Saturday, December 21, 2013

Parelaphostrongylus (Brainworm) Infection in Deer and Elk and the potential for CWD TSE prion consumption and spreading there from ?

Parelaphostrongylus (Brainworm) Infection in Deer and Elk and the potential for CWD TSE prion consumption and spreading there from ?



Greetings everyone et al, and Merry Christmas,


I am hoping, and praying, that 2014 will bring forth much needed funding for the TSE prion scientist around the globe.


I brought up a concern for a worm long ago, that gets in the brains of cervids, and then the worm gets excreted via feces, and then deer forage and eat that worm. if the host cervid of this worm has CWD, could this later transmit CWD?


I was concerned about this long ago, still am. I was curious what any else might think about this potential mode of transmission with cwd ?


there is much cwd risk factor now with soil, and now the potential exists via plants, so I was just pondering out loud here, is it possible that some cwd is being spread, by the Parelaphostrongylus (Brainworm), after sucking up on a CWD infected cervids brain, and then being discarding via feces by that same CWD infected cervid, soaking up the prions via the feces, laying in wait, for a CWD free cervid to come scoop up and eat that Parelaphostrongylus (Brainworm), that has been extremely exposed to the TSE prion ?



kind regards, terry




Parelaphostrongylus (Brainworm) Infection in Deer and Elk



Murray Woodbury DVM, MSc.


Specialized Livestock Research and Development Program


Department of Large Animal Clinical Sciences


Western College of Veterinary Medicine


University of Saskatchewn


Saskatoon,Saskatchewan S7N 5B4




 The parasite Parelaphostrongylus tenuis (P. tenuis) is also known as brain worm, meningeal worm, Pneumostrongylus tenuis, Odocoileostrongylus tenuis, Elaphostrongylus tenuis, or Neurofilaria cornellensis. Infection frequently results in clinical disease called moose sickness, moose disease, moose neurological disease, cerebrospinal parelaphostrongylosis, or cerebrospinal nematodiasis. The existence of this parasite in eastern, but not western, North America and the implications of it's movement west has severely affected live animal trade in the farmed cervid industry of Canada. Etiology


 Parelaphostrongylosis is caused by the roundworm, Parelaphostrongylus tenuis. The major host for this parasite is the white-tailed deer where it is carried without causing clinical signs of disease.


Geographic distribution


P. tenuis is present in eastern and central Canada including Nova Scotia, New Brunswick, southern Quebec, Ontario, Manitoba, and eastern Saskatchewan (5). It is also present in twenty eight of the eastern and central United States (1). It is generally absent from coastal plains of the southeastern United States and St. Croix of the Virgin Islands (14).


The parasite continues to spread extensively as white-tailed deer expand their range in response to environmental changes such as deforestation, agriculture and burning (5). Currently, the meningeal worm is not present in western North America, however it is present in deer of the aspen parkland, and there is no apparent barrier to its continued spread west toward the foothills of the Rockies through such a corridor (5). Biologically, the meningeal worm requires several criteria to be met for survival including the presence of adequate numbers and overlapping populations of definitive (white-tail deer) and intermediate hosts (terrestrial snails and slugs) in sufficient densities to allow for establishment. It also needs a suitable climate for survival of free-living stages of the parasites and suitable numbers of the hosts involved (1). Ecologically, the prairie habitat and its dry conditions may affect the survival of the first stage larvae and this may have some impact on controlling the range of the nematode (9). In addition, the parasite is believed to be associated with certain major soil types in combination with other environmental attributes. However, what constitutes the barrier to generalized distribution is unknown (4).




 Prevalence of the meningeal worm ranges from less than 1% to greater than 85% throughout North America (1). Within Canada, the prevalence for adult worms in the cranial cavities of deer are as follows: Manitoba 10%, Ontario 41- 61%, Quebec 30%, New Brunswick 60%, and Nova Scotia 51% (1). The prevalence of meningeal worms in aberrant hosts is generally unknown, however surveys have been undertaken to determine the prevalence in such hosts (1).




 The life cycle of the meningeal worm is indirect with a typical prepatent period of 82 to 91 days. However, the length may be inversely related to the number of larvae ingested, and may be considerably longer in individual deer (10). P. tenuis is a true lungworm in that it requires both a definitive host, the white-tailed deer, and an intermediate host, a snail or slug. Deer become infected by accidentally ingesting gastropods (snails) containing infective third-stage larvae (L3) which are found on vegetation (4). Larvae are freed from the gastropod tissue by digestion, and during the following ten days they penetrate the abomasal wall, and migrate across the peritoneal cavity to gain access to the central nervous system, likely through lumbar nerves (4). Once they invade neural tissue, larval development occurs primarily in the dorsal horns of the spinal cord. Fourth stage larvae (L4) emerge about 25 days after initial ingestion (4). The L4 larvae leave the neural tissue and migrate to the subdural space by day 40, after which they molt to the immature adult stage (4). Once mature, some nematodes migrate to the venous sinuses of the cranium (4). Some worms may deposit eggs on the meninges, but most deposit eggs directly into the venous circulation where they are transported to the heart and lungs as emboli (4). Eggs lodge in the lungs where they are incorporated into fibrous nodules. These eggs embryonate into first-stage larvae (L1), move into the alveoli, and up the bronchial escalator where they are coughed up and swallowed to be excreted out in the mucous coat on the feces (4). The excreted L1 penetrate the foot of a terrestrial gastropod, where they grow and molt twice to become the infective L3.


The time required for these two molts to occur is variable and highly dependent on environmental conditions but it may be as short as three to four weeks at summer temperatures. Larvae cease to develop when snails are hibernating but development continues normally once snails become active (10). Laboratory and field studies have shown that larvae are capable of overwintering in the intermediate host (4).


Experimentally, a wide range of terrestrial gastropods may be infected, however only a few species are generally involved in natural transmission. This is likely related to preference of certain gastropods for favorable microenvironments of forested areas with specific moisture content, evaporation, and temperature (13). Commonly, gastropod availability in open meadows is less than forested areas, reducing the likelihood of exposure to particular gastropods for animals that utilize these areas to graze (13). Typically, white-tailed deer spend most of their time in forested areas where gastropods are found whereas elk spend most of their time in meadows and open fields (4). Other equally important factors may include seasonal movement patterns in deer, wapiti or gastropods, food preferences and selectivity for gastropods by the host animal (13).


The early phase of the meningeal worm life cycle in aberrant hosts parallels that in white-tailed deer, however the development of the larvae in the central nervous system tends to produce neurologic signs and even death (4). Meningeal worm larvae tend to be unusually active and damaging in neural tissue of aberrant hosts. Some larvae fail to leave the neural parenchyma which results in damage as the larvae matures and migrates, while other larvae invade the ependymal canal or reinvade the spinal cord or brain after maturation (10). The pathogenesis of the meningeal worm in fallow deer is different from other cervids in that infective larvae penetrate the small intestine rather than the abomasum (4).


Other species affected


 A wide variety of species are susceptible to infection with P. tenuis, namely, moose, elk, caribou, reindeer, mule deer, black-tailed deer, mule deer/white-tailed deer hybrids, fallow deer, red deer, red deer/elk hybrids, domestic sheep and goats, llamas, guinea pigs, and several bovid and cervid species in zoos (1). It appears that reindeer, caribou, llamas, and domestic goats are very susceptible to meningeal worm infection (1). It is speculated that caribou and reindeer may be more likely to acquire infected gastropods because of their feeding habits (4).


Clinical signs


 The natural host for this infection is the white-tailed deer, and although the parasite normally migrates to the meninges in this species, the deer typically displays few clinical signs. Lack of apparent disease even with neurological invasion has been attributed to the manner in which the larvae reside in the neuropil of white-tail deer (4). In naturally and experimentally infected white-tail deer, temporary lameness of the forelimb, circling, and rapid oscillation of the eyeballs have been observed (1). Most white-tailed deer survive infection without exhibiting clinical signs, however large larval burdens could precipitate serious signs or even death.


