final exam Flashcards
defense mechanisms against spontaneous abortion bact
physical barrier: vaginal epithelium, muscle contractions
innate immunity: cytokines, neuts, macs
Adaptive immunity: must tolerate sperm/fetus
Hormonal influences: estrogen increases T-cell function
Listeria
“silage sickness”
facultative intracellular, facultative anaerobe, flagella, gram - rod.
L’monocytogens
ubiquitous in environment- entry is feed or enviro
mucous membrane->ascend nerves to CNS->meningoencephalitis
1 billion is infectious dose
zoonotic
Listeria virulence factors/ pathogenesis
- internalins (invades cell)
- listeriolysin (allow listeria to escape phagosomes)
- hijacks actin filament
- multiples/destroys host cell, release bacteria
listeria abortion
suppurative inflammation and necrosis of placenta, septic lesions of multi organs
last trimester (8-9th months), 6-8 days post disease onset, no clinical signs
autolysis
fetus has suppuritive foci on liver, fibrinous polyserositis
listeria bacteriology
small colonies, B-hemolytic, catalase positive, motile at 25 degrees C, CAMP positive
PCR can be positive but not allive
definitive diagnosis = bacteria isolation
listeria antibiotics
Penicillin, ampicillin,, sulfonamides, tetracycline
Brucelloisis: general, entry, multiplication
gram - coccobaccilus, facultative intracellular, capnophilic, nonmotile
wildlife reservoir, not environment
entry: ingestion, dose: 10^3-10^7 CFU, venereal transmission
penetrate Mucous epithelium, phagocytosis of organism through surface protein, decreases pH, stimulates protein production, replication in ER, causes lymphadenitis
Brucelloisis: abortion
tropism for gravis uterus adn male repro due to erythritol (sugar)
placentitis ~4-5 week PI, -> fetal bronchopneumonia _> abort 24-72 hrs after death
cow may become long-term carrier
Brucelloisis: diagnosis
cows who aborted will not abort again, but transmit to calves who will abort their first calf,
-serum agglutination tests (IgG, IgM - screening on milk)
-PCR- any positive is significant
reportable disease, zoonotic
no treatment for ag
tetrocyclines/aminoglycosides for canine
barriers against mastitis
Physical: sphincter muscles, keratin plug, flushing of milk
immune: macs (66088% of mammary gland)
mediators: lactoferrin, lysozome
humoral immune response neutralizes
2 sources of mastitis
Contagious pathogens: S. aureus, step agalactiae, mycoplasma bovis
Environmental pathogens: e. coli, klebsiella
mastitis virulence and spread
adhesins, capsule, exotoxins, endotoxins (gm-)
leukocytes release chemoattractants _> polymorphonuclear neuts (PMN) destroy bacti -> destroy epithelial cells -> decrease milk -> NAGase and LDH relased ->PMN destroyed by macs -> dead epithelial cells slough -> increases SCC
mastitis diagnostics
SCC or cali matitis test
direct microscopy (gm stain)
bacti culture - most useful
ID contagious bs enviro
mastitis: contagious pathogens
staph aureus,
strep agalactiae - penecillin
Mycoplasma bovis - incurable, use adhesins, phopholipase
primary reservoir is cow, obligate parasites
usually subclinical or chronic
mastitis: environmental pathogens
E. coli is most common, 80-90% of clinical mastitis, ~10% endotoxemia
does not adhere to mammary epithelium doesn’t spread into mammary parenchyma
nasocomial
new infection acquired during hospital stay
iatrogenic
acquired directly from action of vet or staff
sterlization
destroy all living organisms including spores, on inanimate objects
disinfection
destroy all vegetative organisms, not spores on inanimate objects
antisepsis
treatment of living tissue to destroy all vegetative organisms
goal of surgical prep
decrease bacti number to decrease infectious dose
infection rate doubles every hour in surgery
peri-operative
for wounds, recurrent UTI, patients with high susceptibility to infection
1st line Ab
75-85% effective, older drugs lower cost
penecillin, trimethoprim/sulfa, gentamicin
