagenicity

Laboratory studies of a variety of organisms have shown that glyphosate-containing products cause genetic damage:

* In fruit flies, Roundup and Pondmaster (an aquatic herbicide consisting of glyphosate and a trade secret surfactant)37 both increased the frequency of sex-linked, recessive lethal mutations. (These are mutations that are usually visible only in males because two damaged genes are required in order to be expressed in females.) In this study, the frequency of lethal mutations was between 3 and 6 times higher in fruit flies that had been exposed to glyphosate products during their larval development than in unexposed flies.38

* A laboratory study of human lymphocytes (one type of white blood cell) showed an increase in the frequency of sister chromatid exchanges following exposure to high doses of Roundup.39 (Sister chromatid exchanges are exchanges of genetic material during cell division between members of a chromosome pair. They result from point mutations.)

* In Salmonella bacteria, Roundup was weakly mutagenic at high concentrations. In onion root cells, Roundup caused an increase in chromosome aberrations.40

Glyphosate alone has rarely caused genetic damage in laboratory tests. None of the mutagenicity studies required for registration of glyphosate have shown it to be mutagenic. Tests included studies of mutations in hamster ovary cells, bacteria, and mouse bone marrow cells.4 Glyphosate was also not mutagenic in other studies of rats, mice,2 and onion cells40 but caused chromosome stickiness and fragmentation in water hyacinth root cells.41

Reproductive Effects

Laboratory studies have demonstrated a number of effects of glyphosate on reproduction, including effects on mothers, fathers, and offspring.

In rat feeding studiess, glyphosate reduced sperm counts (at the two highest doses tested) and lengthened the estrous cycle, how often a female comes into heat (at the highest dose tested).29 Other effects on mother rats in laboratory tests include soft stools, diarrhea, breathing rattles, red nasal discharge, reduced activity, growth retardation, decreased body weights, and increased mortality.2 Effects on offspring included an increase in fetal loss, a decrease in the number of embryos successfully implanted into the uterus, a decrease in the number of viable fetuses, a slight decrease in litter size, a decrease in fetal and pup weights, and an increase in problems with breast bone formation.2 Effects were observed at the highest doses tested (1500 and 3500 mg/kg of body weight per day).2

In a study of rabbits using doses that were lower than those used in the rat studies above, glyphosate caused diarrhea, nasal discharge, and death in mothers.2 The only effect on offspring was a decrease in fetal weight in all treated groups.42

A study in which glyphosate was fed to rats for three generations after which the offspring were examined for birth defects found kidney damage at a relatively low dose (30 mg/kg of body weight). However, a second study (only two generations long) did not find similar effects, and EPA called the damage in the first study "spurious."4 From a public health perspective, however, a new three generation study is crucial.

Toxicology of Glyphosate’s Major Metabolite

In general, studies of the breakdown of glyphosate find only one metabolite, aminomethylphosphonic acid (AMPA).2 (See Figure 5.) Although AMPA has low acute toxicity (its LD50 is 8,300 mg/kg of body weight in rats)20 and is only slightly irritating to eyes,43 it causes a variety of toxicological problems. In subchronic tests on rats, AMPA caused decreased weight gain in males; an increase in the acidity of urine in both males and females; an increase in the activity of an enzyme, lactic dehydrogenase, in both sexes; a decrease in liver weights in males at all doses tested; and excessive cell division in the lining of the urinary bladder and in part of the kidney in both sexes.20 AMPA is much more persistent than glyphosate; studies in eight states found that the half-life in soil (the time required for half of the original concentration of a compound to break down or dissipate) were between 119 and 958 days.2

Quality of Toxicology Testing

Tests done on glyphosate to meet registration requirements have been associated with fraudulent practices.

Laboratory fraud first made headlines in 1983 when EPA publicly announced that a 1976 audit had discovered "serious deficiencies and improprieties" in toxicology studies conducted by Industrial Biotest Laboratories (IBT).44 Problems included "countless deaths of rats and mice that were not reported," "fabricated data tables," and "routine falsification of data."44

IBT was one of the largest laboratories performing tests in support of pesticide registrations.44 About 30 tests on glyphosate and glyphosate-containing products were performed by IBT, including 11 of the 19 chronic toxicology studies.45 A compelling example of the poor quality of IBT data comes from an EPA toxicologist who wrote, "It is also somewhat difficult not to doubt the scientific integrity of a study when the IBT stated that it took specimens from the uteri (of male rabbits) for histopathological examination."46 (Emphasis added.)

