Introduction

• Cause: Toxoplasma gondii.
• Signs: chronic disease most common and can be subclinical. Anorexia, lethargy, pyrexia in acute disease. Central nervous system signs (altered mentation, ataxia, seizures) often associated with chronic disease.
• Diagnosis: serological testing, PCR on cerebrospinal fluid (CSF), post-mortem and histopathological examination.
• Treatment: only of value in acute disease. Sulfadiazine with pyrimethamine.
• Prognosis: fair in chronic disease, acute disease can carry a guarded to poor prognosis.

Pathogenesis

Etiology

• Toxoplasma gondii.
• Protozoan parasite, from the Phylum Apicomplexa, Family Sarcocystiidae.
• Asexual lifestage occurs in the intermediate host, which can be any mammalian or avian species. 
• Sexual lifestage occurs in the definitive host, the domestic cat and other felids

Predisposing factors

General

• Ingestion of food or water contaminated with cat feces, or ingestion of infected prey animals.
• Clinical disease most common in immunocompromised or young animals with immature immune systems.

Specific

• Animals born to a dam with active infection during the gestation period.

Pathophysiology

• The domestic cat and other felids are the final hosts where gametology (sexual reproduction) of the organism occurs.
• Unsporulated oocysts are released into the external environment via feline feces.
• Under suitable environmental conditions, the oocysts become sporulated.
• The intermediate host can become infected by one of two modalities:
  • Ingestion of contaminated food or water containing sporulated oocysts:
    • Sporozoites within the oocyst are liberated within the intestinal tract and rapidly penetrates intestinal epithelial cells.
    • Tachyzoites define the stage of rapid asexual multiplication within infected host cells followed by host cell rupture and invasion to other tissues via the lymphatic and hematogenous route.
    • The intermediate host typically survives this acute phase of toxoplasmosis and produce antibodies that limit the invasiveness of the tachyzoites.
    • Tissue cysts are formed as a result; typically in muscle, but can also occur in the lungs, visceral organs, and the central nervous system.
    • Cysts contain thousands of bradyzoites, where multiplication of the organism is slowed due to the acquired immunity of the intermediate host.
    • Tissue cysts can rupture if the immunity of the intermediate host wanes.
    • Bradyzoites are released and resume the invasive characteristics of tachyzoites.
  • Ingestion of undercooked meat or prey carcasses containing Toxoplasma cysts. Digestion of the cyst wall in the intestinal tract releases bradyzoites, which resume the invasive characteristics of tachyzoites.
• Clinical signs in the intermediate host are associated with the extra-intestinal phase of development.

Timecourse

• Sporulation of toxoplasma oocysts occurs in 1-5 days after passage in feces of affected felids.
• Clinical signs associated with acute disease typically develop around one week after infection:
  • Sudden death in young or immunocompromised animals may be seen without other clinical signs.

Epidemiology

• Acute disease most common in young animals with immature immune systems and immunocompromised individuals.
• Reactivation of chronic toxoplasmosis in healthy animals can occur with immunosuppression later in life.
• Naïve populations or species-specific immune response deficiencies may increase vulnerability to clinical disease.

Diagnosis

Treatment

Prevention

Outcomes