DISEASES

Diseases of koalas are covered in detail in Blanshard and Bodley (2008) and Ladds (2009). Gamma herpesvirus, KoRV, cryptococcosis, chlamydiosis, haemoprotozoa and neoplasia are covered in other chapters.

4.1 Gastrointestinal disease

4.1.1 Caeco-colic dysbiosis/typhlocolitis syndrome

Aetiology and pathogenesis

CDTS refers to the spectrum of disorders associated with alterations in homeostasis, changes in caeco-colic motil­ity, water content, microbial composition, chemistry and epithelial function, and inflammatory changes in the caecum and proximal colon. It can affect both adult and juvenile koalas. The spectrum of conditions observed within CDTS ranges from mild dysbiosis to severe, fatal typhlocolitis. The aetiology and pathogenesis of CDTS are poorly understood and there are likely multiple aeti­ologies and pathogenic mechanisms involved.

These may include, but are not limited to:

• candidiasis/Candida spp. overgrowth - common in convalescing koalas and, if untreated or associated with severe or chronic stress or the use of corticoster­oids, can lead to invasive infections causing multifocal ulceration of the caeco-colic lining

• dysbiosis associated with antibiotic use - resulting in thinning and eventual loss of the mucobacterial lining of the caecum (Plate 33.16) and proximal colon (McKenzie 1978)

• severe stress associated with hospitalisation - reduced food intake resulting in caeco-colic ileus, which left untreated may lead to candidiasis, dysbiosis and advanced CDTS

• inappropriate combined use of NSAIDS and corticos­teroids - leading to fatal caeco-colic ulceration

• Clostridium spp. overgrowth and toxaemia - often in extreme cases of dysbiosis and following potent or high-dose antibiotics

• acute and massive fluid accumulation (oedema, ascites, pleural effusion and associated multi-systemic organ failure) - the mechanism in CDTS is unclear, but may be the result of severe vascular/endothelial damage by microbial toxins and/or a combination of mechanisms in severe cases (e.g.

• other potential, though less discernible aetiologies include chlamydial infection of the GIT (Burach et al. 2014; Hanger and Loader 2014), which may contribute to the pathogenesis of chronic plasmacytic enteritis and immunodeficiency and other conditions related to KoRV infection.

Clinical signs and diagnosis

Clinical signs seen in mild cases of CDTS include inap­petence, mild to moderate depression, weight loss and loss of body condition, mild to moderate dehydration, reduced faecal pellet output and small, hard, irregularly shaped faecal pellets (Fig. 33.3). Affected koalas may also change their eating behaviour, including choosing leaf sticks and mature leaf in preference to fresh tip, or eating bark. More severe cases are associated with severe depres­sion, bruxism, diarrhoea or significant reduction of or no faecal pellet output, dehydration, unpleasant odour,

Fig. 33.3. Normal adult faecal pellets (left); small, misshapen, dry pellets from an adult koala (Phascolarctos cinereus) with candidiasis and dysbiosis (right).

Fig. 33.4. Transverse sonographic image of the caecum showing the 'wagon-wheel' pattern suggestive of oedema of the longitudinal laminae.

generalised or dependent oedema, bloating and death. On palpation of the abdomen, mild or early cases may show no change in caeco-colic fill or consistency, whereas in advanced and/or severe cases, a variety of abnormalities may be palpable. These include: reduced caeco-colic fill (the abdomen, rather than round and full as in a normal koala, feels empty); ability to palpate the caeco-colic wall as a thin, membranous structure; palpation of obstipated faecal masses; palpation of the oedematous, thickened caeco-colic wall; and findings consistent with ascites.

Leucocytosis may be observed in mild cases, but pro­found leucopenia and hypoproteinaemia may be seen in severe cases. Transabdominal sonography may show a slight or pronounced ‘wagon-wheel’ pattern of the caecum and proximal colon when viewed in transverse section (Fig. 33.4). This is the result of oedema of the lon­gitudinal laminae (Plate 33.17) and/or dehydration and inspissation of the mucobacterial lining of the caecum and proximal colon, causing the longitudinal laminae to be clearly visible and thickened sonographically (in normal koalas, the caeco-colic laminae are barely visible sonographically). In some cases there may be atony and increased fluidity of the caeco-colic contents (Plate 33.18), which is reflected as decreased motility and reduced echogenicity of the caeco-colic contents. Radiography may identify gas within the lumen of the caecum.

