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Impact of Endometriosis on Women’s Lives: a Qualitative Study

A qualitative descriptive design was conducted using semi-structured focus group discussions with 35 Australian women with endometriosis, in three age groups. All tape-recorded discussions were transcribed verbatim and read line by line to extract meaningful codes and categories using NVivo 9 software through a thematic analysis approach. Categories were then clustered into meaningful themes. (Source: bmcwomenshealth.biomedcentral.com)

Is Antibiotic Resistance Inevitable?


Yes. Historically, the discovery of the sulfa drugs in the 1930 s and the subsequent development of penicillin during World War II ushered in a new era in the treatment of infectious diseases. Infections that were common causes of death and disease in the pre-antibiotic era - rheumatic fever, syphilis, cellulitis and bacterial pneumonia - became treatable, and over the next 20 years most of the classes of antibiotics that find clinical use today were discovered and changed medicine in a profound way. The availability of antibiotics enabled revolutionary medical interventions such as cancer chemotherapy, organ transplants and essentially all major invasive surgeries from joint replacements to coronary bypass. Antibiotics, though, are unique among drugs in that their use precipitates their obsolescence. Paradoxically, these cures select for organisms that can evade them, fueling an arms race between microbes, clinicians and drug discoverers. (Source: bmcbiol.biomedcentral.com)

How Do Successful Antibiotics Work and What Is the Basis of Resistance to Them?

Antibiotics target essential bacterial physiology and biochemistry, causing microbial cell death or the cessation of growth. There are five major antibiotic targets: the bacterial cell wall, the cell membrane, protein synthesis, DNA and RNA synthesis, and folic acid (vitamin B9) metabolism (Figure 1). These bacterial targets are different or nonexistent in eukaryotic cells (including those of humans), which means that antibiotics are relatively nontoxic drugs. For example, the β-lactam antibiotics such as penicillins, cephalosporins and carbapenems block the synthesis of the bacterial cell wall. This structure is absent in higher organisms but is essential for bacterial survival. The bacterial ribosome is the target of the tetracycline, aminoglycoside, macrolide and other antibiotics, and is sufficiently different from the eukaryotic ribosome that cross-inhibition does not occur. (Source: bmcbiol.biomedcentral.com)

Has the Problem of Antibiotic Resistance Worsened Over Time?

Resistance to antibiotics was recorded even before the first clinical use of penicillin in the early 1940 s. In the intervening years, resistance to all classes of antibiotics has emerged, and there are no antibiotics for which resistance does not exist. There are two general strategies for resistance. One comprises mechanisms that transfer resistance vertically from a bacterium to its progeny. Examples are mutations in chromosomal genes that give rise to drug-insensitive products, such as the point mutations in the genes encoding DNA gyrase or topoisomerase IV that result in resistance to fluoroquinolone antibiotics such as ciprofloxacin. The second strategy includes the actions of genes that can be transmitted both vertically to progeny and horizontally to other bacteria, even those of different genera. These genes are located on mobile genetic elements such as plasmids, which can carry one or more resistance genes. Many of the β-lactamase genes that confer resistance to the penicillin, cephalosporin, penem and monobactam antibiotics are located on such elements, as is the glycopeptide-resistance gene cluster vanHAX, which provides resistance to vancomycin. The prevalence and mobility of resistance genes in previously sensitive pathogenic bacteria has now reached crisis levels in many cases because new antibiotics are no longer being developed at a rate that can keep pace with microbial evolution. (Source: bmcbiol.biomedcentral.com)



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