In this cross-sectional study of the Ghanaian population with dyspepsia, we found a high prevalence of H. pylori, 71.1%, by rapid-urease CLO testing. Furthermore, the prevalence of H. pylori harboring the virulence factors, cagA and vacAs1, were found to be 74.8 and 69.2% respectively. The prevalence of vacAs1m1 was 25.2% while vacAs1m2 was 8.2%. Regarding the cagA gene, the hydrophilic region was more likely to be detected in duodenal ulcers while the region of internal duplication was associated with erosive gastritis, suggesting the effect of these genotypes in disease development. The significant association between cagA-(hydrophilic region) and duodenal ulcer persisted following multivariate analysis.
Majority of vacAs1+ samples were cagA
+ which was consistent with other studies [6, 11]. The expression of cagA gene is closely associated with that of vacuolating cytotoxin A (vacA) . H. pylori cagA had a high prevalence in this study, 74.8%. This was demonstrated in other studies in Nigeria 90% , South Africa 95% . Most H. pylori strains can be classified into two major groups. Type 1 have the gene coding for cagA and co-express cagA and vacA. Type 2 do not have the cagA gene and do not express cagA or vacA . However, an intermediate phenotype has been identified expressing cagA independent of vacA or vice versa . In Ghana the infecting Helicobacter pylori are seen to be of type 1.
The vacuolating cytotoxin A contains at least two variable regions, the signal (s) region which encodes the signal peptide and the middle (m) region . The s region has two sub-types s1 and s2 while the m region has m1 and m2 . The amount of cytotoxin produced is highest in the vacAs1m1 allele followed by the vacAs1m2 . The frequency of vacAs1 and m1 vary across populations. The vacAs1 and m1 genes have been detected at a higher frequency in isolates from patients with DU in comparison with vacAs2 and m2, mostly in countries with a relatively low prevalence of H. pylori infection but also in South America and South Africa where the infection is endemic .
In our study population, vacAs1m1 genotype had a prevalence of 25.2%. Other African studies in Nigeria and Ethiopia had vacAs1m1 prevalence of 24 and 48% respectively . Infection with H. pylori strains having the vacA s1m1 genotype (compared with s1m2 and s2m2) have also been associated with an increased risk of duodenal ulcer disease  as evident in this study. However, other reports from H. pylori endemic countries have not shown a significant association between vacAs1 or vacAs1m1 and gastro-duodenal disease . A complex interplay of host genetic factors, environmental factors and other virulence factors of H. pylori are therefore important in determining the risk of gastro-duodenal disease .
CagA demonstrates considerable diversity in its 3′ region. Its most hydrophilic region contains amino acid repeats including Glu-Pro-Ile-Tyr-Ala (EPIYA) . In addition, the adjacent region of internal duplication has been shown to contain sequences derived from the duplication of three discrete segments of DNA (D1, D2 and D3) [6, 7]. In this study, patients with duodenal ulcer were more likely to have detectable H. pylori cagA-(hydrophilic region) while H. pylori cagA-(internal duplication region) was associated with erosive gastritis. The PCR products of the region of internal duplications of cagA+ differ in size varying from 450 to 558 bps. H. pylori has been shown to express both gene regions in majority (98%) of patients . However, in this study, cagA-(internal duplication region) was more prevalent than cagA-(hydrophilic region), (68.6% vs 48.4%) and 42.1% had both gene regions. This significant association between cagA-(hydrophilic region) and duodenal ulcer persisted following multivariate analysis.
Differences in cagA gene in our study population imply heterogeneity in the cag-pathogenicity island which may have an impact on clinical disease. This study however had limitations; PCR analysis was done on genomic DNA isolated from gastric biopsies which may have underestimated the vacA and cagA prevalence in the study population due to potential PCR inhibitors. Further evaluation would be required to characterize H. pylori bacterial diversity including cag-pathogenicity island gene polymorphisms and their impact on gastro-duodenal disease.