helicobacter

Question 1

Helicobacter pylori: basic morphology?

Answer 1

Small, curved/spiral, gram-negative rod; microaerophilic.

Question 2

H. pylori: motility feature?

Answer 2

Highly motile with rapid corkscrew motion.

Question 3

H. pylori flagella characteristics?

Answer 3

Multiple, polar, sheathed flagella.

Question 4

How do H. pylori forms change with culture age?

Answer 4

Curved/spiral in fresh cultures; spherical (coccoid) forms in older cultures.

Question 5

Key lab tests H. pylori is positive for?

Answer 5

Urease-positive, oxidase-positive, catalase-positive.

Question 6

Why is urease critical for H. pylori survival?

Answer 6

Generates ammonium ions that buffer gastric acidity.

Question 7

Where is H. pylori mainly located in the stomach?

Answer 7

Primarily in the mucous layer; can adhere to mucosal epithelial cells.

Question 8

What epithelium does H. pylori colonize (and not colonize)?

Answer 8

Colonizes gastric-type epithelium (antrum/fundus); does NOT colonize intestinal epithelium.

Question 9

Where can H. pylori be found ectopically?

Answer 9

Duodenum or esophagus (when gastric-type epithelium is present).

Question 10

Is H. pylori invasive (does it invade tissue)?

Answer 10

No; it induces changes via extracellular products and direct contact, not tissue invasion.

Question 11

Why do spiral shape + flagella matter in pathogenesis?

Answer 11

Aid motility through viscous gastric mucus for colonization.

Question 12

Major adhesin BabA binds what receptor?

Answer 12

Fucosylated Lewis b receptor on gastric epithelial cells.

Question 13

SabA binds what receptor?

Answer 13

Sialyl Lewis X receptors.

Question 14

HopQ binds what host molecules?

Answer 14

Carcinoembryonic antigen–related cell adhesion molecules (CEACAMs).

Question 15

Other named adhesins besides BabA/SabA/HopQ?

Answer 15

AlpA and AlpB.

Question 16

What is the cag pathogenicity island (cag PAI)?

Answer 16

A ~35–40 kb region linked to increased pathogenicity; includes cagA.

Question 17

How is CagA delivered into host cells?

Answer 17

Translocated via a type IV secretion system.

Question 18

What does CagA do inside host cells?

Answer 18

Alters signaling pathways, cell shape, and cytokine production → inflammation.

Question 19

Clinical outcomes associated with CagA+ strains?

Answer 19

More severe disease; higher risk of duodenal ulcers and gastric cancer.

Question 20

VacA encodes what?

Answer 20

A vacuolating cytotoxin (secreted pore-forming protein).

Question 21

VacA polymorphism regions?

Answer 21

s, m, and i regions.

Question 22

Which VacA genotype is linked to more severe outcomes?

Answer 22

s1 genotype (often linked with cagA+ strains).

Question 23

VacA s1 vs s2 activity in cellular assays?

Answer 23

s1 active; s2 inactive.

Question 24

What is HtrA in H. pylori?

Answer 24

A protease that helps H. pylori access basolateral gastric epithelial cells.

Question 25

How does H. pylori downregulate host inflammatory recognition?

Answer 25

Modified LPS with reduced proinflammatory activity and flagellin poorly recognized by TLR5.

Question 26

What molecular mimicry helps H. pylori persist?

Answer 26

Expression of Lewis antigens matching gastric epithelial Lewis antigens.

Question 27

Other immune evasion mechanism involving lipids?

Answer 27

Cholesterol glucosylation contributes to immune evasion.

Question 28

What immune cells are commonly seen in H. pylori gastritis?

Answer 28

Lymphocytes, monocytes, plasma cells; sometimes neutrophils and eosinophils.

Question 29

Common gastric pattern in children with H. pylori?

Answer 29

Follicular lymphoid pattern.

Question 30

Hormone change often seen in colonized individuals?

Answer 30

Higher gastrin levels (decrease after eradication).

Question 31

How can increased gastrin contribute to duodenal ulcers?

Answer 31

Increases parietal cell mass and acid output → duodenal ulceration.

Question 32

Global reservoir of H. pylori?

Answer 32

Humans are the major (likely sole) reservoir.

Question 33

Main transmission routes of H. pylori?

Answer 33

Fecal–oral and oral–oral; also possible via vomitus-oral contact or improperly cleaned endoscopes.

Question 34

Is sexual transmission common?

Answer 34

No, it does not occur frequently.

Question 35

Where has H. pylori been detected that supports oral/oral transmission?

Answer 35

Dental plaque and saliva (DNA detectable); also isolated from feces (esp. children).

Question 36

What social setting increases colonization rates?

Answer 36

Suboptimal sanitation; institutions/orphanages; family clustering.

Question 37

When is H. pylori usually acquired?

Answer 37

Early childhood (not typically during the first year of life).

Question 38

How long can H. pylori persist once acquired?

Answer 38

Decades or a lifetime.

Question 39

Prevalence pattern in developing countries by age 10?

Answer 39

>70% colonized by age 10.

Question 40

Trend in developed countries over past decades?

Answer 40

Prevalence declining (improved sanitation, smaller families, antibiotic exposure).

