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Fulltext Comparing the genomes of Helicobacter pylori clinical strain UM032 and Mice-adapted derivatives

Khosravi Y, Rehvathy V, Wee WY, Wang S, Baybayan P, Singh S, et al.

Gut Pathog, 2013;5:25.
PMID: 23957912 DOI: 10.1186/1757-4749-5-25

Helicobacter pylori is a Gram-negative bacterium that persistently infects the human stomach inducing chronic inflammation. The exact mechanisms of pathogenesis are still not completely understood. Although not a natural host for H. pylori, mouse infection models play an important role in establishing the immunology and pathogenicity of H. pylori. In this study, for the first time, the genome sequences of clinical H. pylori strain UM032 and mice-adapted derivatives, 298 and 299, were sequenced using the PacBio Single Molecule, Real-Time (SMRT) technology.

Matched MeSH terms: Helicobacter pylori
Fulltext Clinical and histopathological relevance of helicobacter pylori BabA2 genotype

Tariq Elhashim, M. Imad Mustafa Mahmud, Nasser Amjad, Norra Harun, Imad M. Alani

International Medical Journal Malaysia, 2016;15(2):43-49.
MyJurnal

Introduction: H. pylori BabA is an outer membrane protein that mediates bacterial adherence to the gastric
epithelium, triggers several pathways during the course of infection, and thus contributes to the disease
development. Considering the variability in the presence of BabA coding gene (babA2) among H. pylori
clinical strains, the aim of this study was to assess the relationship between the genotype status of H. pylori
babA2 and the severity of clinical and histopathological outcomes. Methods: Gastric mucosal biopsy
specimens were collected from 30 CLO test-positive patients, 16 with gastritis and 14 with peptic ulcer
disease. Polymerase chain reaction was carried out to detect the presence of H. pylori-specific glmM gene
and BabA coding gene (babA2). Histopathological examination was performed to evaluate the severity of H.
pylori-associated gastric disease according to the Updated Sydney Classification System. Results: The glmM
and babA2 genes were present in 100% and 86.7% of the tested H. pylori strains, respectively. Although
higher degrees of inflammatory activity and H. pylori density were noted in babA2-positive biopsy
specimens, there was no statistically significant association between babA2 genotype status and the severity
of gastric disease. Conclusion: The babA2 genotype status of H. pylori may not be considered as a sole
marker for determining the infection outcomes.

Matched MeSH terms: Helicobacter pylori
Genetic diversity and virulence characteristics of Helicobacter pylori isolates in different human ethnic groups

Hanafiah A, Lopes BS

Infect Genet Evol, 2020 Mar;78:104135.
PMID: 31837482 DOI: 10.1016/j.meegid.2019.104135

Helicobacter pylori is the most predominant bacterium in almost 50% of the world's population and colonization causes a persistent inflammatory response leading to chronic gastritis. It shows high genetic diversity and individuals generally harbour a distinct bacterial population. With the advancement of whole-genome sequencing technology, new H. pylori subpopulations have been identified that show admixture between various H. pylori strains. Genotypic variation of H. pylori may be related to the presence of virulence factors among strains and is associated with different outcomes of infection in different individuals. This review summarizes the genetic diversity in H. pylori strain populations and its virulence characteristics responsible for variable outcomes in different ethnic groups.

Matched MeSH terms: Helicobacter pylori
Analysis of core protein clusters identifies candidate variable sites conferring metronidazole resistance in Helicobacter pylori

Chua EG, Debowski AW, Webberley KM, Peters F, Lamichhane B, Loke MF, et al.

