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Bacteriology (mine) > Gram Positive Rods > Flashcards

Gram Positive Rods Flashcards

1
Q

What are the virulence factors for B. Cereus?

A
  1. emetic enterotoxin (cerulide): vomiting, nausea, cramps in less than 6hrs (lasts for 8-10hrs)
  2. diarrheal enterotoxins: profuse watery diarrhea, nausea, cramps in aboout 8hrs and lasts about 24 hours
  3. hemolysin (cereolysin): punches holes in RBCs membranes -> zone of clearing; similiar to streptolysin in structure/function
  4. proteases and phospholipases (collagenase and serine protease): eye and skin infections allowing dissemination through tissue (associated with nonsterile gauze and alcohol pads)
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2
Q

What’s the pathogenesis of emetic enterotoxins of B cereus?

A

binds 5-hydroxytryptamine (5-HT) receptor and stimulates afferent vagus n. causing stomach to contract quickly and eject toxins

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3
Q

What’s an important characteristic of cerulide?

A

heat-STABLE and proteolytic resistant peptide

(this is why cooking/microwaving/heating does not kill toxin)

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4
Q

How does diarrheal enterotoxin work?

A

just like cholera toxin!

stimulates adenylate-cyclase-cAMP in intestinal epithelial cells causing it to secrete fluids (dysregulation of Cl- secretion causing increase Cl- followed by water)

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5
Q

What’s significant characteristic of diarrheal enterotoxins?

A

large, heat labile protein complex -> will get destroyed if reheat food

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6
Q

Define panophthalmitis.

A

really bad inflammation and infection with proteases chewing up retina as a result of B. cereus getting into vitreal cavity

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7
Q

What are the disseminated infections seen in B. cereus?

A

septicemia, endocarditis, meningitis, etc. seen in immunosuppressed, IV drug users, and patients with indwelling shunts

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8
Q

What’s unique about emetic gastroenteritis?

A

an intoxication (not infection): toxins cause disease so more like poisoning

(extreme overdose of toxin can cause liver failure)

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9
Q

Why do diarrheal gastroenteritis appear AFTER emetic?

A

toxins are NOT premade!

bacteria has to enter intestine before secrete toxin

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10
Q

What culture is NOT done for B. Cereus?

A

fecal! bc it’s part of normal flora

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11
Q

How can spore stains be used to ID B.cereus?

A

spores DON’T STAIN bc spore coat doesn’t pick up reagents (will see gram + rod w/ white, unstained portion inside)

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12
Q

What’s the treatment for B. Cereus?

A
  1. for gastroenteritis: treat symptoms (so rehydrate and replenish electrolytes); no antibiotics bc self-limiting
  2. others: vancomycin, clindamycin, gentamicin (aminoglycoside), or ciprofloxacin
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13
Q

What is B. cereus resistant to?

A

have chromosomally encoded beta lactamase so resistant to beta-lactams, penicillin, and cephalosporin

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14
Q

What is listeria monocytogenes resistant to?

A

aminoglycosides bc they’re intracellular pathogens

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15
Q

What are the virulence factors for listeria monocytogenes?

A
  1. internalin A: adhesion and invasion of eukaryocytic cells by binding E-cadhedrin to be taken into endocytic vacuoles
  2. listeriolysin O (LLO): punches holes into phospholipid layers (hemolysin similar to streptolysin and pneumolysin) allowing bacteria to escape to cytoplasm from vacuoles before lysosomal fusion
  3. other hemolysin (phospholipase C’s): acts synergistically with LLO; affecting signal transduction pathways (short-circuiting intercellular communication networks)
  4. actA: directs host cell actin to polymerize behind it and propel bacterium in cytoplasm (flagella for environment; actA rockets intracellularly)
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16
Q

Where can we find Listeria normally?

A

soil, water, intestinal tracts of animals and man

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17
Q

What is essential for effective immune response to Listeria?

A

cell-mediated! (bc its intracellular)

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18
Q

What’s seen first after Listeria infection?

A

symptoms appear several weeks after, first flu-like (fever, chills, muscle aches, malaise, etc) then GI issues

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19
Q

What’s seen in pregnant women infected by Listeria?

A

may have mild symptoms or none at all

BUT: bacteria cross placenta (pale placenta) to infect fetus resulting in neonatal disease (granulomatosis infantiseptica- fetus with granulomas all over) or fetal death/miscarriage

20
Q

What is seen in neonates and elderly infected with Listeria?

