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ID Week 5 > ICL 2.18: E. Coli > Flashcards

ICL 2.18: E. Coli Flashcards

1
Q

what is the microbiology of Escherichia?

A

gram (-) rod

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2
Q

what is the microbiology of Klebsiella?

A

gram (-) rod

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3
Q

what is the microbiology of proteus?

A

gram (-) rod

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4
Q

what is the microbiology of yersinia?

A

gram (-) rod

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5
Q

what is the reservoir and diseases associated with escherichia?

A

reservoir = ileum and colon of vertebrates

diseases = *UTI, *septicemia, *neonatal meningitis, diarrhea

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6
Q

what is the reservoir and diseases associated with proteus?

A

reservoir = colon of vertebrates, water, soil

diseases = *UTI, septicemia, pneumonia

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7
Q

what is the reservoir and diseases associated with Klebsiella?

A

reservoir = colon of vertebrates, water, sewage

diseases = Pneumonia, septicemia, opportunistic infections in immunocompromised patients

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8
Q

what is the reservoir and diseases associated with yersinia?

A

reservoir = rodents, pigs, water

diseases = *plague, bloody diarrhea, diarrhea, pseudoappendicitis, mesenteric adenitis syndrome

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9
Q

which bacteria are in the enterobacteriaceae family that are no in the GI tract?

A
  1. K1EC
  2. UPEC
  3. Proteus
  4. Klebsiella
  5. Yersinia pestis
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10
Q

what’s are antigens associated with enterobacteriaceae?

A
  1. LPS
  2. O antigen
  3. K antigen
  4. H antigen
  5. pili/fimbriae

the major antigens are used to type via serology –> O antigen: E. coli O157:H7

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11
Q

what is the function of LPS in enterobacteriaceae?

A

LPS binds to TLR4 on host cells which induces cytokines like TNF-alpha

TNF-alpha causes inflammation, fever, DIC, shock

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12
Q

what is the function of O antigen in enterobacteriaceae?

A

it’s part of LPS

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13
Q

what is the function of K antigen in enterobacteriaceae?

A

it’s the capsule!!

it blocks Ab and complement binding (serum resistance)

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14
Q

what is the function of H antigen in enterobacteriaceae?

A

it’s the flagella!!

provides motility

except Klebsiella and Yersinia

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15
Q

what is enterobacteriaceae phase variation?

A

the bacteria can change what is expressed under certain conditions

aka it can turn off/on virulence factors

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16
Q

what can enterobacteriaceae ferment?

A

glucose

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17
Q

are enterobacteriaceae anaerobic or aerobic?

A

aerobic but can be facultative anaerobic

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18
Q

what disease does e. coli K1 most often cause?

A

neonatal meningitis

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19
Q

which pathogen is causing this?

CJ is a 3-day-old baby boy born at term (40 weeks gestation)

Brought to ER for a fever of 101∘F and irritability

Mother states that all symptoms started 6-8 h prior to arrival @ ER

He has not been feeding well since.

The pregnancy was uneventful; delivery was vaginal without prolonged rupture of membranes.

However, she had a fever during labor, for which she was given antibiotics.

On examination, CJ had a full anterior fontanelle and increased tone in all four extremities

WBC: 19,000/µL

Differential: 60% neutrophils, 20% bands, 20% lymphocytes.

CSF: 1500 WBC /µL with 85% PMNs

Gram stain of CSF: showed Gram negative rods

A

E. coli K1

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20
Q

when are E. coli K1 infections most common?

A

E. coli K1 causes neonatal bacterial meningitis

it’s more common in the first month than at any other time of life

it’s rare but occurs in 15% of neonates with bacteremia

mortality has dropped a lot however survivors are still at high risk for neurologic sequelae and lifelong impairment as a result of infectious insult to developing brain

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21
Q

what are the risk factors that could cause neonatal bacterial meningitis?

A
  1. Low birth weight
  2. Pre-term birth
  3. Premature membrane rupture
  4. Traumatic delivery –> sepsis
  5. Fetal hypoxia
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22
Q

what are the common clinical signs of neonatal bacterial meningitis?

