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DISEASES

7.1 Gastrointestinal disease

7.1.1 Mycotic stomatitis

Mycotic stomatitis occurs most commonly in echidnas in managed care with concurrent disease or general debili­tation or as a primary condition.

The presenting sign is excessive time taken to consume food (up to 2 hr). It is proposed that tongue pathology interferes with prehen­sion of the artificial diet. Ptyalism may occur unrelated to feeding or as the unsuccessful feeding event progresses. The food becomes slimy with saliva, further making it even less likely to stick to the tongue. It is not known if ptyalism is caused by oral pain or a response to the echidna trying to eat unsuccessfully, thereby promoting saliva production, or both. Appetite is often unaffected.

Abnormalities on oral examination include ptyalism and oral mucosa that easily bleeds. The tongue can be hyperaemic or pale, swollen, ulcerated and there may be loss of dorsal papilla. Cream-coloured plaques or mucoid accumulations may be present. Deeper examination of the oral cavity can be facilitated with the use of an endo­scope or otoscope.

Diagnosis is based on findings described in Table 29.2. Candida albicans is most commonly cultured, with C. glabrata and C. parapsilois occurring less commonly (Plate 29.1).

Treatment is topical and systemic antifungal therapy (see section 6.2). Candida albicans does not have predict­able susceptibility. If culture and susceptibility testing are unavailable, C. albicans is more often susceptible to amphotericin B, fluconazole and posaconazole (Ostrosky- Zeichner et al. 2003; Badiee and Alborzi 2011).

Supportive care is very important and includes fluid therapy, analgesia and caloric support. Affected echidnas may initially require daily gavage to administer medica­tion and food.

7.1.2 Ulcerative gastritis

Ulcerative gastritis is a common finding in echidnas in managed care.

It occurs both as an acute condition, mostly associated with concurrent disease or debilitation, and as a chronic disease. Clinical signs include weight loss or failure to gain weight in young echidnas, variable appetite and lethargy, and rarely, vomiting. Mycotic sto­matitis and ulcerative gastritis often occur concurrently.

Diagnosis is based on cytology of gastric aspirates (see Table 29.2). Candida spp. include C. albicans and C. glabrata and bacteria include Escherichia spp., Enterococ­cus spp., Klebsiella spp. and Lactobacillus spp. (Plate 29.2). These are considered normal flora of other mammalian species, but are possibly pathogenic in echidnas when compared with the normal gastric flora of primarily gram-positive cocci in free-ranging echidnas (Table 29.2).

Gross necropsy findings include mucosal ulceration, congestion, haemorrhage, fibrinous plaques and gastric wall thickening. Histopathological changes include mild focal to severe, extensive superficial suppurative inflam­mation of the squamous epithelium with erosion and colonisation or invasion with bacterial rods and yeasts, typically Candida spp. The epithelial changes are vesicu- lopustular and erosive (ARWH 2024 case nos 2480.1, 9239.2, 10783.1). Chronic changes include marked epithe­lial hyperplasia and submucosal fibrosis (ARWH 2024 case nos 2488.1, 8895.4, 11453.1). Inflammation can extend into the lamina propria, with the development of submucosal cysts, and into the distal oesophagus.

The microscopic features of echidna gastritis are most akin to those present in ruminal acidosis (Tong et al. 2017). Review of over 60 necropsies (1978-2018) from the ARWH reveal that these lesions are much more common in echid­nas that are in rehabilitation or managed care for more than 14 d, than they are in free-ranging echidnas. Artificial diets are therefore a likely cause (Shaw 2022). It is notewor­thy that since Taronga echidnas transitioned from a meat­mix diet to Wombaroo Echidna Diet (Wombaroo Food Products, Mount Barker, Australia) cases of ulcerative gas­tritis appear to have ceased.

Healthy stomachs were found to be lined by a consistent layer of coccoid bacteria, but inflamed stomachs had lost that layer and cocci were replaced by large numbers of rod bacteria and fungal bodies, suggesting that altered gastric microbiome, or dys­biosis, may play a role in the development of gastritis and/ or may be secondary to the inflammation (ARWH 2024; Tong et al. 2017). It is possible that free-ranging echidnas benefit from regular inoculation of the stomach from more frequent ingestion of the GIT microbiome of ants, termites and associated termite mounds and soils (Shaw et al. 2017).

