Category: EARTH TRUTH



Enoch and Elijah – Witnesses to

POLE SHIFTS

Thursday, October 16, 2014 6:56

(Before It’s News)

Enoch and Elijah – Witnesses to Pole Shifts?

The early theologians Irenaeus and Hippolytus may have been the last heirs to the uncorrupted oral tradition of the Apostles, and both of them said that Enoch and Elijah were the two witnesses we will see in the future preaching and dying on the streets of Jerusalem in the end times.  The Bible tells us that their presence will be a sign that the Second Coming is imminent.  I believe their stories also tell of pole shifts in our past, and lend additional support to the idea that they will be a witness to an upcoming pole shift, when we receive “a new heaven and a new earth.”

The Bible tells us that Enoch lived a total of 365 years.  This lifespan brings two obvious ideas to mind: first, that no one normally lives that long – and second, that the years of Enoch’s life match the number of days in a year.  If this is meant to draw our attention to the sun and the number of days it takes for the earth to orbit the sun, what else might we take from the story of Enoch to apply to the sun?

Enoch’s life is broken down into two portions: at the age of 65 he fathered Methuselah, then continued to live another 300 years before he “walked with God” and was “translated away so that he did not see death.” (Hebrews 11:5)  The word “translated” comes from the Greek “metatithemi” which means “taken to another place.”  Because I have spent many years researching topics like pole shifts, this makes me think the story of Enoch may incorporate a coded message about a pole shift event in the distant past when the sun (symbolized by Enoch in this story) would have been positioned in the sky next to the galactic center (God) when it suddenly shifted its apparent position in the sky and was “taken to another place.”

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I also suspect that the way the Bible breaks down Enoch’s life into two unequal portions might be similar to the way the Maya broke their year down based on the dates on which the sun passes directly overhead in the zenith.  Every spring equinox in March, the sun is directly above the equator at noon.  Lands north of the equator and south of the Tropic of Cancer witness the sun directly overhead at noon at some point prior to the first day of summer.  For example, at Chichen Itza, where the Maya built the great Pyramid of Kukulkan, the sun is directly overhead on May 22.  The sun appears to keep moving north until summer, then starts to fall southwards again.  Chichen Itza experiences a second solar zenith on July 19.  At another Mayan city (Izapa – which is farther south, at a different latitude) where this pattern was first recognized, the two zenith dates are 105 days apart, and the Maya there broke the year into 105 and 260 portions based on the spread of the zenith passage dates at Izapa’s latitude.  What latitude, I wondered, would experience zenith passage dates 65 days apart – and could such zenith dates possibly point us to the previous position of Jerusalem, before the last pole shift?

A little research led me to a chart labelled “Zenith passage dates of the Sun for Observers in Different Latitudes” in Anthony Aveni’s Skywatchers of Ancient Mexico.  Just below 20 degrees north there are 65 days between zenith dates.  Could this be the latitude the holy site we now know as Jerusalem used to be located at prior to the last major shift of the earth’s crust relative to its axis of rotation?  Could the location of this ancient holy site possibly even explain why the Maya had a special term for the 65 day period (Aveni calls it the Cociyo) when neither Izapa nor Chichen Itza experience zeniths 65 days apart?

At first glance, this seems to be a dead end and a bad theory, because we know from other data that the previous North Pole was located on the west side of Hudson Bay.  When the North Pole was there, the land that is now called Jerusalem was approximately eleven and a half degrees north latitude, not just under twenty degrees north latitude.   Jerusalem, at its former latitude, had zenith passage dates well over 100 days apart.  However, I soon noticed that the change in latitude – the northward movement Jerusalem experienced as a result of the last pole shift – is approximately 19.8 degrees.  Which means that Enoch’s being taken away in a “translation” and the years of his life may be astronomical references to a pole shift after all.

the image above may approximate the next position of the “new earth” if the North Pole is near Lake Baikal, as Professor Charles Hapgood suggests it might be in his books.

I believe that cosmic events emanating from the galactic center cause recurring, periodic, and predictable pole shifts on earth.  At the same time I believe the sun will appear to be dark (Revelation 6:12 “the sun became black as sackcloth”) for three days, at the point in the year when it appears at the crossing point of the galactic axis and the ecliptic – the apparent path of the sun and planets.  I suspect it is no coincidence that Jesus died on a cross and was dead for three days and that we are told the sun went dark when he died.  Jonah was in darkness in the belly of the whale for three days, and I believe this is a reference to the sun going dark as it passes through the cosmic leviathan of the Milky Way’s central bulge along the galactic axis.

Elijah encountered “a chariot of fire.”   The Book of Enoch mentions “the sun… and the chariot in which it rises.” (Enoch 72:5)  We can safely assume Elijah represents another heavenly body which encountered the sun. “And Elijah went up by a whirlwind into heaven” just after he walked past Bethel (Beth-El = the house of God = the galactic center) and crossed the Jordan River (the Milky Way) and encountered the chariot of fire (the sun.)  So this occurred when the sun (and some other heavenly body – I suggest Jupiter) had just passed the galactic center and the axis of the Milky Way.  2 Kings 2:17 describes the men sent out to look for Elijah after he disappeared – “They searched three days but could not find him.”  Another symbolic reference to the three days of darkness and confusion.

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And then one of the even stranger comments in the Bible appears in 2 Kings 2:24 “Two female bears came out of the woods and tore up forty-two lads” from Bethel who had previously mocked Elijah’s son.  Now I have been to that part of Israel.  I have stood in the Jordan River.  Trees are scarce, and I never saw “woods” or a forest dense enough that bears could emerge and suddenly surprise anyone.  And even if we grant that there had been thick woods and a pair of real bears, can you imagine 42 young men not scattering and running off in different directions?  Surely a bear could kill a lad or two, but forty-two of them?  As C.M. Houck commented in The Celestial Spheres: Keys to the Suppressed wisdom of the Ancients: “How could two bears possibly manage to outrun, catch, and destroy forty-two terrified, hyperactive juvenile delinquents?  They couldn’t.  This is sacred language.”  And what I think he means is that this is another astronomical reference, this time to the two “polar bears” – the constellations Ursa Major and Ursa Minor – the Big Bear and Little Bear near the celestial North Pole.  I suggest that during the last pole shift, it was noticed that these “bears” seemed to suddenly move far faster than usual into the sky, corresponding with the sudden disappearance of 42 visible stars which unexpectedly fell below the opposite horizon.

In my last book, End Times and 2019, I conclude that the Bible, the Maya, and the Egyptians all left clues pointing to the next pole shift coinciding with the end of the Tribulation and Judgment Day in late December, 2019.  I suggest that Jupiter is the astronomical representation of the prophet Elijah, that the Sun represents Jesus, and that the conjunction of Jupiter and the Sun on Judgment Day represents Elijah anointing Jesus Christ as King.  I believe that Enoch and Elijah have been portrayed as witnesses to a previous pole shift, and that their stories give us clues about that last pole shift.  I believe they will be the two end times witnesses of the tribulation, and that they will witness during the reign of the Antichrist, just before the next catastrophic pole shift in 2019.  If you appreciate my application of “forensic astronomy” to Bible prophecy as detailed above, you will probably appreciate both my previous book – End Times and 2019 – and my new book focusing on events in the middle of the final seven years in June 2016 – Antichrist 2016-2019.

— contributed by David Montaigne, October 2014

author of  End Times and 2019   and   Antichrist 2016-2019

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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.

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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.

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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.”

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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.”

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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.

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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.

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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.

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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.

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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.”

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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

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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.

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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.

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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.

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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.

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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).

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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.

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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%.

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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.

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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.)

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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.

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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.

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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.
 
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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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)

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  • 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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.”

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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.

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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.”

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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.

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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.”

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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.

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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.

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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.

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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.”

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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).

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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

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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.

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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.

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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.

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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.

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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.

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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).

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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.

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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%.

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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.

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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.)

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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.

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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.

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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.

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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.

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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.
 
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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.

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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.

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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.

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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?

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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

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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.

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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.

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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."

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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)

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  • 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.)

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.”

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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.

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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.”

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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.

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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.”

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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.

