Category: Nature Medicine


It’s all scripted! Ebola outbreak and impossibly rapid vaccine response clearly scripted; U.S. govt. patented Ebola in 2010 and now owns all victims’ blood


It’s all scripted! Ebola outbreak

and impossibly rapid vaccine

response clearly scripted; U.S.

govt. patented Ebola in 2010

and now owns all victims’ blood

September 21, 2014 2:39 pm EST

By Mike Adams | Natural News

On the very same day that vaccine maker GlaxoSmithKline is being fined $490 million by Chinese authorities for running an illegal bribery scheme across China [3], the media is announcing the “astonishing” launch of human trials for an Ebola vaccine.

Care to guess who will be manufacturing this vaccine once it is whitewashed and rubber-stamped as “approved?” GlaxoSmithKline, of course. The same company that also admitted to a massive criminal bribery network in the United States, where felony crimes were routinely committed to funnel money to over 40,000 physicians who pushed dangerous prescription drugs onto patients.

This is the company that is now — today! — injecting 60 “volunteers” with an experimental Ebola vaccine.

Spontaneous vaccine development a scientific impossibility

“Normally it would take years of human trials before a completely new vaccine was approved for use,” reports the BBC. [1] “But such is the urgency of the Ebola outbreak in west Africa that this experimental vaccine is being fast tracked at an astonishing rate.”

Yes, it’s astonishing because it’s impossible.

As any vaccine-related virologist already knows, the process of going from an in-the-wild infection of Ebola to a manufactured vaccine ready for human trials simply cannot be achieved in a matter of a few weeks or months. Apparently, we are all to believe that a spontaneous scientific miracle has now taken place — a literal act of vaccine magic — which has allowed the criminal vaccine industry to skip the tedious R&D phases and create a vaccine ready for human trials merely by waving a magic wand.

“The first of 60 healthy volunteers will be injected with the vaccine,” says the BBC today, and vaccine pushers are of course lining up to proclaim the vaccine miracle which has spontaneously appeared before them like a burning bush:

Professor Adrian Hill, director of the Jenner Institute in Oxford, who is leading the trial, said: “This is a remarkable example of how quickly a new vaccine can be progressed into the clinic, using international co-operation.”

Near-proof that this was all scripted

The far more likely explanation, of course, is that all this was scripted in advance: the outbreak, the international cry for help, the skyrocketing of the stock price for Tekmira (which has received financial investments from Monsanto), the urgent call for a vaccine and now the spontaneous availability of human vaccine trials. It’s all beautifully scripted from start to finish, better than a Shakespearean tragedy played out on the international stage.

The “heroes” of this theater have been pre-ordained to be drug companies and vaccines, and it is already written in the script that vaccines will be heralded as lifesaving miracles of modern science even if they infect people and cause widespread damage as has now happened to young girls in Colombia who are being hospitalized en masse after being injected with HPV vaccines. [2]

Incredibly, the official response from vaccine-pushing health authorities in Colombia is that all these girls who are suffering from paralysis are merely “imagining” their symptoms and suffering from “mass hysteria.” Obviously, if vaccines are created by the gods of modern science — the new cult of our delusional world — then they must be perfect and infallible. Therefore, anyone who suffers side effects of such perfect vaccines must obviously be imagining things. Such is the delusional dogma of modern vaccine pushers.

This will be the exact same explanation leveled against anyone who suffers harmful effects from an Ebola vaccine, too. After all, the discovery of vaccine side effects simply isn’t in the script being played out before us. Therefore, it cannot be allowed, and any person who actually suffers side effects will be immediately deemed to be mentally ill. (Yes, this is how insane and Orwellian the vaccine industry has become. All who do now bow down to the voodoo of dangerous vaccines are labeled mental patients and then treated with psychiatric drugs. The vaccine industry has quite literally become the Heaven’s Gate Cult of modern medicine…)

The United States government now owns the patent on Ebola

This plot gets even more interesting when you realize that a patent on Ebola was awarded to the United States government just four years ago, in 2010.

That patent, number CA2741523A1, is available here.

Astonishingly, the patent claims U.S. government ownership over all variants of Ebola which share 70% or more of the protein sequences described in the patent: “[CLAIMS] …a nucleotide sequence of at least 70%-99% identity to the SEQ ID…”

Furthermore, the patent also claims ownership over any and all Ebola viruses which are “weakened” or “killed,” meaning the United States government is literally claiming ownership over all Ebola vaccines.

What this means, of course, is that the U.S. government can demand royalties on all Ebola vaccines.

Even more Orwellian is the fact that the U.S. government can use this patent to halt all other research for treatments or cures for Ebola.

Patent monopoly gives U.S. government legal right to block all non-vaccine Ebola treatments, cures or research

Do you remember the massive medical controversy over the BRCA1 gene tied to breast cancer in women? One corporation claimed patent ownership over the gene and then they used that patent to shut down all other research, testing or diagnosis of breast cancer related to that gene. To date, nearly 20% of the human genome has been claimed as “owned” by corporations, universities and even the government.

The controversy went all the way to the U.S. Supreme Court which ultimately ruled that human genes cannot be patented. But the Supreme Court decision actually protected patents on gene sequences for viruses and other pathogens.

The truth of the matter is that anyone who owns the Ebola gene patent can legally use that patent to shut down all research on Ebola, including research for non-vaccine medical treatments and cures. This is how medical monopolies are reinforced: by monopolizing all the research and all the “cures.”

Even more frightening, the “ownership” over Ebola extends to Ebola circulating in the bodies of Ebola victims. When Dr. Kent Brantly was relocated from Africa to the CDC’s care in Atlanta, that entire scene was carried out under the quasi-legal justification that the U.S. government “owned” the Ebola circulating in Dr. Brantly’s blood. Thus, one of the very first things that took place was the acquisition of his blood samples for archiving and R&D by the CDC and the U.S. Department of Defense.

(Only the gullible masses think that was about saving the life of a doctor. The real mission was to acquire the Ebola strain circulating in his body and use it for weaponization research, vaccine research and other R&D purposes.)

