Anaerobic Soft Tissue Infections Flashcards

1
Q

important pathogens in soft tissue infections

A
  • staph aureus
  • strep pyogenes
  • anaerobes
  • if immunocompromised: pseudomonads, enterobacteriaceae
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2
Q

c tetani bacteriology

A
  • spores are environmental- soil, dust, manure, some human skin and GI
  • gram pos
  • spore forming
  • transmitted to humans by soil contamination of wounds- splinters, thorns, punctures, IV drugs, septic surgery, septic handling of umbilical cord
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3
Q

c tetani pathogenesis

A
  • insertion beneath skin surface limits air contact
  • spores germinate
  • vegetative cells release exotoxin tetannospasmin
  • 4 types of disease: neonatal, cephalic, local, generalized
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4
Q

neonatal tetanus

A
  • contamination of umbilical cord + lack of maternal immunization
  • > 90% mortality in second week of life
  • developmental delays common in survivors
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5
Q

cephalic tetanus

A
  • rare, contamination of head wounds

- patient presents with cranial nerve palsy

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6
Q

local tetanus

A

-wound contamination–> rigidity in a single muscle group, something stops it

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7
Q

generalized tetanus

A
  • bacteria form a locus of infection
  • exotoxin tetanospasmin enters bloodstream
  • full body sx cause morbidity
  • > 50% untreated mortality from respiratory failure
  • 21-31% treated mortality
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8
Q

how does c tetani exotoxin work?

A
  • germinating cells secrete toxin
  • AB subunit- B delivers A to the nerve end and opens a pore for it
  • A enters motor neuron and does retrograde axonal transport as far as it can in 2-14 days to the spinal cord
  • is a protease and cleaves synaptobrevin in inhibitory nerves of CNS- therefore there is not inhibitory action and always contractin
  • vesicles containing GABA and glycine cannot be delivered
  • loss of central inhibitory activity on motor and autonomic neurons
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9
Q

c tetani diagnosis on exam

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

c tetani diagnosis on lab

A
  • few useful tests
  • terminal sport gives tennis racket appearance on microscopy
  • bloodwork can confirm vaccination, rule out strychnine poisoning
  • imaging studies unremarkable
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11
Q

c tetani trt

A
  • tetanus antitoxin (human Ig) neutralizes toxin, shortens course of disease, may lessen severity, ships from the CDC
  • antibiotics of questionable value
  • can use metronidazole
  • airway support, IV nutrition
  • benzos to prevent spasms, can supplement with narcotics and hypnotics, inhalation aids, neuromuscular relaxants
  • blocking agents
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12
Q

c tetani prevention

A
  • universal vaccination with tetanus toxoid in childhood (DTaP) according to standard schedules, adults get booster every 10 years
  • unvaccinated adults can receive vaccine at any time
  • deep puncture wounds should be cleaned, debrided, and vaccine booster given
  • deep and clearly dirty wounds gall for immune globulin in addition
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13
Q

c botulinum bacteriology

A
  • environmental
  • gram pos, spore forming
  • most common presentation is foodborne, botulism intoxication by ingestion of contaminated food
  • most common sources are alkaline veggies (home canned) and raw fish (smoked or Inuit freeze dried
  • spores survive sterilization of pre prepared foods, will germinate if subsequently vacuum packed
  • germinating cells infected by lysogenic phage release one of 8 botulinum toxins
  • A and B are most toxic
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14
Q

c botulinum pathogenesis

A
  • cooking inactivates the toxin in contaminated foods- eating without cooking leads to disease
  • germinating bacteria die in GI, but exotoxin readily absorbed from gut
  • carried in blood to peripheral nerves
  • travels to STIM motor neurons at NMJ in the peripheral nervous system
  • acts as protease, cleaving synaptobrevin
  • different location than tetani- major effect is on release of Ach
  • flaccid paralysis results, if respiratory system- immediate artificial ventilation needed
  • affected nerve terminals suffer irreversible loss of function, recovery waits for new ones to sprout
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15
Q

