Gram Positive Bacteria Answers – Flashcards

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single greatest biological warfare threat
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bacillus anthracis
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bacillus anthracis characteristics and identifying features
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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)

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bacillus anthracis epidemiology
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commonly infects grazing herbivores

more serious w/o animal vaccination

human-->human transmission: RARE

human infection (US): RARE

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bacillus anthracis virulence factors
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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)

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entry/action of anthrax toxin: PA binds anthrax receptor --> processed by furin on cell surf
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--> 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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[image]
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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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[image]
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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

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intestinal anthrax
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cause: eating anthrax-infected meat

fatality: 25-60%

symptoms: severe GI difficulty, vomiting blood, diarrhea, acute inflamm

(Bacillus anthracis)

;

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anthrax hemorrhagic meningitis
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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

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identify cutaneous anthrax specimens
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vesicular stage: vesicular fluid

eschar stage: eschar material

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identify gastrointestinal anthrax in these specimen:
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blood, stool, rectal swab
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identify inhalational anthrax in these specimen:
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blood ; sputum
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[image]
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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

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identifying features of Bacillus cereus
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beta hemolytic on sheep blood agar

string of pearls test-

motile

glutamyl-polypeptide capsule-

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Bacillus cereus virulence factors (2 toxins)
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heat-labile (diarrheal): stim adenylate cyclase (=; cAMP); SLOW onset

heat-stable (emetic): RAPID onset

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ALL gram+ anaerobic spore formers
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Clostridium

part of normal colonic flora

most abundant: C. ranosum, then C. perfringes

most pathogenic: C. perfringes

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Clostridium perfringes epidemiology
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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

;

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pathogenesis of C. perfringes
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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)

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types of diseases caused by C. perfringes
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1. soft tissue infections: cellulitis, suppurrative myositis, myonecrosis (gas gangrene)

2. gastroenteritis: food poisoning, necrotizing enteritis

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[image]
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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)

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suppurative myositis
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suppuration in muscle planes w/o necrosis or systemic symptoms
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gas gangrene=clostridial myonecrosis

what does the "gas" come from?

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organism replication (there will be crepitus present)

extensive hemolysis

bacteria present

inflammatory cells absent

symptoms: shock, renal failure, death w/in 2d

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tx of clostridial myonecrosis
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surgical debridement & frequently amputation
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2nd or 3rd most common cause of food poisoning in the US
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Clostridium perfringes, usually type A

induces Ca++ dependent alteration in permeability

symptoms: epigastric pain, nausea, cramps, watery diarrhea

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other gastroenteritis caused by C. perfringes (other than food poisoning)
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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%

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septicemia from Clostridium perfringes
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bacteremia: in pts w/ myonecrosis & necrotizing enteritis
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[image]
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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)

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Clostridium tetani characteristics & epidemiology
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motile, spore forming, gram+ rod, anaerobe

common in soil

most cases (developing countries): newborns

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2 potent toxins of C. tetani
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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

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C. tetani virulence factors
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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

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generalized tetanus
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C. tetani

most common

masseter muscles (trismus, lockjaw); risus sardonicans

early signs: drooling, irritability, back spasm (opisthotonus)

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localized tetanus
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clostridium tetani

confined to musculature of 1* site of infection

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cephalic tetanus
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Clostridium tetani

head is the 1* site of infection

poor prognosis

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neonatal tetanus
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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)

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name the 4 types of C. botulinum diseases (all paralytic diseases)
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1. foodborne botulism 

2. infant botulism

3. wound botulism

4. inhalational botulism

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foodborne botulism
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C. botulinum

characteristic: symmetric descending paralysis

*flaccid paralysis

initially: blurred vision, constipation, abd px, no fever

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bioterrorism concern
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inhalational botulism caused by Clostridium botulinum <= toxin can be aerosolized 
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Clostridium difficile epidemiology
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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
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spores survive gastric acidity (germinate in LGT)

2 toxins: enterotoxin A & cytotoxin B (disrupt epithel cell barrier)

*pseudomembranes seen on colon endoscopy

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steps to C. difficile colitis:
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1. exposure to antibiotics

2. exposure to C. difficile capable of producing toxins

3. inadequate immune response (antibodies to toxin A-protective)

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2 most likely causes of colitis:
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1. Clostridium difficile

2. Staphylococcus aureus

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