**1. Introduction**

Canine parvovirus (CPV-2) is a member of the *Parvoviridae* family, *Parvovirinae* subfamily, and *Protoparvovirus* genus. It causes severe, acute hemorrhagic gastroenteritis and myocarditis infection in dogs [1]. It is the most important enteric virus affecting domestic and wild carnivores throughout the globe [2]. CPV-2 is a nonenveloped virus with a single-stranded negative-sense DNA genome [3]. The genetic diversity of CPV-2 resulted in the emergence of 5 distinct antigenic variants such as CPV-2a, CPV-2b, new CPV-2a, new CPV-2b, and CPV-2c with amino acid differences mainly restricted to the capsid VP2 protein [4]. CPV-2 are ubiquitous and sturdy viruses that remain viable for more than one year in the favorable environment [5, 6] and are transmitted usually by the faeco-oral route [7, 8].

CPV-2 causes 100 percent morbidity and mortality rate of 10 percent and 91 percent in adult and young dogs respectively [9]. However, a mortality of 91 percent was reported in experimentally infected dogs that were not treated [10]. CPV-2 affects predominately the younger dogs between 6 weeks and 6 months [8] with an increased susceptibility to puppies less than 6 months. In dogs over the age of 6 months, sexually intact males are more likely (twice) to develop canine parvovirus enteritis (CPVE) in comparison to intact females [11]. The CPV-2 antibody titer transmitted to the newborn via absorbed colostral antibody is 50–60% of the mother's titer. The half-life of paroviral maternal antibodies is around 10 days [12]. Therefore, puppies are highly susceptible to the CPV-2 infection as the maternal antibody titres start declining. CPVE affects dogs of all ages, although it is more severe in puppies. Puppies can succumb to shock and die within two days after being sick. The most striking symptom of CPV-2 myocarditis is the abrupt mortality in young puppies, generally around the age of 4 weeks [13].

In recent years, CPVE outbreaks caused by multiple CPV-2 variants have been recorded in diverse geographical locations throughout the world. Previously, CPV-2, which could not infect cats, has been replaced by CPV-2 variants that can now infect cats, suggesting that CPV-2 may be capable of spreading between species [14]. Since CPV-2 infects a wide range of wild animals in the order Carnivora, subclinical infection appears to be prevalent. As a result, significant CPV-2 reservoirs in wildlife appear to exist, and transmission of virus between domestic dogs and wildlife appears to be common and bidirectional [15]. Despite the availability of a wide range of immunoprophylactic and antiviral agents to control CPV-2 infections in dogs, many outbreaks have been reported throughout the world, and the disease has remained a major veterinary and economic concern due to the presence of unvaccinated dogs, intervention of active immunization by maternally derived antibodies, and the emergence of a different antigenic variants of CPV-2.
