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Herpesviridae Flashcards

1
Q

Describe the family Herpesviridae morphology & genome.

A

-enveloped, spherical to pleomorphic
-capsid surrounded by layer of globular material = ‘tegument’
-double stranded DNA genome

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2
Q

Describe viral replication of Herpesviridae.

A

-DNA rep & encapsidation in nucleus
-viral envelope acquired by budding thru inner layer of nuclear envelope
-mature virions accumulate in vacuoles in cytoplasm & released by exocytosis or cytolysis

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3
Q

Describe Herpesviridae general characteristics.

A

-dont survive well outside of host
-moist, cool environ conditions promote extended survival
-latent inf animals = reservoir
-persistent inf w periodic or cont shedding in all inf
-reactivation of latent inf associated w stress: inter current inf, shipping, cold, crowding, administer glucocorticoid drugs
-eosinophilic intranuclear inclusion body
-type A cow dry bodies
-form syncytium

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4
Q

Describe the subfamily Alphaherpesvirinae properties.

A

-high cytopathic in cell culture
-short replication cycle
-some like pseudorabies virus (suid herpesvirus 1) have broad host range - most are restricted in their natural host range
-many make localized lesions in skin or mucosa of resp & genital tract
-gen inf characterized by foci of necrosis in any organ or tissue in young/immunocompromised animals
-preg animals = virus across placenta -> abortion w multi focal area of necrosis in fetal organs

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5
Q

Describe a-herpesvirinae - bovine herpesvirus 1.

A

-inf bovine rhinotracheitis (IBR)
-inf pustular vulvovaginitis
-ocular form of IBR
-abortion
-sys disease of newborn calves

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6
Q

Describe bovine herpesvirus 1 subtypes & transmission.

A
  1. Subtypes
    -BHV 1.1 respiratory
    -BHV 1.2 genital
  2. Transmission
    -respiratory & conjunctivitis from droplet
    -genital from coitus or AI w inf semen
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7
Q

Describe BHV1 pathogenesis.

A

-both genital & respiratory form = lesions are focal areas w epi cell necrosis -> ballooning of epi cells
-inclusion in nuclei at periphery of necrotic foci
-inflam resp in necrotic mucosa w formation of overlying accumulation of fibrin & cell debris (pseudomembrane)
-life long latent inf w periodic virus shedding after BHC1 inf
-seropos animals are carriers
-virus reactivated from latency by corticosteroids or stress
*sites of latency:
>trigeminal n = respiratory dx w BHV1
>sciatic n = genital dx w BHV1

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8
Q

Describe BHV1 clinical signs of the respiratory form.

A

-necrotic rhinitis, dust pneumonia
-laryngitis, tracheitis
-inflam nares (red nose) bc hyperemia + grey necrotic foci on mucous
-nasal discharge more profuse & mucopurulent
-fibrinonecrotic rhinitis
-recover 10-14d
-complication from secondary bacterial inf like shipping fever (Mannheimia hemolytica & Pasteurella multocida)
-death from secondary bronchopneumonia

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9
Q

Describe the ocular form of IBR.

A

-conjunctivitis
-dont misdiagnose as pink eye
>IBR lesion confined to conjunctiva & no lesion on cornea except diffuse edema

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10
Q

Describe BHV1 & abortion.

A

-common sequel to natural inf (100d after inf)
-result of modified live virus vacc given to preg animals
-animals in contact w IBR sus preg animals
-fetus in 2nd half of gestation = higher incidence of abortion but early embryonic death also poss
-abortion doesnt correlate w severity of disease in dam but is preceded by pustular vulvovaginitis

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11
Q

Describe BHV1 & systemic disease of newborn calves.

A

-severe in calves >10d = fatal
-inf in utero or right after birth

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12
Q

Describe BHV1 genital disease.

A
  1. Inf pustular vaginitis
    -after coitus
    -freq urination
    -tail held in elevated position & excessive tail switching
    -vag mucosa red & swollen
    -mild vag discharge
    -vulva swollen, red spots, discrete pustules
  2. Balanoposthitis
    -inflam & pustules in mucosa of penis & prepuce
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13
Q

Describe the vaccine of BHV1.

A

-modified live vacc, subunit, inactivated
-parenteral & intranasal
>both stim humoral prod of ab
>parenteral may cause abortion in preg cow
>intranasal safe for preg cow

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14
Q

Describe the subfamily a-Herpesvirinae - BHV2.

