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ABBEY MSII Unit 2 > Micro U2 L10. > Flashcards

Micro U2 L10. Flashcards

1
Q

Clostridium

A

gram+ spore forming rods - anaerobic (c. tetani, c. botulinum, c. perfringens (gas gangrene and food poisoning), c. difficile)

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2
Q

Four presentations of C. tetani

A
  1. neonatal - infected umbilical cord - mother unvaccinated 2. cephalic - rare infection of head causing cranial nerve palsy 3. local - infection of a wound leads to local muscle rigidity 4. generalized - violent full-body muscle spasms and respiratory distress
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3
Q

Transmission of C. tetani

A

soil contaminated puncture wound (2-14 days before symptoms); IV drug users skin popping; contained umbilical cord or circumcision wound

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4
Q

Pathogenesis of C. tetani

A

deep wound limits air contact and blood supple; vegetation cells release tetanospasmin; exotoxin moves by retrograde axonal transport to CNS, protease activity destroys synaptobrevin/VAMP causing spastic paralysis of affected muscle group

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5
Q

Complication of C. tetani

A

respiratory failure

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6
Q

Clinical features of C. tetani

A

strong muscle spasms and paralysis, lockjaw, grimace, exaggerated reflexes, opisthotonus (strong arching of back)

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7
Q

Labs for C. tetani

A

few useful tests - terminal spore gives “tennis racket” appearance on microscopy

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8
Q

Treatment for C.tetani

A

tetanus antitoxin; antibiotics are meh, airway support, benzodiazepines (valium) for muscle spasms, long term physical therapy

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9
Q

Prevention of C. tetani

A

vaccination with tetanus toxoid in childhood and every 10 yrs after; clean deep puncture wounds (and give booster) - deep and clearly dirty-puncture wounds call for immune globulin in addition to cleaning and booster

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10
Q

Transmission of C. botulinum

A

spores survive in inadequate sterilization of foods - releasing one of 8 toxins (A-H) - cooking properly inactivates toxin

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11
Q

What are the MC sources of c. botulinum?

A

alkaline veggies (home-canned beans, peppers, mushrooms) and raw fish

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12
Q

Pathogenesis of C. botulinum

A

toxin absorbed from gut, carried in blood to peripheral nerve synapses - bacteria itself is usually killed in gut. botulinum toxin protease activity destroys synaptobrevin/VAMP - acetylcholine release in peripheral - results in flaccid paralysis

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13
Q

Botox

A

minute amounts of botulinum toxin A - deliberately paralyze muscles of face, hand, anus, neck, eyelid

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14
Q

Clinical features of typical C. botulinum

A

descending weakness and paralysis without fever; blurred/doubled vision; trouble swallowing - happens FAST - hours

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15
Q

Clinical features of wound botulism

A

spores germinate in a contaminated wound - most common with heroin skin-popping

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16
Q

Clinical features of infant botulism

A

spores survive passage through infant’s stomach and germinate in the gut - weakness and paralysis, history of honey - “floppy baby”

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17
Q

Labs for botulism

A

toxin can be demonstrated in suspect food and patient samples - gram + bacteria gets lost quickly (when exposed to air)

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18
Q

Treatment for botulism

A

respiratory support, trivalent horse-sourced antitoxin (for non A&B subtypes - human for A&B), treatment as needed for serum sickness, physical therapy

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19
Q

Prevention for botulism

A

proper sterilization of banned and vacuum-packed foods, adequate cooking, discard swollen cans

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20
Q

C. perfringens gas gangrene transmission

A

myonecrosis = necrotizing faciitis. transmission - spores from soil or vegetative cells from colon enter wounds, usually from war, car accidents, septic abortions (MAJOR wounds)

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21
Q

C. perfringens pathogenesis

A

vegetative cells grow in tissue, esp muscle - produce a variety of toxins to break down blood and tissue - alpha toxin (lecithinase damages cell membranes - degradative enzymes produce gas in tissue

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22
Q

Which clostridium is slightly aero-tolerant?

A

c. perfringens

23
Q

Extoxin onslaught in C. perfringens leads to what?

