IN HUMANS continued
EXTRA-ENTERIC CYCLE (all warm-blooded vertebrates: mammals and birds)
I.H. All warm-blooded animals susceptible
Sporozoites
d oocyst orm)
Faeces
impaired hearing, ocular and neurological abnormalities. 16-18 The severity of clinical disease in congenital toxoplasmosis is inversely related to the stage of gestation at which infection occurs, with the greatest impact seen following infection in the first trimester. 18 • Most postnatal infections in immunocompetent patients are asymptomatic or subclinical, though some patients may present with a glandular-fever like syndrome (fever, fatigue, muscle pain, a sore throat and headache) with lymphadenopathy and mononucleosis. 18 Severe clinical manifestations are rarely seen in immunocompetent patients. Although the clinical course of toxoplasmosis is usually benign, symptoms may take weeks to months to resolve. • Immunocompromised individuals (including HIV/AIDS patients and transplant recipients) are susceptible to severe disease following primary infection. Systemic involvement can include pneumonitis, myocarditis and hepatitis in these patients. • A significant burden of disease related to toxoplasmosis is due to reactivation of latent infections, most commonly in immunocompromised HIV-positive patients. 19 • In HIV-infected patients with a low CD4+ T cell count, toxoplasmosis can cause opportunistic infection, presenting either as a severe systemic primary infection or more commonly an end-organ infection when associated with reactivation of tissue cysts. Affected individuals most commonly present with cerebral toxoplasmosis (toxoplasmic encephalitis) with the presence of characteristic multiple ring- enhancing intracerebral mass lesions involving the cortex and basal ganglia on CT or MRI imaging. 19 Extracerebral localisation following reactivation is less common. • Toxoplasmosis is an unusual but potentially serious complication following organ transplantation. Patients undergoing cardiac transplantation are susceptible to myocardial reactivation of T. gondii as seropositive organ donors can transmit Toxoplasma cysts in transplanted muscle tissue. 20 Pregnant owners should be counselled on appropriate and proportional risk mitigation strategies to minimise the risk of congenital toxoplasmosis
Tachyzoites
that eat infected animals fective in 3–10 days
The tachyzoites invade various tissues (cerebrum, eye, liver, lung, muscle, placenta) where they multiply, causing inflammation, cell death and necrosis
~ 3 weeks
The parasite forms cysts (with bradyzoites) in the host’s tissues where they can stay quiescent for years
• A study from Western Australia reported that seropositivity increased with age, reflecting the accumulated risk of a lifetime of exposure. 13 Interestingly in this study, owning a cat was not associated with an increased risk of infection. CLINICAL DISEASE • Primary infection in pregnant women may lead to congenital toxoplasmosis. The overall rate of vertical transmission following primary infection during pregnancy has been reported as approximately 30%. 14,15 The risk of vertical transmission increases with gestational age, from 6% at 13 weeks to 72% at 36 weeks. 15 • Congenital infection may also occur in immunocompromised (e.g. HIV-positive) pregnant women with reactivated latent infection. • Congenital toxoplasmosis may result in spontaneous abortion or stillbirth. A wide spectrum of clinical signs have been reported in congenitally infected children, including developmental delays,
CONTENTS
Companion Animal Zoonoses Guidelines 91
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