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Distemper. Paul R Earl Facultad de Ciencias Biológicas Universidad Autónoma de Nuevo León San Nicolás, NL 66451, Mexico.

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Distemper

  • Paul R Earl

  • Facultad de Ciencias Biológicas

    • Universidad Autónoma de Nuevo León

  • San Nicolás, NL 66451, Mexico


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Canine distemper (CD), related to measles, is caused by a morbillivirus through sneezing and nasal discharges, and other transmissions of body fluids from saliva to urine. Once the virus CDV has entered the central nervous system (CNS), the dog will likely die. This is a very common and importantdisease, largely preventable by a 3-dose vaccination, live or attentuated. It is absolutely necessary to try to protect dogs against CDV. Of course, almost all dog owners know this disease by its nerve damage. Parvovirus-caused diseases in dogs like the one causing Aleutian disease in mink and panleukonpenia in cats are also well known and preventable.


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One polyvalent vaccine can include CDV, adenovirus Type 2, hepatitis, parainfluenza, parvovirus, Leptospira canicola and L. icterohaemorrhagiae. Another polyvalent vaccine is CDV-Adenovirus Type 2-Coronavirus-Parainfluenza-Parvovirus type 2b vaccine, modified live and killed viruses with the 2 major Leptospira spp.Other viruses like rabies are also sometimes combined as polyvalent vaccines. See http://www.pitt.edu/~super1/lecture/ lec10911/index.htm


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Morbilliviruses hepatitis, parainfluenza, parvovirus, These contain 6 structural proteins. Three internal proteins are associated with the negative-strand genome: the nucleocapsid protein (N), phosphoprotein (P) and large protein (L). On the inner leafet of the envelope there is a matrix protein (M) which probably plays a role in budding and the structural integrity of the virus.


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Protruding from the envelope are 2 glycoproteins (gp), hemagglut-inin (H) protein and fusion (F) protein. Two additional non-structural proteins are generated from the P gene either by translation of an overlapping open reading frame for the C protein or, by insertion of an extra G residue in the P mRNA. mRNA is generated for the V protein, which is amino-coterminal with P protein but which terminates in 70 residues C-terminal. The genes for the N, P, V, C, M, F, H and L proteins are ordered on the 3' to 5' on a negative-stranded genomic template of 15±7±--15±9 kb. The epitopes on the H protein can be of interest when involved in making vaccines.


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Paramyxovirus. University of Warwick. hemagglut-inin (H) protein and fusion (F) protein. Two additional non-structural proteins are generated from the P gene either by translation of an overlapping open reading frame for the C protein or, by insertion of an extra G residue in the P mRNA. mRNA is generated for the V protein, which is amino-coterminal with P protein but which terminates in 70 residues C-terminal. The genes for the N, P, V, C, M, F, H and L proteins are ordered on the 3' to 5' on a negative-stranded genomic template of 15±7±--15±9 kb. The epitopes on the H protein can be of interest when involved in making vaccines.


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Wild animals hemagglut-inin (H) protein and fusion (F) protein. Two additional non-structural proteins are generated from the P gene either by translation of an overlapping open reading frame for the C protein or, by insertion of an extra G residue in the P mRNA. mRNA is generated for the V protein, which is amino-coterminal with P protein but which terminates in 70 residues C-terminal. The genes for the N, P, V, C, M, F, H and L proteins are ordered on the 3' to 5' on a negative-stranded genomic template of 15±7±--15±9 kb. The epitopes on the H protein can be of interest when involved in making vaccines.Distemper is a worldwide disease of many wild and domestic animals. Most carnivores are susceptible to natural CD. Mammalian families that are commonly infected include: Canidae (dog, fox, wolf) Felidae (cat, lion, tiger) Procyonidae (racoon, panda) and Mustelidae (ferret, skunk, weasel, badger), aside from marine mammals like dolphins and whales. The lethal virus in seals is closely related phocine distemper virus, not CDV.


