Virology Exam 2

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year 2 Semester 1

211 Terms

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what is the result of enteric viruses

diarrhea

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what 2 enteric viruses cause systemic infection

  1. parvovirus

  2. FIP (feline infectious peritonitis virus)


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enteric viruses

  1. enveoloped or naked

  2. transmission type

  3. infections

  4. incubation period

  5. when does it cause severe disease


  1. enveloped (except coronavirus)

  2. feccal- oral

  3. localized transient (mostly small intestine)

  4. short

  5. young animals, intestinal immunity not fully formed


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2 sources of transmission of enteric viruses

  1. transient infected animals

  2. environment


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factors of enteric disease severity

  • dose

  • host health/nutrition/stress

  • underlying/ concurrent infections

  • maternal AB/ vaccination

  • genetics of virus and of host


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what anatomical parts do enteric viruses more often infect

small intestine

  1. crypt: germinal differentiating epithelial cells responsible for secretion of electrolytes

  2. villus: differentiated cells used for digestion and absorption



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what does diarrhea lead to

dehydration and acidosis

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what 3 mechanisms do enteric viruses use to cause diarrhea

  1. villous blunting: decrease absorption = osmotic diarrhea

  2. inflammation: vasodialation causing leaky vessesl

  3. viral enterotoxin: rotavirus NSP4



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Effects of Rotavirus NSP4

  • enterotoxin: disrupt Ca homeostasis, increase Ca intracellularly, activate Cl channels, secrete CL into lumen and Na and H2O follow: secretory diarrhea

  • cellular distribution: impair ting junctions = increased permeability

  • signalling effects: stimulate nervous system to increase motility and fluid excretion


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distribution in intestine:

  1. rotavirus

  2. coronavirus


  1. small intestine

  2. small intestine and maybe some colon (more severe)

note: can be segmented or uneven distribution


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rotavirus

  1. enveloped or non enveloped

  2. genome formation

  3. common host- when is it most severe

  4. incubation

  5. mortality/ morbidity

  6. distribution



  1. non enveloped

  2. segmented ds RNA

  3. young, host specific (severe in neonates <2 weeks)

  4. short (days)

  5. high morbidity, low mortality

  6. localized


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likely virus: acute, watery, yellow diarrhea, non bloody

rotavirus

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what is the main cause of death with rotavirus:

dehydration

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Lab diagnostics for rotavirus

  • PCR

  • Ag detection assays

  • serology (limited)

    • too young to produce Ab

    • Maternal Ab change results


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3 main mechanisms of diarrhea from rotaviruses

  1. villous atrophy = malabsorptive diarrhea → infecting enterocytes on vilious tips

  2. NSP4 = secretory diarrhea → ca homeostasis, Cl secretion



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roatvirus treatment

  • self limiting

  • supportive treatment: fluids, electrolytes


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how to avoid rotavirus

you cannot, it is ubiquitious

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preventing rotavirus

  1. decrease exposure

  2. adequate colostrum


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rotavirus vaccines

  1. inactivated: for dam to protect calf

  2. MLV: IM to dam for Ab in colostrum or oral to newborn calf for mucosal immunity


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differnece in vaccine route for rotavirus

  1. IM

  2. oral


  1. humoral immunity, Ag present in systemic lymphoid tissue. Circulating IgG

  2. Ag present in GALT, increase IgA locally


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coronaviruses

  1. common type of disease

  2. genome

  3. enveloped or naked


  1. enteric mostly, some systemic or respiratory

  2. + ssRNA

  3. enveloped



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pathogenesis of coronaviruses 3 characteristics

  1. infect mature vilous enterocytes → atrophy with marked decrease in absorptive capacity

  2. infect small and large intestine

  3. extensive damage in neonates


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3 major clinical syndromes of bovine coronaviruses

  1. (neonatal) dalf dehydration

  2. winter dysentery (adult diarrhea)

  • dairy cattle, blood diarrhea, high morbidity, low mortality, decreased production

  1. bovine respiratory disease (calves and feedlot cattle)

  • lower and upper respiratory infection

  • part of bovine respiratory disease complex



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control of coronavirus

  • vaccinate:

    • MLV or inactivated to dam with second dose <30 days before calving

    • oral MLV to calf (before colostrum)


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feline enteric coronavirus

  1. common?