Abdominocentesis is not always useful, though may indi­cate aseptic or septic peritonitis, particularly in cases of GI perforation.

Pathology

The range of pathology of CDTS reflects the variable aeti­ologies, pathogeneses and chronicities of the disorders that make up the syndrome. In mild cases, such as mild candidal overgrowth, the gross and histological changes are inapparent or very mild (e.g. a reduction in caeco- colic contents). Severe cases may be associated with obsti­pation, ulceration and haemorrhage (Plate 33.19), perforation of the caecum and/or colon and severe oedema (either localised to the caeco-colic wall, through­out the GIT or generalised leading to ascites, pleural effu­sion and SC oedema). Inflammatory changes include chronic plasmacytic enteritis, characterised by infiltrates in the lamina propria and sometimes submucosa of the small and large intestine, together with a variable degree of fibrosis.

Treatment and prevention

Conservative and judicious use of antibiotics and mini­mising stress are critical factors in the prevention of CDTS. Therapy should be directed at rehydration, nutri­tion, improving gut motility and restoring GI flora, with treatments referable to the cause (e.g. oral antifungal therapy for candidal overgrowth [see section 4.1.2], trans- faunation when dysbiosis is caused by antibiotic use) (Table 33.3). Early diagnosis and management are critical to successful treatment. Once severe CDTS is established, antibiotics are likely to be of limited use even when infec­tion or clostridial toxicosis is suspected.

Prognosis

Uncomplicated dysbiosis associated with antibiotic use has a reasonable prognosis if it is detected early and transfau- nation therapy commenced promptly. Once the mucobac- terial lining is damaged or lost, the caecum and proximal colon are extremely susceptible to secondary infection and ulceration. Multifactorial and complicated CDTS carries a poor prognosis, particularly when associated with KoRV- related immune deficiency and leukaemia/lymphoma (see Chapter 34). Further research into the causes, pathogenesis and management of CDTS is warranted.

4.1.2 Candidiasis

Candidiasis, caused by Candida spp. (usually C. albicans) is extremely common in convalescing koalas and hand­reared orphans and is often overlooked until the koala is critically ill and the prognosis is poor. Inappropriate hygiene, inappropriate diet, dysbiosis, debilitation from concurrent injury or disease and stress are likely to con­tribute to candidiasis. The most common sites of candidi­asis are the oral cavity and hindgut. Affected koalas may be inappetent, have reduced faecal output, dysphagia, stomatitis or frequently drop leaves while eating. Severe infections can cause obstipation, CTDS and death.

A diagnosis of candidiasis is based on clinical signs and the identification of Candida organisms in faecal or oral swab preparations. They are ovoid to round, some­times budding, mildly refractile structures on wet prepa­rations (Fig.

Regular faecal examination should be conducted on all convalescing and hand-reared koalas (Table 33.3), with more frequent assessment when inappetent and/or faecal output is reduced. When koalas are observed dropping leaf or have evidence of stomatitis, swabs of each cheek pouch (buccal mucosal pockets dorsal to the maxillary premolar teeth) should be examined. When more than one Candida

Fig. 33.5. Budding Candida (arrow) and non-budding (arrowhead) on faecal wet preparation (?100 magnification).

Fig. 33.6. Normal koala (Phascolarctos cinereus) faecal flora, including 'koala yeast' (arrow), on wet preparation (?40 magnification)

per high-power field, or budding forms of Candida are seen, treatment should commence and continue until two consecutive negative results are achieved 3-5 d apart.

Treatments of choice for candidiasis include nysta­tin, amphotericin B or fluconazole administered PO tid-qid for a minimum of 10 d (see Appendix 4). Oral candidiasis is treated with topical oral antifungal prod­ucts (e.g. miconazole oral gel; Daktarin Oral Gel, Jans- sen-Cilag, NSW) bid-tid for 5-7 d. Nystatin fails to eliminate lower GI candidiasis in ~50% of koalas, requiring a change in therapy to oral amphotericin B or oral fluconazole. Antifungal resistance in C. albicans is well documented (Mishra et al. 2007) and resistance to nystatin has been linked with biofilm production (Chandra et al.