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Vaccination hemagglut-inin (H) protein and fusion (F) protein. Two additional non-structural proteins are generated from the P gene either by translation of an overlapping open reading frame for the C protein or, by insertion of an extra G residue in the P mRNA. mRNA is generated for the V protein, which is amino-coterminal with P protein but which terminates in 70 residues C-terminal. The genes for the N, P, V, C, M, F, H and L proteins are ordered on the 3' to 5' on a negative-stranded genomic template of 15±7±--15±9 kb. The epitopes on the H protein can be of interest when involved in making vaccines.One aim of vaccination (immunization) is to acquaint the dog’s immune system with the pathogen by presenting a killed or modified form of the pathogen. Another aim is to vaccinate the population 'sufficiently' so that an outbreak cannot not occur.The animal will then be protected from becoming ill when exposed to the real thing. The 2 major parts of the immune system are humoral immunity (B lymphocytes that produce antibodies) and cell-mediated immunity (T lymphocytes that destroy defective and infected cells). Vaccination is critical in the prevention and control of disease, and a great success.


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Newborns can respond immunologically, perhaps weakly, at birth. Passive immunity is provided to them by antibodies that are passed mainly in the colostrum from the dam to the offspring in the 1st 24-72 hours after birth. Eight-two percent to 98 % of the maternal antibodies come from the colostrum, while only 2-18 % of antibodies are transferred in utero. The amount of antibody the young receive depends on the antibody titer of the dam, and how much colostrum each newborn receives. Maternal antibodies interfere with the capacity of the young to respond to vaccination by inactivating the vaccine just as if it is the real pathogen.


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Vaccines birthRoutine vaccines include 1/ CDV, 2/ parainfluenza, 3/ adenovirus-2, 4/ parvovirus and 5/ compulsory rabies. Consider also canine corona virus (CCV) that causes enteritis.


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Major CDV, CPV and vaccines of the 2 viruses combined are now given.PFIZER ANIMAL HEALTH (the Vanguard Puppy Vaccine) INTERVET (the Progard Vaccine) MERIAL (the Recombitek C4 and C6 vaccines). Merial is supported by Rhone-Merieux and Merck.FORT DODGE (the Puppy Shot)SCHERING-PLOUGH ANIMAL HEALTH (the Galaxy Vaccine)


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Rabies combined are now given.In all states, rabies vaccinations are required by law. The first rabies vaccination is good for one year. In many states, subsequent vaccinations are good for 3 years. In other states, they are only valid for one year by law. Please check with your vet to determine the legal requirements in your state. Vaccinating your pet for rabies may literally save its life for 2 reasons. Rabies is a threat in many areas, and it is a horrible disease. In addition, an unvaccinated pet who bites a human being is subject to long quarantine periods or even death for the purpose of testing for rabies infection of the brain.


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As rabies can infect ALL MAMMALS and be fatal, its vaccination in dogs, cats & ferrets should be compulsory. Five companies in the US--Fort Dodge, Pfizer, Intervet, Merial, Bayer and Aventis Pasteur--produce 28 rabies vaccines. Also Schering-Plough is marketing vaccines made by other companies. The Imovax rabies vaccine produced by Aventis Pasteur is a sterile, stable, freeze-dried suspension of rabies virus prepared from strain PM-1503-3M obtained from the Wistar Institute of the University of Pennsylvania in Philadelphia.


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Signs of CD vaccination in dogs, cats & ferrets should be compulsory. Five companies in the US--Fort Dodge, Pfizer, Intervet, Merial, Bayer and Aventis Pasteur--produce 28 rabies vaccines. Also Schering-Plough is marketing vaccines made by other companies. The first sign of distemper is eye discharge that may appear watery to pus-containing. Later, dogs develop fever, nasal discharge, coughing, lethargy, reduced appetite, vomiting and diarrhea. Still later, the virus may attack the nervous system, causing seizures, twitching, partial or complete paralysis. CDV causes demyelinating encephalomyelitis. That is, the covering of the neurons is destroyed. Distemper is often fatal. Even if a dog does not die from the disease, CDV can cause irreparable damage to a dog’s nervous system. However, some dogs mount a strong immune response within 2-3 weeks and recover spontaneously.


