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poultry
infectious disease exam 3
| Question | Answer |
|---|---|
| Poxviruses transmission | contact, mechanically by arthropods. several zoonotic |
| Fowlpox | slow spreading. lesions prolif in skin and mucosae of respiratory and digestive tract. virus survive env |
| Fowlpox virus | direct contact, droplet. mechanical w/ mosquito |
| Fowlpox cutaneous form | prolif lesions in featherless skin |
| Fowlpox diphtheritic form | Soft plaques or lesions in the oral or upper respiratory mucosae. virulent strains w/ lesions in internal organs |
| Herpres virus lesion | characteristic eosinophilic intranuclear inclusion bodies. infection becomes latent w/ recurdescence and intermittent or continuous virus shedding |
| Infectious larynotracheitis: Gallid Herpesvirus 1- Acute disease | Highly contagious, respiratory infection. Characterized by severe dyspnea. coughing, rales |
| Infectious larynotracheitis: Gallid Herpesvirus 1- Subacute disease | lacrimation, tracheitis, conjunctivitis, mild rales |
| Infectious larynotracheitis clinical signs | mouth and beak may be blood stained b/c of tracheal exudates. recovered birds remain carriers and are a source of infection as latent viruses can be reactivated. Reportable disease |
| Infectious larynotracheitis control | vaccination and biosecurity. |
| Infectious larynotracheitis vaccine | modified live virus. vaccinate by eye drop, drinking water, aerosol. |
| Mareks Disease: Gallid Herpesvirus 2 | progressive disease but acute paralysis can occur in young chickens. |
| Mareks Disease signs | lympho-proliferative snydromes |
| Lympho-proliferative syndromes | Oncogenic transformation and defective immune surveillance allow transformed cells to form lymphoid tumors. lymphoma involving visceral organs, asymmetric paralysis of wings and legs. Dilation of crop and grasping if vagus nerve is involved. |
| Mareks Disease vaccination | Automated in ovo at 18th day of incubation |
| Turkey Hemorrhagic enteritis virus | causes acute infection in poluts. macroscopic lesions are pathognomonic. immunosuppression (AB and cell mediated), oportunistic bacteria. |
| Turkey Hemorrhagic enteritis virus clinical signs | sudden onset, depressed poults, bloody dropping, death |
| Turkey Hemorrhagic enteritis virus macroscopic lesions | dilated hemorrhagic intestines, splenomegaly. intranusclear inkclusion bodies in spleen cells. |
| Turkey Hemorrhagic enteritis virus vaccine | live attenuated. drinking water. immunity after infection or vaccination is life-long. |
| Chicken infectious anemia virus: Cricoviruses | chicken anemia virus encodes a protein (VP3) that induces apop in chicken lymphocytes. virus resistant to env and disinfectants. vertical transmission |
| Chicken infectious anemia virus pathogenesis | clinical disease during first 2-3 wks of life. virus persists in immunocompetent chicks for 3-4 wks. viruses persists in immunocompromosed chicks for 7wks. age resistance to disease 3 wks. |
| Chicken infectious anemia virus clinical sign | aplastic anemia. peaks 2 wks after infection. SQ and IM hemorrhages. immunosuppression. high mortality due to secondary infections |
| Chicken infectious anemia virus transmission | vertical. laying gen transmits virus into eggs |
| Chicken infectious anemia virus vaccine | live modified virus. immunize parental flocks, passivey protect chicks. |
| Infectious Bursal Disease: Gumboro disease- Birnaviruses | env stable excreted in feces, transmitted by contact, fomites, common vehicle |
| Infectious Bursal Disease | immunosuppressive disease. viral tropism for pre-B lymphocytes of cloacal bursa producing prolonged immunosuppression |
| Newcastle Disease: Paramyxoviruses | APMV-1. |
| APMV1- velogenic viscerotropic | gut hemorrhagic lesion, high mortality |
| APMV1- velogenic neurotropic | respiratory/neurologic signs, high mortality |
| APMV1- Mesogenic | acute respiratory/ nervous signs, low mortality |
| APMV1- Lentogenic | mild/inapparent respiratory infections |
| APMV1- Asymptomatic enteric | avirulent |
| Virulence factors for Newcastle disease | differentiated by ID the aa around the cleavage site of the Fusion protein. The virus can replicate in a wider range of host cells and become systemic |
| Newcastle disease transmission | direct contact w/ feces and respiratory discharge. contamination of env |
| Newcastle disease zoonosis- clinical manifestation | mild conjunctivitis |
| Newcastle disease clinical signs | edema of head (eyes), greenish, dark watery diarrhea. Respiratory and neurological signs. muscle tremors, drooping wings, dragging legs, paralysis. Signs vary w/ species and virulence/ |
| antigenic drift | small changes, point mutations |
| antigenic shift | abrupt changes. genetic reassortment b/w subtypes. direct transfer of virus. re-emergence of virus |
| reservoir for avian influenza | waterfowl and shorebirds. Carry all known H and N antigens. usually low pathogenic AI forms |
| Low pathogenicity avian influenza | causes mild disease in poultry. H1 to H16 subtpyes. |
| High pathogenicity avian influenza | causes severe disease in poultry. H5 and H7. |
| HPAI clinical signs | sudden death, systemic disease, drop in egg production, neurological signs, depression, anorexia, ruffled feathers, combs swollen, cyanotic, conjuctivities and respiratory signs |
| HPAI diagnosis | clinically indistinguishable from virulent Necastle disease |
| HPAI treatment | no specific treatment. usually not treatment. antivirals effective in reducing mortality. not approved for food animals (result in viral resistance). vaccine may not prevent viral shedding |
| avian influenza prevention | All-in/ all-out management. prevent contact w/ wild birds or their water sources |
| corona and toroviruses | virus unstable in env. wide range clinical presentations. many serotypes w/ specific immunity. transmission by direct contact, fomites. |
| infectious Bronchitis | systemic disease after respiratory infection affecting ovaries and kidneys. little gastrointestinal affect even though virus replicates in gut and is excreted for several days |
| infectious Bronchitis spread | as aerosols and through fecal contamination of feed etc. some birds presistently excrete virus after recovery |
| Avian encephalomyelitis (epidemic tremor)- picornavirus | affects young chickens. causes high mortality where no prior immunity in flock. |
| Avian encephalomyelitis (epidemic tremor) pathogenesis | similar to polio in humans |
| Avian encephalomyelitis (epidemic tremor) shedding and transmission | feces during active infection. birds on ground infected by ingestion. vertical transmission |
| Avian encephalomyelitis (epidemic tremor) microscopic lesions found where | brain, ventriculus, proventriculus, heart, pancreas |
| Avian encephalomyelitis (epidemic tremor) gross patho | microscopic changes in CNS/several visceral organs.neuronial degeneration-brain stem. purkinje cell degeneration-cerebellum. glial foci- molecular layer of cerebellum. perivascular cuffings in CNS. lymphoid foci in pancreas, ventriculus, proventric, heart |
| Avian encephalomyelitis (epidemic tremor) vaccine | pullets after 8wks of age. live virus. vaccinate again at least 1 mo before laying |
Created by:
ejohnson17
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