* Deadly animal prion disease appears in Europe

A highly contagious and deadly animal brain disorder has been detected in Europe for the first time. Scientists are now warning that the single case found in a wild reindeer might represent an unrecognized, widespread infection.

Chronic wasting disease (CWD) was thought to be restricted to deer, elk (Cervus canadensis) and moose (Alces alces) in North America and South Korea, but on 4 April researchers announced that the disease had been discovered in a free-ranging reindeer (Rangifer tarandus tarandus) in Norway. This is both the first time that CWD has been found in Europe and the first time that it has been found in this species in the wild anywhere in the world.

“It’s worrying — of course, especially for animals. It’s a nasty disease,” says Sylvie Benestad, an animal-disease researcher at the Norwegian Veterinary Institute in Oslo who, along with colleague Turid Vikøren, diagnosed the diseased reindeer.

A key question now is whether this is a rare — even unique — case, or if the disease is widespread but so far undetected in Europe.

“If it’s similar to our prion disease in the United States and Canada, the disease is subtle and it would be easy to miss,” says Christina Sigurdson, a pathologist at the University of California, San Diego, who has shown that reindeer can contract CWD in a laboratory environment.

Like both bovine spongiform encephalopathy — also known as mad-cow disease — and variant Creutzfeldt-Jakob disease in humans, CWD occurs when cellular proteins called prions bend into an abnormal shape, inducing neighbouring, healthy proteins to do the same. The misfolded proteins aggregate in the brain and sometimes in other tissue, causing weight loss, coordination problems and behaviour changes. There is no cure or vaccine; as far as scientists know, CWD is always fatal.

Although the disease is not known to be transmissible to humans, it is highly contagious among deer, elk and related animals, which can shed infectious misfolded prion proteins in their saliva, urine and faeces. Animals infected with CWD have been found in more than 20 states in the United States and 2 provinces in Canada. The disease has also been detected in captive animals in South Korea, which imported CWD with a shipment of live elk brought into the country for farming in the late 1990s.

The brain of an ill reindeer from Norway was found to contain misfolded proteins called prions. The infected reindeer ended up on Vikøren’s necropsy table thanks to scientists with the Norwegian Institute for Nature Research in Trondheim. They found it as they used a helicopter to track a free-ranging herd from the Nordfjella population in the alpine regions of southern Norway. Their goal was to capture adult female reindeer and collar them for satellite tracking — but when the researchers landed, they discovered a sick animal that could not move and soon died.

During the necropsy, Benestad tested for the abnormally folded proteins as a matter of routine. Eventually, a total of three different antibody-based tests all confirmed the presence of prions.

“I was very afraid,” Benestad says. During her long career as a prion researcher she has heard scientists from the United States and Canada discuss CWD, how contagious it is and how hard it is to stamp out.

It is a mystery how this disease arrived on a mountaintop in Norway. Benestad and Vikøren think it unlikely that it was it imported. They suspect that it might have arisen spontaneously, or jumped the species barrier from a prion disease in sheep called scrapie, although such a jump has never been seen before.

“The $64,000 question is what is the origin of this case of CWD in Europe,” says Glenn Telling, a prion-disease researcher at Colorado State University in Fort Collins. “What we do know is that once CWD is detected in new locations, it typically takes a foothold in that location, and is difficult to eradicate.”

Nature doi:10.1038/nature.2016.19759  Nature  Original web page at Nature


Plague-riddled prairie dogs a model for infectious disease spread

Every now and then, colonies of prairie dogs are wiped out by plague, an infectious disease most often associated with the Black Death of the 14th century.

Plague doesn’t usually kill people these days, but it’s alive and well among the millions of ground-dwelling rodents of Colorado and other western states, notably the black-tailed prairie dog. They’re resilient critters, though: following wholesale destruction of colonies, they seem to repopulate with a vengeance.

Colorado State University biologists say this sporadic ebb and flow of prairie dog plague is an ideal model for the study of rare infectious zoonotic disease — disease that can jump from wildlife to humans — like MERS (Middle East Respiratory Syndrome) and Ebola.

Plague, in all its terrible forms, is caused by the Yersinia Pestis bacterium, usually spread through flea bites. Last year in Colorado, there were a handful of human cases, including at least two deaths.

A multi-year, CSU-led study that involved trapping and testing thousands of prairie dogs across the Pawnee National Grassland, and tens of thousands of their plague-carrying fleas, was conducted by CSU biologists Daniel Salkeld and Michael Antolin, and is published Jan. 13 in BioScience.

Research scientist Salkeld and Antolin, professor and chair of biology in the College of Natural Sciences, assert that the swirl of ecological factors driving plague outbreaks in prairie dogs can lend key insights into the study of zoonotic diseases. Such diseases, among them Ebola, which swept through west Africa in 2014, are notoriously hard to study. Their outbursts are sporadic at best, making their spread trajectories elusive.

“Plague is deadly — it’s not like the common cold. It kills its host,” Salkeld said. “It affects different hosts, including rats, prairie dogs and grasshopper mice. It is reasonably rare to watch an outbreak, and doing so can give us insight into other rare diseases like Ebola.”

Throughout their analysis of plague in prairie dogs, they concluded that such diseases may “smolder” unnoticed in a population for years, rather than jump from species to species immediately before an outbreak. They also found that investigations occurring after outbreaks can be too shallow or yield false information about which host was chiefly responsible.

In other words, there’s no simple transmission model of diseases like Ebola and plague. Throughout their study, Salkeld and Antolin found that grasshopper mice and coyotes that scavenge plague-killed prairie dogs can speed transmission of the disease by spreading the disease-carrying fleas.

They also found that an outbreak in a prairie dog colony might go unnoticed for years, because the animals are dying underground. Furthermore, the mechanism that drives the spread of plague during the the smoldering, unnoticed period might be different than during a full-blown epidemic.

Ecological conditions come in bursts, too — for plague, a cool, wet season is best for the pathogen to proliferate. Prairie dogs are well adapted to surviving drought. “Prairie dogs spread like crazy during drought in Colorado,” Antolin said. “Without plague, they would probably spread faster during wet periods.”

The parallels with Ebola are without question, Antolin said. Ebola became a pandemic due to a combination of factors, including exposure of the virus in densely populated urban centers with little access to health care and sanitation. Similarly, the Black Death in medieval Europe spread due to things like concentrations of people living with animals; the pathogen was given a pathway to persist.

In the case of Ebola, they argue that the sampling of fruit bats after human outbreaks may have biased subsequent investigations toward bat-Ebola virus ecology, and other, possible host species may have been overlooked.

The researchers hope their study leads to better measures for modeling and predicting infectious disease transmission, but there are still open questions about the human-wildlife interface of disease. In future studies, Salkeld will continue to investigate this question with other human-wildlife diseases, including Lyme disease and Colorado tick fever.  Science Daily  Original web page at Science Daily


Researchers identify areas of plague risk in western United States

Researchers at SUNY Downstate Medical Center have identified and mapped areas of high probability of plague bacteria in the western United States. Their findings were published in a recent edition of the journal PeerJ.

This investigation predicted animal plague occurrence across western states based on reported occurrences of plague in sylvan (wild) and domestic animal hosts. Plague is a disease caused by Yersinia pestis, a bacterium found in rodents and their fleas in many areas around the world.

“This study used surveillance data of plague in wild and domestic animals in the American West to identify and map those areas with the greatest potential for human exposure to this infection, which can be particularly deadly when transmitted to humans,” said Michael Walsh, PhD, MPH, assistant professor in the Department of Epidemiology and Biostatistics in the School of Public Health at SUNY Downstate.

“The findings can be used by public health agencies to target specific areas for enhanced plague surveillance within areas and counties predicted to be at high risk, as well as by other research teams to direct the sampling of local wildlife populations for the identification of Yersinia pestis in wild animals that find themselves in close proximity to humans and human developed landscapes,” he added.

According to the federal Centers for Disease Control and Prevention (CDC), plague was first introduced into the United States in 1900, by rat-infested steamships that had sailed from affected areas. Epidemics occurred in port cities, with the last urban plague epidemic in the United States occurring in Los Angeles from 1924 through 1925. Plague then spread from urban rats to rural rodent species, and became entrenched in many areas of the western United States. Since that time, plague has occurred as scattered cases in rural areas. Most human cases in the United States occur in two regions: Northern New Mexico, northern Arizona, and southern Colorado; and California, southern Oregon, and far western Nevada.

The CDC also notes that in recent decades, an average of seven human plague cases has been reported each year (range: 1-17 cases per year). Plague has occurred in people of all ages (infants up to age 96), though 50% of cases occur in people ages 12-45.

The authors note in their article that while zoonotic (animal) transmission to humans is much less common in modern times, significant plague risk remains in parts of the western U.S. Moreover, risk to some threatened species that are part of the epizootic cycle can be quite substantive.

This investigation attempted to predict the risk of plague across the western US by modeling the ecologic niche of plague in sylvan and domestic animals identified between 2000 and 2015. An algorithm was used to predict this niche based on climate, altitude, land cover, and the presence of an important enzootic (carrier) species, Peromyscus maniculatus (a rodent commonly known as the North American deermouse).

This model demonstrated good predictive ability and identified areas of high risk in central Colorado, north-central New Mexico, and southwestern and northeastern California.

The presence of P. maniculatus, altitude, precipitation during the driest and wettest quarters, and distance to artificial surfaces, all contributed substantively to maximizing the gain function. These findings add to the known landscape epidemiology and infection ecology of plague in the western U.S. and may suggest locations of particular risk to be targeted for wild and domestic animal intervention.  Science Daily  Original web page at Science Daily


* Missing mice: gaps in data plague animal research

Reports of hundreds of biomedical experiments lack essential information. Two studies have unveiled widespread flaws in the reporting of animal experiments — the latest in a series of papers to criticize shoddy biomedical research.

Whereas reports of clinical trials in major medical journals routinely state how many patients die or drop out of analysis during the course of a study, animal studies generally fail to report this figure — or drop animals without saying why, according to a team led by Ulrich Dirnagl at the Charité Medical University in Berlin. That lapse could significantly bias results, the team reports in the journal PLoS Biology.

In a second study in the same journal, a team led by John Ioannidis, an epidemiologist at Stanford University in California who has repeatedly called for more reproducible and transparent research, criticizes the lack of data availability and detailed protocols in biomedical papers.

Dirnagl’s team reviewed 100 reports published between 2000 and 2013 describing 522 experiments that used rodents to test cancer and stroke treatments, and compared the numbers of animals reported in the papers’ methods and results sections. Some two-thirds of the experiments did not state whether they had dropped any animals from their final analysis. Of those that did report numbers, around 30% (53 experiments) reported that they had dropped rodents from their study analysis, but only 14 explained why.

The researchers used computer simulations to show that the levels of attrition they saw might seriously affect the results of the studies. If biomedical scientists were biased in how they dropped animals — excluding outliers that gave extreme data values, for instance — then results would be fourfold more likely to find a statistically significant result that was in fact just due to chance, and could overstate the actual effectiveness of treatments by as much as 175%, the team says.

Ioannidis’s team, meanwhile, examined a random sample of PubMed articles published from 2000 to 2014. They found that none of the 268 biomedical papers made its full data available, and all but one lacked details needed for other researchers to replicate the work. In 2000, more than 90% of examined papers lacked conflict-of-interest statements, compared with about one-third in 2014.

“I have to say I am distressed but not surprised,” says Malcolm Macleod, a stroke researcher and trial-design expert at the University of Edinburgh, UK. “These important findings are further evidence of the challenges we face in improving the quality of biomedical research.”

Both papers reinforce earlier studies that have criticized poorly designed and reported animal experiments. A study led by Macleod last year, for example, looked at over 2,500 preclinical research papers and found that many of the studies described were poorly designed; the majority did not report using recommended methods to avoid bias.

