DISEASES

Due to their semi-fossorial, semi-aquatic and semi­nocturnal behaviour, it can be challenging to assess the health of free-ranging platypuses. Consequently, there is a risk of underestimating both the diversity and severity of disease processes to which platypuses may be susceptible.

3.1 Mucormycosis

Mucormycosis is a disease caused by the dimorphic fungus Mucor amphibiorum. The fungus is endemic in Australia, infecting free-ranging frogs and toads in Qld and NT, and platypuses in Tas. Platypuses are the only non-anuran and only mammal host known to be natu­rally infected with M. amphibiorum (Connolly 2015). The fungus causes a severe granulomatous and often ulcera­tive dermatitis in platypuses (see Chapter 12), which may progress to involve underlying muscle and occasionally disseminate to internal organs, particularly the lungs, leading to death. In the absence of the systemic spread of the organism, death can also result from secondary bac­terial infections, flystrike or impaired thermoregulation and mobility. Lesions in some individuals have been observed to improve and many affected platypuses remain systemically well. The route of infection is thought to be via skin wounds (spurring, bites from water rats, ectoparasites, other trauma), although inhalation and ingestion have also been proposed (Gust and Griffiths 2009; Connolly 2015).

The sudden emergence of mucormycosis in Tasma­nian platypuses in 1982 may have resulted from acciden­tal introduction of the fungus with ‘banana box frogs’ from Qld to a naive population.

Definitive diagnosis of mucormycosis requires both lesions suggestive of mucormycosis and a positive culture of M. amphibiorum. Additional confirmation is possible through the identification of spherules on wet or histo­logic sections, or by detection of M. amphibiorum anti­bodies by ELISA (Connolly 2009). Differential diagnoses include but are not limited to Mucor cicinelloides, Corynebacterium ulcerans, Dermatophilus congolensis and poxvirus.

Geraghty et al. (2011) investigated the influence of mucormycosis on the haematological, plasma biochemi­cal and other indicators of health in free-ranging platy­puses across Tas. There were no differences in haematological or biochemical measures between healthy individuals and those with mucormycosis. However, ulceration was associated with living at higher altitudes, low tail fat content and low trypanosome load.

Table 28.2. Diseases and infectious agents of platypus other than mucormycosis

428 CurrentTherapyin MedicineofAustraIian Mammals

¹Macgregorefa/. 2010; ²Loewenstein etal. 2008; ³Lunn etal. 2016; ⁴R Booth pers.comm.; ⁵MeIbourneZoo clinical records; ⁶Chapter 26; ⁷KesseII etal. 2014; ⁸ARWH 2018 case no. 7962/1; ⁹Gofton etal. 2018; ¹⁰WhinfieId 2024; ¹¹AustraIia ZooWiIdIife Hospital records

Booth and Connolly 2008; Spratt etal.

28 - Platypus 429

plasma GGT and platelet counts compared with animals from catchments with no evidence of infection. The study also generated haematological and biochemical reference intervals for Tasmanian platypuses (see Appendix 1).

3.2 Other diseases

Several surveys of free-ranging platypus populations have found evidence of exposure to infectious pathogens, but clinical disease associated with these infections is uncom­monly detected. Several infectious diseases involving one or a small number of animals, either in managed care or free-ranging, have been reported and include, but are not limited to Aeromonas hydrophila, Escherichia coli, salmo­nellosis, theileriosis, dermatomycosis, non-mucor foot granulomas, sparganosis, toxoplasmosis, angiostrongylia- sis (Whinfield 2024; Australia Zoo Wildlife Hospital records) and trombiculid mites (Ladds 2009; Macgregor et al. 2017a). Infectious diseases in platypuses in managed care are rare. A survey of infectious agents in Tasmanian platypuses revealed that more than 90% were infected with Theileria spp., trypanosomes and ticks, while the prevalence of other pathogens screened for was generally low (from ulcerative mycosis (Stew­art et al. 1999). A zoo-housed 12-yr-old female platypus with a >3 mo history of weight loss, elongated, brittle, split, flaking nails of the manus (from which a fungus of the Fusarium solani complex was cultured) and white, irregular, crumbling keratin of the mandibular and max­illary secateuring ridges was euthanased after developing progressive neurological signs (tremors, circling, rolling). Histologically the superficial keratin of the oral keratinous plates (rostral secateuring and caudal grind­ing) was fragmented, with associated aggregation of keratinous debris, parakeratosis and pigmented and non­pigmented fungal bodies. The most significant pathology was a non-suppurative encephalomyelitis. Mucor circinel- loides was isolated from brain and caudal oral grinding plates. The encephalomyelitis was morphologically con­sistent with mycotic encephalitis (random, multifocal distribution of granulomatous infiltrates); however, fungal elements were not seen in sections examined (ARWH 2018 case no. 11213.1).