In 1991, laboratory fraud returned to the headlines when EPA alleged that Craven Laboratories, a company that performed contract studies for 262 pesticide companies including Monsanto, had falsified test results.47 "Tricks" employed by Craven Labs included "falsifying laboratory notebook entries" and "manually manipulating scientific equipment to produce false reports."48 Roundup residue studies on plums, potatoes, grapes, and sugarbeets were among the tests in question.49

The following year, the owner/president of Craven Laboratories and three employees were indicted on 20 felony counts. A number of other employees agreed to plead guilty on a number of related charges.50 The owner was sentenced to five years in prison and fined $50,000; Craven Labs was fined 15.5 million dollars, and ordered to pay 3.7 million dollars in restitution.48

Although the tests of glyphosate identified as fraudulent have been replaced, these practices cast shadows on the entire pesticide registration process.

References

1. Monsanto, the Agricultural Group. Undated. Roundup into the twenty-first century. St. Louis, MO.

2. World Health Organization, United Nations Environment Programme, the International Labour Organization. 1994. Glyphosate. Environmental Health Criteria #159. Geneva, Switzerland.

3. U.S. Environmental Protection Agency. 1986. Pesticide fact sheet: Glyphosate. No. 173. Washington, D.C.: Office of Pesticide Programs. (June.)

4. U.S. EPA. Office of Pesticide Programs. Special Review and Reregistration Division. 1993. Reregistration eligibility decision (RED): Glyphosate. Washington, D.C. (September.)

5. Monsanto Company Agricultural Products. 1992. Accord label. St. Louis, MO. (December 1.)

6. Carlisle, S.M. and J.T. Trevors. 1988. Glyphosate in the environment. Water, Air, and Soil Pollution 39:409-420.

7. Aspelin, A.L. 1994. Pesticide industry sales and usage: 1992 and 1993 market estimates. U.S. EPA. Office of Prevention, Pesticides and Toxic Substances. Office of Pesticide Programs. Biological and Economic Analysis Division. Washington, D.C. (June.)

8. Whitmore, R.W., J.E. Kelly, and P.L. Reading. 1992. National home and garden pesticide use survey. Final report, Vol. 1: Executive summary, results, and recommendations. Research Triangle Park, NC: Research Triangle Institute.

9 California Environmental Protection Agency. Dept. of Pesticide Regulation. Information Services Branch. 1994. Pesticide use report: Annual 1992. Indexed by chemical. Sacramento, CA. (February.)

10. Cremlyn, R.J. 1991. Agrochemicals: Preparation and mode of action. Chichester, U.K: John Wiley & Sons. Pp.257-258.

11. Gilchrist, D.G. and T. Kosuge. 1980. Aromatic amino acid biosynthesis and its regulation. In Miflin, B.J. (ed.) The biochemistry of plants. New York: Academic Press. Pp. 507-513

12. Metzler, D.E. 1977. Biochemistry: The chemical reactions of living cells. Pp. 849-850. New York, NY: Academic Press.

13. Su, L.Y. et al. 1992. The relationship of glyphosate treatment to sugar metabolism in sugarcane: New physiological insights. J. Plant Physiol. 140:168-173.

14. Hietanen, E., K. Linnainmaa, and H. Vainio. 1983. Effects of phenoxy herbicides and glyphosate on the hepatic and intestinal biotransformation activities in the rat. Acta Pharma. et Toxicol. 53:103-112.

15. U.S. Dept. of Agriculture. Forest Service. Pacific Northwest Region. 1994. Glyphosate herbicide information profile. (October.)

16. Olorunsogo, O.O., E.A. Bababunmi, and O. Bassir. 1977 Proc. 1st Intern. Cong. of Toxicol. (Toronto, Canada). Cited in Olorunsogo, O.O., E.A. Bababunmi, and O. Bassir. 1979. Effect of glyphosate on rat liver mitochondria in vivo. Bull. Environ. Contam. Toxicol. 22:357-364.

17. Olorunsogo, O.O. 1976. Ph.D. thesis, University of Ibadan, Ibadan, Nigeria. Cited in Olorunsogo, O.O., E.A. Bababunmi, and O. Bassir. 1979. Effect of glyphosate on rat liver mitochondria in vivo. Bull. Environ. Contam. Toxicol. 22:357-364.

18. Martinez, T.T., W.C. Long, and R. Hiller. 1990. Comparison of the toxicology of the herbicide Roundup by oral and pulmonary routes of exposure. Proc. West. Pharmacol. Soc. 33:193-197.

