PATHOGENESIS AND PATHOLOGY
Intracellular coccidial replication results in cell rupture to release zoites, gametes and oocysts, causing inflammation, haemorrhage and tissue necrosis. Coccidia must actively invade and rupture enteric cells to produce the oocysts that are shed in faeces.
Infection without clinical disease is common, given the high prevalence of faecal oocysts in healthy echidnas (Debenham et al. 2012). Parasitaemia without clinical disease is also common (section 5.2). Enteric coccidiosis is either subclinical or clinical. Development of clinical enteric with or without systemic coccidi- osis is dependent upon the infective dose, immune status, presence of concurrent disease in the echidna, and the presence of environmental risk factors (Table 30.1).Enteric coccidiosis is a consequence of intestinal coc- cidial replication resulting in haemorrhage, inflammation and cell death (ARWH 2024). With heavy infections, the enteric epithelium may be grossly thickened by the presence of all life-cycle stages within the villous-crypt unit (Whittington and Obendorf 2012). Enteric changes can be acute, subacute or chronic. Inflammation may be focal, segmental or extensive, and non-suppurative, plasmacytic-lymphocytic, haemorrhagic and necrotis- ing. In some cases, intestinal tissue can remain intact with minimal inflammation despite an extreme coccid- ial burden and large numbers of oocysts excreted (ARWH 2024 case no. 10783). Enteric coccidiosis is reported to cause severe pain and fluid loss in marsupials, resulting in shock and death (Carmichael 1998). It is reasonable to assume an equivalent clinicopathological course in echidnas and aggressive therapy is indicated (see section 6).
Systemic coccidiosis occurs when intestinal merozo- ites enter the enteric blood vessels, invade monocytes and disseminate to organs where asexual and sexual reproduction results in inflammation and tissue necrosis (Fig. 30.1) (Whittington and Obendorf 2012). Meronts (schizonts) and zoites have been reported in almost every organ, including stomach, liver, pancreas, spleen, heart, lung, brain, sclera and bone marrow (ARWH 2024). Histopathological changes include interstitial pneumonia, oedematous haemorrhagic pneumonia, lymphocytic- neutrophilic-histiocytic pneumonia, lymphoid necrosis, splenitis, non-suppurative granulomatous hepatitis, fibrinous hepatitis, hepatocellular necrosis, plasmacytic- neutrophilic hepatitis, myocarditis with subendothelial necrosis, non-suppurative interstitial nephritis, necrotis- ing glomerulonephritis, encephalitis and cerebral oedema
(Whittington and Obendorf 2012; ARWH 2024). Systemic lesions are acute and often fatal.
4.