Researchers work on lowering greenhouse gas emissions from poultry houses

The University of Delaware’s Hong Li is part of a research team looking at how adding alum as an amendment to poultry litter reduces ammonia and greenhouse gas concentrations and emissions, specifically carbon dioxide, in poultry houses.

Li partnered with researchers at the United States Department of Agriculture (USDA), the University of Tennessee and Oklahoma State University for the project and the results of the research were recently published in the Journal of Environmental Quality.

Li, assistant professor in the Department of Animal and Food Sciences (ANFS) in UD’s College of Agriculture and Natural Resources, said that the project is ongoing and that the main challenge for the poultry industry is controlling nutrient emissions from poultry houses and conserving energy while also providing for the welfare of the birds inside the houses.

Acid-based chemical compounds, alum and PLT — another amendment — that are added to the bedding material in poultry houses prior to the birds entering have proven to be a very effective tool in controlling ammonia emissions.

“In the poultry industry, ammonia is a major concern. Ammonia during the growth period is high, especially during the wintertime. Ammonia can do a lot of damage to the animal, especially the respiratory system, and can effect overall animal health and welfare,” said Li.

Also, if ammonia is emitted to the air from the poultry house, it is a precursor of fine particles and there are national Clean Air Act regulations from the Environmental Protection Agency that have strict guidelines for controlling emissions.

“We need to control the ammonia, not only for the animal health but also for the public health. That’s why I’m doing the research, to reduce the ammonia emissions and improve the animal health and the public air quality, especially for the rural areas, to make sure our agriculture is sustainable,” said Li.

Li said that there are several products on the market to control ammonia in poultry houses and alum is the preferred product for growers in Arkansas, where the study was conducted.

While adding alum to poultry litter is known to reduce ammonia concentration in poultry houses, its effects on greenhouse gas emissions had been unknown.

Li’s role in the study was on the engineering side and he helped Philip Moore, one of the authors of the paper and a pioneer researcher on alum in poultry production with the USDA, develop an automatic air sampling system to evaluate the emissions reduction by using alum in the broiler house.

“We not only looked at ammonia reduction, we also looked at the whole environmental footprint — how the alum could potentially impact the greenhouse emissions — and the results showed that we reduced quite a bit of carbon dioxide emissions,” said Li.

The carbon dioxide was reduced in two ways. First, because alum is an acidic product, it reduces microbial activity in the litter and reduces the ammonia emissions.

Ammonia comes from uric acid being broken down by bacteria and enzymes. Once the uric acid is broken down, two products are created — one is ammonia and one is carbon dioxide.

“By reducing the bacterial activity, we reduce ammonia and also we reduce the carbon dioxide; that’s one aspect of how we reduce carbon dioxide,” said Li.

Second, by using acid-based litter amendments in poultry litter, growers can reduce the ventilation rate and reduce fuel used for heating the poultry houses, especially during the winter.

“In the broiler industry, we want to control ammonia to improve animal health and welfare. They have to keep the bird comfortable with optimum temperatures. However, if you want to have lower ammonia, you have to bring in more fresh air, remove more of the ammonia-laden air. As a result, you have to over ventilate the house,” Li said.

“That means you have to burn more fuel to keep the house warm. By using the acid-based litter amendments, we can reduce the ventilation rate and the fuel use, which reduces the carbon dioxide emission from the house through the heating process. Basically, if we reduce the microbial activity and also reduce the heating, we can generate lower carbon dioxide emissions.”  Science Daily  Original web page at Science Daily


* When chickens go wild

“Don’t look at them directly,” Rie Henriksen whispers, “otherwise they get suspicious.” The neuroscientist is referring to a dozen or so chickens loitering just a few metres away in the car park of a scenic observation point for Opaekaa Falls on the island of Kauai, Hawaii.

The chickens have every reason to distrust Henriksen and her colleague, evolutionary geneticist Dominic Wright, who have travelled to the island from Linköping University in Sweden armed with traps, drones, thermal cameras and a mobile molecular-biology lab to study the birds.

As the two try to act casual by their rented car, a jet-black hen with splashes of iridescent green feathers pecks its way along a trail of bird feed up to a device called a goal trap. Wright tugs at a string looped around his big toe and a spring-loaded net snaps over the bird. After a moment of stunned silence, the hen erupts into squawking fury.

Opaekaa Falls, like much of Kauai, is teeming with feral chickens — free-ranging fowl related both to the domestic breeds that lay eggs or produce meat for supermarket shelves and to a more ancestral lineage imported to Hawaii hundreds of years ago.

These modern hybrids inhabit almost every corner of the island, from rugged chasms to KFC car parks. They have clucked their way into local lore and culture and are both beloved and reviled by Kauai’s human occupants. Biologists, however, see in the feral animals an improbable experiment in evolution: what happens when chickens go wild?

The process of domestication has moulded animals and their genomes to thrive in human environments. Traits that ensure survival in the wild often give way to qualities that benefit humans, such as docility and fast growth. Feralization looks, on its surface, like domestication in reverse. But closer inspection suggests that the chickens of Kauai are evolving into something quite different from their wild predecessors, gaining some traits that reflect that past, but maintaining others that had been selected by humans. In this way, they are similar to other populations of animals, including dogs, pigs and sheep, that have broken free of captivity and flourished.

By looking at feral animals, some evolutionary biologists hope to determine how domestic animals and their genes change in response to natural pressures. The research could also help to inform tricky conservation questions about how such animals affect native species, and ultimately whether and how to control them.

The natural history of the Kauai fowl makes them an important test case. “People have a really complicated relationship with the chickens,” says Eben Gering, an evolutionary ecologist at Michigan State University’s Kellogg Biological Station in Hickory Corners, who is in Kauai with Henriksen and Wright. “Some people absolutely want them gone. Some consider them an integral part of the local culture.”

The Polynesian mariners who first settled the Hawaiian Islands about 1,000 years ago brought what they needed to start civilization anew. Staple plants such as taro, sweet potato and coconut palm made the trans-Pacific voyage, as did domestic dogs, pigs and, naturally, their prized chickens.

The Polynesian poultry probably bore little resemblance to the birds that provide much of the world’s protein today. Archaeological and genetic evidence suggests that they were more like red junglefowl (Gallus gallus) — small, furtive birds that still roam the forests of southeast Asia and are ancestral to all domestic chickens.

By the time that Captain James Cook landed in Waimea in southern Kauai in 1778, the Polynesian chickens had already, in essence, become feral. They wandered freely between Native Hawaiian villages and the neighbouring forest. Later, European and US settlers imported predators such as mongooses, which devastated birds of all kinds. Polynesian chickens were all but wiped out everywhere but Kauai and neighbouring Niihau, where the predators were never introduced.

On Kauai, chickens flourished. Although the birds’ numbers have not been tracked precisely, many residents contend that the population surged after hurricanes in 1982 and 1992 blew modern chickens from people’s back yards into the forests, where they encountered the descendants of the Polynesian chickens.

Gering says it is possible that interbreeding between the two populations allowed the birds’ numbers to swell. And during his first trip to the island in 2013, he and Wright noticed1 that many of the feral chickens they encountered had flecks of the white feathers common in modern domestic breeds, in addition to the darker plumage usually seen in wild populations. Many had yellow legs (red-junglefowl legs are grey). And some of the roosters’ crows sounded conspicuously like the drawn out cock-a-doodle-doo of their barnyard brethren, rather than the truncated calls of red junglefowl.

DNA from 23 chickens revealed just how far domestic-chicken genes had infiltrated1. The birds’ nuclear genomes seemed to be a mixture of genes from red-junglefowl-like Polynesian chickens and domestic chickens, whereas their maternally inherited mitochondrial markers traced back to European and Pacific domestic poultry. Gering and Wright think that a single hybrid population of feral chickens now roams Kauai, bearing a mixture of traits from modern and ancient birds.

In unpublished work, the two have scoured the birds’ genomes for stretches of DNA with very little variation across the population. This homogeneity suggests that a gene has surged through the population in the recent past, probably because it offers some benefit. If feralization were domestication played backwards, then these ‘selective sweeps’ might appear around the DNA sequences that distinguish domestic chickens from red junglefowl. Instead, the researchers have found that most of the swiftest-evolving genes in the Kauai chickens are distinct from those suspected involved in modern domestication.

In some cases, genes from the Polynesian chickens are helping the hybrid feral chickens to adapt to Kauai’s habitats. For example, modern domestic fowl have been bred not to sit on, or brood, their eggs (making the eggs easier to collect). But in the wild, this trait puts unhatched chicks at risk. Wright and Gering found that feral chickens possess red-junglefowl gene variants that are linked to brooding.

But some genes of domestication do seem to be handy outside the coop. A variant linked to increased growth rates and reproduction in domestic chickens, for example, persists in the Kauai population, even though the average adult feral chicken is half the weight of a month-old bird bred for meat.

“You won’t see a bird as healthy-looking as that,” Wright says of the hen that he and Henriksen had captured at Opaekaa Falls. “Her plumage is perfect.” In the basement of a rented house on Kauai, the researchers have set up a makeshift laboratory where they photograph the bird, draw its blood and then kill it and prepare it for dissection. Wright starts with the hen’s Brazil-nut-sized brain.

Their unpublished research has shown that the brains of domestic chickens are smaller than those of junglefowl, relative to their body size, and organized differently. The team hopes to identify the genes responsible for these changes and others, such as the diminished visual-processing systems of domestic birds. Life in the wild has also altered the reproductive systems of the feral chickens. Domestic breeds lay eggs almost daily, but breeding seasonally could allow feral chickens to reapportion the minerals devoted to eggs (which come from spongy tissue in the centre of their bones) to making their skeletons more robust. The researchers sample the hen’s femur and also find that its ovaries are empty of egg follicles, which could be a sign of seasonal breeding.

Feralization has garnered much less attention from scientists than domestication (which gets a nod in chapter one of Charles Darwin’s 1859 On the Origin of Species). But swapping of domestic and wild genes has been happening all over the world for thousands of years. A feral-sheep population that has lived on the island of St Kilda in the Scottish Outer Hebrides for as long as 4,000 years acquired beneficial alleles that determine coat colour from a modern domestic sheep breed some 150 years ago. A 2009 study in Science found that some wolves in Yellowstone National Park, Wyoming, carry a domestic-dog version of a gene linked to dark coats that shows hallmarks of positive selection, possibly helping wolves from the Arctic to adapt to forested environments. “People would have thought that genes to live in a farm and house aren’t going to be any good in the wild, but that’s not necessarily true,” says Jonathan Losos, an evolutionary ecologist at Harvard University in Cambridge, Massachusetts.

And like Kauai’s feral chickens, other feral animals such as dingoes in Australia and urban pigeons practically everywhere have not evolved back to the state of their wild ancestors — even if certain traits may trend in that direction.

Like chickens, other domesticated animals tend to have smaller brains than their wild cousins, relative to body size. And brain regions involved in processing things such as sight, sound and smell are among the most diminished, perhaps because humans bred animals to be docile and less wary of their surroundings. Feral pigs in Sardinia seem to have regained large brains and high densities of neurons involved in olfaction, but not the abilities that come with them: their neurons do not express a protein that has been linked to the exquisite sense of smell in closely related wild boars. Likewise, feral dogs, cats and pigs often lack the savvy of their wild brethren and still depend on human niches for their survival, notes Melinda Zeder, an archaeologist at the Smithsonian Institution’s National Museum of Natural History in Washington DC. Packs of feral dogs, for instance, do not form the complex hierarchies that make wolves such fearsome predators. “There’s no leadership the way you get in a wolf pack. It’s just a bunch of shitty friends ,” says Greger Larson, an evolutionary geneticist at the University of Oxford, UK, who is part of a team examining the mixed ancestry of Kauai’s feral pigs.