19. Martinez, T.T. and K. Brown. 1991. Oral and pulmonary toxicology of the surfactant used in Roundup herbicide. Proc. West. Pharmacol. Soc. 34:43-46.

20. Agriculture Canada. Food Production and Inspection Branch. Pesticides Directorate. 1991. Discussion document: Pre-harvest use of glyphosate. Ottawa, Ontario, Canada. (November 27.)

21. U.S. EPA. Office of Pesticides and Toxic Substances. 1982. Memo from William Dykstra, Toxicology Branch, to Robert Taylor, Registration Division. (April 29.)

22. Tai, T. 1990. Hemodynamic effects of Roundup, glyphosate and surfactant in dogs. Jpn. J. Toxicol. 3(1): 63-68. Cited in World Health Organization, United Nations Environment Programme, the International Labour Organization. 1994. Glyphosate. Environmental Health Criteria #159. Geneva, Switzerland.

23. Sawada, Y., Y. Nagai, M. Ueyama, and I. Yamamoto. 1988. Probable toxicity of surface-active agent in commercial herbicide containing glyphosate. Lancet 1(8580):299.

24. Tominack, R.L. et al. 1991. Taiwan National Poison Center: Survey of glyphosate-surfactant herbicide ingestions. Clin. Toxicol. 29(1):91-109.

25. Temple, W.A. and N.A. Smith. 1992. Glyphosate herbicide poisoning experience in New Zealand. N.Z. Med. J. 105:173- 174.

26. Talbot, A.R. et al. 1991. Acute poisoning with a glyphosate-surfactant herbicide (‘Roundup’): A review of 93 cases. Human Exp. Toxicol. 10:1-8.

27. Menkes, D.B., W.A. Temple, and I.R. Edwards. 1991. Intentional self-poisoning with glyphosate-containing herbicides. Human Exp. Toxicol. 10:103-107.

28. Jamison, J.P., J.H.M. Langlands, R.C. Lowry. 1986. Ventilatory impairment from pre-harvest retted flax. Brit. J. Ind. Med. 43:809-813.

29. U.S. Dept. of Health and Human Services. Public Health Service. National Institutes of Health. NTP technical report on toxicity studies of glyphosate (CAS No. 1071-83-6) administered in dosed feed to F344/N rats and B6C3F1 mice. (NIH Publication 92-3135). Toxicity Reports Series No. 16. Research Triangle Park, NC: National Toxicology Program.

30. U.S. EPA. Office of Toxic Substances. 1980. EPA Reg. #524-308; glyphosate; 3-month mouse feeding study. Memo from William Dykstra, Health Effects Division, to Robert Taylor, Registration Division. Washington, D.C. (September 29.)

31. U.S. EPA. Office of Pesticides and Toxic Substances. 1985. Glyphosate; EPA Reg.#524-308; Mouse oncogenicity study. Washington, D.C. (April 3.)

32. U.S. EPA. Office of Pesticides and Toxic Substances. 1982. EPA Reg. #524-308; Lifetime feeding study in rats with glyphosate. Memo from William Dykstra, Health Effects Division to Robert Taylor, Registration Division. Washington, D.C. (February 18.)

33. U.S. EPA. Office of Pesticides and Toxic Substances. 1983. Glyphosate; EPA Reg. #524-308; A lifetime feeding study of glyphosate in Sprague-Dawley rats; a preliminary addendum to review dated 2/18/83. Memo to Robert Taylor, Registration Division. Washington, D.C. (February 15.)

34. U.S. EPA. Office of Pesticides and Toxic Substances. 1985. Glyphosate Q Evaluation of kidney tumors in male mice. Chronic feeding study. Memo from L. Kasza, Toxicology Branch, to W. Dykstra, Toxicology Branch. Washington, D.C. (December 4.)

35. U.S. EPA. Office of Pesticides and Toxic Substances. 1991. Second peer review of glyphosate. Memo from W. Dykstra and G.Z. Ghali, Health Effects Division to R. Taylor, Registration Division, and Lois Rossi, Special Review and Reregistration Division. Washington, D.C. (October 30.)

36. U.S. EPA Office of Pesticides and Toxic Substances. 1985. Use of historical data in determining the weight of evidence from kidney tumor incidence in the glyphosate two-year feeding study; and some remarks on false positives. Memo from Herbert Lacayo to Reto Engler (both Office of Pesticide Programs, Health Effects Division). Washington, D.C. (February 26.)

