Deadly Canine Distemper: A Global Multispecies Disease

ABSTRACT

Canine distemper (CD) is a multispecies, deadly, and contagious viral disease; mainly it affects canines, characterized by multisystemic involvement such as respiratory, nervous, gastrointestinal, immune, and cutaneous system. Canine distemper virus (CDV) belongs to Morbillivirus genus and this vims is closely related to measles, rinderpest, Peste-des-petits-ruminant virus, and recently added species namely, Cetacean morbillivirus, phocine distemper virus, and Feline morbillivirus. Due to its high mutation and host variation, CDV is considered to be a deadly and dangerous disease among all carnivores. After the epidemics of Serengeti Lion population with CD, proved the role of CD in felines too. Genetic relatedness between CDV and measles enlighten scientific community to better understand the pathogenesis of measles in human population. Speculative information on multiple sclerosis in human and CDV connection signifies the role of CD with zoonotic threat in near future. Understanding the CDV in multiple species along with its associated epidemiological factors is of prime importance to counteract the future challenges of Morbillivirus diseases.

14.1 GENERAL INFORMATION

In 1905, Henri Care described the first incidence of Canine Distemper (CD) in France (Sykes, 2013). CD is the worldwide contagious disease of domestic dogs (Canis fmniliaris) due to its high case fatality rate next to rabies (Swango, 1995). Domestic ferrets (Mustela putorius ftiro) with CDV possessing 100% case fatality rate (Davidson, 1986) whereas 50-70% of domestic dogs with CDV infection may remain subclinical and or asymptomatic earners (Greene and Appel, 1990). CDV is closely related to human measles virus which suggested using the dog as sentinel model to study the pathogenesis of measles virus. The nondomestic animals for instance raccoon infects the domestic dogs which may cause severe interspecies transmission of CDV. Among the wildlife population, CDV may highly be influenced by catastrophic outbreaks with high mortality (Sykes, 2013).

After the CDV outbreak documentation from Baikal and Caspian seals and large felids in the Serengeti Park, dogs and wolves were identified as a potential vector for this infectious disease transmission (Beineke et al., 2015). Due to the expanding host range of CDV and its survival and maintenance within wildlife reservoir hosts considerably hampers the CDV disease control programs.

14.2 VIRUS

Morbilliviruses belong to the family Paramyxoviridae includes various pathogenic viruses, that is, measles virus, rinderpest virus, CDV, and Peste- des-petits-ruminants virus which causes devastating disease in both humans and animals (Beineke et al., 2015). CDV is a short-lived vims in the environment and can survive at a lower temperature (e.g., 48 h at 25°C and 14 days at 5°C) (Shen and Gorham, 1980; Deem et al., 2000). CDV is an enveloped virus and can also easily be destroyed by heat, diying, and disinfectants (Sykes, 2013). The phylogenetic association of phocine distemper vims (PDV) and CDV revealed that PDV emerged from the CDV several thousands of years ago by contact with terrestrial carnivores (Barret, 1999).

14.3 TRANSMISSION

CDV is a highly contagious airborne disease and the major transmission is through aerosolization of respiratory exudates containing a virus, although other body excretions and secretions (e.g., Urine) are also highly contagious to susceptible host if aerosolized (Deem et al., 2000). CDV is mainly transmitted through droplet nuclei and large size particle aerosol transmission. After aerosol infection of CDV, it is primarily replicated in lymphatic tissues of the respiratory tract and subsequently reaches the various portion of the body including the cells of lower respiratory and gastrointestinal parts, lymphoid system, urinary bladder, and the central nervous system (CNS). In general, nervous signs may be observed in the chronic form of distemper along with or without other clinical manifestations (Appel, 1987; Elia et al., 2006) CDV is also transmitted by transplacental mode in domestic dogs (Krakowka et al., 1977; Sykes, 2013) and vector-mediated transmission (Fleas) in mink (Trebbien et al., 2014). High population densities, predation, and crowding around water bodies is also a significant factor in CDV incidence among wildlife population species (Noon et al., 2003;Nagao et al., 2012)

14.4 PREVALENCE

Globally many researchers have documented the presence of CDV. In Texas (Guo et al., 1986), Santa Maria, Sal Cape Verde (Headley and Graca, 2000), Soul area, Korea (Kim et al., 2001), Warshaw, Poland (Jozwik and Frymus, 2002), Argentina (Calderon et al., 2007), Sao Paulo, Brazil (Alcalde et al., 2013), Chile (Acosta-Jamett et al., 2011; Garde et al., 2013; Acosta-Jamett et al., 2015), and India (Latha et al., 2007; Bora and Pathak, 2009; Pawar et al., 2011; Dongre et al., 2013; Ashmi et al., 2017; Buragohain et al., 2018).

