Cutaneous and Respiratory Lesions in Bushfire-Affected Koalas.

In the wake of increasingly frequent bushfires emerging as a threat to wildlife worldwide, koalas have notably been the most rescued species in Australia. However, our understanding of burns and their severity in koalas is limited; hence, this study investigated the histopathological features and depth of burns in koala skin, as well as the presence of smoke-induced respiratory tract damage. In four bushfire-affected koalas that had been euthanised on welfare grounds, skin burns in various body regions were scored based on clinical appearance as superficial, partial thickness, or full thickness. Histological sections of affected regions of skin were assessed as Grades I-IV and showed that furred regions on the ear margins and dorsum were histologically more severe, at Grade III, compared with the clinical score. There was a similar finding for footpad burns, which were the most common body region affected. In the respiratory tract, pulmonary oedema and congestion were evident in all koalas. Overall, the results highlight that cutaneous burn lesions on furred and palmar/plantar surfaces can have higher severity based on the burn depth than is clinically apparent. Therefore, there is a need to consider this when developing treatment plans and establishing prognosis for burnt koalas at triage, as well as that a high likelihood of pulmonary oedema exists.

Therapeutics in Herd/Flock Medicine.

When treatment is required for a herd/flock health concern, a range of factors must be considered to determine the preferred treatment strategy. If a group treatment strategy is pursued, considerations to optimize the likelihood of safe and effective group treatment include taxon-specific pharmacokinetics/pharmacodynamics, the formulation of prescribed medication, the type and amount of food, the number and type of water sources, enclosure design, size and demography of the group, weather conditions, and health status of individuals in the group. In addition, antimicrobial stewardship principles and relevant legislation/regulation must be at the forefront of decision making.

Horner Syndrome With Ipsilateral Wing Paresis in a Wild, Juvenile Yellow-Tailed Black Cockatoo (Calyptorhynchus funereus).

A juvenile yellow-tailed black cockatoo (Calyptorhynchus funereus) was presented with paresis of the right wing, ptosis, and miosis of the right eye; feather erection of the right side of the head and neck; and a penetrating injury over the right pectoral muscle. Temporary reversal of ptosis, miosis, and feather erection after administration of phenylephrine drops confirmed a diagnosis of Horner syndrome. Computed tomographic imaging revealed a fractured rib, traumatic lung lesions, and subcutaneous emphysema. The right-sided Horner syndrome and wing paresis were attributed to a sympathetic nerve trauma of the eye and feathers and to the brachial plexus, respectively. This report describes the diagnosis and resolution of ptosis and miosis within 8 weeks and recovery of feather symmetry and wing function within 11 weeks of the cockatoo's initial presentation with a conservative-management treatment plan.

Psittacid Adenovirus-2 infection in the critically endangered orange-bellied parrot (Neophema chrysogastor): A key threatening process or an example of a host-adapted virus?

Psittacid Adenovirus-2 (PsAdv-2) was identified in captive orange-bellied parrots (Neophema chrysogastor) during a multifactorial cluster of mortalities at the Adelaide Zoo, South Australia, and an outbreak of Pseudomonas aeruginosa septicaemia at the Tasmanian Department of Primary Industries, Parks, Water and Environment captive breeding facility, Taroona, Tasmania. This was the first time that an adenovirus had been identified in orange-bellied parrots and is the first report of PsAdv-2 in Australia. To investigate the status of PsAdv-2 in the captive population of orange-bellied parrots, 102 healthy birds from five breeding facilities were examined for the presence of PsAdv-2 DNA in droppings and/or cloacal swabs using a nested polymerase chain reaction assay. Additionally, eight birds released to the wild for the 2016 breeding season were similarly tested when they were recaptured prior to migration to be held in captivity for the winter. PsAdv-2 was identified in all breeding facilities as well as the birds recaptured from the wild. Prevalence of shedding ranged from 29.7 to 76.5%, demonstrating that PsAdv-2 is endemic in the captive population of orange-bellied parrots and that wild parrots may have been exposed to the virus. PsAdv-2 DNA was detected in both cloacal swabs and faeces of the orange-bellied parrots, but testing both samples from the same birds suggested that testing faeces would be more sensitive than cloacal swabs. PsAdv-2 was not found in other psittacine species housed in nearby aviaries at the Adelaide Zoo. The source of the infection in the orange-bellied parrots remains undetermined. In this study, PsAdv-2 prevalence of shedding was higher in adult birds as compared to birds less than one year old. Preliminary data also suggested a correlation between adenovirus shedding prevalence within the breeding collection and chick survival.

The role of lead in a syndrome of clenched claw paralysis and leg paresis in Swamp Harriers (Circus approximans).

We investigated the hypothesis that lead poisoning was the cause of the clinical syndrome of clenched feet paralysis and leg paresis in wild raptors. Swamp Harriers (Circus approximans) are one of three extant native raptor species in New Zealand. Harriers with the syndrome were found to have statistically significantly higher blood lead concentrations than those without clenched feet (t-test; t=-4.06, df=5, P=0.01). However, elevated blood lead concentrations were also present in 60% of wild harriers without the clinical syndrome of clenched feet paralysis and leg paresis. There were features of the response to chelation treatment, electroneurodiagnostics, and pathology that were inconsistent with lead poisoning as reported in other birds of prey. We conclude that lead may be a factor in the expression of this clinical syndrome of clenched claw paralysis but that other factors not identified in our study play a role in the expression of the disease.

Evidence of lead exposure in a free-ranging population of Kea (Nestor notabilis).

Kea (Nestor notabilis) are high country parrots endemic to New Zealand. The foraging behavior and inquisitive nature of Kea have led to incidences of foreign substance ingestion, including lead. Between April 2006 and November 2007, 38 Kea in Aoraki/Mount Cook National Park, New Zealand, were captured, and blood was sampled for blood lead analysis. All birds sampled had detectable blood lead with concentrations ranging from 0.028 mg/l to 3.43 mg/l (mean+/-SE, 0.428+/-0.581 mg/l). A retrospective analysis of necropsy reports and archived samples from 15 wild Kea from various South Island locations also was carried out. Seven of these birds (five from the Aoraki/Mount Cook area) died with clinical signs consistent with lead toxicosis and had liver and/or kidney lead levels reported to cause lead toxicity in other avian species. All seven of these birds also had lead inclusions (Ziehl-Neelson positive intranuclear inclusion bodies) in the renal tubular epithelial cells. These are considered diagnostic of lead toxicity in other species. This study showed that lead exposure is ubiquitous in the sampled population and may be an important contributing factor in Kea morbidity and mortality. As a result of these findings, lead abatement in areas frequented by Kea is being initiated.