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Micro Final > Bailey Material > Flashcards

Bailey Material Flashcards

1
Q

Name the 4 species of Shigella

A

S. dysenteriae
S. flexneri
S. Boydii
S. Sonnei

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2
Q

which shgiella species causes the most severe disease?

A

S. dysenteriae

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3
Q

is the shigiella inoculum size small or large?

A

small

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4
Q

How is acid resistance induced with Shigella?

A

is induced upon antibiotic growth conditions

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5
Q

List of five steps of invasion by Shigella

A

Only basolateral surface of cells are susceptible
expression of invasion plasmid antigen
lysing of phagosomal vesicles, replicate intracellularly
expression of IcsA (an ATPAse)which facilitates intracellular spread + causes actin polimerization

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6
Q

Describe M cells

A

M cells (micro fold cells) are cells found in the Peyers patches. they transport organisms and particles from the gut lien to immune cells across the epithelial barrier, and thus are important in stimulating mucosal immunity

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7
Q

describe ulcer formation due to Shigella

A

epithelial cells in the lumen die and are sloughed off causing an ulcer

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8
Q

describe the stool from shigella infection

A

Neutrophilles enter colonic tissue and can be seen in the tstoll. end result is an inflammatory diarrhea with leukocytes in stool.

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9
Q

what species produces shiva toxin?

A

S. dysenteria

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10
Q

describe the effects of shiva toxin

A

it kills intestinal epithelial cells and disrupts Na absorption (this is important bc results in watery diarrhea bc water exits cells)

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11
Q

whats the most common disease caused by salmonella?

A

Gastroenteritis

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12
Q

what species causes Typhoid fever

A

salmonella Typhi and Salmonela paratyphi

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13
Q

what is the innoculum size for salmonella?

A

large

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14
Q

what is the primary virulence factor of salmonella and what induces its expression?

A

it expresses multiple virulence proteins found on pathogenicity islands. A low pH induces their exp.

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15
Q

describe the invasion process of salmonella

A

it invades the apical surface of intestinal epithelial cells–> causes inc. in cellular Calcium.

  1. invasion occurs via bacterial mediated endocytosis
  2. invasion induces “cell ruffling” and signal transduction activation and uptake into vesicles
  3. salmenella travrses to the basal membrane of the intestinal epithelial cell within a vesicle
  4. salmonella is released from vesicle into lamina propria where it is taken up by macrophages.
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16
Q

which salmonella species can replicate in the macrophage?

A

S. Typhoid serovars

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17
Q

where are S. typhi found during the carrier state?

A

Asymptomatic carries with colonized gallbladder

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18
Q

what happens when S. typhi re-infects the intestines?

A

causes inflammation and ulceration of peters patches which results in diarrhea hemmorages and perforation

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19
Q

what are the similarities between the 2 invasive enteric pathogens? (shigella and salmonella)

A

both are invasive, so:
1. stool is small volume
2.stool is bloody
3immune cells leukocytes in stool
4.primarily causing diseases in colon.
both are able to respond to environmental changes to know when within the host are ready to cause disease.
1.shigella able to respond to anaerobic environment to induce acid restance
2.salmonella able to respond to acidic environmen to allow expression of virulence proteins.

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20
Q

what are the 3 major differences b/t the 2 invasive enteric bacteria shigellla and salmonela?

A

1.innocluation size (acid sensitivity)
shigella: little/small
salmonella: large
2.Bacteremia (bacteria in blood) is only seen in salmonella bc shigella is localized.
3.species causing severe disease are very dissimilar:
salmonella typhi are able to replicate within the macrophage and spread
shigella dysenter produces shia toxin

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21
Q

How area invasive enteric pathogens diagnosed?

A

based on symptoms and on stool cultures (Agar to distinguish between shigella and salmonella)

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22
Q

what is the 1st step in treatment of invasive enteric pathogens?

A

oral rehydration

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23
Q

what might a doctor prescribe for salmonella gastroenteritis?