• 14.5 DIAGNOSIS OF CDV
• 14.5.1 PCR

In the diagnosis of CD, reverse-transcriptase polymerase chain reaction (PCR) (RT-PCR) is routinely used and recommended by various researchers throughout the world (Frisk et al., 1999; Von Messling et al., 1999; Rzezutka and Mizak, 2002; Saito et al., 2006). Owing to the difficulties in virus isolation by cell culture, lymphocytes, and macrophages from the affected animal would help in increasing the sensitivity of CDV isolation through cell culture. In CD-infected animals for the purpose of antemortem and differentiation with other similar clinical sign diseases, PCR will be an appropriate test for diagnosis (Deem et al., 2000). The varieties of suitable biological sample usage in CDV molecular diagnosis and they stated that due to the high viral load present in the following samples, that is, urine, tonsil, conjunctival swab, and whole blood these are recommended to be used in real-time RT-PCR (Elia et ah, 2006). In a descriptive study conducted by Frisk et al. (1999) and Saito et al. (2006) from the typical CD dogs CSF samples using PCR and they found negative for CD. They postulated that CDV is not necessary to be always present in CSF which may be the possibility of false negative results while using CSF samples.

In RT-PCR. the diagnosis can be made using the following samples ocular and nasal discharges, saliva, and feces (Kim et ah, 2001). There are variety of diagnostic aid in CD disease that detection of antiCDV IgM antibody, Fluorescent Antibody test, and virus isolation. Due to time-consuming, lack of sensitivity, and cross-reaction with vaccinated animals sample makes it a low preference diagnostic aid among the above said diagnostic aids in the routine diagnosis of CD. RT-PCR is best available antemortem diagnostic tool in CD (Saito et ah, 2006). In this diagnostic method, the only disadvantage is that the recent vaccination history also would give false positive which suggest that it’s always necessary to ensure the recent vaccination history of animals while doing RT-PCR. Some authors have used urine as a sample of choice in diagnosing CD by RT-PCR (Gebara et ah, 2004; Saito et ah, 2006). Urine is the best sample of choice in the diagnosis of CD and it gives the diagnostic sensitivity near to CSF samples (Saito et ah, 2006).

In a better way, to increase the diagnostic sensitivity the samples must be drawn from different anatomical locations of dogs consisting of blood, buffy coat, skin biopsies, urine, conjunctival swabs, and CSF (Sykes, 2013). However, the low level of RNA from clinical samples, due to RNA labile nature, degradation of viral nucleic acids during sample collection, and transport to the laboratory, the low incidence of disease may be reported by RT-PCR.

Throughout the world, the wild-virus strains are highly documented and, however, cross-neutralizing antibodies analysis revealed that it’s not enough to state the change of existing vaccines in CDV (Sykes, 2013).

14.6 VACCINE-INDUCED CDV INFECTION IN WILD SPECIES

There are many reports with the incidence of vaccine-induced CDV infection in wild species, that is, Lesser Panda (Bush et al., 1976); European Mink (Mustela lutreola) (Sutherland-Smith et al., 1997; Ek-Kommonen et al., 2003); Maimed Wolf (Thomas-Basker, 1985); Captive red pandas (Bush and Roberts, 1977); Black-footed ferrets (Carpenter et al., 1976); Gray foxes (Halbrooks et al., 1981); Kinkajous (Potos Jlavus) (Kazacos et al., 1981); South American bush dog (Speothos venaticus) (Mclnnes et al., 1992); African hunting dogs (Lycaon Pictus) (Durchfeld et al., 1990).

