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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
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