A

Antibiotics not indicated but 2nd generation fluoroquinolones can be used effectively

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24
Q

what might a doc prescribe for typhoid fever

A

Fluoroquinoloes or surgical removal of gallbladder

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25
Q

is there a vaccine for either of the invasive gram negative patrons?

A

generally no but there is a vaccine for capsule of typhi

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26
Q

what are the 6 gram negative prolific colonizers of mucosal surfaces?

A 
vibrio spp
salmnola sp
proteus sp
escherichia sp
Klebsiella 
shigella sp
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27
Q

what is a mucosal surface?

A

surface that interacts with air and has associated glands for secreting mucosa

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28
Q

what are the 3 defenses of mucosal surfaces?

A

innate immunity
adaptive immunity
non-specific barrier defenses

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29
Q

describe gram neg invasive enteric pathogen outbreak in 2011

A

in Germany in 2011 E-coli o103:H4 outbreak from alfalfa sprouts caused over 800 cases of Hemolytic uremic syndrome and 32 deaths

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30
Q

what are the 7 ways (7 Fs) fir transmission of gram neg mucsal pathogens to pass from feces to mouth?

A 
fecal
food
fluids 
fingers
flies
fomites
fornication
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31
Q

describe differences in innoculum size

A

for some bacteria as few as 50-100 organisms is enough to cause disease (i.e shigella dysenteriae , e1eL); for other bacteria, millions of organisms are needed to cause disease (i.e ETEC, EPEC, and vibrio sp)

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32
Q

describe the natural barrier defenses of mucosal surfaces

A

natural barrier defenses:

  1. secretory substances
  2. antatomical + physiological barrier
  3. indigenous microbiotia
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33
Q

describe the secretory antimicrobial compound, lysozyme aka muramidase

A

lysozyme cleaves (Beta 1,4 -glycosidic) linkages b/t NAG+ NAM –> manily effective against gram +

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34
Q

what are the 5 main secretory antimicrobial compounds of mucosal surfaces?

A 
lysozyme (muramidase)
lactoferrin
cathelicidin
defensins
secretory immunoglobulins
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35
Q

describe the secretory antimucorbial compound, lactoferrin

A

bacteriostatic effects via sequestering iron, goal is to collect all iron+male availability of free iron low for bacteria

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36
Q

Describe the secretory anti microbial compound, cathelicidin

A

its a positively charged Antimicrobial cationic peptide that disrupts the negatively charged lipid membranes of gram negative bateria

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37
Q

Describe the secretory antimicrobial compound, defensins

A

they are positively charged antimicrobial cationic peptides that create pores in microbes

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38
Q

what is the difference between alpha-defensins and beta-defensins?

A

alpha ones are produced by neutrophils and paneth cells in intestine, and beta ones area produced by epithelial cells

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39
Q

Describe the secretory antimicrobial compound, immunoglobulines

A

secretory IgA pathogens which disrupts their ability of the pathogen to adhere

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40
Q

what are the 4 natural antimicrobial and physiological properties that assist with creating and physical barrier along mucosal surfaces?

A
  1. acidity
  2. motility
  3. mucous layer with underlying glycocalyx
  4. tight junctions
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41
Q

Describe how acidity acts as a natural barrier along mucosal surfaces

A

pH range varies in GI tract from a low pH1 in the stomach to a basic pH of 9 in the duodenum. most microbes cannot withstand a low pH but if microbes are acid resistant then they will be unable to survive in the high pH of the duodenum.

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42
Q

Describe how motility acts as a natural barrier along mucosal surfaces

A

a constant flow of chyme and muscular movements can actually tip off the microbes that try to adhere

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43
Q

describe how the mucous layer with underlying glycol calyx acts asa natural barrier along mucosal surfaces

A

the very viscous layer of mucous is very hard for microbes to pass thru. if they are able to pass, then they must also get across the glycocalyx

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44
Q

describe how tight junctions act as natural barriers for mucosal surfaces

A

epithelial cells are bound to each other thru tight jxns so microbes must figure out a way to invade the epithelial cells ( thru or in between)

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45
Q

describe the role of indigineous microbiota in protection of mucosal surfaces

A

there are lots of commensal microbiota especially in the illiim and colon, which help to protect mucosal surfaces from infection by out competering bad bacteria for nutrients and adherence

