No full-text available
To read the full-text of this research,
you can request a copy directly from the authors.
Emergence of canine parvovirus subtype 2b (CPV-2b) infections in Australian dogs
Abstract and Figures
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.
Figures - uploaded by Nicholas Clark
Author content
All figure content in this area was uploaded by Nicholas Clark
Content may be subject to copyright.
... Epidemiological surveys regarding the distribution of the CPV-2 variants in different countries have shown that CPV-2a is the predominant variant in most of Asia and in European countries, and is the only variant reported in New Zealand. The CPV-2b variant was found to be the predominant antigenic variant in Ireland, the UK, the U.S.A., African countries, several Asian countries and Australia [11]. The CPV-2c variant has mainly been found in European countries and South America, and it has recently been detected in the Australian dog population [12]. ...
... From the sequence analysis, CPV-2b was more genetically stable than CPV-2a but showed the highest fraction of non-synonymous mutations, highlighting a significant phenotypic effect of the accumulated mutations over time. A similar situation was observed in Australia where CPV-2b subtypes have continued to evolve at a relatively rapid rate in recent years [11]. ...
... Finally, from its remergence in recent years, CPV-2b has shown a new and distinctive profile of the VP2 protein, characterised by Asn 517-to-Ser and Ala 371-to-Gly changes. Additional studies are warranted to confirm an increased diffusion of the variants CPV-2b and 2c at the expense of the CPV-2a on the Italian mainland and in many other countries [11,37]; monitoring of the evolution and spread of the new CPV-2 variants should be a key aim of ongoing research. ...
Background:
Canine parvovirus type 2 (CPV-2) is the most important enteric virus infecting canids. It is a rapidly evolving virus; after its emergence in the 1970s, new antigenic variants (called CPV-2a, 2b and 2c) emerged and replaced the original antigenic type. The three antigenic variants are globally distributed with different frequencies and levels of genetic variability. This study focused on VP2 gene sequence analysis and the phylodynamics of CPV-2 which were detected in 123 dogs showing clinical signs of gastroenteritis collected in Italy from 1994 to 2017.
Results:
For the most part, the sick dogs were young, and a third of them (32.5%) had been vaccinated. No statistical association was found between the CPV-2 antigenic variants, and sex, age, breed and vaccination status. Sequence analysis showed that all three antigenic types circulated in Italy; the CPV-2a type was the prominent genotype, followed by CPV-2c and CPV-2b, with notable differences regarding regional bases and significant fluctuations over time. Nucleotide sequence data showed high genetic heterogeneity with 67 nucleotide sequence types (ntSTs) identified, corresponding to 21 amino acid sequence types (aaSTs). The aaSTs and ntSTs obtained were distributed differently among the three CPV-2 antigenic variants: CPV-2a grouped 12/21 (57.1%) aaSTs and 41/67 (61.2%) ntSTs; CPV-2b grouped 5/21 (23.8%) aaSTs and 6/67 (8.9%) ntSTs, and CPV-2c grouped 4/21 (19.1%) aaSTs and 20/67 (29.9%) ntSTs. Canine parvovirus 2a was characterised by the highest genetic variability while CPV-2c was characterised by notable stability with a predominant amino acid profile during the entire sampling time. Canine parvovirus 2b re-emerged in recent years, showing a new and distinctive amino acid profile of the VP2 protein.
Conclusions:
The findings of the present study provided new insights regarding the phylodynamics and evolution of CPV-2 in Italy, pointing out notable differences at the local level in the distribution of the CPV-2 variants and the selection of genetic subtypes. The evolution of CPV-2 has raised questions regarding the efficacy of vaccination; therefore, continuous monitoring regarding the evolution and spread of new CPV-2 variants should be a key aim of ongoing research.
... 62 These 'early finish' claims were subsequently introduced to Australia. Immunisation failures are documented in Australia, 4,52,[68][69][70] though it is likely that most failure cases remain unreported or unrecognised. Early 'vaccine breakdowns' (118 cases [2%] of the 1980 CPV survey) 4 were attributed to maternally derived antibody (MDA) interference or other age-related factors resulting in lack of adequate immunity following vaccination. ...
... 70 Later in 2017, another industrysponsored research team reported 59% CPV-2a and 41% CPV-2b cases from 284 faecal samples from dogs across Australia between 2008 and 2016. 68 This paper was limited to suspected vaccinationfailure cases and unvaccinated dogs so might not be nationally representative. Variant distribution appears to be changing across Australia, and this might shed light on risk factors for viral transmission or mutation. ...
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.
... The Vanguard series of vaccines have been demonstrated to provide efficacy against all the core viral antigens in laboratory challenge studies, including against CPV-2a, CPV-2b, and CPV-2c variants (44,46,54,58). Although all three variants of CPV have been reported in Australia, CPV-2a and CPV-2b remain the predominant variants (10,28,50,55). ...
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.
... The results presented here reinforced that North America was the origin of the CPV-2 with dissemination events to other continents after the 1970s and a high rate of evolution after the 1990s. These findings are in line with previous results that evaluated sequences from around the world and that demonstrated a CPV-2 common ancestor in the 1970s (Lin et al., 2017;Clark et al., 2018;Kulkarni et al., 2019). CPV-2 has also high nucleotide substitution rates as approximately 10 −4 per site per year as compared to those observed in other DNA viruses (Shackelton et al., 2005). ...
Canine parvovirus type 2 (CPV-2) is a relevant pathogen for dogs and causes a severe disease in carnivore species. CPV-2 reached pandemic proportions after the 1970s with the worldwide dissemination, generating antigenic and genetic variants (CPV-2a, CPV-2b, and CPV-2c) with different pathobiology in comparison with the original type CPV-2. The present study aimed to assess the current global CPV-2 molecular phylogeny and to analyze genetic diversity and temporal spreading of variants from Brazil. A total of 284 CPV-2 whole-genome sequences (WGS) and 684 VP2 complete genes (including 23 obtained in the present study) were compared to analyze phylogenetic relationships. Bayesian coalescent analysis estimated the time to the most recent common ancestor (tMRCA) and the population dynamics of the different CPV-2 lineages in the last decades. The WGS phylogenetic tree demonstrated two main clades disseminated worldwide today. The VP2 gene tree showed a total of four well-defined clades distributed in different geographic regions, including one with CPV-2 sequences exclusive from Brazil. These clades do not have a relationship with the previous classification into CPV-2a, CPV-2b, and CPV-2c, despite some having a predominance of one or more antigenic types. Temporal analysis demonstrated that the main CPV-2 clades evolved within a few years (from the 1980s to 1990s) in North America and they spread worldwide afterwards. Population dynamics analysis demonstrated that CPV-2 presented a major dissemination increase at the end of the 1980s / beginning of the 1990s followed by a period of stability and a second minor increase from 2000 to 2004. These results describe the current global CPV-2 phylogenetic genetic diversity in the World and Brazil.
... Inside the bone marrow, the virus continues spreading infection causing damage to the body immune cells making the defence system of the body weak. So, it can also cause leukopenia due to bone marrow infection [21] . [ 18,11] . ...
Canine parvovirus type 2 (CPV-2) infection is a lethal disease of dogs with higher mortality in puppies worldwide. It is crucial to find out a simple, accurate, portable, and economic CPV-2 detection method, with suitability for on-site detection. CRISPR-Cas13a is an RNA-activated ribonuclease (RNase) capable of crRNA processing and foreign RNA degradation upon binding. In this study, we expressed LwCas13a protein in a prokaryotic expression system and purified it by nickel column. CRISPR-Cas13a was then combined with recombinase polymerase amplification (RPA) to establish a molecular system for the nucleic acid detection, termed as specific high sensitivity enzymatic reporter unlocking (SHERLOCK) that can be employed for rapid and analytically sensitive nucleic acid detection. Harnessing SHERLOCK, we established a system for the on-site detection of CPV-2 DNA. The main results are listed below:
1. The IPTG induced Cas13a protein expressed by E. coli was collected, and confirmed by SDS-PAGE with clear protein bands.
2. For checking the activity and specificity of Cas13a we made four groups, two negative controls and two experimental groups. The results showed that the fluorescence values of the experimental groups were significantly higher than the negative control groups, validating that Cas13a protein has RNase activity, and possess excellent specificity for the target.
3. To evaluate the minimum detection limit and time of the detection system, we used known sample concentrations with different time intervals. To improve the detection sensitivity of the system, RPA and T7 in vitro transcription were harnessed, enabling the detection of CPV-2 DNA at concentration as low as 100 aM within 30 minutes.
In short, we established a system for the detection of CPV-2 virus with significant sensitivity and specificity. In future, our system can be used for the rapid on-site detection of CPV-2 during the disease outbreak.
... While we cannot fully exclude this possibility because vaccination history was not available for any of the CPV-2c positive dogs in the current study, both CPV-2a and CPV-2b were detected in samples from vaccinated dogs, which does not seem to support such views. It does, however, highlight the dynamic state of the local CPV-2 evolution, which can be further illustrated by the detection of only CPV-2c viruses from the Colombo district in the current study or a recent replacement of CPV-2a with CPV-2b and introduction of CPV-2c in Australia [27,37]. ...