Wright and Henriksen take less than an hour to dissect the captured hen and preserve samples of its brain, bone, liver and other tissue for gene-expression studies. They will use the RNA molecules expressed in different tissues to come up with a list of genes that might influence traits that distinguish the feral chickens from domestic birds and red junglefowl. They are eager to add to their study sample, and they jump at an offer to visit a nearby farm to collect more chickens.

“They are a scourge. They are vermin. They cost us thousands and thousands of dollars every year,” says the farm’s owner (who asked not to be named). The birds scratch at tree saplings on his orchard, exposing the roots and killing fruit trees before they can mature. He patrols his property in a beaten-up luxury sedan with a high-powered air rifle and a hired hand who gets US$5 per kill. Every few months, he invites hunters with night-vision goggles to visit and pick off the birds as they roost.

Few Kauaians share his malice towards feral chickens. Many locals give them a ‘no-big-deal’ shrug when asked. And the island’s many tourists tend to view the birds with curiosity followed by mild annoyance after a couple of 3 a.m. wake-up calls. Feral-chicken merchandise — postcards, kitchen chopping boards, T-shirts — are ubiquitous. A popular children’s television show hosted by a character called Russell the Rooster has been on air for nearly two decades.

“Before deciding how important it is to conserve them, manage them or cull them, it would at least be good to know about their impact.”

As descendants of the birds imported by the Polynesians, Kauai’s feral chickens occupy a zoological purgatory somewhere between native plants and animals and the dreaded invasive species that plague island habitats such as Hawaii. “It’s much more complicated than just a feralized chicken,” says Gering. “Even though junglefowl were not here before the Polynesians colonized the island, they have been a part of this ecosystem for much longer than the domestic chickens.”

The chickens enjoy semi-official protection as ‘wild chickens’ in nature preserves. But if the same birds wander into developed areas or private property, they are considered ‘free-flying domestic chickens’ with no sanctuary. “Locals are free to take them (if they come onto your property) and put them in the pot,” says a State of Hawaii website. (Gering and Wright, with a freezer full of the animals, consider making ‘feral coq au vin’.)

Kauai may have no shortage of feral chickens now, but if mongooses arrive on the island or political winds change, they could be at risk. Hawaii’s most populous island, Oahu, has mounted a controversial culling campaign against its feral chickens (whose ancestry is uncertain). But Gering thinks that the Kauai chickens’ long tenure and unique cultural position makes some form of conservation worth considering. “Before deciding how important it is conserve them, manage them or cull them, it would be good to at least know about their impact,” he says. Researchers want to know about everything from the animals and plants that the birds eat to how they alter landscapes — information that Gering hopes to gather on future trips to the island.

Kauai’s chickens are hardly the only creatures to occupy a nebulous space between native and alien. When Przewalski’s horses, which live on the Mongolian steppe, were first described in the late nineteenth century, they were believed to be the planet’s last wild, undomesticated horses. But a 2015 genome study found that the 2,100 or so remaining horses carry substantial amounts of domestic-horse DNA. They also show significant signs of inbreeding, owing to a captive-breeding programme begun in the 1940s.

Some conservationists view domestic genes as pollutants that are tarnishing the genomes of wild animals such as wolves, coyotes and even the red junglefowl native to southeast Asia. Some even contend that there are no ‘pure’ red junglefowl left.

“What feral animals make us do is reconsider this all-too-obvious, all-too-easy and all-too-wrong dichotomy between wild and domestic,” says Larson. And the ability of supposedly wild animals to thrive in a world increasingly altered by human activity may be due in part to the domestic genes that they now carry. What better way to adapt to human-moulded environments than to borrow traits from human-moulded creatures?

“Cock-a-doodle-doo,” announces a rooster masked by dense forest in Kokee State Park, an achingly beautiful nature reserve on Kauai’s western coast, on a sunny autumn morning. A faint but unmistakable “cock-a-doodle-doo” volleys back, from maybe a kilometre away.

“What feral animals make us do is consider this all-too-easy dichotomy between wild and domestic.” Although the birds are a fixture even in this rich and remote landscape, most of the chickens in the reserve stick near the car parks and picnic areas, where human hand-outs are easy to come by. The park’s birds are among the most brazen and comfortable around humans in all of Kauai, and it’s hard to enjoy a meal in Kokee’s central meadow without attracting the attention of a flock or two. But “give them a chase and they’ll disappear down a 300-metre ravine that’s so thick with vegetation it’s impossible to follow”, says Gering. “That’s not something I think about barnyard chickens as being able to do.”

A park website discourages visitors from feeding the chickens, in the hope of reducing their numbers and their dependence on humans. This interest in ‘rewilding’ the feral chickens is probably motivated by the desire to reduce their numbers through methods other than culling. It may well be a matter of time before feral animals fully shed their yokes and evolve into creatures less dependent on humans — but perhaps it will never happen. “The environmental niches that feralized animals are exploiting are very different and bear a human stamp that wasn’t there when their ancestors developed,” says Zeder. “Why should anyone expect a feralized animal to go out and become the noble savage animal again?” Wright, however, thinks there is a possibility that if the chickens in Kokee are left alone for long enough, they may well become not a facsimile of their red-junglefowl ancestors, but some other kind of creature just as deserving of being called wild. Whatever wild means.

Nature 529, 270–273 (21 January 2016) doi:10.1038/529270a Nature  Original web page at Nature


US government approves transgenic chicken

Transgenic chickens are the latest animals engineered to produce ‘farmaceutical’ drugs.

The US Food and Drug Administration (FDA) has approved a chicken that has been genetically engineered to produce a drug in its eggs. The drug, Kanuma (sebelipase alfa), is a recombinant human enzyme marketed by Alexion Pharmaceuticals. It replaces a faulty enzyme in people with a rare, inherited condition that prevents the body from breaking down fatty molecules in cells.

Following its approval by the FDA on 8 December, Kanuma joins a small group of ‘farmaceuticals’ on the US market. In 2009, the agency approved genetically modified goats that produce an anticoagulant called ATryn (antithrombin) in their milk. And last year, the FDA authorized a drug for treating hereditary angioedema that is produced by transgenic rabbits.

The FDA’s latest decision “shows that the ATryn goats weren’t just a one-off”, says Jay Cormier, a lawyer at Hyman, Phelps and McNamara in Washington DC and a former scientific reviewer for the FDA. “The process can function for more than just one particular unique case.”

The agency moved quickly to consider Kanuma, giving it a priority review, orphan-drug status and a breakthrough-therapy designation. The disease that it is designed to treat, lysosomal acid lipase deficiency, causes fat to accumulate in the liver, spleen and vasculature. A form of the disease that strikes infants is quickly fatal. A second form that affects older patients causes liver enlargement, fibrosis and cirrhosis, as well as cardiovascular disease.

“Before we had this drug, we didn’t have any treatment for the patients that really addressed the underlying biochemical defect in the disorder,” says Barbara Burton, a paediatrician with the Northwestern University Feinberg School of Medicine in Chicago, Illinois. Clinicians could only provide nutrition and supportive care to infants, says Burton, who worked with Alexion to conduct the clinical trials. Older patients are treated with statins — which do not address the fatty build-up in the liver.

Unlike the genetically engineered AquAdvantage salmon that was approved by the FDA last month, the transgenic chickens that produce Kanuma are not intended to enter the food supply. But just as with the AquAdvantage salmon, the FDA considers the chicken’s genetic modifications to be an ‘animal drug’.

Because every cell in the modified chicken contains altered DNA, the FDA “asserts its jurisdiction over the entire chicken”, says Cormier. Under its process for considering animal drugs, the FDA examined whether altering the chickens’ DNA would harm them, and whether the modified DNA was stable as it passed to new generations of chickens. The FDA says that the chickens are not likely to accidentally enter the food supply or adversely affect the environment because they are raised in indoor facilities.

William Muir, a geneticist at Purdue University in West Lafayette, Indiana, praised the FDA’s decision to approve the transgenic chickens. “The floodgates are opening,” he says, “and I can’t wait to see what comes next.”

Nature doi:10.1038/nature.2015.18985  Nature  Original web page at Nature


Why we’re smarter than chickens

Toronto researchers have discovered that a single molecular event in our cells could hold the key to how we evolved to become the smartest animal on the planet. Benjamin Blencowe, a professor in the University of Toronto’s Donnelly Centre and Banbury Chair in Medical Research, and his team have uncovered how a small change in a protein called PTBP1 can spur the creation of neurons — cells that make the brain — that could have fuelled the evolution of mammalian brains to become the largest and most complex among vertebrates.

The study is published in the August 20 issue of Science.

Brain size and complexity vary enormously across vertebrates, but it is not clear how these differences came about. Humans and frogs, for example, have been evolving separately for 350 million years and have very different brain abilities. Yet scientists have shown that they use a remarkably similar repertoire of genes to build organs in the body. So how is it that a similar number of genes, that are also switched on or off in similar ways in diverse vertebrate species, generate a vast range of organ size and complexity?

The key lays in the process that Blencowe’s group studies, known as alternative splicing (AS), whereby gene products are assembled into proteins, which are the building blocks of life. During AS, gene fragments — called exons — are shuffled to make different protein shapes. It’s like LEGO, where some fragments can be missing from the final protein shape.

AS enables cells to make more than one protein from a single gene, so that the total number of different proteins in a cell greatly surpasses the number of available genes. A cell’s ability to regulate protein diversity at any given time reflects its ability to take on different roles in the body. Blencowe’s previous work showed that AS prevalence increases with vertebrate complexity. So although the genes that make bodies of vertebrates might be similar, the proteins they give rise to are far more diverse in animals such as mammals, than in birds and frogs. And nowhere is AS more widespread than in the brain.

“We wanted to see if AS could drive morphological differences in the brains of different vertebrate species,” says Serge Gueroussov, a graduate student in Blencowe’s lab who is the lead author of the study. Gueroussov previously helped identify PTBP1 as a protein that takes on another form in mammals, in addition to the one common to all vertebrates. The second form of mammalian PTBP1 is shorter because a small fragment is omitted during AS and does not make it into the final protein shape.

Could this newly acquired, mammalian version of PTBP1 give clues to how our brains evolved? PTBP1 is both a target and major regulator of AS. PTBP1’s job in a cell is to stop it from becoming a neuron by holding off AS of hundreds of other gene products.

Gueroussov showed that in mammalian cells, the presence of the second, shorter version of PTBP1 unleashes a cascade of AS events, tipping the scales of protein balance so that a cell becomes a neuron. What’s more, when Gueroussov engineered chicken cells to make the shorter, mammalian-like, PTBP1, this triggered AS events that are found in mammals.

“One interesting implication of our work is that this particular switch between the two versions of PTBP1 could have affected the timing of when neurons are made in the embryo in a way that creates differences in morphological complexity and brain size,” says Blencowe, who is also a professor in the Department of Molecular Genetics.

