Resistance Mechanisms In Bacteria Research Articles

S13.1 What is a biofilm?

This chapter tries to give an answer to the important question asked today whether the use of biocides in the food industry can result in bacterial resistance to biocides and thereby give rise to biocide antibiotic cross- and coresistance. To avoid the development of resistant bacteria the importance of thorough cleaning and correct disinfection of the equipment is emphasized, because if eliminating all bacteria from the equipment, there will be no development of resistance. The aim to achieving this is to try to remove all bacteria from the equipment and the product-contact surfaces. An overview is given of the most important biocides used, their mode of action, the various mechanisms of resistance in bacteria to biocides, and suggested solutions to the problem of biocide resistance in bacteria.

Dealkylation of organotin compounds by biological dithiols: toward the chemistry of organotin toxicity.

In this Communication, we report evidence for the dealkylation of trialkyltin compounds by a short linear peptide extracted from a small membrane protein (stannin) involved in cellular apoptosis and containing a CXC motif. We show that (a) organotin binding induces the formation of a beta-turn in the linear peptide, (b) both cysteines are necessary for the dealkylation reaction, and (c) stable 1:1 complexes are formed between the peptide and diorganotins that can be observed by ESI-MS. Organotin degradation by biological dithiols may be responsible for both the delayed activity of these toxins in humans and the organotin resistance mechanisms in bacteria.

Monitoring and identifying antibiotic resistance mechanisms in bacteria

Sub-therapeutic administration of antibiotics to animals is under intense scrutiny because they contribute to the dissemination of antibiotic-resistant bacteria into the food chain. Studies suggest that there is a link between the agricultural use of antibiotics and antibiotic-resistant human infections. Antibiotic-resistant organisms from animal and human wastes reenter the human and animal populations through a number of pathways including natural waters, irrigation water, drinking water, and vegetables and foods. Antibiotic usage in the United States for animal production (disease prevention and growth promotion) is estimated to be 18 million pounds annually. As much as 25 to 75% of the antibiotics administered to feedlot animals are excreted unaltered in feces. Because about 180 million dry tons of livestock and poultry waste is generated annually in the United States, it is not surprising that animal-derived antibiotic-resistant organisms are found contaminating groundwater, surface water, and food crops. It is extremely important to clearly understand the molecular mechanisms that could potentially cause lateral or horizontal gene transfer of antibiotic resistance genes among bacteria. Once the mechanisms and magnitude of resistance gene transfer are clearly understood and quantified, strategies can be instituted to reduce the potential for dissemination of these genes.

Antibiotic resistance mechanisms in bacteria of oral and upper respiratory origin

Over the past 20 years, antibiotic resistance has increased in virtually every species of bacteria examined. In this paper, the main mechanisms of antibiotic resistance currently known for antibiotics used for treatment of disease caused by oral and upper respiratory bacteria will be reviewed, with an emphasis on the most commonly used antibiotics. The possible role that mercury, which is released from silver amalgams, plays in the oral/respiratory bacterial ecology is also discussed, as it relates to possible selection of antibiotic resistant bacteria.

Copper resistance mechanisms in bacteria and fungi

Copper resistance mechanisms in bacteria and fungi

Copper resistance mechanisms in bacteria and fungi.

Copper is both an essential micronutrient and a toxic heavy metal for most living cells. The presence of high concentrations of cupric ions in the environment promotes the selection of microorganisms possessing genetic determinants for copper resistance. Several examples of chromosomal and plasmid copper-resistance systems in bacteria have been reported, and the mechanisms of resistance have started to be understood at the molecular level. Bacterial mechanisms of copper resistance are related to reduced copper transport, enhanced efflux of cupric ions, or copper complexation by cell components. Copper tolerance in fungi has also been ascribed to diverse mechanisms involving trapping of the metal by cell-wall components, altered uptake of copper, extracellular chelation or precipitation by secreted metabolites, and intracellular complexing by metallothioneins and phytochelatins; only the metallothionein chelation mechanism has been approached with molecular detail.

Gentamycin resistance in Nicotiana conferred by AAC(3)-I, a narrow substrate specificity acetyltransferase.

Acetylation of the amino group in position 3 of the 2-desoxystreptamine moiety [AAC(3)] of gentamycin is a potent and wide-spread resistance mechanism in bacteria. Several marker genes coding for AAC(3) enzymes with varying substrate ranges or differing molecular properties have been identified. The enzymes AAC(3)-I and AAC(3)-II have a narrow substrate range and confer resistance to gentamycin and its close structural derivatives only, whereas genes encoding AAC(3)-III and AAC(3)-IV enzymes have a broad substrate range, modifying kanamycins, tobramycin, neomycin and paromomycin [1, 2]. Genes encoding AAC(3)-III and AAC(3)-IV enzymes were expressed in plants and shown to confer resistance to gentamicin, kanamycin (one of the genes), and possibly to other antibiotics [3]. Resistance to more than one antibiotic limits the use of the chimeric marker gene. We report that the narrow substrate range AAC(3)-I enzyme from the transposable element Tn21 [2] also provides a useful gentamycin resistance marker in plants. Materials and methods

Multiple antibiotic resistance in a bacterium with suppressed autolytic system.

Suppression of the activity of the cellular autolytic system of pneumococci causes simultaneous resistance against penicillin, D-cycloserine and phosphonomycin. This phenomenon represents a novel type of drug resistance mechanism in bacteria.