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MSII Microbiology > Unit 2 - Bacterial Infections of Soft Tissue: Anaerobes > Flashcards

Unit 2 - Bacterial Infections of Soft Tissue: Anaerobes Flashcards

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1
Q

what are important pathogens in soft tissue infections?

A
  1. Staph (aureus, pyogenes) and Strep - opportunistic normal flora already on site, so most common offenders
  2. Anaerobes
  3. Immunocompromised or recently infected have pseudomonas or enterobacteriaceae
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2
Q

explain Clostridium tetani bacteriology?

A

G+, spore-forming rods

  • spores are environmental (soil, dust, manure, some human skin or GI)
  • transmitted to humans by soil contamination of wounds (splinters, thorns, punctures, IV, septic surgery, septic handling of umbilical cord)
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3
Q

explain the pathogenesis of C. tetani?

A

insertion beneath skin surface limits air contact

  • spores germinate (anaerobic)
  • vegetative cells release exotoxin tetanospasmin (AB subunit)
  • B (100kDa large subunit) delivers A (50kDa small subunit) to motor neuron
  • A travels 2-14 days to spinal cord via retrograde axonal transport
  • -protease activity cleaves synaptobrevin (VAMP) in inhibitory motor nerves of CNS, thus blocking release of glycine and GABA at spinal synapses
  • -loss of central inhibitory activity on motor and autonomic neurons leads to spastic paralysis of affected muscle group and respiratory failure with high mortality
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4
Q

what happens in neonatal tetanus?

A

contamination of umbilical cord and lack of maternal immunization

  • > 90% mortality in second week of life
  • developmental delays common in survivors
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5
Q

what happens in cephalic tetanus?

A

rare contamination of head wound causes cranial nerve palsy

-low mortality as long as it remains local

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6
Q

what happens in local tetanus?

A

wound contamination/infection causes local muscle rigidity in a single muscle group
-low mortality as long as it remains local

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7
Q

what happens in generalized tetanus?

A

violent full-body muscle spasms and respiratory distress cause morbidity

  • bacteria form locus of infection
  • exotoxin tetanospasmin enters bloodstream
  • > 50% untreated mortality from respiratory failure
  • 21-31% treated mortality
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8
Q

what do all cases of C. tetani have?

A

all cause tetanus (lockjaw)

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9
Q

what is included in the diagnostic exam for C. tetani?

A
  • sore throat, headache
  • local rigidity, difficulty swallowing
  • often afebrile
  • strong muscle spasms, paralysis
  • trismus (lockjaw)
  • risus sardonicus (permanent grimace)
  • exaggerated reflexes
  • opisthotonus (strong back arching)
  • fractures, tendon ruptures from spasms
  • spatula test
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10
Q

what is the spatula test?

A

used in C. tetani testing

-patient will bite down rather than gag when posterior pharyngeal wall is stimulated

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11
Q

what are lab diagnostics for C. tetani? which ones are useful?

A

only a few useful tests

  • terminal spore gives “tennis racquet” appearance in microscopy
  • bloodwork can confirm vaccination, rule out strychnine poisoning
  • lumbar puncture is unnecessary
  • imaging studies unremarkable
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12
Q

what is treatment for C. tetani?

A
  1. tetanus antitoxin (human-sourced immune globulin) neutralizes toxin
    - shortens course of disease, may lessen severity, but must ship from CDC
  2. antibiotics of questionable value (wound often clears on presentation, but may use metronidazole)
  3. airway support, IV nutrition
  4. benzodiazepines (valium) prevent spasms
  5. long-term physical therapy to recover muscle tone and control
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13
Q

prevention of C. tetani? what happens if you’re punctured?

A

universal vaccination with tetanus toxoid (formaldehyde-treated toxin) in childhood (DTaP) and every 10 years after

  • unvaccinated adults receive vaccine at any time
  • deep puncture wounds should be cleaned and debrided, and vaccine booster given
  • if the puncture is clearly dirty, call for immune globulin + cleaning + booster
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14
Q

what is the bacteriology of C. botulinum?

A

G+, spore forming, environmental (soil)

-germinating spores infected by lysogenic phase release 1 of 8 botulinum toxins (A to H), with A and B most toxic

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15
Q

what are the most common sources of foodborne botulism?

A

alkaline vegetables (home-canned beans, peppers, mushrooms) and raw fish (smoked or freeze-dried)

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16
Q

what is the pathogenesis of C. botunlinum?