Gastroenterol Rep (Oxf), 2019 Feb;7(1):42-49.
PMID: 30792865 DOI: 10.1093/gastro/goy048

Background: Metronidazole is one of the first-line drugs of choice in the standard triple therapy used to eradicate Helicobacter pylori infection. Hence, the global emergence of metronidazole resistance in Hp poses a major challenge to health professionals. Inactivation of RdxA is known to be a major mechanism of conferring metronidazole resistance in H. pylori. However, metronidazole resistance can also arise in H. pylori strains expressing functional RdxA protein, suggesting that there are other mechanisms that may confer resistance to this drug.
Methods: We performed whole-genome sequencing on 121 H. pylori clinical strains, among which 73 were metronidazole-resistant. Sequence-alignment analysis of core protein clusters derived from clinical strains containing full-length RdxA was performed. Variable sites in each alignment were statistically compared between the resistant and susceptible groups to determine candidate genes along with their respective amino-acid changes that may account for the development of metronidazole resistance in H. pylori.
Results: Resistance due to RdxA truncation was identified in 34% of metronidazole-resistant strains. Analysis of core protein clusters derived from the remaining 48 metronidazole-resistant strains and 48 metronidazole-susceptible identified four variable sites significantly associated with metronidazole resistance. These sites included R16H/C in RdxA, D85N in the inner-membrane protein RclC (HP0565), V265I in a biotin carboxylase protein (HP0370) and A51V/T in a putative threonylcarbamoyl-AMP synthase (HP0918).
Conclusions: Our approach identified new potential mechanisms for metronidazole resistance in H. pylori that merit further investigation.

Matched MeSH terms: Helicobacter pylori
Rapid urease test in the diagnosis of Helicobacter pylori infection

Rosaida MS, Goh KL

JUMMEC, 2000;5:11-16.

Many tests are available for the diagnosis of H. pylori infection. Broadly they can be divided into invasive- endoscopy biopsy based tests and non-invasive tests. Of the endoscopy biopsy based tests the rapid urease tests (RUT) have been found to be the most convenient, accurate and inexpensive tests and they have therefore been recommended by several consensus panels and working parties as the test of choice during endoscopy. Several RUTS are available; some are commercial: CLO test, Pyloritek, Helicobacter urease test, H. yylori test and others- "homemade". We strongly recommend the "homemade" 1 min rapid urease test using an unbuffered solution as originally described by Arvind et al. This test has been shown to be easy to prepare, inexpensive and accurate on field-testing. Several factors affect the accuracy of the RUT. The larger the size of biopsy samples, the quicker is the postive reaction time. With the CLO test, warming the tests to 37'C has also been shown to hasten the reaction time. The effect of blood on the RUT poses an important problem in testing. It is vitally important to determine the H. yylori status in patients with bleeding peptic ulcers as the recurrence of bleeding has been shown to be markedly reduced or virtually abolished with H. yylori eradication. While the results of studies have not been entirely consistent, it is likely that presence of blood does reduce the sensitivity of the RUT. It is therefore sensible that in patients with bleeding ulcers, the RUT should not be the sole endoscopy biopsy test used and that samples should also be taken for histological examination.

Matched MeSH terms: Helicobacter pylori
Fulltext Novel essential amino acid-sulfanilamide hybrid as safe anti-ulcerogenic agent with anti-helicobacter pylori activity

Awaad AS, Alafeefy AM, Alasmary FAS, El-Meligy RM, Zain ME, Alqasoumi SI

Saudi Pharm J, 2017 Nov;25(7):967-971.
PMID: 29158702 DOI: 10.1016/j.jsps.2017.02.012

A novel and safe essential amino acid (Leucine) incorporating sulfanilamide was synthesized, and evaluated for its anti-ulcerogenic activity and in vitro anti-Helicobacter pylori activity. The new molecule showed a dose dependent activity against absolute ethanol-induced ulcer in rats, it produced percent protection of control ulcer by 66.7 at dose 100 mg/kg. In addition it showed a potent anti-Helicobacter pylori activity in vitro against 7 clinically isolated strains. The minimum inhibitory concentration (MIC) ranged from 12.5 to 50 μg/ml. The preliminary safety studies and toxicity profile are optimistic and encouraging.

Matched MeSH terms: Helicobacter pylori
Fulltext What indigestion means to the malays?

