Friday, February 28, 2014

Giant crocodile takes to surf, prompting beach closure in Australia

Experts hope to capture and relocate 12-foot reptile, to keep waters safe

giant crocodile
Photo showing giant crocodile in surf at Cable Beach is courtesy of Sharon Scoble.

It’s hard to imagine a creature more menacing than a great white shark swimming in the surf, but a giant crocodile comes close.
An estimated 12-foot crocodile was spotted cruising in the swells this past week at Cable Beach in Broome, Western Australia, prompting officials to close the beach to swimmers and surfers for a day.
It’s unclear what lured the reptile into the surf zone, but the unusual sighting generated quite the spectacle.
Photo showing giant crocodile in surf at Cable Beach is courtesy of Sharon Scoble.
Photo showing giant crocodile in surf at Cable Beach is courtesy of Sharon Scoble.
Sharon Scoble, a Broome local, captured the images that accompany this report after receiving a call from her son, who spotted the croc while driving to the beach.
Scoble told Perth Now: “It was absolutely awesome. But it wouldn’t have been so awesome if I was swimming and noticed it.”
The croc remained in the surf zone for most of the day, before presumably finding its way back to one of the creeks. (The Broome region’s saltwater crocodiles typically remain in inland waterways.)
Photo showing giant crocodile in surf at Cable Beach is courtesy of Sharon Scoble.
Photo showing giant crocodile in surf at Cable Beach is courtesy of Sharon Scoble.
“Rangers were making sure no one was going near it,” Scoble said.
Dave Woods, a Parks and Wildlife officer, said this croc might be the same animal that appeared in the surf in December.
Woods added that the croc has been targeted for capture and will be relocated to a remote wilderness park, leaving Cable Beach swimmers with only one genuine worry: sharks.

Sunday, February 23, 2014

Mysterious polio-like illness affects kids in California

Doctors believe they've identified as many as 25 California children suffering from a mysterious, polio-like virus capable of paralyzing limbs.

A mysterious polio-like syndrome has affected as many as 25 California children, leaving them with paralyzed limbs and little hope of recovery.
"What's we're seeing now is bad. The best-case scenario is complete loss of one limb, the worst is all four limbs, with respiratory insufficiency, as well. It's like the old polio," said Keith Van Haren, a pediatric neurologist at Lucile Packard Children's Hospital in Palo Alto, Calif.
The first known case appeared in 2012. Sofia Jarvis in Berkeley began to experience wheezing and difficulty breathing. The 2-year-old spent days in the intensive care unit at Children's Hospital Oakland. Doctors thought she had asthma.
On a follow-up visit, her mother Jessica Tomei, 37, realized something else was wrong.
"As we were leaving the doctor's office, I noticed that she went to grab something with her left arm and she stopped, midway," Tomei said.
Eventually Sofia was brought to Van Haren's clinic with "a unique set of symptoms." She was treated with steroids and intravenous immunoglobulin therapy, used to reduce the severity of infections by giving the body antibodies to protect against bacteria and viruses. "None of it helped," said Van Haren, a neurology professor at the Stanford University School of Medicine.
"He told us right away that the prognosis was really poor and that she's not going to get better," Tomei said.
The diagnosis proved correct. Today, at age 4, Sofia's left arm is paralyzed and she has some weakness in her left leg as well as slight breathing issues.
Still, parents shouldn't panic. "This is really very rare," Van Haren said. "But we are asking any families who notice a sudden onset of weakness to see their doctors immediately. Their doctors should contact the California Department of Public Health."
California is working with the Centers for Disease Control and Prevention in Atlanta to see if there are cases outside California. So far none have been reported.
Overall Sofia's family is grateful. "She's still with us, she's still running around, she's going to preschool," her mother said.
The case galvanized Van Haren and other neurologists, who worried a new disease had appeared. When they began to go through recent medical files, they found two more cases, both in the San Francisco Bay area.
"We don't have a final case count, but it's probably in the neighborhood of 25 cases, all in California," said Van Haren. The median age of those stricken is 12.
"The California Department of Public Health has asked health care providers to report any polio-like cases they might identify and send specimens so that we can better assess the situation," said Carol Glaser, chief of the encephalitis and special investigation section of the California Department of Public Health in Sacramento.
The children don't have polio, but their symptoms look much like the disease that terrified generations of parents beginning in the 1890s.
Patients lose the ability to move their arms or legs, which "just dangle, like empty balloons," Van Haren said. Because the children can't move their limbs, the muscles atrophy and the limb shrivels.
Polio is a highly infectious disease caused by the polio virus. It invades the nervous system and in one in 200 cases causes irreversible paralysis, according to the World Health Organization. It was not until the introduction of the Salk vaccine in 1954 that any protection against it was available.
Testing confirmed that the children in California "definitely do not have polio," Van Haren said.
"The cause of most of these cases is not known. Some clinical and laboratory features, such as the pattern of inflammation seen in the spinal cord on MRI, are consistent with a viral process," said Glaser.
Van Haren suspects the culprit is an enterovirus. That is a family of viruses that includes polio but also the milder hand, foot and mouth disease, common in infants and children.
Unfortunately while there's a vaccine for the polio virus, "we don't have vaccines for the other enteroviruses," Van Haren said.
"In the past decade, newly identified strains of enterovirus have been linked to polio-like outbreaks among children in Asia and Australia," he said. The California cases highlight the possibility of an emerging infectious polio-like syndrome in California.
While there haven't been reports of the illness outside California, Van Haren thinks that's only because no one is looking for it. He believes once doctors nationwide begin to, they'll find other cases.
"My goal is to get the word out to other neurologists, to make them aware of this," he said.
The Stanford group will be presenting a case report at the American Academy of Neurology meeting in Philadelphia in April.
Tomei wants parents to be aware of this new outbreak because it took so long for doctors to think of polio or polio-like diseases in Sofia's case
"The younger doctors have just never seen polio," she said. "Maybe collaborating between the younger generation and the older generation who actually went through polio will help us catch more cases."

Saturday, February 22, 2014

Study: Nearly Half Of Water Taps May Contain Bacteria That Causes Legionnaires’ Disease

(credit: Sean Gallup/Getty Images)
(credit: Sean Gallup/Getty Images)
PHILADELPHIA (CBS) – The data is scary: Nearly half of water faucets sampled across the United States tested positive for the bacteria that causes Legionnaires’ disease.
While the study was small — researchers only sampled 67 public and private water sources such as kitchen sinks and drinking fountains – it’s the first one to chart the presence of the potentially deadly bacteria in water taps.
According to the EPA, the organization that conducted the research, 32 taps contained the bacteria, and 11 of those contained it in multiple samples.
Legionnaires’ disease is a severe form of pneumonia that causes chills, fever, headache, a cough and more. It can be deadly.
The study was published on Feb. 18 in the journal Environmental Science & Technology.

Uh-Oh: Giant Squid Sightings Considered an ‘Omen’ by Japanese Fishermen

Giant squid were once the stuff of sea monster legend.
With their eyes (the biggest in the animal kingdom) and tentacles (they're more predatory than previously believed), these sea-dwelling creatures eluded humans for centuries, making their first cameo just two years ago. Now, giant squid are turning up with regularity off the Japanese coast. And like Captain Ahab before him, one Japanese fisherman suspects something fishy: It must be “some kind of omen.”
Such was the concern of Shigenori Goto, who “had seen no giant squid before in [his] 15-year fishing career.” Two weeks ago, he caught a 13-footer at Sadogashima Island.
“When I hauled up the net,” he told local reporters, “the squid slowly came floating up.”
The strange occurrences began earlier this year. A giant squid was caught in a stationary net near Sadogashima Island; another was found in a similar situation in the town of Iwami a few days later. Then, on Jan. 19, tentacles—presumably from a giant squid—washed up off the shore of Kashiwazaki, another coastal city.
Able to regenerate limbs, giant squid have tentacles that can extend up to 33 feet. The mollusks usually live about 2,000 feet below sea level, where water temperatures typically run 10 degrees Celsius.
So why are more giant squid being seen by humans? Tsunemi Kuboder of the country’s National Museum of Nature and Science, has a theory: With ocean temperatures dropping in the region this year, the giant squid may be abandoning the chilly ocean depths for the surface, where the water is warmer.

Friday, February 21, 2014

How do you weaponize a rabbit?

A bacteria found in rabbits could be turned into a potent bioweapon by terrorists. In fact, it's been done before.
Who's the cutest threat to our safety? 
Who's the cutest threat to our safety?  (Thinkstock)
There are four major infectious agents that officials fear terrorists will turn into potent bioweapons. The first three you know — smallpox, anthrax, and the plague. The fourth? An itty bitty bacterium that wikes to wive in bunny wabbits.
Don't let its host of choice fool you — tularemia is a serious disease. Humans can contract the nastiness through the bites of ticks and flies or handling the corpses of infected bunnies. Failure to cook said bunnies thoroughly will also make you sick. And that's not all. Back in 2000, 15 residents of Martha's Vineyard came down with "rabbit fever" in a single season — an outbreak thought to have started when someone ran over an infected rabbit with a lawnmower.
Obviously, if an errant brush hog can transmit the disease, a terrorist with an aerosol device could wreak some serious havoc. This isn't merely the plot of a Tom Clancy novel. The United States, Russia, and Japan have all been experimenting with tularemia's use as a bioweapon since at least World War II. That's why researchers at the Lawrence Livermore National Laboratory (LLNL) are peering into the bacterium's inner workings to learn how we might fight such an outbreak. And they're finding tularemia to be a rather sneaky microbe.
In humans and rabbits, tularemia evades the immune system by hiding out in white blood cells — the very sentries we rely upon to hunt invaders. Common signs of the disease include ulcers at the site of insect bites, swollen lymph nodes, and flu-like symptoms such as fever, muscle aches, and fatigue. If left untreated, rabbit fever can kill, as it did with one of the cases in the Martha's Vineyard outbreak.
But as potentially dangerous as tularemia is, there's still a great deal we don't know about it. For instance, until Amy Rasley and her team at LLNL started studying the bacteria, we had no clue how it survived in the environment — i.e., outside of humans, bunnies, and ticks. But Rasley's research has shown that when tularemia is in a bind, it can seek refuge in an amoeba, which are surprisingly similar physiologically to our white blood cells. Once inside, the bacterium becomes encapsulated in dormant cysts where it can remain until better opportunities arise.
Oh, but that's not nearly all. One of Rasley's colleagues, Geoffrey Feld, has been using x-ray crystallography to unravel the secrets of tularemia's survival trick. (Feld discussed the LLNL team's findings last weekend at an annual meeting of the Biophysical Society.) It seems tularemia is capable of secreting special proteins that might actually trigger the amoeba's cyst-making response. In other words, the bacterium does its best Frank Underwood impression and tricks the amoeba into giving it an office.
"If we're able to better characterize these proteins," said Feld in an interview, "then maybe we can start thinking about new countermeasures against tularemia based on how they work."
More research will be needed, of course, but the findings are promising — and welcome, given how little we know about the bacteria. Though the Centers For Disease Control and Prevention reports an average of just 130 human cases of tularemia each year, the agency takes the potential for its use in bioterrorism very seriously.
As an epidemiologist with the CDC's Division of Vector-Borne Diseases, Kiersten Kugeler says tularemia is a cause for concern because it's both highly infectious and widely available in nature. "CDC operates a national program for bioterrorism preparedness and response which includes stockpiling antibiotics to treat infected persons," she said. And just last week the CDC announced a cooperative effort with other federal agencies, international organizations, and foreign governments to launch the Global Health Security Agenda, which Kugeler said is designed to "standardize and unify response to disease outbreaks and close gaps in surveillance and response."
In other words, the CDC's got your back when it comes to a doomsday scenario involving tularemia. Furthermore, Kugeler says terrorists would require technology of "substantial sophistication" to weaponize rabbit fever on a large scale.
Then again, sometimes the simplest methods work best. There's some evidence to suggest that the Hittites used rabbit fever against their enemies over 3,300 years ago — making it the first known instance of bioterrorism. The Hittites' method? Leaving infected rams along the roads traveled by their enemies. After all, who can resist a free ram?