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46
Q

why do most diseases occur in the illiim and colon

A

1.motility decreases around illiim
2pH becomes neutral around illiim
3.environmental becomes anaerobic around ilium

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47
Q

what re the 3 major ways that pathogenic bacteria overcome innate barrier defenses

A

acid resistance
fimbrial pili
bacterial structures

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48
Q

How does acid resistance help pathogenic bacteria to overcome innate barrier defenses

A

Microbes with low infectious doses tend to be acid resistant and therefore can survive in harsh environment of the stomach and some of small intestine (e.g shigella sp. enteroinvasive E.coli)

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49
Q

How do fimbriaw/pili help pathogenic bacteria to overcome innate barrier defenses

A

Adhesins on fibrial / pili are VIP bc they allow bacteria to adhere to tissue and therefore resist being shed. The negatively charged bacteria would be repelled by positively charged mucosal surface but adhesions negate this because adhesions have specific receptors for host cells which allow them to adhere strongly

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50
Q

what are the 5 bacterial structures used by gram - pathogenic bacteria to overcome innate barrier defenses of the host

A
  1. cell membrane sensitivities to bactericidal compounds
  2. cationic amino acids
  3. siderophores
  4. capsule
  5. mechanisms for neutralizing macrophages
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51
Q

How do cationic amino acids help pathogenic bacteria overcome innate barrier defenses of host

A

bacteria put anionic AA into the cell men of the host to reduce the effects of host cationic antimicrobial peptides (defensins and cathelicidin)

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52
Q

how to Siderophores help pathogenic bateria overcome the innate barrier defenses of the host?

A

siderophores sequester iron in low iron environments (e.g enterobacctin produced by E.coli) to negate the effects of host lactoferin

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53
Q

in what 2 ways do pathogenic bacteria avoid being phagocytosed

A
  1. development of a capsule to resist phagocytosis

2. development of me chasms capable of neutralizing the pahocytic compartment of macrophages

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54
Q

why are macrophages an important part of mucosal immunity

A

macrophages recognize microbes via pattern recognition of the macrophages and the ability to kill many microbes

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55
Q

describe how activation of PRRs on macrophages also initiates the inflammatory response

A

inflammatory cytokines TNF, IL1 IL2 and chemokines would be activated and start recruitment upon activation of TLRs esp TLR4

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56
Q

what is the downside to initiating the inflammatory response

A

inflm response such as TNF can disrupt (loosen) the tight jxns b/t epithelial cells which creates a pathway for pathogen invasion

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57
Q

where are the densest cluster of lymph noes found

A

near mucosal tissue

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58
Q

what are the 2 main gram neg toxin producing bacterial pathogens of mucosal surfaces

A
  1. vibrio sp

2. enterotoxigenic ecoli etec

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59
Q

what are 5 major symptoms of a gram neg toxin producing bacterial infection

A
  1. infection of small intestine
  2. copoious amounts of watery stool
  3. no blood in stool
  4. no leukocytes in stool
  5. no tissue damage bc no invasion
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60
Q

what are 4 species of vibrio

A
  1. cholerae
  2. parahaemolytics
  3. vulvinticus
  4. alginolyticus
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61
Q

which form of vibrio causes the most severe disease

A

v.cholerae

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62
Q

name 3 physical characteristics of v.cholerae

A
  1. gram neg
  2. rod
  3. single flagella
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63
Q

what was different b/t the new 0139ElTor strain of v.cholerae and the original ElTor strain

A
  1. mutated the 01 antigen (different antigicity that human immune system hadn’t previously encountered
  2. 0139 was a new LPS serotype
  3. 0139 is encapsulated
  4. 0139 was an epidemic that affected ALL age groups
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64
Q

what are the 3 major virulence factors for V.cholerae

A
  1. flagella
  2. pili
  3. cholera toxin
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65
Q

why is having flagella a particularly important virulence factor for v.cholerae?

