| Canine
and feline distemper are diseases affecting many wild
and domestic carnivores. Although both these diseases can cause acute
illness and death, canine and feline distemper should not be confused, as
they are caused by two distinctly different viral agents.
The
following chart indicates the animals which are susceptible to infection by
canine and feline distemper.
|
Family |
Canine
Distemper |
Feline
Distemper |
|
Canidae
wolf, coyote, fox, domestic dog |
yes |
no |
|
Felidae
bobcat, lynx, domestic cat |
no |
yes |
|
Procyonidae
raccoon |
yes |
yes |
|
Mustelidae
ferret, mink, weasel, martin, fisher,
otter, badger, skunk, wolverine |
yes |
yes |
Description
Canine
distemper is a highly contagious disease of carnivores caused by a
paramyxovirus. The virus is widespread and mortality in juveniles is higher
than in adults. The canine distemper virus is very resistant to cold and
the majority of distemper cases in domestic dogs are seen in the fall and
winter. In wild animals, since the juveniles are more susceptible to
infection, the majority of cases are seen in the spring and summer, but
cases are observed year round. |
|
Transmission
Transmission
occurs via an aerosol-droplet route, direct contact, or possibly by contact
with contaminated objects. It is uncertain whether carrier or unapparent
infections exist. The virus is shed in the faeces and urine of infected
individuals and some evidence exists for transplacental transmission. The
usual route of infection is through the upper respiratory tract, following
inhalation of infective virus. Occasionally infection occurs from ingestion
of infective material. Following entry into the upper respiratory tract,
the virus is spread to the tonsils and lymph nodes, where viral replication
occurs. The virus then enters the blood stream where it is transported to
epithelial cells throughout the body, including the intestinal and
respiratory tract.
Clinical
Signs and Pathology
Typical
signs of canine distemper seen in the domestic dog include respiratory and
intestinal problems such as coughing, diarrhoea, vomiting, nasal and ocular
discharge, anorexia, and hyperkeratosis of the nasal planum and foot pads.
Central nervous system signs may follow the above clinical signs. In wild
carnivores, signs of abnormal behaviour and apparent lack of fear,
suggestive of rabies, may be the only signs grossly visible. Often the
animals are presented with a purulent conjunctivitis and nasal discharge
and the eyelids may be adhered together with crusty exudate. Neurological
disturbances are often seen such as aggressiveness, disorientation, lack of
alertness, convulsive movements of the head and paws, and aimless
wandering. There may be evidence of diarrhoea, laboured breathing and an
unkempt appearance to the fur. Due to the diarrhoea and vomiting, the
animal may be dehydrated and exhibit excessive thirst. Weakness and
emaciation have been associated with canine distemper, but often animals
will be acutely affected and be presented in good nutritional condition.
The
pathological lesions of canine distemper include pulmonary congestion and
consolidation leading to focal pneumonitis. Eosinophilic rounded or ovoid
bodies with refractile particles are found in the epithelial cells of skin,
bronchi, intestinal tract, urinary tract, bile duct, salivary glands,
adrenal glands, central nervous system, lymph nodes and spleen. At the time
of necropsy, an enlarged spleen is usually seen.
Diagnosis
Presumptive
diagnosis is based on clinical signs, the demonstration of inclusion bodies
in neutrophils on blood smear and inclusion bodies in conjunctival smears.
Definitive diagnosis is based on laboratory analysis of affected tissues by
fluorescent antibody techniques.
In
wild carnivores, the presenting signs are often neurological and the
disease must be differentiated from rabies and other encephalitides. Other
diseases which may mimic distemper include tularaemia, listeriosis,
Chastek's paralysis (in captive mink and fox), histoplasmosis (raccoons)
and poisonings.
Treatment
and Control
No
treatment other than supportive care exists for canine distemper. Control
of canine distemper outbreaks includes the removal of carcasses of animals
which have died from the disease, vaccination of susceptible domestic
species to decrease the number of susceptible hosts, and a reduction in
wildlife populations which also reduces the number of potential hosts. The
virus is inactivated by heat, formalin, and Roccal R.
Significance In
Michigan, USA die-offs of raccoons due to canine distemper occur yearly. The
impact of this disease on other wildlife populations is not known at this
time. Unvaccinated domestic dogs are fully susceptible to the canine
distemper virus, therefore, annual vaccination is recommended.
