Prevalence, familial clustering, and influencing factors of Helicobacter pylori infection in Western Fujian Province households

Abstract

BACKGROUND

The epidemiological status of family-based Helicobacter pylori (H. pylori) infection in Western Fujian Province is unclear. H. pylori infection is a major global public health concern and is closely associated with various gastrointestinal and systemic diseases. Familial clustering has been increasingly recognized as an important transmission pattern; however, region-specific data are limited. To our knowledge, this study represents the first family-based epidemiological investigation of H. pylori infections in Western Fujian Province (Minxi). We hypothesized that H. pylori infection exhibits significant familial clustering and is associated with modifiable lifestyle factors in this region.

AIM

To investigate H. pylori prevalence, familial clustering, and infection-associated factors in Western Fujian Province to inform prevention and control strategies.

METHODS

This observational study used stratified sampling to recruit households from seven districts and counties in the Minxi region between January and December 2025. Overall, 415 households (1427 individuals) were included. Standardized questionnaires were used to collect basic demographic characteristics and dietary and hygiene-related information. All participants underwent the ¹³C-urea breath test to determine H. pylori infection status. Univariate and multivariate analyses were conducted to identify factors associated with H. pylori infection, and a binomial goodness-of-fit test assessed familial clustering.

RESULTS

The overall and household H. pylori infection rates were 34.0% and 56.6%, respectively. Not using communal chopsticks and spoons [odds ratio (OR) = 2.669, 95% confidence interval (CI): 1.209-5.895, P < 0.05] and infrequent dishware disinfection (OR = 6.919, 95%CI: 3.897-12.283, P < 0.05) were independently associated with H. pylori infection at the household level. Among adults, insufficient awareness of H. pylori, beer consumption, and frequent spicy-food intake were independently associated with H. pylori infection. No family history of H. pylori infection; low-salt diet; frequent garlic consumption; limited intake of strong tea, coffee, and milk tea; and, adequate sleep were associated with lower infection prevalence. In minors, frequent object biting and dental caries were independently associated with H. pylori infection. No family history of H. pylori infection, independent use of tableware, low consumption of smoked and fried foods, and low-salt diet were associated with lower infection prevalence. H. pylori infection exhibited significant familial clustering (χ² = 134.751, P < 0.05).

CONCLUSION

H. pylori infection in Western Fujian Province exhibits high prevalence and familial clustering and is associated with multiple lifestyle factors. Given the cross-sectional design of this study, causal inferences cannot be drawn; nonetheless, these findings support the need for targeted, family-based prevention and control strategies and warrant further investigation through prospective longitudinal studies.

Key Words: Helicobacter pylori infection; Familial clustering; ¹³C-urea breath test; Risk factors; Minxi region

Core Tip: Current research on the familial clustering of Helicobacter pylori (H. pylori) infection, its prevalence (particularly among minors), and its influencing factors remains limited, with no reported studies in Western Fujian Province. This study identified an overall H. pylori infection rate of 34.0% in Western Fujian Province, including 34.5% among adults and 31.1% among minors. H. pylori infection was associated with household hygiene practices and individual dietary hygiene behaviors, and familial clustering of H. pylori was observed. These findings suggest that family-based prevention and control strategies may be more effective for managing H. pylori infection.

INTRODUCTION

Helicobacter pylori (H. pylori) is a gram-negative microaerophilic pathogenic bacterium characterized by an S-shaped or curved morphology that primarily colonizes the human gastric epithelium. In 1994, the World Health Organization (WHO) and the International Agency for Research on Cancer categorized H. pylori as a group 1 human carcinogen. Globally, H. pylori infection represents the third leading risk factor for cancer-related mortality, making it one of the most prevalent bacterial infections worldwide[1].

H. pylori is implicated in a broad spectrum of gastroduodenal disorders, including chronic active gastritis, atrophic gastritis, gastric polyps, colorectal polyps, peptic ulcers, mucosa-associated lymphoid tissue lymphoma, and non-cardia gastric cancer. As outlined in the Kyoto Consensus[2], H. pylori infection is the predominant etiological factor for gastric cancer, with approximately 90% of gastric cancer cases attributable to this infection. A population-based study on H. pylori-associated gastric cancer in China[3] reported that, among the 478000 newly diagnosed gastric cancer cases in China in 2020, 70% were H. pylori-positive. H. pylori infection increases the risk of non-cardia gastric cancer by over sixfold and cardia gastric cancer by more than threefold. Beyond its established correlation with the initiation and progression of gastrointestinal diseases, recent accumulating evidence indicates that H. pylori infection may also be associated with the pathogenesis of hematological and rheumatic diseases[4,5], cardiovascular diseases[6,7], respiratory diseases[8], and neurological disorders[9,10]. The underlying mechanisms may involve H. pylori infection mediated chronic inflammation, dysregulated lipid metabolism, oxidative stress, and endothelial dysfunction.

Data from recent global epidemiological studies indicate that nearly half of the world’s population is currently infected with H. pylori[11], with an average infection rate of approximately 41.5% in China[12]. A meta-analysis conducted in 2021 focusing on pediatric H. pylori infections in China reported an overall prevalence of 30.3% among children and adolescents[13]. The high prevalence of H. pylori infection has therefore emerged as a major public health challenge in China and worldwide. Although the precise transmission routes of H. pylori have not been fully elucidated, human-to-human transmission is universally recognized as the primary mode of transmission[14], and H. pylori infection exhibits a notable tendency toward familial clustering[15-19]. In response to this familial clustering feature, China issued the 2021 China Consensus Report on Family-Based H. pylori Infection Control and Management[20] and the 2022 Sixth National Consensus Report on H. pylori Infection Management[21], both of which recommend population-level and family-oriented prevention and control strategies to reduce H. pylori-associated disease burden. Early intervention aimed at preventing individual infections and interrupting intrafamilial cross-transmission is expected to yield substantial public health benefits.

To date, familial clustering, prevalence (especially among minors), and risk factors associated with H. pylori infection in other parts of China have been studied, but no relevant studies have been conducted in Western Fujian Province. Owing to the distinctive geographical and cultural characteristics of this region, investigating the prevalence, familial clustering patterns, and risk factors of H. pylori infection in Western Fujian Province is of considerable academic and practical importance. Therefore, this study was designed to assess the H. pylori infection status and lifestyle-related risk factors among family members in Western Fujian Province; to systematically elucidate the epidemiological characteristics, familial clustering patterns, and influencing factors of H. pylori infection in this region; and, to specifically analyze the prevalence of H. pylori infection among minors. The findings of this study are expected to enhance public awareness regarding familial H. pylori prevention, reduce the incidence of both individual and familial infections, and provide evidence-based guidance for the development and optimization of H. pylori eradication and control strategies.

MATERIALS AND METHODS

Study population and design

This family-based survey was conducted across seven districts and counties in Western Fujian Province from January 2025 to December 2025. Totally 1427 individuals from 415 households in the region were randomly selected using a stratified sampling approach to participate in the survey. The inclusion criteria were as follows: (1) Family members residing in Western Fujian Province, with a minimum cohabitation period of 6 months and at least two family members; (2) Family members who consented to and cooperated with the ¹³C breath test and questionnaire survey; and (3) Minors who provided parental consent and signed an informed consent form.

