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Also known as: '''''Canine Distemper — CDV'''''

|Also known as:

|'''Canine Distemper''' <BR> '''CDV'''

==Description==

==Description==

Canine distemper is a contagious, febrile disease of canids and other carnivores caused by Canine Distemper Virus. Canine distemper virus is a member of the Paramyxoviridae family and the morbillivirus genus. The Paramyxoviridae have a helical nucleocapsid surrounded by an envelope which possesses spiked glycoproteins responsible for haemagglutinin, neuraminidase and haemolytic activities. The genome of the Paramyxoviridae is single-stranded, negative-sense RNA which is used as a template for the production of messenger (positive-sense) RNA and further genomic material. Paramyxoviridae are sensitive to heat, dessication and most disinfectants, and so are not resistant in the environment. The Paramyxovididae family is divided to two sub-families, the Paramyxovirinae and the Pneumovirinae. It is within the Paramyxovirinae sub-family that morbilliviruses fall, along with respiroviruses, henipaviruses, rubulaviruses and avulaviruses. As well as canine distemper virus (CDV), the morbilliviruses include rinderpest, peste de petits ruminants, measles, phocine distemper and dolphin distemper.

Canine distemper is a contagious, febrile disease of canids and other carnivores caused by Canine Distemper Virus. Canine distemper virus is a member of the [[:Category:Paramyxoviridae|Paramyxoviridae]] family and the [[:Category:Morbilliviruses|morbillivirus]] genus.  

      

      

Canine distemper virus is spread by direct and indirect contact via ingestion or inhalation of aerosolised droplets. Initial infection of the nasal cavity, pharynx and lungs is followed by a macrophage-associated viraemia to local lymph nodes where the virus replicates. Within one week, all lymphoid tissue is infected and a secondary viraemia distributes the virus to the surface epithelium of the respiratory, gastrointestinal and urogenital tracts, and the grey and white matter of the CNS. In early infection, a fever of 1-2 days duration and lymphopenia (due to replication in lymphoid tissue) may be the only clinical findings, and further signs depend on both the virus strain and the immune response mounted. In the event of a strong humoral and cellular response, disease may remain subclinicals, and if a weak immune response is mounted infection is generally subacute. If the immune response fails, acute death occurs 2-4 weeks post-infection, commonly due to convulsions or other CNS disturbances.

Canine distemper virus is shed in all excretions and secretions, and is spread by direct and indirect contact via ingestion or inhalation of aerosolised droplets. Initial infection of the nasal cavity, pharynx and lungs is followed by a macrophage-associated viraemia to local lymph nodes where the virus replicates. Within one week, all lymphoid tissue is infected, causing [[lymphopenia]]. A second viraemic stage then distributes the virus to the surface epithelium of the respiratory, gastrointestinal and urogenital tracts, endocrine tissue and the grey and white matter of the CNS. A biphasic pyrexia is typical of distemper infection: the first fever occurs 3-6 days post-infection and is associated with lymphopenia, and the second peak coincides with widespread viraemia. Further signs depend on both the virus strain and the immune response mounted. In the event of a strong humoral and cellular response, disease may remain subclinical, and if a weak immune response is mounted infection is generally subacute. If the immune response fails, acute disease and potentially death ensues. When clinical disease manifests, this is initially characterised by lethargy, dehydration, anorexia, and weight loss followed by more specific signs depending on the principally affected organ.

==Signalment==

==Signalment==

==Diagnosis==

==Diagnosis==

 

*'''Immunocytochemistry''' of inclusion bodies

Although a presumptive diagnosis is frequently made on the basis of clinical signs in a young unvaccinated dog, there are several methods of investigating and confirming canine distemper.

**Intracytoplasmic inclusions may be found in most affected tissues

**Inclusions persist longest in the brain (may be intranuclear) and the alveolar macrophages

===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 congested 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, as CDV is highly immunosuppressive. 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 unerupted tooth enamel is common following infection, causing "distemper rings". Pustular dermatitis may also be seen on the abdomen of infected puppies. In pregnant animals, transplacental infection can result in abortions, stillbirths, or the birth of persistent excretors of virus, depending on the stage of gestation.

dehydration, anorexia, and weight loss followed by a more

 

Many infected dogs develop CNS signs after the initial 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 cortex, 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 progress to white matter disease. In this, multifocal lesions mean that the signs are variable: cerebellovestibular signs are common, as well as paresis, ataxia and myoclonus. Once white matter disease has developed, some dogs die with a non-inflammatory, demyelinating disease 4-5 weeks after initial systemic infection. Other animals may recover with minimal injury to the CNS but may suffer neuromuscular tics or "chewing gum" seizures for life.