infant botulism

A
  • child <1 year consumes contaminated uncooked food, usually honey
  • spores germinate in GI and secrete exotoxin
  • loss of muscle tone, floppy baby, breathing problems
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16
Q

wound botulism

A
  • like tetanus, wound becomes contaminated from soil, spores germinate and secrete exotoxin
  • IV drug use or immunosuppressed
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17
Q

c botulinum diagnosis exam

A
  • foodborne: descending weakness and paralysis, N/V/D without fever. typical pt is adult, obtain hx of suspect foods
  • wound botulism:history of soil contaminated wound, IV drug use, rarely C section. infection may not be obvious at wound site
  • infant- average age 3 mo. weakness, paralysis, breathing trouble. hx of honey
  • sx for all progress in hours/days
  • check for trouble swallowing, double vision, fixed/dilated pupils, extremely dry mouth
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18
Q

c botulinum diagnosis in lab

A
  • culture not usually useful, can sometimes be grown from wound or GI tract samples
  • gram positivity may be lost after 18 hrs in culture
  • toxin cab be demonstrated in suspect food and pt samples
  • nerve study usually unremarkable
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19
Q

treatment for c botulinum

A

-admit for rigorous supportive care:
resp, need may be sudden or prolonged
-heptavalent horse sourced antitoxin inactivates toxin in bloodstream, available from CDC
-trt as needed for serum sickness from horse dander
-serum sickness in 20% of admins, do not use preventatively
-gastric lavage or induced vomiting for preventative
-enema may be used to flush unabsorbed toxin
-antibiotics not necessary
-report to health authorities
-also debride and high dose IV penicillin
-long term treatment- full recovery requires 1-12 months, PT and OT, psych consult and pastoral care for depression

20
Q

prevention of c botulinum

A
  • proper sterilization of canned and vacuum packed foods
  • adequate cooking
  • discard swollen cans
21
Q

botox

A
  • minute amounts of botulinum toxin A may be used to deliberately paralyze muscles
  • face
  • hand
  • anus
  • neck
  • eyelid
22
Q

c perfringens-gas gangrene bacteriology

A
  • myonecrosis- necrotizing fasciitis
  • may also be caused by other clostridia (bifermentans, septicum, sporogenes, novyu, fallax, histoyticum, tertium
  • gram pos spore forming rod
  • anaerobic environment required for replication and exotoxin production, relatively aerotolerate during host jumps
23
Q

c perfringens-gas gangrene pathogenesis

A
  • spores from soil or vegetative cells from GI enter wouds (war, car accident, septic abortion) where necrotic tissue, foreign bodies, premature closure disrupt blood flow and enhance germination
  • vegetative cells grow in deep tissue, esp muscle
  • produce at least 20 exotoxins
  • alpha-lecithinase, necrotizing, hemolytic, cardiotoxic
  • others include hemolysins, cytolysins, collagenases, proteases, hyaluronidase, deoxyribonuclease
  • degradative enzymes produce gas in tissue
  • exotoxin hemolysis can lead to anemia and kidney failure
  • failure of heart and kidneys lead to shock and death
  • 25% mortality, higher if trt delayed
24
Q

c perfringens-gas gangrene diagnosis exam

A
  • pain, edema, cellulitis at a recent wound or surgical site
  • skin color bronze then blue/black
  • site tender to palpitation disproportionate to wound appearance
  • occasionally develops at site of malignancy or other serious underlying condition
  • incubation period usually short but may last weeks
  • may also be crepitation, hemolysis, jaundice, blood tinged exudates
  • tach
  • altered mental status
  • hemolytic anemia. hypotension
  • acute resp distress syndrome
  • renal failure
  • shock
  • radiography may show feathering pattern of gas in soft tissue
  • CT scanning most helpful for abd cases
  • US detects gas too
  • surgical exploration needed to confirm myonecrosis
  • high mortality risk associated with any delay and likely need for surgical trt justify the procedure
  • biopsies show widespread myonecrosis, destruction of CT
25
Q

