Definition

• An acute to subacute, contagious, febrile, and often fatal disease with respiratory, urogenital, gastrointestinal, ocular, and CNS manifestations.
• Caused by CDV, a Morbillivirus in the Paramyxoviridae family.
• Affects many different species of the order Carnivora; mortality rate varies greatly among species.

Pathophysiology

• Natural route of infection-airborne and droplet exposure; from the nasal cavity, pharynx, and lungs, macrophages carry the virus to local lymph nodes, where virus replication occurs; within 1 week, viral shedding occurs (mainly in respiratory exudates but also urine) and virtually all lymphatic tissues become infected; spreads via viremia to the surface epithelium of respiratory, gastrointestinal, and urogenital tracts and to the CNS.
• Fever for 1–2 days and lymphopenia may be the only findings during initial period; further disease progression depends on the virus strain and the host's immune response.
• Strong cellular and humoral immune response-host may remain subclinical.
• Weak immune response-subacute infection; host may survive longer.
• Failure of immune response-acute death of host within 2–4 weeks after infection; convulsions and other CNS disturbances frequent causes of death. Viral excretion can occur up to 2–3 months but usually shorter.

Systems Affected

• Multisystemic-all lymphatic tissues; surface epithelium in the respiratory, alimentary, and urogenital tracts; endocrine and exocrine glands.
• Nervous-skin; gray and/or white matter of brain and/or spinal cord in the CNS.

Incidence/Prevalence

• Dogs-restricted to sporadic outbreaks.
• Wildlife (raccoons, skunks, fox, tigers)-fairly common.

Geographic Distribution

Worldwide

Signalment

Signs

• Fever-first peak 3–6 days after infection, may pass unnoticed; second peak several days later (and intermittent thereafter), usually associated with nasal and ocular discharge, depression, and anorexia.
• Gastrointestinal and/or respiratory signs-follow, often exacerbated by secondary bacterial infection.
• CNS-many infected dogs; often, but not always, after systemic disease; depends on the virus strain; either acute gray or white matter disease.
• Gray matter disease: affects cerebral cortex, brainstem, and spinal cord and may cause a non-suppurative meningitis, seizures, stupor, hysteria, and ataxia. Dogs may die in 2–3 weeks; some dogs recover (associated with prompt humoral and cell-mediated immunity), others progress to develop white matter disease.
• White matter disease: variable signs of multifocal disease, commonly cerebellovestibular signs, spinal cord paresis and ataxia, occasionally myoclonus; some dogs die 4–5 weeks after initial infection with non-inflammatory, demyelinating disease; some dogs may recover with minimal CNS injury.
• Optic neuritis and retinal lesions may occur; sometimes infected scleral blood vessels from anterior uveitis.
• Hardening of the footpads (hyperkeratosis) and nose-some virus strains; but relatively uncommon.
• Enamel hypoplasia of the teeth after neonatal infection common.

Causes

• CDV, a Morbillivirus within the Paramyxoviridae family; closely related to measles virus, rinderpest virus of cattle, and phocine (seal) and dolphin distemper viruses.
• Incompletely attenuated vaccines (rare).
• Secondary bacterial infections frequently involve the respiratory and gastrointestinal systems.

Risk Factors

Contact of non-immunized animals with CDV-infected animals (dogs or wild carnivores).

Differential Diagnosis

• Diagnosis usually based on clinical suspicion (typical history in a 3- to 6-month-old unvaccinated puppy showing multifocal signs).
• Kennel cough-can mimic the respiratory disease.
• Enteric signs-differentiate from canine parvovirus and coronavirus infections, parasitism (giardiasis), bacterial infections, gastroenteritis from toxin ingestion, inflammatory bowel disease.
• CNS form-differentiate from autoimmune meningoencephalitis (granulomatous meningoencephalomyelitis, necrotizing encephalitis), protozoal (e.g., toxoplasmosis, neosporosis), fungal (e.g., cryptococcosis), and rickettsial (e.g., ehrlichiosis, Rocky Mountain spotted fever) meningoencephalitis.

CBC/Biochemistry/Urinalysis

Lymphopenia during early infection; intracytoplasmic inclusions in WBCs and RBCs.

Other Laboratory Tests

• Serology-limited value; positive antibody tests do not differentiate between vaccination and exposure to virulent virus; patient may die from acute disease before neutralizing antibody is produced; IgM responses may occur up to 3 months after exposure to virulent virus and for up to 3 weeks after vaccination.
• CDV antibody in CSF-indicative, but not always diagnostic, of distemper encephalitis.

