intestinal viruses Flashcards
why is viral diarrhea more common in young animals
- 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
what is the most common route of infection for GI viruses
fecal oral route
outline the fecal-oral route cycle of viral transmission
- ingestion
- replication in intestine
- excretion of virus in feces
how might an animal ingest viruses that are shed within the feces
- 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
list common features of enteric virus infections
- 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
list mechanisms of viral diarrhea
- increased secretion (cl imbalance)
- increased cell permeability
- altered gut motility
- decreased absorption
list viruses that cause major clinical signs associated with the GIT
- rotaviruis
- parvovirus
- coronavirus
- paramycovirus
- pestivirus
what are the basic features of roatviruses
- icosahedral
- non enveloped
- outer, middle and inner capsid
- core contains a ddsRNA segmented genome (leads to reasortment)
- very stable in environment
if there are multiple virus strains and a segmented genome what might this mean about the effectiveness of an immune response
- 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
how might a new strain of rotavirus arrive on a farm
- bought anials is the most likely source
- could come from fomites
how are rotaviruses spread
fecal/oral transmission
explain what happens on a cellular level in a rotavirus infection
- infection of enterocytes at the tips of the villi in the small intestine
- villi become shorter
- reduced lactase production and impaired Na transport
rotavirus reduces lactase production in the GIT. why is that important in young animals especially
- primarily feed on milk so need lactase to digest lactose
- causes scours
what happens to villi in a rotavirus infection
enterocytes damaged due to virus infection causing lysis
how does rotavirus enter cells
- virus binds to sialic acid, then integrins, then other proteins on the cell surface
what is the clinical importance of rotavirus
- 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
how is rotavirus diagnosed
- 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
how is rotavirus controlled
- 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
list basic features of parvoviruses
- icosahedral
- no envelope
- small linear ssDNA genome
- infect and kill ACTIVELY REPLICATING cells
- persists for long periods in the environment
why are young animals more susceptible to severe parvovirus infections
parvoviruses infect actively dividing cells. young animals have more of them, therefore more cells to infect
list variants of parvoviruses that are of veterinary important
- feline panleukopenia virus
- canin parvovirus
- porcine parvovirus
- mink enteritis virus
- aleutian disease
- goose parvovirus
where on the villi does parvovirus infect and what are the impacts
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
discuss feline parvovirus
- 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)
list clinical signs of feline parvovirus
- 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
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)
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
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
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
suggest where canine parvovirus originated
variant of FPV, 99% genetically identical with only few amino acid differences
list basic features of coronaviruses
- positive sense ssRNA
- enveloped (but still survive relatively well in environment)
- nested RNA genome
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
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
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
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
list disease signs of canine coronavirus
- normally mild, self limiting diarrhea
- may be lethargic and inappetant
- loose feces +/- mucus +/- blood
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
how is canine coronavirus treated, diagnosed and controlled
- non specific supportive tx
- vaccines not currently availible in the uk
- can diagnose with PCR
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
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)
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
how do you diagnose dry FIP
- challenging
- often made at post mortem
why does FIP arise
- probable mutation of virus
- stress?
- viral load?
- not well understood
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
list pestiviruses of veterinary importance
- bovine viral diarrhea
- border disease virus in sheep
- classical swine fever
list basic features of pestiviruses
- positive sence ssRNA genome
- cytoplasmic replication
- icosahedral capsid
- enveloped
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
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
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
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
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)
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)
list important genera of the paramyxoviridae family
- morbillivirus
- rebulavirus
- respirovirus
- pneumovirus
- metapnemovirus
list basic features of paramyxoviridae viruses
- large enveloped virus
- negative sense ssRNA
- sensitive to heat, detergent, desiccation etc
- cytoplasmic replication
- release by budding
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)
what is peste de petit
- goat plague
- rinderpest for small ruminants
- mucosal erosions and profuse diarrhea
- high mortality
- not eradicated but notifiable
canine distemper is caused by which genera of paramyxoviridae
morbillivirus
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
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
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
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