In various cervids, camelids and other wild and domesticated ruminants, very few P. tenuis larvae are required to produce a severe debilitating neurological disease. The disease is expressed by locomotor incoordination, lameness, stiffness, listlessness, progressive hindquarter weakness, circling, abnormal position of the head and neck, blindness, and paralysis (1). Caribou and reindeer also consistently exhibit exophthalmos or a "bug eyed" appearance (4). Naturally infected elk become less wary, leave the herd and remain near roads, fields or woodland clearings (14). Llamas infected with P. tenuis display a sudden onset of weakness or ataxia and at least one of paraparesis (generalized weakness), ataxia, exaggerated patellar reflexes, conscious proprioceptive deficits (can't place feet correctly) or increased extensor tone (rigid muscles) in the rear limbs (6). Cerebrospinal fluid aspirates in infected llamas typically reveal increased protein and eosinophils (6). Fallow deer fawns given high doses of infective larvae die sooner with signs associated with severe peritonitis resulting from perforation of the intestinal wall, compared to fawns given low doses of infective larvae which die later with signs associated with paralysis and inability to rise (8). There is also a continuum of responses to meningeal worm infection in elk: those exposed to large numbers of infective larvae die; those exposed to low numbers survive, often without infection; and those exposed to intermediate numbers often develop patent non-fatal infections (9). Apparently, severity of clinical signs, resolution of clinical signs and death are dose dependent.




 In white-tail deer, lesions associated with developing larvae are relatively minor. Uncoiled larvae are generally located in cell-free tunnels in the dorsal horns of the spinal cord surrounded by compressed neural tissue (4). In white matter, scattered myelin sheath degeneration may be present, with foreign body reactions around pieces of cuticle and hemorrhages associated with larval migration, however, neural parenchyma quickly assumes a normal appearance once larvae have left (4). Lesions associated with the adult meningeal worms in the cranium are unremarkable (4). Lesions in the lungs consist of tiny discolored spots uniformly distributed throughout the parenchyma and under the pleura (10). Nodules may be found within the lungs due to a foreign-body reaction that occurs around the remains of hatched eggshells (4). Congestion, hemorrhages, and eosinophilic and lymphocytic infiltration is common in areas where eggs or larvae have been in the lungs (4). Alveoli may collapse and disappear resulting in subsequent fibrosis of the region which may show as respiratory signs in naturally infected white-tailed deer (4).


Gross pathologic changes in infected aberrant host animals include extensive central nervous system lesions including focal hemorrhages, neuronal degeneration, tracking lesions in the brain and spinal cord, and yellowish accumulations streaked with blood adjacent to the worms (1). Meningeal worms can be found free in the cranial cavity or on the spinal cord or may be embedded in nervous tissue (1).


As identified previously, larval penetration of the small intestine occurs in fallow deer. It is believed that fallow deer are apparently unable to limit the phase of nematode migration through the small intestine, even though they are capable of mounting a substantial immune response against the meningeal worm once it is within the central nervous system (4). This results in colitis and fatal peritonitis, which is different than the pathology seen in all other cervids (4). In fallow deer, the mucosa of the greater curvature of the abomasum is hyperemic with scattered focal hemorrhages, the small intestine is filled with black-red fluid, and the intestinal wall is slightly thickened with rugose congested mucosae (8). Fibrinous adhesions are present throughout the peritoneal cavity.


Microscopic lesions in aberrant hosts include small hemorrhages, masses of parasite eggs, infiltrations of eosinophilic leukocytes, and congestion of very small blood vessels (1). Additional microscopic lesions identified in llamas include multifocal random areas of cavitation, axonal swelling, linear cavities containing a variable number of lipid-laden macrophages and necrosis (6).




 Presently, the only definitive method for diagnosing P. tenuis infections is recovery and identification of adult worms from the central nervous system at necropsy (1).


The current diagnostic technique used in live animals is recovery of first-staged larvae in feces or lung tissue using modified Baermann techniques. Unfortunately, other protostrongylid nematodes shed similar cork-screw shaped dorsal spiny-tailed larvae which may make it difficult to definitively identify Parelaphostrongylus tenuis (1). Additionally, the first-stage larvae of P. tenuis are resistant to dessication and freezing (4) and may be readily washed off feces by water or rain (10) making it difficult to recover larvae using this method. Detection of low-levels of infection by this method is complicated by the parasite's long reproductive period which necessitates repeated testing of feces from suspected animals for several months. It is known that the number of larvae shed fluctuates by season with more larvae shed in winter-spring than in summer-autumn and the normal host, the white-tailed deer, tends to shed more larvae than the aberrant hosts such as elk (1). Also, animals infected with only one worm, or worms of the same gender, will not shed larvae (12). It is also possible that immunological factors and age of the host may play a role in the levels of larval shedding (1).


Attempts to diagnose P. tenuis by measuring total protein concentration and enzyme activity within the cerebrospinal fluid of domestic goats and white-tailed deer showed inconclusive results (7). It is clear that parelaphostrongylosis is accompanied by seroconversion, and that both species develop a significant antibody response in cerebrospinal fluid, however the inability to detect antibodies during the prepatent period hinders the application of this technique as a diagnostic aid (7).


A primary objective of a study undertaken in 1996 was to develop simple and reliable blood tests to detect meningeal worm infection in game-farmed animals (3). The blood tests were based on the reaction between unique somatic antigens to P. tenuis located in or on the worm to antibodies from the blood of infected animals (3). A unique 37 kDa antigen of the third-stage larva, which is also present in adult P. tenuis, serves as a serodiagnostic antigen to develop an enzyme-linked immunosorbent assay as a reliable diagnostic test for P. tenuis infection in white-tailed deer (12). However, the use of native 37kDa antigens from either L3 or adults for developing serological tests is impractical because the antigen is in low concentration in the parasite and would be difficult to obtain. (12) Currently the antigen is being cloned and expressed using recombinant DNA technology (12). Serological diagnosis of P. tenuis should offer many advantages over the currently used method of fecal analysis (12), especially with respect to differentiation of P. tenuis from other protostrongylids.


Differential diagnoses


P. tenuis can be confused with other neurological disorders such as trauma, brain abscesses, tumors, tick paralysis, listeriosis, degenerative myelopathy, rabies and other parasites that cause cerebrospinal nematodiasis. Copper deficiency may cause progressive ataxia, and chronic capture myopathy may have external manifestations similar to some stages of P. tenuis infection (11).




 There are no drugs known to be effective against meningeal worms once they invade the central nervous system (1).


Kocan treated deer with 0.1 mg/kg of ivermectin subcutaneously at 1, 10 and 30 days after exposure to meningeal worm larvae and only prevented infection in deer treated 1 day after exposure (2). Once the larvae emerge from the gastrointestinal tract and enter the central nervous system by six days post-exposure, ivermectin has no effect because it does not readily cross the blood brain barrier except at very high dosages (2). Larvae still penetrating the abomasum, however, are readily killed (2). Treatment of deer with mature worms reduces the number of larvae shed in feces, indicating that ivermectin is effective against first-stage larvae in the lungs and perhaps on egg production or viability, however live adult worms still persist in the central nervous system (2).


According to masters thesis work by Sikarskie at Michigan State University, limited clinical trials of the use of oral albendazole feed at 25 mg/kg in the feed for two weeks, killed adult worms in the meninges of white-tailed deer (11).


Llamas infected with P. tenuis have been treated with anthelmintics including ivermectin and fenbendazole to kill the larval stages of the parasite and anti-inflammatory drugs such as flunixin, phenylbutazone or dexamethasone to decrease the inflammation in the neural tissue associated with migrating or dead larvae (6). In all instances, the animals deteriorated and required euthanasia in spite of treatment.




