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9 Cards in this Set
- Front
- Back
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What are some general features of the family paramyxoviridae?
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-large pleomorphic enveloped viruses
-unsegmented, negative-sense, single stranded RNA -helically symmetrical nucleocapsid -replicate in the cytoplasm and bud through the cell membrane -genomes are not infectious as viral proteins are needed to initiate replication -generally unstable in the environment -protective antibody is directed against both the haemagglutinin/neuraminidase protein, which is used in attachment, and the fusion protein, which is used for penetration and cell-to-cell spread of virus by fusion of adjacent cell membranes -antibody against both proteins is needed for optimal immunity -the fusion protein must be cleaved for the released virus to be infectious, and virulence is related to the sequence of the fustion protein at the cleavage site -there are 2 subfamilies of the family Paramyxoviridae: ●Paramyxovirinae: that includes the genera Respirovirus, Rubelavirus, Morbillivirus and Henipavirus ●Pneumovirinae: that contains the genera Pneumovirus and Metapneumovirus -cause rinderpest, peste des petits ruminants, canine distemper, Newcastle disease, and a range of respiratory disease in animals |
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Describe the genus Rubulavirus
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-contains Newcastle disease (avian paramyxovirus 1), avian paramyxovirus 2-9 which cause respiratory disease in chickens, canine parainfluenze virus 2 which causes respiratory disease in dogs and plays a role in predisposing dogs to chronic tracheobronchitis (kennel cough) caused by the bacterial pathogen Bordetella bronchiseptica, porcine rubulavirus which is an exotic pathogen of pigs, human mumps virus (which infects salivary glands) and human parainfluenza viruses 2-4.
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Describe the disease, pathogenesis, epidemiology, diagnosis and control of Newcastle disease
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-one of the most important infectious diseases of poultry trhoughout the world
✩DISEASE -affects chickens, turkeys, pheasant, pigeons, quail and guinea fowl, ostriches and many wild birds -mild disease in geese & ducks -can cause conjunctivitis in humans -stains are classified as velogenic (highly virulent), mesogenic or lentogenic (mildly virulent) based on the speed that they kill chickens or eggs under defined conditions, and are also classified on the basis of their tissue tropism -INCUBATION PERIOD: 5-6 days ●Viscerotropic Velogenic Strains: sudden, RAPIDLY SPREADING disease with depression, anorexia, increased respiration rate, prostration, bright green diarrhoea, dehydration, edema, cyanosis and death in a few days -birds that don't die may have neurological signs -mortality may be over 90% ●Neurotropic Velogenic Strains: initially severe coughing, gasping, and respiratory distress, progressing over a few days to head tremors, limb paralysis and torticollis -mortality is generally 10-20% ●Mesogenic Strains: coughing with depression, weight loss, and reduced egg production -some birds may develop neurological signs late in the course of the disease -mortality is about 10% ●Lentogenic Strains: SUBCLINICAL, but there may be mild respiratory signs, anorexia and a drop in egg production -there are no neurological signs and little mortality ✩PATHOGENESIS -virus initially replicates in the epithelia of the GI and respiratory tracts, rapidly esablishing viraemia and spreading to the spleen and bone marrow, then replicating further before producing a secondary viremia -the virus then colonises the lung, intestine & CNS -NEUROTROPIC & MESOGENIC FORMS → respiratory distress is due to congestion of the lungs, exudation and hemorrhage into the trachea and damage to the respiratory centre of the brain -VISCEROTROPIC FORM → hemorrhage and necrosis in the upper GI tract and petechial hemorrhages in other organs -enodthelial necoris, thrombosis, edema and hemorrhage may occur in many organs -in the brain there is hyperplasia of the vascular endothelium, lymphocytic infiltration and neuronal