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Pathology vaccination in dogs, cats & ferrets should be compulsory. Five companies in the US--Fort Dodge, Pfizer, Intervet, Merial, Bayer and Aventis Pasteur--produce 28 rabies vaccines. Also Schering-Plough is marketing vaccines made by other companies. Aerosol transmission from respiratory secretions is the main route of transmission. Virus shedding begins about 7 days post infection. Lymphopenia is always present during the early infection.The virus spreads first to local lymph nodes. Within 7 days, it spreads to all lymphatic tissues. During this period of 3-6 days postinfection, the 1st rise of temperarure occurs along with the appearance of interferon in the circulation.


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Depending on the virus strain, the signs may be more related to acute grey matter or subacute white matter disease. Seizures and myoclonus with hyperesthesia and depression predominate in grey matter disease. Incoordination ataxia, paresis, paralysis and muscle tremors occurs in white matter disease. Meningeal signs of hyperesthesia and cervical rigidity may be seen in both. Optic neuritis and retinal lesions also may occur. Hard footpads and hardness of the nose are produced sometimes.


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The clinical course, severity of the disease and neuropathology vary with the virus strain. Dogs either die within 3 weeks or recover. Lesions in the neuraxis are those of a encephalomyelitis. With some less aggressive strains, demyelination can be the predominant finding. Some dogs succumbed, generally around 28-42 days postinfection, while others recover. Strains like R252 and A75-17 induce delayed, white matter disease with a mixed pattern of mortalities, persistent infections or recoveries. Neutralizing antibody responses often correlates with the disease course. Dogs which die have low serum titers or lack antibody. Recovering dogs have the earliest and highest titers.


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Canine distemper encephalomyelitis is the most common form of CDV infection and often begins as gastrointestinal and respiratory disturbances: vomiting, diarrhea, coughing and seromucopurulent eye-nose discharges. Hyperkeratosis of the footpad may be seen. Many animals have conjunctivitis and chorioretinitis. Cortical and subcortical signs include generalized seizures and sometimes personality changes, such as depression and disorientation. Signs of localization in the brain stem include incoordination, falling, turning to one side and nystagmus.


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Neuronal changes including nuclear pyknosis and shrunken cells, chromatolysis and neuronophagia are found in the cerebral cortex, pontomedullary nuclei, Purkinje cells and gray matter of the spinal cord. In some dogs, hippocampal cells can be selectively involved. Intranuclear and intracytoplasmic inclusions bodies may be present in neuronal cells, astrocytes, histiocytes, meningeal cells, and ependymal cells. The distribution of inclusion bodies in distemper virus encephalitis is erratic, and their presence is not an indication of the severity of the disease process. Changes in the white matter vary according to the duration and intensity of the infection.


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Demyelinating lesions can be focal or disseminated. Nerve fibers may undergo degeneration, resulting in the formation of swollen axonal ovoids. Pronounced gliosis may be evident in association with these changes. In many severe lesions, there is evidence of tissue necrosis, edema and macrophage infiltration. These lesions are often situated in the cerebellar peduncles or in the central white matter. Also, CDV can produce chronic multifocal encephalomyelitis. Dogs may have such symptoms for months.


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Courtesy of Michael Oglesbee fibers may undergo degeneration, resulting in the formation of swollen axonal ovoids. Pronounced gliosis may be evident in association with these changes. In many severe lesions, there is evidence of tissue necrosis, edema and macrophage infiltration. These lesions are often situated in the cerebellar peduncles or in the central white matter.


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Courtesy of Michael Oglesbee fibers may undergo degeneration, resulting in the formation of swollen axonal ovoids. Pronounced gliosis may be evident in association with these changes. In many severe lesions, there is evidence of tissue necrosis, edema and macrophage infiltration. These lesions are often situated in the cerebellar peduncles or in the central white matter.


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Courtesy of Michael Oglesbee fibers may undergo degeneration, resulting in the formation of swollen axonal ovoids. Pronounced gliosis may be evident in association with these changes. In many severe lesions, there is evidence of tissue necrosis, edema and macrophage infiltration. These lesions are often situated in the cerebellar peduncles or in the central white matter.


