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Update on Canine Parvovirus Infection: A Review from the Literature


Update on Canine Parvovirus Infection: A Review from the Literature

Md. Mukthar Mia1 and Mahamudul Hasan2*

1Department of Poultry Science, Faculty of Veterinary, Animal and Biomedical Sciences, Sylhet Agricultural University, Sylhet-3100; 2Faculty of Veterinary, Animal and Biomedical Sciences, Sylhet Agricultural University, Sylhet-3100.

Abstract | Canine parvovirus (CPV) enteritis is a highly contagious, virulent, acute, and fatal gastrointestinal viral disease that fundamentally transforms the pups and collapses the body’s posthaste branching organs, such as bone marrow, lymph node, and the flimsy cell of the intestine, causing bloody diarrhea amidst a high mortality and morbidity rate. CPV is distributed in the family Parvoviridae beneath the subfamily Parvovirinae that pertains to the genus Protoparvoviorus with a high genomic replacement unlike other DNA virus; the organism is primarily segmented into three forms acknowledged as (CPV-2a, CPV-2b, and CPV-2c), which resembles to be liable for the infection’s statewide spread. For transmission, the fecal-oral pathway is deemed the most obvious route than other permissible routes. Moreover, spreading through contact interactions, environmental pollutants, and the host reservoir, like a stray dog, could be feasible. Distressingly, such a pathogen is currently endemic in Asian nations, including India, Bangladesh, Sri Lanka and China. Thus, the literature review encompassed comprehensive knowledge concerning contemporary disease occurrence with causes and transmission imperative for management practice. Besides, the study converged on afresh advanced treatment procedures, vaccine progressions, and public awareness efforts, which can be a baseline for the policymaker, veterinarians and pet owner to limit further outbreaks.

Editor | Muhammad Abubakar, National Veterinary Laboratories, Park Road, Islamabad, Pakistan.

Received | December 07, 2020; Accepted | June 24, 2021; Published | July 08, 2021

*Correspondence | Mahamudul Hasan, Faculty of Veterinary, Animal and Biomedical Sciences, Sylhet Agricultural University, Sylhet-3100; Email:

Citation | Mia, M.M. and M. Hasan. 2021. Update on canine parvovirus infection: A review from the literature. Veterinary Sciences: Research and Reviews, 7(2): 92-100.


Keywords | Canine parvovirus, Epidemiology, Transmission, Vaccine, Prevention


Companion animals, such as dogs and cats, serve an important meaning in our communities. Therefore, people want to keep them for physiological, social, and emotional explanations (Robertson et al., 2000). Dissimilarly, new emerging disease like the Canine parvoviral (CPV) infection rapidly transmits among the dog populations of developing countries globally, although few studies have conducted regarding the prevalence of the listed virus from those regions. CPV is a DNA virus (small, non-enveloped with single-stranded genome) that belonged to the family Parvoviridae under the subfamily Parvovirinae and the genus Protoparvovirus, conferring to the recent cataloging. The genomic structure of the DNA molecule includes approximately 5,000 nucleotides with dual interpretation edges (ORFs), including ORF1 and ORF2, which encrypt two non-structural proteins (NS1, NS2). Rest two structural proteins identified as VP1 and VP2 encode and from another merging of the similar mRNAs (Decaro and Buonavoglia, 2012).

Throughout the first half of the 1980s, CPV-2 strain rapidly and entirely replaced into the novel CPV-2a; moreover, between 1991 and 2001, CPV-2b and CPV-2c verities were recognized in the dog population (Zhou et al., 2017). However, though the three alternatives are disseminated worldwide, the ancient CPV-2 variety no longer transmits nowadays (Decaro et al., 2020; Decaro and Buonavoglia, 2017). Considering the significant symptom, the common viral cause of bloody diarrhea spreads rapidly with high morbidity (near about 100%) and mortality rate (approximately 10%) (Schoeman et al., 2013; Shackelton et al., 2005). Analyzing the risk factors, including the age, resilient grade of the dogs, season, the quantity of virus, virulence, and pre-existing parasitic (bacterial or viral) infection, are the foremost clinical manifestation of CPV enteritis (McAdaragh et al., 1982). To be somewhat more specific, clinically, there are two forms of this disease, the enteric form characterized by acute fever, lethargy, anorexia, vomiting, and bloody diarrhea; whereas another type identified as a cardiac form that scarcely finds in neonates causing the failure of the respiratory and cardiovascular manifestations, with the infestation in utero (Schatzberg et al., 2003; Shima et al., 2015). In case of transmission, though the dogs can be infected by pathogens found on fomites, such as shoes, clothes, human fingers, food dishes, and other cookware, CPV can be spread predominantly by the fecal-oral route and from the contaminated of prone dogs (Bajehson, 2010).