As scientists continue to sift through countless molecular events occurring in our cells, they’ll keep finding clues as to how our bodies and minds came to be. “This is the tip of an iceberg in terms of the full repertoire of AS changes that likely have contributed major roles in driving evolutionary differences,” says Blencowe.  Science Daily  Original web page at Science Daily


* Some vaccines support evolution of more-virulent viruses

Scientific experiments with the herpesvirus such as the one that causes Marek’s disease in poultry have confirmed, for the first time, the highly controversial theory that some vaccines could allow more-virulent versions of a virus to survive, putting unvaccinated individuals at greater risk of severe illness. The research has important implications for food-chain security and food-chain economics, as well as for other diseases that affect humans and agricultural animals.

“The challenge for the future is to identify other vaccines that also might allow more-virulent versions of a virus to survive and possibly to become even more harmful,” said Andrew Read, an author of the paper describing the research, which will be published in the July 27, 2015 issue of the scientific journal PLoS Biology. Read is the Evan Pugh Professor of Biology and Entomology and Eberly Professor in Biotechnology at Penn State University.

“When a vaccine works perfectly, as do the childhood vaccines for smallpox, polio, mumps, rubella, and measles, it prevents vaccinated individuals from being sickened by the disease, and it also prevents them from transmitting the virus to others,” Read said. These vaccines are a type that is “perfect” because they are designed to mimic the perfect immunity that humans naturally develop after having survived one of these diseases. “Our research demonstrates that another vaccine type allows extremely virulent forms of a virus to survive — like the one for Marek’s disease in poultry, against which the poultry industry is heavily reliant on vaccination for disease control,” said Venugopal Nair, who led the research team in the United Kingdom where the experimental work related to this study was carried out. Nair is the head of the Avian Viral Diseases program at the Pirbright Institute, which also hosts the OIE Reference Laboratory on Marek’s disease. “These vaccines also allow the virulent virus to continue evolving precisely because they allow the vaccinated individuals, and therefore themselves, to survive, Nair said.

Less-than-perfect vaccines create a ‘leaky’ barrier against the virus, so vaccinated individuals sometimes do get sick, but typically with less-virulent symptoms. Because the vaccinated individuals survive long enough to transmit the virus to others, the virus also is able to survive and to spread throughout a population. “In our tests of the leaky Marek’s-disease virus in groups of vaccinated and unvaccinated chickens, the unvaccinated died while those that were vaccinated survived and transmitted the virus to other birds left in contact with them,” Nair said. “Our research demonstrates that the use of leaky vaccines can promote the evolution of nastier ‘hot’ viral strains that put unvaccinated individuals at greater risk.”

The theory tested by the research team was highly controversial when it first was proposed over a decade ago. The team’s experiments now show, for the first time, that the modern leaky vaccines, widely used in the agricultural production of poultry, can have precisely the effect on evolution of more-virulent strains of the virus that the controversial theory predicted.

Marek’s disease used to be a minor disease that did not do much harm to chickens in the 1950s, but the virulence of the virus has evolved and today it even is capable of killing all the unvaccinated birds in poultry flocks, sometimes within 10 days. “Even though the Marek’s disease virus is much nastier now than it was in the 1950s, it is becoming increasingly rare and now it causes relatively minor problems in the poultry industry because almost every chicken in agricultural production worldwide is vaccinated against the disease,” Read said. If you can vaccinate all the individuals in a population against a virus, it does not matter if the virus has become super virulent so long as the vaccine continues to be effective.”

The virus for Marek’s disease is very virulent, but the virus causing avian influenza can be even worse. “The most-virulent strain of avian influenza now decimating poultry flocks worldwide can kill unvaccinated birds in just under three days,” Read said. The vaccine against avian influenza is a leaky vaccine, according to Read. “In the United States and Europe, the birds that get avian influenza are culled, so no further evolution of the virus is possible,” Read said. “But instead of controlling the disease by culling infected birds, farmers in Southeast Asia use vaccines that leak — so evolution of the avian influenza virus toward greater virulence could happen.”

The research has implications for human health, as well. The World Health Organization recently reported laboratory-confirmed cases in China of human infection with the avian influenza virus, including a number of deaths. “We humans never have experienced any contagious disease that kills as many unvaccinated hosts as these poultry viruses can, but we now are entering an era when we are starting to develop next-generation vaccines that are leaky because they are for diseases that do not do a good job of producing strong natural immunity — diseases like HIV and malaria,” Read said.

“Vaccines for human diseases are the least-expensive, most-effective public-health interventions we ever have had,” Read said. “But the concern now is about the next-generation vaccines. If the next-generation vaccines are leaky, they could drive the evolution of more-virulent strains of the virus.” He said it is critical now to determine as quickly as possible that the Ebola vaccines that now are in clinical trials are not leaky — that they completely prevent the transmission of the Ebola virus among people. “We do not want the evolution of viral diseases as deadly as Ebola evolving in the direction that our research has demonstrated is possible with less-than-perfect, leaky vaccines,” Read said.

The researchers recommend rigorous testing and vigilant monitoring of next-generation vaccines to prevent the runaway evolution of more-virulent strains of viruses that their research has confirmed can occur with leaky vaccines. “If some day we have a malaria vaccine or an HIV vaccine, of course we should use those vaccines, but we would be in significant danger if those vaccines turned out to be leaky and we had not developed effective ways to eradicate any strains that might become more virulent,” Read said.

Read also recommends vaccination for individual protection. “When evolution toward more-virulent virus strains takes place as a result of vaccination practices, it is the unvaccinated individuals who are at the greatest risk. Those who are not vaccinated will be exposed, without any protection, to the hottest strains of a virus. Our research provides strong evidence for the importance of getting vaccinated.” Science Daily Original we page at Science Daily


* New method may eliminate antibiotic use in livestock

A University of Wisconsin-Madison animal scientist has developed an antibiotic-free method to protect animals raised for food against common infections. The innovation comes as growing public concern about antibiotic resistance has induced McDonald’s, Tyson Foods and other industry giants to announce major cuts in antibiotic use in meat production. About 80 percent of antibiotics in the United States are used by farmers, because they both protect against disease and accelerate weight gain in many farm animals.

The overuse of antibiotics in agriculture and medicine has created a public health crisis of drug-resistant infections, such as multidrug resistant staphylococcus aureus (MRSA) and “flesh-eating bacteria.” “You really can’t control the bugs forever; they will always evolve a way to defeat your drugs,” says Mark Cook, a professor of animal science and entrepreneur. Cook’s current work focuses on a fundamental immune “off-switch” called Interleukin 10 or IL-10, manipulated by bacteria and many other pathogens to defeat the immune system during infection. He and animal science associate researcher Jordan Sand have learned to disable this switch inside the intestine, the site of major farm animal infections such as the diarrheal disease coccidiosis.

Cook vaccinates laying hens to create antibodies to IL-10. The hens put the antibody in eggs that are then sprayed on the feed of the animals he wants to protect. The antibody neutralizes the IL-10 off-switch in those animals, allowing their immune systems to better fight disease. In experiments with 300,000 chickens, those that ate the antibody-bearing material were fully protected against coccidiosis. Smaller tests with larger animals also show promise. Dan Schaefer, a professor of animal science, and his graduate research assistant, Mitch Schaefer, halved the rate of bovine respiratory disease in beef steers by feeding them the IL-10 antibody for 14 days.

“That’s a very enticing early result,” Dan Schaefer says. “Bovine respiratory disease is the number one health risk for feeder cattle coming into a confinement situation.” He is planning a larger trial in collaboration with colleagues at other universities. In a test in newborn dairy calves, Sheila McGuirk, a professor of medical sciences at the School of Veterinary Medicine, found less than half as much respiratory disease among calves that ate the antibody for 10 days compared to those that did not. The treated calves also showed less shedding of Cryptosporidium parvum, a protozoa that causes diarrhea, although the trend was not statistically significant. “These diseases cause long-term reproduction, production and growth impairments in livestock,” says McGuirk. “The affected animals are suboptimal in health, performance and profitability. To have something affordable, safe and nonantibiotic that controls these very important diseases is absolutely awesome. We are eager to study this further.”

In the past few years, scientists have learned that a large group of pathogens — including bacteria, single- and multicelled parasites, protozoa, even certain viruses — make a chemical called macrophage migratory inhibition factor, or MIF, which activates the IL-10 mechanism to shut down the host animal’s immune system. “This apparently arose deep in the evolutionary past, and it’s wholesale piracy of the immune system,” says Sand. “People have manipulated the immune system for decades, but we are doing it in the gut. Nobody has done that before,” Cook says.

Cook and Sand, who have been working on the IL-10 system since 2011, are forming Ab E Discovery LLC to commercialize their research. One of the four patents they have filed through the Wisconsin Alumni Research Foundation has just been granted, and WARF has awarded a $100,000 Accelerator Program grant to the inventors to pursue the antibiotic-replacement technology. Cook previously founded Isomark LLC, which is developing a technology for early detection of infection in human breath.

The benefits of reducing farm usage of antibiotics should extend to workers’ families and the wider population. Significantly more people working in conventional chicken farms carry multidrug-resistant pathogens than those who work in antibiotic-free farms, Sand notes. A nonantibiotic method to prevent pathogens from shutting down the immune system seems far less conducive to resistance than the current routine feeding of antibiotics, Cook says. “We are not focused on the pathogens. We are focused on what they are trying to do to the immune system. We are getting encouraging data from dairy and beef. We have conducted experiments involving 300,000 chickens in commercial farms, half receiving the product. We know it works. The market is interested, and now it’s a matter of making a product.”  Science Daily  Original web page at Science Daily


Vaccines developed for H5N1, H7N9 avian influenza strains

Researchers have developed vaccines for H5N1 and H7N9, two new strains of avian influenza that can be transmitted from poultry to humans. The strains have led to the culling of millions of commercial chickens and turkeys as well as the death of hundreds of people. Wenjun Ma, assistant professor of diagnostic medicine and pathobiology at Kansas State University, left, and Jürgen Richt, Regents distinguished professor of veterinary medicine and director of the U.S. Department of Homeland Security’s Center of Excellence for Emerging and Zoonotic Animal Diseases, have developed vaccines for H5N1 and H7N9, two emerging strains of avian influenza. The strains are zoonotic and can be transmitted from chickens to pigs and humans.

A recent study with Kansas State University researchers details vaccine development for two new strains of avian influenza that can be transmitted from poultry to humans. The strains have led to the culling of millions of commercial chickens and turkeys as well as the death of hundreds of people. The new vaccine development method is expected to help researchers make vaccines for emerging strains of avian influenza more quickly. This could reduce the number and intensity of large-scale outbreaks at poultry farms as well as curb human transmission.

It also may lead to new influenza vaccines for pigs, and novel vaccines for sheep and other livestock, said Jürgen Richt, Regents distinguished professor of veterinary medicine and director of the U.S. Department of Homeland Security’s Center of Excellence for Emerging and Zoonotic Animal Diseases. Richt and his colleagues focused on the avian influenza virus subtype H5N1, a new strain most active in Indonesia, Egypt and other Southeast Asian and North African countries. H5N1 also has been documented in wild birds in the U.S., though in fewer numbers.

