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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. Emerging disease: Infections that newly appear in a population, or have existed but are increasing in incidence or geographic range.

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)

Chronic wasting disease (CWD)


CWD : It is a progressive, fatal, degenerative and transmissible spongiform encephalopathy characterized by vacuoles in the brain. Host range:

Mule deer,

white-tailed deer

elk

Geographical distribution
CWD Other emerging diseases

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. CWD is approximately present in 5% mule deer, 2% in white-tailed deer, and <1% in elk.

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

PrPC

PrPSc

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. Prions can remain infective in the soil for several years.

In 2011 researchers had discovered prions spreading through airborne transmission on aerosol particles.

Pathogenesis

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

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

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.

Yellow and gelatinous bone marrow.

Aspiration pneumonia.

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).

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

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 (1011) 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. Preventing the spread of chronic wasting disease beyond historically infected areas. Enforcing illegal feeding regulations and transport laws restricting the movement of deer, and elk from infected areas. Continuing research in conjunction with other agencies and states to further knowledge to manage affected deer and elk. There is still a large need for research on the disease as many questions go unanswered.

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

References
Anderson CA, P Bosque, CM Filley, DB Arciniegas, B K KleinschmidtDemasters, W J Pape,and KL Tyler.(2007). Colorado surveillance program for chronic wasting disease transmission to humans: lessons from 2 highly suspicious but negative cases. Arch Neurol.;64:439-41. Angers RC, SR Browning, TS Seward, CJ Sigurdson, MW Miller, EA Hoover, and GC Telling.(2006) Prions in skeletal muscles of deer with chronic wasting disease. Science.;311:1117. Baeten LA, BE Powers, JE Jewell, TR Spraker, and MW Miller.(2007) A natural case of chronic wasting disease in a freeranging moose (Alces alces shirasi). J Wildl Dis.;43:309-14. Glenn Millhauser http://www1.ucsc.edu/currents/01-02/06- 03/prion.html A. Aguzzi, M Heikenwalder, and G. Miele (2004) Progress and problems in the biology, diagnostics, and therapeutics of prion diseases. Clin Invest.;114:153-160. Hueston W and Bryant CM. (2005). Transmissible spongiform encephalopathies. J Food Science; 70 (5):R77-R87.

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

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