  2. often presentation

  3. typical life cycle

  4. mutations

  5. cells it infects

  6. shedding

  7. prognosis

  8. lesion


  1. common

  2. subclinical, self limiting diarrhea in kittens

  3. repeated cycles of infection and re infection - maintained in cat groups

  4. persistance increases risk for FIP mutation

  5. mature enterocytes

  6. high fecal shedding

  7. excellent

  8. villous atrophy


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What is FIP and what is the pathogenesis

  1. systemic disease mutated from FeCov

  2. allow infection of macrophages and monocytes

  3. infected macrophages disseminate virus = systemic inflammation


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how is FIP transmitted between cats

it is not, FeCov can be transmitted

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FIP

  1. common patient

  2. predisposition?

  3. notable clinical signs

  4. 2 types


  1. young < 2, male often with many cats

  2. genetic

  3. unknown origin fever, pear shaped body

  4. effusive/ wet, non effusive/ dry


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wet FIP

  1. common?

  2. pathogenesis

  3. content of effusion


  1. common

  2. vasculitis and increased permiability from inflammation from Macs cause leaking into the body cavity

  • peritoneal = distension

  • pleural: respiratory distress

  1. high protein, low cellularity, yellow, viscous


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what tests should be done on a young cat with a fever

FIV/FeLV


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what test should be done on a young cat with uveitis

  • FECV serology

  • RT-PCR (blood)



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dry FIP

  1. key characteristic appearance

  2. common locations

  3. clinical signs


  1. pyogranulomatous inflammation around blood vessels and tissues (white spots)

  2. kidney, liver, LN, CNS, eyes (small blood vessels)

  3. depend on organs, non specific



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how to diagnose FIP

  1. presumptive: signs, history, blood work, imagins, effusion

  2. confirmatory: FCoV does not mean FIP

  3. serology: test for Ab against FeCoV, not distinguish from FIP

  4. RT-PCR: detect FeCoV RNA, does not mean FIP

  5. Histopath (difinitive diagnosis) - postmortum


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best locations for RT-PCR for FIP

  1. effusion (best), if positive with this, likely FIP

  2. FNA affected tissue

  3. CSF: for neurologic signs

  4. Aq humor (ocular dz)

  5. whole blood (less useful)


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FIP vaccination

  • nor recommended

  1. low protection for FIP (could reduce severity)

  2. modified live → could revert

  3. many cats = already have FeCoV exposure


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FIP prognosis

grave

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parvo

  1. enveloped or naked

  2. genome

  3. requirement

  4. 2 types


  1. naked

  2. ssDNA

  3. rapidly dividing cells - replicate in nucleus

  4. CPV 1 (minute virus), CPV 2 (canine parvovirus)


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CPV 1: minute virus of canines - describe


origional, cause muld to subclinical signs

Puppies: myocarditis

adults: reprodtive loss

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CPV 2: canine parvovirus

  1. origin

  2. effects


  1. mutant of feline panleuk virus

  2. severe enteritis in puppies


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CPV 2 impact on young dogs and cats - what cells

  1. intestinal crypt cells: villous atrophy → hemorrhage

  2. bone marrow prevursor cells: leukopenia / immune supression

  3. proliferating lymphoid cells: lymphoid depletion = immunosupression


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what does CPV 2 do uniquely in young puppies

attach developing cardiomyocytes= myocarditis

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what doe CPV 2 attack uniquely in neonate/fetal kittens

developing CB cells = CB hypoplasia

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CPV 2 lab findings

  • luekopenia

  • anemia

  • hypoprotenemia

  • hypoglycemia

  • coagulation abnormalities



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most common CPV 2 patient

puppy 6 wks - 6 months (when maternal Ab wanes)

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source of CPV 2

environment, transient infected animals

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CPV 2 vaccination

  • inactivated and MLV = effective (in DAPP)

  • can still have fecal shedding from vaccinated dogs = immunize other dogs

  • not vaccinate puppies or pregnant


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dosing for CPV 2 vaccine

3 doses 6-16 weeks, 2-4 weeks apart because you do not know the level of the maternal Ab

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what is the window of susceptability

maternal AB wane to unprotective but before the vaccine induced immunity is fully developed

= greatest risk of infection C

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CPV 2 treatment

  1. agressive supportive care

  2. antimicrobial (secondary bacterial infection)

  3. blood/plasma transfusion


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diagnosis of CPV 2

  1. ELISA SNAp - detect Ag in feces

  2. PCR = sensitive, feces

  3. IHC (post mortem)


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what does it mean if CPV IFA is positive for IgM and negative for IgG

acute, primary infection, unvaccinated

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why is there hypoprotenemia and hypoglycemia with CPV

intestinal crypt necrosis

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feline panleukopenia

  1. common patient

  2. common lesion

  3. main lab characteristic

  4. neonatal/utero infection


  1. young, unvaccinated, when maternal Ab decreases

  2. intestinal crypt destruction

  3. panleukopenia, damaged bone marrow and lymphoid tissue

  4. CB disease (target rapid dividing cells of CB = hypoplasia)


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how to diagnose feline panleuk

  1. clical suspicion

  2. lab tests

  • CBC : severe paleukopenia

  • Ag detection in SNAP of feces

  • PCR (Sen and SP)

  • serology: FPLV IFA- detect Ab

  • Histopath: crypt necrosis, villous collapse, lymphoid depletion


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Canine Adenovirus (CAV 1)

  1. naked or enveloped

  2. genome

  3. location of replication

  4. disease name

  5. common?


