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Canine parvovirus type 2 (CPV-2) remains one of the most significant viral pathogens in dogs in Australia and worldwide despite the availability of safe and effective CPV vaccines. At least three different variants of CPV-2 have emerged and spread all around the world, namely CPV-2a, CPV-2b, and CPV-2c. The ability of the current vaccines containing either original CPV-2 type or CPV-2b variant to cross protect the heterologous variants has been well demonstrated in laboratory studies, despite some concerns regarding the vaccine efficacy against the emerging variants. Vanguard®, a series of multivalent vaccines, has been in the market for a considerable period of time and demonstrated to provide efficacy against all three types of CPV variants CPV-2a, CPV-2b, and CPV-2c. The purpose of this study was to evaluate the ability of the recently registered Vanguard C4 vaccine to induce cross-neutralizing antibodies against the Australian isolates of CPV-2a, CPV-2b, and CPV-2c variants. Blood samples collected from dogs vaccinated with Vanguard C4 were analyzed by virus neutralizing assays developed for each of three CPV variants. The results of the study demonstrated that Vanguard vaccine induced cross-neutralizing antibodies against the Australian isolates of CPV-2a, CPV-2b, and CPV-2c, thus offering cross protection against all three Australian CPV variants. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Canine parvovirus (CPV) is an important cause of serious and often fatal disease in dogs worldwide, however, a national survey of CPV cases in Australia has not been conducted since 1982. For this study we surveyed the entire Australian veterinary clinic population and achieved a response rate of 23.5% (534 unique veterinary clinics). Respondents reported 4,451 CPV cases in 2015 and 4,219 cases in 2016; the estimated total CPV case load across Australia was 20,661 in 2015 and 20,110 in 2016. The overall reported euthanasia rate was 41%. Geospatial analysis revealed large numbers of CPV cases in rural and remote areas of Australia. Where cases occurred in capital city areas, these were found in peri‐urban areas, away from the inner city. The median cost to treat CPV cases was $A1,500 per patient. A significant difference in the cost of treating cases was found between Australian states; Western Australia (median $A2,500) was the most expensive state. There was a strong correlation between cost of treatment and rate of euthanasia without treatment reflecting the important role of affordability in disease‐related euthanasia. These findings highlight the considerable impact of the evolving CPV situation in Australia, particularly in regional and rural areas. This survey is the most comprehensive epidemiological investigation of canine parvoviral‐related disease, to date, globally and provides a process for national disease surveillance. [ABSTRACT FROM AUTHOR]

The first detection of canine parvovirus type-2 (CPV-2) was in the early 1970s, when it was known to cause severe gastroenteritis in dogs. However, it has evolved over the years into CPV-2a within 2 years, into CPV-2b after 14 years, into CPV-2c after 16 years and more recently CPV-2a-, 2b- and 2c-like variants reported in 2019, with a global distribution. Reports on the molecular epidemiology of this virus are missing in most African countries. The report of clinical cases among vaccinated dogs in Libreville in Gabon triggered the execution of this study. The objective of this study was to characterize circulating variants from dogs showing clinical signs suggestive of CPV that were examined by a veterinarian. A total of eight (8) fecal swab samples were collected, and all had positive PCR results. Sequencing, Blast analysis and assembly of two whole genomes and eight partial VP2 sequences were performed, and the sequences submitted to GenBank. Genetic characterization revealed the presence of CPV-2a and CPV-2c variants with predominance of the former. Phylogenetically, the Gabonese CPVs formed distinct groups similar to Zambian CPV-2c and Australian CPV-2a sequences. The antigenic variants CPV-2a and CPV-2c have not yet been reported in Central Africa. However, these CPV-2 variants circulate in young, vaccinated dogs in Gabon. These results suggest additional epidemiological and genomic studies are required in order to evaluate the occurrence of different CPV variants in Gabon and effectiveness of the commercial vaccines used against protoparvovirus in the country.