Lee YY, Chua AS

J Neurogastroenterol Motil, 2013 Jul;19(3):295-300.
PMID: 23875095 DOI: 10.5056/jnm.2013.19.3.295

Despite being a large ethnic group within the South-East Asia, there is a paucity of reported literatures on dyspepsia in the Malay population. Recent population-based studies indicate that uninvestigated dyspepsia, based on the Rome II criteria, is reported in 12.8% and 11.6% of Malays in the urban and rural communities respectively. Organic causes of dyspepsia including upper gastrointestinal tract cancers, its precancerous lesions, and erosive diseases are uncommon which is largely due to an exceptionally low prevalence of Helicobacter pylori infection in this population. On the other hand, functional dyspepsia and irritable bowel syndrome are relatively common in the Malays than expected. Within a primary care setting, functional dyspepsia, based on the Rome III criteria, is reported in 11.9% of Malays, of which epigastric pain syndrome is found to be more common. Married Malay females are more likely to have functional dyspepsia and psychosocial alarm symptoms. Also based on the Rome III criteria, irritable bowel syndrome, commonly overlapped with functional dyspepsia, is reported in 10.9% of Malays within a community-based setting. Rather than psychosocial symptoms, red flags are most likely to be reported among the Malays with irritable bowel syndrome despite having a low yield for organic diseases. Based upon the above observations, "proton pump inhibitor test" is probably preferable than the "test and treat H. pylori" strategy in the initial management of dyspepsia among the Malays.

Matched MeSH terms: Helicobacter pylori
Why do we still have Helicobacter Pylori in our Stomachs

Abadi AT, Ierardi E, Lee YY

Malays J Med Sci, 2015 Sep;22(5):70-75.
PMID: 28239271

The existence of any infectious agent in a highly acidic human stomach is contentious, but the chance finding of Helicobacter pylori is by no means an accident. Once H. pylori colonises the gastric mucosa, it can persist for a lifetime, and it is intriguing why our immune system is able to tolerate its existence. Some conditions favour the persistence of H. pylori in the stomach, but other conditions oppose the colonisation of this bacterium. Populations with high and extremely low prevalence of H. pylori provide useful insights on the clinical outcomes that are associated with this type of infection. Adverse clinical outcomes including peptic ulcer disease and gastric cancer depend on a delicate balance between a harmless inflammation and a more severe kind of inflammation. Is the only good H. pylori really a dead H. pylori? The jury is still out.

Matched MeSH terms: Helicobacter pylori
Fulltext Preliminary study suggests low incidence of gastric carcinoma in kelantan relates to low rate of helicobacter pylori infection

Kaur G, Raj SM

Malays J Med Sci, 2001 Jan;8(1):31-3.
PMID: 22973153 MyJurnal

Helicobacter pylori-associated gastric carcinoma is generally more common in the antrum/body and is of the intestinal type. The aim of this study was to determine the pattern of gastric carcinoma in an area known to have a low prevalence of H. pylori. Pathology records of gastric carcinoma diagnosed at Hospital University Sains Malaysia between 1995 and 1999 were retrieved and studied. There were a total of 23 cases. The median age was 60 years. Eighteen patients were Malay and 5 were Chinese. The most common location of the tumour was the cardia/gastrooesophageal junction (61%, 14/23 patients). The majority was of the intestinal type (69.6%, 16/23). The frequency of gastric carcinoma appears to be exceptionally low in the area of study. The Chinese population was over-represented. The higher frequency of tumour in the cardia/gastro-oesophageal junction as compared to the antrum and body is in sharp contrast to most other studies. This reaffirms the notion that Helicobacter pylori infection is a causative agent for non-cardia gastric carcinomas.

Matched MeSH terms: Helicobacter pylori
Fulltext Streptococcus mitis induces conversion of Helicobacter pylori to coccoid cells during co-culture in vitro