A

flagella allows v.cholerae to be motile this is especially important bc their nature niche is sea water

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66
Q

why is having poi an important virulence factor for v cholerae

A

pili have adhesions which are very important for adhering to mucosal tissue. theses pili are only expressed once V.cholera made a shift from saltwater to the reduced ion levels of the human body this also causes/induces toxin expression

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67
Q

what does phage encoded mean in regards to cholera toxin (ctx)

A

ctx is phage encoded implying that different strains can obtain this gene to produce cholera toxin

68
Q

how does ctx work

A

binds to its receptor and activates adenylate cyclase (remains active) to produce los of cAMP. so that negative feedback inhibition is no longer working. high levels of cAMP cause epithelial cells to secrete Cl ion and also blocks the absorption of Na so that water flows out into the lumen resulting in watery secretory diarrhea

69
Q

on what basis are e.coli grouped?

A

e.coli are grouped based on what kind of disease they cause

70
Q

what are the 3 major categories of ecoli..give examples

A
  1. secretory diarrhea ETEC, EPEC
  2. Dysentery-like EHEC
  3. urinary tract infections UPEC
71
Q

what is the most common cause of traveler’s diarrhea

A

Enterotoxigenic ecoli

72
Q

describe the infectious dose of ETEC

A

etec has large infectious dose because its very susceptible to acid

73
Q

what is the role of CFA for ETEC

A

Colonization Factor Antigen (CFA) on the fibriae of ETEC helps the negatively charged bacteria to adhere to the negatively charged host cell on mucosal tissue

74
Q

what 2 toxins are produced by ETEC

A
  1. heat-liable toxin (LT) –> degrades upon heating

2. heat-stable toxin (ST) –> stable upon heating

75
Q

what is the mechanism for heat liable toxin

A

LT activates adenylate cyclase (AC) increasing cAMP production causing the epithelial cells to secrete Cl and also stops absorption of Na so water flows into lumen causing water diarrhea

76
Q

what is the mechanism for Heat-stable toxin

A

ST activated Guanylate cyclas (GC) resulting in increased cGMP and disrupts the absorption of Na and secretion of Cl causing water to follow into the lumen

77
Q

what is the importance of adenylate/guanylate cyclase

A

ATP-AC/ GTP-CC –> cAMP/cGMP

78
Q

what is the importance of cAMP/cGMP

A

causes cell to stop absorbing Na

79
Q

which ETEC toxin is similar to cholera toxin

A

LT heat-liable toxin

80
Q

what is the single most important factor in the treatment of v.cholorea

A

oral rehydration

81
Q

why is it important to first rule out v.cholorae when diagnosing non invasive bacterial pathogens

A

bc oral rehydration is most important tx for v.cholorae and tetracyclines are used to treat vibrio while 2nd generation fluoroquinolones are used to treat ETEC

82
Q

what are the 4 ways to rule out v.cholorear when testing for non invasive bacterial pathogens

A
  1. ask if pt has eaten shellfish or been to an endemic area
  2. Thiosulfate-citrate-bile-sucrose (TCBS) agar
  3. agglutination test (El Tor strain)
  4. serological testing
83
Q

what are the hybrid misfits

A

enteropathogenic ecoli EPEL and enterohemorrhagic ecoli EHEC

84
Q

where to EPEC and EHEC colonize

A

lower small intestinal /upper large intesitine

85
Q

what kind of lesion results from EHEC or EPEC colinization

A

attaching and effacing lesion

86
Q

where might you find blood with EHEC infection

A

stool and possibly urine

87
Q

what is the infectious dose sign for ePEC

A

large infectious dose size therefore highly acid sensitive/susceptible

88
Q

what lind of diarrhea is assoc with EPEC

A

non inflammatory secretory diarrhea

89
Q

is EPEC a toxin producer?

