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.

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.

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.

24 Psittacid Adenovirus-2 (PsAdv-2) was identified in captive orange-bellied parrots ( 25 Neophema chrysogastor) during a multifactorial cluster of mortalities at the Adelaide Zoo, 26 South Australia, and an outbreak of Pseudomonas aeruginosa septicaemia at the Tasmanian 27 Department of Primary Industries, Parks, Water and Environment captive breeding facility, 28 Taroona, Tasmania. This was the first time that an adenovirus had been identified in orange-29 bellied parrots and is the first report of PsAdv-2 in Australia. To investigate the status of 30 PsAdv-2 in the captive population of orange-bellied parrots, 102 healthy birds from five 31 breeding facilities were examined for the presence of PsAdv-2 DNA in droppings and/or 32 cloacal swabs using a nested polymerase chain reaction assay. Additionally, eight birds 33 released to the wild for the 2016 breeding season were similarly tested when they were 34 recaptured prior to migration to be held in captivity for the winter. PsAdv-2 was identified in 35 all breeding facilities as well as the birds recaptured from the wild. Prevalence of shedding 36 ranged from 29.7 to 76.5%, demonstrating that PsAdv-2 is endemic in the captive 37 population of orange-bellied parrots and that wild parrots may have been exposed to the 38 virus. PsAdv-2 DNA was detected in both cloacal swabs and faeces of the orange-bellied 39 parrots, but testing both samples from the same birds suggested that testing faeces would 40 be more sensitive than cloacal swabs. PsAdv-2 was not found in other psittacine species 41 housed in nearby aviaries at the Adelaide Zoo. The source of the infection in the orange-42 bellied parrots remains undetermined. In this study, PsAdv-2 prevalence of shedding was 43 higher in adult birds as compared to birds less than one year old. Preliminary data also 44 suggested a correlation between adenovirus shedding prevalence within the breeding 45 collection and chick survival. 46