A
  1. Bovine ulcerative mammilitis
    -host: cattle, heifer (2 wk after calving)
    -transmission:
    >direct & fomites thru trauma to skin
    >mech transmission via stable flies & arthropods
    -CS:
    >severe = teat swollen & painful, skin blue, exudes serum, formation of raw ulcer
    >mastitis
  2. Pseudo lumpy skin disease
    -host: cattle
    -South Africa
    -mech transmission via arthropods
    -CS: fever, skin nodules on faces neck, back, perineum
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15
Q

Describe the subfamily a-Herpesvirinae - porcine herpesvirus 1/suid herpesvirus 1.

A

‘Pseudorabies (Aujeszky disease, Mad itch)’
-host:
>primarily pigs
>range of secondary hosts = horse, cattle, sheep, goat, dogs, cats, feral
>humans refractory to inf

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16
Q

Describe pseudorabies transmission in primary VS secondary hosts.

A
  1. Primary
    -recovered pigs = primary reservoir & latent carrier for life
    -rodent (rat) = reservoir
    -transmission route:
    >virus shed in saliva, nasal discharge, milk of inf pig
    >virus not shed in urine or feces
    >licking, biting, aerosol, ingestion, water, feed
  2. Secondary
    -dog & cat = ingest inf pig meat or rodent
    -cattle = direct contact w inf pig, oral & nasal route
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17
Q

Describe pseudorabies in pigs.

A
  1. Pathogenesis
    -primary site of viral rep in URT
  2. Spread
    -virus rep in tonsil & nasopharynx
    -spread via lymphatics to LN
    -viremia w virulent strains w virus in diff organs
  3. Spread in CNS
    -via axon of cranial n
    -prefer neurons of pons & medulla
  4. CNS lesions
    -ganglioneuritis
    -nonsuppurative meningoencephalitis
    -perivascular cuffing
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18
Q

Describe pseudorabies clinical signs in pigs.

A

-non immune piglet = 100% mortality rate
-non immune preg sow = 50% abortion rate
-older piglet, growers, adult pig = mild dz (mortality rate 2%)
-pruritis in 2ndary host (rare in pig)
-piglet born to non immune sow = (most sus) signs of CNS disease -> in coordination of hind limbs, fitting, tremors & paddling
-weaned & growing pig
>central nervous signs reduced & inc in resp sign
-non immune preg sow:
>inf before 30d of gestation = death & reabsorption of embryo
>inf in late preg = mummified, macerated, still born, weak, or normal swine
>20% sows aborting are infertile next breeding but eventually conceive
-necropsy finding:
>gross lesion absent/minimal
>serous to fibrinous rhinitis common & necrotic tonsillitis

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19
Q

Describe pseudorabies in secondary hosts.

A

*host: ruminant, dog, cat, shoat, horse
*CS: pruritus, hyper acute, rapid progress, high mortality
1. Cattle (Mad itch)
-pruritis
-frenzied
-progressive involvement of CNS, stage of paralysis, ataxia
-death from resp failure
2. Dogs
-frenzy w pruritis
-self mutilation
-paralysis of jaw & pharynx w drooling
-plaintive howl
-dont attack
3. Cats
-dx progress rapid that pruritis not seen

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20
Q

Describe the vaccine of pseudorabies in pigs.

A

-vacc swine in enzootic area reduce loss
-vacc dont prevent inf or establish latent inf by wild type virus but can alleviate CS in pigs of certain age
-recombinant DNA, deletion mutants, live attenuated, inactivated

21
Q

Describe subfamily a-herpesvirinae - equine herpesviruses.

A
  1. Equine herpes virus 1
    -endemic worldwide
    -inhalation, direct/indirect contact w nasal discharge, aborted fetus, placenta/fluid
  2. Equine herpes virus 4
22
Q

Describe the latency of EHV1.

A

-latent EHV1 in tissue of CNS (neuron cell body - trigeminal ganglia) & lymph system (leukocytes & lymphocytes) w/o CS
-immunosuppressed = virus reactivated causing CS or shedding

23
Q

Describe EHV1 pathogenesis.

A

Immunosuppresion

24
Q

Describe EHV1 other diseases.

A
  1. Respiratory diease
    -young horse
    -rhinopneumonitis
  2. Encephalomyelopathy (EHM)
    -any age or breed
25
Q

Describe EHV1 reproductive form.

A

-abortion occur early in gestation but majorly in last trimester (8-10mo)
-repro efficiency not compromised
-case of abortion sporadic
-lg # of sus mare exposed to aborted conceptus -> outbreak of abortion (3 yr cycle)
-natural immunity to EHV1 last 2-3yr

26
Q

Describe EHV4 general characteristics.

