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micro immuno 2 > Vibrio cholera and E. coli (ETEC) Proteus, UPEC, Klebsiella and Helicobacter pylori MM (3/1/18) > Flashcards

Vibrio cholera and E. coli (ETEC) Proteus, UPEC, Klebsiella and Helicobacter pylori MM (3/1/18) Flashcards

1
Q

which pathogenic E. Coli can lead to water diarrhea that lasts for weeks

A

Enteroaggregative

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2
Q

Toxin-produce bacterial pathogens

A

Vibrio Spp

Enterotoxigenic E coli(

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3
Q

calling signs of toxin-producting bacterial pathogens

A 
small intestine location
lots of water in stool
no blood in stool
no leukocytes in stool
no tissue damage
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4
Q

morphology of vibrio

A

curved, gram-

highly motile

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5
Q

location of vibrio

A

saltwater

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6
Q

4 species of Vibrio

A
  • V. cholerae - diarrhea, “cholera gravis”
  • V. parahaemolyticus - diarrhea
  • V. vulnificus - tissues and blood
  • V. alginolyticus - tissues and blood
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7
Q

pH of Vibrio Cholerae

A

8-9.5

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8
Q

what toxin does vibrio cholerae form

A

cholera toxin

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9
Q

two main biotypes that can cause cholera

A

classical

el tor - o1 antigen, and 0139 (New)

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10
Q

what does vibrio cholerae form in environment

A

biofilms

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11
Q

virulence factors for V. cholerae

A

flagella
pili to adhere to mucosal tissue
cholera toxin

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12
Q

why would V. cholerae express the pili and toxin

A

shift from salt to the body (lower ions) cause pili to come out and produce toxin

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13
Q

main regulator of pathogenicity island of V. cholerae

A

ToxR

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14
Q

where the cholera toxin comes from

A

phage encoded

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15
Q

what is the cholera toxin

A

A-B type ADP-ribosylating toxin

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16
Q

Cholera tox lead to what

A

excessive accumulation of cAMP which cuase hypersecretion of chloride, potassium and bicarbonate followed by water by osmotic pressure

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17
Q

how is cholera spread

A

contaminated water and by humans

under cooked crab/shrimp

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18
Q

incubation period of cholera

A

2 days

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19
Q

inoculum needed to fcause disease in cholera

A

high number

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20
Q

Colonize location of cholera

A

small intestine

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21
Q

what types of cholera produce CT

A

o1 and o139, rest dont cause cholera

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22
Q

Cholera leads to

A

loss of water(liters) per day
Rice water stools
hypokalemia and metabolic acidosis : large amound of k and bicarb is loss with water
can kill

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23
Q

cholera immunity

A

Nonspecific important

SIga against O antigen, B subunit of cholera toxin, and toxin coregulated pilus

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24
Q

why use selective media to look at cholera

A

lots of stuff in your poo

use addition biochem tests to ID strain

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25
Q

treating cholera

A

Oral and IV solution of glucose and physiological concentration of Na and Cl, and higher levels of K and HCO3
early intervention is key
also can use antibiotics to decrease time

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26
Q

what is the leading cause of morbidity and mortality in children under 2 in developing countires, ie travelers diarrhea

A

Enterotoxigenic E. Coli (ETEC)

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27
Q

how is Enterotoxigenic E. Coli (ETEC) spread

A

contaminated food/water (usually human orign)

uncooked/undercooked foods at greatest risk

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28
Q

inoculum of Enterotoxigenic E. Coli (ETEC)

A

10^8 to 10^10 in adults

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29
Q

where does Enterotoxigenic E. Coli (ETEC) colonize

A

proximal small intestine

adhere to cause disease

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30
Q

Virulence factors of Enterotoxigenic E. Coli (ETEC)

A

colonizing factor pili

toxins: heat-labile toxin (LT) and Heat-Stable toxin (ST)

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31
Q

What is HEat-Labile toxin (LT) from Enterotoxigenic E. Coli (ETEC)

A

A-B toxin

leads to secretion of Cl, and block of NaCl reabsorption in enterocytes

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32
Q

what is Heat stable toxin (ST) in Enterotoxigenic E. Coli (ETEC)

