Mad pig press release
Add pigs to feed ban?
Mad pig disease?
Species barrier? Killer flu came from pigs
Pig genes Isolated from the Deadly 1918 Flu Virus
Original article on "Spanish" Influenza Virus
Massive disease outbreak in Taiwan pigs
New pig species found in Vietnam
Human prion compared to pig
Human prion compared to cow
Human prion compared to sheep
Pig prion compared to cow
A coalition of veterinarians, inspectors and consumer organizations today called for the U.S. Department of Agriculture (USDA) and the Food and Drug Administration (FDA) to address long-dormant questions about whether public health concerns from England's "Mad Cow Disease" also apply to hogs. The British beef scare has sparked national policy reform proposals to protect American consumers and markets. In a letter today to USDA Secretary Dan Glickman, the groups called for USDA to "take serious public health action this time before there is a tragedy." Groups included the Government Accountability Project, a whistleblower support organization, the National Association of Federal Veterinarians, leadership of the National Joint Council of Food Inspection Locals, Community Nutrition Institute, Humane Farming Association, National Consumers League, and Safe Tables Our Priority (S.T.O.P.), a national support organization for families victimized by food poisoning.
Consumers Union simultaneously recommended that the Food and Drug Administration include hogs in its proposed ban on animal protein in animal feed. The FDA's proposal is supposed to prevent spread of Transmissible Spongiform Encephalopathies (TSE), the scientific name for the disease. "Ignoring hogs could be the Achilles heel of U.S. efforts to protect Americans from TSE threats like Mad Cow Disease," warned GAP Legal Director Tom Devine. "The credibility of the President's Food Safety initiative is at stake."
GAP's Food Safety Director Felicia Nestor explained that the group acted on concerns from government veterinarians that USDA has not followed through responsibly to resolve questions raised by a 1979 study, which suggests TSE's could exist in hogs. The vets renewed their concerns after the Mad Cow Disease outbreaks in Great Britain.
Nestor explained that current and planned policy has three public health loopholes - 1) inadequate ante-mortem inspection. The government reassures consumers that its inspection system will catch sick animals before slaughter. In reality up to 95% of livestock are uninspected for relevant disease symptoms, a rate which draft regulations threaten to increase; 2) inadequate postmortem laboratory testing, which does not check for TSE in hogs; and 3) overly-narrow boundaries for feed bans, that could permit hogs to spread the disease. "These three public health loopholes are three strikes against consumers," warned Nestor. She added, "Diseased animals can still be a human health hazard. Until USDA publishes credible scientific research, it is inexcusable to cut back the government's early warning system for TSE or similar threats."
WASHINGTON -- A coalition of consumer groups, veterinarians, and federal meat inspectors asked the federal government on Thursday to improve its meat inspection system and to take other measures to help prevent the spread of mad cow disease.
Earlier this year, the Food and Drug Administration proposed a ban on using tissue from animals that chew their cud -- cows, sheep, goats, deer, and elk -- in animal feed. The coalition asked on Thursday that hogs be added to that list. There is strong evidence that mad-cow disease, bovine spongiform encephalopathy, spreads through contaminated animal protein. Mink are included in the ban because they have carried a similar ailment.
Hogs have been excluded because the government says it has no evidence that the animals have ever had the disease. But the coalition says there is evidence that hogs can develop a form of the disease. The Consumer Policy Institute of Consumers Union, part of the coalition, has asked the government to institute the same kind of ban that is in effect in England: one that prohibits the use of protein from all mammals in the feed of any food animal.
No case of mad-cow disease has ever been detected in the United States [sic -- webmaster] , but it has afflicted more than 165,000 cattle [sic -- webmaster] in Britain since it was discovered in 1986.
Thomas Billy, administrator of the Agriculture Department's Food Safety and Inspection Service, said that further measures were not necessary. He said that the agency was concerned about the possible risk in hogs used in feed but that there was "no evidence that argues for broadening what we are doing."
Dr. Stephen Sundlof, director of the center for veterinary medicine at the FDA, said that the agency "would take the evidence presented today into consideration." The problem with a wider ban, he said, is that officials would have to find some way to dispose of the animal renderings that are now used in feed.
In asking for a wider ban, Consumers Union and the Government Accountability Project, a Washington-based whistleblower support organization, cited evidence from 1979 suggesting unusual symptoms in the central nervous systems of young hogs. At the time, scientists were not aware of mad-cow disease. But after the announcement by the British government last year that there may be a link between mad-cow disease and the human ailment Creutzfeldt-Jakob disease, which is always fatal, some government scientists recommended a re-examination of the 1979 slides from the hogs.