A

‘Equine viral rhinopneumonitis’
antigenically related to EHV1
1. Transmission
-sporadic
-<2yr
-cause lifelong latent inf that can be reactivated
-droplet inf from inf horse & older horse = in apparent viral shedding
2. Pathogenesis
-cause less severe tissue destruction than EHV1
-rarely cause abortion, viremia, death
3. CS
-URT disease (rhinopharyngitis & tracheobronchitis)
4. Vaccine
-prevent early inf of suckling foals + latency of inf in preg mare
-live attenuated, inactivated EHV1 + combined w EHV1 & EHV4
-immunity is short lived

27
Q

Describe subfamily a-herpesvirinae - K9 herpesvirus 1.

A

‘Hemorrhagic disease of puppies’ (fading puppy syn)
1. Host
-dogs, wild canidae = fatal
2. Transmission (neonates)
-contact w inf oral, nasal, vag secretion of dam
-contact w secretion of littermate
-in utero
-from passage of birth canal
-contact w inf fomite (rare)
(Older dogs)
-venereal
-contact w saliva, nasal discharge, urine of inf dog/puppy

28
Q

Describe CHV pathogenesis in puppies.

A
  1. In utero
    -abortion, still birth, infertility
    -survive = pups develop CHV1 inf in 9d from birth
  2. Systemic neonatal inf
    -pup <1wk most sus to fatal gen inf
    -initial rep in nasal epi, tonsil, pharynx
    -mucosal invasion -> leukocyte (Mac) associated viremia
    -virus rep in endothelial cell
    -diffuse necrotizing vasculitis, multi hemorrhagic necrosis in organs
    -thrombocytopenia, DIC
  3. CNS inf
    -meningoencephalitis in oro nasal inf pup
    -virus travel up nerve axon to CNS
    -pup die from sys illness before neuro sign seen
29
Q

Describe the factors governing systemic neonatal infection of CHV1.

A
  1. Body temp of puppies is critical
    -CHV1 rep at 33c = temp of outer genital & URT
    -hypothalamic thermoreg center of pup not operative fully until 2-3 wk of age
    -pup depend on temp of maternal contact
    -more severe hypothermia = more severe rapid course of dz
  2. Maternal immunity
    -maternal Ab = protection
    -pup from seroneg bitch = vulnerable to severe form of dz
30
Q

Describe CHV1 clinical signs in puppies.

A

-painful crying, ab pain, anorexia, dyspnea, pass soft odorless green stool, no elevation in body temp
-survive sys dz = persistent neurological sign like ataxia, blindness

31
Q

Describe CHV1 clinical signs of adults.

A
  1. Adult genital inf
    A) bitch
    -gen asymp or limited to vag hyperemia
    -vesicular vaginitis w discharge = lesion
    -in utero inf = abortion, still birth, mummy fetus, infertility
    B) male dog
    -balanoposthitis
  2. Adult respiratory inf
    -old dogs = mild resp inf (rhinitis & pharyngitis)
  3. Ocular inf = conjunctivitis
32
Q

Describe the control of CHV1.

A

-reduce hypothermia w heated whelping box, infrared lamp
-low prevalence of severe illness in pups (<20%) & paucity of CS in adult animal = lack of avail vacc

33
Q

Describe the subfamily a-herpesvirinae - feline herpesvirus 1 transmission.

A

‘Feline rhinotracheitis’
*one of the 2 most common cause of inf respiratory dz in cats: FHV1 & feline calcivirus (FCV)
Transmission
-FHV1 shed in ocular, nasal, oral secretion
-spread by direct contact w inf cat
-aerosol route not imp
-natural route = oral, nasal, conjunctiva
-all recovered cats = latent inf carrier
-reactivate from stress or steroids = shedding in oronasal & conjuctival secretion

34
Q

Describe FHV1 pathogenesis.

A

-virus rep in mucosa of nasal septum, turbinates, nasopharynx, tonsil
-viremia rare bc viral rep restricted to area of low temp = URT
-inf lead to area of multifocal epi necrosis, inflam, fibrinous exduation
-secondary bacterial inf cause complication

35
Q

Describe clinical signs in FHV1.

A
  1. Kitten (up to 4wk)
    -URT dz
    -rhinotracheitis
    -fatal bronchopneumonia from secondary bacterial inf
    -conjunctivitis & ulcerative keratitis
  2. Cats (>6mo)
    -mild or subclinical dz
  3. Preg
    -abortion around week 6
    -no evidence of virus crossing placenta
    -severe sys effect of illness & not direct effect of virus
    *conjunctivitis: hyperemia & serous ocular discharge
    *ulcerative keratitis
    *severe necrohemorrhagic rhinitis
    *multifocal necrohemorrhagic palatitis
36
Q

Describe FHV1 vaccine.

