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Numerous raised plaques were observed on the feet of a red-billed gull (Chroicocephalus novaehollandiae scopulinus) that had been found dead. The plaques consisted of thickened epidermis with cell changes indicative of papillomavirus (PV) infection prominent within affected areas. Evidence suggesting progression to neoplasia was visible in one lesion. A DNA sequence that was most similar, but only 68.3% identical, to duck PV type 3 was amplified from the papillomas, suggesting a novel PV type. Lesions containing PV DNA have only previously been reported in three avian species. This is the first evidence that PVs could cause neoplasia in birds.

We investigated an epidemic mortality cluster of yellow-eyed penguins (Megadyptes antipodes) that involved 67 moribund or dead birds found on various beaches of the Otago Peninsula, New Zealand, between 21 January and 20 March 2013. Twenty-four carcases were examined post-mortem. Histological lesions of pulmonary, hepatic and splenic erythrophagocytosis and haemosiderosis were found in 23 of 24 birds. Fifteen birds also had haemoglobin-like protein droplets within renal tubular epithelial cells. Despite consistent histological lesions, a cause of death could not be established. Virology, bacteriology and molecular tests for avian influenza, avian paramyxovirus-1, avipoxvirus, Chlamydia psittaci, Plasmodium spp., Babesia spp., Leucocytozoon spp. and Toxoplasma gondii were negative. Tissue concentrations of a range of heavy metals (n = 4 birds) were consistent with low level exposure, while examination of proventricular contents and mucus failed to detect any marine biotoxins or Clostridium botulinum toxin. Hepatic concentrations of total polycyclic aromatic hydrocarbons (PAHs) (n = 5 birds) were similar to background concentrations of polycyclic aromatic hydrocarbons previously found in yellow-eyed penguins from the South Island of New Zealand, but there were significantly higher concentrations of 1-methylnapthelene and 2-methylnapthelene in the birds found dead in this mortality cluster. The biological significance of this finding is unclear. A temporal investigation of the epidemic did not indicate either a common source or propagative epidemic pattern. Although our investigation did not definitively implicate a toxic or infectious agent, we could not rule out causes such as toxic marine organisms or mycoplasmosis. Further investigations should therefore by carried out in the event of future mortality clusters.

A 12-day-old Brown Kiwi (Apteryx mantelli) was presented with anorexia, torticollis, head-tilt, and coelomic distension. Radiographs showed an ill-defined, fat-opaque, coelomic mass displacing viscera craniodorsally. Curvilinear mineral opacities were superimposed over the ventral aspect of the mass. Computed tomography demonstrated the presence of mineral within the periphery of a fat attenuating mass consistent with a retained yolk sac. A deutectomy (yolk sac excision) was performed. Histopathology of the excised tissue confirmed the diagnosis of a retained yolk sac with multifocal mineralization., (© 2014 American College of Veterinary Radiology.)

Four cases of fatal toxoplasmosis in three endemic New Zealand avian species are reported. Between 2009 and 2012, two kereru (Hemiphaga novaeseelandiae), one North Island brown kiwi (Apteryx mantelli), and one North Island kaka (Nestor meridionalis) were submitted for necropsy examination. On gross postmortem, the kiwi had marked hepatosplenomegaly while the kaka and two kereru had swollen, slightly firm, deep-red lungs. Histologically there was extensive hepatocellular necrosis in the liver of the kiwi while the kaka and kereru showed severe fibrinous bronchointerstitial pneumonia. In the kiwi, protozoal organisms were present within both hepatocytes and Kupffer cells of the liver and within the epithelial cells and macrophages of the interstitium of the lungs in the kaka and two kereru. The diagnosis of toxoplasmosis was confirmed with immunohistochemistry and PCR of paraffin-embedded formalin-fixed tissue of the liver, lungs, or both. Genotyping of up to seven markers revealed that an atypical Type II isolate of Toxoplasma gondii was present in at least three of the cases. This study provides evidence that T. gondii can cause mortality in these endemic species and suggests further research is needed to determine the full extent of morbidity and mortality caused by this parasite in New Zealand's unique avifauna.

Avian malaria is caused by intracellular mosquito-transmitted protist parasites in the order Haemosporida, genus Plasmodium. Although Plasmodium species have been diagnosed as causing death in several threatened species in New Zealand, little is known about their ecology and epidemiology. In this study, we examined the presence, microscopic characterization and sequence homology of Plasmodium spp. isolates collected from a small number of New Zealand introduced, native and endemic bird species. We identified 14 Plasmodium spp. isolates from 90 blood or tissue samples. The host range included four species of passerines (two endemic, one native, one introduced), one species of endemic pigeon and two species of endemic kiwi. The isolates were associated into at least four distinct clusters including Plasmodium (Huffia) elongatum, a subgroup of Plasmodium elongatum, Plasmodium relictum and Plasmodium (Noyvella) spp. The infected birds presented a low level of peripheral parasitemia consistent with chronic infection (11/15 blood smears examined). In addition, we report death due to overwhelming parasitemia in a blackbird, a great spotted kiwi and a hihi. These deaths were attributed to infections with either Plasmodium spp. lineage LINN1 or P. relictum lineage GRW4. To the authors' knowledge, this is the first published report of Plasmodium spp. infection in great spotted and brown kiwi, kereru and kokako. Currently, we are only able to speculate on the origin of these 14 isolates but consideration must be made as to the impact they may have on threatened endemic species, particularly due to the examples of mortality.