Meningitis

Severe necrotizing vasculitis of the central nervous system resulting in signs of meningitis inflammation has been recognized in Bernese Mountain Dogs. Young dogs 3 to 12 months of age are most commonly affected. There is no apparent sex predilection.

Affected dogs experience a sudden onset of the classic signs of meningitis, including fever, cervical rigidity, spinal pain, and stilted gait. The signs may be episodic initially, resolving without treatment in mildly affected dogs with pain-free intervals lasting days to months. Most dogs, however, are severely affected and require treatment. Progression to signs of parenchymal nervous system involvement, including paralysis, blindness, and seizures, has occurred in some dogs in which therapy was not instituted. Most affected dogs have peripheral neutrophilia. Cerebrospinal fluid analysis reveals moderately increased protein and an extreme neutrophilic pleocytosis of 50 to 2000 cells/ul. No infectious agents have been isolated.

Immunosuppressive treatment with prednisone at 2 to 4 mg/kg/day results in rapid resolution of clinical signs in most dogs. After 2 weeks the corticosteroid dosage should be decreased slowly until the dog is maintained on 1 mg/kg of prednisone every other day. Long term therapy is necessary to maintain remission of clinical signs. Resolution of the disorder after 4 to 6 months of treatment without the need for continuing medication is common. Some dogs, however, have had relapses when the corticosteroid dose was reduced, requiring prolonged high-dose corticosteroid treatment or the addition of a more potent immunosuppressive drug. Although experience is limited, administration of azathioprine (imuran) at a dose of 2 mg/kg every 24 hr in these cases has met with

some success. Approximately 10% of dogs require lifelong treatment (Presthus, personal communication, 1990). In spite of aggressive therapy, a few dogs have been euthanized because of recurrences and progressive parenchymal involvement.

At necropsy an extensive suppurative leptomeningitis is found in association with severe arthritis and fibrinoid necrosis of vessel walls. Tissue ischemia and hemorrage account for the neurologic signs. The etiology of the central nervous system vasculitis in these dogs has not been determined. No underlying concurrent disease process has been uncovered, and there is little evidence for a systemic or generalized immune disorder.

This aseptic suppurative meningitis syndrome is common in the Bernese Mountain Dog breed, with an estimated 1 to 2% of the breed affected (Presthus, personal communication, 1990). Many affected dogs have been closely related, and in most affected litters, approximately one quarter of the pups will be affected. Test mating of affected dogs has produced affected puppies. A syndrome with very similar clinical and pathologic features has been described as a rere disorder in young German shorthaired

pointers (Meric, 1988).

Source: Current Veterinary Therapy XI, Small Animal Practice; Kirk R, Bonagura J. (editors)

Philadelphia, PA: WB Saunders; 1992: pg 1008

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Articles Published in the October 1994 THE ALPENHORN

Bernese Mountain Dog Aseptic Meningitis

Canine meningitis and meningoencephalomyelitis may occur as a result of infection with bacterial, viral, protozoal, mycotic, rickettsial, or parasitic pathogens. Syndromes of canine meningitis that have no identifiable infectious etiology and are thought to have an immunological basis have also been recognized. These syndromes are being diagnosed with increasing frequency, and include granulomatous meningoencephalomyelitis (GME) and a steroid-responsive aseptic suppurative meningitis of young dogs. In addition to these clinical syndromes, a group of breed-specific meningitis disorders has been recognized. Bernese Mountain Dogs are one of these breeds. This aseptic suppurative meningitis syndrome is common in the Bernese Mountain Dog breed, an estimated 1 to 2 percent of the breed being affected (Presthus, 1990) Many affected dogs have been closely related, and in most affected litters approximately one quarter of the pups will be affected. Test mating of affected dogs has produced affected puppies.

BMD Aseptic Meningitis-Severe necrotizing vasculitis of the central nervous system resulting in signs of meningeal inflammation has been recognized in Bernese Mountain Dogs. Young dogs 3 to 12 months old are most commonly affected and there is no apparent sex predilection. Affected dogs experience sudden onset of the classic signs of meningitis, including fever, cervical rigidity, spinal pain, and stilted gait. Signs may be episodic initially, resolving without treatment in mildly affected dogs with pain-free intervals lasting days to months. Most dogs, however, are severely affected and require treatment. Progression to signs of parenchymal nervous system involvement, including paralysis, blindness, and seizures has occured in some dogs in which therapy was not instituted. Most affected dogs have peripheral neutrophilia. Cerebrospinal fluid analysis reveals moderately increased protein and an extreme neutrophilic pleocytosis of 50 to 2000 cells/ul. No infectious agents have been isolated. The cluster of cases in related young BMDs indicated the need for careful observation and data collection in order to address the issue of possible genetic susceptibility. Necrotizing vasculitis involving the meninges has been reported in other breeds of dogs and may be part of a more widespread vasculitis sometimes associated with immune complex deposition in the walls of the involved vessels.

