is an inflammation of the blood vessels. The vessels become damaged,
and small holes in the vessels allow for tiny amounts of blood to leak
from the vessel. This is often seen as pinpoint sized red spots
(petechiae) on the gums
or the whites of the eyes. Vasculitis may be caused by a variety of
infectious diseases or by immune mediated disease where the body's own
immune system begins to attack the body instead of attacking germs.
Origin and Development:
Necrotizing vasculitis of the
extradural and intradural spinal meningeal arteries has been reported
to occur in young dogs of several breeds. Pathologic changes that have
include fibrinoid generation, intimal and medial necrosis, inflammatory
infiltration, periadventitial accumulation of inflammatory cells,
meningeal fibrosis, and hyalinization and mineralization of meningeal
arterial walls. Neurologic deficits may result from the rupture of
structurally weakened blood vessels causing extensive meningeal
hemorrhage, and compression of the
spinal cord. Thrombosis of vessels and infarction of the spinal cord my
be contributing factors. Subsequent meningeal fibrosis around nerve
and spinal cord also may result in axonal degeneration. Pathologic
are seen throughout the spinal cord. Similar lesions also have been
in the cardiac arteries of several dogs. The origin of this disease has
The occurrence of this disease in three Bernese Mountain dog litter
mates suggests a genetic predisposition to the disease. This disease
been recognized in an inbred colony of beagle dogs. Immune-mediated
mechanisms are suspected in the pathogenesis of the disease.
Lymphocytic thyroiditis and renal amyloidosis, which are also thought
to have an immunologic basis, were found in several dogs. Infectious
agents have not been isolated, although a viral-induced immune-mediated
reaction is a possible cause. Antinuclear antibody was not present in
three dogs tested. Vasculitis of spinal arteries has also been reported
as part of polysystemic necrotizing vasculitis in an older dog.
Affected dogs are four to 12 months of age. Clinical signs include
fever, anorexia, cervical rigidity, hunched posture, apparent spinal
pain, shifting lameness, apparent pain on opening the mouth, and in
some animals, neurologic deficits, including paraparesis, tetraparesis,
and paraplegia. Clinical
finds usually are indicative of meningitis and, in some animals, of
multifocal or diffuse myelopathy.
Affected animals may have peripheral mature neutrophilic leukocytosis.
Cerebrospinal fluid (CSF) generally has a marked pleocytosis (may be
greater than 10,000 WBC/microliter) with predominantly mature nontoxic
netrophils present. Bacterial or fungal organisms have not been
identified in white blood cells of CSF. Cerebrospinal fluid protein
concentration is also elevated. Blood and CSF bacterial (aerobic and
anaerobic) cultures are negative.
This disease cannot be distinguished from other meningitides (including
viral, bacterial, or fungal meningitis, GME or aseptic suppurative
on the basis of clinical and CSF findings.
Treatment with corticosteroids usually results in rapid improvement in
clinical signs. However, relapses commonly occur when treatment is
discontinued. Neurologic deficits may persist despite treatment in dogs
with severe neurologic abnormalities. Treatment for longer than six
months may result in permanent resolution of clinical signs. A dose of
cortiosteroids sufficient to produce a a remission of clinical signs
(1-2 mg/lb Prednisone) is given initially, followed by maintenance oral
therapy at a dose tapered slowly to be the
lowest dose possible that controls clinical signs (preferably every
day dosage). It has been suggested that corticosteroid therapy should
continued until clinical signs have resolved and results of CSF
are normal. If signs recur, the dose should again be increased.
therapy does not result in improvement of clinical signs. As this
is often indistinguishable from septic meningitis, treatment with a
antibiotic that reaches satisfactory concentrations in the CSF is
initially in animals in which the diagnosis is uncertain.
Source: Textbook of Veterinary Medicine
The above information is simply
informational. It's intent is not to replace the advice of a
veterinarian nor to assist you
in making a diagnosis of your pet. Please consult with your own
veterinarian for confirmation of any diagnosis. Your pets life may
depend on it.