14.3.97 Dateline documentary on BSE in the US
Abstracts relevent to Dateline show
Mystery of CWD in US deer, elk explained?
Is US gov't trying very hard to document US BSE?
Backgrounder on Bone Meal
Dr. Richard Marsh obituary
Secret TSE epidemic in US pigs questioned.
Victims Association concerned about US blood supply
Webmaster's recollections from the Dateline TV show of March 14, 1997 -- transcript to be posted. Friday's broadcast was actually Dateline's second: in April 1996, a show discussed Dr. Marsh's mink findings and questions about USDA's BSE surveillance program.
Dateline: US at risk for BSE and CJD
The show was well-done, carefully researched, and quite current:
... historic video clips of kuru; first transmission and symptoms of chimp;
... first showing of video clip of results of 1979 first scrapie-to-cow transmission in US;
... transmission was by intra-cerebral injection and second passaging (cattle-to-cattle) was seen.
Tape of Gibbs and quote from Gajdushek, each suggesting that home gardeners in US are getting CJD from MBM used in their rose gardens, from the dust. Gibbs stated that in every single case of sporadic CJD where he personally knew the individual, intensive rose gardening with bone meal was in the picture.
Stone Phillips stated point-blank on the show that the American Red Cross has secretly sequestered 2 million units of various blood products, because of uncertain provenance with regard to donors and CJD.
There is a new book out, Deadly Feast. The American author, Richard Rhodes, is making the round of talk shows such as this and has a direct pipeline to Gujdushek, even in prison. He reiterated Gibbs' warnings about pigs (but see below).
Steve Eckert, the producer of NBC Dateline, has provided some helpful corrections and additions to our initial account of the program. (The Dateline show caused a quadrupling of Mad Cow Disease daily Web visitation -- more so than after Oprah.) An exact transcript of the broadcast concerning bone meal and rose gardening:
STONE PHILLIPS NARRATION: Rhodes ends his book with the question: could breathing the dust from that bone meal transmit the disease? With millions of gardeners using it with no apparent problem, to even pose the question seems outlandish. But the government's chief researcher on these brain diseases, the cautious Dr. Gibbs, told Dateline that the few people he's known personally who've died of CJD had one unusual thing in common.
DR. GIBBS: They all used bone meal. But I can't say that there's a relationship between the bone meal and the disease in humans.
STONE PHILLIPS: But it's kind of spooky to hear that.
DR. GIBBS: Kind of spooky, yeah.
RICHARD RHODES: I was sitting with Dr. Gajdusek, and he finally leaned forward and said: "Do you use bone meal on your roses?" I was startled. And I said, yes I do use bone meal on my roses. And he said: "I wouldn't if I were you."
The producer continues:
"In fairness, these important qualifiers:
-- from the start Dr. Gibbs said he was only talking about a few cases, not a full study .
-- Dr. Gibbs clearly stated that, in spite of his personal observation, he could NOT claim there was a relationship between bone meal fertilizer and human cases of CJD.
Dr. Gibbs comments were worth reporting not ot because they proved a connection, but because they made Rhodes' question to Gajdusek -- which, at first glance, had seemed so outlandish -- was that far-fetched after all." --------
The 1979 video clip of sheep-to-cow was from an exeriment in Mission, Texas. It apparently has never been made public before and was obtained under Freedom of Information Act but the results were no 'secret.' The program made clear that transmission was from [intra-cerebral] injection and not from feed. Brain tissue from the infected Mission cattle were later injected into other cattle to determine if second passage was possible, with positive results. The 1979 experiment is discussed in later publications by the Cutlip-Robinson group, relevent abstracts below.
You can order a Dateline videotape containing the clips by visiting or see what they posted on the showTranscripts: $6 each, payable by check only: Burrelle's at (800) 777-TEXT. Or write to: Burrelle's Box 7 Livingston, NJ 07039
The simple history of scrapie-to-cattle research in the U,S. seems to be:
Dr. Wilbur Clark at the USDA's scrapie research station in Texas injected cattle, starting in 1979. Several fell ill, but because the brain lesions were subtle, researchers apparently weren't sure what they had. Several years later, Joe Gibbs tested the cattle brains chemically, found PrP-res in the symptomatic cattle (but not others), and thus confirmed transmission.