A

hemolytic anemia, kidney and heart failure, shock and death

24
Q

alpha toxin

A

lecithinase - damages cell membranes including erythrocytes (reason for necrotoxic, cardiotoxic, and hemolysis

25
Q

Clinical features of C. perfringens

A

pain/tenderness disproportionate to wound appearance, edema, color change (brown -> blue/black) and cellulitis at wound - may also have crepitation, hemolysis, jaundice, blood-tinged exudates

26
Q

X-ray of c. perfringens

A

foreign body or “feathered” appearance of gas produced in tissue by bacterial fermentation

27
Q

Treatment of C. perfringens

A

immediate surgical removal of diseased tissue followed by IV penicillin G and clindamycin (protein synthesis inhibitor)

28
Q

Lab for C. perfringens

A

can see gram + rods

29
Q

C. perfringen food poisoning transmission

A

soil-borne spores contaminate food - inadequate cooking - surviving spores germinate and grow in reheated foods esp meat

30
Q

Pathogenes of C. perfringens food poisoning

A

germinating cells multiply in small bowel - enterotoxins cause diarrhea, disrupting tight junctions (type A exotoxin)

31
Q

Diagnosis of C. perfringens food poisoning

A

8-16 h incubation; watery diarrhea, cramps, little vomiting - resolves in 24 hours

32
Q

C. difficile caused by

A

pseudomembranous colitis - gram +

33
Q

Transmission of C. difficile

A

normal gut flora for 3% population - 30% in hospital - fecal-oral esp nosocomial

34
Q

Pathogenesis of C. difficile

A

recent course of antibiotics or cancer chemotherapeutics suppressing other normal flora; germinating cells release exotoxins

35
Q

Exotoxins release by C. difficile and their effects

A

A- disrupts tight junctions (like C. perfringens). B - depolymerizes actin - kills surrounding cells and causes plaques) - combo cause intestinal inflammation and swelling

36
Q

Clinical features of C. difficile

A

nonbloody cramping diarrhea: mucoid, greenish, malodours (STINKY); fever; on sigmoidoscopy, patches of dead and dying cells appear as yellow-white plaques (pseudomembranes)

37
Q

Labs for C. difficile

A

toxins in stool filtrate - ELISA for toxin or cytotoxicity test - neutrophils in stole

38
Q

Treatment for C. difficile

A

withdraw initial antibiotic, replace fluid, oral metronidazole or vancomycin, surgical resection/removal of colon may be required

39
Q

Bacteroides and prevotella bacteriology

A

Gram NEGATIVE anaerobic, non spore forming, normal flora

40
Q

B fragilis normal flora spot

A

colon and vagina

41
Q

B corrodens and P melaninogenica normal flora spot

A

mouth

42
Q

Pathogenesis of bactericides and prevotella

A

non-communicable - anaerobes escape normal location through break in mucosal surface and set up abscess in new location

43
Q

How do abscesses complicate antibiotic treatment of bactericides and prevotella?

A

polymicrobial infection due to facultative anaerobes in abscesses which use up the oxygen

44
Q

What is a more antibiotic-resistant strain anaerobic bacteria?

A

b. fragilis (vagina and colon)

45
Q

Clinical features of Bacteroides and Prevotella

A

peritonitis or localized abscess and pelvic abscess, necrotizing faciitis, bacteremia

46
Q

How to tell the difference clinically between B. fragilis and P. melaninogenica

A

B fragilis below the diaphragm and p. melaninogenica above

47
Q

Labs for bacteroides and prevotella

A

isolate on anaerobic blood agar plates - p. melaninogenica produces black colonies - identify by sugar fermentation and gas chromatography of acids produced

48
Q

Treatment of bactericides and prevotella

A

metronidazole (used for anaerobes), combine with aminoglycides to kill facultatives in abscess, surgical care for abscess unless in lung

49
Q

Prevention of bactericides and prevotella

A

perioperative cephalosporin

50
Q

Actinomyces israelii bacteriology

A

gram + rodes, normal flora of mouth, cells form long, branching filaments that resemble hyphae of fungi - non communicable

51
Q

Actinomyces israelii pathogenesis

A

bacteria escape mouth during trauma (broken jaw, dental extraction) - bacteria grow in hard filamentous nodules nearby, surrounded by inflammation

52
Q

Clinical features of actinomyces israelii

A

hard, non-tender swelling in face, neck chest, abdomen - may also form in abdomen of a woman with a long-term IUD or after ruptured appendix, diverticulitis - pus draining through sinuses and contains hard yellow sulfur granules with “molar tooth appearance”

53
Q

Actinomyces israelii lab

A

biopsy and/or pus sample contains branching gram + rods with sulfur granules - grows in anaerobic conditions

54
Q

Treatment of actinomyces israelii

A

long course penicillin G - surgically drain the nodule if necessary

ABBEY MSII Unit 2 (19 decks)

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