The exclusion criteria were as follows: (1) Patients with severe cardiovascular or cerebrovascular diseases (e.g., acute myocardial infarction, cerebral hemorrhage, cerebral infarction, or other conditions severely impairing the daily living ability) or acute infectious diseases; (2) Those who had used antibiotics or bismuth agents within the last 4 weeks, proton pump inhibitors, glucocorticoids, gastric mucosal protectants, or traditional Chinese medicine within 2 weeks; (3) Women who were pregnant or lactating; and (4) Individuals who were unable to cooperate with the examination or questionnaire.

All participants voluntarily participated in the study and provided written informed consent. This study was reviewed and approved by the Medical Ethics Committee of Longyan First Affiliated Hospital of Fujian Medical University, No. LYREC2024-k019-01.

Questionnaires for family members

A standardized questionnaire was administered, and the study investigators explained the purpose and requirements to participants prior to obtaining informed consent. Trained staff distributed the questionnaire and guided participants in completing it on-site, with all data collected at the household level. The survey included basic personal information of family members, such as sex, age, marital status, education level, occupation, and personal lifestyle habits, as well as common family issues.

H. pylori testing for all family members

All participants underwent H. pylori testing on the morning of the examination day, either after an over nigh fasting or after at least 2 hours of fasting and water restriction. The basic information of each participant was recorded on the blue and pink airbags, respectively. Participants maintained normal exhalation and blew air into the blue airbag until it was full, after which the bag was immediately sealed; this sample was recorded as the 0-minute exhalation. A capsule containing ¹³C-urea (75 mg) and 50 mL of cool water was then administered orally. After resting quietly for 30 minutes, the same procedure was repeated for the pink airbag, and the sample was recorded as the 30-minute exhalation.

After sample collection, the corresponding air collection bag was inserted into a preheated detector. The instrument automatically performed the analysis and printed the results, which were recorded by the investigator. The results of the ¹³C-urea breath test were expressed as the delta over baseline (DOB) value, calculated as the difference between the δ‰ of ¹³C-carbon dioxide measured at the 30 minutes and the δ‰ at the 0-minute point: DOB = δ‰ (30 minutes) - δ‰ (0 minute). DOB ≥ 4.0‰ indicated a positive H. pylori status, whereas a DOB < 4.0‰ indicated a negative H. pylori status.

Definitions

Households with positive H. pylori infection: At least one household member tested positive for H. pylori during the survey period[19].

Household structure types: Spousal households were defined as family units composed of both spouses[22]. Nuclear families included couples and their unmarried children. Stem families comprised two or more generations of couples without intergenerational gaps. Other types included household structures not classified into the above three categories.

Smokers: According to the WHO criteria, individuals with continuous or cumulative smoking duration ≥ 6 months are defined as smokers. Second-hand smoke exposure was defined as exposure of non-smokers to tobacco smoke from smokers for at least 15 minutes per day on more than 1 day per week. Smoking intensity was assessed using the smoking index (SI), calculated as the number of cigarettes smoked per day multiplied by the number of years of smoking. An SI ≤ 200 indicates light smoking; 200-400, moderate smoking; and ≥ 400, heavy smoking[23].

Alcohol consumers: WHO criteria define individuals who consume alcohol at least twice per week for ≥ 1 year as alcohol consumers. Alcohol intake is calculated as follows: Daily alcohol intake (g) = daily alcohol consumption (mL) × alcohol concentration (%) × 0.8 (alcohol density). Daily alcohol intake ≤ 25 g was classified as low; 26-39 g, moderate; and ≥ 40 g, high[24].

Statistical analysis

Data were compiled in Excel and analyzed using IBM SPSS Statistics for Windows version 25.0. Continuous variables were presented as mean ± SD, whereas categorical variables were expressed as percentages (%). Between-group comparisons were performed using the χ² test. Preliminary screening for significant factors was conducted using one-way analysis, followed by multivariate logistic regression analysis to calculate the odds ratio (OR) and 95% confidence interval (CI). The family clustering of H. pylori infection was evaluated using the goodness-of-fit test for the binomial distribution. P < 0.05 was considered statistically significant.

RESULTS

General characteristics of enrolled individuals

This study included 415 eligible households, comprising 1427 individuals aged 3-91 years, with a mean age of 40.8 ± 18.8 years. Among them, 485 (34.0%) tested positive for H. pylori infection, whereas 942 (66.0%) tested negative. The cohort included 690 (48.4%) males and 737 (51.6%) females, with 1208 adults (84.7%) and 219 minors (15.3%). The overall H. pylori infection rate was 34.0%, with rates of 34.5% among adults and 31.1% among minors. The infection rate was 41.4% among smokers, 41.8% among individuals exposed to secondhand smoke, 33.3% among those who washed their hands before meals or after using the toilet, 43.0% among individuals with gastrointestinal symptoms, 45.7% among those with a family history of H. pylori infection, and 54.6% among those with halitosis. These groups exhibited a higher risk of H. pylori infection. No statistically significant differences in H. pylori infection rates were observed according to sex, age, or place of residence (Table 1).

Table 1 Relationship between general characteristics and Helicobacter pylori infection among 1427 individuals.

Influencing factor	Number of respondents	Number of infected cases	Infection rate (%)	χ2 value	P value
Sex				0.003	0.957
Male	690	235	34.1
Female	737	250	33.9
Age				0.995	0.319
Adult	1208	417	34.5
Minor	219	68	31.1
Residence				0.019	0.889
Rural	529	181	34.2
Urban	898	304	33.9
Smoking				8.120	0.004
Yes	268	111	41.4
No	1159	374	32.3
Secondhand smoke exposure				22.253	0.000
Yes	519	217	41.8
No	908	268	29.5
Hand washing before meals and after defecation				4.975	0.026
Yes	1353	451	33.3
No	74	34	45.9
Gastrointestinal symptoms				28.808	0.000
Yes	509	219	43.0
No	918	266	29.0
Family history of H. pylori infection				129.322	0.000
Yes	854	390	45.7
No	573	95	16.6
Halitosis				201.576	0.000
Yes	610	333	54.6
No	817	152	18.6

P < 0.05 indicating a statistically significant difference. H. pylori: Helicobacter pylori.

Household risk factors for H. pylori infection

Univariate analysis of demographic characteristics revealed no significant association between household H. pylori infection and administrative district or place of residence. However, significant associations were observed with household size, family structure, per capita monthly income, shared use of chopsticks and spoons, shared tableware, shared drinking cups, shared toothbrush cups, and frequency of dishware disinfection (P < 0.05; Table 2).

Table 2 Single factor analysis of demographic characteristics associated with Helicobacter pylori infection in households.

