Anaerobic Soft Tissue Infections Flashcards
(47 cards)
1
Q
important pathogens in soft tissue infections
A
- staph aureus
- strep pyogenes
- anaerobes
- if immunocompromised: pseudomonads, enterobacteriaceae
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
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
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
5
Q
cephalic tetanus
A
- rare, contamination of head wounds
- patient presents with cranial nerve palsy
6
Q
local tetanus
A
-wound contamination–> rigidity in a single muscle group, something stops it
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
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
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
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
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
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
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
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
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
16
Q
wound botulism
A
- like tetanus, wound becomes contaminated from soil, spores germinate and secrete exotoxin
- IV drug use or immunosuppressed
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
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
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
c perfringens-gas gangrene lab diagnosis
- 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
c perfringens-gas gangrene trt and prevention
- 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
c perfringens type A food poisoning bacteriology
- 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
c perfringens type A food poisoning pathogenesis
- 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
c perfringens type A food poisoning diagnosis exam
- 8-16 hr incubation
- watery cramps, diarrhea, cramps, little vomiting
- resolve in 24 hrs
30
c perfringens type A food poisoning diagnosis lab
- no individual tests required
| - organisms can be cultured from uneaten food to trace and outbreak
31
c perfringens type A food poisoning trt and prev
- symptomatic support- don't stop diarrhea
| - thorough cooking
32
c difficile bacteriology
- 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
c diff pathogenesis
- 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
c diff diagnosis exam
- 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
c diff lab diagnosis
- 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
c diff trt
- 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
bacterioids and prevotella bacteriology
- 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
bacteroides and prevotella pathogenesis
- 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
bacteroides and prevotells diagnosis exam
- 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
bacteroides and prevotella lab
- 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
bacteroides and prevotella trt and prev
- 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
actinomyces bacteriology
- 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
actinomyces pathogenesis
- 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
actinomyces head and neck exam
- 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
actinomyces abd exam
- 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
actinomyces lab diagnosis
- 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
actinomyces trt
- long course of penicilling G may suffice
| - surgical drainage may be needed