Canine parvovirus (CPV) is a highly contagious and often fatal disease reported worldwide. Outbreaks occur throughout Australia, and it has been suggested that disproportionally more CPV cases occur in rural locations. However, evidence to support this suggestion—and possible reasons for such a predisposition—has not existed until now. In this study a total of 4870 CPV cases reported from an Australian disease surveillance system between September 2009 and July 2014 were analysed. Australian postcodes were classified as rural or urban (based on human population density) and reported CPV cases were then categorised as rural or urban based on their reported home postcode. Parvovirus cases were predominately young (<12 months), entire, unvaccinated, mixed-breed dogs. More than twice as many of the reported cases were from a rural area (3321 cases) compared to an urban area (1549 cases). The overall case fatality rate was 47.2%; it was higher for those CPV cases reported from urban areas (50.6%) than rural areas (45.5%). A greater proportion of rural cases were younger, entire dogs compared to urban cases. The final multivariable model of CPV cases being reported from a rural area included age (<12 months) and vaccination status (never vaccinated) as significant predictors. Poor socioeconomic status might be a reason for the decision of rural owners not to vaccinate their dogs as readily as urban owners. The excess reporting of rural CPV cases compared to urban cases and the predictive risk factors identified in this study can be used by veterinarians to reduce the incidence of CPV by educating owners about the disease and promoting better vaccination programs in rural areas. This study also supports that the increased risk of CPV in rural areas may necessitate a need for increased vigilance around preventing CPV disease spread, additional care with puppies which are the most susceptible to this disease and tighter vaccination protocols, compared to urban areas. [ABSTRACT FROM AUTHOR]

Abstract: Canine parvovirus (CPV) is a highly contagious cause of serious and often fatal disease in dogs worldwide despite the availability of safe and efficacious vaccines. Although a number of studies have focussed on identifying risk factors in disease development, risk factors associated with death from CPV are largely unknown. In this study we analysed a total of 1451 CPV cases reported from an Australian surveillance system – using univariate and multivariate techniques – to determine significant risk factors associated with death and euthanasia. A crude case fatality rate of 42.3% was estimated – higher than has been reported previously. We found that 3.3% of CPV cases had a history of vaccination in the previous 12 months, despite having completed the primary puppy vaccination course. The majority (89.5%) of these cases occurred in dogs <12 months of age, indicating failure of the primary vaccination course to provide protective immunity (most likely due to interference of the vaccine antigen with maternal antibodies but other reasons are discussed). Extending the age at which the final puppy vaccination is administered might be one of several strategies to consider. The final multivariate model showed that in non-litter CPV cases, risk of death was significantly associated with season of diagnosis (summer) and pedigree type (hounds and non-sporting dogs). Euthanasia in non-litter CPV cases was significantly associated with season of diagnosis (summer), state of residence (Northern Territory/South Australia/Tasmania combined), age (

To identify clusters of canine parvoviral related disease occurring in Australia during 2010 and investigate the role of socio-economic factors contributing to these clusters, reported cases of canine parvovirus were extracted from an on-line disease surveillance system. Reported residential postcode was used to locate cases, and clusters were identified using a scan statistic. Cases included in clusters were compared to those not included in such clusters with respect to human socioeconomic factors (postcode area relative socioeconomic disadvantage, economic resources, education and occupation) and dog factors (neuter status, breed, age, gender, vaccination status). During 2010, there were 1187 cases of canine parvovirus reported. Nineteen significant (P< 0.05) disease clusters were identified, most commonly located in New South Wales. Eleven (58%) clusters occurred between April and July, and the average cluster length was 5.7 days. All clusters occurred in postcodes with a significantly (P < 0.05) greater level of relative socioeconomic disadvantage and a lower rank in education and occupation, and it was noted that clustered cases were less likely to have been neutered (P = 0.004). No significant difference (P> 0.05) was found between cases reported from cluster postcodes and those not within clusters for dog age, gender, breed or vaccination status (although the latter needs to be interpreted with caution, since vaccination was absent in most of tlfe cases). Further research is required to investigate the apparent association between indicators of poor socioeconomic status and clusters of reported canine parvovirus diseases; however these initial findings may be useful for developing geographically- and temporally-targeted prevention and disease control programs. [ABSTRACT FROM AUTHOR]