Many research journals have endorsed voluntary reporting guidelines for animal studies, but adoption is spotty.

The PLoS Biology papers come as a part of a special section on ‘meta-research’: research about how research is done. The number of meta-research studies is increasing, says Marcus Munafò, a biological psychologist at the University of Bristol, UK, who writes about ways to improve scientific rigour. “These studies illustrate what the scope of the problem is,” he says, adding that they should be welcomed as an opportunity to boost scientific quality.

Nature doi:10.1038/nature.2015.19101   Nature  Original web page at Nature


Cattle disease spread by vets, not cows

A cattle disease that affected more than 5,000 cows, over 500 of which were killed, was probably spread by vets farmers and cattle traders in Germany, according to one of the first research articles published in the new open access journal Heliyon. The authors of the study, from Friedrich-Loeffler-Institute (FLI), Germany, say farmers and people who visit farms should take biosecurity measures like wearing disposable clothes where there is a risk of infection.

One of the most important infectious diseases in cattle, Bovine Viral Diarrhea (BVD) leads to severe disease and significant economic losses globally. Caused by the Bovine Viral Diarrhea Virus (BVDV), BVD suppresses the immune system and causes a variety of symptoms, including respiratory problems, infertility, and abortion.

Because of its biological and economic significance, an attempt has been made to eradicate BVD in Germany. This has in some farms resulted in a cattle population that has neither been exposed to the virus nor vaccinated, making it more susceptible to infection.

In 2012 a highly virulent type of BVDV virus (BVDV-2c) was introduced into a cattle farm in Germany and transmitted to other farms. This led to several outbreaks and a high number of deaths among the 5,325 affected cattle on 21 farms. “A dairy farmer first noticed a reduction in milk yield, respiratory symptoms, nasal discharge, fever, sporadic diarrhea and sudden deaths — these symptoms were also noted on other farms as the infection spread, but did not immediately indicate BVD as the cause,” said Dr. Jörn Gethmann, lead author of the study from Friedrich-Loeffler-Institute. “We were surprised by the high morbidity and mortality an induced by a BVDV strain in this outbreak.”

The researchers supported the competent local authorities in tracing the spread of the virus. They visited eight farms and obtained data on a further 13 farms. They discovered that the virus was not transmitted directly by infected cattle, but mostly by people such as vets and traders who were moving between farms. “We were surprised to see the effective transmission to other farms without persistently infected animals involved,” commented Dr. Gethmann.

Lab analyses revealed the source of the outbreak was a BVD type 2c virus that has a particular addition to its genome. The virus appears to be associated with more severe symptoms than BVD; the fatality rate was up to 60% and between 2.3% and 29.5% of the cattle on each farm died during the outbreak.

Once the cause was identified, swift measures were taken to control the outbreak. Veterinary authorities imposed trade restrictions on affected farms. People who had been in contact with infected cattle were generally advised to increase biosecurity measures, for example by wearing disposable clothing. On some farms, affected animals were vaccinated against BVD to reduce clinical signs as an ’emergency measure’.

This approach stopped the further spread of the disease. However, the researchers say it is important to revisit control programs regularly and adapt them to the changing situation, for example with new virulent strains arising.

“The results of our study may help to revise existing BVD control regulations and increase biosecurity in cattle farms, in particular by reducing the risk of disease transmission through person contacts and trade,” said Dr. Gethmann. “We also hope our study will inform farmers about the risks of the introduction of new BVD types into their farms.”  Science Daily  Original web page at Science Daily


A lion tale: Humans cause most mountain lion deaths in Southern California

The biggest threat to Southern California mountain lions is us, confirms a comprehensive 13-year study of the population’s mortality and survival from the University of California, Davis. The study, published in the journal PLOS ONE, combined genetic and demographic data to determine that even though hunting mountain lions is prohibited in California, humans caused more than half the known deaths of mountain lions studied. Most were killed through vehicle collisions, depredation permits, illegal shootings, public-safety removals or human-caused wildfire. Annual survival rates were only about 56 percent.

Exacerbating the problem is an interstate highway, I-15, a major thoroughfare connecting San Bernardino, Riverside and San Diego counties that has proven nearly impossible for the mountain lions to cross. It bisects the study area, which stretches from Orange County, south to the Mexican border and east to the Salton Sea. Crossing the interstate, especially for the animals of breeding age, is important for this population’s declining genetic diversity — and long-term health and survival. Most of the available mountain lion habitat in Southern California is sandwiched between the greater Los Angeles and San Diego areas, home to a growing population of about 20 million people.

Lead author Winston Vickers, an associate veterinarian with the UC Davis Wildlife Health Center at the UC Davis School of Veterinary Medicine, said fragmentation of mountain lion populations by highways is happening to a serious degree in the Santa Ana mountain range, as well as elsewhere in Southern California, such as the Santa Monica Mountains. In the Santa Anas, fragmentation and genetic restriction are compounded by unusually low survival rates. This raises significant concerns about the future persistence of this population.

“Nowhere in the U.S., outside of the endangered Florida panther, have mountain lion populations been documented that are this cut off and with survival rates this low,” Vickers said. “This means that the odds of an individual animal making it across I-15, surviving to set up a territory, successfully breeding, and then their offspring breeding so the genes are spread throughout the population is harder to have happen naturally than one would expect.

During the 13-year study, the researchers detected only one mountain lion that made it across I-15 moving east to west, the direction needed to improve genetic diversity for the Santa Ana Mountains population. That male lion, M86, successfully bred and produced at least four offspring before he died. Of those four, one was poisoned, one was hit by a car, and another was taken into captivity for being too familiar with people. The fourth lion produced kittens, two of which she raised to adulthood, and one of which, F126, is known to still be alive.

“So all the genetic hopes of this population may be pinned on this one animal, F126 — a female we know is circulating,” Vickers said. “Given the odds of that female producing kittens, and those kittens producing kittens, it will take generations and generations to see if his effort, M86’s, in crossing the road was worth it.”

The situation for mountain lions in the Santa Anas, particularly, has become so dire that translocation — such as was done for the endangered Florida panther — may be necessary to prevent further genetic decline, the study warned. However, developing means to connect the population more naturally is preferable, Vickers said, such as by creating safe crossings along targeted highways.

“This population has one foot on the banana peel and one foot on the edge,” Vickers said of Santa Ana mountain lions. “Whatever we can do, we should do. Other populations are going the same direction, they’re just not as far down the road.”  Science Daily  Original web page at Science Daily


South Korean MERS outbreak spotlights lack of research

The world is watching South Korea as the latest outbreak of Middle East respiratory syndrome (MERS) unfolds. But how exactly the virus jumps to humans in the first place is still unknown, and clues to that puzzle lie thousands of kilometres away.

The cluster of hospital-associated cases in South Korea — the largest MERS outbreak outside the Middle East — has so far killed 7 people and infected 95, according to the World Health Organization (WHO). Hundreds of schools have been shut. Although the causal coronavirus, MERS-CoV, is considered a potential pandemic threat, specialists told Nature that they expect authorities to quickly bring this outbreak under control.

A much bigger challenge than emergency response, they say, is how to stop MERS being transmitted from animals to people in the Middle East, where it is endemic in camels. “The focus on South Korea would be better directed towards Saudi Arabia,” says David Heymann, a researcher at the London School of Hygiene and Tropical Medicine and chair of Public Health England, to stop the cases that continue to spark new outbreaks at the source.

Since it was first detected in Saudi Arabia in 2012, MERS-CoV has infected around 1,200 people worldwide, roughly 450 of whom have died, according to the WHO. The virus is thought to originate in bats and to jump to humans through an intermediate animal, such as camels. It does not easily spread between people, partly because it infects deep areas of the lungs, and is not coughed out. Most of the human infections, however, were the result of human-to-human spread, which can occur in hospitals when certain medical procedures combine with poor infection control to disseminate the virus. The latest clusters began when a South Korean man returned to Seoul from the Middle East, and visited four health-care facilities before he was diagnosed.

There is always a chance that as the virus spreads, it could acquire mutations that allow it to spread more easily between humans. But on 6 June, the South Korean health ministry announced that it had sequenced the virus in the current outbreak and that it was almost identical to past sequences from the Middle East. On the same day, the Chinese Center for Disease Control and Prevention posted a separate sequence to the publicly available GenBank database, from a man infected in the South Korean outbreak who then travelled to China, where he felt ill. Christian Drosten, director of the Institute of Virology at the University of Bonn Medical Centre in Germany has analysed this sequence and says that it is shows only minor mutations compared with Middle Eastern strains, none in areas of the genome thought to influence infectiousness.

A stream of new cases in South Korea might create the impression that the disease is out of control. But all cases reported so far have clear transmission routes from the initial infection, says Ian Lipkin, an outbreak specialist at Columbia University in New York. The country is now intensively tracing and isolating the contacts of those infected, and implementing strict infection controls in hospitals. Were cases springing up outside of hospitals that would be cause for worry, but that is not happening, says Lipkin.

In the Middle East, however, the virus continues to jump from camels to humans leading to hospital outbreaks. Heymann, who in 2003 led the global effort to contain severe acute respiratory syndrome, or SARS, says that authorities in the Middle East should do more to investigate how people catch the virus from camels.

Such studies would involve investigating the recent activities of infected people, finding out, for instance, whether they had had contact with animal carcasses or bodily fluids, had consumed fluids such as camel milk or urine, or had been near bat colonies. “It’s frustrating that all cases from animal infections have not been properly investigated,” says Peter Ben Embarek, leader of the WHO’s MERS team at the agency’s headquarters in Geneva, Switzerland. One obstacle is cultural, in that Saudis tend to be averse to discussing what they consider private matters, he says. The outbreak in South Korea will probably put pressure on Middle Eastern countries to accelerate research and control of MERS, says Drosten.

Another outstanding mystery is why human cases have not been detected in African countries with large camel populations: Somalia has 7 million camels, and Kenya 3 million, dwarfing Saudi Arabia’s population of 260,000. “MERS is circulating in camels in many parts of Africa,” says Ben Embarek, “so camel-wise, it’s the same picture as in the Middle East.” One possibility is that human cases are going undetected because of poor surveillance. Another possibility is that cases in Africa are less likely or less serious, because MERS tends to cause serious illness only in people who have diseases that result from modern lifestyles, such as diabetes, which are more common in Saudi Arabia.

Nature 522, 139–140 (11 June 2015) doi:10.1038/522139a  Nature Original web page at Nature


Artificial intelligence joins hunt for human–animal diseases

Model predicts that the midwestern United States and Central Asia are at high risk for outbreaks of rodent-borne pathogens. The Northern flying squirrel carries diseases that can pass from animals to humans. Lyme disease, Ebola and malaria all developed in animals before making the leap to infect humans. Predicting when such a ‘zoonotic’ disease will spark an outbreak remains difficult, but a new study suggests that artificial intelligence could give these efforts a boost.

A computer model that incorporates machine learning can pinpoint, with 90% accuracy, rodent species that are known to harbour pathogens that can spread to humans, researchers report this week in the Proceedings of the National Academy of Sciences. The model also identified more than 150 species that are likely to be disease reservoirs but have yet to be confirmed as such. Central Asia and the midwestern United States were among the regions with the greatest concentrations of potential reservoir species. That surprised lead author Barbara Han, an ecologist at the Cary Institute of Ecosystem Studies in Millbrook, New York. “I had thought, ‘Didn’t we discover everything here already?’” she says.

Han and her colleagues began by training their model to identify characteristics that are common to the 217 rodent species that are known to carry zoonotic diseases. They set the model to analyse databases of animal traits, such as species’ geographic ranges, reproductive behaviour and whether they are a reservoir for any zoonotic disease. The model repeatedly divided species in those databases into groups based on arbitrarily selected traits — searching for patterns about which factors make a species more likely to carry pathogens that can infect humans. Eventually, the model developed a set of rules that could identify known carrier species with 90% accuracy.