Due to the similarity of some of the clinical
signs of canine distemper and rabies, affected animals should be handled
with caution until a diagnosis is confirmed. Canine distemper is of no
public health significance to humans. |
|
CANINE DISTEMPER
Distemper is caused by a Morbillivirus that affects carnivores and certain Felidae. The disease is characterized by a biphasic temperature reaction, lymphopaenia, generalised catarrhal inflammation, and neurological complications. Canine distemper virus is an immunosuppressive virus that affects both T and B cell function.
Pathogenesis
Aerosol droplets attach to epithelial cells of the upper respiratory tract. Within 24 hours the virus multiplies in tissue macrophages and spreads via local lymphatics to tonsils and bronchial lymph nodes. From here the virus spreads to bone marrow, thymus and spleen. Within 4-6 days virus multiplication occurs within lymphoid follicles in the spleen, lamina propria of the stomach and small intestine, mesenteric lymph nodes and Kupffer cells. This stage corresponds with the initial fever and lymphopaenia. 8 to 14 days later spread to epithelial and CNS tissues occurs through infected lymphocytes and macrophages. This happens in dogs with insufficient cell mediated immunity and humoral immune response.
Virus, either free or lymphocyte associated, may enter the CNS by entering into mononuclear cells in the meninges, choroid plexus, epithelial cells of the fourth ventricle and ependymal cells lining the ventricular system. From these sites virus may enter the CSF from where it spreads to the cerebral cortex, optic tracts and nerves, cerebral peduncles, and spinal cord. The type of lesion produced and the course of infection within the CNS depends on the age and immunocompetence of the host, as well as the neurotropic and immunosuppressive properties of the virus.
Young dogs can develop acute (non-inflammatory) demyelinating encephalomyelitis. Chronic encephalitis can either be a polioencephalomalacia or a diffuse sclerosing panencephalitis ("Old dog encephalitis"). The pathogenesis of this appears to be based on an immunological reaction against the basic protein in myelin that is triggered by the distemper virus. The lesion is characterised by perivascular lymphocytic/plasmacytic cuffing of vessels at the junction of the grey and white matter. There is a uniform, diffuse sclerosis of the cerebral white matter, as well as demyelination. 'Old-dog encephalitis' is similar to subacute sclerosing panencephalitis caused by measles infection in children.
Chronic neurological disease with distemper is associated with viral persistence. It has been proposed that defective interfering viral particles may play a role in the pathogenesis. Viral infection within neurons is non-productive as nucleocapsids are produced but not released from the surface of the cell. However, under the influence of a triggering mechanism complete virions can again be produced.
Clinical signs
The clinical signs of distemper are varied and include:
- Sub-clinical to severe multi-systemic signs that can involve the respiratory and gastro-intestinal systems.
- Neurological signs.
- Myoclonus.
- Fading puppy syndrome.
- Enamel hypoplasia.
- Ophthalmological lesions.
Antemortal diagnosis
Clinical signs especially with a poor/no vaccination history are indicative of the disease. The diagnosis can occasionally be made by finding distemper inclusions in lymphocytes, neutrophils and erythrocytes on peripheral blood smear.
Direct immunofluorescence for presence of antigen from smears of conjunctival, tonsillar and genital epithelium, and buffy coat. Viral inclusions can also be demonstrated by immunoperoxidase staining of skin biopsies.
Serological tests such as serum virus neutralization, ELISA, and IFA. The presence of IgM antibodies in the serum is indicative of either acute infection or recent vaccination. IgM antibodies appear in the sera approximately 7 days following exposure to vaccine virus or natural infection and decline to undetectable levels after approximately 4 weeks. IgG titres begin to decline after five to six months. In the absence of re-exposure, IgG titres can drop to undetectable levels by 14-18 months.
IgG in the CSF can be regarded as a sensitive and specific indicator of distemper encephalitis. IgG is produced locally in the CNS and will not be present in vaccinated dogs. Contamination of the CSF tap with whole blood can be a problem, but simultaneous measurement of parvovirus antibody titres in the CSF and blood can help rule this out. Other typical CSF changes are raised protein and lymphocytic pleocytosis.
Therapy
There is no specific therapy and thus therapy is dependent on good nursing care, antibiotics for secondary infections, maintenance of fluid and electrolyte balance, nutritional support, and seizure control.
Remo Lobetti, BVSc, MMedVet (Med), DECVIM (Internal Medicine)
Internist, Bryanston Veterinary Hospital, Professor, Department of Companion Animal Clinical Studies, Faculty of Veterinary Science, University of Pretoria
Onderstepoort, Bryanston, South Africa
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