final exam

Question 1

defense mechanisms against spontaneous abortion bact

Answer 1

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

Question 2

Listeria

Answer 2

“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

Question 3

Listeria virulence factors/ pathogenesis

Answer 3

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

Question 4

listeria abortion

Answer 4

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

Question 5

listeria bacteriology

Answer 5

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

Question 6

listeria antibiotics

Answer 6

Penicillin, ampicillin,, sulfonamides, tetracycline

Question 7

Brucelloisis: general, entry, multiplication

Answer 7

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

Question 8

Brucelloisis: abortion

Answer 8

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

Question 9

Brucelloisis: diagnosis

Answer 9

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

Question 10

barriers against mastitis

Answer 10

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

Question 11

2 sources of mastitis

Answer 11

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

Question 12

mastitis virulence and spread

Answer 12

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

Question 13

mastitis diagnostics

Answer 13

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

Question 14

mastitis: contagious pathogens

Answer 14

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

Question 15

mastitis: environmental pathogens

Answer 15

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

Question 16

nasocomial

Answer 16

new infection acquired during hospital stay

Question 17

iatrogenic

Answer 17

acquired directly from action of vet or staff

Question 18

sterlization

Answer 18

destroy all living organisms including spores, on inanimate objects

Question 19

disinfection

Answer 19

destroy all vegetative organisms, not spores on inanimate objects

Question 20

antisepsis

Answer 20

treatment of living tissue to destroy all vegetative organisms

Question 21

goal of surgical prep

Answer 21

decrease bacti number to decrease infectious dose

infection rate doubles every hour in surgery

Question 22

peri-operative

Answer 22

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

Question 23

1st line Ab

Answer 23

75-85% effective, older drugs lower cost

penecillin, trimethoprim/sulfa, gentamicin

Question 24

2nd line Ab

Answer 24

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

amikacin, vancomycin

Question 25

Mycotic infections general

Answer 25

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

Question 26

moulds

Answer 26

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

Question 27

Yeast

Answer 27

unicellular, budding, moist colonies | 37 degrees C on animal tissue

Question 28

mycotic multiplication

Answer 28

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

Question 29

mycotic diagnosis

Answer 29

serology or skin test is presumptive diagnosis | definitive diagnosis: cultivation: 3-4 weeks

Question 30

polyene | Amphotericin B

Answer 30

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

Question 31

Azoles | Miconazole

Answer 31

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

Question 32

pyrimidine | flucytosine

Answer 32

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

Question 33

Grisans | Griseofulvin

Answer 33

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

Question 34

Cutaneous mycoses | geophilic, zoophilic, anthropophilic

Answer 34

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

Question 35

Cutaneous mycoses: multiplication and damage

Answer 35

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

Question 36

Cutaneous mycoses: diagnosis and treatment

Answer 36

``` 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 ```

Question 37

Subcutaneous mycoses

Answer 37

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

Question 38

Cryptococcosis

Answer 38

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

Question 39

Coccidiodomycosis

Answer 39

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

Question 40

Anaerobic Bacti

Answer 40

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

Question 41

Contagious Ovine foot rot

Answer 41

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

Question 42

clean-contaminated

Answer 42

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

Question 43

"golden period"

Answer 43

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

Question 44

Primary infection

Answer 44

bacti-initiate/cause pathology | single species, Ab along is effective

Question 45

secondary infection

Answer 45

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

Question 46

colonization vs infection

Answer 46

colonization: no disease