Chronic Wasting Disease Emerging threat to wildlife
Presented by : Anand Prabhakar Sarode En. No.: V/05/0149 Course No.: VPP – 691 Course teacher: Dr. V. P. Pathak.

Department of Vet. Pathology, PGIVAS, Akola

Outline
Introduction Distribution History

Symptoms
Lesions

Diagnosis
Treatment
Etiology

Prevention
Pathogenesis

Conclusions

Introduction Wildlife: The term wildlife refers to all the plants and animals on the planet that are not domesticated by humans. . or have existed but are increasing in incidence or geographic range. Emerging disease: Infections that newly appear in a population.

“Emerging” Wildlife Diseases Anthrax (bison) Adenovirus (Long-tailed ducks) Avian vacuolar myelinopathy Botulism Coccidiomycosis (sea otters) Chytridiom ycosis (amphibians) Chronic Wasting Disease Ehrlichiosis Epizootic Hemorrhagic Disease (deer) Harmful algal blooms Hantavirus Lead toxicity Leyogonimus polyoon infection (Coots) Lyme disease Monkey-pox in Prairie dogs Morbillivirus in cetaceans Mycoplasmosis in finches Myxozoan parasite (ducks) Newcastle disease (cormorants) Plague (black-footed ferrets) Salmonellosis in redpolls West Nile Virus Toxoplasmosis (sea otters) Tularemia in Prairie dogs White-Nose syndrome (bats) .

Host range: . degenerative and transmissible spongiform encephalopathy characterized by vacuoles in the brain. Mule deer. white-tailed deer elk .Chronic wasting disease (CWD) CWD : It is a progressive. fatal.

Geographical distribution CWD Other emerging diseases .

and <1% in elk.History First case -1990: Northeastern Colorado and Southeastern Wyoming. where the disease is now endemic CWD has been diagnosed in wild deer and elk in at least 14 states in the United States and two Canadian provinces. 2% in white-tailed deer. . CWD is approximately present in 5% mule deer.

PrPC PrPSc .Etiology Prion: Infectious protein particle without a nucleic acid genome.

Transmission Direct (animal-to-animal contact) Indirect (soil or other surface to animal) Prions are likely shed through the saliva and feaces. and urine of deer. In 2011 researchers had discovered prions spreading through airborne transmission on aerosol particles. . Prions can remain infective in the soil for several years.

Pathogenesis .

.

. .There is conformational or shape difference between PrPc and PrPsc.

Clinical Features: Adults: 17 months to15 years Most 3-5 years Sex: males. max: unknown . females No strict seasonality Clinical duration: months to year Incubation period: min: 17 months.

Symptoms of CWD Nervous symptoms Drooping of head and ears Rough dull coat Excessive salivation Severe emaciation & dehydration .

Gross Lesion Dehydration Total loss of body fat. Muscular atrophy in terminal cases. .

Aspiration pneumonia.Yellow and gelatinous bone marrow. Adrenal cortical hypertrophy .

HISTOPATHOLOGY Diencephalon. Olfactory cortex Nuclei of the medulla oblongata Lesions are basically bilaterally symmetrical and characteristically affect some areas of the brain to a greater extent than other areas. .

Lesions are detectable first in the dorsal motor nucleus of the vagus nerve (DMNV). .

characterized by microcavitation of grey matter and/or white matter.Typically there are changes of spongiform encephalopathy. .

Intraneuronal vacuolation and neuronal degeneration .

Amyloid plaques are readily detected by immunohistochemistry .

Immunohistochemistry has detected PrPCWD in the - lymph nodes pituitary - Adrenal medulla The islets of Langerhans in the pancreas. .

Diagnosis Research is being conducted to develop live-animal diagnostic tests for CWD. Postmortem examination Testing. .

.Immunohistochemistry to test brain The parasympathetic vagal nucleus in the dorsal portion of the medulla oblongata at the obex is the most important site.

Obex .

.Retropharyngeal lymph node.

Multifocal granular immunoreactivity with antiprion MAb in cells of the germinal center. .

.Surround Optical Fiber Immunoassay (SOFIA) Use to detection of PrPSc even when initially present at only one part in a hundred thousand million (10−11) in brain tissue.

Differential diagnosis Hemorrhagic disease (epizootic hemorrhagic disease and bluetongue) Meningeal worm (Parelaphostrongylus tenuis) Locoweed intoxication in elk. .

Treatment No treatment is available. . Affected animals that develop pneumonia may respond temporarily to antibiotic treatment.

How to combat CWD? Quarantining or killing of every affected animal and burning of all carcasses. . There is still a large need for research on the disease as many questions go unanswered. and elk from infected areas. Continuing research in conjunction with other agencies and states to further knowledge to manage affected deer and elk. Preventing the spread of chronic wasting disease beyond historically infected areas. Enforcing illegal feeding regulations and transport laws restricting the movement of deer.

Indian wildlife is likely to suffer from this infection. There is urgent need of improving diagnostic and screening facilities in wildlife territory. It is spreading over a wide geographical range since from emergence.Conclusions CWD is an emerging disease in wild life which is causing heavy mortality in cervidae family. .

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.Contd… McKenzie D. . K. Genava Williams ES. and J M Aiken (2007). production and stockpiling of bacteriological (Biological) and toxin weapons and on their distribution. 67th North American Wildlife and Natural Resources Conference. Pradhan H. Meeting of experts of the state parties to the convention on the prohibition of the development. M. R J Chappell. Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil Particles. (2002). C J Johnson.W. Williams and ET Thorne. PLoS Pathog. 3 (7): e93. J A Pedersen. (2004).

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