Mark Kelman

Canine parvovirus (CPV) has been reported throughout the world since the late 1970s. Published information was reviewed to draw insights into the epidemiology, pathogenesis, diagnosis, treatment and outcomes of CPV disease in Australia and the role of scientific research on CPV occurrence, with key research discoveries and knowledge gaps identified. Australian researchers contributed substantially to early findings, including the first reported cases of parvoviral myocarditis, investigations into disease aetiopathogenesis, host and environmental risk factors and links between CPV and feline panleukopenia. Two of the world's first CPV serological surveys were conducted in Australia and a 1980 national veterinary survey of Australian and New Zealand dogs revealed 6824 suspected CPV cases and 1058 deaths. In 2010, an Australian national disease surveillance system was launched; 4940 CPV cases were reported between 2009 and 2014, although underreporting was likely. A 2017 study estimated national incidence to be 4.12 cases per 1000 dogs, and an annual case load of 20,110 based on 4219 CPV case reports in a survey of all Australian veterinary clinics, with a 23.5% response rate. CPV disease risk factors identified included socioeconomic disadvantage, geographical location (rural/remote), season (summer) and rainfall (recent rain and longer dry periods both increasing risk). Age <16 weeks was identified as a risk factor for vaccination failure. Important knowledge gaps exist regarding national canine and feline demographic and CPV case data, vaccination coverage and population immunity, CPV transmission between owned dogs and other carnivore populations in Australia and the most effective methods to control epizootics.

Canine parvovirus (CPV) is a major enteric pathogen of dogs worldwide that emerged in the late 1970s from a feline parvovirus (FPV)-like ancestral virus. Shortly after its emergence, variant CPVs acquired amino acid (aa) mutations in key capsid residues, associated with biological and/or antigenic changes. This study aimed to identify and analyse CPV variants and their capsid mutations amongst Australian dogs, to gain insights into the evolution of CPV in Australia and to investigate relationships between the disease and vaccination status of dogs from which viruses were detected. CPV VP2 sequences were amplified from 79 faecal samples collected from dogs with parvoviral enteritis at 20 veterinary practices in five Australian states. The median age at diagnosis was 4 months (range 1-96 months). Only 3.7% of dogs with vaccination histories had completed recommended vaccination schedules, while 49% were incompletely vaccinated and 47.2% were unvaccinated. For the first time, CPV-2b has emerged as the dominant antigenic CPV variant circulating in dogs with parvoviral enteritis in Australia, comprising 54.4% of viruses, while CPV-2a and CPV-2 comprised 43.1% and 2.5%, respectively. The antigenic variant CPV-2c was not identified. Analysis of translated VP2 sequences revealed a vast repertoire of amino acid (aa) mutations. Several Australian CPV strains displayed signatures in the VP2 protein typical of Asian CPVs, suggesting possible introduction of CPV strains from Asia, and/or CPV circulation between Asia and Australia. Canine parvoviruses were identified containing aa residues typical of FPV at key capsid (VP2) positions, representing reverse mutations or residual mutations retained from CPV-2 during adaptation from an FPV-like ancestor, suggesting that evolutionary intermediates between CPV-2 and FPV are circulating in the field. Similarly, intermediates between CPV-2a-like viruses and CPV-2 were also identified. These findings help inform a better understanding of the evolution of CPV in dogs.

Canine parvovirus (CPV) is an important cause of disease in domestic dogs. Sporadic cases and outbreaks occur across Australia and worldwide and are associated with high morbidity and mortality. Whether transmission of CPV occurs between owned dogs and populations of wild dogs, including Canis familiaris, Canis lupus dingo and hybrids, is not known. To investigate the role of wild dogs in CPV epidemiology in Australia, PCR was used to detect CPV DNA in tissue from wild dogs culled in the peri-urban regions of two Australian states, between August 2012 and May 2015. CPV DNA was detected in 4.7% (8/170). There was a strong geospatial association between wild-dog CPV infections and domestic-dog CPV cases reported to a national disease surveillance system between 2009 and 2015. Postcodes in which wild dogs tested positive for CPV were 8.63 times more likely to also have domestic-dog cases reported than postcodes in which wild dogs tested negative (p = 0.0332). Phylogenetic analysis of CPV VP2 sequences from wild dogs showed they were all CPV-2a variants characterized by a novel amino acid mutation (21-Ala) recently identified in CPV isolates from owned dogs in Australia with parvoviral enteritis. Wild-dog CPV VP2 sequences were compared to those from owned domestic dogs in Australia. For one domestic-dog case located approximately 10 km from a wild-dog capture location, and reported 3.5 years after the nearest wild dog was sampled, the virus was demonstrated to have a closely related common ancestor. This study provides phylogenetic and geospatial evidence of CPV transmission between wild and domestic dogs in Australia.