At that point, Hourrigan wrote up the original Clark results, and Gibbs reported finding the marker protein. Cutlip followed up in Iowa with a new sheep-to-cattle experiment; and Robinson & others used the Texas cattle brains for a second passage experiment in Pullman.
How hard is USDA really looking for US BSE?19 Mar 1997 Dr. Janice Miller
We work very closely with the pathologists at the National Veterinary Services Laboratories Pathobiology Laboratory [APHIS] and they were aware of our results long before they were published. The problem APHIS has is that most of the specimens they receive from cattle with CNS signs have been collected by non-USDA people (state veterinay diagnostic or public health laboratories) and they have been fixed in formalin, as is standard practice for tissues to be examined by histopathology.
Unfortunately, that is not a good fixation method for detecting the intraneuronal PrP staining that we found in cattle inoculated with sheep scrapie. If you read the Materials and Methods section of that paper you will see that the brains we examined by immunohistochemistry were fixed in PLP with an extremely low percentage of paraformaldehyde, 0.25%. Using this fixative, as we described in our 1993 paper, the PrP which appears in the neuron cell bodies of normal brains is destroyed by formic acid treatment, whereas the abnormal PrP in neurons of affected cattle remains immunoreactive.
The problem with tissue fixed in formalin (we collected tissues in that fixative also) is that the hydrated autoclaving procedure used to "unmask" PrP in formalin-fixed tissue reveals some PrP staining in neuron cell bodies of normal (control) brains. Therefore, the question then becomes quantitative and highly subjective. At which point does the pathologist think he is seeing more than a normal amount? I believe a person would have to look at an awful lot of normal brains before feeling very comfortable about saying a brain had "more than normal" amounts of intraneuronal PrP.
I advised the APHIS pathologists that I thought they should be very careful about trying make such an assessment. So, what are their options? They would need fresh brain specimesns for a good western blot analysis and that would be difficult since they don't control the laboratories submitting material; furthermore, western blots are extremely expensive to run and I'm pretty sure they don't have the resources to do many of those anyway.
The option they chose was to use the immunohistochemical test that we used for our experimental cattle, but applying it only to brains that were collected in the special PLP fixative by APHIS personnel. The brains that fit this category are those collected from selected slaughter plants that kill lots of "downer cows".
They felt the history of those cows most closely fit the kind of syndrome that we saw in the cattle inoculated with U.S. sheep scrapie. I can't tell you how many of them have been examined in that way but if you want that information you could contact Dr. Arthur Davis, Chief, Pathobiology Laboratory, National Veterinary Services Laboratories, APHIS, Ames, Iowa 50010. His phone number is 515-239-8521 and the fax number is 515-239-8527.
This is a very complex problem and seems to get more so every day.
Encephalopathy in cattle experimentally infected with the scrapie agent.Am J Vet Res 56: 606-612 (1995) Clark WW, Hourrigan JL, Hadlow WJ USDA, Animal and Plant Health Inspection Service, Veterinary Services, Mission, TX 78572, USA.Ten 8- to 10-month-old cattle were each inoculated intramuscularly, subcutaneously, intracerebrally, and orally with the scrapie agent to determine whether cattle are susceptible to it. Two inocula, both 10% homogenates of cerebrum, were used. One inoculum was from a sheep used for the second experimental ovine passage of the agent from 4 naturally affected Suffolk sheep. The other inoculum was from a goat used for the first experimental caprine passage of the agent from 2 naturally affected dairy goats living with the Suffolk sheep, the source of their infection. Between 27 and 48 months after inoculation, neurologic disease was observed in 1 of 5 cattle given the sheep brain homogenate and in 2 of 5 given the goat brain homogenate. In all 3 affected cattle, the disease was expressed clinically as increasing difficulty in rising from recumbency, stilted gait of the pelvic limbs, disorientation, and terminal recumbency during a 6- to 10-week course. Neurohistologic changes, though consistent with those of scrapie, were slight and subtle: moderate astrocytosis with sparse rod cells, some neuronal degeneration, a few vacuolated neurons, and scant spongiform change. Clinically and neurohistologically, the experimentally induced disease differed from bovine spongiform encephalopathy. The differences emphasize that such infections in cattle induce diverse responses, presumably depending largely on the strain of the agent. Pathologists should keep this variability in mind when looking for microscopic evidence of a scrapie-like encephalopathy in cattle.