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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.

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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.

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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.”

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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).

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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.

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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.

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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).

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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

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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.

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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.

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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.

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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.

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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.

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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.

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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).

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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.

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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%.

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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.

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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.)

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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.

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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.

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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.

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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.

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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.
 
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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.

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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.

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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.

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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?

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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)

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  • 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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.


Russia Issues Grim Report On North American Magnetic Anomaly

Posted by EU Times on Jun 12th, 2014

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A grim report prepared by Commander-in-Chief of the Air Force Lieutenant-General Viktor Bondarev on the just completed scientific mission of North America carried out by 4 Tupolev Tu-95 strategic aircraft and 2 Ilyushin Il-78 aerial refueling tankers that “electronically swept” for “magnetic anomalies” from Alaska to California warns that a “catastrophic event” may be nearing for this region.

US officials, it should be noted, characterized this purely scientific mission as a “bombing run” that came within 50 miles of California, but which their Air Forces were able to repel by their launching of F-15 fighter jets.

This report, however, states that this scientific mission was necessitated by a “severe mysterious magnetic anomaly” detected by the Kosmos 2473 satellite on 3 June occurring in the Yellowstone region of the Western United States which resulted in what is called an “earthquake swarm.”

Most important to note about the 3 June Yellowstone “magnetic anomaly”, this report continues, are that satellite measurements show it being precipitated by the mysterious earthquake swarm hitting the Brooks Range mountains in Alaska, and which seismologists are still at a loss to explain.

The information relating to the linking of these two “events”, this report says, was further verified by the United States Geological Survey (USGS) magnetic anomaly maps and data for North America showing a strange magnetic “disturbance/ripple” emanating from Brooks Range and ending at Yellowstone on 3 June, both of these areas, it is important to note, being part of the Rocky Mountains that stretch more than 4,830 km (3,000 miles) from the northernmost part of British Columbia, in western Canada, to New Mexico, in the southwestern United States.

Of grave concern to Russian military authorities relating to these “events”, General Bondarev says in his report, was the “catastrophic effect” they had on the advanced “magnetoceptioninertial navigation systems employed by many US-NATO-Russian warplanes which use these highly sophisticated aircraft flight devices.

Though no Russia military aircraft were near the “disturbed magnetic zone” emanating our from Yellowstone on 3 June, this report says, two US military aircraft were at its “boundaries” in the Southern California region on 4 June while this “event” was still “active” causing them both to crash.

The two US fighter jets crashing on 4 June, this report continues, were identified as a US Navy F-A-183 that went down when the pilot was attempting to land aboard the carrier Carl Vinson, and a US Marine Harrier AV-8B jet that crashed into a residential community in Imperial, about 90 miles east of San Diego, both of them occurring within hours of each other.

This report notes that no civilian aircraft would have been affected by this “magnetic anomaly” as only the most advanced military aircraft employ these “geomagnetic-satellite” coordinated flight systems which enable them to “hug the terrain” not unlike the magnetic systems used by birds and insects to navigate.

Russian concerns relating to “magnetic anomalies”, it is important to note, are related to the rapidly shifting north magnetic pole which since 2005 has been moving at a rate of 40 kilometers (25 miles) a year from Arctic Canada toward Siberia.

Frightening independent research from last year (2013) further warns that this shift is still picking up speed and according to this researcher should reach Siberia in at least within 2 years. [See video HERE (banned in US)]

One of the effects of the rapidly shifting magnetic north pole being noticed the most, this report notes, are the airport runway systems being disrupted because of it, and as we can read one such 2011 example which occurred in the US:

“Tampa International Airport was forced to readjust its runways Thursday to account for the movement of the Earth’s magnetic fields, information that pilots rely upon to navigate planes. Thanks to the fluctuations in the force, the airport has closed its primary runway until Jan. 13 to change taxiway signs to account for the shift, the Federal Aviation Administration said.

The poles are generated by movements within the Earth’s inner and outer cores, though the exact process isn’t exactly understood. They’re also constantly in flux, moving a few degrees every year, but the changes are almost never of such a magnitude that runways require adjusting, said Paul Takemoto, a spokesman for the FAA.”

The most chilling aspects of General Bondarev’s report relating to these “events” are the equations he uses in postulating that what is now occurring in North America with these “mysterious magnetic anomalies” occurring over a large expanse of the Rocky Mountains, and when combined with the rapidly shifting magnetic north pole and growing evidence of global climate change, give “huge credibility” to what is called “The Expanding Earth Theory”.

The expanding Earth or growing Earth hypothesis asserts that the position and relative movement of continents is at least partially due to the volume of Earth increasing and stands in contrast to that of plate tectonics, but which new findings relating to “aether theories” and dark matter, General Bondarev summarizes, means “grave consideration” must be given to the words of University of California, Davis, cosmologist Dr. Andreas Albrecht who warned: “We’ve hit some really profound problems with cosmology Ð with dark matter and dark energy, that tells us we have to rethink fundamental physics and try something new.

Or in simple terms, this report ends, “We may be on the verge of a catastrophic North American “event” that could possibly change the world forever, we should be prepared.”

YELLOWSTONE ERUPTION OF MEGAVOLCANO

YELLOWSTONE ERUPTION OF MÉGAVOLCAN

Published June 9, 2014 | by Team Pleinsfeux

The American government  is working on a secret escape plan in case of a mega volcano eruption at Yellowstone ?

  • Conspiracy theorists claim that American citizens could be moved to Australia, Brazil and   Argentina.

  • The last eruption may have occurred there 70,000 years.

  • The volcano could be reclassified as “off”, despite the fact that researchers have recently found that it is 2.5 times larger than they thought.

On May 8, 2014

It has been suggested that millions of citizens of the United States could end up in Brazil, Australia or Argentina if the Yellowstone supervolcano eruption happened.

The news site “Praag” edited in South Africa, argues that the African National Congress would have been offered $ 10 billion a year for 10 years for the construction of temporary housing for Americans if rash, in this As part of the development of current emergency plans.

Bloggers and conspiracy theorists have spent weeks discussing these plans since the videos of animals fleeing the region have been revealed, although park rangers said they were actually frightened by tourists.

PREVIOUS KICKS

  1. According to U.S. Geological Survey, there were three major eruptions of Yellowstone supervolcano over the past million years.

  2. The first would have a league there are about 2.1 million years, while the second took place there 1.3 million years.

  3. The last major eruption took place there 640.000 years.

“It was a kind of spring day, and they were frisky. Contrary to online reports, this is an all-in-natural and not the end of the world phenomenon,” said the spokeswoman, Amy Bartlett.

If the largest volcano in the world was rash, most of the United States would be covered with ashes. However, researchers say there are no signs of an imminent eruption.

“The chance of that happening in our lives is extremely insignificant,” said Peter Cervelli, deputy director for science and technology at the Science Center of the volcanoes of the “United States Geological Survey,” California.

A recent study on the important supervolcano of Yellowstone National Park in the United States, researchers have recently found to be 2.5 times larger than they thought, could actually be dead very soon.

The researchers analyzed the water and gas, and believe that it could already be on its deathbed.

According to Ken Sims, of the University of Wyoming, air and water samples taken from the largest volcano in the world suggests that it might be dying.

The team examined the acidity in water samples and radon in the air as part of their study on the status of Yellowstone.

At Yellowstone, as with other volcanoes, some scientists theorize that the earth’s crust fractures and cracks in a concentric pattern, also known as fractures rings. At some point, these cracks reach the magma reservoir and release the pressure, and the volcano explodes. The enormous amount of released material causes the collapse of the volcano in a huge crater, a caldera.

They also analyzed how water and gas mix in the amount of land in order to improve methods of predicting eruptions and to identify the most volatile areas of the park.

Currently, the park is classified as dormant, as there would have been no eruption since 70,000 years.

If it becomes an extinct volcano, it will never erupt again.

In early November, a team of researchers from the University of Wyoming, led by Ken Sims, has distributed tarpaulins on the snowy ground near the white terraces, outside of “Mammoth Hot Springs” where pools are stacked like small mountains filled with crystal clear water.