With the advent of advanced molecular techniques there has been renewed research interest in organisms found in platypuses. Using genomic mining, Cui and Holmes (2012) found evidence for an endogenous papillo­mavirus-like element in the platypus genome. Paparini et al. (2013, 2014, 2015) used genomic studies to identify two piroplasm genotypes (possibly representing two species previously thought to be the single species of Theileria ornithorhynchi) and four closely related genotypes of Trypanosoma binneyi. Paparini et al. (2014) were also the first to report leeches on platypuses and provided evi­dence that leeches may have originally transmitted T. binneyi from fish to platypuses (see Chapter 26). Gofton et al. (2018) used bacterial 16S rRNA (16S) next-generation sequencing and genus-specific PCR to profile bacterial communities in platypus blood samples and platypus ticks and identified a high prevalence of Ehrlichia sequences. They demonstrated that the platypus Ehrlichia is clearly distinct from all other Ehrlichia spp. and pro­posed a separate species, Ehrlichia ornithorhynchi.

3.2.1 Emaciated juveniles

Juvenile platypuses leave the nesting burrow at about 4 mo of age, from December to May, with earlier emergence in Qld and later in Vic. and Tas.; however, there is consid­erable overlap from north to south. Weaning is likely an abrupt process for at least some individuals. Some young platypuses will then disperse, either within or between adjacent river basins, with some remaining within their natal area and others travelling considerable distances. Platypuses have been reported to cover distances of up to 8 km overland, sometimes negotiating steep terrain. There is a greater propensity for males to disperse over longer distances than females (Furlan et al. 2013). Over­land travel, particularly, requires greater energetic cost and has higher risk of misadventure. The timing of dis­persal is not well understood but likely does not occur immediately after burrow emergence.

Some platypuses that come into care are dispersing juveniles that may simply have dispersed into less appro­priate locations (such as urban backyards), while others are weak, emaciated and dehydrated. Some may be injured, have high tick and theileria burdens or suffering infections (e.g. fungal dermatopathies), although many are not. For those in which injury and disease are ruled out, return to a suitable habitat close to their point of origin as soon as possible after a brief period of supportive care should be a priority (Booth and Connolly 2008; R Booth pers. comm.). However, most juvenile platypus admissions are clustered between December and February (Whinfield 2024), coin­ciding with the timing of weaning and first emergence from the natal burrow. It is speculated that a proportion of juvenile platypuses are unable to cope with the abrupt weaning process or may emerge from the burrow in poor condition. These juveniles are typically in poor body con­dition, have variable waterproofing and may have concur­rent disease processes. Anaemia appears to be a common clinical finding in these juveniles (Whinfield 2024). Microcytic, hypochromic non-regenerative anaemia, characteristic of iron deficiency anaemia, has been observed. The underlying aetiology may involve parasit­ism. Immune-mediated haemolytic anaemia has also been reported in juvenile platypuses, possibly associated with Theileria ornithorhynchi (Kessell et al. 2014).

Hospitalisation of sick and injured platypuses is chal­lenging. They require a dry nest box, shallow-water feed­ing tank (warm water up to 30°C may be preferred by individuals in very poor body condition or with poor water proofing), a range of food items each day (food preference may change daily) and a narrow ambient air temperature range (22-26°C). Preferred food items when first coming into care include earthworms, bloodworms, blackworms, fly pupae, live crickets and mealworms. Very small soft crustaceans, very small yabbies, fish and insect larvae harvested from freshwater ponds can be offered as the animal gains strength. Alternatively, in very weak individuals, especially those with poor water­proofing, food (such as blackworms) can be offered in a shallow, palm-sized dish of water while the platypus is gently restrained on the lap. This approach reduces the energy expenditure of both swimming and thermoregu­lation. Some individuals fail to adapt to a managed care environment, with persistent attempts at escape sapping any remaining energy reserves. In these cases sedation with diazepam may be useful (see Appendix 3). Those that die without obvious pathology are likely to have suc­cumbed to complete depletion of all energy reserves.

Frequent provision of a high-energy diet is therefore important. Some platypuses do not feed readily in the early stages of care and tube or cheek pouch feeding is required (Booth and Connolly 2008; R Booth pers. comm.). A high-energy, easily digestible diet (e.g. Hills a/d, Hills Pet Nutrition, Sydney, NSW) can be instilled into the cheek pouches in 1-2 mL increments via a syringe and feeding tube. The tube is placed in the side of the mouth and inserted into the diagonally opposite cheek pouch. The cheek pouch gradually empties as the platy­pus ingests the content and can be refilled q 4-6 hr. As anaemia appears to be relatively common in compro­mised juvenile platypuses, a PCV/TPP/smear on arrival is recommended. However, as blood requires anaesthesia to collect, it should only be attempted once the animal has been stabilised. Regular monitoring of PCV, TPP and blood glucose during the stabilisation phase is important (see Appendix 1). However, this must be balanced with the stress of sample collection. Blood glucose of curves were described for five variables (PCV, RBC count, Hb, albumin and magnesium). They found evidence that seasonal changes in blood parameters reflect metabolic changes associated with seasonal environmental temperature variation. This has implica­tions for diagnostic interpretation (Macgregor et al. 2017b). Stewart et al. (2021) investigated PCV and six serum chemistry analytes and found a number of seasonal changes and associations with river catchment, sex and age. The causes of these spatial differences remain largely unknown, a reflection of natural variability and the range of environmental stressors affecting platypus populations.

5.