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239 Cards in this Set
- Front
- Back
what are the 2 types of viral vaccines? |
1. conventional vaccines
2. recombinant DNA-derived vaccines |
|
what are the 2 types of conventional viral vaccines? |
1. live
2. inactivated (killed) |
|
what is it called when they took lesions from cadavers, emulsified them and then rubbed them into scarrified areas to prevent smallpox? |
variolation |
|
what was the problem with the treatment for smallpox around 1000 AD? |
still had 1-2% of people develop disease and die |
|
who noticed that a certain group of people did not develop smallpox and who was this group? |
Edward Jenner (1770s)
dairy farmers and their families |
|
T/F - cowpox virus and smallpox virus are antigenically similar viruses |
true |
|
what is another name for the cowpox virus? |
vaccinia virus
(vacca = latin for cow) |
|
"to reduce in virulence" |
attenuate |
|
what is the most common vaccine type currently used in vet med? |
laboratory-attenuated (modified live) |
|
what is an example of a wild-type (virulent) virus vaccine? |
smallpox |
|
what is an example of an attenuated virus vaccine? |
cowpox vaccine |
|
what are some examples of modified live vaccines? |
rabies, canine distemper, canine parvo, feline herpies, feline calicivirus, human rotovirus |
|
flowchart for modified-live viruses |
1. passage in unnatural host
2. adaptive mutations
3. progressive adaptation to unnatural host cell with loss of adaptive/virulence for natural host |
|
describe formation of canine distemper vaccine |
*modified live vaccine
serially passage in ferrets = loss of virulence in dogs but 1% still got distemper
passage in embryonated chicken eggs lead to safe and effective vaccine |
|
name a temperature-sensitive virus |
equine influenza virus
*virus grown to replicate poorly at core body temp (cold-adapted) |
|
how do inactivated viruses work? |
1. virus propagated (make a lot of it)
2. virus inactivated (formalin, heat, uv light, etc.)
3. adjuvant added (stimulates immune response) |
|
"a chemical that stimulates immune response to antigen" |
adjuvant |
|
what are some examples of an inactivated viral vaccine? |
FeLV, FIV, rabies, canine coronovirus, equine influenza, canine parvovirus 2 |
|
what is the goal of vaccination? |
to stimulate acquired immune responses that provide protected immunity
*induce B & T lymphocytes to differentiate and produce antigen specific IgG, IgA, cytotoxic T cells & corresponding populations of memory B & T lymphocytes |
|
where is IgG found?
where is IgA found? |
blood, lymph
mucosal surfaces |
|
what is the most important thing in determining which type of vaccine to use? |
pathogenesis (systemic vs. localized) |
|
which type of antibody is most important for:
1. systemic infections
2. localized infections |
1. IgG
2. IgA |
|
rotavirus & coronovirus are [systemic/localized] infections |
localized |
|
canine parvovirus 2 is a [systemic/localized] infection |
systemic |
|
protective immunity requirements of IgG |
*soluble viral antigens - processed/presented in lymph nodes and/or spleen
*exogenous antigen |
|
protective immunity requirements of IgA |
*contact submucosal lymphoctyes - MALT |
|
protective immunity requirements of cytotoxic T cells |
*infected cells - viral antigens must be synthesized in infected cell & presented at cell surface by MHCI antigens
*endogenous antigen |
|
inactivated vaccines produce primarily _________ and provide protective immunity for ___________ infections |
IgG
systemic infections |
|
live vaccines produce primarily ___________ and provide protective immunity for ____________ infections |
IgG, IgA, cytotoxic T cells
systemic AND local |
|
what is different about vacccines for influenza virus and rotavirus? |
they have restricted tropism so they cannot replicate after injection and spread |
|
T/F IgG antibodies are readily transferable from blood to intestines but much less so from blood to lungs |
False
IgG transfers most readily to lungs, then nasal passages, then intestines |
|
advantages of live viral vaccines |
- require single dose (self-amplifying)
- stimulate protective immunity comparable with natural infection |
|
disadvantages of live viral vaccines |
- may cause disease
- possible reversion to virulence (mutation)