“H5N1 is a zoonotic pathogen, which means that it is transmitted from chickens to humans,” Richt said. “So far it has infected more than 700 people worldwide and has killed about 60 percent of them. Unfortunately, it has a pretty high mortality rate.” Researchers developed a vaccine for H5N1 by combining two viruses. A vaccine strain of the Newcastle disease virus, a virus that naturally affects poultry, was cloned and a small section of the H5N1 virus was transplanted into the Newcastle disease virus vaccine, creating a recombinant virus. Tests showed that the new recombinant virus vaccinated chickens against both Newcastle disease virus and H5N1.

Researchers also looked at the avian flu subtype H7N9, an emerging zoonotic strain that has been circulating in China since 2013. China has reported about 650 cases in humans and Canada has reported two cases in people returning from China. About 230 people have died from H7N9. “In Southeast Asia there are a lot of markets that sell live birds that people can buy and prepare at home,” Richt said. “In contrast to the H5N1 virus that kills the majority of chickens in three to five days, chickens infected with the H7N9 virus do not show clinical signs of sickness. That means you could buy a bird that looks perfectly healthy but could be infected. If an infected bird is prepared for consumption, there is a high chance you could get sick, and about 1 in 3 infected people die.”

Using the same method for developing the H5N1 vaccine, researchers inserted a small section of the H7N9 virus into the Newcastle disease virus vaccine. Chickens given this recombinant vaccine were protected against the Newcastle disease virus and H7N9. “We believe this Newcastle disease virus concept works very well for poultry because you kill two birds with one stone, metaphorically speaking,” Richt said. “You use only one vector to vaccinate and protect against a selected virus strain of avian influenza.” Using the Newcastle disease virus for vaccine development may extend beyond poultry to pigs, cattle and sheep, Richt said.  Science Daily  Original web page at Science Daily


How did the chicken cross the sea?

Michigan State University researcher Eben Gering has collaborated with a team in a study of the mysterious ancestry of the feral chicken population that has overrun the Hawaiian Island of Kauai. Their results, published in the current issue of Molecular Ecology, may aid efforts to curtail the damage of invasive species in the future, and help improve the biosecurity of domestic chicken breeds. Domesticated chickens, humanity’s leading source of animal protein, are fighting rapidly evolving pathogens and fertility issues likely caused by inbreeding. The Red Junglefowl, the chicken’s closest living relative, is believed to have been introduced to Hawaii by ancient Polynesians, and is threatened by habitat loss and the contamination of gene pools from hybridization in its native Asian range. In Kauai, a feral hybrid of the Red Junglefowl and the domesticated chicken has presented the researchers with an opportunity to study the potential practical application of invasive genetics.

“It is crucial that we identify and conserve the genetic variation that still remains in the Red Junglefowl. This variation could soon be essential for the improvement or evolutionary rescue of commercial chicken breeds,” said Gering, a postdoctoral research associate in the Department of Zoology. Through investigating the murky genetic origins of the chickens, the team sought to gain insights into the ongoing evolution of the population. “We are eager to learn which combinations of genes and traits are emerging from this ‘evolutionary experiment,’ and to see whether our findings can translate to gains in the sustainability or efficacy of egg and poultry production,” Gering said. Gering and his team found that some chickens were a perfect match for genetic data from ancient Kauai cave bones that predate Captain Cook’s 1778 discovery of Hawaii. Others, however, had genotypes that are found in chicken breeds developed recently in Europe and farmed worldwide.

The team also found evidence for a population increase in the chickens in Kauai that coincided with storms that locals believe released chickens and caused feralization over the last few decades. Taken together, the data suggest that the population may have hybrid origins, resulting from interbreeding between the ancient Red Junglefowl and their domestic counterparts. Additional clues were found in the appearance and behavior of the chickens, which display physical traits and coloration ranging from those of ancient jungle birds to more recent domesticated breeds. Acoustic properties of rooster crows likewise ranged from those typical of the Red Junglefowl to the familiar sound heard on a domestic farm. But why do these variations matter? Studying the evolutionary forces at play among the feral chicken population may lead to the ability to create hardier breeds of domestic chickens. “Darwin drew heavily from his studies of domesticated species to develop his theory of evolution,” Gering said. “This can provide important insights into evolution in action within human altered landscapes, and may even someday help build a better chicken. And that would be something to crow about.”  Science Dail  Original web page at Science Daily


Timing of Influenza A(H5N1) in Poultry and Humans and Seasonal Influenza Activity Worldwide, 2004–2013

Co-circulation of influenza A(H5N1) and seasonal influenza viruses among humans and animals could lead to co-infections, reassortment, and emergence of novel viruses with pandemic potential. We assessed the timing of subtype H5N1 outbreaks among poultry, human H5N1 cases, and human seasonal influenza in 8 countries that reported 97% of all human H5N1 cases and 90% of all poultry H5N1 outbreaks. In these countries, most outbreaks among poultry (7,001/11,331, 62%) and half of human cases (313/625, 50%) occurred during January–March. Human H5N1 cases occurred in 167 (45%) of 372 months during which outbreaks among poultry occurred, compared with 59 (10%) of 574 months that had no outbreaks among poultry. Human H5N1 cases also occurred in 59 (22%) of 267 months during seasonal influenza periods.

To reduce risk for co-infection, surveillance and control of H5N1 should be enhanced during January–March, when H5N1 outbreaks typically occur and overlap with seasonal influenza virus circulation. Co-circulation of influenza A viruses in human and animal reservoirs can provide opportunities for these viruses to reassort and acquire genetic material that facilitates sustained human-to-human transmission, a necessary trait of pandemic viruses.

One influenza strain at the forefront of pandemic preparedness planning is highly pathogenic avian influenza (HPAI) A(H5N1) virus. Asian-lineage H5N1 viruses emerged in domestic birds in Southeast Asia in 1996 and are now endemic in 5 countries. As of December 2013, H5N1 virus outbreaks have been documented among domestic poultry and wild birds in >60 countries. The spread of H5N1 among the world’s domestic poultry population increases the risk for H5N1 to infect humans. Humans are at risk for H5N1 infection if they have direct or close contact with infected domestic poultry, such as by handling sick animals or their byproducts, caregiving, slaughtering, and butchering; infection can also occur through some forms of indirect contact (e.g., proximity to live poultry or wet markets).

During 2003–2013, more than 645 human cases of HPAI H5N1 were confirmed; the case-fatality rate was ≈60% . H5N1 viruses have not yet acquired the ability to be transmitted between humans beyond 3 generations, therefore failing to show sustained human-to-human transmission. However, these viruses have wide geographic distribution and the potential to reassort with human seasonal influenza viruses. These characteristics mean that clarifying the timing of H5N1 outbreaks among poultry and infections in humans may be useful for prevention and control activities.

Recently published data suggest a seasonal pattern to H5N1 virus infection among domestic and wild birds. Park et al. noted that H5N1 outbreaks among poultry and infections in humans in Southeast Asia occurred in the cooler months during 1997–2006. Other studies from Southeast Asia have suggested that decreasing temperatures may correlate with an increase in the number of H5N1 outbreaks among birds . Although ecologic studies suggest that H5N1 virus activity may occur during predictable times of the year, a systematic analysis of global poultry and human H5N1 data has not tested this hypothesis. In this study, we explored whether H5N1 outbreaks among domestic poultry and human H5N1 cases occurred in temporal proximity, occurred during certain climate conditions, or overlapped with human seasonal influenza epidemics. Emerging Infectious Diseases  Original article at Emerging Infectious Diseases


Pet foods: Not all brands follow meat regulations

Researchers in ChapmanUniversity’s Food Science Program have just published a study on pet food mislabeling. The study focused on commercial pet foods marketed for dogs and cats to identify meat species present as well as any instances of mislabeling. Of the 52 products tested, 31 were labeled correctly, 20 were potentially mislabeled, and one contained a non-specific meat ingredient that could not be verified. “Although regulations exist for pet foods, increases in international trade and globalization of the food supply have amplified the potential for food fraud to occur,” said Rosalee Hellberg, Ph.D., and co-author on the study. “With the recent discovery of horsemeat in ground meat products sold for human consumption in several European countries, finding horsemeat in U.S. consumer food and pet food products is a concern, which is one of the reasons we wanted to do this study.” Chicken was the most common meat species found in the pet food products. Pork was the second most common meat species detected, and beef, turkey and lamb followed, respectively. Goose was the least common meat species detected. None of the products tested positive for horsemeat. Of the 20 potentially mislabeled products, 13 were dog food and 7 were cat food. Of these 20, 16 contained meat species that were not included on the product label, with pork being the most common undeclared meat species. In three of the cases of potential mislabeling, one or two meat species were substituted for other meat species. In the study, DNA was extracted from each product and tested for the presence of eight meat species: beef, goat, lamb, chicken, goose, turkey, pork, and horse. “Pet food safety was another area of concern, particularly with pet foods that are specifically formulated to address food allergies in both cats and dogs,” continued Dr. Hellberg. The pet food industry is a substantial market in the United States. Nearly 75 percent of U.S. households own pets, totaling about 218 million pets (not including fish). On average, each household spends $500 annually on their pets, equating to about 1 percent of household expenditures. In the past five years, pet industry expenditures have increased by $10 billion, with $21 billion spent on pet food alone in 2012. The foods developed for pets are regulated by both federal and state entities. The U.S. Food and DrugAdministrationCenter for Veterinary Medicine regulates animal feed and pet foods. While the U.S. Department of Agriculture regulates the interstate transportation and processing of animal products, as well as the inspection of animal product imports and exports. While a seemingly high percentage of pet foods were found to be potentially mislabeled in this study, the manner in which mislabeling occurred is not clear; nor is it clear as to whether the mislabeling was accidental or intentional and at which points in the production chain it took place. The study was published in the journal Food Control and was completed with Chapman undergrad student Tara Okuma.  Science Daily  Original web page at Science Daily



Highly pathogenic fowlpox virus in cutaneously infected chickens, China

We investigated an acute outbreak of the cutaneous form of fowlpox among chickens in China in November 2009. Using pathologic and virologic methods, we identified a novel type of fowlpox virus that carried an integrated genomic sequence of reticuloendotheliosis virus. This highly pathogenic virus could lead to severe ecologic effects and economic losses. Fowlpox has been reported worldwide as a mild to severe poultry disease. Caused by fowlpox virus (FWPV), the disease is primarily found in 2 forms, cutaneous and diphtheritic. The cutaneous form is usually mild and characterized by multifocal cutaneous lesions on unfeathered areas of the skin. The more severe diphtheritic form is characterized by fibrous necrotic proliferative lesions on the mucous membranes of the respiratory and gastrointestinal tracts and causes more deaths than the cutaneous form, usually resulting from asphyxiation. In recent years, fowlpox outbreaks in poultry flocks have been gradually increasing because of an emerging novel type of FWPV. The pathogenic traits of this virus type are likely enhanced by integrated reticuloendotheliosis virus (REV) sequences of various lengths in the FWPV genome. Although this variant FWPV has been found widely, the reported illness and death rates from the cutaneous form of fowlpox in chickens have not reached 100%. We investigated a severe outbreak of cutaneous fowlpox in a poultry flock in northeastern China in which all infected chickens died. The flock had not been vaccinated with an FWPV vaccine. Clinical signs, including listlessness, anorexia, and typical skin pock lesions, were observed in all infected chickens. Lesions types varied in size and type: ulcerated, multifocal, or coalescing proliferative cutaneous exanthema variolosum. The lesions appeared on the skin in unfeathered areas of the backs, the eyelids, and the wings. All of the birds died within 10 days after clinical signs first appeared. Postmortem examinations were performed for      pathologic evaluation. Samples submitted for histopathologic examination included skin from the varioliform exanthema areas, trachea, thymus gland, bursa of fabricius, and internal organs. Microscopic examination of skin lesions showed swelling, vacuolation, and characteristic eosinophilic cytoplasmic inclusion bodies in the stratified squamous epithelial cells of the folliculus pili. No obvious lesions were observed in other organs. Read more:  Emerging Infectious Diseases