“I got radium,” said Ken Sims, a professor of geology and geophysics of the “University of Wyoming and National Geographic Explorer.”

“We should take samples there. “

Ken Sims knelt beside a mound delicate formations and released their machines boxes backpack: There was a radon detector with lights and a recorder to tape measures, a detector pH to record acid levels.

Both should help me learn how water and gas interact.

“It looks like boiling,” said Ken Sims. “But in fact, it is steam or CO2. “

The area is of outstanding natural beauty: The Yellowstone caldera in Wyoming is the largest super-volcano in the world.

Ken Sims studied the rate at which water and gas mix ascending to the surface.

His research could eventually help scientists understand what causes eruptions of steam.

If they know how fast steam and water interact in the park, they could better predict when an area becomes more volatile.

Despite fears that the supervolcano may be off, the park is one of the research laboratories of the most famous in the world, attracting internationally renowned scientists to study everything from earthquakes to the origins of life, until the power of this volcano lies beneath the soil.

“Yellowstone is so superior in many ways, that sometimes you cry responses to what is happening elsewhere,” said Jacob Lowenstern, scientist in charge of the Yellowstone Volcano Observatory.

The unique park has a quagmire of molten rocks and crystals as the first national park in the country 40 miles (64 km.) Long molten rocks and crystals.

Instead of a cone with a hole, the caldera is an interconnected maze of gas and water covering nearly 60 miles (about 96 km.) In the northwestern corner of Wyoming with parts in Montana and Idaho.

More than 10,000 pots of mud, rivers and geysers boiling, act as valves to release pressure of nature, preventing the heated exploding monster.

And, they move.

“Mammoth Terraces” in the northern part of the park can grow vertically up to 3 meters per year and extend horizontally further.

The rise of the water dissolved calcium in the surface and the CO2 bubble is left behind and the white calcium carbonate.

The terraces rise until the vents become blocked and the gas pressure forces the opening of a weakness elsewhere.

“The intense heat of the Yellowstone volcano is driving the hydrothermal system,” said Henry Heasler, geologist of the park.

“It gets hot and rises, and the magma chamber, or reservoir, is at a relatively shallow depth. “

MERS “Middle Eastern Respiratory Syndrome”


A NEW VIRUS IS A "THREAT TO THE WORLD"

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Published June 24, 2013 | by Sentinel

Virus from the Middle East began to claim lives

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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.

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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."

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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.

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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;

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"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.

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"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.

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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?

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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.

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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.

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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.

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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)…

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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


Obama Brings Ebola Into America After Signing Executive Order to Detain Sick Americans
Officials are importing Ebola into the U.S. which doctors have failed to contain in Africa

Obama Brings Ebola Into America After Signing Executive Order to Detain Sick Americans

Image Credits: Sebástian Freire / Flickr (Medical workers)

by Kit Daniels | Infowars.com | August 2, 2014


Despite the fact that doctors in Africa cannot keep Ebola from spreading, United States officials brought an affected patient into the country only days after President Obama signed an executive order mandating the detention of Americans who show signs of “respiratory illness.”

The first known Ebola patient on U.S. soil, Dr. Kent Brantly, was flown into Emory University Hospital in Atlanta, Georgia, today after contracting the disease in Liberia during the latest outbreak in West Africa which has claimed the lives of over 700.

“Video from Emory showed someone wearing a white, full-body protective suit helping a similarly clad person emerge from the ambulance and walk into the hospital early Saturday afternoon,” CNN reported.

This has stoked concerns among the American public that Ebola could now spread inside the U.S., especially since the virus has been difficult to contain in Africa.

“It sounds like the perfect script for a horror movie: A virus with no vaccine and no cure kills hundreds of people; despite containment efforts, it keeps spreading, but it’s actually all too real in West Africa, where doctors have said Ebola is now ‘out of control,’” wrote Sheila M. Eldred for Discovery News.

Hospitals in America may not fare any better considering that antibiotic-resistant “nightmare bacteria” spread from one medical facility in 2001 to 46 states by 2013.

“Allegedly the Ebola carriers will be quarantined in special rooms, but we already know that American hospitals cannot even contain staph infections,” columnist Paul Craig Roberts wrote. “What happens to the utensils, plates, cups, and glasses with which the ebola infected persons eat and drink and who gets to clean the bed pans?”

“One slip-up by one person, one tear in a rubber glove, and the virus is loose.”

This really highlights the reckless nature of the global elite and government officials for importing a virus into the country which has no specific treatment and a mortality rate of up to 90%.

Similarly, state-funded universities and other facilities across the U.S. are maintaining weaponized viruses for so-called “bio-defense” under the Project Bioshield Act passed by Congress in 2004, but because these facilities are only moderately secure for the most part, there is a real risk that a deadly virus could escape into the public and affect millions of Americans in an outbreak on the same level as the pandemics which killed 80% of Native American populations by the 19th century.

The National Research Council found that one of these laboratories in Kansas, for example, has a 70% chance that a virus will spread from its lab in the next 50 years, even though the facility is designated as “maximum security.”

And it should also be pointed out that this is just one lab out of many in the nation, a good percentage of which have even less security.

There is no doubt that an accidental or an orchestrated release of a virus from one of these labs could result in the deaths of millions as well as a draconian government response to the outbreak, including martial law, through both the Model State Emergency Health Powers Act drafted in 2001 and President Obama’s latest executive order which mandates the apprehension and detention of Americans who merely show signs of “respiratory illness.”

Simply put, instead of preventing Ebola and other viruses from spreading within the U.S., Obama is readying his administration for a power grab if a major pandemic breaks out throughout the country.

 

What Exactly is Ebola Virus

Ebola virus disease

From Wikipedia, the free encyclopedia

  (Redirected from Ebola Virus)

"Ebola" redirects here. For other uses, see Ebola (disambiguation).

Ebola virus disease

Classification and external resources

640px-7042_lores-Ebola-Zaire-CDC_Photo

1976 photograph of two nurses standing in front of Mayinga N., a person with Ebola virus disease; she died only a few days later due to severe internal hemorrhaging.

 

Ebola virus disease (EVD) or Ebola hemorrhagic fever (EHF) is the human disease caused by the Ebola virus. Symptoms typically start two days to three weeks after contracting the virus, with a fever, sore throat, muscle pains, and headaches. Typically nausea, vomiting, and diarrhea follow, along with decreased functioning of the liver and kidneys. At this point, some people begin to have problems with bleeding.[1]

The disease may be acquired upon contact with blood or bodily fluids of an infected animal (commonly monkeys or fruit bats).[1] It is not naturally transmitted through the air.[2] Fruit bats are believed to carry and spread the virus without being affected. Once human infection occurs, the disease may spread between people as well. Male survivors may be able to transmit the disease via semen for nearly two months. In order to make the diagnoses, typically other diseases with similar symptoms such as malaria, cholera and other viral hemorrhagic fevers are first excluded. Blood samples may then be tested for viral antibodies, viral RNA, or the virus itself to confirm the diagnosis.[1]

Prevention includes decreasing the spread of disease from infected monkeys and pigs to humans. This may be done by checking such animals for infection and killing and properly disposing of the bodies if the disease is discovered. Properly cooking meat and wearing protective clothing when handling meat may also be helpful, as is wearing protective clothing and washing hands when around a person with the disease. Samples of bodily fluids and tissues from people with the disease should be handled with special caution.[1]

There is no specific treatment for the disease; efforts to help persons who are infected include giving either oral rehydration therapy or intravenous fluids.[1] The disease has high mortality rate: often killing between 50% and 90% of those infected with the virus.[1][3] EVD was first identified in Sudan and the Democratic Republic of the Congo. The disease typically occurs in outbreaks in tropical regions of Sub-Saharan Africa.[1] Between 1976, when it was first identified, through 2013, fewer than 1,000 people a year have been infected.[1][4] The largest outbreak to date is the ongoing 2014 West Africa Ebola outbreak, which is affecting Guinea, Sierra Leone, and Liberia.[5] As of July 2014 more than 1320 cases have been identified.[5] Efforts are ongoing to develop a vaccine; however, none yet exists.[1]

Signs and symptoms

Symptoms_of_ebola

Symptoms of Ebola.[6]

Signs and symptoms of Ebola usually begin abruptly with an influenza-like stage characterized by feeling tired, fever, headaches, and joint, muscle, and abdominal pain.[7][8] Vomiting, diarrhea and loss of appetite are also common.[8] Less common symptoms include: sore throat, chest pain, hiccups, shortness of breath and trouble swallowing.[8] The average time between contracting the infection and the start of symptoms is 8 to 10 days, but can occur between 2 and 21 days.[8] Skin manifestations may include a maculopapular rash (in about 50% of cases).[9] Early symptoms of EVD may be similar to those of malaria, dengue fever, or other tropical fevers, before the disease progresses to the bleeding phase.[7]

Bleeding

In the bleeding phase internal and subcutaneous bleeding may present itself through reddening of the eyes and bloody vomit.[7] Bleeding into the skin may create petechiae, purpura, ecchymoses, and hematomas (especially around needle injection sites).