Gastritis is often associated with systemic coccidiosis (Whittington and Obendorf 2012) and has been reported in hand-reared juveniles on high carbohydrate milk

Disease/infectious agent Diseaseaetiology Clinical signs and pathology Diagnosis Treatment
Endoparasites Flagellates Asymptomatic, diarrhoea Faecal examination Metronidazole if significant infection and clinical
Trichostrongyloides: Nicollina,

Tachynema, Tasmanema spp.1,2

Subclinical, diarrhoea. Non-suppurative enteritis if high burden.1,2 Death has been reported in free-ranging echidnas (Tachyglossus aculeatus) from trichostrongyloidosis3 Ivermectin, fenbendazole
Ectoparasites Mites: Odontacarus echidnus2 Dermatopathy (direct association with mites unconfirmed) Skin scrape, sticky tape cytology Ivermectin, fipronil, Selamectin
Ticks: Bothriocroton co neo Ior* (formerly

Aponomma),4 Ixodes spp.,* Haemaphysalis spp.

*Carries a novel Borrelia sp. (Candidatus Borellia tachyglossi4) that may have public health significance

None, dermatitis, anaemia with heavy burdens Presence of ticks
Fleas: Echidnophaga ambulans, Bradiopsylla echidnae None, pruritus Presence of fleas
Sparganosis Plerocercoids of Spirometra ernaceieuropaei5 SC masses, Intrathoracic and abdominal masses, fatal disseminated disease.1 Characterised by fibrous tissue and inflammatory infiltrate; presence of plerocercoids Clinical signs, necropsy, histopathology Surgical debulking
Salmonellosis Salmonella bovis-morbificans, S. Zanzibar, S. typhimurium, S. havana, S. Chester, S. dublin, S saint-paul, S. orion, S. arizona2'6'7 Subclinical, liquid to haemorrhagic diarrhoea, lethargy, weakness, septicaemia, death. Granulomatous hepatitis, suppurative enteritis and intussusception, peritonitis, multiorgan focal necrosis3,8 Faecal culture, necropsy Antibiotics, supportive care
Mycobacteriosis Mycobacterium chelonae, M. Intracellulare Incidental finding in lung at necropsy.9 Multifocal Pyogranulomatous abscessation1 Necropsy, culture None
Botryomycosis Staphylococcus aureus, β-haemolytic

Streptococcus spp.7,8,10

Soft-tissue swelling, necrosis. Pyogranulomatous reaction Biopsy, culture Antibiotics, analgesia
Bronchopneumonia Bacterial and fungal, Edswardiella spp.
often Secondaryto other diseases and beaktrauma2
Haemorrhagic nasal discharge, death. Pleural effusion, pulmonary oedema, purulent bronchiolitis, necrotising pneumonia Radiographs, computed tomography Antibiotics, antifungal therapy, nebulisation

29 - Short-beaked echidna 447

Table 29.3. (continued)

Disease/infectious agent Disease aetiology Clinical signs and pathology Diagnosis Treatment
Septicaemia Staphylococcus spp., Streptococcus spp., Aeromonas spp., Proteus spp.2 Can occur Secondaryto beak trauma, systemic Coccidiosis Lethargy, inappetence, death Blood culture, necropsy Antibiotics
Dermatophytosis Microsporum gypseumβ,u Circular alopecia, quill epilation, quill breakage KOH preparation, fungal culture, histopathology Topical enilconazole, miconazole, terbinafine, itraconazole PO
Mycotic dermatitis Malassezia spp.6 Multifocal, circular areas of alopecia, associated with exudative dermatitis Ifsecondary pyoderma (seen Injuvenileechidnas) Cytology, culture Topical miconazole or terbinafine, itraconazole PO
Alternaria sp. in a free-ranging echidna1 Quill loss, folliculitis Histopathology None
Cryptococcosis Cryptococcus neoformans Sudden death.
Concomitanttoxoplasmosis.

