Bailey Material Flashcards
(166 cards)
1
Q
Name the 4 species of Shigella
A
S. dysenteriae
S. flexneri
S. Boydii
S. Sonnei
2
Q
which shgiella species causes the most severe disease?
A
S. dysenteriae
3
Q
is the shigiella inoculum size small or large?
A
small
4
Q
How is acid resistance induced with Shigella?
A
is induced upon antibiotic growth conditions
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
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
7
Q
describe ulcer formation due to Shigella
A
epithelial cells in the lumen die and are sloughed off causing an ulcer
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.
9
Q
what species produces shiva toxin?
A
S. dysenteria
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)
11
Q
whats the most common disease caused by salmonella?
A
Gastroenteritis
12
Q
what species causes Typhoid fever
A
salmonella Typhi and Salmonela paratyphi
13
Q
what is the innoculum size for salmonella?
A
large
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.
15
Q
describe the invasion process of salmonella
A
it invades the apical surface of intestinal epithelial cells–> causes inc. in cellular Calcium.
- invasion occurs via bacterial mediated endocytosis
- invasion induces “cell ruffling” and signal transduction activation and uptake into vesicles
- salmenella travrses to the basal membrane of the intestinal epithelial cell within a vesicle
- salmonella is released from vesicle into lamina propria where it is taken up by macrophages.
16
Q
which salmonella species can replicate in the macrophage?
A
S. Typhoid serovars
17
Q
where are S. typhi found during the carrier state?
A
Asymptomatic carries with colonized gallbladder
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
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.
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
21
Q
How area invasive enteric pathogens diagnosed?
A
based on symptoms and on stool cultures (Agar to distinguish between shigella and salmonella)
22
Q
what is the 1st step in treatment of invasive enteric pathogens?
A
oral rehydration
23
Q
what might a doctor prescribe for salmonella gastroenteritis?
A
Antibiotics not indicated but 2nd generation fluoroquinolones can be used effectively
24
Q
what might a doc prescribe for typhoid fever
A
Fluoroquinoloes or surgical removal of gallbladder
25
is there a vaccine for either of the invasive gram negative patrons?
generally no but there is a vaccine for capsule of typhi
26
what are the 6 gram negative prolific colonizers of mucosal surfaces?
```
vibrio spp
salmnola sp
proteus sp
escherichia sp
Klebsiella
shigella sp
```
27
what is a mucosal surface?
surface that interacts with air and has associated glands for secreting mucosa
28
what are the 3 defenses of mucosal surfaces?
innate immunity
adaptive immunity
non-specific barrier defenses
29
describe gram neg invasive enteric pathogen outbreak in 2011
in Germany in 2011 E-coli o103:H4 outbreak from alfalfa sprouts caused over 800 cases of Hemolytic uremic syndrome and 32 deaths
30
what are the 7 ways (7 Fs) fir transmission of gram neg mucsal pathogens to pass from feces to mouth?
```
fecal
food
fluids
fingers
flies
fomites
fornication
```
31
describe differences in innoculum size
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)
32
describe the natural barrier defenses of mucosal surfaces
natural barrier defenses:
1. secretory substances
2. antatomical + physiological barrier
3. indigenous microbiotia
33
describe the secretory antimicrobial compound, lysozyme aka muramidase
lysozyme cleaves (Beta 1,4 -glycosidic) linkages b/t NAG+ NAM --> manily effective against gram +
34
what are the 5 main secretory antimicrobial compounds of mucosal surfaces?
```
lysozyme (muramidase)
lactoferrin
cathelicidin
defensins
secretory immunoglobulins
```
35
describe the secretory antimucorbial compound, lactoferrin
bacteriostatic effects via sequestering iron, goal is to collect all iron+male availability of free iron low for bacteria
36
Describe the secretory anti microbial compound, cathelicidin
its a positively charged Antimicrobial cationic peptide that disrupts the negatively charged lipid membranes of gram negative bateria
37
Describe the secretory antimicrobial compound, defensins
they are positively charged antimicrobial cationic peptides that create pores in microbes
38
what is the difference between alpha-defensins and beta-defensins?
alpha ones are produced by neutrophils and paneth cells in intestine, and beta ones area produced by epithelial cells
39
Describe the secretory antimicrobial compound, immunoglobulines
secretory IgA pathogens which disrupts their ability of the pathogen to adhere
40
what are the 4 natural antimicrobial and physiological properties that assist with creating and physical barrier along mucosal surfaces?
1. acidity
2. motility
3. mucous layer with underlying glycocalyx
4. tight junctions
41
Describe how acidity acts as a natural barrier along mucosal surfaces
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.