The aim of the study was to identify canine parvovirus type 2 (CPV-2) subtypes circulating among a selected population of domestic dogs and cats in Sri Lanka and to investigate the evolutionary patterns among Sri Lankan viruses in the context of contemporary global CPV-2 sequences. Altogether, 40/61 (65.6%) samples tested were positive for CPV-2 DNA, including 31/48 (64.6%) dogs and 9/13 (69%) cats. All three subtypes (CPV-2a, CPV-2b and CPV-2c) were detected, with CPV-2a being most common. International median joining haplotype network of 291 CPV-2 sequences suggested that there was little barrier for CPV-2 moving between different geographical regions worldwide, including Sri Lanka, and that there was no correlation between the genetic structure within the molecular network and the decade of sample collection. By contrast, there was correlation between CPV-2 subtype and genetic structure, both within the international network and within the network built from 31 Sri Lankan CPV-2 sequences only. The structure within the latter was not correlated with the location of the veterinary clinic where the samples were submitted, the age or species of the host. Altogether, we have shown that there is considerable variability of CPV-2 genotypes circulating in Sri Lanka, which is likely driven by both local evolution and introduction from other countries. The similarity of CPV-2 obtained from cats and dogs suggests that cats may play a role in the epidemiology of CPV-2 in Sri Lanka.
... Up-to-date, it is clearly showed that CPV-2a spreads worldwide and is the key ancestor for the later variants, designated as CPV-2b, CPV-2c or new CPV-2a, which are distributed variably (Voorhees et al., 2020). Current epidemiological surveys show that the CPV-2a variant predominantly circulates in most Asia and in European countries while the CPV-2b variant is a major antigenic variant in Iceland, the UK, the USA, Africa and some Asian countries (Clark et al., 2018). The last variant of CPV-2, CPV-2c, first detected in Italy in 2001 with a specific 426Glu mutation in the VP2 (Buonavoglia et al., 2001). ...
Canine parvovirus type 2 (CPV‐2) is a small, single‐stranded DNA virus causing fatal hemorrhagic enteritis in dogs. Currently, CPV‐2 is classified into CPV‐2a, CPV‐2b, and CPV‐2c based on genetic variation in the VP2 gene. The CPV‐2c variant has become ubiquitous worldwide and gained attention for monitoring parvoviral evolution. In this study, we characterized the full‐length genome sequences of CPV‐2c strains obtained from 59 dogs in Vietnam. Molecular analysis revealed that Vietnamese CPV‐2c shared a common evolutionary pattern with the Asian CPV‐2 clade, which is marked by genetic signature patterns in the structural and nonstructural proteins. In addition, these Vietnamese CPV‐2c strains exhibited unique Thr112Ile and Ile447Met mutations in the VP1 and VP2 sequence, respectively. Interestingly, phylogenetic analysis indicated that the mutations of amino acid residues in both the structural and nonstructural genes have contributed to the emergence of a new clade, designated here as the Asia‐IV clade. The substitution rates, estimated from a dataset containing 199 sequences over the last 42 years, confirmed that CPV‐2 showed a high rate of nucleotide substitution, at about 2.49 x 10‐4 nucleotide substitutions per site per year (nt/s/y), with VP1/2 and NS1/2 estimates of 3.06 x 10‐4 and 3.16 x 10‐4 nt/s/y, respectively. Even though no evidence of genetic recombination in these Vietnamese CPV‐2c strains was established, potential positive selection sites were observed in both the structural and nonstructural genes, suggesting the viral evolutionary process has occurred in both the structural and nonstructural proteins. Genetic and evolutionary analysis of the full‐length genome sequence is necessary to gain evolutionary insight of CPV‐2.
... This study did not assess the genotype of CPV vaccine used by veterinarians or the predominant antigenic variant in the areas surveyed, which could be a risk factor for immunisation failure. However, the authors considered this risk unlikely at the time of the survey, as in Australia CPV-2a/b were the predominant variants (Clark et al., 2018;Meers et al., 2007), and it is generally considered that all current vaccines protect against these variants (Day et al., 2007). A single study has since reported CPV-2c detection in 3 cases from Adelaide, Australia (Woolford et al., 2017), however further national studies have not been able to replicate these results yet (Kwan et al., 2020). ...
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 to 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 use 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.
... Amplification was performed with an initial denaturation step of 10 min, followed by 35 cycles of amplification (94 C for 1 min, 60 C for 1 min, 72 C for 2 min), with a final extension step of 72 C Phylogenetic reconstructions were carried out as described previously. 42 Briefly, evolutionary analyses were conducted by estimating a joint phylogenetic tree from multiple gene partitions in a Bayesian framework using BEAST v1.10.3. This method can account for varying evolutionary histories among different genes (including variation in mutation rates, substitution models and selective forces) while attempting to estimate the true phylogenetic relationships among groups of related organisms. ...
Objective
To determine the current porcine circovirus type 2 (PCV2) genotypes circulating in pigs in Queensland (QLD).
Methods
The PCV2 infection status of pigs was determined by real‐time PCR testing of 210 lymph nodes and 30 serum samples derived from 45 QLD farms. PCV2‐positive samples from 22 pigs from 15 farms were subjected to conventional polymerase chain reaction (PCR) and sequencing of the full PCV2 genome. Phylogenetic analysis of 17 of these sequences in relation to published PCV2 sequences was then performed, and the genotypes were compared.
Results
PCV2 DNA was detected in 95 lymph nodes and 15 serum samples. Phylogenetic analysis of 17 PCV2 sequences demonstrated that seven belonged to genotype PCV2b, two to PCV2d, one to PCV2f and seven to an “intermediate group” that clustered with PCV2d on the full genome analysis.
Conclusion
This work confirms earlier studies reporting the presence of PCV2b in Australia. It is the first study to report that PCV2d and PCV2f are also present in this country. PCV2d is currently a fast‐spreading genotype globally, with reported high virulence. The potential implications of these findings with respect to pathogenicity and vaccine efficacy require further investigation.
... The virus was designated as CPV2, at that time, due to the existence of minute virus of canine, known as CPV1 [4]. During the 80s, the original virus (CPV2) circulating globally acquired mutations, which led to the emergence of two antigenic subtypes (CPV2a and CPV2b) and replacement of the prototype CPV2 with the appearance of an additional antigenic subtype (CPV2c) in 2000 in Italy [5]. ...
Aim:
This study aimed to detect and characterize current genotypes of canine parvovirus (CPV) in Egypt during 2018.
Materials and methods:
A total of 50 fecal swabs were collected from clinically infected domestic dogs of 2-5 months of age, suspected to suffer from CPV infection, from Cairo and Giza Governorates. The samples were subjected to qualitative antigen detection using the rapid test, followed by isolation on Madin-Darby Canine Kidney (MDCK) cells, molecular characterization with partial amplification of VP2 gene using polymerase chain reaction (PCR), followed by sequencing and phylogenetic analysis.
Results:
Out of 50 fecal samples, 20 samples were positive (40%) by Rapid CPV/canine coronavirus Ag Test Kit. These positive samples were cultured successfully on MDCK cells. Nine randomly chosen samples out of 30 apparently negative samples were amplified using PCR with primers Hfor and Hrev to yield a typical 630 bp fragment. Then, six randomly chosen samples out of nine were amplified using PCR with primers Pbs and Pbas to yield a typical 427 bp fragment. Sequencing, BLAST analysis and assembly of the two fragments (630 bp and 427 bp) to produce 912 bp fragments, in the six samples, revealed two serotypes CPV-2b and CPV-2c. The obtained strains were submitted to GenBank and given accession numbers MK642272, MK642273, MK642274, MK642275, MK642276, and MK642277. Phylogenetic analysis of the Egyptian strains serotype 2b illustrated that they were closely related to Thailand strains (accession numbers KP715709, KP715694, KP715701, and KP715700); while Egyptian strains serotype 2c was closely related to Thailand strains (accession numbers MH711894 and MH711902), Taiwanese strain (KU244254), Chinese strain (MF467242), and Vietnamese strain (accession number LC216910).
Conclusion:
The current research recommends further epidemiological studies to assess the extent of the occurrence of different serotypes of CPV in Egypt and the efficiency of imported and locally produced vaccines in protection against CPV infection.
... It has been suggested that vaccine strain may be a risk-factor for vaccination failure and that newer CPV variants may be less protected by the 'original' CPV2 strain vaccines (Cavalli et al., 2008;Decaro et al., 2009;Pratelli et al., 2001), however recent Australian research demonstrated no difference in failure rates between the two commercially available strains (Altman et al., 2017). The reported disease occurrence rate of wild CPV strains in Australia, CPV2a and CPV2b, was 54% and 46% respectively between 2007 and 2016 (Clark et al., 2018), although 3 cases of CPV2c have also been reported from Adelaide in 2015 (Woolford et al., 2017). Ongoing monitoring of vaccine strain usage and vaccination failures will help determine if vaccine strain is a risk factor for vaccination failure. ...
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.
