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365 Cards in this Set
- Front
- Back
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BVD virus family/genus
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flaviviridae/pestivirus
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how many genotypes of BVDV are there?
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2
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how many biotypes of BVDV are there?
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two- NCP and CP
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BVDV is related antigenically to ____ and ___
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classical swine fever/hog cholera and border disease virus
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what is the major source of infection for BVD?
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persistently infected cattle that secrete the virus constantly
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what species can be subclinically infected with BVDV?
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wild ruminants, sheep, goats, pigs
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BVD transmission
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direct contact- mucosal contact with infected urine, feces, excretions, fomites. Fetus can be infected transplacentally
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BVD incubation period
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typically about a week
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what animals are most susceptible to "benign" infection of BVD
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immunocompetent, seronegative calves (3-8 monthsi f they had maternal ab) and young adults)
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what BVD type causes peracute highly fatal diarrhea?
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BVD type II
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clinical signs of peracute highly fatal diarrhea
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resp infection, profuse diarrhea, high fever. Oral erosions/mucosal lesions possible
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fatal mucosal disease is seen only in
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PI animals
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what percent of PI calves will die of mucosal dz between 8mo and 2 years of age?
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50%
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clinical signs of fatal mucosal disease
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profuse watery diarrhea, anorexia, mucopurulent nasal discharge, erosive/ulcerative stomatitis, emaciation, dehydration, with death occuring within a few days/weeks
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what type is TCP/hemorrhagic dz associated with?
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ncp BVDV type 2 virus
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clinical signs of TCP/hemorrhagic dz?
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bloody diarrhea, petechial and echymotic hemorrhages on the mucosal surfaces, epistaxis and prolonged bleeding at injection site. Platelet count less than 25K
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signs of BVD repro failure?
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conception failure, fetal mummification, abortion, premature births and stillbirths
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signs of BVD congenital abnormalities?
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occurs when virus infects fetus during period of organogenesis. Cerebellar hypoplasia and hydranencephaly is common; calves unable to stand/walk after birth. Retinal atrophy and dysplasia, optic neuritis, microphthalmia, can lead to various degrees of blindness
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chronic BVD infection and unthrifty PI calves
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animals that do not completely recover from infection can develop intermittent diarrhea, emaciation, bloat, hoof deformities, erosive stomatitis, and scabby lesions in perineum, scrotum and interdigital cleft
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calves born PI may be:
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smaller than others and fail to grow normally. They may appear unthirfity for several months until they develop fatal pneumonia or fatal mucosal dz.
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calves born PI are sero_____ for BVDV
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seronegative
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where will you primarily see immunosuppression resulting in respiratory dz with secondary bacterial infection
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seen primarily in feedlots when calves are grouped together and stressed
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pathological signs of BVD immunosuppresion --> resp dz/secondary bacterial infection
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abnormalities generally confined to alimentary tract. Shallow erosions seen in mouth, esophagus, forestomach, abomasum and cecum. In mouth, mucosa has a cooked appearance with grayish colored epithelium.
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histology of BVD immunosuppresion --> resp dz/secondary bacterial infection
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peyers patches depleted of lymphocytes with little inflammation in ulcer vicinity
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pathogenesis of BVDV
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bvdv replicates on the mucosal surface and tonsils, spreads to the lymphnodes where they infect lymphocytes and then spreads to all the lymphoid tissues and organs..
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what is the basis for all the BVD lesions observed?
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necrosis of the lymphocyte associated gut wall tissues and of the mucosal epithelium
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what happens to cattle exposed to BVD at estrus?
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failure of conception
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imsemination of seronegative cattle with BVD infected semen can lead to ________________ initially. However, after the animal has seroconverted______________.
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poor conception initially; conception is normal and calf is born healthy
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BVD infection during the embryonic period (0-45d) learsd to
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decreased conception rate and return to estrus
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BVD infection of fetus during early fetal life (45-125d)
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can lead to death of the fetus (mummification/abortion), congenital abnormalities or persistent ifnection
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when will a fetus become persistently infected with BVD?
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when infected during the 45-125d period with a NCP strain
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why does a fetus become persistent infected?
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the fetus recognized the virus as "self"
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when will PI calves develop mucosal dz?
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when the 1) ncp virus mutates into a cp virus or 2) they are infected with a CP virus that is homologous to the NCP virus
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what age range does mucosal dz occur in?
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first 2 years of lfie
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Will PI calves develop a normal immune response to other strains of BVD that are antigenically DIFFERENT from the one they are persistently infected with?
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yes!
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infection of the fetus during the period 125-175 d of gestation
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results in congenital defects
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infection of the fetus after 180d of infection
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results in fully competent immune response by the fetus with elimination of the virus. Calf is born with antibodies to the virus and is virus free
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lab signs of BVDV acute mucosal dz
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leukopenia
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what tests will ID BVD virus in tissue culture cells?
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FA or IPX
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NCP BVD does not cause____
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CPE
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what sample is best for virus isolation and why?
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whole blood; virus is in lymphocytes
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BVD virus ID in tissues
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FA, IHC or PCR. "ear notch sample"
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serology for BVD
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paired samples taken 3-4 weeks apart.
