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SA DX & TX II > Exam 3 - Liver Infection > Flashcards

Exam 3 - Liver Infection Flashcards

1
Q

what is the etiology of FIP in cats?

A

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

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2
Q

T/F: the mutated form of feline coronavirus is not transmitted to new cats

A

true

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3
Q

what is the epidemiology of FIP?

A

enteric coronavirus spread through fecal oral transmission - facilitated by indoor housing, dense husbandry

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4
Q

what cats are at risk for FIP?

A

kittens & purebreds

second smaller peak around 10 years of age

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5
Q

what cats are at risk for FIP?

A

kittens & purebreds

second smaller peak around 10 years of age

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6
Q

what clinical signs are seen in most cats with feline coronavirus?

A

mild clinical illness & asymptomatic shedding

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7
Q

T/F: a vast majority of cats are seropositive for feline coronavirus

A

true

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8
Q

T/F: different sub-strains of FCoV are more or less likely to mutate

A

true

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9
Q

what is the pathogenesis of feline coronavirus?

A

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

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10
Q

what is shedding like for cats with feline coronavirus?

A

most shed for 2-3 months

minority become lifelong carriers of FCoV

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11
Q

do lifelong carriers of FCoV often develop FIP?

A

nope - very seldom do

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12
Q

what are the potential outcomes for a cat infected with feline coronavirus?

A

resistant to infection: 5-10%

transient infection: 70%

persistent infection/carrier status: 13%

FIP: 1-3%

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13
Q

what is the pathogenesis of FIP influenced by?

A

influenced by the viral load, viral strain, genetic background of host, & stress

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14
Q

what is the pathogenesis of FIP?

A

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)

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15
Q

why is there a difference in clinical signs seen between the wet & dry forms of FIP?

A

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

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16
Q

what clinical signs are seen in wet FIP?

A

pleural effusion, abdominal effusion, & high protein-low-cellularity effusion (modified transudate)

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17
Q

why is the dry form of FIP hard to diagnose?

A

they lack the characteristic effusion - fluid gives us the best diagnostic capabilities!!!

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18
Q

what clinical signs are associated with the dry form of FIP?

A

vague pyrexia, weight loss, & inappetence

icterus & liver disease

iritis, uveitis

variable neurologic signs

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19
Q

what pathology is seen in this photo? what is it associated with?

A

iritis - dry form of FIP

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20
Q

what found on necropsy is supportive of the diagnosis of FIP?

A

perivascular pyogranulomatous inflammation is definitive

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21
Q

how do we diagnose FIP? what are the limitations of it?

A

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

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22
Q

why is serology not the best for diagnosing FIP?

A

vast majority of cats are positive from prior exposure or illness

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23
Q

how is wet FIP diagnosed ante-mortem?

A

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

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24
Q

how is the dry form of FIP diagnosed ante-mortem?

A

…find something to PCR or IFA

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25
Q

what are your highly sensitive tests for diagnosing FIP? what are the highly specific tests used?

A

sensitive - FCoV serology/titers & fecal RT-PCR

specific - PCR for mutated FCoV & IFA for FCoV-infected macrophages in fluid

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26
Q

why does a positive serology test for FCoV predict nothing?

A

most shedders of the disease are not sick

chronic shedders are less likely to develop FIP

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27
Q

T/F: there is no available therapy for clearing FCoV+ cats

A

true

28
Q

what is the classic treatment used for FIP? what is the prognosis?

A

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

29
Q

what is the emerging treatment for FIP?

A

GS-441524 - nucleoside analogue which can be administered orally

active metabolite of the injectable prodrug remdesivir (aka GS-5734)

30
Q

what vaccine is available for FCoV?

A

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

31
Q

what is this? what does it contain?

A

toxoplasma gondii oocyst - contains sporozoites

32
Q

what is this? what part of the lifestage is it?

A

tachyzoites - dividing & active in cells

33
Q

what is this? what life stage is it in?