Although more recent readings of the slides have been inconclusive, experts in the field say that the evidence suggests transmissible spongiform encephalopathy. The coalition also noted that mad-cow disease had been experimentally induced in pigs. It is asking the Agriculture Department to conduct further research and to step up inspections at hog slaughterhouses.
Veterinarians and consumer organizations urged the Agriculture Department to determine quickly if American pork products might be tainted by a ``mad-pig disease.'' A leader of the coalition said Thursday there is no evidence to support a conclusion that U.S. hogs are contaminated with anything similar to the fatal ``mad-cow disease'' that has infected many British cattle and resulted in human deaths.
``But it is irresponsible not to take a look,'' said Tom Devine, an official of the Government Accountability Project.
However, Thomas J. Billy, administrator of USDA's Food Safety and Inspection Service, said that while the agency is ready to continue and even expand its work on cattle to prevent an outbreak of mad-cow disease in the United States, it has no evidence pigs might also be capable of being infected.
``At this time there is no scientific justification for using our resources to look at pigs,'' Billy said in an interview. But he said the agency would gladly reconsider that position if such evidence were discovered. Billy noted that while some 250,000 cows were infected in England ``they have not had a single case of infection in the pigs.'' And he said that when pigs were exposed to infected animal tissue they did not develop the disease.
The coalition, which was organized by Devine's group, said its concern arises from a Agriculture Department study of hogs in a New York slaughterhouse that showed symptoms of disorders of the central nervous system.
At a news conference, members of the coalition said the study produced evidence of a disorder in young hogs similar to those associated with an epidemic of mad-cow disease in Britain. There is no recorded case of mad-cow disease in the United States.
``We are seeking answers to very serious public health questions,'' Devine said. ``The credibility of the present food safety (inspection system) is at stake.''
Coalition members signed a letter to Agriculture Secretary Dan Glickman outlining their concerns and calling on the department to act ``before there is a tragedy.'' They said USDA should upgrade the inspection of animals before they are slaughtered to pinpoint any that may have diseases of the central nervous system.
They said the long-dormant 1979 study should be reopened and include any implications for public health, and that swine should be included with cows and sheep in research on factors known to cause mad-cow disease.
Mad-cow disease has been linked by the British government to the practice of mixing ground-up sheep into feed for cattle. Mad-cow, in turn, is suspected as the cause of a new strain of Creutzfeldt-Jakob disease, a fatal brain-wasting disease in humans.
As described in the letter to Glickman, the swine study began in late 1978 when a veterinarian for the Food Safety and Inspection Service noted unusual symptoms of the central nervous system in hogs being received at the New York slaughterhouse. Because the animals came from several sources and the plant did not routinely deal with diseased animals, the veterinarian believed the condition might affect animals being slaughtered nationwide.
There was no follow-up, the letter said. But it said that once the characteristics of mad-cow disease were publicized, some of those involved with the study reviewed the evidence and sent photographs of the brains of animals to experts who saw similarities to mad-cow disease but reached no concrete conclusions. None of the veterinarians involved in the 1979 study were present at the news conference. Nor did any sign the letter to Glickman.
Coalition members signing the letter were representatives of the Government Accountability Project; the Center for Science in the Public Interest; the Community Nutrition Institute; the Consumer Federation of America; the Humane Farming Association; the national Association of Federal Veterinarians; the National Consumers League; the National Joint Council of Food Inspection Locals; and Safe Tables Our Priority.
SCIENTISTS have confirmed that the flu virus which swept around the world in 1918, killing 20 million people, originated in pigs. Samples taken from the lungs of a young soldier who died in the epidemic provided enough genetic material to prove the hypothesis, says a report in Science. The investigation, by a team at the US Armed Forces Institute of Pathology, was made more difficult by the way flu stores its gene information in the form of RNA (ribonucleic acid), not the more stable DNA.
Most flu viruses are believed to originate in birds, usually ducks. They are passed to pigs, which is why so many originate in China, where ducks and pigs are raised in close proximity. The new investigation shows that the 1918 virus, a particularly virulent one, was completely novel. Hardest hit by it were young adults, usually the most resistant to flu infection. The American team is to continue examination of the RNA samples to try to find the cause.
John Oxford, of the London Hospital Medical College, has begun a similar examination. A Canadian team plans to dig up seven miners believed to have died of the 1918 flu, who are buried in frozen ground in Norway. They hope the bodies will be so well preserved that better samples can be obtained.