 Prevention of pasture contamination by white-tailed deer, and mollusk management are the recommended procedures for controlling P. tenuis in wild populations of white-tailed deer (4, 11). Control of the gastropod intermediates is not feasible nor practical because gastropods are present in a wide variety of environmental locations not readily reached by non-specific molluscicides and would not be desirable because gastropods are very important to the ecosystem (10). Controlling the nematode in the definitive host is also not a viable option because there are no known drugs effective against P. tenuis, and anthelmintic treatment of wild populations is generally not feasible (10). Double fencing and establishment of a sanitary central region, cordon sanitaire, has been used in quarantine stations to prevent access of either white-tailed deer or gastropods (11). The ground of the cordon sanitaire must be regularly harrowed or ploughed to keep it free of vegetation, with periodic application of molluscicides to prevent gastropod migration (11).




 The geographical distribution of P. tenuis is very important to wildlife officials and game farm producers because it can cause significant mortality among cervids. It has been suggested that parelaphostrongylosis may be responsible for the decline of moose in some areas of the United States and Canada and is a major factor preventing the establishment of moose, elk, and caribou in areas populated by white-tailed deer (14). Presently, P. tenuis, is considered the greatest threat to game farm animals and provincial wildlife populations if it is accidentally introduced into Saskatchewan populations (1). Concern centers on the potential for translocating and establishing the parasite in nonendemic areas as a result of natural range expansion or translocation of infected hosts (4). Research has illustrated that the meningeal worm can successfully complete its life cycle in elk and that the larvae from such infections are viable and can serve as a source for subsequent infections in white-tailed deer and other elk (9). Current recommendations are that until reliable diagnostic procedures are available, importation of game species from areas where the parasite occurs should not occur (1). One must recognize that should the meningeal worm be introduced into an area free from the disease, it will be extremely difficult, if not impossible, to eradicate (1).


In order to establish quarantine protocols, research would need to be conducted to determine when and how frequently fecal sampling (1) or serological testing would need to be done. Contaminated enclosures used for holding ungulates would need to be kept free of white-tailed deer for a least one to two years and perimeter fences would need to be free of vegetation that could harbor gastropods which could travel into the pens to infect the enclosed animals (10).


Even if the worm did not cause devastation to common native species it would likely have a tremendous economic impact because of mortality, morbidity, responses to public inquiry, lost natural resources and potential threats to the domestic animal industry (1). Domestic goats appear to be exquisitely sensitive, often dying within a few days of infection, while sheep are considerably less susceptible (10). It is believed that cattle are one of the most resistant of the domestic species, although meningeal worms have been recovered from the central nervous system of healthy individuals and adult worms may reach the CNS before the cattle die (10). Although the role of aberrant hosts in sustaining P. tenuis populations or their role in translocating the parasite is not currently known, introduction of this parasite to domestic farms could have a substantial economic impact.


There is no indication that this parasite poses a risk to humans because it is not infective to humans and meat of infected animals is safe for human consumption (14).


Future research According to W.M. Samuel at the University of Alberta, a variety of questions need to be answered in relation to this parasite (1). These include: Do free-ranging elk in eastern North America shed larvae in their feces? What are the specific boundaries of the meningeal worm distribution and what mechanisms delineate this geographic distribution? How susceptible are various native wild and domestic hosts to the meningeal worm? Hopefully, the answers to these questions will soon become clear and with the development of effective diagnostic tests Parelaphostrongylus tenuis infections will be readily prevented, treated or controlled.




1.The review of wildlife disease status in game animals in North America, Saskatchewan Game Farmers Association and The Saskatchewan Game Farming Technical Advisory Committee, 1992. 2.Kocan AA. The use of ivermectin in the treatment and prevention of infection with Parelaphostrongylus tenuis (Dougherty) (Nematoda: Metastrongyloides) in white-tailed deer (Odocoileus virginianus Zimmerman). Journal of Wildlife Diseases 1985; 21(4): 454-455. 3.Development of blood tests for Elaphostrongylus cervi and Parelaphostrongylus tenuis in game-farmed animals. Agriculture Development Fund. 1996. Agriculture and Agri-Food Canada. 4. Fowler ME, Miller RE. Zoo & Wild Animal Medicine Current Therapy 4. Philadelphia: W. B. Saunders, 1999. 5. Bindernagel JA, Anderson RC. Distribution of the meningeal worm in white-tailed deer in Canada. Journal of Wildlife Management 1972; 36(4): 1349 - 1353. 6.Scarratt WK, Karzenski SS, Wallace MA, et al. Suspected Parelaphostrongylosis in five llamas. Progress in Veterinary Neurology 1996; 7(4): 124 - 129. 7.Dew TL, Bowman, DD, Grieve RB. Parasite-specific immunoglobulin in the serum and cerebrospinal fluid of white-tailed deer (Odocoileus virginianus) and goats (Capra hircus) with experimentally induce parelaphostrongylosis. Journal of Zoo and Wildlife Medicine 1992; 23:281 - 287. 8.Pybus MJ, Samuel WM, Welch DA, et al. Mortality of fallow deer (Dama dama) experimentally infected with meningeal worm, Parelaphostrongylus tenuis. Journal of Wildlife Diseases 1992; 28(1): 95 - 101. 9.Samuel WM, Pybus MJ, Welch DA, Wilke CJ. Elk as a potential host for meningeal worm:implications for translocation. Journal of Wildlife Management 1992; 56(4): 629 - 639. 10.Davidson WR, Hayes FA, Nettles VF, et al. Lungworms (Anderson RC, Prestwood AK) In Diseases and Parasites of White-tailed Deer. Tallahassee: Tall Timbers Research Station,1981. 11.Haigh JC, Hudson RJ. Farming Wapiti and Red Deer. St. Louis: Mosby, 1993. 12.Ogunremi O, Lankester M, Kendall J, Gajadhar A. Serological diagnosis of Parelaphostrongylus tenuis infection in white-tailed deer and identificiation of a potentially unique parasite antigen. Journal of Parasitology; 85(1): 122 - 127. 13.Raskevitz RF, Kocan AA, Shaw JH. Gastropod availability and habitat utilization by wapiti and white-tailed deer sympatric on range enzootic for meningeal worm. Journal of Wildlife Diseases 1991; 27(1): 92 - 101. 14.


Subject: Transmission of TSEs through ectoparasites i.e. P. tenuis and CWD


Date: May 3, 2007 at 9:05 am PST




SEAC 97/2


Annex 2






Other organisms


Transmission of TSEs through ectoparasites has been postulated by Lupi5. Post et al6 fed larvae of meat eating and myiasis causing flies with brain material from scrapie infected hamsters. Two days after eating infected material, the larvae showed high amounts of PrPSc by Western blot. In further studies, the inner organs of larvae, which had been fed with scrapie brain, were extracted and fed to hamsters. Six out of eight hamsters developed scrapie. Two out of four hamsters fed on scrapie infected pupae subsequently developed scrapie.



I AGAIN raise the possibility of that damn brain eating worm in elk and CWD transmission via elk, deer, and other critters eating that worm. ...tss


Immunodiagnosis of experimental Parelaphostrongylus tenuis infection in elk


Oladele Ogunremi, Murray Lankester, and Alvin Gajadhar Centre for Animal Parasitology, Canadian Food Inspection Agency, 116 Veterinary Road, Saskatoon, Saskatchewan S7N 2R3 (Ogunremi, Gajadhar); Department of Biology, Lakehead University, 955 Oliver Road, Thunder Bay, Ontario P7B 5E1 (Lankester).


