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

Posted Dec 21 2013 12:43pm
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

 

 Introduction

 

 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

 

 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).

 

Transmission

 

 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.

 

Pathology

 

 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).

 

Diagnosis

 

 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).

 

Treatment

 

 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.

 

Control

 

 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).

 

Significance

 

 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.

 

References

 

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. http://www.dnr.state.mi.us/Wildlife/Divi...Publications/Disease_Manual/BRAINWM.html

 


 

 

 

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

 


 

 

PRION2013 CONGRESSIONAL ABSTRACTS CWD

 

 

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

 


 

 

A CONTRIBUTION TO THE NEUROPATHOLOGY OF THE RED-NECKED OSTRICH (STRUTHIO CAMELUS) - SPONGIFORM ENCEPHALOPATHY

 


 

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.

 


 

 

SE1806

 

TRANSMISSION STUDIES OF BSE TO DOMESTIC FOWL BY ORAL EXPOSURE TO BRAIN HOMOGENATE

 

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.).

 

snip...

 

94/01.19/7.1

 


 


 

 

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.

 


 

 

OPINION on : NECROPHAGOUS BIRDS AS POSSIBLE TRANSMITTERS OF TSE/BSE ADOPTED BY THE SCIENTIFIC STEERING COMMITTEE AT ITS MEETING OF 7-8 NOVEMBER 2002

 

OPINION

 

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.

 

C:\WINNT\Profiles\bredagi.000\Desktop\Necrophagous_OPINION_0209_FINAL.doc

 


 

 

snip...

 

skroll down to the bottom ;

 


 

 

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'

 


 

 

see full text and more ;

 

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

 


 

 

UPDATED DATA ON 2ND CWD STRAIN

 

Wednesday, September 08, 2010

 

CWD PRION CONGRESS SEPTEMBER 8-11 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

 

*** FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2013 UPDATE

 


 

 

 

 

 

 

TSS
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