37. Monsanto Co. 1988. Material safety data sheet: Pondmaster aquatic herbicide. St. Louis, MO. (April.)

38. Kale, P.G. et al. 1995. Mutagenicity testing of nine herbicides and pesticides currently used in agriculture. Environ. Mol. Mutagen. 25:148-153.

39. Vigfusson, N.V. and E.R. Vyse. 1980. The effect of the pesticides, Dexon, Capton and Roundup on sister-chromatid exchanges in human lymphocytes in vitro. Mutation Research 79:53-57.

40. Rank, J. et al. 1993. Genotoxicity testing of the herbicide Roundup and its active ingredient glyphosate isopropylamine using the mouse bone marrow micronucleus test, Salmonella mutagenicity test, and Allium anaphase-telophase test. Mut. Res. 300:29-36.

41. Goltenboth, F. 1977. The effect of glyphosate and ametryn on the root tip mitosis of water hyacinth. Proc. Asian Pac. Weed Sci. 6th Conf. 2:255. Cited in Hess, F.D. 1989. Herbicide interference with cell division in plants. Chapter 5 of Bgez, P and Sandmann, G. (eds.) Target sites of herbicide action. Boca Raton, FL: CRC Press, Inc.

42. U.S. EPA. Office of Toxic Substances. 1980. EPA Reg. #524-308; glyphosate; submission of rat teratology, rabbit teratology, dominant lethal mutagenicity assay in mice. Memo from W. Dykstra, Health Effects Division, to Robert Taylor, Registration Division. Washington, D.C. (Undated.)

43. U.S. EPA. Office of Pesticides and Toxic Substances. 1986. Guidance for the reregistration of pesticide products containing glyphosate as the active ingredient. Washington, D.C. (June.)

44. U.S. Congress. House of Representatives. Committee on Government Operations. 1984. Problems plague the Environmental Protection Agency’s pesticide registration activities. House Report 98-1147. Washington, D.C.: U.S. Government Printing Office.

45. U.S. EPA. Office of Pesticides and Toxic Substances. 1983. Summary of the IBT review program. Washington, D.C. (July.)

46. U.S. EPA. 1978. Data validation. Memo from K. Locke, Toxicology Branch, to R. Taylor, Registration Branch. Washington, D.C. (August 9.)

47. U.S. EPA. Communications and Public Affairs. 1991. Note to correspondents. Washington, D.C. (March 1.)

48. U.S. EPA. Communications, Education, And Public Affairs. 1994. Press advisory. Craven Laboratories, owner, and 14 employees sentenced for falsifying pesticide tests. Washington, D.C. (March 4.)

49. U.S. EPA. Communications and Public Affairs. 1991. Press advisory. EPA lists crops associated with pesticides for which residue and environmental fate studies were allegedly manipulated. Washington, D.C. (March 29.)

50. U.S. Dept. of Justice. United States Attorney. Western District of Texas. 1992. Texas laboratory, its president, 3 employees indicted on 20 felony counts in connection with pesticide testing. Austin, TX. (September 29.)

========================================================

| Northwest Coalition for Alternatives to Pesticides |

| P.O. Box 1393 Eugene, OR 97440 |

| Phone: (541) 344-5044 |

| email: ncap@igc.apc.org |

========================================================

** Pesticide Action Network North America (PANNA) **

Phone: (415) 541-9140

Fax: (415) 541-9253

*For general information about PANNA, send an email: panna@panna.org

http://www.panna.org/panna/

========================================================

Glyphosate Weedkiller in Our Food and Water?

Colin Todhunter
Infowars.com
June 17, 2013

Historians may look back and write about how willing we are to sacrifice our children and jeopardize future generations with a massive experiment that is based on false promises and flawed science just to benefit the bottom line of a commercial enterprise.” So said Don Huber in referring to the use of glyphosate and genetically modified crops. Huber was speaking at Organic Connections conference in Regina, Canada, late 2012.

Huber is an emeritus professor in plant pathology at Purdue University in the US and has worked with the Department of Homeland Security to reduce the impact of plant disease outbreaks. His words are well worth bearing in mind given that a new study commissioned by Friends of the Earth Europe (FoE) and GM Freeze has found that people in 18 countries across Europe have been found to have traces of glyphosate in their urine (1).

Friends of the Earth Europe commissioned laboratory tests on urine samples from volunteers in 18 countries across Europe and found that on average 44 percent of samples contained glyphosate. The proportion of positive samples varied between countries, with Malta, Germany, the UK and Poland having the most positive tests, and lower levels detected in Macedonia and Switzerland. All the volunteers who provided samples live in cities, and none had handled or used glyphosate products in the run-up to the tests.

