INFECTIOUS DISEASE

1.1 Plasmodium

Infection with a Plasmodium sp. was diagnosed in a wild- caught adult female Leadbeaters possum (Gymnobelideus Ieadbeateri) with non-specific illness and failure to adapt to managed care (Scheelings et al.

Histological examination of lung tissue revealed a mixed inflammatory response within the alveoli and dilated lymphatic vessels around airways. The bronchi­oles contained oedema fluid and within erythrocytes there were small protozoan parasites. Transmission elec­tron microscopy confirmed intra-erythrocytic parasites suggestive of a plasmodial organism. Sections of tissue were further tested with a Plasmodium genus-specific PCR assay, which confirmed infection with a Plasmodium species. Speciation of the organism was not possible. This case remains the first report of a Plasmodium infection in a native Australian mammal and its significance remains unknown.

1.2 Klossiellosis

The apicomplexan coccidian genus Klossiella contains parasites of vertebrate hosts with a predilection for renal tubular tissue. There is global distribution and typically, high host-specificity. An unidentified Klossiella sp. was identified in two sugar gliders (Petaurus breviceps) housed in managed care (Ardiaca et al. 2016). In both cases, death was acute following a 12-24 hr illness. Infec­tion with Klossiella resulted in mild interstitial nephritis that was of questionable clinical significance (Ardiaca et al.

1.3 Ophidascariasis

Death from Ophidascaris robertsi infection has been reported in a sugar glider bred in managed care (Agun- dez et al. 2014). The animal presented in shock, with marked cachexia and dehydration. Despite aggressive treatment it died soon after presentation. At necropsy there was a single, large nematode free in the abdominal cavity with an additional two nematodes in the right atrium and right ventricle. The parasites were identified as third-stage larvae of the ascaridoid parasite O. rob­ertsi. The definitive host for this parasite is the Australian carpet python (Morelia spilota). It has a com­plex life history, with second-stage larvae having a wide host range, including earthworms, snails, other inverte­brates, fish, tadpoles, reptiles, birds and mammals. Development of third-stage larvae only occurs in birds and mammals after ingesting an intermediate host with second-stage larvae (Sprent 1963). Given that the glider was bred in managed care and had never left the pet shop where it lived, infection was possibly acquired from ingesting an intermediate host (likely an invertebrate) that had been exposed to faeces of wild-caught carpet pythons that also resided within the premises (Agundez et al. 2014).

1.4 Parasites of the eastern pygmy-possum (Cercartetus nanus)

A summary of the parasites inhabiting the eastern pygmy-possum has been compiled (Harris and Vilcins 2007). However, no assessment was made on the signifi­cance that these infections had on the health of possums and so their pathogenicity remains unknown.

1.5 Angiostrongylus cantonensis

Angiostrongylus cantonensis infection was diagnosed in 4 of 31 (13%) common brush-tailed possums (Trichosurus vulpecula) that died in the Sydney area (Ma et al. 2013). Diagnosis was made based on the histopathological appearance of the brain or spinal cord, as well as the mor­phological characteristics of nematodes.

1.6 Mycobacterium ulcerans (Buruli ulcer)

Mycobacterium ulcerans is an environmental organism responsible for distinctive cutaneous ulcerative lesions in both humans and animals. It has a worldwide distribu­tion but infections are predominately reported in sub­Saharan Africa and Australia (O’Brien et al. 2014). Internationally, the disease is referred to as Buruli ulcer (BU). BU was first reported 60 yr ago and there have been sporadic outbreaks in humans and a variety of domestic and free-ranging animals in south-eastern Vic. since then (Carson et al. 2014). In Vic., clinical manifes­tation of the disease is known as Bairnsdale ulcer (Carson et al. 2014).

Disease has been reported in three species of free- ranging possums from south-eastern Australia. These include the eastern ring-tailed possum (Pseudocheirus peregrinus), common brush-tailed possum and moun­tain brush-tailed possum (T. cunninghami). It is likely that these species are the most important native reser­voirs for human infection (Carson et al. 2014; Roltgen and Pluschke 2015). Infection in all species is most com­monly seen in adults, with lesions appearing as solitary or multiple cutaneous ulcers on the face, limbs or tail (Fig. 38.1). Differences in pathogenicity exist between the species, with the disease being mild and self-limiting in both brush-tailed species (O’Brien et al. 2014). Con­versely, in eastern ring-tailed possums, disease may be apparent at multiple cutaneous sites and in some

Fig. 38.1. A Bairnsdale ulcer on the tail of an eastern ring-tailed possum (Pseudocheirusperegrinus). Photo: Kath Handasyde

instances may result in systemic disease and death (Hobbs et al.