affected organ. Development of a biphasic fever

can be observed 3–6 days pi (Krakowka et al., 1980) and

coincide with the first viremia that results in a generalized

infection of all lymphoid tissues including spleen, thymus,

tissues(MALT) and macrophages in the lamina propria of the

by spread of cell free virus as well as leukocyte and

thrombocyte associated infectious pathogens. The second

viremia follows several days later, frequently associated

with high fever, and results in infection of parenchymal and

Møller et al., 1989; Okita et al., 1997). Thus, CDV can be

found in cells of the respiratory, gastrointestinal and urinary

According to clinical features a catarrhal and nervous

form, and a chronic nervous manifestation can be distinguished.

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

found in every secretion and excretion of the body. This

including onset of a cutaneous rash, serous nasal and ocular

discharge, conjunctivitis and anorexia, followed by gastrointestinal

and respiratory signs, which are often complicated

by secondary bacterial infections and neurological

disturbances (Krakowka et al., 1985). Nervous signs are

diverse and progressive (Parker, 1978; Greene and Appel,

1998) and include myoclonus, nystagmus, ataxia, postural

reaction deficits and tetraparesis or plegia (Koutinas et al.,

2002; Vandevelde and Zurbriggen, 2005; Amude et al.,

2007).

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

Appel, 1998; Gro¨ne et al., 2003a; Schobesberger et al.,

2005). Moreover, some infected animals display a delayed

progression of the disease and a moderate immune

response with subtle early clinical signs. Later, as a

consequence of viral persistence in the CNS, overt CNS

but some recover, and may display lifelong residual signs

such as a persistent myoclonus.

Canine distemper is usually an acute, febrile disease, especially of young dogs, although older unprotected dogs are also susceptible. The first clinical manifestation of distemper is a diphasic febrile response. The first response may be overlooked, but the second generally occurs 2 - 3 days later in conjunction with other clinical signs, which initially include congested conjunctiva and nasal mucosa with subsequent serous to mucopurulent discharges. Pneumonia, depression, anorexia, vomiting, and diarrhea usually follow. Neurologic disturbances, such as neuromuscular tics, "chewing gum" seizures, and paresis are frequent sequelae in dogs that recover from acute disease.

Canine distemper is often fatal, but an increased production of virus-neutralising antibodies can promote 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 usually culminate in the death of the dog.

Hyperkeratosis of the nose and digital pads ("hard pad") develops in some cases. Pustular dermatitis may be seen affecting the abdomen of puppies.

Gross necropsy lesions characteristic of pneumonia and enteritis may be present. Thymic atrophy may be noted in young dogs. Microscopic lesions are widespread in visceral organs and the brain and characteristic viral inclusion bodies are commonly found in brain, lung, stomach, and urinary bladder.

Dogs that recover may years later develop what has been called "old dog encephalitis" as a result of a persistent infection. This manifestation is usually recurrent, with a few to several episodes of neurological manifestations within weeks to months that usually end with death of the dog.

===Laboratory Tests===

    * 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.

With the exception of lymphopenia during early infection, routine haematology and biochemistry do not show any typical changes. Serology is also of limited value for several reasons. Firstly, a patient may die before an antibody response is mounted; secondly, a positive antibody titre does not discriminate between infected and vaccinated animals; and thirdly, IgM may remain high for up to three weeks following vaccination and for three months after infection. Detection of canine distemper virus antibody in the cerebrospinal fluid is, however, indicative of distemper encephalitis.

**Eruptions on the skin including hyperkeratosis of the nose and pads (hardpad)

**[[PNS Repsonses to Injury - Pathology#Segmental Demyelination|Demyelination]] (especially in cerebellum) -> incoordination or muscle tremors -> paralysis and coma or convulsions -> death

**Secondary pyogenic infections associated with immunosuppression and damage to epithelia

**The severity of the disease may vary; if enough neutralising antibody develops in the early stages, the virus maybe kept restricted largely to the lymph nodes

*Involvement of central nervous system generally results in death

*Can contribute to [[Canine Infectious Tracheobronchitis|Infectious Canine Tracheitis]]

There are a number of tests available to confirm the diagnosis of canine distemper. Immunohistochemistry can be used to detect viral antigen in samples of skin, nasal mucosa or footpad epithelium, and viral antigen or inclusions may be demonstrated in buffy coat cells, urine sediment and conjunctival or vaginal imprints. However, negative results do not rule out a diagnosis of distemper. RT-PCR can also be performed on buffy coat, urine sediment, conjuncival swabs or cerebrospinal fluid. A retrospective diagnosis can be made post-mortem on the basis of histopathology, immunofluorescence or immunohistochemistry, virus isolation or RT-PCR. The preferred tissues for these techniques are lung, stomach, urinary bladder, lymph nodes and brain.