Then the researchers used their model to analyse the disease-transmitting potential of the world’s 2,277 rodent species. They identified more than 150 species — including some voles, squirrels and guinea pigs — that are not known reservoirs of zoonotic diseases but seem likely to be, based on factors identified by the model. Felicia Keesing, a biologist at Bard College in New York, likes the study’s use of animal traits such as litter size or frequency of reproduction to identify disease risks. That could lead to more targeted disease surveillance than previous work that focused on the locations of past outbreaks. “We can predict not just where, but in what” species the next illness could arise, she says.

Sophisticated machine learning is beginning to be used more widely across ecology. Such work has uncovered hidden patterns in everything from the dispersal of invasive plants to the flight paths of birds. Studying ecology mostly used to be about going into the field and gathering data, says Reuben Keller, an invasive-species researcher at Loyola University Chicago in Illinois. Now, he says, “ecologists are increasingly learning how to deal with all the data we’ve gathered in rigorous ways”.

Nature doi:10.1038/nature.2015.17568  Nature  Original web page at Nature


* Humans, livestock in Kenya linked in sickness and in health

If a farmer’s goats, cattle or sheep are sick in Kenya, how’s the health of the farmer? Though researchers have long suspected a link between the health of farmers and their families in sub-Saharan Africa and the health of their livestock, a team of veterinary and economic scientists has quantified the relationship for the first time in a study. Writing in the journal Plos One, authors say the study offers a unique view of human health through the lens of animal health.

After tracking 1,500 households and their livestock in 10 western Kenyan villages for one year, researchers found a strong relationship between the number of illnesses among family members and the number of livestock sicknesses and deaths in the same household. Using hut-to-hut visits and free hotline numbers for farmers to call on mobile phones, researchers obtained data on 6,400 adults and children, along with more than 8,000 cattle, 2,400 goats, 1,300 sheep and 18,000 chickens. Analysis of that data revealed this: For every 10 cases of animal illness or death that occurred, the probability of human sickness in the same household shot up by 31 percent.

“Our findings help to understand, in quantitative terms, the complex pathways that link livestock health to the health and welfare of the humans who own them,” said Kenya-based lead author Thumbi Mwangi, an infectious disease epidemiologist at Washington State University’s Paul G. Allen School for Global Animal Health. “It’s important because an estimated 300 million people living in sub-Saharan Africa depend on their livestock as a main source of livelihood and nutrition,” he said. Human health and animal health are connected by three pathways, Mwangi and his co-authors state: socio-economic, where healthy and productive livestock result in higher household incomes and increased access to education and health care; nutritional, where healthy livestock increase access to animal source foods, which, in turn, lowers malnutrition and disease; zoonotic, where healthy livestock are less likely to transmit zoonotic diseases–those that spill over from animals to humans, including food-borne infections.

Livestock benefit families in multiple ways but the negative side of disease must also be considered, the authors argue. They studied 1,500 households spanning a rural region stricken by poverty and infectious diseases. Using bi-weekly home survey visits by veterinary teams and toll-free calls from farmers, the researchers found that households with livestock experiencing high numbers gastrointestinal and respiratory syndromes “have high numbers of the similar syndromes in humans.”

What’s not known is whether animals suffering from those ailments are passing the pathogens directly to the people who own them. It’s also possible that the environment where they live fosters propagation of those pathogens, the scientists write. In their next phase of study, they will try to pinpoint the underlying causes.  Science Daily  Original web page at Science Daily


* Ebola: New studies model a deadly epidemic

On Dec. 26, 2013, a two-year-old boy living in the Guinean village of Meliandou, Guéckédou Prefecture was stricken with a rare disease, caused by the filament-shaped Ebola virus. The child is believed to be the first case in what soon became a flood-tide of contagion, ravaging the West African countries of Guinea, Sierra Leone and Liberia, infecting, according to the World Health Organization, over 21,000 cases as of Jan. 21, with nearly 9000 confirmed deaths–the actual toll likely much higher. Now, researchers from Arizona State University and Georgia State University are trying to better understand the epidemiology and control of Ebola Virus Disease in order to alleviate suffering and prevent future disease outbreaks from reaching the catastrophic proportions of the current crisis. In reports appearing in the February 2015 issue of the British medical journal The Lancet Infectious Disease, ASU researchers report on new efforts to model the impact of timely diagnostic testing on the spread of Ebola across populations. A better understanding of viral dissemination and techniques for disease management are vital if a similar calamity is to be avoided in the future.

Researchers from the Biodesign Institute, and the Simon A. Levin Mathematical, Computational and Modeling Sciences Center present a new study: Modelling the effect of early detection of Ebola. The study examines the levels of detection and patient isolation required to shut down transmission of Ebola. In related research, Gerardo Chowell, a newly appointed faculty member in the School of Public Health at Georgia State University and adjunct faculty member in the ASU’s Simon A. Levin Mathematical, Computational and Modeling Sciences Center, together with Cécile Viboud from the from the National Institutes of Health discuss recent large-scale modeling efforts to explain the spatial-temporal patterns of spread of the epidemic in Liberia. Chowell is also co-author of Ebola control: rapid diagnostic testing, which appears in the Lancet’s correspondence section.

The Ebola virus has become notorious, not only for its highly contagious and lethal nature, but for the nightmarish assortment of symptoms collectively known as hemorrhagic fever. These may include vomiting of blood, bleeding from the eyes, ears, nose, mouth, rectum, internal bleeding, excruciating pain and the liquidization of internal organs. The three West African nations centrally affected by the epidemic were acutely unprepared for the crisis. Treatment centers were rapidly swamped with severely ill patients. Resources for proper care, isolation of infected patients and even basic means of sterilization were soon depleted. Health care workers were especially vulnerable to infection. A number of exacerbating factors contributed to the outbreak and rapid spread of Ebola in the region. Timber and mining activities have impacted densely forested regions and brought fruit bats–believed to be a natural reservoir for the virus–in closer contact with humans. Infected animals consumed as bush meat may also have planted early seeds of the disease in the vulnerable population. Long periods of civil unrest have left the area deeply impoverished and the health infrastructure fractured. Meliandou, the town identified as ground zero, is situated in a forested area at the convergence point of Guinea, Liberia and Sierra Leone. Populations move fluidly across these porous borders, as impoverished residents are often on the move in search of work. These conditions created a perfect storm for the aggressive virus.

An additional factor fueling the explosive spread of Ebola in West Africa was the delayed and inadequate response to the crisis on the part of developed countries and global health organizations. As the authors of the Lancet modeling study emphasize, breaking the chain of Ebola transmission presents intimidating challenges. After the development of symptoms, the virus is highly contagious and each new contact presents an opportunity for further spread of the disease. Tracking all contacts of infected individuals can be a daunting challenge, even in first world settings, with low case numbers. In the absence of a vaccine or reliable therapeutic for Ebola, diagnosis of the disease at a pre-symptomatic stage and rapid isolation of infected individuals are the surest means for arresting further disease transmission.

According to Biodesign’s Karen Anderson, PhD., “Early detection of Ebola infection provides the opportunity and time to safely isolate and treat individuals before they become contagious. Our findings show two key things: first, that the predicted impact of early diagnostic tests depends on existing public health measures. Second, there appears to be a tipping point, where early diagnosis of high-risk individuals, combined with adequate isolation, can markedly decrease the predicted number of infected individuals.” Stopping an epidemic in its tracks requires a reduction in a critical value known as the reproductive ratio or R0– a measure of new infections generated by a single case over the course of the infectious period. The higher the number for R0, the more difficult an epidemic is to contain. A technique known as polymerase chain reaction (PCR) can be used for pre-symptomatic identification of the Ebola virus. The current study models the expected outcomes on viral transmission of Ebola using PCR-based pre-symptomatic diagnosis and isolation of infected patients within 3 days of the onset of symptoms. “Our results underscore the dramatic impact that diagnostic capacity can bring about during an Ebola epidemic to quickly identify Ebola cases before these start new chains of transmission in the community or health care settings,” according to Diego Chowell, lead author of the study. Carlos Castillo-Chavez, director of the Simon A. Levin Mathematical, Computational and Modeling Sciences Center, emphasises the power of mathematical modeling for understanding and limiting the scale of epidemics: “Finding that small differences in isolation effectiveness may have a large impact on epidemic size highlights the importance of evaluating novel diagnostic technologies at the population level using mathematical models,” he says. “An intervention may not work or be effective unless it is effectively used beyond a tipping point.” The authors urge the implementation of the strategy of pre-symptomatic diagnosis and rapid isolation, targeting high-risk individuals, including care givers and health care workers.

In his comment to the Lancet, Geraldo Chowell examines another mathematical model, put forward by Merler and his colleagues. This study models the course of the Ebola epidemic in Liberia, based on population structure and geography, including location of households, hospitals, and Ebola treatment units. Chowell notes that the establishment of new treatment centers, isolation of new patients and distribution of household protection kits all likely played a role in curtailing the spread of Ebola in Liberia, relative to neighboring states of Guinea and Sierra Leone. “Carefully calibrated mathematical models have potential to guide public health authorities to effectively respond to disease epidemics,” Chowell says. “In the context of the Ebola epidemic in West Africa, several key factors, including delays in responding to the epidemic, behavior changes and increased public health infrastructure in the region in order to trace contacts of infected individuals and break chains of transmission through effective isolation have played a major role in shaping the trajectory of this epidemic.” The desperate need for early diagnosis of Ebola was further emphasized in Chowell’s correspondence, which points out that most West African Ebola patients remained undiagnosed in their communities and the average time from symptom onset to diagnosis was about 5 days–a prescription for rapid, far-flung transmission of the disease. While underscoring the diagnostic power of PCR, Chowell notes that such tests presently require transportation to a laboratory or transit center, causing critical delays in diagnosis and treatment and heightening transmission risks. His recommendation is to supplement these efforts with the distribution of point-of-care rapid tests that could be used in households for early protection. Chowell and his colleagues conducted a simulation based on reducing the time between symptom onset and diagnosis, using rapid testing. The results were dramatic. If 60 percent of Ebola patients can be rapidly diagnosed and isolated (within 1 day of symptom onset), the proportion of the population eventually infected (known as the attack rate) drops from 80 percent to nearly zero.

While authors of the current Lancet papers model Ebola transmission and propose strategies to address future epidemics, ASU has also been on the forefront of efforts toward Ebola therapeutics and eventual vaccines. Charles Arntzen, Ph.D., offered a prescient warning back in 2011 that the next outbreak of Ebola could be far more devastating than those in the past, if sufficient resources were not immediately brought to bear. Regrettably, Arntzen’s prediction became a reality with the recent epidemic, far surpassing in death toll and geographic extent all previous Ebola outbreaks combined. Arntzen’s earlier study in the Proceedings of the National Academy of Science described an experimental cocktail of monoclonal antibodies produced from tobacco plants, which showed considerable promise in animal studies. The recent West African epidemic provided an unprecedented opportunity to test the effectiveness of the drug formula, developed with Arntzen’s longtime collaborators at San Diego based MAPP Pharmaceuticals. Two health care workers returning to the U.S. after having been stricken with Ebola in Africa were treated with the drug, known as ZMapp. Both survived, offering the tantalizing potential for a safe, highly effective vaccine against the disease. Arntzen’s efforts also highlighted the potential of similar plant-made pharmaceuticals. A number of these are currently being investigated at the Biodesign Institute by Qiang “Shawn” Chen, Ph.D., a researcher in the Center for Infectious Diseases and Vaccinology. Chen hopes to apply similar techniques to produce therapeutics against other diseases, including West Nile Fever, a focus of current research.