A

Binds to cells, leading to signal cascade that ends with fluid and electrolite section

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33
Q

immunity to Enterotoxigenic E. Coli (ETEC)

A

LT and CF-specific SIgA with no inflammation/tissue destructure

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34
Q

how to identify secretary diarrhea aganets

A

Rule out V. Cholera
Innoculate plates with diluted stool samples
not very rich medium, so fastidious G- wont grow
aerobic incubation kills anaerobes

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35
Q

how to rule out Vibrio cholera from diarrhea agents

A

check if eaten shelfish or in endemic area
Thiosulfate-Citrate - bile-sucrose (TCBS) agar)
Agglutination test (EI Tor strain)
Serological testing

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36
Q

how to treat secretory diarrhea

A

oral rehydration: mix of sugar and water
antibiotics shorten duration and reduce serverity(tetracyclines for vibrio infections, 2nd gen flouroquinolones for ETEC)

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37
Q

Bacterial of invasive bacterial pathogens

A

Salmonella spp, and shigella spp

38
Q

Characteristics of invasive bacterial pathogens

A 
large intestine
small volume of stool
bloody stool
leukocytes in stool
tissue ulcerations
39
Q

bacteria that are toxin producing bacterial pathogen

A

vibrio spp (primarily v. cholerae) and Entertoxigenic E coli (EtEC)

40
Q

characterisitcs of Toxin-Producing bacterial pathogens

A 
Small intesine
lost of watery stool
blood in stool
no leukocytes in stool
no tissue damage
41
Q

characteristics of Enterohemorrhagicic E coli and Enteropathogenic E coli

A

Lower small intestine/upper large intesting
Colonization causes attaching and effacing lesion
blood in stool (also urin with EHEC)

42
Q

most common form of bacterial infection of an organ system

A

UTI (not including adults

43
Q

inflammation in the bladder

A

cytis

44
Q

who is more likely to get a UTI

A

women (shorter uethra so bacteria have to travel less far)

45
Q

Uncomplicated UTI

A

all normal defenses intake
no recent hospital admission
in lower urinary tract
usually EPEC or other commensal E. COli

46
Q

Complicated UTI

A

structural abnormality in urinary tract
recently in hospital
will spread to kindney
other enterobacteriacea

47
Q

natural defenses of urinary tract

A 
complete voidance of bladder
peristalsis
ureterovesicle valves
mucous layer
pH
48
Q

cause of pyelonephrities

A 
Cystitis spread to kidney via retrograde flow from bladder to kidney
-neurological disorders
-ureteroviscle valves not fully formed
-pregnancy hormones change peristalsis
Urethral catheters
Urinary tract stones
49
Q

what cuase 90% of infectious cystists and pyelonephritis in US

A

E. Coli (oringate from intesnite) (Uropathogenic E. Coli)

50
Q

virulence of UPE

A

type 1 pili
P pili for ascending infection
invade superficial epithelial cells
alpha-hemolysin and cytotoxic necrotizing factors cause injury

51
Q

Proteus causes what type of UTI’s

A

uncomplicated and nosocomical infections

usually for abnormal urinary tract strucutre

52
Q

P. mirabilis UTI vs. E. Coli UTI severity

A

P. mirabilis more severe(more virulence)

53
Q

virulence factors of P. mirabilis

A 
Flagella
Adhesion on fimbriea for urinary eptihelium
hemolysins
IgA protease
Urease
54
Q

roll of Urease

A

raise pH of urin to create Nh3 and Co2 and grows better in less acidic encironment

