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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
how does E. coli K1 get across the BBB?
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!
26
what is the E. coli K1 trojan horse mechanism?
E. coli binds to and invades macrophages in order to cross the blood brain barrier
27
what is the capsule of E. coli K1 made of?
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!
28
how do you diagnose an E. coli K1 infection?
* 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)
29
what CBC lab results will you see with an E. coli K1 infection?
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.
30
how do you treat E. coli K1 infection?
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
which two bacteria cause UTIs?
1. UPEC = uropathogenic E. coli | 2. proteus mirabilis
32
are men or women more susceptible to UTIs?
women they have a shorter urethra and urethra is closer to anus
33
what are the two types of UTIs that can be caused by UPEC?
1. cystitis (95%) | 2. pyelonephritis (5%)
34
what is cystisis?
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
what is pyelonephritis?
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
which pathogen is responsible for most community-acquired UTIs?
uropathogenic E. coli = UPEC the other enterobacteriaceae like *staphylococcus, enterobacter, proteus and klebsiella can also cause UTIs but not as common
37
how does UPEC bind to cells?
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
which cells does UPEC infect?
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
what are the virulence factors associated with UPEC?
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
what are the steps in the acute infection cycle of UPEC?
1. attachment 2. intracellular biofilm community formation 3. IBC maturation 4. exfoliation 5. quiescent reservoir or start back at attachment
41
is proteus mirabilis motile?
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
what role does urease play in proteus mirabilis?
proteus mirabilis has urease which breaks down urea into calcium phosphate and uric acid this unfortunately can lead to lots of kidney stones!!!
43
how do you diagnose a UTI from either UPEC or proteus mirabilis?
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
how do you treat a UTI from either UPEC or proteus mirabilis?
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
where is Klebsiella pneumoniae found in nature?
relatively ubiquitous in environment found in water, soil, contaminated food, and intestinal flora
46
which diseases is K. pneumoniae associated with?
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
which disease is Klebsiella granulomatis associated with?
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
what are the virulence factors associated with Klebsiella pneumoniae?
1. capsule = major virulence determinant 2. LPS 3. adhesins 4. siderophores
49
what is the function of the K. pneumoniae capsule?
it's an acidic polysaccharide capsule that's very thick it's antiphagocytic and inhibits activation of C3b
50
what is the function of the K. pneumoniae LPS?
causes sepsis it also helps with immunological masking by blocking C1q and C3b binding
51
what are the symptoms of a Klebsiella pneumoniae infection?
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
what is the hallmark buzzword associated with klebsiella pneumoniae?
blood-tinged, thick sputum = "currant jelly"
53
what's the microbiology of klebsiella pneumoniae? how do you grow it?
short gram (-) rods nonmotile lactose fermenting urease (+)
54
what do you see when you grow klebsiella pneumoniae?
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
how do you diagnose k. pneumoniae?
1. symptoms 2. positive CXR 3. positive blood and sputum cultures
56
how do you treat K. pneumoniae?
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
which pathogen is responsible for the black plague?
yersinia pestis it literally killed 1/3 of europes population in the 1300s
58
what are the two diseases that yersinia pestis causes?
1. bubonic plague (not as bad) 2. pneumonic plague (you're screwed) both transmitted via the oriental rat flea to humans
59
what are the steps in the transmission of the bubonic plague?
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
where are yersinia pestis infections common in the US? the world?
4 corners and out west in general however in the world in general, we're worried about Madegascar
61
what are the symptoms of yersinia pestis infection?
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
what do the virulence factors of yersinia pestis do?
yersinia outer proteins (Yops): 1. block phagocytosis 2. block platelet activation
63
which cells does yersinia pestis infect?
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
how does LPS in yersinia pestis help with immune invasion?
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
how does a yersinia pestis infection progress?
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
how do you diagnose yersinia pestis infection?
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
how do you treat yersinia pestis infections?
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
what is used for yersinia pestis prophylaxis?
doxycyline
69
FLASHCARD: E. coli K1
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
FLASHCARD: UPEC
uropathogenic E. coli major cause of community-acquired UTIs uses adhesins (pili) to attach to and invade facet cells
71
FLASHCARD: proteus mirabilis
another cause of UTIs swarming motility (hyperflaggelated) and urease --> kidney stone formation check susceptibility; treat UTI with β-lactams, trimethoprim-sulfamethoxazole, or fluoroquinolone
72
FLASHCARD; Klebsiella pneumoniae
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
FLASHCARD: yersinia pestis
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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