EPIDEMIOLOGY

The life cycle of T. gondii is divided into sexual and asex­ual replication phases with three infectious stages: sporo­zoites, tachyzoites and bradyzoites. Sexual replication occurs in the feline intestine following ingestion of either environmental oocysts or bradyzoites (or tachyzoites) present in the tissues of infected IH.

The asexual replication phase occurs in IH, including herbivorous and carnivorous species, which are infected via different pathways. Herbivorous IH are exposed fol­lowing ingestion of vegetation, soil or water contaminated with sporulated oocysts. Following ingestion of oocysts, sporozoites invade intestinal cells within 24 hr and subse­quently divide, via an asexual process known as endody- ogeny, to become tachyzoites. The tachyzoite is the infectious stage that multiplies rapidly inside the host’s body during the acute phase of the disease. Following dis­semination throughout the body, tachyzoites differentiate into slowly replicating bradyzoites and subsequently form tissue cysts.

Carnivorous IH are exposed following ingestion of bradyzoites (or tachyzoites) in infected prey and in this instance bradyzoites, rather than sporozoites, invade the intestinal epithelial cells to initiate asexual replication. Experimental studies in eastern barred bandicoots (Per- ameles gunnii) suggest that earth worms, a major dietary component of this species, may act as mechanical vectors of T. gondii, passaging oocyst-contaminated soil through their alimentary tracts (Bettiol et al. 2000b).

Exposure pathways have not been definitely identified for Australian marine mammals, although infection via contaminated coastal freshwater runoff is considered likely and was identified as a potential risk factor in Aus­tralian hump-backed dolphins (Sousa sahulensis), an Indo-Pacific bottle-nosed dolphin (Tursiops aduncus), Risso’s dolphins (Grampus griseus) and a long-nosed fur seal (Arctocephalus forsteri) with toxoplasmosis (Jardine and Dubey 2002; Bowater et al. 2003; Donahoe et al. 2014; Cooper et al. 2016). Elevations in mean T. gondii serum antibodies were observed in dugongs (Dugong dugon) fol­lowing a flood event (Wong et al. 2020). Benthic inverte­brates and filter-feeding fish have been postulated as potential sources of oocysts for some Australian marine mammals.

Risk factors for infection in Australian mammals remain largely unknown. However, Groenewegen et al. (2017) demonstrated an association between T. gondii- associated mortality and eastern barred bandicoots inhabiting lower topographic sites in an island popula­tion established by assisted colonisation.

Because T. gondii replicates both sexually and asexu- ally, both clonal and recombinant lineages may occur.

The incidence of morbidity and mortality in Austral­ian mammals following infection with T. gondii is unknown, but the presence of antibodies to T. gondii in a range of species demonstrates that exposure is not invari­ably fatal (Hartley and English 2005; Parameswaran et al. 2009b; Fancourt et al. 2014; Mayberry et al. 2014). Con­versely, Obendorf et al. (1996) found evidence to suggest eastern barred bandicoots were highly susceptible to infection and toxoplasmosis was identified as a signifi­cant cause of mortality during translocation of eastern barred bandicoots to an island where a high prevalence of T. gondii infection in feral cats was subsequently demon­strated (Groenewegen et al. 2017; Adriaanse et al. 2020). The outcome for the host following exposure is likely influenced by the virulence and strain of T. gondii involved, the inoculation dose and immune status of the host (Hillman et al. 2016). Differential interferon-gamma and tumour necrosis factor-alpha-driven cytokine responses have been demonstrated in managed fat-tailed dunnarts (Sminthopsis crassicaudata) experimentally infected with T. gondii and Neospora caninum (Donahoe et al. 2017). Infected dunnarts were able to mount a more effective immune response to T. gondii, providing evi­dence that host immune response is also important in determining the outcome of infection.

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