Changes

===Clinical Signs===

===Clinical Signs===

Canine distemper is characterised by a biphasic fever, with the first peak 3-6 days post-infection and the second peak several days later and intermittently thereafter. The second peak of pyrexia is usually associated with the onset of other clinical signs. These initially include conjested conjunctiva and nasal mucosa leading to serous ocular and nasal discharges that become mucopurulent. The animal is depressed and anorexic, and vomiting, diarrhoea and pneumonia commonly follow. These gastrointestinal and respiratory signs are often complicated by secondary bacterial infections. Lesions may occur on the retina and optic neuritis can develop. Some strains of CDV cause hyperkeratosis of the footpads and the nose, and retinal lesions and optic neuritis can occur. In neonates, hypoplasia of the tooth enamal is common following infection, causing "distemper rings". Pustular dermatitis may also be seen on the abdomen of infected puppies.

Canine distemper is characterised by a biphasic fever, with the first peak 3-6 days post-infection and the second peak several days later and intermittently thereafter. The second peak of pyrexia is usually associated with the onset of other clinical signs. These initially include conjested conjunctiva and nasal mucosa leading to serous ocular and nasal discharges that become mucopurulent. The animal is depressed and anorexic, and vomiting, diarrhoea and pneumonia commonly follow. These gastrointestinal and respiratory signs are often complicated by secondary bacterial infections. Lesions may occur on the retina and optic neuritis can develop. Some strains of CDV cause hyperkeratosis of the footpads and the nose, and retinal lesions and optic neuritis can occur. In neonates, hypoplasia of the tooth enamal is common following infection, causing "distemper rings". Pustular dermatitis may also be seen on the abdomen of infected puppies.  

Many, but not all, infected dogs develop CNS signs after systemic disease but this is dependent on the strain of the virus. Either the white matter or the grey matter may be affected. Grey matter disease affects the cerebral coretx, brainstem and spinal cord, and may give a non-suppurative meningitis, seizures, stupor, hysteria or ataxia. Dogs with grey matter disease may die within 2-3 weeks, recover, or alterntatively progress to white matter disease. In this, mutlifocal lesions mean that the signs are variable: cerebellovestibular signs are common, as well as spinal cord paresis, ataxia and occasionaly myoclonus. Once white matter disease has developed, some dogs die with a non-inflammatory, demyelinating disease 4-5 weeks after intial systemic infection. Other animals may recover with minimal injury to the CNS but may still suffer neuromuscular tics or "chewing gum" seizures.

Many, but not all, infected dogs develop CNS signs after systemic disease but this is dependent on the strain of the virus. Either the white matter or the grey matter may be affected. Grey matter disease affects the cerebral coretx, brainstem and spinal cord, and may give a non-suppurative meningitis, seizures, stupor, hysteria or ataxia. Dogs with grey matter disease may die within 2-3 weeks, recover, or alterntatively progress to white matter disease. In this, mutlifocal lesions mean that the signs are variable: cerebellovestibular signs are common, as well as spinal cord paresis, ataxia and occasionaly myoclonus. Once white matter disease has developed, some dogs die with a non-inflammatory, demyelinating disease 4-5 weeks after intial systemic infection. Other animals may recover with minimal injury to the CNS but may still suffer neuromuscular tics or "chewing gum" seizures.

Dogs that recover from acute canine distemper infection may develop "old dog encephalitis" years later. This is a result of persistent infection and manifests with several episodes of neurological abnormalities over weeks to months, before the dog ultimately dies.

Although canine distemper is often fatal, in some cases an increased production of virus-neutralising antibodies promotes the recovery of the animal. However, CDV can persist in the uvea, CNS, lymphoid organs and footpads despite elimination from most organs and the blood. This can result in "old dog encephalitis" in dogs that recovered from acute canine distemper years previously. In this, several neurological episodes occur over weeks to months, and end in the death of the dog.

 

Moritz et al., 1998, 2000, 2003). At the acute stage, virus is

found in every secretion and excretion of the body. This

In some cases, an improved immune response especially

an increased production of virus-specific neutralizing

antibodies can promote the recovery of the animal.

However, despite elimination of the virus from several

organs and the peripheral blood, CDV can persist in certain

tissues including uvea, CNS, lymphoid organs and footpads

(Appel, 1970, 1987; Zurbriggen et al., 1995a,b; Greene and

progression of the disease and a moderate immune

response with subtle early clinical signs. Later, as a

disturbances can be observed resulting in the nervous form

 

 

 

    * A laboratory diagnosis may not be feasible. A presumptive diagnosis is frequently made on the basis of clinical signs in a young unvaccinated dog. Nonetheless, the vaccinated status does not assure protection since many cases of distemper have been reported in well vaccinated dogs.

    * A reliable way to diagnose canine distemper is the demonstration of viral infected cells by immunofluorescence. Examination of conjunctival scrapings and blood smears is useful during early stages of the illness, but false negative results are likely to occur as the disease progresses. Tests are accurate when performed on appropriate necropsy tissues.

    * Microscopic lesions of demyelination in the cerebellum and characteristic inclusion bodies in various tissues are diagnostically significant. The inclusions are primarily intranuclear in the brain and intracytoplasmic in other tissues.

 

 

===Laboratory Tests===

===Laboratory Tests===