A
  1. cooking inactivates toxin in contaminated foods, but w/o prior cooking its toxigenic
  2. germinating bacteria die in GI, but exotoxin is readily absorbed from cut, and carried to peripheral nerve synapses
  3. travels to stimulatory motor neurons at NMJ in PNS
  4. acts as protease to cleave synaptobrevin (VAMP)
    -unlike by tetanospasmin, its major effect is on release of ACh
  5. results in flaccid
    paralysis
    -if respiratory system affected, need artificial ventilation
    -affected nerve terminals suffer irreversible loss of function, thus recovery waits for new ones to sprout
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17
Q

what is infant botulism?

A

< 1 yo eats contaminated uncooked food (usually honey)

  • spores survive passage through stomach, and germinate in gut
  • weakness and paralysis (floppy baby) and breathing problems
  • symptoms progress for hours-days
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18
Q

what is wound botulism?

A

like tetanus, wound becomes contaminated from soil, and spores germinate and secrete exotoxin

  • common if IV drug use (heroin skin-popping) or immunosuppressed
  • rarely Cesarean
  • infection may not be obvious at wound site
  • symptoms progress in hours-days
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19
Q

explain what botox is

A

minute amounts of botulinum toxin A (not B)
-used to deliberately paralyze muscles of face, hand, anus, neck, or eyelid, where uncontrolled muscle contraction is the problem

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20
Q

what does typical botunlium look like

A

descending weakness and paralysis

  • N/V, diarrhea, no fever
  • typical patient is adult, thus obtain history of suspect food
  • symptoms for all progress in hours-days
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21
Q

what should you check for when suspecting botulism?

A
  1. trouble swallowing
  2. double vision
  3. fixed/dilate pupils
  4. extremely dry mouth
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22
Q

what are labs for botulism?

A
  1. culture not usually useful, can sometimes be grown from wound or GIT samples
  2. G+ may be lost after 18 hours in culture
  3. toxin can be demonstrated in suspect food and patient samples
  4. nerve studies usually unremarkable
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23
Q

what is treatment for botulism?

A

admit for rigorous supportive care

  • respiratory support (need may be sudden and/or prolonged)
  • heptavalent horse-sourced antitoxin inactivates toxin in bloodstream (available from CDC)
  • -treatment as needed for serum sickness from horse dander (in 20% of administrations, so NOT for prevention)
  • long-term physical therapy to recover muscle tone/control (full recovery takes 1-12 months)
  • antibiotics not necessary (but can be requested by parent)
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24
Q

what can be used as prevention of botulism?

A
  1. gastric lavage or induced vomiting
  2. enema to flush unabsorbed toxin
  3. proper sterilization of canned and vacuum-packed foods
    - adequate cooking, discarding swollen cans
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25
Q

explain the bacteriology of C. perfringens?

A

gas gangrene = myonecrosis = necrotizing faciitis

  • may be caused by other Clostridia
  • G+, spore-forming rod
  • anaerobic environment required for repication and exotoxin production
  • -relatively aerotolerant during host jumps
26
Q

explain the transmission of C. perfringens?

A

spores from soil or vegetative cells from colon enter wounds, usually from war, car accidents, septic abortions, etc.

27
Q

explain the pathogenesis of C. perfringens?

A
  1. vegetative cells grow in deep tissue, especially muscle
  2. produce >20 exotoxins to break down blood and tissue
    - alpha toxin (lecithinase) is necrotizing, hemolytic, and cardiotoxic (damages cell membranes, including erythrocytes
    - also includes hemolysins, cytolysins, collagenases, proteases, hyaluronidase, and deoxyribonuclease
  3. degradative enzymes produce gas in tissue
    - exotoxin hemolysis can lead to anemia and kidney failure, leading to shock/death
  4. 25% mortality, higher if treatment is delayed
28
Q

what is the exam for C. perfringens?

A
  1. pain, edema, and cellulitis at recent wound/surgical site that is disproportionate to wound appearance
    - skin turns bronze, then blue-black
    - occasionally develops at site of malignancy or other serious underlying condition
  2. may be crepitation, hemolysis, jaundice, blood-tinged exudates
    - tachycardia, altered mental state, hypotension, ARDS, renal failure and shock
  3. X-ray may show foreign body or “feathered” appearance of gas made in tissue by fermentation
29
Q

what is needed to confirm myonecrosis in gas gangrene?

A

surgical exploration

-high mortality risk associated with any delay, and likely need for surgical treatment to justify procedure

30
Q

what would biopsies show in gas gangrene?

A
  1. widespread myonecrosis
  2. destruction of CT
  3. paucity of neutrophils
31
Q

what does gas gangrene show in lab?