90
Q

what is the disease causing mechism for EPEC

A

it is the colonization itself that causes the diseases / characteristic intimate adherence pattern aka “ attaching and effacing lesion” NOT a toxin, NOT invasion

91
Q

what are the 3 steps for intimate adherence pattern of colonization aka attaching and effacing lesion

A
  1. bundle formin pili
  2. type 3 secretion of Tir into host epithelial cells
  3. Tir binding to intimin
92
Q

what is the fxn of budge forming pilus for EPEC

A

Bfs assists in adherence from a relatively long distance

93
Q

what is the result of type III secretion of TIR into host cell

A

Tir binds to intimin on epec resulting in pedestal formation due to stimulation of actin polymerization in the host cell. formation of pedestal actually leads to the disease

94
Q

describe pedestal formation assoc with EPEC

A

its due to rearrangement of epithelial cells into pedestal structure which causes diarrhea bc the microvilli are used for putting the bacteria on a pedestal instead of for its usual purpose

95
Q

how does enteropathogenic Ecoli induce diahrrea

A

1.malabsorption due to microvilli disruptions
stops absorption of Na , starts secretion of Cl and thus causes water to follow into lumen
2. disruption of epithelial tight jxn causes tissue to become leaky
3.for EPEC, there is no toxin production

96
Q

who are most susceptible to EPEC

97
Q

what is the major difference between EPEC and EHEC

A

enterohemorrhagic ecoli EHEC binds exactly the same as EPEC only that EHEC can produce a toxin which leads to bloody stool or even urine

98
Q

what genes are unique to EHEC

A

has set of EPEC genes called Eae genes so it produces an effacing lession

99
Q

what toxin is produced by EHEC

A

shigella like toxin aka vero toxin

100
Q

what/who is the primary resorvior for EHEC

A

cattle are primary resorvoir

101
Q

what is the most common strand of EHEC

A

ecoli 0157:H7

102
Q

what kind of lesion does EHEC cause

A

attaching effacing lesion (gastroenteritis)

103
Q

what does shiga-like toxin attack

A

small blood vessels of large intestines

104
Q

what are 2 major diseases that result from shiga-like toxin in EHEC

A
  1. hemorrhagic olitis affects small blood vessels in colon

2. hemolytic uremic syndrome (HUS) can affect small blood vessels of the kidney if soreads

105
Q

how does EHEC cause on attaching and effacing lesion

A

same 3 steps as w/EPEC

106
Q

does inflammation enhance or reduce the effects of shiva-like toxin

A

inflmmatory cytokines IL1 , TNF-alpha engance/ intensifies the effects of the shiga-like toxin

107
Q

why is tx of EHEC with antibiotics considered to be controversial

A

bc it stimulates the verotoxin production

108
Q

what organ besides the colon is susceptible to shiva-like toxin

A

the kidneys

109
Q

how does shigalike toxin affect the kidneys

A

blood vessels in the kidney are especially susceptible to shiva-like toxin so after cytokine storm shigalike toxin is more apt to spread to kidneys

110
Q

what is the most common form of bacterial infection besides mouth and most frequent cause for doctors visits by adults

A

UTIS urinary tract infections

111
Q

what is the term for inflammation of bladder

112
Q

why are UTIs more common in women

A
  1. anatomical reasons

2. during pregnancy, hormones cause dilation and decreased peristalsis of the ureters

113
Q

why does age affect the incidence of UTIs in men

A

incidence of UTI goes up w/age in men bc the antimicrobial substance produced by the prostate gland becomes less active with age.

114
Q

what is an uncomplicated UTI

A
  1. all normal defense mechanisms are intact
  2. no recent hospital admissions
  3. disease limited to lower urinary tract
115
Q

what is a complicated UTI

A
  1. some structural abnormality in urinary tract
  2. recent admission to hosp
  3. disease most likely will spread to kidneys
116
Q

what is cystitis

A

inflammation in the bladder

117
Q

what is pyelonephritis

A

inflammation of the kidney (retrograde flow of urine from bladder to kidneys)