The influenza outbreak of 1918, the "Spanish" flu, was the worst pandemic disease outbreak in history and killed more than 20 million people. Taubenberger et al. (p. 1793; see the news story by Pennisi, p. 1739) sequenced viral RNA fragments obtained from a preserved lung sample of an individual whose death occurred at an early stage when influenza virus would still have been present. The analysis suggests that the strain was an H1N1 subtype that is closely related to classic swine influenza virus, as opposed to the avian subgroup. Such sequence data may help in predicting the virulence of future outbreaks.
Global killer. The 1918 flu decreased life expectancy Pathologist Jeffery Taubenberger, molecular biologist Ann Reid, and their colleagues at the Armed Forces Institute of Pathology in Washington, D.C., report that they have isolated pieces of five flu genes from the private's lungs. While the genes collected so far portray the killer as a run-of-the-mill swine flu, its deadly secrets may emerge as Taubenberger and Reid collect more of the viral genome and other researchers apply the same methods to other preserved tissue from the 1918 epidemic.
This report "probably won't make as big a splash as cloning that sheep, [but] if we can get a handle on what caused those deaths, that is important," says historian Alfred Crosby, author of the book, America's Forgotten Pandemic: The Influenza of 1918. Knowing what a killer flu virus looks like, for instance, could enable health officials to spot particularly dangerous flu strains as they emerge and "help us prepare for what we need to be prepared for," says Nancy Cox, a virologist from the Centers for Disease Control and Prevention (CDC) in Atlanta.
For the current work, Taubenberger and Reid began with several dozen samples of lung tissues taken from soldiers who died of the 1918 flu and preserved in their institute's archives. These, they realized, could be analyzed by modern polymerase chain reaction (PCR) methods, which can amplify extremely small quantities of DNA and RNA, thus providing sufficient amounts of material for sequence analysis. From the beginning, though, the researchers knew success was a long shot.
Typically, the flu virus infects the respiratory system, replicates, and then is shed into the air via the lungs, all in just a few days. Thus, unless one of the soldiers had died very soon after infection, all traces of the virus would probably have vanished by the time an autopsy was performed. What's more, the flu virus stores its genetic information on single strands of RNA, which is much more susceptible to degradation by cellular enzymes than DNA. "So you have to look for little pieces," Taubenberger explains. These problems had already proved insurmountable once before. Several years ago, virologist Robert Webster of St. Jude Children's Research Hospital in Memphis, Tennessee, had failed in an attempt to pull genetic material from archived samples.
To increase their chance of finding viral RNA, the researchers worked for a year refining their PCR procedure. In addition, they carefully examined each of the lung-tissue specimens under a microscope to find ones with indications of viral infections, such as lung air spaces filled with fluid and blood and damaged cells in the bronchial epithelial linings. Of the 28 tissue samples examined, Taubenberger says, the private's "was the only case with all the features of viral pneumonia."
His was also the only specimen in which they could identify flu-virus RNA sequences, including segments of five genes: those encoding hemagglutinin and neuraminidase--proteins that help the virus get into a cell--and three structural proteins. From the hemagglutinin and neuraminidase gene fragments, the researchers were able to confirm earlier conclusions about the virus's source.
Influenza viruses are thought to pass into pigs from birds, usually ducks, that are kept in close proximity to swine in some parts of the world, particularly China. Subsequent genetic changes enable the virus to move from pigs into people. However, there had been some speculation that the 1918 flu virus might have been so deadly because it was an avian virus, and these data indicate that isn't the case.
Because the flu-virus genes from the private closely resemble those of viruses isolated from pigs, the researchers concluded that his virus had been in the pig population for a while. That is also in line with previous antibody studies of blood taken from people who had lived through the 1918 pandemic, indicating that this killer plague was a classical swine flu. "What this says is we had better watch what's happening in the pig populations of the world," Webster says, because it seems that ever-changing flu viruses in those animals are the source of new flu viruses in humans. Currently, both the CDC and the World Health Organization devote most of their flu-surveillance efforts to monitoring for new flu strains in people, not animals.
The work does not support another supposition about the virus, however. Virologists have suggested that the extreme virulence of the 1918 flu virus may have resulted from the same genetic change that enabled an avian flu virus to kill whole flocks of chickens overnight in Mexico 2 years ago (Science, 17 March 1995, p. 1594). The deadly mutation altered a segment of the hemagglutinin protein, probably increasing the virus's ability to infect cells. But Taubenberger's group found no such change in the specimen they examined.
Hoping to find more clues to these and other mysteries, such as why young adults, usually the most resistant to flu infections, were the hardest hit in 1918, Taubenberger and Reid are continuing to isolate more of the viral RNA from the private's tissue samples. At the same time, they plan to use PCR to make lots of copies of all the viral RNA bits they recover. From these, they will create a cDNA library so as to have an unlimited supply of that genetic material.