A
  1. large G+ rods
  2. hemolytic anemia, renal failure
    - chemistry profile for metabolic acidosis and/or renal failure
    - ELISA for alpha-toxin and PCR for clostridial DNA useful, but not widely available
  3. anerobic culture can retroactively identify species by sugar fermentation and organic acid production, hemolysis on blood agar, lecithinase test on egg yolk agar

*DO NOT WAIT FOR LABS TO PROCEED WITH EXPLROATORY SURGERY

32
Q

treatment and prevention of gas gangrene?

A

TRT: both surgery and antibiotics

  • pencillin G + clindamycin, or clindamycin + metronidazole
  • protein-synthesis inhibitors shut down exotoxin production
  • additional antibiotics may be needed for coincident infections (esp. if ICU)

PVT: clean and debride wounds

33
Q

what is C. perfringens food poisoning?

A

same bacteria, but different place

  • similar to botulism, except more in reheated foods (especially meat)
  • surviving environmental spores germinate and grow to large numbers in food
34
Q

explain the pathogenesis of C. perfringens food poisoning?

A
  1. germinating cells multiply in small bowel

2. type A enterotoxin destroys tight junctions between epithelial cells in gut, causing diarrhea and abdominal pain

35
Q

what is the diagnostic exam for C. perfringins food poisoning?

A
  1. 8-16 hour incubation
  2. watery diarrhea, cramps, and little vomiting
  3. resolves in 24 hours
    - typical 24 hour stomach bug
36
Q

what are the labs for C. perfringens food poisoning?

A

no individual tests required

-organisms can be cultured from uneaten food to trace an outbreak

37
Q

what is treatment and prevention for C. perfringens food poisoning?

A

TRT: don’t stop diarrhea, just let it flush out of body
PVT: thorough cooking

38
Q

explain C. difficile bacteriology?

A

G+ spore forming rod

-causes pseudomembranous colitis –> CDAD (associated diarrhea)

39
Q

how is C. diff transmitted?

A
  1. normal gut flora for 3% of general population, 30% of hospitalized
  2. fecal-oral route, especially nosocomial from spores on hsopital instruments and hands of health care workers
40
Q

explain C. diff pathogenesis?

A
  1. recent course of antibiotics or cancer chemotherapeutics suppresses other normal flora, allowing C. diffi to overgrow
  2. germinating cells release exotoxins
    - A: disrupts tight junctions, causing intestinal swelling and inflammation
    - B: major toxin that disrupts cytoskeleton by depolymerizing actin, killing surrounding cells
    - mortality between 2-6%
41
Q

diagnostic exam of C. diff?

A
  1. nonblood cramping diarrhea (mucoid, greenish, malodorous)
  2. fever, abdominal tenderness
  3. history of recent antibiotic use, cancer chemotherapeutics, or immunosuppressants
  4. geriatric patients are at higher risk for both disease and poor outcome
  5. recent GI drugs and procedrues predisposing
42
Q

what will sigmoidoscopy show for C. diff?

A
  1. patches of dead/dying cells appear as yellow-white plaques (pseudomembranes)
  2. biopsy shows focal necrosis in glandular crypts with neutrophilic infiltration and fibrin plugging of capillaries in lamina propria and mucus hypersecretion in adjacent crypts, leading to formation of crypt abscesses
  3. toxic megacolon or colonic perforation may occur (use imaging studies to diagnose these)
43
Q

what will C. diff show in labs?

A
  1. bloodwork (WBC and serum creatinine both elevated)
  2. can be cultured from stool, but slow
  3. toxins in stool filtrate
    - ELISA for toxins A/B (quick, but not very sensitive and must test for both)
    - cytotoxicity test (observe that untreated stool filtrate, but not treated, will kill human cells in culture; takes 24-48 hours)
  4. neutrophils may be present in stool
44
Q

explain treatment of C. difficile?

A
  1. withdraw initial antibiotic (20% of cures)
  2. replace fluids
  3. give oral metronidazole or vancomycin (unless very mild)
  4. don’t treat diarrhea (let toxins flush)
  5. surgical resection or removal of colon may be required
    - episodes of colitis may recur
    - alternatively use bacteriotherapy to supply colon with normal flora by enema
45
Q

what are bacteroides and prevotella bacteriology?

A

AGNB (anaerobic G- bacilli)

  • non-spore forming
  • opportunistic pathogens (breach normal area)
  • fastidious in culture
46
Q

where is B. fragilis usually? where does it infect?

