- Hello Jeff - I haven't had time to read the entire article
but it does look like Elk did have changes in both gray and white brain
matter due to infection of prion disease.
-
- It also shows that the US military HAS been experimenting
with captive deer and elk regarding prion disease. If you remember I had
been trying to find the neurological experiment conducted by US Army cofinanced
by Burroughs Welcome back in the 60s at the same time CWD emerged.
-
- I am getting close to proving my theory that CWD escaped
that Colorado wildlife station in the mid-sixties.
-
- Patty
-
- http://www.afip.org/vetpath/WSC/wsc99/99wsc27.htm
-
- Results AFIP Wednesday Slide Conference - No. 27
- 26 April 2000
- Conference Moderator:
- MAJ Jo Lynne Raymond
- Department of Veterinary Pathology
- Armed Forces Institute of Pathology
- Washington, DC 20306-6000
- Return to WSC Case Menu
- Case I - 99/1240 (AFIP 2694720)
-
- Signalment: Three to four-year-old ox.
-
- History: Six out of 65 intensively housed cattle, 1-4
years old, kept in different pens, developed severe nervous symptoms characterised
by staggering, circling, blindness, head-pressing and collapse within 2-3
days of receiving a home-mixed salt lick consisting of 50% coarse feed-grade
sodium chloride and 50% calcium diphosphate.
-
- The outbreak occurred during mid-winter, when the feeding
of salt lick was resumed after an interval of about 2 months during which
time lick constituents were unavailable on the farm. A concentrated production
ration containing 1% salt was fed during the same period. As far as could
be established, there was also restricted access to drinking water in some
of the pens. Three of the most severely affected animals were euthanized
by intravenous injections of barbiturate for necropsy, histopathological
and toxicological examinations.
-
- The remaining 3 animals were successfully treated by
parenteral administration of diuretics, corticosteroids, B-complex vitamins,
as well as by dosing regulated quantities of water and supportive oral
remedies via stomach tube. In the latter animals the nervous symptoms and
blindness persisted for about 2 weeks after which complete recovery occurred.
-
- Gross Pathology: There was marked congestion and edema
of the brain and meninges, as well as petechiae and ecchymoses within the
gray- and white matter of the cerebrum, cerebellum and brain stem, and
a moderate to severe congestion of the abomasal mucosa.
-
- Laboratory Results: Sodium levels were determined in
the brain of 3 cases by atomic absorption photospectrometry. In 2 cases,
the levels were exceedingly high, viz. 3060 ppm and 3885 ppm, and in the
third slightly high, 1839 ppm. According to Osweiler, levels of >2000
ppm is supportive of sodium toxicosis.
-
- Determinations for organophosphate and organochlorine
pesticides and lead, as well as bacteriological examinations on the brain
of one of the animals were negative.
-
- Contributor's Diagnosis and Comments: HE stained transverse
sections (3 different sections, marked A, B and C) of the dorsolateral
cerebrum, approximately at the level of the midbrain are presented.
-
- Morphologic Diagnosis: Poliomalacia, multifocal, acute,
moderate, with vasculitis, fibrinoid, multifocal, moderate and leucocytosis,
(neutrophilic and monocytic); microhaemorrhages, scattered, multifocal,
mild.
-
- Histopathological changes are present within the meninges
and gray and white matter and comprised varying degrees of vasculitis and
edema with accompanying neuronal and glial cell changes. The vascular changes
included: endothelial cell swelling, medial fibrinoid change and accumulation
of a homogenous eosinophilic material within lumens of capillaries, venules
and arterioles, mononuclear leucocyte (neutrophil and occasionally eosinophil)
infiltrations into the walls of some vessels (more pronounced in sections
marked 99/1240 C), or extravasations into the extravascular spaces.
-
- Marked edema with dilatation of perivascular spaces,
vacuolation of gray and white matter, as well as eosinophilic degeneration
and necrosis of neurons, and glial cell cytoplasmic swelling are evident
within the gray matter of the cerebral and cerebellar cortices. Degenerative
and necrotic changes of neurons comprise swelling, chromatolysis, increased
eosinophilia, fading of nuclear membranes and nuclear pyknosis. Perivascular
and neuropil hemorrhages are occasionally present in both the gray and
white matter.
-
- The clinical signs and histopathological changes of the
poliomalacia described here, appear to be similar to those of cerebrocortical
necrosis (CCN) associated with thiamine deficiency in cattle and sheep,
as well as lead poisoning in cattle. However, the extremely high levels
of sodium detected in the brains of two of three of the animals that were
euthanized together with a history of salt engorgement as well as possible
water deprivation, favors a diagnosis of water deprivation/sodium ion toxicosis.
-
- In contrast to pigs where eosinophilic meningoencephalitis
is common and together with laminar neuronal changes is regarded to be
pathognomonic for salt poisoning in this species, eosinophils are only
rarely encountered in cases of salt poisoning in cattle and sheep.