A

bradyzoites - encysted & quiescent

34
Q

what species are the definitive host for toxoplasma gondii? what about intermediate host?

A

domestic cat/ wild felidae

all other warm-blooded animals

35
Q

what is the etiology of toxoplasma gondii?

A

obligate intracellular coccidian

36
Q

what are the 3 life stages of toxoplasma gondii?

A
  1. sporozoites - in protective oocysts
  2. tachyzoites - dividing & active in cells
  3. bradyzoites - encysted & quiescent
37
Q

how do cats pick up toxoplasma gondii?

A

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

38
Q

what is the infective stage of toxoplasma gondii?

A

sporozoites

39
Q

how long does it take for oocysts of toxoplasma gondii to sporulate in the environment after they are passed in feces?

A

1-5 days

40
Q

what is the life cycle of toxoplasma gondii?

A

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!!!!

41
Q

what is the pathogenesis of toxoplasma gondii in everyone else (not cats)?

A

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

42
Q

does shedding occur in humans/dogs with toxoplasma gondii?

A

no

43
Q

T/F: toxoplasma gondii never undergoes sexual reproduction outside of the cat

A

true

44
Q

what can happen if a dog eats cat poop from a cat with toxoplasma gondii?

A

oocyst perhaps is mature enough to be infective

may pass out again in dog feces

may infect dog tissues

45
Q

what happens if a host species becomes infected with toxoplasma gondii during pregnancy & parasitemia occurs?

A

regardless of host species (human, sheep, etc) & regardless of means of infection (oocysts, tissue cysts)

tachyzoites in parasitemia are attracted to fetus!!!!

46
Q

what can happen if a human eats meat contaminated with toxoplasma gondii?

A

bradyzoites (less likely tachyzoites) in cysts become active & infect cells & spread through out the body

but never undergo sexual reproduction outside of the cat

47
Q

when would the natural host not show any clinical signs associated with toxoplasma gondii?

A

if the parasite is successful & the natural host is participating in the gi transmission cycle

48
Q

T/F: cats shedding t. gondii are seldom clinically sick

A

true

49
Q

when may we see clinical signs in animals with t. gondii?

A

immunosuppressed animals (including cats) & people

spread & proliferation occurs throughout the body causes clinical signs

50
Q

what clinical signs are seen in kittens with t. gondii?

A

kittens may be stillborn or die before weaning

51
Q

what clinical signs are seen in adult cats with t. gondii?

A

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

52
Q

what clinical signs are seen in dogs with t. gondii?

A

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

53
Q

when would you use a fecal float to diagnose t. gondii?

A

in the definitive host only - just cats

54
Q

this parasite is morphologically indistinguishable from neospora & hammondia spp., what is it?

A

toxoplasma gondii

55
Q

why is a fecal float not the most useful diagnostic test for t. gondii infections?

A

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

56
Q

what systemic diagnostics are used for patients with suspected t. gondii infections?

A

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

57
Q

why is antibody class for t. gondii infections not predictive?

A

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

58
Q

T/F: animals infected with t. gondii have cysts & positive serology titers for life

A

true - 30% of US cats/dogs/women are seropositive for t. gondii

59
Q

what serology tests are used for t. gondii infections?

A

ELISA, MAT, & agglutination tests

60
Q

does positive serology of t. gondii correlate with shedding of oocysts?

A

no

61
Q

how are serology titers for t. gondii interpreted?

A

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

62
Q

what other fluids/tissues can be sampled for diagnostics for t. gondii?

A

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)

63
Q

what is the general goal of treatment for t. gondii infection?

A

suppression of replication more likely than complete kill - remember the lifecycle, you will minimize tachyzoites but bradyzoite cysts will likely remain

64
Q

what therapy is used for treating t. gondii infections?

A

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

65
Q

how are t. gondii infections prevented?

A

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

SA DX & TX II (62 decks)

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