Mycotic pulmonary interstitial pneumonia,1 pulmonary necrosis, alveolar pneumonia, minimal inflammation12

Necropsy, histopathology None
Viruses Herpesvirus2

Poxvirus1,8

Death (n = 2)

Pouch lesions. Free-ranging juvenile with marked hyperkeratosis

Histopathology, electron microscopy, PCR None
Cryptosporidia Cryptosporidium fayerir3 Anorexia, concurrent disease Faecal examination, direct fluorescent antibody test None
Toxoplasmosis Toxoplasma gondii Neurological abnormalities. Non-suppurative encephalitis, hepatitis, splenitis, nephritis3 Associated with cryptococcosis in one case12 Necropsy, modified agglutination test, indirect fluorescent antibody test, ELISA (serum), PCR on fresh tissue, histopathology, immunohistochemistry, PCR (on fixed tissue) None reported but Ifsuspected in a live animal treatments used in other species could be trialled

1Whittington and Obendorf 2012; 2MiddIeton 2008; 3McOrist and Smales 1986; 4Loh etal. 2017; 5Spratt and Beveridge 2017, ARWH 2024 case no. 8895.4; 6Taronga Zoo records; 7ARWH 2024; 8Whittington 1994; 9ARWH 2024 case no. 10611.1; 10DoneIeyand Sprohnle-Barrera 2021; 11Whittington 1993; 12PhiIIips 2000; 13SIapeta etal. 2017, ARWH 2024 case no. 8060.1

448 CurrentTherapyin MedicineofAustraIian Mammals

Disease/agent Aetiology Clinical signs and pathology Diagnosis TreatmentZcomment
Gastric impaction Sinewy meat in diet, trichobezoars (fur ingestion from conspecific or overgrooming), phytobezoars (bamboo, coconut husk or mulch fibres) Inappetence, distended abdomen, vomiting, lethargy Clinical examination, radiography, contrast radiography, endoscopy, necropsy2 Surgery, correct diet
Hypervitaminosis D Increased serum 25(OH)-D from dietary excess (supplementation of adult diet or milk replacer in echidnas in managed care)3,4 Asymptomatic in adults. Sudden death in hand-reared juveniles with findings of metastatic calcification on necropsy1,2 Serum levels, physical exam, radiographs, necropsy Echidnas have low serum vitamin D and a reduced dietary requirement. Calcium absorption is independent of vitamin D, so milk replacer may have levels that exceed requirement.4 Risk Ofclinical disease in hand-reared echidnas
Dermatopathy (see

Chapter 12)

Nutritional aetiology suspected but not confirmed. Extensive investigations have not identified an aetiology

Seborrhoea6

Alopecia, quill changes and epilation. Orthokeratotic hyperkeratosis. Secondary infections in epidermis, spines and follicles. Similar but less severe changes reported in free-ranging echidnas5

Increased scale in hand-reared juveniles

Clinical signs. Fungal culture if suspect dermatophytosis Self-limiting. Systemic antibiotics if evidence Ofsecondary bacterial folliculitis

Topical keratolytics, Omega 3,6 oil

Foot pad dermatitis Surface insult and secondary bacterial infection Increased scale, erythema, ulceration Clinical signs Topical barrier cream or silver sulfadiazine; improve substrate - leaf litter, recycled paper cat litter
Recurrent blepharoconjunctivitis lmmune-mediated7 Non-seasonal periocular alopecia, blepharoedema, serous ocular discharge, chemosis, conjunctival hyperaemia and secondary entropion and trichiasis. Severe chemosis with any handling of eyelids. Mild chronic periadnexal inflammation, moderate chronic epidermal hyperplasia Ophthalmicexamination under anaesthesia. Intradermal allergen testing - strong reactions to all allergens including negative saline control, therefore of little use8 Parenteral treatments as topical application difficult. Prednisolone 5 mg PO sid 5 d, then taper dose. Removetrichiasis
Keratoconjunctivitis2 Unknown Ocular discharge, corneal opacity, corneal ulceration Ophthalmic examination Topical treatment under anaesthesia
Cataracts Unknown, trauma Cataracts Physical examination None, blind echidnas do well in managed care; monitor IOP

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Table 29.4. (continued)

bgcolor=white>History, clinical signs
Disease/agent Aetiology Clinical signs and pathology Diagnosis TreatmentZcomment
Burns (see Chapter 27) Bush fires Burnt spines, inappetence, lethargy, malodour. Burn severity is worse than what is observed on the surface. Necrosis may take a few weeks to be clinically evident Clinical signs Supportive care, antibiotics and analgesia for mild cases, euthanasia of severe cases
Skin erythema - periocular, ventrum, base of beak during anaesthesia Unknown, possible vasodilation Occurs post anaesthesia induction Erythema None, resolves
Hyperthermia Result of a combination of low Tb, heterothermy and exposure to high Ta without opportunity for behavioural thermoregulation Ataxia, inappropriate mentation, muscle fasciculations, tachycardia, tachypnoea, diarrhoea, haematuria and body temperature >37oC Active cooling with water or dilute alcohol and SC fluids. Wet towels inhibit evaporative cooling and should not be used. Monitor echidnas when Ta exceeds 35oC

1ARWH 2024 case nos 9239.2,11024.1; 2MiddIeton 2008; 3ScheeIings and Haynes 2012; 4ScheeIings et al. 2017; 5Whittington and Obendorf 2012; 6Whittington 1993; 7ARWH 2024 case no. 2452.2; 8LJ Vogelnest pers. comm. Ta, ambient temperature; Tb, basal body temperature.