Elk infected with the meningeal worm, Parelaphostrongylus tenuis (Protostrongylidae), do not consistently excrete larvae in feces, making the current method of diagnosing live animals using the Baermann fecal technique unreliable. Serological diagnosis could prove more useful in diagnosing field-infected animals but depends on the identification and availability of good quality antigen. To mimic field infections, 2 elk were inoculated with 6 infective L3 larvae of P. tenuis, and another 2 with 20 L3 larvae. Fecal samples were examined for nematode larvae using the Baermann technique and serum samples taken were tested for anti-P. tenuis antibody with ELISAs by using the excretory-secretory (ES) products of L3, and sonicated adult worms as antigens. One animal passed first-stage larvae in its feces 202 days post inoculation, but passed none thereafter. The remaining 3 inoculated animals did not pass larvae. In contrast to parasite detection, antibodies against larval ES products were detected in all animals starting from 14 to 28 days post inoculation and persisted until the termination of the experiment on day 243 in 2 animals that harbored adult worms. Antibodies against somatic antigens of the adult worm were not detected until day 56 but also persisted until the end of the experiment in the animals with adult worms. In 2 elk that had no adult worms at necropsy, anti-ES antibodies were detected transiently in both, while anti-adult worm antibodies were present transiently in one. These findings confirm the superiority of P. tenuis larval ES products over somatic adult worm antigens as serodiagnostic antigens, as previously observed in studies of infected white-tailed deer, and extend the application of the newly developed ELISA test in diagnosing and monitoring cervids experimentally infected with P. tenuis.



Subject: TSE & insects as a vector of potential transmission


Date: October 26, 2006 at 12:50 pm PST


i try to keep an open mind about any other routes and sources that we may be overlooking. i mean, there is enough TSE protein in circulation now VIA the FDA, just in 2006 alone, and the oral route has been proven with BSE, and the non-forced oral consumption of scrapie to primate, as to not worry about a natural route of a few worms that have maybe been feasting on a deer that's brain is infected with CWD, then excreted out, and then passed on to another worm hungry deer looking for that feast. i suppose maybe just another potential route and source for a TSE, and possibly even a 'double dose' so to speak from not only the worm in the feces (maybe triple with feces), but the soil as well (see soil and prion study as well below) following that are some other studies that may be of interest ; Myiasis as a risk factor for prion diseases in humans


Journal of the European Academy of Dermatology and Venereology Volume 20 Page 1037 - October 2006 doi:10.1111/j.1468-3083.2006.01595.x Volume 20 Issue 9




Myiasis as a risk factor for prion diseases in humans


O Lupi *




Prion diseases are transmissible spongiform encephalopathies of humans and animals. The oral route is clearly associated with some prion diseases, according to the dissemination of bovine spongiform encephalopathy (BSE or mad cow disease) in cattle and kuru in humans. However, other prion diseases such as scrapie (in sheep) and chronic wasting disease (CWD) (in cervids) cannot be explained in this way and are probably more associated with a pattern of horizontal transmission in both domestic and wild animals. The skin and mucous membranes are a potential target for prion infections because keratinocytes and lymphocytes are susceptible to the abnormal infective isoform of the prion protein. Iatrogenic transmission of Creutzfeldt–Jakob disease (CJD) was also recognized after corneal transplants in humans and scrapie was successfully transmitted to mice after ocular instillation of infected brain tissue, confirming that these new routes could also be important in prion infections. Some ectoparasites have been proven to harbour prion rods in laboratory experiments. Prion rods were identified in both fly larvae and pupae; adult flies are also able to express prion proteins. The most common causes of myiasis in cattle and sheep, closely related animals with previous prion infections, are Hypoderma bovis and Oestrus ovis, respectively. Both species of flies present a life cycle very different from human myiasis, as they have a long contact with neurological structures, such as spinal canal and epidural fat, which are potentially rich in prion rods. Ophthalmomyiases in humans is commonly caused by both species of fly larvae worldwide, providing almost direct contact with the central nervous system (CNS). The high expression of the prion protein on the skin and mucosa and the severity of the inflammatory response to the larvae could readily increase the efficiency of transmission of prions in both animals and humans.



International Journal of Dermatology Volume 42 Page 425 - June 2003 doi:10.1046/j.1365-4362.2003.00345.x Volume 42 Issue 6




Could ectoparasites act as vectors for prion diseases?


Omar Lupi, MD, PhD




Prion diseases are rare neurodegenerative diseases of humans and animals with a lethal evolution. Several cell types found on the human skin, including keratinocytes, fibroblasts and lymphocytes, are susceptible to the abnormal infective isoform of the prion protein, which transforms the skin to produce a potential target for prion infection. Iatrogenic transmission of Creutzfeldt-Jakob disease was also recognized after corneal transplants in humans, and scrapie was successfully transmitted to mice after ocular instillation of infected brain tissue, confirming that these new routes, as well as cerebral inoculation and oral ingestion, could be important in prion infections. Animal prion infections, such as scrapie (sheep) and "mad cow disease" (cattle), have shown a pattern of horizontal transmission in farm conditions and several ectoparasites have been shown to harbor prion rods in laboratory experiments. Fly larvae and mites were exposed to brain-infected material and were readily able to transmit scrapie to hamsters. New lines of evidence have confirmed that adult flies are also able to express prion proteins. Because ocular and cerebral myiases and mite infestation are not rare worldwide, and most cases are caused by fly larvae or hay mites that usually affect sheep and cattle, it is important to discuss the possibility that these ectoparasites could eventually act as reservoirs and/or vectors for prion diseases.



P. tenuis – The White-tailed Deer Parasite


“Brain worms” (meningeal worms) can affect sheep, goats, llamas, alpacas, moose and other exotic small ruminants


M. Kopcha, D.V.M., M.S., J. S. Rook, D.V.M. & D. Hostetler, D.V.M MSU Extension & Ag. Experiment Station Michigan State University College of Veterinary Medicine


Many livestock producers are familiar with internal parasites that invade the digestive system (the abomasum, small or large intestines), liver, and lungs. An internal parasite which may not be so well-recognized is one that invades the central nervous system (brain and spinal cord). Commonly called the “brain worm” or meningeal worm (the meninges are a thin membrane that covers the brain and spinal column), the scientific name for this parasite is Parelaphostroneylus tenuis (P. tenuis), and its natural host is the White-tailed deer. Usually, P. tenuis completes its life cycle in the deer (Figure 1) without causing noticeable problems. However, when P. tenuis is ingested by unnatural, or aberrant hosts such as, llamas, sheep, goats, moose, elk, caribou, and other susceptible ruminants, the parasite moves into the brain and/or spinal cord, damaging delicate nervous tissue. Neurologic problems result.


White-tailed deer may he parasitized by P. tenuis year-round. However, the neurologic disease seen in aberrant hosts has a seasonal occurrence that starts in the late summer and continues until a hard freeze occurs. A cool, moist summer and/or a mild winter may extend the period during which the disease occurs. How does it occur?


To understand this disease and how to prevent or minimize its occurrence, it is important to understand the life cycle of P. tenuis in the White-tailed deer and what happens when the parasite is ingested by susceptible ruminants. The life cycle is as follows (Figure 1): adult meningeal worms live in the deer's central nervous system (brain and spinal cord) and produce eggs which hatch into larvae. The larvae migrate from the deer's central nervous system to the lungs, where they are coughed into the mouth, swallowed and passed from the intestinal tract with the manure. This portion of the life cycle takes approximately three months (Figure 1 - numbers 1 and 2). After excreted in the manure, larvae must continue their development in an intermediate host (certain land-dwelling snails and slugs) for another three to four weeks until they reach their infective stage (Figure 1 - numbers 3 and 4). White-tailed deer become infested with P. tenuis by eating these snails or slugs that contain the infective stage of the larvae (Figure 1 - number 5). Once ingested, the larvae migrate through the deer’s gut and eventually move into their central nervous system where they mature into adults, produce eggs,


Figure 2 The Angora goat in the center of the picture had a mild lameness in its left forelimb (arrow). The presumptive diagnosis was meningeal worm infestation. Mild cases such as this one may recover spontaneously.


Figure 3 This Angora goat was probably affected with meningeal worms and was able to use its hindlimbs, but was unable to rise onto its forelimbs.


Figure 4 This alpaca had been paralyzed by meningeal worms. Notice that despite the paralysis, the animal appears alert. This is typical for a brain worm infestation that affects the spinal cord and not the brain. Figure 6: This Suffolk sheep was one of several sheep from a flock that were affected with Parelaphostrongylus tenuis. The posture that this animal is displaying is referred to as a “dogsitting” position.