... When sanitation rates are poor and burdens are high, ecological risk factors that influence vegetation or water properties, both of which impact parasite survival and/or infectivity, become especially important. The widespread availability of satellite imagery has played a key role in identifying ecological correlates of geographical distributions and infection rates for an incredible diversity of pathogens [29,[65][66][67][68][69]. For human helminth parasites, numerous geostatistical analyses have delineated spatial clusters of high infection risk, further indicating a strong role of environmental forces [29,65,70,71]. ...
Background
Schistosomiasis is a neglected tropical disease caused by Schistosoma parasites. Intervention relies on identifying high-risk regions, yet rapid Schistosoma diagnostics (Kato-Katz stool assays (KK) and circulating cathodic antigen urine assays (CCA)) yield different prevalence estimates. We mapped S. mansoni prevalence and delineated at-risk regions using a survey of schoolchildren in Rwanda, where Schistosoma mansoni is an endemic parasite. We asked if different diagnostics resulted in disparities in projected infection risk.
Methods
Infection data was obtained from a 2014 Rwandan school-based survey that used KK and CCA diagnostics. Across 386 schools screened by CCA (N = 19,217). To allow for uncertainty when interpreting ambiguous CCA trace readings, which accounted for 28.8% of total test results, we generated two presence-absence datasets: CCA trace as positive and CCA trace as negative. Samples (N = 9,175) from 185 schools were also screened by KK. We included land surface temperature (LST) and the Normalized Difference Vegetation and Normalized Difference Water Indices (NDVI, NDWI) as predictors in geostatistical regressions.
Findings
Across 8,647 children tested by both methods, prevalence was 35.93% for CCA trace as positive, 7.21% for CCA trace as negative and 1.95% for KK. LST was identified as a risk factor using KK, whereas NDVI was a risk factor for CCA models. Models predicted high endemicity in Northern and Western regions of Rwanda, though the CCA trace as positive model identified additional high-risk areas that were overlooked by the other methods. Estimates of current burden for children at highest risk (boys aged 5–9 years) varied by an order of magnitude, with 671,856 boys projected to be infected by CCA trace as positive and only 60,453 projected by CCA trace as negative results.
Conclusions
Our findings show that people in Rwanda’s Northern, Western and capital regions are at high risk of S. mansoni infection. However, variation in identification of environmental risk factors and delineation of at-risk regions using different diagnostics likely provides confusing messages to disease intervention managers. Further research and statistical analyses, such as latent class analysis, can be used to improve CCA result classification and assess its use in guiding treatment regimes.
... Canine parvovirus (CPV) is one of the most important gastrointestinal pathogens of domestic dogs, responsible for morbidity and mortality worldwide (Clark et al., 2018). In Australia, the annual CPV caseload has been estimated to be approximately 20,000, with an euthanasia rate of 41% and an estimated treatment cost of $A1,500 per patient (Kelman et al., 2019). ...
Canine parvovirus (CPV) is an important and often fatal pathogen of domestic dogs. It is resistant in the environment and cross-species transmission has been indicated in some canid populations, but never in Australia. The aim of this study was to determine if an association exists between 1. reported CPV cases in domestic dogs, and 2. the wild canid distribution in New South Wales (NSW), Australia. Reported CPV cases, and reports of the presence of wild dogs and the red fox (Vulpes vulpes), were extracted from a voluntary surveillance database and a voluntary pest reporting system, respectively. A total of 1,984 CPV cases in domestic dogs, and 3,593 fox and 3,075 wild dog sightings were reported between 2011 and 2016. Postcodes in which CPV cases were reported were significantly (P = 0.0002) more likely to report wild dogs (odds ratio 2.07, 95% CI 1.41–3.03). Overall, CPV cases were significantly (P < 0.05) correlated with both fox reports (rSP 0.225) and wild dog reports (rSP 0.247). The strength of association varied by geographical region and year; the strongest correlations were found in the mid-North Coast region (rSP 0.607 for wild dogs) and in 2016 (rSP 0.481 for foxes). Further serological and virological testing is required to confirm the apparent and plausible association between domestic CPV cases and wild canid distribution found in this study. Keywords: Microbiology, Ecology, Wildlife ecology, Viral disease, Epidemiology, Animal behavior, Virologycanine parvovirus, Protoparvovirus, Wild dog, Fox, Vulpes vulpes, Spatial analysis, Australia
... In addition to delineating regions in need of intervention, a key aim of infectious disease modelling is to uncover ecological drivers of observed infection patterns [51][52][53][54]. Capabilities to uncover ecological correlates of pathogen distributions and infection rates have greatly improved with the widespread availability of satellite imagery [16,25,51,55]. Here, we identified NDWI as an important predictor of infection probability for all three STH parasite groups. ...
Soil-transmitted helminth (STH) infections are globally distributed intestinal parasite infections caused by Ascaris lumbricoides, Trichuris trichiura, and hookworms (Ancylostoma duodenale and Necator americanus). STH infection constitutes a major public health threat, with heavy burdens observed in many of the world’s tropical and subtropical regions. Mass drug administration and sanitation improvements can drastically reduce STH prevalence and associated morbidity. However, identifying targeted areas in need of treatment is hampered by a lack of knowledge on geographical and population-level risk factors. In this study, we applied Bayesian geostatistical modelling to data from a national school-based STH infection survey in Rwanda to (1) identify ecological and population-level risk factors and (2) provide comprehensive precision maps of infection burdens. Our results indicated that STH infections were heterogeneously distributed across the country and showed signatures of spatial clustering, though the magnitude of clustering varied among parasites. The highest rates of endemic clustering were attributed to A. lumbricoides infection. Concordant infection patterns among the three parasite groups highlighted populations currently most at-risk of morbidity. Population-dense areas in the Western and North-Western regions of Rwanda represent areas that have continued to exhibit high STH burden across two surveys and are likely in need of targeted interventions. Our maps support the need for an updated evaluation of STH endemicity in western Rwanda to evaluate progress in MDA efforts and identify communities that need further local interventions to further reduce morbidity caused by STH infections.
... Since its global emergence, highly contagious CPV-2 causes acute gastroenteritis and lymphopenia in young dogs and is endemic in the most wild and domestic dog populations. Now, new antigenic types, CPV-2a, 2b, and 2c, are circulating worldwide Mohan Raj et al., 2010;Decaro and Buonavoglia, 2012;Sharma et al., 2016;Zhao et al., 2017;Mira et al., 2018;Clark et al., 2018). Genetic variation among CPV-2 isolates has been used to further classify the virus among these three antigenic variants that differ in their amino acid sequences and VP2 gene structure (Amrani et al., 2016;Buonavoglia et al., 2001;Mira et al., 2018;Mohan Raj et al., 2010). ...
... In fact, Ohneiser et al. (2015) discovered a monophyletic group of locally evolving CPV-2a variants, without evidences of ongoing viral exchange with other countries. The monophyletic nature of New Zealand CPV-2a conflicts with what is observed for this variant in this and other studies (Clark et al., 2018;Grecco et al., 2018). However, the actual evolutionary and clinical consequences of the coexistence of both imported and locally evolving viruses, remain to be elucidated. ...
Canine parvovirus is one of the most frequent pathogens of young dogs, causing severe clinical manifestations. Its phenotypic variability led to an antigenic-based classification into different variants, which have been reported worldwide. To update the Italian distribution of CPV, a molecular survey was performed on 100 geographically-annotated samples collected from 2008 to 2015 by full VP2 sequencing. All three antigenic variants (CPV-2a, 2b, 2c) were detected during the studied period, being CPV-2a the most prevalent (60%). Locally, CPV appeared widely distributed, without any regional or temporal clustering, demonstrating an outstanding and uncontrolled within-country viral spreading. The Italian sequences were also contextualized in the International scenario. The analysis of CPV worldwide molecular epidemiology highlighted the remarkable genetic heterogeneity of the circulating strains and their broad distribution. In fact, a frequent viral exchange among Countries, was proven both over short and long distances, involving haplotypes persisting through time. The reported information on viral dissemination patterns appears crucial for understanding the introduction routes of new variants or strains, which could complicate the epidemiological scenario, affect the disease patterns, show possible differential virulence and clinical relevance of emerging strains especially, and impair the vaccine efficacy.
... The extent of carnivore species diversity in the UK is higher than Australia and New Zealand but lower than that in Europe and North America. Molecular surveillance of CPVs in Australia and New Zealand, has shown a 'lag' in CPV evolution, with CPV-2a being reported as the dominant subtype in Australia until 2011-2013, and the only subtype in NZ until at least 2009, likely reflecting both geographical isolation and the absence of endemic species which facilitate viral evolution (Ohneiser et al., 2015;Clark et al., 2018). ...