According to the latest reports from the World Health Organization, the Ebola epidemic appears to be weakening its grip on the region. For the first time since June 2014, there have been fewer than 100 new weekly cases reported in the 3 countries most affected, signaling what health care workers hope is the final phase of Ebola’s devastating reign. Increased vigilance and new tools at both the epidemiological and therapeutic ends of the spectrum are vitally needed, if another epidemic–perhaps of even greater scale–is to be prevented. Science Daily Original web page at Science Daily


Study maps travel of H7 influenza genes

Certainly one reason is that influenza viruses have a history of jumping from other animals to humans, which, when the trans-species virus is new to the human population, generally means that human immune systems have no natural resistance. Another reason is that influenza viruses, with their rapidly mutating single-strand RNA genomes, are highly variable over time. Now a more complex and daunting view is emerging that shows viruses’ constant variability — and sometimes deadly innovation — happens as a result of these two factors, combined with influenza’s tendency to swap genes among viruses and also to move between geographically separate populations through traveling or migrating hosts. A new report published online on January 21, 2015 in the journal Cladistics sees H7 influenza not just as a steadily changing virus, but as regularly shuffling combinations of genetic segments, each of which has its own history of travel among hosts and geographic places. A host can often be infected with more than one type of virus and, as viruses replicate in the host’s cells, the genetic segments of the progeny viruses can be shuffled into new combinations. In essence, the influenza viruses are made of set of generally interchangeable parts that periodically assemble a virus newly suited to evade hosts’ immune systems. “A case in point is the China-Taiwan H7N9 outbreak, which was caused by a virus made of genetic segments previously circulating in chickens in China and ducks in Korea,” the authors note. “Some segments have historical international connections to and from China-Taiwan to neighboring countries.” Appearing in the journal’s February 2015 issue, the study, “Phylogenetic visualization of the spread of H7 influenza A viruses” uses genomic analysis to look at the phylogenetic history of genes that assort with H7 influenza. H7 viruses infect a variety of birds and periodically infect humans including the recent human cases of H7N9 in China, Hong Kong, and Taiwan. The paper’s authors are University of North Carolina’s Daniel A. Janies and Chris Krueger, and Laura W. Pomeroy, Igor O. Voronkin, Jori Hardman, Yuqi Zhang, Izzet Senturk, Kamer Kaya and Ümit Çatalyürek from the Ohio State University. Contrary to traditional opinion that H7 is a restricted in geographic scope, the authors show regular transit in genes that assort with H7 viruses across vast geographic distances. “We find multiple occurrences of transboundary and transcontinental spread, both within and between the previously observed American and Eurasian clusters,” the authors say “H7 strains have a long history,” said UNC Charlotte’s Janies. “There are isolates of H7 going back to 1902. But the recent H7N9 virus is a new constellation of genes — a new disease, based not only on H7, but other strains of influenza” The view that individual influenza genes have moved between species and across great geographic distances, complicates the issue of viral adaptation and evolution. Concurrent with reassortment of genes into new sets, a specific gene’s mutation rate can be rapid, and thus the possibilities for dangerous new viral adaptations are constant. Despite the dynamic nature of the virus, most research labs construct phylogenetic trees gene-by-gene. However these trees are difficult to interpret. Janies and colleagues have developed new computing techniques that combine viral genomic data and geographic metadata to create visualizations of viral traffic across the planet ( The results, called transmission graphs, allow public health scientists to identify hubs for the transport of the disease where countermeasures will have the most durable effect on the global spread of the disease. Janies argues a new approach is needed in how we study and monitor widespread zoonotic viruses like influenza that frequently cross species and geographic boundaries. While the global health community jumps into action when outbreaks in humans occur, if the outbreak is stopped it does not mean that the danger has fully subsided because the reservoirs for the viruses may be distributed elsewhere among animals and geography. “There’s an unlearned lesson: even if people say the disease went away, often it hasn’t — the virus can be hanging around in places and hosts at which we are not looking, it’s hanging around in chickens, it’s hanging around in pigeons — our tools enable researchers to know where to focus efforts for the best chance to break the transmission network.” Janies said, noting that the wildlife biologists and veterinary doctors who know and observe animal diseases often do not often belong to the same communication networks as physicians. “The viruses don’t care what discipline in which you work. You are going to have patients and problems caused by the viruses crossing over geographic boundaries, host boundaries and disciplinary boundaries,” he said. “When a host is co-infected, the genes assemble themselves into novel viruses to which people may not be immune. It’s not just that the genes mutate, it’s that the whole deck gets shuffled. That’s what happened with H7N9 recently and pandemic H1N1 from 2009. New combinations are important things for which to watch, no matter where they occur.”  Science Daily  Original web page at Science Daily


Ebola by the numbers: The size, spread and cost of an outbreak

The Ebola outbreak in West Africa continues to rage, with the number of people infected roughly doubling every 3–4 weeks. More than 8,000 people are thought to have contracted the disease, and almost half of those have died, according to the World Health Organization. Although these estimates are already staggering, the situation on the ground means that not all cases and deaths are being reported, so the true extent is likely to be much greater. Outside of Africa, a health-care worker in Texas has become infected while treating a patient who was hospitalized in Dallas after travelling from Liberia and who has now died. And a nurse in Madrid has contracted the virus after caring for a missionary who had become infected while caring for patients in West Africa. Health-care workers remain one of the groups at highest risk of exposure: by 8 October, 416 had become infected and 233 had died.  The spread beyond the epicentre of Guinea, Liberia and Sierra Leone remains limited. Apart from the people in Dallas and Spain, only two other exported cases are known: one in Nigeria and one in Senegal. A man who travelled to Lagos from Liberia sparked a further 19 cases in Nigeria, but that outbreak was curtailed by the swift actions of the authorities in tracing and monitoring those who had contact with the infected man. Similar public-health measures stopped further cases in Senegal after an infected man travelled from Guinea to Dakar.  Within the epicentre, authorities have made some progress in slowing transmission — but the disease is resurgent in places where it had seemed under control, such as in Conakry, Guinea’s capital. Meanwhile, the estimated cost of fighting the disease is spiralling upward. UN secretary-general Ban Ki-moon warned on 9 October that “at least a 20-fold surge in assistance” was needed to confront the outbreak. But “things will get worse before they get better”, he warned. Just how much worse will depend on the international community — which has been widely criticized for its belated response, and its slow translation of pledges into concrete action.  Nature  Original web page at Nature


* Avian influenza virus isolated in harbor seals poses a threat to humans

A study led by St. Jude Children’s Research Hospital scientists found the avian influenza A H3N8 virus that killed harbor seals along the New England coast can spread through respiratory droplets and poses a threat to humans. The research appears in the current issue of the scientific journal Nature Communications. The avian H3N8 virus was isolated by scientists investigating the 2011 deaths of more than 160 harbor seals. Researchers discovered the virus had naturally acquired mutations in a key protein that previous laboratory research had shown allowed the highly pathogenic avian H5N1 virus to spread though respiratory droplets. Scientists reported that the avian H3N8 seal virus infected and grew in human lung cells. Researchers also found that the virus spread in ferrets though respiratory transmission, which is uncommon for avian flu viruses and raises concerns about possible person-to-person airborne spread of the harbor seal virus. Investigators found no evidence of human immunity to the strain. This study highlights a gain-of-function experiment that occurred in nature and shows us there are avian flu viruses out there beyond H5N1 and H7N9 that could pose a threat to humans,” said corresponding author Stacey Schultz-Cherry, Ph.D., a member of the St. Jude Department of Infectious Diseases. In recent years, human cases of highly pathogenic avian H5N1 and H7N9 flu have been confirmed in countries around the world, with mortality rates approaching 60 percent. “Avian H3N8 viruses are established in horses and dogs. This study raises a red flag about the threat this strain poses to humans exposed to animals infected with the virus,” Schultz-Cherry said. While no human illness was linked to the 2011 harbor seal virus, a different flu virus has spread from infected seals to humans who came in close contact with the animals. Avian H3N8 is also believed to have triggered a human flu pandemic in the 1880s. The findings reinforce the need for continued surveillance of flu viruses circulating in wild and domestic animals to understand the risk the viruses pose to humans, said the study’s first author Erik Karlsson, Ph.D., a St. Jude postdoctoral fellow. The H3N8 harbor seal virus caught the attention of researchers when sequencing showed the virus included two particular mutations in the hemagglutinin (HA) protein and a change in the PB2 gene. HA is carried on the surface of the flu virus. The virus depends on HA to bind to and infect cells. The PB2 mutation was associated with more severe illness in mice. The HA and PB2 changes were among a handful of genetic alterations that in 2012 other scientists reported were sufficient to allow the highly pathogenic H5N1 to spread in ferrets via respiratory droplets.

In this study, two of the three animals exposed to the harbor seal virus via respiratory transmission became infected, although symptoms were mild. Airborne transmission did not occur with the five other avian viruses tested, but two of the viruses spread in ferrets that shared cages. Both viruses were close genetic relatives of the harbor seal virus. Scientists want to understand the genetic changes that make respiratory transmission of avian H3N8 virus possible and the likelihood that related flu viruses will or have acquired those alterations. Researchers also checked blood samples from 102 individuals vaccinated against seasonal flu strains between 2009 and 2011, including the human H3N2 flu strain. There was no evidence that seasonal flu vaccines protected against the harbor seal virus. “The transmissibility of the seal H3N8 virus coupled with the apparent lack of immunity makes this strain a concern,” researchers noted.  Science Daily  Original web page at Science Daily


Largest ever Ebola outbreak is not a global threat

Deadly Ebola probably touched down in Lagos, Nigeria, the largest city in Africa, on 20 July. A man who was thought to be infected with the virus had arrived there on a flight from Liberia, where, along with Guinea and Sierra Leone, the largest recorded Ebola outbreak is currently raging. The Lagos case is the first to be internationally exported by air travel and today the UK foreign secretary announced that he would chair a government meeting on Ebola. As long as the virus continues to infect people in Liberia, Guinea and Sierra Leone, there is a small risk of more long-distance exports of the disease. But, as Nature’s Declan Butler explains, Ebola does not pose a global threat. The World Health Organization still considers the Lagos case a “probable” infection because it has not yet confirmed that the 40-year-old Liberian man had Ebola. He was quarantined upon arrival at the airport and taken to hospital, where he died on 25 July. Assuming he had Ebola, if proper control measures were taken at the airport and at the hospital, the risk that health-care workers or others will become infected as a result of contact with him is low. The European Centre for Disease Prevention and Control classifies people sharing public transport with someone infected as having a “very low” risk of catching the virus. Healthcare workers and doctors, several of whom have now been infected and died as a result of caring for people in the current outbreak, are at much higher risk and the WHO advises that they take strict precautions, which greatly lowers the risk. The ECDC also says the probability of an infected person getting on a flight in the first place is low, given the small overall number of Ebola cases. Moreover, functional health systems should be able to prevent onward spread from any exported cases. Overall, the World Health Organisation estimates that there is a high risk of spread to countries bordering those with existing outbreaks, a moderate risk to countries further afield in the sub-region, but that there is little chance of spread overseas. There is no reason to assume that an exported case — be it to Lagos, a city of 17 million people, or any other place — will spark new outbreaks, because Ebola is not highly contagious.