4.1.3 Gastrointestinal torsion and intussusception

Both GI torsion and intussusception have been reported in koalas (Blanshard and Bodley 2008; Joyce-Zuniga et al. 2014). Presentation varied from inappetence and reduced faecal pellet production to abdominal distension, stretch­ing and open-mouth gasping. Prognosis is poor, with recurrence common after surgical correction (50%) and >80% mortality. Most individuals die shortly after onset of clinical signs or soon after surgical intervention (see Chapter 10). The aetiology remains unclear and may be related to overall GI health, alterations to GI function fol­lowing a change in eucalypt species and stress (Joyce- Zuniga et al. 2014).

4.2 Respiratory diseases

4.2.1 Bordetellosis

A zoo colony of 13 koalas in south-east Qld succumbed to an outbreak of bordetellosis caused by Bordetella bron- chiseptica. Despite multiple courses of antibiotics (trimeth- oprim-sulfonamide, gentamicin and chloramphenicol), nebulisation and vaccination, 7 of the 13 koalas died or were euthanased. Histopathology revealed severe, chronic, diffuse histiocytic interstitial pneumonia with bronchiolar and type II alveolar epithelial hyperplasia and moderate fibrosis, suggestive of toxicity or viral infection. Herpesvi­ruses were excluded by PCR. Although the initial outbreak was attributed to B. bronchiseptica, a secondary viral pneumonia was suspected (C Lacasse pers. comm.). Subse­quent to this and other similar outbreaks of bordetellosis in zoo koalas, the frequency of booster vaccination in some Qld facilities has been increased to q 6 mo. Although not fully protective, this new regimen has reduced clinical signs and prevented fatalities where further outbreaks occurred (M Pyne pers. comm.).

4.2.2 Verminous pneumonia

A severely emaciated free-ranging adult male koala from south-east Qld with severe dyspnoea and lethargy and radiographic evidence of extensive pulmonary disease was euthanased because of poor prognosis. Histopathol­ogy of the lung revealed numerous small nematodes con­sistent with Durikainema sp. within the pulmonary vessels and vascular intimal hyperplasia, some eosino­philic vasculitis and occasional thrombosis. Mild to mod­erate multifocal histiocytic interstitial pneumonia/ alveolitis and haemosiderosis consistent with cardiac failure was also present. Durikainema sp. have been iden­tified in several koalas from NSW but not Qld, and described as Durikainema phascolarcti n. sp (Spratt and Gill 1998). Previous infections have not been associated with pulmonary inflammation, but were suggested to potentially impede cardiopulmonary function through obstruction of pulmonary vessels (Spratt and Gill 1998).

4.3. Urinary tract disease

4.3.1. Oxalate nephrosis in free-ranging and rehabilitating koalas

a. Aetiology and pathogenesis

Oxalate nephrosis is frequently reported in free-ranging rescued and managed koalas from the Mount Lofty Ranges in SA (Speight et al. 2013a). Approximately 55% (32/51) of koalas examined from this region were affected with gross and/or histopathological evidence of renal oxalate deposition. Affected individuals were usually res­cued after being found on the ground in poor condition or polydipsic (N Speight pers. comm.). Gross appearance of the kidneys at necropsy included pale yellow crystal precipitation, particularly at the renal papilla. Renal his­topathology included tubular loss, cortical fibrosis, tubule dilation, glomerular atrophy and crystal-associated inflammation. A genetic predisposition to endogenous oxalate overproduction is suspected in South Australian koalas, with eucalypt leaf oxalate levels (usually <1%) thought to have a secondary rather than primary role (Speight et al. 2013b). Histological surveys of renal tissues collected from Vic. koalas between 2010 and 2017 found renal changes consistent with oxalate nephrosis in approximately 14% of cases. All were from French Is. or populations with French Is. origins and not from Str- zelecki populations (Speight et al. 2020a). There does not appear to be an association with oxalate nephrosis and low/absent Oxalobacter formigenes abundance in SA koalas (Speight et al. 2019.).

