Page 814 - Clinical Small Animal Internal Medicine

782 Section 8 Neurologic Disease

infectious agents have been incriminated and include are occasionally obtained in dogs with chronic CDV
VetBooks.ir viruses (distemper, rabies, parvovirus, parainfluenza, encephalomyelitis. Identification of neutralizing CDV
antibodies in serum is of questionable value in previ-
herpes, feline leukemia, feline immunodeficiency virus),
bacteria, rickettsia (Ehrlichia, Rocky Mountain spotted
bodies in CSF can be complicated if CSF is contaminated
fever), protozoal (Toxoplasma, Neospora), fungi (blasto- ously vaccinated dogs, and demonstration of CDV anti-
mycosis, histoplasmosis, cryptococcosis, aspergillosis, with peripheral blood. Several PCR techniques have
coccidioidomycosis), and spirochetes (Lyme disease, been described for the detection of CDV in various tis-
leptospirosis). Adding to this list, a number of parasites sues and body fluids, some of which are now commer-
have been reported to affect the brain during aberrant cially available, and these can be applied to CSF; this is
migration (Toxocara, heartworm, Cuterebra larvae) and probably the most specific and sensitive test for the
the incidence of these depends mainly on geographic antemortem diagnosis of CDV encephalomyelitis
location. CSF and infectious titers or DNA testing regardless of the clinical form of disease present.
performed on serum or CSF are the most reliable ante- The chronic form of the disease is typically slowly
mortem diagnostic tests for identifying infectious CNS progressive, although clinical signs may be well tolerated
diseases. for long durations. Therapy is mainly supportive and
symptomatic. Overall, prognosis is poor although the
Canine Distemper Virus Encephalomyelitis disease is not fatal in all dogs and some may recover.
Canine distemper virus (CDV) is a paramyxovirus that
commonly infects the CNS of dogs and other carnivores. Feline Infectious Peritonitis (FIP)
Unvaccinated and vaccinated dogs are at risk for this Two biotypes of feline coronavirus (FCoV) exist: feline
disease, and although the prevalence of infection seems infectious peritonitis virus (FIPV) that causes FIP, and
to be decreasing in some countries, sporadic outbreaks feline enteric coronavirus (FECV) that induces mild
have been reported in several countries, particularly enteritis from which cats typically recover. FIPV has
where vaccination coverage is incomplete. Systemic been shown to arise within individual patients from a
signs of disease such as respiratory and gastrointestinal spontaneous mutation of existing FECV infection. FIP
involvement are reported to precede the neurologic signs is a clinical disease that arises due to infection of mac-
by 2–3 weeks. However, many dogs have no previous rophages by FIPV, which subsequently results in the
history of disease prior to the onset of neurologic signs. immune‐mediated formation of pyogranulomatous
Many dogs probably develop transient CNS infections lesions with an affinity for serosal, pleural, uveal,
without concurrent clinical signs. Lesions may be found meningeal, and ependymal membranes (surface‐related
in gray (polioencephalomyelopathy, PEM) and/or white disease).
matter (leukoencephalomyelopathy, LEM). Since the The neurologic clinical variant of FIP is the most com-
lesions are predominantly demyelinating in nature, it has mon infectious cause of meningoencephalomyelitis in
been proposed as a model for the study of multiple scle- the cat, as well as being the most prevalent spinal cord
rosis. PEM is more frequently seen in immature dogs disease of cats. Although the effusive form is about four
while a combination of PEM and LEM is more common times more common than the noneffusive form, neuro-
in mature animals. logic involvement is more common with the noneffusive
Infected dogs can present with a variety of neurologic (or “dry”) form of the disease and develops in cats with
signs that tend to be progressive. Clinical signs in dogs humoral immunity, but with partial cell‐mediated
with chronic CDV encephalomyelitis may have a chronic immunity (immunity sufficient to induce granuloma-
insidious or waxing and waning course, and are often not tous inflammatory reaction around virus present in
associated with systemic signs of CDV. The classic syn- macrophages, but not quite adequate to eliminate the
drome of distemper myoclonus (repetitive and continual infection). The pathogenesis involves FIP virus inducing
myoclonic jerks that affect the whole body or just one a pyogranulomatous and immune complex‐mediated
body part with a characteristic 1 Hz frequency) can be vasculitis involving the meninges, ependymal lining,
pathognomonic. periventricular brain tissue, and choroid plexus of the
The diagnosis of CDV can be difficult. CSF analysis is CNS. As a result, clinical signs most commonly arise as
often the most helpful diagnostic test. However, an a result of hydrocephalus secondary to obstruction of
inflammatory response is often lacking in the acute the ventricular pathways.
stage of the disease, with mononuclear pleocytosis Cats with FIP are typically young (<3 years of age),
more often observed in the chronic stage. pure‐bred, from multiple cat households and the disease
Immunofluorescent staining of conjunctival tissues, is more common in sexually intact males. The main
urine sediment, tracheal wash or CSF leukocytes for route of infection with FCoV is oronasal from contact with
CDV antigen is variably successful, but positive results infected feces. Asymptomatic carriers are not common.