42
Describe how motility acts as a natural barrier along mucosal surfaces
a constant flow of chyme and muscular movements can actually tip off the microbes that try to adhere
43
describe how the mucous layer with underlying glycol calyx acts asa natural barrier along mucosal surfaces
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
44
describe how tight junctions act as natural barriers for mucosal surfaces
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)
45
describe the role of indigineous microbiota in protection of mucosal surfaces
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
46
why do most diseases occur in the illiim and colon
1.motility decreases around illiim
2pH becomes neutral around illiim
3.environmental becomes anaerobic around ilium
47
what re the 3 major ways that pathogenic bacteria overcome innate barrier defenses
acid resistance
fimbrial pili
bacterial structures
48
How does acid resistance help pathogenic bacteria to overcome innate barrier defenses
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)
49
How do fimbriaw/pili help pathogenic bacteria to overcome innate barrier defenses
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
50
what are the 5 bacterial structures used by gram - pathogenic bacteria to overcome innate barrier defenses of the host
1. cell membrane sensitivities to bactericidal compounds
2. cationic amino acids
3. siderophores
4. capsule
5. mechanisms for neutralizing macrophages
51
How do cationic amino acids help pathogenic bacteria overcome innate barrier defenses of host
bacteria put anionic AA into the cell men of the host to reduce the effects of host cationic antimicrobial peptides (defensins and cathelicidin)
52
how to Siderophores help pathogenic bateria overcome the innate barrier defenses of the host?
siderophores sequester iron in low iron environments (e.g enterobacctin produced by E.coli) to negate the effects of host lactoferin
53
in what 2 ways do pathogenic bacteria avoid being phagocytosed
1. development of a capsule to resist phagocytosis
| 2. development of me chasms capable of neutralizing the pahocytic compartment of macrophages
54
why are macrophages an important part of mucosal immunity
macrophages recognize microbes via pattern recognition of the macrophages and the ability to kill many microbes
55
describe how activation of PRRs on macrophages also initiates the inflammatory response
inflammatory cytokines TNF, IL1 IL2 and chemokines would be activated and start recruitment upon activation of TLRs esp TLR4
56
what is the downside to initiating the inflammatory response
inflm response such as TNF can disrupt (loosen) the tight jxns b/t epithelial cells which creates a pathway for pathogen invasion
57
where are the densest cluster of lymph noes found
near mucosal tissue
58
what are the 2 main gram neg toxin producing bacterial pathogens of mucosal surfaces
1. vibrio sp
| 2. enterotoxigenic ecoli etec
59
what are 5 major symptoms of a gram neg toxin producing bacterial infection
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
60
what are 4 species of vibrio
1. cholerae
2. parahaemolytics
3. vulvinticus
4. alginolyticus
61
which form of vibrio causes the most severe disease
v.cholerae
62
name 3 physical characteristics of v.cholerae
1. gram neg
2. rod
3. single flagella
63
what was different b/t the new 0139ElTor strain of v.cholerae and the original ElTor strain
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
64
what are the 3 major virulence factors for V.cholerae
1. flagella
2. pili
3. cholera toxin
65
why is having flagella a particularly important virulence factor for v.cholerae?
flagella allows v.cholerae to be motile this is especially important bc their nature niche is sea water
66
why is having poi an important virulence factor for v cholerae
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
67
what does phage encoded mean in regards to cholera toxin (ctx)
ctx is phage encoded implying that different strains can obtain this gene to produce cholera toxin
68
how does ctx work
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
on what basis are e.coli grouped?
e.coli are grouped based on what kind of disease they cause
70
what are the 3 major categories of ecoli..give examples
1. secretory diarrhea ETEC, EPEC
2. Dysentery-like EHEC
3. urinary tract infections UPEC
71
what is the most common cause of traveler's diarrhea
Enterotoxigenic ecoli
72
describe the infectious dose of ETEC
etec has large infectious dose because its very susceptible to acid
73
what is the role of CFA for ETEC
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
what 2 toxins are produced by ETEC
1. heat-liable toxin (LT) --> degrades upon heating
| 2. heat-stable toxin (ST) --> stable upon heating
75
what is the mechanism for heat liable toxin
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
what is the mechanism for Heat-stable toxin
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
what is the importance of adenylate/guanylate cyclase
ATP-AC/ GTP-CC --> cAMP/cGMP
78
what is the importance of cAMP/cGMP
causes cell to stop absorbing Na
79
which ETEC toxin is similar to cholera toxin
LT heat-liable toxin
80
what is the single most important factor in the treatment of v.cholorea
oral rehydration
81
why is it important to first rule out v.cholorae when diagnosing non invasive bacterial pathogens
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
what are the 4 ways to rule out v.cholorear when testing for non invasive bacterial pathogens
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
what are the hybrid misfits
enteropathogenic ecoli EPEL and enterohemorrhagic ecoli EHEC
84
where to EPEC and EHEC colonize
lower small intestinal /upper large intesitine
85
what kind of lesion results from EHEC or EPEC colinization
attaching and effacing lesion
86
where might you find blood with EHEC infection
stool and possibly urine
87
what is the infectious dose sign for ePEC
large infectious dose size therefore highly acid sensitive/susceptible
88
what lind of diarrhea is assoc with EPEC
non inflammatory secretory diarrhea
89
is EPEC a toxin producer?
