Canine Distemper
Dr. Pallvi Slathia1, Dr. Riya Abrol2
1Department of Veterinary Microbiology, College of Veterinary Science, SKUAST-Jammu,
2Ph.D. Student, Department of Veterinary Pathology, College of Veterinary Science, SKUAST-Jammu,
Abstract: The most prevalent and contagious disease affecting domestic dogs (Canis familiars) worldwide, canine distemper (CD), is an acute, highly contagious viral illness that affects both carnivores and domestic dogs of all ages. Its mortality rate is second only to that of rabies. The canine distemper virus is a Morbillivirus belonging to the Paramyxoviridae family. It is a rather large (150-250 nm) single-stranded RNA virus with a lipoprotein envelope. Young, unvaccinated dogs frequently contract canine distemper within their first year of life. Other body excretions and secretions, such as urine, can infect susceptible hosts if aerosolized and transferred by direct touch. The transmission is through aerosolization of respiratory exudates harbouring virus. Canine distemper infection is not curable; therapy focuses more on preventing secondary complications and providing supportive care.
Introduction: The etiological agent of canine distemper is the canine distemper virus (CDV), also known as canine morbillivirus and a member of the Paramyxoviridae family. Since 1760, it has been recognised as a highly infectious and severely febrile disease in dogs. Infections of the respiratory, gastrointestinal, urinary, lymphatic, cutaneous, skeletal, and central nervous systems (CNS) are caused by various cell tropism (epithelial, lymphoid, and neurological) that is connected with it (Lempp et al 2014). Members of the Canidae, Procyonidae, and Mustelidae are just a few of the many carnivore families that can contract the canine distemper virus (CDV). Typically occurring in the first year of life, CD is frequent in young, unvaccinated dogs, while numerous cases are also reported in adulthood. Some of the highest fatality rates for infectious diseases in dogs are caused by canine distemper.
Transmission: Direct contact between the susceptible dog and infected dogs or wildlife is the most frequent cause of infection. The main way that CDV spreads is through the aerosolization of respiratory exudate that contains the virus, but other bodily excretions and secretions, such urine, might infect hosts who aren’t susceptible if they are exposed to them. Its IP spans a period of roughly 1 week to 1 month. Canine distemper is extremely contagious, and virus shedding may occur 60 to 90 days after infection. There is evidence that domestic dogs can get a transplacental infection. It is unknown whether vertical transmission can occur in non-domestic species or its epidemiologic significance in CD. The virus can survive at lower temperatures, despite often having a brief lifespan in the environment. Additionally spread through either direct contact or spores (Pearson and Gorham, 1987).
Pathogenesis: The virus often enters through the upper respiratory tract’s epithelium, growing in macrophages before spreading to the tonsils and local lymph nodes, where it can replicate within two to four days of infection. Within a week, CDV multiplies in lymphoid organs such the lamina propria of the stomach and small intestine, Kupffer’s cells in the liver, mesenteric lymphnodes, and spleen. Leukopenia and fever are linked to viral spread due to T and B cell suppression. The virus eventually infects epithelial cells all across the body. Dogs with significant humoral and cellular immunity may exhibit clinical symptoms, but most tissues will be cleared of the virus in 3 weeks. The host immune response that is humoral and cell-mediated determines the pathogenesis between 9–14 days. Canines with the neurological condition could develop due to the virus’s epithelial damage, the footpads and nose have hyperkeratosis (thickening). As a result of this canine form, the term “hardpad disease” has become a widespread alternate term for canine distemper. Less than 50% of adult dogs with CDV infection pass away from it; but, in puppies, the mortality rate can reach as high as 80% (Williams, 2001).
Clinical Signs: After the incubation period of 3-6 days of canine distemper virus infection, a brief fever and leukopenia (defined by lymphopenia) may appear; these clinical symptoms may go unrecognised or may be accompanied by malnutrition. A second fever that may be accompanied by lethargy, anorexia, serous nasal discharge, mucopurulent ocular discharge, and other symptoms appears after the first one has subsided for a few days. Following may be GI and respiratory symptoms that are occasionally complicated by subsequent bacterial infections, as well as pustular dermatitis. Encephalomyelitis may accompany these symptoms, follow a systemic illness, or develop in the absence of systemic symptoms. Dogs who survive the acute phase may develop hyperkeratosis of the footpads and nasal epithelium, as well as enamel hypoplasia in teeth that have not fully erupted (Gelatt et al.,1985).