Canine parvovirus 2 (CPV-2), a highly contagious virus, affects dogs worldwide. Infected animals present severe and acute gastroenteritis which may culminate in death. CPV-2 VP2 protein is responsible for important biological functions related to virus-host interactions. Herein we obtained VP2 full-length gene sequences from Brazilian dogs with bloody diarrhea (n=15) and vaccine strains (n=7) produced by seven different laboratories and marketed in Brazil. All wild sequences and one vaccine strain were classified as CPV-2b and six vaccines were the classic CVP-2. Mutations in VP2 protein from vaccine and wild strains obtained in Brazil and worldwide were analyzed (n=906). Amino acid sequences from vaccine strains remarkably diverge from each other, even that classic CPV-2. Phylogenetic analysis based on VP2 gene and conducted with sequences displaying mutations in epitope regions previously described shows that vaccine strains are distantly related from the wide range of wild CPV-2. The impact of amino acid mutations over VP2 protein structure shows that vaccine and wild strains obtained in this study diverge in loop 3, an epitope region that plays a role in the CPV-2 host range. This is the first analysis of CPV-2 VP2 from commercial vaccine strains in Brazil and wild ones from Minas Gerais State, Brazil, and the first detailed attempt to vaccinal VP2 molecular and structural analyses.
Canine parvovirus (CPV) is a major cause of hemorrhagic diarrhea and mortality in puppies worldwide. There are 2 types of Parvovirus which affects canines: Canine parvovirus 2 (CPV-2) and Canine parvovirus 1 (CPV-1) or the Minute Virus of Canine (MVC). CPV-2 originated from Feline panleukopenia virus and has undergone genetic variation to give rise to its three variants (CPV-2a, CPV-2b and CPV-2c). Amino acid substitutions in VP2 capsid protein have led virus to adapt new host range. The original CPV-2 was known to be dominant in Japan, Belgium, Australia as well as USA and later circulated throughout the world. Clinically, CPV-2 infection is characterized by anorexia, lethargy, depression, vomiting, leukopenia and severe hemorrhagic diarrhea. Several diagnostic tests have been developed to detect parvoviral infections which are categorized into immunological tests (latex agglutination test, SIT-SAT and ELISA etc.) and molecular based tests (PCR, mPCR and RT-PCR etc.). To control and manage the disease several treatments like fluid therapies, antibiotics, and adjunctive treatments are available and some are in various stages of development. Apart from this, many vaccines are also commercially available and some are in developmental stages. The present review contains detailed information regarding structural biology, occurrence, pathogenesis, clinical diagnosis, treatments and prevention in order to understand the need and the growing importance of CPV-2.
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 5 Australian states. The median age at diagnosis was 4 months (range 1 to 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 aa mutations. Several Australian CPV strains displayed signatures in the VP2 protein typical of Asian CPVs, suggestion 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 capsid (VP2) key 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.
[Background] Spillover of parasites at the domestic animal - wildlife interface is a pervasive threat to animal health. Cat and dog fleas (Ctenocephalides felis and C. canis) are among the world’s most invasive and economically important ectoparasites. Although both species are presumed to infest a diversity of host species across the globe, knowledge on their distributions in wildlife is poor. We built a global dataset of wild mammal host associations for cat and dog fleas, and used Bayesian hierarchical models to identify traits that predict wildlife infestation probability. We complemented this by calculating functional-phylogenetic host specificity to assess whether fleas are restricted to hosts with similar evolutionary histories, diet or habitat niches.
[Results] Over 130 wildlife species have been found to harbour cat fleas, representing nearly 20% of all mammal species sampled for fleas. Phylogenetic models indicate cat fleas are capable of infesting a broad diversity of wild mammal species through ecological fitting. Those that use anthropogenic habitats are at highest risk. Dog fleas, by contrast, have been recorded in 31 mammal species that are primarily restricted to certain phylogenetic clades, including canids, felids and murids. Both flea species are commonly reported infesting mammals that are feral (free-roaming cats and dogs) or introduced (red foxes, black rats and brown rats), suggesting the breakdown of barriers between wildlife and invasive reservoir species will increase spillover at the domestic animal - wildlife interface.
[Conclusions] Our empirical evidence shows that cat fleas are incredibly host-generalist, likely exhibiting a host range that is among the broadest of all ectoparasites. Reducing wild species’ contact rates with domestic animals across natural and anthropogenic habitats, together with mitigating impacts of invasive reservoir hosts, will be crucial for reducing invasive flea infestations in wild mammals.
Canine parvovirus (CPV) outbreaks can have a devastating effect in communities with dense dog populations. The interior region of Alaska experienced a CPV outbreak in the winter of 2016 leading to the further investigation of the virus due to reports of increased morbidity and mortality occurring at dog mushing kennels in the area. Twelve rectal-swab specimens from dogs displaying clinical signs consistent with parvoviral-associated disease were processed using next-generation sequencing (NGS) methodologies by targeting RNA transcripts, and therefore detecting only replicating virus. All twelve specimens demonstrated the presence of the CPV transcriptome, with read depths ranging from 2.2X - 12,381X, genome coverage ranging from 44.8-96.5%, and representation of CPV sequencing reads to those of the metagenome background ranging from 0.0015-6.7%. Using the data generated by NGS, the presence of newly evolved, yet known, strains of both CPV-2a and CPV-2b were identified and grouped geographically. Deep-sequencing data provided additional diagnostic information in terms of investigating novel CPV in this outbreak. NGS data in addition to limited serological data provided strong diagnostic evidence that this outbreak most likely arose from unvaccinated or under-vaccinated canines, not from a novel CPV strain incapable of being neutralized by current vaccination efforts.
The US swine industry has been impaired over the last 25 years by the far-reaching financial losses caused by the porcine reproductive and respiratory syndrome (PRRS). Here, we explored the relations between the spatial risk of PRRS outbreaks and its phylodynamic history in the U.S during 1998-2016 using ORF5 sequences collected from swine farms in the Midwest region. We used maximum entropy and Bayesian phylodynamic models to generate risk maps for PRRS outbreaks and reconstructed the evolutionary history of three selected phylogenetic clades (A, B and C). High-risk areas for PRRS were best-predicted by pig density and climate seasonality and included Minnesota, Iowa and South Dakota. Phylodynamic models demonstrated that the geographical spread of the three clades followed a heterogeneous spatial diffusion process. Furthermore, PRRS viruses were characterized by typical seasonality in their population size. However, endemic strains were characterized by a substantially slower population growth and evolutionary rates, as well as smaller spatial dispersal rates when compared to emerging strains. We demonstrated the prospects of combining inferences derived from two unique analytical methods to inform decisions related to risk-based interventions of an important pathogen affecting one of the largest food animal industries in the world.
Canine parvovirus (CPV-2) is an important cause of hemorrhagic enteritis in dogs. In Australia the disease has been associated with CPV-2a and CPV-2b variants. A third more recently emerged variant overseas, CPV-2c, has not been detected in surveys of the Australian dog population. In this study, we report three cases of canine parvoviral enteritis associated with CPV-2c infection; case 1 occurred in an 8-week-old puppy that died following acute hemorrhagic enteritis. Cases 2 and 3 were an 11-month-old female entire Saint Bernard and a 9-month-old male entire Siberian husky, respectively, both which had completed vaccination schedules and presented with vomiting or mild diarrhea only. Full genomic sequencing of parvoviral DNA from cases 1, 2, and 3 revealed greater than 99% homology to known CPV-2c variants and predicted protein sequences from the VP2 region of viral DNA from all three cases identified; glutamic acid residues at the 426 amino acid residue, characteristic of the CPV-2c variant. Veterinary professionals should be aware that CPV-2c is now present in Australia, detected in a puppy and vaccinated young adult dogs in this study. Further characterization of CPV-2c-associated disease and its prevalence in Australian dogs requires additional research.
Is the origin of gibbon ape leukemia virus (GALV) human after all? When GALV was discovered and found to cause neoplastic disease in gibbons, it stimulated a great deal of research including investigations into the origins of this virus. A number of publications have suggested that the GALV progenitor was a retrovirus present in one of several species of South East Asian rodents that had close contact with captive gibbons. However, there are no published retroviral sequences from any South East Asian species to support this view. Here we present an alternative hypothesis that the origin of GALV is a virus closely related to Melomys burtoni retrovirus, and that this virus infected human patients in Papua New Guinea from whom biological material was obtained or in some way contaminated these samples. This material we propose contained infectious MbRV-related virus that was then unwittingly introduced into gibbons which subsequently developed GALV infections.