Figure 5: This alpaca displayed weakness in both hindlimbs and was unable to stand without assistance. The presumptive diagnosis was brain worm infestation. This animal eventually recovered. and the cycle begins again.


When P. tenuis-infected snails and slugs are ingested by aberrant hosts, the larvae migrate into the brain and/or spinal cord, but do not mature into adults. Instead, these immature larvae wander through the central nervous system causing inflammation and swelling which damages sensitive nervous tissue producing a variety of neurologic signs. Because these larvae do not mature into adults in aberrant hosts, they cannot produce eggs that would mature into larvae which would then pass outside the animal with the feces. This is why sheep, goats, llamas and other unnatural hosts are considered dead-end hosts for P. tenuis. Dead end hosts infected with P. tenuis larva cannot spread the disease to other aberrant hosts or back to deer - i.e. infected sheep or goats can not bring the disease to your flock or herd. The neurologic signs observed in infected llamas, sheep, goats and others depend upon the number of larvae present in the nervous tissue and the specific portion of the brain or spinal cord that has been affected. For example - a mild infestation in a very local area may produce a slight limp (Figure 2)) or weakness in one or more legs (Figure 3,4,5, & 6). A more severe infestation may cause an animal to become partially or completely paralyzed. If the parasites are located only in the spinal cord, an affected animal will appear bright and alert, and have a normal appetite, despite the altered gait or paralysis. When larvae migrate through the brain, they may cause blindness, a head tilt, circling, disinterest in or inability to eat, or other signs that can mimic brain diseases caused by bacteria, viruses, nutritional deficiencies, trauma, or toxins. Table I lists some of the diseases that P. tenuis can mimic when the parasites migrate through nervous tissue.


Table 1_Included in this table are various diseases that can look similar to “brain worm” infestation. Also listed are the target species that are susceptible to each of the diseases.


Species Disease Llamas and Alpacas Sheep Goats Listeriosis X X X Caprine Arthritis- Encephalitis X Scrapie X Rare* Rabies X X X Trauma X X X Copper Deficiency X X X Vitamin E/Selenium Deficiency X X X Spinal Cord or Brain Abscess X X X Polioencephalomalacia X X X


Could it happen on my farm?


Animals pastured in lowland areas frequented by infected White-tailed deer are prime candidates for exposure to snails containing P. tenuis larvae. When such animals develop neurological problems during the late summer through early winter in the Upper Midwest (the season for exposure may be longer in other parts of the country), “brain worms” are a likely possibility.


Presently there is no definitive test that can be performed on a live animal to confirm P. tenuis infestation. Since the larvae do not mature to adulthood in aberrant hosts, and therefore, cannot produce eggs or pass larvae in the feces, a fecal examination is not useful. Also, these parasites cannot be detected by blood testing. A test that can help support suspicions of brain worm infestation is evaluation of cerebrospinal fluid (CSF), which is the fluid that bathes the brain and spinal cord. Disease that occurs in these areas may cause changes in the CSF detectable by various tests. Normal CSF contains very few cells and little protein. An animal that has parasites migrating in the brain or spinal cord, often will have a larger number of cells, especially a certain type of cell called an eosinophil. Also, the protein concentration may be increased. Therefore, finding eosinophils in a CSF tap taken from an animal with neurologic abnormalities is very supportive evidence for “brain worm” infestation. If eosinophils are not found, this does not rule out the possibility of a “brain worm” problem. Currently, the only way to confirm this diagnosis is by finding the parasite in the nervous system, which requires a necropsy examination.


Obtaining CSF from sheep, goats, and llamas is somewhat more involved than obtaining a blood sample. Two areas used most often for CSF collection are just behind the poll or over the hips, in the area called the lumbosacral junction. We prefer the lumbosacral site because the test can be performed using local anesthetic only (rarely would a tranquilizer be required), and the animal can be standing or lying down, whichever is most comfortable. The head site usually requires that the animal be heavily tranquilized or anesthetized.


The procedure can be performed in a hospital setting or on the farm, and must be done in a sterile manner. This includes removal of the hair or wool from a small area where the puncture will be made, scrubbing the site with surgical disinfectant and rinsing with alcohol. Sterile gloves and equipment are used.


After the site has been scrubbed, an injection of a local anesthetic is placed under the skin and into the deeper tissues where the spinal needle will be placed. The needle is inserted through the anesthetized area. The animal may notice slight discomfort when the needle enters the spinal canal. However, having a quiet person at the animal's head (in some cases the best person is the owner or handler) will provide a calming effect. The needle does not penetrate the spinal cord. In many animals, the cord ends just ahead of where the needle is placed. Once fluid has been obtained, the needle is withdrawn. The amount of fluid collected depends on the animal's size. Usually, 5 to 8 cc's are withdrawn and submitted to a clinical laboratory for analysis. This is a very safe procedure if performed properly.


What about treatment?


Many different drugs including thiabendazole, levamisole, fenbendazole, albendazole, and ivermectin have been used in an attempt to treat “brain worm” infestation. However, to date, no controlled studies have confirmed or refuted the efficacy of various treatment recommendations. Some anthelmintics can kill P. tenuis larvae while they migrate from the stomach to the brain or spinal cord, but are unable to enter the central nervous system because of a structure called the blood-brain barrier. Therefore, they do not have an effect on parasitic larvae once the parasite has migrated across the blood-brain barrier and is in the central nervous system. Other anthelmintics may be able to kill the larvae regardless of their location in the body. An important point to remember is that once the parasite begins to migrate within the nervous tissue, damage occurs that is usually irreversible. Although some drugs may kill the worms, thus pre venting further damage, treatment does not repair nervous tissue. Some animals with mild clinical signs may recover without treatment. At this time, the best recommendation for treatment is "do no harm." Perhaps some medications are helpful, however, remember that drugs used at higher-than-usual levels or more frequently than usual may cause toxicity problems.


The best approach to “brain worm” infestation is prevention. This s achieved by keeping the life cycle in mind. Animals kept in pastures that have wetlands and White-tailed deer should be removed from these pastures in the late summer and until the first hard freeze. If this is not possible, strategic deworming is the second best approach. This would involve either continuously providing an anthelmintic in feed or mineral mix throughout the “brain worm” season, or deworming with an oral or injectable product every 10 to 14 days - starting in late summer and continuing through early to mid-winter, depending on the severity of the freezing temperatures.


The 10- to 14-day schedule recommendation is based on experimental evidence that demonstrated the parasites' ability to reach the brain and/or spinal cord in this amount of time after an animal eats the snails containing P. tenuis larvae. Thus, this is a "window of opportunity" to kill the worms before they enter the central nervous system where they may be "safe" or protected from the killing effect of drugs that cannot cross the blood-brain barrier. While clinical cases of meningeal worm infestation are rare, “brain worms” could affect your animals if they have access to wetlands harboring P. tenuis-infected White-tailed deer. Wetlands contain a population of snails and slugs needed to complete the parasite's life cycle if it is the season when P. tenuis infestation occurs. Remember: the success of treatment is variable - prevention is the best means of control.






P.121: Efficient transmission of prion disease through environmental contamination


Sandra Pritzkow, Rodrigo Morales, and Claudio Soto Mitchell Center for Alzheimer’s disease and related Brain disorders; University of Texas Medical School at Houston; Hourston, TX USA


Chronic wasting disease (CWD) is a prion disorder effecting captive and free-ranging deer and elk. The efficient propagation suggests that horizontal transmission through contaminated environment may play an important role. It has been shown that infectious prions enter the environment through saliva, feces, urine, blood or placenta tissue from infected animals, as well as by carcasses from diseased animals and can stay infectious inside soil over several years.


