CANINE DISTEMPER

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), most Procyonidae (eg, raccoon, coatimundi), and some Viveridae (binturong).

Etiology and Pathogenesis:

Canine distemper is caused by a paramyxovirus closely related to the viruses of measles and rinderpest. The enveloped virus is sensitive to lipid solvents and most disinfectants and 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 spread of virus to various tissues is moderated by the level of specific humoral immunity in the host during the viremic period.

Clinical Findings:

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, and anorexia. GI and respiratory signs may follow and are usually complicated by secondary bacterial infections. An acute encephalomyelitis may occur in association with or following the systemic disease, or in the absence of systemic manifestations. Hyperkeratosis of the footpads (“hardpad” disease) and epithelium of the nasal plane may be seen. Neurologic signs are frequently seen in those dogs with hyperkeratosis. CNS signs include the following: 1) localized involuntary twitching of a muscle or group of muscles (myoclonus, chorea, flexor spasm, hyperkinesia), such as in the leg or facial muscles; 2) paresis or paralysis, often most noticeable in the hindlimbs as ataxia, followed by tetraparesis and tetraparalysis; and 3) convulsions characterized by salivation and often chewing movements of the jaw (“chewing-gum fits”). The seizures become more frequent and severe, and the dog may fall on its side and paddle its legs; involuntary urination and defecation (grand mal seizure, epileptiform convulsion) often occur. A dog may exhibit any or all of these neurologic signs in addition to others in the course of the disease. Infection may be mild and inapparent or lead to severe disease manifest by 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. 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 adult dogs without a history of signs related to systemic canine distemper. The development of neurologic signs is often more progressive. Although canine distemper antigen has been detected in the brain of some dogs with ODE by fluorescent antibody staining, dogs with ODE are not infectious and replication-competent virus has not been isolated. Genetic methods may be needed to document infection. The disease is caused by an inflammatory reaction associated with persistent canine distemper virus infection in the CNS. Lesions: 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 may also be present. 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, demyelination, perivascular cuffing, nonsuppurative leptomeningitis, and intranuclear inclusion bodies predominately within glial cells.

Diagnosis:

Distemper should be considered in the diagnosis of any febrile condition in puppies with multisystemic manifestations. While the typical clinical case is not difficult to diagnose, the characteristic signs sometimes fail to appear until late in the disease. The clinical picture may be modified by concurrent toxoplasmosis, neosporosis, coccidiosis, parasitoses, 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. At necropsy, diagnosis is usually confirmed by histologic lesions or immunofluorescent assay for viral antigen in tissues, or both. In dogs with multisystemic signs, conjunctival, tracheal, vaginal, or other epithelium, or the buffy coat of the blood can be examined by immunofluorescent assay. These samples are usually negative when the dog is showing only neurologic manifestations or when circulating antibody is present (or both). The diagnosis can then be made by serologic demonstration of virus-specific IgM or an increased ratio of CSF to serum virus-specific IgG.

Treatment:

Treatments are directed at limiting secondary bacterial invasion, supporting fluid balance, and controlling nervous manifestations. Antibiotics, balanced electrolyte solutions, parenteral nutrition, dietary supplements, antipyretics, nasal preparations, analgesics, and anticonvulsants are used. No single treatment is specific or uniformly successful. Dogs may recover completely from systemic manifestations, but good nursing care is essential. Despite intensive care, some dogs do not make a satisfactory recovery. Unfortunately, treatment for acute neurologic manifestations of distemper is unsuccessful. If the neurologic signs are progressive or severe, the owner should be appropriately advised. 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.

Prevention:

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 2- to 4-wk intervals until 16 wk old. Measles virus induces immunity to canine distemper virus in the presence of relatively greater levels of maternal distemper antibody. An MLV measles vaccine and a combination of MLV measles and MLV canine distemper vaccine are available. Measles vaccines must be administered IM. Pups 6-7 wk old should receive the measles or combination vaccine and 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 can produce postvaccinal illness in some immunosuppressed dogs. A recombinant canarypox vector vaccine expressing distemper virus proteins is available. Annual revaccination has been suggested because of the breaks in neurologic distemper that can occur in stressed, diseased, or immunosuppressed dogs. Longer than yearly intervals of administration have been suggested with MLV vaccines; however, this should be tempered with the prevalence of the disease and other potential risk factors.