intestinal viruses Flashcards

1
Q

why is viral diarrhea more common in young animals

A
  • antibodies arent developed against viruses yet
  • suckling from teats exposes young animals to unclean environments
  • gastric acid and mucosal integrity probably not fully developed yet
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2
Q

what is the most common route of infection for GI viruses

A

fecal oral route

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3
Q

outline the fecal-oral route cycle of viral transmission

A
  1. ingestion
  2. replication in intestine
  3. excretion of virus in feces
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4
Q

how might an animal ingest viruses that are shed within the feces

A
  • can be she in high levels in diarrhea which can be explosive leading to aerosols
  • contamination of food, water and fomites (clothes, material etc)
  • poor disinfection of the environment may fail to stop the disease from spreading
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5
Q

list common features of enteric virus infections

A
  • infection dose is often small
  • normally have a short incubation and the life cycle is lytic causing an acute infection and damaging cells
  • large amounts of virus shed in feces
  • viruses are generally tough and capable of surviing the low ph of the stomach an the environment
  • secondary bacterial infection is common
  • may have multiple viral infections at once (esp if young or in herd)
  • diarrhea common (+/- vomiting, but differs between species)
  • deaths from dehydration mostly (+/- acid base imbalance
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6
Q

list mechanisms of viral diarrhea

A
  • increased secretion (cl imbalance)
  • increased cell permeability
  • altered gut motility
  • decreased absorption
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7
Q

list viruses that cause major clinical signs associated with the GIT

A
  • rotaviruis
  • parvovirus
  • coronavirus
  • paramycovirus
  • pestivirus
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8
Q

what are the basic features of roatviruses

A
  • icosahedral
  • non enveloped
  • outer, middle and inner capsid
  • core contains a ddsRNA segmented genome (leads to reasortment)
  • very stable in environment
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9
Q

if there are multiple virus strains and a segmented genome what might this mean about the effectiveness of an immune response

A
  • lots of virus variation
  • protection only against closely related cirus after infection means that reinfection with other strains is possible
  • vaccine protection is limited to strains closely related to the vaccine strain of the virus
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10
Q

how might a new strain of rotavirus arrive on a farm

A
  • bought anials is the most likely source
  • could come from fomites
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11
Q

how are rotaviruses spread

A

fecal/oral transmission

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12
Q

explain what happens on a cellular level in a rotavirus infection

A
  • infection of enterocytes at the tips of the villi in the small intestine
  • villi become shorter
  • reduced lactase production and impaired Na transport
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13
Q

rotavirus reduces lactase production in the GIT. why is that important in young animals especially

A
  • primarily feed on milk so need lactase to digest lactose
  • causes scours
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14
Q

what happens to villi in a rotavirus infection

A

enterocytes damaged due to virus infection causing lysis

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15
Q

how does rotavirus enter cells

A
  • virus binds to sialic acid, then integrins, then other proteins on the cell surface
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16
Q

what is the clinical importance of rotavirus

A
  • affects piglets, calves and foals
  • leads to pasty/watery diarrhea
  • secondary infection with E. coli, other viruses, coccidia, leads to more severe disease
  • leads to reluctance to suckle and dehydration
  • pigs infected with rotavirus take 5 day longer to reach 25 kg weight
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17
Q

how is rotavirus diagnosed

A
  • collect samples from feces or gut contents (at PM)
  • detection of viral antigen via ELISA or latex agglutination test
  • detection of viral RNA via RT-PCR
  • virus often present in healthy animals!
  • post mortem exam detects pathological damage to tissue
  • rapid fixation of intestinal tissue post-euth is very important to detect pathological changes
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18
Q

how is rotavirus controlled

A
  • importance of getting young animals colostrum
  • dont mix groups
  • good hygiene (disinfection, removal of feces in farrowing units, prevent food/water contamination)
  • vaccines availible for cows and horses (NOT PIGS)
  • aim of vaccine is to increased colostral Ab
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19
Q

list basic features of parvoviruses

A
  • icosahedral
  • no envelope
  • small linear ssDNA genome
  • infect and kill ACTIVELY REPLICATING cells
  • persists for long periods in the environment
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20
Q

why are young animals more susceptible to severe parvovirus infections

A

parvoviruses infect actively dividing cells. young animals have more of them, therefore more cells to infect

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20
Q

list variants of parvoviruses that are of veterinary important

A
  • feline panleukopenia virus
  • canin parvovirus
  • porcine parvovirus
  • mink enteritis virus
  • aleutian disease
  • goose parvovirus
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21
Q

where on the villi does parvovirus infect and what are the impacts

A

the dividing stem cells of the crypt
- villi tip cells turnover normally but are not replaced because the virus has killed the stemcells
- leads to stunted villi, malabsorption, maldigestion, crypt dilation and necrosis