450 CurrentTherapyin MedicineofAustraIian Mammals

formulae or in adults supplemented with carbohydrate rich milks (see section 7.2).

Treatment is similar to that for mycotic stomatitis with the addition of antibiotics. Cultures of gastric aspirates have shown a consistent susceptibility to amoxicillin-cla- vulanic acid and enrofloxacin (P Thompson pers. comm.). Transfaunation from healthy echidnas has been success­fully used to re-establish a more balanced microbiome in compromised individuals.

7.1.3 Diarrhoea

Diarrhoea is relatively common in echidnas in managed care. In the majority of cases the animal is otherwise well and diarrhoea is usually transient and/or diet associated. Historically, a range of meat, milk, glucose and oil-based gruels was fed, which invariably resulted in soft faeces. The addition of soil to the gruel improved faecal consist­ency. Newer diets have resulted in a significant improve­ment in faecal consistency (Stannard et al. 2017; see Chapter 14) (Complete Echidna Diet, Vetafarm, Wagga Wagga, NSW; Wombaroo Echidna Diet, Wombaroo Food Products, Mount Barker, Australia). Rescued free-ranging echidnas can develop diarrhoea while transitioning to an artificial diet. Echidnas with diarrhoea as a result of infec­tions are often unwell, with general malaise and weight loss. Faecal consistency is variable, ranging from grade 4 to 5, and can be accompanied by a large amount of gas in the faeces.

Diagnostic work-up should occur without delay if the echidna is unwell, if there is a change in consistently firm faeces, or if there is faecal blood. It will include a careful review of history, clinical examination under anaesthesia, radiography, which may reveal excessive GIT gas or consti­pation (causing paradoxical diarrhoea), haematology and biochemistry, and faecal examination (wet preparation, floatation, modified Romanowsky and Gram stains and culture). Non-budding yeasts, coccidia, flagellates and strongyle larvae and eggs are often found in healthy echid­nas. A high coccidia, flagellate or strongyle burden in an echidna with diarrhoea may be significant and treatment is recommended. Enteric pathogens found in echidnas with diarrhoea include Aeromonas hydrophila, Salmonella spp., Proteus spp. and Candida albicans, C. barcarensis and C. borborygmi (Whittington 1994; Ladds 2009). Non-infec- tious non-dietary causes of diarrhoea may include envi­ronmental or social stressors, toxins or irritants.

Treatment is specific in cases where an infectious cause is identified. Supportive therapies include SC crystalloid fluids, antidiarrhoeal preparations, analgesia and faecal transfaunation.

Treatment of intractable diarrhoea can be frustrating. Specific treatments for high burdens of flagellates or nematodes are not effective at resolving diarrhoea in all cases. In such cases where the diarrhoea persists, it is rea­sonable to assume the infectious agents may not have been the primary cause of diarrhoea. Anecdotally flu­conazole has been most effective in resolving diarrhoea associated with Candida spp. (Taronga Zoo records). Antidiarrhoeal suspensions and barium sulfate have been effective in some cases and transfaunation in many cases.

7.2 Failure to thrive in hand-reared echidnas

Wherever possible, puggles should be mother-reared, but zoo-bred puggles with poor weight gain or rescued free- ranging puggles will require hand-rearing or supplemen­tal feeding. Hand-reared puggles are susceptible to slow weight gain, stunted growth and recurrent GI disease (see section 7.1). Potential causes include nutritional deficien­cies, inadequate passive transfer of immunity, inappro­priate milk formula, lack of access to antimicrobial proteins in the mother’s milk (Kumar et al. 2019), or enteric infections. Feeding milk replacer to a weaned juvenile or sub-adult with a stomach that is already physi­ologically functioning as a fermentation chamber (see section 2.1) will result in ulcerative gastritis and possible subsequent scarring that then affects digestion through­out life (M Shaw pers. comm.). The simple carbohydrates within the milk, combined with an absence of fibre, pro­mote dysbiosis favouring acid-producing bacteria, further lowering the pH allowing these bacteria to thrive. Severe or recurrent gastritis has resulted in gastric fibrosis (ARWH 2024 case no. 2488.1). Some hand-reared echid­nas are predisposed to recurrent infectious disease, most notably coccidiosis and mycotic stomatitis or gastritis. Permanent stunting may occur as a result.