We hypothesize that environmental components getting in contact with infectious prions can also play a role for the horizontal transmission of prion diseases. To study this issue, surfaces composed of various environmentally relevant materials were exposed to infectious prions and the attachment and retention of infectious material was studied in vitro and in vivo. We analyzed polypropylene, glass, stainless steel, wood, stone, aluminum, concrete and brass surfaces exposed to 263K-infected brain homogenate. For in vitro analyses, the material was incubated in serial dilutions of 263K-brain homogenate, washed thoroughly and analyzed for the presence of PrPSc by PMCA. The results show that even highly diluted PrPSc can bind efficiently to polypropylene, stainless steel, glass, wood and stone and propagate the conversion of normal prion protein. For in vivo experiments, hamsters were ic injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters, inoculated with 263K-contaminated implants of all groups, developed typical signs of prion disease, whereas control animals inoculated with non-contaminated materials did not.


In addition, in order to study the transmission in a more natural setting, we exposed a group of hamster to habit in the presence of spheres composed of various materials that were pretreated with 263K prions. Many of the hamsters exposed to these contaminated materials developed typical signs of the disease that were confirmed by immunohistological and biochemical analyses.


These findings suggest that various surfaces can efficiently bind infectious prions and act as carriers of infectivity, suggesting that diverse elements in the environment may play an important role in horizontal prion transmission.


P.146: Kinetics and cell association of chronic wasting disease prions shed in saliva and urine of white-tailed deer


Nicholas J Haley,1,2 Scott Carver,3 Clare E Hoover,1 Kristen A Davenport,1 Candace K Mathiason,1 Glenn C Telling,1 and Edward A Hoover1


1Department of Microbiology, Immunology, and Pathology, College of Veterinary Medicine and Biomedical Sciences; Colorado State University; Fort Collins, CO USA; 2Department of Diagnostic Medicine and Pathobiology, College of Veterinary Medicine; Kansas State University; Manhattan, KS USA; 3School of Zoology; University of Tasmania; Hobart, Tasmania, Australia


Chronic wasting disease, a transmissible spongiform encephalopathy (TSE) of deer, elk, and moose, is unique among prion diseases in its relatively efficient horizontal transmissibility. Recent studies have shown that excreta—saliva, urine, and feces—from CWD-positive cervids may play an important role in horizontal transmission of CWD, and although the precise onset of shedding in these excreta is unknown, it is thought to occur long before the onset of clinical symptoms. High levels of prion seeding activity have been demonstrated in excretory tissues of deer, including tongue, salivary glands, kidney, and urinary bladder, though the origin(s) and cellular nature of infectious prions in excreta is unknown. We hypothesized that excretory shedding of CWD prions in saliva and urine would coincide with the appearance of PrPd appearance in peripheral lymphatic tissues, and that infectivity would associate with cellular preparations of these excreta. Following intracerebral inoculation of susceptible Tg[CerPrP] mice, we observed efficient transmission in saliva collected as early as 12 months post-exposure, coinciding with peripheral PrPd appearance in tonsil biopsies; while urine collected at terminal disease was only minimally infectious in transgenic mice. We also found that acellular preparations of saliva, and cellular preparations of urine, were capable of transmitting CWD infection to transgenic Tg[CerPrP] mice with incubation periods similar to that of whole saliva or urine; saliva and urine from CWD-negative deer failed to induce prion disease in these mice. Infectious titers were determined for obex and bodily fluids, and were similar to those previously described. These findings extend our understanding of CWD shedding in white-tailed deer, and offer insight into the source and cellular associations of infectious CWD prions in excreta.


P.178: Longitudinal quantitative analysis of CWD prions shed in saliva of deer


Davin M Henderson, Nina Garbino, Nathaniel D Denkers, Amy V Nalls, Candace K Mathiason, and Edward A Hoover Prion Research Center, College of Veterinary Medicine and Biomedical Sciences, Colorado State University; Fort Collins, CO USA


Background/Introduction. Chronic Wasting Disease (CWD) is an emergent rapidly spreading fatal prion disease of cervids (deer, elk and moose). CWD has now been identified in 22 States (including two new states within the last year), 2 Canadian provinces, and South Korea. Shedding of infectious prions in excreta (saliva, urine, feces) may be an important factor in CWD transmission. Here we apply an adapted version of a rapid in vitro assay [real-time quaking-induced conversion (RT-QuIC)] to determine the time of onset, length, pattern, and magnitude of prion shedding in saliva of infected deer.


Materials and Methods. The RT-QuIC assay was performed as previously described in Henderson et al. PLoS-One (2013). Saliva samples were quantitated by comparison to a RT-QuIC reaction rate standard curve of a bioassayed obex sample from a terminally ill cervid.


Results. To better understand the onset and length of CWD prion shedding we analyzed >150 longitudinally collected, blinded, then randomized saliva samples from 17 CWD-infected and 3 uninfected white-tailed deer. We observed prion shedding, as detected by the RT-QuIC assay, as early as 3 months from inoculation and sustained shedding throughout the disease course in both aerosol and orally exposed deer. We estimated the infectious lethal dose of prions shed in saliva from infected deer by comparing real-time reaction rates of saliva samples to a bioassayed serially diluted brain control. Our results indicate that as little as 1 ml of saliva from pre-symptomatic infected deer constitutes a lethal CWD prion dose.


Conclusions. During the pre-symptomatic stage of CWD infection and throughout the course of disease deer may be shedding multiple LD50 doses per day in their saliva. CWD prion shedding through saliva and excreta may account for the unprecedented spread of this prion disease in nature. Acknowledgments. Supported by NIH grant RO1-NS-061902 and grant D12ZO-045 from the Morris Animal Foundation.



*** We conclude that TSE infectivity is likely to survive burial for long time periods with minimal loss of infectivity and limited movement from the original burial site. However PMCA results have shown that there is the potential for rainwater to elute TSE related material from soil which could lead to the contamination of a wider area. These experiments reinforce the importance of risk assessment when disposing of TSE risk materials.


*** The results show that even highly diluted PrPSc can bind efficiently to polypropylene, stainless steel, glass, wood and stone and propagate the conversion of normal prion protein. For in vivo experiments, hamsters were ic injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters, inoculated with 263K-contaminated implants of all groups, developed typical signs of prion disease, whereas control animals inoculated with non-contaminated materials did not.








Conclusions. To our knowledge, this is the first established experimental model of CWD in TgSB3985. We found evidence for co-existence or divergence of two CWD strains adapted to Tga20 mice and their replication in TgSB3985 mice. Finally, we observed phenotypic differences between cervid-derived CWD and CWD/Tg20 strains upon propagation in TgSB3985 mice. Further studies are underway to characterize these strains.


We conclude that TSE infectivity is likely to survive burial for long time periods with minimal loss of infectivity and limited movement from the original burial site. However PMCA results have shown that there is the potential for rainwater to elute TSE related material from soil which could lead to the contamination of a wider area. These experiments reinforce the importance of risk assessment when disposing of TSE risk materials.


The results show that even highly diluted PrPSc can bind efficiently to polypropylene, stainless steel, glass, wood and stone and propagate the conversion of normal prion protein. For in vivo experiments, hamsters were ic injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters, inoculated with 263K-contaminated implants of all groups, developed typical signs of prion disease, whereas control animals inoculated with non-contaminated materials did not.


Our data establish that meadow voles are permissive to CWD via peripheral exposure route, suggesting they could serve as an environmental reservoir for CWD. Additionally, our data are consistent with the hypothesis that at least two strains of CWD circulate in naturally-infected cervid populations and provide evidence that meadow voles are a useful tool for CWD strain typing.


Conclusion. CWD prions are shed in saliva and urine of infected deer as early as 3 months post infection and throughout the subsequent >1.5 year course of infection. In current work we are examining the relationship of prionemia to excretion and the impact of excreted prion binding to surfaces and particulates in the environment.


Conclusion. CWD prions (as inferred by prion seeding activity by RT-QuIC) are shed in urine of infected deer as early as 6 months post inoculation and throughout the subsequent disease course. Further studies are in progress refining the real-time urinary prion assay sensitivity and we are examining more closely the excretion time frame, magnitude, and sample variables in relationship to inoculation route and prionemia in naturally and experimentally CWD-infected cervids.


