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American crows (Corvus brachyrhynchos) and potential spreading of CWD through feces of digested infectious carcases

Posted Nov 01 2009 10:00pm
Could Crows Play a Role in Spreading CWD

was presented by Dr. Kurt VerCauteren, NWRC, WS-APHIS- USDA. From the first observations (40 years ago) of CWD in mule deer (Odocoileus hemionus) and Rocky Mountain elk (Cervus elaphus nelsoni) in Northern Colorado, the disease has been identified in an increasing geographic area. Mechanisms for the spread of CWD are incompletely understood. Birds have been identified as potential vectors for a number of diseases, where infected material is ingested and the disease agent is later shed in new areas after flying substantial distances. We hypothesized that avian scavengers have the potential to disseminate 200 prions associated with transmissible spongiform encephalopathies (TSEs), like CWD, by a similar process. As prions are resistant to destruction, it is reasonable that infectious material could pass through the digestive tract of scavenging birds. Our objective was to determine if TSE-positive brain material from mice (i.e., mouse-adapted scrapie) could pass through the digestive tract of American crows (Corvus

American crows (Corvus brachyrhynchos) and potential spreading of CWD through feces of digested infectious carcasses

brachyrhynchos) and still be infectious to mice. Our experimental design included treatment groups of mice inoculated intraperitoneally with: 1) normal mouse brain, 2) infected mouse brain, 3) gamma-irradiated feces from crows gavaged with normal mouse brain, and 4) gamma-irradiated feces from crows gavaged with infected mouse brain. Our preliminary results indicate feces from each of 20 crows gavaged with infected mouse brain were infectious for mice (proportion of crows=1.00, 95% CI: 0.83-1.00) and average longevity for mice was 213 days (95% CI: 210-216). Longevity of mice inoculated with infected mouse brain was slightly less (198 days, 95% CI: 188-207). Most mice inoculated with normal brain, or feces from crows gavaged with normal brain, were still alive 1 year post inoculation with no evident clinical signs of TSE disease in any control mice. Our results demonstrate that a common, migratory North American scavenger, the American crow, can pass infective prions in feces and, therefore, could play a role in the spatial dissemination of prion disease....

Chronic wasting disease (CWD), first identified in Wisconsin in 2002, is an infectious transmissible spongiform encephalopathy (TSE) afflicting members of the taxonomic family Cervidae, and causes neurodegeneration and ultimately death. As a proxy for mortality or harvest of CWD-infected deer, we placed disease-free white-tailed deer (Odocoileus virginianus) carcasses and gut piles in the environment and monitored scavenger activity and carcass removal from September to April in 2003 through 2005. We recorded 14 species of scavenging mammals (six species of visitors), and eight species of scavenging birds (14 species of visitors). Prominent scavengers included American crows (Corvus brachyrhynchos), raccoons (Procyon lotor), and Virginia opossums (Didelphis virginiana). We found no evidence that deer directly consumed conspecific remains, but they visited carcasses and gut piles. Domestic dogs (Canis familiaris), cats (Felis sylvestris catus), and cows (Bos spp.) either scavenged or visited carcass sites, which may have increased exposure risk of CWD to humans and human food supplies. Deer carcasses persisted for a median of 18 to 101 days, while gut piles lasted for a median of three days. Habitat did not influence carcass consumption/decomposition, but mammalian and avian scavenger activity and higher temperatures (proxy for microbial and arthropod activity) were associated with greater rates of carcass removal. Our findings suggest that infected deer carcasses can function as an environmental source of CWD prions to mammalian and avian scavengers. We discuss the implications of these results in a broader context of CWD spread, and suggest preemptive management strategies for mitigating impacts of CWD contaminated deer remains in the environment....