degeneration ✩EPIDEMIOLOGY -highly contagious and outbreaks can be EXPLOSIVE, but are modulated by antibody, which may result from prior exposure to lentogenic viruses -transmission by INHALATION of AEROSOLS and INGESTION, with virus excreted in faeces and from the respiratory tract of infected birds -airborne transmission over short distances can occur -contact with contaminated personnel, equipment, feed, trucks and cages may also transmit disease -WILD BIRDS may be an important RESERVOIR -recent outbreaks in Australia may have resulted from mutation of an endemic lentogenic strain in the fusion protein cleavage region -Australia and many other countries are free of velogenic NDV ✩DIAGNOSIS -virus is isolated in the allantoic sac of embryonated eggs and presence of virus is demonstrated by haemagglutination and haemagglutination inhibition -pathogenicity tests are performed in eggs, by intracerebral inoculation of day old chicks of by intravenous inoculation of 6-10 week old birds -RT-PCR and sequencing of the fusion protein and haemagglutinin can be used to predict virulence -antibody can be detected by haemagglutinin inhibition ✩CONTROL -in many countries thoguhout the world control is by serological testing and slaughter of any birds in contact with a serologically positive animal -variants of the endemic Australian strain have been selected for temperature resistance and used as an oral vaccine, mixed with food, for protection of village poultry -ENDEMIC countries → ATTENUATED VACCINE |
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Describe the genus Morbilliviruses
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-includes Rinderpest, Peste de Petit Ruminant, Canine Distemper, and Phocine, Dolphin and Porpoise Distemper
-it also includes human measles virus -ALL of these viruses have a tropism for the EPITHELIUM of the REPIRATORY and GASTROINTESTINAL tracts, and to some extent the central nervous system, producing disease characterized by GASTROENTERITIS, PNEUMONIA, and NEUROLOGICAL DISEASE |
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Describe the disease, pathogenesis, epidemiology, diagnosis, and control of the disease Rinderpest
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✩DISEASE
-very high morbidity and mortality -in European cattle breeds morbidity can be 100% and mortality 90-100% -affected cattle have an initial fever, followed by mucopurulent nasal and ocular discharge -within 1-2 days necrotic foci develop on the nasal, oral and urogenital mucosa -these then progress to erosions -animals develop laboured respiration and haemorrhagic diarrhoea -most animals die in 6-12 days after the start of clinical signs -cattle and buffalo are most susceptible, but some breeds of pigs, antelope, giraffe and warthogs are also susceptible ✩PATHOGENESIS -enters via INHALATION and initially replicates in the tonsils and local lymph nodes -viraemia develops in 2-3 days, then virus localises in lymph nodes, spleen, bone marrow, and the mucosal epithelium of the GI and respiratory tract -virus replication in the mucosal epithelium causes necrosis and erosions -leukopaenia develops as a result of replication and destruction of lymphoid tissue -the profound immunosuppression that develops promotes secondary infection with other viruses and bacterial pathogens -death within 12 days (dehydration & wasting, secondary infection) ✩EPIDEMIOLOGY -HIGHLY CONTAGIOUS -transmission is predominantly by AEROSOL -virus is shed in expired air, respiratory secretions, faeces, urine, and other secetions, and SHEDDING commences BEFORE CLINICAL SIGNS are seen, but there is no chronic carrier state -infection requires close contact -virus is labile in environment -one serotype but different strains -eradicated ✩DIAGNOSIS -antigen can be detected in tissue (ie spleen, lymph nodes, or secretions) by immunochemical tests and virus can be isolated in cell culture -antibodies are detected by ELISA or serum neutralization ✩CONTROL -control in most countries is by quarantine measures -a cell culture attenuated vaccine is used in endemic countries and is very effective -lasting immunity to vaccine, no carries, no animal reservoir, good diagnostic tests |
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What is Pest de Petit Ruminants?
