Bacterial Infections of Soft Tissue: Anaerobes Flashcards
C. tetani bacteriology
spores are environmental. Gram +. transmitted to humans by soil contamination of wounds
C. tetani pathogenesis
insertion beneath skin surface limits air contact. spores germinate and vegetative cells release exotoxin tetanospasmin.
neonatal tetanus
contamination of umbilical cord + lack of maternal immunization. 90%+ mortality in second week of life. developmental delays common in survivors
cephalic tetanus
rare, contamination of head wounds. patient presents with cranial nerve palsy.
local tetanus
wound contamination -> rigidity in a single muscle group.
generalized tetanus
bacteria form a locus of infection, and exotoxin tetanospasmin enters bloodstream. full-body symptoms cause morbidity. >50% untreated mortality from respiratory failure. 21-31% treated mortality
tetanospasmin structure and function
2 subunits, large and small. large subunit is a ferry for the small unit. it opens a pore in the cell for the small unit to get in to the presynaptic motor neuron. cleaves synaptobrevin (VAMP) causing vesicles containing GABA and glycine not to be released. loss of inhibitory action = constant contraction
C. tetani exam
sore throat, headache, local rigidity, strong muscle spasms. Trismus (lockjaw), grimace, opisthotonus (arching of back). spatula test: patients bite instead of gag when posterior pharyngeal wall is stimulated
c. tetani lab
terminal spores give tennis racket on microscopy. bloodwork can confirm vaccination, rule out strychnine poisoning. no need for lumbar puncture. imaging studies unremarkable
c. tetani treatment
tetanus antitoxin neutralizes toxin. metronidazole doesnt do much. valium to prevent spasms, other muscle relaxants can help
C. tetani prevention
tetanus toxoid vaccine. booster every 10 years. adults can receive vaccine at any time. deep puncture should be cleaned and debrided and vaccine booster given. deep and clearly dirty wounds call for immune globulin and booster of vaccine
c. botulinum bacteriology
environmental. gram +, spore forming. foodborne botulism is most common presentation. spores survive inadequate sterilization. germinating cells release one of 8 botulinum toxins: A-H. A and B are the most toxic.
c botulinum pathogenesis
cooking inactivates toxin. germinating bacteria die in GI, but exotoxin is readily absorbed from the gut. carried in blood to peripheral nerve synapses. acts as protease cleaving synaptobrevin (VAMP). flaccid muscles.
infant botulism
chile
wound botulism
wound contaminated with soil. spores germinate and secrete exotoxin. IV drug use or immunosuppressed show this. rarely seen in C sections. infection may not be obvious at would site.