Defense & Barriers 2: FIP Flashcards
FIP IS ____, NOT ____
what does this mean for cats that are FIP- living with cats that are FIP+?
why does this kind of transmission NOT occur?
SPORADIC, SPREAD
CATS ARE NOT AT A HIGHER LIKELIHOOD OF DEVELOPING FIP/CLINICAL SIGNS ASSOCIATED W/ DZ if they live with FIP+ cats, just higher risk of INFECTION
VIRULENT STRAINS OF FELINE ENTERIC CORONAVIRUS CANNOT REPLICATE IN GI TRACT so no CAT-CAT transmission
3 qualities of FELINE ENTERIC CORONAVIRUS…
obviously, causes what disease?
3 qualities?
1. Large, enveloped ssRNA virus
2. Has outer “spikes” that make crown appearance
3. EASILY DISINFECTED but MAY SURVIVE ON FOMITES
FELINE ENTERIC CORONAVIRUS CAUSES FIP
INTERNAL MUTATION hypothesis for FIP TRANSMISSION (3)
(1) A LOW-PATHOGENICITY feline enteric coronavirus mutates into a VIRULENT STRAIN
(2) VIRULENT STRAIN causes INFECTION/MULTIPLICATION in MACROPHAGES to EVADE HOST IMMUNE RESPONSE
(3) Then causes SYSTEMIC PYOGRANULOMATOUS VASCULITIS that then makes pet SICK
DIFFERENT VIRAL STRAIN hypothesis for FIP transmission? (1, hint is that 3 things change likelihood of transmission)
GENETIC PREDISPOSITION + VIRULENCE OF STRAIN + ENVIRONMENT can influence FIP infection likelihood
SIGNALMENT in cats for FIP? (3, first one has something specific)
- BIMODAL AGE DISTRIBUTION
–> Most are YOUNG (3 mos –> 3 year) or GERIATRIC (>10 years) - PUREBRED cats more likely
- SIBLINGS of cats that have FIP MIGHT BE AT GREATER RISK
pathogenesis/steps of FIP infection? (6 steps, including when a certain sign appears in relation to clinical signs, and last step isn’t REALLY a step)
word reminders:
feces
systemic pyo…
shedding
macrophages
incubation period
viral replication
- CORONAVIRUS spread via ORONASAL EXPOSURE to FECES or FOMITES
- Virus then REPLICATES in TIPS OF INTESTINAL VILLI
- Fecal SHEDDING of virus starts 1 WEEK AFTER INFECTION (and can continue for life for some cats)
- Virus then enters MACROPHAGES and has LONG INCUBATION PERIOD (6-18 months after initial infection)
- End result = SYSTEMIC PYOGRANULOMATOUS VASCULITIS
–> this can occur MONTHS BEFORE clinical signs visible - What happens next DEPENDS ON IMMUNE RESPONSE OF CAT
NON-EFFUSIVE FIP…
called “what?”
= what is it?
what it OVERALL LEADS TO? (1 main point, 5 sub locations)
what can occur in GI?
“dry”
= when there’s a PARTIAL CELL-MEDIATED IMMUNE RESPONSE to the virus
OVERALL LEADS TO = (+/- PYO)GRANULOMATOUS inflammation in MULTIPLE ORGANS…
1. Mesenteric LNs
2. Kidneys
3. Liver
4. Brain
5. Eyes
in GI?
–> GRANULOMAS can form in intestinal wall particularly along ILEOCECAL JUNCTION
EFFUSIVE FIP…
called “what?”
what is it?
how does it manifest grossly? (hint: 2 locations)
pathogenesis/steps? (3)
when compared to NON-EFFUSIVE form of disease?
many cats have ____ forms of the disease
“wet”
what is it?
= when there’s NO IMMUNE RESPONSE
how does it manifest grossly?
= causes HIGH PROTEIN/LOW CELLULARITY EXUDATES in THORAX or ABDOMEN
pathogenesis/steps?
1. INCREASED expression of VEGF (Vascular Endothelial Growth Factor)
2. INCREASED VEGF leads to increased VASCULAR PERMEABILITY
3. INCREASED PERMEABILITY leads then to VASCULITIS
compared to NON-EFFUSIVE form?
–> MORE SEVERE FORM OF DISEASE THAN DRY, often disease progresses from DRY to WET
many cats have BOTH forms of the disease!
FIP IS THE ___ MOST COMMON CAUSE OF ____ ___ AFTER ____ & ____
FIP IS THE THIRD MOST COMMON CAUSE OF PERICARDIAL EFFUSION after HCM and NEOPLASIA
FIP IS THE ____ ____ INFECTIOUS CAUSE OF ____ IN ____
MOST COMMON, PYREXIA, CATS
CLINICAL signs in FIP…
what kinds are MOST COMMON? (overall name, then 3 examples)
what are 2 RARER clinical signs?
2 other possible clinical signs?
NON-SPECIFIC SIGNS ARE COMMON…
1. Lethargy
2. Fever
3. Inappetence
2 RARE clinical signs?
1. Neurologic
2. Pericardial effusion
2 other clinical signs?
1. Ocular changes (uveitis, retinal)
2. Lameness
PYREXIA is more common with the ____ form of FIP
EFFUSIVE/WET
in cats with PROTEIN-LOSING NEPHROPATHY upon bloodwork, what CLINICAL SIGN and subsequent DISEASE should we suspect?