- unstable (can be inactivated)
- adverse reactions (anaphylaxis, autoimmune) |
|
advantages of inactivated viral vaccines |
- safe
- stable |
|
disadvantages of inactivated viral vaccines |
- multiple doses usually required
- poor stimulators of IgA & cytotoxic T cells
- adverse reactions (injection-site fibrosarcomas) |
|
_____________ is the principal concern with live virus vaccines, while ___________ is the principal concern with inactivated virus vaccines |
safety
efficacy |
|
what are the 3 main types of recombinant DNA technology vaccines? |
1. recombinant DNA-subunit vaccines
2. gene-deleted vaccines
3. virus-vectored vaccines |
|
3 advantages of recombinant DNA technology for making vaccines |
1. safe AND effective
2. useful for viruses that cannot be propagated outside animal host (hepB; rota; papilloma)
3. allow differentiation of vaccinated vs. naturally-infected animals |
|
in recombinant DNA-derived vaccines, genetic materials are manipulated via _______________ |
restriction endonucleases |
|
what is important about restriction endonucleases? |
they cleave a specific sequence of DNA |
|
T/F - recombinant DNA-derived vaccines provides antiviral immunity and protective antigens |
true |
|
"viral proteins that stimulate protective immunity responses" |
protective antigens |
|
T/F - not all protective antigens are surface proteins |
false - they ALL are |
|
what is the protective antigen in the rabies virus? |
G protein |
|
what is the protective antigen in feline lukemia virus? |
gp70 |
|
"to carry or transport" |
vector |
|
what do recombinant DNA subunit vaccines utilize in vaccines? |
plasmids |
|
what is the process for making recombinant DNA subunit vaccines? |
1. foreign gene inserted into plasmid
2. recombinant plasmid introduced into E. coli
3. expression of plasmid genes + specific protective antigen protein + adjuvant |
|
which type of immune response do you get from recombinant DNA subunit vaccines? |
IgG |
|
"not required for virus replication in host cells" |
nonessential gene |
|
how do gene-deleted virus vaccines work? |
take away nonessential genes that are virulent so that you can make live vaccines but there is no chance for virulence
*safe AND effective |
|
explain gene-deleted virus vaccine for pseudorabies |
- thymidine kinase = virulent & nonessential - several surface genes code for attachment proteins - vaccine TK-/gpE- is avirulent due to removal of thymidine kinase - also removed nonessential attachment protein gpE so they could differentiate vaccinated vs naturally infected animals |
|
what are the methods for eradicating pseudorabies from a herd? |
1. depopulation/repopulation
2. gene-deleted vaccines with test and removal program *remove pigs with gpE antibody because those are the naturally infected ones |
|
describe virus-vectored vaccines |
- gene coding protective antigen is inserted into genome of a virus (vector) - altered virus replicates in inoculated host: expresses vector genes & protective antigen gene - antigen presentation leads to IgG, IgA, cytotoxic T cells |
|
what are the requirements for a virus-vectored vaccine viral vector? |
1. large genome with non-essential genes
2. infectious for intended species
3. safe for intended species |
|
what are some viral vectors used for virus-vector vaccines? |
poxvirus, herpesvirus, adenovirus, togavirus, retravirus |
|
is vaccinia virus a useful vector for virus-vector vaccines? |
Good: wide host range, large genome
Bad: not safe for humans |
|
what is the only vaccinia-vectored vaccine in use? |
vaccinia vectored rabies G protein vaccine
- gene coding rabies G protein inserted into DNA - expressed during vaccinia virus replication - marketed by merial |
|
what is a safe alternative to vaccinia virus for virus-vectored vaccines? |
canary poxvirus
- avian poxviruses produce nonproductive infection in mammals (do NOT assemble) - does NOT require adjuvant |
|
advantages of canary poxvirus-vectored vaccines |
1. no lesion
2. no virus shedding
3. no adjuvant |
|
examples of virus-vectored vaccines being used |
1. vaccinia + rabies G protein - wildlife 2. canary poxvirus + rabies G protein - cats 3. canary poxvirus + feline lukemia virus - cats 4. canary poxvirus + west nile virus - horses |
|