All people infected show some symptoms of circulatory system involvement, including impaired blood clotting.[9] Bleeding from puncture sites and mucous membranes (e.g. gastrointestinal tract, nose, vagina and gums) is reported in 40–50% of cases.[10] Types of bleeding known to occur with Ebola virus disease include vomiting blood, coughing it up or defecating it. Heavy bleeding is rare and is usually confined to the gastrointestinal tract.[9][11]

In general, the development of bleeding symptoms often indicates a worse prognosis. However, contrary to popular belief, bleeding does not lead to hypovolemia and is not the cause of death (total blood loss is low except during labor). Instead, death occurs due to multiple organ failure (MOF) due to fluid redistribution, low blood pressure, disseminated intravascular coagulation, and focal tissue death.

Causes

EbolaCycle

Life cycles of the Ebolavirus

EVD is caused by four of five viruses classified in the genus Ebolavirus, family Filoviridae, order Mononegavirales. These four viruses are Bundibugyo virus (BDBV), Ebola virus (EBOV), Sudan virus (SUDV), Taï Forest virus (TAFV). The fifth virus, Reston virus (RESTV), is not thought to be disease-causing in humans. During an outbreak those at highest risk are health care workers and close contacts of those with the infection.[12]

Transmission

It is not entirely clear how Ebola is spread.[13] EVD is believed to occur after an ebola virus is transmitted to an initial human by contact with an infected animal’s bodily fluids. Human-to-human transmission can occur via direct contact with blood or bodily fluids from an infected person (including embalming of an infected dead person) or by contact with contaminated medical equipment, particularly needles and syringes.[14] Transmission through oral exposure and through conjunctiva exposure is likely[15] and has been confirmed in non-human primates.[16] The potential for widespread EVD infections is considered low as the disease is only spread by direct contact with the secretions from someone who has symptomatic disease.[14] The quick onset of symptoms makes it easier to identify sick individuals and limits a person’s ability to spread the disease by traveling. Because bodies of the deceased are still infectious, some doctors had to take measures to properly dispose of dead bodies in a safe manner despite local traditional burial rituals.[17]

Medical workers who do not wear appropriate protective clothing may also contract the disease.[18] In the past, hospital-acquired transmission has occurred in African hospitals due to the reuse of needles and lack of universal precautions.[19]

EVD is not naturally transmitted through the air.[2] They are, however, infectious as breathable 0.8–1.2 micrometre laboratory generated droplets;[20] because of this potential route of infection, these viruses have been classified as Category A biological weapons.[21] Recently the virus has been shown to travel without contact from pigs to non-human primates.[22]

Bats drop partially eaten fruits and pulp, then land mammals such as gorillas and duikers feed on these fallen fruits. This chain of events forms a possible indirect means of transmission from the natural host to animal populations, which have led to research towards viral shedding in the saliva of bats. Fruit production, animal behavior, and other factors vary at different times and places that may trigger outbreaks among animal populations.[23]

Reservoir

1280px-Bushmeat_-_Buschfleisch_Ghana

Bushmeat being prepared for cooking in Ghana, 2013. Human consumption of equatorial animals in Africa in the form of bushmeat has been linked to the transmission of diseases to people, including Ebola.[24]

Bats are considered the most likely natural reservoir; plants, arthropods, and birds have also been considered.[25] Bats were known to reside in the cotton factory in which the first cases for the 1976 and 1979 outbreaks were employed, and they have also been implicated in Marburg virus infections in 1975 and 1980.[26] Of 24 plant species and 19 vertebrate species experimentally inoculated with EBOV, only bats became infected.[27] The absence of clinical signs in these bats is characteristic of a reservoir species. In a 2002–2003 survey of 1,030 animals including 679 bats from Gabon and the Republic of the Congo, 13 fruit bats were found to contain EBOV RNA fragments.[28] As of 2005, three types of fruit bats (Hypsignathus monstrosus, Epomops franqueti, and Myonycteris torquata) have been identified as being in contact with EBOV. They are now suspected to represent the EBOV reservoir hosts.[29][30]

Between 1976 and 1998, in 30,000 mammals, birds, reptiles, amphibians, and arthropods sampled from outbreak regions, no ebolavirus was detected apart from some genetic traces found in six rodents (Mus setulosus and Praomys) and one shrew (Sylvisorex ollula) collected from the Central African Republic.[26][31] Traces of EBOV were detected in the carcasses of gorillas and chimpanzees during outbreaks in 2001 and 2003, which later became the source of human infections. However, the high lethality from infection in these species makes them unlikely as a natural reservoir.[26]

Transmission between natural reservoir and humans is rare, and outbreaks are usually traceable to a single case where an individual has handled the carcass of gorilla, chimpanzee, or duiker.[32] Fruit bats are also eaten by people in parts of West Africa where they are smoked, grilled or made into a spicy soup.[30][33]

Virology
Genome

Ebola_virus_virion

Electron micrograph of an Ebola virus virion

Like all mononegaviruses, ebolavirions contain linear nonsegmented, single-strand, non-infectious RNA genomes of negative polarity that possesses inverse-complementary 3′ and 5′ termini, do not possess a 5′ cap, are not polyadenylated, and are not covalently linked to a protein.[34] Ebolavirus genomes are approximately 19 kilobase pairs long and contain seven genes in the order 3′-UTRNPVP35VP40GPVP30VP24L5′-UTR.[35] The genomes of the five different ebolaviruses (BDBV, EBOV, RESTV, SUDV, and TAFV) differ in sequence and the number and location of gene overlaps.

Structure

Like all filoviruses, ebolavirions are filamentous particles that may appear in the shape of a shepherd’s crook or in the shape of a "U" or a "6", and they may be coiled, toroid, or branched.[35] In general, Ebolavirions are 80 nm in width, but vary somewhat in length. In general, the median particle length of ebolaviruses ranges from 974 to 1,086 nm (in contrast to marburgvirions, whose median particle length was measured at 795–828 nm), but particles as long as 14,000 nm have been detected in tissue culture.[36]

Replication

The ebolavirus life cycle begins with virion attachment to specific cell-surface receptors, followed by fusion of the virion envelope with cellular membranes and the concomitant release of the virus nucleocapsid into the cytosol. The viral RNA polymerase, encoded by the L gene, partially uncoats the nucleocapsid and transcribes the genes into positive-strand mRNAs, which are then translated into structural and nonstructural proteins. Ebolavirus RNA polymerase (L) binds to a single promoter located at the 3′ end of the genome. Transcription either terminates after a gene or continues to the next gene downstream. This means that genes close to the 3′ end of the genome are transcribed in the greatest abundance, whereas those toward the 5′ end are least likely to be transcribed. The gene order is, therefore, a simple but effective form of transcriptional regulation. The most abundant protein produced is the nucleoprotein, whose concentration in the cell determines when L switches from gene transcription to genome replication. Replication results in full-length, positive-strand antigenomes that are, in turn, transcribed into negative-strand virus progeny genome copy. Newly synthesized structural proteins and genomes self-assemble and accumulate near the inside of the cell membrane. Virions bud off from the cell, gaining their envelopes from the cellular membrane they bud from. The mature progeny particles then infect other cells to repeat the cycle.[37]