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Parvoviridae fibers may undergo degeneration, resulting in the formation of swollen axonal ovoids. Pronounced gliosis may be evident in association with these changes. In many severe lesions, there is evidence of tissue necrosis, edema and macrophage infiltration. These lesions are often situated in the cerebellar peduncles or in the central white matter. Members of the family Parvoviridae are small eukaryotic DNA viruses that infect a variety of animal species, including humans. The genome is minus-sense, single-stranded DNA and the virus has no envelope.Canine parvovirus (CPV), feline panleukopenia virus (FPV) and viruses similar to FPV like blue fox parvovirus, the raccoon parvoviruses and mink enteritis virus are all host variants of the carnivore parvoviruses.CPV evolved as a new pathogen in dogs in1976 from FPV. The new virus hit an unprotected population, caused a dramatic pandemic and infected virtually all populations of domestic and wild carnivores worldwide.


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Ferrets fibers may undergo degeneration, resulting in the formation of swollen axonal ovoids. Pronounced gliosis may be evident in association with these changes. In many severe lesions, there is evidence of tissue necrosis, edema and macrophage infiltration. These lesions are often situated in the cerebellar peduncles or in the central white matter. Etiology. CDV, Morbillivirus, pantropic virus replicates in epithelium and lymphoid tissues.Transmission. Aerosol.Clinical. Mucopurulent oculonasal discharge, papular rash under chin, perianal, inguinal; “orange” hyperkeratotic planum nasale and footpads, photophobia, acute mortality; central nervous signs, tremors, convulsions, coma. Disease progression 10-40 days with profound immunosuppression Pathology. Bilateral nasal and ocular discharge, suppurative bronchopneumonia, acute death without gross lesions; eosino-phillia, 2-5 µm intranuclear and intracytoplasmic inclusions especially in the cells of the urinary bladder, renal pelvis, biliary epithelium, neurons. Encephalitis with demyelination.


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Aleutian disease fibers may undergo degeneration, resulting in the formation of swollen axonal ovoids. Pronounced gliosis may be evident in association with these changes. In many severe lesions, there is evidence of tissue necrosis, edema and macrophage infiltration. These lesions are often situated in the cerebellar peduncles or in the central white matter. Etiology. Parvoviridae, Aleutian disease virus.Transmission. Orofecal, aerosol, in utero; shed subclinically for months, persists in the environment.Clinical. Plasma cell proliferation, hypergammaglobulinemia >20% serum protein, glomerulonephritis, vasculitis, insidious 2 year progressive disease,Pathology. Prominent plasmacytic infiltrate in renal interstitium, portal triads, spleen, membranous glomerulonephritis, tubular protein casts, splenomegaly, pale, tan kidneys.


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Coronavirus fibers may undergo degeneration, resulting in the formation of swollen axonal ovoids. Pronounced gliosis may be evident in association with these changes. In many severe lesions, there is evidence of tissue necrosis, edema and macrophage infiltration. These lesions are often situated in the cerebellar peduncles or in the central white matter. Etiology. Coronaviridae, Epizootic Catarrhal Enteritis.Transmission. orofecal, prolonged shedding.Clinical. high morbidity, low mortality, vomiting and dark green diarrhea with abundant mucus;Pathology. Often no gross lesions, clear fluid lumen content; vacuolar degeneration and necrosis of apical enterocytes, marked villous atrophy, fusion, blunting; later, enteritis with marked lymphocytic infiltration.


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Parvovirus fibers may undergo degeneration, resulting in the formation of swollen axonal ovoids. Pronounced gliosis may be evident in association with these changes. In many severe lesions, there is evidence of tissue necrosis, edema and macrophage infiltration. These lesions are often situated in the cerebellar peduncles or in the central white matter. Found throughout the world, parvovirus is a highly contagious disease agent that attacks the intestinal tract, the white blood cells and sometimes the heart. It is spread through contact with the feces of infected dogs and can be carried on shoes, crates, equipment, or on the hair or feet of infected dogs. One infected dog at a show, a canine expo, a shelter or any other facility where dogs congregate can spread the virus to hundreds of unprotected dogs.Symptoms of parvo appear 5-7 days after exposure and include depression, loss of appetite, vomiting and severe diarrhea.