Experimental work increasingly suggests that non-random pathogen associations can affect the spread or severity of disease. Yet due to difficulties distinguishing and interpreting co-infections, evidence for the presence and directionality of pathogen co-occurrences in wildlife is rudimentary. We provide empirical evidence for pathogen co-occurrences by analysing infection matrices for avian malaria (Haemoproteus and Plasmodium spp.) and parasitic filarial nematodes (microfilariae) in wild birds (New Caledonian Zosterops spp.). Using visual and genus-specific molecular parasite screening, we identified high levels of co-infections that would have been missed using PCR alone. Avian malaria lineages were assigned to species level using morphological descriptions. We estimated parasite co-occurrence probabilities, while accounting for environmental predictors, in a hierarchical multivariate logistic regression. Co-infections occurred in 36% of infected birds. We identified both positively and negatively correlated parasite co-occurrence probabilities when accounting for host, habitat and island effects. Two of three pairwise avian malaria co-occurrences were strongly negative, despite each malaria parasite occurring across all islands and habitats. Birds with microfilariae had elevated heterophil to lymphocyte ratios and were all co-infected with avian malaria, consistent with evidence that host immune modulation by parasitic nematodes facilitates malaria co-infections. Importantly, co-occurrence patterns with microfilariae varied in direction among avian malaria species; two malaria parasites correlated positively but a third correlated negatively with microfilariae. We show that wildlife co-infections are frequent, possibly affecting infection rates through competition or facilitation. We argue that combining multiple diagnostic screening methods with multivariate logistic regression offers a platform to disentangle impacts of environmental factors and parasite co-occurrences on wildlife disease. Experimental work increasingly suggests that non-random pathogen associations can affect the spread or severity of disease. Yet due to difficulties distinguishing and interpreting co-infections, evidence for the presence and directionality of pathogen co-occurrences in wildlife is rudimentary. We provide empirical evidence for pathogen co-occurrences by analysing infection matrices for avian malaria (Haemoproteus and Plasmodium spp.) and parasitic filarial nematodes (microfilariae) in wild birds (New Caledonian Zosterops spp.). Using visual and genus-specific molecular parasite screening, we identified high levels of co-infections that would have been missed using PCR alone. Avian malaria lineages were assigned to species level using morphological descriptions. We estimated parasite co-occurrence probabilities, while accounting for environmental predictors, in a hierarchical multivariate logistic regression. Co-infections occurred in 36% of infected birds. We identified both positively and negatively correlated parasite co-occurrence probabilities when accounting for host, habitat and island effects. Two of three pairwise avian malaria co-occurrences were strongly negative, despite each malaria parasite occurring across all islands and habitats. Birds with microfilariae had elevated heterophil to lymphocyte ratios and were all co-infected with avian malaria, consistent with evidence that host immune modulation by parasitic nematodes facilitates malaria co-infections. Importantly, co-occurrence patterns with microfilariae varied in direction among avian malaria species; two malaria parasites correlated positively but a third correlated negatively with microfilariae. We show that wildlife co-infections are frequent, possibly affecting infection rates through competition or facilitation. We argue that combining multiple diagnostic screening methods with multivariate logistic regression offers a platform to disentangle impacts of environmental factors and parasite co-occurrences on wildlife disease.
The most important enteric virus infecting canids is canine parvovirus type 2 (CPV-2). Canine parvovirus is the etiologic agent of a contagious disease, mainly characterized by clinical gastroenteritis signs in younger dogs. CPV-2 emerged as a new virus in the late 1970s, which could infect domestic dogs, and becoming distributed in the global dog population within 2 years. A few years later the virus original type was replaced by a new genetic and antigenic variant, called CPV-2a. Around 1984 and 2000 virus variants with the single change to Asp or Glu in the VP2 residue 426 were detected (sometimes termed CPV-2b and CPV-2c). The genetic and antigenic changes in the variants have also been correlated with changes in their host range; in particular in the ability to replicate in cats and also host range differences in canine and other tissue culture cells. CPV-2 variants have been circulating among wild carnivores and have been well-documented in several countries around the world. Here we review and summarize the current information about the worldwide distribution and evolution of CPV-2 variants since they emerged, as well as the host ranges they are associated with.
Unlabelled:
Influenza A viruses (IAVs) are maintained mainly in wild birds, and despite frequent spillover infections of avian IAVs into mammals, only a small number of viruses have become established in mammalian hosts. A new H3N2 canine influenza virus (CIV) of avian origin emerged in Asia in the mid-2000s and is now circulating in dog populations of China and South Korea, and possibly in Thailand. The emergence of CIV provides new opportunities for zoonotic infections and interspecies transmission. We examined 14,764 complete IAV genomes together with all CIV genomes publicly available since its first isolation until 2013. We show that CIV may have originated as early as 1999 as a result of segment reassortment among Eurasian and North American avian IAV lineages. We also identified amino acid changes that might have played a role in CIV emergence, some of which have not been previously identified in other cross-species jumps. CIV evolves at a lower rate than H3N2 human influenza viruses do, and viral phylogenies exhibit geographical structure compatible with high levels of local transmission. We detected multiple intrasubtypic and heterosubtypic reassortment events, including the acquisition of the NS segment of an H5N1 avian influenza virus that had previously been overlooked. In sum, our results provide insight into the adaptive changes required by avian viruses to establish themselves in mammals and also highlight the potential role of dogs to act as intermediate hosts in which viruses with zoonotic and/or pandemic potential could originate, particularly with an estimated dog population of ∼ 700 million.
Importance:
Influenza A viruses circulate in humans and animals. This multihost ecology has important implications, as past pandemics were caused by IAVs carrying gene segments of both human and animal origin. Adaptive evolution is central to cross-species jumps, and this is why understanding the evolutionary processes that shape influenza A virus genomes is key to elucidating the mechanisms underpinning viral emergence. An avian-origin canine influenza virus (CIV) has recently emerged in dogs and is spreading in Asia. We reconstructed the evolutionary history of CIV and show that it originated from both Eurasian and North American avian lineages. We also identified the mutations that might have been responsible for the cross-species jump. Finally, we provide evidence of multiple reassortment events between CIV and other influenza viruses (including an H5N1 avian virus). This is a cause for concern, as there is a large global dog population to which humans are highly exposed.
We review the literature to distinguish reports of vertebrate wildlife disease emergence with sufficient evidence, enabling a robust assessment of emergence drivers. For potentially emerging agents that cannot be confirmed, sufficient data on prior absence (or a prior difference in disease dynamics) are frequently lacking. Improved surveillance, particularly for neglected host taxa, geographical regions and infectious agents, would enable more effective management should emergence occur. Exposure to domestic sources of infection and human-assisted exposure to wild sources were identified as the two main drivers of emergence across host taxa; the domestic source was primary for fish while the wild source was primary for other taxa. There was generally insufficient evidence for major roles of other hypothesized drivers of emergence.
Copyright © 2015 Elsevier Ltd. All rights reserved.
Canine parvovirus (CPV), a fast-evolving single-stranded DNA virus, comprises three antigenic variants (2a, 2b, and 2c) with different frequencies and genetic variability among countries. The contribution of co-infection and recombination to the genetic variability of CPV is far from being fully elucidated. Here we took advantage of a natural CPV population, recently formed by the convergence of divergent CPV-2c and CPV-2a strains, to study co-infection and recombination. Complete sequences of the viral coding region of CPV-2a and CPV-2c strains from 40 samples were generated and analyzed using phylogenetic tools. Two samples showed co-infection and were further analyzed by deep sequencing. The sequence profile of one of the samples revealed the presence of CPV-2c and CPV-2a strains that differed at 29 nucleotides. The other sample included a minor CPV-2a strain (13.3% of the viral population) and a major recombinant strain (86.7%). The recombinant strain arose from inter-genotypic recombination between CPV-2c and CPV-2a strains within the VP1/VP2 gene boundary. Our findings highlight the importance of deep-sequencing analysis to provide a better understanding of CPV molecular diversity.
Maximum likelihood or restricted maximum likelihood (REML) estimates of the
parameters in linear mixed-effects models can be determined using the lmer
function in the lme4 package for R. As for most model-fitting functions in R,
the model is described in an lmer call by a formula, in this case including
both fixed- and random-effects terms. The formula and data together determine a
numerical representation of the model from which the profiled deviance or the
profiled REML criterion can be evaluated as a function of some of the model
parameters. The appropriate criterion is optimized, using one of the
constrained optimization functions in R, to provide the parameter estimates. We
describe the structure of the model, the steps in evaluating the profiled
deviance or REML criterion, and the structure of classes or types that
represents such a model. Sufficient detail is included to allow specialization
of these structures by users who wish to write functions to fit specialized
linear mixed models, such as models incorporating pedigrees or smoothing
splines, that are not easily expressible in the formula language used by lmer.
[Extract] Effective surveillance is crucial for early detection and successful mitigation of emerging diseases [1]. The current global approach to surveillance for wildlife diseases affecting biodiversity ("biodiversity diseases") is still inadequate as demonstrated by the slow characterization and response to the two recent devastating epidemics, chytridiomycosis and white-nose syndrome [2]–[5]. Current surveillance for wildlife disease usually targets diseases that affect humans or livestock, not those impacting wildlife populations. Barriers to effective surveillance for biodiversity diseases include a relative lack of social and political will and the inherent complexity and cost of implementing surveillance for multiple and diverse free-ranging populations. Here we evaluate these challenges and the inadequacies of current surveillance techniques, and we suggest an integrated approach for effective surveillance.
