Bacteria bacterial inactivation

Different mechanisms to explain the disinfection ability of photocatalysts have been proposed [136]. One of the first studies of Escherichia coli inactivation by photocatalytic Ti02 action suggested the lipid peroxidation reaction as the mechanism of bacterial death [137]. A recent study indicated that both degradation of formaldehyde and inactivation of E. coli depended on the amount of reactive oxygen species formed under irradiation [138]. The action with which viruses and bacteria are inactivated by Ti02 photocatalysts seems to involve various species, namely free hydroxyl radicals in the bulk solution for the former and free and surface-bound hydroxyl radicals and other oxygen reactive species for the latter [139]. Different factors were taken into account in a study of E. coli inactivation in addition to the presence of the photocatalyst treatment with H202, which enhanced the inactivation... 

If this enhancement of dimerization in UV-exposed DNA is transposed to the more normal situation that applies when bacteria are treated with a silver salt such as AgN03, then it is tempting to speculate that interaction of DNA with Ag is a primary target site. It would, however, be premature to propose that such an interaction is necessarily responsible for bacterial inactivation, although it must clearly play some role. 

Three common food borne pathogenic bacteria were transformed with plasmids carrying the lux genes in order to evaluate wet and dry surface pasteurisation of food surfaces. The work was carried out within the Bugdeath programme, an EU Framework V collaborative project to develop predictive models for the surface pasteurisation of raw food materials, based on accurate data obtained from real food samples, heated in standardised, precisely controlled conditions. Previous models, based on indirect viable counts of bacteria, have been shown to be poor predictors of bacterial inactivation and recovery during heat treatment. 

Smiddy et al. (2005) confirmed higher baro-resistance of bacteria in oysters than in bnffer, which indicated that stndies of high-pressure-induced bacterial inactivation in bnffer systems may not predict inactivation of microorganisms in foods. Calci et al. (2005) indicated that 6-log redaction of Hepatitis A virus could be achieved via application of high pressure (350-400 MPa). Li et al. (2009) demonstrated that high-pressnre treatment (400 MPa, 5 min, 0°C) of oysters contaminated with murine norovirns-1 could reduce the levels of contaminant to undetectable levels. 

Formaldehyde vapour generated from formaldehyde solution is an effective space disinfectant for decontaminating rooms or buildings. It inactivates vegetative bacteria, bacterial spores, and viruses. Formaldehyde... 

As a result of hospital infections caused by the increased resistance of bacterial strands to antibiotics inducing infections for which they are not effective, such as methiciUin-resistant Staphylococcus aureus (MRSA), Pseudomonas aeruginosa, and certain strands of Escherichia coli, there is a need to develop new robust antibacterial films.These films should reduce or abate pathogenic bacteria resistant to synthetic antibiotics when administered for a long time. The films should have fast bacterial reduction kinetics, be uniform, adhese to the support, and have low cytotoxicity. That is the focus of this study addressing silver (Ag)-nitride/oxynitride bacterial inactivation films. Nitrides/oxynitrides have been shown to be resistant composites and have no or extremely low cytotoxic activity. 

Figure 10.3 X-ray photoelectron spectroscopy of TiN (3 min) in contact with bacteria for 3 s (a) time = 0 min and (h) time 120 min, showing the shift in deconvoluted peaks after bacterial inactivation.

Fig. 10.24 present E. coli bacterial results on TaN, Ag-TaN and TaON, and Ag-TaON films. The effects of the light dose and bacterial reduction by Ag sputtered on polyester by itself are considered. Bacterial inactivation becomes faster for increasing TaN-sputtering times. Fig. 10.24(a) shows that sputtering TaN for 120 s inactivated bacteria within 300 min. Fig. 10.24(a), trace 5 shows that in the dark there was no bacterial inactivarion on Ag-TaN polyester. Ag-TaN showed faster bacterial inactivation compared with TaN films and inactivated E. coli within 120 min for a 120-s co-sputtered sample. Fig. 10.24(a), trace 3 shows bacterial inactivation for Ag-TaN—Ag-surfaces co-sputtered for 60s. Because the E. coli inactivation time... 

Recently it has been proposed that bacterial inactivation by HOCl is the result of inhibition of DNA replication. When bacteria are exposed to HOCl, there is a precipitous decline in DNA synthesis that precedes inhibition of protein synthesis, and closely parallels loss of viability. During bacterial genome replication, the origin of replication (oriC in E. coli) binds to proteins that are associated with the cell membrane, and it was observed that HOCl treatment decreases the affinity of extracted membranes for oriC, and this decreased affinity also parallels loss of viability. A study by Rosen et al. compared the rate of HOCl inhibition of DNA replication of plasmids with different replication origins and found that certain plasmids exhibited a delay in the inhibition of replication when compared to plasmids containing oriC. Rosen s group proposed that inactivation of membrane proteins involved in DNA replication are the mechanism of action of HOCl. 

The antibacterial effectiveness of penicillins cephalospotins and other P-lactam antibiotics depends upon selective acylation and consequentiy, iaactivation, of transpeptidases involved ia bacterial ceU wall synthesis. This acylating ability is a result of the reactivity of the P-lactam ring (1). Bacteria that are resistant to P-lactam antibiotics often produce enzymes called P-lactamases that inactivate the antibiotics by cataly2ing the hydrolytic opening of the P-lactam ring to give products (2) devoid of antibacterial activity. 

After 30 hours, the maximum and critical fermentation is underway and the pH must remain above 4.0 for optimal fermentation. However, accompanying bacterial contamination from various sources such as yeast contamination, improper cleaning procedures, slow yeast growth, or excessive temperatures can result in a pH below 4.0. The remaining amylase enzymes, referred to as secondary conversion agents, are inactivated and can no longer convert the dextrins to maltose. Under these circumstances, the fermentor pH continues to drop because of acid production of the bacteria, and the pH can drop to as low as 3.0. The obvious result is a low ethanol yield and quaUty deterioration. 

At 70—140°C, peroxide is vaporised. Peroxide vapor has been reported to rapidly inactivate pathogenic bacteria, yeast, and bacterial spores in very low concentrations (133). Experiments using peroxide vapor for space decontamination of rooms and biologic safety cabinets hold promise (134). The use of peroxide vapor and a plasma generated by radio frequency energy releasing free radicals, ions, excited atoms, and excited molecules in a sterilising chamber has been patented (135). 

Studies on the mechanism of action of /3-lactam antibiotics have shed considerable light on how these agents kill bacteria. They also help explain qualitative differences between various agents and why there is a correlation between the reactivity of the /3-lactam and antibacterial activity. However, it is also clear that reactivity is only one factor in determining how effectively a given /3-lactam antibiotic will inactivate bacterial enzymes (82BJ(203)223). 

Because the natural penicillins have been used for many years, drug-resistant strains of microorganisms have developed, making the natural penicillins less effective than some of the newer antibiotics in treating a broad range of infections. Bacterial resistance has occurred within tire penicillins. Bacterial resistance is the ability of bacteria to produce substances that inactivate or destroy the penicillin. One example of bacterial resistance is tiie ability of certain bacteria to produce penicillinase, an enzyme that inactivates penicillin. The penicillinase-resistant penicillins were developed to combat this problem. 

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