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Treatment failure is a major cause of concern for the Helicobacter pylori-related gastroduodenal diseases like gastritis, peptic ulcer, and gastric cancer. Curcumin, diferuloylmethane from turmeric, has recently been shown to arrest H. pylori growth. The antibacterial activity of curcumin against 65 clinical isolates of H. pylori in vitro and during protection against H. pylori infection in vivo was examined. The MIC of curcumin ranges from 5 g/ml to 50 g/ml, showing its effectiveness in inhibiting H. pylori growth in vitro irrespective of the genetic makeup of the strains. The nucleotide sequences of the aroE genes, encoding shikimate dehydrogenase, against which curcumin seems to act as a noncompetitive inhibitor, from H. pylori strains presenting differential curcumin MICs showed that curcumin-mediated growth inhibition of Indian H. pylori strains may not be always dependent on the shikimate pathway. The antimicrobial effect of curcumin in H. pylori-infected C57BL/6 mice and its efficacy in reducing the gastric damage due to infection were examined histologically. Curcumin showed immense therapeutic potential against H. pylori infection as it was highly effective in eradication of H. pylori from infected mice as well as in restoration of H. pylori-induced gastric damage. This study provides novel insights into the therapeutic effect of curcumin against H. pylori infection, suggesting its potential as an alternative therapy, and opens the way for further studies on identification of novel antimicrobial targets of curcumin.

Antibiotic resistance, virulence gene, and molecular profiles of Shiga toxin-producing Escherichia coli (STEC) non-O157 strains isolated from human stool samples, cow stool samples, and beef samples over a period of 2 years in Calcutta, India, were determined. Resistance to one or more antibiotics was observed in 49.2% of the STEC strains, with some of the strains exhibiting multidrug resistance. The dominant combinations of virulence genes present in the strains studied were stx 1 and stx 2 (44.5% of strains) and stx 1 , stx 2 , and hlyA (enterohemorrhagic E. coli hemolysin gene) (19% of strains). Only 6.4% of the STEC strains harbored eae. The diversity of STEC strains from various sources was assessed by random amplification of polymorphic DNA (RAPD). STEC strains that gave identical or nearly similar DNA fingerprints in RAPD-PCR and had similar virulence genotypes were further characterized by pulsed-field gel electrophoresis (PFGE). Identical RAPD and PFGE profiles were observed in four sets of strains, with each set comprising two strains. There was no match in the RAPD and PFGE profiles between strains of STEC isolated from cows and those isolated from humans. It appears that the clones present in bovine sources are not transmitted to humans in the Calcutta setting although these strains showed evolutionary relatedness. Maybe for this reason, STEC has still not become a major problem in India.During the past decade, Shiga toxin-producing Escherichia coli (STEC) has evolved from a clinical novelty to a global public health concern. STEC infections have been reported from over 30 countries and can cause a spectrum of human illness ranging from symptom-free carriage to severe bloody diarrhea and even life-threatening sequelae such as hemolyticuremic syndrome (HUS) (4, 31). STEC is a serologically diverse group of food-borne, zoonotic pathogens, of which the serotype O157:H7 has been epidemiologically significant worldwide because of its notoriety of being associated with lifethreatening disease (18). However, in some geographic areas, non-O157 strains are more commonly isolated from persons with diarrhea or HUS than are O157 STEC strains (40).The ability of STEC to cause serious disease in humans is related to the production of one or more Shiga-like toxins (Stx1, Stx2, or their variants), which inhibits protein synthesis of host cells, thus leading to cell death (26, 27). Additional virulence factors-including the presence of a pathogenicity island designated the locus of enterocyte effacement (LEE) and especially eae, one of the constituent genes of LEE, which is responsible for attaching and effacing lesions (17, 28)-are also shown to be necessary for STEC infection. The large plasmid of STEC O157 carries determinants characteristic for STEC that presumably harbor additional virulence factors:hlyA (the enterohemorrhagic E. coli hemolysin gene), which acts as a pore-forming cytolysin on eukaryotic cells (38); the bifunctional catalase peroxidase (KatP) (6); the etp gene cluster (36); and the secreted serin...

Antimicrobial susceptibilities of Vibrio cholerae strains isolated from cholera patients admitted to the Infectious Diseases Hospital, Calcutta, India for 6 years were analysed to determine the changing trends; 840 V. cholerae strains isolated in 1992-1997 were included in this study. Among V. cholerae serogoup O1 and O139, ampicillin resistance increased from 1992 (35 and 70%, respectively) to 1997 (both serogroups 100%). Resistance to furazolidone and streptomycin was constantly high among V. cholerae O1 strains with gradual increase in resistance to other drugs such as ciprofloxacin, co-trimoxazole, neomycin and nalidixic acid. V. cholerae O139 strains exhibited susceptibilities to furazolidone and streptomycin comparable with those of O1 strains. However, after initial increase in resistance to chloramphenicol and co-trimoxazole, all the V. cholerae O139 strains became susceptible to these two drugs from 1995 onwards. Both V. cholerae O1 and O139 remained largely susceptible to gentamicin and tetracycline. V. cholerae non-O1, non-O139 strains, in contrast, exhibited high levels of resistance to virtually every class of antimicrobial agents tested in this study especially from 1995. Kruskal-Wallis one-way analysis showed that V. cholerae O1 Ogawa serogroup exhibited significant yearly increase in resistance to nine antibiotics followed by non-O1 non-O139 and O139 strains to six antibiotics and two antibiotics respectively. Interesting observation encountered in this study was the dissipation of some of the resistant patterns commonly found among V. cholerae non-O1 non-O139 or O1 serogroups to the O139 serogroup and vice versa during the succeeding years.

A total of 32 Vibrio cholerae isolates were collected during a recent large cholera outbreak in Eastern India. Biochemical and serological studies revealed that all of the isolates belonged to serogroup O1, biotype El Tor, serotype Ogawa. Two multiplex PCR assays confirmed the presence of various toxigenic and pathogenic genes -ace, ctxAB, hlyA, ompU, ompW, rfbO1, rtx, tcp, toxR and zot -in all of the isolates. Sequencing of the ctxB gene from the isolates revealed a novel mutation in the gene. Sequencing also confirmed the presence of altered cholera toxin B of the classical biotype in all of the El Tor isolates, suggesting infection of isolates by classical CTXW. The molecular diversity of V. cholerae isolates studied by enterobacterial repetitive intergenic consensus sequence PCR, BOX-PCR and randomly amplified polymorphic DNA analysis uniformly showed the clonal relationship among the outbreak V. cholerae O1 isolates. The results of this study suggest that cholera-causing V. cholerae strains are constantly evolving in epidemic areas, highlighting the potential of the emergence of more virulent strains.