A
  1. Temperature instability (fever or hypothermia)
  2. Irritability or lethargy
  3. Poor feeding or vomiting
  4. Findings of a full, but not bulging, fontanelle
  5. normal neck flexion are common at
    initial presentation
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23
Q

which two pathogens are common causes of neonatal meningitis?

A
  1. E. coli K1 = early onset (3-7 days)

2. Group B Strep = late onset

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24
Q

what are the steps that happen during E. coli infection?

A

(1) Mucosal colonization in nose/mouth
(2) Invasion of bloodstream
(3) Survival and multiplication causing high-level bacteremia
(4) Crossing the blood–brain barrier
(5) Invasion of the meninges and the central nervous system.

(6-9) lead to neuronal injury (10)

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25
Q

how does E. coli K1 get across the BBB?

A

it needs a high degree of bacteremia

then E. coli binds to and invades the brain micro-vascular epithelial cells through ligand-receptor interactions

then there’s host cytoskeletal rearragnements and activation of different signalling pathways

E. coli invades the cells but doesn’t grow intracellularly

this is transcellular traversal!

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26
Q

what is the E. coli K1 trojan horse mechanism?

A

E. coli binds to and invades macrophages in order to cross the blood brain barrier

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27
Q

what is the capsule of E. coli K1 made of?

A

poly-sialic acid

this helps it evade the immune system because it mimics our systems sialic acid = molecular mimicry*

it also binds factor H which blocks alternative complement pathway –> when factor H is bound to a cell it tells the immune system not to kill it!

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28
Q

how do you diagnose an E. coli K1 infection?

A
  • bacterial isolation from the CSF by culture and/or visualization by Gram stain
  • increased CSF WBCs (typically >1000/µL) with a predominance of neutrophils
  • elevated CSF protein (>150 mg/dL in preterm and >100 mg/dL in term infants)
  • decreased CSF glucose (<20 mg/dL [1.1 mmol/L] in preterm and <30 mg/dL [1.7 mmol/L] in term infants)
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29
Q

what CBC lab results will you see with an E. coli K1 infection?

A

WBC: 19,000/µL

differential: 60% neutrophils, 20% bands, 20% lymphocytes.

CSF: 1500 WBC /µL with 85% PMNs

gram stain of CSF: showed Gram negative rods

culture of CSF: grew E. coli. The E. coli was resistant only to ampicillin.

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30
Q

how do you treat E. coli K1 infection?

A

if you see gram (-) rods in CSF, consider E. coli, pseudomonas aeruginosa, and K. pneumoniae

you can then treat with:

  1. ampicillin (if it’s not resistant)
  2. cefotaxime = broad spectrum cephalosporin
  3. gentamicin = aminoglycoside
31
Q

which two bacteria cause UTIs?

A
  1. UPEC = uropathogenic E. coli

2. proteus mirabilis

32
Q

are men or women more susceptible to UTIs?

A

women

they have a shorter urethra and urethra is closer to anus

33
Q

what are the two types of UTIs that can be caused by UPEC?

A
  1. cystitis (95%)

2. pyelonephritis (5%)

34
Q

what is cystisis?

A

a type of UTI caused by UPEC

it’s an uncomplicated bladder infection that causes a burning sensation, frequent micturation, incomplete voiding, suprapubic pain

is commonly caused by recent sexual intercourse; this is why you’re supposed to pee after sex!

35
Q

what is pyelonephritis?

A

a type of UTI caused by UPEC

leads to kidney infections!!! so more severe than cystitis

symptoms include chills.. high fever, nausea, arthralgia/myalgia, flank pain

untreated, it can lead to renal failure, bacteremia, septic shock

36
Q

which pathogen is responsible for most community-acquired UTIs?

A

uropathogenic E. coli = UPEC

the other enterobacteriaceae like *staphylococcus, enterobacter, proteus and klebsiella can also cause UTIs but not as common

37
Q

how does UPEC bind to cells?

A

several adhesins bind to surface facet cells of bladder, upper urinary tract and prevent bacteria being voided with urine

these adhesins include:

  1. type 1 pili
  2. pyelonephritis-associated pili
  3. Dr/AFA pili
38
Q

which cells does UPEC infect?