Imaging

• Radiographs-may determine the extent of pneumonia.
• CT and MRI-may or may not disclose lesions. MRI sensitive for visualization of demyelination.

Diagnostic Procedures

• Immunohistochemical detection in haired skin, nasal mucosa, and footpad epithelium.
• Viral antigen or viral inclusions-in buffy coat cells, urine sediment, conjunctival or vaginal imprints (negative results do not rule out the diagnosis).
• RT-PCR-on buffy coat, urine sediment cells, conjunctival swabs and CSF.
• CSF-moderate pleocytosis of mononuclear cells (lymphocytes and macrophages), CDV-specific antibody, interferon, and viral antigen early in disease course.
• Post-mortem diagnosis-histopathology, immunofluorescence and/or immunocytochemistry, virus isolation, and/or RT PCR; preferred tissues from lungs, stomach, urinary bladder, lymph nodes, and brain.

Pathologic Findings

Appropriate Health Care

Inpatients and in isolation, to prevent infection of other dogs. Unlike systemic signs, presenting neurologic signs are usually not reversible.

Nursing Care

• Symptomatic.
• Intravenous fluids-with anorexia and diarrhea.
• Once fever and secondary bacterial infections are controlled, patients usually begin to eat again.
• Clean away ocular discharges.

Activity

Limited

Diet

Depends on the extent of gastrointestinal involvement

Client Education

• Inform client that mortality rate is about 50%.
• Inform client that dogs that appear to recover from early catarrhal signs may later develop fatal CNS signs.

Drug(s) Of Choice

• Antiviral drugs-none known to be effective.
• Broad-spectrum antibiotics-to reduce secondary bacterial infection, because CDV is highly immunosuppressive. Ampicillin, tetracycline, and chloramphenicol are good choices.
• Anticonvulsant therapy-phenobarbital, potassium bromide; to control seizures.

Contraindications

Corticosteroids-use anti-inflammatory doses with caution; may provide short-term control; immunosuppressive doses may enhance viral dissemination.

Precautions

Tetracycline and fluorinated quinolones-best avoided in young and growing animals.

Patient Monitoring

• Monitor for CNS signs, because seizures often follow.
• Monitor for signs of pneumonia or dehydration from diarrhea in the acute phase of the disease.

Prevention/Avoidance

• Vaccination is key.
• Isolate puppies to prevent infection from wildlife (e.g., raccoons, foxes, skunks) or from CDV-infected dogs.
• Recovered dogs are not carriers.

Possible Complications

Possibility of occurrence of CNS signs for 2–3 months after catarrhal signs have subsided.

Expected Course and Prognosis

• Depends on the strain and the individual host response-subclinical, acute, subacute, fatal, or nonfatal infection.
• Mild CNS signs-patient may recover; myoclonus may continue for several months or indefinitely.
• Death-2 weeks to 3 months after infection; mortality rate approximately 50%.
• Euthanasia-owner may elect if or when neurologic signs develop; indicated when uncontrollable seizures occur.
• Fully recovered dogs do not shed CDV.

Associated Conditions

• Persistent or latent Toxoplasma gondii infections-reactivated because of the immunosuppressive state.
• Respiratory infections with Bordetella bronchiseptica (a major cause of kennel cough).

Age-Related Factors

• Young puppies-more susceptible; mortality rate is higher.
• Non-immunized old dogs-highly susceptible to infection and disease.

Zoonotic Potential

• Possible that humans may become subclinically infected with CDV; immunization against measles virus also protects against CDV infection.
• Once speculated that CDV triggers MS but several studies have refuted this proposition.

Pregnancy/Fertility/Breeding

In utero infection of fetuses-occurs in antibody-negative bitches; rare; may lead to abortion or to persistent infection; infected neonates may develop fatal disease by 4–6 weeks of age.

Synonyms

• Canine distemper
• Hard pad disease
• Hundestaupe
• Maladie de Carré

See Also

Myoclonus (although not unique to CDV)

Abbreviations

• CDV = canine distemper virus
• CNS = central nervous system
• CSF = cerebrospinal fluid
• CT = computed tomography
• MLV-CD = modified live virus of canine distemper
• MRI = magnetic resonance imaging
• MS = multiple sclerosis
• RT-PCR = reverse transcriptase polymerase chain reaction

Internet Resources

http://www.ivis.org/advances/Vite/braund27/chapter_frm.asp?LA=1#Distemper_Encephalomyelitis.

Client Education Handout Available Online