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ABSTRACT: Cats are susceptible to feline panleukopenia virus (FPV) and canine parvovirus type 2 (CPV-2). Therefore, coinfection and superinfection with multiple parvovirus strains may occur, resulting in high heterogeneity and recombination. Considering the importance of cats as a potential source of genetic diversity for parvoviruses, we investigated the frequency of parvovirus infection in cats using their blood and fecal samples and performed molecular characterization of parvovirus strains circulating in cat populations. Accordingly, the fecal and blood samples of 60 cats with gastroenteritis symptoms were collected from Turkey’s Burdur, Isparta, and Izmit provinces. Of these 15 fecal samples tested as parvovirus-positive by PCR, 14 were confirmed to have been infected with true FPV strains by sequencing analysis. Through the phylogeny analysis, those were located in the FPV cluster, closely related to CPV-2, and one was discriminated in the CPV-2b cluster. Additionally, sequence analysis of the VP2 gene of CPV and FPV revealed that the FPV strains detected in Turkey and the vaccine strains were highly related to each other, with a nucleotide identity of 97.7- 100%. Furthermore, 13 variable positions were detected in VP2 of the field and reference FPV strains. Three synonymous mutations were determined in the VP2 gene. Some amino acid mutations in the VP2 protein-affected sites were considered responsible for the virus’s biological and antigenic properties. The partial sequence analysis of the VP2 gene revealed that four FPV strains detected in Turkey have a single nucleotide change from T to G at the amino acid position 384 between the nucleotides 3939-3941, which was reported for the first time. Therefore, these four isolates formed a different branch in the phylogenetic tree. The results suggest that both FPV and CPV-2b strains are circulating in domestic cats in Turkey and cats should be considered as potential sources of new parvovirus variants for cats, dogs and other animals.

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 type 2 (CPV‐2) emerged as dog pathogen in the late 1970s, causing severe and often fatal epizootics of gastroenteritis in the canine population worldwide. Although to date CPV‐2 is circulating in all continents, most of the current studies have analysed the amino acid changes accounted in the VP2 gene sequence, with limited information on virus introductions from other countries. The aim of this study was to analyse the genetic features of CPV‐2c strains currently spreading in Italy. Swabs and tissue samples were collected from dogs suspected of CPV infection. The nearly complete genome sequence from the CPV‐positive samples was obtained. The co‐circulation of two different but related CPV‐2c strains, with amino acid changes characteristic of CPV strains of Asian origin (NS1: 60V, 544F, 545F, 630P – NS2: 60V, 151N, 152V ‐ VP2: 5A/G, 267Y, 297A, 324I, 370R), were observed. The phylogenetic analyses inferred from the NS1 and VP2 gene sequences confirmed the relationship with Asian CPV‐2c strains. This study reports the spread of novel CPV‐2c mutants in Italy and supports further studies to evaluate the coexistence of genetically divergent CPV strains in the same geographical environment. [ABSTRACT FROM AUTHOR]

Eighty-three wild and domestic carnivores of nine species from Janos Biosphere Reserve (JBR), Mexico, were tested by serologic and molecular assays to determine exposure and infection rates of carnivore protoparvovirus 1. Overall, 50.8% (33/65) of the wild carnivores and 100% (18/18) of the domestic dogs tested were seropositive for Canine protoparvovirus 1 (CPV), while 23% (15/65) of the wild carnivores and 22.2% (4/18) of the domestic dogs were PCR positive for CPV. Phylogenetic analysis confirmed circulation of CVP-2 with residues 426 Asn (CPV2a = 1/19) and 426 Glu (CPV-2c = 18/19) among carnivores in JBR. The prevalence of both PCR positivity and antibodies to CPV varied significantly among wild host species. Of the six identified haplotypes, three were unique to kit foxes (Vulpes macrotis) (the species with higher haplotype richness) and two to striped skunks (Mephitis mephitis). The remaining haplotype was shared among all carnivore species including dogs suggesting non-host specificity and bidirectional and continuous viral transmission cycle in the JBR. The phylogenetic similarity of CPV strains from dogs and wild carnivores and the higher prevalence of CPV in wild carnivores captured near towns relative to those captured far from towns suggest that dogs might be an important source of CPV infection for wild carnivores in the JBR. We provide evidence that cross-species transmission occurs at the domestic–wildlife interface in JBR. [ABSTRACT FROM AUTHOR]

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.

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. [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]

Feline panleukopenia (FPL) is caused by a Carnivore protoparvovirus infection. Feline parvovirus (FPV) causes most cases. When Canine parvovirus 2 (CPV-2) first emerged, it could not replicate in cats. All current CPV variants (CPV-2a-c) can infect cats to cause subclinical disease or FPL. Feline panleukopenia has re-emerged in Australia in shelter cats associated with failure to vaccinate. Parvoviruses can remain latent in mononuclear cells post-infection. Molecular methods such as polymerase chain reaction are used to determine the infecting strain. Current perspectives on causes, epidemiology, diagnosis, treatment, prognostic indicators, and management of outbreaks in shelters are reviewed., (Copyright © 2019 Elsevier Inc. All rights reserved.)