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
2
Q
what is the most common route of infection for GI viruses
A
fecal oral route
3
Q
outline the fecal-oral route cycle of viral transmission
A
- ingestion
- replication in intestine
- excretion of virus in feces
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
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
6
Q
list mechanisms of viral diarrhea
A
- increased secretion (cl imbalance)
- increased cell permeability
- altered gut motility
- decreased absorption
7
Q
list viruses that cause major clinical signs associated with the GIT
A
- rotaviruis
- parvovirus
- coronavirus
- paramycovirus
- pestivirus
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
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
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
11
Q
how are rotaviruses spread
A
fecal/oral transmission
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
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
14
Q
what happens to villi in a rotavirus infection
A
enterocytes damaged due to virus infection causing lysis
15
Q
how does rotavirus enter cells
A
- virus binds to sialic acid, then integrins, then other proteins on the cell surface
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
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
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
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
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
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
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
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)
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
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
