Clinical diseases that follow Helicobacter pylori infection are associated with expression of the cagA gene, a part of cytotoxin-associated gene pathogenicity island (cag-PAI). This study aims to determined whether or not the presence of cagA is associated with the presence of complete cag-PAI and to evaluate inflammatory changes associated with the five loci in the cag-PAI of H. pylori comprising cagA, cagA promoter region (cagAP), cagE, cagT and the left end of the cagA gene (LEC). H. pylori isolates were obtained from patients with dyspeptic symptoms. Clinical strains of H. pylori were screened by the polymerase chain reaction (PCR) for respective genes of the cag-PAI. Of 115 H. pylori isolates, 31 (28%) were positive for the five cag-PAI loci. H. pylori isolates with intact cag-PAI were associated with gastric carcinoma (GC; n=9 [60%]) and gastric ulcer (GU; n=5 [45%]) compared to non-ulcer dyspepsia (NUD; n=14 [18%]) (P=0.001 and P=0.049, respectively). In patients with intact cag-PAI, acute on chronic inflammation was present in 25 (81%) and was more common than chronic inflammation (P=0.013). The cagE and cagAP had deletions in 25 (37%) and 23 (35%) cases, respectively. The cagAP region was significantly associated with GC (n=12 [80%], P<0.001) and GU (n=9 [82%], P=0.001) compared to NUD (n=24 [30%] and with significant acute on chronic inflammation (n=40 [80%], P=0.007). The distribution of vacAs1a with intact cag-PAI in GC was 9 (60%) and in NUD was 10 (13%) (P<0.001). The presence of the cagA gene does not signify presence of an intact cag-PAI. Most of the H. pylori isolates studied had partial cag-PAI with missing cagE and cagA promoter regions.