http://www.usaha.org/meetings/2008/2008_USAHA_Proceedings.pdf





Greetings,

THIS potential vector of transmission is very disturbing. I don't know what the flight paths, and or travel of either species of birds, or if there are others, there are many birds that eat meat and or are scavengers. But the disturbing part is the amount of territory they can cover and spread their feces. PLUS, this goes back to what the late Dr. Gibbs told me, and what the late Harash Narang book showed, Dr. Gibbs stating that the TSE agent could spread through the digestinal track, and survive, and could still have the potential to spread, and Harash Narang's book 'The Link', page 135, where a farmers around Kent have chickens with BSE. MAFF was aware of this and was suppose to do some studies? BUT, regardless whether or not these birds become clinical and die, the fact that the above studies showed that the TSE agent survived the digestinal tract, and went on to further infect mice via feces, is very disturbing, and further enhances transmission studies must be done asap. PLUS, this should be the final straw for chicken litter being fed back to cattle and other food producing animals for humans and animals. AND not to forget the Red Necked Ostrich and BSE? ...TSS

January 2, 2000

U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well

Our feeding and rendering practices have mirrored that of the U.K. for years, some say it was worse. Everything from the downer cattle, to those scrapie infected sheep, to any roadkill, including the city police horse and the circus elephant went to the renders for feed and other products for consumption. Then they only implemented a partial feed ban on Aug. 4, 1997, but pigs, chickens, dogs, and cats, and humans were exempt from that ban. So they can still feed pigs and chickens those potentially TSE tainted by-products, and then they can still feed those by-products back to the cows. I believe it was Dr. Joe Gibbs, that said, the prion protein, can survive the digestinal track. So you have stopped nothing.


http://www.bmj.com/cgi/eletters/320/7226/8/b#EL1




http://chronic-wasting-disease.blogspot.com/2009/07/deer-carcass-decomposition-and.html




http://madcowspontaneousnot.blogspot.com/




http://stanford.wellsphere.com/cjd-article/deer-carcass-decomposition-and-potential-scavenger-exposure-to-chronic-wasting-disease/744792





ALSO; in Harash Narang's book THE LINK (i believe he went to work for NIH on TSEs, not sure if he is still there) there is a part about BSE IN HENS (page 135), that a farmer in kent in Nov. 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 experiencing 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 (Fig. 15). 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, similar to those seen in BSE, became common sparked off by the slightest provocation. Three other farmers from the UK are known to have reported having hens with similar symptoms...

with this agent, i would not rule out anything or any species...TSS


From: TSS
Subject: TRANSMISSION STUDIES OF DOMESTIC FOWL AND OSTRICH......
Date: May 9, 2002 at 7:36 am PST

######## Bovine Spongiform Encephalopathy #########

Greetings List Members,

just reading over a few old documents, i am pondering a few things out loud here, hope some find them interesting...TSS

snip...

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...

snip...

94/01.19/7.1


http://www.bse.org.uk/files/yb/1994/01/19007001.pdf




also,

TRANSLATION

F437/91

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

* The Red-Neck Ostrich 'THE AUTOPSY' & TSEs

THE AUTOPSY

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'

######## BSE #########

TRANSLATION

F437/91

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

H A Schoon, Doris Brunckhorst and J Pohienz Institute of Pathology, Veterinary University of Hannover

Introduction

Since the first appearance of BSE in Great Britain in l985 {review in TRUYEN & KAADEN, l990), research into the incidence, diagnosis, differential diagnosis and epidemiology of spongiform encephalopathies in humans and animals has been a focus of medical and public interest. In view of the growing number of reports of "new" spontaneously or experimentally susceptible species (cats: WYATT et al, l990; pigs: DAWSON et al, 1990), and of the associated questions with regard to the causal agent and in particular its transmissibility, it seems essential that agnopathogenetic individual cases should also be described. We therefore report below the preliminary findings of morphological examinations of three red-necked ostriches in 1986, 1988 and 1989, taking account of differential diagnostic factors.