1)Hourrigan JL Experimentally induced bovine spongiform encephalopathy in cattle in Mission, Tex., and the control of scrapie. J Am Vet Med Assoc 1990;196;1678-9
2) Gibbs CJ Jr. Experimental transmission of scrapie to cattle. Lancet, 1990; 335;1275
Intracerebral transmission of scrapie to cattle.J Infect Dis 169: 814-820 (1994) Cutlip RC, Miller JM, Race RE, Jenny AL, Katz JB, Lehmkuhl HD, DeBey BM, Robinson MM USDA, Agriculture Research Service, National Animal Disease Center, Ames, IA 50010.To determine if sheep scrapie agent(s) in the United States would induce a disease in cattle resembling bovine spongiform encephalopathy, 18 newborn calves were inoculated intracerebrally with a pooled suspension of brain from 9 sheep with scrapie. Half of the calves were euthanatized 1 year after inoculation. All calves kept longer than 1 year became severely lethargic and demonstrated clinical signs of motor neuron dysfunction that were manifest as progressive stiffness, posterior paresis, general weakness, and permanent recumbency. The incubation period was 14-18 months, and the clinical course was 1-5 months. The brain from each calf was examined for lesions and for protease-resistant prion protein. Lesions were subtle, but a disease-specific isoform of the prion protein was present in the brain of all calves. Neither signs nor lesions were characteristic of those for bovine spongiform encephalopathy.
Experimental infection of cattle with the agents of transmissible mink encephalopathy and scrapie.J Comp Pathol 113: 241-251 (1995) Robinson MM, Hadlow WJ, Knowles DP, Huff TP, Lacy PA, Marsh RF, Gorham JR USDA-ARS Animal Disease Research Unit, Washington State University, Pullman 99164-7030, USA.Cattle are susceptible to experimental infection with the Stetsonville isolate of the transmissible mink encephalopathy (TME) agent. To determine if they are susceptible to other TME isolates, two groups of calves were inoculated intracerebrally with homogenate of mink brain containing the Hayward isolate or the Blackfoot isolate. For comparison, a third group was inoculated with a brain homogenate from a steer infected with the Stetsonville isolate in its primary cattle passage and a fourth group was inoculated with a pool of brain homogenate from three cattle experimentally infected with a sheep and goat scrapie agent in its primary cattle passage. Clinical signs of neurological disease appeared in each steer of every group between 15 and 25 months after inoculation. An encephalopathy characterized by severe spongiform change and pronounced astrocytosis occurred in the three groups inoculated with the TME agent. In contrast, the neurohistological changes in the steers inoculated with the cattle-passaged scrapie agent were slight and subtle. Analysis of the octapeptide repeat region of the bovine protease-resistant protein (PrP) gene showed that variations in incubation period, clinical signs, and neurohistological changes were unrelated to the homozygous or heterozygous condition of six or six/five octapeptide repeats.
Experimental infection of mink with bovine spongiform encephalopathy.J Gen Virol 75: 2151-2155 (1994) Robinson MM, Hadlow WJ, Huff TP, Wells GA, Dawson M, Marsh RF, Gorham JR USDA-ARS Animal Disease Research Unit, Pullman, Washington 99164-7030.To determine whether the aetiological agent of bovine spongiform encephalopathy (BSE) is pathogenic for mink, standard dark mink were inoculated with coded homogenates of bovine brain from the U.K. Two homogenates were from cows affected with BSE. The third was from a cow that came from a farm with no history of having had BSE or having been fed ruminant-derived, rendered by-products, the proposed vehicle for introduction of the BSE agent. Each homogenate was inoculated intracerebrally into separate groups of mink and a pool of the three was fed to a fourth group. Signs of neurological disease appeared in mink an average of 12 months after intracerebral inoculation and 15 months after feeding. Decreased appetite, lethargy and mild to moderate pelvic limb ataxia were the predominant clinical signs, quite unlike the classic clinical picture of transmissible mink encephalopathy (TME).