A

3 types for FHV1 & FCV
1. MLV parenterally
2. MLV intranasal
3. Inactivated vacc parenterally

37
Q

Describe subfamily a-Herpesvirinae avian diseases.

A
  1. Infectious laryngotracheitis
    >Gallid herpesvirus 1
  2. Mareks disease
    >gallid herpesvirus 2
38
Q

Describe infectious laryngotracheitis (ILT) transmission.

A
  1. Inhalation *
  2. Droplets to conjunctiva
  3. Ingestion
  4. Recovered & vacc chickens serve as carriers of ILT & shed virus when subj to stress
  5. Fomites; contaminated litter or farm workers
  6. Mech transmission esp thru scavenger birds, domestic dogs, wild animals that feed on improperly disposed dead bird
39
Q

Describe ILT pathogenesis.

A

-laryngotracheitis
-diphtheritic membrane formation that form second tube for the length of trachea, blocking air passage = death from asphyxia
-persist -> trigeminal ganglion = target ILT viral latency
-hemorrhagic tracheitis
-necrotizing hemorrhagic tracheitis
-tracheal plug

40
Q

Describe the severe form of ILT.

A

-resp distress = head shaking w coughing
-neck raised & head extend during inspiration = pump handle respiration
-cough = blood mucus

41
Q

Describe ILT clinical signs.

A

-strains of low virulence w conjunctivitis, ocular discharge, swollen infra orbital & nasal sinus w dec egg prod
-mild enzootic form most common & severe epizootic form is uncommon

42
Q

Describe the diagnosis of ILT.

A

-necropsy: tracheal plug (diphtheric membrane)
-detect typical intranuclear inclusions in respiratory tissues
-virus isolation in nasal mucosa
-virus grow in CAM

43
Q

Describe the treatment & prevention of ILT.

A
  1. Control
    -slaughter inf birds & disinf
    -implement farm biosecurity measures
  2. Vaccine (3)
    A) chick embryo origin (CEO)
    >can revert to virulence & cause ILT
    >better immunity
    B) tissue culture origin (TCO)
    >via eye drops/water/spray mass & doesnt revert to virulence
    >immunity is limited BUT SAFER !!! use this
    C) pox vectored recombinant vaccine
44
Q

Describe Mareks disease.

A

GHV2
-host: chicken, turkey, quail, pheasants
-transmission:
>contagious
>inhale inf feather debris, chicken dander or dust
>cell free virus release from feather follicles highly inf but labile
>virus in desquamated cells (dander) less inf but survive in environ for months (dust/litter)

45
Q

Describe MD 4 pathotypes of GHV2.

A
  1. Mild [mMDV]
    -neural MD
    -preventable w HVT vacc
  2. Virulent [vMDV]
    -neural & visceral lymphomas
    -preventable w HVT vacc
  3. Very virulent [vvMDV]
    -neural & visceral lymphomas
    -oncogenic in HVT vacc chicken
    -preventable w bivalent vacc
  4. Very virulent plus [vv+MDV]
    -neural & visceral lymphomas
    -virus oncogenic in chickens vacc w bivalent vacc
46
Q

Describe the pathogenesis of MD.

A

-virus is slowly cytopathic & remain associated w cells
-cell free inf virus impossible to obtain, except in dander from feather follicles
-lesion in MD from infiltration & in situ prolif of transformed T lymphocytes
-cell lysis results in inflam response

47
Q

Describe the clinical signs of MD.

A
  1. Neurolymphomatosis
    -enlarge nerve trunks
    -nerve lose striation
    -edematous, grey, yellow
    -lameness, droopy wings, paresis of legs, limber neck, torticollis, in coordination
  2. Visceral lymphomatosis
    -diffuse or nodular lymphoid tumor in organs like liver, spleen, gonads, heart, lung, kidney, muscle, proventriculus
    -bursa rarely tumorous & more atropic = absence of tumors help distinguish disease from lymphoid leukosis
  3. Ocular lymphomatosis
    -gray iris
    -interfere w normal pupilllar constrict & dilation
    -partial/total blindness
  4. Cutaneous lymphomatosis
    -plucking of feathers = nodular lesion on skin
    -enlarged feather follicles ‘skin leukosis’
48
Q

Describe MD vaccine.

A

-turkey herpesvirus HV
-bivalent vaccine = HVT + SB-1 or 301B/1 strains of gallid herpesvirus 3 (serotype 2, avirulent strain)
-most protective vacc = CVI988/Rispens
>attenuated MD mixed w HVT at vaccination

Virology (24 decks)

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