Influencing factor	Number of households surveyed	Number of H. pylori-positive households	Positive rate (%)	χ2 value	P value
Jurisdiction				11.038	0.087
Xinluo District	127	79	62.2
Yongding District	48	24	50.0
Shanghang County	60	31	51.7
Changting County	60	30	50.0
Wuping County	40	19	47.5
Liancheng County	40	30	75.0
Zhangping City	40	22	55.0
Residence				0.076	0.783
Urban	269	151	56.1
Rural	146	84	57.5
Household size				21.593	0.001
2	1001	401	40.0
3	135	75	55.6
4	1072	692	64.5
5	49	32	65.3
6	19	14	73.7
7	5	5	100.0
Family structure				20.740	0.000
Spousal family	841	301	35.7
Nuclear family	1942	1152	59.3
Stem family	1132	762	67.3
Other family types	24	14	58.3
Per capita monthly household income (Chinese yuan)				27.204	0.000
≤ 1500	191	161	84.2
1501-3000	1761	1181	67.0
3001-5000	2012	962	47.8
> 5000	192	52	26.3
Separate chopsticks and spoons				29.494	0.000
No	352	219	62.2
Yes	63	16	25.4
Shared tableware				27.520	0.000
No	98	33	33.7
Yes	317	202	63.7
Shared drinking cups				5.949	0.015
No	348	188	54.0
Yes	67	47	70.1
Shared toothbrush cups				18.027	0.000
No	361	190	52.6
Yes	54	45	83.3
Frequency of tableware disinfection (time/week)				70.894	0.000
< 1	2531	1811	71.5
1-2	532	282	52.8
≥ 3	1092	262	23.9

¹Represent the baseline group within the current influencing factor category.

²Groups that showed statistically significant differences from group labeled 1.

P < 0.05 indicating a statistically significant difference. A special symbol in statistics indicating no statistical difference between groups with the same number and a statistically significant difference between groups with different numbers. H. pylori: Helicobacter pylori.

Multivariate logistic analysis was performed using variables that were statistically significant in the univariate analysis. The results demonstrated that not using communal chopsticks and spoons (OR = 2.669, 95%CI: 1.209-5.895, P < 0.05) and infrequent dishware disinfection (OR = 6.919, 95%CI: 3.897-12.283, P < 0.05) were independent risk factors for H. pylori infection in households. By contrast, a spousal family structure (OR = 0.293, 95%CI: 0.099-0.866, P < 0.05) and the independent use of toothbrush cups (OR = 0.289, 95%CI: 0.121-0.690, P < 0.05) were identified as protective factors against H. pylori infection (Table 3).

Table 3 Results of multivariate logistic analysis of factors associated with household Helicobacter pylori infection.

Variable	β	SE	Wald	P value	OR	95%CI
Household size	0.478	0.497	0.922	0.337	1.612	0.608-4.274
Spousal family	-1.226	0.553	4.926	0.026	0.293	0.099-0.866
Per capita monthly household income	1.803	1.026	3.090	0.079	6.066	0.813-45.272
Shared chopsticks and spoons	0.982	0.404	5.897	0.015	2.669	1.209-5.895
Shared tableware (no)	-0.590	0.322	3.348	0.067	0.554	0.295-1.043
Shared drinking cups (no)	-0.094	0.357	0.069	0.792	0.910	0.452-1.833
Shared toothbrushing cups (no)	-1.240	0.443	7.829	0.005	0.289	0.121-0.690
Tableware disinfection < 1 time/week	1.934	0.293	43.628	0.000	6.919	3.897-12.283

P < 0.05 indicating a statistically significant difference. OR: Odds ratio; CI: Confidence interval.

Risk factors for H. pylori infection in adults

A total of 1208 adults were enrolled in the analysis, including 562 males (46.5%) and 646 females (53.5%). The prevalence of H. pylori infection among adults was 34.5% (417/1208). One-way analysis was conducted to evaluate the H. pylori infection status based on demographic characteristics (sex, age, and place of residence), lifestyle factors, and dietary habits. The results revealed that adult H. pylori infection was associated with family role; awareness of H. pylori; smoking status; SI; second-hand smoke exposure; type of alcoholic beverage consumed; alcohol intake; history of gastrointestinal disease; gastrointestinal symptoms; family history of H. pylori infection; consumption of spicy foods; consumption of pickled foods; salt intake; consumption of vegetables and fruits; consumption of whole grains; garlic consumption; consumption of strong tea, coffee, or milk tea; the use of communal chopsticks and spoons when dining out; sleep duration; three-meal rhythm; tooth brushing frequency; toothbrush replacement frequency; and halitosis (P < 0.05). No significant associations were found between H. pylori infection and sex, age, place of residence, marital status, occupation, educational level, hand hygiene, oral diseases, consumption of dairy and soy products, or frequency of business travel (Tables 4 and 5).

Table 4 Relationship between Helicobacter pylori infection and different demographic characteristics in adults.

Influencing factor	Number of respondents	Number of infected cases	Infection rate (%)	χ2 value	P value
Sex				0.015	0.904
Male	562	195	34.7
Female	646	222	34.4
Age				4.392	0.356
18-35	313	114	36.4
36-50	387	130	33.6
51-65	395	143	36.2
66-75	96	25	26.0
> 75	17	5	29.4
Residence				0.168	0.682
Rural	754	257	34.1
Urban	454	160	35.2
Family role				14.805	0.011
Parents	6081	2211	36.3
Spouse	1742	412	23.6
Grandparents	1491	551	36.9
Children	2531	931	36.8
Grandchildren	17	3	17.6
Others	7	4	57.1
Marital status				0.929	0.818
Married	952	330	34.7
Unmarried	188	64	34.0
Divorced	26	7	26.9
Widowed	42	16	38.1
Occupation				4.705	0.453
Worker (staff, professional and technical personnel)	521	178	34.2
Civil servant	56	19	33.9
Farmer	244	90	36.9
Retired	99	31	31.3
Student	78	20	25.6
Freelancer (self-employed, unemployed)	210	79	37.6
Educational level				2.290	0.318
Primary school and below	182	69	37.9
Junior high school/senior high school/technical secondary school	462	165	35.7
College and above	564	183	32.4
Awareness of H. pylori				69.758	0.000
Unaware	6611	2961	44.8
Partially aware	5172	1112	21.5
Fully aware	30	10	33.3

¹Represent the baseline group within the current influencing factor category.

²Groups that showed statistically significant differences from group labeled 1.

P < 0.05 indicating a statistically significant difference. A special symbol in statistics indicating no statistical difference between groups with the same number and a statistically significant difference between groups with different numbers. H. pylori: Helicobacter pylori.

Table 5 Relationship between adult Helicobacter pylori infection and individual lifestyle and diet.