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differentials for BVDV
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diseases causing erosios and diarrhea (MCF and rinderpest) the vesicular dzs, BT, BPS, diseases causing diarrhea with no mouth infections and helminth infections
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treatment and control of BVD
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detect/eliminate PI animals from herd. Vaccinate, prevent intro of PI animals into non infected herd
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MCF is aka
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alcelaphine herpesvirus 1 and ovine herpesvirus 2
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MCF stands for
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malignant catarrhal fever
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MCF is one of the most important dzs of
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farmed deer
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MCF is a _________________________ infectious disease of cattle and deer
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sporadic, acute highly fatal
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characteristics of MCF
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development of an erosive stomatitis, gastroenteritis, erosions of the upper respiratory tract, keratoconjunctivitis, encephalitis and lymphadenopathy.
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MCF is characterized by ___ morbidity and ____ case fatality
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low; high
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MCF virus family/genus
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herpesviridiae ; gamma herpesvirus
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what species does alcelaphine herpes virus type 1 infect?
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wildebeest
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what are the two recognized MCFforms?
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African and sheep associated/US-eruopean
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wildebeest and sheep are ____ carriers of MCF
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inapparent
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how is mcf transmitted to cattle?
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via direct contact (AHV1 with wildebeest placenta/new born calves). OHV2 not associated with lambing
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cattle to cattle MCF transmission
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cannot be accomplished except by blood transfusion- not contagious between cattle
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MCF incubation period
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3-8 weeks
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most common form of MCF
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head and eye form
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characteristics of head and eye form of MCF
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sudden onset high fever (106-107), extreme depession anorexia, photophobia with blepharospasm, profuse mucopurulent ocular/nasal discharges, bilater corneal opacity and diarrhea. Generalize lymphadenopathy- lymph nodes unusually large. Lameness often noted due to coronitis
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where does corneal opacity begin and where does it progress?
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at the limbus and progresses centrally
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when does death occur after onset of MCF signs?
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within 7-10d
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can MCF present with CNS signs?
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yes- incoordination, muscle tremor, and head pressing
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what MCF form is common deer?
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peracute and alimentary tract form
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characteristics of peracute and alimentary tract form of MCF?
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high fever, dyspnea and acute gastroenteritis. Death occurs in 1-3 d
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characteristics of the mild form of mcf?
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transient fever and mild erosion
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pathogenesis of MCF
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virus infects lymphocytes, causes a florid lymphoproliferative and vascular lesions. Widespread proliferation of lymphocytes and multifocal areas of necrosis centered around small arteries that undergo fibrinoid necrosis of the muscle wall
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pathognomic lesions of MCF
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necrotizing vasculitis and perivascular cuffing- very evident in brain
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mcf lesions may be ______ _____ as a result of ____ attackign and killing the vascular endothelial cells
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immune mediated; CTLs
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what is very important in diagnosis of MCF?
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clinical signs
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what is important for histopath dx?
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various organs in formalin
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blue tongue virus family.genus
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reoviridae/orbivirus
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reo virus is an _NA virus
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RNA
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_______of genes can occur between serotypes
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reassortment
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BTV distribution
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worldwide- tropical/subtropical countries
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species susceptible to BTV? Which can have significant disease
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ruminants- domestic and wild (cattle, sheep, goats, deer, elk, etc). Only sheep and WTD get significant disease
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what species can serve as a reservoir and amplifying host for BTV?
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cattle
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where in the US is BT prevelant?
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southern/western states
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why do BT outbreaks occur in the summer and fall?
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insect vector- culicoides- is active
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can BT infections occur transplacentally?
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yes, for some serotypes
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how else can BT be transmitted?
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via semen
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when will bulls excrete virus in their semen?
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only at the time they are viremic
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BT incubation period
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1 week
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clinical signs of BT in sheep
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high fever --> anorexia, nasal discharge and excessive salivation. Nasal discharge becomes mucopurulent. Reddening of nasal and buccal mucosa followed by excoriation of buccal mucosa. Tongue/gums swollen and purple/blue. Oral lesions (erosions/ulcerations-catarrhal stomatitis). diarrhea. lameness due to coronitis.
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a very long ____ period is typical of BT
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convalescent
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fetal malformation most often associated with btv is
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hydranencephaly of the cerebral hemispheres and arthrogryposis
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what clinical sign of BTV is seen in deer?
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acute hemorrhagic dz
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where does BTV replicate?
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macrophages, dendritic cells and vascular endothelium
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BT virus mediated vascular injury leads to
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thrombosis of the small arteries resulting in infarcts --> widespread petechial hemorrhages and necrosis in most organs with extensive edema
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pathological lesions of BTV
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arteritis
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what lesion is rarely notced in cattle?
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arteritis
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how do the lungs of sheep with BTV appear?
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heavy with frothy fluid in air passages
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what is pathognomic for BTV?
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hemorrhagic lesion at the base of the pulmonary artery
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what sample should be collected for BTV isolation?
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blood with anticoagulant
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btv can be detected in blood and tissue samples by
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rt-pcr
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can pregnant animals be vaccinated for BTV?
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not with a MLV vaccine
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EHD stands for
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epizootic hemorrhagic dz
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EHD is very similar to _____ except that it does not ________
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Blue tongue; affect sheep
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EHD virus is an ____virus
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orbivirus
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there are ___ serotypes of EHD
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ten
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EHD is spread by _______ and is seen seasonally in
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culicoidies; late summer and fall
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only ____ get acute hemorrhagic dz from EHD - most are found dead
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WTD
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clinical signs of EHD in deer
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lung edema, widespread hemorrhage
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EHD is _____ in cattle but clinical disease is ____
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common; rare
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What cells does EHD infect?
