Coronaviridae Flashcards
name four significant group 1a coronaviruses
- Feline enteric coronavirus (AKA Fel. Infectious Peritonitis)
- Canine coronavirus
- Transmissible gastroenteritis virus of swine
- porcine respiratory coronavirus
name the significant virus from group 1b coronavirus
porcine epidemic diarrhea virus
name 4 major viruses from group 2a coronviruses
- porcine hemagglutinating encephalomyelitis virus
- mouse hepatitis virus
- sialodacryoadenitis virus of rats
- bovine coronavirus
name the major group 2b coronavirus
SARS
name the 2 major group 3 coronaviruses
- avian infectious bronchitis virus
- turkey coronavirus (bluecomb)
describe coronaviridae structure
- enveloped, with large club shaped spikes
- icosahedral internal core structure enclosing a helical nucleocapsid (coronavirus) OR a tightly coiled tubular nucleocapsid bent into a donut shape (torovirus)
describe coronaviridae genome
single molecule of linear, positive sense ssRNA
coronaviridae replication occurs in the ________. virions are formed by ______ into the _____ and are released by _______.
cytoplasm; budding; endoplasmic reticulum; exocytosis
what is TGE? what is its etiology?
Transmissible gastroenteritis; highly infectious viral disease of pigs, characterized by vomiting, dehydration, diarrhea, and high mortality in piglets. older pigs are also susceptible, but usualy milder clinical signs.
caused by TGE virus, group 1a coronavirus
describe the two forms of TGE
epidemic: virus first introduced into susceptible herd, observed usually in winter. rapid spread, high morbidity and mortality in piglets.
endemic: virus persists in partially immune herd, or due to concurent porcine respiratory coronavirus (PRCV) infection (deletion mutant of TGE virus). less severe form, lower mort and morb
t/f TGE has been reported in the usa
true!
what is the major route of transmission for TGE?
unclear, but appears to be mainly fecal-oral. aerosol also occurs
describe the pathogenesis of TGE
tge virus affects intestinal villi (blunting and fusion) –> villus atrophy = malabsorption –> diarrhea
what is the incubation period for TGE? onset?
24-48 hrs. onset is sudden.
describe the clinical findings of TGE
- profuse diarrhea in piglets
- vomiting
- depression/dehydration
- watery, yellow-green stool, offensive odor
- feces may contain clots of undigested milk
- distended intestine; translucent wall
- dilated stomach
- bloated gut
- gases present in gut, atrophy of villi
how do we diagnose TGE?
- necropsy and histopath (atrophied/fused/blunted villi)
- fluorescent antibody assay (FA), immunohistochemistry (IHC)
- detection of nucleic acid by reverse transcriptase PCR
describe control during/after outbreak of TGE
- isolation of sows due to farrow
- discontinuation of selling and purchasing breed stock
- partial culling
- biosecurity measures
- all-in all-out management system
- complete depopulation and establishment of a new herd
- vaccination of pregnant sows and neonatal pigs
what is PED? What is its etiology?
Porcine epidemic diarrhea
Group 1B coronavirus
PED is spread via _______. Causes acute outbreaks of _______.
fecal-oral route.
severe diarrhea, vomiting, high morbidity and variable mortality.
similar clinical signs to TGE
what is vomiting & wasting dz in pigs?
Porcine Hemagglutinating Encephalomyelitis
group 2a coronavirus
hemagglutination of rbc’s
describe the transmission and pathogenesis of porcine hemagglutinating encephalomyelitis
aerosol route –> replication in nasal mucosa –> replication in small intestine, lungs, tonsils –> spread to CNS via peripheral NS –> replicate in the brainstem, cerebrum, cerebellum.
-In piglets <4 wks, the virus will also replicate in the distal vagi ganglion, leading to vomiting, as well as the vagal nerves in the gut, causing malnutrition and characteristic lesions in the intramural plexi.
clinical findings in vomiting/wasting dz form of porcine hemagglutinating encephalomyelitis? what’s the other form?