Influencing factor	Number of households surveyed	Number of H. pylori-positive households	Positive rate (%)	χ2 value	P value
Smoking				5.841	0.016
No	997	329	33.0
Yes	211	88	41.7
SI				6.118	0.047
Mild smoking	10661	3551	33.3
Moderate smoking	32	13	40.6
Heavy smoking	1102	492	44.5
Second-hand smoke exposure				18.476	0.000
No	746	223	29.9
Yes	462	194	42.0
Alcohol type				28.840	0.000
Liquor	1341	681	50.7
Red wine	25	12	48.0
Rice wine	46	20	43.5
Beer	691	311	44.9
None	9342	2862	30.6
Alcohol consumption (g/day)				16.368	0.000
Low dose	11431	3811	33.3
Medium dose	35	16	45.7
High dose	302	202	66.7
Hand washing after meals and defecation				2.547	0.110
No	64	28	43.8
Yes	1144	389	34.0
History of gastrointestinal diseases				6.664	0.010
No	799	296	37.0
Yes	409	121	29.6
Gastrointestinal symptoms				24.942	0.000
No	731	212	29.0
Yes	477	205	43.0
Family history of H. pylori infection				99.189	0.000
No	441	73	16.6
Yes	767	344	44.9
History of long-term medication				1.599	0.206
No	1101	386	35.1
Yes	107	31	29.0
Family history of upper gastrointestinal diseases				0.541	0.462
No	1077	368	34.2
Yes	131	49	37.4
Spicy food intake (time/week)				136.234	0.000
< 1	8691	2241	25.8
1-3	1592	662	41.5
> 3	1803	1273	70.6
Pickled food intake (time/week)				15.626	0.000
< 1	8721	2741	31.4
1-3	2862	1172	40.9
> 3	502	262	52.0
Salt intake (g/day)				205.886	0.000
< 6	831	177	21.3
≥ 6	377	240	63.7
Fruit and vegetable intake (time/week)				14.076	0.001
< 1	291	181	62.1
1-3	921	401	43.5
> 3	10872	3592	33.0
Whole grain intake (time/week)				23.802	0.000
< 1	6931	2791	40.3
1-3	3372	922	27.3
> 3	1782	462	25.8
Milk and dairy product intake (time/week)				4.821	0.090
< 1	6991	2591	37.1
1-3	2862	872	30.4
> 3	223	71	31.8
Soybean and soybean product intake (time/week)				2.392	0.302
< 1	370	139	37.6
1-3	629	206	32.8
> 3	209	72	34.4
Soup consumption (time/week)				0.343	0.842
< 1	56	21	37.5
1-3	126	45	35.7
> 3	1026	351	34.2
Garlic intake (time/week)				145.004	0.000
< 1	6831	3291	48.2
1-3	2092	562	26.8
> 3	3163	323	10.1
Strong tea/coffee/milk tea consumption (time/week)				10.674	0.005
< 1	9181	2951	32.1
1-3	169	67	39.6
> 3	1212	552	45.5
Use of separate chopsticks and spoons when dining out				21.219	0.000
No	840	325	38.7
Yes	368	92	25.0
Frequency of dining out (time/week)				4.530	0.104
< 1	806	263	32.6
1-3	258	95	36.8
> 3	144	59	41.0
Sleep duration (hours/day)				20.096	0.000
< 4	11	3	27.3
4-6	2151	861	40.0
6-8	6931	2591	37.4
> 8	2892	692	23.9
Breakfast habit and eating rhythm				9.947	0.007
No, irregular	83	34	41.0
Yes, irregular	752	372	49.3
Yes, regular	10501	3461	33.0
Toothbrushing frequency (time/day)				31.144	0.000
1	3251	1521	46.8
2	8212	2512	30.6
> 2	622	142	22.6
Toothbrush replacement frequency (months/time)				41.913	0.000
≤ 3	6711	1901	28.3
4-6	2631	891	33.8
> 6	2742	1382	50.4
Business trip frequency (day/month)				2.280	0.320
< 1	1177	409	34.7
1-5	22	7	31.8
> 5	9	1	11.1
Oral diseases (dental caries, dentures, periodontitis)				2.415	0.120
No	763	251	32.9
Yes	445	166	37.3
Halitosis				198.442	0.000
No	6781	1221	18.0
Yes, noticed by others	942	382	40.4
Yes, noticed by oneself	4363	2573	58.9

¹Represent the baseline group within the current influencing factor category.

²Groups that showed statistically significant differences from group labeled 1.

³Groups that showed statistically significant differences compared to both groups labeled 1 and 2.

P < 0.05 indicating a statistically significant difference. A special symbol in statistics indicating no statistical difference between groups with the same number and a statistically significant difference between groups with different numbers. H. pylori: Helicobacter pylori; SI: Smoking index.

Multivariate logistic analysis showed that family role was associated with a lower risk of H. pylori infection in grandchildren, with adults being the most at-risk (OR = 0.113, P < 0.05). Individuals without halitosis (OR = 0.251, P < 0.05) had a lower risk of H. pylori infection than those with halitosis. Poor awareness of H. pylori (OR = 2.191, P < 0.05), beer consumption (OR = 2.537, P < 0.05), and frequent consumption of spicy foods (OR = 2.346, P < 0.05) were identified as independent risk factors for H. pylori infection. Protective factors included no history of H. pylori infection (OR = 0.296, P < 0.05); adherence to a low-salt diet (OR = 0.326, P < 0.05); frequent garlic consumption (OR = 0.352, P < 0.05); reduced intake of strong tea, coffee, and milk tea (OR = 0.506, P < 0.05); and, adequate sleep (OR = 0.525, P = 0.003; Table 6).

Table 6 Results of multivariate logistic analysis on factors influencing Helicobacter pylori infection in adults.

Influencing factor	β	SE	Wald	P value	OR	95%CI
Family role-grandchildren	-2.184	0.825	7.004	0.008	0.113	0.022-0.568
Awareness of H. pylori-unaware	0.784	0.191	16.877	0.000	2.191	1.507-3.186
Smoking	0.375	0.388	0.933	0.334	1.455	0.680-3.111
SI	-0.246	0.445	0.307	0.579	0.782	0.327-1.868
Secondhand smoke exposure	0.000	0.194	0.000	1.000	1.000	0.684-1.463
Alcohol type-beer	0.931	0.359	6.737	0.009	2.537	1.256-5.125
Alcohol consumption	-0.587	0.585	1.007	0.316	0.556	0.176-1.751
History of gastrointestinal diseases	0.936	0.199	22.051	0.000	2.549	1.725-3.766
Gastrointestinal symptoms	-0.166	0.179	0.867	0.352	0.847	0.597-1.202
Family history of H. pylori infection-no	-1.216	0.193	39.761	0.000	0.296	0.203-0.433
Spicy food intake > 3 times/week	0.853	0.319	7.144	0.008	2.346	1.255-4.383
Pickled food intake	0.282	0.206	1.864	0.172	1.325	0.885-1.986
Salt intake < 6 g/day	-1.121	0.191	34.576	0.000	0.326	0.224-0.474
Fruit and vegetable intake	0.404	0.557	0.525	0.469	1.498	0.503-4.463
Whole grain intake	0.266	0.198	1.799	0.180	1.304	0.885-1.923
Garlic intake > 3 times/week	-1.043	0.296	12.423	0.000	0.352	0.197-0.629
Strong tea/coffee/milk tea consumption < 1 time/week	-0.682	0.246	7.688	0.006	0.506	0.312-0.819
Separate chopsticks and spoons when dining out	-0.102	0.192	0.281	0.596	0.903	0.619-1.317
Sleep duration > 8 hours/day	-0.645	0.220	8.633	0.003	0.525	0.341-0.807
Regular three meals a day	0.423	0.315	1.808	0.179	1.526	0.824-2.828
Toothbrushing frequency	0.586	0.418	1.960	0.162	1.796	0.791-4.078
Toothbrush replacement frequency	0.392	0.238	2.716	0.099	1.480	0.928-2.360
Halitosis-no	-1.381	0.188	54.191	0.000	0.251	0.174-0.363

P < 0.05 indicating a statistically significant difference. OR: Odds ratio; CI: Confidence interval; H. pylori: Helicobacter pylori; SI: Smoking index.