  1. naked

  2. ds DNA

  3. nucleus (intranuclear inclusions)

  4. canine infectious hepatitis

  5. uncommon (in vaccinated)


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canine adenovirus pathogenesis


systemic infection with viremia

and

infect hepatocytes and endothelial cells → wide spread activation of clotting = microthrombi and organ damage = DIC

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canine adenovirus major cell targets

  1. hepatocytes

  2. vascular endothelial cells

  3. renal tubular epithelium


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common unique symptom of canine adenovirus

“blue eye” / corneal edema

  • type 3 hypersensitivity = immune complex disposition

  • can occur in recovery

  • transient, self limiting

  • inflammatory


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CAV 1 vaccination

  • use CAV 2 vaccine (DAPP)

  • CAV 1 vaccine can cause blue eye and excretions in urine


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family of herpes viruses

orthohperesviridae

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herpesvirus

  1. naked or enveloped

  2. transmission

  3. genome

  4. replication location

  5. durration of infection


  1. enveloped

  2. close contact

  3. ds DNA

  4. nucleus

    1. for life, latency


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for hepresviruses, does replication require clinical disease

no

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hepresvirus treatment

antivirals

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alphaherpesvirinae

  1. replication

  2. site of replication

  3. site of latency

  4. disease

  5. primary cite of infection


  1. fast with necrosis

  2. epithelial cells

  3. PNS neurones

  4. causes Dz and cell lysis

  5. epithelium


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3 main organ systems target by alphahrpesvirinae

  1. respiratory (usualy location of start)

  2. reproduction

  3. CNS



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Equine alphaherpes virus: 2 types

  1. EHV 1: respiratory disease, abortion, perinatal mortality, CNS

  • respiratory epithelium, sensory neurons (PNS), lymphocytes, endothelium

  1. EHV 4: respiratory disease

  • respiratory epithelium, sensory neurons


differ in cell tropism


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describe EHV 1 and 4 latency

  • in neurons of sensory ganglia innervating nasopharyngeal mucosa

  • reactivate in adult horse ± clinical signs


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what is the most important agent of acute respiratory disease in horses

EHV 4

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EHV respiratory infections

  1. localised upper respiratory infection

  • non specific signs, nasal discharge, regional lymphadenopathy, subclinical and self limiting

  1. lower respiratory infection: rare

  • in immune deficient individuals


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extrarespiratory pathogeneisis with EHV

endothelial cell infection leading to vasculitis and ischemia

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EHV abortion

  1. what type

  2. how

  3. what can it lead to


  1. EHV 1 mostly

  2. -

  • uterine vasculitis (enough alone)

  • can cross placenta to infect fetus (not always)- causing disseminated disease in fetus

  1. abortion storms- whole group aborts, less now with vaccination and management



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what is seen in EHV necropsy of fetus

could be uninfected or

disseminated disease and wide spread petechial hemorrhage


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EHV -1 Perinatal mortalitiy

  1. common?

  2. describe

  3. cause


  1. uncommon

  2. foal born at term but dead or weak and die soon

  3. due to sever lower respiratory infection and disseminated systemic infection



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EHV 1 neurologic disease

  1. name

  2. key lesions

  3. common signs


  1. equine herpes myeloencephalitis

  2. vasculitis and ischemia

  3. inability to rise from sitting, paralysis, recumbency



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EHV 1 hypervirulent strains - describe

  • cause outbreaks in high morbidity and mortality

  • increased replication rate

  • unknown why



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EHV 1 differentials

  1. respiratory disease (cannot clinically distinguish)

  2. neurologic disease: rabies, west nile, etc



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EHV testing

  1. PCR for viral DNS from nasal secretions early one and blood with viremia

  2. serology: compounded to see if infection or vaccine

  3. histopathology: aborptions


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significance in controling EHV

  • it is reportable in WA

  • there are vaccines



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EHV vaccination

  • common

  • cross protect 1 and 4

  • not prevent infection or protect from neuro disease

  • prevent disease outbreaks

  • short protection: need revaccination



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Bovine alphaherpes virus

  1. name

  2. major cause of what

  3. difference from EHV -1

  4. aborptions

  5. CNS disease


  1. bovine herpesvirus 1 (BHV -1)