History/subjects

The three ostriches (Flock A: Ostrich 1, female, adult, 150 kg; Flock B: Ostrich 2, female, adult, 80 kg; Ostrich 3: male, juvenile, 60 kg) came from two zoos in North West Germany and were euthenised because of their hopeless prognosis. Preliminary reports indicated that all three birds had presented protracted central nervous symptoms with ataxia, disturbance of balance and discoordinated feeding behaviour. Ostrich 2 had also exhibited pronounced lameness of the left lower limbs and the juvenile bird was suffering from perosis. The birds were fed on vegetable material, supplemented by commercial compound poultry feed and ''raw meat'', some of which was ''obtained from local small emergency slaughterers''. Comparable clinical pictures with fatal outcome in individual birds had occurred in both flocks: in a male bird at the same time (Flock A) and in several ostriches over recent years (Flock B).

Methods

Autopsy was followed in all three cases by histopathological examination of the following tissues: heart (several locations including coronary arteries and aorta), right and left pulmonary lobes, liver, kidneys, limb musculature, peripheral nerves (brachial plexus, sciatic nerve, in each case both left and right) and brain (left and right cerebral hemispheres, two samples each from the cranial/caudal third, two sagittal sections of the cerebellum, two cross-sections of the brain stem at the level of the optical lobes, four cross-sections from the medulla oblongata). The tissue material was fixed in formalin and embedded in Paraplast by the conventional method and the sections were evaluated using the following staining techniques and histochemical reactions: all organs: haematoxylin eosin staining; brain: PAS reaction (McManus), Ziehl/Neelsen staining (mod. Pearse), iron method (Lillie) for detection of neuromelanin, Turnbull's reaction (Bancroft & Stevens), alkaline Congo red method (Puchtler) (of SCOON & SCHINKEL, 1986), myelin sheath staining (Spielmeyer) (ROMEIS, 1968). In addition, unstained sections were examined by fluorescence microscopy (to detect autofluorescing lipofuscin granula) and the following lipid stains were applied to cryostat sections of liver, and of heart and skeletal musculature: Sudan III, Sudan black, oil red.

Findings

Ostrich 1

Brain: whilst only middle grade oedematisation of the neuropil was noted in the cerebral and cerebellar region, major changes were detected in the brain stem and medulla oblongata (Figures 1-3): in addition to pronounced vacuolation of the grey matter, optically vacant, ovoid to spherical vacuoles of differing sizes occurred bilaterally symmetrically in numerous neurons of the brain centres nucleus ruber, vestibular nucleus and reticular formation, in certain cases compressing the Nissl substance into a narrow fringe. In addition, fine granular pigments were found in the perikaryon of the neurons (with and without vacuoles), which showed a golden brown coloration in the haematoxylin eosin specimen, gave positive reactions to both PAS and Ziehl-Neelsen and also exhibited a yellowish-green spontaneous autofluorescence. Lillie staining to detect neuromelanin gave a negative result. The pigments thus exhibited the characteristics of lipofuscin (SCHOON & SCHINKEL, 1986). Ferruginous pigments and histochemically detectable amyloids were absent. Mild gliosis, isolated necrotic neurons and neuronophagia were observed only in the cranial locations of the brain stem.

Other findinqs: The ostrich exhibited marked adiposity and multiple pressure sores of both lower limbs. Moderate steatosis was found in the heart and skeletal musculature and in the liver. Multifocal arteriosclerotic plaques were also noted in the coronary and limb arteries.

Ostrich 2

Brain: Histopathological changes in the brain of this ostrich were limited to the medulla oblongata and were qualitatively consistent with those found in Ostrich 1, although confined, bilaterally symmetrically, to small localised areas and affecting only individual neurons. Gliosis reaction was almost entirely absent.

Other findinqs: The carcase was moderately well nourished and exhibited multifocal dermal and muscular necroses on both lower limbs in conjunction with lateral chronically destructive tarsitis and coxitis. In the internal organs, parenchymatous degeneration of the liver and kidneys and multifocal arteriosclerotic plaques in the coronary arteries were noted.