55
Q

Urease effect on renal cells

A

toxic and creates cystals for identification clincally

56
Q

diagnosis of UTI

A

hard to positively ID causative agent of UTI

count bacteria

57
Q

healthy individual bacteriuria

A

less than 10^5 CFU/ml

58
Q

CFU with individual with dysuria

A

greater than 10^2

59
Q

what is dysuria

A

painful urination

60
Q

what is pyuria

A

WBC/pus in urin

61
Q

Proteus can be diagnoses by

A

Consistently alkaline urine

Production of urease

62
Q

treating a UTI

A 
antimicrobials (trimethoprim-sulgamethoxazole first choice)
3 days for acute cystitis
10-14 days for polynephritis
prophylactic treatment
asymptomatic bacteriuria(pregnant)
63
Q

morphology of Klebsiella

A

nonmotile, capsule

64
Q

how does klebsiella adhere

A

pili

65
Q

capsule with colonies of Klebsiella

A

large mucoid colonies (interferes with complement activation

66
Q

where does Klebsiella infect

A

respiratory and urinary epithelium

67
Q

klebsiella virulence factors

A

pili (type 1 and type 3 )
enterotoxin similar to ST and LT
aerobactin
Antiphagocytic capsule

68
Q

roll of type 1 pili

A

adherence to urinary tract epithelial cells

69
Q

roll of type 3 pili

A

important for adherence to respirator tract epithelial cells

70
Q

enterotoxin of Klebsiella leads to

A

similar to ST and LT to induce secretory diarrhea

71
Q

roll of aerobactin

A

iron sequestering PR

72
Q

the primary virulence factory

A

antiphagocytic capsule

73
Q

Klebsiella antibiotic resistance

A

very resistant, especially type 258

74
Q

Klebsiella resistance to antibiotics is implicated where

A

hospital acquired respirator, UTI and Bloodstream Infections

75
Q

what was Helicobacter pylori originally classified as

A

campylobacter (motile, curved, G- rod)

microaerophilic

76
Q

growth of Helicobacter pylori

A

slow growth (3-5 days) but infection can last for days

77
Q

where does Helicobacter pylori colonize

A

in stomach, secreting urease to raise pH

78
Q

how does Helicobacter pylori cause apoptosis of host cell

A

Vacuolating cytotoxin

79
Q

how is helicobacter pylori transmitted

A

likely feca-oral and even oral-oral

80
Q

where si Helicobacter pylori found

A

30-50% of people in developing countries, and nearly all of devlping nations

81
Q

Helicobacter pylori is the precursor of

A

Gastritis, gastric ulcer, and duodenal ulcar

82
Q

the only class one carcinogen

A

Helicobacter pylori

83
Q

how does Helicobacter pylori act as a class I carcinogen

A

Cag+ strains lead to the developmeny of gastric adenocarinoma by triggering growth-promoting oncogenic signals

84
Q

Infection cycle of H. Pylori

A
  • H. pylorisecretes urease in order to raise the pH in the stomach (via ammoniaproduction).
  • Uses flagella to propel itself into the mucus layer where it secretes more urease.
  • Outer membrane proteins are used to adhere to gastric epithelial cells.
  • Type IV secretion system injects VacAand Cag into gastric epithelial cells.
  • Inflammatory response likely contributes to epithelial cell death and ulcer formation.
85
Q

how to kill H. Pylori

A

readily killed by gastric acid

IL-8 come because of inflammatory effector moelcules

86
Q

what all causes the problem with H. pylori ulcer

A

inflammation, cytotoxin, and downregulation of domatostatin-producing D cells

87
Q

what can H. pylori infection lead to

A

peptide ulcer
chronic supericical gasritis
lymphoproliterative disease
chronic astrophic gastritis

88
Q

clinical manifestation of H. Pylori

A 
can be silent of nausea and upper ab pain
belching
heartburn
dysphagia
globus sensation
89
Q

best way to test for H. Pylori

A

Urea breath test: injest labeled urea

urease in stomach break it down into a labeled CO2 that is exhauled and quantified

90
Q

probelm with treating H> pylori

A

intense with many side effects

91
Q

how to treat H. pylori

A

First Line
•Proton pump inhibitor
•Antibiotic cocktail
•usually clarithromycin and metronidazole or amoxicillin
•250-1000 mg twice a day for 7-10 days
Second Line
•Proton pump inhibitor
•bismuth subsalicylate
•tetracycline 500 mg four times a day for 14 days
•metronidazole 500 mg three times a day for 14 days

micro immuno 2 (8 decks)

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