Thursday, February 20, 2014

Scientists Discover How HIV Becomes Drug Resistant

By David Heitz
Wed, Feb 19, 2014

For the first time, scientists have determined how HIV is able to duck a commonly used drug.
Researchers from the University of Pittsburgh School of Medicine presented their findings today at the Biophysical Society annual meeting in San Francisco. Cell biologist Sanford Leuba and colleagues studied the molecular activity of efavirenz, an antiretroviral drug that is one of a class of drugs called non-nucleoside reverse transcriptase inhibitors, or NNRTIs. Efavirenz is sold under the brand name Sustiva, or Atripla when used in combination with another drug.
NNRTIs work by keeping HIV from piercing CD4+ “helper” cells and hijacking their genetic material to turn them into machines used for copying the virus. But the virus has found ways to adapt to NNRTIs and become resistant to them in some patients.
Leuber told Healthline that his team made the discovery by studying a “tour de force of expressions” previously found by their colleague Nicolas Sluis-Cremer. Sluis-Cremer is an internationally recognized expert on reverse transcription who also studies HIV drug resistance.
The Future of HIV Prevention: Truvada for PrEP
NNRTIs normally create a tiny “salt bridge” that keeps HIV from performing reverse transcription on cells. Reverse transcription is required for HIV to enter and corrupt the CD4+ cell with its genetic information. The salt bridge prevents HIV from fully grasping the cell, much like a hand that cannot close to fully clench an object.
Instead, the viral cell slides against the healthy cell, and this sliding keeps it from replicating. But Leuber and his colleagues now know that the sliding sometimes continues until the salt bridge eventually breaks, or is unable to form, allowing HIV to get inside the cell.

A 'Eureka' Moment

Leuber told Healthline there was “a screaming moment” when this mutation was first observed in the laboratory. “My interests are watching proteins move in real time on nucleic acid,” he said, adding that he did not know this could be done with HIV reverse transcription until now.
Dr. Daniel Kuritzkes, a professor of virology at Harvard University who also studies how HIV develops resistance to antiretroviral medications, told Healthline that Leuber's research is “interesting, but not earth-shattering.”
Kuritzkes said that the discovery has greater implications for the field of biochemistry than for advancing patient treatment. “But the truth is that the more we understand about the mechanisms of action for drug resistance, the better we may be able to design molecules that can overcome those mechanisms," he said.
"What people would ideally want are molecules that anticipate the mechanism of resistance and have patterns of escape.”
45 HIV/AIDS Terms You Should Know 

One in Six Carry Drug Resistant HIV Strain

More than 16 percent of Americans with HIV carry a strain of the virus that is resistant to certain drugs, according to research presented in March 2013 at the Conference on Retroviruses and Opportunistic Infections in Atlanta, Ga. In half of those cases, the virus is resistant to NNRTIs.
Although the majority of patients taking antiretroviral drugs do well, “for a significant subgroup of patients who have trouble taking their medications regularly, these people can get into trouble with resistance,” Kuritzkes said. “Resistance to non-nucleosides is a problem.”
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Tuesday, February 18, 2014

Can 'Robotic' Pills Replace Injections?

Entrepreneur Mir Imran Hopes to Change Diabetes Treatment

Feb. 17, 2014 7:05 p.m. ET

The adage "Take two aspirin and call me in the morning" is destined for a futuristic makeover. Doctors may just as easily recommend swallowing sophisticated gadgets instead.
That is the hope of prolific inventor Mir Imran, who has created a robotic pill to replace injectable drugs for chronic conditions such as diabetes. The gadget, in preclinical studies and backed by Google Inc. GOOG +0.73% 's venture-capital unit, consists of an ingestible polymer and tiny hollow needles made of sugar that are designed to safely deliver drugs to the small intestine.
Such a pill would have seemed unthinkable years ago. But advancements in technology and scientific research have recently led to two federally approved robotic pills.
The Food and Drug Administration earlier this month cleared the PillCam, a pill-sized camera from Given Imaging Ltd. GIVN 0.00% that photographs human insides in a hunt for colon polyps. Another company, Proteus Digital Health Inc., received clearance a year and a half ago to put ingestible sensors inside pills to help patients and doctors determine how many they have taken.
Mr. Imran's pill hasn't yet been tested in humans, so it is probably still at least a year away from even seeking federal approval. It also would require substantial financing to manufacture millions of pills. But if it is successful, the gadget has the potential to disrupt a multibillion-dollar market for injectable drugs and make life easier for millions of sufferers of conditions such as diabetes and rheumatoid arthritis.
Mr. Imran is a safer bet than most entrepreneurs. The Indian-born founder of the research lab and business incubator InCube Labs in Silicon Valley has founded more than 20 medical-device startups, a dozen of which have been acquired by companies such as Medtronic Inc. MDT -1.03% He owns over 300 patents and helped develop the first implantable cardioverter defibrillator to correct irregular heartbeats.
Rani Therapeutics, the startup formed at InCube Labs to commercialize the robot pill, last year raised funds from Google Ventures and angel-investment fund VentureHealth.
Blake Byers, the Google Ventures general partner who spearheaded the investment, says Mr. Imran may be achieving one of the "holy grails" for biotechnology by figuring out how to deliver protein-based drugs such as basal insulin to the body without the use of a syringe.
"This investment is not exactly in our wheelhouse, but we're open to people who can change our minds," Mr. Byers said. "This one really stood out as a huge clinical need; $110 billion is spent in the U.S. every year on biologics, all of them injectable."
Drugs used to treat a variety of chronic conditions, including diabetes, rheumatoid arthritis, osteoporosis and multiple sclerosis, can't be delivered in pill form because stomach acids break down the proteins.
Mr. Imran's idea is an "autonomic robotic delivery system" that can stay intact in the stomach and small intestine long enough to deliver enough of the drug. The body's natural digestive processes activate the pill to perform a series of functions even without any electronics.
As the pH level, or acidity, builds up in the intestine, the outer layer of the polymer pill casing dissolves, exposing a tiny valve inside the device that separates two chemicals, citric acid and sodium bicarbonate.
When the valve becomes exposed, the chemicals mix together to create carbon dioxide. This acts as an energy source, gently inflating a balloon-like structure that is outfitted with needles made of sugar and preloaded with drugs.
The needles push into the intestinal wall, which has no pain receptors. Once lodged there, they detach from the gadget and slowly dissolve, while the balloon and polymer casing pass from the body.
In numerous attempts over the past 40 years to make insulin and other drugs available in pill form, pharmaceutical companies have been able to create coatings so tough that pills can reach the small intestine. But once there, they are attacked by enzymes, which has compromised the pills and prevented significant amounts of the drug from reaching the patient.
In preclinical studies, Rani Therapeutics has shown that its robotic pill can boost drug absorption at least as high as syringes can, Mr. Imran said.
"I am guardedly optimistic, and I say guardedly because there is still a lot of work left to do," said Elliott Sigal, who several months ago retired from drug maker Bristol-Myers Squibb Co. His 16-year run at the drug maker included top posts in drug discovery and development and a nearly 10-year tenure as the head of research and development.
"Rani's engineering-based approach to this is very innovative," said Mr. Sigal, who doesn't have a financial stake in the business. "He is getting results that I have not seen before. It hasn't been tried in human patients yet, and things do sometimes fail at that level. But if the [trials] data continues, there will be a great deal of pharma interest."
Mr. Imran said pharmaceutical companies, which would license the technology for use with their own drugs, have already expressed interest. He declined to give further details.
Rani Therapeutics will spend another year testing the robot pill, he said, in the hope that it will have definitive clinical data in 2015.
If the data back up his claim about the pill, it could not only help millions of patients ditch their syringes and stick-pens, but it could remove another barrier for a range of early-stage treatments that currently have no safe avenue into the body, said Google Ventures' Mr. Byers.

Monday, February 10, 2014

NY Mall Warning: Shoppers Possibly Exposed to Measles

Monday, Feb 10, 2014  |  Updated 12:46 PM EST

Shoppers at a New York mall, particularly those at an AT&T store and a Best Buy, were possibly exposed to measles, a county health department warned Friday.
A case of measles has been identified in Rockland County, and anyone at the Palisades Center Mall on Sunday between 11 a.m. and 1 p.m. could have been exposed, the county Department of Health said. 
The health department said people who shopped on the first floor of the mall and at those two electronics stores are at the greatest risk of exposure.
It's a painful, contagious disease that many people mistake for the common cold. 
Despite news of the measles case, the parking lot at Palisades Mall was packed Friday night. One shopper who contracted it 25 years ago called it "scary."
"No one should have to go through it," said Leanne O'Brien of Newburgh.
Bruce Pratt of Munsie also had the measles decades ago and still remembers the pain it caused. 
"I had a cold, rash on my stomach and little spots, and you cough a lot," he said. 
Babies under 6 months old, pregnant women and those with immune system problems may be at risk. Anyone who has not had a measles vaccination and who was shopping at the mall during those times should also contact a doctor, the health department said.
People who have had two doses of measles, mumps and rubella vaccine are not at risk of contracting measles, authorities said. Most New Yorkers have been vaccinated, the health department said.
Symptoms of measles include fever and rash but many people who contract it may think it may dismiss the warning signs. 
"They may just think they have a cold, so they may have not broken out with the rash, and they don't know they have it and can expose a lot of people," said Dr. Len Horovitz at Lenox Hill Hospital. 
Anyone who suspects they may have been exposed and have symptoms should call their physician before seeking care so that others are not exposed in a waiting room, the health department said.
- Brynn Gingras contributed to this report.

Saturday, February 8, 2014

Virus Advances Through East Caribbean

MIAMI — A painful mosquito-borne virus common in Africa and Asia has advanced quickly throughout the eastern Caribbean in the past two months, raising the prospect that a once-distant illness will become entrenched throughout the region, public health experts say.
Chikungunya fever, a viral disease similar to dengue, was first spotted in December on the French side of St. Martin and has now spread to seven other countries, the authorities said. About 3,700 people are confirmed or suspected of having contracted it.
It was the first time the malady was locally acquired in the Western Hemisphere. Experts say conditions are ripe for the illness to spread to Central and South America, but they say it is unlikely to affect the United States.
“It is an important development when disease moves from one continent to another,” said Dr. C. James Hospedales, the executive director of the Caribbean Public Health Agency in Trinidad. “Is it likely here to stay? Probably. That’s the pattern we have observed elsewhere.”

