Effect of Helicobacter pylori and Helminth Coinfection on the Immune Response to Mycobacterium tuberculosis.

Tuberculosis remains one of the main causes of morbidity and mortality worldwide despite decades of efforts to eradicate the disease. Although the immune response controls the infection in most infected individuals (90%), the ability of the bacterium to persist throughout the host's life leads to a risk of reactivation. Underlying conditions including human immunodeficiency virus (HIV) infection, organ transplantation, and immunosuppressive therapies are considered risk factors for progression to active disease. However, many individuals infected with Mycobacterium tuberculosis may develop clinical disease in the absence of underlying immunosuppression. It is also possible that unknown conditions may drive the progression to disease. The human microbiota can be an important modulator of the immune system; it can not only trigger inflammatory disorders, but also drive the response to other infectious diseases. In developing countries, chronic mucosal infections with Helicobacter pylori and helminths may be particularly important, as these infections frequently coexist throughout the host's life. However, little is known about the interactions of these pathogens with the immune system and their effects on M. tuberculosis clinical disease, if any. In this review, we discuss the potential effects of H. pylori and helminth co-infections on the immune response to M. tuberculosis. This may contribute to our understanding of host-pathogen interactions and in designing new strategies for the prevention and control of tuberculosis.

Detection of pathogenic Leptospira in ornamental water fountains from urban sites in Cali, Colombia.

Leptospirosis is a disease endemic to both rural and urban areas of tropical countries and resource-poor communities. Little information is available on the presence of Leptospira spp. in urban water sources. A study was conducted to detect pathogenic Leptospira in ornamental water fountains in Cali, Colombia. Twenty-seven water fountains were tested for pathogenic Leptospira using a multiplex PCR assay targeting the secY and the flaB genes. Pathogenic Leptospira was confirmed in 11 (41%) ornamental water fountains. Plazas, building exteriors, and sidewalks presented the highest proportion (67%) of pathogenic Leptospira-positive water fountains. Urban ornamental water fountains might be sources of pathogenic Leptospira and might pose a risk to humans who come into close contact, although relevance from a public health perspective is yet to be established.

Effect of treatment failure on the CagA EPIYA motif in Helicobacter pylori strains from Colombian subjects.

AIM: To evaluate effect of treatment failure on cagA and vacA genotypes in Helicobacter pylori (H. pylori) isolates from Colombia. METHODS: One hundred and seventy-six participants infected with H. pylori from Colombia were treated during 14 d with the triple-standard therapy. Six weeks later, eradication was evaluated by 13C-Urea breath test. Patients with treatment failure were subjected to endoscopy control; biopsies obtained were used for histopathology and culture. DNA from H. pylori isolates was amplified using primers specific for cagA and vacA genes. The phylogenetic relationships among isolates obtained before and after treatment were established by conglomerate analysis based on random amplified polymorphic DNA (RAPD) fingerprinting. RESULTS: Treatment effectiveness was at 74.6%. Of the participants with treatment failure, 25 accepted subjected to a second endoscopy. Prevalence of post-treatment infection was 64% (16/25) and 40% (10/25) by histology and culture, respectively. Upon comparing the cagA and vacA genotypes found before and after therapy, multiple cagA genotypes (cagA-positive and cagA-negative) were found before treatment; in contrast, cagA-negative genotypes decreased after treatment. vacA s1m1 genotype was highly prevalent in patients before and after therapy. The 3'cagA region was successfully amplified in 95.5% (21/22) of the isolates obtained before and in 81.8% (18/22) of the isolates obtained after treatment. In the isolates obtained from patients with treatment failure, it was found that 72.7% (16/22) presented alterations in the number of EPIYA motifs, compared to isolates found before treatment. CONCLUSION: Unsuccessful treatment limits colonization by low-virulence strains resulting in partial and selective eradication in mixed infections, and acts on the cagA-positive strains inducing genetic rearrangements in cagA variable region that produces a loss or gain of EPIYA repetitions.

Genomic variability of Helicobacter pylori isolates of gastric regions from two Colombian populations.

AIM: To compare the genomic variability and the multiple colonization of Helicobacter pylori (H. pylori) in patients with chronic gastritis from two Colombian populations with contrast in the risk of developing gastric cancer (GC): Túquerres-Nariño (High risk) and Tumaco-Nariño (Low risk). METHODS: Four hundred and nine patients from both genders with dyspeptic symptoms were studied. Seventy-two patients were included in whom H. pylori was isolated from three anatomic regions of the gastric mucosa, (31/206) of the high risk population of GC (Túquerres) and (41/203) of the low risk population of GC (Tumaco). The isolates were genotyped by PCR-RAPD. Genetic diversity between the isolates was evaluated by conglomerates analysis and multiple correspondence analyses. RESULTS: The proportion of virulent genotypes of H. pylori was 99% in Túquerres and 94% in Tumaco. The coefficient of similarity of Nei-Li showed greater genetic diversity among isolates of Túquerres (0.13) than those of Tumaco (0.07). After adjusting by age, gender and type of gastritis, the multiple colonization was 1.7 times more frequent in Túquerres than in Tumaco (P = 0.05). CONCLUSION: In Túquerres, high risk of GC there was a greater probability of multiple colonization by H. pylori. From the analysis of the results of the PCR-RAPD, it was found higher genetic variability in the isolates of H. pylori in the population of high risk for the development of GC.

In vitro effect of amoxicillin and clarithromycin on the 3' region of cagA gene in Helicobacter pylori isolates.

AIM: To evaluate the in vitro effect of amoxicillin and clarithromycin on the cag pathogenicity island (cag PAI). METHODS: One hundred and forty-nine clinical isolates of Helicobacter pylori (H. pylori) cultured from gastric biopsies from 206 Colombian patients with dyspeptic symptoms from a high-risk area for gastric cancer were included as study material. Antimicrobial susceptibility was determined by the agar dilution method. Resistant isolates at baseline and in amoxicillin and clarithromycin serial dilutions were subjected to genotyping (cagA, vacA alleles s and m), Glu-Pro-Ile-Tyr-Ala (EPIYA) polymerase chain reaction and random amplified polymorphic DNA (RAPD). Images of the RAPD amplicons were analyzed by Gel-Pro Analyzer 4.5 program. Cluster analyses was done using SPSS 15.0 statistical package, where each of the fingerprint bands were denoted as variables. Dendrograms were designed by following Ward's clustering method and the estimation of distances between each pair of H. pylori isolates was calculated with the squared Euclidean distance. RESULTS: Resistance rates were 4% for amoxicillin and 2.7% for clarithromycin with 2% double resistances. Genotyping evidenced a high prevalence of the genotype cagA-positive/vacA s1m1. The 3' region of cagA gene was successfully amplified in 92.3% (12/13) of the baseline resistant isolates and in 60% (36/60) of the resistant isolates growing in antibiotic dilutions. Upon observing the distribution of the number of EPIYA repetitions in each dilution with respect to baseline isolates, it was found that in 61.5% (8/13) of the baseline isolates, a change in the number of EPIYA repetitions lowered antibiotic pressure. The gain and loss of EPIYA motifs resulted in a diversity of H. pylori subclones after bacterial adjustment to changing conditions product of antibiotic pressure. RAPD PCR evidenced the close clonal relationship between baseline isolates and isolates growing in antibiotic dilutions. CONCLUSION: Antibiotic pressure does not induce loss of the cag pathogenicity island, but it can lead--in most cases--to genetic rearrangements within the 3' region cagA of the founding bacteria that can affect the level of tyrosine phosphorylation impacting on its cellular effects and lead to divergence of cagA-positive subclones.