July 22, 2014  Original web page at Emerging Infectious diseases


* Chicken project gets off the ground

Modern chickens are descended primarily from the red junglefowl. The meat and eggs of domestic chickens are a source of protein for billions. Yet how and when the birds were domesticated remains a mystery. The answers to these questions could reveal a wealth of information about the genetics of domestication, as well as human behaviour, and how we can improve our husbandry of the birds. In a bid to learn more about the chicken and its lineage, the UK government is funding a £1.94-million (US$3.3-million) effort to determine how the chicken went from being a wild fowl roaming the jungles of southeast Asia several thousand years ago to one of the world’s most abundant domesticated animals. The Cultural and Scientific Perceptions of Human–Chicken Interactions project — ‘Chicken Coop’ for short — will examine human history from the perspective of the fowl. “No one ever considers chickens, which is a massive mistake,” says Holly Miller, an archaeologist at the University of Nottingham, UK. She was one of two dozen researchers, from anthropologists to geneticists, who attended the second meeting of the five-month-old project at the University of Roehampton, UK, last week. Another was Greger Larson, an evolutionary geneticist at Durham University, UK, who is a senior scientist on the project. He says that researchers studying domestication tend to overlook chickens in favour of other domesticated animals, such as dogs, cows and pigs. But no domestic animal has been moulded and remoulded by humans as extensively as chickens, says Larson. The animals have been bred for eating, egg-laying and fighting. And in the case of one particularly vocal breed, the creatures have even been strapped to the masts of Polynesian boats to act as foghorns. “Chickens are polymaths,” he says. Larson, who studies DNA from the remains of ancient chickens, discovered last year that modern chickens can be deceptive. Previous studies have compared the DNA of modern chicken breeds with that of species of guinea fowl that contributed to the gene pool of early chickens, such as the red junglefowl. The work identified variants in two genes that are common in contemporary chickens but not in guinea fowl.

One variant — when present in two copies — gives domestic chickens their familiar yellow skin and legs when they consume a diet rich in carotenoids; this trait is almost universal in European chickens. The other is a variant of the thyroid-stimulating hormone receptor gene (TSHR) that may alter the seasonal mating patterns of chickens and allow them to lay eggs all year round. It is universal in modern breeds such as Rhode Island Reds and broiler chickens. Because these mutations are so common in contemporary chickens, Larson’s team and others assumed that humans influenced these traits through selective breeding early in the course of domestication. But DNA from chickens recovered at archaeological sites across Europe, spanning the period from around 280 bc to ad 1800, has turned that idea on its head. In an analysis published last month, Larson’s team reported that none of 25 ancient chickens would have had yellow legs, and that just 8 out of 44 birds carried two copies of the TSHR variant3. So even 200 years ago, chickens may have been very different from those we know today. With the help of other Chicken Coop members, Larson is also trying to get to grips with the wider evolutionary forces that shaped modern chickens. He hopes to determine why, for instance, chickens have not been wiped out by disease. This might have been expected because their very rapid selection — much of which has taken place since 1900 — should have led to inbreeding and, by whittling down immune genes, a reduced ability to respond to infections. Other members of Chicken Coop are tackling different aspects of the bird’s past. Miller plans to analyse the diet of ancient chickens, using chemical isotopes in their bones and egg shells, to reveal information on the resources available to the humans who kept them. Another team, at the University of Leicester, UK, will compare chicken bones from archaeological sites with bones of modern breeds. Known pathologies in today’s birds can then be used to determine how diseases and breeding changed through time. John Hutchinson, an evolutionary biomechanist at the RoyalVeterinaryCollege in London, thinks that a better understanding of the bird’s history will help people to address some of the problems facing chickens and the poultry industry, such as avian influenza and leg weakness among broiler chickens. Research on ancient breeds could help us to “refresh the genetics” of broilers, he suggests. Last month, Hutchinson ran a conference, Towards the Chicken of the Future, to tackle such issues. “Science has got us into this problem through intense selection,” he says. “It can maybe help us out of it.” Nature 509, 546 (29 May 2014) doi:10.1038/509546a  Nature

June 24, 2014  Original web page at Nature


Barnyard chickens living just a few hundred years ago looked far different from today’s chickens

Analyzing DNA from the bones of chickens that lived 200-2300 years ago in Europe, researchers report that just a few hundred years ago domestic chickens may have looked far different from the chickens we know today. The results suggest that some of the traits we associate with modern domestic chickens — such as their yellowish skin — only became widespread in the last 500 years, much more recently than previously thought. “It’s a blink of an eye from an evolutionary perspective,” said co-author Greger Larson at DurhamUniversity in the United Kingdom. The study is part of a larger field of research that aims to understand when, where and how humans turned wild plants and animals into the crops, pets and livestock we know today. Generally, any mutations that are widespread in domestic plants and animals but absent from their wild relatives are assumed to have played a key role in the process, spreading as people and their livestock moved across the globe. But a growing number of ancient DNA studies tell a different tale. Chickens are descended from a wild bird called the Red Junglefowl that humans started raising roughly 4,000-5,000 years ago in South Asia. To pinpoint the genetic changes that transformed this shy, wild bird into the chickens we know today, researchers analyzed DNA from the skeletal remains of 81 chickens retrieved from a dozen archeological sites across Europe dating from 200 to 2,300 years old. The researchers focused on two genes known to differ between domestic chickens and their wild counterparts: a gene associated with yellow skin color, called BCDO2, and a gene involved in thyroid hormone production, called TSHR. Though the exact function of TSHR is unknown, it may be linked to the domestic chicken’s ability to lay eggs year-round — a trait that Red Junglefowl and other wild birds don’t have.

When the team compared the ancient sequences to the DNA of modern chickens, only one of the ancient chickens had the yellow skin so common in chickens today. Similarly, less than half of the ancient chickens had the version of the TSHR gene found worldwide in modern chickens. The results suggest that these traits only became widespread within the last 500 years — thousands of years after the first barnyard chickens came to be. “Just because a plant or animal trait is common today doesn’t mean that it was bred into them from the beginning,” Larson said. “It demonstrates that the pets and livestock we know today — dogs, chickens, horses, cows — are probably radically different from the ones our great-great-grandparents knew,” he added. “…They are subjected to the whim of human fancy and control, so radical change in the way they look can be achieved in very few generations.” Science Daily

May 13, 2014  Original web page at Science Daily


Vietnam on high alert over flu risk

The H7N9 avian-influenza virus that has killed more than 100 people in China in the past year has for the first time been detected in a province bordering Vietnam, raising the prospect that the disease may take hold across Asia and beyond. It was found in poultry in the live-bird markets of southern China’s Guangxi province in late January, and has caused three known human cases in the region. The news comes as a surge in human H7N9 flu cases in China since the start of the year shows signs of abating, possibly because of the re­introduction of control measures. Vietnam, which had already prepared response plans for such an H7N9 outbreak, has placed itself on high alert. “There is a very high likelihood of H7N9 entering the poultry sector in Vietnam,” says Peter Horby, a researcher at the Oxford University Clinical Research Unit in Hanoi. H7N9 flu was first detected in China in March last year, and almost all of the human cases were reported the following month. They subsequently dropped off sharply after the prompt, temporary closure of live-bird markets, which were quickly identified as the places where most human infections occurred. Researchers say that the surge in cases since the start of the year is probably due to the arrival of winter and the intense poultry trading at live markets in the run-up to the Chinese New Year on 31 January.

So far, more than 200 human cases of H7N9 flu have been registered in China this year, compared with around 160 recorded in 2013. This year’s outbreak has been centred in many of the same eastern provinces as last year’s, although with a coastal and southerly shift. Zhejiang and Guangdong provinces are the worst affected. Last week, the first human case of H7N9 flu was detected in Jilin province in the far north of the country, raising a further risk of spread to North Korea and Russia, which border the province.  Nature

March 18, 2014  Original web page at Nature


Full genome of influenza A (H7N9) virus derived by direct sequencing without culture

An epidemic caused by influenza A (H7N9) virus was recently reported in China. Deep sequencing revealed the full genome of the virus obtained directly from a patient’s sputum without virus culture. The full genome showed substantial sequence heterogeneity and large differences compared with that from embryonated chicken eggs. Recently, a novel influenza A (H7N9) virus infected humans in China, leading to great concerns about its threat to public health. However, almost all the current genomes of the novel subtype H7N9 virus have been sequenced after culture in embryonated chicken eggs or mammalian cells. Switching the evolutionary selection pressure from in vivo human respiratory tract to embryonated chicken eggs might introduce mutations into the final genome sequences during culture. We report determination of the full genome of the influenza A (H7N9) virus derived directly by deep sequencing, without virus culture, from a sputum specimen of an infected human. Deep sequencing provides a direct way to evaluate the genome characteristics and potential virulence and transmissibility of the novel influenza A (H7N9) virus.

Emerging Infectious Diseases
September 3, 2013

Original web page at Emerging Infectious Diseases


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


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


Putting the clock in ‘cock-a-doodle-doo’

Of course, roosters crow with the dawn. But are they simply reacting to the environment, or do they really know what time of day it is? Researchers reporting on March 18 in Current Biology, a Cell Press publication, have evidence that puts the clock in “cock-a-doodle-doo” (or “ko-ke-kok-koh,” as they say in the research team’s native Japan). “‘Cock-a-doodle-doo’ symbolizes the break of dawn in many countries,” says Takashi Yoshimura of Nagoya University. “But it wasn’t clear whether crowing is under the control of a biological clock or is simply a response to external stimuli.” That’s because other things — a car’s headlights, for instance — will set a rooster off, too, at any time of day. To find out whether the roosters’ crowing is driven by an internal biological clock, Yoshimura and his colleague Tsuyoshi Shimmura placed birds under constant light conditions and turned on recorders to listen and watch. Under round-the-clock dim lighting, the roosters kept right on crowing each morning just before dawn, proof that the behavior is entrained to a circadian rhythm. The roosters’ reactions to external events also varied over the course of the day.

In other words, predawn crowing and the crowing that roosters do in response to other cues both depend on a circadian clock. The findings are just the start of the team’s efforts to unravel the roosters’ innate vocalizations, which aren’t learned like songbird songs or human speech, the researchers say. “We still do not know why a dog says ‘bow-wow’ and a cat says ‘meow,’ Yoshimura says. “We are interested in the mechanism of this genetically controlled behavior and believe that chickens provide an excellent model.”

Science Daily
April 2, 2013

Original web page at Science Daily


How size of hen’s comb is linked to ability to lay more eggs

A lone rooster sees a lot of all the hens in the flock, but the hen with the largest comb gets a bigger dose of sperm — and thus more chicks. This sounds natural, but behind all this is humanity’s hunger for eggs. or thousands of years, people have tinkered with the development of domestic chickens. Through selective breeding for a few characteristics such as large muscle mass and increased egg-laying, we have at the same time caused numerous other radical changes in appearance and behaviour. A research group at Linköping University in Sweden has now shown how the size of a hen’s comb is bound up with the ability to lay more eggs. The results have been presented in the scientific journal PLoS Genetics. Compared with the original wild jungle hen, domestic hens have larger combs as well as denser bones. This influences egg-laying, as the hen’s bone tissues provide calcium for the eggshells. The greater the bone mass, the more eggs she can lay.

