Spoligotype Diversity of Mycobacterium tuberculosis over Two Decades from Tiruvallur, South India.

Geographically, most tuberculosis (TB) cases in 2018 were reported from India. This TB burden is compounded by MDR-TB and XDR-TB. The strategies for the management and control of TB in the community depend on an understanding of the mode of spread of the different strains of TB isolates in the community. To determine the distribution and trends of M. tb strains over the time period in the community due to treatment, we carried out the present study on changes over two decades. Design/Methods. A total of 1218 M. tb isolates (year: 2001-2018) from Tiruvallur, India, were genotyped by spoligotyping after DNA extraction and subjected to anti-TB drug susceptibility testing for the first-line anti-TB drugs. Results. On analysis with the SpolDB4 database, majority (2001-2003: 53.32% and 2015-2018: 46.3%) of the isolates belonged to East African Indian (EAI) lineage, and the orphans designated in comparison to SpolDB4 stood 33% among 2001-2003 strain collection and 46.3% among 2015-2018 strain collection. 10.2% (2001-2003) and 9.26% (2015 to 2018) of isolates were monoresistant to isoniazid (H). MDR strains were less common among EAI strains (3.2%) compared to non-EAI strains (10.32%). Conclusions. EAI is the most predominant lineage in Tiruvallur, despite the presence of highly transmissible lineages like Beijing for the last two decades. The prevalence of MDR-TB is below the national average of 2-3% among the new TB cases in the last two decades. The reason can be attributed to the well-established nature of the locally circulating strains in this region which are not associated with drug resistance.

Effect of secoverine on colonic myoelectric activity in diverticular disease of the colon.

The effect of secoverine on colonic smooth muscle was measured in patients with diverticular disease and in healthy subjects. The frequency of slow wave activity was determined using the fast Fourier transform (FFT) and peak identification analysis (SWSA). The mean slow wave frequency was similar (6 cycles/minute) in healthy subjects using both analytic methods. The slow wave frequency in patients with diverticular disease was similar to that in healthy subjects. The peak frequency measured with SWSA was uniformly higher than that measured with FFT. Secoverine, a muscarinic antagonist, did not affect the slow wave frequency. Eating a 1000-kcal meal initiates an increase in colonic spike activity (22 +/- 2 spike potential/30 min) (P less than 0.001) in healthy subjects during the immediate postprandial period. The gastrocolonic response in patients with diverticular disease was prolonged for 60 min. Secoverine inhibited the gastrocolonic response in patients with diverticular disease. These studies suggest patients with diverticular disease have a similar slow wave frequency as healthy subjects, the gastrocolonic response is prolonged in patients with diverticular disease, and secoverine inhibits the colonic response.

Comparison of intraluminal and intravenous mediators of colonic response to eating.

Eating a 1000-kcal mixed meal stimulates an increase in distal colonic motility. Fat is the dietary component which is the major stimulant of colonic spike activity. In this study the colonic spike activity increased similarly after the mixed meal [19.1 +/- 2.4 spike potentials (SP)/30 min] and after the fat meal (19.4 +/- 5.4 SP/30 min). Fat stimulated a concentration-dependent increase in colonic motility only when in contact with the gastroduodenal mucosa. Intravenous administration of Liposyn (100 kcal/hr) did not stimulate an increase in colonic spike activity (3.3 +/- 1.3 SP/30 min) despite greater increase in plasma total fatty acid levels than after the oral ingestion of fat. In contrast both the oral ingestion and the intravenous administration of an amino acid mixture (Aminosyn) inhibited the gastrocolonic response after the 1000-kcal mixed meal. Thus, these studies demonstrate: (1) fat stimulates colonic motility only through direct mucosal contact, and (2) a mixture of amino acid inhibits colonic motility through either mucosal contact or by circulating in the plasma. The exact neurohumoral mechanisms involved in both of these effects is unknown at present.