Risk factors for H. pylori infection in minors

A total of 219 participants aged < 18 years were included (128 males and 91 females). The H. pylori infection rate in this group was 31.1% (68/219). H. pylori infection in minors was significantly associated with a family history of H. pylori infection, shared utensils, consumption of smoked or fried foods, salt intake, dental caries, halitosis, and object-biting behavior (P < 0.05). No statistically significant associations were observed with sex, age, place of residence, family role, personal hygiene habits, dietary patterns, learning methods, and sleep duration (Table 7).

Table 7 Single factor analysis of Helicobacter pylori infection factors in adolescents.

Influencing factor	Number of households surveyed	Number of H. pylori-positive households	Positive rate (%)	χ2 value	P value
Sex				0.006	0.940
Male	128	40	31.3
Female	91	28	30.8
Age				1.126	0.569
3-6	37	9	24.3
7-12	112	35	31.3
13-17	70	24	34.3
Residence				0.496	0.481
Rural	75	21	28.0
Urban	144	47	32.6
Family role				0.028	0.867
Children	127	40	31.5
Grandchildren	92	28	30.4
Family history of H. pylori infection				32.110	0.000
No	132	22	16.7
Yes	87	46	52.9
Hand washing before and after meals				2.807	0.094
No	10	6	60.0
Yes	209	62	29.7
Hand washing after defecation				1.213	0.271
No	7	4	57.1
Yes	212	64	30.2
Shared tableware (including straws)				6.519	0.011
No	82	17	20.7
Yes	137	51	37.2
Toothbrushing frequency (time/day)				0.450	0.502
≤ 1	83	28	33.7
> 1	136	40	29.4
Toothbrush replacement frequency (months/time)				1.261	0.532
≤ 3	161	49	30.4
4-6	39	11	28.2
> 6	19	8	42.1
Eating rhythm				1.017	0.313
No	28	11	39.3
Yes	191	57	29.8
Smoking or secondhand smoke exposure				3.113	0.078
No	162	45	27.8
Yes	57	23	40.4
Gastrointestinal symptoms				2.823	0.093
No	187	54	28.9
Yes	32	14	43.8
Beverage consumption				2.670	0.102
No	47	10	21.3
Yes	172	58	33.7
Beverage type				1.870	0.393
None/electrolyte drink/soda water	54	13	24.1
Milk tea/fruit tea/coffee	49	15	30.6
Carbonated beverage	116	40	34.5
Smoked and fried food intake (time/week)				4.125	0.042
< 1	202	59	29.2
≥ 1	17	9	52.9
Pickled food intake (time/week)				0.021	0.885
< 3	207	65	31.4
≥ 3	12	3	25.0
Salt intake (g/day)				29.664	0.000
< 6	183	43	23.5
≥ 6	36	25	69.4
Fruit and vegetable intake (time/week)				3.543	0.060
< 3	14	8	57.1
≥ 3	205	60	29.3
Whole grain intake (time/week)				1.524	0.217
< 3	181	53	29.3
≥ 3	38	15	39.5
Milk and dairy product intake (time/week)				0.085	0.771
< 3	30	10	33.3
≥ 3	189	58	30.7
Soybean and soybean product intake (time/week)				2.606	0.106
< 3	151	52	34.4
≥ 3	68	16	23.5
Soup consumption (time/week)				2.090	0.148
< 3	28	12	42.9
≥ 3	191	56	29.3
Garlic intake (time/week)				1.216	0.270
< 3	205	66	32.2
≥ 3	14	2	14.3
Snack consumption (time/week)				1.616	0.446
< 1	13	4	30.8
1-3	94	25	26.6
> 3	112	39	34.8
Sleep duration (hours/day)				0.361	0.548
≤ 8	64	18	28.1
> 8	155	50	32.3
Staying up late				0.357	0.550
No	179	54	30.2
Yes	40	14	35.0
Dental caries				28.960	0.000
No	135	24	17.8
Yes	84	44	52.4
Halitosis				17.362	0.000
No	1391	301	21.6
Yes, noticed by others	412	172	41.5
Yes, noticed by oneself	392	212	53.8
Learning mode				0.123	0.726
Day school	194	61	31.4
Boarding	25	7	28.0
Object biting				17.032	0.000
No	1831	521	28.4
Occasionally	261	71	26.9
Frequently	102	92	90.0
Independent sleep				0.423	0.525
No	81	23	28.4
Yes	138	45	32.6
Playing in public places (times/week)				1.169	0.280
< 3	85	30	35.3
≥ 3	134	38	28.4
Mouth-to-mouth kissing				2.145	0.143
No	213	64	30.0
Yes	6	4	66.7

¹Represent the baseline group within the current influencing factor category.

²Groups that showed statistically significant differences from group labeled 1.

P < 0.05 indicating a statistically significant difference. A special symbol in statistics indicating no statistical difference between groups with the same number and a statistically significant difference between groups with different numbers. H. pylori: Helicobacter pylori.

Multivariate logistic analysis revealed that frequent object biting (OR = 39.300, P < 0.05) and dental caries (OR = 3.506, P < 0.05) were independent risk factors for H. pylori infection in adolescents. Conversely, the absence of a family history of H. pylori infection (OR = 0.141, P < 0.05), independent use of tableware (OR = 0.335, P < 0.05), low consumption of smoked or fried foods (OR = 0.181, P < 0.05), and adherence to a low-salt diet (OR = 0.231, P < 0.05) were protective factors against H. pylori infection (Table 8).

Table 8 Multivariate analysis of Helicobacter pylori infection in adolescents.

Variable	β	SE	Wald	P value	OR	95%CI
Family history of H. pylori infection-no	-1.967	0.406	23.447	0.000	0.140	0.063-0.310
Shared tableware-no	-1.094	0.451	5.887	0.015	0.335	0.138-0.810
Smoked and fried food intake < 1 time/week	-1.711	0.638	7.182	0.007	0.181	0.052-0.632
Salt intake < 6 g/day	-1.466	0.521	7.916	0.005	0.231	0.083-0.641
Halitosis	0.995	0.601	2.736	0.098	2.704	0.832-8.788
Dental caries-yes	1.254	0.467	7.221	0.007	3.506	1.404-8.754
Object biting-frequently	3.671	1.159	10.033	0.002	39.300	4.054-381.012

P < 0.05 indicating a statistically significant difference. OR: Odds ratio; CI: Confidence interval; H. pylori: Helicobacter pylori.