-
- The pathogenesis of the edema underlying the poliomalacia
is attributed to passive diffusion of sodium into the brain substance from
the blood and cerebrospinal fluid when the sodium levels in these compartments
rise. This is counteracted by an energy dependent process (anaerobic glycolysis),
which is inhibited by high levels of sodium entering the brain, resulting
in trapping of sodium ions within the brain. When water intake and renal
excretion of sodium reduces the blood sodium levels to normal, an osmotic
gradient results which leads to cerebral edema.
-
- Sodium chloride poisoning has been classified as acute/direct
salt poisoning where there has been ingestion of excessive salt in feed
or drinking water or as delayed/indirect when there has been a restriction
in water intake with or without ingestion of excessive salt. These cases
probably resemble indirect salt poisoning due to the delay in onset of
clinical symptoms (a few days) and gastrointestinal symptoms, although
there was no definite evidence of water restriction in all the cases affected.
-
- Hypernatremia with resultant brain edema and neurological
disease has also been induced in calves by injudicious use of sodium bicarbonate
and oral electrolyte solutions during treatment of diarrhoea with dehydration
and acidosis.
-
- AFIP Diagnosis: Cerebral cortex: Neuronal necrosis, laminar
and segmental, with fibrinoid vascular necrosis and edema, breed not specified,
bovine.
-
- Conference Note: The contributor has provided an excellent
discussion of this case.
-
- Contributor: Pathology Section PO Box 12502 Onderstepoort
0110 South Africa.
-
- References:
- 1. Angelos JM, Smith BP, George LW: Treatment of hypernatremia
in an acidotic neonatal calf. J Amer Vet Med Assoc 214:1364-1367, 1999
- 2. Butler R: Salt poisoning/water deprivation in sheep?
Control & Therapy series: Post Graduate Foundation in Veterinary Science
of the University of Sydney, Australia: Mailing 207:1078, 1999
- 3. Jubb KVF, Huxtable CR: The Nervous System. In: Pathology
of Domestic Animals, eds Jubb KVF, Kennedy PC, Palmer N, vol 1, 4th ed,
pp. 340-347. Academic Press, San Diego, 1993
- 4. Osweiler GD, Carr TF, Sanderson TL: Water deprivation-sodium
ion toxicosis in cattle. J Vet Diag Invest 7:583-585, 1995
- 5. Osweiler GD: Toxicoses resulting from sodium-water
imbalance. In: Toxicology, pp. 355-357. Williams & Wilkins, Philadelphia,
USA, 1996
- 6. Penrith M-L: A case of salt poisoning in grower pigs.
Newsletter of the Veterinary Laboratory Diagnosticians Group S Afri Vet
Assoc 3:2-3, 1995
- 7. Scarratt WK, Collins TJ, Sponenberg DP: Water deprivation-sodium
chloride intoxication in a group of feeder lambs. J Amer Vet Med Assoc
186:977-978, 1985
- 8. Summers BA, Cummings JF and De Lahunta A: Salt poisoning.
In: Veterinary Neuropathology, pp. 254-255. Mosby, St Louis, MO, 1995
- 9. Trueman KF, Clague DC: Sodium chloride poisoning in
cattle. Aust Vet J 5: 89-93, 1978
- 10. Van Leeuwen JA: Salt poisoning in beef cattle on
coastal pasture on Prince Edward Island. Can Vet J 40: 347-348, 1999
-
-
- Case II - TAMU 99-1 (AFIP 2694696)
-
- Signalment: Five-year-old, Aberdeen Angus bull
-
- History: Lesions of 3 months duration on all four distal
limbs
-
- Gross Pathology: Gray, proliferative, symmetric, moist
lesions were observed in circumferential bands extending 15-cm proximally
from the coronary band on both front feet. Nodular, dry alopecic lesions
were seen on the fetlocks of both rear limbs and the distal scrotal skin.
Serpentiginous, dry alopecic lesions were on the sternal skin.
-
- Contributor's Diagnosis and Comments: Chronic proliferative
dermatitis/pododermatitis with epithelial and mesenchymal proliferation,
epidermal hydropic degeneration, focal vasculitis and intraepithelial inclusion
bodies, hyperkeratosis, bacterial colonies
-
- Etiology: uncharacterized bovine parapoxvirus
-
- This case represents a good example of an unpublished
condition! There are numerous parapox virions in the lesions (parapox are
different in appearance from other poxviruses on EM), and the lesions are
typical of poxvirus diseases. Of course, cutaneous lesions are not usually
described in cattle with parapoxvirus. The recognized parapoxviruses include:
contagious ecthyma of sheep, bovine papular stomatitis, parapoxvirus of
red deer and pseudocowpoxvirus.
-
- At necropsy, the serpentiginous lesions of the sternal
skin made us suggest parapoxvirus in the gross report (honest!). Some of
the gross lesions looked like papillomas, and the moist lesions of the
front limb were reminiscent of the lesions in cattle attributed variably
to spirochetes (none seen) or papillomavirus. Vasculitis can be seen with
lumpy skin disease and bovine papular stomatitis and is seen in this case.
In order to find out if this is a new parapox disease, samples have to
be typed, but the lab that does this is in New Zealand, and we could not
legally send the material into that country.
