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
how is feline parvovirus controlled
- 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
how is feline parvovirus diagnosed
- 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
infection of actively dividing cells in canine parvoviruse leads to what
- 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
discuss mycarditis in puppies with canine parvovirus
- 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
suggest where canine parvovirus originated
variant of FPV, 99% genetically identical with only few amino acid differences
29
list basic features of coronaviruses
- positive sense ssRNA - enveloped (but still survive relatively well in environment) - nested RNA genome
30
where on the intestinal villi do coronaviruses target and why
- mature enterocytes in middle (not tip or crypt) - virus spike proteins bind to aminopeptidase N, a protein highly expressed in mature enterocytes
31
discuss clinical signs and features of transmissible gastroenteritis virus | porcine coronavirus
- highly contagious - young pigs - diarrhea/vomiting - rapid dehydration - mortality rate up to 100% in newborn piglets
32
discuss porcine epidemic diarrhea virus | porcine coronavirus
- 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
discuss betacoronaviruses
- 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
list disease signs of canine coronavirus
- normally mild, self limiting diarrhea - may be lethargic and inappetant - loose feces +/- mucus +/- blood
35
discuss severe disease of canine coronavirus
- 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
how is canine coronavirus treated, diagnosed and controlled
- non specific supportive tx - vaccines not currently availible in the uk - can diagnose with PCR
36
discuss feline coronavirus infection
- 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
discuss feline infectious peritonitis
- 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
what might lead you to suspect a case of wet FIP and what are the clinical signs
- effusion in a body cavity (ascites, pleural effusion) - pot belly, with evident fluid on ballottment - dyspnoea
39
how do you diagnose dry FIP
- challenging - often made at post mortem
40
why does FIP arise
- probable mutation of virus - stress? - viral load? - not well understood
41
how are coronaviruses controlled
- 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
list pestiviruses of veterinary importance
- bovine viral diarrhea - border disease virus in sheep - classical swine fever
43
list basic features of pestiviruses
- positive sence ssRNA genome - cytoplasmic replication - icosahedral capsid - enveloped
44
discuss clinical signs of bovine viral diarrhea
- diarrhea (usually mild) - decreased fertility/milk yield - abortion - congenital defects - stunted calves - immunosupression (associated with respiratory disease outbreaks) - mucosal disease
45
there are two genotypes of BVD. what are the differences
- 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
discuss the challenge of persistant BVD infection
- 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
if a cow is infected with BVD after the development of fetal immunocompetence, what are the impacts
- calf born with congenital defects - calf aborted depends on amount of virus exposed to
48
discuss Mucosal disease in BVD infections
- 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
how is BVD controlled
- 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
list important genera of the paramyxoviridae family
- morbillivirus - rebulavirus - respirovirus - pneumovirus - metapnemovirus
51
list basic features of paramyxoviridae viruses
- large enveloped virus - negative sense ssRNA - sensitive to heat, detergent, desiccation etc - cytoplasmic replication - release by budding
52
what is rinderpest and list clinical signs
- 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
what is peste de petit
- goat plague - rinderpest for small ruminants - mucosal erosions and profuse diarrhea - high mortality - not eradicated but notifiable
54
canine distemper is caused by which genera of paramyxoviridae
morbillivirus
55
what demographic is affected by canine distemper and how is it transmitted
- 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
list clinical signs of canine distemper
- pyrexia - depression - ocular and nasal discharge - cough - vomiting/diarrhea - hyperkeratosis of nose/pads if immune system responds poorly, development of neuro signs
57
discuss newcastle disease
- 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
discuss strains of newcastle disease
- 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