Pathophysiology

600px-Ebola_Pathenogensis_path.svg

Pathogenesis schematic

Endothelial cells, mononuclear phagocytes, and hepatocytes are the main targets of infection. After infection, a secreted glycoprotein (sGP) known as the Ebola virus glycoprotein (GP) is synthesized. Ebola replication overwhelms protein synthesis of infected cells and host immune defenses. The GP forms a trimeric complex, which binds the virus to the endothelial cells lining the interior surface of blood vessels. The sGP forms a dimeric protein that interferes with the signaling of neutrophils, a type of white blood cell, which allows the virus to evade the immune system by inhibiting early steps of neutrophil activation. These white blood cells also serve as carriers to transport the virus throughout the entire body to places such as the lymph nodes, liver, lungs, and spleen.[38]

The presence of viral particles and cell damage resulting from budding causes the release of cytokines (to be specific, TNF-α, IL-6, IL-8, etc.), which are the signaling molecules for fever and inflammation. The cytopathic effect, from infection in the endothelial cells, results in a loss of vascular integrity. This loss in vascular integrity is furthered with synthesis of GP, which reduces specific integrins responsible for cell adhesion to the inter-cellular structure, and damage to the liver, which leads to coagulopathy.[39]

Diagnosis

The most important method of diagnosis EVD is the medical history, especially travel and occupational history and the person’s exposure to wildlife. EVD can be confirmed by isolating ebolaviruses from or by detection of ebolavirus antigen or genomic or subgenomic RNAs in patient blood or serum samples during the acute phase of EVD. Ebolavirus isolation is usually performed by inoculation of grivet kidney epithelial Vero E6 or MA-104 cell cultures or by inoculation of human adrenal carcinoma SW-13 cells, all of which react to infection with characteristic cytopathic effects.[40][41]

Filovirions can easily be visualized and identified in cell culture by electron microscopy due to their unique filamentous shapes, but electron microscopy cannot differentiate the various filoviruses alone despite some overall length differences.[36] Immunofluorescence assays are used to confirm ebolavirus presence in cell cultures. During an outbreak, virus isolation and electron microscopy are most often not feasible options. The most common diagnostic methods are therefore RT-PCR in conjunction with antigen-capture ELISA, which can be performed in field or mobile hospitals and laboratories.[42] Indirect immunofluorescence assays (IFAs) are not used for diagnosis of EVD in the field anymore.

Classification

465px-Filovirus_phylogenetic_tree

Phylogenetic tree comparing the Ebolavirus and Marburgvirus. Numbers indicate percent confidence of branches.

The genera Ebolavirus and Marburgvirus were originally classified as the species of the now-obsolete Filovirus genus. In March 1998, the Vertebrate Virus Subcommittee proposed in the International Committee on Taxonomy of Viruses (ICTV) to change the Filovirus genus to the Filoviridae family with two specific genera: Ebola-like viruses and Marburg-like viruses. This proposal was implemented in Washington, DC on April 2001 and in Paris on July 2002. In 2000, another proposal was made in Washington, D.C., to change the "-like viruses" to "-virus" resulting in today’s Ebolavirus and Marburgvirus.[43]

Rates of genetic change are 100 times slower than influenza A in humans, but on the same magnitude as those of hepatitis B. Extrapolating backwards using these rates indicates that Ebolavirus and Marburgvirus diverged several thousand years ago.[44] However, paleoviruses (genomic fossils) of filoviruses (Filoviridae) found in mammals indicate that the family itself is at least tens of millions of years old.[45] Fossilized viruses that are closely related to ebolaviruses have been found in the genome of the Chinese hamster.[46]

Differential diagnosis

The symptoms of EVD are similar to those of Marburg virus disease.[47] It can also easily be confused with many other diseases common in Equatorial Africa such as other viral hemorrhagic fevers, falciparum malaria, typhoid fever, shigellosis, rickettsial diseases such as typhus, cholera, gram-negative septicemia, borreliosis such as relapsing fever or EHEC enteritis. Other infectious diseases that should be included in the differential diagnosis include the following: leptospirosis, scrub typhus, plague, Q fever, candidiasis, histoplasmosis, trypanosomiasis, visceral leishmaniasis, hemorrhagic smallpox, measles, and fulminant viral hepatitis.[citation needed] Non-infectious diseases that can be confused with EVD are acute promyelocytic leukemia, hemolytic uremic syndrome, snake envenomation, clotting factor deficiencies/platelet disorders, thrombotic thrombocytopenic purpura, hereditary hemorrhagic telangiectasia, Kawasaki disease, and even warfarin poisoning.[48][49][50][51]

Prevention

Biosafety_level_4_hazmat_suit

A researcher working with the Ebola virus while wearing a BSL-4 positive pressure suit to avoid infection

Behavioral changes

Ebola viruses are contagious with prevention predominantly involves behavior changes, proper personal protective equipment, and disinfection. Governments and individuals often quarantine the area where the disease is occurring; while the lack of roads and transportation may help.[52]

Techniques to avoid infection involve not contacting infected blood or secretions, including from those who are dead.[13] This involves suspecting and diagnosing the disease early and using standard precautions for all patients in the healthcare setting.[53] Recommended measures when caring for those who are infected include: wearing protective clothing including: masks, gloves, gowns and goggles, equipment sterilization and isolating them.[13]

Due to lack of proper equipment and hygienic practices, large-scale epidemics have occured mostly in poor, isolated areas without modern hospitals or well-educated medical staff. Traditional burial rituals, especially those requiring embalming of bodies, should be discouraged or modified.[53] Airline crews who fly to areas of these areas of the world are taught to identify Ebola and are to isolate anyone who has symptoms.[54]

Vaccine

No vaccine is currently available for humans.[1][55][56] The most promising candidates are DNA vaccines[57] or vaccines derived from adenoviruses,[58] vesicular stomatitis Indiana virus (VSIV)[59][60][61] or filovirus-like particles (VLPs)[62] because these candidates could protect nonhuman primates from ebolavirus-induced disease. DNA vaccines, adenovirus-based vaccines, and VSIV-based vaccines have entered clinical trials.[63][64][65][66]

Vaccines have protected nonhuman primates. Immunization takes six months, which impedes the counter-epidemic use of the vaccines. In 2003, a vaccine using an adenoviral (ADV) vector carrying the Ebola spike protein therefore was tested on crab-eating macaques. The monkeys twenty-eight days later were challenged with the virus and remained resistant.[58] A vaccine based on attenuated recombinant vesicular stomatitis virus (VSV) vector carrying either the Ebola glycoprotein or the Marburg glycoprotein in 2005 protected nonhuman primates,[67] opening clinical trials in humans.[63] The study by October completed the first human trial, over three months giving three vaccinations safely inducing an immune response. Individuals for a year were followed, and, in 2006, a study testing a faster-acting, single-shot vaccine began; this new study was completed in 2008.[64] Trying the vaccine on a strain of Ebola that more resembles the one that infects humans is the next step.[citation needed]

On 6 December 2011, the development of a successful vaccine against Ebola for mice was reported. Unlike the predecessors, it can be freeze-dried and thus stored for long periods in wait for an outbreak.[68] An experimental vaccine made by researchers at Canada’s national laboratory in Winnipeg was used in 2009 to pre-emptively treat a German scientist who might have been infected during a lab accident.[69] However, actual EBOV infection could never be demonstrated without a doubt.[70] Experimentally, recombinant vesicular stomatitis Indiana virus (VSIV) expressing the glycoprotein of EBOV or SUDV has been used successfully in nonhuman primate models as post-exposure prophylaxis.[71][72][clarification needed]

Laboratory

Ebola viruses are World Health Organization Risk Group 4 pathogens, requiring biosafety level 4-equivalent containment. Laboratory researchers must be properly trained in BSL-4 practices and wear proper personal protective equipment.