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endothelial cells of blood vessels and causes an arteritis
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name four important vesicular dzs
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vesicular stomatitis, vesicular exanthema of swine, foot and mouth dz, swine vesicular dz
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how can these four dzs be differentiated?
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they can't
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which vesicular dz is present in the US?
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VESV- vesicular exanthema of swine
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san miguel sea lion disease is very similar to
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VES- endemic in sea mammals off the coast of california
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VSV is a ____ belonging to the virus family ____
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vesiculovirus; rhabdoviridiae
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species affected by VSV? Characteristics of dz?
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horses, cattle and pigs (influenza like dz in humans). Development of v esicles in mouth, feet and on teats.
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when do outbreaks of VSV occur?
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clustered outbreaks in summer/fall- coincide with vector transmission (sand flies and blackflies)
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how is VSV transmitted during an outbreak
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through mucosa or broken skin. Saliva and vesicular fluid from infected animals is highly infectious
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VSV incubation period
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about a week
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VSV clinical signs
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fever anorexia and excess salivation to start- mild fever with profuse ropy saliva. In horses and cattle see vesicles on dorusm of tongue (most pronounced in horse), dental pads, buccal mucosa, teats, and coronary bands. Ruptured vesicles leave shallow erosions/ulcers. Lameness often noted. Swine- vesicles on snout and feet.
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VSV morbidity/mortality
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10-80%/ 0%
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a vet must report any condition with _____________ to USDA/APHIS
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vesicular lesions
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VESV incubation period? It caused by a ____Virus
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18-72 hours; calici
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VESV is characterized by
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formation of vesicles on the snout, in the mouth and on the feet
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why is VESV so important?
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because it cannot be differentiated from other vesicular dz
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how is VESV dxed?
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rt-pcr and virus isolation on fluid from vesicles
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is VESV zoonotic?
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yes
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How can VESV and SMSV be distinguished?
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virus neutralization test
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what does SMSV cause
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abortions and vesicular lesions on flippers of sea lions
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what is one of the most important economic and political diseases in the world?
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FMD
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FMD is an ____ belonging to the family ____
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aphtovirus; picornaviridae
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how many types of FMD are there
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7 major, over 70 subtypes
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what animals are affected by FMD?
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cloven foot- cattle, pigs, sheep/goats, wild rums
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cattle recovered from FMD may remain carries with virus recovered In the
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epithelial cells lining the pharynx and esophagus
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fmd transmission
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in acutely ill animals, virus in saliva and most body fluids (incl semen). Spread by direct contact with infected animals and fomites, by inhalation (aerosols from milk trucks, wind), by ingestion (garbage feeding)
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FMD incubation period
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2-4 days
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FMD clinical signs
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cattle- lameness, lip smacking, salivation, vesicles may appear in mouth, on muzzle, on feet, on teats and udder. Vesciles start as blanched areas, rupture and heal completely in 2 weeks. In calves, death may occur from myocarditis. In pigs- lameness and vesicles on snout
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what sample should be submitted for FMD dx?
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vesicular fluid and epithelial covering
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what can help differentiate between the vesicular diseases?
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animal incoluation with vesicular fluid
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what happens after animals recover from FMD
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good immunity- type specific
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FMD vaccine?
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inactivated virus
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VIA antigen
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virus infection associated antigen- the rna polymerase enzyme synthesized during virus replication.
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SVD (swine vesicular dz) an ____ in the family ____
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enterovirus; picornaviridae
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pseudorabies in pigs causes
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encephalitis and reproductive failure
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pseudorabies in other species
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encephalitis and marked local pruritis (Frenzied animal)
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pseudorabies family/genus
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herpesviridae, alphaherpesviridae
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principal natural host, that maintains the virus latently
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pig (Domestic and feral)
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where does PRV go latent?
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principally in the neurons of the trigeminal ganglia
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what other animals can harbor and transmit the virus, and act as carriers?
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brown rat and raccoons may harbor and transmit the virus to pigs, domestic cats and dogs, but only for short periods. They are not carriers
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principle route for transfer of pseudorabies between pigs
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naso-oropharyngeal route
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after the virus recrudesces from neurons to replicate in nasal passages and oropharynx, where is PRC present?
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in saliva and nasal secretions
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is pseudorabies zoonotic?
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no
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clinical signs in adult pigs
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vague, mild, often unobserved. Some sows some vomiting, anorexia, depression, and incoordination. 50% pregnant sows will abort and have increased SMEDI
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clinical signs in young piglets
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high mortality if less than 3wks. Dz starts with coughing and sneezing, then consipation, incoordination, listlessness, tremors, convulsions and death within 72 hrs
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once pr becomes established on a farm, the suckling pigs are _____
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immune from the ab received in the colustrom and the CNS form is no longer recognized
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clinical signs in older weaned pigs
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vomiting, constipation, incoordination with 2% mortality
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do pigs with pseudorabies have pruritis?
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no
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pseudorabies in cattle
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"mad itch" intesnse pruritis, typically flank and hind legs. Itching causes frenzy. May see pharyngeal paralysis with salivation, mania, bellowing and convulsions. Death within 48 hours.
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prv in dogs and cats
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intense pruritis., usually of head regiong. Salivation (bulbar paralysis). Generalized convulsions. NO AGGRESSION. Howling, mewing, vomiting, diarrhea common
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where does prv replicate in pigs?
