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.
c. botulinum exam
foodborne: descending weakness and paralysis. nausea, vomiting, diarrhea without fever. get history of suspect foods. check for trouble swallowing, double vision, fixed/dilated pupils, dry mouth
c. botulinum lab
cultures not usually useful, can sometimes be grown from wound or GI tract. gram positivity may be lost after 18 hours in culture. toxin can be demonstrated in suspect food and patient samples. nerve studies usually unremarkable.
c. botulinum treatment
admit for rigorous supportive care. respiratory support. for infant type A and B can get antitoxin. for adult and non AB, horse sourced antotoxin. can get serum sickness from antitoxin. induce vomiting / gastric lavage. enema. for wound also give IV penicillin
c. botulinum long term treatment
full recovery in 1-12 months. physical and occupational therapy. psych consult and pastoral care for depression.
what toxin is used in facial botox?
toxin A. small amounts!!!
c. perfringens bacteriology
gas gangrene = myonecrosis = necrotizing faciitis. gram + spore forming rod. anaerobic environment required for replication and exotoxin production, relatively aerotolerant during host jumps
c. perfringens pathogenesis
spores from soil or vegetative cells from GI enter wounds. necrotic tissue, foreign bodies, premature closure disrupt bloodflow and enhance germination. vegetative cells grow in deep tissue, especially muscle. produce >20 exotoxins. alpha toxin: lecithinase, necrotizing, hemolytic, cardiotoxic. degradative enzymes make gas in tissue. can lead to anemia and kidney failure.
c. perfringens exam
pain, edema, and cellulitis at recent wound or surgical site. skin turns bronze then blue/black. site tender. short incubation but can be weeks. tachycardia. acute respiratory distress. shock, renal failure.
c. perfringens radiology
feathering of gas in soft tissue. CT scan help in abdominal cases. ultrasound can see gas.
myonecrosis
surgical exploration needed.
c. perfringens lab
smears from tissue and exudate show large gram + rods. hemolytic anemia, increased lactate dehydrog, toxic shock. metabolic acidosis and renal failure. ELISA for alpha toxin and PCR for clostridial DNA. anaerobic culture can retroactively identify species.
c. perfringens treatment and prevention
penicillin G + clindamycin. protein synth inhibitors shut down exotoxin production. additional antibiotics may be needed. ICU admit often needed. clean and debride wounds to prevent
c. perfringens type A food poisoning
soil borne spores contaminate food. inadequate cooking doesnt kill. large numbers grow in reheated food. multiply in smal bowel. CPE enterotoxin of type A strains destroys tight junctions and causes diarrhea and ab pain.
c. difficile bacteriology
gram + spore forming rod. causes pseudomembranous colitis = C. difficile associated diarrhea = antibiotic associated colitis = c. diff colitis. transmission: normal flora in 30% of hospitalized. fecal-oral.
c. diff pathogenesis
recent antibiotics or chemo allow c. diff to overgrow. release exotoxin A, disrupting tight junctions. exotoxin B is major toxin, disrupts cytoskeleton by depolymerizing actin and killing surrounding cells.
c. diff exam
nonbloody cramping diarrhea. green and smelly. fever, history of chemo or immunosuppressant/antibiotics. sigmoidoscopy shows patches of dead and dying cells as yellow/white plaques. focal necrosis of glandular crypts with neutrophilic infiltration and fibrin plugging of capillaries. can lead to abscesses
c. diff lab
WBC and creatinine elevated. can be cultured from stool but is slow. ELISA for toxins A and B. not sensitive. cytotoxicty test. sensitive but slow (untreated stool filtrate kill human cells in culture). neutrophils in stool
c. diff treatment
withdraw intitial antibiotic. replace fluids. give oral metronidazole or vancomycin. let toxins flush. surgical resection or removal of colon possible. fecal bacteriotherapy may prove effective
actinomyces bacteriology
gram + folamentous rods. non spore forming. anaerobic to microaerophilic. normal flora of mouth and vag. cells form long branching filaments. polymicrobial infections. rare.
actinomyces pathogenesis
bacteria escape proper compartment during accidental or surgical trauma. grow in hard filamentous nodules. slow and invasive growth. non-communicable
actinomyces exam
head/neck: hard nontender swelling in neck/face/chest. untreated leads to more spots. pus draining through sinuses with hard yellow sulfur granules. history of dental work or bad teeth
abodmen: slow growing tumor. nonspecific abdominal symptoms. usually need surgery to rule out cancer. 8yrs + of IUD or bowel surgery
actinomyces lab
biopsy or pus sample contains branching gram + rods with sulfur granules. can be cultured but takes 3 weeks to grow. IF testing available. PCR in pipeline
actinomyces treatment
long course of penicillin G may suffice. surgical draining of nodule may be needed
