IN ANIMALS continued
PREVALENCE AND RISK FACTORS • Pooled global meta-analysis from 1967-2017 estimated 52% of cats in Australia as seropositive to T. gondii . 4 A 2020 Australian study reported 39% seroprevalence of T. gondii in owned domestic cats in Australia. 5 • Feeding companion animals raw meat diets (kangaroo, lamb and other pasture-consuming species) is considered a major risk factor for T. gondii infections. It is reported that up to 59% of cats in Australia are fed raw meat diets. 5 • The prepatent period in cats depends on the stage of T. gondii ingested (3-10 days after ingestion of bradyzoites and 18 days or more after ingestion of tachyzoites). 6 • Only about 1% of the feline population are found to be shedding oocysts at any given time. 7 Duration of shedding is relatively short (1-3 weeks) and cats that have previously shed T. gondii typically do not re-shed oocysts unless re-infected or immunocompromised. 3,7 CLINICAL DISEASE • The majority of infections with T. gondii are asymptomatic in cats. Clinical disease is considered rare and more commonly seen in immunocompromised cats and young kittens. Cats with iatrogenically induced immunosuppression, feline infectious peritonitis, feline immunodeficiency virus and feline leukaemia virus can be predisposed to systemic toxoplasmosis, with immunosuppression leading to recrudescence of latent infection. 8,9 • Non-specific clinical signs and multi-system infection characterise the clinical presentation in non-immune adult cats. Pneumonia is the predominant sign of generalised toxoplasmosis in cats. Acute respiratory distress syndrome and septic shock may also occur. In cats with severe neurological or respiratory signs, toxoplasmosis can be fatal. Common sites of involvement include the central nervous system, musculature, lungs and eyes. 3,9
• It is rare for dogs to present with clinical toxoplasmosis in the absence of underlying immunosuppressive disease. 3 Clinical signs may relate to hepatic, pulmonary, ocular or neurological involvement, resulting in fever, cough, jaundice, seizures and cranial nerve deficits. Screening dogs with neurological signs for T. gondii infection is recommended. 3 • If infection occurs for the first time in immuno-naive pregnant cats, or if pregnant cats have a reactivation of latent infection (for example due to immunosuppression), tachyzoites can cross the placenta to infect the foetus. Clinical toxoplasmosis in transplacentally infected kittens can vary in severity depending on the stage of gestation, and may include foetal death and abortion in early pregnancy or the birth of stillborn or deformed kittens with infection later in pregnancy. Live born congenitally infected kittens, or those infected lactogenically, frequently die of pulmonary or hepatic disease. 3,9 Congenital infection is rarely reported in pups. DIAGNOSIS • As active shedding only occurs for 1-3 weeks after initial exposure, oocysts are rarely found in cat faeces via faecal flotation. Serological testing can determine if a cat is positive (exposed, asymptomatic or clinical) or negative (susceptible to infection). Cases of severe clinical systemic toxoplasmosis may be diagnosed by: - High-to extreme IgM anti- T. gondii antibody titres. - Rising paired IgG anti- T. gondii antibody titres. - Detecting presence of the organism’s DNA in body fluids (cerebrospinal fluid, aqueous humour or bronchoalveolar lavage fluid) or tissue via PCR. 8,9 • In older dogs that are iatrogenically or naturally immunosuppressed, concurrent testing and measurement of anti- Neospora caninum antibody titres is strongly recommended as clinical signs may be indistinguishable from those of toxoplasmosis.
TRANSMISSION
• The most common route of transmission to humans is through consumption of tissue cysts in raw or undercooked meat contaminated with T. gondii. • Human infection can occur through accidental ingestion of sporulated oocysts shed in the faeces of cats, for example when gardening or consuming vegetables, fruit or water contaminated with oocysts.
CONTENTS
Companion Animal Zoonoses Guidelines 89
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