Determining a juvenile echidna’s age and whether it is weaned is challenging. It is usually straightforward in zoo-born echidnas because their age is usually known. However, growth curves for nursing echidnas are only linear for puggles between 5 and 55 d (Rismiller and McKelvey 2003). Therefore using body mass as a measure for estimating age in puggles >300 g is considered inac­curate (Griffiths 1978; Rismiller and McKelvey 2003). Further complicating age determination is differences in pelage growth. Puggles may present with fully developed pelage yet still be small (e.g. 400-500 g). As a guide, all puggles without a fully developed pelage and with no radiographic or faecal evidence of mineralised ingesta (i.e. soil/invertebrates) can be considered unweaned. Young echidnas with a fully developed pelage and evi­dence of mineralised ingesta may either be exploratory foraging and ingesting both milk and invertebrates or fully weaned. Behavioural cues may indicate whether an echidna is weaned or not. Puggles or juveniles that turn onto their sides to feed with or without kneading with their fore feet are very likely unweaned (A Sehlmeier pers. comm.). If unsure it is safer to feed an adult diet. Although milk replacer may cause gastritis in the adult stomach, offering an adult diet to an unweaned echidna is unlikely to have an adverse effect on gastric health. The addition of termites, ants or termite mound is recommended.

Frequency of milk feeds (usually q 3-5 d) will depend upon whether the young is pre- or post-emergent (see section 3) and should be individually titrated. Overfeed­ing can cause gastric distension, stasis and death (ARWH 2024 case nos 8935, 9024). Puggles (pre-emer- gent) can be fed as long as they do not have a distended abdomen, are defecating and are showing interest. When showing interest, warm in hand, and allow an ad lib milk feed, after which they may sleep for a few days before again showing interest in feeding. Post-emergent juveniles that have been forced to emerge prematurely (dug up, inadequate milk supply, dam failed to return) can be fed more frequently to meet increased energy demands from activity (e.g. a zoo-born post-emergent juvenile needing hand-rearing at 140 d (662 g) required feeding q 2 d). Based on free-ranging echidna behaviour, adult diet should routinely be made available to juve­niles from when they reach 1 kg or around 120 d, with ongoing access to milk either from the mother or milk formula (G Morrow pers. comm.). Weaning should take place over a minimum of 3-4 wk. It can take between 12 and 82 d for post-emergent juveniles to fully accept an artificial diet (Ferguson and Laming 2022). In the case of poor acceptance, adult diet is added gradually to milk formula. Milk formula is withdrawn once juveniles are ingesting an adult echidna diet, defecating and gaining weight consistently.

Weight can plateau or decrease by up to 20% in wean­ing zoo-housed echidnas for up to 4 wk during this period (B Finlaysonpers. comm.; Ferguson and Turner 2013) and is not unexpected because young free-ranging echidnas lose weight after weaning (Morrow and Nicol 2012). Weaned zoo-bred echidnas all lost weight after separation from their mothers, taking on average 3.5 wk to regain lost weight (Ferguson and Laming 2022).

If weight gain is persistently low in sub-adults, increase the amount fed or feed ad lib. Additives such as olive oil can adversely affect palatability and consistency whereas avocado, ground termite mound, termites and nutritional supplements (Megaderm, Virbac, Wetherill Park, NSW) may improve palatability for some echidnas. The addition of fruit, including paw-paw, or milk formula is not rec­ommended because it may cause gastritis. Faecal trans- faunation has resulted in improved weight gains in sub-adults. This provides natural GIT microbes thought necessary for transition to adult diets.

Hand-rearing is discussed in Middleton (2008) and Chapter 15.