Though the strain of Ebola in the current outbreak appears to kill 56% of the people it infects, to become infected in the first place, a person’s mucous membranes, or an area of broken skin, must come into contact with the bodily fluids of an infected person, such as blood, urine, saliva, semen or stools, or materials contaminated with these fluids such as soiled clothing or bed linen. By contrast, respiratory pathogens such as those that cause the common cold or flu are coughed and sneezed into the air and can be contracted just by breathing or touching contaminated surfaces, such as door knobs. A pandemic flu virus can spread around the world in days or weeks and may be unstoppable whereas Ebola only causes sporadic localised outbreaks that can usually be stamped out. In principle, it should be straightforward to bring an Ebola outbreak under control via public health measures alone, namely, identifying all people who have been infected and isolating them, monitoring all those that they have been in contact with for 21 days (the maximum incubation period), as well as promoting basic infection control measures. What’s more, since people infected with Ebola do not infect others until they have symptoms, it is easier to trace their contacts than it is for some other diseases. Ebola is out of control in these countries because the sheer size of the outbreak is stretching response teams, and also because of local sociocultural factors. Local health authorities and international organisations such as WHO and Médecins Sans Frontières (also known as Doctors Without Borders) are struggling to control the spread in these areas because of a lack of trust and cooperation among the affected populations. Doctors and health workers have sometimes been blocked from accessing affected places because of opposition from villagers who fear the medics will bring the disease. According to the WHO, not all people who are infected are getting or seeking care, and so are passing the virus on to family and other close contacts. Another major driver of new infections is that families are often continuing to perform traditional burial rites that involve mourners having direct contact with the bodies of the dead – and unfortunately all too often Ebola. It is larger than any other outbreak in recorded history. The WHO reports that as of 23 July, there were 814 lab-confirmed infections, including 456 deaths. If ‘probable’ and ‘suspected’ cases are included, these numbers rise to 1,201 infections, including 672 deaths — but some of these may have been caused by other diseases. Only 7 other of the few dozen past outbreaks have involved more than 100 cases, and before now, the largest outbreak was in Uganda between 2000 and 2001, in which 425 people were infected and 224 died.

Since Ebola first appeared in 1976, only 19 outbreaks have had more than 10 victims, and around 2,000 people in total have died from the disease. By comparison, malaria kills some 3,200 people a day, and diarrhoeal diseases some 4,000. Snakes and other venomous animals cause some 55,000 deaths a year — 27 times more than the entire number of people killed by Ebola in 38 years. There are no licensed drugs or vaccines for Ebola, although candidates are in development. New treatments would help reduce the high mortality rate of the disease – which has ranged in past outbreaks from 25% to 89%, with an average of around 62%. Jeremy Farrar, head of the UK Wellcome Trust in London, has argued for the use of experimental, unapproved drugs in the current outbreak. But other scientists have said that with distrust of health workers already hampering efforts to bring the outbreak under control, such measures could be counterproductive by creating suspicion and so further undermining trust. Outreach, in particular involving local community leaders, will be vital to persuade people to trust health workers and to follow public-health advice. Authorities need to win over public trust, persuade people to bury their dead safely, and continue to step up local and regional efforts to trace and isolate people who are infected and their contacts.

Nature doi:10.1038/nature.2014.15640  Nature Original web page at Nature


* Biologist warn of early stages of Earth’s sixth mass extinction event

In a new review of scientific literature and analysis of data published in Science, an international team of scientists cautions that the loss and decline of animals is contributing to what appears to be the early days of the planet’s sixth mass biological extinction event. Since 1500, more than 320 terrestrial vertebrates have become extinct. Populations of the remaining species show a 25 percent average decline in abundance. The situation is similarly dire for invertebrate animal life. And while previous extinctions have been driven by natural planetary transformations or catastrophic asteroid strikes, the current die-off can be associated to human activity, a situation that the lead author Rodolfo Dirzo, a professor of biology at Stanford, designates an era of “Anthropocene defaunation.” Across vertebrates, 16 to 33 percent of all species are estimated to be globally threatened or endangered. Large animals — described as megafauna and including elephants, rhinoceroses, polar bears and countless other species worldwide — face the highest rate of decline, a trend that matches previous extinction events. Larger animals tend to have lower population growth rates and produce fewer offspring. They need larger habitat areas to maintain viable populations. Their size and meat mass make them easier and more attractive hunting targets for humans. Although these species represent a relatively low percentage of the animals at risk, their loss would have trickle-down effects that could shake the stability of other species and, in some cases, even human health. For instance, previous experiments conducted in Kenya have isolated patches of land from megafauna such as zebras, giraffes and elephants, and observed how an ecosystem reacts to the removal of its largest species. Rather quickly, these areas become overwhelmed with rodents. Grass and shrubs increase and the rate of soil compaction decreases. Seeds and shelter become more easily available, and the risk of predation drops. Consequently, the number of rodents doubles — and so does the abundance of the disease-carrying ectoparasites that they harbor. “Where human density is high, you get high rates of defaunation, high incidence of rodents, and thus high levels of pathogens, which increases the risks of disease transmission,” said Dirzo, who is also a senior fellow at the Stanford Woods Institute for the Environment. “Who would have thought that just defaunation would have all these dramatic consequences? But it can be a vicious circle.”

The scientists also detailed a troubling trend in invertebrate defaunation. Human population has doubled in the past 35 years; in the same period, the number of invertebrate animals — such as beetles, butterflies, spiders and worms — has decreased by 45 percent. As with larger animals, the loss is driven primarily by loss of habitat and global climate disruption, and could have trickle-up effects in our everyday lives. For instance, insects pollinate roughly 75 percent of the world’s food crops, an estimated 10 percent of the economic value of the world’s food supply. Insects also play a critical role in nutrient cycling and decomposing organic materials, which helps ensure ecosystem productivity. In the United States alone, the value of pest control by native predators is estimated at $4.5 billion annually. Dirzo said that the solutions are complicated. Immediately reducing rates of habitat change and overexploitation would help, but these approaches need to be tailored to individual regions and situations. He said he hopes that raising awareness of the ongoing mass extinction — and not just of large, charismatic species — and its associated consequences will help spur change. “We tend to think about extinction as loss of a species from the face of Earth, and that’s very important, but there’s a loss of critical ecosystem functioning in which animals play a central role that we need to pay attention to as well,” Dirzo said. “Ironically, we have long considered that defaunation is a cryptic phenomenon, but I think we will end up with a situation that is non-cryptic because of the increasingly obvious consequences to the planet and to human wellbeing.”  Science Daily  Original web page at Science Daily


US disease agency suspends pathogen shipments

Workers at the US Centers for Disease Control and Prevention in Atlanta, Georgia, accidentally shipped highly dangerous H5N1 influenza virus to another government laboratory in March, the agency revealed today. The news comes weeks after the CDC announced that dozens of its employees were potentially exposed to anthrax because its staff did not follow established laboratory safety guidelines. In response to the incidents, the CDC today imposed a moratorium on shipments from its high-biosecurity facilities and shut down the laboratories responsible for the anthrax and H5N1 incidents, pending an investigation. “I’m disappointed by what happened and frankly I’m angry,” agency director Thomas Frieden said at a press conference. After news of the anthrax exposure broke on 19 June, the CDC began investigating why its lab workers did not follow proper procedure to inactivate Bacillus anthracis spores before shipping them to another lab on the agency’s Atlanta campus. The receiving lab was not equipped to handle the pathogen, and once the mistake was discovered, more than 70 people were pre-emptively treated for anthrax infection. The CDC now says that the lab never needed to work with B. anthracis in the first place; another bacterium would have sufficed to test the diagnostic equipment that the lab was evaluating. The good news, Frieden says, is that the CDC now does not believe that anyone was actually exposed to anthrax spores. But the agency’s ongoing investigation has revealed more bad news: on 12–13 March, the CDC’s influenza lab contaminated a harmless flu strain with the highly dangerous H5N1 variety, and sent it to a laboratory operated by the US Department of Agriculture (USDA) in Athens, Georgia. The mistake was discovered on 23 May, but Frieden says that he was not notified until 9 July. “Why it took six weeks for that to be made apparent, I can think of no valid explanation,” he says. The USDA lab was equipped to handle highly infectious agents, and the agency is confident that there were no exposures. According to a CDC report released on 11 July, at least five such incidents have happened in the past decade, in which CDC shipments of potentially viable pathogens — including those that cause botulism, anthrax and brucellosis — were improperly inactivated or wrongly believed to be harmless. “These are wakeup calls,” Frieden says. “These are events that tell us we have a problem, and we are going to fix it.”

The CDC says that it will work with an external scientific advisory panel to examine safety procedures at all of its high-level biosafety labs before resuming any shipments to internal or external labs. The influenza and anthrax labs are shut indefinitely, pending completion of the investigations, but Frieden expects that the influenza lab will reopen in time for tracking the flu season this autumn. The agency is also instituting new safety measures, including a review of its training procedures and appointing CDC health-care safety expert Michael Bell to act as a single point of accountability for future biosafety incidents. Frieden also says that employees who are found to have knowingly violated lab safety procedures will face disciplinary action. News of the CDC troubles “points out that accidents can happen anywhere”, even at the agency charged with overseeing US biosecurity, says Michael Osterholm, a public-health expert at the University of Minnesota in Minneapolis. He sees the H5N1 incident as a reason to question ‘gain-of-function’ research that involves engineering disease-causing viruses to make them more deadly, in order to understand what might happen if such viruses evolved naturally to become more pathogenic. If there is any silver lining to the CDC incidents, Osterholm says, “it’s that we will have a heightened level of lab safety and a discussion that I think has been long overdue.” The CDC’s actions come on the heels of another biosafety scare earlier this week, when unauthorized vials of smallpox were found in a cold storage room on the National Institutes of Health campus in Bethesda, Maryland. The CDC said today that its tests show that virus samples from at least two of the twelve vials were able to successfully infect and replicate in cultured human cells. Frieden says that the vials will now be destroyed with the World Health Organization in attendance as a witness. “That’s what should have been done a couple decades ago,” he says.

Nature doi:10.1038/nature.2014.15544  Nature  Original web page at Nature


Declines in large wildlife lead to increases in disease risk

In the Middle Ages, fleas carried by rats were responsible for spreading the Black Plague. Today in East Africa, they remain important vectors of plague and many other diseases, including Bartonellosis, a potentially dangerous human pathogen. Research by Hillary Young, assistant professor in UC Santa Barbara’s Department of Ecology, Evolution and Marine Biology, directly links large wildlife decline to an increased risk of human disease via changes in rodent populations. The findings appear today in the Proceedings of the National Academy of Sciences Early Online Edition. With an East African savanna ecosystem as their research site, Young and her colleagues examined the relationship between the loss of large wildlife — defaunation — and the risk of human disease. In this case, they analyzed Bartonellosis, a group of bacterial pathogens which can cause endocarditis, spleen and liver damage and memory loss. “We were able to demonstrate that declines in large wildlife can cause an increase in the risk for diseases that are spread between animals and humans,” said Young. “This spike in disease risk results from explosions in the number of rodents that benefit from the removal of the larger animals.” The researchers discovered this effect by using powerful electric fences to experimentally exclude large species like elephants, giraffe and zebra from study plots in Kenya. Inside these plots, rodents doubled in number. More rodents meant more fleas, and genetic screens of these fleas revealed that they carried significantly numbers of disease-causing pathogens. The study was concentrated in an area where rodent-borne disease is common and sometimes fatal. According to Young, these rodent outbreaks and associated increases in disease risk may be exacerbating health problems in parts of Africa where diminishing wildlife populations are rife.

“This same effect, however, can occur almost anywhere there are large wildlife declines,” Young said. “This phenomena that we call rodentation — the proliferation of rodents triggered by large wildlife loss — has been observed in sites around the world.” Downturns in wildlife numbers can cause rodent increases in a variety of ways, including by providing more access to food and better shelter. “The result is that we expect that the loss of large animals may lead to a general increase in human risk of rodent borne disease in a wide range of landscapes,” Young said. “In this study, we show the causal relationship between disturbance and disease is alarmingly straightforward,” she added. “We knock out the large members of ecosystems, and the small species, which generally interact more closely with humans, dramatically increase in number, ultimately brewing up more disease among their ranks. The study provides ecosystem managers with yet another reason to protect large and at-risk wildlife species. “Elephants are an irreplaceable part of our global biodiversity portfolio,” Young said, “but they also appear to be circuitously protecting us from disease.”  Science Daily

May 27, 2014  Original web page at Science Daily




Whole genome sequencing provides researchers with a better understanding of bovine TB outbreaks

The use of whole bacterial genome sequencing will allow scientists to inexpensively track how bovine tuberculosis (TB) is transmitted from farm to farm, according to research presented this week at the Society of General Microbiology Autumn Conference. Bovine TB is primarily a disease of cattle, caused by the bacterium Mycobacterium bovis. The disease is hugely expensive, costing the Government over £91 million in England in 2010/11. Researchers from the University of Glasgow, working in collaboration with the Agri-Food and Biosciences Institute and the Department of Agriculture and Rural Development, Northern Ireland, sequenced the genomes of 147 M. bovis samples, collected over a decade of outbreaks in Northern Ireland. By combining the genomic sequences of the bacteria with information about when and where the sample was isolated, in addition to data on the movement of cattle from farm to farm, the researchers were able to build a detailed forensic map of bovine TB spread. The results showed that, even on a scale of few kilometres, M. bovis samples from neighbouring farms were more closely genetically related than geographically distant farms that had had cattle moved between them. This finding confirms that, while long distance spread via cattle movements plays a role, local transmission mechanisms appear to drive the spread of the disease, although the researchers are unable to determine what these are at the present time.

