Ongoing Investigation into the Cause of Seasonal Hindlimb Paralysis Syndrome in Carnaby’s Cockatoos (Zanda latirostris) in Western Australia

Flaminia J Coiacetto

Carnaby’s Hindlimb Paralysis Syndrome (CHiPS), characterised by bilateral leg paralysis that occasionally ascends to include wing paralysis, has been described in endangered populations of Carnaby’s cockatoos since 2012. The annual outbreaks of paralysis typically occur between January to March within the Southern Wheatbelt region in Western Australia with approximately 15-25 cases documented per year. Affected birds are either found paralysed with severe debilitation or dead in nest hollows or are presented to the Perth Zoo Veterinary Department. Previous investigations involving clinical, clinicopathologic and radiologic evaluation, epidemiologic studies, limited gross and histologic necropsy examination, direct and indirect toxicology assays suggested a possible toxic aetiology, particularly an organophosphate toxicosis. The aim of this PhD was to systematically describe the gross and histologic necropsy changes associated with CHiPS, and to investigate the role of acute organophosphate toxicosis and organophosphate induced delayed neuropathy (OPIDN) in the pathogenesis of CHiPS using direct toxicology and indirect toxin biomarker studies. Full gross necropsy and histopathology examinations were performed on 17 CHiPS cases and 11 non-CHiPS animals for reference. Histopathology included examination of all major organs as well as brain, spinal cord, brachial plexus, sciatic nerve and wing and leg muscles. Luxol fast blue counterstained with cresyl violet histochemistry was also performed to investigate for evidence of demyelination. Gross and histopathology examination did not elucidate a definitive cause of the clinical signs seen in CHiPS cases. There were no significant gross or histopathologic changes within the brain, spinal cord, sciatic nerve, or brachial plexus that could explain the leg paralysis. The most significant changes were seen in the leg and wing muscles with a monophasic to polyphasic myopathy present in the leg muscles of 15 out of the 17 CHiPS cases and in the wing muscles in 11 of those cases. Based on the above findings, the most likely differentials include neurotoxicoses (e.g. organophosphate and carbamate toxicoses), neuro-myotoxicosis (e.g. ionophore toxicosis), and less likely nutritional myopathy (e.g. vitamin E/selenium deficiency) or botulism. An acute organophosphate toxicosis was investigated using brain acetylcholinesterase (AChE) and blood butyrylcholinesterase (BChE). Brain AChE was evaluated in 18 CHiPS cases compared to 11 non-CHiPS animals and a previously described reference interval, and blood BChE was evaluated in 31 CHiPS cases compared to 51 non-CHiPS animals. As blood BChE had not been previously evaluated in this species, a validation study was performed to investigate the accuracy of the assay for the evaluation of BChE measurement in blood from Carnaby’s cockatoos. This study found no evidence of changes in blood BChE or brain AChE that indicate an acute organophosphate toxicosis as the cause of CHiPS. These results render an acute organophosphate toxicosis unlikely. Based on the results from the BChE validation study, the authors can recommend this assay for the evaluation of BChE measurement in plasma and serum from Carnaby’s cockatoos with results showing excellent accuracy and precision. Direct toxicology testing for a suite of neurotoxins demonstrated no evidence of detectable toxin residues in necropsy tissues from 10 CHiPS cases. OPIDN was investigated using neuropathy target esterase (NTE) inactivation assays. NTE assays were performed on brain from 17 CHiPS cases and compared with results from 11 non-CHiPS animals. This study demonstrated a statistically significant difference in brain NTE activity between the two groups with a reduction in CHiPS cases. Whilst definitive diagnosis of OPIDN would require the generation of a reference interval to compare these values against, this evidence is strongly suggestive of either OPIDN or a carbamate toxicosis as the cause of CHiPS. The conclusions from the study as a whole were that the top differentials for CHiPS were OPIDN, ionophore toxicosis or a combination of both given the evidence that organophosphates can potentiate the neurotoxic effects of ionophores.

Ongoing Investigation into the Cause of Seasonal Hindlimb Paralysis Syndrome in Carnaby’s Cockatoos (Zanda latirostris) in Western Australia

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