EPIDEMIOLOGY
Eimeria spp. have a direct life cycle. As with most Eimeria spp., E. echidnae and E. tachyglossi are transmitted horizontally (faecal-oral) through ingestion of faeces, substrate or mechanical hosts such as earthworms or insects.
The life cycle and pathogenesis of E. echidnae is described in Fig. 30.1.Although enteric coccidia are common in free-ranging echidnas, disease is rare, with only mild enteritis having been reported (Middleton 2008; ARWH 2024). Conversely, significant clinical disease is observed in echidnas held in managed care, with disease most frequently occurring in rescued free-ranging echidnas, either during their initial hospitalisation or within the first 6-12 mo of permanent care. Disease is reported more commonly in sub-adults but also occurs in long-term zoo-housed adults (Dubey and Hartley 1993; Middleton 2008; Taronga Zoo records).
Debenham et al. (2012) investigated the prevalence and intensity of Eimeria spp. in long-term zoo-housed adult echidnas compared with free-ranging echidnas and echidnas held short-term in managed care over an 18-mo period. The latter two groups included animals that were injured, sick, or orphaned puggles or juveniles.
Fig. 30.1. Life cycle and pathogenesis of Eimeria echidnae in the short-beaked echidna (Tachyglossus aculeatus). Illustration: Angie Jarman
Table 30.1. Pathogen-host-environment factors that may influence development of clinical coccidiosis in short-beaked echidnas (Tachyglossus aculeatus)
| Pathogen factors | Host factors | Environmental factors |
| • Introduction of a novel coccidian species or strain (e.g. E. tachyglossi shed by a recently free-ranging echidna when introduced to an established zoo group) • Infective dose • Geographical differences in virulence of some coccidian strains | • Genetic susceptibility • Dysbiosis • Immune compromise (e.g. concurrent infection [e.g. Salmonella spp., Candida spp.], poor nutrition)• Lack of immunity (e.g. inadequate passive transfer of immunity in handreared echidnas, lack of exposure to oocysts in naive zoo-housed adults) • Exposure to stressors (e.g. free-ranging echidna brought into care, sudden changes in diet or routine, overcrowding, noise/disturbance, transportation) | • Poor hygiene • Conditions favouring sporulation (e.g. moderate-cool temperature and moisture/ humidity) • Sudden change in diet or routine • Confinement in small areas • Overcrowding • Noise, disturbance • Transportation • High ambient temperature >35°C • Environmental oocyst load (see section 7.2) |
Key findings included:
• low-to-moderate numbers of E. echidnae oocysts were shed in faeces throughout the year by 79-85% of healthy, zoo-housed, adult echidnas without causing clinically apparent disease.
• approximately one-third of adult and sub-adult free- ranging and short-term managed care echidnas shed E. tachyglossi oocysts in their faeces, with the majority of these animals also shedding E. echidnae.
• E. tachyglossi oocysts were not found in long-term managed care echidnas. The reason for this is unclear.
• no significant difference in coccidian oocyst prevalence found in short-term managed care echidnas (83%, n = 6) and free-ranging echidnas (60%, n = 10).
• different intensity of oocyst shedding between age groups. Adults shed low-to-moderate numbers, post- emergent juveniles and sub-adults (0.8-2.5 kg) shed moderate to very high numbers and all pre-emergent juveniles (<0.8 kg) were negative for oocysts. This is consistent with the echidna life cycle where pre-emer- gent juveniles are restricted to the burrow until emergence at 0.8-1 kg (Augee et al. 2006; Morrow et al. 2009). Once juveniles exit the burrow and forage in soil, they are exposed to oocysts for the first time.
Coc- cidial infection intensity is therefore expected to be greatest in sub-adults and decrease in adults as they establish immunity (Debenham et al. 2012).• shedding intensity was not influenced by season or monthly mean minimum temperature.
• no difference between shedding intensity in echidnas housed indoors or outdoors, but the prevalence of faecal oocysts was significantly greater in outdoor enclosures (97%) compared with indoor enclosures (71%). Outdoor enclosures are exposed to rain and increased humidity, which then facilitates sporulation, increasing infection risk.
The interaction of pathogen-host-environment factors (Table 30.1) determines the degree of pathogenicity and severity of clinical signs of coccidiosis (Ladds 2009). What is a benign parasite in free-ranging populations may become a significant pathogen in managed populations because of the interaction of factors unique to the managed care environment.
Coccidiosis may occur as an outbreak within a managed care group or as sporadic, individual cases. An outbreak occurred at Taronga Zoo, affecting eight echidnas, three of which died. Three factors were identified as contributing to the outbreak: the enclosure population doubled from four to eight in the month leading up to the outbreak; the index case was shedding large numbers of oocysts; and there was a period of wet weather just before the first animals became unwell. Conversely, an outbreak at Perth Zoo in which three of four echidnas died had no identifiable triggers (S Vitali pers. comm.).
Comorbidities that occur commonly with clinical coc- cidiosis include septicaemia, stomatitis and gastritis caused by fungal and gram-negative bacterial infection (see Chapter 29), interstitial pneumonia and renal tubular degenerative changes (Middleton 2008; Whittington and Obendorf 2012; Taronga Zoo records).
3.