Anyone infected with Ebola now deemed to be carrying “government property” in the form of a patented virus

This brings us to the quarantine issue. As the whole world knows by now, the entire nation of Sierra Leone is now under a state of medical martial law, where Ebola victims are now being hunted down like fugitives in door-to-door manhunts. [4]

Simultaneously, the United States government is now operating under Obama’s executive order #13674, signed on July 31, 2014, which allows the U.S. federal government to arrest and quarantine any person who shows symptoms of infectious disease. [5]

This executive order allows federal agents to forcibly arrest and quarantine anyone showing symptoms of:

…Severe acute respiratory syndromes, which are diseases that are associated with fever and signs and symptoms of pneumonia or other respiratory illness, are capable of being transmitted from person to person, and that either are causing, or have the potential to cause, a pandemic, or, upon infection, are highly likely to cause mortality or serious morbidity if not properly controlled.

Part of the legal argument for justifying such a quarantine in the case of Ebola goes like this: If you are carrying Ebola in your body, then you are in possession of U.S. government property!

The fact that the virus is replicating in your body is, legally speaking, a violation of patent law. Because you are providing a host environment for the replication of the virus, you technically are breaking federal laws that restrict the copying and distributed of patented properties, which in this case include the Ebola virus.

Thus, the government has every right to “relocate” you and prevent you from violating patent law by replicating, distributing or spreading THEIR intellectual property (i.e. the Ebola virus).

Lest you think this legal argument sounds insane, just remember that the legal system is full of lawyers who make far more insane arguments on a daily basis, including the argument that human genes could be patented in the first place. And medical officials also make insane, irrational arguments almost constantly, including the argument that all those girls in Colombia who are suffering convulsions and paralysis from the HPV vaccine are merely “imagining” their symptoms. Such explanations flatly defy any attachment to sane thinking.

Ultimately, the patent on the Ebola virus provides the legal justification for forced government quarantines — and even medical research — on Ebola victims.

“Ebola is a genetically modified organism”

What I’ve outlined in this story is just a small taste of the crime against humanity which is taking place right before our eyes. I am now convinced that this Ebola outbreak is very likely not an accident, and many scientists in Africa wholeheartedly agree that the outbreak is actually the deployment of a biological weapon.

“Ebola is a genetically modified organism (GMO),” declared Dr. Cyril Broderick, Professor of Plant Pathology, in a front-page story published in the Liberian Observer. [6]

He goes on to explain:

[Horowitz] confirmed the existence of an American Military-Medical-Industry that conducts biological weapons tests under the guise of administering vaccinations to control diseases and improve the health of “black Africans overseas.”

SITES AROUND AFRICA, AND IN WEST AFRICA, HAVE OVER THE YEARS BEEN SET UP FOR TESTING EMERGING DISEASES, ESPECIALLY EBOLA

The World Health Organization (WHO) and several other UN Agencies have been implicated in selecting and enticing African countries to participate in the testing events, promoting vaccinations, but pursuing various testing regiments.

AFRICAN LEADERS AND AFRICAN COUNTRIES NEED TO TAKE THE LEAD IN DEFENDING BABIES, CHILDREN, AFRICAN WOMEN, AFRICAN MEN, AND THE ELDERLY. THESE CITIZENS DO NOT DESERVE TO BE USED AS GUINEA PIGS!

Africa must not relegate the Continent to become the locality for disposal and the deposition of hazardous chemicals, dangerous drugs, and chemical or biological agents of emerging diseases. There is urgent need for affirmative action in protecting the less affluent of poorer countries, especially African citizens, whose countries are not as scientifically and industrially endowed as the United States and most Western countries, sources of most viral or bacterial GMOs that are strategically designed as biological weapons. It is most disturbing that the U. S. Government has been operating a viral hemorrhagic fever bioterrorism research laboratory in Sierra Leone.

The world must be alarmed. All Africans, Americans, Europeans, Middle Easterners, Asians, and people from every conclave on Earth should be astonished. African people, notably citizens more particularly of Liberia, Guinea and Sierra Leone are victimized and are dying every day.

Learn the truth at BioDefense.com

If you really want to learn the truth about all this, listen to the free Pandemic Preparedness audio course available right now at www.BioDefense.com

All MP3 files are freely downloadable, and new episodes are being posted every few days.

Also check out these 11 horrifying truths about Ebola that you’re not supposed to know.

Nearly one million people have now visited www.BioDefense.com since its launch last week. Find out there what the mainstream media won’t dare tell you. Your life may quite literally depend on it.

Sources for this article include:
[1] http://www.bbc.com/news/health-29230157

[2] http://news.yahoo.com/mystery-illness-plague…

[3] http://www.bbc.com/news/business-29274822

[4] http://www.naturalnews.com/046945_medical_ma…

[5] http://www.federalregister.gov/articles/2014…

[6] http://www.liberianobserver.com/security/ebo…

[7] http://www.google.com/patents/CA2741523A1

[8] http://www.naturalnews.com/036417_Glaxo_Merc…

[9] http://www.naturalnews.com/046259_ebola_outb…

[10] http://www.naturalnews.com/040400_gene_paten…

[11] http://www.naturalnews.com/028492_BRCA1_huma…

[12] http://www.thecommonsenseshow.com/2014/09/17…

This article originally appeared on Natural News.

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


Ebo-Lie: Man Living In Ghana

Confirms Ebola Is A Hoax!

Saturday, November 1, 2014 12:05

(Before It’s News)

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

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

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

REASONS:

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

Reason 1:

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

Reason 2:

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

Reason 3:

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

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

Reason 4:

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

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

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

The original piece written by him can be found here.

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

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

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

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

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

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

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

 

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

Patent applicants are clearly described on the patent as including:

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

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

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

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

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

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

Sources: Listed within the article

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

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


Countries that have confirmed cases of Ebola

Below is a list of countries that have confirmed cases of Ebola: Is Mainstream media facilitating mass murder by omitting facts?