Ostrich 3

Brain: Whilst no histopathological changes were found in the cerebrum and cerebellum of this ostrich, a high grade spongious dispersion of the neuropil existed in all locations examined in the brain stem and medulla oblongata (status spongiosus, Figure 4). Individual neurons contained optically vacant vacuoles of varying size, whilst numerous nerve cells exhibited clear signs of nuclear degeneration, in particular in the form of nuclear pyknosis. Low grade gliosis was also noted in all locations.

Other findinqs: The left lower limb of this bird exhibited defective positioning of the tarsal joint resulting from axial distortion of the long bones with applanation of the lateral [Rollkamm - word not found] and resultant instability of the tendons and inward turning of the tarsus.

Discussion

Although ostriches are widely kept in zoos, there are virtually no detailed descriptions of central nervous disorders with associated locomotor disfunction in this species. Neurological symptoms have been reported in connection with an outbreak of Newcastle Disease (KLOPPEL, 1969) and bacterial meningitis has been described (GRZIMEK, 1953), whilst other, sporadic cases have remained etiologically unexplained (ZUKOWSKY, 1959; LANDOWSKI, 1965). Disfunctions of the locomotor system of extracerebral origin occur predominantly in juvenile ostriches, emus and rheas in connection with muscular disease, perosis and trauma (FROIKA, 1982, 1983; MIHALIK & SRANK, 1982; SCHRODER & SEIDEL0 1989). One of the ostriches we examined was suffering from perosis, another from unilateral tarsitis and coxitis. All three, however, exhibited neuropathological findings consisting of a gradual, bilaterally symmetrical, spongiform encephalopathy of varying degree in the brain stem and medulla oblongata. No descriptions of such findings in this species appear in any of the literature we have been able to obtain.

These histopathologically confirmed brain changes are not consistent either with those caused by the classic viral infections in domesticated and wild birds or with those described by GRATZL & KOHLER (1957) and CHEVILLE (1966) as typical of Vitamin E deficiency-related encephalopathy in chicks. Instead, at the light microscopy level, both in qualitative terms and in the pattern of distribution in the central nervous system, there is a high degree of coincidence with findings which occur in transmissible spongiform encephalopathies in mammals (scrapie, BSE, transmissible mink encephalopathy, chronic wasting disease of captive mule deer and elk) (HADLOW, 1961; BURGER & HARTSOUGH, 1965; HARTSOUGH & BURGER, 1965; WILLIAMS & YOUNG, 1980; WELLS et al, 1987, 1989).

The sporadic occurrence of vacuoles in individual neurons of the nucleus ruber in cattle was interpreted species-specifically as an artefact by FRANKHAUSER et al (1972). We are unable to judge whether a similar conclusion is also appropriate in the case of the ostrich, since our experience is based on only a small number of neuropathologically investigated cases. However, examination of the brains of twelve other ostriches which came to autopsy after death from extracerebral causes did not reveal any such findings. FRANKENHAUSER et al (1972) also emphasise that none were observed by them either in small ruminants or in the horse or the dog.

It is not possible at this time to determine whether and to what extent our neuropathological findings in an omnivorous bird, the ostrich, are etiopathogenetically consistent with those of the spongiform encephatopathies of mammals. There are no indications whatever in the relevant literature of even a hypothetical susceptibility in birds, although it must be said by way of qualification that clinical manifestations would be most unlikely in short-lived farm poultry, given the long incubation period. Moreover, Germany was officially free of scrapie and BSE at the time the condition appeared in the ostriches. The question of possible contamination of carcase meal is discussed in the work of TRUYEN & KAADEN (1990).

