Canine distemper is a highly contagious, systemic, viral disease of dogs seen worldwide.
Clinically, canine distemper is characterized by:
, , Its epidemiology is complicated by the large number of species susceptible to infection. The disease is seen in Canidae (dog, fox, wolf, raccoon dog), Mustelidae (ferret, mink, skunk, wolverine, marten, badger, otter), most Procyonidae (raccoon, coatimundi), some Viveridae (binturong, palm civet), Ailuridae (red panda), Ursidae (bear), Elephantidae (Asian elephant), primates (Japanese monkey), and large Felidae. Domestic dogs (including feral populations) are considered to be the reservoir species in most, if not all, locations. Antigenic drift and strain diversity is increasingly documented in association with outbreaks in wild species, domestic dogs, and exotic animals held in zoos and parks.
Canine distemper virus, or CDV, is a paramyxovirus closely related to the viruses of measles and rinderpest. The fragile, enveloped, single-strand RNA virus is sensitive to lipid solvents, such as ether, and most disinfectants, including phenols and quaternary ammonium compounds. It is relatively unstable outside the host. The main route of infection is via aerosol droplet secretions from infected animals. Some infected dogs may shed virus for several months.
The virus initially replicates in the lymphatic tissue of the respiratory tract. A cell-associated viremia results in infection of all lymphatic tissues, which is followed by infection of respiratory, GI, and urogenital epithelium, as well as the CNS and optic nerves. Disease follows virus replication in these tissues. The degree of viremia and extent of viral spread to various tissues is moderated by the level of specific humoral immunity in the host during the viremic period.
A transient fever usually occurs 3–6 days after infection, and there may be a leukopenia (especially lymphopenia) at this time; these signs may go unnoticed or be accompanied by anorexia. The fever subsides for several days before a second fever occurs, which may be accompanied by serous nasal discharge, mucopurulent ocular discharge, lethargy, and anorexia. GI and respiratory signs, typically complicated by secondary bacterial infections, may follow; rarely, pustular dermatitis may be seen. Encephalomyelitis may occur in association with these signs, follow the systemic disease, or occur in the absence of systemic manifestations. Dogs surviving the acute phase may have hyperkeratosis of the footpads and epithelium of the nasal planum, as well as enamel hypoplasia in incompletely erupted teeth.
Overall, a longer course of illness is associated with the presence of neurologic signs; however, there is no way to anticipate whether an infected dog will develop neurologic manifestations.
Classic neurologic signs include:
Other neurologic signs include:
Localized involuntary twitching of a muscle or group of muscles (myoclonus, chorea, flexor spasm, hyperkinesia) and convulsions characterized by salivation and, often, chewing movements of the jaw (“chewing-gum fits”) are considered classic neurologic signs. Emerging viral strains may be associated with greater neurotropism; increased morbidity and mortality from neurologic complications has been observed.
A dog may exhibit any or all of these multisystemic signs during the course of the disease. Infection may be mild and inapparent or lead to severe disease with most of the described signs. The course of the systemic disease may be as short as 10 days, but the onset of neurologic signs may be delayed for several weeks or months as a result of chronic progressive demyelination within the CNS.
Clinicopathologic findings are nonspecific and include lymphopenia, with the possible finding of viral inclusion bodies in circulating leukocytes very early in the course of the disease. Thoracic radiographs may reveal an interstitial pattern typical of viral pneumonia.
Chronic distemper encephalitis (old dog encephalitis, [ODE]), a condition often marked by ataxia, compulsive movements such as head pressing or continual pacing, and incoordinated hypermetria, may be seen in fully vaccinated adult dogs without a history suggestive of systemic canine distemper infection. Although canine distemper antigen has been detected in the brains of some dogs with ODE by fluorescent antibody staining or genetic methods, dogs with ODE are not infectious, and replication-competent virus has not been isolated. The disease is caused by an inflammatory reaction associated with persistent canine distemper virus infection in the CNS, but mechanisms that trigger this syndrome are unknown.
