Micro U2 L10.

Question 1

Clostridium

Answer 1

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

Question 2

Four presentations of C. tetani

Answer 2

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

Question 3

Transmission of C. tetani

Answer 3

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

Question 4

Pathogenesis of C. tetani

Answer 4

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

Question 5

Complication of C. tetani

Answer 5

respiratory failure

Question 6

Clinical features of C. tetani

Answer 6

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

Question 7

Labs for C. tetani

Answer 7

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

Question 8

Treatment for C.tetani

Answer 8

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

Question 9

Prevention of C. tetani

Answer 9

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

Question 10

Transmission of C. botulinum

Answer 10

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

Question 11

What are the MC sources of c. botulinum?

Answer 11

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

Question 12

Pathogenesis of C. botulinum

Answer 12

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

Question 13

Botox

Answer 13

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

Question 14

Clinical features of typical C. botulinum

Answer 14

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

Question 15

Clinical features of wound botulism

Answer 15

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

Question 16

Clinical features of infant botulism

Answer 16

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

Question 17

Labs for botulism

Answer 17

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

Question 18

Treatment for botulism

Answer 18

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

Question 19

Prevention for botulism

Answer 19

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

Question 20

C. perfringens gas gangrene transmission

Answer 20

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

Question 21

C. perfringens pathogenesis

Answer 21

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

Question 22

Which clostridium is slightly aero-tolerant?

Answer 22

c. perfringens

Question 23

Extoxin onslaught in C. perfringens leads to what?

Answer 23

hemolytic anemia, kidney and heart failure, shock and death

Question 24

alpha toxin

Answer 24

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

Question 25

Clinical features of C. perfringens

Answer 25

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

Question 26

X-ray of c. perfringens

Answer 26

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

Question 27

Treatment of C. perfringens

Answer 27

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

Question 28

Lab for C. perfringens

Answer 28

can see gram + rods

Question 29

C. perfringen food poisoning transmission

Answer 29

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

Question 30

Pathogenes of C. perfringens food poisoning

Answer 30

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

Question 31

Diagnosis of C. perfringens food poisoning

Answer 31

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

Question 32

C. difficile caused by

Answer 32

pseudomembranous colitis - gram +

Question 33

Transmission of C. difficile

Answer 33

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

Question 34

Pathogenesis of C. difficile

Answer 34

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

Question 35

Exotoxins release by C. difficile and their effects

Answer 35

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

Question 36

Clinical features of C. difficile

Answer 36

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

Question 37

Labs for C. difficile

Answer 37

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

Question 38

Treatment for C. difficile

Answer 38

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

Question 39

Bacteroides and prevotella bacteriology

Answer 39

Gram NEGATIVE anaerobic, non spore forming, normal flora

Question 40

B fragilis normal flora spot

Answer 40

colon and vagina

Question 41

B corrodens and P melaninogenica normal flora spot

Answer 41

mouth

Question 42

Pathogenesis of bactericides and prevotella

Answer 42

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

Question 43

How do abscesses complicate antibiotic treatment of bactericides and prevotella?

Answer 43

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

Question 44

What is a more antibiotic-resistant strain anaerobic bacteria?

Answer 44

b. fragilis (vagina and colon)

Question 45

Clinical features of Bacteroides and Prevotella

Answer 45

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

Question 46

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

Answer 46

B fragilis below the diaphragm and p. melaninogenica above

Question 47

Labs for bacteroides and prevotella

Answer 47

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

Question 48

Treatment of bactericides and prevotella

Answer 48

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

Question 49

Prevention of bactericides and prevotella

Answer 49

perioperative cephalosporin

Question 50

Actinomyces israelii bacteriology

Answer 50

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

Question 51

Actinomyces israelii pathogenesis

Answer 51

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

Question 52

Clinical features of actinomyces israelii

Answer 52

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”

Question 53

Actinomyces israelii lab

Answer 53

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

Question 54

Treatment of actinomyces israelii

Answer 54

long course penicillin G - surgically drain the nodule if necessary