• 14.7 EPIDEMIOLOGICAL ATTRIBUTES
• 14.7.1 AGE

Vulnerability of young ones to CD was documented by several authors and they also added that due to sudden declining of MDA facilitate the infection when it’s contacted with infected animals (Swango, 1989; Shell, 1990; Headley and Graca, 2000; Tarafder and Samad, 2010; Dongre et al., 2013). Some researchers found the increased susceptibility of CD between 4 and 24 months than other age groups (Patroneck et al., 1995; Ek-Kommonen et al., 1997; Headley and Graca, 2000; Martella et al., 2008; Acosta-Jamett et al., 2011; Garde et al., 2013). Active immunization may occur only when the MDA level is too low especially 3-6 months of age. Due to lack of vaccination or earlier vaccination of CDV may facilitate the chance of disease occurrence in 4-24 months age (Jozwik and Frymus, 2002; Latha et al., 2007). In contrary to this, some of the workers found that no significant association between age and the occurrence of CD (Twark and Dodds, 2000; Cattet et al., 2004). However, in endemic countries it’s not easy to determine that period and age susceptibility might be due to the population community and exposure to the amount of pathogen and it is varied between time and location (Garde et al., 2013). On the other hand, the higher prevalence of CDV in adults than young ones might be due to following possible reasons, that is, increased constant endemic pressure, variation in the exposure level to different population, increase in disease exposure with age, and recent outbreak nature (Acosta-Jamett et al., 2015).

14.8 BREED

Dolichocephalic breeds are much prone to encephalitis than brachycephalic breeds (Gorham, 1995; Headley and Graca, 2000). There are many documentation of higher positivity of CD in mixed than purebred throughout the world (Alex and Dhanapalan, 1994; Patronek et al., 1995). Due to behavioral adaptation, the dogs roaming in streets may predispose the chance of exposure from infected dogs than purebreds (Patronek et al., 1995). In contrary to this, Twark and Dodds (2000) reported that there is no significant association between breed and CD occurrence.

14.9 SEX

Many researchers have documented that there is no influence of gender in the occurrence of CD (Gorham, 1966; Guo et al., 1986; Patronek et al., 1995; Headley and Graca, 2000; Twark and Dodds, 2000; Cattet et al., 2004; Eghafona et al., 2007; Latha et al., 2007). In other hand, Alex and Dhanapalan (1994) and Buragohain et al. (2018) reported the highest prevalence of CD in male animals which may be due to high male population in the city and behavioral character of male dog lead to getting more disease.

14.10 IMMUNE STATUS (VACCINATED/UNVACCINATED)

Annual vaccination in dogs to maintain protective antibody in suspected population is the recommended strategy in different parts of the world (McCaw et al., 1998; Latha et al., 2007; Jerret and Ramsey, 2001; Garde et al., 2013). The published data onmatemal antibody interference with vaccination suggested that final CDV booster should be practiced around 18-20 weeks and 10 weeks of age, respectively, for raccoons and ferrets (Pare et al., 1999; Gorham, 1999). Domestic dog should be vaccinated every 3-4 week between 6th and 16th week of age whereas in colostrums deprived puppy, first dose should be given around 2 week of age followed by two booster with the interval of 3-4 weeks due to lack of maternally derived antibodies supply from dam and around 4-6 weeks of age (Appel, 1977; Deem et al., 2000). The variation in the CDV outbreaks recommended the importance of tailoring vaccination schedules required to particular species and modification of vaccination schedule needed during the epidemics of CD outbreaks.

Several reports were published in the occurrence of the CD even in vaccinated animals (Gouveia et al., 1987; Ek-Kommonen et al., 1997; Headley and Graca, 2000). The increased morbidity rate of canine distemper even in vaccinated animals alarm us to move with CDV regional-specific strain vaccines rather than prototypes (Ikeda et al., 2001).

14.11 SEASON/MONTH

In developing countries like India, there is a high chance of free-ranging dogs in rural and urban cities which make the dog population to be a sentinel to many infectious diseases to domestic as well as wildlife species (Jackman and Rowan, 2007; Ashmi et al., 2017). Though the vaccination measures were practiced in developing countries due to the higher population density of free-ranging dogs, it doesn’t ensure adequate herd immunity (Jackman and Rowan, 2007). In this situation, the sudden stochastic disaster could be easier to transmit the disease to other suspected population (Latha et ah, 2007; Bilxenkrone-Moller et al., 1993). Hence, an adequate understanding of infectious disease occurrence nature should be always studied continuously in all epidemiological circumstances (Garde et al., 2013).

Regarding the seasonal influence of CD epidemics, winter plays a major role in disease outbreaks (Ho and Babiuk, 1979; Alex and Dhanapalan, 1994; Gorham, 1966; Headley and Graca, 2000; Latha et al., 2007; Bora and Pathak, 2009; Tarafder and Samad, 2010). Due to virus, survival in the colder season may be favorable and also colder environment induces immunosuppression in neonates (Reeder and Kramer, 2005) and recently weaned animals which also contributed to the epidemics. Also due to the dispersal of dust and dirt more in a diy environment (winter) which makes easy transmission of the virus particle to distant places (Buragohain et ah, 2018). In opposite to this higher positivity of CD during summer is also noted (Patronek et al., 1995).