In contrast, clinical oxalate nephrosis is rarely observed in free-ranging koalas from other parts of Australia. How­ever, it is relatively common in free-ranging koalas in Qld undergoing treatment and rehabilitation. Possible causal mechanisms include: loss of oxalate-degrading bacteria through antibiotic therapy; high levels of oxalate or oxalo- genic compounds/precursors in browse; and chronic stress or other factors related to managed care affecting the GI microbiome. A single aetiology seems unlikely, as some clinicians report a seasonal or weather-related varia­tion in frequency of cases (C Lacasse and A Robbins pers. comm.). This suggests a concomitant variation in oxalate or oxalogenic substances in the browse may be a contrib­uting factor; however, facilities housing both zoo-based koalas and caring for sick and injured free-ranging koalas often feed the same range and species of browse to both cohorts, with only the free-ranging koalas succumbing to the condition. Oxalobacter formigenes is susceptible to doxycycline and quinolone antibiotics such as enrofloxa- cin and their use may predispose treated koalas to oxalate nephrosis; however, it is also seen after treatment with chloramphenicol (A Robbins and J Loader pers. comm.). Mild oxalate nephrosis has been detected as an incidental finding in otherwise healthy free-ranging koalas and as an incidental necropsy finding. Rescued free-ranging koalas that develop oxalate nephrosis during care often do not have pre-existing renal functional abnormalities in blood and urine analysis or sonographic abnormalities at admis­sion. At one treatment facility in Qld, >70% of cases occurred in koalas undergoing treatment for chlamydio- sis. Affected koalas commonly displayed acute (<5 d) and dramatic weight loss (400-1000 g), reduced appetite and dehydration. Mortality was ~50% and appeared to be highest in koalas affected within the first 2 mo of care.

The primary pathogenic mechanism in koalas is physi­cal damage and associated inflammation in the renal parenchyma caused by the deposition of calcium oxalate crystals. In severe cases, renal failure or secondary septi­caemia and death can occur. The pathogenesis of hyper­oxaluria in some individuals (but not others on similar diets and in similar conditions) and/or the failure of inhibition of crystal nucleation, aggregation and growth, leading eventually to tissue deposition, are poorly under­stood in koalas.

b. Diagnosis

Definitive diagnosis of oxalate nephrosis is confirmed by ultrasound examination (observable renal medullary and/or cortical hyperechogenicity and loss of parenchy­mal detail [Fig. 33.7]) and crystalluria, consistent with calcium oxalate crystals. Hyperechoic deposits (Fig. 33.8) within the renal cortex and/or medulla are intermittently seen during ultrasound examinations of free-ranging koalas in south-east Qld and northern NSW.

Clinically affected koalas may or may not be azotae- mic; however, urine specific gravity is usually <1.035. The majority (93%) of koalas from SA that were affected by oxalate nephrosis were azotaemic (urea >6.6 mmol/L and creatinine >150 μmol∕L) and azotaemic animals had a urine specific gravity <1.035. All koalas from the Mount Lofty Ranges were hyperoxaluric when compared with koalas from other regions (Qld) and urinary crystals were consistent with calcium oxalate but with an atypical ‘spiky bowtie’ morphology (Speight et al. 2014). Elevated SDMA levels have been observed in a proportion of

Fig. 33.7. Hyperechoic medulla and cortex with loss of parenchymal detail in the kidney of a koala (Phascolarctos cinereus) with oxalate nephrosis.

Fig. 33.8. Hyperechoic deposits (arrows) in the renal medulla of a healthy free-ranging koala (Phascolarctos cinereus).

affected koalas from the Mt. Lofty ranges (Speight et al. 2020b). Urinary crystals in koalas from Qld were typi­cally rectangular or oval (Plate 33.15), consistent with calcium oxalate monohydrate. In advanced cases, koalas develop renal failure, electrolyte imbalance, caecal stasis and oedema and sometimes septicaemia. Anecdotally, total blood calcium is often low in affected individuals and can be used as a prognostic indicator. Hypocalcaemic koalas may also have varying degrees of hypoproteinae- mia, associated with a poorer prognosis.