-
- A couple of interesting features of ovine parapoxvirus
infection are that the virus is resistant to both alpha and gamma interferon,
and is believed capable of modulating the Th-1 immune response of the infected
host through an IL-10-like gene product of the virus. The virus also makes
an endothelial growth factor. Parapoxviruses are suggested to occur in
musk ox, gray seals, and the Japanese serow (these have not been confirmed
in THE lab). This group of viruses is responsible for a nuisance category
(due to the mild signs) of zoonoses called "farmyard pox". This
type of human pox is described to occur also in handlers of reindeer and
other cervids.
-
- AFIP Diagnosis: Haired skin: Dermatitis, proliferative,
chronic-active, focally extensive, severe, with hyperkeratosis, epithelial
ballooning degeneration, and eosinophilic intracytoplasmic inclusion bodies,
Aberdeen Angus bull, bovine.
-
- Conference Note: Parapoxvirus is a genus of the family
Poxviridae. Parapoxviruses are large, enveloped, highly epitheliotropic,
DNA viruses that are cocoon shaped and measures 260 x 160 nm. There are
over 100 polypeptides in the virion. The core proteins include a transcriptase
and several other enzymes. There is extensive cross-neutralization and
cross-protection between viruses belonging to the same genus, but not between
those of different genera. Even though parapoxviruses exhibit a highly
restricted host range, most can infect humans, producing generally benign
cutaneous lesions limited to the site of inoculation.
-
- By electron microscopy parapoxviruses are ovoid with
a regular spiral arrangement of "tubules" (surface rodlets) on
the outer membrane. There is no nucleocapsid conforming to either icosahedral
or helical symmetry; hence it is called a "complex" virion. An
outer membrane encloses a dumbbell-shaped (biconcave) central core and
two "lateral bodies" of unknown nature.
-
- Some sections contain an organizing thrombus in the subcutis.
-
- Contributor: Texas A&M University, Department of
Veterinary Pathobiology, College of Veterinary Medicine, Texas A&M
University, College Station, TX 77843-4467.
-
- References:
- 1. Haig DM: Poxvirus interference with the host cytokine
response. Vet Immunol & Immunopath 63(1-2):149-56, 1998
- 2. Haig DM, Mercer AA: Ovine diseases. Orf. Vet Res.
29(3-4):311-26, 1998
- 3. Murphy FA, Gibbs EBJ, Horzinek MC, Studdert MJ: Veterinary
Virology, 3rd ed., pp. 278-291. Academic Press, San Diego, CA, 1999
- 4. Robinson AJ, Mercer AA: Parapoxvirus of red deer:
Evidence for its inclusion as a new member in the Genus Parapoxvirus. Virolo
208(2):812-815, 1995
- 5. Smith KJ, Skelton HG, James WD, Lupton GP: Parapoxvirus
infections acquired after exposure to wildlife. Arch of Dermatol 127(1):79-82,
1991
-
-
- Case III - 989-4037 (AFIP 2694690)
-
- Signalment: Tissue is from a 5-year-old female mule deer
(Odocoileus hemionus).
-
- History: This mule deer was showing signs of weakness,
excessive salivation and emaciation.
-
- Gross Pathology: Gross lesions included extensive serous
atrophy of adipose tissues, mild muscular atrophy, bronchopneumonia, mild
gastric ulceration and enlarged adrenal glands.
-
- Laboratory Results: Pasteurella sp. was isolated from
the pneumonic portion of the lung. No significant growth was cultured from
the gastric ulcer.
-
- Case 27-3. This photomicrograph is of the dorsal motor
nucleus of the vagus nerve of this deer stained with a monoclonal antibody
(Mab 89/160.1.5). The positive red staining is interpreted to be scrapie-associated
prion protein or an antigenically similar protein that has been found with
chronic wasting disease of deer and elk. (Legend and image from Colorado
State University Diagnostic Lab, Ft. Collins, CO, USA and reproduced with
permission.)
-
- Contributor's Diagnosis and Comments: Spongiform encephalopathy,
severe, brain, compatible with chronic wasting disease (etiology-thought
to be a prion protein).
-
- This slide is from the obex region of the medulla oblongata
of the brain stem of a 5-year-old female mule deer. The primary histological
lesions at this level of the medulla oblongata are found within the dorsal
motor nucleus of the vagus nerve with milder lesions of the hypoglossal
nucleus, nucleus of the spinal tract of the trigeminal nerve, nucleus ambiguus
and the olivary nuclei. The histological lesions are characterized by intracytoplasmic
neuronal vacuolation, microcavitation of the neuropil and mild astrocytosis.
Many of the sections contain variably-sized areas of mineralization at
the vagal nucleus. This is a common incidental finding with no known association
with the observed vacuolar changes. This condition is confined to North
Central Colorado and Southeast Wyoming
-
- MORE INFORMATION ON THAT WEBPAGE WITH PICTURES.
-
- My guess is the bovine polio-like illness is triggered
by mad cow.
-
- Patty
- Patricia A. Doyle, PhD
- Please visit my "Emerging Diseases" message
board at: http://www.clickitnews.com/ubbthreads/postlist.php?Cat=&Board=emergingdiseases
- Zhan le Devlesa tai sastimasa
- Go with God and in Good Health
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