Treatment

Ebola_outbreak_in_Gulu_Municipal_Hospital

A hospital isolation ward in Gulu, Uganda, during the October 2000 outbreak

No ebolavirus-specific treatment exists.[56] Treatment is primarily supportive in nature and includes minimizing invasive procedures, balancing fluids and electrolytes to counter dehydration, administration of anticoagulants early in infection to prevent or control disseminated intravascular coagulation, administration of procoagulants late in infection to control hemorrhaging, maintaining oxygen levels, pain management, and administration of antibiotics or antimycotics to treat secondary infections.[73][74][75] Early treatment may increase the chance of survival.[76]

Prognosis

The disease has a high mortality rate: often between 50 percent and 90 percent.[1][3] If an infected person survives, recovery may be quick and complete. Prolonged cases are often complicated by the occurrence of long term problems, such as inflammation of the testicles, joint pains, muscle pains, skin peeling, or hair loss. Eye symptoms, such as light sensitivity, excess tearing, iritis, iridocyclitis, choroiditis and blindness have also been described. EBOV and SUDV may be able to persist in the semen of some survivors, which could give rise to infections and disease via sexual intercourse.[1]

Epidemiology

For more about specific outbreaks and their descriptions, see List of Ebola outbreaks.

CDC_worker_incinerates_med-waste_from_Ebola_patients_in_Zaire

CDC worker incinerates medical waste from Ebola patients in Zaire in 1976

While investigating an outbreak of Simian hemorrhagic fever virus (SHFV) in November 1989, an electron microscopist from USAMRIID discovered filoviruses similar in appearance to Ebola in tissue samples taken from crab-eating macaque imported from the Philippines to Hazleton Laboratories Reston, Virginia.[78]

Blood samples were taken from 178 animal handlers during the incident.[79] Of those, six animal handlers eventually seroconverted. When the handlers did not become ill, the CDC concluded that the virus had a very low pathogenicity to humans.[80]

Because of the virus’s high mortality, it is a potential agent for biological warfare.[81]

Given the lethal nature of Ebola, and since no approved vaccine or treatment is available, it is classified as a biosafety level 4 agent, as well as a Category A bioterrorism agent by the Centers for Disease Control and Prevention. It has the potential to be weaponized for use in biological warfare.[82] The BBC reports in a study that frequent outbreaks of Ebola may have resulted in the deaths of 5,000 gorillas.[83]

2007 to 2011

As of 30 August 2007, 103 people (100 adults and three children) were infected by a suspected hemorrhagic fever outbreak in the village of Kampungu, Democratic Republic of the Congo. The outbreak started after the funerals of two village chiefs, and 217 people in four villages fell ill. The World Health Organization sent a team to take blood samples for analysis and confirmed that many of the cases were the result of Ebolavirus.[84][85] The Congo’s last major Ebola epidemic killed 245 people in 1995 in Kikwit, about 200 miles (320 km) from the source of the August 2007 outbreak.[86]

On 30 November 2007, the Uganda Ministry of Health confirmed an outbreak of Ebola in the Bundibugyo District. After confirmation of samples tested by the United States National Reference Laboratories and the Centers for Disease Control, the World Health Organization confirmed the presence of a new species of Ebolavirus, which was tentatively named Bundibugyo.[87] The epidemic came to an official end on 20 February 2008. While it lasted, 149 cases of this new strain were reported, and 37 of those led to deaths.

An International Symposium to explore the environment and filovirus, cell system and filovirus interaction, and filovirus treatment and prevention was held at Centre Culturel Français, Libreville, Gabon, during March 2008.[88] The virus appeared in southern Kasai Occidental on 27 November 2008,[89] and blood and stool samples were sent to laboratories in Gabon and South Africa for identification.

On 25 December 2008, it was reported that the Ebola virus had killed 9 and infected 21 people in the Western Kasai province of the Democratic Republic of Congo.[90] On 29 December, Doctors Without Borders reported 11 deaths in the same area, stating that a further 24 cases were being treated. In January 2009, Angola closed down part of its border with the Democratic Republic of Congo to prevent the spread of the outbreak.[91]

On 12 March 2009, an unidentified 45-year-old scientist from Germany accidentally pricked her finger with a needle used to inject Ebola into lab mice. She was given an experimental vaccine never before used on humans. Since the peak period for an outbreak during the 21-day Ebola incubation period had passed as of 2 April 2009, she had been declared healthy and safe. It remains unclear whether or not she was ever actually infected with the virus.[92]

In May 2011, a 12-year-old girl in Uganda died from Ebola (Sudan subspecies). No further cases were recorded.[93]

2012 outbreaks

In July 2012, the Ugandan Health Ministry confirmed 13 deaths due to an outbreak of the Ebola-Sudan variant[94] in the Kibaale District.[95] On 28 July, it was reported that 14 out of 20 (70% mortality rate) had died in Kibaale.[96] On 30 July, Stephen Byaruhanga, a health official in Kibaale District, said the Ebola outbreak had spread from one remote village to several villages.[97]

The World Health Organization‘s (WHO) global and alert response network reported on August 3 that the suspected case count had risen to 53, including 16 deaths. Of these cases, five were confirmed by UVRI as Ebola cases. There were no confirmed cases outside of Kibaale District except for a patient who was medically evacuated to Kampala District and then died. WHO and CDC support was on the ground in Uganda supporting the government response. There were no confirmed cases outside of Uganda.[98] Included among populations confirmed to be affected were prisoners in Kabbale prison. [99] Dr. Joaquim Saweka, the WHO representative to Uganda, reported that the outbreak was under control and that everyone known to have had contact with a known Ebola patient was in isolation.[100]

On 8 August, the Ugandan Ministry of Health recorded 23 probable and confirmed cases, including 16 deaths. Ten cases were confirmed by the Uganda Virus Research Institute as Ebola. 185 people who came into contact with probable and confirmed Ebola cases were followed during the incubation period of 21 days.[101]

On 17 August, the Ministry of Health of the Democratic Republic of the Congo reported an outbreak of the Ebola-Bundibugyo variant[102] in the eastern region.[103] By 21 August, the WHO reported a total of 15 cases and 10 fatalities.[104] No evidence suggested that this outbreak was connected to the Ugandan outbreak.[105] By 13 September 2012, the WHO revealed that the virus had claimed 32 lives and that the probable cause of the outbreak was tainted bush meat hunted by local villagers around the towns of Isiro and Viadana.[106]

2014 outbreak
Main article: 2014 West Africa Ebola outbreakpIn February 2014, a strain of the Ebola Virus appeared in Guinea. This is the first Ebola virus outbreak registered in the region. As of April 10, 157 suspected and confirmed cases and 101 deaths were reported in Guinea, 22 suspected cases in Liberia including 14 deaths, 8 suspected cases in Sierra Leone including 6 deaths, and 1 suspected case in Mali.[107][108] Investigations on these are under way.[109][110][111]By late June 2014 the death toll had reached 390 with over 600 cases reported.[112] By 23 July 2014, the World Health Organization had reported 1201 confirmed cases including 672 deaths since the epidemic began in March.[113] On July 31 2014, WHO reports the death toll has reached 826 from 1440 cases. [114]

Emory University Hospital was the first US hospital to care for patients exposed to Ebola.[115] Two American medical providers, Kent Brantly and Nancy Writebol, were exposed while treating infected patients in Liberia. Arrangements were made for them to be transported to Emory via speciality aircraft. Emory Hospital has a specially built isolation unit set up in collaboration with the CDC to treat patients exposed to certain serious infectious diseases.[116][117][118] On 2 August 2014 Brantly was flown in to Dobbins Air Force Base in Marietta, Georgia, and transferred to Emory Hospital.[119]

History

For more about the outbreak in Virginia, see Reston virus.

1280px-EbolaSubmit2

Cases of ebola fever in Africa from 1979 to 2008.

Ebola virus first emerged in 1976 in outbreaks of Ebola hemorrhagic fever in Zaire[120] and Sudan.[121] The strain of Ebola that broke out in Zaire has one of the highest case fatality rates of any human virus, roughly 90%.[122]

The name of the disease originates from one of those first recorded outbreaks in 1976 in Yambuku, Democratic Republic of the Congo (then Zaire), which lies on the Ebola River.[120]

In 1990, Hazelton Research Products’ Reston Quarantine Unit in Reston, Virginia suffered a mysterious outbreak of fatal illness among a shipment of Crab-eating Macaque monkeys imported from the Philippines. The company’s veterinary pathologist sent tissue samples from dead animals to the United States Army Medical Research Institute of Infectious Diseases (USAMRIID) at Fort Detrick, Maryland, where a laboratory test known as an ELISA assay showed antibodies to Ebola virus.