After having spotted a clear correlation between comb size and bone mass in chickens from a cross between red junglefowl and domestic chicken, the research group — under the leadership of evolutionary geneticist Dominic Wright — set up a study where such chickens were crossed for several generations. In this way the genome was split up into smaller and smaller regions, which allowed the “mapping” of the functions of individual genes. In the eighth generation, the researchers found an area that had a strong effect on the weight of the comb — but also on bone mass and fertility. The genetic variation has gradually decreased over the course of domestication. In domestic chickens there are now some 40 known small regions with stable genes that potentially govern their typical “domestic” characteristics. LiU researchers have now discovered two “pleiotropic” genes: two genes connected to each other that influence several characteristics simultaneously. By regulating the production of cartilage, they influence combs (which consist of cartilage throughout) as well as bone growth (where cartilage is the base material) and, ultimately, egg production. “The original hens have smaller combs, thinner legs, and lay fewer eggs. When people bred for the characteristic of laying many eggs, the comb grew automatically,” Dominic Wright says. In nature, the comb is an example of a sexual ornament. Individuals — often males — with the most impressive ornaments are favoured by females, thereby obtaining more numerous offspring than their competitors. In domesticated animals, sexual selection — like natural selection — has lost its role, as it was humans who determine breeding.

Science Daily
September 18, 2012

Original web page at Science Daily


Vaccines backfire: Veterinary vaccines found to combine into new infectious viruses

Research from the University of Melbourne has shown that two different vaccine viruses- used simultaneously to control the same condition in chickens- have combined to produce new infectious viruses, prompting early response from Australia’s veterinary medicines regulator. The vaccines were used to control infectious laryngotracheitis (ILT), an acute respiratory disease occurring in chickens worldwide. ILT can have up to 20% mortality rate in some flocks and has a significant economic and welfare impact in the poultry industry. The research found that when two different ILT vaccine strains were used in the same populations, they combined into two new strains (a process known as recombination), resulting in disease outbreaks. Neither the ILT virus or the new strains can be transmitted to humans or other animals, and do not pose a food safety risk.

The study was led by Dr Joanne Devlin, Professor Glenn Browning and Dr Sang-Won Lee and colleagues at the Asia-Pacific Centre for Animal Health at the University of Melbourne and NICTA’s Victoria Research Laboratory and is published July 13, 2012 in the journal Science. Dr Devlin said the combining of live vaccine virus strains outside of the laboratory was previously thought to be highly unlikely, but this study shows that it is possible and has led to disease outbreaks in poultry flocks. “We alerted the Australian Pesticide and Veterinary Medicines Authority (APVMA) to our findings and they are now working closely with our research team, vaccine registrants and the poultry industry to determine both short and long term regulatory actions,” she said. “Short-term measures include risk assessment of all live virus vaccines currently registered by the APVMA in regard to the risk of recombination and could include changes to product labels, which may result in restrictions on the use of two vaccines of different origins in the one animal population.”

The ILT vaccines are ‘live attenuated vaccines’, which means that the virus has some disease-causing factors removed but the immune system still recognises the virus to defend against a real infection. “Live vaccines are used throughout the world to control ILT in poultry. For over 40 years the vaccines used in Australia were derived from an Australian virus strain. But following a vaccine shortage another vaccine originating from Europe was registered in 2006 and rapidly became widely used,” Dr Devlin said. “Shortly after the introduction of the European strain of vaccine, two new strains of ILT virus were found to be responsible for most of the outbreaks of disease in New South Wales and Victoria. So we sought to examine the origin of these two new strains.” The team sequenced all of the genes (the genome) of the two vaccines used in Australia, and the two new outbreak strains of the virus. Following bioinformatic analysis on the resulting DNA sequence, in conjunction with Dr John Markham at NICTA’s Victoria Research Laboratory, they found that the new disease-causing strains were combinations of the Australian and European origin vaccine strains. “Comparisons of the vaccine strains and the new recombinant strains have shown that both the recombinant strains cause more severe disease, or replicate to a higher level than the parent vaccine strains that gave rise to them,” Dr Lee said.

Professor Glenn Browning said recombination was a natural process that can occur when two viruses infect the same cell at the same time. “While recombination has been recognised as a potential risk associated with live virus vaccines for many years, the likelihood of it happening in viruses like this in the field has been thought to be so low that it was considered to be very unlikely to lead to significant problems,” he said. “Our studies have shown that the risk of recombination between different vaccine strains in the field is significant as two different recombinant viruses arose within a year. We also demonstrated that the consequences of such recombination can be very severe, as the new viruses have been responsible for the deaths of thousands of Australian poultry.” “The study suggests that regulation of live attenuated vaccines for all species needs to take into account the real potential for vaccine viruses to combine. Measures such as those now being taken for the ILT vaccines will need to be implemented.”

Science Daily
July 24, 2012

Original web page at Science Daily


Men can rest easy: Sex chromosomes are here to stay

Fears that sex-linked chromosomes, such as the male Y chromosome, are doomed to extinction have been refuted in a new genetic study which examines the sex chromosomes of chickens. The study, published May 12 in the journal Proceedings of the National Academy of Sciences (PNAS), looked at how genes on sex-linked chromosomes are passed down generations and linked to fertility, using the specific example of the W chromosome in female chickens. The results confirm that although these chromosomes have shrunk over millions of years, and have lost many of their original genes, those that remain are extremely important in predicting fertility and are, therefore, unlikely to become extinct. Professor Judith Mank, from the UCL Department of Genetics, Evolution and Environment and senior author said: “Y chromosomes are here to stay, and are not the genetic wasteland that they were once thought to be.” W chromosomes in female chickens are entirely analogous to Y chromosomes in men in that they are sex-limited and do not re-combine when males and females reproduce, as the other regions of the genome do. Recombination allows chromosomes to break up linked genes, which makes selection more effective and helps get rid of faulty mutations. Some scientists think that Y and W chromosomes are doomed because of this lack of recombination.

The study, which involved researchers at UCL, Oxford and the Swedish Agricultural University, compared DNA regions on the W chromosome in different breeds of chickens, whose fertility rates are very easy to measure simply by counting eggs. Genetic information from two breeds, the Minorca and Leghorn, which lay more than 250 eggs per year, were compared with two breeds selected for male traits (fighting and plumage) called Yokohama and Old English Game. The researchers also looked at Red Jungle Fowl, a wild ancestor of chickens. The researchers measured gene expression levels from the W-linked genes in all the breeds, and showed that selection for laying lots of eggs has led to elevated gene expression for almost all the W-linked genes in the layer breeds. At the same time, relaxed female selection in the fighting and plumage breeds has led to a loss of W gene expression. This means that female-specific selection related to fertility acts to shape the W chromosome, and that the chromosome is able to respond to that selection despite all the problems with the lack of recombination. Professor Mank said: “We have shown that Y and W chromosomes are very important in fertility — the Y in males and the W in females. It is the ability of the W-linked genes to evolve that is the key to their survival, and which suggests that both the Y and the W chromosomes are with us for the long haul.”

Science Daily
May 29, 2012

Original web page at Science Daily


Influenza virus A (H10N7) in chickens and poultry abattoir workers, Australia

In March 2010, an outbreak of LPAI A (H10N7) was identified in a biosecure intensive commercial poultry enterprise in New South Wales, Australia. For 8–14 days, 10–25 birds died each day, compared with the normal number of 2–6 birds per day. An egg production decrease of up to 15% was documented in the affected flocks. In contrast to other reported poultry outbreaks, respiratory signs were absent in the flock. All cloacal and tracheal swabs from 10 dead and 10 live birds submitted for influenza virus exclusion were positive by an influenza A matrix gene quantitative real-time reverse transcription PCR, and virus was detected at various levels (cycle threshold [Ct]). The influenza A viruses were then subtyped from swabs by using a microarray assay (Clondiag, Jena, Germany) that enabled the rapid identification of influenza virus A (H10N7). The virus was readily cultured from swabs in embryonated chicken eggs and in MDCK cell cultures. Several viral genome segments were sequenced, which enabled confirmation of the virus as LPAI A (H10N7) and performance of phylogenetic analysis. A fluorescence-based neuraminidase inhibition assay showed the isolate to be sensitive to the antiviral drugs oseltamivir and zanamivir (mean 50% inhibitory concentration ± SD 0.5 ± 0.1 nmol/L and 1.8 ± 0.3 nmol/L, respectively).

Serologic testing was conducted by using an influenza A nucleoprotein–based blocking ELISA and a subtype H10–specific hemagglutination inhibition test; results showed widespread infection in the affected flock, with 18 of 20 samples seropositive. Sampling across a 4 additional flocks on site showed that an additional 9 of 40 birds were seropositive for influenza A subtype H10. Ten days after the outbreak was confirmed, 3 previously seronegative flocks from the site were sent to an abattoir; 1 day earlier, they had passed state government clinical inspection, including inspection and examination of production and mortality records. Within a week, 7 workers at the abattoir showed signs of conjunctivitis; 2 also reported rhinorrhea and 1 a sore throat. Conjunctival swabs were collected from 6 of the workers and nose and throat swabs from all 7. Influenza A RNA was detected by PCR 4 days after abattoir exposure in conjunctival swabs from a worker who reported conjunctivitis, rhinorrhea, and sore throat (Ct 31.8) and 7 days after abattoir exposure from the nose/throat swab of another worker who reported only conjunctivitis with onset 2 days earlier (Ct 35). Partial sequence analysis of the hemagglutinin genes from both samples (GenBank accession nos. CY063325 and CY063326) confirmed the presence of influenza A subtype H10; the partial sequences were identical to the subtype H10 chicken isolate, although no virus was cultured from the workers.

The conjunctivitis and other reported symptoms among the 7 workers were mild and of short duration, and there was no evidence of seroconversion by hemagglutination inhibition or virus neutralization tests in any of the workers from whom convalescent-phase blood was collected, including the 2 with confirmed influenza A subtype H10 infection. These findings are consistent with the mild symptoms and lack of serologic evidence reported in humans after experimental infection with influenza A (H10N7), which may indicate the limited ability of the virus to multiply and stimulate a detectable immune response in humans. Other studies have reported no evidence of elevated subtype H10–specific antibody titers among poultry abattoir workers, although serologic evidence of subtype H10 infection was detected among turkey farmers in the absence of clinical symptoms. Although 4 farm staff members from the site of the initial infections reported conjunctivitis and other symptoms to health care workers, influenza was not confirmed. The abattoir workers with laboratory-confirmed influenza A subtype H10 infection handled offal and giblets in a section of the abattoir where automated evisceration usually took place; however, because of the size of the birds, evisceration was manually assisted on the day that these flocks were slaughtered.