Hannah Trewby, who is presenting this work says, “The inclusion of whole genome information in our data will give us unprecedented insight into how bovine TB spreads, and will help us to develop better control methods for the disease.” The role of infected wild badgers in spreading bovine TB remains controversial. This work will help to clarify the role that badgers may have in spreading the disease and continue to build a sound scientific evidence base on which control measures can be built. Professor Rowland Kao, the Principle Investigator of the project, explains, “Our results suggests that the establishment and local persistence of the pathogen in cattle has a distinct spatial signature — we believe that explaining this signature is the key to quantifying the role that badgers play in the persistence of bovine TB in Britain and Ireland. While we do not yet have sufficient data to be definitive, it is clear that whole genome sequencing of the bacterium will play an important part in solving this puzzle. Given the extensive collection of samples already collected from cattle and badgers, we are optimistic that this approach will help accumulating the right scientific evidence over the coming years to tackle this important problem.”

Science Daily
September 17, 2013

Original web page at Science Daily


Emergence of H7N9 avian flu hints at broader threat

Evolutionary path shows related virus can infect some mammals, raising concerns about spread. Samples taken from ducks in Chinese poultry markets, like this bird in Changsha, revealed the presence of H7 influenza viruses. The H7N9 influenza virus did not emerge alone. Researchers have traced the evolution of the deadly avian flu currently spreading in China, and have found evidence that it developed in parallel with a similar bird flu, H7N7, which can infect mammals. Although there is no evidence that this H7N7 strain will infect humans, the authors of a study published today in Nature1 say that their finding reinforces the idea that H7 avian viruses are constantly mixing and exchanging genetic material — a process known as reassortment — in Asian poultry markets. This raises the threat that H7N7 will reassort and become able to spread to humans. “H7 is out there in China and not just in the form of this H7N9,” says Richard Webby, a co-author of the study and an influenza specialist at St. Jude Children’s Research Hospital in Memphis, Tennessee. Ducks, in particular, act as living mixing bowls for avian viruses. Domestic species encounter a large catalogue of wild-bird viruses, which swap genes to form versions that can spread to chickens and to humans.

Better surveillance of Chinese bird populations is needed to monitor the emergence of dangerous viruses such as H7N9, says lead author Yi Guan, an influenza specialist at the University of Hong Kong. In China, the virus has infected 135 people and resulted in 44 deaths since February. “This is a very different influenza ecosystem from other countries,” says Guan. Guan’s team sampled wild birds and poultry markets around Shanghai in April, weeks after the H7N9 outbreak began there. The researchers collected throat and intestinal swabs from 1,341 birds, including chickens, ducks, geese, pigeons, partridges and quails, plus 1,006 water and faecal samples from bird markets. About 10% of samples tested positive for an influenza virus; of those, 15% were an H7 virus. When the team sequenced the two viruses’ genomes and compared them to other bird-flu strains, they found H7N9 and H7N7 to be hybrids of wild Eurasian waterfowl strains, such as H7N3 and H11N9. The scientists think that those viruses swapped genes in domestic ducks before spreading to chickens, where they traded genes with a common chicken virus, H9N2. That improved the viruses’ ability to spread in chickens, which live in close contact with humans. So far, the latest H7N7 strain has not infected a human. But Guan and his team found that ferrets could become infected with the virus, suggesting that a spread to humans is possible.

“It really shows that the emergence of these types of viruses can happen at any time,” says Camille Lebarbenchon, a viral ecologist at the University of Reunion Island in St Denis, France, who has also studied the evolution of H7N9 using archived viral sequences. David Morens, an influenza researcher and senior adviser at the US National Institutes of Health in Bethesda, Maryland, says that the evolutionary pathway that the viruses followed suggests that more surveillance and better sanitation practices at poultry markets are crucial to monitoring risks to human health. But Ian Lipkin, an epidemiologist at Columbia University in New York City, says that surveillance is not a foolproof solution. “It’s inevitable that something is going to slip through the cracks.”

September 3, 2013

Original web page at Nature


H7N9 influenza: History of similar viruses gives cause for concern

The H7N9 avian flu strain that emerged in China earlier this year has subsided for now, but it would be a mistake to be reassured by this apparent lull in infections. The virus has several highly unusual traits that paint a disquieting picture of a pathogen that may yet lead to a pandemic, according to lead scientists from the National Institute of Allergy and Infectious Diseases. David Morens, Jeffery Taubenberger, and Anthony Fauci, in a paper published in mBio®, the online open-access journal of the American Society for Microbiology, describe the history of H7 viruses in animal and human disease and point out that H7 influenza has a tendency to become established in bird, horse, and swine populations and may spillover repeatedly into humans. “The evidence as a whole is complex and the implications of past outbreaks for predicting the future course of the current H7N9 epizootic (an epidemic among animals) are uncertain,” write the authors. The outbreak of H7N9 earlier this year led China to temporarily close scores of live poultry markets in an effort to limit the spread of the virus. Although this previously unrecognized strain of avian influenza A has now been associated with 132 confirmed human infections and 39 related deaths (as of June 14), the rate at which new cases are recognized has dwindled in recent weeks.

In their minireview, Morens, Taubenberger and Fauci point out that despite this apparent hiatus, viruses like H7N9, which have subtype 7 hemagglutinin, are a cause for heightened concern because of several highly unusual characteristics. First, H7 viruses have repeatedly been involved in numerous explosive poultry outbreaks including incidents in New York, Canada, Mexico, the Netherlands, and Italy, and in almost all of these cases the virus eventually spilled over into humans. Also, H7 viruses have the ability to mutate from a low pathogenicity form to a high pathogenicity form in birds, a scenario that can lead to large-scale culling and ultimately to human exposure to the virus among poultry workers. H7N9 also shares many characteristics with another influenza strain that continues to spillover into humans: highly pathogenic avian influenza H5N1. Among other commonalities, both viruses have a clinical picture that includes bilateral pneumonia, acute respiratory distress syndrome, and multi-organ failure, and it appears they are both currently unable to easily infect most humans but cause severe disease in individuals with uncharacterized genetic susceptibilities. The fact that many H7 viruses tend to infect conjunctival cells is also cause for concern. Some, but not all, cases of human H7 infection feature prominent signs and symptoms in the eyes, including itching, swelling, and tearing, that could enhance person-to-person spread in an H7N9 outbreak.

The authors point out that many H7 viruses have adapted to infect mammals, including horses and pigs, which raises the possibility that H7N9 could adapt in a similar fashion. The possibility that H7N9 might infect pigs is particularly troubling, as swine are considered a “mixing vessel” for viruses – a breeding ground for novel viral reassortants like the 2009 H1N1 pandemic influenza strain commonly known as “swine flu”. The sum of these observations is this: we do not know what H7N9 will do next. Although avian influenza viruses have not caused widespread human transmission in 94 years of surveillance, there have been numerous instances of avian influenza spillover and H7N9 “might arguably be more likely than other avian viruses to become human-adapted,” write the authors. Regardless of its future, H7N9 certainly holds lessons for preventing human and animal pandemics. All the unknowns surrounding the virus make a strong case for enhancing basic and applied research into the evolution of influenza viruses and for better integration of influenza virology within human and veterinary public health efforts. “We have a unique opportunity to learn more of influenza’s many secrets, and thereby enhance our ability to prevent and control an important disease that seems destined to appear again and again, in multiple guises, far into the foreseeable future,” write the authors.

EurekAlert! Medicine
July 23, 2013

Original web page at EurekAlert! Medicine


New test for H7N9 bird flu in China may help slow outbreak, prevent pandemic

Breaking research appearing online today in Clinical Chemistry, the journal of AACC, demonstrates that a recently developed diagnostic test can detect the new strain of influenza (H7N9) currently causing an outbreak in China. Since the end of March, 31 people have died from H7N9 infection, and the number of confirmed cases has climbed to 129. Evidence suggests that most H7N9 infections have arisen from poultry-to-human transmission, and that passage of the virus between humans is limited. However, researchers have also found mutations in the virus that are known to help avian viruses adapt to mammalian hosts. If these mutations lead to sustained human-to-human transmission, a serious pandemic could occur. In this study, Wong et al. designed a diagnostic test with high specificity for the H7N9 virus that does not cross react with distantly related viruses, including all previously known avian and mammalian H7 viruses. They also show that this one-step quantitative real-time PCR assay enables specimen processing in about 3 hours. According to the authors, this new test should also detect viruses closely related to the H7N9 virus.

If confirmed, this capability could prove vital; it’s likely that the H7N9 virus is evolving rapidly, and there could be multiple introductions of avian H7N9 viruses from animals to humans. The test also demonstrates a detection limit of ~0.04 median tissue culture infective dose (TCID50) per reaction. This means that it should be sensitive enough to identify patients with active virus replications. “These results suggest that the established assay should be suitable for screening H7N9 viruses in human samples,” said lead investigator Leo Poon, PhD, of the University of Hong Kong, though additional evaluation using clinical specimens from H7N9 patients is needed. If validated, this diagnostic test could help health officials avert a potential pandemic by allowing them to monitor the spread of the virus. The test could also identify H7N9 patients in the early stages of infection, improving their chances of responding to clinical treatments.

Science Daily
May 28, 2013

Original web page at Science Daily


Bird flu in live poultry markets are the source of viruses causing human infections

On 31 March 2013, the Chinese National Health and Family Planning Commission announced human cases of novel H7N9 influenza virus infections. A group of scientists, led by Professor Chen Hualan of the Harbin Veterinary Research Institute at the Chinese Academy of Agricultural Sciences, has investigated the origins of this novel H7N9 influenza virus and published their results in Springer’s open access journal Chinese Science Bulletin (SpringerOpen). Following analysis of H7N9 influenza viruses collected from live poultry markets, it was found that these viruses circulating among birds were responsible for human infections. These results provide a basis for the government to take actions for controlling this public health threat. The novel H7N9 influenza virus was identified in China as the agent, that causes a flu-like disease in humans, resulting in some deaths. A total of 970 samples were collected from live poultry markets and poultry farms located in Shanghai and Anhui Province. Samples analyzed included drinking water, feces, contaminated soil, and cloacal and tracheal swabs. Of these samples, 20 were positive for the presence of H7N9 influenza viruses. All of the positive samples originated from live poultry markets in Shanghai. Of these 20 positive samples, 10 were isolated from chickens, 3 from pigeons, and 7 were from environmental samples. The complete genome of three H7N9 isolates, from a chicken, pigeon, and environmental sample, was sequenced and deposited into the GISAID database (

Genetic analysis of these isolates revealed high homology across all eight gene segments. The analysis of these novel H7N9 influenza virus isolates showed that that the six internal genes were derived from avian H9N2 viruses, but the ancestor of their hemagglutinin (HA) and neuraminidase (NA) genes is unknown. HA receptor-binding specificity is a major molecular determinant for the host range of influenza viruses. Within the HA protein of novel H7N9 viruses, there was a leucine residue at position 226, which is characteristic of the HA gene in human influenza viruses. This finding implies that H7N9 viruses have partially acquired human receptor-binding specificity. The authors conclude: “We suggest that strong measures, such as continued surveillance of avian and human hosts, control of animal movement, shutdown of live poultry markets, and culling of poultry in affected areas, should be taken during this initial stage of virus prevalence to prevent a possible pandemic. Additionally, it is also imperative to evaluate the pathogenicity and transmissibility of these H7N9 viruses, and to develop effective vaccines and antiviral drugs so as to reduce their adverse effects upon human health.

