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USMLE Step I Microbiology > Other Gram + Bacteria > Flashcards

Other Gram + Bacteria Flashcards

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USMLE® Step 1 flashcards Biology 101 flashcards
1
Q

properties of Enterococci

A
  • gram + cocci
  • catalase -
  • PYR +
  • variable hemolysis
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2
Q

Entercocci (E. faecalis and E. faecium):

where are they normal?

what are they resistant to?

what do they cause?

A
  • normal colonic flora
  • penicillin G resistant
  • cause:
    • UTI
    • biliary tract infections
    • subacute endocarditis (following GI/GU procedures)
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3
Q

what do vancomycin resistant enterococci (VRE) cause?

A
  • cause nosocomial infection
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4
Q

enterococci vs. nonenterococcal group D

A

enterococci are hardier than non enterococci group D

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5
Q

what do you grow enterococci in in the lab?

A
  • 6.5% NaCl and bile
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6
Q

properties of Bacillus anthracis

A
  • gram +
  • spore forming rod that produces anthrax toxin
  • ONLY bacterium with a polypeptide capsule (contains D-glutamate)
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7
Q

cutaneous anthrax

A
  • painless papule surrounded by vesicles –> ulcer with black eschar (painless, necrotic) –> uncommonly progresses to bacteremia and death
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8
Q

pulmonary anthrax

A
  • inhalation of spores –> flu like symptoms that rapidly progress to fever, pulmonary hemorrhage, mediastinitis, and shock
  • also known as woolsorter’s disease
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9
Q

properties of Bacillus cereus

A
  • gram + rod
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10
Q

what does Bacillus cereus cause?

A
  • food poisoning
  • “Reheated rice syndrome”
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11
Q

Bacillus cereus and Reheated Rice Syndrome

A
  • spores survive cooking rice
    • keeping rice warm results in germination of spores and enterotoxin formation
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12
Q

Bacillus cereus emetic type

A
  • usually seen with rice and pasta
  • nausea and vomiting within 1-5 hours
  • caused by cereulide–a preformed toxin
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13
Q

Bacillus cereus diarrheal type

A
  • causes watery, nonbloody diarrhea and GI pain within 8-18 hours
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14
Q

properties of Clostridia (with exotoxins)

A
  • gram +
  • spore forming
  • oligate anaerobic rods
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15
Q

C. tetani–toxin and mechanism

A
  • toxin: tetanospasmin–an exotoxin causing tetanus
  • tetanus toxin (and botulinum toxin) are proteases that cleave SNARE proteins for neurotransmitters
    • blocks release of inhibitor neurotransmitters, GABA and glycine, from Renshaw cells in the spinal cord
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16
Q

C. tetani–effects

A
  • tetanospasmin causes
    • spastic paralysis
      • “tetanus is tetanic paralysis”
    • trismus (lockjaw)
    • risus sardonicus–raised eyebrows and open grin
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17
Q

C. tetani:

how to prevent?

how to treat?

A
  • prevention:
    • tetanus vaccine
  • treatment:
    • antitoxin +/- vaccine booster
    • diazepam–for muscle spasms
    • wound debridement
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18
Q

C. botulinum–toxin and mechanism

A
  • toxin: heat labile toxin–botulinum toxin
  • mechanism:
    • inhibits ACh release at the neuromuscular junction, causing botulism
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19
Q

C. botulinum:

in adults?

in babies?

A
  • adults:
    • disease is caused by ingestion of preformed toxin
  • babies:
    • ingestion of spores (ie. in honey) leads to disease
      • Floppy Baby Syndrome
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20
Q

C. botulinum–treatment

A
  • antitoxin
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21
Q

where does C. botulinum come from?

A
  • Botulinum is from bad bottles of food, juice, honey
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22
Q

C. botulinum–effects

A
  • flaccid paralysis
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23
Q

C. botulinum and botox

A
  • local botox injections used to treat foca ldystonia, achalasia, and muscle spasms
  • also used for cosmetic reduction of facial wrinkles
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24
Q

C. perfringens–toxin, effects

A
  • produce alpha toxin (lecithinase, a phospholipase)
    • spores can survive in undercooked food
      • so, when ingested, bacteria release heat labile enterotoxin –> food poisoning
  • can cause myonecrosis (gas gangrene) and hemolysis
    • “Perfringens perforates a gangrenous leg”
25
Q

C. difficile–diagnosis

A
  • diagnosis by detecting one or both toxins in stool by PCR
26
Q

C. difficile–toxin

A
  • 2 possible toxins
    • toxin A–enterotoxin
    • toxin B–cytotoxin
27
Q

C. difficile toxin A

A
  • enterotoxin
  • binds ot the brush border of the gut
28
Q

C. difficile toxin B

A
  • cytotoxin
  • causes cytoskeletal disruption via actin depolymerization –> diarrhea –> pseudomembranous colitis
29
Q

what is often the cause of C. difficile infection?

A
  • often the C. difficile infection is secondary to antibiotic use, especially clindamycin or ampicillin
  • associated with PPI use
30
Q

C. diffiicile–effects

A
  • diarrhea
    • “Difficile causes diarrhea”
31
Q

C. difficile–treatment

A
  • metronidazole or oral vancomycin
  • for recurrent cases, consider repeating prior regimen, fidazomicin, or fecal microbiota transplant
32
Q

properties and mechanism of Corynebacterium diphtheriae

A
  • gram + rod
    • “coryne = club shaped”
  • potent exotoxin inhibits protein synthesis via ADP ribosylation of EF-2
    • “ABCDEFG”
      • ADP ribosylation
      • Beta prophage
      • Corynebacterium
      • Diphtheriae
      • Elongation Factor 2
      • Granules
33
Q

what does Corynebacterium diphtheriae cause and how?