c perfringens-gas gangrene lab diagnosis

A
  • microscopy: smears from tissue and exudate show large gram pos rods
  • bloodwork for hemolytic anemia, increased LDH, TSS
  • chem profile for metabolic acidosis and/or renal failure
  • ELISA for a toxin and PCR for clostridial DNA are useful but not widely avaiable
  • anaerobic culture can retroactively identify species by sugar fermentation and organic acid production
  • hemolysis on blood agar, lecintinase test
  • DON’T WAIT FOR LABS BEFORE SURGERY
26
Q

c perfringens-gas gangrene trt and prevention

A
  • surgery and antibiotics
  • penicillin G and clinda, or clinda and metronidazole
  • protein synthesis inhibitors shut down exotoxin production (clinda, chloramphenicol, rifampin, tetra)
  • additional antibiotics may be needed for coincident infections
  • ICU admit often needed for complications
  • prevention- clean and debride wounds
27
Q

c perfringens type A food poisoning bacteriology

A
  • soil borne food sports contaminate food
  • inadequate cooking fails to kill them
  • spores germinate and grow to lg numbers in reheated foods, esp meat
28
Q

c perfringens type A food poisoning pathogenesis

A
  • germinating cells multiply in the small bowel

- CPE enterotoxin type A strains destroy tight junctions between epithelial cells in gut, causing diarrhea and abd pain

29
Q

c perfringens type A food poisoning diagnosis exam

A
  • 8-16 hr incubation
  • watery cramps, diarrhea, cramps, little vomiting
  • resolve in 24 hrs
30
Q

c perfringens type A food poisoning diagnosis lab

A
  • no individual tests required

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

31
Q

c perfringens type A food poisoning trt and prev

A
  • symptomatic support- don’t stop diarrhea

- thorough cooking

32
Q

c difficile bacteriology

A
  • gram pos spore forming rods
  • causes pseduomembranous colitis- C diff associated diarrhea, antibiotic associated colitis
  • transmission:
  • normal gut flora for 3% of general pop, 30% for hospitalized
  • fecal oral, esp nosocomial from spores on hosp instruments or on hands of health care workers
33
Q

c diff pathogenesis

A
  • recent course of antibiotics or cancer chemo suppresses other normal flora, allows overgrowth of c diff
  • germinating cells release exotoxin A, which disrupts tight junctions, causing intestinal swelling and inflammation
  • exotoxin b is major toxin, disrupts cytoskeleton by depolymerizing actin, kills surrounding cells
  • A more virulent and drug resistant strain emerged in 01-02, cases doubled in 00-03 and have continued to rise
  • mortality increased from 6 %
34
Q

c diff diagnosis exam

A
  • nonbloody cramping diarrhea, mucoid, greenish, malodorous
  • fever, abd tenderness
  • hx of antibiotic use, chemo or immunosuppressants
  • geriatric patients at higher risk for disease and poor outcome
  • recent GI drugs and procedures are also predisposing
  • patches of dead and dying cells appear as yellow-white plaques
  • biopsy during sigmoidoscopy, focal necrosis in glandular crypts with neutrophilic infiltration and fibrin plugging of caps in lamina propria and mucous hypersecretion in adjacent crypts
  • leads to crypt abscess
  • toxic megacolon or colonic perf can occur, imaging studies diagnose these
35
Q

c diff lab diagnosis

A
  • WBC and serum creatinine elevated
  • can be cultured from stool, but slow
  • toxins in stool filtrate
  • ELISA for toxins A and B, quick but not sensitive
  • cytotox test- observe untreated stool filtrate but not stool filtrate treated with antibodies agains c diff toxins, kill human cells in culture
  • sens but slow- 24-48 hrs
  • PCR tests soon
  • neutrophils may be present in stool
36
Q

c diff trt

A
  • withdraw initial antibiotic, cures 20%
  • replace fluids
  • unless disease was very mild, give oral metronidazole or vanco
  • do not trt diarrhea
  • surgical resection or removal of colon may be required
  • episodes od colitis may recur
  • alternative approach may be fecal bacteriotherapy
37
Q