general characteristics of picornaviridae virus family |
1. non-enveloped
2. single stranded RNA |
|
pathogenesis for picornavirdae viruses |
1. oral exposure 2. replication in intestinal epithelia, lymphoid tissue 3. viremia 4. spread to either brain & spinal grey matter (polioencephalomyelitis) or skin (vesicular lesions)
|
|
family and genre of Porcine teschen virus 1 |
picornaviride, teschovirus |
|
describe porcine teschen virus 1 |
1. Europe - highly virulent - polioencephamyelitis, paralysis, high mortality - inactivated & modified live vaccines 2. USA - less virulent - harmless GI inhabitant - no vaccination currently |
|
family and genre of avian encephalomyelitis virus |
picornaviridae, tremovirus |
|
describe avian encephalomyelitis virus |
- CNS disease in baby chicks - rarely seen in adults (decreased egg production) - transmitted by feces and eggborne - controlled via vaccination of breeding flock *attenuated vaccine given to adults but not safe for babies; maternal immunity passed to offspring
|
|
what is the "epidemic tremor disease" in chicks? |
avian encephalomyelitis virus |
|
family and genus of duck/turkey hepatitis virus |
picornaviridae, avihepatovirus |
|
describe duck/turkey hepatitis virus |
- 1 serotype - hepatitis/encephalitis in ducklings - adults can harbor virus but not affected by it - rapid transmission through clutch (100%) - controlled via attenuated vaccine to breeding flock |
|
family and genus for swine vesicular disease enterovirus |
picornaviridae, enterovirus |
|
describe swine vesicular disease virus, type 9 |
- occurs outside of the US - vesicles - excreted in feces - recovered pigs immune; minor production loss - can NOT distinguish it from FMDV - stable at low pH, ambient temp, easily transmitted in meat (salami) |
|
why is it so important to keep swine vesicular disease virus, type 9 out of the US? |
you cannot distinguish it from FMDV |
|
progression of vesicular disease |
1. macule 2. papule 3. vesicle 4. pustule 5. ulcer |
|
family and genus of seneca valley virus |
picoranviridae, senecavirus |
|
describe seneca valley virus |
- oncolytic potential in humans - vesicular disease - several incidents in NC in 2012 - still very new virus
*resembles FMDV |
|
family and genus for equine rhinitis A virus |
picornaviridae, apthovirus |
|
describe equine rhinitis A virus |
- sporadic acute febrile respiratory outbreaks - sub-clinical infections very common - experimental infection establishes persistent infection
|
|
pathogenesis of equine rhinitis A virus |
1. infects phyarnx
2. upper and lower airways
3. mild to severe respiratory disease
4. viremia - possibly kidney/bladder |
|
family and genus for foot and mouth disease |
picornaviridae, apthovirus |
|
FMDV - who does it affect? |
- cloven-footed animals - cattle, sheep, swine, wild ruminants (deer) - greatest losses in cattle and swine - low mortality but HIGH morbidity |
|
FMDV - transmission |
***highly contagious
- spreads rapidly via aersol & saliva - can spread great distances - high titer droplets, very stable and short incubation period - can be in meats, hide and milk |
|
FMDV - pathogenesis |
exposure - replication in epithelium (pharynx) - viremia
1-heart (muscle) --> rare
2-epithelia (mouth, muzzle, feet, teats, udder) - vesicles & ulcers |
|
FMDV - viral excretion |
- begins 24 hours prior to clinical disease - lasts several days to > month - can persist in cattle for up to 2 years > become carriers and can continue to spread the infection (debatable) |
|
serotype definition |
in vitro, antiserum which is neutralizing for one serotype is very much less neutralizing for another serotype |
|
subtype definition |
sufficiently different from each other to make immunity in vivo subtype specific and immunity lasts only about one year |
|
where is FMDV endemic? |
1. Africa, Asia - inactivated vaccines specific to local strains
2. South America - vaccinate in most countries |
|
where is FMDV low incidents? |
Continental Europe - control by vaccination in some countries |
|
what parts of the world are FMDV free? |
North & Central America; Carribean; Australia; New Zealand; Scand - no vaccinations |
|
impediments to successful vaccination programs for FMDV |
1. immunity is subtype specific
2. only lasts 1 year = expensive!