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oropharynx
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after replication, where does is spread?
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to cranial nerves, travels to the ganglia and the brain stem
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in pigs, what happens when an immune response occurs?
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virus replication is arrested and pigs become latently infected
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in animals besides pigs, how does PRV travel from site of infection to the CNS?
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via sensory nerves
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tests/samples to diagnose PRV
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FA-frozen tissue sections; IHC on FF tissue. PCR on tissues/nasal secretions/saliva. Virus isolation from throat swabs/tonsils/brain. Serology- ELISA
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how was PRV eradicated from domestic commercial herds in the US?
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test and slaughter policy
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will vaccines prevent infection with PRV?
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yes, except for virulent wild type virus
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is PRV a notifiable dz?
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yes
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porcine teschovirus type 1 virus family
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picornviridae
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porcine teschovirus type 1 causes
|
encephalomyelitis in pigs with high mortaility recorded in piglets (kills 50-90% affected animals)
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porcine teschovirus type 1 transmission
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fecal oral
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porcine teschovirus type 1 is aka
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porcine poliomyelitis / viral encephalomyeltitis
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PTV-1 severe form
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young piglets up to 3 wks old develop fever and anorexia followed by CNS signs- convulsions, hind leg paralysis, opisthotonus, and paddling movements
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PTV1 less severe form
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pigs develop fever and ataxia with eventual recovery
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where does PTV1 replicate?
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in the intestines
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what is required for CNS dz with PTV1
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viremia!
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PTV1 diagnosis / tissue samples
|
RT-PCR on brain tissue. FA and IHC on tissue sections
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porcine hemagglutinating encephalomyelitis virus is caused by a ____ which posses_____
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porcine coronovirus which possesses hemgglutinins
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porcine hemagglutinating encephalomyelitis virus transmission
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oral and respiratory routes with virus in feces
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porcine hemagglutinating encephalomyelitis virus infection:
|
inapparent in adults. In susceptible piglets less than 3 weeks old- repeated vomiting after suckling, emciation ,and death. Can be similar to PTV-1
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where does procine hemagglutinating encephalomyelitis virus replicate?
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nasal mucosa, tonsils, small intestine and then spreads to CNS
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porcine hemagglutinating encephalomyelitis virus diagnosis
|
demonstrating virus in tonsils and CNS by FA, or by isolating virus in TC and doing hemagglutination or HI test. Or RT-PCR
|
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porcine hemagglutinating encephalomyelitis virus control
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expose sows to virus prior to farrowing
|
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encephalomyocarditis virus is caused by a ____ in the family_____
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cardiovirus; picornavirus
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natural reservoir of encephalomyocarditis virus
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rodents/rats
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virus transmission of encephalomyocarditis virus
|
eating infected rats or food contaminated by rodent feces
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encephalomyocarditis virus is only a significant pathogen of
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pigs and elephants
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encephalomycoarditis virus clinical signs
|
SMEDI in sows. Causes death in piglets and finishing pigs, acompanied by trembling and incoordination. Suddent deaths in elepahnts comin in contact with infected rats
|
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EMCV pathological lesions
|
coagulative necrosis in heart= "Tiger heart". In pigs also see encephalomyelitis.
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TGE is caused by a porcine ______
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coronavirus
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TGEV shares antigens with
|
FIP, canine coronavirus and human coronavirus
|
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TGE transmission
|
fecal oral, readily transmitted by contaminated fomites
|
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what is the only natural host of TGE?
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swine
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TGE in adults
|
subclinical, usualy, but they are an important source of infection of the piglets since they gcan shed TGEV for up to 3 months after recovering from infection
|
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TGE incubation period
|
12-18 hours (Results in explosive outbreaks)
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what seasons is TGE more prevalent in?
|
winter and spring
|
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TGE epizootic/acute dz associated with epidemic outbreaks
|
on farms that have never experienced TGE before. Virus introduced by replacement pigs, visitors, pigs in contact with outside pigs, etc. Sudden onset diarrhea/vomiting in suckling piglets. Yellow, watery, putrid, diarrhea (may contain milk). Piglets dehydrate rapidly and die in 2-5 days.
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TGE enzootic form of the dz assoc with endemic infections
|
seeon on large farms with continuous farrowing system. Affects weaned piglets. Sporadic diarrhea and some vomiting for 3-4 d
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TGEV infects and kills the ______ ____ at the tips of the villi of the _______ resulting in ____ ____
|
columnar epithelium, small intesting, shortened villi
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TGE results in loss of digestive enzymes, decreased capacity of epithelial cells to absorb water and nutrients resulting in
|
diarrhea- dehydration, electrolyte problems, lack of nutrients, death.
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the main reason for TGE diarrhea is
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osmotic effect
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enteric _____ proliferate in intestine and ____ worsens the condition
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bacteria; toxemia
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piglets that survive TGE often delveop
|
secondary bacterial infection- causes permanent damage to intestinal epithelium (results in malabsorption)
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epidemic outbreaks are followed by
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development of immunity in pigs throughout the whole herd, and TGE disappears from the farm
|
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endemic infections on large farms
|
constant source of infection to keep the outbreak going.
