Gram Positive Bacteria Answers – Flashcards
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Unlock answerssingle greatest biological warfare threat |
bacillus anthracis |
bacillus anthracis characteristics and identifying features |
gram+ rods non-motile nonfastidious non-hemolytic
spore-forming (resistant to heat, UV, gamma-radiation, & disinfectants; may be dormant for decades; "medusa head" on agar surf) |
bacillus anthracis epidemiology |
commonly infects grazing herbivores more serious w/o animal vaccination human-->human transmission: RARE human infection (US): RARE |
bacillus anthracis virulence factors |
2 large plasmids account for ALL virulence: 1. pXO1: toxin proteins (PA; LF; EF) combine to form binary exotoxins = lethal toxin/LeTx (PA+LF); edema toxin/EdTx (PA+EF) *individually, toxin proteins harmless 2. pXO2: genes encode protein for capsule syn *unique capsule: polyglutamate (antiphag) |
entry/action of anthrax toxin: PA binds anthrax receptor --> processed by furin on cell surf |
--> PA oligomerizes => EF/LF binding sites --> toxins endocytosed --> PA conform chg w/ pH chg --> toxins in cytosol
EF (adenylate cyclase): releases cAMP LF (protease): degrades MAPKK |
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cutaneous anthrax common affected areas: head, neck, & extrem description: nondescript 1* lesion (painless papule, no pus) progression: w/in 2-3d vesicles --> central necrosis & drying => eschar (usually surrounded by eroded areas/edema- may be self-limiting) left untx: bacteremic/fatal |
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inhalational anthrax (woolsorter's disease) initial symptoms: flu-like (fever, cough, myalgia, malaise) characteristic: widened mediastinum (this is where the org is prolif ; prod toxins) progression: 1-3d fulminant course (dyspnea, strident cough, chills, usually fatal) associated: gastrointestinal ; leptomeningeal lesions ;= hematogenous spread |
intestinal anthrax |
cause: eating anthrax-infected meat fatality: 25-60% symptoms: severe GI difficulty, vomiting blood, diarrhea, acute inflamm (Bacillus anthracis) ; |
anthrax hemorrhagic meningitis |
fatality: 100% symptoms: lots of edema, blood CSF (w/ gram+) "Cardinal's cap" appearance (lots of hemorrhage of leptomeninges) spreads: to CNS from any kind of anthrax infection |
identify cutaneous anthrax specimens |
vesicular stage: vesicular fluid eschar stage: eschar material |
identify gastrointestinal anthrax in these specimen: |
blood, stool, rectal swab |
identify inhalational anthrax in these specimen: |
blood ; sputum |
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id bacillus anthracis on sheep blood agar non-motile non-hemolytic irregularly round medusa head colony (comma shaped projection) PLET for isolation bicarbonate agar =; capsule formation |
identifying features of Bacillus cereus |
beta hemolytic on sheep blood agar string of pearls test- motile glutamyl-polypeptide capsule- |
Bacillus cereus virulence factors (2 toxins) |
heat-labile (diarrheal): stim adenylate cyclase (=; cAMP); SLOW onset heat-stable (emetic): RAPID onset |
ALL gram+ anaerobic spore formers |
Clostridium part of normal colonic flora most abundant: C. ranosum, then C. perfringes most pathogenic: C. perfringes |
Clostridium perfringes epidemiology |
most predominant (spores/vegetative bacteria): serotype A in human fecal flora ; in soil (most virulent) growth time: very fast (3xs faster than E. coli) infections endo/exogenous ; |
pathogenesis of C. perfringes |
growth requirements: ~14 AAs ; 6 other factors (most body fluids are deficient of these materials EXCEPT necrotic tissues) *produces ~12 toxins ;(alpha toxin=gas gangrene) |
types of diseases caused by C. perfringes |
1. soft tissue infections: cellulitis, suppurrative myositis, myonecrosis (gas gangrene) 2. gastroenteritis: food poisoning, necrotizing enteritis |
