Livestock Health, Management and Production › High Impact Diseases › Contagious diseases ›
Rabies
Rabies
Author: Prof Darryn Knobel
Adapted from: Swanepoel, R. (2004). Rabies. In Infectious diseases of livestock, 2nd edition (J.A.W.
Coetzer & R.C. Tustin, eds). Oxford University Press, Cape Town, pp. 1123-1182.
DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS
Clinical signs and pathology
Rabies should be suspected in cases of abnormal behaviour in animals, particularly when the affected
animal comes from an area where the disease is known to be active, or when there is a history that
suggests possible exposure to infection. Currently there are no reliable ante mortem tests for rabies
infection. Confirmation of a diagnosis therefore relies on demonstrating the presence of the virus or
antigen in the brain tissue post mortem. Animals with clinical signs suggestive of rabies, or displaying
any progressive neurological disease in a rabies-endemic area, should be euthanized for
examination. In certain circumstances where a dog has bitten humans or another animal/s, authorized
persons (state veterinary officials) may confine the animal and keep it under observation for 10-14
days (the maximum time period measured between the presence of virus in salivary glands and the
eventual onset of clinical signs). If the animal remains alive and healthy at the end of this period of
observation, it can be concluded that the probability that the animal was infectious at the time that it
inflicted the bite was very slight. Animals displaying signs of illness consistent with rabies during the
period of observation must however be euthanized and brain samples submitted for laboratory
examination. In cases where they are suspected of exposing humans to infection, wild animals, feral
dogs, or stray dogs whose owner cannot be traced, should be euthanized for examination.
Animals should be killed in such a manner as to avoid damaging the cranium. Protective clothing to
be worn while collecting specimens should include gloves, an impermeable apron and a face mask or
visor, and personnel should be immunized. The hippocampus is commonly used for the diagnosis of
rabies, but the distribution of virus antigen varies and it should be routine to take tissue samples from
a variety of sites in the brain. Brain specimens to be submitted for laboratory examination include 10–
20 mm3 blocks of cerebrum, cerebellum, hippocampus, medulla, thalamus and brain stem preserved
in duplicate in 50 per cent glycerol-saline solution for virological examination and in ten per cent
buffered formalin for histopathological examination. Where small animals are involved, half of the
brain (sectioned sagittaly) may simply be placed in the glycerol-saline preservative and the other half
in the formalin. If preservative is not available, specimens may be stored in empty containers on ice
and submitted to the laboratory without delay. Adequate samples for making an accurate diagnosis
may also be collected in wide-bore, plastic drinking straws by a method which obviates the need to
skin the head and saw the cranium open: the occipital foramen is exposed with a knife and the
sample is collected by inserting the straw through the foramen and pushing it with a slight twisting
motion towards one of the eyes. The end of the straw containing the plug of brain tissue is cut off into
the container with preservative. Occasionally, virus antigen or infectivity may be demonstrated in
salivary glands and not brain, and it is recommended that samples of submaxillary salivary gland
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Livestock Health, Management and Production › High Impact Diseases › Contagious diseases ›
Rabies
should also be submitted in glycerol-saline and formalin preservatives. Specimen containers are
sealed tightly and packed in sufficient absorbent material to soak up the entire liquid contents of the
container.
Laboratory confirmation
Confirmation of a clinical diagnosis of rabies cannot be made by gross pathology or histology. The
fluorescent antibody test (FAT) is the standard diagnostic test used to confirm a diagnosis. The FAT
demonstrates the presence of rabies virus antigen in brain smears by means of immunofluorescence
using antirabies fluorescein conjugate. The FAT takes only one to three hours to perform, and is of
comparable sensitivity to mouse inoculation, with a concordance of 95 to 99 per cent between the two
methods when the immunofluorescence test is performed by experienced investigators. The use of
the FAT is limited by the costs of acquiring and maintaining a fluorescence microscope. A direct rapid
immunohistochemical test (DRIT), employing a short formalin fixation of brain impression smears and
requiring no specialized equipment, was shown to be 100% sensitive and specific when compared to
the FAT. Supplementary tests include viral isolation in cell culture, mouse inoculation, polymerase
chain reaction, and immunohistological tests. Histopathology on formalin-impregnated brain sections
is not always informative for rabies infection but may help to exclude conditions in the differential
diagnosis of rabies.
Differential diagnosis
Diseases which may be or have been, confused with rabies in southern Africa include distemper,
infectious canine hepatitis, ehrlichiosis, cerebral babesiosis, toxoplasmosis, cerebral cysticerosis
(caused by Taenia solium), tetanus, diminazine toxicity, pesticide (such as metaldehyde) and
strychnine poisonings in dogs; cerebral theileriosis and babesiosis, thrombotic meningoencephalitis
(caused by Haemophilus somnus) sporadic bovine encephalomyelitis (caused by Chlamydophila
pecorum), botulism, lead, urea, chlorinated hydrocarbon and organophosphate poisonings, and
cerebrocortical necrosis (caused by thiamine deficiency) in cattle; coenurus cerebralis (Taenia
multiceps coenuriasis) in sheep; heartwater and a variety of plant poisonings (such as those caused
by Homeria and Morea spp., Matricaria nigellifolia, Cestrum spp., Cynanchum spp., Dipcadi glauca)
and the mycotoxicosis, diplodiosis, caused by the fungus Diplodia maydis in domestic ruminants;
encephalomyelitis caused by equid herpesvirus 1 infection, tetanus, leukoencephalomalacia (caused
by fumonisin B1 produced by the fungus Fusarium moniliforme) and poisoning by Senecio spp. in
horses; and pesticide poisonings in all animals.
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