14.12 THERAPY

Though it’s not a curable disease in dogs, still many supportive therapies is tried to enhance the life span as empirical approach. The broad spectrum antibiotics and fluid therapy were regularly practiced. Some of the homeopathy medicines were tried in CD dogs, that is, Comum Maculatum also useful in reducing the post-hind paralysis and other neurological manifestations of CD (Karen, 2011). Even after using rapid diagnosis teclmique and high standard care given to treatment, it’s not enough to say about the recovery of annuals despite its lead to high mortality (Martella et al., 2008). In vitro efficacy of ribavirin and 5-ethynyl-l-/?-D- ribofuranosylimidazole-4-carboxamide (EICAR) as antiviral therapy in CD also reported (Sykes, 2013). Zhao et al. (2017) conducted an analytical study on gut microbial fauna assessment in CDV-infected and noninfected Giant Panda from China and reported that CDV-infected animals gut fauna revealed the changes in gut microbial diversity with a reduced level of dominating bacteria, that is, Escherichia and Clostridium. This fauna microbial diversity identification may be useful in planning better nutrition to overcome this disease fatal nature with broad supportive nature.

14.13 CLINICAL SIGNS

Acute generalized CD infections were highly related to the respiratory and gastrointestinal systems and include conjunctivitis, pneumonia, diarrhoea (often hemorrhagic), anorexia, and severe dehydration and also they narrated the neurological manifestation of CD which may occur 1-3 weeks after recovery from acute generalized infection (Vandervelde and Cachin, 1993; Appel, 1987; Deem et al., 2000). In chronic progressive neurological dysfunction may occur in over 6 year age group of dogs mostly and also the least clinical signs of CD diseases as digital hyperkeratosis, optic neuritis, chorioretinitis, uveitis and in young dogs juvenile cellulitis, metaphyseal bone lesions, and enamel hypoplasia may be noted (Dubielzig et al., 1981; Malik et al., 1995).

In comparison with all other signs, the following signs are considered to be characteristic suggestive signs of CD, that is, myoclonus (Greene and Apple, 1998; Saito et al., 2006; Sykes, 2013) and “Chewing gum fits” (Breazile et al., 1966; Deem et al., 2000). In other hand, Garde et al. (2013) reported that “None of the clinical signs are considered to be pathognomic signs” due to the wide variation of CD nature pertaining to individual dog’s immunity, type of virus infected, secondary bacterial infection involvement, and vaccination history. The enlisted influencing factor toward the clinical progression pattern of CDV in individual animals were virus strain virulence, environmental conditions, animals age, and immune status and infected species identity (Deem et al., 2000).

In domestic dogs, acute generalized CD infection would be routinely diagnosed by typical clinical signs whereas in nondomestic species suspected cases would be differentiated from rabies, feline panleukopenia, toxoplasmosis, canine parvovirus, lead poisoning, and bacterial enteritis (Deem et al., 2000). CD-infected ferrets and mink would have the suspected clinical signs like digital, nasal, and eyelid hyperkeratosis (Pearson and Gorham, 1987). The broad clinical manifestations of the CD with varying clinical signs lead to difficulty in differentiating with other respiratory diseases (Jones et al., 1997). The diagnosis of CD in acute or subacute stages can be done with typical clinical signs such as conjunctivitis, bronchitis, catarrhal pneumonia, gastroenteritis, and neurological disturbances. Some other diseases which mimic the similar signs may reduce the clear diagnosis arrival, that is, early stage of kernel cough, chronic distemper encephalitis, parainfluenza virus 2, canine coronavirus, infectious canine hepatitis virus, and canine parvovirus (Kim et al., 2001). CDV is the major immunosuppressant disease in dogs which makes host with increased vulnerability to secondary pathogen infection that lead to increased CDV associated death (Pawar et al., 2011).

Based on the virus strain, the proliferation of CDV in various brain cells was also one of the clinical sign variations reported instance Synder Hill strain mainly produce neurological signs (Sykes, 2013). In the ocular form of CDV characterized by uveitis, chorioretinitis, keratoconjunctivitis sicca (KCS), keratitis, and optic neuritis lead to blindness. The common copathogen in CDV in dogs was Bordetella bronchiseptica and other opportunistic pathogens were toxoplasmosis, salmonellosis, nocadiosis, and generalized demodecosis. Similarly, in mink, Pneumocystis carinii and in raccoon, neopsorosis were reported as a copathogenic infection with CDV (Sykes, 2013).