Therefore, investigation to detect modes of transmission and make the dog owners more aware of preventive strategies is paramount to reduce its accelerated occurrence. This paper aims to focus on epidemiology, mode of transmission, pathogenesis, treatment, and vaccination to take any action before implementing somewhat control programs for curbing further outbreaks.

Epidemiology and risk factor

In 1978, CPV-2 became considered the cause of significant canine enteropathy and cardiomyopathy (Goddard and Leisewitz, 2010). The original CPV-2 strain has now been exposed worldwide and categorized into CPV-2a and CPV-2b antigenic forms. In Italy and different parts of the world, CPV-2c, a supplementary antigenic variant, was identified for the first time in 2000. Besides, CPV-2c has previously been isolated sporadically in the United Kingdom, Greece and Bulgaria, where there was a more conspicuous incidence of CPV-2a/ 2b appearance (Filipov et al., 2011). A preceding study informed that the oldest CPV-2c strain was discovered in 1996 (Decaro et al., 2007a), describing that perhaps the variant had been circulating in Germany for four years before its discovery in Italy in 2000 (Decaro and Buonavoglia, 2012). Besides, Tunisia has a tremendous occurrence for all three kinds outside Europe (Touihri et al., 2009). Additionally, in North America (Hong et al., 2007), type 2b and 2c isolates are more prevalent, whereas CPV-2c is more familiar in South America, excluding Brazil, where almost all propagating strains were classified as CPV-2a (Castro et al., 2011). In contrast, within Asia (Nandi et al., 2010) and Australia (Meers et al., 2007), CPV-2a is the most typical variety, with hardly a few CPV-2c strains detected in India (Nandi et al., 2010).

Throughout the last decade, CPV was reported from Pakistan, China, Nigeria, Tunisia, Egypt, Bangladesh and India, whereas the notable prevalence rate was inscribed from Egypt and Tunisia, respectively 59.75% and 32.2% (Table 1). Analyzing the risk factors, varied reasons like age, sex and breed are mainly susceptible to CPV-2 infection (Castro etal., 2007; Gombač et al., 2008). In Table 1, most of the evidence designates


Table 1: Prevalence with risk factors of CPV since 2010 to present.



Total preva-lence (%)

Prevalence (%)








<1 year

>1 year


















(Umar et al., 2015)













(Luo et al., 2017)













(Tion et al., 2018)













(Tagorti, 2018)













(Sayed-Ahmed et al., 2020)













(Roy et al., 2018)


Jabalpur (India)











(Khare, 2019)


that the proportion of CPV contamination is very eminent in male individuals rather than female; meanwhile, the puppies below one year aged and pure breed dogs are more receptive to the viral infection. Therefore, the study is in line with the previous study reported that young puppies are vulnerable to infection due to the biological half-life of the parvovirus maternal antibody (only around ten days), and this natural resistance emanates from the mother, rendering puppies more prone to infections (Roy et al., 2018). However, (Nandi and Kumar, 2010) proclaimed that CPV has also a devastating effect on pure breeds like Rottweilers, German Shepherd, English Springer Spaniels, and Doberman Pinchers.


CPV is a highly contagious disease that can transmit from the fecal waste of diseased individuals, whose severity can alter from slight to over 90% if the individuals do not get treatment or receive any faulty treatment (Kumrul et al., 2017). Going dipper, CPV is resistant to disinfectant with extremely stable power to stay in the environment for a long period (Khatri et al., 2017). The incubation period of this virus is 4-5 days (Bajehson, 2010). Excluding the fecal-oral route, the feces of dogs, pet shops, kennels, breeding equipment, and veterinary clinic can act as a secondary source of infection among the canine population (Bajehson, 2010; Behdenna et al., 2019; Nandi and Kumar, 2010). Likewise, dogs can also infect by fomites, including shoes, human hands, clothing, food bowls, and other utensils when they usually lick those items (Decaro et al., 2005). In addition, direct interaction or pollution of the atmosphere can also aid CPV transmission (Bagshaw et al., 2014; Behdenna et al., 2019).

Moreover, street dogs can act as a reservoir and perform a crucial role for operating the life cycle of the pathogen (Islam et al., 2014). A recent study held in Australia also reported that feral dogs in a particular area could be responsible for the growing infection rate of the pet dogs in those areas, but further investigation is important for evaluating the transmission (Kelman et al., 2020). In the case of cross-transmission, (Behdenna et al., 2019) stated that dogs serve as a vector of infection for lions in unidirectional cross-species transmission, and lions do not maintain CPV infection independently of dogs. Despite the unusual direct contact of domestic dogs and lions, several other carnivorous animals could serve as intermediate hosts (Craft et al., 2017).