bacterioids and prevotella bacteriology

A
  • AGNB- anaerobic gram ned bacilli, also includes fusobacter
  • non spore forming
  • normal flora of mucus membranes–> opportunistic pathogens
  • B fragilia-normally colon, infections in abd
  • B corrodens and P melaninogenica- normally mouth and vagina–> infections in resp tract
  • fastidious in culture
  • trt complicated by 3 factors:
    1. slow growth
    2. antibiotic resistance
    3. polymicrobial nature of infection, 5-10 org at site, only one has to secrete beta lactamase to protect whole colony from penicillin
38
Q

bacteroides and prevotella pathogenesis

A
  • anaerobes escape normal location through a break in mucosal surface
  • set up abscess in new location, particularly when local tissue trauma impairs the blood supply
  • abscesses often also include facultative anaerobes which use up the oxygen, then the anaerobes grow well
  • B fragilis: polysaccharide capsule, some produce enterotoxin and cause diarrhea, more antibiotic resistance than most anaerobes
  • several strains of each produce hyaluronidase, collagenase, phospholipase
39
Q

bacteroides and prevotells diagnosis exam

A
  • hx of tissue trauma, cancer, other major illness affecting blood flow (colitis, vascular disease), surgery, immunosuppression
  • painful abscess
  • infections of ears or resp sys can progress to meningitis or brain abscess
  • dental infections can spread to deep neck space
  • osteomyelitis of long bones following break
  • pelvic abscess following escape from colon
  • abscess in vagina can progress to PID
  • superficial skin infections or diabetic foot ulcers can progress to cellulitis, gas gangrene
  • bacteremia is possible and dangerous
  • imaging studies can reveal abscesses and gas in tissue
  • usually b fragilis if below the diaphragm and p melaninogenica if above
40
Q

bacteroides and prevotella lab

A
  • collect by a method that bypasses normal flora and maintains anaerobic conditions (needle aspiration)
  • culture promptly on anaerobic blood agar plates with kanamycin and vanomycin or in anaerobic liquid media
  • culture requires 2-4 days
  • p melaninogenica produces black colonies
  • ID by sugar fermentation and gas chromatography of acids produced
  • PCR tests in pipeline
  • antimicrobial susceptibility testing is recommended but difficult
41
Q

bacteroides and prevotella trt and prev

A
  • metronidazole or cefoxitin, clinda, chloramphenicol kill the anaerobes
  • combine with aminoglycosides to kill facultatives in abscess
  • surgical care- drain/debride abscess unless in lung, relieve instructions
  • infection will persist if locus not surgically removed
  • prev-preoperative cephalosporin
42
Q

actinomyces bacteriology

A
  • gram pos filamentous rods
  • non spore forming
  • anaerobic to microaerophilic
  • normal flora of mouth, vagina
  • cells form long, branching filaments that resemble the hyphae of fungi
  • infections are polymicrobial, 5-10 org
  • infections are rare, esp in pop with good hygiene
43
Q

actinomyces pathogenesis

A
  • bacterial escape compartment during accidental or surgical trauma
  • grow in hard, filamentous nodules nearby, surrounded by IF
  • non-communicable
  • good prognosis-low pathogenicity, slow growth, little antibiotic resistance
44
Q

actinomyces head and neck exam

A
  • hard, non tender swelling in face, neck, chest
  • untreated, spots increase in size and number
  • pus draining through sinuses
  • pus contains hard yellow sulfur granules
  • history of dental work, poor dental hygiene, can spread to head or bloodstream if untreated
45
Q

actinomyces abd exam

A
  • slow growing tumor
  • nonspecific abd symptoms- weight loss, fatigue, discomfort, nausea
  • usually diagnosed on exploratory surgery to rule out malignancy
  • history of >8 year IUD or remote bowel surgery
46
Q

actinomyces lab diagnosis

A
  • biopsy or needed aspirated pus sample contains branching gram pos rods with sulfur granules
  • can be anaerobically cultured if sample is appropriately handled, but may take 3 weeks to grow
  • IF testing available if needed
  • PCR in pipeline
47
Q

actinomyces trt

A
  • long course of penicilling G may suffice

- surgical drainage may be needed