Canine distemper is a highly contagious, systemic, viral disease of dogs seen worldwide. Clinically, it is characterized by a diphasic fever, leukopenia, GI and respiratory catarrh, and frequently pneumonic and neurologic complications. The disease is seen in Canidae (dogs, foxes, wolves), Mustelidae (eg, ferret, mink, skunk, wolverine, marten, badger), most Procyonidae (eg, raccoon, coatimundi), some Viveridae (binturong), red pandas (Ailuridae), Elephantidae (Asian elephant), primates (Japanese monkey), and large Felidae.
Etiology and Pathogenesis
Canine distemper is caused by a paramyxovirus closely related to the viruses of measles and rinderpest. The fragile enveloped 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.
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 lasts <1 wk. This 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 (“hardpad” disease) 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. CNS signs include circling, head tilt, nystagmus, paresis to paralysis, and focal to generalized seizures. 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.
A dog may exhibit any or all of these multisystemic signs over the course of the disease. Infection may be mild and inapparent or lead to severe disease with most of the above 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 brain 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, broncho-pneumonia, enteritis, and skin pustules may also 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 brain of dogs with neurologic complications include neuronal degeneration, gliosis, noninflammatory demyelination, perivascular cuffing, nonsuppurative leptomeningitis, and intranuclear inclusion bodies predominately within glial cells.
Distemper should be considered in the diagnosis of any febrile condition in puppies with multisystemic manifestations. Characteristic signs sometimes fail to appear until late in the disease and the clinical picture may be modified by concurrent toxoplasmosis, neosporosis, coccidiosis, parasitism, and numerous viral and bacterial infections. Distemper is sometimes confused with other systemic infections such as leptospirosis, infectious canine hepatitis, or Rocky Mountain spotted fever. Intoxicants such as lead or organophosphates can cause simultaneous GI or neurologic sequelae. A febrile catarrhal illness with neurologic sequelae justifies a clinical diagnosis of distemper.
In dogs with multisystemic signs, smears of conjunctival, tracheal, vaginal, or other epithelium; the buffy coat of the blood; urine sediment; or bone marrow aspirates can be examined by immunofluorescent assay or reverse transcriptase PCR. Virus-specific IgM serology is also useful early in the course of disease. 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 virus-specific IgM serology as described above.
Treatments are symptomatic and supportive, aimed at limiting secondary bacterial invasion, supporting fluid balance, and controlling nervous manifestations. Broad-spectrum antibiotics, balanced electrolyte solutions, parenteral nutrition, antipyretics, analgesics, and anticonvulsants are used, and good nursing care is essential. No single treatment is specific or uniformly successful. Experimental in vitro work with antiviral agents shows promise, but is not yet commercially available.
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. Dogs with some of the more chronic progressive or vaccine-induced forms of neurologic disease may respond to immunosuppressive therapy with anti-inflammatory or greater dosages of glucocorticoids.
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 2 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 now available and has been shown to be safe and effective. Historically, annual revaccination has been standard because of the breaks in protection that can occur in stressed, diseased, or immunosuppressed dogs, and vaccines have been labeled for annual use. Increasing evidence supports the finding that immunity induced by MLV distemper vaccines lasts 3 yr or longer. 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.
Last full review/revision March 2012 by Kate E. Creevy, DVM, MS, DACVIM