Ecological fitting refers to interspecific associations characterized by ecologically specialized, yet phylogenetically conservative, resource utilization. During periods of biotic expansion, parasites and hosts may disperse from their areas of origin. In conjunction with ecological fitting, this sets the stage for host switching without evolving novel host utilization capabilities. This is the evolutionary basis of emerging infectious diseases (EIDs). Phylogenetic analysis for comparing trees (PACT) is a method developed to delineate both general and unique historically reticulated and non-reticulated relationships among species and geographical areas, or among parasites and their hosts. PACT is based on ‘Assumption 0’, which states that all species and all hosts in each input phylogeny must be analysed without modification, and the final analysis must be logically consistent with all input data. Assumption 0 will be violated whenever a host or area has a reticulated history with respect to its parasites or species. PACT includes a Duplication Rule, by which hosts or areas are listed for each co-evolutionary or biogeographical event affecting them, which satisfies Assumption 0 even if there are reticulations. PACT maximizes the search for general patterns by using Ockam's Razor – duplicate only enough to satisfy Assumption 0. PACT applied to the host and geographical distributions of members of two groups of parasitic helminths infecting anthropoid primates indicates a long and continuous association with those hosts. Nonetheless, c. 30% of the host associations are due to host switching. Only one of those involves non-primate hosts, suggesting that most were constrained by resource requirements that are phylogenetically conservative among primates (ecological fitting). In addition, most of the host switches were associated with episodes of biotic expansion, also as predicted by the ecological fitting view of EIDs.
Summary: The two main functions of bioinformatics are the organization and analysis of biological data using computational resources. Geneious Basic has been designed to be an easy-to-use and flexible desktop software application framework for the organization and analysis of biological data, with a focus on molecular sequences and related data types. It integrates numerous industry-standard discovery analysis tools, with interactive visualizations to generate publication-ready images. One key contribution to researchers in the life sciences is the Geneious public application programming interface (API) that affords the ability to leverage the existing framework of the Geneious Basic software platform for virtually unlimited extension and customization. The result is an increase in the speed and quality of development of computation tools for the life sciences, due to the functionality and graphical user interface available to the developer through the public API. Geneious Basic represents an ideal platform for the bioinformatics community to leverage existing components and to integrate their own specific requirements for the discovery, analysis and visualization of biological data.Availability and implementation: Binaries and public API freely available for download at http://www.geneious.com/basic, implemented in Java and supported on Linux, Apple OSX and MS Windows. The software is also available from the Bio-Linux package repository at http://nebc.nerc.ac.uk/news/geneiousonbl.Contact:
peter@biomatters.com
Understanding the evolutionary history of living organisms is a central problem in biology. Until recently the ability to infer evolutionary relationships was limited by the amount of DNA sequence data available, but new DNA sequencing technologies have largely removed this limitation. As a result, DNA sequence data are readily available or obtainable for a wide spectrum of organisms, thus creating an unprecedented opportunity to explore evolutionary relationships broadly and deeply across the Tree of Life. Unfortunately, the algorithms used to infer evolutionary relationships are NP-hard, so the dramatic increase in available DNA sequence data has created a commensurate increase in the need for access to powerful computational resources. Local laptop or desktop machines are no longer viable for analysis of the larger data sets available today, and progress in the field relies upon access to large, scalable high-performance computing resources. This paper describes development of the CIPRES Science Gateway, a web portal designed to provide researchers with transparent access to the fastest available community codes for inference of phylogenetic relationships, and implementation of these codes on scalable computational resources. Meeting the needs of the community has included developing infrastructure to provide access, working with the community to improve existing community codes, developing infrastructure to insure the portal is scalable to the entire systematics community, and adopting strategies that make the project sustainable by the community. The CIPRES Science Gateway has allowed more than 1800 unique users to run jobs that required 2.5 million Service Units since its release in December 2009. (A Service Unit is a CPU-hour at unit priority).
The emergence of canine parvovirus (CPV) represents a well-documented example highlighting the emergence of a new virus through cross-species transmission. CPV emerged in the mid-1970s as a new pathogen of dogs and has since become endemic in the global dog population. Despite widespread vaccination, CPV has remained a widespread disease of dogs, and new genetic and antigenic variants have arisen and sometimes reached high frequency in certain geographic regions or throughout the world. Here we review our understanding of this emergence event and contrast it to what is known about the emergence of a disease in mink caused by mink enteritis virus (MEV). In addition, we summarize the evolution of CPV over the past 30 years in the global dog population, and describe the epidemiology of contemporary parvovirus infections of dogs and cats. CPV represents a valuable model for understanding disease emergence through cross-species transmission, while MEV provides an interesting comparison.
Canine parvovirus type 2 (CPV2) emerged in 1978 as a highly contagious and very serious disease in dogs. The characterization of CPV2 antigenic types is exclusively based on the identification of the amino acid residue at position 426 of the capsid protein VP2. Currently, three antigenic types CPV-2a (asparagine N(426)), CPV-2b (aspartic acid D(426)) and CPV-2c (glutamic acid E(426)) are circulating worldwide. In Tunisia, despite the fact that many clinical and few serological investigations clearly indicate that CPV is widespread and of major concerns in the local dog population, no molecular and antigenic type characterization of circulating variants has been carried out. This investigation showed that most of clinically presumed CPV infections were confirmed by classical or real-time PCR. When no real-time PCR facilities were affordable, classical PCR as reported here in association with restriction fragment length polymorphism (RFLP) with MboI and MboII can be very useful for screening and diagnosing CPV infections. A total of 50 variants were characterized by sequencing and an almost even representation of the different antigenic types, including CPV-2c and slightly more type 2b, were evidenced. Characterization of the Tunisian variants by MGB probe assays as reported was inefficient for most of CPV-2a variants because of their typical nucleotide mutation C(1269). Phylogenetic analysis showed that the Tunisian variants underwent evolution for a relatively long period of time inside the country. The analysis also showed some crossings of the different antigenic types, leaving both genotypic and phenotypic characteristic mutations.
Analysis of canine parvovirus (CPV) isolates with a panel of monoclonal antibodies showed that after 1986, most viruses isolated from dogs in many parts of the United States differed antigenically from the viruses isolated prior to that date. The new antigenic type (designated CPV type 2b) has largely replaced the previous antigenic type (CPV type 2a) among virus isolates from the United States. This represents the second occurrence of a new antigenic type of this DNA virus since its emergence in 1978, as the original CPV type (CPV type 2) had previously been replaced between 1979 and 1981 by the CPV type 2a strain. DNA sequence comparisons showed that CPV types 2b and 2a differed by as few as two nonsynonymous (amino acid-changing) nucleotide substitutions in the VP-1 and VP-2 capsid protein genes. One mutation, resulting in an Asn-Asp difference at residue 426 in the VP-2 sequence, was shown by comparison with a neutralization-escape mutant selected with a non-CPV type 2b-reactive monoclonal antibody to determine the antigenic change. The mutation selected by that monoclonal antibody, a His-Tyr difference in VP-2 amino acid 222, was immediately adjacent to residue 426 in the three-dimensional structure of the CPV capsid. The CPV type 2b isolates are phylogenetically closely related to the CPV type 2a isolates and are probably derived from a common ancestor. Phylogenetic analysis showed a progressive evolution away from the original CPV type. This pattern of viral evolution appears most similar to that seen in some influenza A viruses.
Canine parvovirus (CPV) is a significant pathogen of domestic and free-ranging carnivores all over the world. It suddenly appeared at the end of the 1970s and most likely emerged as a variant of the well known feline panleukopenia virus (FPV). During its adaptation to the new host, the domestic-dog, the virus has changed its antigenic profile twice giving rise to two new antigenic types, CPV-2a and CPV-2b. These new types have replaced the original type CPV-2 in the United States of America, Europe and Japan. However, no data about the prevalence of the new antigenic types on the African continent are available. In this study, 128 recent parvovirus isolates from South Africa and Namibia were antigenically typed with type-specific monoclonal antibodies. No original CPV-2 viruses were found and its complete replacement by the new antigenic types conforms to the situation in other parts of the world. The predominant strain found in southern Africa was CPV-2b (66%), which differs from the situation in Europe and Japan where CPV-2a is the most prevalent type. Analysis of the capsid protein DNA-sequences of four selected African isolates gave no hint of a specific African parvovirus lineage.
Canine parvovirus type 2 (CPV2) emerged in 1978 as causative agent of a new disease of dogs. New antigenic variants (biotypes), designated CPV2a and CPV2b, became widespread during 1979 to 1980 and 1984, respectively. At the present time the original CPV2 has disappeared in the dog population and has been replaced by the two new viruses. In the present study the comparison of neutralizing antibody titers in two groups of pups (18 pups in each group) inoculated with CPV2 and CPV2b modified live virus vaccines is reported. Using the hemagglutination inhibition (HI) test, relevant differences between antibody titers, against either the homologous or the heterologous virus, were not constantly observed. Using the neutralization (Nt) test, however, the pups inoculated with CPV2 had antibody titers which were approximately 30 times higher to the homologous virus (mean, 4,732) than to the heterologous virus (CPV2b) (mean, 162). The results of these experiments support two conclusions: (i) the HI test may not always accurately evaluate the true immune status of dogs with respect to CPV, and (ii) dogs inoculated with CPV2 vaccine develop relatively low Nt antibody titers against the heterologous virus (CPV2b). These data may suggest an advantage for new vaccines, considering that most presently licensed vaccines are produced with CPV2, which no longer exists in the dog population.
