Exam 3 - Liver Infection Flashcards
what is the etiology of FIP in cats?
ssRNA coronavirus - common enteric virus of cats
FIP develops in a minority due to a novel genetic mutation after infection that stimulates an excessive immune response
T/F: the mutated form of feline coronavirus is not transmitted to new cats
true
what is the epidemiology of FIP?
enteric coronavirus spread through fecal oral transmission - facilitated by indoor housing, dense husbandry
what cats are at risk for FIP?
kittens & purebreds
second smaller peak around 10 years of age
what cats are at risk for FIP?
kittens & purebreds
second smaller peak around 10 years of age
what clinical signs are seen in most cats with feline coronavirus?
mild clinical illness & asymptomatic shedding
T/F: a vast majority of cats are seropositive for feline coronavirus
true
T/F: different sub-strains of FCoV are more or less likely to mutate
true
what is the pathogenesis of feline coronavirus?
direct or indirect fecal-oral route that is very durable in the environment (use bleach when cleaning) causing mild diarrhea or nothing in most cats or rare severe diarrhea
what is shedding like for cats with feline coronavirus?
most shed for 2-3 months
minority become lifelong carriers of FCoV
do lifelong carriers of FCoV often develop FIP?
nope - very seldom do
what are the potential outcomes for a cat infected with feline coronavirus?
resistant to infection: 5-10%
transient infection: 70%
persistent infection/carrier status: 13%
FIP: 1-3%
what is the pathogenesis of FIP influenced by?
influenced by the viral load, viral strain, genetic background of host, & stress
what is the pathogenesis of FIP?
feline coronavirus in the cat mutates & leaves the GI tract & invades monocytes
replicates outside of the GI tract & monocytes extravasate & go anywhere
immune response against mutated FIPV -
strong cell-mediated immunity: prevents FIP
weak cell-mediated immunity/strong humoral - wet FIP
moderate immune response - dry FIP (immune-privileged sites)
why is there a difference in clinical signs seen between the wet & dry forms of FIP?
multi-systemic pyogranulomatous vasculitis occurs everywhere in wet form of FIP - why we see effusion
in the dry form - limited vessels are affected in limited sites
what clinical signs are seen in wet FIP?
pleural effusion, abdominal effusion, & high protein-low-cellularity effusion (modified transudate)
why is the dry form of FIP hard to diagnose?
they lack the characteristic effusion - fluid gives us the best diagnostic capabilities!!!
what clinical signs are associated with the dry form of FIP?
vague pyrexia, weight loss, & inappetence
icterus & liver disease
iritis, uveitis
variable neurologic signs
what pathology is seen in this photo? what is it associated with?
iritis - dry form of FIP
what found on necropsy is supportive of the diagnosis of FIP?
perivascular pyogranulomatous inflammation is definitive
how do we diagnose FIP? what are the limitations of it?
very high titers of serology supports diagnosis: > 1:1600, but it can also be high in high-density housing
fecal RT-PCR to detect gi disease/shedders - highly sensitive tests
why is serology not the best for diagnosing FIP?
vast majority of cats are positive from prior exposure or illness
how is wet FIP diagnosed ante-mortem?
minimum database - lymphopenia is common & hyperglobulinemia often with low albumin is highly suggestive
effusion - high protein (globulin) & low cell count
positive PCR for mutated FCoV - highly specific
positive IFA for FCoV-infected macrophages in fluid -highly specific
how is the dry form of FIP diagnosed ante-mortem?
…find something to PCR or IFA
what are your highly sensitive tests for diagnosing FIP? what are the highly specific tests used?
sensitive - FCoV serology/titers & fecal RT-PCR
specific - PCR for mutated FCoV & IFA for FCoV-infected macrophages in fluid
why does a positive serology test for FCoV predict nothing?
most shedders of the disease are not sick
chronic shedders are less likely to develop FIP
T/F: there is no available therapy for clearing FCoV+ cats
true
what is the classic treatment used for FIP? what is the prognosis?
suppress the excessive immune response - prednisolone commonly used but evidence for benefit is minimal
no better evidence for anything else - interferon-omega or polyprenyl immunostimulant (-> Th1 -> CMI)
POOR PROGNOSIS
what is the emerging treatment for FIP?
GS-441524 - nucleoside analogue which can be administered orally
active metabolite of the injectable prodrug remdesivir (aka GS-5734)
what vaccine is available for FCoV?
single MLV IN product licensed for kittens > 16 weeks (but most are already infected by then) but not protection has been proven for vaccinates housed in known FCoV seropositive groups
what is this? what does it contain?
toxoplasma gondii oocyst - contains sporozoites
what is this? what part of the lifestage is it?
tachyzoites - dividing & active in cells
what is this? what life stage is it in?
bradyzoites - encysted & quiescent
what species are the definitive host for toxoplasma gondii? what about intermediate host?
domestic cat/ wild felidae
all other warm-blooded animals
what is the etiology of toxoplasma gondii?
obligate intracellular coccidian
what are the 3 life stages of toxoplasma gondii?