*May be involved in [[Pancreatitis, Chronic Interstitial|chronic interstitial pancreatitis]]

*May cause [[Bones Developmental - Pathology#Retention of elongated primary trabeculae|growth retardation lattice]]

*May also trigger latent [[Toxoplasma|Toxoplasmosis]] due to suppressing effect on lymphoid tissue

===Diagnostic Imaging===

===Diagnostic Imaging===

===Pathology===

===Pathology===

*[[Nasal Cavity Inflammatory - Pathology#Infectious causes of rhinitis|Rhinitis]]

 

*Although many organs can be affected by CDV, a relatively constant feature is the respiratory signs which occur in varying severity

On post-mortem examination, the thymus is often found to be greatly reduced in size and gelatinous in young dogs. There is patchy consolidation of the lungs due to interstitial pneumonia, and signs of catarrhal enteritis may be present. Mucopurlent discharges are commonly seen from the eyes and nose and bronchopneumonia is sometimes present. Skin pustules and hyperkeratosis of the footpads and nose are seen occasionally.

*A syndrome of catharral oculonasal discharge, [[Nasopharynx Inflammatory - Pathology#Infectious causes of pharyngitis|pharyngitis]] and [[Bronchi and Bronchioles Inflammatory - Pathology#Infectious causes of bronchitis or bronchiolitis|bronchitis]] is relatively common in the initial stages

 

*Since one of the primary sites of action of this virus is lymphoid tissue, the resultant immunosuppression -> predisposition to secondary bacterial infection

Microscopically, eosinophilic intra-cytoplasmic inclusion bodies are often found in the bronchial, gastric and urinary epithelium. They may also be seen in leukocytes and lymphoid tissue. In the CNS, inclusion bodies are frequently intra-nuclear in both neurons and glial cells. Demyelination may also be seen. When inclusion bodies are not evident, immunofluorescence or immunohistochemistry may be used to detect canine distemper virus antigen. Virus isolation or RT-PCR can also be carried out post-mortem using lung, stomach, urinary bladder, lymph nodes or brain sample.

*May cause [[Lungs Inflammatory - Pathology#Interstitial pneumonia|interstitial pneumonia]] where [[Degenerations and Infiltrations - Pathology#Cellular Inclusions|inclusions]] are found within alveolar macrophages

**Necrosis of pneumocytes, necrotising bronchiolitis, alveolar oedema, thickening of alveolar walls and type II pneumocyte hyperplasia

==Treatment==

==Treatment==

*Live attenuated virus vaccines given at 10 and 12 weeks of age

Dogs suffering distemper should be treated in isolation with barrier nursing to prevent spread to other dogs. Treatment is supportive, including intravenous fluid therapy to correct the deficit cause by vomiting and diarrhoea and antiobitics to reduce secondary infections. Anticonvulsants such as phenobarbital and potassium bromide may be necessary to control seizures. Although corticosteroids may alleviate clinical signs in the short term, they should be used with caution as they augment the immunosuppression caused by CDV and may enhance viral dissemination. Animals should be rested and fed a diet appropriate to the severity of their gastrointestinal signs.

**Some now given at 7 and 10 weeks to allow socialisation

*Live attenuated vaccines may kill some wildlife therefore '''Iscom vaccine''' is used in seal sanctuaries

    * Modified live vaccines are administered to dogs between six and 16 weeks of age, usually at 2 - 3 week intervals. This multiple dose regimen is necessary because the maternal antibody in puppies greatly hampers the efficacy of vaccination by neutralizing viral antigen.

    * Dogs older than three months with unknown immune status should be vaccinated twice, 2 - 4 weeks apart, all dogs should receive periodic (one to two years-interval ) boosters.

|literature search = [http://www.cabdirect.org/search.html?q=%28%28title%3A%28distemper%29+AND+%28diagnosis%29%29%29+AND+%28%28title%3A%28distemper%29+AND+%28treatment%29%29%29 Distemper diagnosis and treatment]

==Links==

==Links==

==References==

==References==

#Carter, GR and Wise, DJ (2005) '''A Concise Review of Veterinary Virology''', ''International Veterinary Information Service''.

#Carter, GR and Wise, DJ (2005) '''A Concise Review of Veterinary Virology''', ''International Veterinary Information Service''.

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[[Category:Respiratory Viral Infections]]

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