Pathogens that can be transmitted between different host species are of fundamental interest and importance from public health, conservation and economic perspectives, yet systematic quantification of these pathogens is lacking. Here, pathogen characteristics, host range and risk factors determining disease emergence were analysed by constructing a database of disease-causing pathogens of humans and domestic mammals. The database consisted of 1415 pathogens causing disease in humans, 616 in livestock and 374 in domestic carnivores. Multihost pathogens were very prevalent among human pathogens (61.6%) and even more so among domestic mammal pathogens (livestock 77.3%, carnivores 90.0%). Pathogens able to infect human, domestic and wildlife hosts contained a similar proportion of disease-causing pathogens for all three host groups. One hundred and ninety-six pathogens were associated with emerging diseases, 175 in humans, 29 in livestock and 12 in domestic carnivores. Across all these groups, helminths and fungi were relatively unlikely to emerge whereas viruses, particularly RNA viruses, were highly likely to emerge. The ability of a pathogen to infect multiple hosts, particularly hosts in other taxonomic orders or wildlife, were also risk factors for emergence in human and livestock pathogens. There is clearly a need to understand the dynamics of infectious diseases in complex multihost communities in order to mitigate disease threats to public health, livestock economies and wildlife.
Canine parvovirus (CPV) is an emerging DNA virus that was first observed to cause disease in canines in 1978 and has since become a ubiquitous pathogen worldwide. CPV emerged from feline panleukopenia parvovirus (FPLV) or a closely related virus, differing at several key amino acid residues. Here we characterize the evolutionary processes underlying the emergence of CPV. Although FPLV has remained an endemic infection in its host populations, we show that, since the 1970s, the newly emerged CPV has undergone an epidemic-like pattern of logistic/exponential growth, effectively doubling its population size every few years. This rapid population growth was associated with a lineage of CPV that acquired a broader host range and greater infectivity. Recombination played no role in the emergence of CPV. Rather, any preexisting variation in the donor species and the subsequent rapid adaptation of the virus to canines were likely dependent on a high rate of mutation and the positive selection of mutations in the major capsid gene. Strikingly, although these single-stranded viruses have a DNA genome and use cellular replication machinery, their rate of nucleotide substitution is closer to that of RNA viruses than to that of double-stranded DNA viruses.
• adaptation
• emergence
• mutation rate
• phylogeny
• natural selection
Emerging pathogens potentially undergo rapid evolution while expanding in population size and geographic range during the course of invasion, yet it is generally difficult to demonstrate how these processes interact. Our analysis of a 30-yr data set covering a large-scale rabies virus outbreak among North American raccoons reveals the long lasting effect of the initial infection wave in determining how viral populations are genetically structured in space. We further find that coalescent-based estimates derived from the genetic data yielded an amazingly accurate reconstruction of the known spatial and demographic dynamics of the virus over time. Our study demonstrates the combined evolutionary and population dynamic processes characterizing the spread of pathogen after its introduction into a fully susceptible host population. Furthermore, the results provide important insights regarding the spatial scale of rabies persistence and validate the use of coalescent approaches for uncovering even relatively complex population histories. Such approaches will be of increasing relevance for understanding the epidemiology of emerging zoonotic diseases in a landscape context.
• invasion
• phylogeography
• Procyon lotor
• wildlife disease
• zoonoses
Canine parvovirus (CPV) type 2 (CPV-2) emerged around 1978 as a major pathogen of dogs worldwide. In the mid-1980s, the original CPV-2 had evolved and was completely replaced by 2 variants, CPV-2a and CPV-2b. In 2000, a new variant of CPV (named CPV-2c) was detected in Italy and now cocirculates with types 2a and 2b in that country. The CPV-2c has also been reported from single outbreaks in Vietnam and Spain. This study was conducted to determine if CPV-2c occurs in the United States. Thirty-three fecal samples were collected from dogs in 16 states between April 2006 and April 2007 and were tested for CPV using real-time polymerase chain reaction (PCR). Positive samples were further tested using conventional PCR and minor-groove binding TaqMan PCR assays to determine the viral type and to differentiate vaccine strains from field strains. Twenty-seven samples were positive for CPV, 7 of which were CPV-2c from 5 states: Arizona, California, Georgia, Oklahoma, and Texas. Of the 7 isolates, 4 differed from European CPV-2c isolates by 2 additional single-nucleotide mutations at positions 4076 and 4104, the latter of which produces a ThrAla change at residue 440 located near a major antigenic site. The coast-to-coast geographic distribution of the states in which CPV-2c was detected strongly suggests that this new CPV variant is probably widespread in the United States. The continuous evolution of CPV requires that monoclonal antibody-based and nucleic acid-based diagnostic assays should be periodically checked for sensitivity on prevalent CPV strains.
Infections with Trypanosoma spp. have been associated with poor health and decreased survival of koalas (Phascolarctos cinereus), particularly in the presence of concurrent pathogens such as Chlamydia and koala retrovirus. The present study describes the application of a next-generation sequencing (NGS)-based assay to characterise the prevalence and genetic diversity of trypanosome communities in koalas and two native species of ticks (Ixodes holocyclus and I. tasmani) removed from koala hosts. Among 168 koalas tested, 32.2% (95% CI: 25.2-39.8%) were positive for at least one Trypanosoma sp. Previously described Trypanosoma spp. from koalas were identified, including T. irwini (32.1%, 95% CI: 25.2-39.8%), T. gilletti (25%, 95% CI: 18.7-32.3%), T. copemani (27.4%, 95% CI: 20.8- 34.8%) and T. vegrandis (10.1%, 95% CI: 6.0-15.7%). Trypanosoma noyesi was detected for the first time in koalas, although at a low prevalence (0.6% 95% CI: 0-3.3%), and a novel species (Trypanosoma sp. AB-2017) was identified at a prevalence of 4.8% (95% CI: 2.1- 9.2%). Mixed infections with up to five species were present in 27.4% (95% CI: 21-35%) of the koalas, which was significantly higher than the prevalence of single infections 4.8% (95% CI: 2-9%). Overall, a considerably higher proportion (79.7%) of the Trypanosoma sequences isolated from koala blood samples were identified as T. irwini, suggesting this is the dominant species. Co-infections involving T. gilletti, T. irwini, T. copemani, T. vegrandis and Trypanosoma sp. AB-2017 were also detected in ticks, with T. gilletti and T. copemani being the dominant species within the invertebrate hosts. Direct Sanger sequencing of Trypanosoma 18S rRNA gene amplicons was also performed and results revealed that this method was only able to identify the genotypes with greater amount of reads (according to NGS) within koala samples, which highlights the advantages of NGS in detecting mixed infections. The present study provides new insights on the natural genetic diversity of Trypanosoma communities infecting koalas and constitutes a benchmark for future clinical and epidemiological studies required to quantify the contribution of trypanosome infections on koala survival rates. © 2017 Barbosa et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
The range of hosts a pathogen infects (host specificity) is a key element of disease risk that may be influenced by both shared phylogenetic history and shared ecological attributes of prospective hosts. Phylospecificity indices quantify host specificity in terms of host relatedness, but can fail to capture ecological attributes that increase susceptibility. For instance, similarity in habitat niche may expose phylogenetically unrelated host species to similar pathogen assemblages. Using a recently proposed method that integrates multiple distances, we develop a new index to assess the relative contributions of host phylogenetic and functional distances to pathogen host specificity (functional-phylogenetic host specificity). We apply this index to a dataset of avian malaria parasite (Plasmodium and Haemoproteus spp.) infections from Melanesian birds to show that multi-host parasites generally use hosts that are closely related, not hosts with similar habitat niches. We also show that host community phylogenetic ß diversity (Pßd) predicts parasite Pßd, and that individual host species carry phylogenetically clustered Haemoproteus parasite assemblages. Our findings were robust to phylogenetic uncertainty, and suggest that phylogenetic ancestry of both hosts and parasites play important roles in driving avian malaria host specificity and community assembly. However, restricting host specificity analyses to either recent or historical timescales identified notable exceptions, including a 'habitat specialist' parasite that infects a diversity of unrelated host species with similar habitat niches. This work highlights that integrating ecological and phylogenetic distances provides a powerful approach to better understand drivers of pathogen host specificity and community assembly. This article is protected by copyright. All rights reserved.
More than thirty years have passed since canine parvovirus (CPV) emerged as a significant pathogen and it continues to pose a severe threat to world canine populations. Published information suggests that flies (Diptera) may play a role in spreading this virus; however, they have not been studied extensively and the degree of their involvement is not known. This investigation was directed toward evaluating the vector capacity of such flies and determining their potential role in the transmission and ecology of CPV. Molecular diagnostic methods were used in this cross-sectional study to detect the presence of CPV in flies trapped at thirty-eight canine facilities. The flies involved were identified as belonging to the house fly (Mucidae), flesh fly (Sarcophagidae) and blow/bottle fly (Calliphoridae) families.