Treatment and management

Treatment is challenging and generally unsuccessful in advanced cases, so prevention and early detection and treatment are important. Supplementation with oral cal­cium may help to bind oxalate in the GIT and reduce absorption of unbound oxalate. Hypocalcaemic koalas and those with cortical and medullary hyperechogenicity on ultrasound examination have been supplemented with low doses of oral calcium (1-2 g of calcium carbonate powder sid). Supplementation may result in temporary hypercalcaemia causing diarrhoea and inappetence and in these circumstances the dose should be reduced or therapy discontinued. Administration of caecal contents (pap) together with fluid support has been effective in some koalas that had received antibiotics for chlamydial infections, presumably by restoring oxalate-degrading bacteria to the gut (Loader J and Robbins A, pers. comm.). Given the difficulty in obtaining and storing fresh caecal contents, treatment (or prevention) with O. formigenes- containing probiotics may be worthwhile as an alterna­tive (L. Vogelnest pers. comm.), but to date this has not been used and its efficacy is speculative. Management of dehydration by administration of IV and SC fluids is required. Adding vitamin B complex to IV fluids may assist in the metabolic processing of oxalate. Dietary management for treatment and prevention should include feeding a high diversity of freshly cut eucalypt and non- eucalypt browse species. This allows selection of lower- risk browse by the koala and appears to be important to treatment success. The installation of overhead water misters in koala enclosures may reduce the incidence of oxalate nephrosis.

4.3.2. Non-Chlamydial cystitis

a. Fungal cystitis

Fungal cystitis was reported in six adult free-ranging koalas admitted to a south-east Qld wildlife facility for treatment of chlamydial cystitis. Following completion of chlamydial treatment (chloramphenicol ± prednisolone), all koalas were dysuric, haematuric and pyuric, and most still had marked sonographic thickening of the bladder wall (3-11 mm). Fungal hyphae or yeasts were observed on Diff-Quik-stained smears of urine sediment collected via cystocentesis (Plates 33.12 and 33.13). None had detectable fungal elements on urine sediment examina­tions at admission. Solid pellets of sediment were detect­able on ultrasound examination of the bladder of some individuals. Urinary cultures yielded C. albicans and Aspergillus fumigatus (not concurrently). Treatment suc­cess was achieved in 50% of cases after trialling multiple regimens. Treatment failure is likely attributable to poor oral absorption of most antifungal drugs, efficient drug metabolism in the liver by cytochrome P450 (see Chapter 11) and perhaps resistance of some organisms following multiple ineffective antifungal regimens. Greatest success is likely achieved through aggressive, prompt and long­term treatment regimens of IV fluconazole bid or ampho­tericin B q 48 hr for a minimum of 4-6 wk.

b. Bacterial cystitis

Bacterial cystitis is likely a result of ascending infection from the urogenital sinus and is often associated with common GI bacteria. Urinary sediment examination of koalas with bacterial cystitis is likely to have coccobacilli or rods (not seen in chlamydial cystitis) and may be asso­ciated with concurrent crystalluria, pyuria and the pres­ence of hyaline and granular casts. In one free-ranging koala joey, bacterial cystitis caused by Escherichia coli was associated with sulfonamide (Plate 33.14), ammonium urate and calcium oxalate crystalluria and the presence of hyaline and granular casts. The joey deteriorated despite treatment and was subsequently euthanased. Renal histo­pathology revealed tubulointerstitial nephritis with low numbers of intratubular oxalate crystals and mild tubular mineralisation.

4.4 Ophthalmic disorders

4.4.1 Keratomycosis

Keratitis and corneal ulceration in koalas, refractory to topical antimicrobials, may be caused by fungal infection. Keratomycosis primarily affects the corneal epithelium and stroma, and occurs most frequently following ocular trauma with vegetable matter (Sonal 2011). Culture may confirm fungal infection; however, the epithelium overly­ing some fungal infections may heal, sealing in the infection with negative fungal cultures. The topical anti­fungal drug of choice is undiluted fluconazole IV solution 200 mg/100 mL (Diflucan, Pfizer Australia, West Ryde, NSW) applied topically to the affected eye qid. Efficacy may be hindered by poor penetration, especially with intact epithelium or endothelial plaque. Regular epithe­lial debridement may be required to improve drug contact with the fungus. A compounded topical preparation of DMSO 10%, norfloxacin 5% and ketoconazole 2% has improved treatment success. Without aggressive long­term therapy, prognosis is poor and enucleation of the affected eye or euthanasia may be required.

4.4.2 Anterior chamber collapse syndrome

A case of anterior chamber collapse syndrome following suspected corneal trauma has been reported in an adult free-ranging koala (Liddle et al. 2014). The globe was markedly buphthalmic with increased intraocular pres­sure. Glaucoma was secondary to the initial anterior chamber collapse. Enucleation was performed because of poor vision and to alleviate ongoing discomfort and risk of proptosis.