However, recent studies indicated that thermal persistence and enhanced potential exposure of CPV pathogen could be responsible for the extended drought periods. Moreover, a strong correlation between CPV frequency and rainfall distribution periods has been indicated (Clark et al., 2018; Decaro et al., 2020; Rika-Heke et al., 2015). Furthermore, the parasitic and other particular causes can also predispose puppies to parvoviral infection, including premature weaning, overcapacity, starvation, and additional anxiety factors (Gamage et al., 2020; Mylonakis et al., 2016). Thus, comprehending the exact cause of a disease is essential to its prevention.


The virus comes in contact when the dog cleans its own body or eats food off the ground or floor through the mouth. Following entered the virus into a dog, it takes (3-7) days development to show signs and symptoms. Then, it replicates an immense number within the lymph node (Khatri et al., 2017; Nandi and Kumar, 2010). A few days later, significant masses of viruses in the bloodstream are discharged, and the pathogen invades 3-4 days later in bone marrow (fast dividing cell). Then the virus delicates the intestinal cells and formed broad inclusion bodies (eosinophilic intranuclear) by multiplying viruses. After that, privileged the bone marrow, the pathogen abolishes the new cells of the defense system. Alongside, it commences to knock out the best defensive mechanism of the body. Afterward, the pathogen causes the vastest shocking consequences in the gastrointestinal tract, and due to inflammation of the bone marrow, CPV infection is signalized by a reduction in white blood cells. The typical intestine has small finger-like protuberances called villi. These tiny fingers are immensely strengthened in the surface areas that make it difficult to access liquid and nutrient absorption in the gastrointestinal tract. The villi are compact transitory cells that are readily replaced by the new cells. The rapidly dividing portion at the base of the villi known as the Crypts of Lieberkühn acts as a source of the new cells that provide the actual number of cells in the villi (Nandi and Kumar, 2010). The parvovirus raided the crypt and remodeled the villi into blunted shape, and makes it unable to engross nutrients; thus, diarrhea results due to a reduction of new cells from the crypt and addresses the easy entry of bacteria causing widespread infection. The etiology of recurrent enteropathies in dogs is associated with Enterobacteriaceae (Proteobacteria phylum) (Cassmann et al., 2016; Park et al., 2019); belatedly, extreme fluid loss leads to bloody diarrhea and vomiting until shock and death (Nandi and Kumar, 2010).


For fluid therapy, after accessing the vascular balance, a crystalloid isotonic solution should be administrated, and the initial fluid application volume delimits the degree of interstitial dehydration, whether the hypovolemia present. For the consequence of hypothermia, tachycardia, bradycardia, hypotension, and overdue capillary refill time, it is more gratifying to give intravenous (IV) solution as promptly as practicable in boluses (20 ml/kg) (Decaro et al., 2007b). Besides, serum glucose concentration needs to be monitored regularly and supplemented as necessary for hypoglycemia. Furthermore, for decreasing the serum glucose level (below 60 mg/dL tailed by the adding of 2.5% to 5% dextrose solution in crystalloid fluids), it is mandatory to the administration of IV dextrose solution (Vet One Dextrose 50%) besides bolus (1-2 ml/kg 25% dextrose) (Mazzaferro, 2020).

In patients with CPV, use of antiemetics is vital to use antiemetic drugs for lessening vomiting. Administration of anthelmintic in pups with CPV enteritis showed lessened clinic stay time in patients who have endured antiemetics (Mantione and Otto, 2005). Coequally active in minimizing the number of vomiting incidents in another study was also antiemetics, mainly metoclopramide (0.5 mg/kg IV every 8 hours). Moreover, administration of ondansetron (0.5 mg/kg) through IV route after every 8 hours and maropitant (1 mg/kg) subcutaneously after every 24 hours are also recommended (Mazzaferro, 2020; Yalcin and Keser, 2017).

For antibiotic treatment, administration of Ampicillin (20-40) mg/kg, Ampicillin-sulbactam (30–50) mg/kg, Cefovecin 8 mg/kg, Cefoxitin from cephalosporin group (20–30) mg/kg body weight, Enrofloxacin 10 mg/kg body weight, and Metronidazole 10 mg/kg via IV route except for Cefovecin (subcutaneous) is highly effective (Mazzaferro, 2020). Moreover, in analgesia, vomiting and potential with ileus intussusception may cause abdominal pain in many patients with CPV infection (Mylonakis et al., 2016). Partial inhibitors like as buprenorphine (0.01-0.02 mg/kg IV every 8 hours) or else butorphanol (0.1-0.2 mg/kg/hour) can be suggested to genuine agonists, including methadone (0.1-0.2 mg/kg IV every 6 hours), hydromorphone (0.1 mg/kg intravenous, intramuscular every 8 hours) morphine (0.1-0.2 mg/kg, intravenous, intramuscular, or subcutaneous every 8 hours), or fentanyl (1-5 mg/kg/hour IV) (Marquez et al., 2015; Mazzaferro, 2020). Furthermore, the current findings examining the rectal application to puppies with CPV enteritis of 10 g of fecal content from the recovered dog, diluted in 10 ml of sterile 0.9% saline, demonstrated the earlier onset of diarrheal resolution increased survival in the fecal transplant community (Pereira et al., 2018). Finally, to lessen the fever, diarrhea, vomiting, and mortality and increases appetite, transgenic feline omega-interferon (1–5 106 IU/kg/d IV for three days) can be provided (De Mari et al., 2003; Mazzaferro, 2020).