  2. bovine respiratory co plex and secondary bacterial pneumonia

  3. not infect endothelium and rare meningoencephalitis

  4. always due to fetal infection

  5. BHV 5 infects neurons



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components )viruses and bacteria) of bovine respiratory complex

viruses:

  • BHV-1,

  • bovine parainfluenza,

  • bovine respiratory synscitial virus

bacteria:

  • mannhemia haemolytica,

  • histophilus sommi,

  • pasteurella multocida


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Feline Alphaherpisvirus

  1. name

  2. type of pathogen

  3. common clinical signs

  4. viremia

  5. common sign in kittens


  1. feline herpesvirus 1

  2. upper respiraotry (part of feline respiratory disease complex)

  3. conjuncitivitis, ulceration, abortions

  4. rare

  5. hypothermia



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feline alphaherpesvirus vaccination

  • FVRCP

  • modified life/ inactivated

  • SQ or internasal


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diagnosis of feline herpesvirus 1

PCR of nasal swab

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treatment for feline herpesvirus 1

  • supportive care

  • antivirals


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main differential for feline herpesvirus 1

feline calicivirus

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feline calicivirus

  1. naked or enveloped

  2. genome

  3. key lesion

  4. location of persistence

  5. localization

  6. unique locations


  1. naked

  2. RNA

  3. stomatitis with ulcers

  4. tonsils and oropharynx

  5. upper respiratory tract

  6. some strains can cause disease in joints and lungs



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hypervirulent strains of feline calicivirus

  • infect endothelial cells = hemorrhage

  • can be in fully vaccinated animals



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canine alphaherpesvirus - young dog infection


  • neonatal: fata multisystematic hemorrhage and necrosis

  • cause hypothermia

  • in utero = abortion

  • turkey egg kidney is common necropsy find


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caine alphaherpesvirus - in adult dogs

apathogenic or mild rhinotrachitis

  • not have much disease



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non human primate alphaherpesvirus

  1. name

  2. species

  3. common lesion

  4. concerns

  5. seroprevelence



  1. macacine herpesvirus 1 (B virus)

  2. macaques

  3. oral and gingival ulcers

  4. fatal zoonosis: encephalitis in people

  5. high in captive and wild populations



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do herpesviruses jump hosts?

not often, but when they do they are lethal

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betaherpesvirinae

  1. replication

  2. location of latency

  3. disease

  4. location of exposure


  1. slow, less damage

  2. secretory epithelium (often salivary gland)

  3. only in immmunecompromised hosts, no cell lysis

  4. ubiquitous - but not likely the main cause od disease


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elephantid herpesvirus 1

  1. name

  2. cell tropism

  3. results

  4. patient

  5. treatment

  6. type of virus


  1. endotheliotrophic elephant herpesvirus

  2. endothelial cells

  3. highly fatal from hemorrhage disease

  4. young asian elephants

  5. antiviral therapy, rapid intervention

  6. betaherpesvirus


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non human primate betaherpesvirus

  1. name

  2. patient

  3. disease

  4. diagnose


  1. Rheus Cytomegalovirus

  2. endemic to macaques

  3. in immunosupressed and recurrent (asymptomatic in immunocompetent)

  4. not testable


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gamaherpesvirinae

  1. replication

  2. site of latency

  3. disease

  4. results

  5. location in the environment


  1. slow

  2. lymphocytes

  3. no cell lysis, disease in non adapted hosts

  4. lymphoid dysregulation, proliferation and neoplasia

  5. ubiquitous in mammals though mostly non pathogenic


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Equine herpesvirus 5

  1. type of herpesvirus

  2. appearance

  3. other name

  4. pathogenesis

  5. cellular appearance


  1. gamma

  2. progressive, nodular fibrosis, with enlarged LN

  3. equine multinodular pulmonary fibrosis

  4. unknown

  5. see inclusions



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malignant catarrhal fever

  1. causitive agent

  2. 2 types

  3. who are they dangerous to

  4. type of herpesvirus


  1. genus macavirus

  2. -

  • ovine herpesvirus 2: common in sheep, ubiquitous in domestic sheep

  • alcelaphine herpesvirus 1, wildebeasts

  1. cattle

  2. gamma


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what virus do all sheep have

ovine herpesvirus 2 (gamma herpesvirus)

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Malignant catarrhal Fever - describe transmission from natural host


  • no disease in natural host

  • replication in nasopharynx

  • shed in nasal secretions

  • close contract trasnmission

  • sheep shed at 6-9 months old most