3. DIVA - need to develop recombinant DNA vaccines |
|
why is FMDV your worst nightmare? |
1. HIGHLY contagious 2. DEBILITATING 3. Immunity: - specific across 70 subtypes - short-lived - does not prevent "carrier" state |
|
how many serotypes and subgroups does FMDV have? |
7 serotypes
70 subgroups |
|
3 families of viruses that appear similar and regular in shape under electron microscopy
what are their physical characteristics? |
1. togaviridae 2. arteriviridae 3. flaviviridae
RNA genome; enveloped |
|
3 viruses in family togaviridae |
1. eastern equine encephalitis
2. western equine encephalitis
3. venezuelan equine encephalitis |
|
are EEE, WEE and VEE zoonotic? |
yes
- humans, equines, most exotic avian species |
|
how are EEE, WEE & VEE transmitted? |
mosquitoes |
|
describe EEE/WEE transmission |
enzootic cycle: birds (preferred)
epizootic: exotic birds
dead-end: humans, equine |
|
describe VEE transmission |
enzootic cycle: rodents
epizootic: equine
dead-end: humans |
|
pathogenesis of EEE/WEE/ZEE |
1. local replication 2. systemic spread 3. lymphoid & other organs 4. viremia 5. +/- CNS invasion/encephalitis |
|
clinical signs of EEE/WEE/ZEE |
- fever - anorexia - neurologic signs > severe depression, wide stance, dropping head - death |
|
rank EEE, WEE and ZEE in order of mortality rate |
1. EEE
2. VEE
3. WEE |
|
what is the sentinel program? |
chickens are sent out to a variety of locations and checked periodically for antibodies to specific viruses
they are resistant to the viruses so can alert the presence of the virus via their blood without getting sick themselves |
|
how do we control EEE/WEE/VEE? |
1. vaccinate - killed bivalent/trivalent in spring - modified-live VEE vaccine - canarypox cevtored vaccine
2. outbreaks - restrict mvmt; pesticide spray; vaccinate |
|
name 2 viruses in arteriviridae family |
1. equine arteritis virus
2. porcine respiratory & reproductive syndrome (PRRS) |
|
how are arteriviridae viruses transmitted? |
aerosol or venereal |
|
pathogenesis of equine arteritis virus |
1. infects macrophages in lungs 2. spread to lymph nodes 3. viremia 4. infects endothelial cells in small artery walls 5. infects epithelium of seminiferous tubules *persistent shedding |
|
clinical signs of equine arteritis virus |
- most infections are sub-clinical - mild to moderate disease > fever, depression, anorexia, edema of limbs, genitalia & abdomen, nasal & lacrimal discharge - **ABORTION |
|
how do we control equine arteritis virus? |
- modified-live vaccine > vaccinate breeding animals
- current programs in NY & KY to vaccinate stallions and test for carrier status |
|
what is the "blue ears" virus? |
porcine respiratory & reproductive syndrome (PRRS) |
|
pathogenesis of porcine respiratory & reproductive syndrome |
1. infects lung macrophages 2. viremia 3. spreads to other tissues including bulbourethral gland in boar *persistently shed |
|
clinical signs for porcine respiratory & reproductive syndrome |
- mostly subclinical - mild to moderate disease > fever, anorexia, respiratory disease, secondary bacterial disease (pneumonia) - *ABORTIONS & STILLBIRTHS |
|
how do we control porcine respiratory & reproductive syndrome? |
- inactivated and live vaccines - don't seem to be very effective, possibly because of antigenic variations between strains |
|
2 types of flaviviridae viruses |
1. pestiviriuses
2. flaviviruses |
|
3 kinds of pestiviruses
(what family are these in?) |
1. bovine virus diarrhea virus (type 1 & 2)
2. classic swine fever virus (hog cholera)
3. border disease
(flaviviridae) |
|
bovine virus diarrhea - disease "flowchart" |
1. types - type 1 or type 2 2. disease syndromes - acute: bovine virus diarrhea - persistent: mucosal disease 3. viral biotypes - non-cytopathic (normal) - cytopathic (mutant that can arise) |
|
bovine virus diarrhea - acute infection - pathogenesis |
1. oronasal uptake of infectious secretions 2. local mucosal infection (nasal/ocular discharge, salivation, stomatitis) 3. spread to lymphoid tissue (immune suppression - shipping fever) 4. spreads to GI epithelium (explosive D+) |
|
describe bovine virus diarrhea infection in a pregnant cow: cytopathic biotype |
1. early - mid gestation > abortion, mummification, congenital defects