The Influence of the Biotech Sector on Safety and Regulation

Although ‘weedkiller in urine’ sounds alarming, Tom Sanders, head of the nutritional sciences research division at King’s College London, says the levels found are unlikely to be of any significance to health because they are 300 times lower than the level which might cause concern. Alison Haughton, head of the Pollination Ecology Group at Rothamsted Research, said that if FoE and GM Freeze want their work to have scientific credibility and provide a genuine contribution to the debate on pesticide residues, they should submit their work for publication in a peer-reviewed journal.

Valid points, you might think. But FoE believes that there is sufficient evidence to suggest environmental and health impacts from glyphosate warrant concern. It wants to know how the glyphosate found in human urine samples has entered the body, what the impacts of persistent exposure to low levels of glyphosate might be and what happens to the glyphosate that remains in the body. New research published in the journal Entropy sheds disturbing light on such concerns (discussed later in this article).

In 2011, Earth Open Source said that official approval of glyphosate had been rash, problematic and deeply flawed. A comprehensive review of existing data released in June 2011 by Earth Open Source suggested that industry regulators in Europe had known for years that glyphosate causes birth defects in the embryos of laboratory animals. Questions were raised about the role of the powerful agro-industry in rigging data pertaining to product safety and its undue influence on regulatory bodies (2).

In the same vein, FoE says there is currently very little testing for glyphosate by public authorities, despite its widespread use, and authorities in Europe do not test for glyphosate in humans and tests on food are infrequent. Glyphosate was approved for EU-wide use in 2002, but FoE argues that the European regulatory agencies did not carry out their own safety testing, relying instead on data provided by the manufacturers.

Of course there are certain scientists (usually with links to the agro-industry) who always seem to be strident in calling for peer-reviewed evidence when people are critical of the biotech sector, but then rubbish it and smear or intimidate the scientists involved when that occurs, as has been the case with Dr Arsad Pusztai in the UK or Professor Seralini in France. It is therefore quite revealing that most of the data pertaining to glyphosate safety came from industry studies, not from peer-reviewed science, and the original data are not available for independent scrutiny.

Increasing Use

With references to a raft of peer-reviewed studies, FoE also brings attention to the often disturbing health and environmental dangers and impacts of glyphosate-based herbicides throughout the world (1). The FoE study also highlights concerns around the increasing levels of exposure to glyphosate-based weed killers, particularly as the use of glyphosate is predicted to rise further if more genetically modified (GM) crops are grown. It is after all good for business. And the biggest producer of glyphosate is Monsanto, which sells it under the brand name ‘Roundup’.

“The figures don’t lie; GMOs drive glyphosate sales.” (3)

Despite its widespread use, there is currently little monitoring of glyphosate in food, water or the wider environment. The FoE commissioned study is the first time monitoring has been carried out across Europe for the presence of the weed killer in human bodies. FoE Europe’s spokesperson Adrian Bebb argues that there is a serious lack of action by public authorities and indicates that this weed killer is being widely overused.

This certainly needs to be addressed not least because the prediction concerning increasing exposure to glyphosate is not without substance. The introduction of Roundup Ready crops has already resulted in an increase of glyphosate use. Using official US government data, Dr Charles Benbrook, research professor at the Center for Sustaining Agriculture and Natural Resources at Washington State University, states that since 1996 the glysophate rate of application per crop year has tripled on cotton farms, doubled in the case of soybeans and risen 39 percent on corn (4). The average annual increase in the pounds of glyphosate applied to cotton, soybeans, and corn has been 18.2 percent, 9.8 percent, and 4.3 percent, respectively, since herbicide tolerant crops were introduced.

Glyphosate is used on many genetically modified crops. 14 new GM crops designed to be cultivated with glyphosate are currently waiting for approval to be grown in Europe. Approval of these crops would inevitably lead to a further increase of glysphosate spraying. In the US, biotech crops, including corn, soybeans, canola and sugarbeets, are planted on millions of acres annually.

Increasing Dangers

Evidence suggests that Roundup could be linked to a range of health problems and diseases, including Parkinson’s, infertility and cancers, according to a new peer-reviewed report, published recently in the scientific journal Entropy (5). The study also concluded that residues of glyphosate have been found in food.

