Chapter 277 Familiarity with Toxoplasma gondii is important for all small animal practitioners because of pet ownership issues, as well as the occasional association of T. gondii with clinical illness in cats and dogs. The life cycle, diagnosis, treatment, and prevention of feline and canine toxoplasmosis has been reviewed extensively over the years (Dubey et al, 2009; Lappin, 2010). In addition, the American Association of Feline Practitioners and the Centers for Disease Control and Prevention have provided information concerning cat ownership as it relates to T. gondii and other infectious agents (Brown et al, 2003; Kaplan et al, 2009). This chapter emphasizes some of the most important points about this disease and provides recently published information concerning the zoonotic and clinical considerations for this protozoan. Fatal toxoplasmosis can develop during acute dissemination and intracellular replication of tachyzoites; hepatic, pulmonary, CNS, and pancreatic tissues commonly are involved (Dubey et al, 2009). Transplacentally or lactationally infected kittens develop the most severe signs of extraintestinal toxoplasmosis and generally die of pulmonary or hepatic disease. Common clinical findings in cats with disseminated toxoplasmosis include depression, anorexia, fever followed by hypothermia, peritoneal effusion, icterus, and dyspnea. If a host with chronic toxoplasmosis is immunosuppressed, bradyzoites in tissue cysts can replicate rapidly and disseminate again as tachyzoites; this is common in humans with acquired immune deficiency syndrome (AIDS). Disseminated toxoplasmosis has been documented in cats concurrently infected with feline leukemia virus (FeLV), FIV, and feline infectious peritonitis virus. Commonly used clinical doses of glucocorticoids do not appear to predispose to activated toxoplasmosis. However, administration of cyclosporine to cats or dogs with renal transplantations or dermatologic disease has been associated with fatal disseminated toxoplasmosis (Barrs, Martin, and Beatty, 2006; Bernstein et al, 1999). Cats started on cyclosporine before exposure to T. gondii are most likely to develop significant illness, particularly if the trough blood level is higher than the normal range. Administration of cyclosporine at 7.5 mg/kg PO daily for 42 days failed to reactivate T. gondii in one experimental model performed by the author. T. gondii antigens or DNA can be detected in the blood of healthy or clinically ill cats and dogs; the source of the organism is likely bradyzoites from tissue cysts (Lee et al, 2008). The combination of T. gondii–specific antibody detection in aqueous humor or CSF and organism DNA amplification by PCR is the most accurate way to diagnose ocular or CNS toxoplasmosis in cats (Powell et al, 2010). CNS toxoplasmosis and neosporosis can appear clinically similar in dogs; thus the author frequently combines PCR testing for both organisms on CSF samples from dogs with inflammatory CNS disease.
Toxoplasmosis
Clinical Features of Feline Infection
Clinical Diagnosis
Toxoplasmosis
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