Objectives To determine the prevalence of canine vector-borne diseases (CVBD: Babesia spp., Anaplasma spp., Ehrlichia spp., haemotropic mycoplasmas and Hepatozoon) in Australian dogs; namely, dogs from pounds in south-east Queensland and an indigenous Aboriginal community in the north-east of the Northern Territory. Design and procedure Blood samples were collected from 100 pound dogs and 130 Aboriginal community dogs and screened for the CVBD pathogens using polymerase chain reaction (PCR). All positive PCR products were sequenced for species confirmation. Results In total, 3 pound dogs and 64 Aboriginal community dogs were infected with at least one CVBD pathogen. Overall, B. vogeli was detected in 13 dogs, A. platys in 49, M. haemocanis in 23, Candidatus Mycoplasma haematoparvum in 3 and C. M. haemobos in 1 dog. Co-infections were detected in 22 Aboriginal community dogs. Conclusions This study found B. vogeli, A. platys and haemotropic mycoplasma infections to be common in dogs in subtropical and tropical areas of Australia. This study also reports for the first time the prevalence and genetic characterisation of haemotropic mycoplasmas in dogs in Australia. [ABSTRACT FROM AUTHOR]

• Surveillance for parvoviruses in faeces from cats in multicat environments (MCE) was performed. • Parvoviral DNA was detected using a TaqMan real-time PCR. • Parvoviral DNA was detected in 6.61 % of faecal samples from cats in MCE in Italy and Australia. • Parvoviral variants were typed using a minor-groove binding real-time PCR. • Viruses detected in positive samples were FPV in 90.3 % and CPV in 12.9 %. Whether subclinical shedding of canine parvovirus (CPV) by cats might contribute to the epidemiology of canine CPV infections, particularly in facilities housing both cats and dogs, requires clarification. Conflicting results are reported to date. Using conventional PCR (cPCR) to amplify the VP2 gene, shedding of the CPV variants (CPV-2a, 2b, 2c) by healthy cats in multi-cat environments was reportedly common in Europe but rare in Australia. The aim of this study was to determine whether low-level faecal CPV shedding occurs in multi-cat environments in Australia and Italy using a TaqMan real-time PCR to detect Carnivore protoparvovirus 1 (CPV and feline parvovirus, FPV) DNA, and minor-groove binder probe real-time PCR assay to differentiate FPV and CPV types and to characterize CPV variants. In total, 741 non-diarrhoeic faecal samples from shelters in Australia (n = 263) and from shelters or cat colonies in Italy (n = 478) were tested. Overall, Carnivore protoparvovirus 1 DNA was detected in 49 of 741 (6.61 %) samples. Differentiation was possible for 31 positive samples. FPV was most common among positive samples (28/31, 90.3 %). CPV was detected in 4/31 samples (12.9 %) including CPV-2a in one sample, CPV-2b in another and co-infections of FPV/CPV-2b and CPV-2a/CPV-2b in the remaining two samples. A high rate of subclinical FPV infection was detected in one shelter during an outbreak of feline panleukopenia, during which 21 of 22 asymptomatic cats (95.5 %) sampled were shedding FPV. Faecal shedding of CPV by cats in multi-cat environments is uncommon suggesting that domestic cats are not significant reservoirs of CPV. [ABSTRACT FROM AUTHOR]