Science Daily
May 28, 2013

Original web page at Science Daily


Insight on pandemic flu

Pandemic flu continues to threaten public health, especially in the wake of the recent emergence of an H7N9 low pathogenic avian influenza strain in humans. A recent study published in PLoS ONE, a peer-reviewed scientific journal, provides new information for public health officials on mitigating the spread of infection from emerging flu viruses. Dr. Henry Wan, associate professor at the Mississippi State University College of Veterinary Medicine led a study with researchers from Georgia Institute of Technology, Marshall University, and Universidad Miguel Hernández in Spain called “A perspective on multiple waves of influenza pandemics” that brings new insight into the H1N1 pandemic of 2009, and may help officials prepare for future pandemics. During the 2009 H1N1 pandemic, along with the last three flu pandemics of 1918, 1957, and 1968, the United States experienced multiple peaks, or waves, of infection. Normal seasonal flu outbreaks have only one peak of infection–the number of cases starts very low, increases to a maximum, then decreases to a very low level, and remains at a low level until the next flu season. In this study, the team developed models to explain possible causes of the multiple peaks in pandemic flu, which are largely unknown.

“With the H1N1 pandemic in 2009, we experienced multiple waves of infection,” Dr. Wan said. “The first wave began in March 2009 and peaked in late June and early July. Then there were fewer cases in August and then a second, larger wave hit in late October and early November. But China only experienced a single wave of infection. So we created infection models and analyzed the outcomes.” The models showed that border control had some small effects on outbreaks. “In 2009, China instituted strict border controls at the onset of the outbreak,” said first author Dr. Anna Mummert, assistant professor of mathematics at Marshall University. “We developed models explaining the occurrence of the multiple peaks and tested border control strategies to determine if a strict border control in the United States could reduce the total number of infections.” Four of the models indicated that if that stricter border control is related to fewer waves of infection. “What was really remarkable was that all of the models showed that strong border control would not have decreased the total number of infections,” said Dr. Howie Weiss, professor in Georgia Tech’s School of Mathematics or College of Sciences. The effects of vaccinations were studied in the models, and the authors concluded that the actual H1N1 vaccination distribution schedule played only a small role in curtailing the outbreak. While it has been thought that the timing of school vaccinations played a large role in producing the second wave of infections, the models did not show a strong link, but indicated that an earlier vaccination schedule could have helped. The research team plans further collaboration in understanding influenza viruses and their spread. “We are fortunate to have each other’s expertise in mathematical modeling and infectious diseases,” Wan said. “Our goal is to provide timely information to health organizations and others who work on infectious disease prevention.”

Science Daily
May 14, 2013

Original web page at Science Daily


African forest elephant population plummeting

The population of African forest elephants plummeted 62% in the past decade, according to a new study. The figure, which the authors blame on ivory poachers, comes as policymakers discuss ways to curb the ivory market at the Convention on International Trade in Endangered Species of Wild Fauna and Flora (CITES) meeting in Thailand. “Hopefully these numbers will help convince decision-makers that there is a problem,” says wildlife biologist Fiona Maisels of the Wildlife Conservation Society and the University of Stirling in the United Kingdom, first author of the new paper. Forest elephants, which often live closer to human populations than the larger savanna elephants, have been particularly hard-hit by ivory poachers. After declines in the elephant population last century, a 1989 international ban on ivory initially led to signs of a resurgence in the animals. Since then, anecdotal evidence and surveys taken in individual parks suggested that heightened demand for ivory in China has once again led an uptick in elephant slaughters. “We knew it was bad, but their habitat is all under forest coverage, so you can’t just go out and do aerial surveys like you can for savanna elephants,” Maisels says.

To get a more complete picture, Maisels and a team of more than 60 researchers from around the world helped coordinate and assemble data from 80 individual surveys taken from 2002 through 2011 in central African locales that are known to be the primary habitats for forest elephants. Some sites were in formally protected areas; others were in spots that conservationists would like to see protected in the future. In each of the locations, which spanned Cameroon, Gabon, the Central African Republic, the Democratic Republic of the Congo, and the Republic of the Congo, trained biologists surveyed land for elephant dung, an indicator of the elephant population in the area. “This is the first time we’ve managed to do a comparison of all these sites in a very coordinated way,” Maisels says. When the team crunched the numbers, it found that just during the 10-year span covered in the new surveys, the elephant population declined by 62% and the land area inhabited by elephants dropped by 30%. Areas lacking guards, closest to roads, and in countries with high levels of corruption had the most elephant population decline, the researchers reported today in PLOS ONE.

“I think these numbers are either very accurate or even a bit conservative,” says biologist Richard Ruggiero, the chief of the Near East, South Asia, and Africa Branch in the U.S. Fish and Wildlife Service’s Division of International Conservation in Arlington, Virginia, who was not involved in the new work. Because many of the surveys took place in protected areas, he says, they could overestimate elephant populations—elephants often flee into the protected zones to escape nearby poaching. “These surveys are as good as they can be,” Ruggiero adds. “They are certainly very objective and very rigorous.” Estimates on the absolute population of elephants at any given time must be taken with a grain of salt, he says, but overall trends seen over years of sampling the same areas in a standardized way are generally more accurate. The new numbers are not surprising to conservationists who work in the area, both Ruggiero and Maisels say, but are needed to convince others of the problems and provide a starting point to see the effect of future conservation efforts. “When you’re on the ground and you know what to look for, you don’t need a survey to see what’s happening,” Ruggiero says. “But unless you can put a more or less objective metric on it, you’re not going to get this in front of the people who need to see it.” The challenge now, Maisels says, is for those countries represented at the CITES meeting, which lasts until 14 March, to put together new policies to curb the ivory trade. The key, she thinks, will be to stop the trade within China, lowering the demand for ivory and the price. Previous programs aimed at this aspect of the market have been more successful than those specifically aiming to stop the poaching, she says.

March 19, 2013

Original web page at ScienceNow


Livestock density as risk factor for livestock-associated methicillin-resistant Staphylococcus aureus, the Netherlands

To determine whether persons living in areas of high animal density are at increased risk for carrying livestock-associated methicillin-resistant Staphylococcus aureus (LA-MRSA), we used an existing dataset of persons in the Netherlands with LA-MRSA carriage and controls who carried other types of MRSA. Results of running univariate and multivariate logistic regression models indicated that living in livestock-dense areas increases the odds of nasal carriage of LA-MRSA. We found that doubling pig, cattle, and veal calf densities per municipality increased the odds of LA-MRSA carriage over carriage of other types of MRSA by 24.7% (95% CI 0.9%–54.2%), 76.9% (95% CI 11.3%–81.3%), and 24.1% (95% CI 5.5%–45.9%), respectively, after adjusting for direct animal contact, living in a rural area, and the probable source of MRSA carriage. Controlling the spread of LA-MRSA thus requires giving attention to community members in animal-dense regions who are unaffiliated with livestock farming.

Emerging Infectious Diseases
November 13, 2012

Original article at Emerging Infectious Diseases


UK badger cull tentatively supported by science

Somewhere beneath England’s rolling fields, there’s a badger with a price on its head. Sometime in the next two weeks, it will likely become the first of hundreds to be shot dead as part of a pilot cull licensed by the UK government to curb the spread of bovine tuberculosis to cattle – despite the fact that the badgers are protected under UK law. Farmers in England and Wales are keen to get on with the controversial cull. They have seen the annual slaughter of cattle with bovine TB soar from 6000 in 1998 to 34,000 in 2011, and have long argued that badgers are at least partly responsible. They infect cattle by contaminating pastures, feeding areas, and even the air with Mycobacterium bovis – the bacteria that causes TB both in badgers and in cows. Now, for the first time, an independent scientific group has presented evidence in support of a cull – five years after it suggested that culling would not work. James Small’s farm in Somerset has just reopened after a 6-month lockdown triggered when one of his cows tested positive. He says that bovine TB is every cattle farmer’s worst nightmare – both in the UK and elsewhere. “It’s terrifying. Until the disease has really progressed in your cows, there are no visible signs,” he says. “We got the all clear in September after tests for the herd were negative for the necessary 120 days, but the test days were really stressful, not knowing what the vets would find.” Small is relieved that one of two pilot studies to evaluate badger culling is set to go ahead, although his farm lies outside both of the proposed field-trial areas. Others are appalled by the decision. Queen guitarist Brian May launched an online petition to stop the cull, which has amassed 150,000 signatures to date.

At first glance, the new pilot studies appear to fly in the face of previous science. In 2007, interim conclusions of the Randomised Badger Culling Trial (RBCT) – a £50-million experiment to assess the merits of a badger cull – suggested that culling would not work. Killing badgers reduced the number of infected cattle herds within the RBCT study area by some 23 per cent compared with unculled areas, but these gains were offset by a 24 per cent rise in herd losses in a 2-kilometre-wide ring surrounding the culled area. Researchers called this phenomenon the “perturbation effect”. Infected badgers in the culling area fled to the sanctuary of the surrounding unculled zone, taking TB with them. So strong was the perturbation effect that the increased herd losses in the peripheral area effectively cancelled out gains within the culled area. In fact, the 2007 conclusions suggested that just 14 herd infections would have been avoided after a sustained badger cull covering 1000 square kilometres of farmland for five years. But continued monitoring of the same sites where the RBCT took place has changed the picture, strengthening the justification for culling after all. Christl Donnelly, an epidemiologist at Imperial College London, was a member of the team that performed the original 2007 analysis. She has periodically collected data from the study region since 2006. The improvements seen within the study area have persisted.

Between 2006 and 2011 there were 28 per cent fewer TB infections there than might otherwise have been expected. What’s more, the boost seen in TB levels in the unculled outer ring was not sustained. In fact, between 2006 and 2011 there were 4 per cent fewer TB cases than expected from controls within the outer ring (PLoS One, Armed with the new data, scientists advising the UK government concluded that culling over four years in a hypothetical area of 150 square kilometres – killing an estimated 1000 to 1500 badgers – could achieve a net reduction of herd infections of around 16 per cent within nine years. This, they calculated, equates to preventing 47 out of 292 TB infections that would result in a farm being locked down. “The data that have accumulated have pushed us more towards a position to cull,” says Donnelly. At a pivotal meeting in December 2011, scientific experts advising the UK government’s Department for the Environment, Food and Rural Affairs (DEFRA) on bovine TB concluded that culling might play a role, alongside existing measures to physically exclude badgers from farms, frequently test cattle for TB and restrict movement of affected herds.

New Scientist
October 30, 2012

Original web page at New Scientist


Genome of malaria-causing parasite sequenced: Even when on different continents, organism features same mutations

Scientists at Case Western Reserve University and the Cleveland Clinic Lerner Research Institute have discovered that the parasite that causes the most common form of malaria share the same genetic variations — even when the organisms are separated across continents. The discovery raises concerns that mutations to resist existing medications could spread worldwide, making global eradication efforts even more difficult. The researchers, including Cleveland-based David Serre and Peter Zimmerman, Didier Menard (Institut Pasteur-Cambodia) and Arsene Ratsimbasoa (Madagascar National Malaria Control Program) are the first to sequence the genome of the parasite Plasmodium vivax, taken from patients at coverage needed to verify genome-wide DNA sequence variation. The genome contains all of the organism’s inheritable information. The ability to sequence is crucial to understanding the hard-to-study parasite, which annually causes up to 250 million cases of malaria and places an economic burden, mostly on the poor, in excess of $1.4 billion by some estimates. The researchers report their findings in the Sept. 6 issue of the online journal PLoS Neglected Tropical Diseases.

