Canine Distemper (CD)

Canine Distemper (CD) also known as Carre’s disease, Hard-pad disease and Canine influenza.

Canine Distemper (CD) is a highly contagious, systemic, viral disease of dogs and other carnivores, clinically characterized by diphasic fever, leukopenia, GI and respiratory catarrh, and frequently causes pneumonic and neurologic complications.

Etiology

Canine Distemper (CD) is caused by genus Morbilivirus, family Paramyxoviridae, a single stranded enveloped RNA virus called canine distemper virus (CDV).
This virus is antigenically related to rinderpest, peste des petits ruminants and measles viruses.
There is only one serotype causing this disease in canines, which contains three strains, namely A, B and C. The strains A and B were more virulent than C strain. All these strains vary in their pathogenicity and tissue trophism.
It is relatively fragile in an environment.
The virus is sensitive to lipid solvents, such as ether, phenols and quaternary ammonium compounds.

Epidemiology

World wide in distribution.
Canine distemper virus causes higher morbidity and mortality than any other virus that infects dogs.
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.

Host affected

The disease is seen in dog, fox, wolf, raccoon, ferret, mink, skunk, wolverine, marten, badger, otter binturong, palm civet, red panda, bear and large felines.
The disease is more common in dogs at 3-6 months of age.
The incidence of disease is gradually decline as age increases.

Source of infection

Some infected dogs may shed virus from secretion for several months.

Transmission

Inhalation of aerosol droplets secreted from an infected animal.
Direct contact with an infected animal.

Pathogenesis

Virus initially replicates in the lymphatic tissue (tonsil and bronchial lymph node) 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 manifestation

Incubation period is one week but may extend to 4 weeks or more
The severity and duration of illness depends on virulence of virus, age and immune status of infected animal.
Fever is biphasic (initial elevation of temperature may not be noticed). During the second period of pyrexia, oculonasal discharge, pharyngitis and tonsilar enlargement are noticed.
The second rise of temperature is accompanied by rhinitis, conjunctivitis, gastroenteritis and bronchopneumonia.
Coughing, vomition and diarrhoea are consequence of secondary infections.
A skin rash or pustules may be present on the abdomen.
Some affected dog have hyperkeratosis of nose and foot pads so, it is called as hard pad disease.
Neurological signs include paresis, myoclonus and seizures .
Convulsions may begin as petit mal ‘chewing gum fits’ where the animal may salivates and makes chewing movements with the jaws before convulsions, after that convulsions become more frequent and severe resulting in grand mal epileptiform of seizures.
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.
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.
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.

Clinical signs of canine distemper manifested as five different forms:

Pulmonary form

A coryza like syndrome is characterized by oculonasal discharge, pharyngitis and bronchitis are seen.
Bronchopneumonia is the common feature.
The pulmonary form is more prevalent than digestive form.
The pneumonic condition may persist for a long period.

Gastrointestinal form

This form is characterized by loss of appetite, vomition and abdominal pain.
The faeces is semisolid or loose and foul smelling.
The diarrheic faeces may contain blood.
The hemorrhagic enteritis is commonly seen in young pup.

Ocular form

This is manifested as swollen eyelids, conjunctivitis and purulent discharge from the eyes.
Ulceration of the cornea and transient keratitis may also be observed.

*Keratitis in Canine Distemper (CD) in a Dog*

Nervous form

The affection of the nerve cells lead to neurological disorders.
These are characterized by restlessness, excitement, chewing movements, excessive salivation and convulsion.
The nervous manifestations are noted when the animal can resist the primary infection and suffer from secondary complication.
Lymphopenia is the distinct feature of distemper but this may not occur in dogs with delayed encephalitis.
A condition known as “old dog encephalitis” characterized by mental disorders, motor deterioration and death as clinical features.
The nervous form may be characterized by jerky movements of group of muscles.

The muscular spasms may be observed in the lips, cheeks, jaws, head and neck or limb muscles.

Cutaneous form

There is appearance of rash, vesicles and pustules on the body of the affected dog especially on the ventral aspect of the abdomen and on the inner parts of the thigh.
In some cases the skin of the foot pads and nose may become hard due to hyperkeratitis and the condition is ascribed as hard pad disease.

Clinical pathology

Lymphopenia.
Viral inclusion bodies in circulating leukocytes during very early course of the disease.
Thoracic radiographs may reveal an interstitial pattern typical viral pneumonia.

Necropsy Finding

Thymic atrophy.
Histopathology: interstial pneumonia, intracytoplasmic and intranuclear inclusion bodies in respiratory, urinary and GI epithelium.
Non inflammatory demyelination, nonsuppurative leptomeningitis, and intranuclear inclusion bodies predominately within glial cells.

Sample collection

Smears from conjunctival, tracheal, vaginal, or other epithelium, buffy coat, urine sediments and bone marrow aspirates.

Diagnosis

Based on clinical signs and necropsy findings.
Immunofluorescent assay or reverse transcriptase (RT- PCR) are commonly used for diagnosis of canine distemper virus.
Commercially available quantitative RT-PCR and two-step RT-PCR is commonly used to distinguish vaccine strains from emerging wild-type strains.
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.
ELISA can be performed to detect antibodies in serum and CSF. The antibody titre is relatively higher in CSF compared to blood. It is useful to differentiate vaccinated from infected animal.

Differential diagnosis

Leptospirosis
Infectious canine hepatitis
Rocky mountain spotted fever
Organophosphorus and lead poisoning

Treatment

Treatments are symptomatic and supportive, aimed at limiting secondary bacterial invasion, supporting fluid balance, and controlling neurologic 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 these agents have not yet been widely used.
Some dogs with chronic progressive or vaccine-induced forms of neurologic disease may respond to immunosuppressive therapy with anti-inflammatory drugs or greater dosages of glucocorticoids.

Antibiotics

Ampicillin, Amoxicillin 20 mg/kg b.wt TID for 7 days.
Doxycycline 5-10 mg/kg b.wt BID for 7 days.
Chloramphenicol 40-50 mg/kg b.wt TID for 7 days.
Cephapirin 10-30mg/kg b.wt I/M or I/V TID for 3-5 days.

Anticonvulsive agents

Phenobarbital 10-20mg/Kg IV once then followed by 2-8 mg/Kg b.wt orally.
Seizures are best managed with parenteral diazepam 0.5-2.0 mg/Kg rectally or slow IV for status epilepticus.

Anti-inflammatory agents

For CNS edema- Dexamethasone 1-2 mg/Kg b.wt.
For optic neuritis- 0.1 mg/Kg b.wt for 3-5 days.

Other supportive therapy

Parenteral antiemetics.
Lacated ringer’s solution IV.
B-vitamins.
Ascorbic acid/Vitamin A 20000 IU for 5 days.

Prevention

Pups are vaccinated with MLV vaccine at 6 wk old and at 3- to 4-wk intervals until 16 wk old and then annual revaccination every year.
Onderstepoort and Rockborn strain is commonly used as vaccine strain.
The rockborn strain causes greater chance of virus induced illness than onderstepoort.
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.
Disinfection of a CDV contaminated environment can be accomplished with commonly used disinfectants because the enveloped virus destroyed outside the host.
Measurement of serum neutralizing antibody titer is more accurate for withstanding the infection after vaccination.
Serum neutralizing antibody titer equal to or greater than 100 is protective when the dog received maternal antibody.
Serum neutralizing antibody titer 20 is considered protective when measuring vaccination response (when dog not received maternal antibody through milk).