Multiple, epizootic outbreaks of feline panleukopenia (FPL) caused by feline parvovirus (FPV) occurred in eastern Australia between 2014 and 2018. Most affected cats were unvaccinated. We hypothesised that low population immunity was a major driver of re-emergent FPL. The aim of this study was to (i) determine the prevalence and predictors of seroprotective titres to FPV among shelter-housed and owned cats, and (ii) compare the prevalence of seroprotection between a region affected and unaffected by FPL outbreaks. FPV antibodies were detected by haemagglutination inhibition assay on sera from 523 cats and titres ≥1:40 were considered protective. Socioeconomic indices based on postcode and census data were included in the risk factor analysis. The prevalence of protective FPV antibody titres was high overall (94.3%), even though only 42% of cats were known to be vaccinated, and was not significantly different between outbreak and non-outbreak regions. On multivariable logistic regression analysis vaccinated cats were 29.94 times more likely to have protective FPV titres than cats not known to be vaccinated. Cats from postcodes of relatively less socioeconomic disadvantage were 5.93 times more likely to have protective FPV titres. The predictors identified for FPV seroprotective titres indicate targeted vaccination strategies in regions of socioeconomic disadvantage would be beneficial to increase population immunity. The critical level of vaccine coverage required to halt FPV transmission and prevent FPL outbreaks should be determined.

Case summary: A 12-year-old male neutered Tonkinese cat was presented for acute ataxia, weakness, altered mentation and generalised tremors. The cat had been administered oral spinosad (140 mg; 33.5 mg/kg) 48 h prior to the onset of clinical signs, and an oral anthelmintic containing milbemycin oxime (16 mg; 3.8 mg/kg) and praziquantel (40 mg; 9.6 mg/kg) 12 h before the onset of clinical signs. On physical examination, dull-to-obtunded mentation, tetraparesis, ataxia and mild tremors of facial, limb and trunk muscles were noted. Serum biochemical changes and urinalysis were consistent with haemoconcentration. The results of a complete blood count, urine culture and serology for feline leukaemia virus, feline immunodeficiency virus and cryptococcal antigen were negative. The patient was monitored in hospital and all clinical signs resolved within 24 h. Relevance and novel information: The neurological signs in this case were consistent with macrocyclic lactone neurotoxicity, which is suspected to have occurred from an adverse drug interaction between spinosad and milbemycin oxime. This report serves to highlight the potential for this adverse drug interaction between these commonly used prophylactic drugs.