• 11 % of Australian veterinary hospitals reported >40 canine parvovirus cases in 2016. • Socioeconomic disadvantage was the strongest risk factor for canine parvovirus. • Euthanasia is the leading cause of fatality for canine parvovirus related disease. • Hottest month of the year is associated with canine parvovirus case occurrence. • Low rainfall is associated with higher canine parvovirus cases. Infection of canids with canine parvovirus (CPV) can result in severe, often fatal disease. This study aimed to examine climatic, socioeconomic and geographic risk factors for CPV infection and CPV-associated euthanasia in Australia. Australian veterinary hospital responses (534; 23.5 %) to a national veterinary survey of CPV case occurrences and euthanasias in 2016 were used. Severe caseloads (>40 cases per annum) were reported by 26 (11 %) hospitals (median 60 cases; IQR 50–110). Case reporting, case numbers, and without-treatment euthanasia were significantly associated with disadvantage across all Socio-Economic Index for Areas quintiles (p < 0.0001) – the greater the disadvantage, the more reports. Strong negative correlations were found between case numbers and the Index of Relative Socioeconomic Disadvantage (r SP = –0.3357, p < 0.0001) and also between euthanasia and the Index of Education and Occupation (r SP = –0.3762, p < 0.0001). Hospitals in more remote areas were also more likely to report cases and to euthanize without treatment (p < 0.0001). Of the climate variables, temperature of the hottest month was most strongly positively correlated with case numbers (r SP = 0.421, p < 0.0001), and lower annual rainfall was associated with more case-reporting hospitals (p < 0.0001). These results confirm that socioeconomic disadvantage is a significant risk-factor for CPV infection and outcome, and high temperature may also contribute to risk. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Aim: To describe faecal PCR (fPCR) results and clinical findings of dogs seen at a university teaching hospital for diarrhoea., Design: Retrospective case series (April 2015 to July 2018)., Procedure: Data were collected from the hospital electronic medical records. Data extracted included signalment, history, clinical signs, treatment, fPCR panel results, other faecal diagnostic test results and antimicrobial use., Results: One hundred and sixty-eight dogs with diarrhoea had a fPCR panel submitted. Most dogs (115, 68.5%) had diarrhoea of 3 days or less duration. Clostridium perfringens alpha toxin gene was most frequently detected (156, 92.9%) by fPCR, followed by Campylobacter spp. (55, 32.7%), canine parvovirus (CPV) (29, 17.3%), Salmonella spp. (14, 8.3%) and Giardia spp. (9, 5.4%). For the 45 dogs that had a negative point-of-care CPV test, 13 were CPV fPCR positive; some of which were adult dogs with current vaccination status. A total of 94/168 (56%) dogs received antimicrobials at some time during the treatment of diarrhoea., Conclusion: Faecal PCR panels can identify dogs with enteric organisms in their faeces that traditional faecal diagnostics may miss, thus contributing additional information to the diagnostic process. Nonetheless, fPCR results should be interpreted in light of the clinical findings, and particular consideration given to avoiding inappropriate use of antimicrobials. This study highlights that testing for C. perfringens alpha toxin gene is not likely to be diagnostically helpful, and that adult dogs with diarrhoea might be identified as CPV positive with PCR testing, despite a negative point-of-care CPV test result and a current vaccination status., (© 2020 Australian Veterinary Association.)

Canine parvovirus (CPV) is a cause of severe disease in dogs globally, yet is preventable by vaccination. A range of vaccination protocols are used by veterinary practitioners with evidence suggesting some protocols provide better protection than others in high infection-risk situations. This study investigated associations between veterinarians' vaccination recommendations and hospital remoteness, socioeconomic disadvantage, CPV caseload, and veterinarian perceptions and demographics. A national Australian veterinary survey in 2017 received 569 practitioner responses from 534 unique hospitals (23.6 % response rate). Respondents from major city hospitals had the lowest perceptions of the national CPV caseload (p < 0.0001). Those from hospitals with mild to moderate caseloads (6-40 cases per annum) recommended more frequent puppy revaccination - which is considered more protective - than those with the highest caseload (p = 0.0098), which might increase vaccination failure risk. Respondents from the most socioeconomically disadvantaged regions were over-represented in recommending annual revaccination of adult dogs; those from the least disadvantaged regions were over-represented in recommending triennial revaccination (p < 0.0001). Hospitals with higher CPV caseloads, greater socioeconomic disadvantage or increased remoteness did not favor two puppy vaccination protocols that are considered more protective (younger first vaccination age or older final vaccination age), despite these regions presenting higher CPV caseload risk. Titer testing to determine whether to revaccinate was more likely to be used in major city hospitals (p = 0.0052) and less disadvantaged areas (p = 0.0550). University of graduation was associated with CPV caseload, remoteness and level of socioeconomic disadvantage of the region where the graduate worked. University of graduation was significantly associated with age for final puppy vaccination and titer-testing recommendations. Graduates from one university were over-represented in recommending an earlier (10-week) finish protocol and titer testing, compared to all other universities. Year and university of graduation, and respondent's age were associated with a number of vaccination protocol recommendations suggesting that inherent biases might affect veterinarians' decisions. Emphasis on currently recommended vaccination protocols in undergraduate curricula and more protective vaccination protocol use in higher-risk regions could reduce immunization failure and CPV caseload., Competing Interests: Declaration of Competing Interest The lead author is a founder and director of Paws for A Purpose Ltd, an Australian charity created to try and help reduce CPV cases as part of its charitable purpose. The authors otherwise have no conflicts of interest to report., (Copyright © 2020 Elsevier B.V. All rights reserved.)

