The principal aim of this study was to optimize the diagnosis of canine neuroangiostrongyliasis (NA). In total, 92 cases were seen between 2010 and 2020. Dogs were aged from 7 weeks to 14 years (median 5 months), with 73/90 (81%) less than 6 months and 1.7 times as many males as females. The disease became more common over the study period. Most cases (86%) were seen between March and July. Cerebrospinal fluid (CSF) was obtained from the cisterna magna in 77 dogs, the lumbar cistern in f5, and both sites in 3. Nucleated cell counts for 84 specimens ranged from 1 to 146 150 cells μL−1 (median 4500). Percentage eosinophils varied from 0 to 98% (median 83%). When both cisternal and lumbar CSF were collected, inflammation was more severe caudally. Seventy-three CSF specimens were subjected to enzyme-linked immunosorbent assay (ELISA) testing for antibodies against A. cantonensis; 61 (84%) tested positive, titres ranging from <100 to ⩾12 800 (median 1600). Sixty-one CSF specimens were subjected to real-time quantitative polymerase chain reaction (qPCR) testing using a new protocol targeting a bioinformatically-informed repetitive genetic target; 53/61 samples (87%) tested positive, C T values ranging from 23.4 to 39.5 (median 30.0). For 57 dogs, it was possible to compare CSF ELISA serology and qPCR. ELISA and qPCR were both positive in 40 dogs, in 5 dogs the ELISA was positive while the qPCR was negative, in 9 dogs the qPCR was positive but the ELISA was negative, while in 3 dogs both the ELISA and qPCR were negative. NA is an emerging infectious disease of dogs in Sydney, Australia.

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Objective The objective of the present study was to investigate the frequency of abnormal clinicopathological parameters in a population of client‐owned clinically healthy middle‐aged dogs and cats. Materials and methods Biochemical and haematological profiles, urinalysis and total T4 were measured in clinically healthy middle‐aged dogs (age, 5–8 years) and cats (age, 6–9 years) presenting to veterinary practices for routine procedures. Results Of the 406 dogs, only 55 had no abnormalities identified in the testing panel. Most changes were minor or considered artifactual; however, changes that were diagnostic of significant disease or warranting additional evaluation were identified in 25 dogs (6.2%). Of the 130 cats, only 26 had no abnormalities identified in the testing panel. Most changes were minor or considered artifactual; however, changes diagnostic of significant disease or warranting additional evaluation were identified in 25 cats (19.2%). Significant abnormalities included anaemia, inflammation and evidence of liver, kidney and pancreatic disease. Conclusion Biochemical and haematological testing as part of regular preventive health checks may facilitate early detection of diseases before they present clinically, allowing earlier intervention and better health outcomes.

The histopathological and electronmicroscopic features of a novel parasitic infection causing seasonal epizootics of central nervous disease in Nankeen kestrels (Falco cenchroides) from Western Australia is described. Thorough necropsy, haematological and transmission electronmicroscopical examinations were performed on thirteen affected kestrels between 1996 and 1999. All had an extensive vasculocentric granulomatous meningoencephalomyelitis, pectenitis and proliferative arteritis with endothelial parasitic cysts measuring 40 to 60 m m in diameter. Arterioles in the brain, optic papillae, pecten and kidney were most consistently affected. In some birds there was severe haemorrhage from the pecten. Less commonly, parasitic cysts were seen in the arterioles of the lung, liver, heart and intestines. Endothelial schizonts contained many spherical merozoites measuring 1 m m in diameter that were also present free within the lumen of affected arterioles. Haematological examination in three of seven affected kestrels tested demonstrated rare, basophilic intracytoplasmic inclusions in leucocytes with distorted nuclei consistent with Leucocytozoon-like gametocytes. Day-old chickens inoculated with brain homogenate failed to develop similar lesions.