Canine Distemper Overview

By Kate E. Creevy , DVM, MS, DACVIM, Texas A&M University

Last full review/revision Mar 2018 | Content last modified Mar 2018

Canine distemper is a highly contagious, systemic, viral disease of dogs seen worldwide.

Clinically, canine distemper is characterized by:

a diphasic fever

leukopenia

GI and respiratory catarrh, and

frequently, pneumonic and neurologic complications

, , 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.

Etiology and Pathogenesis:

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.

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 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:

localized involuntary muscle twitching (myoclonus, chorea, flexor spasm, hyperkinesia)

convulsions, including salivation and chewing movements of the jaw (chewing-gum fits)

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Other neurologic signs include:

circling

head tilt
nystagmus

paresis to paralysis

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. 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.

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 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:

neuronal degeneration

gliosis

noninflammatory demyelination

perivascular cuffing

nonsuppurative leptomeningitis, and

intranuclear inclusion bodies predominately within glial cells

Diagnosis of Canine Distemper :

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:

leptospirosis

infectious canine hepatitis

Rocky Mountain spotted fever

CookiesIntoxicants 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:

smears of conjunctival, tracheal, vaginal, or other epithelium

the buffy coat of the blood

urine sediment, or

bone marrow aspirates

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.

Treatment of Canine Distemper :

Treatments are symptomatic and supportive, aimed at limiting secondary bacterial invasion, supporting
fluid balance, and

controlling neurologic manifestations.

Treatment includes:

broad-spectrum antibiotics

balanced electrolyte solutions

parenteral nutrition

antipyretics, analgesics, and anticonvulsants, and

good nursing care

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.

Prevention of Canine Distemper :

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

© 2020 Merck Sharp & Dohme Corp., a subsidiary of Merck & Co., Inc., Kenilworth, NJ, USA)

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.

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