Has anybody had any dealing with this?  My young GWP is having tests at the moment for this.

Tracy

Bumped you to the top again...
I know some people on here have had dogs suffer from Meningitis but what type i don't know, lets hope they spot your post here.
Again i'll contact my friend for you as per msg on FB

Thanks Sue,

He has had a better night and temp is going down, but still in a lot of pain. Just waiting for all the test results to come back now.

Tracy

Is thsi the same as IMPA?

Your poor dog, at least mine doesn't appear to be in pain it is all so worrying isn't it

Good luck with the tests, I hope you can find a solution for your dog and that he improves

Polyarthritis, Nonerosive, Immune-Mediated

BASICS

DEFINITION
Nonerosive polyarthritis is an immune-mediated inflammatory disease of joints which does not cause erosive change. Nonerosive immune-mediated arthropathies include idiopathic polyarthritis, systemic lupus erythematosus (SLE), polyarthritis associated with chronic disease (chronic infectious, neoplastic or enteropathic disease), polyarthritis-polymyositis syndrome, polyarthritis-meningitis syndrome, polyarteritis nodosa, familial renal amyloidosis in Chinese shar pei dogs, lymphocytic-plasmacytic synovitis, villonodular synovitis, juvenile-onset polyarthritis of Akitas, and the proliferative form of feline chronic progressive polyarthritis (FCPP).

Pathophysiology
The pathogenesis involves a type III hypersensitivity reaction. Immune complexes form and become deposited within the synovial membrane. An inflammatory response and complement activation ensues leading to clinical signs of arthritis. In SLE patients, nuclear material from various cells becomes antigenic leading to formation of autoantibodies (antinuclear antibody).

Systems Affected
Musculoskeletal--diarthrodial joints

Genetics
Not known to be hereditary

Incidence/Prevalence
Idiopathic polyarthritis is the most common form of immune-mediated, nonerosive polyarthritis in dogs. The other forms are uncommon.

Geographic Distribution N/A

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SIGNALMENT

Species Dogs and cats

Breed Predilections
* Idiopathic polyarthritis affects both large and small-dog breeds, but is more common in the former. It is uncommon in cats. Breeds that appear to be overrepresented include German shepherds, Doberman pinschers, retrievers, spaniels, pointers, toy poodles, Lhasa apsos, Yorkshire terriers, and Chihuahuas.
* In contrast to rheumatoid arthritis, SLE has a tendency to affect larger-breed dogs. Breeds reported more often include collies, German shepherds, poodles, beagles, and Shetland sheepdogs.
* Doberman pinschers appear to have a high sensitivity to developing polyarthritis secondary to administration of sulfa drugs.
* Polyarthritis-meningitis syndrome has been reported in the Weimaraner, German shorthaired pointer, boxer, Bernese mountain dog, and Japanese Akita.
* Amyloidosis and synovitis are prominent features of a syndrome affecting young shar pei dogs.
* Juvenile-onset polyarthritis has been reported in akitas.

Mean Age and Range
Most dogs affected with nonerosive immune-mediated polyarthritis are young to middle-aged.

Predominant Sex
Male cats have been reported to be exclusively affected by FCPP.

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SIGNS

General Comments
Clinical signs of nonerosive and erosive forms of immune-mediated polyarthritis can be similar initially. As erosive polyarthritis becomes chronic, it is easily distinguished.

Historical Findings
* Dogs and cats affected by immune-mediated arthritis typically show an acute onset of a single or multiple limb lameness. The lameness may shift from leg to leg. No history of trauma is usually present.
* Other systemic clinical signs may also be present, including vomiting, diarrhea, anorexia, pyrexia, polyuria, polydipsia, or clinical signs associated with systemic infectious (e.g., pyometra, prostatitis, diskospodylitis) or neoplastic disease.
* These diseases are often cyclic and may appear to respond to antibiotic therapy when in actuality the disease may be spontaneously undergoing remission. Some affected animals are being treated with antibiotics (sulfur-containing antibiotics) at the time arthritis ensues.