Below is a list of countries that have confirmed cases of Ebola:
· Every country in Africa
· Spain
· Italy
· France
· Germany
· Poland
· Greece
· Turkey
· Saudi Arabia
· Yemen
· Oman
· Iran
· Kuwait
· Vietnam
· Myanmar
· India
· Indonesia
· Australia
· China
· Brazil
· Venezuela
· Mexico
· United States
· Canada
What you’re seeing here is the initial global footprint of the Ebola virus. It is most likely that each one of the above countries has more than one case; and, they are struggling to maintain the public’s confidence. We should see a second global wave of Ebola cases following a brief incubation period. The secondary global outbreak will be under-reported, as well. Around the end of October/beginning of November, during the tertiary wave, it will become apparent this is a global pandemic that has spiraled completely out of control.
At this point, economies will start to falter, airline travel will decline rapidly, and governments around the world will blame each other for lack of truthfulness.
One may appropriately expect the spread of Ebola through the international community to look like the spread of Enterovirus-68 in the United States:
1. Initial outbreaks played down and under-reported.
2. Initial reporting suggests the government and health agencies are responding appropriately.
3. Spread has reached several states.
4. Number infected suggests it is completely out of control.
5. Confirmation that it is completely out of control.
6. Increase in morbidity and mortality.
7. Public panic ensues.
It is possible the spread of Ebola will burn through the population like the flu-both have similar infection mechanisms and life expectancies in the external environment. Let’s pray this assessment is completely wrong!

Oct 6, 2014


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

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

High security laboratory

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

marburg

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

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

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

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

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

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

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

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

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

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

bird_flu

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

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

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

F2.medium

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

H5N1virus

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

h5n1

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

bird-flu-0002

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

Influenza A Pandemics

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

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

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

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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.

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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.

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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.)

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.


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.

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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.

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.

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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.

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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.

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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.

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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.

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.
 
featured-image-2
 
Antibodies to Cedar virus were shown to cross react with, but not cross neutralize Hendra or Nipah virus. Despite this close relationship, when Cedar virus was tested in experimental challenge models in ferrets and guinea pigs, we identified virus replication and generation of neutralizing antibodies, but no clinical disease was observed. As such, this virus provides a useful reference for future reverse genetics experiments to determine the molecular basis of the pathogenicity of the henipaviruses.

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

 3246969817

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

photo1

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

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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.

Tuberculosis550_ab

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

tuberculosis_incidence_global_2011

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

Mycobacterium_tuberculosis

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

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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
800px-Tick-Borne_Encephalitis_Virus

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

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

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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.)

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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

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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.

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.

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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.

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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.

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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.

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.

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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?

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.

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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.

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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.

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.


 

cancer

Chemotherapy backfires – causes healthy cells to feed growth of cancer tumors

Tuesday, August 07, 2012
by Mike Adams, the Health Ranger
Editor of NaturalNews.com

Learn more: http://www.naturalnews.com/036725_chemotherapy_cancer_tumors_backfires.html#ixzz22yleICAl

(NaturalNews) Ever since chemotherapy was introduced into the practice of western medicine, doctors and oncologists have been trying to answer this nagging question: Why does chemotherapy seem to work at first, but then cancer tumors cells grow back even more aggressively while the body becomes resistant to chemotherapy?
It turns out that chemotherapy damages healthy cells, causing them to secrete a protein that accelerates the growth of cancer tumors. (http://ca.news.yahoo.com/chemotherapy-backfire-boost-cancer-growth-st…)
This protein, dubbed “WNT16B,” is taken up by nearby cancer cells, causing them to “grow, invade, and importantly, resist subsequent therapy,” said Peter Nelson of the Fred Hutchinson Cancer Research Center in Seattle. He’s the co-author of the study that documented this phenomenon, published in Nature Medicine.
This protein, it turns out, explains why cancer tumors grow more aggressively following chemotherapy treatments. In essence, chemotherapy turns healthy cells into WNT16B factories which churn out this “activator” chemical that accelerates cancer tumor growth.
The findings of the study were confirmed with prostate cancer, breast cancer and ovarian cancer tumors. This discovery that chemotherapy backfires by accelerating cancer tumor growth is being characterized as “completely unexpected” by scientists.

The chemotherapy fraud exposed

As NaturalNews has explained over the last decade, chemotherapy is medical fraud. Rather than boosting the immune response of patients, it harms the immune system, causing tumors to grow back. This latest researching further confirms what we’ve known for years in the holistic health community: That chemotherapy is, flatly stated, poison. It’s not “treatment,” it’s not medicine, and it’s not prevention or a cure. It’s poison with virtually no medicinal value except in perhaps one to two percent of cancer cases.
The No. 1 side effect of chemotherapy is, by the way, cancer. Cancer centers should technically be renamed “poison centers” because they are in the business of poisoning patients with a toxic cocktail of chemicals that modern science reveals to be a cancer tumor growth accelerant!
Learn more: http://www.naturalnews.com/036725_chemotherapy_cancer_tumors_backfires.html#ixzz22ylTmtzw

The $200 Billion Scam

By Jeff Kamen

Why the government tries to bury the real cures.

Kathy Keeton‘s successful battle against cancer is more than personal good news–it has blown open a Washington scandal of astonishing proportions.