Tracking Outbreaks

Reports of locally acquired Chikungunya virus as of January 2014

Chikungunya fever is particularly troublesome for places such as St. Martin, a French and Dutch island 230 miles east of Puerto Rico, where two million tourists visit annually. In an effort to keep the disease from affecting tourism and crippling the island economy, local governments began islandwide campaigns of insecticide fogging last week and house-to-house cleanups of places where mosquitoes could breed.
The French side of St. Martin to the north has had 476 confirmed cases, the largest cluster in all of the islands, while the Dutch side has had 40 cases, according to the Caribbean Public Health Agency.
Already, the travel search engine Kayak said there was a 75 percent decline in searches for St. Martin in the past three weeks, compared to the same period last year.
Searches for Martinique, which has had 364 confirmed chikungunya cases, were down 18 percent.
“When I read about chikungunya, I thought: ‘There’s a mosquito in St. Martin waiting for me, rubbing its little feet together waiting to get a hold of me,’ ” said Betsy Carter, a New York City novelist who was scheduled to travel to St. Martin with two other couples in January. “So we all decided not to go.”
Ms. Carter was particularly nervous, because she had contracted a different disease from a sand fly a few years ago in Belize, which caused half her hair to fall out. Despite having bought insurance, last month the three couples lost $9,000 they paid to stay at Dreamin Blue, a luxurious villa overlooking Happy Bay.
“The owners said they would spray the house,” Ms. Carter said. “But what if you want to leave the house?”
Public health and tourism officials on the islands are urging visitors to wear long sleeves and insect repellent high in DEET.
“Not a lot of bookings were canceled, but there were a few people not understanding exactly what this was, thinking it was a pandemic on a large scale,” said Kate Richardson, a spokeswoman for the French St. Martin’s tourism board. “People got a bit scared, and a few of them have declined to take their trips.”
She said the hotel association had not reported the number of cancellations.
Chikungunya (pronounced chik-en-GUN-ya) causes high fever and muscle pain, symptoms similar to those caused by dengue fever, which has swept the Caribbean for several years. While dengue can be fatal and chinkungunya rarely is, experts said the effects of chikungunya, such as pain in the small joints, tend to last longer, sometimes for months.
Ann M. Powers, a vector-borne disease specialist at the Centers for Disease Control and Prevention, said past outbreaks in other nations had incapacitated people because the pain in their wrists and ankles was so severe.
“They miss school and work,” she said. “It’s quite a drain on resources and the work force.”
Nora E. Kelly, an Ontario restaurant comptroller, is leaving for St. Martin on Sunday with a group of 28 friends who have tracked the disease closely and loaded up on insect repellent.
“It’s been a miserable winter,” Ms. Kelly said. “Chikungunya is not going to stop me from getting on that plane in a million years.”
The health ministry in Sint Maarten, the Dutch side of the Caribbean island, said no Canadian, European or American tourist at a resort had fallen ill.
“In order to keep the virus under control, various proactive steps have been taken and continue to be taken by both the Dutch and French authorities,” Lorraine Scot, a spokeswoman for the ministry, said in a statement.
Those steps include fogging, surveillance of suspected cases, biological lab investigations and a public-awareness campaign alerting people to the dangers of standing water, where mosquitoes lay their eggs.
The virus has also been detected in the British Virgin Islands, Dominica, French Guiana, Guadeloupe and St. Barthélemy.
“It certainly has the potential to move to a lot of other places in the Western Hemisphere,” Ms. Powers said. “All of Central America and big parts of South America would certainly be susceptible.”
The disease is not likely to spread to the United States, because it is carried by two species of mosquito that prefer warm climates.
Chikungunya was first identified in Tanzania in 1952. The name translates to “that which bends up” in the Kimakonde language of Mozambique.
According to the World Health Organization, since 2005, nearly two million cases have been reported in India, Indonesia, Malvides, Myanmar and Thailand.
An epidemic hit Northern Italy in 2007, and in 2006 thousands were sickened in Réunion, a French island east of Madagascar.
Correction: February 8, 2014
Because of an editing error, an earlier version of a picture caption misstated the name of a species of mosquito that carries Chikungunya fever. It is Aedes aegypti, not aegpyti.

Truvada for PrEP: Experts Weigh In on the Newest Way to Prevent HIV/AIDS

Truvada (emtricitabine and tenofovir disoproxil fumarate), manufactured by Gilead Sciences, is the first drug approved to reduce the risk of HIV infection. In a pre-exposure prophylaxis, or PrEP, regimen, HIV-negative people who are at high risk may take a daily dose of Truvada, which has been proven to lower their infection risk if they are exposed to the virus.
PrEP treatment is meant to be employed alongside other prevention methods, such as safer sex practices, risk-reduction counseling, and regular HIV testing.
In giving the green light to Truvada on July 16, 2012, FDA Commissioner Dr. Margaret A. Hamburg said, "Every year, about 50,000 U.S. adults and adolescents are diagnosed with HIV infection, despite the availability of prevention methods and strategies to educate, test, and care for people living with the disease. New treatments as well as prevention methods are needed to fight the HIV epidemic in this country."
See the Infographic: Truvada PrEP for Men Who Sleep with Men

A Work in Progress

Dr. Kenneth Mayer, a visiting professor at Harvard Medical School and the medical research director at Boston’s Fenway Institute (a research center dedicated to providing medical services to LGBT communities), expressed a favorable opinion about Truvada for HIV prevention—while emphasizing that the drug’s use for this purpose is in its infancy.
“It has potential to help people,” he told Healthline. “Several randomized control trials show that it decreases HIV incidence, but it’s not a simple matter. It’s in its early days, and it’s very analogous to the early days of hormonal contraception. The initial hormonal contraception was only progestin. It was a very high dose, and that had more side effects … people got smarter about how to give it less frequently and to modulate the chemicals.”
In trials, Truvada has proved, overall, to be safe and well tolerated, though a small minority of people did show some side effects. And many medical experts and HIV experts have raised serious concerns about the ability of high-risk patients to consistently take a pill every day—if it’s not taken daily, it loses efficacy, and there are fears that poor adherence to a daily schedule could lead to HIV infections and Truvada-resistant strains of HIV.
Dr. Mayer said that it is important for healthcare providers to determine patients’ motivations and their willingness to be monitored: “It’s not a vaccine," he explained. "It’s a commitment to taking pills on a regular basis."
Thomas D. Chiampas, Pharm.D., BCPS, AAHIVP, a clinical assistant professor and clinical pharmacist at the University of Illinois College of Pharmacy, was initially skeptical about the use of Truvada for PrEP. But after reading the results of studies and talking to preceptors and students, he echoed Dr. Mayer’s sentiments.
“I do think Truvada for PrEP, when safe for the patient and taken appropriately with 100 percent medication adherence, does have the potential to diminish HIV transmission and thus AIDS infections. At our clinics we only see HIV-positive individuals; therefore, we do not prescribe Truvada for PrEP," he said. "I do believe more education is needed about Truvada for PrEP—in particular, appropriate prescribing duration, assessment of risk factors, assessment of adherence, and lab monitoring,” he said.

A Numbers Game

According to several accounts, 1,774 people filled prescriptions for Truvada for PrEP between January 2011 and March 2013. But while those numbers may seem low, many others are receiving the medication through ongoing clinical trials.
Get the Inside Story: Q&A with PrEP Patient Michael Rubio
And at about $13,000 a year, Truvada for PrEP does not come cheap. While most insurance companies in the U.S. cover Truvada, affordability can be an issue if a person has a high-copay insurance plan. “For many people, it’s not necessarily expensive, but it does involve people being motivated consumers, since a physician might have to get prior approval with some insurance companies,” said Dr. Mayer.

Education Is Key

There is some agreement among the medical community that riskier sexual behavior is on the rise, and that more education about HIV and AIDS prevention is crucial.
Fenway Health is one of several groups that have received non-restricted educational and research grants from Gilead Sciences, according to Dr. Mayer. “We’ve used some of the funding to convene a conference about best practices in HIV prevention and have developed some educational materials for people in the community, so they can be informed consumers. Their goal is not to push people to use PrEP, but [to let them] know about it. Obviously, it’s not the answer for some people,” he said.
Fenway has also conducted research on whether people are starting to use the medication, what people know about it, and what concerns they have.
One eye-opening finding of the focus group is that some people are not comfortable talking about their sexual behavior with their doctors, according to Dr. Mayer.
“This medication is not something that you would give to everybody,” said Dr. Mayer. “It is individuals who are having unprotected sexual behavior with any regularity, particularly if they have a known HIV-infected partner, who are the key targets for using PrEP. There are a number of people who said, ‘Well, I wouldn’t be comfortable divulging my behavior to my doctor, so I don’t know how I would ask for it.’ That was one concern.”
“The focus group findings also revealed that even though the drugs’ side effect profile is quite low, some individuals felt that any risk of any side effect was unacceptable if they were otherwise healthy,” he added.

What Are the Side Effects?

Acknowledging that tenofovir has been associated with kidney problems in HIV-infected people, Dr. Mayer believes that this side effect is not a major drawback if patients are monitored.
“The kidney problems that people are monitored for tend to be self-limited. You stop the medication, and the creatinine [which is evidence of kidney dysfunction] goes back to normal, so it’s not as if people automatically go into irreversible kidney failure," Dr. Mayer explained. "But what it means is, particularly if they have preexisting kidney disease, or, for example, untreated hypertension for a long time, if they go on the medication, they need to be carefully monitored. We do kidney function within a month after people start the medication, and then if it looks good, we do quarterly monitoring of kidney function. So that’s an important side effect. It’s uncommon though; it was in the 1 percent to 2 percent range that people had to stop the medication because of kidney problems in the course of the trials.”
Other side effects reported in trials include weight loss (2 percent), nausea (2 percent), and headache (4 percent), according to Fenway Medical.

Complacent Attitudes and Risky Behaviors?

Many medical professionals agree that the current generation of sexually active young adults is more complacent about HIV and AIDS than the generation before it.
For much of the 1980s and early 1990s, the lack of effective treatments for AIDS made the disease more frightening. But current therapies are so effective that HIV/AIDS is widely seen as a manageable health condition, not the death sentence it once was. And this may lead to young people being lax when it comes to safe sex practices.
Dr. Mayer explains, “Young people may feel invulnerable and the epidemic may be quieter for them, because they don’t know people with AIDS. Years ago, the drugs had more side effects and people were sicker. In many cities, you could spot people that you had the sense might have AIDS … and that’s not the case anymore.”
As such, one major concern for medical professionals is whether using Truvada will lead to riskier sexual practices—and thereby increase people’s risk for other STDs.
Maurizio Bonacini, M.D., is an associate clinical professor at the University of California, San Francisco, and the director of the HIV-Liver program at California Pacific Medical Center. He is adamantly opposed to Truvada for AIDS prevention: “I found it appalling that Truvada was approved to prevent HIV. So now we will have people that have high risk sex taking a tablet with questionable adherence, and placing themselves at risk for HBV [hepatitis B], HCV [hepatitis C], HAV [hepatitis A], HSV [herpes simplex virus], HPV [human papillomavirus], and whatever other acronym that will spell health trouble,” he said
Fred Mayer, R.Ph., the president of Pharmacists Planning Service Inc. (PPSI), a California non-profit corporation that offers a large number of health-awareness programs to promote public health and education, gave a thumbs-up to Truvada for prevention, but feels that there is not enough of a promotional push for using the drug in conjunction with condoms and other safer sex practices.
“I think any new development in prescription drugs, especially for AIDS, is great as a consumer advocate," Mayer said. "The only downside I see as a consumer advocate with a public health pharmacy organization is they are promoting this drug as an AIDS preventative and should be promoting this drug with the use of condoms, for prevention of STDs, STIs, chlamydia, et cetera,” he said.
Chiampas agrees: “People think, ‘OK, it’s a pill I can take.’ But adherence counseling, follow-up for labs and assessments, pregnancy tests, hepatitis tests, sexually transmitted diseases, HIV—all of those tests need to be drawn every two to three months to six months out for safety concerns.”

New Avenues for Education and Counseling

In terms of public health initiatives, social media presents new opportunities and new challenges. In the recent past, materials for people who are at high risk for AIDS were provided at places where they congregated. “For example, [if] gay men meet in a bar or club, you can do lot of education, you can have materials in the club—people would know where to go to recruit people for trials and studies,” said Dr. Mayer.
But as more and more people are socializing and finding sexual partners on their handheld devices, outreach can be more difficult.
“We’ve learned to be creative,” said Dr. Mayer. “The challenge is that organizations that in the past helped instill a sense of community… are not as strong anymore, because people are meeting partners online. On the other hand, with the Internet you can also offer a lot of education materials and you can educate people in the privacy of their home. It’s a matter of figuring out creative ways.”
Josh Robbins, an HIV activist and patient advocate and blogger, has recently launched a digital LGBT PrEP Guide for HIV Prevention at I'm Still Josh. “I fall short of endorsing PrEP because I don’t believe that’s the best place for our voice,” said Robbins. "What I believe in is giving people the power to be informed and then to make an educated decision with their physician or healthcare provider."
Robbins explained, "I’m not saying PrEP is right for everybody, but I’m not saying you should ignore PrEP. It is important, maybe, for me to say that, because the FDA has neither tested nor approved a condom for anal sex. PrEP is the only FDA-approved prevention method. It is the only one in the arsenal when we talk about what do we have for the prevention of HIV… as long as you have an educated discussion with a physician or whoever is the stakeholder in helping you make a decision, then, whether I agree with your decision or not, at the end of the day I’m glad that you had that discussion.”
Chiampas and one of his colleagues are planning to conduct a survey for general practitioners to see how comfortable they feel about Truvada. “Our concerns are the appropriate monitoring and follow-up, as well as counseling," he said.
He added that people on a PrEP regimen should be seen by a healthcare provider every two to three months, to be tested for HIV, kidney function, pregnancy, and other things. “The adherence issue cannot be stressed enough,” he said. “But when taken with 100 percent adherence, Truvada for PrEP was very effective in preventing HIV transmission between homosexual, heterosexual, and injection drug-use populations.”
And all the experts stress that although PrEP is an effective option, there is no 100 percent guaranteed way to prevent sexually transmitted HIV infection.

