Peracetic acid is an oxidant that produces hydroxyl radicals that subsequently attack essential cell components such as DNA. Peracetic acid resistance mechanisms might therefore consist of systems involved in DNA repair, such as the SOS response. Recently, it was shown for L. monocytogenes that its SOS response was important for oxidative stress resistance ( van der Veen et al., 2010), and

that the SOS response was specifically activated during continuous flow biofilm formation and not during static biofilm formation ( van der Veen and Abee, 2010). Whether selleck the SOS response is activated during mixed species biofilm formation remains to be elucidated. In contrast to L. monocytogenes and other low GC Gram-positives, L. plantarum contains a specific oxidative stress resistance mechanism that

includes accumulation of high concentrations of intracellular manganese ions, acting as radical scavengers ( Archibald and Fridovich, 1981). Our results showed that peracetic acid resistance of L. plantarum grown in biofilms was increased in BHI-Mn-G but not in BHI-Mn pointing to a more prominent role of acid adaptation in peracetic acid resistance. In conclusion, our approach highlighted Pictilisib concentration the impact of mixed species biofilm formation on disinfection resistance. In future studies we will investigate the specific factors involved in mixed species biofilm formation, including intra- and interspecies communication, and the mechanisms that confer disinfection resistance. “
“Clostridium perfringens is an anaerobic, Gram-positive, spore-forming, rod-shaped and non-motile bacterium widely found in soil, water, air, and in the gastrointestinal tract of humans and animals,

which can contaminate raw and processed foods, particularly meat, meat products and poultry. This bacterium produces over 13 different toxins and is commonly classified into five types (A, B, C, D and E) depending on the production of four major lethal toxins including alpha, beta, epsilon and iota ( Juneja et al., 2003 and Carman et al., 2008). Foodborne illness occurs after the ingestion of food contaminated with a large number (106–107 cells/g) of type A Parvulin viable vegetative cells carrying the cpe gene encoding the C. perfringens enterotoxin (CPE). Foodborne illness is the result of CPEs that are produced during in vivo sporulation, which usually occurs in the small intestine and is stimulated by acid conditions. Approximately 8 h to 12 h after eating contaminated food, the symptoms start with acute abdominal pain, nausea and diarrhea. The contaminated food is almost always heat-treated, which kills competing flora, while the C. perfringens spores survive and germinate ( Mcclane and Rood, 2001, Brynestad and Granum, 2002, Byrne et al., 2008 and Juneja et al., 2009). C.