Canine parvovirus enteritis disease is extremely virulent and contagious; prevention is imperative to assure the good health of the puppy and dog. The virus is remarkably hardy and can live in feces and soil (organic material) for more than one year (Bajehson, 2010). Besides, CPV is versatile, environmentally stable, and can survive in favorable conditions for many months (Bajehson, 2010; Decaro et al., 2020). Thus, for indoor decontamination, about one month, the pathogen loses its virulence; it should perhaps be safe to insert a new puppy indoors, one month after the conclusion of the active infection. On the contemporary, if the exterior is poisoned and cold, one should perpetually wait to heat it before a regulated manner adopting a newborn pup. Shaded areas for seven months and zones with adequate daylight should be known as polluted (Houston et al., 1996; Nandi and Kumar, 2010). Though CPV can resist broadly used disinfectants, likely quaternary ammonium compounds), a sodium hypochlorite solution (0.75%) verified respectable effectiveness against the pathogen (Cavalli et al., 2018; Decaro et al., 2020).

Additionally, mechanical refinement through irrigation after drying the permissible area may also be supportive. Spreading peroxymonosulfate (organic matter) has relatively good action on filthy areas (Nandi and Kumar, 2010). Segregating an at-risk puppy is the best way to avoid infection from CPV exposure. Vaccinated adults’ dog (with normal feces) can spread the CPV pathogen via the possible path of contamination. So, to minimize contamination, the risk puppy should not expose till the puppy has acquired its complete spectrum of vaccines. Barrier methods, including protective gloves, hat, gown, and booties, must be worn in the diarrheic patient, including the negative response of fecal ELISA test, once treating the patient to prevent cross-contamination as well as the advancement of the disease (Mazzaferro, 2020).

Vaccine development

Though the control of canine parvovirus is a global challenge, the most important criterion for minimizing the transmission of infection in dogs is vaccination (Decaro et al., 2020). For all dogs, irrespective of situations or geographic region, a core vaccination is important because the vaccine can protect the animals from dangerous and serious diseases (Day et al., 2016). Though the vaccination program is increasing, the CPV infection among licensed and confined dogs was 4.12 times among one thousand dogs, according to the latest study of veterinary hospitals in Australia (Kelman et al., 2019). In the circumstance of the vaccine category, modified live vaccine (MLV), frequently uses because, by duplicating inside the host, it can induce a durable, lifelong response without causing any tissue harm or clinical signs. Currently, only two CPV forms, the inventive CPV-2 stain, besides its additional variant CPV-2b comprise the CPV MLV vaccine formulations in most countries. However, the MLV can be synthesized in the intestinal mucosa and can be shed (feces of immunized dogs) for at least 3-4 weeks after vaccination (Freisl et al., 2017; Zhou et al., 2017). This vaccine is also responsible for causing viremia (Decaro et al., 2020; Freisl et al., 2017). However, for heightening equally antibody and cell-mediated immune responses, Modified Live Virus (MLV) vaccines are used to protect CPV.

Moreover, it offers decent, lifelong coverage against subsequent obstacles of virulent viruses (Ford et al., 2017). On the other hand, the “World Small Animal Veterinary Association” Vaccination Community is not strongly suggesting CPV MLV vaccines for wild animals. Also, it is restricted in pups (age less than 4-6 weeks) and at the time of pregnancy because of the potentially harmful impact of vaccines (Day et al., 2016; Decaro et al., 2020).

To better overcome MDA intervention, it is now suggesting trial and marketable vaccines for oral and intranasal administration, but all commercially viable CPV vaccines offer parenteral route administration (Cavalli et al., 2020). Failures in immunization may be vaccinated or host-related, and inappropriate vaccine schedules, vaccine processing or implementation defects, and the defects of vaccine immunogenicity are causes of vaccine-related failures (Altman et al., 2017; Decaro et al., 2020). On the other hand, age, hereditary factors, and compromised fitness, diet, or immune status are correlated with host-related factors (Wiedermann et al., 2016).