Microscopic changes in brain sections of most affected mink were those of a scrapie-like spongiform encephalopathy. Vacuolar change in grey matter neuropil was accompanied by prominent astrocytosis. Varying greatly in severity from one mink to another, the degenerative changes occurred in the cerebral cortex, dorsolateral gyri of the frontal lobe, corpus striatum, diencephalon and brainstem. Although resembling TME, the encephalopathy was distinguishable from it by less extensive changes in the cerebral cortex, by more severe changes in the caudal brainstem and by sparing of the hippocampus. The results of this study extend the experimental host range of the BSE agent and demonstrate for the first time the experimental oral infection of mink with a transmissible spongiform encephalopathy agent from a naturally infected ruminant species.
Veteran researcher Dr. Richard Marsh at U. Wisconsin was rumored to be, but in fact was not, suffering from CJD. \
Marsh had told friends that little or no safety precautions in handling TSEmaterial were taken in the early days at NIH labs. He cannot speak to the public without written clearance from the Attorney General of the State of Wisconsin because of a lawsuit threatened on the University by the rendering industry. Wisconsin is a big dairy state.
Richard Marsh, 58, Cow-Disease ResearcherBy FORD BURKHART March 27, 1997 NY Times
Richard F. Marsh, whose research in veterinary science at the University of Wisconsin at Madison led him to sound an alarm about the risks of mad cow disease a decade before the outbreak of the disease in Britain last year, died on Sunday at his home in Middleton, Wis. He was 58. The cause was cancer, his family said.
Dr. Bert Mitchell, associate director of the Center for Veterinary Medicine in the National Institutes of Health in Bethesda, Md., credited Marsh with bringing up the possibility in 1985 that the disease could pass from animal to animal through tissue used in feed.
In his research, Marsh observed diseases in minks and learned from a mink rancher that the animals had been fed with a food supplement made from cattle parts. He theorized there was a pathway for transmission of cattle diseases that the industry was unaware of and urged a ban on such feeding. The disease, mink spongiform encephalopathy, destroys brain tissue in a manner similar to the way mad cow disease affects cattle.
He lived to see the first steps toward a federal ban on the feeding of tissue from cud-chewing animals, or ruminants, like cattle and sheep, to other ruminants. The ban is expected to become law by this summer, federal officials said. The mad cow disease, or bovine spongiform encephalopathy, has been tentatively linked to the fatal Creutzfeldt-Jakob disease, a variant of which British experts have confirmed in about a dozen cases. A colleague at Wisconsin, Dr. Judd Aiken, said Marsh had alerted the veterinary field to the virtual impossibility of killing, by sterilizing the tissue used in animal feed, the agent that is believed to cause mad cow disease. "He showed these things are iron-clad agents," Aiken said.
He said Marsh had shown that the symptoms of these cattle diseases were slow in developing. An infected calf can look normal, perhaps for as long as five to eight years without a signal of the dangerous agents, until a mature cow begins to stagger or become aggressive. So Marsh lobbied for a ban even in absence of symptoms in cattle.
Marsh received a doctorate in veterinary medicine from Washington State University in 1963. He worked at the U.S. Public Health Service from 1968-70, then joined the University of Wisconsin, working there until his death.
Mystery of CWD explained?Listserve Opinion 15 March 1997
Heard at a meeting: Chronic wasting disease, the TSE of elk and mule deer, currently affects several per cent of wild herds in Colorado and southern Wyoming. There is no winter range for these animals any more and as they come down out of the mountains, they cause damage to hay and alfalfa ranches occupying their winter habitat. To mitigate, Colorado Fish and Game supplies feed. Apparently this included rendered bovine material in the form of 'cake' for protein. Sheep material is possible but maybe less likely since it is a tiny portion of US rendered meal.
This scenario, while unproven, strikes me as a whole lot more likely than natural endemicity at these levels, transmission by mites, or horizontal or vertical passage. It would also explain why Colorado Fish and Game is telling hunters that tainted elk brain is safe to handle and eat -- to avoid riling the public over their earlier tragic blunder. Not unlike what MAFF did in England.
