Avian malaria caused by Plasmodium species is a known cause of mortality in avifauna worldwide, however reports within New Zealand kiwi (Apteryx spp.) are scant. Postmortem reports from kiwi were obtained from the Massey University/Te Kunenga ki Pūrehuroa School of Veterinary Science Pathology Register from August 2010–August 2020. Gross lesions were described from postmortem reports, and archived H.E.-stained slides used for histological assessment. Nested PCR testing was performed on formalin-fixed paraffin-embedded tissue samples to assess the presence of Plasmodium spp. and Toxoplasma gondii DNA and cases with a PCR-positive result were sequenced to determine the lineage involved. Of 1005 postmortem reports, 23 cases of confirmed or suspected avian malaria were included in this study. The most consistent gross lesions included splenomegaly, hepatomegaly, and interstitial pneumonia with oedema. Histological lesions were characterised by severe interstitial pneumonia, pulmonary oedema, interstitial myocarditis, hepatic sinusoidal congestion and hypercellularity, and splenic macrophage hyperplasia and hyperaemia/congestion with numerous haemosiderophages. Cytoplasmic meronts were consistently found within endothelial cells of a variety of tissues, and within tissue macrophages of the liver, lung and spleen. A diagnosis of avian malaria was confirmed via PCR testing in 13 cases, with sequencing revealing P. matutinum (LINN1) and P. elongatum (GRW6) as the species involved. This is the largest case series describing the pathology of avian malaria as a cause of mortality in endemic New Zealand avifauna.

To examine and assess causes of mortality of kiwi (Apteryx spp.) submitted to Massey University between 2010 and 2020 across the five recognised species according to location, age group and captivi...

This report details investigations into nine cases of neurological disease and/or sudden death in 8-13-week-old puppies between 2021 and 2024. Aside from two pairs of littermates, cases were unrelated. The puppies had an onset of clinical signs 9-23 days following at least one "on-label" dose of a commercially available quadrivalent vaccine containing live attenuated canine distemper virus (CDV). Eight of the nine cases displayed signs typical of "classic distemper," including seizures, circling, tremors, hypersalivation, progressive neurological deficits, pyrexia, and/or respiratory and gastrointestinal signs. Pathological and molecular investigations were undertaken in eight cases. Mononuclear/lymphohistiocytic encephalitis or meningoencephalitis with or without neuronal intranuclear inclusion bodies was present in seven cases. Five cases had bronchopneumonia. Other lesions included poliomyelitis, necrotising enteritis and myocardial necrosis or myocarditis. PCR for CDV was positive on tissues from seven cases, and immunohistochemistry for CDV was positive on neural tissues in six cases. Whole genome sequencing of PCR amplicons demonstrated a Rockborn-like strain with 99.9% homogeneity between samples from four cases and a vial of vaccine. Based on the combination of case history, pathological findings, molecular test results and/or whole genome sequencing, a diagnosis of post-vaccinal canine distemper was confirmed in six cases and presumed in two. Outbreaks of canine distemper have been stemmed by widespread vaccination starting in the mid-twentieth century. Consequently, confirmed cases of natural CDV have not been reported in New Zealand since an outbreak in the 1980s, and CDV is considered a "notifiable organism" as per the Biosecurity Act 1993. This is the first case series to report genomic investigation of post-vaccinal canine distemper in New Zealand puppies and highlights a rare adverse event associated with routine vaccination. Our results suggest that puppies with neurological, respiratory and/or gastrointestinal disease with an onset within 6 weeks of vaccination with live attenuated CDV should be reported and investigated accordingly.

Cutaneous lesions due to papillomavirus (PV) infection are well described in cats. However, there are few reports of similar lesions in the oral cavity. In this case series, 7 cats with in situ carcinomas of the oral mucosa are reported. Lesions appeared histologically like cutaneous Bowenoid in situ carcinomas, and PV-induced cell changes were visible within lesions from 6 cats. A PV etiology was further supported by intense p16 ^CDKN2A protein immunolabeling within all lesions. Five lesions contained Felis catus papillomavirus (FcaPV) type 3 DNA, while 2 contained FcaPV1 DNA. Cats had clinical signs of drooling and oral pain for over 6 months prior to diagnosis, and the dorsal surface of the tongue was most often affected. Four cats had multiple oral lesions, and 2 cats had oral and skin lesions. Of the 6 cats for which clinical outcome was known, 3 are still alive at least 6 months after diagnosis, 2 died of unrelated causes 7 and 14 months after diagnosis, and 1 cat was euthanatized due to oral pain 18 months after diagnosis. Results suggest PV-associated oral in situ carcinoma is a specific disease entity of cats. Lesions are slowly progressive with pain management allowing long survival times. No cases were known to progress to invasive squamous cell carcinoma, and feline oral squamous cell carcinomas appear to infrequently develop as a progression from these lesions. Due to the marked difference in biological behavior, diagnosticians should differentiate PV-associated oral in situ carcinomas and oral squamous cell carcinomas in cats.