Serological testing may be a valuable tool for evaluating the feasibility of vaccination in rising kennels to explore diseased animals and determine the letdown influences to vaccinate (Rota et al., 2019). In most studies, CPV seroprevalence already published within the last twenty years, ranging from 86% to 98.5% in typically vaccinated owned dogs (Killey et al., 2018; Riedl et al., 2015; Rota et al., 2019). On the other hand, unvaccinated homeless dogs showed a seroprevalences rate of 67% to 84% (Spindel et al., 2018). 70-75% vaccination coverage recommended for the lowest possible in owned dog population groups to avoid disease outbreaks (Decaro et al., 2020; Riedl et al., 2015).

Vaccination protocol

Protocols for CPV vaccination are a customized action with various variables, including age, breed, dog’s way of living, and the occurrence of diseases in a specific geographic area. Therefore, some general guidelines for the canine core vaccinations that include MLV CPV and Canine Distemper are recommended to use, but no standard vaccination policy can cover all possible circumstances (Decaro et al., 2020). The minimum age for beginning the primary CPV vaccinated protocol is 6-8 weeks. Then a revaccination period of (2-4) weeks protocol is recommended until the age of 16 weeks or even later after vaccination. Dogs must undergo a booster as a pup within one year of the primary vaccine course (Decaro et al., 2020; Ford et al., 2017).

Economic impact

People from poor and under developing countries are not highly familiar with pure breed pet dog rearing. The price of a puppy is very high, though a few people are starting to make dog farms for business purposes. As the canine parvovirus is a contagious disease, the contaminated dog can easily spread the virus in the environment. If the outbreak of the disease rises bit by bit, individuals do not express interest in chasing the puppy. Then, not only for those who engage with the pet dog selling trade but also for the economy created for this business, detrimental factors can arise. Besides, the cost of animal diseases will increase the expenditure on treatment, which typically increases expenses. To sum up, animal disease output depends on the expenses regarding the animal disease, deaths, decreased productivity, and declines in commerce and other receipts (Rushton, 2008).


The authors are thankful to the all members of Department of Medicine, Sylhet Agricultural University, for providing guidelines.

Novelty Statement

Previously, many studies reported scattered top to bottom information about CPV. However, our study reviewed the history of the most contagious CPV disease’s contemporary prevalence with risk factors, the adversarial impact on dogs, newly ascertained dynamic transmission with treatment procedures, and significant economic repercussions. Furthermore, our study affirmed that the CPV is fast progressing in impoverished and developing countries due to a lack of awareness.

Author’s Contribution

MH: Conceptualization, writing original draft preparation and writing, reviewing and editing.

MMM: Supervision, writing, reviewing and editing.

Conflict of interest

The authors have declared no conflict of interest.


Altman, K.D., Kelman, M. and Ward, M.P., 2017. Are vaccine strain, type or administration protocol risk factors for canine parvovirus vaccine failure? Vet. Microbiol., 210: 8–16.

Bagshaw, C., Isdell, A.E., Thiruvaiyaru, D.S., Brisbin, I.L. and Sanchez, S., 2014. Molecular detection of canine parvovirus in flies (Diptera) at open and closed canine facilities in the eastern United States. Prev. Vet. Med., 111(3–4): 276–284.

Bajehson, D.B., 2010. molecular characterization of canine parvovirus strains from domestic dogs in South Africa and Nigeria. PhD thesis, University of Pretoria, South Africa.

Behdenna, A., Lembo, T., Calatayud, O., Cleaveland, S., Halliday, J.E.B., Packer, C., Lankester, F., Hampson, K., Craft, M.E., Czupryna, A., Dobson, A.P., Dubovi, E.J., Ernest, E., Fyumagwa, R., Hopcraft, J.G.C., Mentzel, C. and Viana, M., 2019. Transmission ecology of canine parvovirus in a multi-host, multi-pathogen system. Proc. Biol. Sci., 286(1899): 20182772.

Cassmann, E., White, R., Atherly, T., Wang, C., Sun, Y., Khoda, S., Mosher, C., Ackermann, M. and Jergens, A., 2016. Alterations of the ileal and colonic mucosal microbiota in canine chronic enteropathies. PLoS One, 11(2): 1–18.

Castro, T.X., Costa, E.M., Leite, J.P., Labarthe, N.V. and Garcia, R.C.N.C., 2011. Monitoring of canine parvovirus (CPV) strains detected in vaccinated puppies in Brazil. Res. Vet. Sci., 90(2): 336–340.

Castro, T.X., Miranda, S.C., Labarthe, N.V., Silva, L.E. and Cubel, G.R.C.N., 2007. Clinical and epidemiological aspects of canine parvovirus (CPV) enteritis in the State of Rio de Janeiro: 1995-2004. Arquivo Brasileiro Med. Vet. Zoot., 59(2): 333-339.