118
Q

what is the most common bacterial pathogen that causes uncomplicated UTI

119
Q

what is the most common bacterial pathogen that causes complicated UTI

A

psuedomonas aeruginosa

120
Q

what are the natural barrier defenses found in the urinary tract

A
  1. complete voidance of the bladder
  2. peristalsis uninductional contraction
  3. ureterovesicle valves
  4. mucous layer
  5. normal microbiota like lactobacillus
  6. pH reduction
121
Q

name 6 reasons why cystitis can progress to pyelonephritis

A
  1. retrograde flow of urine bladder –> kidneys
  2. neurological disorders leading to poor emptying of the bladder
  3. children having incomplete closure of the ureterovesicle valves
  4. during pregnancy hormones causing dialation and decreased peristalsis of the ureters
  5. uretheral cathedars
  6. urinary tract stones causing some bacteria like proteus sp to neutralize the pH of urine and cause the formation of “struvite” calculi insoluble precipitate that can damage vesicles.
122
Q

what kind of UTI does UPEC cause

A

uncomplicated UTI

123
Q

How does UPEC adhere to urinary tract tissue?

124
Q

with UPEC what kind of adhesion is needed for adhesion resulting in acute cystitis uncomplicated UTI

A

FimH (fibrial antigen)

125
Q

with UPEC what kind of adhesion is needed for adhesion resulting in pyelonephritis

A

P fimbrial

126
Q

what are the 2 adhesions UPEC requires for adhesion

A

FimH and P fibrae

127
Q

why is aerobactin import in for UPEC to produce

A

aerobactin is a sidrophore used by UPEC for sequestering iron

128
Q

why is hemolysin important for UPEC to produce

A

hemolysin is used by UPEC to lyse RBCs to host (assoc with pyelonephtritis) leading to bloody urine

129
Q

what kind of UTI does proteus mirabilis cause

A

causes both complicated and uncomplicated uti

130
Q

what pathogen is most likely to be the cause of UTIs resulting from abnormal urinary tract structure

A

Proteus Mirabilis

131
Q

does Proteus Mirabilis cause a more or less severe UTI compared to ecoli

A

Proteus Mirabilis UTIs tend to be more severe than those caused by ecoli due to additional virulence factors

132
Q

what are the 5 virulence factors assoc with Proteus Mirabilis

A
  1. flagella
  2. Hemolysin
  3. Adhesins
  4. IgA protease
  5. Urease
133
Q

why are flagella an important virulence factor for Proteus Mirabilis

A

flagella allow Proteus Mirabilis to be highly motile and thus capable of swimming in bladder and up ureters

134
Q

why are the adhesions of Proteus Mirabilis considered an important virulence factor

A

they are specific for adhesion of urinary epithelium in particular

135
Q

why is IgA protease an important virulence factor for Proteus Mirabilis

A

IgA protease degrades IgA which makes it easier for Proteus Mirabilis to adhere to tissues

136
Q

which virulence factor is the #1 reason that Proteus Mirabilis is dangerous

137
Q

why is urease an important virulence factor for Proteus Mirabilis

A
  1. urease is an enzyme that raises the pH of urine by converting urea to NH3+CO2 . this creates a better (more alkaline) environment for the bacteria to grow in .
  2. urease is toxic to renal cells
  3. urease enhances the formation
138
Q

why is the production of urease dangerous in the urinary system

A

leads to chronic infection

139
Q

how are UTIs diagnosed

A

by counting the bacteria in the urine

140
Q

when would antibiotics be prescribed for a healthy individual (i.e asymptomatic with a uti)

A

health (asymptomatic) individual bacteriurea > or = to 100,000 CFU/mL

141
Q

when would antibiotics be prescribed for a symptomatic individual with a uti

A

individual with dysuria > or = to 100 with pyuria

142
Q

how can Proteus Mirabilis, specifically, be diagnosed

A
  1. consistently alkaline urine

2. prodcution of urease

143
Q

how does treatment of uti due to Proteus Mirabilis differ when the infection is in kidney vs bladder

A

tx with Trimethoprim-Sulfamethoxazole at high dose for a short amount of time for bladder but at low dose for a long period for infection in kidney

144
Q

Is Klebsiella pneumoniae mobile or immobile and why

A

Klebsiella pneumoniae is immobile due to its large capsule with no flagella

145
Q

what kind of disease assoc with the lungs results from Klebsiella

A

Klebsiella bacterial pneumoniae: fluid fills the lungs (usually assoc with immune compromised patients)

