Description: Beagles and occasionally other breeds of dogs can develop a syndrome of recurrent intermittent pain and fever that persist for 3-7 days in young animals. The pain can be intense and diffuse, or can be more localized in areas like the shoulder, neck, hip or along the back.

There can be associated neurologic deficits. Nonregenerative anemia, hypoalbuminemia, and a mature neutrophilia are common. Histology shows periarteritis in the heart and meninges, and subdural and extradural spinal cord hemorrhage. This may be an autoimmune disease. Some cases undergo spontaneous regression. There is often a neutrophilic pleocytosis of the CSF, combined with an inability to identify an infectious agent in the spinal fluid. Treatment with corticosteroids is effective in some dogs, but long-term treatment may be needed to maintain remission; treatment was discussed by Scott-Moncrieff.

Signs: Abnormal anal, perineal, tail reflexes; Abnormal hindlimb reflexes; Abnormal proprioceptive positioning; Anorexia; Back pain; Diarrhea; Dullness; Dyspnea; Fever; Forelimb lameness; Forelimb pain; Forelimb spasms; Generalized lameness or stiffness; Generalized weakness; Head, face, neck spasms; Hemiparesis;, Hindlimb atrophy; Hindlimb hypoesthesia; Hindlimb lameness; Hindlimb pain; Hyperesthesia; Increased respiratory rate; Kyphosis, Melena or occult blood in feces, stools; Pain on external abdominal pressure; Pain, chest, thorax, ribs, sternum; Pain, neck, cervical, throat; Pain, scrotum; Paraparesis; Pelvic or hip pain; Reluctant to move; Skin edema; Skin pain; Stiffness or extended neck; Tail weakness; Tail, anal hypoesthesia; Tetraparesis; Trembling; Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift; Urinary incontinence; Weight loss.

References:

SNYDER PW ET AL. Pathologic features of naturally occurring juvenile polyarteritis in beagle dogs. Vet Pathol 1996; 32:337-345

SCOTT-MONCRIEFF JCR ET AL. Systemic necrotizing vasculitis in nine young beagles. JAVMA 1992; 201:1553-1558.

Source: Cornell University College of Veterinary Medicine

More Information About Necrotizing Vasculitis...

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 been describe include fibrinoid generation, intimal and medial necrosis, inflammatory cell 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 also be contributing factors. Subsequent meningeal fibrosis around nerve roots and spinal cord also may result in axonal degeneration. Pathologic changes are seen throughout the spinal cord. Similar lesions also have been found in the cardiac arteries of several dogs. The origin of this disease has not been determined.

The occurrence of this disease in three Bernese Mountain dog litter mates suggests a genetic predisposition to the disease. This disease has also 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.

Clinical Findings: 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.

Diagnosis: 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 meningitis) on the basis of clinical and CSF findings.

Treatment: 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 other day dosage). It has been suggested that corticosteroid therapy should be continued until clinical signs have resolved and results of CSF analysis are normal. If signs recur, the dose should again be increased. Antibiotic therapy does not result in improvement of clinical signs. As this condition is often indistinguishable from septic meningitis, treatment with a broad-spectrum antibiotic that reaches satisfactory concentrations in the CSF is suggested initially in animals in which the diagnosis is uncertain.

Source: Textbook of Veterinary Medicine

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