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Emergency presentations of 4 dogs with suspected neurologic toxoplasmosis

Authors


Address correspondence and reprint requests to:
Dr. Jeremy M. Tarlow, Cobb Emergency Veterinary Clinic, 630 Cobb Parkway North, Marietta, GA 30062. E-mail: jtarlow@hotmail.com

Abstract

Objective: To review the signalment, clinical signs, abnormal laboratory data, therapeutics, and response to therapy of dogs with clinical signs consistent with toxoplasmosis infection.

Series summary: A retrospective review was performed on the records of 4 dogs presented to the Animal Emergency Center between January 1998 and February 2000 exhibiting neurologic signs and having elevated titers for Toxoplasma gondii. A tentative diagnosis of toxoplasmosis was based upon one of the following criteria: (1) a serial 4-fold or greater change in serum T. gondii IgG titers; 2) serially decreasing serum T. gondii IgM titers with concurrent increasing serum T. gondii IgG titers; or 3) positive cerebrospinal fluid (CSF) T. gondii titers. In addition, inclusion of cases was limited to dogs that showed improvement of neurologic signs following treatment with antiprotozoal drugs. Trimethoprim–sulfamethoxazole treatment was associated with successful elimination of clinical signs in all of the dogs. Two of the dogs developed side effects potentially attributed to the trimethoprim–sulfamethoxazole (TMS), and antiprotozoal treatment was continued using clindamycin.

Unique information presented: Toxoplasmosis is an important differential diagnosis in any dog that presents as an emergency with central or peripheral neurologic signs. Affected dogs need not be immunocompromised for clinical signs of toxoplasmosis to occur. Appropriate treatment with TMS or clindamycin can lead to resolution of clinical signs.

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