4.5 Other disorders

4.5.1 Trauma and predation

Trauma is common in free-ranging koalas and is usually the result of motor vehicle collisions, dog attacks and burns. Natural predation by carpet pythons (Morelia spi- lota) is also a notable cause of mortality in free-ranging koala populations in SEQ (Robbins et al. 2019). In zoo­housed koalas, injuries from conspecific aggression are the most common cause of trauma. Although inter-male fighting injuries are usually not life-threatening, severe injuries may cause abscesses, bone infection and occa­sionally death (Hanger et al. 2017).

Injuries from dog attacks may be inconspicuous, unless puncture wounds occur over areas of muscle or bone such as the rump, limbs, neck or head. Blood or saliva is sometimes visible on the fur, but this may be less obvious over the abdomen, during damp weather or if the koala has been in contact with the ground. During dry weather, fur that has been contaminated with saliva may stick together, creating in a ‘paint brush’ appear­ance to the fur tips (Fig. 33.9). This effect, and subtle abrasions on shaved skin, may be the only indication of a dog attack (Figs 33.10 and 33.11). Underlying soft tissue damage and fractures are often extensive and severe, and external lesions often belie the severity of internal damage (Fig. 33.12).

Fig. 33.9. 'Paint-brush' tipping of the fur following a dog attack, showing the tips of the fur stick together with saliva.

Fig. 33.10. Subtle indications of a dog attack include fine abrasions visible on shaven skin (particularly of the abdomen). This may be the only indication of a dog attack in a koala (Phascolarctos cinereus).

Signs of predation by carpet pythons are often subtle, but include a U-shaped primary bite site, slicking of fur from python saliva (especially around the face) and dif­fuse, uniform pulmonary congestion consistent with a fatal constriction. Other lesser observed signs include vascular injection of the SC tissue, petechial and ecchy- motic haemorrhages at or around the bite or constriction site, and the presence of shed python teeth in bite wounds (Robbins et al. 2019).

Koala habitat may be severely impacted by fire and koalas often require intensive and prolonged treatment and rehabilitation. Post release monitoring of koalas affected by fire indicates that they can be successfully reintroduced to burnt landscapes post fire (Lane et al. 2023). Burn injuries and smoke inhalation sustained in bushfires may be severe and euthanasia is usually indi­cated in koalas with extensive, full-thickness burns and severe respiratory signs (Baek et al. 2023). See Chapter 27 for management of burn injuries.

Fig. 33.11. Shaving the fur from an area with saliva may reveal only minor abrasions on the skin (a). This belies the often severe trauma beneath (b).

Fig. 33.12. Severe caecal trauma may occur in koalas (Phascolarctos cinereus) attacked by dogs despite few external signs of injury.

4.5.2 Hip and shoulder dysplasia

Metabolic bone disease has been proposed as the patho­genic mechanism of hip and shoulder dysplasia in young koalas without sufficient exposure to natural ultraviolet light in zoo facilities in the USA (Pye et al. 2008; Pye et al. 2013; Pye 2009). In koala joeys, hip and shoulder dyspla­sia was prevented by regular exposure to natural sunlight and supplementary feeding with milk protein-based powder containing vitamin D (Portagen, Mead Johnson Co., Evansville, IN, USA) administered to the dam during gestation, pouch rearing and to the joey following pouch emergence (G Pye pers. comm.).

4.5.3 Diabetes

Diabetes mellitus in koalas has been infrequently reported (Blanshard and Bodley 2008). In free-ranging koalas undergoing managed care, hyperglycaemia is occasionally observed. In a retrospective study of 17 hyperglycaemic koalas, 75% (13/17) were male, all were undergoing or had completed chlamydial treatment with systemic antibiotics and six had received oral prednisolone during treatment. Affected koalas displayed rapid loss of body condition (within days), despite normal or increased appetite. Blood glucose varied from 10 to 26 mmol/L, with some having glucosuria. A total of 12 koalas were treated (5 were not treated, because of poor prognosis or concurrent disease) with insulin (Caninsulin®, MSD Animal Health, NJ, USA) at 0.25-0.5 IU∕kg SC sid-bid. Eight koalas responded to therapy, with six recovering fully and were released fol­lowing resolution of hyperglycaemia and underlying ill­ness. There was no apparent correlation between the degree of hyperglycaemia and response to therapy or clinical outcome. Necro' 1 ’,i< ni.ii' of the koalas that failed to respond to treatment revealed moderate to severe diffuse pancreatic islet cell vacuola­tion, with pyknosis and mild reduction in the number of islet cells and mild to moderately reduced immunohisto­chemical staining for insulin (J Mackie pers. comm) Taken together, the clinicopathological findings suggest that the pathogenesis of diabetes mellitus in koalas in managed care may involve transient, stress-related insulin resistance (potentially exacerbated by prednisolone ther­apy). Subsequent hyperglycaemia and hyperinsulinaemia may cause islet toxicity with vacuolation and ultimately islet exhaustion and decreased insulin production, rather than insulin deficiency per se (J Mackie pers. comm.).