Repeated retching and vomiting, rapid emaciation.
Neonatal pigs become dehydrated, cyanotic, and comatose and die.
Anterior abdomen distended from impaired emptying and accumulation of gas
other form is encephalomyelitic: nonsuppurative encephalomyelitis and neuro signs
describe bovine coronavirus transmission and path
fecal-oral mainly, but also aerosol
main form: virus replicates in small and large intestine, leads to villus atrophy/fusion/blunting… diarrhea, malabsorption, and dehydration
other form: replicates in upper respiratory tract. produces mild URT dz, rhinitis, tracheitis.
bovine coronavirus mainly affects what age of calves?
1-2 weeks. in general though, calves 1 day to 3 months of age
what is the main clinical sign of bovine coronavirus in calves?
profuse liquid diarrhea, explosive outbreaks in a herd.
how do use vaccinations for bovine coronavirus?
commercial bovine rotavirus/coronavirus/E.coli and somtimes C. perfringens combined vaccine. given to healthy pregnant cows, and revaccinated before each subsequent calving.
increases protective antibodies against corona/rota/E.coli in colostrum and milk. provides passive immunity to calf once it consumes the colostrum and milk
what is the etiology of winter dysentery in cows?
bovine coronavirus. group 2a
what age of cow does winter dysentery affect?
Disease occurs in mature cattle, most common in recently calved, lactating cows. Young cattle may be infected, but normally exhibit mild clinical signs
pathogenesis of winter dysentery?
basically same as with coronavirus infection in calves… diarrhea
clinical signs of winter dysentery in cows?
sudden, explosive outbreak of diarrhea. short course, dark green to black feces, presence of blood flecks, dehydration, decrease milk production, some coughing.
etiology of feline infectious peritonitis?
feline coronavirus (group 1a)
FIP is a highly fatal ______ mediated disease of cats and wild felids.
immune
t/f - FIP is poorly understood and prevention is difficult.
True
describe FIP transmission
infected cat or chronic carrier sheds FCoV in feces –> mainly fecal oral transmission to uninfected cat.
also inhalation and transplacental are possible.
name the possible outcomes and frequency of FCoV infections
- Resistant (5-10%)
- Transient infection - diarrhea(70%)
- Persistent carrier (5-10%)
- Feline infectious peritonitis (1-3%)
FIP FCoV has an affinity for what cell?
macrophages
what kind of immune response allows the prevention of FIP?
a strong cell-mediated response
what kind of immune response will result in the Effusive (wet) form of FIP? What are the signs in the dz?
a weak CMI and strong humoral (Ab) response.
peritonitis, pleuritis, vasculitis, intravascular coagulation, ascites, glomerulonephritis
what kind of immune response allows for the non-effusive(dry) form of FIP? what are the signs of the dz?
an intermediate response.
small granulomas, ocular lesions, CNS involvement.
Describe the role of mutations in FIP/FCoV
Usually, when FCoV infects a healthy cat, it’s an avirulent/low virulence strain of the virus. Usually leads to mild diarrhea or something, as the virus affects the villi.
However, FCoV will often mutate in the body, usually just stays low virulence. Sometimes though, the mutation leads to a really virulent strain, with affinity for the macrophages; which would be FIP virus. Severe dz. infect and replicate in macrophage
describe how FIP enters the macrophage and alters host immune response
virus infects macrophage through the CD13 receptor on the macrophage. –> macrophage becomes activated, carries virus throughout body. –> macrophage releases inflammatory mediators/cytokines –> macrophages skew the immune response from a Th1(cell mediated) response to a Th2(humoral) response, as well as causing lymphocyte apoptosis (and subsequently lymphopenia=reduced lymphocytes) due to TNF release
what is the role of the FIPV spike-specific antibody?