No obvious breach of biosecurity occurred on the farm. The water supply to the farm was chlorinated town water; no large dams were on site, only small paddock dams for cattle. The sheds were birdproof and protected by additional bird netting. A feed mill supplied the feed, which was delivered into silos through blow pipes from outside the perimeter fence. Litter (wood shavings) was delivered in enclosed bales. Workers showered on the way in and out of facilities; disinfectant foot baths were placed at the entrance of each shed, and staff were required to use the separate footwear provided inside the shed. Staff were not allowed to have birds or pigs at home. During 2010, the number of wild waterfowl observed on the affected site was unusually low. Surveillance of poultry flocks within a 2-km radius of the affected farm did not detect any serologic or virologic evidence of subtype H10 infection. Ongoing surveillance of wild waterfowl in New South Wales reported influenza virus A (H10N7) in other areas in the previous year (K.E. Arzey, unpub. data); however, during 2007–2008, onsite surveillance detected no evidence of influenza A infection among wild waterfowl (G.G. Arzey, unpub. data).

Emerging Infectious Diseases
May 15, 2012

Original web page at Emerging Infectious Diseases


Poultry culling and Campylobacteriosis reduction among humans, the Netherlands

In the Netherlands during March–May 2003, an outbreak of avian influenza (H7N7) virus among poultry led to the culling of >30 million birds. The outbreak, and thus the culling, was confined to a relatively small area of 50 × 30 km in the center of the country. A few years after the avian influenza outbreak, it became apparent that the incidence of campylobacteriosis among humans had decreased during 2003 and that the extent of this decrease varied by region. Because the avian influenza outbreak strongly affected the poultry industry in 2003, a link was suspected. Consumption of poultry and direct contact with poultry are generally accepted as dominant risk factors for sporadic Campylobacter spp. infections among humans. In the Netherlands, the strongest reduction in campylobacteriosis cases occurred in the laboratory service areas overlapping the culling area and the areas where the slaughterhouses were closed. Also, sales of poultry meat dropped most in these areas, although not proportional to the reduction in campylobacteriosis, and recovered quickly after June; the reduction in campylobacteriosis occurred at least up to the end of the year. Moreover, culling was mainly among layer hens (54%) and only 8% among broilers. In the Netherlands, meat from spent hens (layer hens that are no longer economically productive) is not consumed as fresh meat.

Environmental pathways of human Campylobacter spp. infection remain less understood and might play a major role in rural areas. These pathways remain to be clarified, although some studies have implicated aerosols and flies as vectors for environmental transmission. Campylobacter spp. have been detected in the air up to 30 m downwind of and in puddles near broiler houses. A US study among chicken catchers and poultry plant workers at 1 plant found colonization with Campylobacter spp. among 41% and 63% of these persons, respectively. Surprisingly, 9 community members who lived near, but did not work at, the US plant had positive Campylobacter spp. test results. In the Netherlands, culling was conducted in a relatively small area, at farms under strict biosecurity measures, and was followed by intensive cleaning and disinfection of the farms and an extended period when farms were empty. Furthermore, in the Netherlands, sales of broiler meat decreased by <12%, whereas in Belgium, 100% of broiler meat was withdrawn from the market. In this retrospective study, measures of environmental dissemination of Campylobacter spp. were lacking. The use of aggregated data makes it impossible to prove a causal link between the culling of poultry and the decrease in campylobacteriosis incidence. Nevertheless, on the basis of the combined information, we hypothesize a relationship between the reduced environmental contamination by poultry farms and slaughterhouses and the reduced number of campylobacteriosis cases in humans in the same region. Because slaughterhouses were closed and disinfected farms were empty or closed for everyone except attendants under strict hygiene measures, a temporal, lower environmental load of Campylobacter spp. was probably achieved. We are not aware of any other events in this period that might explain the regional and temporary decrease in campylobacteriosis incidence. However, unobserved effects, such as improved kitchen hygiene resulting from regional consumers’ awareness of a link between poultry meat and infectious diseases, are also possible explanations.

Our hypothesis of secondary exposure to Campylobacter spp. through dissemination from poultry farms or slaughterhouses has public health implications. Even if poultry meat at retail is free of Campylobacter spp., campylobacteriosis could occur earlier through exposure during production; thus, control should start at this step of the food chain. More research, including microbiological, analytical, and risk assessment studies, needs to be done to prove or disprove the role of dissemination in the spread of Campylobacter spp. and to clarify the possible mechanisms of environmental transmission.

Emerging Infectious Diseases
March 20, 2012

Original web page at Emerging Infectious Diseases


New study identifies emergence of multidrug-resistant strain of Salmonella

A new study has identified the recent emergence of a multidrug-resistant strain of Salmonella that has a high level resistance to ciprofloxacin, a common treatment for severe Salmonella infections. The study, led by François-Xavier Weill, MD, and Simon Le Hello, PharmD, at the Pasteur Institute in France, is published in The Journal of Infectious Diseases and is now available online. Salmonella infection represents a major public health problem worldwide. An estimated 1.7 million such infections occur in North America each year. More than 1.6 million cases were reported between 1999 and 2008 in 27 European countries. Although most Salmonella infections produce only mild gastroenteritis, elderly and immunocompromised patients are especially at risk for life-threatening infections. These cases are typically treated with antimicrobials called fluoroquinolones, such as ciprofloxacin.

Dr. Weill and colleagues studied information from national surveillance systems in France, England and Wales, Denmark, and the United States. The data showed that a multidrug-resistant strain of Salmonella, known as S. Kentucky, infected 489 patients in France, England and Wales, and Denmark between 2000 and 2008. In addition, researchers reported that the first infections were acquired mainly in Egypt between 2002 and 2005, while since 2006 the infections have also been acquired in various parts of Africa and the Middle East. The absence of reported international travel in approximately10 percent of the patients suggests that infections may have also occurred in Europe through consumption of contaminated imported foods or through secondary contaminations. In this study, multidrug-resistant S. Kentucky was isolated from chickens and turkeys from Ethiopia, Morocco, and Nigeria, suggesting that poultry is an important agent for infection. The common use of fluoroquinolones in chicken and turkey production in Nigeria and Morocco may have contributed to this rapid spread.

This study highlights the importance of public health surveillance in a global food system. According to Dr. Le Hello, “We hope that this publication might stir awareness among national and international health, food, and agricultural authorities so that they take the necessary measures to control and stop the dissemination of this strain before it spreads globally, as did another multidrug-resistant strain of Salmonella Typhimurium DT104, starting in the 1990s.” The investigators from the Pasteur Institute and its international network, the Centers for Disease Control and Prevention in the U.S., the Health Protection Agency in the United Kingdom, and the Statens Serum Institute and Technical University of Denmark reported that they will continue to monitor this multidrug-resistant strain as well as help strengthen the capacities of national and regional laboratories in the surveillance of Salmonella and other major foodborne pathogens through the World Health Organization Global Foodborne Infections Network.

Craig Hedberg, PhD, from the University of Minnesota School of Public Health, noted in an accompanying editorial that the ability to integrate public health surveillance is limited by differences in national surveillance systems. The study by Dr. Le Hello and colleagues reported that the percentage of Salmonella isolates submitted from clinical laboratories to national health reference laboratories ranged from 65 percent in France to 99 percent in Denmark. “Given the medical costs and public health impact associated with the spread of multidrug-resistant organisms,” Dr. Hedberg noted, “the potential benefits of such a system should far outweigh its costs.” Fast facts: 1.This study found that a multidrug-resistant strain of Salmonella, known as S. Kentucky, infected 489 patients in France, England and Wales, and Denmark between 2000 and 2008. 2. Poultry appears to be a major vehicle for spreading these infections. 3.International public health surveillance systems are needed to limit the spread of such multidrug-resistant organisms.

Science Daily
August 23, 2011

Original web page at Science Daily


US meat and poultry is widely contaminated with drug-resistant Staphylococccus aureus bacteria

Drug-resistant strains of Staphylococcus aureus, a bacteria linked to a wide range of human diseases, are present in meat and poultry from U.S. grocery stores at unexpectedly high rates, according to a nationwide study by the Translational Genomics Research Institute (TGen) Nearly half of the meat and poultry samples — 47 percent — were contaminated with S. aureus, and more than half of those bacteria — 52 percent — were resistant to at least three classes of antibiotics, according to the study published April 15 in the journal Clinical Infectious Diseases. This is the first national assessment of antibiotic resistant S. aureus in the U.S. food supply. And, DNA testing suggests that the food animals themselves were the major source of contamination.

Although Staph should be killed with proper cooking, it may still pose a risk to consumers through improper food handling and cross-contamination in the kitchen. Researchers collected and analyzed 136 samples — covering 80 brands — of beef, chicken, pork and turkey from 26 retail grocery stores in five U.S. cities: Los Angeles, Chicago, Fort Lauderdale, Flagstaff and Washington, D.C. “For the first time, we know how much of our meat and poultry is contaminated with antibiotic-resistant Staph, and it is substantial,” said Lance B. Price, Ph.D., senior author of the study and Director of TGen’s Center for Food Microbiology and Environmental Health. “The fact that drug-resistant S. aureus was so prevalent, and likely came from the food animals themselves, is troubling, and demands attention to how antibiotics are used in food-animal production today,” Dr. Price said. Densely-stocked industrial farms, where food animals are steadily fed low doses of antibiotics, are ideal breeding grounds for drug-resistant bacteria that move from animals to humans, the report says. “Antibiotics are the most important drugs that we have to treat Staph infections; but when Staph are resistant to three, four, five or even nine different antibiotics — like we saw in this study — that leaves physicians few options,” Dr. Price said.

“The emergence of antibiotic-resistant bacteria — including Staph — remains a major challenge in clinical medicine,” said Paul S. Keim, Ph.D., Director of TGen’s Pathogen Genomics Division and Director of the Center for Microbial Genetics and Genomics at Northern Arizona University (NAU). “This study shows that much of our meat and poultry is contaminated with multidrug-resistant Staph. Now we need to determine what this means in terms of risk to the consumer,” said Dr. Keim, a co-author of the paper. The U.S. government routinely surveys retail meat and poultry for four types of drug-resistant bacteria, but S. aureus is not among them. The paper suggests that a more comprehensive inspection program is needed. S. aureus can cause a range of illnesses from minor skin infections to life-threatening diseases, such as pneumonia, endocarditis and sepsis.

Science Daily
May 3, 2011

Original web page at Science Daily


Novel picornavirus in turkey poults with hepatitis, California, USA

To identify a candidate etiologic agent for turkey viral hepatitis, we analyzed samples from diseased turkey poults from 8 commercial flocks in California, USA, that were collected during 2008–2010. High-throughput pyrosequencing of RNA from livers of poults with turkey viral hepatitis (TVH) revealed picornavirus sequences. Subsequent cloning of the ≈9-kb genome showed an organization similar to that of picornaviruses with conservation of motifs within the P1, P2, and P3 genome regions, but also unique features, including a 1.2-kb sequence of unknown function at the junction of P1 and P2 regions. Real-time PCR confirmed viral RNA in liver, bile, intestine, serum, and cloacal swab specimens from diseased poults. Analysis of liver by in situ hybridization with viral probes and immunohistochemical testing of serum demonstrated viral nucleic acid and protein in livers of diseased poults. Molecular, anatomic, and immunologic evidence suggests that TVH is caused by a novel picornavirus, tentatively named turkey hepatitis virus.
Turkey viral hepatitis (TVH) is a highly infectious disease affecting young turkey poults. The disease is often subclinical, causing minor histologic lesions, and becomes overt when the animals are stressed, resulting in varying rates of illness and death. Mortality rates of up to 25% have been reported. Diagnosis is based on characteristic lesions in the liver, which include multifocal necrosis and mononuclear inflammatory cell infiltrates. Similar lesions may be found in the pancreas. Clinical signs include anorexia, depression, diarrhea, and weight loss compatible with a diagnosis of enteritis, the second most common diagnosis made in turkey poults throughout the United States. Although we cannot with confidence estimate the specific burden of TVH, its economic effects are likely substantial; in the United States, turkey production was valued at $3.71 billion in 2007. The identification of a pathogen and development of specific diagnostics will lead to better understanding of the economic consequences and other effects of TVH.