Shortly afterward, a US Army team headquartered at USAMRIID went into action to euthanize the monkeys which had not yet died, bringing those monkeys and those which had already died of the disease to Ft. Detrick for study by the Army’s veterinary pathologists and virologists, and eventual disposal under safe conditions.

The Philippines and the United States had no previous cases of Ebola infection, and upon further isolation researchers concluded it was another strain of Ebola, or a new filovirus of Asian origin, which they named Reston ebolavirus (REBOV) after the location of the incident.[123]

Some scientists also believe that the Plague of Athens, which wiped out about a third of its inhabitants during the Peloponnesian War, may have been caused by Ebola. However, these studies are conflicting, and point to other possible diseases such as typhoid.[124]

Other animals

In general, outbreaks of EVD among human populations result from handling infected wild animal carcasses. In general, declines in animal populations precede outbreaks among human populations. Since 2003, such declines have been monitored through surveillance of animal populations with the aim of predicting and preventing EVD outbreaks in humans.[125] Recovered carcasses from gorillas contain multiple Ebola virus strains, which suggest multiple introductions of the virus. Bodies decompose quickly and carcasses are not infectious after three to four days. Contact between gorilla groups is rare, suggesting transmission among gorilla groups is unlikely, and that outbreaks result from transmission between viral reservoir and animal populations.[126]

Outbreaks of EVD may have been responsible for an 88% decline in tracking indices of observed chimpanzee populations in 420 square kilometer Lossi Sanctuary between 2002 and 2003.[126] Transmission among chimpanzees through meat consumption constitutes a significant 5.2 (1.3–21.1 with 95% confidence) relative risk factor, while contact between individuals, such as touching dead bodies and grooming, do not.[127]

Domestic animals

Ebola virus can be transmitted to dogs and pigs.[128] While dogs may be asymptomatic, pigs tend to develop symptomatic disease.

Recent research

Hyperimmune equine immunoglobulin raised against EBOV was used in Russia to treat a laboratory worker who accidentally infected herself with EBOV. The treatment, however, was unsuccessful in saving her life.[129][clarification needed] Other promising experimental therapeutic regimens rely on antisense technology. Both small interfering RNAs (siRNAs) and phosphorodiamidate morpholino oligomers (PMOs) targeting the EBOV genome could prevent disease in nonhuman primates.[130][131]

Researchers from the U.S. Army Medical Research Institute of Infectious Diseases also found that FDA-approved estrogen receptor drugs used to treat infertility and breast cancer (clomiphene and toremifene) inhibit the progress of Ebola virus in infected mice.[132] Ninety percent of the mice treated with clomiphene and fifty percent of those treated with toremifene survived the tests.[132] The authors of the study concluded that given their oral availability and history of human use, these drugs would be excellent candidates for repurposing efforts to treat Ebola virus infection in remote geographical locations, either on their own or together with other antiviral drugs.

During an outbreak in the Democratic Republic of the Congo in 1995, seven of eight patients having received blood transfusions from convalescent individuals survived.[133] However, this potential treatment is considered controversial.[134]

A study in 2012 found a plant based treatment, which successfully provided protection in monkeys, administered post exposure.[135]

Antibodies against Ebola Zaire and Reston viruses have been found in fruit bats in Bangladesh, thus identifying potential virus hosts and signs of the filoviruses in Asia.

 

Why Experts Were Surprised That Ebola-Infected Doctor Could Walk Into a Hospital

Aug 2, 2014, 5:16 PM ET

By GILLIAN MOHNEY via World News

PHOTO: An ambulance arrives with Ebola victim Dr. Kent Brantly, right, to Emory University Hospital, Saturday, Aug. 2, 2014, in Atlanta.

Plane Carrying American Ebola Victim Lands in Georgia

Next Video Ebola Infected Aid Workers to Be Treated in Emory Isolation Room

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The fact that an Ebola-infected American was able to walk into a Georgia hospital today after his return to the United States surprised even medical experts familiar with the ravages of the deadly disease.

Dr. Kent Brantly arrived at Emory University Hospital today after being evacuated from Monrovia, Liberia where he was being treated for Ebola. Although Brantly had shown signs of the disease for the past week, he managed to walk into the hospital with the support of medical personnel.

All three wore protective gear to contain the deadly virus.

Brantly, along with missionary Nancy Writebol, was infected with the disease after working with Ebola-infected patients in Liberia’s capital city. This current Ebola outbreak is the worst on record and has killed more than 700 in three countries in West African and infected more than 1,300.

Before Brantly arrived in Atlanta, not much about his condition had been made public. According to Samaritan’s Purse, the aid organization he was working for, Brantly was in "serious but stable" condition before being flown to the U.S.

Get All the ABC News coverage on the Ebola Outbreak Including Videos, News, and Explainers

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Nearly 1 in 3 of all Ebola deaths in the last 40 years… have occurred since March

What is Ebola? How does it spread? Who is at risk? What you need to know

Is it safe to bring Ebola patients to the US?

When the doctor was able to walk into the hospital, at least two experts said they were surprised but pleased that the doctor seemed to be doing well.

This strain of the Ebola virus has a fatality rate of approximately 60 percent and past outbreaks had fatality rates as high as 90 percent.

Dr. William Schaffner, an infectious disease specialist at Vanderbilt University School of Medicine, said he felt "guardedly optimistic," since Ebola usually advances quickly and Brantly had shown signs of the disease for at least a week.

"The first thing we all said ‘Whoa he’s not on a vent,’" Schaffner said of realizing that Brantly did not need a ventilator to help him breathe. "In general [with] Ebola is … you progress on a downhill course. If you’re at this point and you’re holding your own you’re entitled to be optimistic."

PHOTO: Dr. Kent Brantly speaks with a worker outside the ELWA Hospital in Monrovia, Liberia

Courtesy Samaritans Purse

PHOTO: Dr. Kent Brantly speaks with a worker outside the ELWA Hospital in Monrovia, Liberia

While the incubation period can last from eight to 21 days, once someone develops symptoms they can be sick for a wider range of time. Schaffner explained that when someone shows signs of Ebola they tend to go downhill fairly rapidly and consistently.

Scaffner explained that once a person shows signs of Ebola the symptoms don’t usually disappear until the person overcomes the virus. As a result, they don’t usually have periods where they could appear healthy and relapse.

Schaffner said the fact that Brantly appeared to be well enough to walk, indicates that at least for the moment his heart rate, respiratory rate and other vital signs were not critical.

Dr. Stephen Morse, a professor of Epidemiology at the Columbia University Mailman School of Public Health, said although it does not guarantee Brantly will fully recover, the fact that he could walk 10 days after showing Ebola symptoms is a "good sign."

"If you can walk in, that’s a very good sign. I was surprised but pleasantly," Morse said of seeing Brantly walk to the hospital entrance.

PHOTO: The Ebola-stricken Americans will be treated this isolation rooms and others similar to it.

Jack Kearse/Emory University

PHOTO: The Ebola-stricken Americans will be treated this isolation rooms and others similar to it.

Morse said that Brantly was obviously not out of the woods and that he would be under constant monitoring to ensure his blood pressure, lung function, kidney function and other vitals remained steady.

"If he really does get better, we want to know his secret," Morse said.

After Brantly’s arrival, his wife Amber Brantly released a statement saying she is relieved her husband has arrived in the U.S.

"It was a relief to welcome Kent home today," Amber Brantly said in a statement. "I spoke with him, and he is glad to be back in the U.S. I am thankful to God for his safe transport and for giving him the strength to walk into the hospital."

 

2nd American With Ebola Expected to Arrive in U.S. Tuesday
Odd of a pandemic in America increases

2nd American With Ebola Expected to Arrive in U.S. Tuesday

Image Credits: Public domain

by ABC News | August 3, 2014


The plane carrying the second American patient who contracted Ebola while working in Liberia will leave the U.S. for the West African country later today and is expected to return Tuesday, a U.S. official told ABC News.