She wears fitted black pants and an ivory blouse accented by wisps of silk, which the warm wind wraps tightly around her dancer’s body. A man walking his white miniature French poodle directly in her path cannot keep from staring, and she has to tack around him to rendezvous with the sleek limo waiting at the corner for her and the solidly built man who follows a few paces back. *She is one of those graceful women you usually see only in the pages of high-fashion magazines. The angular bone structure, the edgy style, the controlled, hard-bodied personal power, is all hallmarks of her thoroughbred beauty. Such women compel us, but also keep us at a distance. You could empathize with the guy with the dog, who for a moment couldn’t move when she appeared out of nowhere and seemed to float straight at him. He probably missed the strange-looking leather case hanging from her right shoulder. A slim tube runs from the box discreetly into her clothing and then into her. It is a self-administered pain-control unit. Whenever the pain from the cancer she is fighting becomes too much to bear, she presses a button and another dose of medication pushes into her bloodstream, driving back the agony one more time. Kathy Keeton, Vice-Chairman of General Media International and wife of Penthouse Publisher Bob Guccione, enters the limo, curls into the deep leather seat, and reaches with her right hand to smooth her husband’s windblown hair. He has just closed the door, ordered the driver to head for Kennedy Airport, and asked after the comfort of a guest who is sitting on the floor in front of them, struggling to insert a balky cassette into a tape recorder. As the low-tech problem is being solved, Keeton stares out the window, watching the East Side of Manhattan pass in review. It was six months since they were at Cannes, on the eve of the opening of the 1995 film festival. There, suddenly, Kathy had become ill – deeply, nauseatingly ill. At first she figured it was food poisoning. Nothing else made much sense. Only six weeks earlier she had passed her annual physical, including a mammogram, with a perfect score. What would you expect from the founder of Longevity magazine and a global advocate of healthy living, who not only talked the talk but also danced the steps of vigorous exercise and high-fiber diet. Nevertheless she fell deeper into the unexplained illness, and Bob flew them home immediately.

Within hours of landing in New York City, Kathy was seen byher family physician, which probed, listened, and did not like what he suspected. He did some tests, told her to come back in a few hours, and then ordered her to see a specialist a few blocks away. Minutes later Kathy Keeton walked into the oncologist’s office, was directed to a small cubicle, where she removed and folded her clothes, put on a hospital gown, and waited for the doctor to examine her and tell her what was happening to her. In that moment of waiting Kathy began to know in her gut that something truly awful was wrong.

“I’m sorry,” she remembers her doctor saying. “It’s a very rare form of the disease. It’s called galloping breast cancer, because it starts by spreading rapidly from what had only recently appeared to be perfectly healthy tissue. The mammogram we took six weeks ago was not in error. The cancer simply wasn’t detectable at that time. It’s the nature of this kind of cancer that it takes off at a gallop, and metastasizes quickly So we need to act quickly, get you started on chemotherapy at once. We have some of the best people in the world in this field here at Mount Sinai, and I urge you to let me get you into their expert care. There is no time to waste. This form of cancer is often fatal, and quickly so. Untreated, you have six weeks to live. We really must move aggressively with the chemo.” In this circumstance most people immediately surrender to the direction of their doctors and undergo one of the great gambles of modern medicine. They begin a regimen of cell-poisoning chemotherapy, hoping that the powerful drugs will kill their tumors. Along the way the chemo usually shatters the life of the patient with waves of horrendous nausea and pain.

Many cannot bear the suffering, and choose to drop the chemo and be sedated until the inevitable occurs. For those who endure the chemo the outlook is not good, statistically. Only about 20 percent of patients are cured. The rest die anyway

Kathy and her husband knew a lot about all of this, years before it happened to her. Their magazines reported on cancer research and controversy. For more than a decade Kathy and Bob had published investigative stories about the work of Joseph Gold, M.D., a former U.S. Air Force research physician and now director of the Syracuse (New York) Cancer Research Institute.

Gold had discovered that small doses of hydrazine sulfate, a chemical used in rocket fuel, could function as an effective anti-cancer drug, and did so without any of the side effects of standard chemotherapy. Gold’s discovery, which first attracted the attention and support of the cancer establishment in the mid-1970s, just as quickly earned the enmity of the chemotherapists who had taken over the leadership of the federal war on cancer. If Gold’s experimental drug turned out to be as efficacious as initial studies and case reports indicated, there would be a lot less demand for chemotherapy. Further complicating matters, hydrazine sulfate is dirt cheap, unlike standard cytotoxic chemotherapy agents. The price of a single dose of chemo would buy a ten-year supply of hydrazine sulfate.

Kathy and Bob decided to hold off the Mount Sinai team, and called in Dr. Gold to see if, after all those years of supporting hydrazine sulfate in their magazines, the drug might work for them.

Gold examined Kathy and recommended a course of hydrazine sulfate. The Mount Sinai team warned Kathy that hydrazine sulfate would be a waste of her rapidly diminishing time. Kathy and Bob put up a united front, demanding that their doctors support Dr. Gold’s recommendations and make sure the hydrazine sulfate was properly dispensed to her in the hospital and subsequently at home, according to the established, published protocol. The doctors watched disapprovingly as, taking her first hydrazine capsule, Kathy waited and prayed.

Her diary entry for Saturday, August 11, 1995:
Joe Gold is my shepherd, I shall not die,
He leadeth me thru green pastures.
Yea, though I walk through the valley of
the shadow of the Crab, his care and
his calls shall comfort me, and / shall
dwell in the house of Hydrazine forever

In the pursuit of this story what has been uncovered is a skein of lies and betrayal-not by politicians or C.I.A. spooks, but by physicians and health-care investigators, many of whose salaries your federal taxes pay. It begins with the National Cancer Institute, pulls in the Food and Drug Administration, and ends up-perhaps most shockingly-with the U.S. General Accounting Office, Congress’s own investigative agency.

In the 25 years since the federal government declared war on cancer, an estimated $200 billion has been spent by U.S. taxpayers and private investors on research that has produced so little bang for the buck that it makes the Pentagon’s $600 toilet seats look like bargains for every American home. The cancer industry has become a huge jobs program for brilliant, even highly motivated, doctors and other scientists, whose efforts are misguided by the economic forces behind the industry. Directly put, it’s in the interests of all the fat cats in government and private enterprise who earn their living and status from what is largely a failed enterprise, to stick with it. That is why a drug like hydrazine sulfate is dumped on by the cancer establishment, instead of given legitimate support and honest evaluation.

The GAO–with its proud past of fair, impartial audits of the performance of other federal agencies-appears to have done something underhanded in the case of hydrazine sulfate. It has demonstrated a level of incompetence and avoidance of controversy that’s stunningly atypical of this investigative agency and its track record of unflinching pursuit of the truth without fear or favor. In fact the tenor of the incompetence leads to the inescapable conclusion that a deliberate deceptions cover-up-was perpetrated to save other federal officials and the government itself from a scandal of astonishing proportions.

