Exam 1 - infectious diseases and abx Flashcards
What is the etiologic agent of feline infectious peritonitis?
Feline coronavirus (+ssRNA, enveloped)
What are the two presentations of feline coronavirus?
GI disease and FIP
What is the theory of FIP pathogenesis (what makes it different from standard FeCoV infection)?
Mutation in FeCoV strain allows for macrophage tropism
What signalment is typical of FIP?
3 months - 3 years
purebred cats
overcrowded/stressful environment
How is FeCoV transmitted?
Oronasal exposure to feces/fomites
Describe the pathogenesis of FIP in the body.
Macrophage infection –> systemic pyogranulomatous vasculitis
Wet form associated with inadequate CMI –> exudation of plasma proteins
Dry form associated with partially protective CMI –> granuloma/pyogranuloma formation
Describe the concept of “antibody dependent enhancement” (ADE) in relation to FIP
Sub-neutralizing antibodies accelerate the disease process
M0s bind to Ab-virus complex > more viral infection of macrophages
What clinical signs are associated with FIP?
Vague: lethargy, anorexia, weight loss, chronic fever
Wet-specific: high protein fluid accumulation in body cavities
Dry-specific: pyogranulomatous lesions in eyes, CNS, LNs
How is FIP diagnosed?
Chem - hyperglob and hypoalb (alb:glob <4 highly predictive), hyperbili
Polyclonal gammopathy
*Immunohistochem is GS, but can only be done post-mortem
*IFA serum ELISA is GS for FeCoV Ab detection but does NOT predict FIP
rt-PCR - sensitive for FIP with effusion sample
How is FIP treated?
Prednisone (immunosuppressive dose) - NOT curative
Intracavitary dexamethasone for effusions
How is FIP prevented?
Test queen before kittens born - if + remove kittens at 4-6 weeks
Vaccination is non-core and not recommended
What is the prognosis for FIP?
Poor (9-38 days)
NPIs: hyperbili, lymphopenia, large volumes of effusion
What is the etiology of infectious canine hepatitis?
Canine adenovirus 1 (CAV-1) (dsDNA, non-enveloped)
Why is infectious canine hepatitis rarely seen in the US?
Cross vaccination with CAV-2
How is infectious canine hepatitis transmitted?
oronasal with urine contact
What is the pathogenesis and CS associated with infectious canine hepatitis?
Infection of hepatocytes and endothelial cells
Blue eye
Glomerulonephritis
Icterus
How is canine distemper virus transmitted?
Aerosol, respiratory secretions
What signalment is typical with canine distemper virus?
Puppies 3-6 months (d/t loss of maternal Ab)
Describe the pathogenesis of canine distemper.
Local tissue M0 infection > lymphoid infection and viremia > *epithelial cell and CNS infection
Variable immune response may lead to viral persistence (hard pad dz, optic neuritis, KCS, etc.), or widespread tissue infection (GI, genitourinary, respiratory, skin, and CNS infection)
What three presentations of CNS disease are seen with canine distemper?
- Acute CDV encephalitis (acute, non-inflammatory demyelination in puppies d/t viral replication)
- Subacute and chronic (demyelinating immune reaction in older dogs, not associated with viral replication)
- “Old dog encephalitis” (chronic active and progressive inflammation of cerebrum/brainstem grey matter, occurs weeks to years after infection)
What clinical signs are associated with canine distemper?
Cough, runny nose, respiratory distress
Seizures
Diarrhea, vomiting, tenesmus, intussuseption (ddx parvo)
Chorioretinitis (gold medallion lesions)
Nasal and digital hyperkeratosis
Progressive encephalitis with repetitive motions
How is canine distemper diagnosed?
Primarily clinical suspicion!
ELISA IgM - acute cases
ELISA IgG - past or present infeciton or vaccination
How is canine distemper treated/prevented?
No treatment.
Vaccination VERY effective!
How is rabies transmitted?
Saliva - salivary shedding can occur before CS apparent!
Describe the pathogenesis of rabies.