A

normally in colon and vagina

-causes infections in abdomen (below diaphragm)

47
Q

where is B. corrodens and P. melaninogenica usually? where does it infect?

A

normally in mouth and vagina

-causes infections in respiratory tract (above diaphragm)

48
Q

why is treatment of AGNB complciated?

A

bacteroides and prevotella treatment complicated by 3 factors:

  1. slow growth
  2. antibiotic resistance
  3. polymicrobial nature of infection (5-10 organisms at site, only one has to secrete beta-lactamase to protect whole colony from penicillins)
49
Q

explain the pathogenesis of AGNB?

A
  1. non-communicable
  2. anaerobes escape normal location through break in mucosal surface (injury, surgery)
  3. set up abscess in new location, particularly where local tissue trauma impairs blood supply
  4. abscess often includes faculative anaerobes which use up O2, then anaerobes grow well
  5. several strains produce hyaluronidase, collagenase, and phospholipase (exotoxin tissue-degrading enzymes)
50
Q

describe B. fragilis morphology?

A

AGNB (Bacteroides)

  • polysaccharide capsule
  • some make enterotoxin and cause diarrhea
  • more antibiotic-resistant than most anaerobes
51
Q

describe the diagnostic exam for AGNB?

A
  1. history of tissue trauma, cancer, or other major illnesses affecting blood flow (colitis, vascular disease), surgery, immunosuppression
  2. painful abscess (peritonitis or localized)
    - pelvic abscess (escape from colon), necrotizing faciitis, bacteremia, PID (if vaginal abscess)
  3. infections of ears or respiratory system can progress to meningitis or brain abscess
  4. dental infections can spread to deep neck space
  5. osteomyelitis of long bones following break
52
Q

what do labs say for AGNB?

A
  1. collect via method that bypasses normal flora and maintains anaerobic conditions (needle aspiration)
  2. isolate on anaerobic blood agar blates with kanamycin and vancomycin, for 2-4 days
  3. identify by sugar fermentation and gas chromatography of acids produced
  4. antimicrobial susceptibility testing is recommended, but difficult
53
Q

what does P. melaninogenica produce in culture?

A

black colonies

54
Q

what are minor anaerobic pathogens that produce look-alike abscesses to AGNB?

A
  1. fusobacterium
  2. peptostreptococcus
  3. prevotella
55
Q

what is treatment for AGNB? prevention?

A

TRT: metronidazole or cefoxitin, clindamycin, chloramphenicol

  • combine with aminoglycides to kill faculatives in abscess
  • surgical care: drain/debride abscess unless in lung, relieve obstructions (infection persists if locus is not surgically removed)

PRT: perioperative cephalosporin

56
Q

explain actinomyces bacteriology?

A

G+ filamentous rods that are non-spore forming

  • anaerobic to microaerophilic
  • normal flora of mouth, vagina
  • cells from long, branching filaments that resemble hyphae of fungi
  • infections are polymicrobial, 5-10 organisms
  • infections are rare, especially in population w/ good dental hygiene
57
Q

describe the pathogenesis of actinomyces?

A
  1. bacteria escape proper compartment during accidental or surgical trauma
  2. grow in hard, filamentous nodules nearby, surrounded by inflammation
  3. non-communicable
  4. good prognosis; low pathogenicity, slow growth, and little antibiotic resistance
58
Q

what are the 2 presentations for actinomyces?

A
  1. head/neck

2. abdomen

59
Q

describe the diagnostic exam for head/neck actinomyces?

A
  1. hard, non-tender swelling in face, neck, chest
  2. untreated spots increase in size/number
  3. pus draining through sinuses (contains hard, yellow sulfur granules)
  4. history of dental work, poor dental hygiene, can spread to head or bloodstream of untreated
60
Q

describe the diagnostic exam for abdomen actinomyces?

A
  1. slow-growing tumor
  2. nonspecific abdominal symptoms (weight loss, fatigue, discomfort, nausea)
  3. usually diagnosed on exploratory surgery to rule out malignancy
  4. hsitory of > 8 year IUD or remote bowel surgery (perforated appendix, diverticulitis)
61
Q

what is actinomyces labwork?

A
  1. biopsy and/or needle-aspirated pus sample contains branching G+ rods with sulfur granules
  2. can be anaerobically cultured if sample is appropriately handled, but may take 3 weeks to grow
  3. IF testing available if needed
62
Q

treatment for actinomyces?

A
  1. long course of penicillin G

2. surgical drainage of nodule may be needed

MSII Microbiology (23 decks)

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