The Future of HIV/AIDS Prevention

Now that the darkest days of the AIDS crisis have passed, what does the future of treatment and prevention of HIV look like?
Dr. Mayer sees the glass as half full. “We are at an interesting point, a watershed moment where we have proof-of-concept that treating people earlier will make them less infectious, and we have proof-of-concept that for high-risk people, taking medication on a daily basis before and after high-risk behavior will make them less likely to become infected. We have new tools in the last few years, but they are not being implemented as quickly as many of us would like. It is going to take time. A lot of it is professional education in the media, a lot of it is public education, continuing the discussion.”
He adds, “None of us who work in this area think that we are going to necessarily give the same medication the same way over the next decade. There are a number of different studies looking at: Can you give less drug? Should you give different drugs that have different side effect profiles? Can you give the medication in different ways ... such as gels, vaginal rings, and injectables? It’s a very interesting time.”
Chiampas sums up the future in these words: “We think a lot of patients … will be going to their general family medicine provider and they might say, ‘I’m not positive, but I’m not in a monogamous relationship, so can I get this drug?’ or ‘My partner is HIV positive and his provider only deals with HIV patients, so can I get it through you?’ That’s where a lot of the education might be targeted.”
Finally, Dr. Mayer points out that the Centers for Disease Control and Prevention’s (CDC) guidance on the use of PrEP addresses heterosexual couples as well as women who want to conceive a child.
“One study in Africa enrolled [HIV-status] discordant heterosexual couples," he said. "It was quite a large study with almost 5,000 participants. Part of the package insert and CDC guidance is for heterosexual couples using this medication. It’s part of a larger piece. There are also studies that show that people who are infected who go on treatment become less infectious. The whole idea now is using antiretrovirals for prevention. Part of this is treating infected people earlier and working with them to maintain adherence so they are less likely to transmit."
"The other part of the equation is to identify the riskiest uninfected people and to offer them PrEP so they don’t become infected in the first place.”

Is an AIDS Cure Hiding in the Blood of 'Elite Controllers?'

Some people contract HIV and never get sick. These people are called “controllers,” and studying them has long been a focus for researchers seeking a cure for the disease.
Now, an ambitious plan called The Immunity Project has released a white paper outlining how they plan to create an HIV vaccine—free for the entire world population—based on the computerized analysis of blood from HIV controllers.
Although their work has created some eye rolls in the HIV research community, big names have stepped up with funding. Microsoft has donated $1 million toward the effort, for example. But The Immunity Project has turned to crowdfunding to come up with the more than $400,000 needed to keep its work moving forward. With 15 days to go, more than $130,000 still is needed to advance trials using human blood in mice.
A non-profit organization, The Immunity Project has partnered with Until There's a Cure, and also receives support fromY Combinator, an incubator for innovative start-up companies.
Read More: Experts Weigh In on Truvada for HIV Prevention

Who Are the Controllers?

Dr. Reid Rubsamen, who founded a drug delivery company called Aradigm, Inc., serves as CEO of The Immunity Project. Aradigm specializes in inhaled medications, which is how Rubsamen would like to see The Immunity Project's vaccine administered.
The Immunity Project uses a computerized method to figure out how controllers evade AIDS. The key is the way the controllers' cells manage to alert their immune systems to attack the HIV virus.
By expressing certain proteins, the controllers' cells send out a signal showing the immune system the best location to attack on the surface of HIV cells.
“These beneficial targets have been identified by researchers in university laboratories and private industry who have used computer-assisted statistical analysis to essentially reverse engineer the targets on the HIV virus preferred by the controller's T-cells,” Rubsamen told Healthline. “We believe that controllers are an important part of moving forward with vaccine development because they are clearly doing something right in defending against the virus.”
Although everyone's patterns of protein expression are different, The Immunity Project intends to create a “cocktail” based on some of the most popular genotypes from people who are able to withstand the virus long-term.
Some people have greater natural control over the HIV virus than others.
Dr. Jay Levy, a scientist at the AIDS Research Institute at the University of California, San Francisco, has been studying controllers for many years. Some go two years without much of the virus being detected in their blood, while others go 10 years or more, he said. Some patients have “blips” where the virus appears and then disappears.
Levy said that less than 1 percent of people with HIV are "elite" controllers who never get sick, while as many as 5 percent are virus controllers to a lesser degree.
How Far Have We Come? Know the History of HIV

Taking Advantage of the 'Innate Immune System'

Levy believes researchers should turn their attention to the “innate immune system,” which is the non-specific immunity every person is born with and uses to fight off infections.
Levy wants to better understand how “natural killer,” or NK, cells limit HIV infection and disease. In his laboratory, he is examining cell non-cytotoxic anti-HIV responses, or CNAR.
After studying people infected with HIV who have remained healthy for 10 years or longer, he determined that they all have white blood cells called CD-8 lymphocytes. Now, Levy's laboratory wants to find the protein the lymphocyte naturally produces and use it to create treatments for HIV and other diseases.
It's not an easy task. Levy likened it to trying to find biomarkers for cancer, although companies have sprung up nationwide for just that purpose.
“It's such a communication system,” Levy said of the immune system. “It's the beauty of nature.”
The problem, he said, is that companies simply aren't funding research into immune therapies. He likened our knowledge of such therapies to being in “third or fourth grade.”
Read this article at

Exclusive: AIDS patients in Obamacare limbo as insurers reject checks

U.S. President Obama speaks during a visit to Michigan State University in Lansing
By Sharon Begley and Julie Steenhuysen

NEW YORK (Reuters) - Hundreds of people with HIV/AIDS in Louisiana trying to obtain coverage under President Barack Obama's healthcare reform are in danger of being thrown out of the insurance plan they selected in a dispute over federal subsidies and the interpretation of federal rules about preventing Obamacare fraud.
Some healthcare advocates see discrimination in the move, but Blue Cross and Blue Shield of Louisiana says it is not trying to keep people with HIV/AIDS from enrolling in one of its policies under the Affordable Care Act, also known as Obamacare.
The state's largest carrier is rejecting checks from a federal program designed to help these patients pay for AIDS drugs and insurance premiums, and has begun notifying customers that their enrollment in its Obamacare plans will be discontinued.
The carrier says it no longer will accept third-party payments, such as those under the 1990 Ryan White Act, which many people with HIV/AIDS use to pay their premiums.
"In no event will coverage be provided to any subscribers, as of March 1, 2014, unless the premiums are paid by the subscriber (or a relative) unless otherwise required by law," Blue Cross Blue Shield of Louisiana spokesman John Maginnis told Reuters.
The dispute goes back to a series of statements from Centers for Medicare and Medicaid Services (CMS), the lead Obamacare agency.
In September, CMS informed insurers that Ryan White funds "may be used to cover the cost of private health insurance premiums, deductibles, and co-payments" for Obamacare plans.
In November, however, it warned "hospitals, other healthcare providers, and other commercial entities" that it has "significant concerns" about their supporting premium payments and helping Obamacare consumers pay deductibles and other costs, citing the risk of fraud.
The insurers told healthcare advocates that the November guidance requires them to reject payments from the Ryan White program in order to combat fraud, said Robert Greenwald, managing director of the Legal Services Center of Harvard Law School, a position Louisiana Blue still maintains.
"As an anti-fraud measure, Blue Cross and Blue Shield of Louisiana has implemented a policy, across our individual health insurance market, of not accepting premium payments from any third parties who are not related" to the subscriber, Maginnis said.
On Friday, CMS spokeswoman Tasha Bradley told Reuters that, to the contrary, Ryan White grantees "may use funds to pay for premiums on behalf of eligible enrollees in Marketplace plans, when it is cost-effective for the Ryan White program," meaning that having people with HIV/AIDS enroll in insurance under Obamacare could save the government money.
"The third-party payer guidance CMS released (in November) does not apply to" Ryan White programs.
Maginnis did not respond to further requests, sent after business hours, for comment on CMS's Friday statement.
Hundreds of indigent HIV/AIDS patients are dependent on Ryan White payments for Obamacare because they fall into a gap. They are not eligible for Medicaid, the joint federal-state health insurance program for the poor, because Louisiana did not expand the low-income program, and Obamacare federal subsidies don't kick in until people are at 100 percent of the federal poverty level.
Before Obamacare, the 1990 Ryan White Act offered people with HIV/AIDS federal financial help in paying for AIDS drugs and health insurance premiums, especially in state-run, high-risk pools.
Obamacare, which bans insurers from discriminating against people with preexisting conditions, was designed to replace these high-risk pools.
Starting on October 1, AIDS advocates and others in Louisiana "were enrolling anyone and everyone we could" through the Obamacare exchange, said Lucy Cordts of the New Orleans NO/AIDS Task Force.
Last month, her clients and those of other AIDS groups began to hear from Louisiana Blue that their enrollments were in limbo because the company would not accept the Ryan White checks for premium payments.
The only other carrier that is refusing to accept such payments is Blue Cross Blue Shield of North Dakota, according to a CMS official.
North Dakota Blue "restricts premium payment from third parties including employers, providers, and state agencies," said spokeswoman Andrea Dinneen, but "is currently reviewing its eligibility policies with respect to recipients of Ryan White Program funding."
Healthcare advocates are worried that the refusal to accept Ryan White payments is an effort by insurers to keep AIDS patients from enrolling in their plans and last month began pressing the issue, including with the office of Democratic Senator Mary Landrieu.
In an email reviewed by Reuters, a healthcare expert on Landrieu's staff wrote, "BCBS LA told me their decision was not due to the CMS guidance or any confusion (as we thought before) but was in fact due to adverse selection concerns. I have also recently learned North Dakota's BCBS plan has implemented the same policy."
Jessica Stone, the Landrieu staff member, declined to elaborate on the email further or to discuss her interactions with Louisiana Blue.
Adverse selection refers to the situation where an insurer attracts patients with chronic conditions and expensive care. Louisiana Blue's action "sure looks to us like discrimination against sick people," said John Peller, vice president for policy at the AIDS Foundation of Chicago.
Asked if it were engaging in efforts to avoid adverse selection by refusing to accept Ryan White payments for would-be customers with HIV/AIDS, Louisiana Blue said it was not trying to keep such customers out of its plans. "We welcome all Louisiana residents who chose Blue Cross and Blue Shield of Louisiana," said Maginnis.
(Reporting by Sharon Begley and Julie Steenhuysen; Editing by Peter Henderson and Prudence Crowther)

Friday, February 7, 2014

Scientists blown away by Tasmania's giant jellyfish


SYDNEY (Reuters) - Residents of a sleepy hamlet in Tasmania found a previously unknown kind of giant jellyfish washed up on a beach, prompting excitement among scientists in Australia as they work to formally name and classify the creature.
About 1.5 meters (five feet) across, the white jellyfish with a pink spot in the middle is believed to be a relative of the lion's mane species popularly known as a "snotty" as it resembles mucus.
"There's the excitement, that it's a new species and then there's the 'Oh my God factor' that it happens to be the size of a Smart car," Lisa-ann Gershwin, a scientist at the government's Commonwealth Scientific and Industrial Research Organisation, told Reuters. "It's like Disneyland for marine biologists."
A family walking along the beach found the giant jellyfish in late January and sent a photo to the research organisation in Hobart, Australia's southernmost city. Scientists believe the jellyfish was later washed out to sea.
Gershwin and other scientists are also trying to discover why there has been an enormous rise in jellyfish populations in the waters around Tasmania this year.
"There's something going on that's causing a whole lot of species to bloom in staggering numbers and we don't know why yet," she said. "It's so thick with jellyfish that it's like swimming in bubble tea."
(Reporting by Pauline Askin; Editing by John O'Callaghan and Ron Popeski)

Sunday, February 2, 2014

Deadly Viruses


They aren’t living, or non-living: They’re the perfect parasites
Viruses are everywhere
Over 5,000 have been described in detail
Millions and Millions Exist
When they’re in the air, or on a doorknob
They’re inert = about as living as a rock.
When they come into contact with host cells
They trigger the cell to engulf them
Or fuse with the cell
Then use the cell’s machinery to reproduce

What is a virus?

