Difference between revisions of "Canine Distemper Virus"
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− | {{ | + | {{unfinished}} |
− | Also known as: ''''' | + | |
+ | {|cellpadding="10" cellspacing="0" border="1" | ||
+ | |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 | + | 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 virus | + | 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 later to 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. |
==Signalment== | ==Signalment== | ||
− | + | As well as the domestic dog, canine distemper virus infection has been found in many species, as detailed in the table below. | |
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− | {|cellpadding="10" cellspacing="0" border="1" width="{{{width| | + | {|cellpadding="10" cellspacing="0" border="1" width="{{{width|50%}}}" align="center" |
| <center><u>'''Canidae'''</u> </center> | | <center><u>'''Canidae'''</u> </center> | ||
| <center><u>'''Procyonidae'''</u> </center> | | <center><u>'''Procyonidae'''</u> </center> | ||
Line 21: | Line 24: | ||
| <center> Ferret <BR> Marten <BR> Mink <BR> Otter <BR> Sable <BR> Wolverine <BR> Badger <BR> Skunk </center> | | <center> Ferret <BR> Marten <BR> Mink <BR> Otter <BR> Sable <BR> Wolverine <BR> Badger <BR> Skunk </center> | ||
|} | |} | ||
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+ | *Dogs, ferrets, seals, lions, mink | ||
+ | *Has been a major pathogen of dogs prior to vaccination | ||
==Diagnosis== | ==Diagnosis== | ||
− | + | *May present as series of infections | |
− | + | *'''Immunocytochemistry''' of inclusion bodies | |
− | + | **Intracytoplasmic inclusions may be found in most affected tissues | |
+ | **Inclusions persist longest in the brain (may be intranuclear) and the alveolar macrophages | ||
+ | **Sections of fixed bronchial tissue, lung, macrophages, bladder may be used or nasal or conjunctival epithelium from live animals | ||
+ | *Giant cells may be seen in the alveol | ||
===Clinical Signs=== | ===Clinical Signs=== | ||
+ | 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. | ||
+ | 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. | ||
− | + | * Clinical specimens: Conjunctival scrapings, blood (buffy coat) smears, lung, urinary bladder, stomach, and brain. | |
+ | * 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. | ||
+ | * The prognosis is poor for dogs with CNS involvement. | ||
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===Laboratory Tests=== | ===Laboratory Tests=== | ||
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===Diagnostic Imaging=== | ===Diagnostic Imaging=== | ||
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===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 | |
− | + | *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 | |
+ | *May cause [[Lungs Inflammatory - Pathology#Interstitial pneumonia|interstitial pneumonia]] where [[Degenerations and Infiltrations - Pathology#Cellular Inclusions|inclusions]] are found within alveolar macrophages | ||
+ | *Gross pathology: | ||
+ | **Oedematous lungs, diffuse interstitial pneumonia | ||
+ | *Micro pathology: | ||
+ | **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 | |
+ | **Some now given at 7 and 10 weeks to allow socialisation | ||
+ | *Homeopathic vaccines do not work | ||
+ | *Live attenuated vaccines may kill some wildlife therefore '''Iscom vaccine''' is used in seal sanctuaries | ||
− | + | Treatment | |
− | + | * Supportive treatment, and antimicrobial therapy to cope with secondary bacterial respiratory infection. | |
− | + | Prevention | |
− | + | * 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. | |
− | + | * Pregnant bitches should not be vaccinated with modified live vaccines. | |
+ | ==Prognosis== | ||
==Links== | ==Links== | ||
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==References== | ==References== | ||
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#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:Morbilliviruses]][[Category: | + | [[Category:Morbilliviruses]][[Category:Dog]] |
− | [[Category: | + | [[Category:To_Do_- Lizzie]] |
[[Category:Respiratory Viral Infections]] | [[Category:Respiratory Viral Infections]] |
Revision as of 15:29, 12 August 2010
This article is still under construction. |
Also known as: | Canine Distemper CDV |
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 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 later to 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.
Signalment
As well as the domestic dog, canine distemper virus infection has been found in many species, as detailed in the table below.
Dingo Fox Jackal Wolf |
Racoon Coati Bassariscus |
Marten Mink Otter Sable Wolverine Badger Skunk |
- Dogs, ferrets, seals, lions, mink
- Has been a major pathogen of dogs prior to vaccination
Diagnosis
- May present as series of infections
- Immunocytochemistry of inclusion bodies
- Intracytoplasmic inclusions may be found in most affected tissues
- Inclusions persist longest in the brain (may be intranuclear) and the alveolar macrophages
- Sections of fixed bronchial tissue, lung, macrophages, bladder may be used or nasal or conjunctival epithelium from live animals
- Giant cells may be seen in the alveol
Clinical Signs
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. 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.
* Clinical specimens: Conjunctival scrapings, blood (buffy coat) smears, lung, urinary bladder, stomach, and brain. * 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. * The prognosis is poor for dogs with CNS involvement.
Laboratory Tests
Diagnostic Imaging
Pathology
- Rhinitis
- Although many organs can be affected by CDV, a relatively constant feature is the respiratory signs which occur in varying severity
- A syndrome of catharral oculonasal discharge, pharyngitis and 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
- May cause interstitial pneumonia where inclusions are found within alveolar macrophages
- Gross pathology:
- Oedematous lungs, diffuse interstitial pneumonia
- Micro pathology:
- Necrosis of pneumocytes, necrotising bronchiolitis, alveolar oedema, thickening of alveolar walls and type II pneumocyte hyperplasia
Treatment
- Live attenuated virus vaccines given at 10 and 12 weeks of age
- Some now given at 7 and 10 weeks to allow socialisation
- Homeopathic vaccines do not work
- Live attenuated vaccines may kill some wildlife therefore Iscom vaccine is used in seal sanctuaries
Treatment
* Supportive treatment, and antimicrobial therapy to cope with secondary bacterial respiratory infection.
Prevention
* 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. * Pregnant bitches should not be vaccinated with modified live vaccines.
Prognosis
Links
References
- Carter, GR and Wise, DJ (2005) A Concise Review of Veterinary Virology, International Veterinary Information Service.