Feline panleukopenia (FPL), a frequently fatal disease of cats, is caused by feline parvovirus (FPV) or canine parvovirus (CPV). We investigated simultaneous outbreaks of FPL between 2014 and 2018 in Australia, New Zealand and the United Arab Emirates (UAE) where FPL outbreaks had not been reported for several decades. Case data from 989 cats and clinical samples from additional 113 cats were obtained to determine the cause of the outbreaks and epidemiological factors involved. Most cats with FPL were shelter-housed, 9 to 10 weeks old at diagnosis, unvaccinated, had not completed a primary vaccination series or had received vaccinations noncompliant with current guidelines. Analysis of parvoviral VP2 sequence data confirmed that all FPL cases were caused by FPV and not CPV. Phylogenetic analysis revealed that each of these outbreaks was caused by a distinct FPV, with two virus lineages present in eastern Australia and virus movement between different geographical locations. Viruses from the UAE outbreak formed a lineage of unknown origin. FPV vaccine virus was detected in the New Zealand cases, highlighting the difficulty of distinguishing the co-incidental shedding of vaccine virus in vaccinated cats. Inadequate vaccination coverage in shelter-housed cats was a common factor in all outbreaks, likely precipitating the multiple re-emergence of infection events.

Feline immunodeficiency virus (FIV), feline calicivirus (FCV), and feline herpesvirus (FHV-1) are common viral infections of domestic cats in Australia. A study was performed to investigate the possible effect of area-based socioeconomic factors on the occurrence of FIV, FCV, and FHV-1 infection in Australian client-owned cats. A total of 1044 cases, reported to a voluntary Australian online disease surveillance system between January 2010 and July 2017, were analysed with respect to their postcode-related socioeconomic factors using the Socio-Economic Indexes For Areas (SEIFA). SEIFA consists of four different indexes which describe different aspects of socioeconomic advantage and disadvantage. Signalment details including age, sex, neuter status, and breed were also considered. A significant correlation was observed between areas of lower socioeconomic status and a higher number of reported cases of FIV infection for all four SEIFA indexes (p ≤ 0.0002). Postcodes with SEIFA indexes below the Australian median (“disadvantaged” areas) were 1.6–2.3 times more likely to have reported cases of FIV infection than postcodes with SEIFA indexes above the median (“advantaged” areas). In contrast, no correlation was observed between the number of reported cases of FCV or FHV-1 infection and any of the four SEIFA indexes (p > 0.05). When signalment data were analysed for the three infections, FIV-infected cats were more likely to be older (p < 0.00001), male (p < 0.0001), neutered (p = 0.03), and non-pedigree (p < 0.0001) compared to FCV and FHV-1 infected cats. Results from this study suggest that area-based disease control strategies, particularly in areas of social disadvantage, might be effective in reducing the prevalence of FIV infection in pet cats in Australia.

The aim of this study was to conduct a comprehensive assessment of feline infectious upper respiratory tract infection (URTI) and disease (URTD) in Australian cats. Laboratory data demonstrating URTI from feline URTD multiplex PCR panel (feline Herpesvirus 1 [FHV-1], feline calicivirus [FCV], Bordetella bronchiseptica, Chlamydophila felis, Mycoplasma felis and H1N1 influenza) submissions in Australia (2013–2015) were obtained. For comparison, reports of feline URTD during the same time period were sourced from a voluntary companion animal disease surveillance system. A total of 3126 samples were submitted for testing; 1533 (49%) were positive. Of these, the most commonly detected agents were M felis (21.5%) and FCV (16.0%) alone, followed by FCV and M felis (13.4%) together as a respiratory infection complex, then FHV-1 (7.0%) alone. During the study period, there were 262 reports of 320 clinical feline URTD cases. Most cases (69%) were reported from New South Wales, M felis and FCV infection. This information can be used by veterinarians to educate clients about prevention and management of this important infectious disease of cats.