ARTHROPOD-BORNE VIRAL
ENCEPHALITIDES
Other arthropod-borne infections of dogs and cats
eliminated by an active immune response and animals in
endemic areas may have detectable antibody titres for life.
The incubation period is short (7–14 days or less).
Clinical signs of TBE are referable to multifocal neurological involvement and include fever, gait abnormalities,
seizures, paresis and peripheral neuropathies, particularly
involving the cranial nerves. Initially, dogs with louping ill
have CNS signs of more localized cerebellar dysfunction,
with ataxia and tremor. Signs are rapidly progressive, with
the development of recumbency, tetraplegia, opisthotonus
and death in some cases. Recovery can occur but it is slow
and may be associated with residual locomotor and
cerebral abnormalities. In a Swedish study, only 8% of
seropositive dogs developed clinical signs and of these,
most recovered from the initial disease over 2–3 months.
Diagnosis
Clinical signs are not pathognomonic for either viral
infection. Clinical pathological parameters and CSF
analysis are compatible with non-suppurative meningoencephalitis. Antemortem diagnosis is most commonly
made by demonstrating rising serum antibody titres.
Serological testing is only available from specialist
laboratories. A single positive test on serum is difficult to
associate with disease due to the high exposure rates in
endemic areas. However, high titres in CSF compared to
serum are supportive for TBE. Histopathological
examination of brain tissue reveals neuronal necrosis and
perivascular lymphoid cuffing that is particularly
prominent in the spinal cord. Viral isolation or
immunohistochemistry on brain tissue provides
postmortem diagnostic confirmation.
Treatment and management
Supportive and symptomatic therapy during the acute
phase of illness is particularly important for recovery of
infected animals. No specific anti-viral chemotherapy has
been recommended. Aggressive control of tick infestation
provides the most effective prevention. In addition,
control of louping ill in sheep will decrease the risk for
working dogs.
Zoonotic potential/public health significance
Humans are accidentally infected with TBE virus through
exposure to infected tick bites in a similar manner to
companion dogs, although humans are more susceptible
to developing clinical signs. About 10–30% of infected
humans, particularly children, develop central nervous
system disease. Clinical progression is usually biphasic,
with a viraemic phase (malaise, fever, lethargy) followed
by a period of clinical remission. Clinical signs are
referable to non-suppurative meningitis, meningoencephalitis or polyradiculoneuritis. Although recovery
occurs in most cases, serious neurological or neuropsychiatric sequelae may persist for prolonged periods.
Recovery is accompanied by lifelong immunity.
Companion dogs are considered a sentinel for human
TBE virus infection.
Occasional clinical signs occur in humans infected with
louping ill virus. The clinical signs are similar to those
seen in TBE, although milder.
Both louping ill and TBE may also have alternative
methods of transmission. Outbreaks of louping ill in
abattoir workers are reported and TBE can be transmitted
through ingestion of infected milk.
West Nile virus encephalitis
West Nile fever is caused by a mosquito-transmitted
flavivirus that has been recognized in Europe and Africa
for several decades but has recently emerged in North
America. It causes neurological disease in humans, horses
and certain species of birds, and is primarily maintained
in wild bird reservoirs. The role of dogs in the
epidemiology of West Nile virus (WNV) is thought to be
minor. Wild and domesticated canids are susceptible to
natural infection, as shown by seropositivity, but clinical
disease is difficult to reproduce experimentally. However,
neurological disease associated with WNV has recently
been reported in susceptible dogs and a wolf in the USA.
Clinical signs included fever, lethargy, ataxia and
multifocal central nervous system signs. Histopathological findings were compatible with viral encephalitis
and diagnosis was confirmed by immunohistochemistry
and in situ PCR.
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