Conclusions. Our results suggested that the odds of infection for CWD is likely controlled by areas that congregate deer thus increasing direct transmission (deer-to-deer interactions) or indirect transmission (deer-to-environment) by sharing or depositing infectious prion proteins in these preferred habitats. Epidemiology of CWD in the eastern U.S. is likely controlled by separate factors than found in the Midwestern and endemic areas for CWD and can assist in performing more efficient surveillance efforts for the region.


Conclusions. During the pre-symptomatic stage of CWD infection and throughout the course of disease deer may be shedding multiple LD50 doses per day in their saliva. CWD prion shedding through saliva and excreta may account for the unprecedented spread of this prion disease in nature.


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Monday, June 23, 2014









*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years***


Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3



New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication



Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production



Detection of protease-resistant cervid prion protein in water from a CWD-endemic area







A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing



Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals



Karen Fernie, Allister Smith and Robert A. Somerville The Roslin Institute and R(D)SVS; University of Edinburgh; Roslin, Scotland UK


Scrapie and chronic wasting disease probably spread via environmental routes, and there are also concerns about BSE infection remaining in the environment after carcass burial or waste 3disposal. In two demonstration experiments we are determining survival and migration of TSE infectivity when buried for up to five years, as an uncontained point source or within bovine heads. Firstly boluses of TSE infected mouse brain were buried in lysimeters containing either sandy or clay soil. Migration from the boluses is being assessed from soil cores taken over time. With the exception of a very small amount of infectivity found 25 cm from the bolus in sandy soil after 12 months, no other infectivity has been detected up to three years. Secondly, ten bovine heads were spiked with TSE infected mouse brain and buried in the two soil types. Pairs of heads have been exhumed annually and assessed for infectivity within and around them. After one year and after two years, infectivity was detected in most intracranial samples and in some of the soil samples taken from immediately surrounding the heads. The infectivity assays for the samples in and around the heads exhumed at years three and four are underway. These data show that TSE infectivity can survive burial for long periods but migrates slowly. Risk assessments should take into account the likely long survival rate when infected material has been buried.


The authors gratefully acknowledge funding from DEFRA.




Sunday, November 3, 2013


*** Environmental Impact Statements; Availability, etc.: Animal Carcass Management [Docket No. APHIS-2013-0044] ***



Singeltary submission ;


Program Standards: Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose


DOCUMENT ID: APHIS-2006-0118-0411


***Singeltary submission


Docket No. 00-108-10 Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose; Program Standards


>>>The CWD herd certification program is a voluntary, cooperative program that establishes minimum requirements for the interstate movement of farmed or captive cervids, provisions for participating States to administer Approved State CWD Herd Certification Programs, and provisions for participating herds to become certified as having a low risk of being infected with CWD<<<


Greetings USDA/APHIS et al,


I kindly would like to comment on Docket No. 00-108-10 Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose; Program Standards.


I believe, and in my opinion, and this has been proven by scientific facts, that without a validated and certified test for chronic wasting disease cwd, that is 100% sensitive, and in use, any voluntary effort will be futile. the voluntary ban on mad cow feed and SRMs have failed terribly, the bse mad cow surveillance program has failed terribly, as well as the testing for bse tse prion in cattle, this too has failed terrible. all this has been proven time and time again via OIG reports and GOA reports.


I believe that until this happens, 100% cwd testing with validated test, ALL MOVEMENT OF CERVIDS BETWEEN STATES MUST BE BANNED, AND THE BORDERS CLOSED TO INTERSTATE MOVEMENT OF CERVIDS. there is simply to much at risk.


In my opinion, and the opinions of many scientists and DNR officials, that these so called game farms are the cause of the spreading of chronic wasting disease cwd through much negligence. the game farms in my opinion are not the only cause, but a big factor. I kindly wish to submit the following to show what these factors are, and why interstate movement of cervids must be banned. ...


snip...see full text and PDF ATTACHMENT HERE ;




Tuesday, December 16, 2014


Evidence for zoonotic potential of ovine scrapie prions Scrapie from sheep could infect humans with 'mad cow disease', study finds



Tuesday, December 16, 2014


Texas 84th Legislature 2015 H.R. No. 2597 Kuempel Deer Breeding Industry TAHC TPWD CWD TSE PRION



Friday, February 08, 2013


*** Behavior of Prions in the Environment: Implications for Prion Biology




Uptake of Prions into Plants




Friday, August 09, 2013


***CWD TSE prion, plants, vegetables, and the potential for environmental contamination




Friday, December 06, 2013 2:39 PM


Procedures for identifying infectious prions after passage through the digestive system of an avian species




Saturday, March 10, 2012


CWD, GAME FARMS, urine, feces, soil, lichens, and banned mad cow protein feed CUSTOM MADE for deer and elk







Sunday, August 25, 2013


***Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood, and mother to offspring transmission




Sunday, July 21, 2013


*** As Chronic Wasting Disease CWD rises in deer herd, what about risk for humans?





Detection of PrPCWD in Rocky Mountain Elk Feces Using Protein Misfolding Cyclic Amplification


Bruce E Pulford,1 Terry Spraker,1 Jenny Powers,2 Margaret Wild2 and Mark D. Zabel1 1Department of Microbiology; Immunology and Pathology; College of Veterinary Medicine and Biomedical Sciences; Colorado State University; 2Biological Resource Management Division; United States National Park Service; CO, USA


Key words: CWD, feces, PMCA, elk


Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy affecting cervids, including mule and white-tailed deer (Odocoileus hemionus and virginianus), elk (Cervus elaphus nelsoni) and moose (Alces alces shirasi). The method of CWD transmission between hosts is unclear, though there is evidence that feces excreted by infected animals may play a role. Recently, CWD prions was detected in feces using bioassays in cervidized mice, which took many months to produce results. In this study, we use a more rapid procedure, protein misfolding cyclic amplification (PMCA), to test elk feces for the presence of PK-resistant cervid PrP (PrPCWD). Feces were collected from symptomatic and asymptomatic elk in several northern Colorado locations, homogenized, mixed with normal brain homogenate from Tg5037 mice (expressing cervid PrP) and subjected to up to 9 rounds of PMCA (1 round = 40 secs sonication/30 mins at 70% maximum power, 24 hours). Western blots were used to detect PrPCWD using BAR-224 anti-PrP antibody. Rectal and CNS tissue from the elk were IHC-labeled and examined for the presence of PrPCWD. Fecal samples from symptomatic and asymptomatic elk that tested positive by IHC showed characteristic PrPCWD bands on western blots following PMCA. In addition, PMCA detected PrPCWD in 25% of fecal samples from IHC-negative animals. These data suggest that PMCA may (1) prove useful as a non-invasive method to supplement or even replace IHC testing of cervids for CWD, and (2) identify additional asymptomatic carriers of CWD, the prevalence of which may be underestimated using IHC.




Detection of subclinical infection in deer orally exposed to urine and feces (1) suggests that a prolonged subclinical state can exist, necessitating observation periods in excess of two years to detect CWD infection, and (2) illustrates the sensitive and specific application of sPMCA in the diagnosis of low-level prion infection. Based on these results, it is possible that low doses of prions, e.g. following oral exposure to urine and saliva of CWD-infected deer, bypass significant amplification in the LRS, perhaps utilizing a neural conduit between the alimentary tract and CNS, as has been demonstrated in some other prion diseases.


In summary, we provide evidence for the presence of infectious prions in the brains of conventional prion-assay-negative deer orally exposed 19 months earlier to urine and feces from CWD-infected donor deer. This apparent low level of prion infection was amplified by sPMCA, confirmed by Tg[CerPrP] mouse bioassay, and detected only in the obex region of the brain. These results demonstrate the potential for CWD prion transmission via urine and/or feces, and highlight the application of more sensitive assays such as sPMCA in identification of CWD infection, pathogenesis, and prevalence.