2. mid - late gestation > normal, healthy calf > immune system has developed enough to clear the infection |
|
describe bovine virus diarrhea infection in a pregnant cow: non-cytopathic biotype |
1. less than 3 months gestation > immune tolerance & persistant infection > seen as "self" > calf born healthy but shedding virus 2. over 3 months gestation > viral clearance > immune response develops to clear infection |
|
how do cows acquire mucosal disease? |
bovine virus diarrhea - persistent non-cytopathic - 100% fatal
1. mutation of non-cytopathic biotype 2. infection of cytopathic biotype from envmt |
|
describe mucosal disease - clinical signs |
- severe disease > fever, ulceration of intestines & mouth, diarrhea with blood, anorexia, nasal discharge
- death in 1-3 weeks |
|
how do we control bovine virus diarrhea? |
- difficult due to persistently infected animals - inactivated & modified-live vaccines - slaughter persistently infected animals but they are hard to identify because they have little or no antibody to the virus |
|
what is the new name for hog cholera? |
classic swine fever |
|
describe classic swine fever |
- worldwide but eradicated from US in 1960s - endothelial damage - petechia, thrombosis & hemorrhage - "button ulcers" in GI - huge economic threat -1998 outbreak in Netherlands - uncooked pork import is big threat |
|
"hairy shaker lamb" syndrome |
border disease |
|
describe border disease |
- infects sheep & goats - transmission & pathogenesis similar to BVD - fetal infection less than 2 mo gestation - signs due to poor growth & CNS infection
|
|
family and genus of west nile virus |
flaviviridae, flavivirus |
|
where and when did west nile virus start? |
1999 - exotic bird deaths in the bronx zoo |
|
describe transmission of west nile virus |
enzootic: birds
epizootic: crows & bluejays
dead-end: humans & equine |
|
how do we control west nile virus? |
- killed vaccine available (yearly) > may not provide protective immunity for entire mosquito season
- recombinant canary-pox virus vaccine (2005) |
|
what family is "true" mucous viruses? |
orthomyxoviridae |
|
what family is "other" mucous viruses? |
paramyxoviridae |
|
family of flu virus
what is the only one that affects animals? |
orthomyxoviridae
influenza A |
|
who does influenza A infect |
- primarily avian species - humans - swine - equine - marine mammals - dogs - cats |
|
describe traits of the influenza virus |
- enveloped - single stranded RNA - 8 segments of RNA "mini genes" - 2 envelope proteins |
|
2 envelope proteins on influenza virus
which one is responsible for attachment?
how many antigenic strains are there of each? |
1. hemagglutinin - H *attachment - 17 types
2. neuraminidase - N - 10 types |
|
nomenclature for classifying influenza viruses |
strain/species it affects/geographic origin of strain/strain #/year it was isolated
A/duck/Alberta/35/76 |
|
point mutations are associated with ______________ of influenza viruses
resassortment is associated with ________________ of influenza viruses |
antigenic drift
antigenic shift |
|
describe antigenic drift of influenza viruses |
- slow - mutations in enveloped proteins - allows escape from immune system
(H3N2 this year) |
|
describe antigenic shift of influenza virus |
- MUST have segmented genome - new antigenic type is created by rare dual infection - does not occur very often - sudden and higher morbidity/mortality - pandemic instead of endemic |
|
2 receptor types of influenza virus |
1. avian
2. mammalian |
|
which receptor type (and where) are present in:
avian - swine - human |
avian - avian
swine - avian & mammalian in URT
humans - avian in LRT; mammalian in URT |
|
pathogenesis of equine & swine influenza |
- local respiratory infection - fever, cough, nasal/ocular discharge, anorexia - secondary bacterial infections > bronchopneumonia |
|
which strand of influenza do cats seem to be susceptible to? |
avian H5N1 |
|
which strand of influenza are dogs susceptible to? |
equine H3N8 |
|
where did the "new" H1N1 originate in 2009? |
Mexico |
|
pathogenesis of influenza in birds |
- subclinical infection in waterfowl - avirulent strains in domestic birds - local infection in respiratory & GI tracts |
|
which influenza virus strain produces a severe systemic disease in birds?