Conclusive diagnosis, especially in these cases, and in spite of the certainty ascribed by WELLS et al (1989) to histopathological diagnosis in cattle, also requires electron microscopic detection of so-called scrapie-associated fibrils (SCOTT et al, 1987; HOPE et al, 1988) and attempts, by inoculation of suspect brain material, to transmit the disease to the mouse (TRUYEN & KAADEN, 1990). Both of these procedures are normally carried out using fresh material, whereas we now have only tissue fixed in formalin and embedded in Paraplast.

Etiological consideration must also be given retrospectively to unidentified toxic influences, unknown species-specific deficiency diseases and unexplained predisposing metabolic conditions.

The etiologically unexplained neuropathological findings reported here, together with the multitude of unanswered questions in this connection, underline the need for further, systematic, standardised studies in this species, based on a larger sample of birds.

Summary and Literature

[Not translated]

Figures

Figure 1: Spongiform encephalopathy with oedematisation and vacuolation of the neuropil and "ballooning" degeneration of virtually all neurons in this area of the brain - brain stem. (H,-E.-Frgb., magnification x 120)

Figure 2: Detail of Figure 1. In 'addition to oedematisation of the neuropil, numerous, optically vacant vacuoles in the neurons, with partial displacement of the Nissl substance - brain stem. (H.-E.-Frgb., magnification x 480)

Figure 3: Medulla oblongara with high grade spongiform dissociation of the neuropil. (H.-E.-Frgb., magnification x 300)

Figure 4: Medulla oblongata. Status spongiosus with neuron degeneration. (H.-E.-Frgb., magnification x 300).

-----------------------------------------------------

even the late great Dr. Gibbs once told me personally that even if the Chicken did not contract a TSE, IF the chicken had been fed the TSE tainted feed and then slaughtered, the agent survives the digestinal tract to pass on to other species through feed...

TSS

Date: Tue, 27 May 2003 08:07:58 -0500 Reply-To: Bovine Spongiform Encephalopathy Sender: Bovine Spongiform Encephalopathy From: "Terry S. Singeltary Sr." Subject: FDA BSE Update - Pet Food from Canadian Manufacturer & MAD DOG DATA

######## Bovine Spongiform Encephalopathy #########

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


http://www.bseinquiry.gov.uk/files/sc/Seac10/tab06.pdf





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


http://ec.europa.eu/food/fs/sc/ssc/out295_en.pdf





FDA asked to ban poultry litter from feed AGAIN 17 Aug 2009
Posted Aug 17 2009 11:07pm


http://stanford.wellsphere.com/cjd-article/fda-asked-to-ban-poultry-litter-from-feed-again-17-aug-2009/772893





Tuesday, October 27, 2009

Petition to Declare Poultry Litter as a Food Additive and to Ban Its Use as Cattle Feed August 12, 2009 UNITED STATES

DEPARTMENT OF HEALTH AND HUMAN SERVICES FOOD AND DRUG ADMINISTRATION


http://madcowfeed.blogspot.com/2009/10/petition-to-declare-poultry-litter-as.html





Sunday, May 17, 2009

WHO WILL WATCH THE CHILDREN ? SCHOOL LUNCH PROGRAM FROM DOWNER CATTLE UPDATE

http://downercattle.blogspot.com/2009/05/who-will-watch-children.html





http://downercattle.blogspot.com/





Sunday, September 6, 2009

MAD COW USA 1997 SECRET VIDEO


http://madcowusda.blogspot.com/2009/09/mad-cow-usa-1997-video.html





U.S.A. HIDING MAD COW DISEASE VICTIMS AS SPORADIC CJD ? see video at bottom


http://creutzfeldt-jakob-disease.blogspot.com/2009/07/usa-hiding-mad-cow-disease-victims-as.html





DAMNING TESTIMONY FROM STANLEY PRUSINER THE NOBEL PEACE PRIZE WINNER ON PRIONS SPEAKING ABOUT ANN VENEMAN see video


http://maddeer.org/video/embedded/prusinerclip.html





Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
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