Meanwhile, Taubenberger hopes that his success will inspire others to comb their archives for other possible samples. Already, before learning of the current work, virologist John Oxford of London Hospital Medical College had begun collecting samples from his own institution and from Australia and Prague for a similar analysis. And a Canadian-led team hopes to dig up seven miners who presumably died of the 1918 flu and have been preserved in their graves in the frozen ground near Spitzbergen, Norway.
Webster worries about the slim chance that those bodies will contain live virus. But it may be worth the risk, he says: "We want to know what killed these people. The potential is there for this kind of virus to return."
The "Spanish" influenza pandemic killed at least 20 million people in 1918-1919, making it the worst infectious pandemic in history. Understanding the origins of the 1918 virus and the basis for its exceptional virulence may aid in the prediction of future influenza pandemics. RNA from a victim of the 1918 pandemic was isolated from a formalin-fixed, paraffin-embedded, lung tissue sample. Nine fragments of viral RNA were sequenced from the coding regions of hemagglutinin, neuraminidase, nucleoprotein, matrix protein 1, and matrix protein 2. The sequences are consistent with a novel H1N1 influenza A virus that belongs to the subgroup of strains that infect humans and swine, not the avian subgroup.
The influenza pandemic of 1918 was exceptional in both breadth and depth. Outbreaks of the disease swept not only North America and Europe but spread as far as the Alaskan wilderness and the most remote islands of the Pacific. Large proportions of the population became ill; 28% of the U.S. population is estimated to have been infected (1). The disease was also exceptionally severe, with mortality rates among the infected of over 2.5%, as compared with less than 0.1% in other influenza epidemics (2, 3). Furthermore, in the 1918 pandemic, most deaths occurred among young adults, a group that usually has a very low death rate from influenza. Influenza and pneumonia death rates for 15- to 34-year-olds were more than 20 times higher in 1918 than in previous years (4). It has been estimated that the influenza epidemic of 1918 killed 675,000 Americans, including 43,000 servicemen mobilized for World War I (5). The impact was so profound as to depress the average life expectancy in the United States by more than 10 years (6).
The unusual severity of the 1918 pandemic and the exceptionally high mortality it caused among young adults have stimulated great interest in the influenza strain responsible for the 1918 outbreak. Characterization of this virus may help to elucidate the mechanisms whereby novel influenza viruses evolve and circulate in humans. Because the first human influenza viruses were not isolated until the early 1930s (7, 8), characterization of the 1918 strain has had to rely on indirect evidence. The natural reservoir for influenza virus is thought to be wild waterfowl. Periodically, genetic material from avian strains emerges in strains infectious to humans.
Because pigs can be infected with both avian and human strains, they are thought to be an intermediary in this process. Influenza strains with recently acquired genetic material are responsible for pandemic influenza outbreaks (9). Analysis of survivor antibody titers from the late 1930s and historical projection of phylogenetic analyses suggest that the 1918 strain was an H1N1-subtype virus, probably closely related to what is now known as classic swine influenza virus (10, 11), which may have emerged from an avian reservoir before the 1918 outbreak.
Although the length of sequence between primers was small, phylogenetic analyses for each gene segment were possible with the use of the corresponding regions of other previously sequenced influenza viruses. Analyses were carried out with two computer software packages: Molecular Evolutionary Genetics Analysis (MEGA), version 1.01 (17), and Phylogenetic Analysis Using Parsimony (PAUP), version 3.1 (18).
Four fragments of the hemagglutinin (HA) gene segment were analyzed. An interprimer sequence of 49 base pairs (bp) (HA137) was initially generated by RT-PCR with primers designed to amplify all H1 sequences. A Basic Local Alignment Search Tool (BLAST) search (19) of the files of the National Center for Biotechnology Information indicated that the sequence was unique. The HA137 sequence of 1918 case 1 was compared to 16 other H1-subtype HA genes and 27 H2-H15-subtype HA genes. Sequences were analyzed by the MEGA program with a neighbor-joining (N-J) algorithm and Jukes-Cantor (J-C) distance or p-distance (the proportion of sites that are different). N-J (100 bootstrap replications) placed 1918 case 1 within the H1-subtype HA genes at the 100% level. On the basis of these analyses, primers for two larger regions of HA were designed (HA33, interprimer length 163 bp; and HA389, interprimer length 138 bp).
Fig. 1. Influenza phylogenetic trees. All trees are N-J trees using p-distance and were constructed with the MEGA program. Bootstrap values (500 replications) are presented for selected nodes. A branch-length scale bar is shown beneath each tree. (A) The hemagglutinin fragment HA33. (B) The neuraminidase fragment NA53. (C) The nucleoprotein segment NP540. Arrows identify 1918 case 1.