14.14 FELIDAE

Serological studies on CDV in cat populations of the United States revealed that 10% of cat populations had Viral Neutralizing Antibodies against CDV (Appel et al., 1974). The epidemics of CDV in 1992 from North America’s large captive felids and they histopathologically confirmed CDV infection in African Lion (Panthera leo), tiger (Panthera tigris), leopard (Panthera pardus), and Jaguar (Panther onca) (Appel et al., 1994). In these epidemics, the severity pattern of CDV pathogenesis with major involvement of gastrointestinal, respiratory, and CNS systemic signs.

The CD infection with multispecies morbidity in the Serengeti ecosystem with 30% of a population of 3000 African lions and they hypothesized that “from unvaccinated dogs, CDV infection might be transmitted to spotted hyenas (Crocuta crocuta) which in turn to lion’s CDV transmission” (Roelke-Parker et al., 1996). As per rare serological studies of CD in cat documented by Appel et al. (1974) and Ikeda et al. (2001), respectively, in 1974 at the United States and in 1982 at Japan suggested that CDV infection was associated with cats for a considerably longer time worldwide. Ikeda et al. (2001) conducted a serological study on CDV in Asian felids and revealed that cat with antibodies had likely been exposed to field strains rather than typical CDV vaccine strains. They also enlisted the risk factor associated with the prevalence of CDV antibodies in Asian felids and the factors were region, individual, and exposure to infected dogs. They additionally added the strong circumstantial evidence of typical CDV transmission from infected dogs to unaffected cats. In this analytical study, they found that there are no relationships between CDV seropositive cat populations with their physical condition except seropositive cases were likely to have an anemic issue than other cats. They also hypothesized the low pathogenic tropism of CDV in cats and the possibility of respiratory and hepatic involvement in seropositive CDV cats.

A phylogenetic and molecular characterization of CDV H gene isolates revealed that “CDV infections in felids are not only incidental or spill over of infections and also it is a part of the regular host spectrum of infectivity” (Terio and craft, 2013).

14.15 HOST RANGE

CD is a most important disease in all families of terrestrial carnivores due to its wide spectrum of host ranges, that is, Canidae, Felidae, Hyaenidae, Mustelidae, Procyonidae, Ursidae, and Viverridae (Deem et al., 2000). Wildlife spillover of CDV infection from domestic dogs prevalence reported by various researcher with epidemiological investigations strongly recommended that the “Domestic dogs with CDV infection may serve as a reservoir for free-ranging wildlife” (Alexander et al., 1995; Roelke-Parker et al., 1996; Deem et al., 2000; Beineke et al., 2015).

A phylogenetic and molecular evolutionary analysis of CDV was conducted by various researchers throughout the world (McCarthy et al., 2007; Bieringer et al., 2013; Nikolin et al., 2012; Origgi et al., 2012; Sattler et al., 2014). They hypothesized that mutation affecting the binding site of the virus (H protein) entry receptors, that is, signaling lymphocytic activation molecule (SLAM), CD 150 and nectin are the associated factors in the emergence of CDV epidemics in new host species.

14.16 NATURAL INFECTION OF CDV IN NON-DOMESTIC CANID SPECIES

There are varieties of documentation of CDV in non-domestic canines, that is, African hunting dogs (Lycaon Pictus) (Van Heerden et al., 1990; Alexander et al., 1993; Alexander et al., 1994; Alexander et al., 1996;); Australian dingos (Cam's dingo) (Armstrong and Anthony, 1942); Kit foxes (Vulpes Macrotis Macrotis) (Armstrong and Anthony, 1942); Bat-Eared foxes (Otocyon megalotis) (Hofmeyer, 1956; Moehhnan, 1983); Raccoon dogs (Nyctereutesprocyonoides) (Armstrong and Anthony, 1942; Machida et al., 1993); Coyotes (Canis latrans) (Gese et al., 1991; Gese et al., 1997; Cypher et al., 1998); Red foxes (Vulpes vulpes) (Armstrong and Anthony, 1942; Little et al., 1998) and Grey foxes (Urocyon cinereargenteus) (Armstrong and Anthony, 1942; Hoff and Bigler, 1974).

14.17 NONCARNIVORE

CD diseases were also reported in noncamivore’s, that is, Collared Peccaries (Javelina; Pecan tajaui) (Appel et al., 1991); Japanese Macaques (Macaca fuscata) (Yoshikawa et al., 1989), and Rhesus Monkey (Sun et al., 2010).