Just a tiny bundle of RNA or DNA and a shell.
That uses host cells to reproduce itself.
And manifest some of the scariest illnesses on the planet.
HIV: the mass killer
Yearly Mortality: 3.1 million
Total Mortality: 25 million+ since 1981
How it works:
Invades important immune system cells and kills them.
Leaves patient open to death by other illnesses with lowered immune function.
Ebola: the rapid killer with no cure
Yearly mortality: Mortality rate: 90% within days[3]
How it works:
[3]Disables tetherin, a protein that disables the spread of the virus from cell to cell. Spreads rapidly to cause hemorrhaging, extreme fever, and death.
Rotavirus: the child-killer
Yearly Mortality:>500,000 children
How it works:
Spread through fecal-oral exposure, often through play surfaces or contaminated water. Diarrhea, vomiting, and abdominal pain can be deadly, particularly in the developing world.[4]
Smallpox: the monarch killer
Mortality rate: Eradicated
20th century mortality rate: 300-500 million
80% of infected children died
20-60% of infected adults.
How it works:
Localizes in the blood vessels of the skin and in the mouth and throat. One of two infectious diseases to be eradicated by humans. Ravaged populations from 10,000 b.c.- 1979. Killing 5 reigning monarchs in the 1700′s.
Hepatitis B: killing your liver
How it works:
The virus enters the bloodstream and heads for the liver. Once in the liver many other viruses activate and spread.[6]
Influenza: the pandemic that’s still around
Yearly Mortality: 500,000 deaths
Pandemics occur around 3 times a century.
How it works:
Attaches itself to receptors on cells in the lungs and air passages. As it takes over their machinery, the cells die. Dead cells cause runny nose, sore throat, and other symptoms.
Hepatitis C
Yearly Mortality: 56,000 deaths
200-300 million people infected.
How it works:
“Hepatitis” means inflammation of the liver, and it is in the liver where the Hepatitis virus replicates itself.
70% of patients develop chronic liver disease.[7] 15% cirrhosis
5% die from liver cancer or cirrhosis
Yearly Mortality: 197,000 deaths
Over last 150 years: 200 million deaths
How it works:
One of the most contagious viruses. Causes rash, high fever, and for weakened immune systems can be deadly.
Hantavirus: Because rats are dirty
yearly mortality: 70,0000 deaths
How it works:
Spread through rodent bites, droppings, or aerosolized rodent fecal matter. Can cause hemorrhaging and death.
Yellow Fever:The reemerging killer
Yearly Mortality: 30,000 deaths
How it works:
An acute hemorrhagic disease sometimes causing jaundice and living damage.
Dengue Fever: the break-bone fever
yearly mortality: 25,000 deaths
How it works:
[8]Spread by mosquitoes. Leads to severe pain in muscles, joints, and behind eyes. Occurs primarily in urban tropical areas.
yearly mortality: 55,000 deaths
How it works:
[9]Enters the body and proceeds to the brain, replacing nerve cells in the process. By proceeding through the salivary glands it increases salivation, causing foaming at the mouth. This helps the virus spread through saliva. The most common form is the encephalitic or “furious” form of rabies in which agitation and aggression is heightened.
Viruses are aren’t truly even alive, but without proper care they can take your life.


From Wikipedia, the free encyclopedia

Classification and external resources
Child with Smallpox Bangladesh.jpg
Child infected with smallpox. Bangladesh, 1973. In ordinary type smallpox the bumps are filled with a thick, opaque fluid and often have a depression or dimple in the center. This is a major distinguishing characteristic of smallpox.
ICD-10 B03
ICD-9 050
DiseasesDB 12219
MedlinePlus 001356
eMedicine emerg/885
MeSH D012899
Smallpox was an infectious disease caused by either of two virus variants, Variola major and Variola minor.[1] The disease is also known by the Latin names Variola or Variola vera, derived from varius ("spotted") or varus ("pimple"). The disease was originally known in English as the "pox"[2] or "red plague";[3] the term "smallpox" was first used in Britain in the 15th century to distinguish variola from the "great pox" (syphilis).[4] The last naturally occurring case of smallpox (Variola minor) was diagnosed on 26 October 1977.[5]
Smallpox localized in small blood vessels of the skin and in the mouth and throat. In the skin it resulted in a characteristic maculopapular rash and, later, raised fluid-filled blisters. V. major produces a more serious disease and has an overall mortality rate of 30–35%. V. minor causes a milder form of disease (also known as alastrim, cottonpox, milkpox, whitepox, and Cuban itch) which kills about 1% of its victims.[6][7] Long-term complications of V. major infection include characteristic scars, commonly on the face, which occur in 65–85% of survivors.[8] Blindness resulting from corneal ulceration and scarring, and limb deformities due to arthritis and osteomyelitis are less common complications, seen in about 2–5% of cases.
Smallpox is believed to have emerged in human populations about 10,000 BC.[4] The earliest physical evidence of it is probably the pustular rash on the mummified body of Pharaoh Ramses V of Egypt.[9] The disease killed an estimated 400,000 Europeans annually during the closing years of the 18th century (including five reigning monarchs),[10] and was responsible for a third of all blindness.[6][11] Of all those infected, 20–60%—and over 80% of infected children—died from the disease.[12] Smallpox was responsible for an estimated 300–500 million deaths during the 20th century.[13][14][15] 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.[5]
After vaccination campaigns throughout the 19th and 20th centuries, the WHO certified the eradication of smallpox in 1979.[5] Smallpox is one of two infectious diseases to have been eradicated, the other being rinderpest, which was declared eradicated in 2011.[16][17][18]


There were two clinical forms of smallpox. Variola major was the severe and most common form, with a more extensive rash and higher fever. Variola minor was a less common presentation, and a much less severe disease, with historical death rates of 1% or less.[19] Subclinical (asymptomatic) infections with variola virus were noted but were not common.[20] In addition, a form called variola sine eruptione (smallpox without rash) was seen generally in vaccinated persons. This form was marked by a fever that occurred after the usual incubation period and could be confirmed only by antibody studies or, rarely, by virus isolation.[20]

Signs and symptoms

Child showing rash due to ordinary-type smallpox (variola major)
The incubation period between contraction and the first obvious symptoms of the disease is around 12 days. Once inhaled, variola major virus invades the oropharyngeal (mouth and throat) or the respiratory mucosa, migrates to regional lymph nodes, and begins to multiply. In the initial growth phase the virus seems to move from cell to cell, but around the 12th day, lysis of many infected cells occurs and the virus is found in the bloodstream in large numbers (this is called viremia), and a second wave of multiplication occurs in the spleen, bone marrow, and lymph nodes. The initial or prodromal symptoms are similar to other viral diseases such as influenza and the common cold: fever of at least 38.5 °C (101 °F), muscle pain, malaise, headache and prostration. As the digestive tract is commonly involved, nausea and vomiting and backache often occur. The prodrome, or preeruptive stage, usually lasts 2–4 days. By days 12–15 the first visible lesions—small reddish spots called enanthem—appear on mucous membranes of the mouth, tongue, palate, and throat, and temperature falls to near normal. These lesions rapidly enlarge and rupture, releasing large amounts of virus into the saliva.[7]
Smallpox virus preferentially attacks skin cells, causing the characteristic pimples (called macules) associated with the disease. A rash develops on the skin 24 to 48 hours after lesions on the mucous membranes appear. Typically the macules first appear on the forehead, then rapidly spread to the whole face, proximal portions of extremities, the trunk, and lastly to distal portions of extremities. The process takes no more than 24 to 36 hours, after which no new lesions appear.[7] At this point variola major infection can take several very different courses, resulting in four types of smallpox disease based on the Rao classification:[21] ordinary, modified, malignant (or flat), and hemorrhagic. Historically, smallpox has an overall fatality rate of about 30%; however, the malignant and hemorrhagic forms are usually fatal.[22]


Ninety percent or more of smallpox cases among unvaccinated persons are of the ordinary type.[20] In this form of the disease, by the second day of the rash the macules become raised papules. By the third or fourth day the papules fill with an opalescent fluid to become vesicles. This fluid becomes opaque and turbid within 24–48 hours, giving them the appearance of pustules; however, the so-called pustules are filled with tissue debris, not pus.[7]
By the sixth or seventh day, all the skin lesions have become pustules. Between seven and ten days the pustules mature and reach their maximum size. The pustules are sharply raised, typically round, tense, and firm to the touch. The pustules are deeply embedded in the dermis, giving them the feel of a small bead in the skin. Fluid slowly leaks from the pustules, and by the end of the second week the pustules deflate, and start to dry up, forming crusts (or scabs). By day 16–20 scabs have formed over all the lesions, which have started to flake off, leaving depigmented scars.[23]
Ordinary smallpox generally produces a discrete rash, in which the pustules stand out on the skin separately. The distribution of the rash is densest on the face; denser on the extremities than on the trunk; and on the extremities, denser on the distal parts than on the proximal. The palms of the hands and soles of the feet are involved in the majority of cases. Sometimes, the blisters merge into sheets, forming a confluent rash, which begin to detach the outer layers of skin from the underlying flesh. Patients with confluent smallpox often remain ill even after scabs have formed over all the lesions. In one case series, the case-fatality rate in confluent smallpox was 62%.[20]
Man suffering from severe hemorrhagic-type smallpox.


Referring to the character of the eruption and the rapidity of its development, modified smallpox occurs mostly in previously vaccinated people. In this form the prodromal illness still occurs but may be less severe than in the ordinary type. There is usually no fever during evolution of the rash. The skin lesions tend to be fewer and evolve more quickly, are more superficial, and may not show the uniform characteristic of more typical smallpox.[23] Modified smallpox is rarely, if ever, fatal. This form of variola major is more easily confused with chickenpox.[20]


In malignant-type smallpox (also called flat smallpox) the lesions remain almost flush with the skin at the time when raised vesicles form in the ordinary type. It is unknown why some people develop this type. Historically, it accounted for 5%–10% of cases, and the majority (72%) were children.[24] Malignant smallpox is accompanied by a severe prodromal phase that lasts 3–4 days, prolonged high fever, and severe symptoms of toxemia. The rash on the tongue and palate is extensive. Skin lesions mature slowly and by the seventh or eighth day they are flat and appear to be buried in the skin. Unlike ordinary-type smallpox, the vesicles contain little fluid, are soft and velvety to the touch, and may contain hemorrhages. Malignant smallpox is nearly always fatal.[20]


Hemorrhagic smallpox is a severe form that is accompanied by extensive bleeding into the skin, mucous membranes, and gastrointestinal tract. This form develops in approximately 2% of infections and occurred mostly in adults.[20] In hemorrhagic smallpox the skin does not blister, but remains smooth. Instead, bleeding occurs under the skin, making it look charred and black,[20] hence this form of the disease is also known as black pox.[25]
In the early, or fulminating form, hemorrhaging appears on the second or third day as sub-conjunctival bleeding turns the whites of the eyes deep red. Hemorrhagic smallpox also produces a dusky erythema, petechiae, and hemorrhages in the spleen, kidney, serosa, muscle, and, rarely, the epicardium, liver, testes, ovaries and bladder. Death often occurs suddenly between the fifth and seventh days of illness, when only a few insignificant skin lesions are present. A later form of the disease occurs in patients who survive for 8–10 days. The hemorrhages appear in the early eruptive period, and the rash is flat and does not progress beyond the vesicular stage.[20] Patients in the early stage of disease show a decrease in coagulation factors (e.g. platelets, prothrombin, and globulin) and an increase in circulating antithrombin. Patients in the late stage have significant thrombocytopenia; however, deficiency of coagulation factors is less severe. Some in the late stage also show increased antithrombin.[7] This form of smallpox occurs in anywhere from 3 to 25% of fatal cases depending on the virulence of the smallpox strain.[22] Hemorrhagic smallpox is usually fatal.[20]