Thymic atrophy is a consistent postmortem finding in infected young puppies. Hyperkeratosis of the nose and footpads is often found in dogs with neurologic manifestations. Depending on the degree of secondary bacterial infection, bronchopneumonia, enteritis, and skin pustules also may be present. In cases of acute to peracute death, exclusively respiratory abnormalities may be found. Histologically, canine distemper virus produces necrosis of lymphatic tissues, interstitial pneumonia, and cytoplasmic and intranuclear inclusion bodies in respiratory, urinary, and GI epithelium.
Lesions found in the brains of dogs with neurologic complications include:
Canine distemper should be considered in the diagnosis of any febrile condition in dogs with multisystemic manifestations. Characteristic signs sometimes do not appear until late in the disease, and the clinical picture may be modified by concurrent parasitism and numerous viral or bacterial infections.
Distemper in dogs can beconfused with other systemic infections:
Intoxicants such as lead or organophosphates can cause simultaneous GI and neurologic signs. A febrile catarrhal illness with neurologic sequelae justifies a clinical diagnosis of canine distemper.
In dogs with multisystemic signs, the following can be examined by immunofluorescent assay or reverse transcriptase (RT) PCR:
Commercially available quantitative RT-PCR can usually distinguish natural infection from vaccinal virus. A combined two-step RT-PCR to distinguish vaccinal strains from emerging wild-type strains has also been described; this assay would be of particular value in epidemiologic investigations or in outbreaks in non-canine species. Antibody titers or ELISA can be performed on CSF and compared with peripheral blood; a relatively higher level in the CSF is typical of natural infection versus vaccination. Viral antigen immunofluorescent assay (IFA) or fluorescent in situ hybridization for viral DNA can be performed on biopsies from the footpads or from the haired skin of the dorsal neck.
At necropsy, diagnosis is usually confirmed by histologic lesions, IFA, or both. These samples are often negative when the dog is showing only neurologic manifestations or when circulating antibody is present (or both), requiring that the diagnosis be made by CSF evaluation or RT-PCR as described above.
Treatments are symptomatic and supportive, aimed at limiting secondary bacterial invasion, supporting fluid balance, and controlling neurologic manifestations.
No single treatment is specific or uniformly successful. Experimental in vitro work with antiviral agents shows promise, but these agents have not yet been widely used.
Unfortunately, treatment for acute neurologic manifestations of distemper is frequently unsuccessful. If the neurologic signs are progressive or severe, the owner should be appropriately advised. With prompt, aggressive care, dogs may recover completely from multisystemic manifestations, but in other cases, neurologic signs may persist after GI and respiratory signs have resolved. Some dogs with chronic progressive or vaccine-induced forms of neurologic disease may respond to immunosuppressive therapy with anti-inflammatory or greater dosages of glucocorticoids.
With the potential increasing virulence of emerging strains and the wide host range of canine distemper virus, widespread vaccination of domestic dogs is essential. Successful immunization of pups with canine distemper modified-live virus (MLV) vaccines depends on the lack of interference by maternal antibody. To overcome this barrier, pups are vaccinated with MLV vaccine when 6 wk old and at 3- to 4-wk intervals until 16 wk old. Alternatively, measles virus vaccine induces immunity to canine distemper virus in the presence of relatively greater levels of maternal distemper antibody. MLV measles vaccine is administered IM to pups 6–7 wk old and is followed with at least two more doses of MLV distemper vaccine when 12–16 wk old.
Many varieties of attenuated distemper vaccine are available and should be used according to manufacturers’ directions. MLV vaccines should not be used in late-pregnant or early-lactation bitches. MLV vaccines can produce postvaccinal illness in some immunosuppressed dogs. A recombinant canarypox vector vaccine expressing distemper virus proteins is licensed for use in ferrets; the American Association of Zoo Veterinarians recommends its extra-label use in many at-risk species held in zoos and parks.
Historically, annual revaccination has been standard because of the breaks in protection that can occur in stressed, diseased, or immunosuppressed dogs, and because vaccines have been labeled for annual use. Substantial evidence supports the finding that immunity induced by MLV distemper vaccines lasts ≥3 yr. However, in most cases, this remains an extra-label use of the vaccine; thus, decisions to revaccinate less often than annually should be considered in light of local prevalence of the disease and other potential risk factors, as well as industry and professional organization recommendations.