2nd line Ab
85-95% effective, restricted for multi-drug resistant,
amikacin, vancomycin
Mycotic infections general
mimic other diseases occur sporadically, have geographical incidence, eukaryotes (righ in ergosterol, high % poysaccharide, capsules)
poorly contagious
moulds
grow by hyphal elongation/division
called mycelium
25 degrees in environment
Yeast
unicellular, budding, moist colonies
37 degrees C on animal tissue
mycotic multiplication
don’t multiple well in body, require free iron, killed by phagocytosis or granuloma formation
mycotic diagnosis
serology or skin test is presumptive diagnosis
definitive diagnosis: cultivation: 3-4 weeks
polyene
Amphotericin B
systemically used and topical nephrotoxic, not water soluble (no oral) poor CSF penetration broad spectrum fungicidal binds ergosterol and disrupts fungal cell membrane
Azoles
Miconazole
fungistatic, broad spectrum PO, IV, systemic and topical less toxic than polyene effective topically for ringworm inhibits ergosterol synthesis
pyrimidine
flucytosine
fungicidal, PO, systemic infections
narrow spectrum (crypto/candida)
enters CSF in high concentration
used with amphotericin B
Grisans
Griseofulvin
fungistatic (block mitosis by inhibiting microtubule assembly)
systemically for superficial infections (dermatophy), ringworm
Oral
teratogenic in pregnant cats
not effective topically
Cutaneous mycoses
geophilic, zoophilic, anthropophilic
dermatophysis, ringworm
geophilic- soil, sporatic, poorly transmitted (microsporum gypseum- #1 in horses)
zoophilic- obligate parasites, spread rapidly among animals, zoonotic (microsporum canis- ringworm)
anthropophilic- obligate animal parasite, on humans (athletes foot
Cutaneous mycoses: multiplication and damage
arthrospores: infective form, enter abraded skin
limited to epidermis by temp & keratin
inflammation - mast cell degranulation, hyperkeratosis
most self limiting
Cutaneous mycoses: diagnosis and treatment
cultivation, skin biopsy, KOH most self limiting in Large animal treatment for small animal topical- organic iodide, bathing 2% lime-sulfer oral- imidazole, grisams PO for 6 weeks
Subcutaneous mycoses
deeper skin, CT, bone, muscle
Pythiosis- horse “swamp cancer”, not fungi, chronic nonhealing, severe granulation tissue lesion, isolation is definitive diagnosis, surgical removal in chronic case, vaccine in acute lesion
Sporotrichosis- subcue abscess horses, dogs, male cats, dimorphic, spreads via lymphatics, recurrent nonhealing wounds, NO glucocorticoids. Can use ketaconazole, itraconazole
Cryptococcosis
most common systemic mycotic infection in cats: C. neophormans
inhaled, no animal-animal transmission, low virulence->inapparent infections (unless FeLV, FIV)
cause nasal granuloma, CNS, or Pneumonia in dogs
latex agglutination test
Itraconazol, amphotericin B, fluorocytosine
Coccidiodomycosis
sever pneumonia/systemic disease, productive cough, fever dogs->pyogranulomatous response
soil, fecal contamination
Tube precipitin (IgM), Complement fixation (IgG)
ID or culture is confirmatory
treat itraconazol/fluconazole
NO corticosteroids
Anaerobic Bacti
ubiquitous, non-pathogenic on own, opportunistic
normal flora, in soil
most infections are endogenous and opportunistic
cytotoxic exotoxins, foul odor, gas in lesion, necrosis
Contagious Ovine foot rot
anaerobic, requires Fusobacterium necrophorum- normal flora ->mild dermatitis
D. nodosus- obligate pathogen, has pili, actual cause of fooot rot
clean-contaminated
traumatic, infected, surgery with viscous entered, sx >3 hours, dentistry
“golden period”
time prior to significant replication, <3 hours, including surgery time (rate doubles per hours)
Primary infection
bacti-initiate/cause pathology
single species, Ab along is effective
secondary infection
most common
multiple species of bati (polymicrobial infections)
must treat underlying cause
colonization vs infection
colonization: no disease
