DIAGNOSIS
5.1 History, clinical signs and faecal oocysts
A history of recent exposure to risk factors (Table 30.1) and disease in other echidnas will increase the index of suspicion of clinical coccidiosis in a sick echidna.
Subjective estimates of faecal oocyst numbers using standard wet preparation or faecal flotation techniques are quick and easy to perform (Fig. 30.2). The presence or number of faecal oocysts is not necessarily indicative of the presence of disease (Middleton 2008; Debenham et al. 2012; Taronga Zoo records; ARWH 2024). Healthy echidnas can shed large numbers of oocysts while acute, fatal coccidiosis can occur before any oocysts are shed in the faeces. Large numbers of oocysts in echidnas with diarrhoea, lethargy and inappetence should be considered significant and treatment initiated.
Fig. 30.2. Coccidial oocysts (arrows) in the faeces of a short-beaked echidna (Tachyglossus aculeatus). It is not possible to distinguish Eimeria echidnae and E. tachyglossi oocysts on wet preparation or floatation, as there is considerable variation in the oocyst size of each species. Note the presence of strongyle-type ova (faecal floatation, ?400 magnification). Image: Taronga Wildlife Hospital
5.2 Haematology and biochemistry
Neutrophilia or neutropenia with or without a left shift may occur in echidnas with clinical coccidiosis. Five echidnas with systemic coccidiosis at Taronga Zoo had a relative and absolute monocytosis of up to 33% and 7.4 ? 109∕L (reference range: monocyte 0-10%, monocytes 0.07-1.5 ? 109∕L [ZIMS 2024]). There was moderate-marked (30100%) intramonocytic Eimeria burden in all five echidnas.
Intramonocytic Eimeria are detected in up to 50% of healthy echidnas (Plate 30.1).
The coccidia occupy up to half the monocyte cytoplasm, displacing the nucleus, and contain numerous blue punctate structures and sometimes an eccentric nucleus. The proportion of parasitised monocytes in healthy echidnas varies between 0.5% and 54%, with parasitaemia of up to 10% more commonly reported (Ploeg et al. 2008). Echidnas with systemic disease commonly have parasitaemia in more than 30% of monocytes and in severe cases up to 100% (Taronga Zoo records; ARWH 2024).Myelocytes and metamyelocytes were observed in blood smears of one echidna that died of overwhelming systemic coccidiosis (ARWH 2024 case no. 10783). A second echidna with fatal systemic coccidiosis had a significant leucocytosis of 105 ? 109∕L comprising immature myeloid or lymphoid cells. Although it is likely these cells reflected bone marrow response to severe systemic inflammation, particularly as the WBC count decreased to 44 ? 109∕L a few days after treatment commenced, leukaemia could not be ruled out (ARWH 2024 case no. 9855).
There are no pathognomonic biochemistry abnormalities. Changes reflect metabolic derangements, dehydration, organ failure and sepsis.
5.3 Necropsy
Gross findings in subclinical enteric coccidiosis in echidnas that have died for other reasons have been described as prominent, pale, ‘frosty’ mucosal patches of the distal two-thirds of the small intestine (Barker et al. 1985; Ladds 2009). Changes associated with clinical enteric coccidio- sis include intestinal wall thickening; multifocal, pale mucosal nodules; haemorrhage; ulceration; and necrosis (Middleton 2008; ARWH 2024). Systemic changes are dependent on the organs affected, but generally include congestion, haemorrhage, necrosis and oedema.
Histopathology confirms enteric or systemic coccidio- sis. Subclinical infection is characterised by an absence of significant inflammation associated with coccidia (Barker et al. 1985). Detailed histopathological descriptions of enteric and systemic coccidiosis can be found in Barker et al.
(1985), Dubey and Hartley (1993), Booth (1999), Rose (1999) and Ladds (2009). Briefly, enteric changes include: haemorrhagic and necrotising enteritis; intestinal mucosal thickening due to the presence of large numbers of coc- cidial life-cycle stages; focal mucosal erosion; villous atrophy; and mononuclear infiltration of the lamina propria (Rose 1999; Ladds 2009). Systemic changes include: presence of various coccidian life-cycle stages scattered throughout the endothelium and parenchyma of the lung, liver, heart, kidney, spleen and GIT (Dubey and Hartley 1993); diffuse mononuclear infiltration within the stroma and blood vessels of the lung (Ladds 2009); foci of necrosis in the spleen and lymph nodules (Rose 1999); foci of necrosis and granulomas in the liver; mononuclear infiltrates with or without neutrophils in myocardium; and renal mononuclear infiltrates with enlarged, hypercellular glomeruli (Ladds 2009). Pathology associated with concurrent disease (e.g. bacterial septicaemia (S. typhimu- rium, Fusobacterium spp.), fungal pneumonia (Cryptococcus spp.), fungal gastritis (Candida spp.) and nephropathy) may also be present (Middleton 2008).6.
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