A

they invade the superficial facet cells in the bladder –> you’ll see gram (-) rods inside the cells

there, they can cause apoptosis and exfoliation, exposing lower layers

the bacteria can also remain dormant inside intracellular vesicles and reactivation can launch recurrent episodes of cystitis

39
Q

what are the virulence factors associated with UPEC?

A
  1. siderophores –> for acquiring Fe
  2. secreted toxins like alpha-hemolysin

these toxins alter host cell signaling cascades, modulate inflammatory responses and trigger apoptosis

40
Q

what are the steps in the acute infection cycle of UPEC?

A
  1. attachment
  2. intracellular biofilm community formation
  3. IBC maturation
  4. exfoliation
  5. quiescent reservoir or start back at attachment
41
Q

is proteus mirabilis motile?

A

yes

hyperflaggelated so they zoom around super quickly (you watched the video of them moving around)

they literally look like swarms on agar surface (ripples)

42
Q

what role does urease play in proteus mirabilis?

A

proteus mirabilis has urease which breaks down urea into calcium phosphate and uric acid

this unfortunately can lead to lots of kidney stones!!!

43
Q

how do you diagnose a UTI from either UPEC or proteus mirabilis?

A
  1. urine dip sticks –> detect nitrite and leukocyte esterase
  2. immersion culture media –> plastic rod coated with 2 culture mediate incubated for 24 hours
44
Q

how do you treat a UTI from either UPEC or proteus mirabilis?

A

normally B-lactams like amoxicillin or cephalosporins are used but resistance is increasing

you could also use Bactrim (trimethoprim-sulfamethoxazole) but the resistance to this is also increasing

or you could use fluoroquinolone like ciprofloxacin or levofloxacin

if it’s a serious or complicated infection, aminoglcosides can be used but their toxicity profiles are concerning and they have to be given parenterally –> they achieve high renal and urine levels which is good to kill the bacteria

45
Q

where is Klebsiella pneumoniae found in nature?

A

relatively ubiquitous in environment

found in water, soil, contaminated food, and intestinal flora

46
Q

which diseases is K. pneumoniae associated with?

A

so the K1 serotype (capsule) is particularly pathogenic

it can cause:

  1. pneumonias –> particularly in alcoholics
  2. UTIs
  3. biliary tract infection –> now leading cause of liver abscesses in US
  4. wounds –>including rare necrotizing fasciitis
  5. ocular neurological problems
47
Q

which disease is Klebsiella granulomatis associated with?

A

it can cause an STD that causes granuloma inguinale = that lesion looking thing by the testicles

surpisingly though, the lesions are painless!

this is endemic in tropical areas

48
Q

what are the virulence factors associated with Klebsiella pneumoniae?

A
  1. capsule = major virulence determinant
  2. LPS
  3. adhesins
  4. siderophores
49
Q

what is the function of the K. pneumoniae capsule?

A

it’s an acidic polysaccharide capsule that’s very thick

it’s antiphagocytic and inhibits activation of C3b

50
Q

what is the function of the K. pneumoniae LPS?

A

causes sepsis

it also helps with immunological masking by blocking C1q and C3b binding

51
Q

what are the symptoms of a Klebsiella pneumoniae infection?

A

primarily pneumonia symptoms such as:

  1. fever
  2. elevated respiration rate
  3. elevated WBCs
  4. elevated PMNs (neutrophils 72%)
  5. decreased p02 (68 mmHg)
  6. CXR shows patchy infiltrate from bronchiole inflammation; sometimes there’s even cavities due to necrosis from the abscess
52
Q

what is the hallmark buzzword associated with klebsiella pneumoniae?

A

blood-tinged, thick sputum = “currant jelly”

53
Q

what’s the microbiology of klebsiella pneumoniae? how do you grow it?

A

short gram (-) rods

nonmotile

lactose fermenting

urease (+)

54
Q

what do you see when you grow klebsiella pneumoniae?

A

mucoid colonies

you’ll literally get like a white string sticking to the stick if you touch an agar that’s growing K. pneumoniae

55
Q

how do you diagnose k. pneumoniae?

A
  1. symptoms
  2. positive CXR
  3. positive blood and sputum cultures
56
Q

how do you treat K. pneumoniae?