The disease has been experimentally reproduced in turkey poults by inoculation with material derived from affected animals. A viral basis for TVH has been presumed since its initial description in 1959 because the causative agent passed through 100-nm membranes, was acid stable, was not affected by antimicrobial drugs, and could be propagated in the yolk sac of embryonated chicken eggs. Icosahedral particles of 24 to 30 nm have been found by electron microscopy (EM) in liver lesions of birds, as well as in embryonated turkey eggs that have been inoculated with material derived from affected birds; however, no agent has been consistently implicated.

Emerging Infectious Diseases
March 22, 2011

Original web page at Emerging Infectious Diseases


Transgenic chickens curb bird flu transmission

GM chickens could pave way for H5N1-resistant flocks if tall political, technical and economic hurdles can be overcome. Researchers have made genetically modified chickens that can’t infect other birds with bird flu. The H5N1 strain of influenza — which raged through southeast Asia a decade ago and has killed hundreds of people to date — remains a problem in some developing countries, where it is endemic. The birds carry a genetic tweak that diverts an enzyme crucial for transmitting the H5N1 strain. Although they die of the disease within days, the molecular decoy somehow impedes the virus from infecting others. The findings are published January 14, 2011 in Science. The researchers say that although large-scale distribution of the genetically modified (GM) birds will one day be feasible, their study is meant only to show proof-of-concept of the technique. “We have more ambitious objectives in terms of getting full flu resistance before we would propose to put these chickens into true production,” says Laurence Tiley, a molecular virologist at the University of Cambridge, UK, and lead investigator for the study. His team is now working on further genetic tweaks that would inhibit the virus in different ways. “It would be a bit like combination drug therapy for HIV,” he says.

Other experts point out that even if the GM chickens carried full resistance to influenza, there are political and economic hurdles to their widespread commercial use — not least the public’s aversion to GM food. “It’s the beginning of something which will require a certain number of years to see whether it is accepted by the public,” says Ilaria Capua, head of virology at the Experimental Animal Health Care Institute of Venice in Legnaro, Italy. H5N1 is endemic in at least five countries, and is particularly threatening in Egypt and Indonesia, says Capua. So far, the virus has not been able to spread from human to human, but some public health experts worry that eventually it will adapt to do so. In developed countries, H5N1 outbreaks are controlled by swiftly culling the animals. In poor countries, however, there are lots of small farms, few health regulations and long-held cultural practices involving birds. “In the developing world, we cannot follow the slaughter strategy used in the developed world,” says Arnold Monto, an epidemiologist at the University of Michigan School of Public Health in Ann Arbor. “Politically they can’t do it, and practically they can’t do it.” Instead, developing countries try to control H5N1 by vaccinating birds. This doesn’t prevent them from silently acquiring mild forms of the disease and, if not monitored well, transmitting it to healthy birds. What’s more, flu viruses mutate quickly and are famous for evading vaccines.

If made commercially available, the GM birds wouldn’t have these issues. They carry a genetic ‘cassette’ dubbed a short-hairpin RNA, which includes genetic sequences that match up with an enzyme that influenza viruses use for replication and packaging. These sequences can bind with the enzyme, somehow stopping it from working with the virus. The enzyme could mutate to evade this decoy, but if it did so it would no longer be able to match up with its binding sites on the virus. So for the virus to escape, it would need to simultaneously change its own genome and that of the enzyme in eight different spots — a highly unlikely event. The chickens were modified by a team led by Helen Sang, a geneticist at the Roslin Institute of the University of Edinburgh, UK. The researchers modified the chickens by injecting a lentivirus carrying the cassette into clusters of cells on top of egg yolks. In some of the resulting chicks, the cassette integrates into germ cells. These animals can be cross-bred to produce chickens that carry the cassette in every cell. The researchers infected decoy-carrying birds with H5N1 and housed them with uninfected birds, some with the transgene and some without. Most of the birds that received the primary infection died, but didn’t pass on the flu to any of their uninfected cage mates.

The researchers found that the amount of virus present in the infected GM birds was not significantly different from that in non-transgenic controls. “It must be something above and beyond the effect on replication that’s having this effect,” says Tiley. It could be, for example, that the hairpin disrupts the packaging of the virus, preventing it from being taken up normally in the next animal. Sang says that using their methods, it costs approximately £50,000 (US$79,000) to produce “a small number of stable transgenic birds you can characterize and breed from”. She and Tiley argue that getting similar transgenic birds into global production would be possible because there are only a handful of companies providing purebred chicken lines. But this approach would not be feasible in poorer countries. “This will only become affordable for the people who are well off,” says Marc Van Ranst, a virologist at the Dutch-speaking Catholic University of Leuven in Belgium. The technique may become most useful not for preventing the spread of H5N1, but for using similar cassettes to create resistance to other common poultry diseases.

January 24, 2010

Original web page at Nature


Selected hens give new genetic insights

Studies of heavy, fast-growing hens and small, slow-growing hens provide important new knowledge on the origin of the genetic variation that has enabled them to adapt rapidly to new extreme environments. The findings, reported in the online journal PLoS Genetics, were made by researchers from the Swedish University of Agricultural Sciences, Uppsala University in Sweden and Virginia Polytechnic Institute and State University (Virginia Tech) in the US. These findings may provide vital information on the evolutionary process, how animal and plant breeding should be conducted, and how epidemic diseases such as obesity and diabetes should be studied. Ever since Darwin presented his theory of evolution, scientists have been trying to understand the mechanisms that enable species to adapt to new habitats. In the next issue of PLOS Genetics researchers from Uppsala and Virginia in the US explain how the genetic variation already present in hundreds of genes in a population enables that population to adapt rapidly to new extreme environments.

To demonstrate this, the researchers used a unique hen model bred in the US. Professor Paul Siegel of Virginia Tech, USA, has been studying the biological effects of selection on the basis of body weight since 1957. Out of a uniform population of hens, he has bred two lines: one for high growth and one for low growth. The heaviest specimens in the high-growth line have been selected for breeding the next generation; the lightest individuals have been selected from the low-growth line. The high-growth line animals now weigh eight times more than the low-growth line counterparts at the age of eight weeks. “Since individuals have been selected on the basis of a single characteristic that we know is governed by both genetic and environmental factors, these hens are an excellent model for studying the number of genes that have contributed to this extreme change in the size of the animals,” explains Professor Örjan Carlborg of SLU, who initiated the genetic studies of the hen lines together with Professor Siegel. By examining the differences between nearly 100,000 genetic markers in the DNA of the two lines, the researchers have succeeded in demonstrating that they now have variants in more than 100 genes.

“We have been able to identify a contribution from so many genes because the selection in the lines has been so intensive over the 50 years that it represents several thousand years of natural selection,” explains Mats Pettersson of SLU, who has conducted the studies together with Anna Johansson, also of SLU. This is the first time it has been possible to demonstrate on such a large scale in experimental data that existing genetic variants are essential if populations are to adapt to new environments by natural or artificial selection. “We have used a new method to ascertain how the gene variants that were present before the breeding programme began have contributed to the change in body size in the two hen lines. Our results show that the majority of the gene variants that have now been fixed in the two lines were present in the original population. This shows that mutations during the selection process are not as important as was previously thought,” says Ms Johansson. The two hen lines also differ in terms of traits other than growth, such as appetite, obesity and immunological defence. The high-growth line are compulsive eaters, whereas the low-growth line are anorexic; the high-growth line are fat, the low-growth line thin, and the high-growth line have poorer immunological defences than the low-growth line. “We have been able to identify many regions in the DNA where the lines differ, which means that we are now better able to examine which of them influence medically important traits: appetite, obesity and immunological defences. This will provide us with new knowledge and may ultimately result in better medicines to combat many of our most prevalent diseases,” says Professor Carlborg.

Science Daily
November 23, 2010

Original web page at Science Daily


Analysis of avian hepatitis E virus from chickens, China

Avian hepatitis E virus (HEV) has been identified in chickens; however, only 4 complete or near-complete genomic sequences have been reported. We found that the near-complete genomic sequence of avian HEV in chickens from China shared the highest identity (98.3%) with avian HEV from Europe and belonged to avian HEV genotype 3. Hepatitis E virus (HEV) is a nonenveloped, positive-sense, single-stranded RNA virus. It has 3 open reading frames (ORFs) and a genome size of 7.2 kb. So far, HEV strains are classified into 4 major genotypes, and genotypes 3 and 4 are probably zoonotic. Avian HEVs have been identified from chickens with big liver syndrome and hepatitis–splenomegaly syndrome. Each syndrome mainly causes increased deaths, reduced egg production, and enlarged liver and spleen; hepatitis–splenomegaly syndrome also causes accumulation of bloody fluid in the abdomen and vasculitis and amyloidosis in the liver. Molecular epidemiologic investigations have shown that avian HEV infection in chickens is endemic to the United States and Spain. Because propagating avian HEV in cell culture or embryonated eggs is difficult, avian HEV is primarily detected by reverse transcription–PCR (RT-PCR). However, only 4 complete or near-complete genomic sequences have been reported to GenBank. We identified and analyzed the near-complete genomic sequence of avian HEV in a chicken flock from the People’s Republic of China.

Avian HEV infection of a chicken flock in Shandong, China, was identified by detection of avian HEV ORF2 antibodies and viral RNA. A near-complete avian HEV genome from the flock was determined, and sequence analysis indicated that this avian HEV strain displayed the highest identity (98.3%) with EaHEV and belonged to avian HEV genotype 3.

Emerging Infectious Diseases
September 14, 2010

Original web page at Emerging Infectious Diseases


Half a billion eggs recalled in US salmonella outbreak

A quadrupling in the usual number of cases of infection with a strain of Salmonella enteritidis in May alerted the US Centers for Disease Control in Atlanta to a possible outbreak. The trail led the CDC and FDA to two Iowa farms now under investigation: Wright County Egg and Hillandale. Although the CDC initially linked around 2000 cases of food poisoning with the outbreak, it is thought 40 times as many people may have been infected. Now the race is on to explain how it happened. “The FDA is evaluating potential causes of contamination in the farms associated with the outbreak,” says Margaret Hamburg, the FDA’s commissioner. “In general, the likely sources of salmonella outbreaks include rodents, shipments of contaminated chicks or hens, lack of biosecurity controls and tainted seed.” Since the Minnesota facility that supplies chicks to the Iowa farms has been certified salmonella-free since 1989, the FDA’s focus has shifted to the pullet houses where chicks are reared to become laying hens. In the UK, salmonella contamination has fallen drastically since 1998, when vaccination of laying hens against S. enteritidis was introduced. The FDA supports voluntary but not mandatory vaccination in the US.

New Scientist
September 14, 2010

Original web page at New Scientist