The theory that CWD in the US originates from BSE cattle rather than scrapie sheep is not so easily testable by current strain typing, since putative US strains of TSE would not necessarily bear any resemblance to the four British strains. Eventually, we might establish the provenance of CWD by this method however.
One thing that nobody discusses is a negative species barrier, ie that the species barrier could actually be _lower_ in the cross species situation, that is, deer/elk could hypothetically be _more_ susceptible to, say, mad cow disease, than another cows.
Response from Colorado Fish & Game:From Mike Miller, CDFG veternarian:
Regulations in Colorado prohibit the public from feeding deer, elk, and other wild ungulates. The Division of Wildlife does have a policy and SOP in place for emergency feeding of select ungulate populations during severe winters; on average, conditions warranting such emergency feeding arise about every 10 years in some western portions of the state. Winters are sufficiently mild along the northern Front Range (where CWD occurs in free-ranging deer and elk) that emergency feeding is unnecessary. Moreover, the formulation of our supplemental ration, published by Baker and Hobbs (1985, J. Wildl. Manage. 49:934-942), does not include animal-derived protein.
The Colorado Division of Wildlife, in consultation with the Colorado Department of Public Health and Environment, actually has provided a considerable amount of information and advice about CWD to hunters and the general public through press releases and brochures. From our recently published 1997 Deer, Elk, Antelope & Black Bear hunting brochure (pg. 12) : "There is also no evidence that it [CWD] affects humans, but the DOW advises hunters to take simple precautions when handling the carcass of a deer or elk harvested in units where CWD occurs. Wear rubber gloves when field dressing carcasses and minimize handling of brain and spinal tissues and wash hands afterward. Hunters should bone out carcasses or at least avoid consuming brain, spinal cord, eyes, spleen and lymph nodes of harvested animals. Hunters should not handle or consume wild animals that appear sick, regardless of the cause."
Response to Colorado Fish & GameMike, here's the way that came out a couple of local newspaper stories. See also main CWD page.Colorado Big-Game Stricken with Mad Cow-like Ailment McClatchy Western News Service ... [approx. spring 1996]
DENVER - Deer and elk in parts of norther Colorado have been stricken with an ailment similar to Great Britain's mad cow disease, but it doesn't affect humans who eat the tainted meat.
"While the disease is similar, there never has been a link found between it and any human health problems," said Mike Miller, a Colorado Division of Wildlife veterinarian.
The so-called chronic wasting disease damages portions of the brains of deer and elk. Affected animals experience progressive weight and muscle loss, bahavioral changes, excessive salivation, incrased drinking, urination, and depression. Chronic wasting disease is always fatal. It's suspected that the disease is transmittted through feces, urine and shedding. The known cases are limited to areas from the Wyoming border south to Lyons and along the South Platte River east to Fort Morgan. When a diseased animal is reported, state wildlife officials capture and destroy it.
Division reminds northeast colorado hunters about deer, elk with CWDOct. 29, 1996 see CDFG Wildlife News for full article. ...
"Nothing has changed regarding the relationship between chronic wasting disease and human illness," said Division Veterinarian Mike Miller said. "There is still no evidence that chronic wasting disease affects people ... We're advising people about chronic wasting disease because we want to err on the side of being conservative without being alarmist," Miller added. "Unfortunately, we can't make absolute guarantees about this or any other disease and we can't prove that something can never happen."
There are significant differences between wasting disease and BSE, Miller explained. State health officials recommended avoiding consumption of viscera or handling viscera from animals with chronic wasting disease. Deer and elk infected with wasting disease show progressive loss of body condition, behavioral changes, excessive salivation, increased drinking and urination, lethargy and eventual death.
"We do not recommend special precautions for healthy appearing deer and elk," the letter states. "However, if in the conduct of a special study, an animal pathology report indicates wasting disease, then the hunter should be advised against eating the meat. This is not to recommend that all deer and elk be examined....nor that entire game management units....be closed to hunting."
The Division asked state health officials for their recommendation at an Aug. 28 meeting that brought together wildlife managers, experts on chronic wasting disease and the Health Department. At that meeting, epidemiologist John Pape and University of Wyoming veterinary pathologist Beth Williams BOTH SAID THEY WOULD EAT VENISON from healthy animals taken in northeastern Colorado. ...
