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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

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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
treating cholera
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
26
what is the leading cause of morbidity and mortality in children under 2 in developing countires, ie travelers diarrhea
Enterotoxigenic E. Coli (ETEC)
27
how is Enterotoxigenic E. Coli (ETEC) spread
contaminated food/water (usually human orign) | uncooked/undercooked foods at greatest risk
28
inoculum of Enterotoxigenic E. Coli (ETEC)
10^8 to 10^10 in adults
29
where does Enterotoxigenic E. Coli (ETEC) colonize
proximal small intestine | adhere to cause disease
30
Virulence factors of Enterotoxigenic E. Coli (ETEC)
colonizing factor pili | toxins: heat-labile toxin (LT) and Heat-Stable toxin (ST)
31
What is HEat-Labile toxin (LT) from Enterotoxigenic E. Coli (ETEC)
A-B toxin | leads to secretion of Cl, and block of NaCl reabsorption in enterocytes
32
what is Heat stable toxin (ST) in Enterotoxigenic E. Coli (ETEC)
Binds to cells, leading to signal cascade that ends with fluid and electrolite section
33
immunity to Enterotoxigenic E. Coli (ETEC)
LT and CF-specific SIgA with no inflammation/tissue destructure
34
how to identify secretary diarrhea aganets
Rule out V. Cholera Innoculate plates with diluted stool samples not very rich medium, so fastidious G- wont grow aerobic incubation kills anaerobes
35
how to rule out Vibrio cholera from diarrhea agents
check if eaten shelfish or in endemic area Thiosulfate-Citrate - bile-sucrose (TCBS) agar) Agglutination test (EI Tor strain) Serological testing
36
how to treat secretory diarrhea
oral rehydration: mix of sugar and water antibiotics shorten duration and reduce serverity(tetracyclines for vibrio infections, 2nd gen flouroquinolones for ETEC)
37
Bacterial of invasive bacterial pathogens
Salmonella spp, and shigella spp
38
Characteristics of invasive bacterial pathogens
``` large intestine small volume of stool bloody stool leukocytes in stool tissue ulcerations ```
39
bacteria that are toxin producing bacterial pathogen
vibrio spp (primarily v. cholerae) and Entertoxigenic E coli (EtEC)
40
characterisitcs of Toxin-Producing bacterial pathogens
``` Small intesine lost of watery stool blood in stool no leukocytes in stool no tissue damage ```
41
characteristics of Enterohemorrhagicic E coli and Enteropathogenic E coli
Lower small intestine/upper large intesting Colonization causes attaching and effacing lesion blood in stool (also urin with EHEC)
42
most common form of bacterial infection of an organ system
UTI (not including adults
43
inflammation in the bladder
cytis
44
who is more likely to get a UTI
women (shorter uethra so bacteria have to travel less far)
45
Uncomplicated UTI
all normal defenses intake no recent hospital admission in lower urinary tract usually EPEC or other commensal E. COli
46
Complicated UTI
structural abnormality in urinary tract recently in hospital will spread to kindney other enterobacteriacea
47
natural defenses of urinary tract
``` complete voidance of bladder peristalsis ureterovesicle valves mucous layer pH ```
48
cause of pyelonephrities
``` 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
what cuase 90% of infectious cystists and pyelonephritis in US
E. Coli (oringate from intesnite) (Uropathogenic E. Coli)
50
virulence of UPE
type 1 pili P pili for ascending infection invade superficial epithelial cells alpha-hemolysin and cytotoxic necrotizing factors cause injury
51
Proteus causes what type of UTI's
uncomplicated and nosocomical infections | usually for abnormal urinary tract strucutre
52
P. mirabilis UTI vs. E. Coli UTI severity
P. mirabilis more severe(more virulence)
53
virulence factors of P. mirabilis
``` Flagella Adhesion on fimbriea for urinary eptihelium hemolysins IgA protease Urease ```
54
roll of Urease
raise pH of urin to create Nh3 and Co2 and grows better in less acidic encironment
55
Urease effect on renal cells
toxic and creates cystals for identification clincally
56
diagnosis of UTI
hard to positively ID causative agent of UTI | count bacteria
57
healthy individual bacteriuria
less than 10^5 CFU/ml
58
CFU with individual with dysuria
greater than 10^2
59
what is dysuria
painful urination
60
what is pyuria
WBC/pus in urin
61
Proteus can be diagnoses by
Consistently alkaline urine | Production of urease
62
treating a UTI
``` antimicrobials (trimethoprim-sulgamethoxazole first choice) 3 days for acute cystitis 10-14 days for polynephritis prophylactic treatment asymptomatic bacteriuria(pregnant) ```
63
morphology of Klebsiella
nonmotile, capsule
64
how does klebsiella adhere
pili
65
capsule with colonies of Klebsiella
large mucoid colonies (interferes with complement activation
66
where does Klebsiella infect
respiratory and urinary epithelium
67
klebsiella virulence factors
pili (type 1 and type 3 ) enterotoxin similar to ST and LT aerobactin Antiphagocytic capsule
68
roll of type 1 pili
adherence to urinary tract epithelial cells
69
roll of type 3 pili
important for adherence to respirator tract epithelial cells
70
enterotoxin of Klebsiella leads to
similar to ST and LT to induce secretory diarrhea
71
roll of aerobactin
iron sequestering PR
72
the primary virulence factory
antiphagocytic capsule
73
Klebsiella antibiotic resistance
very resistant, especially type 258
74
Klebsiella resistance to antibiotics is implicated where
hospital acquired respirator, UTI and Bloodstream Infections
75
what was Helicobacter pylori originally classified as
campylobacter (motile, curved, G- rod) | microaerophilic
76
growth of Helicobacter pylori
slow growth (3-5 days) but infection can last for days
77
where does Helicobacter pylori colonize
in stomach, secreting urease to raise pH
78
how does Helicobacter pylori cause apoptosis of host cell
Vacuolating cytotoxin
79
how is helicobacter pylori transmitted
likely feca-oral and even oral-oral
80
where si Helicobacter pylori found
30-50% of people in developing countries, and nearly all of devlping nations
81
Helicobacter pylori is the precursor of
Gastritis, gastric ulcer, and duodenal ulcar
82
the only class one carcinogen
Helicobacter pylori
83
how does Helicobacter pylori act as a class I carcinogen
Cag+ strains lead to the developmeny of gastric adenocarinoma by triggering growth-promoting oncogenic signals
84
Infection cycle of H. Pylori
* 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
how to kill H. Pylori
readily killed by gastric acid | IL-8 come because of inflammatory effector moelcules
86
what all causes the problem with H. pylori ulcer
inflammation, cytotoxin, and downregulation of domatostatin-producing D cells
87
what can H. pylori infection lead to
peptide ulcer chronic supericical gasritis lymphoproliterative disease chronic astrophic gastritis
88
clinical manifestation of H. Pylori
``` can be silent of nausea and upper ab pain belching heartburn dysphagia globus sensation ```
89
best way to test for H. Pylori
Urea breath test: injest labeled urea | urease in stomach break it down into a labeled CO2 that is exhauled and quantified
90
probelm with treating H> pylori
intense with many side effects
91
how to treat H. pylori
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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