No abstract

Fecal bacteria have traditionally been used as indicator organisms to monitor the quality of recreational waters. Recent work has questioned the robustness of traditional indicators, particularly at seawater bathing beaches. For example, a study of Florida beaches found unexpectedly high abundances of Escherichia coli, fecal coliforms, and enterococci in beach sand. The aim of the present study was to explain these abundances by assessing the survival of E. coli and enterococci in beach sand relative to seawater. We used a combination of quantitative laboratory mesocosm experiments and field observations. Results suggested that E. coli and enterococci exhibited increased survivability and growth in sand relative to seawater. Because fecal bacteria are capable of replicating in sand, at least under controlled laboratory conditions, the results suggest that sand may be an important reservoir of metabolically active fecal organisms. Experiments with "natural" mesocosms (i.e., unsterilized sand or water rich in micropredators and native bacteria) failed to show the same increases in fecal indicators as was found in sterile sand. It is postulated that this was due to predation and competition with indigenous bacteria in these "natural" systems. Nonetheless, high populations of indicators were maintained and recovered from sand over the duration of the experiment as opposed to the die-off noted in water. Indicator bacteria may wash out of sand into shoreline waters during weather and tidal events, thereby decreasing the effectiveness of these indicators as predictors of health risk and complicating the interpretations for water quality managers.

Seven locations were screened for antibiotic-resistant bacteria using a modified agar dilution technique. Isolates resistant to high levels of antibiotics were screened for r plasmids. Low-level resistance (25 micro g x ml(-1)) was widespread for ampicillin, penicillin, tetracycline, vancomycin and streptomycin but not for kanamycin. Resistant populations dropped sharply at high antibiotic levels, suggesting that intrinsic non-emergent mechanisms were responsible for the multiple drug resistance exhibited at low doses. Dairy farm manure contained significantly (P < 0.01) more (%) resistant bacteria than the other sites. Bacteria isolated from a dairy water canal, a lake by a hospital and a residential garden (fertilized by farm manure) displayed resistance frequencies of 77, 75 and 70%, respectively. Incidence of tetracycline resistance was most prevalent at 47-89% of total bacteria. Out of 200 representative isolates analyzed, Pseudomonas, Enterococcus-like bacteria, Enterobacter and Burkholderia species constituted the dominant reservoirs of resistance at high drug levels (50-170 micro g x ml(-1)). Plasmids were detected in only 29% (58) of these bacteria with tetracycline resistance accounting for 65% of the plasmid pool. Overall, resistance trends correlated to the abundance and type of bacterial species present in the habitat. Environmental reservoirs of resistance include opportunistic pathogens and constitute some public health concern.

We have identified the product of the NIL2 gene of Saccharomyces cerevisiae which contains a zinc finger region highly homologous to those of the GATA factors Gln3p and Nil1p as an antagonist of Nil1p and to a lesser extent of Gln3p. The expression of many nitrogen-regulated genes of Saccharomyces cerevisiae requires activation by GATA factor Gln3p or Nil1p and is prevented by the presence of glutamine in the growth medium. Disruption of NIL2 results in a great increase in the expression of NIL1 and of GAP1, the structural gene for the general amino acid permease, in glutamine-grown cells in response to activation by Nil1p. The primary effect of the elimination of Nil2p appears to be an increase in the intracellular level of Nil1p, which in turn is responsible for increased expression of GAP1. Experiments using an artificial UAS (upstream activating site) consisting of three GATAAGATAAG sites revealed that Nil2p exerts its effect by competing primarily with Nil1p and less effectively with Gln3p for these sites. Apparently, the principal role of Nil2p is to prevent activation of transcription by Nil1p unless Nil1p has been converted to a more active state by the absence of glutamine and glutamate.It is now well established that the expression of many genes of Saccharomyces cerevisiae whose products are responsible for the utilization of different nitrogen compounds as sources of nitrogen is activated by two zinc finger proteins that recognize the sequence GATAAG located upstream of these genes (4,5,16,21,23,25). One of these activators is the product of the GLN3 gene, and its ability to activate transcription is opposed by the product of the URE2 gene in response to an increase in the intracellular level of glutamine (2,6,7,13,19,21). The other activator, the product of NIL1 (also called GAT1) has a zinc finger highly homologous to that of Gln3p and is capable of activating some of the same promoters as Gln3p, but its activity appears to be antagonized by an as yet unknown protein in response to the rise in the intracellular concentration of glutamate (5, 25). As a result, transcription of a susceptible gene such as GAP1, coding for the general amino acid permease, is activated almost exclusively by Gln3p during growth with glutamate as the source of nitrogen and almost exclusively by Nil1p during growth with ammonia or urea as the source of nitrogen and is not activated at all during growth in a medium containing glutamine (25).In addition to possessing homologous zinc fingers, Gln3p and Nil1p also resemble one another by possessing highly acidic amino-terminal domains, characteristic of many activators (25). Two other proteins also possess zinc fingers with high homology to those of Gln3p and Nil1p, but they lack the acidic amino-terminal portions (8,25). One of these proteins, the product of DAL80, has been identified as an antagonist of Gln3p in the case of some, but not all, Gln3p-dependent genes (10, 12). Apparently, Dal80p requires two GATAAG sequences located not more than 20 bp apart to be effective (9)....

Invasive candidiasis remains one of the most serious community and healthcare-acquired infections worldwide. Conventional Candida detection methods based on blood and plate culture are time-consuming and require at least 2–4 days to identify various Candida species. Despite considerable advances for candidiasis detection, the development of simple, compact and portable point-of-care diagnostics for rapid and precise testing that automatically performs cell lysis, nucleic acid extraction, purification and detection still remains a challenge. Here, we systematically review most prominent conventional and nonconventional techniques for the detection of various Candida species, including Candida staining, blood culture, serological testing and nucleic acid-based analysis. We also discuss the most advanced lab on a chip devices for candida detection.

Ebola virus disease (EVD) is a devastating, highly infectious illness with a high mortality rate. The disease is endemic to regions of Central and West Africa, where there is limited laboratory infrastructure and trained staff. The recent 2014 West African EVD outbreak has been unprecedented in case numbers and fatalities, and has proven that such regional outbreaks can become a potential threat to global public health, as it became the source for the subsequent transmission events in Spain and the USA. The urgent need for rapid and affordable means of detecting Ebola is crucial to control the spread of EVD and prevent devastating fatalities. Current diagnostic techniques include molecular diagnostics and other serological and antigen detection assays; which can be time-consuming, laboratory-based, often require trained personnel and specialized equipment. In this review, we discuss the various Ebola detection techniques currently in use, and highlight the potential future directions pertinent to the development and adoption of novel point-of-care diagnostic tools. Finally, a case is made for the need to develop novel microfluidic technologies and versatile rapid detection platforms for early detection of EVD.

No abstract

No abstract