The scientists at first were surprised to find little genetic variation specific to different locations among the samples, which came from humans in Madagascar and Cambodia and South America. How can parasites, transmitted by mosquitoes, share genome-wide variations on three continents? “The parasite’s life cycle enables P. vivax to be a microbial globe-trotter,” said Peter Zimmerman, professor of international health, genetics and biology in the Center for Global Health and Diseases at Case Western Reserve University School of Medicine. In parts of the world where Plasmodium vivax malaria is endemic, the primary infection gets into the red blood cells and makes people sick, he explained. When they feel better, people resume their normal activities and travel. But a portion of the infectious form can remain in their liver, where it may lay dormant for months or a year, then re-emerges into the blood when that person is in a different place. “In that new place, local mosquitoes bite, become infected, and start spreading the P. vivax parasite and its genome in locations that can be a long distance away from where the original human infection occurred,” Zimmerman, a senior author of the new study, said. This ability for worldwide travel raises concerns among the researchers. There is no vaccine and there is only one drug that kills the parasite in the liver.

“If drug resistance arises, with modern travel, how long would it be before the resistance is spread over the world?” Zimmerman said. “This data suggests it could quickly become a big problem.” Learning how Plasmodium vivax lives and causes malaria has been challenging because the parasite dies when removed from its host. With improvements in sequencing techniques and reductions in costs, David Serre, Assistant Professor, at the Genomic Medicine Institute, Cleveland Clinic Lerner Research Institute, and Zimmerman decided to try to see if the parasite’s genome could be sequenced and what it might tell. “Our work provides the first report on genome-wide variation of this malaria parasite and provides the malaria research community with more than 80,000 genetic markers that can now be used for trait mapping or population monitoring,” Serre said. “This is a critical step to understand the biology of this parasite that cannot be studied in the laboratory yet affects millions of people each year.” Serre and Ernest R. Chan, a postdoctoral research fellow at the Genomic Medicine Institute, sequenced the genomes of parasites in blood samples taken from two P. vivax malaria patients in Madagascar and three in Cambodia, after first removing the white blood cells. For comparison, they sequenced P. vivax from a monkey that had been infected with a human strain of the parasite found in South America. The results showed the six samples extensively shared alternative forms of the same gene, called alleles.

Sequencing parasite strains straight from humans is a big step forward, Serre said. Most researchers have been studying human strains of ,P. vivax propagated through monkeys. This method is not as reliable as using human samples, because it introduces variability, and is limited to only about a dozen strains that have been adapted to monkeys. Far more strains have been found in humans. The 80,000 genetic markers identified can now be used to search for links to drug-resistant malaria, a growing problem in Southeast Asia; and to study possible new treatments for P. vivax malaria. Zimmerman and Serre are seeking grants to expand their work, sequencing more samples from more locations. The researchers will use the data to perform genetic evolution studies to learn where the parasite originated, how it spreads, and how different strains are geographically distributed. The team will also study evolving P. vivax infection mechanisms. For example, in a classic example of natural selection, African persons do not develop P. vivax malaria, but the disease is prevalent in nearby Madagascar. Serre and Zimmerman believe specific mutations in Malagasy P. vivax strains make the parasite able to infect individuals previously thought to be resistant.

Science Daily
September 18, 2012

Original web page at Science Daily


Health experts narrow the hunt for Ebola

Response efforts to outbreaks of Ebola hemorrhagic fever in Africa can benefit from a standardized sampling strategy that focuses on the carcasses of gorillas, chimpanzees, and other species known to succumb to the virus, according to a consortium of wildlife health experts. In a recently published study of 14 previous human Ebola outbreaks and the responses of wildlife teams collecting animal samples, the authors of the new study conclude that most efforts to collect samples from live animals (i.e. rodents, bats, primates, birds) failed to isolate Ebola virus or antibodies. However, they found that collecting samples from animal carcasses during outbreaks was a more effective method for Ebola detection. The early detection of Ebola in animal populations near a human outbreak is crucial for learning more about this virus, which can strike human populations with a mortality rate of more than 80 percent. “You can’t test every single animal, so we used information from historical outbreaks to figure out how to help the field response team focus their effort,” according to Wildlife Conservation Society (WCS) wildlife epidemiologist Sarah Olson, the lead author of the new report. “It turns out that carcass sampling yields a 50 percent chance of finding Ebola virus or antibodies compared to less than six percent when sampling free-ranging live animals.”

The scientific consortium that participated in the study, published in an online issue of Emerging Health Threats, are key partners in PREDICT, part of USAID’s Emerging Pandemic Threats Program that is improving global capacity to respond to emerging infectious diseases that originate in wildlife. PREDICT is led by the University of California at Davis, in partnership with Ecohealth Alliance, Global Viral Forecasting Initiative, the Smithsonian Institution, and the Wildlife Conservation Society. “The Emerging Pandemic Threats program is a visionary investment by USAID to protect and improve global health because it has made it possible for us to, for the first time, preemptively, and on a global scale, identify novel pathogens in wildlife that could pose pandemic threats to humans,” said Dr. Jonna Mazet, Director of PREDICT and Director of the One Health Institute at the University of California, Davis School of Veterinary medicine. “This study is a great example of how PREDICT is using science to improve our ability to detect lethal diseases, like Ebola.”

The study was designed to develop a set of animal sampling recommendations to maximize the effectiveness of Ebola outbreak response efforts with limited resources. Specifically, the study was prompted by a 2011 outbreak near Kampala, Uganda, in which a 12-year-old girl died from Ebola hemorrhagic fever. PREDICT wildlife veterinarians were sent to the victim’s village to screen wildlife as a potential source of the virus. “This study digests over 30 years of accumulated knowledge so field teams can arrive informed and prepared,” adds WCS epidemiologist and senior author, Damien Joly. The authors also point to some scientific “loose ends” that can be incorporated into future animal sampling efforts during Ebola outbreak response. For instance, despite some evidence of Ebola in dogs and pigs, the number of samples acquired from these animals is limited to just two outbreaks; the authors recommend increasing the number of samples collected from these groups in the future to better determine their role in Ebola outbreaks. The study also confirms that while fruit bats should be a focus of investigation as a potential reservoir for Ebola, field teams need to be prepared to sample hundreds of bats because virus prevalence across all bats sampled to date is very low, estimated at 3 percent.

Science Daily
May 29, 2012

Original web page at Science Daily


Nowhere to hide: Tigers threatened by human destruction of groundcover

The elimination of ground-level vegetation is bringing another of the world’s tiger subspecies to the brink of extinction, according to Virginia Tech and World Wildlife Fund researchers. The Sumatran tiger, native to Indonesia, could be the fourth type of tiger to disappear from the wild. This is due, in part, because of deforestation and the loss of thick groundcover, also known as understory cover, said Sunarto, lead scientist on a study that is the first to systematically investigate the use of both forests and plantation areas for tiger habitat. Although tiger’s prefer forest to plantation areas, the study found that the most important factor was that availability of thick ground-level vegetation which apparently serves as an environmental necessity for tiger habitat, regardless of location. “As ambush hunters, tigers would find it hard to capture their prey without adequate understory cover,” said Sunarto, who earned his doctorate at Virginia Tech and now is a tiger expert for the World Wildlife Fund-Indonesia (WWF-Indonesia). “The lack of cover also leaves tigers vulnerable to persecution by humans, who generally perceive them as dangerous.”

Within forest areas, tigers also strongly prefer sites that have low levels of human disturbance as indicated by their preference for areas closer to forest centers and farther from human activity centers such as bodies of water and areas bordering plantations and towns. Tigers occupy only around 7 percent of their historic range. Estimates place the current wild tiger populations at as few as 3,200 tigers, including only about 400 Sumatran tigers, which are listed as critically endangered on the International Union for Conservation of Nature Red List of Threatened Species. “These study results indicate that to thrive, tigers depend on the existence of large contiguous forest blocks,” said study co-author Marcella Kelly, an associate professor in Virginia Tech’s Department of Fish and Wildlife Conservation and Sunarto’s graduate advisor. The Indonesian government has set aside many areas and national parks for the conservation of endangered species but about 70 percent of tiger habitat in Sumatra, an island in western Indonesia, remains outside these protected areas. The preservation of such habitats, which requires support from government, landowners, and concession holders, is critical for conservation of the species, the study authors emphasize.

A recently published Indonesian presidential decree on land use in Sumatra points out the importance of building wildlife corridors between critical areas, where commitments from concession owners are key to successful implementation. “Even with current legal protection for the species, tigers are not doing well in many places, especially those outside protected areas,” Sunarto said. “As long as forest conversion continues, tigers will require active protection or they will quickly disappear from our planet.” The study concludes that in order to protect tigers, it is critical to stop clearing Indonesia’s remaining natural forests for plantations. With adjustments in management practices on existing plantations to include more understory and riparian forest corridors, tigers could use a mosaic of forest patches across fragmented landscapes. “We hope that plantation managers and concession owners can use the recommendations of this report to apply best management practices to further protect Sumatran tigers from extinction,” said Anwar Purwoto, director of the Forest, Freshwater, and Species Program at WWF¬Indonesia. “Ensuring that tigers are able to roam freely in natural forests and restored habitat is crucial to their survival,” said co-author Sybille Klenzendorf, head of WWF’s species program, who earned her master’s and doctorate degrees in wildlife science from Virginia Tech. “This study is a reminder of just how important it is for us to protect the natural forests that tigers and other animals rely on.” The report was published in the journal PLoS ONE on Jan. 23.

Science Daily
March 20, 2012

Original web page at Science Daily


Latex gloves lead to lax hand hygiene in hospitals, study finds

Healthcare workers who wear gloves while treating patients are much less likely to clean their hands before and after patient contact, according to a study published in the December issue of Infection Control and Hospital Epidemiology, the journal of the Society for Healthcare Epidemiology of America. This failure of basic hand hygiene could be contributing to the spread of infection in healthcare settings, the researchers say. Glove use is appropriate for situations when contact with body fluids is anticipated or when patients are to be managed with contact precautions. However, use of gloves should not be considered a substitute for effective hand hygiene practices taking place before and after patient contact. Although gloves can reduce the number of germs transmitted to the hands, germs can sometimes still get through latex. Hands can also be contaminated by “back spray” when gloves are removed after contact with body fluids.

The researchers, led by Dr. Sheldon Stone of the Royal Free Hospital NHS Trust, observed more than 7,000 patient contacts in 56 intensive care and acute care of the elderly wards in 15 United Kingdom hospitals, making this one of the largest and most detailed studies on gloves and their impact on hand hygiene. Overall, the study found that hand hygiene compliance was “disappointingly low,” at just 47.7 percent. Compliance was even lower in instances where gloves were worn, dipping to just over 41 percent. “The chances of hands being cleaned before or after patient contact appear to be substantially lower if gloves were being worn,” said Dr. Stone, the principal investigator. “We call this the phenomenon of the ‘Dirty Hand in the Latex Glove.'” Though troubling, the results also reveal an opportunity to reduce healthcare associated infections by focusing further hand hygiene improvement efforts on better hand hygiene when using gloves. Doing so may prove the critical step in getting overall hand hygiene levels to the levels needed to prevent transmission of infection, the researchers say. Dr. Stone and his colleagues suggest further study on the behavioral reasons behind why healthcare workers are less likely to wash their hands when wearing gloves. Regardless, the researchers recommend that campaigns such as the World Health Organization’s Clean Care is Safer Care program should emphasize better hand hygiene associated with gloving practices.

EurekAlert! Medicine
November 15, 2011

Original web page at EurekAlert! Medicine