The GAO defied logic, reason, and science to give its blessing to what in fact has to be seen as the NCI’s deliberately biased testing of hydrazine sulfate, which falsely made the drug appear to be without merit. What is so damaging to the GAO is that its investigators did their fact-finding jobs well, but the higher-ups who wrote that agency’s report avoided the inescapable conclusion that the NCI had betrayed the medical community and cancer patients everywhere by rigging the clinical trials.

The GAO’s investigators began their work by going through more than 100 pages of documents and hours of videotape obtained by Penthouse in pursuing this story over the preceding three years. They confirmed many of the allegations brought to them by Penthouse. The crucial consideration is that established medical practice forbids the use of alcohol, tranquilizers, or sleeping pills by patients taking hydrazine sulfate because those “incompatible agents” not only deactivate hydrazine’s therapeutic powers but also can make the sufferers much sicker. The GA0 investigators smoked out the truth that in its initially published study results the NCI chose not to reveal the ingestion of those incompatibles by the participants in its nationwide clinical trials of hydrazine sulfate.

Under pressure from the GAO investigators, doctors who conducted one of the NCI trials admitted in a letter to the Journal of Clinical Oncology that virtually all of the subjects had taken tranquilizers while receiving hydrazine sulfate.

Despite those admissions, the GAO still managed in its report to declare that the NCI’s trials “were not flawed.” That’s the equivalent of describing a car as having a broken transmission, four punctured tires, and useless brakes, but the vehicle is nevertheless just fine, thank you, and quite capable of carrying you safely on the interstate. In this pronouncement the GAO participated in wrecking the hopes of millions of cancer sufferers, dooming many to unnecessary suffering or premature and painful death.

In the “In” baskets of the upper echelons of the GAO there sits a direct challenge to the integrity and credibility of that much-admired organization. It is an unanswered eight-page letter from Dr. Gold, who as a young physician was part of the NASA medical team that made sure Colonel John Glenn was fit for his historic mission. For the past quarter-century Joe Gold has been fighting to win from the American cancer establishment acceptance of the astonishingly effective and inexpensive anti-cancer drug that he developed. For most of those 25 years the most influential people at the NCI and its major grantee institutions have rejected and vilified hydrazine sulfate, which costs less than a dollar a day and has no significant side effects when the established protocol is properly followed.

When the NCI published its deeply flawed taxpayer-funded national tests of the drug, making it appear ineffective, the FDA stopped issuing “compassionate use” permissions for physicians requesting hydrazine sulfate for their patients. That choked off the very limited official supply of the drug, prompting desperate patients-as well as some physicians whose own loved ones’ lives were hanging by a wire-to seek other, unofficial lines of supply.

One respected member of the cancer establishment, medical oncologist Lynn H. Ratner, M.D., who has a private practice in New York, is on the faculty of the Mount Sinai School of Medicine. He runs the cancer-education program for physicians at Lenox Hill Hospital and has decided to go public (see sidebar at end of article) with his own use of hydrazine sulfate.

Dr. Ratner told me in April of this year: “There are over 25 patients taking hydrazine sulfate [in our practice], 15 of them under my direct care…. The drug has helped my patients avert the terrible effects of cachexia [cancer-induced starvation]…. It is important to note that this drug is working against cachexia in all 15 cases that I am personally monitoring.

“It is abundantly clear to me that hydrazine sulfate deserves another clinical trial that would be conducted in a double-blind fashion in good-risk candidates who are not taking other anti-cancer drugs.”

“On the important issue of incompatibility, I think Dr. Gold is right, and the NCI needs to conduct the trials differently. The new clinical trials I am calling for should exclude those substances identified as incompatible, and it should be fair and impartial, without the biases that afflicted previous nationwide multi-institution clinical trials run by the NCI You can’t argue with the kind of success I am seeing in my patients.”

As this article was going to press Dr. Ratner told me he had begun documenting antitumor activity in one patient receiving only hydrazine sulfate.

If there is anyone in your life who has cancer, this article will be very personal indeed. It has been personal for me for a long time. It was nine years ago that I first learned of hydrazine sulfate. It was prescribed for my mother as a last-ditch treatment. She had nothing to lose; she had smoked her way into lung cancer, which ultimately spread to her brain and throughout her body. Erna Kamen was only 64 and an athlete, but none of that helped much. The surgeons and radiation specialists had done everything they could. At one point, to get even more radiation therapy than is generally allowed, she signed a release authorizing the doctors to give her yet another course of radiation. The family joke was that one more treatment and she would glow in the dark. Despite our hopes and prayers, the cancer continued its relent less assault, and further treatment was deemed to be useless.

As the widespread tumors disrupted her system’s capacity to process nutrients, her body shrank. My mom lost massive amounts of weight, along with her mental acuity. She virtually disappeared into her bedclothes. After yet another race to the hospital emergency room, I was told by her oncologist that she had only days to live, and that we should “take her home and make her as comfortable as possible” until she died.

The next day, at the direction of the oncologist, she started hydrazine sulfate. She managed with some water to swallow one capsule. We didn’t have much hope that it would do anything for her. After all, only hours earlier the NCI’s 1-(800)-4-CANCER public-information line had told us that hydrazine sulfate was worthless.

I needed to escape from the mounting emotional pain. So I pulled on shorts and shoes for an hour’s hard run, determined to numb my brain by pounding the concrete drawbridges and blacktop that lead to downtown Sarasota, Florida. Finally exhausted, I returned, showered, and fell into a deep, troubled sleep. Next thing I knew, my mother’s nurse was shaking me awake.

“Is she gone?” I asked
The nurse laughed.