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.

Canine Parvovirus (CPV) causes severe morbidity and mortality in dogs, particularly puppies, worldwide. Although vaccination is highly efficacious in preventing disease, cases continue to occur and vaccination failures are well documented. Maternally derived antibody interference is the leading cause of vaccination failure and age at vaccine administration is a significant risk factor for failure. However, no studies have been performed on practicing veterinarians' usage of and compliance with published vaccination guidelines and label recommendations. Likewise, there are no published studies of veterinarian perceptions on CPV occurrence and mortality and its influence on case outcome. We report a study in which all Australian small companion animal (canine and feline) veterinary hospitals were surveyed, yielding a response rate of 23.5% (534 unique veterinary hospitals). Respondents overall perceived national CPV occurrence ten-times lower (median 2000 cases) than the estimated national caseload (20,000 cases). Respondents from hospitals that did not diagnose CPV perceived national occurrence twenty-times lower (median 1000 cases) than the estimated rate (p < 0.0001). Perceived disease mortality (50%) was 2.74 times higher than that reported (18.2%). In addition, 26.7% of veterinarians reported using serological titer testing to some degree, which some practitioners use in lieu of vaccination if a titer is perceived to reflect sufficient immunity. Based on this study veterinarians appear to be aware of the disease risk in their region but unaware of the burden of CPV disease nationally, and perceive mortality risk higher than it actually is. This might lead to an overestimation of cost to treat, and over-recommendation of euthanasia. Nearly half (48.7%) of respondents recommended final puppy vaccination earlier than guidelines recommend, while 2.8% of respondents recommended a puppy re-vaccination interval longer than supported by vaccine labels and guidelines. Both of these practices may put puppies at risk of CPV infection., (Copyright © 2019 Elsevier B.V. All rights reserved.)

Tracing the temporal dynamics of pathogens is crucial for developing strategies to detect and limit disease emergence. Canine parvovirus (CPV-2) is an enteric virus causing morbidity and mortality in dogs around the globe. Previous work in Australia reported that the majority of cases were associated with the CPV-2a subtype, an unexpected finding since CPV-2a was rapidly replaced by another subtype (CPV-2b) in many countries. Using a nine-year dataset of CPV-2 infections from 396 dogs sampled across Australia, we assessed the population dynamics and molecular epidemiology of circulating CPV-2 subtypes. Bayesian phylogenetic Skygrid models and logistic regressions were used to trace the temporal dynamics of CPV-2 infections in dogs sampled from 2007 to 2016. Phylogenetic models indicated that CPV-2a likely emerged in Australia between 1973 and 1988, while CPV-2b likely emerged between 1985 and 1998. Sequences from both subtypes were found in dogs across continental Australia and Tasmania, with no apparent effect of climate variability on subtype occurrence. Both variant subtypes exhibited a classical disease emergence pattern of relatively high rates of evolution during early emergence followed by subsequent decreases in evolutionary rates over time. However, the CPV-2b subtype maintained higher mutation rates than CPV-2a and continued to expand, resulting in an increase in the probability that dogs will carry this subtype over time. Ongoing monitoring programs that provide molecular epidemiology surveillance will be necessary to detect emergence of new variants and make informed recommendations to develop reliable detection and vaccine methods., (Copyright © 2017 Elsevier B.V. All rights reserved.)