- sporozoites - in protective oocysts
- tachyzoites - dividing & active in cells
- bradyzoites - encysted & quiescent
how do cats pick up toxoplasma gondii?
usually a prey item contains tissue cysts (bradyzoites) in which the cat ingests
cyst is digested in cat’s intestine & bradyzoites invade enteric epithelium & mature through several generations (merozoites are sexual reproduction generation & macrogametes/microgametes fuse to form oocysts)
oocysts sporulate after they are passed in feces taking 1-5 days in the environment to produce infective sporozoites
what is the infective stage of toxoplasma gondii?
sporozoites
how long does it take for oocysts of toxoplasma gondii to sporulate in the environment after they are passed in feces?
1-5 days
what is the life cycle of toxoplasma gondii?
cats - get infected by eating prey with tissue cysts/oocysts which transform into tachyzoites after ingestions which localize in neural & muscle tissue & develop into tissue cyst bradyzoites
cat sheds oocysts & sporulate in 1-5 days becoming infective
other animals/humans accidentally ingest it poop & become infected with it
humans eat contaminated meat
only the cat produces oocyst!!!!
what is the pathogenesis of toxoplasma gondii in everyone else (not cats)?
ingestion of infective oocysts - came from cat’s feces into the environment 1-5 days ago (herbivores eat contaminated grass/plants while humans/dogs eat contaminated produce or bradyzoites in raw meat)
sporozoites invade intestinal epithelium & then divide to form tachyzoites
cell ruptures & tachyzoites spread to new cells or they eventually encyst as bradyzoites
does shedding occur in humans/dogs with toxoplasma gondii?
no
T/F: toxoplasma gondii never undergoes sexual reproduction outside of the cat
true
what can happen if a dog eats cat poop from a cat with toxoplasma gondii?
oocyst perhaps is mature enough to be infective
may pass out again in dog feces
may infect dog tissues
what happens if a host species becomes infected with toxoplasma gondii during pregnancy & parasitemia occurs?
regardless of host species (human, sheep, etc) & regardless of means of infection (oocysts, tissue cysts)
tachyzoites in parasitemia are attracted to fetus!!!!
what can happen if a human eats meat contaminated with toxoplasma gondii?
bradyzoites (less likely tachyzoites) in cysts become active & infect cells & spread through out the body
but never undergo sexual reproduction outside of the cat
when would the natural host not show any clinical signs associated with toxoplasma gondii?
if the parasite is successful & the natural host is participating in the gi transmission cycle
T/F: cats shedding t. gondii are seldom clinically sick
true
when may we see clinical signs in animals with t. gondii?
immunosuppressed animals (including cats) & people
spread & proliferation occurs throughout the body causes clinical signs
what clinical signs are seen in kittens with t. gondii?
kittens may be stillborn or die before weaning
what clinical signs are seen in adult cats with t. gondii?
most commonly have pneumonia!!!!! may be acute/severe
may be accompanied by eosinophilia, CNS infiltration, & hepatic infiltration - may also see pancreatic, cardiac, or ocular infiltration
what clinical signs are seen in dogs with t. gondii?
pulmonary & hepatic infiltrates - may be rapidly fatal
CNS infiltration may cause signs that persist for weeks without progression to a fatal form with signs depending upon the location of the lesion
can range from seizures to paresis of CNS - lower motor neuron weakness/myositis peripherally
when would you use a fecal float to diagnose t. gondii?
in the definitive host only - just cats
this parasite is morphologically indistinguishable from neospora & hammondia spp., what is it?
toxoplasma gondii
why is a fecal float not the most useful diagnostic test for t. gondii infections?
there is only a brief period of shedding after initial infection that is seldom accompanied by clinical signs - if the disease spreads systemically, clinical signs will likely be delayed
what systemic diagnostics are used for patients with suspected t. gondii infections?
CBC, chemistry, urinalysis - results will vary based on organ systems affected
thoracic rads show diffuse interstitial to alveolar pattern with mottled lobar distribution
ocular exam may reveal uveitis and/or chorioretinitis
why is antibody class for t. gondii infections not predictive?
for most infections, IgM is acute & IgG is persistent
cats with t. gondii may never develop an IgM response, & in cats that do, IgM may persist for years & never switch to IgG
T/F: animals infected with t. gondii have cysts & positive serology titers for life
true - 30% of US cats/dogs/women are seropositive for t. gondii
what serology tests are used for t. gondii infections?
ELISA, MAT, & agglutination tests
does positive serology of t. gondii correlate with shedding of oocysts?
no
how are serology titers for t. gondii interpreted?
fourfold rise in titer over 2-3 weeks suggests recent infection
fourfold drop in titer over 2-3 weeks with resolution of clinical signs suggests relevant infection
what other fluids/tissues can be sampled for diagnostics for t. gondii?
csf - titers compared to peripheral blood, but rare cytologic diagnosis
aqueous humor - titers compared to peripheral blood, but rare cytologic diagnosis
tissue samples for biopsy (or at necropsy)
what is the general goal of treatment for t. gondii infection?
suppression of replication more likely than complete kill - remember the lifecycle, you will minimize tachyzoites but bradyzoite cysts will likely remain
what therapy is used for treating t. gondii infections?
clindamycin - up to 25 mg/kg BID for 2-3 weeks, which is much higher than typical antibacterial doses
clinical signs usually improve within 24-48 hours
may use potentiated sulfas or pyrimethamine
how are t. gondii infections prevented?
limit cat predation to limit cat infection & limit handling of 1-5 day old feces
cook your food, cook your pets’ food, & wash your hands well