Khosravi Y, Dieye Y, Loke MF, Goh KL, Vadivelu J

PLoS One, 2014;9(11):e112214.
PMID: 25386948 DOI: 10.1371/journal.pone.0112214

Helicobacter pylori (H. pylori) is a major gastric pathogen that has been associated with humans for more than 60,000 years. H. pylori causes different gastric diseases including dyspepsia, ulcers and gastric cancers. Disease development depends on several factors including the infecting H. pylori strain, environmental and host factors. Another factor that might influence H. pylori colonization and diseases is the gastric microbiota that was overlooked for long because of the belief that human stomach was a hostile environment that cannot support microbial life. Once established, H. pylori mainly resides in the gastric mucosa and interacts with the resident bacteria. How these interactions impact on H. pylori-caused diseases has been poorly studied in human. In this study, we analyzed the interactions between H. pylori and two bacteria, Streptococcus mitis and Lactobacillus fermentum that are present in the stomach of both healthy and gastric disease human patients. We have found that S. mitis produced and released one or more diffusible factors that induce growth inhibition and coccoid conversion of H. pylori cells. In contrast, both H. pylori and L. fermentum secreted factors that promote survival of S. mitis during the stationary phase of growth. Using a metabolomics approach, we identified compounds that might be responsible for the conversion of H. pylori from spiral to coccoid cells. This study provide evidences that gastric bacteria influences H. pylori physiology and therefore possibly the diseases this bacterium causes.

Matched MeSH terms: Helicobacter pylori/physiology*
Helicobacter pylori: molecular detection of vacA gene and vacuolating activity in human gastric adenocarcinoma cells

Alfizah H, Noraziah MZ, Chao MY, Rahman MM, Ramelah M

Clin Ter, 2013;164(4):301-5.
PMID: 24045512 DOI: 10.7417/CT.2013.1577

Helicobacter pylori strains secrete a vacuolating cytotoxin (VacA), plays an important role for the development of peptic ulcer disease and gastro-duodenal diseases. vacA gene is responsible to regulate the activity of the vacuolating cytotoxin. The objective of this study was molecular detection of vacA gene and observes the vacuolating activity on human gastric adenocarcinoma (AGS) cells.

Matched MeSH terms: Helicobacter pylori/genetics*
Fulltext Helicobacter pylori infection--a boon or a bane: lessons from studies in a low-prevalence population

Lee YY, Mahendra Raj S, Graham DY

Helicobacter, 2013 Oct;18(5):338-46.
PMID: 23607896 DOI: 10.1111/hel.12058

Helicobacter pylori (H. pylori) infection is etiologically associated with gastric cancer and peptic ulcer diseases which are both important public health burdens which could be largely eliminated by H. pylori eradication. However, some investigators urge caution based on the hypothesis that eradication of H. pylori may result in an increase in the incidence of gastroesophageal reflux disease, esophageal adenocarcinoma, and childhood asthma. The ethnic Malays of northeastern Peninsular Malaysia have long had a low prevalence of H. pylori infection and, as expected, the incidence of gastric cancer and its precursor lesions is exceptionally low. The availability of a population with a low H. pylori prevalence and generally poor sanitation allows separation of H. pylori from the hygiene hypothesis and direct testing of whether absence of H. pylori is associated with untoward consequence. Contrary to predictions, in Malays, erosive esophagitis, Barrett's esophagus, distal esophageal cancers, and childhood asthma are all of low incidence. This suggests that H. pylori is not protective rather the presence of H. pylori infection is likely a surrogate for poor hygiene and not an important source of antigens involved in the hygiene hypothesis. Helicobacter pylori in Malays is related to transmission from H. pylori-infected non-Malay immigrants. The factors responsible for low H. pylori acquisition, transmission, and burden of H. pylori infection in Malays remain unclear and likely involves a combination of environmental, host (gene polymorphisms), and strain virulence factors. Based on evidence from this population, absence of H. pylori infection is more likely to be boon than a bane.

Matched MeSH terms: Helicobacter pylori/isolation & purification*
Fulltext Commentary: changing aetiology of peptic ulcers

Goh KL, Chan WK

Aliment Pharmacol Ther, 2012 Aug;36(3):291-2; discussion 292-3.
PMID: 22747451 DOI: 10.1111/j.1365-2036.2012.05164.x
Matched MeSH terms: Helicobacter pylori/isolation & purification*
Deleted in Colorectal Cancer (DCC) gene polymorphism is associated with H. pylori infection among susceptible Malays from the north-eastern region of Peninsular Malaysia

Maran S, Lee YY, Xu S, Rajab NS, Hasan N, Mustaffa N, et al.