A

RAPID shift to septicemia or meningitis (stiff neck, headache, confusion, convulsions)

usu too late to treat and patient goes into septic shock -> HIGH MORTALITY RATE

21
Q

What virulence factors cause the beta-hemolysis seen in Listeria?

A

LLO and phospolipase C

22
Q

What should we culture to ID listeria?

A

blood and CSF

23
Q

How do we treat patients infected with Listeria?

A

ampicillin+gentamicin (synergism), amoxicillin (penicillin)

bactrim (sulgamethoxazole w/ trimethroprim)

24
Q

What’s Intralytix?

A

cocktail of phage approved to treat variety of processed meat to prevent listeria

25
Q

What’s the most important virulence factor for Corynebacterium diphtheria?

A

Diptheria Toxin (DTx): A subunit (catalytic) and B subunit (binding)

26
Q

How does the B subunit of Diptheria Toxin work?

A

helps the toxin translocate into cell bc it has translocation and receptor binding regions (for heparin binding epidermal growth factor [HB-EGF] on host)

27
Q

What’s the mecahnism of action of DTx?

A
  1. toxin binds receptor and endocytosed
  2. drop in pH in vesicle causing toxin conformational change allowing A subunit to pop off and enter cytoplasm
  3. in cytoplasm, A subunit catalyzes ADP-ribosylation of elongation factor-2
  4. leads to inactivation of protein shutting down protein synthesis -> CELL DEATH
28
Q

What’s significant about the DTx?

A

VERY POTENT: 1 molecule of A subunit is lethal for cell

29
Q

How is DTx regulated?

A
  1. encoded by lysogenic phage (omega or beta) so has to infect to be pathogenic
  2. toxin production is regulated by iron reponsive protein (DTxR) that’s encoded on bacteria’s chromosome-> low iron turns on toxin production
30
Q

What is the only sole reservoir for Corynebacterium diphtheria?

A

humans! (carried in oropharynx or skin of asymptomatic carriers of unvaccinated hosts)

31
Q

What is seen first after infection with Corynebacterium diphtheria?

A

after 2-6 days, tired, achy, sore throat with exudate -> pseudomembrane (bacteria, lymphocytes, plasma cells, fibrin, dead epithelial cells)

1 in 10 infected -> death

32
Q

What is the cutaneous presentation of Corynebacterium diphtheria?

A

chronic non-healin ulcer (RARE)

33
Q

What makes up the metachromatic granules?

A

phosphates: form of storage vesicle or inclusion body for bacteria

34
Q

What agar can be used to grow Corynebacterium diphtheria?

A

cysteine-potassium telluride agar (appears grey-black)

35
Q

What is this?

A

Listeria (short gram + rods)

36
Q

What is this?

A

C. Diptheria (note the club shaped pleiomorphic rods)

37
Q

What is this?

A

Nocardia on blood agar (note the orange waxy appearance)

38
Q

What is this?

A

Nocardia (note the filamentous rods)

39
Q

Describe the Elek Test.

A
  1. used to determine whether or not strain isolated from throat is making toxin
  2. based on Ag-Ab precipitation reaction (precipitation occurs when antitoxin sees toxin)
40
Q

What is the treatment of choice for C. Diptheria?

A

penicillin (1st) or erythromycin

antitoxin made in horses (used before antibiotics; beware of serum sickness)

41
Q

Is there a vaccine for C. diptheria?

A

toxoid vaccine (“D” of DPT vaccine): toxin that’s heat activated or treated with formalin so not active but still immunogenic

*boosters every 10 years

42
Q

What’s the Schick Test?

A

test immune status against DTx - similar to TB skin test

43
Q

What’s the virulence factor for Nocardia?

A

unknown but knows it grows in non-activated macrophages

44
Q

What’s unique about the pneumonia from nocardia?

A

opacity throughout entire lung field (others only consolidated in single lobe)

45
Q

Describe the brain abscesses from Norcadia spread.

A

well-circumscribed lesions

46
Q

What is collected for Nocardia culture?

A

sputum or abscess

47
Q

What’s the mode of treatment for nocardia?

A

sulfonamides or amikacin + beta lactam

severe cases: ceftriaxone or imipenem

Bacteriology (mine) (6 decks)

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