4.5.4 Kyphosis, scoliosis and osteopathy

Kyphosis and kyphoscoliosis have been seen in free- ranging koalas presented to wildlife facilities in SA (W Boardman pers. comm.) and south-east Qld (T Portas, M Kunde and J Loader pers. comm.). The aetiology is unknown and trauma seems unlikely, because of the con­sistent mid-thoracic location and morphological charac­teristics of the lesion. The spinal deformity is grossly apparent in the advanced stage and is clearly visible radi­ographically, affecting the mid-caudal thoracic vertebrae (Fig. 33.13). Mobility does not appear to be significantly affected in many koalas and most are able to climb and run to adequately survive in the wild, although in one case (D de Villiers pers. comm.) the lesion progressed suf­ficiently to impede mobility and browsing.

Hypertrophic osteopathy secondary to pulmonary actinomycosis was described in 17 koalas from SA.

Fig. 33.13. Kyphosis in a 10-yr-old free-ranging male koala (Phascolarctos cinereus). The koala was ambulatory and able to climb, but was in poor body condition at the time of rescue. Image: Timothy Portas

Periosteal surfaces of the metaphyses and diaphyses of long bones were thickened and roughened with radio­graphic and computed tomography images demonstrat­ing periosteal reaction on the scapula, humerus, ulna, radius, ilium, femur, tibia, fibula, metacarpus, metatarsus and phalanx (Griffith et al. 2021).

4.5.5 Otitis media

Otitis media has been diagnosed in both free-ranging and zoo-based koalas. Lesions in free-ranging koalas are often detected after presentation for other conditions (e.g. trauma, chlamydiosis), but in one case the koala had an obvious mass affecting the face. Otitis media in a koala in managed care was found incidentally during a CT scan to investigate a potential nasal cryptococcal granuloma (C Singleton pers. comm.). Most free-ranging koalas affected by otitis media have concurrent chronic otitis externa (exudate and thickening of ear canal). One had a head tilt and drooping pinna on the affected side and thick nasal discharge. In another case, impaction of the ipsilateral cheek pouch caused by a neurological deficit associated with osteomyelitis was obvious as a gross asymmetry of the face (J Loader and A Robbins pers. comm.). In affected free-ranging koalas, otitis media is identified radiographically as increased density in the right or left tympanic bulla, with localised osteo­myelitis in two cases. Corynebacterium spp. are often cultured from affected ears and otitis media lesions; a mixed infection of Pseudomonas aeruginosa and E. coli was cultured from the ear canal of one case and Yokanella regensburgei was cultured in another case. The latter koala (Y. regensburgei case) was successfully returned to the wild following surgical external ear canal ablation and tympanic bulla osteotomy (Hulst et al. 2015), where it remained healthy for >6 mo of post­release monitoring (Swaffield et al. 2023). Other cases were euthanased because of poor prognosis and/or con­current illnesses.