Immunosuppressive treatment with prednisone at 2 to 4 mg/kg/day results in rapid resolution of clinical signs in most dogs. After 2 weeks, the corticosteroid dosage should be decreased slowly until the dog is maintained on 1 mg/kg of prednisone every other day. Long-term therapy is necessary to maintain remission of clinical signs. Resolution of the disorder after 4 to 6 months of treatment without the need for continuing medication is common. Some dogs have had relapses when the corticosteroid dose was reduced,

requiring prolonged high-dose corticosteroid treatment or the addition of a more potent immunosuppressive drug. Although experience is limited, administration of azathioprine (Imuran) at a dosage of 2 mg/kg every 24 hours in these cases has met with some success. Approximately 10 percent of dogs require lifelong treatment (Presthus, 1990).

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In July 1986 Meric, Child, and Higgins reported on three littermate BMDs with clinical and clinicopathological findings consistent with aseptic suppurative meningitis. The illness begin acutely with fever, pain along the spine, and flaccid paralysis of one or more limbs, variable in severity. A complete blood count showed marked elevation of the white blood count, chiefly neutrophils and monocytes. The serum alkaline phosphatase, SGOT, and cholesterol levels were increased. The cerebrospinal fluid showed increased white blood cells, mostly neutrophils. No infectuous organisms were found on direct examination or culture of cerebrospinal fluid, and blood cultures were negative. Course of illness not affected by antibiotic treatment, but there was dramatic response to corticosteroids. One of the dogs had residual abnormal neurological findings while on corticosteroids, one showed complete resolution of clinical abnormalities but relapsed on withdrawal of corticosteroids, and one remained in remission after corticosteroid withdrawal.
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Presthus reported on 11 closely related BMDs with a similar illness. 3 were examined by the author and histories of the remaining were available to the author for analysis. The 3 examined dogs ranged from 8 months to 23 months. All presented with fever, stiff gait, and cervical pain. No neurological abnormalities were found, but all three had peripheral blood leukocytosis and neutrophilia; two of the 3 had cerebrospinal fluid neutrophilia. One of the 3 dogs had 3 episodes of the condition over a period of one year. This group of affected dogs showed rapid response to corticosteroids; 2 of the 3

achieved prolonged remission off corticosteroids (one also had an ovariohysterectomy). The remaining 8 BMDs, 3 to 13 months, all had stiff gait and fever; 7 of the 8 had cervical pain. Laboratory findings and course were similar to those found in the examined group. It appears 2 of the 3 dogs reported by Meric et al. had a disease more severe than that in the dogs reported by Presthus in that frank paralysis was noted. The overall clinical picture supports the hypothesis that all 14 reported dogs had the same

disease. An autoimmune etiology is suspected but to date unsupported by autoimmune-associated findings.

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Breeders and owners should be aware of a disease effecting Bernese Mountain Dogs. Definitely hereditary so dogs affected should not be used for breeding. Recovery rate is good in most cases. Canine meningitis and meningoencephalomyelitis may occur as a result of infection with bacterial, viral, protozoal, mycotic, rickettsial, or parasitic pathogens. Syndromes of canine meningitis that have no identifiable infectious etiology & are thought to have an immunologic basis have also been recognized. These syndromes being diagnosed with increasing frequency, and include granulomatous meningoencephalomyelitis (GME) and a steroid-responsive aseptic suppurative meningitis of young dogs. In addition to these clinical syndromes, a group of breed specific meningitis disorders has been recognized-Beagles, Bernese Mountain Dogs, Pugs.

BERNESE MOUNTAIN DOG ASEPTIC MENINGITIS

Severe necrotizing vasculitis of the central nervous system resulting in signs of meningeal inflammation has been recognized in Berners. Young dogs 3 to 12 months old most commonly affected. No apparent sex predilection. Affected dogs experience sudden onset of classic signs of meningitis, including fever, cervical rigidity, spinal pain, and stilted gait. Signs may be episodic initially, resolving without treatment in mildly

affected dogs with pain-free intervals lasting days to months. Most dogs, however, are severly affected and require treatment. Progression to signs of parenchymal nervous system involvment, including paralysis, blindness, and seizures, has occured in some dogs in which therapy was not instituted. Most affected dogs have peripheral neutrophilia. Cerebrospinal fluid analysis reveals moderately increased protein and an

extreme neutrophilic pleocytosis of 50 to 2000 cells/ul. No infectious agents have been isolated. Immunosuppressive treatment with prednisone at 2 to 4 mg/kg/day results in rapid resolution of clinical signs in most dogs. After 2 weeks, corticosteroid dosage should be decreased slowly until dog maintained on 1 mg/kg of prednisone every

other day. Long-term therapy necessary to maintain remission of clinical signs. Resolution of disorder after 4 to 6 months of treatment without need for continuing medication is common. Some dogs have had relapses when corticosteroid dose reduced, requiring prolonged high-dose corticosteroid treatment or the addition of a more potent immunosuppressive drug. Although experience is limited, administration

of azathioprine (Imuran) at a dosage of 2mg/kg every 24 hours in these cases has met with some success. Approximately ten percent of dogs require lifelong treatment (Presthus, 1990). This aseptic suppurative meningitis syndrome is common in the Bernese Mountain Dog breed, an estimated one to two percent of the breed being affected. (Presthus, 1990) Many affected dogs have been closely related and in most affected litters approximately one-quarter of the pups will be affected. Test mating of affected dogs has produced affected puppies.

Susan M. Meric, DVM

University of Saskatchewan

Dept. of Veterinary on Internal Medicine

Saskatoon, Saskatchewan