In contrast, CWD prions have been reported in saliva, urine and feces, which are thought to be responsible for horizontal transmission. While the titers of CWD prions have been measured in feces, levels in saliva or urine are unknown. Because sheep produce ~17 L/day of saliva and scrapie prions are present in tongue and salivary glands of infected sheep, we asked if scrapie prions are shed in saliva. We inoculated transgenic (Tg) mice expressing ovine prion protein, Tg(OvPrP) mice, with saliva from seven Cheviot sheep with scrapie. Six of seven samples transmitted prions to Tg(OvPrP) mice with titers of -0.5 to 1.7 log ID50 U/ml. Similarly, inoculation of saliva samples from two mule deer with CWD transmitted prions to Tg(ElkPrP) mice with titers of -1.1 to -0.4 log ID50 U/ml. Assuming similar shedding kinetics for salivary prions as those for fecal prions of deer, we estimated the secreted salivary prion dose over a 10-mo period to be as high as 8.4 log ID50 units for sheep and 7.0 log ID50 units for deer. These estimates are similar to 7.9 log ID50 units of fecal CWD prions for deer. Because saliva is mostly swallowed, salivary prions may reinfect tissues of the gastrointestinal tract and contribute to fecal prion shedding. Salivary prions shed into the environment provide an additional mechanism for horizontal prion transmission.




Conclusions. This study documents the first aerosol transmission of CWD in deer. These results further infer that aerosolized prions facilitate CWD transmission with greater efficiency than does oral exposure to a larger prion dose. Thus exposure via the respiratory mucosa may be significant in the facile spread of CWD in deer and perhaps in prion transmission overall.



Conclusion. Transepithelial transport of prions across nasal cavity mucosa begins within minutes of inhalation and can continue for up to 3 h. While M cells appear to transport prions across the follicular associated epithelium, larger amounts of prions are transported between the cells of the respiratory and olfactory epithelia, where they immediately enter the lymphatic vessels in the lamina propria. Thus, inhaled prions can be spread via lymph draining the nasal cavity and have access to somatic and autonomic nerves in the lamina propria of the nasal cavity. The increased efficiency of the nasal cavity route of infection compared with the oral route may be due to the rapid and prolonged transport of prions between cells of the respiratory and olfactory epithelia.




Now that these experiments are completed we conclude that TSE infectivity is likely to survive burial for long periods of time with minimal loss of infectivity and restricted movement from the site of burial. These experiments emphasize that the environment is a viable reservoir for retaining large quantities of TSE infectivity, and reinforce the importance of risk assessment when disposing of this type of infectious material.






Friday, December 06, 2013 2:39 PM


Procedures for identifying infectious prions after passage through the digestive system of an avian species







4.21 Three cases of SE’s with an unknown infectious agent have been reported in ostriches (Struthio Camellus) in two zoos in north west Germany (Schoon @ Brunckhorst, 1999, Verh ber Erkeg Zootiere 33:309-314). These birds showed protracted central nervous symptoms with ataxia, disturbances of balance and uncoordinated feeding behaviour. The diet of these birds had included poultry meat meal, some of which came from cattle emergency slaughter cases.








1 challenged cock bird was necropsied (41 months p.i.) following a period of ataxia, tremor, limb abduction and other neurological signs. Histopathological examination failed to reveal any significant lesions of the central or peripheral nervous systems...


1 other challenged cock bird is also showing ataxia (43 months p.i.).









A notification of Spongiform Encephalopathy was introduced in October 1996 in respect of ungulates, poultry and any other animal.


4.23 MAFF have carried out their own transmission experiments with hens. In these experiments, some of the chickens exposed to the BSE agent showed neurological symptoms. However MAFF have not so far published details of the symptoms seen in chickens. Examination of brains from these chickens did not show the typical pathology seen in other SE’s. 4.24 A farmer in Kent in November 1996 noticed that one of his 20 free range hens, the oldest, aged about 30 months was having difficulty entering its den and appeared frightened and tended to lose its balance when excited. Having previously experienced BSE cattle on his farm, he took particular notice of the bird and continued to observe it over the following weeks. It lost weight, its balance deteriorated and characteristic tremors developed which were closely associated with the muscles required for standing. In its attempts to maintain its balance it would claw the ground more than usual and the ataxia progressively developed in the wings and legs, later taking a typical form of paralysis with a clumsy involuntary jerky motion. Violent tremors of the entire body, particularly the legs, became common, sparked off by the slightest provocation. This is similar to that seen in many BSE cases where any excitement may result in posterior ataxia, often with dropping of the pelvis, kicking and a general nervousness. Three other farmers and a bird breeder from the UK are known to have reported having hens with similar symptoms. The bird breeder who has been exhibiting his birds for show purposes for 20 years noticed birds having difficulty getting on to their perch and holding there for any length of time without falling. Even though the bird was eating normally, he noticed a weight loss of more than a pound in a bird the original weight of which was 5 pounds. 4.25 Histological examination of the brain revealed degenerative pathological changes in hens with a minimal vacuolation. The presence of PrP immunostaining of the brain sections revealed PrP-sc positive plaques and this must be regarded as very strong evidence to demonstrate that the hens had been incubating Spongiform Encephalopathy.








1. Necrophagous birds as possible transmitters of BSE. The SSC considers that the evaluation of necrophagous birds as possible transmitters of BSE, should theoretically be approached from a broader perspective of mammals and birds which prey on, or are carrion eaters (scavengers) of mammalian species. Thus, carnivorous and omnivorous mammals, birds of prey (vultures, falcons, eagles, hawks etc.), carrion eating birds (crows, magpies etc.) in general could be considered possible vectors of transmission and/or spread of TSE infectivity in the environment. In view also of the occurrence of Chronic Wasting Disease (CWD) in various deer species it should not be accepted that domestic cattle and sheep are necessarily the only source of TSE agent exposure for carnivorous species. While some information is available on the susceptibility of wild/exotic/zoo animals to natural or experimental infection with certain TSE agents, nothing is known of the possibility of occurrence of TSE in wild animal populations, other than among the species of deer affected by CWD in the USA.


1 The carrion birds are animals whose diet regularly or occasionally includes the consumption of carcasses, including possibly TSE infected ruminant carcasses.








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Date: Mon, 11 Jun 2001 16:24:51 –0700


Reply-To: Bovine Spongiform Encephalopathy


Sender: Bovine Spongiform Encephalopathy


From: "Terry S. Singeltary Sr." Subject: The Red-Neck Ostrich & TSEs 'THE AUTOPSY'




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Friday, February 25, 2011 Soil clay content underlies prion infection odds






Wednesday, September 08, 2010









Spiroplasma spp. from transmissible spongiform encephalopathy brains or ticks induce spongiform encephalopathy in ruminants


Frank O. Bastian1, Dearl E. Sanders2, Will A. Forbes2, Sue D. Hagius1, Joel V. Walker1, William G. Henk3, Fred M. Enright1 and Philip H. Elzer1




also, see page 104 here ;



Identifying the role of different organs and organisms in scrapie transmission


Prions can survive for years in soil but how can scrapie be transmitted? A group of teams from France, Iceland and Spain is setting out to study the role of nematode parasites, nasal fly, ticks and mites in the transmission process and to determine to what extent wild rodents could serve as reservoir of prion. It is also examining possible vertical transmission through embryo organs. This work will permit a better understanding of the wide spread of scrapie in naturally infected flocks, taking into account the genetic susceptibility of the hosts.


Manech Blond-face sheep in the French Pyrenees and Latcha Blond-face in Spain are breeds particularly susceptible to scrapie, but the disease occurs only in some French flocks. A comparative survey between infected and non-infected flocks with scrapie will be conducted to compare the infection with parasites such as nematode worms, nasal fly and ticks. Wild rodent populations will be compared as will be mites from fresh grass and hay. These mites will be also studied in infected and non-infected farms in Iceland. Experiments on sheep and mice will provide a better understanding of the role of nematodes. The PrPsc protein will be investigated in these organisms, and mice inoculations are projected to demonstrate the possibility of prion transmission.






also, see ;






Sunday, December 15, 2013












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