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| | ===Transmission=== | | ===Transmission=== |
| | + | Any of the three life stages of T gondii can infect warmblooded |
| | + | vertebrates, including cats and humans. Since |
| | + | tachyzoites are readily inactivated by gastric secretions, |
| | + | most orally acquired infections develop following the |
| | + | ingestion of bradyzoites or sporozoites. Coprophagy is |
| | + | uncommon in cats; the usual source of infection is the |
| | + | ingestion of T gondii bradyzoites during carnivorous |
| | + | feeding. Oocysts can generally be detected in the faeces |
| | + | from three days post-infection (see graph on the right) |
| | + | and oocyst shedding is usually completed by 10 to 21 |
| | + | days post-infection. Only 20 per cent of cats infected by |
| | + | ingestion of sporulated oocysts will shed the organism; |
| | + | the onset of oocyst shedding is between 18 and 44 days |
| | + | post-infection, and the patent period is six to 10 days |
| | + | (Dubey and Lappin 1998). |
| | + | Transplacental infection occurs if a T gondii-naive |
| | + | woman or queen ingests T gondii during gestation. First |
| | + | trimester infections are rare but, when they occur, the |
| | + | sequelae are generally severe. In humans, stillbirth, abortion |
| | + | and severe CNS disease are common. In neonatally |
| | + | infected kittens, interstitial pneumonia, necrotising |
| | + | hepatitis, myocarditis, non-suppurative encephalitis and |
| | + | uveitis are commonly detected after necropsy and histological |
| | + | examination. In humans, the fetus is more likely |
| | + | to be infected if exposed during the second and third |
| | + | trimesters but the resultant disease is usually milder. The |
| | + | same may be true for cats. Previously infected women or |
| | + | queens are unlikely to transmit T gondii to the fetus, |
| | + | even if exposed during gestation. |
| | | | |
| | ==Signalment== | | ==Signalment== |