Familial clustering of H. pylori infection

Among the 415 households included in this study, 235 tested positive for H. pylori, yielding a household H. pylori infection rate of 56.6%. The goodness-of-fit test for the binomial distribution revealed that the distribution of H. pylori infection within households did not conform to a binomial distribution (χ² = 134.751, P < 0.05). The observed frequency of H. pylori infection differed significantly from the expected theoretical frequency, suggesting a clear pattern of familial clustering of H. pylori infections in households (Tables 9 and 10).

Table 9 Distribution of the frequency of household Helicobacter pylori infection.

Number of infected persons in household	Household size
	2	3	4	5	6	7	Total households	Total number of infected persons
0	60	60	38	17	5	0	180	0
1	25	23	21	8	2	0	79	79
2	15	33	20	12	4	2	86	172
3	0	19	20	6	4	0	49	147
4	0	0	8	5	2	3	18	72
5	0	0	0	1	2	0	3	15
Total number of households	100	135	107	49	19	5	415	485
Total population	200	405	428	245	114	35	1427

Table 10 Fit goodness test for the binomial distribution of family clusters in Helicobacter pylori-infected households.

Number of cases per household	Observed frequency (A)	Theoretical frequency (T)	Residual (A-T)
0	180	110.7	69.3
1	79	168.4	-89.4
2	86	98.9	-12.9
3	49	30.4	18.6
≥ 4	21	6.7	14.3

H. pylori infection among family members

A total of 471 couples were included, of whom 86 were both H. pylori-positive, 154 had only one H. pylori-positive partner, and 231 were both negative. The concordance rate for H. pylori infection among couples was 67.3%. McNemar’s test indicated consistency in H. pylori infection status between couples (P > 0.05; Table 11).

Table 11 Helicobacter pylori infection status in spouses.

Wife’s H. pylori status	Husband’s H. pylori status		Total
	Positive	Negative
Positive	86	77	163
Negative	77	231	308
Total	163	308	471

H. pylori: Helicobacter pylori.

Among 414 children with intact families, participants were divided into three groups based on parental infection status: Group 1 (both parents positive), group 2 (one parent positive), and group 3 (both parents negative). The H. pylori infection rates in these groups were 61.3%, 47.6%, and 12.3%, respectively. Infection rates among children with both parents positive and one parent positive were significantly higher than those with both parents negative (χ² = 78.382, P < 0.05; Table 12).

Table 12 Relationship between parental infection status and pediatric Helicobacter pylori infection.

Group	Children’s H. pylori status		Total (number of children)	Children’s H. pylori infection rate (%)
	Positive	Negative
Group 1 (both parents positive)	49	31	80	61.3
Group 2 (one parent positive)	70	77	147	47.6
Father positive	34	43	77	44.2
Mother positive	36	34	70	51.4
Group 3 (both parents negative)	23	164	187	12.3
Total	142	272	414	34.3

H. pylori: Helicobacter pylori.

Similarly, 75 grandchildren with intact families were divided into three groups based on their grandparents’ infection status: Group 1 (both grandparents positive), group 2 (one grandparent positive), and group 3 (both grandparents negative). The H. pylori infection rates among these groups were 57.1%, 43.8%, and 6.9%, respectively. Infection rates among grandchildren with both grandparents positive and one grandparent positive were significantly higher than those with both grandparents negative (χ² = 14.496, P < 0.05; Table 13).

Table 13 Relationship between grandparent infection status and Helicobacter pylori infection in grandchildren.

Group	Grandchildren’s H. pylori status		Total (number of grandchildren)	Grandchildren’s H. pylori infection rate (%)
	Positive	Negative
Group1 (both grandparents positive)	8	6	14	57.1
Group 2 (one grandparent positive)	14	18	32	43.8
Grandfather positive	5	7	12	41.7
Grandmother positive	9	11	20	45.0
Group 3 (both grandparents negative)	2	27	29	6.9
Total	24	51	75	32.0

H. pylori: Helicobacter pylori.

DISCUSSION

H. pylori infection is a chronic condition. Infected individuals develop specific T cells that produce cytokines capable of counteracting the pathogenic effects of H. pylori. H. pylori-induced specific immune responses are predominantly T helper cell (Th) 1-type and can effectively suppress or eradicate infection in early stages[25]. However, failure to eliminate the infection leads to the development of a robust humoral immune response. The failure to clear the infection can be attributed to both bacterial factors (e.g., bacterial antigenic variation, biofilm formation, and colonization) and host immune factors (e.g., immune deviation and tolerance). During the transition from Th1-type to Th2-type immune responses, Th2 responses not only suppress excessively destructive Th1-mediated inflammation facilitating host-H. pylori “coexistence” and preventing fatal outcomes of acute infection but also actively attenuate effective cellular immunity. This process promotes ineffective antibody responses and tissue fibrosis, leading to chronic persistent H. pylori infection and pathological damage. Consequently, these mechanisms contribute to the development of various diseases, including gastric ulcers, duodenal ulcers, and gastric cancer.

Global epidemiological survey data indicate that nearly half of the world’s population is infected with H. pylori. In China, the average H. pylori infection rate is 41.5%, indicating that approximately four in ten individuals are infected. Notably, H. pylori infection exhibits significant familial clustering, with multiple infections among family members being relatively common. The high prevalence of H. pylori infection, both globally and in China, imposes a substantial public health burden. Therefore, understanding the current infection patterns, influencing factors, and familial clustering is essential for improving prevention and control strategies and achieving meaningful social and economic benefits.

Over the past three decades, numerous epidemiological studies on H. pylori infection have been conducted both domestically and internationally. Significant regional disparities were observed, with infection rates ranging from 70.1% in Africa, 69.4% in South America, and 66.6% in West Asia to 24.4% in Oceania. Substantial variations are also observed at the national level, with rates ranging from 18.9% in Switzerland to 87.7% in Nigeria[26]. Stratified analyses of ethnic populations in Malaysia revealed higher H. pylori infection rates among Chinese and Indian populations (40%-50%) compared with those among Malaysians (10%-20%)[27], indicating potential ethnic differences in susceptibility. Regional variations in H. pylori infection rates are also evident in China. Multiple meta-analyses have reported the highest infection rate in the northwestern region (51.8%) and the lowest in the southern region (40%), with specific rates of 45.0% in Lanzhou, 32.5% in Nanjing, and 28.4% in Beijing. Among children, H. pylori infection rates are higher in the northwestern region and lower in the southern region, with economically developed areas generally exhibiting a lower prevalence than underdeveloped regions[13,28-30]. Furthermore, a correlation exists between geographical regions and H. pylori infection rates, with southern provinces generally having lower infection rates than northern and central-western provinces, and coastal regions exhibiting lower rates than the northwestern plateau region. These differences may reflect variations in regional economic development, access to healthcare resources, and antibiotic usage patterns. With improvements in socioeconomic conditions and increased public awareness, the global prevalence of H. pylori infection has declined over time. A 2022 meta-analysis revealed a decrease in the global H. pylori infection rate from 58.2% during 1980-1990 to 43.1% during 2011-2022[11]. Similarly, in China, the infection rate declined from 58.3% during 1983-1994 to 40.0% during 2015-2019[28]. Despite this downward trend, the prevalence of H. pylori infection remains relatively high and continues to impose a significant public health burden. This study showed that the H. pylori infection rate in the local population was 34.0%, with rates of 34.5% among adults and 31.1% among minors. However, these rates are lower than the national average.