The private air ambulance is scheduled to take off today and arrive in Liberia after one stopover, the official said. The plane will then bring aid worker Nancy Writebol to Dobbins Air Reserve Base in Marietta, Ga., and is expected to land midday Tuesday.

The same plane brought Dr. Kent Brantly to Georgia on Saturday. He’s undergoing treatment at Emory University Hospital, where Writebol will be treated after she arrives in the U.S.

 

Ebola outbreak: Western drugs firms have not tried to find vaccine ‘because virus only affects Africans’, says UK’s top public health doctor

Professor John Ashton accuses pharmaceutical industry of ‘moral bankruptcy’

Jane Merrick Author Biography

Political Editor

Sunday 03 August 2014

Britain’s leading public health doctor today blames the failure to find a vaccine against the Ebola virus on the "moral bankruptcy" of the pharmaceutical industry to invest in a disease because it has so far only affected people in Africa – despite hundreds of deaths.

Professor John Ashton, the president of the UK Faculty of Public Health, says the West needs to treat the deadly virus as if it were taking hold in the wealthiest parts of London rather than just Sierra Leone, Guinea and Liberia. Writing in The Independent on Sunday, Professor Ashton compares the international response to Ebola to that of Aids, which was killing people in Africa for years before treatments were developed once it had spread to the US and UK in the 1980s.

He writes: "In both cases [Aids and Ebola], it seems that the involvement of powerless minority groups has contributed to a tardiness of response and a failure to mobilise an adequately resourced international medical response.

"In the case of Aids, it took years for proper research funding to be put in place and it was only when so-called ‘innocent’ groups were involved (women and children, haemophiliac patients and straight men) that the media, politicians, scientific community and funding bodies stood up and took notice."

The Ebola outbreak has so far claimed the lives of at least 729 people across Liberia, Guinea, Sierra Leone and Nigeria, according to the latest figures from the World Health Organisation (WHO), although the number is likely to be far higher.

Yesterday, a US relief organisation confirmed that two US aid workers who contracted the disease in Liberia had left the country. Dr Kent Brantly was being treated in a specialised hospital unit in Atlanta, Georgia, after becoming the first person with the disease to arrive on US soil yesterday evening. The second aid worker, Nancy Writebol, was due to land on a separate private flight.

On Friday, the WHO warned that the outbreak in West Africa was "moving faster than our efforts to control it". The organisation’s director general, Dr Margaret Chan, warned that if the situation continued to deteriorate, the consequences would be "catastrophic" to human life. Professor Ashton believes that more money must be funnelled into research for treatment.

"We must respond to this emergency as if it was in Kensington, Chelsea and Westminster. We must also tackle the scandal of the unwillingness of the pharmaceutical industry to invest in research [on] treatments and vaccines, something they refuse to do because the numbers involved are, in their terms, so small and don’t justify the investment. This is the moral bankruptcy of capitalism acting in the absence of a moral and social framework."

Western countries are on high alert after Patrick Sawyer, a civil servant for the Liberian government, died last week after arriving at Lagos airport – the first known case in Nigeria. International airline hubs are the focus of attention because of the high volume of passengers flying into and out of West Africa every day. Dubai’s Emirates airline began a ban yesterday on its flights in Guinea over the crisis, with the suspension lasting until further notice.

Professor Ashton welcomed the decision by the Foreign Secretary, Philip Hammond, to convene a meeting of the Government’s crisis committee, Cobra, last week to discuss the UK’s preparedness for cases of Ebola in this country.

Development of a vaccine is in the early stages in the US, but this is on a small scale and there is little hope of one being ready to treat the current outbreak in West Africa. Dr Anthony Fauci, the director of the National Institutes of Health, an agency of the US Department of Health and Human Services, has said it has plans possibly to begin testing an experimental Ebola vaccine on people in mid-September, following encouraging results in pre-clinical trials on monkeys. Earlier this month, the US Food and Drug Administration put a hold on a trial upon healthy volunteers by Tekmira Pharmaceuticals Corporation to ensure their potential Ebola treatment has no ill-effects, as it sought more information to ensure the safety of volunteers.

Professor Ashton said: "The real spotlight needs to be on the poverty and environmental squalor in which epidemics thrive and the failure of political leadership and public health systems to respond effectively. The international community has to be shamed into real commitment… if the root causes of diseases like Ebola are to be addressed."

 

Ebola: covert op in a hypnotized world

Ebola: covert op in a hypnotized world

Image Credits: YouTube

by Jon Rappoport | August 3, 2014


You show people a germ and you tell them what it is and what it does, and people salute. They give in. They believe. They actually know nothing. But they believe.

The massive campaign to make people believe the Ebola virus can attack at any moment, after the slightest contact, is quite a success.

People are falling all over themselves to raise the level of hysteria.

This is what is preventing a hard look at Liberia, Sierra Leone, and the Republic Guinea, three African nations where poverty and illness are staples of everyday life for the overwhelming number of people.

The command structure in those areas has a single dictum: don’t solve the human problem.

Don’t clean up the contaminated water supplies, don’t return stolen land to the people so they can grow food and finally achieve nutritional health, don’t solve overcrowding, don’t install basic sanitation, don’t strengthen their immune systems so they can ward off germs, don’t let the people have power—because then they would throw off the local and global corporate juggernauts that are sucking the land of all its resources.

In order not to solve the problems of the people, a cover story is necessary. A cover story that exonerates the power structure.

A cover story like a germ.

It’s all about the germ. The demon. The strange attacker. (See, for example, this March 27th, Reuter’s article entitled “Beware of bats: Guinea issues bushmeat warning after Ebola outbreak”.)

Forget everything else. The germ is the single enemy.

Forget the fact, for example, that a recent study of 15 pharmacies and 5 hospital drug dispensaries in Sierra Leone discovered the widespread and unconscionable use of beta-lactam antibiotics.

These drugs are highly toxic. One of their effects? Excessive bleeding.

Which just happens to be the scary “Ebola effect” that’s being trumpeted in the world press.

(J Clin Microbiol, July 2013, 51(7), 2435-2438), and Annals of Internal Medicine Dec. 1986, “Potential for bleeding with the new beta-lactam antibiotics”)

Forget the fact that pesticide companies are notorious for shipping banned toxic pesticidesto Africa. One effect of the chemicals? Bleeding.

Forget that. It’s all about the germ and nothing but the germ.

Forget the fact that, for decades, one of the leading causes of death in the Third World has been uncontrolled diarrhea. Electrolytes are drained from the body, and the adult or the baby dies.

Any sane doctor would make it his first order of business to replace electrolytes with simple supplementation—but no, the standard medical line goes this way:

The diarrhea is caused by germs in the intestinal tract, so we must pile on massive amounts of antibiotics to kill the germs.

The drugs kill off all bacteria in the gut, including the necessary and beneficial ones, and the patient can’t absorb what little food he has access to, and he dies.

Along the way, he can also bleed.

But no, all the bleeding comes from Ebola. It’s the germ. Don’t think about anything else.

Forget the fact that adenovirus vaccines, which have been used in Liberia, Guinea, and Liberia (the epicenter of Ebola), have, according to vaccines.gov, the following adverse effects: blood in the urine or stool, and diarrhea.

No, all the bleeding comes from the Ebola germ. Of course. Don’t think about anything else.

Reporter Charles Yates uncovered a scandal in Liberia centering around the Firestone Rubber Plantation—chemical dumping, poisoned water.

And skin disease.

“Rash” is listed as one of the Ebola symptoms.

So is diarrhea.

Liberia Coca Cola bottling plant: foul black liquid seeping into the environment—animals dying.

Chronic malnutrition and starvation—conditions that are endemic in Liberia, Sierra Leone, and Guinea—are the number-one cause of T-cells depletion in the world.

T-cells are a vital component of the immune system. When that system is compromised, any germ coming down the pipeline will cause epidemics and death.

Getting the picture?

Blame it all on the germ.

Allow the corporate-government domination to continue.



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.

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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.

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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 Unfor