Variola virus (Smallpox)
This transmission electron micrograph depicts a number of smallpox virions. The "dumbbell-shaped" structure inside the virion is the viral core, which contains the viral DNA; Mag. = ~370,000x
Virus classification
Group: Group I (dsDNA)
Order: Unassigned
Family: Poxviridae
Subfamily: Chordopoxvirinae
Genus: Orthopoxvirus
Type species
Vaccinia virus
Variola virus
Smallpox is caused by infection with variola virus, which belongs to the genus Orthopoxvirus, the family Poxviridae and subfamily chordopoxvirinae. Variola is a large brick-shaped virus measuring approximately 302 to 350 nanometers by 244 to 270 nm,[26] with a single linear double stranded DNA genome 186 kilobase pairs (kbp) in size and containing a hairpin loop at each end.[27][28] The two classic varieties of smallpox are variola major and variola minor.
Four orthopoxviruses cause infection in humans: variola, vaccinia, cowpox, and monkeypox. Variola virus infects only humans in nature, although primates and other animals have been infected in a laboratory setting. Vaccinia, cowpox, and monkeypox viruses can infect both humans and other animals in nature.[20]
The lifecycle of poxviruses is complicated by having multiple infectious forms, with differing mechanisms of cell entry. Poxviruses are unique among DNA viruses in that they replicate in the cytoplasm of the cell rather than in the nucleus. In order to replicate, poxviruses produce a variety of specialized proteins not produced by other DNA viruses, the most important of which is a viral-associated DNA-dependent RNA polymerase.
Both enveloped and unenveloped virions are infectious. The viral envelope is made of modified Golgi membranes containing viral-specific polypeptides, including hemagglutinin.[27] Infection with either variola major or variola minor confers immunity against the other.[7]


Transmission occurs through inhalation of airborne variola virus, usually droplets expressed from the oral, nasal, or pharyngeal mucosa of an infected person. It is transmitted from one person to another primarily through prolonged face-to-face contact with an infected person, usually within a distance of 6 feet (1.8 m), but can also be spread through direct contact with infected bodily fluids or contaminated objects (fomites) such as bedding or clothing. Rarely, smallpox has been spread by virus carried in the air in enclosed settings such as buildings, buses, and trains.[19] The virus can cross the placenta, but the incidence of congenital smallpox is relatively low.[7] Smallpox is not notably infectious in the prodromal period and viral shedding is usually delayed until the appearance of the rash, which is often accompanied by lesions in the mouth and pharynx. The virus can be transmitted throughout the course of the illness, but is most frequent during the first week of the rash, when most of the skin lesions are intact.[20] Infectivity wanes in 7 to 10 days when scabs form over the lesions, but the infected person is contagious until the last smallpox scab falls off.[29]
Smallpox is highly contagious, but generally spreads more slowly and less widely than some other viral diseases, perhaps because transmission requires close contact and occurs after the onset of the rash. The overall rate of infection is also affected by the short duration of the infectious stage. In temperate areas, the number of smallpox infections were highest during the winter and spring. In tropical areas, seasonal variation was less evident and the disease was present throughout the year.[20] Age distribution of smallpox infections depends on acquired immunity. Vaccination immunity declines over time and is probably lost in all but the most recently vaccinated populations.[7] Smallpox is not known to be transmitted by insects or animals and there is no asymptomatic carrier state.[20]


The clinical definition of smallpox is an illness with acute onset of fever greater than 101 °F (38.3 °C) followed by a rash characterized by firm, deep seated vesicles or pustules in the same stage of development without other apparent cause.[20] If a clinical case is observed, smallpox is confirmed using laboratory tests.
Microscopically, poxviruses produce characteristic cytoplasmic inclusions, the most important of which are known as Guarnieri bodies, and are the sites of viral replication. Guarnieri bodies are readily identified in skin biopsies stained with hematoxylin and eosin, and appear as pink blobs. They are found in virtually all poxvirus infections but the absence of Guarnieri bodies cannot be used to rule out smallpox.[30] The diagnosis of an orthopoxvirus infection can also be made rapidly by electron microscopic examination of pustular fluid or scabs. However, all orthopoxviruses exhibit identical brick-shaped virions by electron microscopy.[7]
Definitive laboratory identification of variola virus involves growing the virus on chorioallantoic membrane (part of a chicken embryo) and examining the resulting pock lesions under defined temperature conditions.[31] Strains may be characterized by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) analysis. Serologic tests and enzyme linked immunosorbent assays (ELISA), which measure variola virus-specific immunoglobulin and antigen have also been developed to assist in the diagnosis of infection.[32]
Chickenpox was commonly confused with smallpox in the immediate post-eradication era. Chickenpox and smallpox can be distinguished by several methods. Unlike smallpox, chickenpox does not usually affect the palms and soles. Additionally, chickenpox pustules are of varying size due to variations in the timing of pustule eruption: smallpox pustules are all very nearly the same size since the viral effect progresses more uniformly. A variety of laboratory methods are available for detecting chickenpox in evaluation of suspected smallpox cases.[20]


Components of a modern smallpox vaccination kit including the diluent, a vial of Dryvax vaccinia vaccine, and a bifurcated needle.
The earliest procedure used to prevent smallpox was inoculation (also known as variolation). Inoculation was possibly practiced in India as early as 1000 BC,[33] and involved either nasal insufflation of powdered smallpox scabs, or scratching material from a smallpox lesion into the skin. However, the idea that inoculation originated in India has been challenged as few of the ancient Sanskrit medical texts described the process of inoculation.[34] Accounts of inoculation against smallpox in China can be found as early as the late 10th century, and the procedure was widely practiced by the 16th century, during the Ming Dynasty.[35] If successful, inoculation produced lasting immunity to smallpox. However, because the person was infected with variola virus, a severe infection could result, and the person could transmit smallpox to others. Variolation had a 0.5–2% mortality rate, considerably less than the 20–30% mortality rate of the disease itself.[20]
Lady Mary Wortley Montagu observed smallpox inoculation during her stay in the Ottoman Empire, writing detailed accounts of the practice in her letters, and enthusiastically promoted the procedure in England upon her return in 1718.[36] In 1721, Cotton Mather and colleagues provoked controversy in Boston by inoculating hundreds. In 1796, Edward Jenner, a doctor in Berkeley, Gloucestershire, rural England, discovered that immunity to smallpox could be produced by inoculating a person with material from a cowpox lesion. Cowpox is a poxvirus in the same family as variola. Jenner called the material used for inoculation vaccine, from the root word vacca, which is Latin for cow. The procedure was much safer than variolation, and did not involve a risk of smallpox transmission. Vaccination to prevent smallpox was soon practiced all over the world. During the 19th century, the cowpox virus used for smallpox vaccination was replaced by vaccinia virus. Vaccinia is in the same family as cowpox and variola but is genetically distinct from both. The origin of vaccinia virus and how it came to be in the vaccine are not known.[20]
An 1802 cartoon of the early controversy surrounding Edward Jenner's vaccination theory, showing using his cowpox-derived smallpox vaccine causing cattle to emerge from patients.
The current formulation of smallpox vaccine is a live virus preparation of infectious vaccinia virus. The vaccine is given using a bifurcated (two-pronged) needle that is dipped into the vaccine solution. The needle is used to prick the skin (usually the upper arm) a number of times in a few seconds. If successful, a red and itchy bump develops at the vaccine site in three or four days. In the first week, the bump becomes a large blister (called a "Jennerian vesicle") which fills with pus, and begins to drain. During the second week, the blister begins to dry up and a scab forms. The scab falls off in the third week, leaving a small scar.[37]
The antibodies induced by vaccinia vaccine are cross-protective for other orthopoxviruses, such as monkeypox, cowpox, and variola (smallpox) viruses. Neutralizing antibodies are detectable 10 days after first-time vaccination, and seven days after revaccination. Historically, the vaccine has been effective in preventing smallpox infection in 95% of those vaccinated.[38] Smallpox vaccination provides a high level of immunity for three to five years and decreasing immunity thereafter. If a person is vaccinated again later, immunity lasts even longer. Studies of smallpox cases in Europe in the 1950s and 1960s demonstrated that the fatality rate among persons vaccinated less than 10 years before exposure was 1.3%; it was 7% among those vaccinated 11 to 20 years prior, and 11% among those vaccinated 20 or more years prior to infection. By contrast, 52% of unvaccinated persons died.[39]
A demonstration by medical personnel on use of a bifurcated needle to deliver the smallpox vaccine, 2002.
There are side effects and risks associated with the smallpox vaccine. In the past, about 1 out of 1,000 people vaccinated for the first time experienced serious, but non-life-threatening, reactions including toxic or allergic reaction at the site of the vaccination (erythema multiforme), spread of the vaccinia virus to other parts of the body, and to other individuals. Potentially life-threatening reactions occurred in 14 to 500 people out of every 1 million people vaccinated for the first time. Based on past experience, it is estimated that 1 or 2 people in 1 million (0.000198%) who receive the vaccine may die as a result, most often the result of postvaccinial encephalitis or severe necrosis in the area of vaccination (called progressive vaccinia).[38]
Given these risks, as smallpox became effectively eradicated and the number of naturally occurring cases fell below the number of vaccine-induced illnesses and deaths, routine childhood vaccination was discontinued in the United States in 1972, and was abandoned in most European countries in the early 1970s.[5][40] Routine vaccination of health care workers was discontinued in the U.S. in 1976, and among military recruits in 1990 (although military personnel deploying to the Middle East and Korea still receive the vaccination.[41]) By 1986, routine vaccination had ceased in all countries.[5] It is now primarily recommended for laboratory workers at risk for occupational exposure.[20]


Smallpox vaccination within three days of exposure will prevent or significantly lessen the severity of smallpox symptoms in the vast majority of people. Vaccination four to seven days after exposure can offer some protection from disease or may modify the severity of disease.[38] Other than vaccination, treatment of smallpox is primarily supportive, such as wound care and infection control, fluid therapy, and possible ventilator assistance. Flat and hemorrhagic types of smallpox are treated with the same therapies used to treat shock, such as fluid resuscitation. People with semi-confluent and confluent types of smallpox may have therapeutic issues similar to patients with extensive skin burns.[42]
No drug is currently approved for the treatment of smallpox. However, antiviral treatments have improved since the last large smallpox epidemics, and studies suggest that the antiviral drug cidofovir might be useful as a therapeutic agent. The drug must be administered intravenously, however, and may cause serious kidney toxicity.[43]


A case of smallpox, 1886
The overall case-fatality rate for ordinary-type smallpox is about 30%, but varies by pock distribution: ordinary type-confluent is fatal about 50–75% of the time, ordinary-type semi-confluent about 25–50% of the time, in cases where the rash is discrete the case-fatality rate is less than 10%. The overall fatality rate for children younger than 1 year of age is 40–50%. Hemorrhagic and flat types have the highest fatality rates. The fatality rate for flat-type is 90% or greater and nearly 100% is observed in cases of hemorrhagic smallpox. The case-fatality rate for variola minor is 1% or less.[23] There is no evidence of chronic or recurrent infection with variola virus.[23]
In fatal cases of ordinary smallpox, death usually occurs between the tenth and sixteenth days of the illness. The cause of death from smallpox is not clear, but the infection is now known to involve multiple organs. Circulating immune complexes, overwhelming viremia, or an uncontrolled immune response may be contributing factors.[20] In early hemorrhagic smallpox, death occurs suddenly about six days after the fever develops. Cause of death in hemorrhagic cases involved heart failure, sometimes accompanied by pulmonary edema. In late hemorrhagic cases, high and sustained viremia, severe platelet loss and poor immune response were often cited as causes of death.[24] In flat smallpox modes of death are similar to those in burns, with loss of fluid, protein and electrolytes beyond the capacity of the body to replace or acquire, and fulminating sepsis.[42]