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pathology of TGE at necropsy
|
thin/transparaent intestinal villi due to villous atrophy
|
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which IG protects piglets as long as they suckle?
|
IgA
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what tests are important in differentiating between different coronaviruses?
|
ELISA and PCR (RT-PCR since coronavirus)
|
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best way to diagnost TGE
|
FA of frozen sections of jejunum
|
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how should sows be vaccinated for TGE?
|
live and inactivated vaccines given 3-4 weeks before farrowing/during pregnancy (MLV CAN BE GIVEN DURING PREG- UNUSUAL)
|
|
|
porcine epidemic diarrhea virus is caused by a
|
coronavirus
|
|
|
which pigs are affected by procine epidemic diarrhea?
|
weaned pigs. Rarely suckling pigs.
|
|
|
PEDV is characterized by
|
profuse watery diarrhea, vomiting, high morbidity, mortality sometimes approaches 80%
|
|
|
porcine rotavirus family/genus
|
reoviridae/rotavirus
|
|
|
when do piglets become infected with rotavirus?
|
3-5 weeks, usually after weaning
|
|
|
when do seropositive sows shed rotavirus in their feces?
|
5 days before until 2 weeks after farrowing
|
|
|
rotavirus is aka
|
white scours/milk scours
|
|
|
porcine rotavirus diarrhea
|
typically profuse, watery, with flecks of undigested milk
|
|
|
rotavirus infects and destroys:
|
the terminally differentiated enterocytes lining the tips of the intestinal villi causing intestinal malabsorption and maldigestion. Villi become shortened and covered with less differentiated cells from the crypts
|
|
|
diagnosing porcine rotavirus
|
ELISA detects virus in feces, and RT-PCR
|
|
|
porcine postweaning multisystemic wasting syndrome is caused by
|
porcine circovirus type 2
|
|
|
PMWS occurs
|
sporadically
|
|
|
clinical signs of PMWS
|
generalized lymphadenopathy, weight loss, lymphopenia. Assoc with respiratory dz complex- broncho-intersitial pneumonia. Assoc with SMEDI in sows
|
|
|
where does porcine circovirus type 2 replicate?
|
macrophages and lymphoid tissues
|
|
|
PCV2 _____ infection with other pathogens
|
exacerbates
|
|
|
infection with other pathogens induce and enhance PCV2 replication through an
|
immune mediated mechanisms
|
|
|
PMWS diagnosis
|
ELISA for serology, PCR for virus ID
|
|
|
porcine reproductive and respiratory syndrome virus is AKA
|
blue ear pig dz
|
|
|
PRRSV is caused by an ___virus
|
arterivirus
|
|
|
PRRSV replicates in _____ and is shed from ____
|
replicates in macrophages in lungs and lymphoid tissues and is shed from all secretions of infected animals, including semen
|
|
|
how does PRRSV establish a permanent infection once introduced in a herd?
|
through virus transmission from infected sows to piglets via placenta and milk
|
|
|
PRRSV in young pigs
|
respiratory dz, anorexia, fever, dyspnea, cyanosis of extremities caused by interstitial pneumonia
|
|
|
PRRSV in sows
|
SMEDI
|
|
|
PRRSV dx
|
serology ELISA, RT-PCR to detect virus in lymphoid tissue. IHC on infected FF Tissues
|
|
|
best way to get rid of PRRSV
|
test and slaughter
|
|
|
swine influenza
|
H1N1 or H3N2
|
|
|
swine influenza is an acute resp dz characterized by
|
sudden explosive onset, high morbidity, extreme weakness and prostration, coughing and thumps
|
|
|
when does swine flu primarily occur
|
fall/winter months
|
|
|
clinical signs of swine flu
|
sudden onset of fever, anorexia followed by etreme prostration, labored breathing, thumps, deep cough, watery discharge from eyes/nose. Disease looks bad but recovery is rapid after a few days.
|
|
|
_____ may exacerbate swine flu
|
secondary bacterial infection (haemophilus)
|
|
|
DX swine flu
|
PCR, serology, viros isolation in nasal secretions
|
|
|
porcine respiratory coronavirus is a variant f
|
TGE virus that has acquired a tropism for the respiratory tract by a deletion in the glycoprotein spike
|
|
|
PRCV infects pigs of ___ ages causing __
|
all; subclinical and mild respiratory dz
|
|
|
PRCV is ____ in swine herds worldwide and is transmitted by
|
enzootic; aerosol
|
|
|
where can virus be detected by RT PCR and ELISA
|
nasal swabs and lung tissue
|
|
|
inclusion body rhinitis is caused by _____ or _____
|
beta herpesvirus or porcine cytomegalovirus
|
|
|
IBR mainly infects ________ and causes _________
|
young pigs less than ten weeks of age; rhinitis and sinusitis
|
|
|
IBR plays a contributory role in the development of
|
atrophic rhinitis
|
|
|
IBR clinical sign
|
sneezing, mucopurulent discharge, piglets do not suckle and remained stunted. IN inclusions present in enlarged cells of inflamed nasal mucosa.
|
|
|
DX IBR
|
detection of inclusions in mucosal cells or from nasal swabs. ELISA test.
|
|
|
porcine parvovirus causes
|
reproductive failure in swine- characterized by embryonic and fetal infections
|
|
|
SMEDI
|
stillbirth, mummified fetuses, embryonic deaths, infertiility
|
|
|
what are the outward clinical signs of PPV in sows?