what is the name for this? |
H5 and H7 viruses
fowl plague |
|
how is influenza virus transmitted? |
- aerosolized respiratory secretions
- avians can shed in feces without any clinical signs in the actual bird |
|
how is influenza virus controlled in equine? swine? avian? |
- frequent vaccination for high risk pop. - inactivated H3/N8 (H7/N7 in older vx) - quarantine in outbreak
|
|
how is influenza virus controlled in swine? |
- no routine vaccination
- vaccinate when there is an outbreak |
|
how is influenza virus controlled in avians? |
- quarantine and eradication if there is an outbreak of disease
- limit contact with wild birds |
|
examples of paramyxoviruses |
- canine distemper - newcastle disease - canine parainfluenza virus - parainfluenza III - bovine respiratory syncytial virus - rinderpest |
|
transmission of paramyxoviruses |
respiratory route via aerosolized secretions |
|
what species are affected by canine distemper virus? |
- dogs - wild canids - skunks - racoons |
|
canine distemper pathogensis |
- infects macrophages of oropharynx - primary viremia: spread to lymphoid tissues - secondary viremia: infects respiratory, GI, urogenital epithelium, skin & CNS |
|
canine distemper virus outcome with healthy immune response |
excellent immune response - subclinical infection
- can still invade CNS - rarely seen 2-8 years later as "old dog encephalitis" |
|
canine distemper virus outcome with moderate immune response |
mild illness
- virus persists in CNS - neurologic signs +/- death 4-9 weeks later *difficult to diagnose |
|
canine distemper virus outcome with poor immune response |
severe disease and death |
|
how do we control canine distemper virus? |
modified live vaccine
- add human measles to early vaccine to generate immune response better |
|
describe caliciviridae |
non-enveloped
single-stranded RNA |
|
4 genre in calciciviridae |
1. vesivirus
2. lagovirus
3. norovirus
4. sapovirus |
|
3 vesivirus diseases |
1. vesicular exanthema of swine
2. san miguel sea lion virus
3. feline calicivirus |
|
family and genus of vesicular exanthema of swine |
caliciviridae, vesivirus |
|
what is the most important reason to worry about vesicular exanthema of swine? |
resemblance to FMDV |
|
describe vesicular exanthema of swine |
- vesicular disease (like FMDV) - currently "foreign animal disease" - isolated in sea lions in 1972 (san miguel) |
|
describe host range in vesiviruses |
*broad host range
- single strain has successfully infected 21 animal hosts - has been eliminated from swine population but still endemic in ocean species, some livestock and cats |
|
family and genus of san miguel sea lion virus |
caliciviridae, vesivirus |
|
what disease did san miguel sea lion virus appear to be the same as? |
vesicular exanthema of swine |
|
family and genus of feline calicivirus |
caliciviridae, vesivirus |
|
what are the 2 major causes of feline respiratory disease? |
1. feline calicivirus
2. feline herpesvirus 1 |
|
how is feline calicivirus transmitted? |
aerosol, fomites, human handlers |
|
clinical signs of feline calicivirus |
- depend on cat breed, age, strain, etc. - conjunctivitis, rhinitis, tracheitis, pneumonia, tounge/ocular lesions - vary from subclinical to pneumonia - high morbidity/mortality in kittens |
|
describe viral shedding in feline calicivirus |
*recovered cats are immune but may shed for life (increases with stress)
- persistant, intermittent, or resistant to disease (no shedding)
*tremendous opportunity for evolution |
|
what is virulent systemic disease? |
- a variant of feline calicivirus - subclinical to pneumonia & death - edema & sores of feet and face
*vaccinated cats were susceptible! |
|
how do we control feline calicivirus? |
- modified-live or inactivated vaccine (FVRCP)
- both types of vaccines provide the same protection
*does not protect against ALL strains |
|
what is the persistence of feline calicivirus? |
continuous shedding, re-infection: great evolution |
|
what are the variants of feline calicivirus? |
spontaneous virulent systemic disease variant(s) |
|
family and genus of rabbit hemorrhagic disease virus |
caliciviridae, lagovirus |
|
describe rabbit hemorrhagic disease virus |
- identified in China (1984) - sudden death within 1 day of fever - hemorrhagic lesions (liver/lung) - young rabbits resistant - used as population control in Australia |
|
family and genus of feline norovirus |
caliciviridae, norovirus |
|
characteristics of reoviridae |
- non-enveloped
- double-stranded RNA
- segmented |
|
5 genre of reoviridae |
1. reovirus 2. rotovirus 3. orbivirus 4. coltivirus 5. aquareovirus |
|
how are reoviridae viruses like influenza? |
*segmented genome allows reassortment between viruses
- only in same genus - new viral disease emerge - not as big of a problem with reoviridae |
|
transmission/pathogenesis of rioviridae |
1. reo/roto - stable at low pH - oral entry - enteric infection - proteolytic activation
2. orbi/colti - not stable at low pH - blood entry - systemic infection - no proteolytic activation |
|
family and genus of avian viral arthritis virus |
reoviridae, reovirus |
|
how many serotypes are there of avian viral arthritis virus?