Reports on the association between H. pylori infection and sex, age, place of residence, and marital status have yielded inconsistent findings across domestic and international studies. Some studies[31,32] indicate higher infection rates among females than males and among married individuals than unmarried individuals. However, most studies have suggested no association between H. pylori infection and sex, place of residence, or marital status[33-35]. Consistent with these findings, our findings demonstrated no significant differences in H. pylori infection rates based on sex, age, place of residence, or marital status in this region. Instead, family role and awareness of H. pylori were identified as factors that influenced H. pylori infection risk. Among family roles, the infection rate among grandchildren was significantly lower than that observed in other groups. This could be because grandchildren typically have fewer social interactions, resulting in reduced exposure to potential sources of infection. Additionally, grandchildren are younger and possess a more robust gastric mucosal barrier, which is less conducive to H. pylori colonization. Furthermore, prolonged exposure, cumulative effects of infection, and weakened immune resistance increase the likelihood of H. pylori infection, contributing to lower infection rates among younger individuals[36-38]. Conversely, increased awareness of H. pylori also facilitates early prevention and treatment, thereby reducing infection rates.

Most domestic and international studies[39-41] have reported that educational level is negatively associated with H. pylori infection, with decreasing infection rates as educational attainment increases. However, we found no such correlation in the present study. Kheyre et al[42] demonstrated that H. pylori infection rates may vary significantly among occupational groups due to differences in work environments and hygiene conditions. Domestic studies have also reported variations in H. pylori infection rates across different occupational groups, with higher rates observed among healthcare workers than among government job holders, education sector employees, and staff in enterprises and institutions; additionally, employed individuals had higher rates than unemployed individuals and freelancers[43,44]. However, the present study did not demonstrate a correlation between educational attainment or occupation and H. pylori infection rates. This discrepancy may reflect societal progress, the advancement of informatization, improvement in health literacy, enhanced awareness of personal protection, and the implementation of more comprehensive preventive measures.

This study further suggests that reduced consumption of strong tea, coffee, and milk tea; decreased intake of smoked and fried foods; adherence to a low-salt diet; and increased garlic consumption are protective factors against H. pylori infection, whereas beer consumption and frequent intake of spicy foods are independent risk factors. Diets high in salt, as well as frequent consumption of strong tea, coffee, milk tea, and smoked or fried foods, may compromise the gastric mucosal barrier. High salt concentrations may increase the secretion of vacuolating cytotoxin by H. pylori, thereby enhancing bacterial invasion and colonization[45,46]. Capsaicin, the active component of chili peppers, can induce inflammation in the gastrointestinal tract, disrupt the gastric environment, and damage the gastric mucosal barrier. It may also alter gastrin secretion, resulting in reduced gastric acid levels, thereby creating a low acidic environment that promotes H. pylori colonization[47]. An association was observed between the consumption of milk tea and coffee and H. pylori infection. The intake of high-sugar foods may contribute to H. pylori infection susceptibility through effects on blood glucose levels. Hyperglycemia can lead to the development of intestinal neuropathy, increased production of pro-inflammatory cytokines, and subsequent neurodegeneration, ultimately reducing local intestinal blood flow and impairing host defenses. Additionally, hyperglycemic states can weaken both cellular and humoral immunity, promote dysbiosis, and reduce resistance to H. pylori infection[48,49]. Previous studies have shown that ethanol, the main component of alcoholic beverages, can disrupt the lipoprotein layer that protects the gastric mucosa, thereby weakening the mucosal defense against H. pylori infection. Furthermore, ethanol promotes gastric acid secretion, directly damaging the gastric mucosal barrier and increasing susceptibility to H. pylori infection[50,51]. However, evidence regarding the impact of different types of alcoholic beverages on H. pylori infection is limited. Although the present study found a higher rate of H. pylori infection among beer consumers, further studies with larger sample sizes are warranted to validate this finding.

Allicin, an active compound in garlic, can inhibit H. pylori response, thereby suppressing H. pylori infection[52]. The mountainous and hilly terrain of Western Fujian Province, combined with historically poor transportation infrastructure and a subtropical monsoon climate characterized by high humidity, has contributed to the development of traditional food preservation practices. These include pickled foods such as dried radishes, dried pork gallbladder, and pickled vegetables, which remain commonly consumed in this region. These dietary habits may represent a significant factor influencing H. pylori infection in this population. The present study found that the H. pylori-positivity rate among individuals with halitosis was significantly higher than that among those without halitosis, indicating an increased risk of H. pylori infection in patients with halitosis. When H. pylori infection is present in the body, gastrointestinal digestion and absorption, as well as gastric motility, may be impaired, leading to prolonged retention of food residues in the gastrointestinal tract. These residues are subsequently decomposed by gastrointestinal bacteria, producing hydrogen sulfide (H₂S) and methyl mercaptan. In addition, H. pylori infection can induce the upregulation of related genes, such as cystathionine γ-lyase and cystathionine β-synthetase, as well as genes encoding inflammatory mediators, thereby increasing endogenous H₂S production and contributing to halitosis[53,54].

Additionally, previous studies have identified adequate sleep duration as a protective factor against H. pylori infection. Insufficient sleep can lead to autonomic nervous system dysfunction, resulting in decreased immune function. The combined effects of these factors contribute to gastrointestinal dysfunction, including increased gastric acid secretion, weakened gastrointestinal motility, and reduced self-repairing capacity[55,56]. The findings of this study also indirectly supports the aforementioned viewpoint perspective. The prevalence of H. pylori infection remains high among adults, and children are also at high risk. Zabala Torrres et al[57] reported that approximately one-third of children worldwide are infected with H. pylori. The present study found that the H. pylori infection rate among minors in the Minxi region was 31.1%, with rates of 24.3%, 31.3%, and 34.3% in the preschool (age: 3-6 years), elementary school (7-12 years), and junior/senior high school (13-17 years) groups, respectively, indicating that the infection rate increased with age. The findings of a cross-sectional study conducted by Huang et al[58] are consistent with ours. The current infection prevalence among minors is concerning. Our team will subsequently expand the sample size of this population and conduct further in-depth research. After adjusting for confounding factors, frequent object biting and dental caries were identified as independent risk factors for H. pylori infection among adolescents, whereas no family history of H. pylori infection, independent use of tableware, reduced consumption of smoked and fried foods, and adherence to a low-salt diet were identified as protective factors. Frequent object biting and dental caries increased the risk of H. pylori infection by 39.3-fold and 3.51-fold, respectively. H. pylori can colonize saliva, periodontal pockets, and dental plaque. Oral H. pylori infection may disrupt the acid-base balance and immunoglobulin activity in the oral cavity and increase the plaque index, thereby impairing oral immunity and promoting the development of dental caries. Oral H. pylori strains share high homology with gastric H. pylori[59-61], and maintaining oral hygiene may reduce the risk of H. pylori infection.