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-closely related to Rinderpest
-"goat plague": acute, contagious disease of small ruminants -transmission by aerosol, requires close contact -similar sings to rinderpest -up to 70% mortality -occurs in Africa -controlled by Rinderpest vaccine (PPRV vaccine developed) |
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Describe the disease, pathogenesis, epidemiology, diagnosis, and control for the disease Canine Distemper
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✩DISEASE
-3-6 days INCUBATION -affected dogs have initial fever, followed by mucopurulent nasal and ocular discharge -animals develop COUGHING, VOMITING, and WATERY DIARRHOEA -later CNS SIGNS develop with spasms, myoclonic contractions, ataxia, paresis and convulsions -approximately 50% of dogs succumb and those that survive have ongoing neurological damage, most frequently leg movements -there are 2 chronic sequalae of distemper -in old dog encephalitis there is progressive loss of neurological function, while in hard pad disease develop hyperkeratosis of the food-pads and nose ✩PATHOGENSIS -virus enters VIA INHALATION and initially replicates in the UPPER RESPIRATORY TRACT or CONJUNCTIVA, then subsequently in the local lymph nodes -viremia develops and virus is carries in lymphocytes and localizes in the reticuloendothelial system -there is a secondary viremia, with virus in circulating lymphocytes and monocytes, and localisation in the mucosal epithelium of the GI and RESPIRATORY tracts, as well as the CNS -an intersitial pneumonia develops, as well as gasteroenteritis, encephalitis, and profound immunosuppression ✩EPIDEMIOLOGY -highly contagious -transmitted predominantly by AEROSOL and DIRECT CONTACT -shed in expired air, respiratory secretions, faeces, urine, and other secretions, and shedding commences before clinical signs are seen -disease tends to occur after maternal antibody has waned -occurs in all Canidae, Procyonidae (racoons & pandas), Mustelidae (ferrets, otters, minks and skunks) ✩DIAGNOSIS -DIFFICULT to isolate in cell culture -best performed using immunohistochemistry to show antigen in impression smears of conjunctiva or peripheral blood lymphocytes, or at post mortem in lung, gastrointestinal mucosa or urinary mucosa ✩CONTROL -fully effective protection is dependent on the development of cell mediated immunity -vaccination with ATTENUATED viruses is very effective -major problem is interference with vaccination by maternal antibody -if antibody titres can be determined the appropriate time to vaccinate can be predicted, alternatively vaccination can be performed at 2-4 weekly intervals from 6-16 weeks to ensure that pups are not left unprotected |
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Describe Henipaviruses
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-since 1994 several severe outbreaks of acute respiratory disease and encephalitis have been seen in domestic animals and also human in contact with animals
-the viruses involved appear to belong to a distinct genus and the reservoir host appears to be fruit bats -the first outbreak, caused by Hendra virus, occurred in horses in Brisbane -horses died of acute pneumonia -the trainer of the affected horses also died of acute respiratory disease -at the same time 2 horses in Mackay died and a man who was assisting his veterinarian wife perform he post mortem developed mild meningoencephalitis, appeard to recover, but then died a year later with severe encephalitis -experimentally the virus has shown to be able to cause disease in cats and guinea pigs as well as horses -horses found to have congested, firm, fluid filled lungs, with dilated lymphatics -thick foamy, haemorrhagic exudate in airways -more recently a very large outbreak of acute fatal respiratory disease was seen in pigs in Malaysia and many of the staff at the piggeries involved also died with acute respiratory disease -the virus involved, Nipah virus, is related to but distinct from Hendra virus |
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What are the facts about Hendra?
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• Seroprevalence varies between bat
colonies (2 – 50%) Suggests non-lethal infection in bats • Detected in foetal/neonatal lung Detected in uterine fluid & renal tissue • No definitive data on bat-to-bat spread • No data on bat-to-horse spread • No evidence of bat-to-human spread Case – fatality rate 57% (4/7) • All associated with close contact with affected horses (endoscopy, treating, nursing or post-mortem examination) •Extremely low risk handling normal horses • 3 outbreaks with >1 horse involved All associated with human fatalities • Sudden death and severe acute respiratory signs -Hendra in 1994: 20 infected 14 died. Tachypnoeic, tachycardic, ataxic, frothy nasal discharge, collapse →7 deaths within 12 hours, (10 < 36 hours) -Rockhampton 2009: Sudden death and respiratory disease • All confirmed cases PCR positive on blood and/or nasal swabs and/or tissue samples from Post Mortem |