Cavalli, A., Desario, C., Marinaro, M., Losurdo, M., Camero, M., Decaro, N., Catella, C., Lanave, G. and Buonavoglia, C., 2020. Oral administration of modified live canine parvovirus type 2b induces systemic immune response. Vaccine, 38(2): 115–118.

Cavalli, A., Marinaro, M., Desario, C., Corrente, M., Camero, M. and Buonavoglia, C., 2018. In vitro virucidal activity of sodium hypochlorite against canine parvovirus type 2. Epidemiol. Infect., 146(15): 2010–2013.

Clark, N.J., Seddon, J.M., Kyaw-Tanner, M., Al-Alawneh, J., Harper, G., McDonagh, P. and Meers, J., 2018. Emergence of canine parvovirus subtype 2b (CPV-2b) infections in Australian dogs. Infect. Genet. Evol., 58(2018): 50–55.

Craft, M.E., Vial, F., Miguel, E., Cleaveland, S., Ferdinands, A. and Packer, C., 2017. Interactions between domestic and wild carnivores around the greater Serengeti ecosystem. Anim. Conserv., 20(2): 193–204.

Day, M.J., Horzinek, M.C., Schultz, R.D. and Squires, R.A., 2016. WSAVA guidelines for the vaccination of dogs and cats. J. Small Anim. Pract., 57(1): 1–45.

De Mari, K., Maynard, L., Eun, H.M. and Lebreux, B., 2003. Treatment of canine parvoviral enteritis with interferon-omega in a placebo-controlled field trial. Vet. Rec., 152(4): 105–108.

Decaro, N., Buonavoglia, C. and Barrs, V.R., 2020. Canine parvovirus vaccination and immunisation failures: are we far from disease eradication? Vet. Microbiol., 247: 108760.

Decaro, Nicola and Buonavoglia, C., 2012. Canine parvovirus-a review of epidemiological and diagnostic aspects, with emphasis on type 2c. Vet. Microbiol., 155(1): 1–12.

Decaro, Nicola and Buonavoglia, C., 2017. Canine parvovirus post-vaccination shedding: Interference with diagnostic assays and correlation with host immune status. Vet. J., 221(2017): 23.

Decaro, Nicola, Desario, C., Addie, D.D., Martella, V., Vieira, M.J., Elia, G., Zicola, A. and Davis, C., 2007. Thompson, G., Thiry, E., others. Molecular epidemiology of canine parvovirus, Europe. Emerg. Infect. Dis., 13(8): 1222.

Decaro, Nicola, Desario, C., Campolo, M., Elia, G., Martella, V., Ricci, D., Lorusso, E. and Buonavoglia, C., 2005. Clinical and virological findings in pups naturally infected by canine parvovirus type 2 Glu-426 mutant. J. Vet. Diagn. Invest., 17(2): 133–138.

Decaro, Nicola, Desario, C., Elia, G., Campolo, M., Lorusso, A., Mari, V., Martella, V. and Buonavoglia, C., 2007. Occurrence of severe gastroenteritis in pups after canine parvovirus vaccine administration: A clinical and laboratory diagnostic dilemma. Vaccine, 25(7): 1161–1166.

Filipov, C., Decaro, N., Desario, C., Amorisco, F., Sciarretta, R. and Buonavoglia, C., 2011. Canine parvovirus epidemiology in Bulgaria. J. Vet. Diagn. Invest., 23(1): 152–154.

Ford, R.B., Larson, L.J., McClure, K.D., Schultz, R.D. and Welborn, L.V., 2017. Canine Vaccination Guidelines. J. Am. Anim. Hosp. Assoc., 53(5): 243–251.

Freisl, M., Speck, S., Truyen, U., Reese, S., Proksch, A.L. and Hartmann, K., 2017. Faecal shedding of canine parvovirus after modified-live vaccination in healthy adult dogs. Vet. J., 219: 15–21.

Gamage, B.G.S.S., Dissanayake, D.R.A., Prasada, D.V.P. and Silva, I.D., 2020. Risk, prognosis and causality of parvo viral enteritis in. dogs in Sri Lanka. Comp. Immunol. Microbiol. Infect. Dis., 72(February): 101496.

Goddard, A. and Leisewitz, A.L., 2010. Canine parvovirus. Vet. Clin. N. Am. Small Anim. Pract., 40(6): 1041–1053.

Gombač, M., Švara, T., Tadić, M. and Pogačnik, M., 2008. Retrospective study of canine parvovirosis in Slovenia. Slovenian Vet. Res., 45(2): 73–78.

Hong, C., Decaro, N., Desario, C., Tanner, P., Pardo, M.C., Sanchez, S., Buonavoglia, C. and Saliki, J.T., 2007. Occurrence of canine parvovirus type 2c in the United States. J. Vet. Diagn. Invest., 19(5): 535–539.

