The Escherichia coli Fur protein, with its iron(II) cofactor, represses iron assimilation and manganese superoxide dismutase (MnSOD) genes, thus coupling iron metabolism to protection against oxygen toxicity. Iron assimilation is triggered by iron starvation in wild-type cells and is constitutive in fur mutants. We show that iron metabolism deregulation in fur mutants produces an iron overload, leading to oxidative stress and DNA damage including lethal and mutagenic lesions. fur recA mutants were not viable under aerobic conditions and died after a shift from anaerobiosis to aerobiosis. Reduction of the intracellular iron concentration by an iron chelator (ferrozine), by inhibition of ferric iron transport (tonB mutants), or by overexpression of the iron storage ferritin H-like (FTN) protein eliminated oxygen sensitivity. Hydroxyl radical scavengers dimethyl sulfoxide and thiourea also provided protection. Functional recombinational repair was necessary for protection, but SOS induction was not involved. Oxygen-dependent spontaneous mutagenesis was significantly increased in fur mutants. Similarly, SOD deficiency rendered sodA sodB recA mutants nonviable under aerobic conditions. Lethality was suppressed by tonB mutations but not by iron chelation or overexpression of FTN. Thus, superoxide-mediated iron reduction was responsible for oxygen sensitivity. Furthermore, overexpression of SOD partially protected fur recA mutants. We propose that a transient iron overload, which could potentially generate oxidative stress, occurs in wild-type cells on return to normal growth conditions following iron starvation, with the coupling between iron and MnSOD regulation helping the cells cope.

The human gut is colonized by a variety of large amounts of microbes that are collectively called intestinal microbiota. Most of these microbial residents will grow within the mucus layer that overlies the gut epithelium and will act as the first line of defense against both commensal and invading microbes. This mucus is essentially formed by mucins, a family of highly glycosylated protein that are secreted by specialize cells in the gut. In this Review, we examine how commensal members of the microbiota and pathogenic bacteria use mucus to their advantage to promote their growth, develop biofilms and colonize the intestine. We also discuss how mucus-derived components act as nutrient and chemical cues for adaptation and pathogenesis of bacteria and how bacteria can influence the composition of the mucus layer.

Waterborne pathogens and related diseases are a major public health concern worldwide, not only by the morbidity and mortality that they cause, but by the high cost that represents their prevention and treatment. These diseases are directly related to environmental deterioration and pollution. Despite the continued efforts to maintain water safety, waterborne outbreaks are still reported globally. Proper assessment of pathogens on water and water quality monitoring are key factors for decision-making regarding water distribution systems’ infrastructure, the choice of best water treatment and prevention waterborne outbreaks. Powerful, sensitive and reproducible diagnostic tools are developed to monitor pathogen contamination in water and be able to detect not only cultivable pathogens but also to detect the occurrence of viable but non-culturable microorganisms as well as the presence of pathogens on biofilms. Quantitative microbial risk assessment (QMRA) is a helpful tool to evaluate the scenarios for pathogen contamination that involve surveillance, detection methods, analysis and decision-making. This review aims to present a research outlook on waterborne outbreaks that have occurred in recent years. This review also focuses in the main molecular techniques for detection of waterborne pathogens and the use of QMRA approach to protect public health.

Mastitis is the most common and detrimental infection of the mammary gland in dairy cows and has a major economic impact on the production of milk and dairy products. Bacterial mastitis is caused by several pathogens, and the most frequently isolated bacterial species are coagulase-negative staphylocci (CNS). Although CNS are considered minor mastitis pathogens, the importance of CNS has increased over the years. However, the mechanism and factors involved in CNS intramammary infection are poorly studied and defined. Biofilms have been proposed as an important component in the persistence of CNS intramammary infection. Biofilms are defined as a cluster of bacteria enclosed in a self-produced matrix. The objectives of this study were to investigate the ability of CNS to form biofilms. A total of 255 mastitis-associated CNS isolates were investigated using a standard microtiter plate biofilm assay. The biofilms of some isolates were also observed by using confocal microscopy. The presence of biofilm-associated genes icaA, bap, aap, embP, fbe, and atlE was determined by PCR in the 255 isolates. The 5 dominant species assayed were Staphylococcus chromogenes (n=111), Staphylococcus simulans (n=53), Staphylococcus xylosus (n=25), Staphylococcus haemolyticus (n=15), and Staphylococcus epidermidis (n=13), and these represented 85% of the isolates. The data gathered were analyzed to identify significant links with the data deposited in the Canadian Bovine Mastitis Research Network database. Overall, Staph. xylosus is the species with the strongest ability to form biofilm, and Staph. epidermidis is the species with the lowest ability to form biofilm. Regardless of the species, the presence of icaA, bap, or the combination of multiple genes was associated with a greater ability to form biofilm. A strong relationship between the strength of a biofilm and days in milk was also noted, and CNS isolated later in the lactation cycle appeared to have a greater ability to form biofilm than those isolated earlier in the lactation cycle. In conclusion, Staph. xylosus is the species with the strongest biofilm formation ability. Furthermore, days in milk and gene combinations are predicted to be the variables with the strongest effect on biofilm formation by CNS.