Clinical Antibiotic Resistance Cases

TABLE 4.6 Quinupristin-Dalfopristin Susceptibility and Genetic Determinants of Resistance in Enterococcus faecium from Different Midwestern U.S. Ecologic Sources 

faecium Source %Susceptibility to Quinupristin-Dalfopristin %Resistance Genes  

The use of disinfectants such as triclosan and quaternary ammonium compounds and triclosan in homes and hospitals also leads to an enhanced selection for antibiotic-resistant bacteria (Russell, 2000 Kiicken et al., 2000 McMurray et al., 1998). Besides introducing resistance to bacteria, some antibiotics can also impose other effects. For example, a recent study by Vehcer et al. (2004) reported an intriguing association between cumulative exposure to all classes of antibiotics and breast cancer. Floroquinolones have also been imphcated in inducing tensions in the cartilage of immature animals (Hunt et al., 2002) and are generally deemed unsuitable for pediatric use. However, their presence in the environment can inadvertently introduce them to such susceptible individuals. 

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The most relevant of the coagulase-positive species is Staphylococcus aureus subsp. aureus (further S. aureus), pathogenic to both humans and animals. It is an extraordinary versatile pathogen and the major causative agent of numerous hospital-and community acqnired infections. The spread, survival and prevalence of antibiotic resistant clones of S. aureus are immensely important problems for human health. Major antibiotic resistance problems are typically associated with methicillin (oxacillin) resistant S. aureus strains (MRSA) and, more recently, vancomycin-intermediate (VISA) and vancomycin-resistant (VRSA) strains. Up to 30% of the hnman population carries S. aureus without any symptoms. In most cases, however, the colonizing strain serves as an endogenous reservoir for clinical infections (von Eiff et al. 2004). The disease spectrum includes abscesses, bacteremia, central nervons... 

The introduction of antibiotics led to an enormous decrease in the morbidity and mortality caused by bacterial infections. Widespread use of antibiotics in the clinic, in animal feed, and in consumer products has resulted in astonishingly rapid evolution of antibiotic resistance, typically within a few decades, or even a few years, after introduction of a new antibiotic. Resistance can occur via multiple mechanisms, including detoxification by enzymes as well as target modification, decreased membrane permeability, and use of efflux pumps to expel antibiotics from cells. In many cases, antibiotic resistance genes are already present in the environment as a result of self-protection mechanisms in organisms that produce antibiotics, or of exposure of... 

Clearly two distinct issues arise from these observations. The first is whether the development of nonsusceptibility to antiseptics by nosocomial pathogens, skin flora, and other microorganisms results in decreased clinical efficacy of the topical antiseptics used in healthcare settings. The second issue is whether the emergence of resistance to the antiseptics will result in cross-resistance to clinically useful antibiotics. The concern in the latter case is that the wide availability and use of antiseptics and the selection pressure they provide will counterselect for antibiotic resistant pathogens. 

COPD exacerbations. Therefore, in exacerbation treatment with antibiotics is justified when the patient has at least two of three features of increased dyspnea, increased sputum volume, and sputum pu-rulence. Antibiotic choice will depend on local experience derived from local bacteriological sensitivity data. Older, less costly compounds such as tetracycline, doxycycline, amoxicillin, erythromycin, cefaclor etc. are often as effective as newer, more expensive ones. If resistant organisms are suspected or when the severity of the patients clinical condition puts them at high-risk of treatment failure, a second or third generation cephalosporin, fluoroquinolone, newer macrolide or broad-spectrum penicillin may be preferred. In cases of recurrent infection prolonged courses of antibiotics continuous or intermittent, may be useful. 

Oral vancomycin, 0.125-0.25 g every 6 hours, is used to treat antibiotic-associated enterocolitis caused by C difficile. Because of the emergence of vancomycin-resistant enterococci and the selective pressure of oral vancomycin for these resistant organisms, metronidazole had been preferred as initial therapy over the last two decades. However, recent clinical data suggest that vancomycin is associated with a better clinical response than metronidazole for more severe cases of C difficile enterocolitis. Therefore, oral vancomycin may be used as a first line treatment for severe cases or for cases that fail to respond to metronidazole. 

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