|
NONE
|
|
|
on farms where the virus is endemic, the disease develops mainly when seronegative pregnant gilts are exposed oronasally to the virus during days ____ of gestation
|
1 thru 70
|
|
|
sows infected at >70d gestation
|
will farrow normal piglets immune to PPV
|
|
|
after PPV infection, ____ develops and
|
viremia develops and the virus crosses the placenta
|
|
|
how can PPV be controlled?
|
exposing gilts to sow feces. MLV vaccine 2 weeks before breeding
|
|
|
dx PPV
|
difficult- submit mummies or aborted fetus. PCR can detect but contamination common. FA test on fresh tissue is possible
|
|
|
porcine teschoviruses types 2-7 and 11-13- where are they found
|
all commercial swine herds worldwide
|
|
|
only virus associated with cNS infection
|
porcine teschovirus type 1
|
|
|
suipoxvirus is a
|
mild disease of young pigs
|
|
|
suipoxvirus characteristics
|
localized cutaneous lesions esp on ventral abdomen. Usually see umbilicated pustules 1-2cm in diameter which crust over and scabs within a week. Recovery within 3 weeks
|
|
|
how is suipoxvirus transmitted
|
by the hog louse- haematopinus suis
|
|
|
classical swine fever is AKA
|
hog cholera
|
|
|
what is the most important dzo f swine worldwide?
|
classical swine fever
|
|
|
why is CSF so important?
|
economically- interferes with trade. Countries that have hog cholera cannot export meat products
|
|
|
CSF virus is a____ in the family ____
|
pestovirus; flaviviridae
|
|
|
how is CSFV transmitted?
|
1) direct contract in sick pigs (virus preseent in all excretions). 2) mechanically via fomates and 3) thru feeding of HCV infected uncooked pork products
|
|
|
clinical signs of CSFV
|
sudden onset of peractue deaths. High fever, depression, conjunctivitis, diffuse purplish discolaration of skin of abdomen and nervous signs (Circuling, convulsions). Death within 5-7 days of onset of fever. Mild strains cause SMEDI
|
|
|
pathological lesions of CSFV
|
extensive diffuse hemorrhages in all organs, splenic infacrtcs and button ulcers in the colon. TURKEY EGG KIDNEY
|
|
|
what causes the widespread hemorrhages seen with CSFV
|
degeneration of endothelial cells of blood vessels
|
|
|
when should HC be suspected?
|
when you see dz characterized by high fever, hemorrhages with purplish discolaration and very high mortality
|
|
|
what samples should be submitted for virus detection?
|
spleen, tonsils, lymph nodes in formalin
|
|
|
two virus that is transmitted via uncooked meat
|
hog cholera nd ASF
|
|
|
african swine fever caused by a large dNA virus-
|
asfarvirus
|
|
|
how do domestic pigs in endemic countries acquire the virus
|
from warthogs via infected Argasid ticks
|
|
|
sylvatic cycle
|
ASFV cycles between warthogs and the argasid tick - ornithodorus moubata
|
|
|
ASF classic form
|
in domestic pigs cahracterized by high morbidity, a short clinical illness (2-3d), fever, cyanosis, skin blotching, incoordination, almost 100% fataility
|
|
|
ASF chronic form
|
low morbidity, low case fatality. Emacation and lameness due to joint swelling
|
|
|
ASF pathological lesions at necropsy
|
extensive hemoorhages on skin and in organs. Enlarged friable spleen, hemorrhagic lymph nodes
|
|
|
what systems does avian influenza affect?
|
respiratory, enteric, nervous
|
|
|
avian influenza in chickens
|
inapparent if LPAI, very severe/high mortality if HPAI
|
|
|
avian influenza virus familky
|
orthomyxoviridae
|
|
|
how many HA and NA types are there?
|
15 HA, 9 NA
|
|
|
HA =
|
hemagglutinin
|
|
|
NA=
|
neuramidase
|
|
|
avian influenza = HA types
|
5, 7, 9
|
|
|
HPAI H5N2 - how did it start?
|
as an LPAI virus that circulating amongst poultry for some time before mutating into the HPAI virus
|
|
|
do most wild, migrating aquatic birds show clinical signs of dz?
|
no
|
|
|
where do avian influenza viruses replicate
|
primarily in the GI Tract of aqutic birds
|
|
|
virus excretion of avian influenza?
|
in feces
|
|
|
where does reassortment occur?
|
in the GI tract
|
|
|
source of infection for avian influenza
|
wild migrating and overwintering aquatic birds that transmit the virus to the susceptible domestric poultry
|
|
|
avian influenza transmission
|
fecal oral - ingestion of the virus. Aerosol can play a role. Virus can be carried and spread through personnel, shoes, clothing, etc
|
|
|
HPAI clinical signs
|
high fever, anorexia, lethargy. Sneezing, coughing, mucoid nasal discharge, respiratory distress, edema of face and head. Diarrhea common. May also show nervous sighs. Death within a few hours of onset of clinical signs
|
|
|
LPAI clinical signs
|
decline in egg production. May have diarrhea and sinusitius (turkeys)
|
|
|
pathological lesions of avian influenza
|
necrosis of various organs. Petechial hemorrhages in the heart m, abdominal fat, and in the mucosa of the proventriculus. Encephalitis often noted
|
|
|
what needs to happen before the influenza virus can infect cells?