Any age dog can get neurologic distemper, even if there were no or just minor systemic symptoms, and older dogs may develop chronic progressive neurologic impairment as a result (usually over 6 years of age). Depending on how the virus affects the CNS, neurologic consequences can manifest as hyperesthesia, cervical rigidity, seizures, cerebellar and vestibular symptoms, paraparesis or tetraparesis with sensory ataxia. Another very strong indicator of CD is the involuntary twitching of muscles in a powerful synchronous contraction, which frequently results in “chewing gum” fits. Digital hyperkeratosis (hard pads) and optic neuritis, chorioretinitis, and uveitis are additional CDV symptoms in domestic dogs. Pneumonia, conjunctivitis, rhinitis, and tracheitis are all symptoms of distemper in puppies. The lungs are usually swollen, and a broncho-interstitial pneumonia is seen under the microscope, along with necrosis of the epithelium lining the tiny airways and thickening of the alveolar walls.
Other neurological symptoms include spinning, head tilting, nystagmus, paresis, and paralysis as well as various types of seizures, from focal to widespread. Greater neurotropism may be linked to newly emerging virus strains. There have been more cases of morbidity and death due to neurological issues. Lymphopenia is one of the non-specific clinicopathologic signs, and it’s likely that very early in the course of the disease, circulating leukocytes contain viral inclusion bodies. A viral pneumonia-specific interstitial pattern may be seen on thoracic radiographs.
Chronic distemper encephalopathy, also known as old dog encephalitis (ODE), can occur in completely immunised adult dogs without a history of systemic canine distemper infection. ODE symptoms include ataxia, compulsive behaviours such head pressing or constant pacing, and uncoordinated hypermetria. Although some dogs with ODE have had canine distemper antigen found in their brains using fluorescent antibody staining or genetic techniques, these dogs are not contagious, and no replication-competent virus has been recovered. The persistent canine distemper virus infection in the CNS causes an inflammatory response that causes the disease; however, it is not known what causes this syndrome (McLachlan and Dubovi, 2011).
Lesions: A common postmortem finding in young puppies with canine distemper virus infection is thymic atrophy. In dogs with neurologic symptoms, hyperkeratosis of the snout and footpads is a common finding. Bronchopneumonia, enteritis, and cutaneous pustules may also exist, depending on the severity of the secondary bacterial infection. It’s possible to find just respiratory anomalies in deaths that were acute or subacute. Histologically, the canine distemper virus causes cytoplasmic and intranuclear inclusion bodies in the respiratory, urinary, and GI epithelium, as well as necrosis of lymphatic tissues, interstitial pneumonia, and these conditions.
Dogs with neurologic issues have many brain lesions, including development of new neurons. Gliosis is characterised by non-inflammatory demyelination, perivascular cuffing and non-suppurative leptomeningitis. Glial cells predominately contain intranuclear inclusion bodies.
Diagnosis: Clinical assessment serves as the initial diagnosis and reverse transcriptase PCR (RT- PCR) and antibody detection as confirmation tests. Any febrile disease in dogs with multisystemic clinical symptoms affecting the respiratory, gastrointestinal, and/or nervous systems should be diagnosed with canine distemper. Dogs that are unvaccinated or whose immunisation status is uncertain should be given special suspicion. The first step is to establish an appropriate index of suspicion based on clinical indicators. In carefully chosen clinical instances, widely accessible RT-PCR and antibody detection assays (ELISA, immunofluorescence assay [IFA]) are utilised to demonstrate the existence of the virus or an immune reaction against it.
IFA or RT-PCR may be used in canines exhibiting multisystemic clinical symptoms to test for: Conjunctival, tracheal, nasal, vaginal, or other epithelial smears, transtracheal wash fluid, urine, bone marrow aspirates, and buffy coat of the blood. Quantitative RT-PCR may be able to evade the issue that commercially available RT-PCR may not be able to distinguish between natural infection and virus produced from a vaccine. A substantially higher level of antibodies in the CSF is indicative of a natural infection than vaccination, and antibody titers or ELISA can be used to compare CSF with peripheral blood. Biopsies from the dorsal neck’s hairy skin or the footpads can be used to detect viral DNA using fluorescent in situ hybridization (FISH) or viral antigen IFA.
Treatment: Canine distemper has no specific therapy. However, they are symptomatic and supportive and are intended to prevent subsequent bacterial invasion, promote fluid balance and manage neurologic symptoms. Good nursing care is crucial, and the use of broad-spectrum antibiotics, balanced electrolyte solutions, parenteral feeding, antipyretics, analgesics, and anticonvulsants is common (Creevy, 2013).
Prevention and control: The best method of preventing canine distemper is immunisation. For dogs and other domestic and nondomestic animals, a number of canine distemper vaccinations are available (Deem et al 2001). Domestic dogs are currently immunised with commercially available vaccines that include the altered live virus (MLV). Puppies receive the MLV vaccine at 6 weeks old and then every 3 to 4 weeks until they are 16 weeks old. UV radiation, heat, desiccation, and conventional disinfectants including formaldehyde, phenolic chemicals, and quaternary ammonium compounds can all severely harm the virus. The virus is also exceedingly fragile. Additionally, it cannot endure the environment for more than a few hours at room temperature (25°C), but it can survive the environment for at least two weeks at temperatures close to freezing (5°C).
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