how many cause disease? |
5
4 - viral arthritis in chickens |
|
pathogenesis of avian viral arthritis virus |
- enters via oral/tracheal/nasal - generalized infection (5-7wk old) - main damage to synovial membrane & tendon sheaths - high morbidity; low mortality - disease 2 wks; virus persists 30 days - can be found in eggs |
|
how do we control avian viral arthritis virus? |
- vaccines in problem areas only
- immunize breeder flocks
- modified-live vaccine (SQ or drinking water) |
|
family and genus of porcine and bovine rotaviruses |
reoviridae, rotavirus |
|
pathogenesis of porcine and bovine rotaviruses |
- orally - stomach - intestine - infects epithelial cells in absorptive portion of villus (NOT crypt cells) - D+ & milk scours - secondary infections make D+ more severe |
|
immunity for porcine and bovine rotaviruses |
- resistance mediated by local immunity > epithelial surface of small intestine (IgA)
- colostrum protection is typically not enough |
|
how do we control porcine and bovine rotaviruses? |
- modified live vaccine
- inactivated vaccines in dam
- less practical: feed susceptible neonates high titer immune colustrum |
|
family and genus of african horse sickness virus |
reoviridae, orbivirus |
|
why do we care about african horse sickness virus? |
*never been seen in western hemisphere
- most important and lethal disease of horses other than EEE & VEE
- restricts importations of horses |
|
transmission of african horse sickness virus |
- NOT directly transmissible from horse-horse - culicoides > virus replicates in them - animals less susceptible may serve as reservoir |
|
pathogenesis of african horse sickness virus |
- replication in local lymph node - transient primary viremia - infection of other lymphoid tissues - secondary viremia - mechanism unknown
*vasculitis |
|
describe the 2 disease forms of african horse sickness virus |
1. acute - highly virulent strain or naive horse - pulmonary edema; death via drowning 2. chronic - poorly virulent strain or previously exposed or genetically resistant - edema of head, neck shoulder; heart lesions *typically see combination of both forms |
|
describe immunity to african horse sickness virus |
- 9 serotypes - immunity to one doesn't preclude infection from another - second infection tends to be less severe/chronic |
|
how do we control african horse sickness virus? |
- control culicoides > pesticide sprays
- south africa has a modified live vaccine with all 9 serotypes |
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family and genus for epizootic hemorrhagic disease virus |
reoviridae, orbivirus |
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describe epizootic hemorrhagic disease virus? |
- infects ruminants worldwide > white-tail deer are most susceptible - spread by culicoides - most infections mild or sub-clinical - indistinguishable from bluetongue virus |
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family and genus of bluetongue virus |
reoviridae, orbivirus |
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what species is most affected by bluetonge virus? |
*sheep
- also infects cattle & goats - death loss mostly in lambs - significant & loss due to export bans |
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pathogenesis of bluetongue disease |
- culicoides bite - regional lymph nodes - blood - vascular endothelial cells - major lesions in upper GI mouth - cyanosis of tongue - lesions in coronary band and btwn toes - can cause intrauterine infection *host remains viremic long after recovery |
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how is bluetongue virus transmitted? |
- culicoides bites
- NOT transmitted in animal products |
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how do we control bluetongue virus? |
- control culicoides (pesticide spray)
- modified-live vaccines available in US for 3 serotypes
- use only in sheep where there is a bigger problem |
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what are the target cells and disease of rotaviruses? |
mature villus epithelium --> repopulation by crypt cells --> D+ & milk scours |
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how does climate affect orbiviruses? |
they are spread by culicoides so once it is cold enough for them to go away, the virus is no longer able to spread |
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what is the impact of viremia in bluetongue virus? |
prolonged viremia facilitates spread |
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characteristics of birnaviridae |
- noneveloped
- double-stranded RNA
- 2 segments |
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3 pathogens of birnaviridae family |
1. infectious bursal disease virus
2. chicken proventricular necrosis virus
3. infectious pancreatic necrosis virus |
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describe infectious pancreatic necrosis virus |
*highly contagious, lethal disease of salmonid fish reared in hatcheries - subclinical in pike, carp and barbels - subclinical in older fish - swollen abdomen, bulging eyes, cutaneous hemorrhages, frantically whirl, lie on bottom - survivors are lifelong carriers - spread in feces, eggs, sperm - no vaccine - rely on water disinfection |
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family of infectious bursal disease virus |
birnaviridae |
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pathogenesis of infectious bursal disease virus |
- 3-6 wk old chicks most susceptible - oral entry; replication in gut-associated macrophages & lymphoid cells - enteric infection = D+ = death of dehydration - primary viremia = bursal l.n. = compromised immune system - secondary viremia = kidneys = immune complex disease |