A
  1. extended spectrum B-lactams = piperacillin or ticarcillin
  2. newer cephalosporins combined with aminoglycosides

ultimately though, antibiotic choice depends on resistance pattern

however, there’s a high mortality rate even with proper therapy

57
Q

which pathogen is responsible for the black plague?

A

yersinia pestis

it literally killed 1/3 of europes population in the 1300s

58
Q

what are the two diseases that yersinia pestis causes?

A
  1. bubonic plague (not as bad)
  2. pneumonic plague (you’re screwed)

both transmitted via the oriental rat flea to humans

59
Q

what are the steps in the transmission of the bubonic plague?

A
  1. flea drinks rat blood that carries yersinia pestis
  2. bacteria multiply in the flea’s gut
  3. gut becomes clogged with bacteria
  4. flea bites human and regurgitates blood into open wound
  5. human is infected
60
Q

where are yersinia pestis infections common in the US? the world?

A

4 corners

and out west in general

however in the world in general, we’re worried about Madegascar

61
Q

what are the symptoms of yersinia pestis infection?

A
  1. buboes = swollen, painful lymph nodes
  2. necrosis secondary to DIC

so because of the DIC, circulation gets cut off to the extremities and you literally get black fingers and toes and that’s how it got its name as the black plague

62
Q

what do the virulence factors of yersinia pestis do?

A

yersinia outer proteins (Yops):

  1. block phagocytosis
  2. block platelet activation
63
Q

which cells does yersinia pestis infect?

A

yersinia pestis binds to APCs like langerhans and alveolar mecrophages

they do this by LPS binding to DC-SIGN/CD209 receptor

this results in delivery of the bacteria to CD4+ lymphocytes in nodes

64
Q

how does LPS in yersinia pestis help with immune invasion?

A

the LPS switching from 6 to 4 carbon chain

when it does this, the 4 chain LPS is no longer recognized by TLR4!

this is how it evades the immune response

65
Q

how does a yersinia pestis infection progress?

A

so for the first 36 hours, there’s no immune response! no inflammation or proinflammator cytokines are released because of the LPS switching that inhibits TLR4

however, after the first 36 hours our immune system somehow figures things out and there’s a very robust inflammatory response

66
Q

how do you diagnose yersinia pestis infection?

A
  1. Y. pestis (unlike other Yersiniae) is NON-motile at all temperatures
  2. Wright’s stain preferentially stains granules at the ends of the bacteria (resembling a closed safety pin)
  3. fluorescent antibody (DFA) assay for F1 glycoprotein of capsule –> this is the key test now*
  4. PCR
67
Q

how do you treat yersinia pestis infections?

A

DOC for all forms is streptomycin

however this drug is hard to get in the US because it has significant toxicity

instead, gentamicin, doxycycline, chloramphenicol are used

68
Q

what is used for yersinia pestis prophylaxis?

A

doxycyline

69
Q

FLASHCARD: E. coli K1

A

one of leading causes of neonatal meningitis; pre-term birth is risk factor

temp instability, irratability or lethargy, full fontanelle; often in first 3-7 days

K1 polysialic acid capsule is major virulence factor; molecular mimicry

treat with ampicillin or cephalosporins and aminoglycosides

70
Q

FLASHCARD: UPEC

A

uropathogenic E. coli

major cause of community-acquired UTIs

uses adhesins (pili) to attach to and invade facet cells

71
Q

FLASHCARD: proteus mirabilis

A

another cause of UTIs

swarming motility (hyperflaggelated) and urease –> kidney stone formation

check susceptibility; treat UTI with β-lactams, trimethoprim-sulfamethoxazole, or fluoroquinolone

72
Q

FLASHCARD; Klebsiella pneumoniae

A

can cause serious pneumonia in older alcoholics; ‘currant jelly’ sputum

no flagella; major virulence factor is its thick K1 capsule

check antibiotic resistance; cephalosporins + aminoglycosides

73
Q

FLASHCARD: yersinia pestis

A

plague; killed 1/3 of Europe in 1300s

major virulence factors include tetra-acylated lipid A, protein capsule, and type III secretion system (TTSS) with Yops

no flagella

wright stain = resembles a safety pin

direct fluorescent antibody

streptomycin (gent, doxy, chlor) treatment early

ID Week 5 (13 decks)

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