Canine toxoplasmosis: a case report

Abstract

Toxoplasmosis, caused by the protozoan Toxoplasma gondii, an obligatory intracellular parasite, is a coccidian that infects warm-blooded animals and humans. Felids are considered the only definitive hosts as they release infective forms, while other hosts are merely intermediaries. Currently, dogs are being studied as potential sentinels for both human and environmental contamination. The vast majority of infections are subclinical, with generalized toxoplasmosis occurring mainly in immunosuppressed individuals. Clinical toxoplasmosis primarily manifests with nonspecific signs including diarrhea, fever, vomiting, respiratory, and neurological alterations such as tremors, ataxia, paresis, tetraparesis, seizures, stiffness, muscle weakness, and dysphonia, varying depending on the site of infection. Antemortem diagnosis can be achieved through the exclusion of differential diagnoses, elevated and increasing antibody levels, along with clinical signs and improvement post-initiation of anti-Toxoplasma therapy. Herein, we present a case of a 6-year-old male neutered canine, of mixed breed, presenting with stiff, ataxic, and paretic pelvic limbs. Preserved proprioception in all four limbs, with decreased muscle tone, intact perineal and cutaneous trunci reflexes, and no cranial nerve abnormalities, which progressed to tetraparesis, loss of various reflexes, and ventroflexion of the neck. The patient had a history of ingesting feces from other animals, primarily its feline cohabitant with unrestricted outdoor access. Treatment with sulfadiazine + trimethoprim was initiated, followed by the addition of clindamycin upon positive results for IgM and IgG toxoplasmosis antibodies. After 28 days of treatment, the patient was discharged with resolution of all clinical signs and hematological abnormalities.