1/12 JSM Veterinary Med Res 2: 12 JSM Veterinary Medicine and Research Submitted: 05 July 2019 | Accepted: 25 August 2019 | Published: 27 August 2019 *Corresponding author: UK De, Division of Veterinary Medicine, Centre for Animal Disease Research and Diagnosis, Indian Veterinary Research Institute, Izatnagar, India, E-mail: sukdebnandi@yahoo.in Copyright: © 2019 Nandi S, 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. Citation: Nandi S, Sharma GK, Gupta V, Deol P, Chander V, et al. (2019) Global Scenario of Canine Parvovirus Mutants: Epidemiology, Diagnostics and Immunoprophylactic Agents. JSM Vet Med Res 2: 12. Global Scenario of Canine Parvovirus Mutants: Epidemiology, Diagnostics and Immunoprophylactic Agents S. Nandi, GK Sharma, Vikas Gupta, Pallavi Deol, Vishal Chander, UK De* and VK Gupta Division of Veterinary Medicine, Centre for Animal Disease Research and Diagnosis, Indian Veterinary Research Institute, Izatnagar, India Abstract Canine parvovirus 2 (CPV-2) is one of the most important enteropathogen of dogs emerged in 1978 and manifested by two forms namely gastroenteritis and myocarditis. It is characterized by depression, loss of appetite, vomiting and leukopenia. CPV-2 is probably evolved from a very closely related virus in cats, feline panleukopenia virus (FPLV) or a closely related carnivore parvovirus. It caused high morbidity of 100% and low mortality of 10% in adult dogs and 91% in pups. Over the years a number of variants namely CPV-2a, CPV-2b, CPV-2c, New CPV-2a, New CPV-2b and Asp300 (2a/2b) have been reported from different countries in the world with varying degree of pathogenic potential. Although CPV-2 differ from FPV by 6 amino acids in the VP2 protein, subsequent variants differ from CPV-2 only in one or two places. Further, CPV-2 affects only dogs, new variants expanded their host range to cat as well. There are a number of different serological and molecular tests (PCR, nested PCR, SYBR Green based real time PCR, Taqman based real time PCR, Minor grove binding assay based PCR) available for prompt, specifc and accurate diagnosis of the disease. Some molecular tests not only detect the CPV-2 but also identify the variant of CPV-2 involved in disease outbreak. Further, both live attenuated and inactivated vaccines are available to control the disease in animals. Besides, new generation vaccines namely recombinant vaccine, peptide vaccine and DNA vaccine have been developed for control of the disease in canines effectively and effciently. However, new generation vaccines have not been issued license to be used in the feld condition. Again, the presence of maternal antibodies often interferes with the active immunization with live attenuated vaccine and there always exists a window of susceptibility in spite of following proper immunization regimen. Lastly, judicious use of the vaccines in pet dogs, stray dogs and wild canids keeping in mind the new variants of the CPV-2 along with the proper sanitation and disinfection practices must be implemented for the successful control the disease. Keywords: Canine parvovirus-2 (CPV-2); CPV-2a; CPV-2b; CPV-2c; New CPV-2a; New CPV-2b; Asp300 (2a/2b); Hemorrhagic enteritis; Myocarditis; Canine; Vaccination; Feline panleukopenia virus (FPV); Raccoon parvovirus (RPV); Mine enteritis virus (MEV); Blue fox parvovirus (BFPV) Introduction CPV-2 is the most important enteric virus affecting domestic and wild carnivores around the world [1]. In the late 1970s from feline panleukopenia virus or related carnivore parvovirus was found to be ancestor of the CPV-2 [2]. There are two forms of the disease : enteritis in dogs of all ages and myocarditis in pups of 6 weeks to 6 months old with 100% morbidity and mortality of 10% in adult dogs and 91% in pups. The virus is very sturdy and usually transmitted by faecal oral route. The virus has be propensity to replicate in the rapidly dividing cells such as lymphoid tissues, intestinal epithelium and bone marrow as well as myocardium in neonatal pups. Vomiting, haemorrhagic diarrhoea, depression, loss of appetite, fever, dehydration are the prominent signs of the disease but myocarditis is seen mainly neonatal pups. Due to infection of bone marrow and lymphoid tissue there is sharp drop of WBC count. Although a galaxy of immunoprophylactic agents are available to prevent the CPV- 2 infections in dogs, lot of outbreaks are still reported in many countries around the world due to presence of unvaccinated dogs, interference of active immunization by maternally derived antibodies and emergence of a number of different mutants over the years. Because of sudden and wide spread outbreaks of severe contagious enteritis in dogs, canine parvovirus (CPV) has become an issue of great concern to veterinarians. The review article is aimed to give an idea about the latest development in the field of newly emergent variants, diagnostics and immunoprophylactics to the scientific fraternities. Etiology The CPV-2 together with FPV, MEV, RPV is under the genus Protoparvovirus and family Parvoviridae according to the ICTV [3]. CPV-2 is a naked virus, 25 nm in diameter and having icosahedral symmetry. The virus has a linear, SS negative sense DNA genome of 5.2 Kb containing 2 ORFs. One of which encodes 2 nonstructural proteins NS1 and NS2 and other two structural proteins VP1 and VP2. The palindromic hairpin of about 150 bases present in the viral genomic DNA is used in the replication of the viral DNA [4]. The viral capsid contains 60 structural subunits of VP2 (54-55 copies) and VP1 (5-6 copies). The VP1 protein is 727 residues in Review Article © Nandi S, et al. 2019