Currently, there is no consensus on the relationship between active or passive smoking and H. pylori infection. Some studies have suggested no association between smoking and H. pylori infection[62,63], whereas others have found a positive correlation[64-66]. Certain studies[67] suggest that nicotine in tobacco stimulates the production of gastric acid, pepsin, and free radicals during smoking, leading to gastroduodenal reflux and enhancing aggressive gastric factors while simultaneously weakening mucosal defenses (including prostaglandin synthesis, mucus production, and epidermal growth factor secretion). These changes facilitate the colonization and growth of H. pylori. However, our study did not find a correlation between smoking or secondhand smoke exposure and H. pylori infection, which is consistent with the findings of Morris et al[64].

Statistical distribution models of disease clustering within families have long been of interest in epidemiology and genetics. Understanding the theoretical distribution of disease occurrence within families provides valuable insights for etiological investigations and the selection of statistical methods. In medicine, the binomial distribution is used to describe the patterns of discrete random events with two mutually exclusive outcomes. Because H. pylori infection has only two outcomes, positive or negative, it can be analyzed using a binomial distribution to investigate familial clustering. Currently, it is widely accepted that diseases without familial clustering follow a binomial distribution[16]. A 2021 large-scale epidemiological study in China surveyed the H. pylori infection status of 10735 families across 29 provinces and revealed a household H. pylori infection rate ranging from 50.27%-85.06%, with an average of 71.21%[18]. In the present study, 235 families were H. pylori-positive and 180 were H. pylori-negative, resulting in a household infection rate of 56.6%. The concordance rate of H. pylori infection among spouses was 67.3%. The H. pylori infection rate among children with both parents positive for H. pylori was 61.3%, which was significantly higher than that among children with both parents negative (12.3%). Furthermore, the H. pylori infection rate among grandchildren with both grandparents positive was 57.1%, which was significantly higher than that among grandchildren with both grandparents negative (6.9%). Additionally, we found that the distribution of H. pylori-infected households did not follow a binomial distribution, suggesting that H. pylori infection exhibited familial clustering. This suggests that the presence of an infected individual in a family increases the risk of H. pylori infection among other family members. This conclusion aligns with the findings of Li et al[14] and Jiang et al[68]. Furthermore, treating all members in a H. pylori-positive household enhances H. pylori eradication rates and reduces recurrence compared with individual-based eradication approaches[69-71]. These findings further validate the concept of familial clustering of H. pylori infection. Our findings provide a theoretical basis for implementing household-based H. pylori prevention and control strategies.

Extensive research has demonstrated that household H. pylori infection is associated with factors such as family economic status, household hygiene practices, family members’ history of H. pylori infection, and family size[22,40,72-75]. The present study identified the communal use of chopsticks and spoons, infrequent utensil disinfection, and family history of H. pylori infection as independent risk factors for household infection, whereas the use of individual toothbrush cups served as a protective factor. These findings align with those of Li et al[76], who reported that independent use of chopsticks significantly reduces bacterial colony counts on food items and lowers cross-infection rates caused by communal dining. The prevailing consensus is that H. pylori transmission primarily occurs through person-to-person contact[77]. H. pylori thrives optimally in a moist, microaerobic environment at 37 °C, exhibiting prolonged survival outside the body. However, it is sensitive to environmental changes and becomes rapidly inactivated at high temperatures[78]. Therefore, frequent utensil disinfection can effectively eliminate bacteria adhering to tableware, reduce exposure to H. pylori, and lower infection risk. Close contact among parents and children within households, as well as use of utensils and toothbrush cups, may facilitate H. pylori retention on daily-use items, promoting oral-oral transmission and increasing H. pylori infection risk[79,80]. Conversely, the simpler the family structure, the lower the exposure to H. pylori, thereby reducing infection risk. Family members infected with H. pylori represent an independent risk factor for household H. pylori infection. H. pylori infection exhibits familial clustering, and close daily contact within households can increase the likelihood of transmission. In the Minxi region, where the Hakka population is predominant, the traditional Tulou residential system, multigenerational living arrangements, and warm hospitality practices further increase the risk of H. pylori infection among local residents.

This study has some limitations. First, although the H. pylori infection status was determined in all participants, this study did not include endoscopic evaluation of gastric mucosal pathology. Key histopathological indicators along the Correa cascade, including chronic atrophic gastritis, intestinal metaplasia, and dysplasia, were not assessed. These lesions are well-established precursors to gastric adenocarcinoma and serve as essential components in gastric cancer risk stratification. The absence of these data limits the clinical interpretation of the observed infection burden in this cohort, as H. pylori-positive individuals cannot be further stratified according to their actual risk of premalignant disease. Consequently, the clinical urgency and intensity of eradication therapy cannot be calibrated based on mucosal pathology status. Future follow-up of this cohort, incorporating standardized upper endoscopy with systematic biopsy (in accordance with the updated Sydney system), would markedly enhance the clinical relevance of these findings and enable the longitudinal assessment of Correa cascade progression in a family-based setting. Second, not all H. pylori strains possess equivalent carcinogenic potential. Strains harboring the cytotoxin-associated gene A (cagA) and those with the vacuolating cytotoxin A (vacA) s1m1 genotype are consistently associated with significantly higher risks of gastric ulcer, atrophic gastritis, and gastric adenocarcinoma compared with cagA-negative or vacA s2m2 strains. Given that household members frequently share homologous H. pylori strains through close interpersonal contact, the observed familial clustering of infection may simultaneously reflect the intrafamilial concentration of high-virulence, high-risk genotypes. In this scenario, family-based transmission would imply not only a quantitative clustering of infection but also a potential qualitative clustering of more pathogenic strains, which could amplify the population-attributable gastric cancer risk within certain households. Virulence genotyping was beyond the scope of the present investigation; however, future family-based studies incorporating strain-level characterization particularly of cagA, vacA, and other established virulence markers would provide a more refined understanding of transmission dynamics and facilitate the development of risk-stratified, family-centered eradication strategies.

Although this cross-sectional investigation explored several factors that influence H. pylori infection, the causal relationship is weakly substantiated and requires confirmation through prospective studies. Additionally, most survey data were collected via questionnaires, which inevitably introduced recall bias during data collection, thereby increasing the uncertainty of the associations.

CONCLUSION

The findings of this study suggest that enhancing public awareness and knowledge of H. pylori infection is essential for effective prevention and control. Individuals with halitosis, dental caries, or a family history of H. pylori infection should undergo early screening. Additionally, reducing the intake of spicy foods, high-salt foods, strong tea, milk tea, coffee, and smoked or fried foods while increasing garlic consumption, implementing family meal segregation, using separate toothbrush cups, and frequently disinfecting tableware can help reduce the risk of H. pylori infection. By encouraging individuals to actively improve their dietary and hygiene habits, early detection and treatment can be achieved, thereby reducing the incidence of gastrointestinal diseases and delaying disease progression, ultimately leading to a life free from H. pylori infection.

ACKNOWLEDGEMENTS

We would like to thank the participants for generously dedicating their time to answering the questionnaire and providing test samples.