Some avian influenza strains of subtypes H5 and H7 are highly pathogenic in certain avian species, including domestic chickens. These strains are characterized by the insertion of coding nucleotides for several basic amino acids at the cleavage site between the HA1 and HA2 subunits of hemagglutinin (20). This insertion makes the mutant cleavage site accessible to intracellular proteases and is responsible for the increased virulence of these strains (21). This mutation has not been described in mammalian influenza isolates nor in any H1-subtype strains. To test the hypothesis that the 1918 strain had a similar mutation, primers spanning the cleavage site were designed (HA980, interprimer length 94 bp). No insertion at the cleavage site was present. The HA980 sequence of 1918 case 1 was compared to 29 other H1-subtype HA genes with the use of the MEGA program with an N-J algorithm and J-C distance; 94 out of 100 bootstrap replications placed the case in the mammalian cluster.
The influenza virus matrix (M) genes are highly conserved. Although the M2 fragment (M811) was found to be unique, neither the 72-bp region of M1 (M149), nor the 79-bp region of M811 contained enough sequence variation to produce a meaningful phylogenetic tree. Our data confirm that the 1918 strain was an H1N1 virus, distinct from all subsequently characterized strains. The 1918 case 1 HA sequences appear to be most closely related to early swine influenza strains, corroborating the archaeserological data from the 1930s. Phylogenetic analyses of all influenza genes consistently suggest a common avian ancestor for both human and swine H1N1 virus lineages (9, 22, 23). It has been suggested that the 1918 strain may itself have been that ancestor (23). The fact that our analyses group the 1918 HA, NA, and NP genes with those of mammalian, not avian, viruses may indicate that an ancestral virus had entered the mammalian population at some point before 1918. REFERENCES AND NOTES
1.W. H. Frost, Public Health Rep. 35, 584 (1920). 2.G. Marks and W. K. Beatty, Epidemics (Scribner, New York, 1976), p. 274. 3.M. J. Rosenau and J. M. Last, Maxcy-Rosenau Preventive Medicine and Public Health (Appleton-Century-Crofts, New York, 1980), p. 116. 4.F. E. Linder and R. D. Grove, Vital Statistics Rates in the United States: 1900-1940 (Government Printing Office, Washington, DC, 1947), pp. 254-255. 5.W. Crosby, America's Forgotten Pandemic: The Influenza of 1918 (Cambridge Univ. Press, Cambridge, 1989), pp. 205-207. 6.R. D. Grove and A. M. Hetzel, Vital Statistics Rates in the United States: 1940-1960 (Government Printing Office, Washington, DC, 1968), p. 309. 7.W. Smith, C. H. Andrewes, P. P. Laidlaw, Lancet 225, 66 (1933) . 8.T. Francis Jr., Science 80, 457 (1934) . 9.R. G. Webster, W. J. Bean, O. T. Gorman, T. M. Chambers, Y. Kawaoka, Microbiol. Rev. 56, 152 (1992) . 10.R. E. Shope, J. Exp. Med. 63, 669 (1936) . 11.R. N. Philip and D. B. Lackman, Am. J. Hyg. 75, 322 (1962). 12.R. E. Shope, Public Health Rep. 73, 165 (1958) . 13.A. I. Braude, C. E. Davis, J. Fierer, Infectious Diseases and Medical Microbiology (Saunders, Philadelphia, PA, 1986), p. 783. 14.H. Chmel, M. Bendinelli, H. Friedman, Pulmonary Infections and Immunity (Plenum, New York, 1994), p. 286. 15.S. B. Wolbach, Johns Hopkins Hosp. Bull. 30, 104 (1919). 16.E. R. LeCount, J. Am. Med. Assoc. 72, 650 (1919) . 17.S. Kumar, K. Tamura, M. Nei, Molecular Evolutionary Genetics Analysis, version 1.01 (Pennsylvania State University, University Park, PA, 1993). 18.D. L. Swofford, PAUP: Phylogenetic Analysis Using Parsimony, version 3.1.1 (Illinois Natural History Survey, Champaign, IL, 1991). 19.S. F. Altschul, W. Gish, W. Miller, E. W. Meyers, D. J. Lipman, J. Mol. Biol. 215, 403 (1990) . 20.C. Röhm, T. Horimoto, Y. Kawaoka, J. Süss, R. G. Webster, Virology 209, 664 (1995) . 21.T. Horimoto and Y. Kawaoka, J. Virol. 68, 3120 (1994) . 22.Y. Kanegae, S. Sugita, K. F. Shortridge, Y. Yoshioka, K. Nerome, Arch. Virol. 134,17 (1994). 23.O. T. Gorman, et al., J. Virol. 65, 3704 (1991) .