An explanatory note:: Fish & Game departments in the western United States derive their revenue in large measure, if not exclusively, from the sale of deer and elk tags and fishing licenses. Should the area of endemic chronic wasting disease have to be closed to hunting, the financial effects on the Colorado Dept. of Fish & Game might be devastating. So the staff is asked to fall on their swords to keep the hunting units open. Notice that Miller and Williams only sald they _would_ eat venison from the area with endemic TSE, not that they actually did in fact eat any. And only from a healthy animal; a good idea, too bad there is no way of telling.
If 3-4% of the herd is manifesting gross clinical symptoms of an easily transmissable spongiform encephalopathy, one might suppose that 30-40% or more are seriously infectious. Does the average Colorado hunter really have access to a P3 containment facitliy to safely dissect out the peripheral nervous system from a slab of venison?
The advice being given out by CDFG is extremely irresponsible and embodies the all-too-familiar failure to distinguish between infectivity and overt illness. In other words, animasl can and do have extremely high infectious titres for TSEs but only years later exhibit symptoms. Indeed, overt manifestations of TSEs result from neuronal cell death, which can be years subsequent to and remote from actual peaking of rogue prion conformer, the likely infectious agent. The species barrier for CWD has been crossed for mink; experimental tests of transmission to humans is out of the question, and the incubation period can be so long that dietary transmission to a hunter from a diseased but asymtomatic elk would not be expected to show up -- yet. And by the time it does, if it does, it is too late for a whole lot of people. -- webmaster
Victims Association concerned about US blood supplyAlphas have genetic alpha1-antitrypsin deficiency [causing elastase problems in lungs]
"The voluntary withdrawal of certain lots of [human-derived alpha 1-protease inhibitor?] Prolastin® by Bayer Corporation in 1994 and again in 1996 has raised concerns and fears about the safety of Prolastin. The lots were tainted by a rare, slow virus-like infectious agent which can cause Creutzfeldt-Jakob disease.
Creutzfeldt-Jakob disease is a degenerative, neurological disorder transmitted via tissue transfer from infected individuals. The incubation period for the disease is thought to be between eighteen months and thirty years. Thus far, there are no documented cases of human to human transmission of Creutzfeldt-Jakob disease through blood or blood products. Studies looking at transmission in a large blood bank have failed to show any association between transfusions of "infected blood" and development of the disease.
Even though the risk of infection is extremely low, Kathy Kane, on behalf of the Alpha1 National Association, is keeping records of all Alphas who have received recalled lots of Prolastin. If you have received recalled lots, please get in touch with her. She will need to know your lot number and how many infusions your received. She can be reached at:61 West Street Hebron, CT 06248. 203-228-3261"
Secret Epidemic in US pigs?
"There is a new book out, Deadly Feast. The American author is making the round of talk shows such as this, has a direct pipeline to Gujdushek, even in prison. He reiterated Gibbs' warnings about pigs. There is reportedly a horrendous uncharacteristiced swine epidemic on-going in the Midwest, carcasses going directly into sewage lagoons without notification or or autopsy, rendering plants refusing to pick them up."Response: Beth Lautner, National Pork Producers 16 Mar 1997:I am a veterinarian who is the Vice President of Swine Health and Pork Safety at the National Pork Producers Council (NPPC). NPPC is the association for the pork producers in the U.S.
There is no "horrendous" swine epidemic occurring in the Midwest. Our office is located in Des Moines, Iowa. Iowa is the largest pork producing state in the U.S. Perhaps this refers to Porcine Reproductive and Respiratory Syndrome (PRRS) in swine herds. PRRS, caused by a RNA virus, has been a clinical syndrome in the U.S. since the late 1980's. It has been reported in almost all countries with pig populations.
Last fall, several swine herds in southeast Iowa developed somewhat more severe symptoms than normally associated with more recent PRRS breaks. This consisted of abortions that could occur in all stages of gestation and some increase in sow mortality.
Comprehensive diagnostics were done to determine if any other agents were present in addition to the PRRS virus detected in these herds. In addition, NPPC asked the U.S. Department of Agriculture's Animal and Plant Health Inspection Service (APHIS) to send a team composed of an epidemiologist, a diagnostician, and a pathoglogist to visit some of the affected herds to determine if there was any possibility of other agents and to determine what the risk factors may be for having this more severe manifestation of PRRS.