Hepatogastroenterology, 2013 Jan-Feb;60(121):124-8.
PMID: 22829558

Using genome-wide case-control association approach, the current study aimed to determine whether genetic polymorphism(s) is/are associated with H. pylori infection among ethnic Malays from the north-eastern region of Peninsular Malaysia, a region with an exceptionally low prevalence for H. pylori infection and gastric cancer.

Matched MeSH terms: Helicobacter pylori*
Extragastrointestinal manifestations of Helicobacter pylori infection: facts or myth? A critical review

Tan HJ, Goh KL

J Dig Dis, 2012 Jul;13(7):342-9.
PMID: 22713083 DOI: 10.1111/j.1751-2980.2012.00599.x

Helicobacter pylori (H. pylori) infection is reported to be associated with many extragastrointestinal manifestations, such as hematological diseases [idiopathic thrombocytopenic purpura (ITP) and unexplained iron deficiency anemia (IDA)], cardiovascular diseases (ischemic heart diseases), neurological disorders (stroke, Parkinson's disease, Alzheimer's disease), obesity and skin disorders. Among these, the best evidence so far is in ITP and unexplained IDA, with high-quality studies showing the improvement of IDA and ITP after H. pylori eradication. The evidence of its association with coronary artery disease is weak and many of the results may be erroneous. The role of H. pylori infection in affecting serum leptin and ghrelin levels has attracted a lot of attention recently and available data to date have been conflicting. There have also been many uncontrolled, small sample studies suggesting an association between H. pylori infection and neurological disorders or chronic urticaria. However, more studies are required to clarify such proposed causal links.

Matched MeSH terms: Helicobacter pylori*
Fulltext Epidemiology of Helicobacter pylori infection in Malaysia--observations in a multiracial Asian population

Goh KL

Med J Malaysia, 2009 Sep;64(3):187-92.
PMID: 20527265

Observations of racial differences in the prevalence of Helicobacter pylori in Malaysia have been intriguing. The Indians and Chinese consistently have a higher prevalence compared to the Malays. The racial cohort theory has been proposed to explain these differences where transmission and perpetuation of infection takes place within a racial group rather than between races, races being separate owing to the low rate of interracial marriages. Studies have demonstrated distinctive bacterial strains between races. Phylogenetic studies have shown that H. pylori isolates amongst Chinese and Indians are distinctive while Malays have Indian and other strains suggesting a more recent acquisition of the bacterium from Indians. H. pylori is recognized as the major causative factor in peptic ulcer disease and gastric cancer. Despite the high prevalence of H. pylori, Indians have a relatively low prevalence of peptic ulcer disease and a low incidence of gastric cancer. This paradox with regards to gastric cancer has been termed the "Indian enigma". Bacterial strain differences between races may be putative but this observation may also indicate gastroprotective environmental factors or a lower genetic susceptibility to develop cancer in the Indians.

Matched MeSH terms: Helicobacter pylori*
Fulltext Development and evaluation of a new growth medium for Helicobacter pylori

Sasidharan S, Uyub AM

FEMS Immunol. Med. Microbiol., 2009 Jun;56(1):94-7.
PMID: 19309485 DOI: 10.1111/j.1574-695X.2009.00554.x