Complications of smallpox arise most commonly in the respiratory system and range from simple bronchitis to fatal pneumonia. Respiratory complications tend to develop on about the eighth day of the illness and can be either viral or bacterial in origin. Secondary bacterial infection of the skin is a relatively uncommon complication of smallpox. When this occurs, the fever usually remains elevated.[20]
Other complications include encephalitis (1 in 500 patients), which is more common in adults and may cause temporary disability; permanent pitted scars, most notably on the face; and complications involving the eyes (2% of all cases). Pustules can form on the eyelid, conjunctiva, and cornea, leading to complications such as conjunctivitis, keratitis, corneal ulcer, iritis, iridocyclitis, and optic atrophy. Blindness results in approximately 35% to 40% of eyes affected with keratitis and corneal ulcer. Hemorrhagic smallpox can cause subconjunctival and retinal hemorrhages. In 2% to 5% of young children with smallpox, virions reach the joints and bone, causing osteomyelitis variolosa. Lesions are symmetrical, most common in the elbows, tibia, and fibula, and characteristically cause separation of an epiphysis and marked periosteal reactions. Swollen joints limit movement, and arthritis may lead to limb deformities, ankylosis, malformed bones, flail joints, and stubby fingers.[7]


Viral evolution

The date of the appearance of smallpox is not settled. It most likely evolved from a rodent virus between 68,000 and 16,000 years ago.[44][45] The wide range of dates is due to the different records used to calibrate the molecular clock. One clade was the variola major strains (the more clinically severe form of smallpox) which spread from Asia between 400 and 1,600 years ago. A second clade included both alastrim minor (a phenotypically mild smallpox) described from the American continents and isolates from West Africa which diverged from an ancestral strain between 1,400 and 6,300 years before present. This clade further diverged into two subclades at least 800 years ago.
A second estimate has placed the separation of variola from Taterapox at 3000–4000 years ago.[46] This is consistent with archaeological and historical evidence regarding the appearance of smallpox as a human disease which suggests a relatively recent origin. However if the mutation rate is assumed to be similar to that of the herpesviruses the divergence date between variola from Taterapox has been estimated to be 50,000 years ago.[46] While this is consistent with the other published estimates it suggests that the archaeological and historical evidence is very incomplete. Better estimates of mutation rates in these viruses are needed.
It seems to have emerged in its endemic form in India 2500–3000 years ago.[47]

Other history

The earliest credible clinical evidence of smallpox is found in the smallpox-like disease in medical writings from ancient India (as early as 1500 BC),[48] Egyptian mummy of Ramses V who died more than 3000 years ago (1145 BC).[9] and China (1122 BC).[49] It has been speculated that Egyptian traders brought smallpox to India during the 1st millennium BC, where it remained as an endemic human disease for at least 2000 years. Smallpox was probably introduced into China during the 1st century AD from the southwest, and in the 6th century was carried from China to Japan.[24] In Japan, the epidemic of 735–737 is believed to have killed as much as one-third of the population.[10][50] At least seven religious deities have been specifically dedicated to smallpox, such as the god Sopona in the Yoruba religion. In India, the Hindu goddess of smallpox, Sitala Mata, was worshiped in temples throughout the country.[51]
Statue of Sopona, the West African god thought to inflict the disease.
The timing of the arrival of smallpox in Europe and south-western Asia is less clear. Smallpox is not clearly described in either the Old or New Testaments of the Bible or in the literature of the Greeks or Romans. While some have identified the Plague of Athens – which was said to have originated in "Ethiopia" and Egypt – or the plague that lifted Carthage's 396 BC siege of Syracuse with smallpox,[2] many scholars agree it is very unlikely such a serious disease as variola major would have escaped being described by Hippocrates if it had existed in the Mediterranean region during his lifetime.[52] While the Antonine Plague that swept through the Roman Empire in AD 165–180 may have been caused by smallpox,[53] Saint Nicasius of Rheims became the patron saint of smallpox victims for having supposedly survived a bout in 450,[2] and Saint Gregory of Tours recorded a similar outbreak in France and Italy in 580, the first use of the term variola;[2] other historians speculate that Arab armies first carried smallpox from Africa into Southwestern Europe during the 7th and 8th centuries.[24] In the 9th century the Persian physician, Rhazes, provided one of the most definitive descriptions of smallpox and was the first to differentiate smallpox from measles and chickenpox in his Kitab fi al-jadari wa-al-hasbah (The Book of Smallpox and Measles).[54] During the Middle Ages, smallpox made periodic incursions into Europe but did not become established there until the population increased and population movement became more active during the era of the Crusades. By the 16th century smallpox had become well established across most of Europe.[24] With its introduction into populated areas in India, China and Europe, smallpox affected mainly children, with periodic epidemics that killed as many as 30% of those infected. The settled existence of smallpox in Europe was of particular historical importance, since successive waves of exploration and colonization by Europeans tended to spread the disease to other parts of the world. By the 16th century it had become an important cause of morbidity and mortality throughout much of the world.[24]
Drawing accompanying text in Book XII of the 16th-century Florentine Codex (compiled 1540–1585), showing Nahuas of conquest-era central Mexico suffering from smallpox.
There are no credible descriptions of smallpox-like disease in the Americas before the westward exploration by Europeans in the 15th century AD.[45] Smallpox was introduced into the Caribbean island of Hispaniola in 1509, and into the mainland in 1520, when Spanish settlers from Hispaniola arrived in Mexico bringing smallpox with them. Smallpox devastated the native Amerindian population and was an important factor in the conquest of the Aztecs and the Incas by the Spaniards.[24] Settlement of the east coast of North America in 1633 in Plymouth, Massachusetts was also accompanied by devastating outbreaks of smallpox among Native American populations,[55] and subsequently among the native-born colonists.[56] Some estimates indicate case fatality rates of 80–90% in Native American populations during smallpox epidemics.[57] Smallpox was introduced into Australia in 1789 and again in 1829.[24] Although the disease was never endemic on the continent,[24] it was the principal cause of death in Aboriginal populations between 1780 and 1870.[58]
Smallpox sufferer in the United States, 1912
By the mid-18th century smallpox was a major endemic disease everywhere in the world except in Australia and in several small islands. In Europe smallpox was a leading cause of death in the 18th century, killing an estimated 400,000 Europeans each year.[59] Through the century smallpox resulted in the deaths of perhaps 10% of all the infants of Sweden every year,[10] and the death rate of infants in Russia may have been even higher.[49] The widespread use of variolation in a few countries, notably Great Britain, its North American colonies, and China, somewhat reduced the impact of smallpox among the wealthy classes during the latter part of the 18th century, but a real reduction in its incidence did not occur until vaccination became a common practice toward the end of the 19th century. Improved vaccines and the practice of re-vaccination led to a substantial reduction in cases in Europe and North America, but smallpox remained almost unchecked everywhere else in the world. In the United States and South Africa a much milder form of smallpox, variola minor, was recognized just before the close of the 19th century. By the mid-20th century variola minor occurred along with variola major, in varying proportions, in many parts of Africa. Patients with variola minor experience only a mild systemic illness, are often ambulant throughout the course of the disease, and are therefore able to more easily spread disease. Infection with v. minor induces immunity against the more deadly variola major form. Thus as v. minor spread all over the USA, into Canada, the South American countries and Great Britain it became the dominant form of smallpox, further reducing mortality rates.[24]


Vaccination during the Smallpox Eradication and Measles Control Program in Niger, February, 1969.
The English physician Edward Jenner demonstrated the effectiveness of cowpox to protect humans from smallpox in 1796, after which various attempts were made to eliminate smallpox on a regional scale. As early as 1803, the Spanish Crown organized a mission (the Balmis expedition) to transport the vaccine to the Spanish colonies in the Americas and the Philippines, and establish mass vaccination programs there.[60] The U.S. Congress passed the Vaccine Act of 1813 to ensure that safe smallpox vaccine would be available to the American public. By about 1817, a very solid state vaccination program existed in the Dutch East Indies.[61] In British India a program was launched to propagate smallpox vaccination, through Indian vaccinators, under the supervision of European officials.[62] Nevertheless, British vaccination efforts in India, and in Burma in particular, were hampered by stubborn indigenous preference for inoculation and distrust of vaccination, despite tough legislation, improvements in the local efficacy of the vaccine and vaccine preservative, and education efforts.[63] By 1832, the federal government of the United States established a smallpox vaccination program for Native Americans.[64] In 1842, the United Kingdom banned inoculation, later progressing to mandatory vaccination. The British government introduced compulsory smallpox vaccination by an Act of Parliament in 1853.[65] In the United States, from 1843 to 1855 first Massachusetts, and then other states required smallpox vaccination. Although some disliked these measures,[49] coordinated efforts against smallpox went on, and the disease continued to diminish in the wealthy countries. By 1897, smallpox had largely been eliminated from the United States.[66] In Northern Europe a number of countries had eliminated smallpox by 1900, and by 1914, the incidence in most industrialized countries had decreased to comparatively low levels. Vaccination continued in industrialized countries, until the mid to late 1970s as protection against reintroduction. Australia and New Zealand are two notable exceptions; neither experienced endemic smallpox and never vaccinated widely, relying instead on protection by distance and strict quarantines.[67]
Smallpox quarantine order, California, ca 1910
The first hemisphere-wide effort to eradicate smallpox was made in 1950 by the Pan American Health Organization.[68] The campaign was successful in eliminating smallpox from all American countries except Argentina, Brazil, Colombia, and Ecuador.[67] In 1958 Professor Viktor Zhdanov, Deputy Minister of Health for the USSR, called on the World Health Assembly to undertake a global initiative to eradicate smallpox. The proposal (Resolution WHA11.54) was accepted in 1959.[69] At this point, 2 million people were dying from smallpox every year. Overall, however, the progress towards eradication was disappointing, especially in Africa and in the Indian subcontinent. In 1966 an international team, the Smallpox Eradication Unit, was formed under the leadership of an American, Donald Henderson.[70] In 1967, the World Health Organization intensified the global smallpox eradication by contributing $2.4 million annually to the effort, and adopted the new disease surveillance method promoted by Czech epidemiologist Karel Raška.[71][72]
Two-year old Rahima Banu of Bangladesh (pictured) was the last person infected with naturally occurring Variola major, in 1975
In the early 1950s an estimated 50 million cases of smallpox occurred in the world each year.[5] To eradicate smallpox, each outbreak had to be stopped from spreading, by isolation of cases and vaccination of everyone who lived close by. This process is known as "ring vaccination". The key to this strategy was monitoring of cases in a community (known as surveillance) and containment. The initial problem the WHO team faced was inadequate reporting of smallpox cases, as many cases did not come to the attention of the authorities. The fact that humans are the only reservoir for smallpox infection, and that carriers did not exist, played a significant role in the eradication of smallpox. The WHO established a network of consultants who assisted countries in setting up surveillance and containment activities. Early on donations of vaccine were provided primarily by the Soviet Union and the United States, but by 1973, more than 80% of all vaccine was produced in developing countries.[67]
The last major European outbreak of smallpox was in 1972 in Yugoslavia, after a pilgrim from Kosovo returned from the Middle East, where he had contracted the virus. The epidemic infected 175 people, causing 35 deaths. Authorities declared martial law, enforced quarantine, and undertook widespread re-vaccination of the population, enlisting the help of the WHO. In two months, the outbreak was over.[73] Prior to this, there had been a smallpox outbreak in May–July 1963 in Stockholm, Sweden, brought from the Far East by a Swedish sailor; this had been dealt with by quarantine measures and vaccination of the local population.[74]
By the end of 1975, smallpox persisted only in the Horn of Africa. Conditions were very difficult in Ethiopia and Somalia, where there were few roads. Civil war, famine, and refugees made the task even more difficult. An intensive surveillance and containment and vaccination program was undertaken in these countries in early and mid-1977, under the direction of Australian microbiologist Frank Fenner. As the campaign neared its goal, Fenner and his team played an important role in verifying eradication.[75] The last naturally occurring case of indigenous smallpox (Variola minor) was diagnosed in Ali Maow Maalin, a hospital cook in Merca, Somalia, on 26 October 1977.[20] The last naturally occurring case of the more deadly Variola major had been detected in October 1975 in a two-year-old Bangladeshi girl, Rahima Banu.[25]
The global eradication of smallpox was certified, based on intense verification activities in countries, by a commission of eminent scientists on 9 December 1979 and subsequently endorsed by the World Health Assembly on 8 May 1980.[5][76] The first two sentences of the resolution read:
"Having considered the development and results of the global program on smallpox eradication initiated by WHO in 1958 and intensified since 1967 … Declares solemnly that the world and its peoples have won freedom from smallpox, which was a most devastating disease sweeping in epidemic form through many countries since earliest time, leaving death, blindness and disfigurement in its wake and which only a decade ago was rampant in Africa, Asia and South America."
—World Health Organization, Resolution WHA33.3[77]