“Gone? Are you kidding? I don’t believe it. She’s trying to sit up in bed, and she wants you to get up there. Listen! That’s her yelling for you to join her for breakfast. She actually wants to eat! “Hydrazine sulfate was my mom’s ticket to renewed life, and it brought her back for about four months, much of which she enjoyed. Although she back 23 pounds, hydrazine sulfate didn’t get a chance to do everything it could for her. She died after her medical team had made a major error in judgment: Her medication was switched, and she was taken off hydrazine sulfate.

Kathy Keeton sits at her computer, answering anxious e-mail queries about the drug. Much of her legendary energy has returned, which she now uses tirelessly to help other patients with cancer. She has hired a staff and provided it with space in the Penthouse offices, from which answers are sent to the thousands of inquiries received by Penthouse each week, as well as information on how to obtain hydrazine sulfate. Kathy has gone public with her experience. She has been in print in dozens of newspapers, on television and radio in the US and Europe. All of which has thrown a spotlight on peer-reviewed medical literature affirming the drugs safety and efficacy at all stages of cancer.

But despite her advocacy of hydrazine sulfate, Kathy is outspoken in her gratitude to the staff at Mount Sinai for helping her fight for her life. “The doctors are really wonderful, and I can’t say enough in praise of the warm and supportive nurses who did everything in their power for me,” she says with passion. “It’s not their fault that the medical establishment they’re part of prevents them from appreciating hydrazine. It’s the NCI that’s the real villain here.”

Almost a decade earlier thousands of people called in to TV stations, seeking information and help, in response to the seven times I appeared on Independent Network News, 1988 to 1990, reporting on the hydrazine-sulfate story and-on four of those broadcasts-the story of my mother.

Feeling the mounting pressure from my broadcasts and from Penthouse’s investigations, as well as ten years of double-blind positive clinical studies reported by UCLA’s Harbor Hospital, the National Cancer Institute finally went forward. Its long-awaited multi-institutional Phase III clinical trials of hydrazine sulfate got under way in 1989 and 1990. I had hoped that my report would in part lead to the rescue of hundreds of thousands of cancer patients who would soon gain access to this low cost, uniquely effective medication. But that sweet dream would become a nightmare.

By April of 1993 1 was writing in Penthouse that the NCI had prejudiced its nationwide testing of hydrazine sulfate by including in its study an unspecified number of cancer patients who had not been kept from using alcohol, tranquilizers, or barbiturates. This was incomprehensible.

Even the FDA itself had long warned physicians administering the drug to make sure patients did not consume alcohol, tranquilizers, or sleeping pills. (For almost ten years the FDA had made hydrazine sulfate available to doctors on a “Compassionate Use” basis.) I brought all this information plus supporting documentation (more than 100 pages) to the House of Representatives subcommittee with oversight responsibility for the NCI.

In Penthouse for July 1994 I wrote about the Russian oncology-research community’s illuminating experience with hydrazine sulfate. There, it has been brought to bear against a broad array of “incurable” cases of lung, lymphatic, and 30 other types of cancer, with surprisingly good results, for what is now almost a quarter century. One of the more startling findings by the Russians is hydrazine sulfate’s effectiveness against cancerous and non-cancerous tumors of the brain. Non-cancerous brain tumors are fearsome because they expand until they crowd out the brain, causing blindness, paralysis, and death. The Russians report that hydrazine-sulfate treatment results in a 45-percent response rate for cancerous brain tumors and a 65-percent response rate for non-cancerous brain tumors. The Russian doctors strictly forbid the use of alcohol, barbiturates, or tranquilizers by patients on the treatment. As one prominent Russian researcher (and former NCI consultant), Michael Gershanovich, M.D., told me: “Why would you want to give these things to patients receiving the hydrazine sulfate? The hydrazine sulfate would not work, and that would be wrong.”

At the Petrov Research Institute of oncology in St. Petersburg I heard a great deal about the Russian doctors’ fear of offending America’s all-powerful, grant-giving NCI -an institution with which the Petrov had enjoyed 17 years of collegial relations via the Joint U.S. – USSR Cancer Agreement.

But in the United States the NCI – sponsored researchers chose not to follow the Russian lead. Patients in the NCI -approved study protocols were permitted to drink alcohol and pop tranquilizers and sleeping pills. No fewer than 94 percent of those in one of the trials are known to have consumed one or more tranquilizers. Which means that only six percent of the subjects-16 of them, in this case-had any realistic chance of benefiting from the hydrazine sulfate. Want to bet that none of the 266 patients in this particular study was told in the required “informed consent statements” that the odds of getting any benefit at all had been reduced to about zero even before he or she swallowed the first capsule? Or been told that the consumption of alcohol, barbiturates, or tranquilizers could not only negate the therapeutic effect of hydrazine sulfate but cause, as the profession gently puts it, “morbidity and mortality”-sickness arid death?

The 16 patients whose charts do not show the presence of any incompatibles totaled roughly one-quarter the number of people in a previous clinical trial at Harbor-UCLA that, through its positive outcome, had inspired much of my reporting. The NCI initially dismissed those results because the number of patients involved was too small, they said, to be statistically significant.

In 1994, a year before the great love of his life would come down with breast cancer, Bob Guccione was a guest along with Dr. Joseph Gold on a talk-radio program I hosted on WWRC in Washington, D.C. On the air Guccione laid out the sorry history of the NCI’s bitter and determined resistance to giving hydrazine sulfate a fair test, and Gold explained how the drug works. The stations phone lines were quickly besieged by impassioned listeners who wanted to know what they could do to help. I suggested that they phone and fax Edolphus Towns (DL-N.Y.), then chairman of the House Intergovernmental Relations Subcommittee, which has the authority to investigate the NCI. Within minutes the congressman’s staff called us, demanding that we stop giving out the number, that the program’s listeners were “making it impossible for us to get our jobs done.” We politely declined to call off our listeners. A second call came from a senior aide to the chairman, who promised to get his boss to read the massive documentation I had submitted to the subcommittee … a year before the broadcast.