A
  • diphtheria via exotoxin encoded by beta prophage
34
Q

Corynebacterium diphtheriae infection–effects

A
  • pseudomembranous pharyngitis (grayish white membrane)
  • lymphadenopathy
  • myocarditis
  • arrhythmias
35
Q

Corynebacterium diphtheriae–diagnosis

A
  • lab diagnosis based on gram + rods with metachromatic (blue and red) granules and + Elek test for toxin
36
Q

how to prevent diphtheria?

A

toxoid vaccine

37
Q

what medium do you use to grow Corynebacterium diphtheriae? what do the colonies look like?

A
  • cystine tellurite agar
  • black colonies
38
Q

properties and mechanism of Listeria monocytogenes

A
  • gram +
  • facultative anaerobe rod
  • form “rocket tails” via actin polymerization that allow intracelllar movement and cell to cell spread across cell membranes, therby avoiding antibody
  • characteristic tumbling motility in broth
39
Q

how does one acquire a Listeria monocytogenes infection?

A
  • acquired by ingestion of unpasteurized dairy products and cold deli meats
  • via transplacental transmission
  • by vaginal transmission during birth
40
Q

what does Listeria monocytogenes cause?

A
  • amnionitis
  • septicemia
  • spontaneous abortion in pregnant women
  • granulomatosis infantiseptica
  • neonatal meningitis
  • meningitis in immunocompromised patients
  • mild, self-limited gastroenteritis in healthy individuals
41
Q

Listeria monocytogenes–treatment

A
  • ampicillin in infants, immunocompromised, and the elderly as empirical treatment of meningitis
42
Q

how are Nocardia and Actinomyces alike?

A
  • both are gram + and form long, branching filaments resembling fungi
    *
43
Q

Nocardia and Actinomyces–differences in their properties and mechanisms

A
  • Nocardia
    • aerobe
    • acid fast (weak)
    • found in soil
  • Actinomyces
    • anaerobe
    • not acid fast
    • normal oral, reproductive, and GI flora
44
Q

Nocardia and Actinomyces–differences in what they cause and treatments?

A
  • Nocardia
    • can cause:
      • pulmonary infections in immunocompromised (can mimic TB but with -PPD)
      • cutaneous infections after trauma in immunocompetent
    • treatment:
      • sulfonamides (TMP-SMX)
  • Actinomyces
    • can cause:
      • oral/facial abscesses that drain thru sinus tracts
      • forms yellow “sulfur granules”
      • can also cause PID with IUDs
    • treatment:
      • penicillin
  • “Treatment is a SNAP: Sulfonamides–Nocardia; A**ctinomyces–P**encillin”
45
Q

primary and secondary tuberculosis

A
  • PPD + if current infection or past exposure
  • PPD - if no infection and in sarcoidosis
  • Interferon gamma release assay (IGRA) has fewer false positives from BCG vaccination
  • causeating granulomas with central necrosis and Langerhans giant cells are characteristic of 2ndary tuberculosis
46
Q

name the types of Mycobacteria

A
  • Mycobacterium tuberculosis
  • M. avium–intracellulare
  • M. scrofulaceum
  • M. marinum
47
Q

what does M. tuberculosis cause?

A
  • TB
    • often resistant to multiple drugs
48
Q

what does M. avium–intracellulare cause?

what is the prophylaxis?

A
  • disseminated, non TB disease in AIDS
    • often resistant to multiple drugs
  • prophylaxis with azithromycin when CD4+ count < 50 cells/mm3
49
Q

what does M. scrofulaceum cause?

A
  • cervical lymphadenitis in children
50
Q

what does M. marinum cause?

A
  • hand infection in aquarium handlers
51
Q

tuberculosis–symptoms

A
  • fever
  • night sweats
  • weight loss
  • cough–nonproductive or productive
  • hemolysis
52
Q

cord factor and mycobacteria

A
  • cord factor creates a “serpentine cord” appearance in virulent M. tuberculosis strains
    • inhibits macrophage maturation
    • induces release of TNF alpha
  • sulfatides (surface glycolipids) inhibit phagolysosomal fusion
53
Q

properties of Mycobacteria

A
  • all are acid fast
    • pink rods at arrow tips
54
Q

what bacterium causes Leprosy (Hansen disease)?

A
  • Mycobacterium leprae
55
Q

properties of Mycobacterium leprae

A
  • acid fast bacillus that like cool temperatures
    • infects skin and superficial nerves–“glove and stocking” loss of sensation
  • cannot be grown in vitro
  • reservoid in the US: armadillos
56
Q

2 forms of Leprosy (Hansen disease)

A
  • lepromatous
  • tuberculoid
57
Q

explain lepramatous Hansen disease

A
  • presents diffusely over the skin, with leonine (lion-like) facies
  • is communicable
  • characterized by low cell mediated immunity with a humoral Th2 response
    • “Lepromatous form can be Lethal”
58
Q

explain tuberculoid Hansen disease

A
  • limited to a few hypoesthetic, hairless skin plaques
  • characterized by high cell mediated immunity with a largely Th1 type immune response
59
Q

what are the treatments for each form of Hansen disease?

A
  • tuberculoid form:
    • dapsone
    • rifampin
  • lepromatous form:
    • same as tuberculoid
    • BUT add clofazimine

USMLE Step I Microbiology (44 decks)

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