4.5.6 Oesophagitis, pharyngitis and tonsillitis

A small number of rescued free-ranging koalas from Qld undergoing rehabilitation have been observed to be coughing while eating, dysphagic and/or displaying regurgitation-like behaviour after eating. Some individu­als appeared to spontaneously recover, but others deterio­rated. No abnormalities or obstructions could be identified within the mouth or oropharynx. One female intermit­tently displaying dysphagia and regurgitation over a 2-wk period was euthanased following sudden aspiration of copious amounts of masticated leaf material. Gross nec­ropsy revealed severe ulceration and abscess formation within the oesophageal sphincter. A large subcapsular haematoma on the liver was also present, suggesting trauma was the cause of both findings. A second female was euthanased following deterioration from pneumonia. Gross necropsy revealed an ulcerated mass in the left aryt­enoid and a second mass at the epiglottis. Severe ulcerative pharyngitis and tonsillitis with infiltrates of histiocytes and Langhans giant cells were seen histologically. Primary mucosal trauma through ingestion of poorly masticated leaf matter or secondary necrosis of traumatised soft tissue following blunt force trauma (e.g. motor vehicle strike) was the suspected aetiology. Koalas displaying signs of coughing, dysphagia or regurgitation should be examined endoscopically to visualise the oropharynx, oesophagus and oesophageal sphincter.

4.5.7 Ptyalism or sialorrhea

Ptyalism has been observed in a small number of rescued free-ranging koalas in south-east Qld undergoing reha­bilitation. The onset of ptyalism has been observed days to months after admission, with no sex or age predilec­tion. Affected koalas eat normally and do not have any oral (mucosal or lingual) injury. Copious amounts of saliva overflow at the commissures of the mouth, induc­ing severe secondary moist dermatitis and alopecia on the neck, chest, abdomen and limbs. Aetiology is unknown, despite extensive gross and histopathological investigation. The condition is often unresponsive to treatment, including antifungals and antibiotics, NSAIDs, prednisolone, atropine, leaf species variation and transferring koalas to outdoor treed/hands-off enclosures. Targeted radiation therapy, intended to induce atrophy of the parotid salivary glands, was tri­alled as a treatment in one koala. Despite repeated treat­ments, this therapy failed to reduce the flow of saliva or size of the glands.

4.5.8 Polyarthritis

Several koalas presented to a wildlife facility in south­east Qld were observed with swellings to one or more joints. The lesions were consistent with polyarthritis at necropsy. One case was emaciated with swelling to the tarsal joint, severe chlamydial cystitis, deep fungal der­matitis and a small bony proliferation on the head (oste­ochondroma). Necropsy revealed thickening and discolouration of the synovial joint fluid and thickening of the joint capsule. Cytology of the joint fluid revealed moderate cellularity, mostly neutrophils (>90%) and activated macrophages, lymphocytes and synovial lining cells. Culture failed to reveal a bacterial agent and bacte­ria were not observed cytologically. The affected syno­vial joint fluid was positive for Chlamydia pecorum on qPCR, suggesting arthritis may be an uncommon mani­festation of C. pecorum infection in koalas (Burnard et al. 2018).

4.5.9 Coccidiomycosis

Disseminated coccidiomycosis was detected in a zoo­housed koala with non-specific illness and signs of weight loss. Lung, liver, spleen, kidney, lymph node, heart, eye and bone marrow were all affected (Burgdorf- Moisuk et al. 2012). The koala was IgM and IgG seron­egative for Coccidioides spp. Pathological examination revealed infiltrates of neutrophils and macrophages, rare multinucleated giant cells and numerous spherical fungal organisms characteristic of Coccidioides spp. Infection may be via inhalation of contaminated soil or entry via a traumatic wound or animal bite (Burgdorf- Moisuk et al. 2012).

4.5.10. Parasitism by Ophidascaris robertsi

Larval forms of the python nemotode Ophidascaris rob­ertsi have been observed obstructing hepatic blood ves­sels in a koala from southeast Qld (Gonzalez-Astudillo et al. 2019). Grossly the liver contained multiple domed regions within the parenchyma containing larval nemo- todes. An encysted larva was also found beside a thoracic vertebra. It is presumed that infection with Ophidascaris robertsi was acquired through ingestion of soil contami­nated with eggs shed in python faeces.

4.5.11 Testicular asymmetry and hypoplasia

Testicular asymmetry and hypoplasia is occasionally observed in free-ranging koalas throughout their range. This could be associated with developmental or infectious aetiologies, including Chlamydia pecorum. Although tes­ticular asymmetry appears relatively common, hypoplas­tic, aplastic or microtestes are rare. Testicular asymmetry does not infer decreased reproductive capacity in koalas unless testicular hypoplasia, aplasia or microtestes are present. Hypoplastic, aplastic or microtestes result from severe disruption and fibrosis of the testicular paren­chyma (Buchanan et al. 2022).