Houston, D.M., Ribble, C.S. and Head, L.L., 1996. Risk factors associated with parvovirus enteritis in dogs: 283 cases (1982-1991). J. Am. Vet. Med. Assoc., 208(4): 542–546.

Islam, M.R., Islam, M.A., Rahman, M.S., Uddin, M.J., Sarker, M.A.S., Akter, L. and Alam, E., 2014. Prevalence of canine parvovirus infection in street dogs in Mymensingh municipality area, Bangladesh. Microb. Health, 3(1): 5–6.

Kelman, M., Harriott, L., Carrai, M., Kwan, E., Ward, M.P. and Barrs, V.R., 2020. Phylogenetic and geospatial evidence of canine parvovirus transmission betweenwild dogs and domestic dogs at the urban fringe in Australia. Viruses, 12(6): 1–13.

Kelman, M., Ward, M.P., Barrs, V.R. and Norris, J.M., 2019. The geographic distribution and financial impact of canine parvovirus in Australia. Transbound. Emerg. Dis., 66(1): 299–311.

Khare, R., 2019. Prevalence of canine parvovirus infection in dogs in Jabalpur (M.P.), 7(June): 1495–1498.

Khatri, R., Poonam, Mohan, H. and Minakshi, C.S.P., 2017. Epidemiology, pathogenesis, diagnosis and treatment of canine parvovirus disease in dogs: A mini review abstract. J. Vet. Sci. Med. Diagn., 6(3): 2.

Killey, R., Mynors, C., Pearce, R., Nell, A., Prentis, A. and Day, M.J., 2018. Long-lived immunity to canine core vaccine antigens in UK dogs as assessed by an in-practice test kit. J. Small Anim. Pract., 59(1): 27–31.

Kumrul, H.M., Nahat, F.W., Bhattacharjee, P.K., Rahman, M.S., Anisur, R.A.K.M., Islam, M.A., Akter, M. and Chae, J.S., 2017. Prevalence of canine influenza infection in pet dogs and canine parvovirus infection in street dogs of bangladesh. J. Vet. Clin., 34(3): 165–171.

Luo, H., Li, K. and Zhang, H., 2017. Epidemiology of Canine distemper and Canine parvovirus in pet dogs in Wenzhou, China. Indian J. Anim. Res., 51(1): 159–161.

Marquez, M., Boscan, P., Weir, H., Vogel, P. and Twedt, D.C., 2015. Comparison of nk-1 receptor antagonist (maropitant) to morphine as a pre-anaesthetic agent for canine ovariohysterectomy. PLoS One, 10(10): 1–10.

Mazzaferro, E.M., 2020. Update on canine parvoviral enteritis. Vet. Clin. N. Am. Small Anim. Pract., 50(6): 1307–1325.

McAdaragh, J.P., Eustis, S.L., Nelson, D.T., Stotz, I. and Kenefick, K., 1982. Experimental infection of conventional dogs with canine parvovirus. Am. J. Vet. Res., 43(4): 693–696.

Meers, J., Kyaw-Tanner, M., Bensink, Z. and Zwijnenberg, R., 2007. Genetic analysis of canine parvovirus from dogs in Australia. Austral. Vet. J., 85(10): 392–396.

Mylonakis, M., Kalli, I. and Rallis, T., 2016. Canine parvoviral enteritis: an update on the clinical diagnosis, treatment, and prevention. Vet. Med. Res. Rep., 7: 91–100.

Mantione, N.L. and Otto, C.M., 2005. Characterization of the use of antiemetic agents in dogs with parvoviral enteritis treated at a veterinary teaching hospital: 77 Cases (1997-2000). J. Am. Vet. Med. Assoc., 227(11): 1787–1793.

Nandi, S. and Kumar, M., 2010. Canine parvovirus: Current perspective. Indian J. Virol., 21(1): 31–44.

Nandi, S., Chidri, S., Kumar, M. and Chauhan, R.S., 2010. Occurrence of canine parvovirus type 2c in the dogs with haemorrhagic enteritis in India. Res. Vet. Sci., 88(1): 169–171.

Park, J.S., Guevarra, R.B., Kim, B.R., Lee, J.H., Lee, S.H., Cho, J.H., Kim, H., Cho, J.H., Song, M., Lee, J.H., Isaacson, R.E., Song, K.H. and Kim, H.B., 2019. Intestinal microbial dysbiosis in beagles naturally infected with canine parvovirus. J. Microbiol. Biotechnol., 29(9): 1391–1400.

Pereira, G.Q., Gomes, L.A., Santos, I.S., Alfieri, A.F. and Costa, J.S.W.M.C., 2018. Fecal microbiota transplantation in puppies with canine parvovirus infection. J. Vet. Int. Med., 32(2): 707–711.