The natural history of M. ulcerans infection and the mode of transmission to humans remain unknown, but punctures of contaminated skin surfaces by arthropod bites may play an important role (Wallace et al. 2017) (see Chapter 16). Typically, M. ulcerans invades the host via cutaneous lesions and it is thought that biting insects may play a role as vectors (Roltgen and Pluschke 2015). Once it has infected an individual, lesions are created by elabora­tion of the cytotoxic and immunosuppressive polyketide toxin, mycolactone (O’Brien et al. 2014). In cases of human infection, the incubation period is estimated to be around 4.5 mo and there is no evidence of human-to- human transmission (O’Brien et al. 2017).

1.7 Listeriosis

Listeria monocytogenes was diagnosed as the cause of death in a free-ranging common brush-tailed possum and two zoo-housed eastern ring-tailed possums (Sangster 2016). The brush-tailed possum was found dead within the grounds of a zoological park and the ring-tailed possums died shortly after presenting with severe cardiovascular collapse. In both species, L. monocytogenes was cultured from lesions. Pathological findings in all cases included suppuration of the brain stem with numerous intracellular clusters of short gram-positive bacilli, in addition to fulmi­nant disease in areas of the thorax and/or abdomen (Plates 38.1 and 38.2) (Sangster 2016). The source of infection was not identified, but may have included contaminated food items or enclosure furnishings and substrate. Listeriosis was also diagnosed in a sugar glider that presented with an acute onset of vomiting, lethargy, dyspnoea and anorexia, with subsequent death. The source of infection could not be identified and conspecifics living with the affected indi­vidual remained unaffected (Nichols et al.

1.8 Helicobacter

A potentially novel Helicobacter species was detected in the distal GIT (colon and rectum) of eastern ring-tailed possums (Coldham et al. 2013). Samples were collected at necropsy of injured or sick animals. Histological exami­nation of the GIT of affected possums revealed no abnor­malities and the significance of infection remains unknown (Coldham et al. 2013).

1.9 Tularaemia

A case of infection with Franciscella tularensis was diag­nosed in a woman bitten on the finger by an eastern ring­tailed possum in Tas. (Jackson et al. 2012). The incident occurred in the daytime and the victim reported that the possum appeared lethargic and unwell. The patient devel­oped an ulcer at the bite site, followed by lymph node enlargement, fevers, rigors, myalgia and night sweats. The possum was not examined for confirmation as the vector and it is not known what effects, if any, tularaemia has on ring-tailed possums. Since this initial case report, F. tularensis subsp. holarctica has been identified in a further two liver samples obtained from eastern ring­tailed possums associated with two separate mass mor­tality events in the Sydney north-shore area (Eden et al. 2017). More than 300 species of animals are recognised as being susceptible to tularaemia (including the opossum in North America) (Jackson et al. 2012). Further research is required to elucidate the role that Australian marsupi­als play in the role of tularaemia infection and care should be taken when handling animals.

1.10 Cryptococcosis

Cryptococcosis was diagnosed as the cause of death in two zoo-housed yellow-bellied gliders (Petaurus australis) and a wild eastern ring-tailed possum. The gliders were found dead in their enclosures without any premonitory signs and the ring-tailed possum was found moribund and died shortly after (ARWH 2018 case nos 5352.1; 11139.1; and 7126.1). On gross necropsy, all animals had abdominal distension with multiple round, cream-pink masses scattered free or adhered to viscera throughout the abdominal cavities.