enhances uptake and replication of FIPV in macrophages.
leads to Ag-Ab complex formation –> complement activation –> vasculitis/edema… effusive (wet) FIP
name some lesions/signs of effusive(wet) FIP
- distended abdomen
- diffuse fibrinous peritonitis
- ascites
- pygranulomatous foci on the serosal surface of intestines
- pyogranulomas in liver
- serofibrinous pleuritis
- abdominal viscera show pyogranulomatous foci
- pyogranulomas on omentum
- thoracic effusion
In non-effusive(dry) FIP, _______ macrophages are infected than in wet FIP.
fewer
what are some signs/lesions of dry FIP?
- granulomatous inflammation/enlarged mesenteric lnn.
- pyogranulomatous lesions on kidney
- granulomatous meningoencephalitis
- granulomatous uveitis
- keratic precipitates on the inner cornea
Describe the Rivalta Test.
Method of diagnosing FIP.
- in a test tube, add 1 drop 98% acetic acid to 5 ml water. Add one drop of effusion(ascites tap) to the tube.
- If drop disappears, and solution is clear, negative for FIP
- If drop retains shape, drops down, or attaches to surface of tube, positive for FIP
what is the main flaw of ELISA, IFA, and virus-neutralization tests for FCoV?
they detect antibodies, but CANNOT differentiate b/w the various strains.
t/f - there is an intranasal vaccine available for FIP
true, but its use is not recommended. controversial
what is the etiology of avian infectious bronchitis?
group 3 coronavirus
IBV - infectious bronchitis virus
avian infectious bronchitis is a common, _____ contagious, acute, and economically important viral disease of _______
highly; chickens
what is S protein of IBV?
antigenically significant, major inducer of protective immunity.
what are IBV protectotypes?
by mutation and recombination, there is genetic variation in the S protein gene of IBV. this variation leads to antigenic variation, and some of these serotypes are known are protectotypes.
a protectotype will provide cross-protection against other IBV serotypes.
name the 5 types of IBV tropism
- Respiratory (most common)
- enterotropic
- nephrotropic (some strains are super nephropathogenic)
- proventricular
- uterotropic
what are the major sources of IBV?
infected chicks, carrier chickens or latent chickens
- coughing (virus in tracheobronchial exudate)
- feces
- egg surface (from oviduct)
routes of transmission for IBV?
aerosol/inhalation
direct contact
contact with contaminated fomites, food, litter, water, etc
t/f - possible outcomes of IBV infection in a healthy bird include nephritis, reproductive disorders, egg decline, and respiratory dz
true. respiratory dz being most common
what 3 things can enhance the severity of bronchitis due to IBV?
immunosuppression, E. coli, or mycoplasma infection
IBV respiratory dz will lead to what in the trachea/bronchi?
congestion/hemorrhages(trachea), inflammation (both), white caseous exudate in syrinx and primary bronchi
what is seen in IBV nephritis?
nephritis, swollen kidney, urolithiasis, distended ureter w urates. visceral gout, urates on liver/heart
what is seen with IBV reproductive disorders?
- soft-shelled, misshapen, discolored eggs
- thin, watery albumin, separation b/w thick and thin albumin absent
- involuted, flaccid ovarian follicles
- stunted, dwarfing of embryo
vaccination of IBV?
- live vaccines: used in meat type (broiler) chickens, and for the initial vaccination and priming of breeders and layers… the Massachusetts (M41) strain, H120, and other vaccines of the massachussetts serotype.
- inactivated: used in layers and breeders
what is the significant torovirus for vet med?
bovine torovirus (Breda virus, BoTV-1 and BoTV-2)
what does bovine torovirus cause?
profuse diarrhea in young calves
what is the pathogenesis of bovine torovirus?
BoTV rapidly infects epithelial cels from the lower half of the villi, extending into the crypts throughout the mid-jejunum, ileum. BoTV also infects colon and cecum epithelium
