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LEARNING OBJECTIVES

1. What is the etiology of rabies and distemper?2.

What is the clinical signs and pathogenesis of rabies and distemper?

3. What are the pathological changes of rabies and distemper?4. How to diagnose rabies and distemper?5. How to treat and control rabies and distemper?

1. Etiology of Rabies and DistemperA. Rabies

Rabies is a disease caused by rabies virus. Rabies virus belongs to

genus Lyssavirus which is a member of the family Rhabdoviridae. The

characteristics of this virus are rod in shape, has envelope, and possess a

linear, non-segmented RNA genome with negative polarity. This virus

present in saliva animal that infected with rabies virus (Quinn, 2002).

B. DistemperCanine distemper is a highly contagious acute febrile disease of dogs

that caused by canine distemper virus. This virus belongs to genus

Morbillivirus which is a member of family Paramyxoviridae. The

characteristics of this virus are pleomorphic, has mucous membrane, has

envelope and contain a single molecule of negative-sense, single-stranded

RNA (MacLahlan & Dubovi, 2011).

2. Clinical Signs and Pathogenesis of Rabies and DistemperA. Rabies

a. Clinical SignThe clinical course in domestic carnivores, which usually lasts

for days or for a few weeks, may encompass prodromal, furious

(excitative) and dumb (paralytic) phases. In certain rabid animals,

some of these phases may not be observed.

- Prodromal PhaseIn the prodromal phase, affected animals are often confused

and disorientated. Wild animals may lose their natural fear of

humans.

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- Furious PhaseThe furious phase is charaterized by an increase in

aggressiveness and hyperexcitability, and there is a tendency to bite

at inanimate objects and at other animals. Affected animals may

roam over long distances. The furious form is observed more often

in cats than in dogs. Foxes rarely exhibit this form of the disease.

- Dumb PhaseIn dumb phase, muscle weakness, difficulty in swallowing,

profuse salivation and dropping of the jaw are the usual features.

These clinical signs may be mistaken for those caused by a foreign

body in the mouth or throat. The term hydrophobia, a synonym for

rabies in humans, relates to the inability to swallow water because

of pharyngeal paralysis.

(Quinn et al, 2002)

b. PathogenesisThe transmission of this virus is usually by bite or an accidental

break in the skin, though it can be introduced by inhalation and through

the mucous membranes of eyes and mouth. The primary replication

occurs in the muscle fibre at the site of inoculation, the virus then

aggregates around the proprio-receptor nerve endings of their

acetylcholine receptors, and migrates along the exoplasm, the

centripetal migration takes place. When the virus enters central

nervous system, usually the spinal cord, its migration to brain is rapid.

Although the ultimate target of the virus is CNS, it also infects salivary

glands by centrifugal movement along the exoplasmic route. And thusthe virus is secreted in saliva (Sharma & Adlakha, 2009).

B. Distempera. Clinical Sign

The incubation period is usually about one week but may

extend to four weeks or more when nervous signs appear without prior

evidence of infection. The pyrexic response to infection is biphasic

although the initial elevation of temperature may not be noticed.

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During the second period of pyrexia, oculonasal discharge, pharyngitis

and tonsillar enlargement become evident. Coughing, vomiting and

diarrhoea are often consequences of secondary infections. A skin rash

and pustules may be present on the abdomen. Some affected dogs have

hyperkeratosis of the nose and footpads, referred to as 'hardpad'.

Common neurological signs include paresis, myoclonus and

epileptiform seizures (Quinn et al, 2002).

b. PathogenesisThis virus has an especially strong tropism for epithelium and

lymphoid tissues. The lungs are also central to the pathogenesis of

CDV infection. Initial replication occurs in macrophages in the

bronchial lymph nodes and tonsils immediately following respiratory

infection. The virus then spread to other lymphoid tissues (lymph

nodes, spleen, thymus, and bone marrow) where further replication

occurs prior to viremia that disseminates CDV to virtually all organs of

the body, including the CNS and eyes (Hirsh et al, 2004).

3. Pathological Changes of Rabies and DistemperA. Rabies

a. MacroscopicNo characteristic gross lesions except some wooden or non

food items present in the stomach of dog. In other animals, lesions of

bite on skin must be present (Chauhan, 2010).

b. MicroscopicThe brains of animals with rabies exhibit variable inflammation

and often only modest histological evidence of neuronal injury. Thepresence of eosinophilic intracytoplasmic inclusions (Negri bodies) in

neurons is characteristic and diagnostic, these being especially

common in neurons in the hippocampus and Purkinje cells in the

cerebellum. Ganglioneuritis occurs in some animals, and involves the

Gasserian ganglion in particular (MacLahlan & Dubovi, 2011).