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clostridial cellulitis doesn't involve muscle/deeper tissue anaerobic less aggressive than gas gangrene after surgery/trauma (dmg to arteries reduces 02 supply) |
suppurative myositis |
suppuration in muscle planes w/o necrosis or systemic symptoms |
gas gangrene=clostridial myonecrosis what does the "gas" come from? |
organism replication (there will be crepitus present) extensive hemolysis bacteria present inflammatory cells absent symptoms: shock, renal failure, death w/in 2d |
tx of clostridial myonecrosis |
surgical debridement & frequently amputation |
2nd or 3rd most common cause of food poisoning in the US |
Clostridium perfringes, usually type A induces Ca++ dependent alteration in permeability symptoms: epigastric pain, nausea, cramps, watery diarrhea |
other gastroenteritis caused by C. perfringes (other than food poisoning) |
necrotizing enteritis (enteritis necroticans, pig-bel) cause: strains prod beta toxin occurs w/: high protein/trypsin inhibitor (sweet potato) incr risk: decr intestinal proteases symptoms: peritonitis, abdom px, vomiting, bloody diarrhea, shock fatality: 50% |
septicemia from Clostridium perfringes |
bacteremia: in pts w/ myonecrosis & necrotizing enteritis |
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Clostridium perfringes non-motile, box-car shaped gram+ rod *rod presence w/o leukocytes in specimen nagler rxn+ (anti-alpha-toxin added to egg yolk agar cultures (on upper half)- prevents visible opacity <= lecithinase action of alpha toxin) |
Clostridium tetani characteristics & epidemiology |
motile, spore forming, gram+ rod, anaerobe common in soil most cases (developing countries): newborns |
2 potent toxins of C. tetani |
1. chromosomally encoded 02 labile hemolysin (tetanolysin): unclear role 2. plasmid encoded 02 labile neurotoxin (tetanospasmin-tetanus toxin): stationary phase, blocks release of inhibitory neurotrans |
C. tetani virulence factors |
common entry to body: implanting spores in wounds under anaerobic conditions: spores germinate --> produce toxins --> retrograde mvmt w/in CNS char sympt: convulsive muscle contraction (lockjaw, back muscles) cause of death: cardiac/respiratory complic |
generalized tetanus |
C. tetani most common masseter muscles (trismus, lockjaw); risus sardonicans early signs: drooling, irritability, back spasm (opisthotonus) |
localized tetanus |
clostridium tetani confined to musculature of 1* site of infection |
cephalic tetanus |
Clostridium tetani head is the 1* site of infection poor prognosis |
neonatal tetanus |
tetanus neonatorum clostridium tetani common 1* infection site: umbilical stump (dirty tools to sever cord) symptoms: excessive crying, trismus, tetanic spasms, opisthotonus fatality: >90% (survivors have developmental defects) |
name the 4 types of C. botulinum diseases (all paralytic diseases) |
1. foodborne botulism 2. infant botulism 3. wound botulism 4. inhalational botulism |
foodborne botulism |
C. botulinum characteristic: symmetric descending paralysis *flaccid paralysis initially: blurred vision, constipation, abd px, no fever |
bioterrorism concern |
inhalational botulism caused by Clostridium botulinum <= toxin can be aerosolized |
Clostridium difficile epidemiology |
spores high conc in hospitals & LTCF (high antibiotic use) risk of infection correl. to length of stay
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virulence of C. difficile |
spores survive gastric acidity (germinate in LGT) 2 toxins: enterotoxin A & cytotoxin B (disrupt epithel cell barrier) *pseudomembranes seen on colon endoscopy |
steps to C. difficile colitis: |
1. exposure to antibiotics 2. exposure to C. difficile capable of producing toxins 3. inadequate immune response (antibodies to toxin A-protective) |
2 most likely causes of colitis: |
1. Clostridium difficile 2. Staphylococcus aureus |