The present study was aimed at modifying the original formulation of Commercial Eugon agar (CEA) to develop a new H. pylori growth medium. Initial studies were carried out to determine the number of H. pylori colonies recovered on in-house H. pylori agar (IHPA), IHPA without L-cysteine and sodium sulfite (IHPA-NC), IHPA without L-cysteine (IHPA-C), IHPA without sodium sulfite (IHPA-N) and CEA as the control. Significant differences (P < 0.001) in the number of colonies recovered were observed between IHPA-N, IHPA-NC and IHPA-C. Incorporation of sodium sulfite decreased the number of colonies recovered, indicating that sodium sulfite was inhibitory to H. pylori growth. Removal of L-cysteine reduced the number of colonies recovered, suggesting that L-cysteine is necessary for the growth of H. pylori. In the subsequent study, incorporation of K(2)HPO(4) further increased the number of colonies recovered compared with IHPA-N (P < 0.001), and 0.25% (w/v) of K(2)HPO(4) yielded the highest numbers of colonies (P < or = 0.04). Finally, thirty other H. pylori clinical isolates were evaluated for their growth in the IHPAP-N, a new medium consisting of 1.5% (w/v) pepticase, 0.5% (w/v) peptone, 0.4% (w/v) sodium chloride, 0.03% (w/v) L-cysteine, 0.55% (w/v) dextrose, 0.25% (w/v) K(2)HPO(4) and 1.5% (w/v) agar. The number of colonies recovered in IHPAP-N was significantly (P < 0.005) higher than that of CEA. IHPAP-N with 0.25% K(2)HPO(4) and without sodium sulfite were adequate solid media for the growth of H. pylori.

Matched MeSH terms: Helicobacter pylori/growth & development*
Further observations in an area with an exceptionally low prevalence of Helicobacter pylori infection

Raj SM, Lee YY, Choo KE, Noorizan AM, Zulkifli A, Radzi M, et al.

Trans R Soc Trop Med Hyg, 2008 Nov;102(11):1163-4.
PMID: 18678380 DOI: 10.1016/j.trstmh.2008.06.015
Matched MeSH terms: Helicobacter pylori/isolation & purification*
Changing epidemiology of Helicobacter pylori in Asia

Tan HJ, Goh KL

J Dig Dis, 2008 Nov;9(4):186-9.
PMID: 18959588 DOI: 10.1111/j.1751-2980.2008.00344.x

As in developed societies, the prevalence of Helicobacter pylori has declined rapidly in Asia. This has been shown in both seroprevalence-based and endoscopy-based studies. While the decline in the incidence of gastric cancer has now been observed, a decrease in peptic ulcer disease has not been so clearly evident. This apparent paradox can be explained by an increase in non-H. pylori associated ulcers - such as those related to non-steroidal anti-inflammatory drugs or idiopathic ulcers. The increase of gastroesophageal reflux disease in Asia has been widely observed and commented on and its relationship to the decline in H. pylori speculated upon. However there have been few conclusive studies from Asia on this subject. While the improved diagnosis and elimination of H. pylori has contributed to its decline, a more basic change involving large segments of the Asian population must be responsible. An improvement in hygiene and living conditions that results from more affluent Asian societies is thought to be a possible cause.

Matched MeSH terms: Helicobacter pylori*
Fulltext Helicobacter pylori infection in peptic ulcer disease: the importance of smoking and ethnicity

Pillay KV, Htun M, Naing NN, Norsa'adah B

Southeast Asian J. Trop. Med. Public Health, 2007 Nov;38(6):1102-10.
PMID: 18613553

This study was conducted to determine the prevalence of Helicobacter pylori (H. pylori) and its associated factors among patients with peptic ulcer disease in Taiping Hospital. Consecutive peptic ulcer disease patients who had undergone esophagogastro-duodenoscopy were included. The H. pylori status was assessed by the rapid urease test. We excluded those who had active bleeding, a perforated peptic ulcer, severe vomiting, a history of gastric surgery, peptic ulcer disease or renal or liver diseases, carcinoma of the stomach, and recent use of antibiotics or proton pump inhibitors. Socio-demography, H. pylori status, medication history and other relevant clinical data were collected from case notes. A total of 416 subjects were selected, 49.7% were positive and 50.3% were negative for H. pylori infection. There were significant associations between H. pylori and age, ethnicity, smoking status and NSAID usage. However, there were no significant relationships between H. pylori status and gender or type of peptic ulcer. Multiple logistic regression showed that other ethnicities than Malays and smokers had a higher risk of H. pylori. Our prevalence rate was low and the identified risk factors were consistent with previous studies. Ethnic differences may be related to genetic and sociocultural behaviors. Quitting smoking may benefit peptic ulcer patients with H. pylori infection.

Matched MeSH terms: Helicobacter pylori/isolation & purification*

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