Anaerobic Soft Tissue Infections Flashcards
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