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22
Q

discuss feline parvovirus

A
  • fecal oral transmission
  • persists in environment for up to a year
  • high titre in feces
  • infects lymph nodes of naso and oro pharynx then spreads to other tissues
  • needs rapidy dividing cells to propagate
  • mainly infects intestinal cells and bone marrow
  • kittens most susceptible however unvaccinated older cats also infeted
  • if queen is infected can lead to wobbly kittens (cerebellar hypoplasia)
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23
Q

list clinical signs of feline parvovirus

A
  • pyrexia
  • vomiting
  • diarrhea
  • dehydration
  • shock and sepsis due to compromised intestinal mucosa
  • mortality rate very high if not rapidly and aggresively treated
  • can cause sudden death in kittens and cats in shelters
  • treatment requires support of circulation/hydration and antibiotics to cover risk of sepsis from secondary bacterial infection
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24
Q

how is feline parvovirus controlled

A
  • maternally derived antibody wanes after ~8 weeks
  • vaccinate (modified and live virus vaccines availible
  • boost vax every 1-3 years
  • prevent exposure of kittens to FPV in environment if prior outbreak on premises (hygiene)
25
Q

how is feline parvovirus diagnosed

A
  • fecal sample for antigen detection (ELISA) or virus DNA (PCR)
  • detect antibody to virus in blood (not really helpful if suspect)
  • supportive evidence (marked leucopenia/neutropenia)

rapid cage side snaps can have false positives

26
Q

infection of actively dividing cells in canine parvoviruse leads to what

A
  • generalised neonatal disease (fading pups)
  • myocarditis in neonatal puppies (uncommon)
  • bone marrow infection = leukopenia
  • intestinal villi infection = enteritis and then V/D
  • intestinal and mesenteric lymphoid tissue infection = immunosupression
27
Q

discuss mycarditis in puppies with canine parvovirus

A
  • heart failure due to myocarditis
  • myocardial cells necrotic
  • inclusion bodies in muyocardial cells
  • influx of inflammatory cells
  • fibrosis (bad for heart cells)
  • leading to massiv enlargment of heart, then heart failure and pulmonary oedema
28
Q

suggest where canine parvovirus originated

A

variant of FPV, 99% genetically identical with only few amino acid differences

29
Q

list basic features of coronaviruses

A
  • positive sense ssRNA
  • enveloped (but still survive relatively well in environment)
  • nested RNA genome
30
Q

where on the intestinal villi do coronaviruses target and why

A
  • mature enterocytes in middle (not tip or crypt)
  • virus spike proteins bind to aminopeptidase N, a protein highly expressed in mature enterocytes
31
Q

discuss clinical signs and features of transmissible gastroenteritis virus

porcine coronavirus

A
  • highly contagious
  • young pigs
  • diarrhea/vomiting
  • rapid dehydration
  • mortality rate up to 100% in newborn piglets
32
Q

discuss porcine epidemic diarrhea virus

porcine coronavirus

A
  • similar to TGEV
  • historically less severe
  • BUT new pathogenic strains reported in asia, NA and ukraine have high mortality in piglets (100%)
  • as a consequence now notifiable in UK
33
Q

discuss betacoronaviruses

A
  • cattle coronavirus
  • calf diarrhea
  • scours in 4d-3week calves
  • leads to dehydration, acidosis, depression and fever
  • recovery within 4-5 days
  • can also cause respiratory signs
  • also causes winter dysentry in housed adult cattle
34
Q

list disease signs of canine coronavirus

A
  • normally mild, self limiting diarrhea
  • may be lethargic and inappetant
  • loose feces +/- mucus +/- blood
35
Q

discuss severe disease of canine coronavirus

A
  • novel virus genotypes due to sponteaneous mutation may rarely produce more severe disease
  • leads to severe systemic disease (v/d but also pyrexia and seizures) with some fatalities
35
Q

how is canine coronavirus treated, diagnosed and controlled

A
  • non specific supportive tx
  • vaccines not currently availible in the uk
  • can diagnose with PCR
36
Q

discuss feline coronavirus infection

A
  • 2 biologically distince phenotypes (FCoV and FIP)
  • enteric virus is mild signs but can become systemic
  • virus can survive up to 7 weeks in cat litter
  • cat ingests pathogen
  • majority of infection is transiet but can shed virus for many months
  • some cats may be carrier state and shed for life
  • minority will develop FIP
37
Q

discuss feline infectious peritonitis

A
  • infection with FCoV
  • develops into feline infectious peritonitis
  • virus replicates in macrophages
  • forms immune complexes
  • leads to vasculitis
  • results in one of 2 variants: wet FIP (effusions) or dry FIP (pyogranulomatous lesions)
38
Q

what might lead you to suspect a case of wet FIP and what are the clinical signs

A
  • effusion in a body cavity (ascites, pleural effusion)
  • pot belly, with evident fluid on ballottment
  • dyspnoea
39
Q

how do you diagnose dry FIP

A
  • challenging
  • often made at post mortem
40
Q

why does FIP arise

A
  • probable mutation of virus
  • stress?
  • viral load?
  • not well understood
41
Q