These residues enhance the damaging effects of other food-borne chemical residues and toxins in the environment to disrupt normal body functions and induce disease, according to the report, authored by Stephanie Seneff, a research scientist at the Massachusetts Institute of Technology, and Anthony Samsel, a science consultant. The study says that negative impact on the body is insidious and manifests slowly over time as inflammation damages cellular systems throughout the body.

In 2010, the provincial government of Chaco province in Argentina issued a report on health statistics from the town La Leonesa. The report showed that from 2000 to 2009, following the expansion of genetically-modified soy and rice crops in the region (and the use of glyphosate), the childhood cancer rate tripled in La Leonesa and the rate of birth defects increased nearly fourfold over the entire province (6).

Professor Huber also notes the health risks associated with the (increasing) use of glyphosate. He says a number of plant pathogens are emerging, which when consumed could impact human health. Based on research that he alludes to (he refuses to make his research public or identify his fellow researchers, who he claims could suffer substantial professional backlash from academic employers who received research funding from the biotechnology industry), Huber notes that the use of glyphosate changes the soil ecology, killing many bacteria, while giving other bacteria a competitive advantage. This makes plants highly susceptible to soil borne diseases. At the same time, glyphosate has a negative effect on a number of beneficial soil organisms (7).

Huber’s concerns about the impact of long term use of glyphosate on soil sterility are similar to concerns expressed by Elaine Ingham, a soil ecologist with the Rodale Institute, and also research carried out in by Navdanya in India (8).

As for GM crops, Huber says they have lower water use efficiency, tend to be nutrient deficient, have increased bud and fruit abortion and are predisposed to infectious diseases and insect damage. He suggests that Roundup Ready crops, treated with glyphosate, have higher levels of mycotoxins and lower nutrient levels than conventional crops.

“… you could say that what you’re doing with glyphosate is you’re giving the plant a bad case of AIDS. You’ve shut down the immune system or the defense system.” Professor Ron Huber (7)

He concludes that, when consumed, the GM crops were more likely to cause disease, infertility, birth defects, cancer and allergic reactions than conventional crops.

Huber claims that consumption of food or feed that was genetically modified could bring the altered genes in contact with the microbes in the guts of the livestock or people who eat them. He feels this increases diseases, such as celiac disease, allergies, asthma, chronic fatigue syndrome, diabetes, gluten intolerance, irritable bowel disease, miscarriage, obesity and sudden infant death syndrome.

While none of these findings conclusively prove that plant (or animal) diseases are caused by the glyphosate, Huber feels safety evaluations have been inadequate, suggesting that previous (GM sector) research was substandard and extremely misleading in its interpretation of results – or worse.

With some hugely powerful players involved here, many of whom have successfully infiltrated important government and official bodies (9), much of the science and the ensuing debate surrounding glyphosate is being manipulated and hijacked by vested interests for commercial gain.

“… publishing in this area can also be difficult. I know from the International Symposium on Glyphosate that they had to find a journal publisher outside this country (the US) to publish the research data and symposium proceedings. It’s pretty hard to get it published in the States. There are also some hazards to publishing if you’re a young researcher doing research that runs counter to the current popular concepts. A lot of research on safety of genetic engineering is done outside of this country because it’s difficult to gain access to the materials, or the statements you have to sign to have access to those materials stating that you won’t publish without permission of the supplier. I think the 26 entomologists who sent their letter to EPA in 2009 stated it aptly when they said that objective data wasn’t available to the EPA because the materials haven’t been available to them or that they’re denied the opportunity to publish their data.” Professor Ron Huber (7)

Notes

1) http://www.foeeurope.org/sites/default/files/press_releases/foee_media_briefing_glyphosate.pdf
2) http://www.huffingtonpost.com/2011/06/24/roundup-scientists-birth-defects_n_883578.html
3) http://www.globalresearch.ca/genetic-engineering-and-corporate-agribusiness-gmos-and-the-impacts-of-glyphosate-herbicide/5337096
4) http://www.organic-center.org/reportfiles/13Years20091126_FullReport.pdf
5) http://www.nationofchange.org/study-links-monsanto-s-roundup-autism-parkinson-s-and-alzheimer-s-1367764115
6) http://www.pagina12.com.ar/diario/elpais/1-147561-2010-06-14.html
7) http://farmandranchfreedom.org/wp-content/uploads/2013/01/don-huber-may2011-acres.pdf
8) http://www.i-sis.org.uk/BtCottonKillsSoilandFarmers.php
9) http://rense.com/general33/fd.htm

This original originally appeared at GlobalResearch.