Question 41

What is the “birth cohort effect” in H. pylori?

Answer 41

Higher prevalence in older adults reflects higher childhood acquisition in earlier birth cohorts.

Question 42

Acute H. pylori acquisition symptoms?

Answer 42

Nausea, upper abdominal pain, vomiting, burping, fever.

Question 43

Typical duration of acute illness after acquisition?

Answer 43

3–14 days; most resolve in <1 week.

Question 44

What physiologic change can last up to 1 year after acute acquisition?

Answer 44

Hypochlorhydria (low stomach acid).

Question 45

Are most acquisitions symptomatic or asymptomatic?

Answer 45

Most are asymptomatic, especially in children.

Question 46

Association of H. pylori with duodenal ulcer disease?

Answer 46

>90% of “idiopathic” duodenal ulcer patients are colonized.

Question 47

How much does prior H. pylori colonization increase duodenal ulcer risk?

Answer 47

About 3–4× increased risk (especially cagA+ strains).

Question 48

Where does H. pylori colonize in the duodenum?

Answer 48

Only in areas of gastric metaplasia.

Question 49

Association of H. pylori with benign gastric ulcers?

Answer 49

~50–80% colonized (higher if NSAID/aspirin excluded).

Question 50

H. pylori and gastric carcinoma relationship?

Answer 50

Chronic gastritis is a risk factor; linked to atrophic gastritis and intestinal metaplasia leading toward cancer.

Question 51

Does eradication reverse intestinal metaplasia?

Answer 51

No; intestinal metaplasia is not reversed (atrophic gastritis may be partially reversible).

Question 52

H. pylori and MALT lymphoma relationship?

Answer 52

Most gastric MALT lymphomas are B-cell lymphomas associated with H. pylori.

Question 53

Effect of eradication on gastric MALT lymphoma?

Answer 53

Eradication can improve/regress tumors in many patients.

Question 54

Inverse relationship: H. pylori vs what esophageal diseases?

Answer 54

GERD, Barrett’s esophagus, and esophageal adenocarcinoma (especially inverse with cagA+ strains).

Question 55

Noninvasive diagnostic tests for H. pylori?

Answer 55

Serology (IgG), urea breath test, stool (fecal) antigen test.

Question 56

Invasive diagnostic method?

Answer 56

Endoscopy with gastric biopsy (histology/culture/rapid urease test).

Question 57

Culture conditions for biopsy specimens?

Answer 57

Incubate 2–5 days at 35–37°C in moist microaerobic atmosphere (~5% O2).

Question 58

Rapid urease test sensitivity timing?

Answer 58

~60% at 1 hour; >90% at 24 hours.

Question 59

What does the urea breath test detect?

Answer 59

Urease activity: urea → labeled CO2 in breath within ~1 hour.

Question 60

When does a negative urea breath test indicate eradication?

Answer 60

Negative 1–3 months after therapy suggests successful eradication.

Question 61

When can stool antigen confirm response after treatment?

Answer 61

As early as 1 month after treatment.

Question 62

What can cause false-negative stool antigen results?

Answer 62

Stool preservatives like formaldehyde.

Question 63

Why can serology remain positive after treatment?

Answer 63

IgG declines slowly; needs ~3–6 months to noticeably decrease.

Question 64

How long after therapy to confirm eradication by biopsy/breath/stool tests?

Answer 64

At least 1 month after therapy.

Question 65

How long after therapy to confirm eradication by serology?

Answer 65

At least 6 months after therapy.

Question 66

When is treatment clearly indicated?

Answer 66

H. pylori–associated peptic ulcer disease (duodenal and gastric if associated), gastric MALT lymphoma, H. pylori+ ITP, post–early gastric cancer resection/high gastric cancer risk.

Question 67

Is treatment always indicated for asymptomatic colonization?

Answer 67

No; most colonized individuals are asymptomatic (treat based on indications like ulcers/cancer risk).

Question 68

Key concept for therapy strategy?

Answer 68

Combination therapy (monotherapy often insufficient).

Question 69

Why are PPIs included in regimens?

Answer 69

Improve eradication by raising gastric pH; may directly inhibit H. pylori and block urease activity.

Question 70

Primary metronidazole/tinidazole resistance rate?

Answer 70

~20–40% primary resistance (noted particularly in young women or prior antiparasitic therapy).

Question 71

Resistance trend for clarithromycin/macrolides/fluoroquinolones?

Answer 71

Increasing resistance.

Question 72

Which resistances are less common?

Answer 72

Amoxicillin and tetracycline resistance are less common.

Question 73

What should be done after treatment failure?

Answer 73

Use a different regimen; consider culture + susceptibility testing before second-line therapy.

Question 74

Potential risks of eradication therapy?

Answer 74

Antibiotic resistance, medication GI side effects, rare antibiotic-associated colitis/candidiasis; increased reflux esophagitis after eradication.

Question 75

Prevention: is H. pylori immunization routine?

Answer 75

No, immunization is not routinely practiced.

Question 76

Vaccine evidence mentioned for H. pylori?

Answer 76

Phase III study in China: recombinant oral vaccine reduced acquisition in children (needs more long-term study).