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immunity for infectious bursal disease virus |
- maternal antibodies for 1-2 weeks
- very young chicks can develop immunity without disease |
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how is infectious bursal disease virus transmitted? |
direct and indirect contact
*highly contagious |
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how do we control infectious bursal disease? |
- natural immunity in young chicks - modified-live or inactivated vx (SQ/water) - antibody-coated virus injected into eggs > requires exact antibody, virus ratio, timing, etc |
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what virus did Dr. Fuller and Dr. Guy discover? |
chicken proventricular necrosis virus
- from transmissible viral proventriculitis - enlargement of proventriculus until it ruptured, usually at production, causing a lot of loss |
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characteristics of coronoviridae |
- enveloped
- single-stranded RNA |
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what kinds of diseases does coronoviridae cause? |
respiratory, GI and systemic |
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why is antigenic cross-reactivity clinically important for coronoviridae viruses? |
- several viruses infect several species *induce antibodies which may exacerbate disease
- some viruses are indistinguishable antigenically *difficult to interpret serum antibody titers |
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describe viral replication in coronaviruses |
- very long RNA genomes - polymerase jumps during synthesis - frequent recombination
*creates recombinant RNA = new viruses! |
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why is recombination important in coronaviruses? |
1. frequent recombination generates new mixed genomes
2. results in frequent mutations
*many viruses may be recombinant or mutant forms derived from each other |
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viral family of transmissible gastroenteritis virus (TGEV) |
coronaviridae |
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describe 2 forms of transmissible gastroenteritis virus |
* highly contagious enteric virus of swine 1. epizootic - susceptible (nonimmune) herd 2. enzootic - persistence of virus in herd due to continuous introduction of susceptible pigs |
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pathogenesis of transmissible gastroenteritis virus |
- fecal-oral route - can be shed for 10 weeks - replicates in absorptive epithelial cells of small intestines |
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determinants of prognosis for transmissible gastroenteritis virus |
adults: repopulate crypt cells; immune response young: 2 possibilities: 1. epizootic - usually fatal 2. enzootic - usually low mortalityho |
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how do we control transmissible gastroenteritis virus? |
- prevent introduction to herd - local eradication - vaccinate sows prior to farrowing > modified live vx - only in previously infected pigs > orally administer live virulent virus to sows (natural or deliberate feedback) |
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variants of transmissible gastroenteritis virus |
1. porcine resp.corona (PRCV) - Europe 1980s - respiratory! 2. north america - same mutation, different strain - PRCV is typically subclinical so now it can protect herds against TGEV |
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family of porcine epidemic diarrhea (PED) |
coronoviridae |
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what is special about porcine epidemic diarrhea? |
- not antigenically related to other coronaviruses - causes acute D+ in pigs of all ages but typically older ones recover - was foreign until 2013 |
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pathogenesis of porcine epidemic diarrhea |
- fecal/oral transmission - short incubation period (12-24 hours) - shed for 7-10 days
*problem with trucks spreading contamination |
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describe canine coronavirus |
- similar to TGE in pigs - all breeds/ages but young more susceptible - ubiquitous - no effective vaccine - can infect cats |
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what is important about feline enteric coronavirus? |
it mutates into feline infectious peritonitis virus |
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2 biotypes of feline coronavirus |
1. feline enteric coronavirus 2. feline infectious peritonitis virus
*anitbodies are indistinguishable |
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evolution of feline infectious peritonitis from feline enteric coronavirus |
1. epidemiology - geography of strain 2. mutation - analysis of natural infection - mutate inside cat since FIP doesn't spread as well 3. tissue tropism - FIP is not as transmissible |
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pathogenesis of feline infectious peritonitis virus |
3 possible forms: 1. effusion (wet) - peritoneal/pleural effusion 2. noneffusive (dry) - pyogranulomatous lesions in kidney, liver, CNS, eyes 3. combination of bothw |
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what determines the pathogenesis of feline infectious peritonitis virus? |
the immunity of the infected host and the virus mutation |
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treatment for feline infectious peritonitis virus |
- purely palliative (no cure) - treat cats otherwise healthy - corticosteroids, antibiotics, nutrients, fluids - potential for reactivation - no vaccine |