how are coronaviruses controlled

A
  • hygiene measures can help reduce environmental contamination with virus
  • vaccines are availible for some diseases which reduce but do not eliminate disease
  • removal of infected animals and maintenance of clean herd/house is possible but may be difficult
42
Q

list pestiviruses of veterinary importance

A
  • bovine viral diarrhea
  • border disease virus in sheep
  • classical swine fever
43
Q

list basic features of pestiviruses

A
  • positive sence ssRNA genome
  • cytoplasmic replication
  • icosahedral capsid
  • enveloped
44
Q

discuss clinical signs of bovine viral diarrhea

A
  • diarrhea (usually mild)
  • decreased fertility/milk yield
  • abortion
  • congenital defects
  • stunted calves
  • immunosupression (associated with respiratory disease outbreaks)
  • mucosal disease
45
Q

there are two genotypes of BVD. what are the differences

A
  • BVD1 = classical form
  • BVD 2 = hemorrhagic syndrome, severe and acute BVD

2 biotypes: NCP (non-cytopathic) and CP (cytopathic. NCP is major cause of BVD and is followed by CP for mucosal disease

46
Q

discuss the challenge of persistant BVD infection

A
  • pregnant heiffer exposed to NCP-BVD within 1st-4th month of gestation
  • calf immunocompetence not developed
  • calf immune system thinks virus is part of self
  • calf becomes persistently infected carrier and sheds NCP-BVD
  • reservoir of virus in herd
47
Q

if a cow is infected with BVD after the development of fetal immunocompetence, what are the impacts

A
  • calf born with congenital defects
  • calf aborted

depends on amount of virus exposed to

48
Q

discuss Mucosal disease in BVD infections

A
  • infrequent consequence of BVD infection
  • develops only in persistent infected animals around 2 years of age
  • requires presence of NCP and antigenically related CP virus
  • NCP virus mutates in PI animal, superinfection of PI animal with another CP virus
  • CP viruses show marked tropism for GALT
  • severe diarrhea
  • marked mucosal hemorrahe
  • fatal - cull animal for welfare reasons AND herd health (super shedder)
49
Q

how is BVD controlled

A
  • eliminate PI animals from herd
  • regular blood sampling of young stock
  • maintain closed herd
    OR
  • maintain herd immunity so that no naive cattle are infected
  • do with vaccination or deliberate infection (Risky)
50
Q

list important genera of the paramyxoviridae family

A
  • morbillivirus
  • rebulavirus
  • respirovirus
  • pneumovirus
  • metapnemovirus
51
Q

list basic features of paramyxoviridae viruses

A
  • large enveloped virus
  • negative sense ssRNA
  • sensitive to heat, detergent, desiccation etc
  • cytoplasmic replication
  • release by budding
52
Q

what is rinderpest and list clinical signs

A
  • cattle plague
  • highly infectious disease of cattle
  • respiratory and ailimentary tract disease
  • very high mobidity and mortality
  • clinical signs: nasal discharge, pyrexia, oral and nasal erosions and ulcerations, diarrhea with mucus blood and debris, dehydration followed by death
  • eradicated in 2011 after global vaccination program
  • notifiable (hopefully never seen again)
53
Q

what is peste de petit

A
  • goat plague
  • rinderpest for small ruminants
  • mucosal erosions and profuse diarrhea
  • high mortality
  • not eradicated but notifiable
54
Q

canine distemper is caused by which genera of paramyxoviridae

A

morbillivirus

55
Q

what demographic is affected by canine distemper and how is it transmitted

A
  • young dogs especialy susceptible
  • transmitted by direct contact
  • virus replicates in upper respiratory tract
  • spreads to tonsils/lymph nodes then systemically spreads to epithelia and CNS
56
Q

list clinical signs of canine distemper

A
  • pyrexia
  • depression
  • ocular and nasal discharge
  • cough
  • vomiting/diarrhea
  • hyperkeratosis of nose/pads

if immune system responds poorly, development of neuro signs

57
Q

discuss newcastle disease

A
  • notifiable
  • avian paramyxovirus
  • shed in all excretions and becomes aerosol
  • virus stable for weeks on carcasses (mechanical transfer)
  • COMMON IN WILD BIRDS
  • zoonotic to the extent of conjunctivitis in humans
  • see hemorrhages in proventriculus and trachea
  • torticollis as neurological sign
  • can control with proper biosecurity, slaughter in the event of outbreak and vaccination of commercial flocks
58
Q

discuss strains of newcastle disease

A
  • lentogenic = mild inapparent infection
  • mesogenic = mild respiratory disease, some death in young birds
  • neurotropic velogenic = acute, severe, fatal with respiratory and nervouse signs
  • viscerotropic velogenic = severe, fatal with hemorrhagic intestinal lesions and respiratory disease

pathogenicity determined by F glycoprotein cleavage