Three former directors of the Global Smallpox Eradication Program read the news that smallpox had been globally eradicated, 1980
The last cases of smallpox in the world occurred in an outbreak of two cases (one of which was fatal) in Birmingham, UK in 1978. A medical photographer, Janet Parker, contracted the disease at the University of Birmingham Medical School and died on September 11, 1978,[77] after which the scientist responsible for smallpox research at the university, Professor Henry Bedson, committed suicide.[4] In light of this incident, all known stocks of smallpox were destroyed or transferred to one of two WHO reference laboratories which had BSL-4 facilities; the Centers for Disease Control and Prevention (CDC) in the United States and the State Research Center of Virology and Biotechnology VECTOR in Koltsovo, Russia.[78]
In 1986, the World Health Organization first recommended destruction of the virus, and later set the date of destruction to be 30 December 1993. This was postponed to 30 June 1999.[79] Due to resistance from the U.S. and Russia, in 2002 the World Health Assembly agreed to permit the temporary retention of the virus stocks for specific research purposes.[80] Destroying existing stocks would reduce the risk involved with ongoing smallpox research; the stocks are not needed to respond to a smallpox outbreak.[81] Some scientists have argued that the stocks may be useful in developing new vaccines, antiviral drugs, and diagnostic tests;[82] however, a 2010 review by a team of public health experts appointed by the World Health Organization concluded that no essential public health purpose is served by the U.S. and Russia continuing to retain virus stocks.[83] The latter view is frequently supported in the scientific community, particularly among veterans of the WHO Smallpox Eradication Program.[84]
In March 2004 smallpox scabs were found tucked inside an envelope in a book on Civil War medicine in Santa Fe, New Mexico.[85] The envelope was labeled as containing scabs from a vaccination and gave scientists at the Centers for Disease Control and Prevention an opportunity to study the history of smallpox vaccination in the U.S.

Society and culture

Biological warfare

The British considered using smallpox as a biological warfare agent at the Siege of Fort Pitt during the French and Indian Wars (1754–63) against France and its Native American allies.[86][87] Although it is not clear whether the actual use of smallpox had official sanction, on June 24, 1763, William Trent, a local trader, wrote, "Out of our regard for them [sc. representatives of the besieging Delawares], we gave them two Blankets and an Handkerchief out of the Small Pox Hospital. I hope it will have the desired effect."[88][89] Historians do not agree on whether this effort to broadcast the disease was successful. It has also been alleged that smallpox was used as a weapon during the American Revolutionary War (1775–83).[90][91]
Subsequently, according to an article in Journal of Australian Studies, in 1789, British marines used smallpox against indigenous tribes in New South Wales.[92] This occasion was also discussed earlier in Bulletin of the History of Medicine[93] and by David Day in his book Claiming a Continent A New History of Australia.[94]
During World War II, scientists from the United Kingdom, United States and Japan (Unit 731 of the imperial Japanese army) were involved in research into producing a biological weapon from smallpox.[95] Plans of large scale production were never carried through as they considered that the weapon would not be very effective due to the wide-scale availability of a vaccine.[96]
In 1947 the Soviet Union established a smallpox weapons factory in the city of Zagorsk, 75 km to the northeast of Moscow.[97] An outbreak of weaponized smallpox occurred during testing at a facility on an island in the Aral Sea in 1971. General Prof. Peter Burgasov, former Chief Sanitary Physician of the Soviet Army and a senior researcher within the Soviet program of biological weapons, described the incident:
On Vozrozhdeniya Island in the Aral Sea, the strongest recipes of smallpox were tested. Suddenly I was informed that there were mysterious cases of mortalities in Aralsk. A research ship of the Aral fleet came to within 15 km of the island (it was forbidden to come any closer than 40 km). The lab technician of this ship took samples of plankton twice a day from the top deck. The smallpox formulation—400 gr. of which was exploded on the island—"got her" and she became infected. After returning home to Aralsk, she infected several people including children. All of them died. I suspected the reason for this and called the Chief of General Staff of Ministry of Defense and requested to forbid the stop of the Alma-Ata—Moscow train in Aralsk. As a result, the epidemic around the country was prevented. I called Andropov, who at that time was Chief of KGB, and informed him of the exclusive recipe of smallpox obtained on Vozrazhdenie Island.[98][99]
Others contend that the first patient may have contracted the disease while visiting Uyaly or Komsomolsk-on-Ustyurt, two cities where the boat docked.[100][101]
Responding to international pressures, in 1991 the Soviet government allowed a joint U.S.-British inspection team to tour four of its main weapons facilities at Biopreparat. The inspectors were met with evasion and denials from the Soviet scientists, and were eventually ordered out of the facility.[102] In 1992 Soviet defector Ken Alibek alleged that the Soviet bioweapons program at Zagorsk had produced a large stockpile—as much as twenty tons—of weaponized smallpox (possibly engineered to resist vaccines, Alibek further alleged), along with refrigerated warheads to deliver it. Alibek's stories about the former Soviet program's smallpox activities have never been independently verified.
In 1997, the Russian government announced that all of its remaining smallpox samples would be moved to the Vector Institute in Koltsovo.[102] With the breakup of the Soviet Union and unemployment of many of the weapons program's scientists, U.S. government officials have expressed concern that smallpox and the expertise to weaponize it may have become available to other governments or terrorist groups who might wish to use virus as means of biological warfare.[103] Specific allegations made against Iraq in this respect, however, proved to be false.[104]
Concern has been expressed by some that artificial gene synthesis could be used to recreate the virus from existing digital genomes, for use in biological warfare.[105] Insertion of the synthesized smallpox DNA into existing related pox viruses could theoretically be used to recreate the virus.[105] The first step to mitigating this risk, it has been suggested, should be to destroy the remaining virus stocks so as to enable unequivocal criminalization of any possession of the virus.[106]

Notable cases

Famous historical figures who contracted smallpox include Lakota Chief Sitting Bull, Ramses V of Egypt,[107] the Kangxi Emperor (survived), Shunzhi Emperor and Tongzhi Emperor (refer to the official history) of China, Date Masamune of Japan (who lost an eye to the disease). Cuitláhuac, the 10th tlatoani (ruler) of the Aztec city of Tenochtitlan, died of smallpox in 1520, shortly after its introduction to the Americas, and the Incan emperor Huayna Capac died of it in 1527. More recent public figures include Guru Har Krishan, 8th Guru of the Sikhs, in 1664, Peter II of Russia in 1730 (died),[108] George Washington (survived), king Louis XV in 1774 (died) and Maximilian III Joseph, Elector of Bavaria in 1777.
Prominent families throughout the world often had several people infected by and/or perish from the disease. For example, several relatives of Henry VIII survived the disease but were scarred by it. These include his sister Margaret, Queen of Scotland, his fourth wife, Anne of Cleves, and his two daughters: Mary I of England in 1527 and Elizabeth I of England in 1562 (as an adult she would often try to disguise the pockmarks with heavy makeup). His great-niece, Mary, Queen of Scots, contracted the disease as a child but had no visible scarring.
In 1767, the 11-year old composer Wolfgang Amadeus Mozart survived a smallpox outbreak in Austria that killed Holy Roman Empress Maria Josepha, who became the second consecutive wife of Holy Roman Emperor Joseph II to die of the disease, as well as Archduchess Maria Josepha. (See Mozart and smallpox.)
In Europe, deaths from smallpox often changed dynastic succession. The only surviving son of Henry VIII, Edward VI, died from complications shortly after apparently recovering from the disease, thereby nullifying Henry's efforts to ensure a male successor to the throne (his immediate successors were all females). Louis XV of France succeeded his great-grandfather Louis XIV through a series of deaths of smallpox or measles among those earlier in the succession line. He himself died of the disease in 1774. William III lost his mother to the disease when he was only ten years old in 1660, and named his uncle Charles as legal guardian: her death from smallpox would indirectly spark a chain of events that would eventually lead to the permanent ousting of the Stuart line from the British throne. William III's wife, Mary II of England, died from smallpox as well.
In Russia, Peter II of Russia died of the disease at 15 years of age. Also, prior to becoming Russian Emperor, Peter III caught the virus and suffered greatly from it. He was left scarred and disfigured. His wife, Catherine the Great, was spared but fear of the virus clearly had its effects on her. She feared for her son and heir Pavel's safety so much that she made sure that large crowds were kept at bay and sought to isolate him. Eventually, she decided to have herself inoculated by a Scottish doctor, Thomas Dimsdale. While this was considered a controversial method at the time, she succeeded. Her son Pavel was later inoculated as well. Catherine then sought to have inoculations throughout her empire stating: "My objective was, through my example, to save from death the multitude of my subjects who, not knowing the value of this technique, and frightened of it, were left in danger." By 1800, approximately 2 million inoculations were administered in the Russian Empire.[109]
In China, the Qing Dynasty had extensive protocols to protect Manchus from Peking's endemic smallpox.
U.S. Presidents George Washington, Andrew Jackson, and Abraham Lincoln all contracted and recovered from the disease. Washington became infected with smallpox on a visit to Barbados in 1751.[110] Jackson developed the illness after being taken prisoner by the British during the American Revolution, and though he recovered, his brother Robert did not.[110] Lincoln contracted the disease during his Presidency, possibly from his son Tad, and was quarantined shortly after giving the Gettysburg address in 1863.[110]
Famous theologian Jonathan Edwards died of smallpox in 1758 following an inoculation.[111]
Soviet leader Joseph Stalin fell ill with smallpox at the age of seven. His face was badly scarred by the disease. He later had photographs retouched to make his pockmarks less apparent.[112]
Hungarian poet Ferenc Kölcsey, who wrote the Hungarian national anthem, lost his right eye to smallpox.[113]

Tradition and religion

The Hindu goddess Shitala was worshipped to prevent or cure smallpox.
As a reaction to the devastation of smallpox, smallpox gods and goddesses were invented as a mechanism to cope with the disease. Two examples of this occurred in China and India. In China, the smallpox goddess was referred to as T’ou-Shen Niang-Niang.[114] The Chinese actively worked to please the goddess and thus keep the disease at bay. For example, the Chinese referred to the smallpox pustules as "beautiful flowers"; this was an attempt to not offend the goddess and keep her happy.[115] The Chinese also took great measure to protect children from the dangers of smallpox by tricking their smallpox goddess. It was believed that the goddess enjoyed passing the disease to attractive children. This transmission was most likely to occur on the last night of the year, so children wore ugly masks to bed to trick the goddess into passing over them.[115] If infection of smallpox did occur, shrines were set up in the homes of the victims. These shrines were worshipped and offerings made to while the victim was sick. If the victim recovered, the shrines were taken away from the home in a special handmade paper chair or boat and burned. If the patient did not recover, the shrine was destroyed and curses were used to remove the goddess from the house.[114]
India’s first records of smallpox can be found in a medical book that dates back to A.D. 400. This book describes a disease that sounds exceptionally like smallpox.[115] India, like China, created a goddess in response to its exposure to smallpox. The Hindu goddess Shitala was both worshipped and feared during her reign. It was believed that this goddess was both evil and kind and had the ability to inflict victims when angered, as well as calm the fevers of the already afflicted.[116] Portraits of the goddess show her holding a broom in her right hand to continue to move the disease and a pot of cool water in the other hand in an attempt to soothe victims.[115] Shrines were created where many India natives, both healthy and not, went to worship and attempt to protect themselves from this disease. Some Indian women, in an attempt to ward off Shitala, placed plates of cooling foods and pots of water on the roofs of their homes.[117]
In medieval times, several countries held a belief in the smallpox demon, who was blamed for the disease. Such beliefs were prominent in Japan, Europe, Africa, and other parts of the world. Nearly all cultures who believed in the demon also believed that it was afraid of the color red. This led to the red treatment, where victims and their rooms would be decorated in red. The practice spread to Europe in the 12th century and was practiced by (among others) Charles V of France and Elizabeth I of England.[2] Given scientific credibility by some studies by Finsen showing red light reduced scarring,[2] the belief persisted until the 1930s.

See also