Enters peripheral nerves and replicates locally > spreads passively by intra-axonal flow
Incubation: dogs and cats (1-6 months), humans (1-12 months)
Enters spinal cord/brainstem ipsilateral to bite > spread to contralateral side > ascends bilaterally to forebrain > progressive LMN disease
Spread to acinar cells of salivary gland
Describe the clinical phases of rabies
- Prodromal (CNS viral spread)
- mood change, variable fever, pupils dilated, pruritis - Furious (forebrain involvement) - common in cats
- hyperesthesia, photophobia, aggression, seizures - Paralytic - common in dogs
- ascending flaccid paralysis - Death - within 2-4 days of clinical onset
How is rabies diagnosed?
Clinical suspicion - any animal that suddenly develops profound behavioral changes and/or LMN paralysis
Histopath: negri bodies and perivascular cuffing
*Direct fluorescent Ab test
What specimens should be sent in suspected rabies cases? How should they be preserved?
Hippocampus, cerebellum, medulla oblongata
Fresh or refrigerated (NOT frozen or in formalin)
A dog who is up-to-date on the rabies vax comes to you after being bitten by a racoon. What do you tell the owners regarding rabies risk/protocol?
Revaccinate
45 day observation period
A cat who was never vaccinated for rabies comes to you after being bitten by a bat. What do you tell the owners regarding rabies risk/protocol?
Vaccinate
180 day observation period
Mrs. Hutchinson’s daughter was bitten by their darling dog, Fluffy, yesterday. Fluffy is healthy but not UTD on the rabies vax and Mrs. H doesn’t want to euthanize. What do you tell her regarding rabies risk/protocol?
DO NOT vaccinate
10 day observation period
How is Clostridium botulinum transmitted?
Food-borne ingestion of preformed toxin
Describe the pathogenesis of C. botulinum infection.
Toxin absorbed in small intestines > lymphatics and bloodstream > neural intoxication:
- toxin binds to cell surface receptors
- internalization of toxin into endosomal compartments
- membrane translocation
- enzymatic cleavage of SNARE proteins (important in release of Ach > paralysis at NMJ)
What clinical signs are consistent with C. botulinum?
Ascending flaccid paralysis - though mentally alert and tail wag maintained!
List some ddx for ascending flaccid paralysis:
- C. botulinum
- Polyradiculoneuritis (Coonhound paralysis) - muscle wasting and hyperesthesia
- Tick paralysis (less CN involvement)
- Myasthenia gravis (will be episodic)
How is C. botulinum infection diagnosed?
Clinical signs
Confirmed by finding toxin in serum/feces/vomit/food sample (mouse inoculation test)
How is C. botulinum treated?
Equine antitoxin (not effective once bound to the nerve) Supportive therapy
What is the prognosis for C. botulinum infection?
Good! Complete recovery in 14-21 days barring secondary infection or respiratory failure
What is the etiology of tetanus?
Clostridium tetani
What are the two tetanus toxins? Which causes clinical signs?
Tetanospasmin - CS!
Tetanolysin
What are the three forms of tetanus?
- Localized disease
- Generalized disease - spastic paralysis
- Cranial nerve tetanus - risus sardonicus, trismus, protrusion of 3rd eyelid, laryngeal spasm
Describe the pathogenesis of tetanus.
Wound contaminated with C. tetani spores > anaerobic environment promotes germination > toxin attaches to peripheral nerves > migrates retrograde to CNS > prevents release of inhibitory neurotransmitters (irreversibly!) > spastic paralysis
How is tetanus treated?
Antitoxin - risk of anaphylaxis
PenG, metronidazole (IV)
Clean/debride wound
Supportive care - quiet, non-stimulating environment
What is the prognosis for tetanus cases?
Complete recovery expected if they can survive the initial period
May take up to 2 weeks before improvement observed
Full recovery within 60 days
Which antibiotics are concentration dependent?
Metronidazole (nitroimidazoles)
Fluoroquinolones
Aminoglycosides
Glycopeptides (Vancomycin)