Authorities closed Taiwan's largest zoo and all five national parks Wednesday to combat an outbreak of hoof-and-mouth disease in pigs that is threatening the island's pork industry. President Lee Teng-hui told members of his ruling party to help the industry by eating more pork and to serve at least two pork courses at official banquets.
The highly contagious disease broke out on the island last week for the first time in 83 years, forcing the government to call out the military to slaughter 50,000 of Taiwan's 11 million pigs. An emergency airlift of 1.5 million vaccine units has been ordered from Britain. So far, the slaughter has failed to halt the spread of the disease, officials said.
Hoof-and-mouth disease causes high fever and blisters in the mouths and hoofs of affected animals. Humans can carry and spread the virus, although they do not develop the sickness. The Taipei Zoo announced a 12-day closure to prevent visitors from spreading the virus to its 360 hoofed animals, including buffalo, giraffe and deer.
The country's five national parks also closed their wildlife reserves just ahead of a week-long spring holiday when many hikers typically visit them. Despite assurances that well-cooked pork is safe to eat, consumers are shunning pork products. Pork has been removed from supermarket shelves, and vendors and restaurants report slumping demand for normally popular pork delicacies.
Taiwan has banned pork exports to Japan, the industry's sole foreign customer, which buys nearly half of Taiwan's $3.2 billion annual pork output. Officials say the disease and damage to related industries could cut this year's projected economic growth rate from 6.2 percent to as low as 4.8 percent. Officials say they believe the disease came from China, either with smuggled pigs or through Taiwanese farmers who visited Chinese pig farms.
TAIPEI Taiwan's fast-moving hog foot and mouth epidemic has spread to more than 1,000 breeding centers, up from just nine when the outbreak was confirmed on March 20, officials said on Friday.
A mass slaughter of all hogs -- healthy or otherwise -- at all farms struck by the deadly contagion continued with experts reporting that over 886,000 pigs would have to be destroyed, the cabinet's Council of Agriculture said. As of late on Friday, the virus had been detected on 1,008 of Taiwan's 25,000 hog farms, though only 160,315 pigs were reported to have been slaughtered, official statistics showed. Some 46,500 pigs had died of the disease, officials said.
"The slaughter must continue," council secretary-general Lee Jen-chyuan told Reuters by telephone. Industry sources quoted by the ruling Nationalist Party on Wednesday estimated that about 15 percent of Taiwan's 11 million swine -- or 1.6 million animals -- would be affected directly. Local media said two U.S. Department of Agriculture experts were flying to Taiwan next week to survey the situation, though Taiwan farm officials have not sought outside help.
Breeders angry about low state compensation for their losses called off plans to march in Taipei's streets on Friday after the council agreed to discuss a possible increase. Council officials persuaded the farmers that coming to Taipei in great numbers could actually spread the virus, which is airborne and can be transmitted by humans. "We realized that it would be dangerous to have pig farmers from infected areas gather at one place," a spokesman for the Republic of China Swine Association told Reuters by telephone. The farm council banned all pork exports after confirming the outbreak on March 20, when the virus had been found in just nine of the island's 25,000 hog breeding farms.
Across the island, masked soldiers in plastic suits have wielded electric prods to stun pigs, then used huge earth movers to dump them into incinerators or giant pits -- often with the pigs still gasping for air. Millions of vaccine doses airlifted to Taiwan this week were being distributed in hopes of checking the contagion's spread, with healthy hogs and other livestock slated for vaccination. The crisis has threatened to slow the island's gathering economic recovery, battered the stock market and promised tens of thousands of layoffs in the huge feedlot and meat-packing sectors, which employ 700,000. The crisis has reduced local demand for animal feed, forcing cancellations of tenders for nearly 200,000 tons of corn and soy since March 20 and, on Friday, the first voiding of an existing contract -- one to import 25,000 tonnes of corn.
Taiwan corn buyers have estimated the crisis would slash the island's feed corn imports by about one-fifth. A Reuters survey of five major grain importers found that all expected significant reductions in corn imports, with most estimating the downturn at about 1.2 million tons of the island's annual imports of 6.5 million tons.
A so-called lost world on the border between Vietnam and Laos has yielded yet another new species of animal, this one a primitive wild pig, researchers reported on Wednesday DNA tests showed the pig, Sus bucculentus, was only distantly related to other pigs in the region, said Colin Grove of the Australian National University in Canberra.