Within a week the chairman ordered the GAO to conduct an investigation into the matters raised by Penthouse. When the GAO’s investigators called upon senior officials of the NCI they ran into anger and resentment. At one point,informed sources say, there was considerable shouting and screaming, and a sense of NCI gloom over the possible outcome of the congressional investigation–a concern over what the costs might be to the powerful men and women who had waged war against the drug and its developer, and therefore against cancer patients. But the NCI brass shouldn’t have lost much sleep. The damage, as it turned out, would be very small indeed, and quite contained. No heads would roll; no blame would be fixed. Business-as-usual would prevail.

This is how it worked: The GAO slapped the wrists of the NCI for sloppy, incomplete record keeping of the drugs other than hydrazine sulfate that were taken by the patients in the clinical trials. As a result, NCI’s team leaders, as indicated, admitted in a letter to the Journal of Clinical Oncology what they hadn’t bothered to disclose in their original report to the medical community-that 94 percent of the patients in one study had received one or more tranquilizers. But if you didn’t already know that tranquilizers (and barbiturates and alcohol) were incompatible with hydrazine sulfate, the NCI letter wouldn’t have helped you to learn that. It simply confessed to not having fully reported on other drugs consumed by patients in the study. The NCI has always rejected the fact that some substances are incompatible with, and therefore deactivate, hydrazine sulfate, and that the mix can be extremely dangerous. Thus the NCI letter didn’t tell the truth, didn’t warn that mixing the incompatibles with the hydrazine sulfate was a time bomb.

Then in late 1995 came the official GAO report. It upheld the NCI’s testing methods in this case, making the GAO’s long awaited probe of the whole affair a veritable whitewash.

The GAO’s report is a stunning defeat for millions of cancer patients and their families in the United States and around the world. To affirm the NCI’s destructive conclusion–to say that the NCI’s hydrazine-sulfate studies “were riot flawed”–the GAO had to buy into the deceptive pronouncements and statistics that are at the core of the NCI’s case.

When Congress ordered the GAO probe it was believed that the GAO would conduct an independent audit of the NCI’s methodology–but hat did not happen. Instead, after an “internal review,” the GAO accepted the NCI’s own “retrospective analyses.”

Penthouse hired independent medical-statistics consultant Richard Wilkins, a former senior biostatistician at a major pharmaceutical manufacturer. He was asked to evaluate the NCI’s retrospective analyses.” Because of my long and emotional investment in the case, I waited with some apprehension for Wilkins’s report. What if it were I who was biased in my reporting? What if all those great results in Russia and America had been flukes?

I shouldn’t have worried. My copy of Wilkins’s conclusions came with a cover letter saying, “You are to be congratulated for bringing the important, indeed truly scandalous, hydrazine sulfate story to the attention of the American people. The enclosed should provide more ammunition for it.”

The hostility toward hydrazine sulfate at the NCI is bone marrow deep. The NCI’s longtime former director, Vincent T. De Vita, Jr., M.D., now head of the Yale University Cancer Center, had long attacked Dr. Gold and belittled his discovery. He told the Washington Post, ” it’s a ho-hum drug,” and the ABC News program “20/20,” “We throw away better drugs than hydrazine sulfate.” A renowned pioneering chemotherapist and a master at the politics of cancer, De Vita is an icon in the cancer establishment, with friendships among the powerful in almost every corner of American and international life. For more than a decade his word on anything having to do with cancer rolled down like thunder across the worldwide medical landscape. So it should not have come as a complete surprise that the GAO’s deck would be stacked against a full and fair assessment of the NCI’s hydrazine-sulfate trials. To come up with anything else would have reflected terribly on the NCI power structure, past and present.

Listen in as Mark Nadel, assistant director of the General Accounting Office, attempts, in a telephone interview with me, to justify the method and administration of the NCI’s clinical trials of hydrazine sulfate: “The reason [the use of tranquilizers) was incompatible, which threw us at first, was that it would heighten the sedative effect [of hydrazine sulfate]. In any case, in the admittedly small number of patients in the trials who did not receive the incompatibles, there was no (positive) effect seen of hydrazine sulfate and the issue of statistical significance shouldn’t blind one to the fact that no (positive) effect was seen.

Nadel must have assumed that I wasn’t paying attention, and that you, the reader, cannot think. Why do major clinical trials routinely embrace hundreds of patients and not just a few dozen? Because statistical significance is at the very core of measuring the success or failure of any experimental medication. For the sake of his report’s credibility, Nadel wants us to ignore the importance of statistics.

Here’s Dr. Gold on that question: “It is impossible to state that no effect was seen, because there weren’t enough patients who did not receive the incompatibles to document whether an effect was seen. Mr. Nadel’s insistence that the issue of statistical significance I shouldn’t blind one’ is stunning, since it is only statistical significance which can confirm any effect in a clinical trial. It is the basis of all clinical trials, and he knows it.

“The fact that hydrazine sulfate heightens the sedative effect of the incompatibles is only a secondary consideration of incompatibility. The primary consideration, which is demonstrated by both published and unpublished studies which were made available to the NCI before the commencement of any of their clinical trials, is that the combination of hydrazine sulfate and tranquilizers nullifies the therapeutic effect of hydrazine sulfate and causes vastly increased risk of additional illness and even death in test subjects.

“Additionally, prior to the commencement of the NCI’s clinical trials of this drug I alerted NCI that hydrazine sulfate is a member of the class of drugs called MAO inhibitors. As such, a patient who also is taking tranquilizers, barbiturates, beer, wine, or hard liquor cannot use it. It also cannot be used by patients who are permitted to eat raisins, yogurt, and a list of other foods containing tyramines (amino-acid derivatives). The NCI made no attempt to monitor any of these things in its studies, which can also have the effect of turning off hydrazine sulfate’s capacity to stop cancer-induced starvation and shrink the tumors themselves.

“Since hydrazine sulfate is an MAO inhibitor, and since MAO inhibitors and tranquilizers are recognized as incompatible, then the NCI studies are by definition intrinsically flawed. The use of incompatible agents constitutes negative-bias factors in a study design, and the effect of negative-bias factors is to produce a negative outcome.”

