Municipal wastewater (MW) contains a conglomeration of human enteric microbiota from a community and, hence, represents a potential surveillance tool for gastrointestinal infectious disease burden at the community level. To evaluate this, the concentration of Salmonella in MW samples from Honolulu, Hawaii, was monitored over a 54-week period, which showed positive and significant linear and rank correlation with clinical salmonellosis case numbers over the same period. Salmonella isolates were obtained from the MW samples and then compared with clinical isolates obtained by the Hawaii Department of Health State Laboratories over the same period. The MW isolate collection contained 34 serotypes, and the clinical isolate collection contained 47 serotypes, 21 of which were shared between the two isolate collections, including nine of the 12 most commonly detected clinical serotypes. Most notably, nine Salmonella strains, including one outbreak-associated Paratyphi B strain and eight other clinically rare strains, were shared and concurrently detected between the MW and the clinical isolate collections, indicating the feasibility of using enteric pathogens in the MW as a timely indication of community enteric disease activity.

This study investigated the flux stability of select chemical and biological sewage markers, including caffeine, total nitrogen (TN), total suspended solids (TSS), E. coli, and enterococci, and their suitability in assessing the severity of rainfall-derived infiltration and inflow (RDII) in a residential sewershed. To quantify and compare marker flux stability, concentrations of the candidate markers in two dry-weather periods were determined and the one-day lag autocorrelation coefficients (r) of their mass fluxes were calculated. TN (r = 0.82-0.88) exhibited higher and more consistent flux stability than TSS (r = 0.49-0.82), caffeine (r = 0.56-0.58), E. coli (r = 0.36-0.87), and enterococci (by culture; r = 0.40-0.52), all of which except enterococci by qPCR (r = -0.10-0.21) showed significant autocorrelation. Sewage flows and marker concentrations were also monitored in two wet-weather periods, and the severity of RDII (R(RDII)) were calculated using either flow measurements or marker concentrations independently. Corresponding to its outstanding flux stability, R(RDII) values estimated by TN predicted all severe RDII instances and gave the highest and most consistent correlation (r = 0.74-0.78) among the different sewage markers. Overall, the study illustrated the feasibility of using the flux stability of sewage markers in assessing the severity of RDII and thereby deterioration levels in sewer systems.

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Background The aim of this study was to assess the effect of antiretroviral therapy (ART) versus HIV on mitochondria in fat. Methods Subcutaneous fat was collected from 45 HIV-infected patients on ART with lipoatrophy, 11 HIV-infected ART-naive patients and nine healthy controls. Three mitochondrial transcripts: NADH dehydrogenase subunit 1 (ND1), cytochrome B (CYTB) and NADH dehydrogenase subunit 6 (ND6) genes were quantitated using TaqMan® probes and normalized to nuclear-encoded ribosomal L13. Results ND1/L13 and CYTB/L13 were lower in HIV-positive patients on ART with lipoatrophy versus ART-naive patients (3.4 versus 7.2 [ P=0.017] and 2.5 versus 4.6 [ P=0.006], respectively). No difference was found between ART-naive patients and controls ( P>0.70). ND6/ L13 was similar between all groups. Dual-energy X-ray absorptiometry-measured limb fat and mitochondrial DNA in fat were also lower in HIV-positive patients on ART with lipoatrophy versus HIV-infected, ART-naive patients (4,382 versus 7,662 g [ P=0.02] and 726 versus 1,372 copies/cell [ P=0.03], respectively), but no difference was found between ART-naive and controls. In a multiple regression analysis, limb fat correlated with all three mitochrondrial RNA, whereas mitochondrial DNA did not correlate with mitochondrial RNA or limb fat. Conclusions In contrast to ART-naive patients, HIV-positive patients on ART with lipoatrophy had significant depletion in mitochondrial DNA in fat and mitochondrial RNAs. This suggests that mitochondrial toxicity in lipoatrophy could be driven by ART and not by HIV itself. In addition, mitochondrial RNA abnormalities, and not mitochondrial DNA depletion, could be a key driving force behind lipoatrophy.

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