7.3 Infectious disease

Infectious disease in echidnas in managed care is common and more prevalent than reported for free-ranging echid­nas. The reasons for the higher prevalence of infectious disease in echidnas in managed care are unclear, but envi­ronmental, nutritional, husbandry and other management factors may play a role. Infectious and non-infectious dis­eases are covered in detail in Middleton (2008) and Ladds (2009). A summary of significant disease of echidnas is provided in Table 29.3. Coccidiosis is discussed in Chapter 30.

7.4 Non-infectious diseases

Selected non-infectious diseases are summarised in Table 29.4.

7.4.1 Trauma

A review of the morbidity and mortality of free-ranging echidnas admitted to the Australian Wildlife Health Centre, Healesville Sanctuary found that 90.1% of echid­nas were admitted because of trauma. Of these, 73.2% were motor vehicle accidents and 14.2% were dog attacks (Scheelings 2016). Overall, there was 50.5% mortality; 38% of echidnas presented with beak fractures, 69.5% of which were either euthanased or died.

Although there is an inherent bias in a retrospective study reviewing wildlife hospital admissions, the results highlight anthropogenic effects on echidnas. Adult echid­nas comprised 77% of admissions and were more com­monly seen from October to January. These findings reflect the biology and behaviour of echidnas where activ­ity is increased in warmer months and adults are more likely to be moving throughout a home range. This review confirms findings in other literature where motor vehicle impacts are the dominant cause of trauma and beak frac­tures are the most common injury (Middleton 2008).

Guidelines for treating beak trauma are summarised in Middleton (2008). Anaesthesia and radiographic assessment of both the beak and the whole echidna is essential (Hulst et al. 2015). Anaesthesia may need to be delayed until significant swelling or haemorrhage has resolved. Echidnas with beak fractures that are open, unstable, significantly displaced or associated with sig­nificant soft tissue trauma should be euthanased (Table 29.1). Multimodal analgesia, fluid therapy, caloric sup­port and broad-spectrum antibiotics are essential when managing beak trauma. Feed from flat, shallow dishes.

Fractures of the appendicular skeleton are less common, a reflection of the robustness of the long bones, compact body shape and protective quills. External fixa­tion is not practical and internal fixation is rarely success­ful (see Chapter 10; ARWH 2024 case no. 11417.1). Anecdotal reports support conservative treatment of limb and pelvic fractures by confinement (M Pyne pers. comm., L Vogelnest pers. comm.).

7.4.2 Neoplasia

Few tumours have been reported in echidnas and are discussed in Chapter 18. Vaasjo et al. (2024) describe an intrathoracic mass in a zoo short-beaked echidna with a long history of intermittent anorexia and lethargy. CT confirmed a contrast-enhanced mass compressing the cranial vena cava and right atrium, and the animal was euthanased. The mass was diagnosed histologically as thyroid adenocarcinoma.

7.4.3 Dorsal alopecia

Characterised by easily epilated hairs and quills with a basal crust and dry, flaky skin. Epilated quills may be normal or have a crimped base. The head and ventral fur is often unaffected although one echidna has been seen by the author with recurrent ventral alopecia, and two cases of total alopecia (quills unaffected) have been reported (C Whitten pers. comm.). Signs appear in warmer months from October, but episodes have been seen in August and September. Cytology, microbiology and histopathology are usually unrewarding. In one adult female the alopecia has recurred annually in 10 of 15 yr (Taronga Zoo records). Multiple investigations did not reveal a cause and all episodes resolved within 3 mo with or without treatment. The histopathological diagnosis was orthokeratotic hyperkeratosis, which is commonly reported in echidnas with generalised dermatopathy (Middleton 2008; ARWH 2024; see Chapter 12). The same female also had a 4-mo episode starting in February concurrently with another non-contact female, both having bred the year before. Interestingly, the offspring of both developed dorsal alopecia simultaneously 1 yr later. This dermatopathy is thought to be a seasonal alopecia that may be hormonally or nutritionally induced.

ACKNOWLEDGEMENTS

I thank Vanessa Barrs, Brett Finlayson, Rebecca Russell- Cook, Gemma Morrow, Michael Pyne, Annabelle Sehlmeier, Michelle Shaw, Paul Thomson, Lydia Tong, Simone Vitali and Linda Vogelnest for providing infor­mation for this chapter. Special thanks to Larry Vogelnest and Tim Portas for the opportunity to contribute and for their patience and their editing and input - which was invaluable.

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Source: Vogelnest L., Portas T. (Eds.). Current Therapy in Medicine of Australian Mammals. CSIRO,2025. — 848 p.. 2025

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