Detection and characterisation of the canine parvovirus (CPV-2) strains that are currently circulating are essential for the understanding of viral evolution and the development of measures to control its spread. In the present study, stool samples from 144 dogs were analysed by polymerase chain reaction (PCR) for CPV-2, and 29.2% (42/144) of them were positive. From the 42 positive strains, 71.4% (30) of the dogs had signs of haemorrhagic gastroenteritis. The sequencing of the 583 bp fragment of the VP2 gene from the positive strains identified 78.6% (33/42) of them as type 2c, 19% (8/42) as type 2b and 2.4% (1/42) as type 2a. A phylogenetic analysis of the variants circulating in the canine population of Brazil showed that they are very similar to those found in other countries and type 2c has become the predominant type circulating in Brazil.
Canine parvovirus type 2 (CPV-2), which causes acute hemorrhagic enteritis in dogs, is comprised of three antigenic variants (2a, 2b, and 2c) that are distributed worldwide with different frequencies. Variant prevalence was analyzed in 150 CPV-2-positive samples collected from the Uruguayan dog population in 2007-2010. Samples were analyzed with polymerase chain reaction, restriction fragment length polymorphism, and sequencing of the coding region for the largest and most variable loop of the VP2 capsid protein. CPV-2c was the only strain detected from 2007 to 2009. Uruguayan CPV-2c showed high homogeneity in both nucleotide and amino acid sequences, indicating a low level of genetic variability. In 2010, an unexpected epidemiological change occurred in Uruguay as a consequence of the appearance of a novel CPV-2a strain. This variant rapidly spread through the Uruguayan dog population and was detected in 20 of the 52 cases (38%) analyzed in 2010. CPV-2a sequences were identical in all field viruses analyzed, and in addition to the characteristic 426Asn residue, the sequences showed amino acid substitutions (267Tyr, 324Ile, and 440Ala) not observed in the Uruguayan CPV-2c. These data and the first detection in April 2010 suggest that the CPV-2a variant recently emerged in Uruguay and underwent clonal expansion. This observation is the first case in which a CPV-2a variant increased its frequency in a dog population where CPV-2c was prevalent. Our results emphasize the dynamic changes in CPV variants and highlight the importance of ongoing surveillance programs to provide a better understanding of virus epidemiology.
Canine parvovirus type 2 (CPV-2) emerged in late 1970s causing severe epizootics in kennels and dog shelters worldwide. Soon after its emergence, CPV-2 underwent genetic evolution giving rise consecutively to two antigenic variants, CPV-2a and CPV-2b that replaced progressively the original type. In 2000, a new antigenic variant, CPV-2c, was detected in Italy and rapidly spread to several countries. In comparison to the original type CPV-2, the antigenic variants display increased pathogenicity in dogs and extended host range, being able to infect and cause disease in cats. Epidemiological survey indicate that the newest type CPV-2c is becoming prevalent in different geographic regions and is often associated to severe disease in adult dogs and also in dogs that have completed the vaccination protocols. However, the primary cause of failure of CPV vaccination is interference by maternally derived immunity. Diagnosis of CPV infection by traditional methods has been shown to be poorly sensitive, especially in the late stages of infections. New diagnostic approaches based on molecular methods have been developed for sensitive detection of CPV in clinical samples and rapid characterisation of the viral type. Continuous surveillance will help assess whether there is a real need to update currently available vaccines and diagnostic tests.
The sequence of the full-length gene encoding for the main capsid protein VP2 of 58 canine parvovirus (CPV) type 2c strains, along with recent CPV-2a/2b strains, was determined and analysed in comparison with reference CPV isolates. The CPV-2c strains displayed a low genetic variability and shared amino acid changes already detected in recent CPV-2a/2b isolates, with a phylogenetic clustering accounting for their geographical distribution. Analysis of the selection pressure driving CPV evolution confirmed that the VP2 gene is under purifying selection. The emergence and global spread of the new CPV variant provides an interesting model to better understand virus evolution.
Fifty-five canine parvovirus type 2 (CPV) samples, 12 fecal specimens and 43 cell culture isolates, were examined for their genetic characteristics of VP2 gene. They were collected from the diseased dogs at various districts of Japan during 27 years from 1980 to 2006. A fragment of VP2 gene was analyzed by restriction fragment length polymorphism assay and DNA sequencing. The original antigenic type 2 of CPV (CPV-2) was no longer found in the samples since 1984, and two antigenic variants CPV-2a and CPV-2b replaced CPV-2 as predominant types for about 5 years from 1982. A new genetic variant of prototype CPV-2a with non-synonymous substitution at the VP2 amino acid residue 297 from Ser to Ala was first detected in 1987. New CPV-2b with the same amino acid substitution at position 297 as new CPV-2a was also detected from the samples collected in 1997. Since then new CPV-2b has been the predominant CPV over the field of Japan. Several additional amino acid substitutions were detected in the VP2 gene of some recent CPV strains. Neither CPV-2c(a), CPV-2c(b), nor "Glu-426" of the antigenic variants previously found outside the country was detected in any samples tested. Reactivity of new CPV-2a and 2b variants against antibodies produced by the current vaccine products was determined by a cross hemagglutination-inhibition test. The recent field CPV isolates reacted more efficiently to the antibodies produced in dogs vaccinated with the new CPV-2b vaccine strain than the conventional CPV-2 vaccine strain.
A schematic presentation of the organization of the genomes of parvo- and dependoviruses is given. For the densoviruses comparable data are not yet available.
To determine breed, sex, and seasonal predisposition for development of canine parvovirus (CPV) enteritis in dogs.
Retrospective case-control study.
Medical records from 283 dogs with confirmed CPV enteritis and from 834 age-matched control dogs that were healthy or had been admitted with nonenteric illness.
Effects of season, breed, sex, and neutering on the risk of developing CPV enteritis were examined by calculation of unadjusted odds ratios and performance of multivariate analysis. Stratified and contingency table analyses were performed to identify interactions and confounding among variables.
Rottweilers, American Pit Bull Terriers, Doberman Pinschers, and German Shepherd Dogs were at increased risk and Toy Poodles and Cocker Spaniels were at decreased risk for developing CPV enteritis, compared with that for mixed-breed dogs. For dogs more than 6 months old, sexually intact males were twice as likely as intact females to develop CPV enteritis. Dogs were 3 times more likely to be admitted with CPV enteritis in July, August, and September, compared with the rest of the year. Dogs were 12.7 times more likely to be admitted with CPV enteritis if they had not been currently vaccinated.
Lack of vaccination is a significant risk factor for development of CPV enteritis. Seasonal, sex, and breed predispositions for the development of CPV enteritis also exist.
The North American raccoon rabies epizootic continues to expand, now affecting most of New England. In 1990, raccoons became the vertebrate most often reported rabid in the United States. Emergence of this zoonosis poses increasing, but poorly defined risks to humans. This study analyzed various demographic, environmental, and behavioral factors associated with animal infection and human exposure before and during the epizootic in Connecticut. Rabies virus infections among terrestrial vertebrates were analyzed from 1985 through 1994. From March 1991, when the first case was diagnosed, through December 1994, 2,522 of 13,147 animals tested were found positive for rabies viral antigen. Forty-seven percent of the raccoons tested were infected, representing 88.0% of all animals found positive. Domestic animals constituted only 1.7% of positive test results, but 40.6% of the tests performed. The epizootic wave of transmission advanced approximately 30 km/year. Most rabies-positive wild animals were taken from private properties, usually near houses. Possible human exposures involved 939 people on 556 occasions through direct contact (20.7%) or indirectly through another animal (79.3%). Of 3,239 domestic animals exposed to rabies-positive wild animals, 18.4% lacked vaccination. Rabies has become enzootic in Connecticut and risk to humans and animals persists. The public health burden is considerable, yet knowledge is lacking to develop sustainable prevention strategies.
To determine the genetic variants of canine parvovirus-2 (CPV) present in domestic dogs in Australia and to investigate 26 cases of apparent vaccine failure.
Thirty-three samples of faeces or intestinal tissues and 16 cell culture virus isolates collected over a period from 1980 to 2005 from five Australian states were analysed. Procedure DNA was extracted from the samples and a 1975 bp fragment of the VP1/2 gene of CPV was amplified by polymerase chain reaction (PCR) and sequenced. Sequences were compared to published strains of CPV-2, CPV-2a, CPV-2b and CPV-2c.
Forty-one of 43 PCR-positive samples contained CPV-2a viruses. One sample collected in 2002 from a pup in northern NSW contained a CPV-2b virus. One sample that had been included in the study as a CPV-antigen negative control sample contained a CPV-2 virus.
CPV-2a remains the predominant genetic variant of CPV in dogs in Australia and has not been replaced by CPV-2b or CPV-2c as in many other countries. The vaccine failures investigated in the study were likely caused not by genetic variation of field viruses but by maternal antibody interference in the response of pups to vaccination.
BEAST: Bayesian evolutionary analysis by sampling trees
- A J Drummond
- A Rambaut
Drummond, A.J., Rambaut, A., 2007. BEAST: Bayesian evolutionary analysis by sampling
trees. BMC Evol. Biol. 7 DOI: 10.1186/1471-2148-1187-1214.
- N J Clark
N.J. Clark et al.
Infection, Genetics and Evolution 58 (2018) 50-55