Grove said the pig had been described more than 100 years ago but then became lost to science. A living version was never seen by scientists. "We here report its re-discovery in the Annamite Range in Laos, an area which is becoming famous for the discovery of new and previously undescribed large mammals," Grove and his colleagues wrote in a letter to the science journal Nature.
Grove said he found one skull from the pig in Beijing's Academia Sinica, with century-old documentation. "A new specimen of Sus bucculentis, a partial skull of a juvenile male, was obtained from indigenous hunters in the Annamite Range, Laos, in January 1995," he added.
They did DNA tests on muscle tissue left on the skull and found a "remarkably" large difference in the DNA between it and other wild and domestic pigs in the region. The Vu Quang area has already yielded several spectacular wildlife finds, including the discovery in 1992 of a deer-like animal known as the saola or Vu Quang ox, and a new freshwater fish last September. "These conclusions underline the significance of the Annamites as a biotically unique region where primitive taxa, long extinct elsewhere, have been able to survive into the late 20th century," Groves wrote.
The Vietnamese government and environmental groups say the region's forests are threatened by loggers. According to the World Wide Fund for Nature, Vietnam has only 19 percent forest cover today compared to 43 percent 50 years ago.
Below I compare GenBank prion amino acid sequences from cow, pig, sheep, and human. The idea is that they are not too different, so species barriers could be small. (But actually this is very hard to predict or anticipate.)
pig-cow 93.8% identity 257 aa vs 256 pig-sheep 94.2 % identity 257 aa vs 256 cow-sheep 98.8 % identity 256 aa vs 256 human-pig 85.2% identity 245 aa vs 256 human-cow 87.9 % identity 245 aa vs 256 human-sheep 87.5 % identity 245 aa vs 256
Difference between human and pig has to be viewed in Courier or similar font to align properly. The differences are mostly found in a hypervariable loop region that is probably not very important in normal prion function.
human to pig 85.2% identity 10 20 30 40 50 262542 M--ANLGCWMLVLFVATWSDLGLCKKRPKPGG-WNTGGSRYPGQGSPGGNRYPPQGGGGW _ .VKSHI.G.I......A...I...........G........................... 60 70 80 90 100 262542 GQPHGGGWGQPHGGGWGQPHGGGWGQ---------GGGTHSQWNKPSKPKTNMKHMAGAA _ ..........................PHGGGGWGQ...S.G..............V.... 110 120 130 140 150 160 262542 AAGAVVGGLGGYMLGSAMSRPIIHFGSDYEDRYYRENMHRYPNQVYYRPMDEYSNQNNFV _ .....................L................Y..........V.Q.....S.. 170 180 190 200 210 220 262542 HDCVNITIKQHTVTTTTKGENFTETDVKMMERVVEQMCITQYERESQAYYQRGSSMVLFS _ .......V.....................I............QK.YE..A...A.VI... 230 240 262542 SPPVILLISFLIFLIVG _ ...........L.....
human cow 87.9% identity 10 20 30 40 50 569305 M--ANLGCWMLVLFVATWSDLGLCKKRPKPGG-WNTGGSRYPGQGSPGGNRYPPQGGGGW _ .VKSHI.S.I......M...V...........G........................... 60 70 80 90 100 569305 GQPHGGGWGQPHGGGWGQPHGGGWGQ--GGG------THSQWNKPSKPKTNMKHMAGAAA _ ..........................PH...GWGQGGS................V..... 110 120 130 140 150 160 569305 AGAVVGGLGGYMLGSAMSRPIIHFGSDYEDRYYRENMHRYPNQVYYRPMDEYSNQNNFVH _ ....................L....N......................V.Q......... 170 180 190 200 210 220 569305 DCVNITIKQHTVTTTTKGENFTETDVKMMERVVEQMCITQYERESQAYYQRGSSMVLFSS _ ......V.E................I...............Q..........A.VI.... 230 240 569305 PPVILLISFLIFLIVG _ ................
human to sheep 87.9% identity 10 20 30 40 50 151611 M--ANLGCWMLVLFVATWSDLGLCKKRPKPGG-WNTGGSRYPGQGSPGGNRYPPQGGGGW _ .VKSHI.S.I......M...V...........G........................... 60 70 80 90 100 151611 GQPHGGGWGQPHGGGWGQPHGGGWGQ--GGG------THSQWNKPSKPKTNMKHMAGAAA _ ..........................PH...GWGQGGS................V..... 110 120 130 140 150 160 151611 AGAVVGGLGGYMLGSAMSRPIIHFGSDYEDRYYRENMHRYPNQVYYRPMDEYSNQNNFVH _ ....................L....N......................V.Q......... 170 180 190 200 210 220 151611 DCVNITIKQHTVTTTTKGENFTETDVKMMERVVEQMCITQYERESQAYYQRGSSMVLFSS _ ......V.E................I...............Q..........A.VI.... 230 240 151611 PPVILLISFLIFLIVG _ ................