Kathy Keeton, whose silken hair, lustrous complexion, and flashing eyes do not look remotely like those of a patient with end-stage breast cancer, gives instructions to one of her assistants. It is spring 1997. She no longer wears the strange leather case that delivers pain medication. Kathy is full of life. Her words flow softly, with the clipped lilt of her native South Africa. She speaks of the information she has disseminated about hydrazine sulfate to cancer patients and their families all over the world. She speaks of the growing number of physicians prescribing this drug as a result of this information. She speaks of the class-action lawsuit her husband is considering launching against the NCI on behalf of all those patients who were cruelly given hydrazine sulfate without clear instructions to avoid alcohol, antidepressants, and/or sleeping pills. Kathy Keeton is a woman with a mission. She feels she has been literally “touched by an angel,” and is now dedicated to giving back by helping those in need.

This reporter has turned over to Congress the Wilkins report, which strips bare the NCI’s “retrospective analyses,” and Penthouse’s and my findings on the GAO’s cover-up of the NCI’s assault on hydrazine sulfate. You can help by writing, faxing, or calling your representatives in the House and Senate. Enclose a copy of this article; urge them to hold public hearings on this cover-up and to demand an impartial, properly administered large-scale clinical trial of hydrazine sulfate.

Every cancer patient on this planet should have the same chance that saved Kathy Keeton.

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http://just-say-no-to-chemo.blogspot.ca/2011/02/suzanne-somers-let-debates-begin.html

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ALTERNATIVE SCIENCE:

Chemo A FRAUD – More Evidence It’s WORTHLESS
Rense.com, March 01, 2008

Chemo Therapy
Chemo Therapy

…..RESULTS: The overall contribution of curative and adjuvant cytotoxic chemotherapy to 5-year survival in adults was estimated to be 2.3% in Australia and 2.1% in the USA. CONCLUSION: As the 5-year relative survival rate for cancer in Australia is now over 60%, it is clear that cytotoxic chemotherapy only makes a minor contribution to cancer survival. To justify the continued funding and availability of drugs used in cytotoxic chemotherapy, a rigorous evaluation of the cost-effectiveness and impact on quality of life is urgently required.”
Chemotherapy…the massive, evil poisoning of the already immuno-suppressed human body…remains one of the most barbaric, criminal undertakings of modern ‘medicine’ against the human species. The cost of the average chemotherapy regimen: $300,000 to $1,000,000. It’s ALL about MONEY and PROFITS. YOU are worthless to the AMA-Pharma death machine. The FAKE war on cancer has raised over a trillion dollars to date and now one out of every TWO Americans will be confronted with cancer at some point. Most of all, the criminal ‘war on cancer’ has made a lot of people wealthy. It is, without question, one of the biggest hoaxes in human history.
There are MANY cures for cancer, from Rife to Essiac to Ozone to Hoxey to Glyconutrients to the simple cessation of poisoning one’s body with meat, dairy and processed foods loaded with MSG and countless other carcinogens. This particular article is but one of many showing that chemo (and radiation) do NOT extend the life of one cancer patient over another with the same cancer who does NOTHING. To devastate a body trying to cope with a disease by poisoning the hell out of it is beyond something from the Dark Ages.
So, when your ‘doctor’ tells you a tumor can be ‘shrunk’ ask him/her how that actually translates to ANY increase in survival. The vast majority of times chemotherapy will only HASTEN death…and utterly destroy the quality of life until then.
While chemo can shrink some tumors, the devastating cycotoxic nature of chemo ‘therapy’ further destroys the patients already compromised and failing immune system causing an even quicker demise. Until and unless the patient takes the responsibility for his or her OWN health and stops poisoning their own body…and begins to study so-called ‘alternative’ approaches to recovery…there is virtually no hope for true healing. Cancer doesn’t just ‘happen’…it is CAUSED by diet, lifestyle, stress, anxiety and environmental toxins in the work place and home.
Do a search for Rife and Ozone and Essiac. Read NotMilk.com and NoMilk.com. Read MadCowboy.com and MeatStinks.com. And others. Educate yourself if you want to live. By all means, see the new Rife Documentary (http://www.zerozerotwo.org) and prepare to be outraged beyond your worst imaginings. -JR
Comment in:
Clin Oncol (R Coll Radiol).
2005 Jun;17(4):294.
The contribution of cytotoxic chemotherapy to 5-year survival in adult malignancies.
Morgan G,
Ward R,
Barton M.
Department of Radiation Oncology, Northern Sydney Cancer Centre, Royal North Shore Hospital, Sydney, NSW, Australia.
gmorgan1@bigpond.net.au
AIMS: The debate on the funding and availability of cytotoxic drugs raises questions about the contribution of curative or adjuvant cytotoxic chemotherapy to survival in adult cancer patients. MATERIALS AND METHODS: We undertook a literature search for randomised clinical trials reporting a 5-year survival benefit attributable solely to cytotoxic chemotherapy in adult malignancies. The total number of newly diagnosed cancer patients for 22 major adult malignancies was determined from cancer registry data in Australia and from the Surveillance Epidemiology and End Results data in the USA for 1998. For each malignancy, the absolute number to benefit was the product of (a) the total number of persons with that malignancy; (b) the proportion or subgroup(s) of that malignancy showing a benefit; and (c) the percentage increase in 5-year survival due solely to cytotoxic chemotherapy. The overall contribution was the sum total of the absolute numbers showing a 5-year survival benefit expressed as a percentage of the total number for the 22 malignancies. RESULTS: The overall contribution of curative and adjuvant cytotoxic chemotherapy to 5-year survival in adults was estimated to be 2.3% in Australia and 2.1% in the USA. CONCLUSION: As the 5-year relative survival rate for cancer in Australia is now over 60%, it is clear that cytotoxic chemotherapy only makes a minor contribution to cancer survival. To justify the continued funding and availability of drugs used in cytotoxic chemotherapy, a rigorous evaluation of the cost-effectiveness and impact on quality of life is urgently required.

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