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B. Distempera. Macroscopic

The macroscopic changes of this disease are catarrhal and

purulent exudate in upper respiratory tract, lobular pneumonia,

congestion and consolidation of lungs, hyperkeratinisation of foot pad

skin, presence of pustules on lower abdomen (Chauhan, 2010).

b. MicroscopicThe microscopic changes of this disease are bronchopneumonia

characterized by infiltration of neutrophils in alveoli around

bronchioles, presence of intracytoplasmic and intra nuclear

eosinophilic inclusions in epithelial cells of upper respiratory passage,

bronchioles, urinary bladder, stomach, skin and in circulating

neutrophils(Chauhan, 2010).

4. Diagnosis Methods of Rabies and DistemperA. Rabies

Early clinical diagnosis of rabies is very critical since there is

probability of human exposure. The clinical signs are helpful but are not

confirmatory. If the animal dies within 2-3 days after showing symptoms

or if the animal dies in the quarantine or the animal has the symptoms,

tissues like brain preserved in glycerine saline should be sent to laboratory

for diagnosis. The laboratory diagnosis includes the following:

a. Search for Negri bodies in sections or impression smears of thecerebellum stained by seller's or Giemsa stain.

b. If Negri bodies are not found, weaned mice are inoculatedintracerebrally. The mice show symptoms within 6-15 days but thesymptoms may be delayed upto 21 days and the mice usually die

within 1-2 days after that. The mouse brains are examined for presence

of Negri bodies from dead as well as from those which survive 5-6

days of inoculation.

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c. The fluorescent antibody test is the preferred method of diagnosis andis about 100% correct. Smears from hippocampus medulla and

cerebrellum are used.

(Sharma & Adlakha, 2009)

B. DistemperThis disease can be diagnose by examining the symptoms and lesions

and several laboratory tests (Chauhan, 2010)

a. Laboratory TestLaboratory diagnosis is necessary to exclude other diseases

with similar clinical manifestations. Virus isolation can be achieved by

co-cultivation of lymphocytes from suspect animals. After initial

isolation, the virus can then be adapted to grow in primary dog lung

cells or conventional cell lines, including MadinDarby canine kidney

or Vero. Immuno-histochemical or fluorescent antibody staining

methods are useful for demonstrating the presence of viral antigen in

impression smears of the conjunctiva and skin biopsies (antemortem)

or sections of lung, intestine, stomach, kidney, brain, and bladder tissue

collected at necropsy. RT-PCR tests can be done on conjunctival

swabs, blood mononuclear cells, any tissue sample that includes

epithelium, and urine. The serological status of dogs can be assessed

with virus neutralization assays, ELISA, or indirect fluorescent

antibody tests (MacLahlan & Dubovi, 2011).

5. Treatment and ControlA. Rabies

Inactivated, live-attenuated and recombinant vaccines have beendeveloped for the parenteral immunization of animals and humans against

rabies. Original vaccines that incorporate nervous tissue containing

inactivated virus cause immunologically mediated nervous disease in some

individuals, and original live-attenuated vaccines that are propagated in

embryonated duck eggs also induce allergic reactions in some immunized

individuals. A considerable number of cell culture derived live-attenuated

and inactivated vaccines are now available and, more recently, highly

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effective recombinant vaccines that express the rabies virus glycoprotein

have been developed. Successful oral vaccination against rabies has been

achieved using either live-attenuated or recombinant vaccines that are

delivered in baits to target wildlife species. Recombinant vaccinia viruses

that express the rabies virus glycoprotein have proven effective in

immunizing foxes and raccoons, but a variety of other virus vectors now

have been developed. The use of vaccine-containing baits has been used to

control and even eliminate rabies from foxes in much of Europe, and

regionally among coyotes, raccoons, and foxes in North America. The

great merit of this approach over animal population reduction is that the

eco niche remains occupied, in this case by an immune population.

B. DistemperFor treatment, hyperimmune serum or immune globulin can be used

prophylactically immediately after exposure. Antibiotic therapy generally

has a beneficial effect by lessening the effect of secondary opportunistic

bacterial infections. Control of canine distemper virus infection is based on

adequate diagnosis, quarantine, sanitation, and vaccination. The virus is

very fragile, and susceptible to standard disinfectants. Thorough

disinfection of premises, however, can be very challenging. Successful

immunization of pups with attenuated canine distemper virus vaccines

depends on the absence of interfering maternal antibody.

(MacLahlan & Dubovi, 2011)

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Reference

Chauhan, R. 2010. Text Book of Veterinary Pathology. ibdc publisher. India

Hirsh, D. MacLahlan, N. Walker, R. 2004. Veterinary Microbiology 2

nd

Edition.Blackwell Publishing. Iowa

MacLahlan, J. Dubovi, E. 2011. FennerVeterinary Virology 4th

Edition. Elsevier.

United Kingdom

Quinn, P. Markey, B. Carter, M. Donnelly, W. Leonard, F. 2002. Veterinary

Microbiology and Microbial Disease. Blackwell Science. USA

Sharma, S. Adlakha, S. 2009. Textbook of Veterinary Virology. International

Book Distributing Co. India