pig to cow 93.8% identity 10 20 30 40 50 60 166351 MVKSHIGGWILVLFVAAWSDIGLCKKRPKPGGGWNTGGSRYPGQGSPGGNRYPPQGGGGW _ .......S........M...V....................................... 70 80 90 100 110 120 166351 GQPHGGGWGQPHGGGWGQPHGGGWGQPHGGGGWGQGGGSHGQWNKPSKPKTNMKHVAGAA _ .....................................-..S................... 130 140 150 160 170 180 166351 AAGAVVGGLGGYMLGSAMSRPLIHFGSDYEDRYYRENMYRYPNQVYYRPVDQYSNQNSFV _ ..........................N...........H..................N.. 190 200 210 220 230 240 166351 HDCVNITVKQHTVTTTTKGENFTETDVKMIERVVEQMCITQYQKEYEAYAQRGASVILFS _ .........E................I..M.............R.SQ..Y.......... 250 166351 SPPVILLISFLLFLIVG _ ...........I.....
Sus scrofa pig 774 Artiodactyla; Suiformes; Suina; Suidae; Sus. MVKSHIGGWILVLFVAAWSDIGLCKKRPKPGGGWNTGGSRYPGQ GSPGGNRYPPQGGGGWGQPHGGGWGQPHGGGWGQPHGGGWGQPHGGGGWGQGGGSHGQ WNKPSKPKTNMKHVAGAAAAGAVVGGLGGYMLGSAMSRPLIHFGSDYEDRYYRENMYR YPNQVYYRPVDQYSNQNSFVHDCVNITVKQHTVTTTTKGENFTETDVKMIERVVEQMC ITQYQKEYEAYAQRGASVILFSSPPVILLISFLLFLIVG Homo sapiens human 2301 Primates; Catarrhini; Hominidae; Homo. MANLGCWMLVLFVATWSDLGLCKKRPKPGGWNTGGSRYPGQGSP GGNRYPPQGGGGWGQPHGGGWGQPHGGGWGQPHGGGWGQGGGTHSQWNKPSKPKTNMK HMAGAAAAGAVVGGLGGYMLGSAMSRPIIHFGSDYEDRYYRENMHRYPNQVYYRPMDE YSNQNNFVHDCVNITIKQHTVTTTTKGENFTETDVKMMERVVEQMCITQYERESQAYY QRGSSMVLFSSPPVILLISFLIFLIVG Ovis aries Sheep gene 771 Artiodactyla; Ruminantia; Pecora; Bovoidea Bovidae; Caprinae; Ovis MVKSHIGSWILVLFVAMWSDVGLCKKRPKPGGGWNTGGSRYPGQ GSPGGNRYPPQGGGGWGQPHGGGWGQPHGGGWGQPHGGGWGQPHGGGGWGQGGSHSQW NKPSKPKTNMKHVAGAAAAGAVVGGLGGYMLGSAMSRPLIHFGNDYEDRYYRENMYRY PNQVYYRPVDQYSNQNNFVHDCVNITVKQHTVTTTTKGENFTETDIKIMERVVEQMCI TQYQRESQAYYQRGASVILFSSPPVILLISFLIFLIVG Bos taurus bovine 771 Artiodactyla; Ruminantia; Pecora; Bovoidea Bovidae; Bovinae; Bos. MVKSHIGSWILVLFVAMWSDVGLCKKRPKPGGGWNTGGSRYPGQ GSPGGNRYPPQGGGGWGQPHGGGWGQPHGGGWGQPHGGGWGQPHGGGGWGQGGSHSQW NKPSKPKTNMKHVAGAAAAGAVVGGLGGYMLGSAMSRPLIHFGNDYEDRYYRENMHRY PNQVYYRPVDQYSNQNNFVHDCVNITVKEHTVTTTTKGENFTETDIKMMERVVEQMCI TQYQRESQAYYQRGASVILFSSPPVILLISFLIFLIVG
References Martin T, 1995 Direct sequencing of PCR amplified pig PrP genes. Biochim. Biophys. Acta 1270, 211-214 (1995) Philpott M, 1993 The dangers of disease transmission by artificial insemination and embryo transfer Br. Vet. J. 149, 339-369 (1993) Dawson M, 1990 Primary parenteral transmission of bovine spongiform encephalopathy to the pig [letter] Vet. Rec. 127, 338 (1990) (no abstract available)