Physical Examination Findings
* Clinical signs include stiffness of gait, lameness, reduced range of motion, crepitus, and joint swelling and pain in one or more joints.
* Lameness can vary in severity from mild, weightbearing lameness to nonweightbearing lameness.
* All diarthrodial joints can be
affected; however, most forms of nonerosive polyarthritis have a predilection for the stifle, elbow, carpus, and tarsus.

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CAUSES
* The cause of most of these diseases is unknown, but an immunologic mechanism is likely.
* Polyarthritis of chronic disease has been associated with antigenic stimulation in the presence of concurrent gastrointestinal disease, neoplasia, urinary tract infection, periodontitis, bacterial endocarditis, heartworm disease, pyometra, chronic otitis media or externa, fungal infections, and chronic Actinomyces infections.
* Polyarthritis can occur secondarily to a hypersensitivity reaction involving the deposition of drug-antibody complexes in blood vessels of the synovium. Antibiotics of the following classes have been suspected of initiating this syndrome: sulfas, cephalosporins, lincomycin, erythromycin, and penicillins.
* Feline leukemia and feline syncytium-forming viruses have been linked to cats with FCPP.

RISK FACTORS N/A

DIAGNOSIS

DIFFERENTIAL DIAGNOSIS
* Early erosive polyarthritides
* Infectious arthritis
* Joint trauma
* Polymyositis

CBC/BIOCHEMISTRY/URINALYSIS
* Complete blood count, serum chemistries, and urinalysis are usually normal.
* The hemogram may show leukocytosis, neutrophilia, and hyperfibrinogenemia.
* Hematologic abnormalities such as thrombocytopenia and hematolytic anemia are seen in only 10 to 20% of all patients with SLE.

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OTHER LABORATORY TESTS
* Either a positive LE preparation or a positive ANA test should be seen in dogs with SLE.
* Serum titers for Borrelia, Ehrlichia, and Rickettsia should be normal.
* Serologic evidence of FeSFV can be found in all affected cats with FCPP; 50% or less of cats will also have exposure to FeLV.

IMAGING
The primary radiographic change associated with nonerosive polyarthritis is joint capsular distension and occasionally enthesiophytosis in prolonged or recurrent cases.

OTHER DIAGNOSTIC PROCEDURES
* Arthrocentesis and synovial fluid analysis are essential for diagnosis. Synovial fluid typically appears cloudy with normal viscosity and has a high number of nondegenerate neutrophils (20,000-200,000 cells/ ml).
* Synovial fluid should be submitted for bacterial culture and sensitivity.
* Synovial biopsy may be helpful for diagnosis.

GROSS AND HISTOPATHOLOGIC FINDINGS
The joint capsule may appear thickened and a synovial effusion is present. Synovial hypertrophy and hyperplasia are associated with mononuclear cell infiltrate. Neutrophils are also seen in the synovial tissues due to chemotaxis.

TREATMENT

INPATIENT VERSUS OUTPATIENT
Outpatient therapy is most common.

ACTIVITY
Exercise should be limited to a level that minimizes aggravation of clinical signs.

DIET
Weight reduction will reduce the stress placed on affected joints.

CLIENT EDUCATION
A poor prognosis for cure and complete resolution should be given to owners.