CLINICAL SIGN = IMMUNE-MEDIATED GLOMERULONEPHRITIS
DISEASE = FIP
BLOODWORK changes with FIP…
ANEMIA is categorized as WHAT? + 3 causes for the anemia in FIP
HYPOALBUMINEMIA can be present due to (4, include reason for each)
ANEMIA is MULTIFACTORIAL, and can be caused by…
1. Anemia of chronic disease
2. Can also have SECONDARY IMHA
3. Can be MICROANGIOPATHIC from VASCULITIS
Hypoalbuminemia can be present because…
1. Liver failure = Liver no longer making albumin
2. Vasculitis = Can LOSE albumin out of blood
3. Protein-losing nephropathy = Albumin lost in glomerular filtrate
4. Negative acute phase protein
BLOODWORK changes in FIP… (5, just parameters)
- ANEMIA
- HYPOALBUMINEMIA
- HYPERBILIRUBINEMIA
- POLYCLONAL GAMMOPATHY
- ALBUMIN:GLOBULIN <1
possible DDxs for FIP?
3 MAIN CATEGORIES
first has 5, second/third have 2
- EFFUSION
–> Lymphoma
–> carcinomatosis
–> other neoplasia
–> CHF
–> Chylothorax - PERITONITIS
–> Pancreatitis
–> Septic abdomen - Other NEURO/OCULAR dz
–> Rabies
–> CNS lymphoma
DIAGNOSIS of FIP…
how do we reach DEFINITIVE diagnosis?
what 5 things can help INCREASE index of suspicion?
should we try to achieve DEFINITIVE diagnosis or just go with INCREASING INDEX OF SUSPICION/why?
DEFINITIVE dx = IMMUNHISTOCHEMISTRY staining for FELINE CORONAVIRUS ANTIGEN within PYOGRANULOMATOUS or GRANULOMATOUS VASCULITIS LESIONS
What can increase index of suspicion?
1. History
2. Signalment
3. B/w findings
4. Ruling out other diseases
5. Consistent diagnostic results
DEFINITIVE DIAGNOSIS is MORE IMPORTANT now that there is a VIABLE TREATMENT OPTION, SO TRY TO GET IT
“CLASSIC” effusion in FIP
gross appearance?
3 cytological findings?
how do we look for ORGANISM in this effusion?
rivalta test?
grossly? = Yellow/sticky
cytological findings…
1. HIGH PROTEIN & LOW CELL COUNT
2. Low cell count because cells are trapped in fibrin clots
3. PREDOMINANT CELLS = MACROPHAGES & NEUTROPHILS
Can do IMMUNOHISTOCHEMISTRY to look for ORGANISM IN EFFUSION via staining
RIVALTA TEST NOT COMMONLY DONE & NOT HELPFUL
PCR for FIP…
= what does it measure/what is it looking to determine?
how likely are we to use this test for FIV diagnosis? (2)
why is PCR better than other assays for FIP
what 3 findings are consistent with HIGHLY SUGGESTIVE FOR FIP?
= MEASURES presence of mRNA to determine if there’s an ACTIVELY REPLICATING VIRUS
how likely to use?
1. THIS IS OUR TEST OF CHOICE FOR FIP because it has HIGH SENSITIVITY & SPECIFICITY
2. Although IMMUNOHISTOCHEMISTRY is even BETTER than PCR, PCR on EFFUSION MORE COMMONLY/EASILY DONE
better than OTHER ASSAYS?
–> Other assays might not distinguish between virulent and avirulent strains
3 findings HIGHLY SUGGESTIVE FOR FIP when VIRAL mRNA found in…
1. EFFUSIONS
2. BLOOD
3. FIP-COMPATIBLE LESIONS
what diagnostic is the GOLD STANDARD for FIP diagnosis? & what’s unique about it?
IMMUNOHISTOCHEMISTRY/STAINING
NOT USED OFTEN bc PCR CAN USE EFFUSION SAMPLE while IMMUNOHISTOCHEMISTRY CANNOT/MIGHT REQUIRE GA depending on where we need to sample from
IMMUNOHISTOCHEMISTRY/STAINING for FIP…
= looking for?
what can we NOT submit as a sample?
= looking for histopathology of SYSTEMIC PERIVASCULAR PYOGRANULOMATOUS VASCULITIS
- CANNOT SUBMIT EFFUSION SAMPLE but PCR CAN, SO NOT USED AS OFTEN
treatment via ANTIVIRALS for FIP…
2 possible methods of action for antivirals?
risk to host?
Can use ANTIVIRALS that either…
1. INHIBIT RNA VIRUS REPLICATION (nucleoside analogues)
2. Or HAMPER CELLULAR PROCESSES THAT VIRUSES USE
risk to host?
However, RISK OF HOST TOXICITY because FIP USES HOST MACHINERY so risk of damaging HOST REPLICATION MACHINERY with antivirals
METHOD OF ACTION for NUCLEOSIDE ANALOGUES for FIP (2)
what kind of drug is this?
method of action?
1. Normally CORONAVIRUS enters cell via binding to RECEPTOR and will use HOST genome to replicate
- But nucleoside analogue will BIND TO RNA POL to PREVENT IT FROM WORKING ON VIRAL RNA and causing VIRAL REPLICATION
THIS IS AN ANTIVIRAL DRUG
BIGGEST INDICATOR of POSITIVE RESPONSE TO TREATMENT in FIP patients?
WEIGHT GAIN
REMDESIVIR for FIP…
what kind of drug? (2)
how is it administered? (2)
what kind of drug?
1. BROAD-SPECTRUM
2. ANTIVIRAL
how is it administered?
1. COMPOUNDED
2. PARENTERALLY
MOLNUPIRAVIR for FIP…
what kind of drug is this?
ANTIVIRAL
issues with trying to USE/GET A HOLD OF REMDESIVIR or MOLNUPIRAVIR? (2)
- BOTH ARE NOT FDA-APPROVED OR AVAILABLE IN US
- Current cost for hospitals is ~$5,000 over 12 WEEKS
