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Bacteriology > final exam > Flashcards

final exam Flashcards

1
Q

defense mechanisms against spontaneous abortion bact

A

physical barrier: vaginal epithelium, muscle contractions
innate immunity: cytokines, neuts, macs
Adaptive immunity: must tolerate sperm/fetus
Hormonal influences: estrogen increases T-cell function

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2
Q

Listeria

A

“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

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3
Q

Listeria virulence factors/ pathogenesis

A
  1. internalins (invades cell)
  2. listeriolysin (allow listeria to escape phagosomes)
  3. hijacks actin filament
  4. multiples/destroys host cell, release bacteria
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4
Q

listeria abortion

A

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

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5
Q

listeria bacteriology

A

small colonies, B-hemolytic, catalase positive, motile at 25 degrees C, CAMP positive
PCR can be positive but not allive
definitive diagnosis = bacteria isolation

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6
Q

listeria antibiotics

A

Penicillin, ampicillin,, sulfonamides, tetracycline

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7
Q

Brucelloisis: general, entry, multiplication

A

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

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8
Q

Brucelloisis: abortion

A

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

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9
Q

Brucelloisis: diagnosis

A

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

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10
Q

barriers against mastitis

A

Physical: sphincter muscles, keratin plug, flushing of milk
immune: macs (66088% of mammary gland)
mediators: lactoferrin, lysozome
humoral immune response neutralizes

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11
Q

2 sources of mastitis

A

Contagious pathogens: S. aureus, step agalactiae, mycoplasma bovis
Environmental pathogens: e. coli, klebsiella

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12
Q

mastitis virulence and spread

A

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

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13
Q

mastitis diagnostics

A

SCC or cali matitis test
direct microscopy (gm stain)
bacti culture - most useful
ID contagious bs enviro

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14
Q

mastitis: contagious pathogens

A

staph aureus,
strep agalactiae - penecillin
Mycoplasma bovis - incurable, use adhesins, phopholipase
primary reservoir is cow, obligate parasites
usually subclinical or chronic

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15
Q

mastitis: environmental pathogens

A

E. coli is most common, 80-90% of clinical mastitis, ~10% endotoxemia
does not adhere to mammary epithelium doesn’t spread into mammary parenchyma

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16
Q

nasocomial

A

new infection acquired during hospital stay

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17
Q

iatrogenic

A

acquired directly from action of vet or staff

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18
Q

sterlization

A

destroy all living organisms including spores, on inanimate objects

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19
Q

disinfection

A

destroy all vegetative organisms, not spores on inanimate objects

20
Q

antisepsis

A

treatment of living tissue to destroy all vegetative organisms

21
Q

goal of surgical prep

A

decrease bacti number to decrease infectious dose

infection rate doubles every hour in surgery

22
Q

peri-operative

A

for wounds, recurrent UTI, patients with high susceptibility to infection

23
Q

1st line Ab

A

75-85% effective, older drugs lower cost

penecillin, trimethoprim/sulfa, gentamicin

24
Q

2nd line Ab

A

85-95% effective, restricted for multi-drug resistant,

amikacin, vancomycin

25
Q

Mycotic infections general

A

mimic other diseases occur sporadically, have geographical incidence, eukaryotes (righ in ergosterol, high % poysaccharide, capsules)
poorly contagious

26
Q

moulds

A

grow by hyphal elongation/division
called mycelium
25 degrees in environment

27
Q

Yeast

A

unicellular, budding, moist colonies

37 degrees C on animal tissue

28
Q

mycotic multiplication

A

don’t multiple well in body, require free iron, killed by phagocytosis or granuloma formation

29
Q

mycotic diagnosis

A

serology or skin test is presumptive diagnosis

definitive diagnosis: cultivation: 3-4 weeks

30
Q

polyene

Amphotericin B

A 
systemically used and topical
nephrotoxic, not water soluble (no oral)
poor CSF penetration
broad spectrum
fungicidal
binds ergosterol and disrupts fungal cell membrane
31
Q

Azoles

Miconazole

A 
fungistatic, broad spectrum
PO, IV, systemic and topical
less toxic than polyene
effective topically for ringworm
inhibits ergosterol synthesis
32
Q

pyrimidine

flucytosine

A

fungicidal, PO, systemic infections
narrow spectrum (crypto/candida)
enters CSF in high concentration
used with amphotericin B

33
Q

Grisans

Griseofulvin

A

fungistatic (block mitosis by inhibiting microtubule assembly)
systemically for superficial infections (dermatophy), ringworm
Oral
teratogenic in pregnant cats
not effective topically

34
Q

Cutaneous mycoses

geophilic, zoophilic, anthropophilic

A

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

35
Q

Cutaneous mycoses: multiplication and damage

A

arthrospores: infective form, enter abraded skin
limited to epidermis by temp & keratin
inflammation - mast cell degranulation, hyperkeratosis
most self limiting

36
Q

Cutaneous mycoses: diagnosis and treatment

A 
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
37
Q

Subcutaneous mycoses

A

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

38
Q

Cryptococcosis

A

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

39
Q

Coccidiodomycosis

A

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

40
Q

Anaerobic Bacti

A

ubiquitous, non-pathogenic on own, opportunistic
normal flora, in soil
most infections are endogenous and opportunistic
cytotoxic exotoxins, foul odor, gas in lesion, necrosis

41
Q

Contagious Ovine foot rot

A

anaerobic, requires Fusobacterium necrophorum- normal flora ->mild dermatitis
D. nodosus- obligate pathogen, has pili, actual cause of fooot rot

42
Q

clean-contaminated

A

traumatic, infected, surgery with viscous entered, sx >3 hours, dentistry

43
Q

“golden period”

A

time prior to significant replication, <3 hours, including surgery time (rate doubles per hours)

44
Q

Primary infection

A

bacti-initiate/cause pathology

single species, Ab along is effective

45
Q

secondary infection

A

most common
multiple species of bati (polymicrobial infections)
must treat underlying cause

46
Q

colonization vs infection

A

colonization: no disease

Bacteriology (2 decks)

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