CLINICAL DISEASE
Herpesvirus infections in Australian marsupials range from subclinical shedding to outbreaks of mortality (Finnie et al. 1976; Dickson et al. 1980; Stalder et al. 2015). Although different herpesvirus infections may exhibit similar clinical presentations, there are no pathognomonic clinical signs within or across marsupial species groups.
MaHV-1 and MaHV-2 have both been associated with significant pathology in macropods in managed care, resulting in widespread mortality (Finnie et al. 1976; Dickson et al. 1980; Acland 1981; Callinan and Kefford 1981; Wilks et al. 1981; Britt et al. 1994). In the initial MaHV-1 outbreak, managed parma wallabies (Nota- macropus parma) with a history of recent translocation developed conjunctivitis, rhinitis, pneumonia, vesicular cloacitis (Fig. 23.1) and pyrexia and many died suddenly. At necropsy, tracheitis, myocarditis and congestion with or without necrosis of the lungs, liver and spleen were observed (Finnie et al. 1976). Similar clinical manifestations have been reproduced experimentally and free- ranging eastern grey kangaroos infected with MaHV-4 also exhibited respiratory signs, including rhinitis and conjunctivitis, and possible neurological signs (Acland 1981; Vaz et al. 2013). Lumholtz’s tree-kangaroos in managed care with confirmed MaHV-4 infection and intranuclear inclusion bodies in liver specimens exhibited respiratory signs including dyspnoea, tachypnoea, oculonasal discharge, lethargy and ulceration of the foot pads prior to death (Shima et al. 2020). An alphaherpesvirus has been implicated in an outbreak of respiratory disease and sudden death in greater bilbies (Macrotis lagotis) in managed care (Besier et al. 2016). Predominant clinical signs included pyrexia, lethargy, serous nasal discharge in one animal and sudden death. Histopathology demonstrated the presence of widespread epithelial erosions and necrosis in the upper respiratory tract and bronchi, alveolar oedema and the presence of eosinophilic intranuclear inclusion bodies.
The liver and adrenal glands were also variably congested with areas of necrosis. Lymphoid depletion was also a common feature (Besier et al. 2016).Although three herpesvirus species have been identified in bare-nosed wombats, there is only one report of associated pathology (Rothwell et al. 1988). Disseminated herpesvirus infection was identified using histopathology and electron microscopy at necropsy in a juvenile handreared bare-nosed wombat following a 4-d period of lethargy and inappetence resulting in hypothermia and death. As the virus could not be cultured the herpesvirus species involved was not identified, but these signs may have been induced by one of three recently identified vombatid herpesviruses (Stalder et al. 2015) or alternatively be a manifestation of cross-species infection with another herpesvirus, because the wombat joey had been in contact with multiple other species (Rothwell et al. 1988).
Gammaherpesvirus infections in Australian marsupials are often subclinical or may be identified in animals with signs of concurrent disease including infection with C. pecorum in koalas, Sarcoptes scabiei in bare-nosed wombats (Vombatus ursinus) and Theileria spp. infections in quokkas (Vaz et al. 2011; Vaz et al. 2012; Stalder et al. 2015; Martinez-Perez et al. 2021). Ulcerative cloacitis has been documented in managed eastern grey kangaroos infected with MaHV-3 (Smith et al. 2008). In small dasyu- rids, including the yellow-footed antechinus (Antechinus flavipes), agile antechinus (A. agilis), dusky antechinus (A. swainsonii) and brush-tailed phascogale (Phascogale tapoatafa), herpesvirus infections may manifest histologically as progressive nuclear and cytoplasmic enlargement, with intracytoplasmic vacuolation and the presence of intranuclear inclusion bodies in the prostate (Plate 23.1) (Barker et al. 1981; Munday and Obendorf 1983; Amery- Gale et al. 2014). Hepatic necrosis and lymphoid depletion were also features in some animals (Amery-Gale et al. 2014). At present, the clinical significance of herpesvirus infection in these animals is unknown. It is likely that severe immune suppression caused by glucocorticoid release is responsible for recrudescence of latent infection preceding the post-mating mortality observed seasonally in male antechinus species (Amery-Gale et al. 2014).
4.