Fig. 38.2. Cryptococcosis in a yellow-bellied glider (Petaurus australis). (a) Large cryptococcomas in the cranial thorax and smaller lesions throughout the lungs; (b) multiple cryptococcomas, some very large, scattered free or adhered to viscera throughout the abdominal cavity. Photos: Larry Vogelnest

1.11 Nidovirus (wobbly possum disease)

A fatal neurological condition of common brush-tailed possums, termed wobbly possum disease (WPD), was first identified in a research facility in NZ in 1995. Simi­lar clinical signs had also been observed in free-ranging possums in both NZ and Australia (Mackintosh et al. 1995; Dunowska et al. 2012; Giles et al. 2016). For 20 yr the aetiological agent of WPD remained a mystery until recent isolation of a novel marsupial nidovirus from archival tissue of WPD-affected animals (Dunowska et al. 2012). Strong experimental evidence for the causative involvement of marsupial nidovirus in the development of WPD was obtained by inoculating four healthy pos­sums with purified nidovirus, with all but one succumb­ing to disease (Giles et al. 2016). Partial genomic sequencing of marsupial nidovirus shows that it is closely related to current members of the Family Arteriviridae (Dunowska et al. 2012).

Initial clinical signs associated with WPD infection include behavioural changes (inappetence, decreased interest in the environment, temperament changes), fol­lowed by a fine head tremor, progressive ataxia, blind­ness and a reluctance to move. Severe neurological impairment followed by death occurs after an incubation of ~2 wk (Perrott et al. 2000a). Close contact is necessary for the spread of WPD and it has been experimentally induced in healthy possums challenged with tissue sus­pensions, blood, urine and mites from WPD-infected possums (Perrott et al. 2000b). Under natural conditions it is hypothesised that WPD may be spread by ingestion of contaminated food, fighting, contamination of wounds with urine or transfer of mites during den- sharing or other social interactions (Perrott et al. 2000b). This hypothesis has been supported by identification of high viral RNA loads in the salivary glands, serum, kidney, bladder and urine (Giles et al. 2018b). Histologi­cally, the disease is characterised by non-suppurative meningoencephalitis and infiltrations of mononuclear inflammatory cells, often associated with blood vessels. Similar inflammatory lesions may be observed in other tissues, including liver, kidney or spleen (Mackintosh et al. 1995). Despite the clinical similarities, it is still unknown if WPD seen in Australia and NZ are the same syndrome with the same aetiological agent. Prospective epidemiological investigations into WPD are now possi­ble with the development of an indirect ELISA based on recombinant nucleocapsid (rN) protein of WPD virus (Giles et al. 2018a). During the development of this test it was discovered that preexisting antibodies to WPD offer no protection to experimental infection (Giles et al. 2018a).

1.12 Poxvirus

An outbreak of infection with an Orthopoxvirus was reported in a zoo-housed population of eastern ring­tailed possums (Vogelnest et al. 2012). Lesions appeared as nodular exophytic masses on the tail and digits. Diag­nosis was confirmed by biopsy and a combination of histopathology and electron microscopy. Affected ani­mals were treated with either topical ointments or enro- floxacin. The lesions in all animals resolved within 2 mo of initial presentation, and there was no detrimental effect on the general health of the possums. All possums lived in outside enclosures and the outbreak occurred in March. An increase in arthropod vector activity may have played an important role in transmission ( Vogelnest et al. 2012).

1.13 Lung worm (Marsupostrongylus spp.) infection

Verminous pneumonia caused by infection with a Mar- supostrongylus spp. nematode was identified as the cause of death in 34 common brush-tailed possums in NSW. Gross pulmonary lesions were variable but consistent with other reports of Marsupostrongylus infection in marsupials (Wai-Shing et al. 2023). Histologically, lesions comprised of interstitial inflammation typified by infiltrates of macrophages, lymphocytes, plasma cells and eosinophils. Adult nematodes were observed in eight possums and were found within alveoli, bronchi­oles and pockets of emphysema (Wai-Shing et al. 2023). The lifecycle of Marsupostrongylus spp. are still unknown but evidence of reproduction within common brush-tailed possums indicates that they are a definitive host. It is likely that possums swallow infective third- stage larvae (either free-living or within intermediate hosts) which then penetrate mucosal surfaces and migrate to the lungs via blood or lymphatic vessels (Wai- Shing et al. 2023). Further research to determine life history traits and epidemiological risk factors are needed to better understand Marsupostrongylus spp. infections in marsupials.

2.