SURGICAL CONSIDERATIONS N/A

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MEDICATIONS

DRUGS AND FLUIDS
* Glucocorticoids (GCC) are usually used for the initial treatment of immune-mediated nonerosive polyarthritis.
* If response is poor, combination chemotherapy using GCC and cytoxic drugs is started. Underlying causes of polyarthritis should be eliminated if possible (i.e. chronic disease, offending antibiotic). Complete remission is usually achieved; however, a recurrence rate of 30 to 50% can be expected once therapy is discontinued.
* Therapy is usually initiated with prednisone at 1.5 to 2.0 mg/kg, PO q12h for 10-14 days. If synovial fluid cell counts return below 4000 cells/ml and mononuclear cells predominate, the dose of prednisone can be slowly tapered over several weeks to 1.0 mg/kg, PO q48h. If clinical signs persist or synovial fluid analysis is abnormal, cytotoxic drugs should be started with prednisone. If clinical signs do not recur while on alternate day GCC therapy for two to three months, the drug can be discontinued. Cytotoxic drugs are used in combination with GCC due to their synergistic effect.
* The most commonly used cytotoxic drugs include cyclophosphamide and the thiopurines, azathioprine and 6-mercaptopurine. Cyclophosphamide is given at 2.5 mg/kg for dogs less than 10 kg, 2.0 mg/kg for dogs between 10 and 25 kg, and 1.75 mg/kg for dogs heavier than 50 kg. This dosage is given PO q24h for four consecutive days of each week. Prednisone is also given as described above; although some clinicians reduce the total daily dose by half.
* If azathioprine or 6- mercaptopurine is used, they are given at 2.0 mg/kg, PO q24h 14-21 days, then q48h. Prednisone is given as with cyclophosphamide; however, it is given on alternating days with the thiopurine. Remission usually occurs in 2 to 16 weeks.
* Cytotoxic drugs are discontinued one to three months after remission is achieved; this is determined by resolution of clinical signs and confirmation of normal synovial fluid analysis.
* Alternate-day GCC therapy (prednisone, 1.0 mg/kg, PO) is generally successful in maintaining remission.
* If clinical signs or synovial neutrophilia recur, long term cytotoxic drug therapy may be necessary. If clinical signs do not recur while on alternate-day GCC therapy for two to three months, the drug can be discontinued. If clinical signs recur when GCC are stopped, treatment should be extended; if remission does not ensue, long-term cytotoxic drug therapy may be needed.
* Treatment of FCPP may help to slow progression. Prednisone (2 mg/kg, q12h) and cyclophosphamide (2.5 mg/kg) are typically used as described above. Treatment of FCPP may help to slow progression. Prednisone (2 mg/kg, q12h) and cyclophosphamide (2.5 mg/kg) are typically used as described above.

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CONTRAINDICATIONS
Cytotoxic drugs should not be used in animals with chronic infections or bone marrow suppression (cats with FCPP).

PRECAUTIONS
Long term administration of GCC can lead to iatrogenic Cushing's disease. Administration of cytotoxic drugs frequently induces bone marrow suppression. Complete blood counts should initially be monitored weekly (see polyarthritis, erosive).

POSSIBLE INTERACTIONS
None known

ALTERNATE DRUGS See above

FOLLOW-UP

PATIENT MONITORING
Clinical deterioration indicates the need for a change in drug selection or dosage.

PREVENTION/AVOIDANCE N/A

POSSIBLE COMPLICATIONS N/A

EXPECTED COURSE AND PROGNOSIS
* Progression of disease is guarded with SLE and FCPP and good with most other nonerosive arthritides.
* Recurrence is seen intermittantly.

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MISCELLANEOUS

ASSOCIATED CONDITIONS N/A

AGE RELATED FACTORS N/A

ZOONOTIC POTENTIAL N/A

PREGNANCY N/A

SYNONYMS N/A

ABBREVIATIONS

FCPP = feline chronic progressive polyarthritis

GCC = glucocorticoids

SLE = systemic lupus erythematosus

References

Beale BS. Arthropathies. In: Bloomberg MS, Taylor RT, Dee J, eds. Canine sports medicine and surgery. Philadelphia: WB Saunders, in press.

Goring RL, Beale BS. Immune-mediated arthritides. In: Bojrab MJ, ed. Disease mechanisms in small animal surgery. Philadelphia: Lea and Febiger, 1993;742-750.

Pedersen NC. Joint diseases of dogs and cats. In: Ettinger SJ, ed. Textbook of veterinary internal medicine. 3rd ed. Philadelphia: WB Saunders, 1989;2329-2377.

Author Brian Beale

Consulting Editor Peter D. Schwarz


Disease & Conditions | Problems & Findings | Lab Tests | EKG | Drugs | Images | Return to top

Dont know if this any help.

I lost a dog to Meningitis, please feel free to pm me for more information.