|
the HA glycoprotein has to be cleaved to HA1 and HA1. this occurs thru the action of proteases located on the cells of the resp and GI Tracts
|
|
|
LPAI viruses have a single basic AA _____ at the cleage site, and the glycosylation of this AA sheilds the cleavage site from cleavage by proteases
|
arginine
|
|
|
why are LPAI viruses essentially restricted to replicating in resp and GI TractS?
|
the HA of LPAI can only be cleaved by trypsin-like enzymes present on the epithelial cells of the resp and GI Tracts
|
|
|
why can HPAI virus HA be cleaved by other proteases?
|
through mutations, they accumulate basic AA just before the cleavage site, "opening" it up.
|
|
|
what can cleave the HA of HPAI intracellularly?
|
endopeptidase furin in the golgi apparatus
|
|
|
DX avian influenza
|
PCR - differentiate HP/LP. Detect LP with HI, ELASA, FAT
|
|
|
reportable? Control?
|
yes! Slaughter/quarentine. NO vaccination.
|
|
|
which avian influenzas are zoonotic?
|
h5n1, h7,n3, h7n7, and h9n2
|
|
|
avian paramyxovirus-1 is aka
|
newcastle disease virus
|
|
|
newcastle disease is associated with
|
high mortality in domestic birds caused by the hihgly virulent strain
|
|
|
how many strains/pathotypes of avian paramyxovirus1 are there?
|
5
|
|
|
viscerotropic velogenic pathotype
|
90-100% mortality, highly virulent, often no clinical signs. When clinical signs are present- starts with resp dz, fever, dullness, thirst, ruffled feathers, hemorrhagic comb, edema of head, resp distress. Can be neuro signs, acute diarrhea
|
|
|
neurotropic velogenic
|
highly virulent, high mortality
|
|
|
mesogenic pathotype
|
less virulent, 25% mortality. Resp signs, reduced egg production (Soft shelled eggs with watery albumin)
|
|
|
avirulent lentogenic pathotype
|
often used as vaccines - no clincal signs of dz
|
|
|
the fifth pathotype?
|
asymptomatic enteric pathotype
|
|
|
what bird species have avian paramyxociruses types 2-9 been isolated from?
|
imported psitacines
|
|
|
most important disease of poultry worldwide?
|
newcastle disease
|
|
|
in the us, what maintains the ND virus?
|
domestic birds and cormorants
|
|
|
infeted birds shed paramyxovirus by
|
aerosolized roplets from the respiratory tracts for several weeks after recovery from infection. Virus also spread via feces, eggs, fomites and contaminated clothing
|
|
|
the greatest risk for transmission of the virus during an nd outbreak is through
|
human activity- mechanical transfer of infective material on equipment, supplies, clothing, shoes and other fomites
|
|
|
ND incubation period
|
7 days
|
|
|
pathological lesions of ND
|
necrosis of various organs. Petechial hemorrhages in the heart m, abdominal fat, and in the mucosa of the proventriculus. Encephalitis often noted
|
|
|
what does the virulence of avian paramyxovirus 1 depend on?
|
the cleavability of the F protein into F1 and F2
|
|
|
what does intracellular cleavage (of AI or ND) mean?
|
the virus leaves the cells as infectious particules and in that way can go viremic and infect cells in all organs of the body
|
|
|
ND diagnosis
|
RT-PCR. IHC, FAT, serology
|
|
|
is there a vaccine available for ND?
|
yes, both live and inact are available. Inact have to be injected. Lentogenic live vaccine can be given in drinking water or by aerosol at 4-6 months.
|
|
|
is VVND a reportable dz?
|
yes
|
|
|
can humans be infected with NDV?
|
yes- conjunctivitis
|
|
|
infectious laryngotracheitis is caused by
|
gallid herpesvirus1
|
|
|
ILT incubation period? Transmission?
|
48 hours, direct contact
|
|
|
ILT characteristics
|
resp distress due to inflammation of larynx and ttrachea. Laryngeal necrosis and inflammation lead to the formation of diphtheric membranes that can occlude the trachea leading to resp distress. Affected chickens cough, shake heads, gasp for air and sneeze. high morbidity, 10-70% mortality.
|
|
|
do birds remain carries of the virus upon recovery?
|
yes
|
|
|
ILT vacination
|
attenuated vaccine via conjunctival sac
|
|
|
infectious bronchitis virus is caused by a
|
coronavirus
|
|
|
incubatoin period? Transmission?
|
48hrs, by aerosol and ingestion of contaminated feed
|
|
|
IBV characteristics
|
acute resp infection with sneezing, coughin, gastpin, and accumulation of excess mucous in bronchi and trachea. High morbidity, 25-30% mortality in young chicks. Layers have subclinical infections with drop in egg product, soft shelled/malformed eggs
|
|
|
IBV vaccine
|
attenuated vaccines in drinking water or as aerosol
|
|
|
mareks dz is aka
|
avian leukosis, range paralysis
|
|
|
mareks dz is caused by
|
gallid herpesvirus2
|
|
|
mareks primary host
|
chickens
|
|
|
markeks is transmitted by ____ but
|
aerosol, but not via droplet aerosol from resp track- via inhallaation of infected cells that line the feather follicles
|
|
|
virus is inhaled and
|
taken up by lung marcophages. Disseminates throughout the body via infected lymphocytes. Virus reaches follicles in the ksin and infects epithelial cells lining the feather follicles.
|
|
|
where does mareks go latent?
