Micro U2 L10. Flashcards
Clostridium
gram+ spore forming rods - anaerobic (c. tetani, c. botulinum, c. perfringens (gas gangrene and food poisoning), c. difficile)
Four presentations of C. tetani
- 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
Transmission of C. tetani
soil contaminated puncture wound (2-14 days before symptoms); IV drug users skin popping; contained umbilical cord or circumcision wound
Pathogenesis of C. tetani
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
Complication of C. tetani
respiratory failure
Clinical features of C. tetani
strong muscle spasms and paralysis, lockjaw, grimace, exaggerated reflexes, opisthotonus (strong arching of back)
Labs for C. tetani
few useful tests - terminal spore gives “tennis racket” appearance on microscopy
Treatment for C.tetani
tetanus antitoxin; antibiotics are meh, airway support, benzodiazepines (valium) for muscle spasms, long term physical therapy
Prevention of C. tetani
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
Transmission of C. botulinum
spores survive in inadequate sterilization of foods - releasing one of 8 toxins (A-H) - cooking properly inactivates toxin
What are the MC sources of c. botulinum?
alkaline veggies (home-canned beans, peppers, mushrooms) and raw fish
Pathogenesis of C. botulinum
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
Botox
minute amounts of botulinum toxin A - deliberately paralyze muscles of face, hand, anus, neck, eyelid
Clinical features of typical C. botulinum
descending weakness and paralysis without fever; blurred/doubled vision; trouble swallowing - happens FAST - hours
Clinical features of wound botulism
spores germinate in a contaminated wound - most common with heroin skin-popping
Clinical features of infant botulism
spores survive passage through infant’s stomach and germinate in the gut - weakness and paralysis, history of honey - “floppy baby”
Labs for botulism
toxin can be demonstrated in suspect food and patient samples - gram + bacteria gets lost quickly (when exposed to air)
Treatment for botulism
respiratory support, trivalent horse-sourced antitoxin (for non A&B subtypes - human for A&B), treatment as needed for serum sickness, physical therapy
Prevention for botulism
proper sterilization of banned and vacuum-packed foods, adequate cooking, discard swollen cans
C. perfringens gas gangrene transmission
myonecrosis = necrotizing faciitis. transmission - spores from soil or vegetative cells from colon enter wounds, usually from war, car accidents, septic abortions (MAJOR wounds)
C. perfringens pathogenesis
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
Which clostridium is slightly aero-tolerant?
c. perfringens
Extoxin onslaught in C. perfringens leads to what?
hemolytic anemia, kidney and heart failure, shock and death
alpha toxin
lecithinase - damages cell membranes including erythrocytes (reason for necrotoxic, cardiotoxic, and hemolysis
Clinical features of C. perfringens
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
X-ray of c. perfringens
foreign body or “feathered” appearance of gas produced in tissue by bacterial fermentation
Treatment of C. perfringens
immediate surgical removal of diseased tissue followed by IV penicillin G and clindamycin (protein synthesis inhibitor)
Lab for C. perfringens
can see gram + rods
C. perfringen food poisoning transmission
soil-borne spores contaminate food - inadequate cooking - surviving spores germinate and grow in reheated foods esp meat
Pathogenes of C. perfringens food poisoning
germinating cells multiply in small bowel - enterotoxins cause diarrhea, disrupting tight junctions (type A exotoxin)
Diagnosis of C. perfringens food poisoning
8-16 h incubation; watery diarrhea, cramps, little vomiting - resolves in 24 hours
C. difficile caused by
pseudomembranous colitis - gram +
Transmission of C. difficile
normal gut flora for 3% population - 30% in hospital - fecal-oral esp nosocomial
Pathogenesis of C. difficile
recent course of antibiotics or cancer chemotherapeutics suppressing other normal flora; germinating cells release exotoxins
Exotoxins release by C. difficile and their effects
A- disrupts tight junctions (like C. perfringens). B - depolymerizes actin - kills surrounding cells and causes plaques) - combo cause intestinal inflammation and swelling
Clinical features of C. difficile
nonbloody cramping diarrhea: mucoid, greenish, malodours (STINKY); fever; on sigmoidoscopy, patches of dead and dying cells appear as yellow-white plaques (pseudomembranes)
Labs for C. difficile
toxins in stool filtrate - ELISA for toxin or cytotoxicity test - neutrophils in stole
Treatment for C. difficile
withdraw initial antibiotic, replace fluid, oral metronidazole or vancomycin, surgical resection/removal of colon may be required
Bacteroides and prevotella bacteriology
Gram NEGATIVE anaerobic, non spore forming, normal flora
B fragilis normal flora spot
colon and vagina
B corrodens and P melaninogenica normal flora spot
mouth
Pathogenesis of bactericides and prevotella
non-communicable - anaerobes escape normal location through break in mucosal surface and set up abscess in new location
How do abscesses complicate antibiotic treatment of bactericides and prevotella?
polymicrobial infection due to facultative anaerobes in abscesses which use up the oxygen
What is a more antibiotic-resistant strain anaerobic bacteria?
b. fragilis (vagina and colon)
Clinical features of Bacteroides and Prevotella
peritonitis or localized abscess and pelvic abscess, necrotizing faciitis, bacteremia
How to tell the difference clinically between B. fragilis and P. melaninogenica
B fragilis below the diaphragm and p. melaninogenica above
Labs for bacteroides and prevotella
isolate on anaerobic blood agar plates - p. melaninogenica produces black colonies - identify by sugar fermentation and gas chromatography of acids produced
Treatment of bactericides and prevotella
metronidazole (used for anaerobes), combine with aminoglycides to kill facultatives in abscess, surgical care for abscess unless in lung
Prevention of bactericides and prevotella
perioperative cephalosporin
Actinomyces israelii bacteriology
gram + rodes, normal flora of mouth, cells form long, branching filaments that resemble hyphae of fungi - non communicable
Actinomyces israelii pathogenesis
bacteria escape mouth during trauma (broken jaw, dental extraction) - bacteria grow in hard filamentous nodules nearby, surrounded by inflammation
Clinical features of actinomyces israelii
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”
Actinomyces israelii lab
biopsy and/or pus sample contains branching gram + rods with sulfur granules - grows in anaerobic conditions
Treatment of actinomyces israelii
long course penicillin G - surgically drain the nodule if necessary