14.18 FELIDAE

There are many reports on wild felines CDV occurrence were reported, that is, Bengal tiger (Blythe et al., 1983); Snow leopard (Panthera uncia) (Fix et al 1989); Siberian tiger (Gould and Fenner, 1983); Lion (Piat, 1950; Appel et al., 1994; Truyen et al., 1998); Iberian lynx (Lynxpardinus) (Meli et al., 2010); Eurasian lynx (Lynx lynx) (Origgi et al., 2012); Canadian lynx (Lynx Canadensis) and Bobcats (Lynx rufus) (Daoust et al., 2009).

14.19 MUSTELIDAE

Among the wide spectrum of CDV infection, Mustelidae are the most susceptible species than others (Deem et al., 2000). Domestic ferrets and black-footed ferrets (Mustela nigripes) are the highly prone species of natural CDV with increased morbidity and case fatality rate than other Mustelidae genus species (Bernard et al., 1984; Davidson, 1986). In Mustelidae family many CD reports are documented throughout the world, that is, American badgers (Taxidea taxus) (Armstrong and Anthony, 1942; Goodrich et al., 1994); Striped skunk (Mephitis mephitis) (Diters and Nielsen, 1978); European mink (Mustela lutrola); American mink (Mustela visoii) (Montali et al., 1994; Pearson and Gorham, 1987; Sutherland-Smith et al., 1997); Eurasian badgers (Meles meles) (Armstrong and Anthony, 1942); European otters (Lutra lutra) (Scott, 1979; Giesel, 1979). In a phylogenetic analysis of various carnivores CDV infection in central Europe revealed a distinct CDV lineage in ferrets, polecats, and martens which alarmed the importance of mustelid-adapted strains (Liermann et al., 1998).

14.20 URSIDAE

Many reports of CDV infection in Ursidae were reported throughout the world, that is, American black bears (Ursns americamis) (Cottrell et al., 2013; Stephenson et al., 2015); Asian black bears (Ursus tibethamis) (Nagao et al., 2012); Polar bears (Ursus maritimus) (Kirk et al., 2010); Grizzly bears (Ursus arctos horribilis) (Philippa et al., 2004), and Marsican brown bears (Ursus arctos marsicanus) (Di Francesco et al., 2015). After the first incidence of CDV infection in wild black bears (Ursus americanus) and further molecular sequencing found that CDV vaccine strain (Rockbom strain) is the etiological agent for that epidemics which suggested that importance of potential virus exchangebetweenvaccinateddomesticanimalsandwildlife(Cottrelletal., 2013).

14.21 VIVERRIDS

Some of the incidence of CDV in Viverrids also documented in various parts of world, that is, Binturong (Arcticis binturong) (Chandra et al., 2000); Masked pahn civet (Paradoxurus hermaphrodites) and Asian palm civet (Paradoxurus hermaphrodites) (Techangamsuwan et al., 2014) and Genet (Genetta Genetta) (Lopez-Pena et al., 2001).

14.22 HYANEIDAE

Alexander et al. (1995) conducted a study on free ranging spotted hyenas in the Masai Mara, Kenya and showed a high title of CDV with clinical signs or mortality during a trend in which domestic dog CD epidemics where noted. They hypothetically documented the association of CD epidemics in hyena and domestic dog.

14.23 MARINE MAMMALS

In marine mammals, PDV was documented with high similarity lineage between CDV (Duignan et al., 2014). In Siberia, Baikal Seals (Phoca Sibirica) reported with CDV also documented (Butina et al., 2010)

14.24 ZOONOTIC POTENTIAL

In an experimental study, reports of asymptomatic human CDV infection signifies the CDV viral host mutation and attaclnnent which make future threads to human (Deem et al, 2000).

14.25 CONCLUSION

There are varieties of incidence of CDV were documented in both carnivores and noncarnivores. It’s thought to be restricted in dogs; recent epidemics suggested increased chance of mutilation and wide host range. These hypothesized data possessing the future infection with human species too. Considering the fact continuous monitoring on CDV with molecular characterization possesses a huge background for combating future epidemics. In a nutshell, canine distemper is a deadly disease with multi-host range of clinical manifestation which needs a systemic and thorough understanding to overcome the epidemic curve peak of CDV.

KEYWORDS

• • morbillivirus
• • CD
• • multiple species
• • combat-deadly disease
• • contagious
• • zoonotic
• • multisystemic involvement

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