|
t-cells
|
|
|
when can paralysis of legs and wings be seen?
|
in birds where the sciaticand brachial nerves have been infiltrated with transofmred t-cells
|
|
|
pathological lesions of markes
|
sciatic and brachial nerves are enlarged and loose their typical striation patterns. In visceral organs, lymphoid tumros cause enlargement of gonads, liver, and spleen
|
|
|
avian encephalomyelitis
|
epidemic tremor. Dz of 1-3wk old chicks. Caused by a picornavirus- replicates in SI And spreads to CNS
|
|
|
EEE in pheasants
|
staggaring and paralysis. High mortality. Introduced through infected mosquitos, spread between pheasants by pecking
|
|
|
infectious bursal dz of chickens is caused by
|
birnavirus- nonenveloped with segmented DS RNA genome
|
|
|
IBD selective replicates in the ____ Where it causes
|
bursa fabricius (where chickens manufacture their b-cells); causes swelling, edema, hypermia, and sub serosal hemorrhages in the gland. Clinical signs = anorexia, slow growth, enhanced susceptibility to secondary infections
|
|
|
pacheco's dz caused by
|
psittacine herpesvirus (At least 3 serotypes)
|
|
|
birds that recover from pachecos are
|
carries and can excrete virus in feces during times of stress - primarily fecal transmission
|
|
|
signs of pachecos
|
lethargy, anorexia, regurg, diarrhea, ruffled feathers, neuro signs. Feces color- dark green to bright yellow. Birds die of massive liver necrosis characterized by enlarged liver, spleen, and kidneys. Multifocla hepatic and splenic necrosis with eosinophilic IN inclusion bodies.
|
|
|
pachecos tx?
|
acyclovir- but can cause liver damage
|
|
|
psittacine beak and feather dz caused by a
|
circovirus
|
|
|
PBFD results in
|
abnormal feather development and beak growth, characteristically seen in young fledging birds during their first feather formation after replacement of the neonatal downs. Beak may become brittle and misformed. In older birds, dystrophic feathers appear on the wings, tail, and crest.
|
|
|
birds affected with PBFD die due to
|
immunosuppresion and secondary infections brought on by the circovirus
|
|
|
where is PBFD present?
|
in the feather dust and droppings of acutely sick birds and in carrier birds with clinical signs
|
|
|
samples tested for PBFD
|
PCR= blood and feces
|
|
|
avian polyoma virus is aka
|
burderigar fledgling dz
|
|
|
APV is an
|
acute generalized dz of fledgling parakeets and most psittacine birds
|
|
|
APV of burdgerigars causes
|
variable morbidity/mortality, with abnormal feather development (French molt). Normal feathers will return with the next molt.
|
|
|
APV of psitacines
|
characterized by acute death in 1-2d, with birds dying with full crop, distended abdomen, diarrhea, reddening of skin. 30-80% mortality
|
|
|
Proventriculus dilation disease / macaw wasting dz
|
caused by a borna virus. Mostly seen in lg macaws. First signs are vomiting/regurg and passage of undigested seed/food. Virus causes lymphoplasmacytic ganglioneuritis and encephalitis- damages nerves enervating the proventriculus
|
|
|
hemorrhagic enteritis of turkeys
|
caused by turkey adenovirus. Acute disease of young turkeys (older than 4wks), characterized by bloody droppings and death. Develop and acute hemoorhagic enteritis
|
|
|
tnramissible enteritis of turkeys / blue comb dz
|
turkey coronavirus. Highly infectious dz of turkeys of all ages characterized by constant chirping, depression and wet feces
|
|
|
duck hepatitis virus
|
acute disease of 2-3 week old ducklings caused by a picornavirus. High morbiidty and mortality. Affected ducklings lag behind, become somnolent, eventually fall on their side, exhibit kicking movements and die with opsithotonus. Liver lesions- enlarged hemorrhagic liver with hepatic necrosis
|
|
|
duck viral enteritis / duck plague
|
caused by anatid herpesvirus 1. acute highly contagious. Sudden death, high mortality, diarrhea. Extensive hemorrages and focal necrosis of internal organs. Vaccine available
|
|
|
inclusion body hepatitis
|
adenovirus, dz of broilers. IN inclusions in liver
|
|
|
rotavirus in chickens
|
diarrhea
|
|
|
chicken infectious anemia
|
caused by circovirus. 2-4week old chickens. Aplastic anemia and profound immunosuppresio. Birds become resistant at 4weeks of age
|
|
|
fowlpox
|
characterized by proliferative cutaneous nodulse in the most unfeathered parts of the body or by lesions in the upperrespiratiry and oral mucosa (Diphtheric form). Causes economic loss. Spread via mosquitos, lice, ticks, direct contact. Vaccine available
|
|
|
avipox
|
resembles fowlpox. Young birds usually most susceptibile, high mortality
|
|
|
avian leukosis and sarcoma
|
retrovirus. Transmitted from hens to chicks through the eggs. Infected chicks remain carriers for life. Also spread thru bird to bird contact. Long incubation period, dz rarely seen before 16 weeks of age. Lymphoid leukosis (big liver dz) is most common outcome in infected chickens. affected birds become progressively weaker and emaciated with enlarged abdomen. tumors/leukemia often seen, included osteopetrosis (thick legs) erythroblastosis and myeloblastosis. necropsy- neoplasms seen, enlarged visceral organs, etc.
|