146
Q

what are the 4 major virulence factors for the Klebsiella pneumoniae

A
  1. pili
  2. enterotoxin
  3. aerobactin
  4. capsule
147
Q

what type of pili are necessary for Klebsiella pneumoniae adhesion to respiratory epithelial cells

A

type III pili

148
Q

what type of pili are necessary for Klebsiella pneumoniae adhesion to urinary tract epithelial cells

A

type I pili

149
Q

how does Klebsiella pneumoniae induce a watery diarrhea

A

caused by its enterotoxin similar to LT and ST of ETEC

150
Q

why is aerobactin an important virulence factor for Klebsiella pneumoniae

A

its an iron sequestering protein

151
Q

why is a capsule an important virulence factor for Klebsiella pneumoniae

A

it gives Klebsiella pneumoniae an antiphagocytic characteristic which prevents the macrophage from engulfing and degrading the bacteria

152
Q

why is the capsule considered #1 virulence factor for Klebsiella pneumoniae

A

bc without it Klebsiella pneumoniae is avirulent

153
Q

why is Heliobacter pylori considered a slow pathogen

A

bc the diseases it caused take a long period of time to do damage and have a long asymptomatic time period

154
Q

where does Heliobacter pylori colonize

A

Antrum of stomach only found in the mucous overlain mucous-secreting cells of the stomach

155
Q

how does Heliobacter pylori transmission differ from other gram negative pathogens that we have studied

A

spread/trasminssion is oral to oral also fecal to oral

156
Q

what are the 4 main diseases that Heliobacter pylori leads to

A
  1. peptic ulcer disease
  2. lymphoproliferative disease (leads to MALT or GALT caners)
  3. chronic superficial gastritis
  4. chronic atrophic gastritis (leads to gastric adenocarcinoma)
157
Q

what is the animal reservoir for Heliobacter pylori

A

none! Heliobacter pylori is only found in humans.

158
Q

all of the diseases resulting from Heliobacter pylori infection are always produced by the development of what

A

chronic superficial gastritis (low inflammation/redness) that can be present for years w/o visible symptoms

159
Q

describe the inflammatory / effector molecules asssoc with Heliobacter pylori

A

inflmmatory effector molecs casue epithelial cells to produce IL8 which recruits neutrophils to the sire of infection which may actually end up further contributing to the formation of an ulcer due to inflammatory effects

160
Q

why is the production of urease an important virulence factor for Heliobacter pylori

A

since Heliobacter pylori is readily killed by gastric acid, urease is essential bc it raises the pH thus creating an alkaline environment which the Heliobacter pylori is able to tolerate

161
Q

how can production of urease be useful for identification of Heliobacter pylori

A

a “urea breath test” (highly able to detect ammonia) is able to be used to indicate the presence of urease which points to the Heliobacter pylori presence

162
Q

why is production of cytotoxin important for Heliobacter pylori

A

cytotoxin is assoc with peptic ulcer disease and induces vacuolation and apoptosis of epithelial cells

163
Q

why is the down regulation of somatostatin producing D-cells important for Heliobacter pylori

A

this causes an up regulation of gastrin (or gastritis) which is an inability to control gastrin this leads to cell proliferation and thus mutation and likely cancer

164
Q

why is an increase in gastrin production important for the development of Heliobacter pylori mediated carcinogenesis

A

incerased gastrin production resulting from Heliobacter pylori infection leads to increased cell proliferation and then increased numbers of host cell mutation

165
Q

in what 3 ways can the enhanced inflammatory response from Heliobacter pylori infection lead to carcinogenesis

A
  1. increase in # of free radicals
  2. increase in gastrin leading to increase in cell proliferation
  3. decrease in ascorbate leading to increase in N-nitrous compounds increasing# of mutations
166
Q

what is atrophic gastritis

A

chronic inflammmatory stomach mucosa caused by the inability to make gastric acids. leads to loss of gastric glandular cells causing digestion problems and greater susceptibility to dietratry carcinogens

Micro Final (13 decks)

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