NO!
90
what is the disease causing mechism for EPEC
it is the colonization itself that causes the diseases / characteristic intimate adherence pattern aka " attaching and effacing lesion" NOT a toxin, NOT invasion
91
what are the 3 steps for intimate adherence pattern of colonization aka attaching and effacing lesion
1. bundle formin pili
2. type 3 secretion of Tir into host epithelial cells
3. Tir binding to intimin
92
what is the fxn of budge forming pilus for EPEC
Bfs assists in adherence from a relatively long distance
93
what is the result of type III secretion of TIR into host cell
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
describe pedestal formation assoc with EPEC
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
how does enteropathogenic Ecoli induce diahrrea
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
who are most susceptible to EPEC
newborns
97
what is the major difference between EPEC and EHEC
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
what genes are unique to EHEC
has set of EPEC genes called Eae genes so it produces an effacing lession
99
what toxin is produced by EHEC
shigella like toxin aka vero toxin
100
what/who is the primary resorvior for EHEC
cattle are primary resorvoir
101
what is the most common strand of EHEC
ecoli 0157:H7
102
what kind of lesion does EHEC cause
attaching effacing lesion (gastroenteritis)
103
what does shiga-like toxin attack
small blood vessels of large intestines
104
what are 2 major diseases that result from shiga-like toxin in EHEC
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
how does EHEC cause on attaching and effacing lesion
same 3 steps as w/EPEC
106
does inflammation enhance or reduce the effects of shiva-like toxin
inflmmatory cytokines IL1 , TNF-alpha engance/ intensifies the effects of the shiga-like toxin
107
why is tx of EHEC with antibiotics considered to be controversial
bc it stimulates the verotoxin production
108
what organ besides the colon is susceptible to shiva-like toxin
the kidneys
109
how does shigalike toxin affect the kidneys
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
what is the most common form of bacterial infection besides mouth and most frequent cause for doctors visits by adults
UTIS urinary tract infections
111
what is the term for inflammation of bladder
cyctitis
112
why are UTIs more common in women
1. anatomical reasons
| 2. during pregnancy, hormones cause dilation and decreased peristalsis of the ureters
113
why does age affect the incidence of UTIs in men
incidence of UTI goes up w/age in men bc the antimicrobial substance produced by the prostate gland becomes less active with age.
114
what is an uncomplicated UTI
1. all normal defense mechanisms are intact
2. no recent hospital admissions
3. disease limited to lower urinary tract
115
what is a complicated UTI
1. some structural abnormality in urinary tract
2. recent admission to hosp
3. disease most likely will spread to kidneys
116
what is cystitis
inflammation in the bladder
117
what is pyelonephritis
inflammation of the kidney (retrograde flow of urine from bladder to kidneys)
118
what is the most common bacterial pathogen that causes uncomplicated UTI
ecoli
119
what is the most common bacterial pathogen that causes complicated UTI
psuedomonas aeruginosa
120
what are the natural barrier defenses found in the urinary tract
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
name 6 reasons why cystitis can progress to pyelonephritis
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
what kind of UTI does UPEC cause
uncomplicated UTI
123
How does UPEC adhere to urinary tract tissue?
