- Swine rabies can be transmitted to pigs by dogs infected with rabies virus. In China and parts of the USA and Brazil, transmission from dogs to pigs has been reported.
- Rabies virus causes acute lethal infection in pigs. Clinical signs in pigs may include aggressiveness, neurological signs, fever, anorexia and progressive paralysis.
- Diagnosis is usually confirmed by fluorescent antibody test on brain tissue post-mortem, though PCR and ELISA methods can also be used. Vaccination of pigs exposed to rabid animals and control of rabies in dog populations is important for prevention.
2. INTRODUCTION
All mammalian species are believed to be susceptible to
rabies virus, although some appear to require higher
infectious doses to develop clinical disease
Rare Reportable
Acute Lethal
Zoonotic
4. Twelve distinct lyssa virus species
can be distinguished within the
genus,
RABV is the most important one for
public and animal health
Lagos haven’t caused diseases or
death in humans
SPECIES
classical rabies virus (RABV),
Lagos bat virus (LBV),
Mokola virus (MOKV),
Duvenhage virus (DUVV),
European bat lyssaviruses type-1
(EBLV-1), (EBLV-2)
Australian bat lyssavirus (ABLV),
Aravan virus (ARAV),
Khujand virus (KHUV),
Irkut virus (IRKV),
West Caucasian bat virus (WCBV),
Shimoni bat virus (SHIBV).
5. Virion consists of 5 viral proteins of which two are of special interest.
The phosphorylated nucleoprotein (N) includes the antibody-binding
epitopes that contribute to the differentiation of the various virus
groups.
Glycoprotein (G) covers the virion, except at the planar end. It is the
only one of the 5 proteins that binds virus-neutralizing antibodies
Variation in its amino acid sequence appears to contribute to the
variation in pathogenicity of the different strains.
6. Classic zoonotic infection, Recognized for over 4,000 years.
Spread from animals (dogs, cats, foxes, bats, etc.) to human
Reservoirs - fox species, jackals and coyotes, raccoons, skunks and
mongooses, and bats.
EPIDEMIOLOGY
7. Attributable to a bite (any penetration of the skin by the teeth)
Secretion of the virus in the animal’s saliva promote the transmission
of the virus.
Non bite exposures eg: contamination of an open wound / a mucous
membrane via scratches/licks
8. Rabies virus propagates in two epidemiologic cycles.
urban cycle, the street virus circulates in feral and domestic dogs
and still puts humans at great risk of exposure -developing countries.
In developed world -shift from urban-sylvatic cycle, in which
distinctive rabies virus variants circulate in specific wildlife reservoirs
within discrete geographic clusters.
EPIDEMIOLOGY
9. Outbreak of swine rabies transmitted by a dog in China the main
clinical signs were aggressiveness and other neurological signs
In USA, in 10 cases of rabies transmitted by wild animals, mainly
raccoons, mongoose and skunks, clinical signs were fever, aggression,
restlessness, anorexia, head rubbing, progressive paralysis,
depression, and vocalization.
In Brazil there are several reports of identification of rabies virus in
swine but there are no reports on the epidemiology.
DISTRIBUTION
10. The incidence of rabies in swine in North America is low.
Two of 2601 rabies cases reported from 1998 through 2003 in Canada
(Canadian Food Inspection Agency 2004)
The geographic distribution of rabies is almost global,
with the exception of island nations in the South Pacific (New Zealand
and others), where rabies has never been recorded.
In Japan, the United Kingdom, Norway, and a few other countries,
rabies has been eradicated
The World Health Organization classifies a country as rabies-free if no
indigenous cases of rabies have been confirmed in any animal species
and humans during the previous 2 years
11.
12. • Swine rabies transmitted by a dog in China.
• In USA, rabies transmitted by wild animals, mainly raccoons,
mongoose and skunks.
• In Brazil there are several reports of identification of rabies virus in
swine originated from dogs and others from vampire bats.
TRANSMISSION
13. The incubation period -few days to several months.
The duration -depends on the virus strain, the site of the bite and
the amount of virus transmitted, and the age and immune status of
the bitten animal.
Rabies spread by infected saliva entering an open cut or wound, or
contacting a mucous membrane, such as those in the mouth, nasal
cavity or eyes.
Following an eclipse phase, in which virus replication occurs,
possibly in myocytes at the bite site, the virus migrates through the
axoplasm of the peripheral or cranial nerves to reach the CNS.