The conclusions of the field team based on histories, clinical signs, and laboratory finds were that these operations were experiencing PRRS as "described initially in the U.S. in 1989 and 1990." Further epidemiological studies are planned to better determine the reason and risk factors for some herds experiencing this more severe form of PRRS. It is speculated that through the widespread use of segregated early weaning technologies, many swine herds no longer have natural immunity to PRRS and when PRRS positive replacement swine are introduced into these herds, we have re-created the syndrome seen in naive herds.
Evidence supporting this theory includes the finding that herds with this more severe manifestation of PRRS are less likely to properly isolate females prior to introduction into the herd and may use more sources of replacement stock. The exact number of herds seeing this more severe form of PRRS is not known exactly, but is estimated to be between 25-100 herds (out of approximately 180,000 herds in the U.S.)
In addition to providing funding for the epidemiological study, NPPC is also providing significant dollars for research on PRRS virus pathogenesis, transmission, detection methodologies, etc. The American Association of Swine Practitioners is also providing some funding for the epidemiological study. There is no uncharacterized epidemic occuring in the Midwest or in other areas of the U.S. or problems with animal disposal related to this as mentioned in the email. Rather we are trying to further identify the management factors including herd immunity that result in PRRS virus infection in swine herds.
These studies have received some attention in the local media and trade press as it is the first national collaborative epidemiological study undertaken by NPPC, the American Association of Swine Practitioners, APHIS, university diagnostic laboratories, university researchers, and private practitioners. We hope that we have developed a model for future collaborative studies that can be used if there is a new emerging disease in the swine population in the U.S. These cases of a more severe form of PRRS have provided an opportunity to test how this collaboration can work to more quickly provide epidemiological information to practitioners and producers. I personally am very excited about this collaboration and pooling of intellectual resources.
For additional information, please contact me by email at or at 1-515-223-2623.
Background on Bone Meal
18 Mar 97 Dave HARLAN, Taylor Byproducts
Background on Bone Meal
It appears that some people are getting the feed supplement 'meat and bone meal' confused with the organic fertilizer 'bone meal'. They are two different products, the latter not containing any specified risk materials (brain, spinal cord and eyes). *IF* people were getting CJD from bone meal used in gardens, then surely every feedmill and rendering plant worker along with every truck driver who hauled any of the material would be dropping like flies due to a much higher exposure. This is not happening.
A little bit of history. Up to 1900 all rendered proteins/minerals were used as fertilizer. The fats were the most valuable portion... used as a fuel for lamps, etc. Around 1900 it was found that hogs would grow significantly faster when their corn diets were supplemented with "meat scraps", an old term for meat and bone meal (MBM). By the mid-50's other sources of nitrogen, phosphorous and potassium (collectively referred to as NPK) were used due to higher production farming. Currently the only fertilizer uses for are for home gardening and 'organic' farming... at least in more developed countries.
Bone meal was used as a mineral supplement for livestock, however, very very limited use today (I have not come across it). I don't think there is much bone meal produced in the US today... bones now mixed with other materials to make MBM. In yesteryears, I think (not sure) steamed bone meal was a by-product of animal glue manufacturing. Collagens were removed from bones to make glue, cooked or steamed bone residue was ground to make bone meal. Not much if any animal glue produced today, think synthetics have taken over.
I understand that in other parts of the world, such as Africa, bones are collected by 'bone pickers', a profession, and sold to bone meal facilities. The resulting product is used as a livestock supplement. The minerals provided by this bone meal (just like you taking a daily vitamin/mineral pill) supplement the diet of animals, including cattle, in these developing countries.
Now, a moral question. Do we, the more affluent societies of the world, not allow less affluent developing countries from utilizing a domestic source of minerals when that source is helping to feed their people? WHO's R-R ban does that! How many people should we starve, how many more acres of land do we take from nature to produce more food. How less efficient should we make animal agriculture? Europe appears headed in that direction. Don't get me wrong, we need to make some major changes, but let's not throw the whole system out the window.