Fimbriae
124
with UPEC what kind of adhesion is needed for adhesion resulting in acute cystitis uncomplicated UTI
FimH (fibrial antigen)
125
with UPEC what kind of adhesion is needed for adhesion resulting in pyelonephritis
P fimbrial
126
what are the 2 adhesions UPEC requires for adhesion
FimH and P fibrae
127
why is aerobactin import in for UPEC to produce
aerobactin is a sidrophore used by UPEC for sequestering iron
128
why is hemolysin important for UPEC to produce
hemolysin is used by UPEC to lyse RBCs to host (assoc with pyelonephtritis) leading to bloody urine
129
what kind of UTI does proteus mirabilis cause
causes both complicated and uncomplicated uti
130
what pathogen is most likely to be the cause of UTIs resulting from abnormal urinary tract structure
Proteus Mirabilis
131
does Proteus Mirabilis cause a more or less severe UTI compared to ecoli
Proteus Mirabilis UTIs tend to be more severe than those caused by ecoli due to additional virulence factors
132
what are the 5 virulence factors assoc with Proteus Mirabilis
1. flagella
2. Hemolysin
3. Adhesins
4. IgA protease
5. Urease
133
why are flagella an important virulence factor for Proteus Mirabilis
flagella allow Proteus Mirabilis to be highly motile and thus capable of swimming in bladder and up ureters
134
why are the adhesions of Proteus Mirabilis considered an important virulence factor
they are specific for adhesion of urinary epithelium in particular
135
why is IgA protease an important virulence factor for Proteus Mirabilis
IgA protease degrades IgA which makes it easier for Proteus Mirabilis to adhere to tissues
136
which virulence factor is the #1 reason that Proteus Mirabilis is dangerous
urease
137
why is urease an important virulence factor for Proteus Mirabilis
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
why is the production of urease dangerous in the urinary system
leads to chronic infection
139
how are UTIs diagnosed
by counting the bacteria in the urine
140
when would antibiotics be prescribed for a healthy individual (i.e asymptomatic with a uti)
health (asymptomatic) individual bacteriurea > or = to 100,000 CFU/mL
141
when would antibiotics be prescribed for a symptomatic individual with a uti
individual with dysuria > or = to 100 with pyuria
142
how can Proteus Mirabilis, specifically, be diagnosed
1. consistently alkaline urine
| 2. prodcution of urease
143
how does treatment of uti due to Proteus Mirabilis differ when the infection is in kidney vs bladder
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
Is Klebsiella pneumoniae mobile or immobile and why
Klebsiella pneumoniae is immobile due to its large capsule with no flagella
145
what kind of disease assoc with the lungs results from Klebsiella
Klebsiella bacterial pneumoniae: fluid fills the lungs (usually assoc with immune compromised patients)
146
what are the 4 major virulence factors for the Klebsiella pneumoniae
1. pili
2. enterotoxin
3. aerobactin
4. capsule
147
what type of pili are necessary for Klebsiella pneumoniae adhesion to respiratory epithelial cells
type III pili
148
what type of pili are necessary for Klebsiella pneumoniae adhesion to urinary tract epithelial cells
type I pili
149
how does Klebsiella pneumoniae induce a watery diarrhea
caused by its enterotoxin similar to LT and ST of ETEC
150
why is aerobactin an important virulence factor for Klebsiella pneumoniae
its an iron sequestering protein
151
why is a capsule an important virulence factor for Klebsiella pneumoniae
it gives Klebsiella pneumoniae an antiphagocytic characteristic which prevents the macrophage from engulfing and degrading the bacteria
152
why is the capsule considered #1 virulence factor for Klebsiella pneumoniae
bc without it Klebsiella pneumoniae is avirulent
153
why is Heliobacter pylori considered a slow pathogen
bc the diseases it caused take a long period of time to do damage and have a long asymptomatic time period
154
where does Heliobacter pylori colonize
Antrum of stomach only found in the mucous overlain mucous-secreting cells of the stomach
155
how does Heliobacter pylori transmission differ from other gram negative pathogens that we have studied
spread/trasminssion is oral to oral also fecal to oral
156
what are the 4 main diseases that Heliobacter pylori leads to
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
what is the animal reservoir for Heliobacter pylori
none! Heliobacter pylori is only found in humans.
158
all of the diseases resulting from Heliobacter pylori infection are always produced by the development of what
chronic superficial gastritis (low inflammation/redness) that can be present for years w/o visible symptoms
159
describe the inflammatory / effector molecules asssoc with Heliobacter pylori
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
why is the production of urease an important virulence factor for Heliobacter pylori
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
how can production of urease be useful for identification of Heliobacter pylori
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
why is production of cytotoxin important for Heliobacter pylori
cytotoxin is assoc with peptic ulcer disease and induces vacuolation and apoptosis of epithelial cells
163
why is the down regulation of somatostatin producing D-cells important for Heliobacter pylori
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
why is an increase in gastrin production important for the development of Heliobacter pylori mediated carcinogenesis
incerased gastrin production resulting from Heliobacter pylori infection leads to increased cell proliferation and then increased numbers of host cell mutation
165
in what 3 ways can the enhanced inflammatory response from Heliobacter pylori infection lead to carcinogenesis
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
what is atrophic gastritis
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