Riedl, M., Truyen, U., Reese, S. and Hartmann, K., 2015. Prevalence of antibodies to canine parvovirus and reaction to vaccination in client-owned, healthy dogs. Vet. Rec., pp. 1–8.

Rika-Heke, T., Kelman, M. and Ward, M.P., 2015. The relationship between the Southern Oscillation Index, rainfall and the occurrence of canine tick paralysis, feline tick paralysis and canine parvovirus in Australia. Vet. J., 205(1): 87–92.

Robertson, I.D., Irwin, P.J., Lymbery, A.J. and Thompson, R.C.A., 2000. The role of companion animals in the emergence of parasitic zoonoses. Int. J. Parasitol., 30(12–13): 1369–1377.

Rota, A., Dogliero, A., Muratore, E., Pregel, P., Del Carro, A. and Masoero, L., 2019. Serological survey of canine parvovirus 2 antibody titres in breeding kennels in northern Italy. BMC Vet. Res., 15(1): 1–5.

Roy, S., Ahmed, S.U., Alam, S., Chowdhury, Q.M.M.K., Rahman, M.S., Popy, F.Y., Sharma, B., Basit, M.S.I. and Ahmed, J., 2018. Prevalence of canine parvoviral enteritis in pet dogs at Dhaka city of Bangladesh. Int. J. Biol. Res., 6(1): 14–17.

Rushton, J., 2008. The economics of animal health and production. CABI, UK.

Sayed-Ahmed, M.Z., Elbaz, E., Younis, E. and Khodier, M., 2020. Canine parvovirus infection in dogs: Prevalence and associated risk factors in Egypt. World’s Vet. J., 10(4): 571–577.

Schatzberg, S.J., Haley, N.J., Barr, S.C., Parrish, C., Steingold, S., Summers, B.A., DeLahunta, A., Kornegay, J. N. and Sharp, N.J.H., 2003. Polymerase Chain Reaction (PCR) amplification of parvoviral DNA from the brains of dogs and cats with cerebellar hypoplasia. J. Vet. Int. Med., 17(4): 538–544.

Schoeman, J.P., Goddard, A. and Leisewitz, A.L., 2013. Biomarkers in canine parvovirus enteritis. N. Z. Vet. J., 61(4): 217-222.

Shackelton, L.A., Parrish, C.R., Truyen, U. and Holmes, E.C., 2005. High rate of viral evolution associated with the emergence of carnivore parvovirus. Proc. Natl. Acad. Sci. U.S.A., 102(2): 379–384.

Shima, F.K., Apaa, T.T. and Mosugu, J.I.T., 2015. Epidemiology of canine parvovirus enteritis among hospitalized dogs in effurun/Warri metropolitan region of Delta State, Nigeria. OALib, 2(1): 1–7.

Spindel, M.E., Krecic, M.R. and Slater, M.R. and Vigil, N., 2018. Evaluation of a community’s risk for canine parvovirus and distemper using antibody testing and GIS mapping of animal shelter intakes. J. Appl. Anim. Welfare Sci., 21(4): 362-374.

Tagorti, G., 2018. Prevalence of canine parvovirus infection in Grand Tunis, Tunisia. J. Adv. Vet. Anim. Res., 5(1): 93–97.

Tion, M.T., Apaa, T.T., Saganuwan, A.S., Nwankwo, H.C., Tughgba, T., Anumtyo, T.M., Amine, A.A., Nguetyo, S.A. and Igoh, A.-I., 2018. The epidemiology of canine parvovirus enteritis in dogs of makurdi. J. Homepage World Vet. J., 8(3): 48–54.

Touihri, L., Bouzid, I., Daoud, R., Desario, C., El-Goulli, A.F., Decaro, N., Ghorbel, A., Buonavoglia, C. and Bahloul, C., 2009. Molecular characterization of canine parvovirus-2 variants circulating in Tunisia. Virus Genes, 38(2): 249–258.

Umar, S., Ali, A., Younus, M., Maan, M.K., Ali, S., Khan, W.A. and Irfan, M., 2015. Prevalence of canine parvovirus infection at different pet clinics in Lahore, Pakistan. Pak. J. Zool., 47(3): 657–663.

Wiedermann, U., Garner-Spitzer, E. and Wagner, A., 2016. Primary vaccine failure to routine vaccines: Why and what to do? Hum. Vaccines Immunother., 12(1): 239–243.

Yalcin, E. and Keser, G.O., 2017. Comparative efficacy of metoclopramide, ondansetron and maropitant in preventing parvoviral enteritis-induced emesis in dogs. J. Vet. Pharmacol. Therapeut., 40(6): 599–603.

Zhou, P., Zeng, W., Zhang, X. and Li, S., 2017. The genetic evolution of canine parvovirus. A new perspective. PLoS One, 12(3): 1–13.

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