PATHOGENESIS
14. Once it’s in the brain it multiplies quickly, and that’s when clinical
signs appear
virus moves centrifugally into non-nervous tissues, including the
salivary glands and eyes. Virus may be shed in saliva of infected
animals prior to, at, or after onset of clinical disease (Rupprecht et al.
2002).
Once symptoms appear, rabies is always fatal.
The lag time between inoculation and neural invasion may be the
grace time during which post-exposure prophylactic treatment is
most likely to be effective (Acha and Szyfres 2003).
PATHOGENESIS
15. • nonspecific respiratory, GIT or CNS disease signs,
including initial behavioral changes may appear
• animal is agitated and aggressive, and which
progresses through seizures to coma and death
• characterized by paralysis, coma, and death
Prodromal phase
Furious phase
Dumb phase
CLINICAL SIGNS
16. Reported clinical signs include
uneasiness,
dullness
incoordination,
excitement with a tendency to root or attack,
drooling/salivation, marked thirst, anorexia,
grunts and vocalizations or squealing,
twitching of nose and rapid chewing movements
convulsions, fever, and
general paralysis proceeding into coma and death
CLINICAL SIGNS
17. Post Mortem Diagnosis
(FAT) for rabies – gold standard test
Antigen may be detected in all parts of the CNS of infected animals,
in corneal impressions, and in skin biopsies
Test is the most sensitive -impression smears from the medulla
oblongata, cerebellum, and hippocampus (Ammon’s horn), in which
the greatest antigen quantities can be expected
False-negative FAT have been reported in swine in such cases rabies
can confirmed by mouse inoculation tests
DIAGNOSIS
18. Direct immunofluorescence testing
ELISA
PCR
Negri bodies, which are eosinophilic inclusions in the cytoplasm of
nerve cells and dendrites of infected animals, are frequently absent in
rabid swine
19. • In case of exposure, unvaccinated livestock should be slaughtered
immediately:
• “If the animal is slaughtered within 7 days of being bitten, its tissues
may be eaten without risk of infection, provided that liberal portions
of exposed area are discarded” (National Association of State Public
Health Veterinarians 2004).
PREVENTION & CONTROL
20. • Temperature: Does not survive for more than 24 hours in dead
animals when temperatures reach 21°C (70°F), but is highly resistant
for extended periods at low or freezing temperatures
• pH: Sensitive to very low pH (below 3) or very high pH (greater than
11)
• Chemicals/ Disinfectants: Inactivated by sodium hypochlorite, 45–
75% ethanol, iodine preparations, quaternary ammonium
compounds, formaldehyde, phenol, ether, trypsin, β-propiolactone,
and some other detergents
• Survival: Does not survive well outside its host (in dried blood and
secretions) as it is susceptible to sunlight and desiccation. It is also
susceptible to ultraviolet radiation
RESISTANCE TO PHYSICAL &
CHEMICALACTION
21. • Mitmoonpitak et al. (2002) reported
• that, following severe rabies exposure involving deep bite wounds on
nose, shoulder, vulva, and tail from a rabid dog, 11 pigs received either
vaccine alone (inactivated, Rabisin manufactured by Rhone Merieux,
France) or vaccine with equine rabies immunoglobulin (ERIG, 40 IU/kg
bodyweight; Pasteur Merieux Connaught, France).
• All treated pigs had detectable antibodies to rabies by 14 days post
treatment, and all pigs survived for 1 year following the exposure. Thus,
post-exposure rabies treatment of valuable farm animals may be a safe
and effective alternative to immediate slaughter
22. • Rabies vaccines are defined as a standardized formulation containing
defined amounts of immunogens. These immunogens are either
inactivated (killed), live-attenuated or biotechnology-derived.
• Live-attenuated vaccines have been widely used for injection in
domestic animals. However, several of these products have been
documented to cause rabies in vaccinated animals
• The rabies virus glycoprotein biotechnology-derived vector vaccines
are not live rabies virus vaccines. They are prepared by inserting non-
infectious rabies virus nucleic acid coding for rabies virus glycoprotein
into a vector.
PROPHYLAXIS
23. • Management control and prevention
• Since it is a zoonotic infection - the affected pig – isolation .
• Beware that other pigs may be incubating the disease. Inspect them all
frequently and if any behave suspiciously separate them
• Slaughtering of affected pigs
• In regions where rabies is common, farm staff and the farm dogs should
be vaccinated.