Antibiotic resistance clinical

The antimicrobial properties of conductive functionalised-polyaniline (f-PANI) have been investigated by exploring their interaction with different bacteria. It was observed that low concentrations of PANI strongly inhibited the growth of wild-type Escherichia coli. Pseudomonas aeruginosa and Staphylococcus aureus as well as several antibiotic-resistant clinical pathogens [18]. 

That bacterial resistance predates the era of clinical use of antibiotics by several hundred millions of years is the recent result of genomic sequence data mining from antibiotic-producing microorganisms. These are supposed to be the inventors of antibiotic resistance genes which they had developed to protect themselves from the lethal action of their own antibiotics [4]. 

Overproduction of the chromosomal genes for the dihydrofolate reductase (DHFR) and the dihydroptero-ate synthase (DHPS) leads to a decreased susceptibility to trimethoprim and sulfamethoxazol, respectively. This is thought to be the effect of titrating out the antibiotics. However, clinically significant resistance is always associated with amino acid changes within the target enzymes leading to a decreased affinity of the antibiotics. 

P. acnes is an anaerobic diphteroid that populates the androgen-stimulated sebaceous follicles and is a normal constituent of the cutaneous microflora even if acne is not infectious, the commensal P. acnes acts in acne pathogenesis. Three pieces of evidence support the role of P. acnes in acne 1) higher counts of P. acnes in individuals with acne than in those without acne 2) correlation between the reduction of P. acnes counts and the clinical improvement of the disease and 3) correlation between development of acne and presence of antibiotic-resistant P. acnes organisms. P. acnes products mediate the formation of comedones and contribute to their rupture, leading to extrusion of... 

Bacterial resistance to antibiotics has been recognized since the first drugs were introduced for clinical use. The sulphonamides were introduced in 1935 and approximately 10 years later 20% of clinical isolates of Neisseria gonorrhoeae had become resistant. Similar increases in sulphonamide resistance were found in streptococci, coliforms and other bacteria. Penicillin was first used in 1941, when less than 1 % of Staphylococcus aureus strains were resistant to its action. By 1947,3 8% of hospital strains had acquired resistance and currently over 90% of Staph, aureus isolates are resistant to penicillin. Increasing resistance to antibiotics is a consequence of selective pressure, but the actual incidence of resistance varies between different bacterial species. For example, ampicillin resistance inEscherichia coli, presumably under similar selective pressure as Staph, aureus with penicillin, has remained at a level of 30-40% for mai years with a slow rate of increase. Streptococcus pyogenes, another major pathogen, has remained susceptible to penicillin since its introduction, with no reports of resistance in the scientific literature. Equally, it is well recognized that certain bacteria are unaffected by specific antibiotics. In other words, these bacteria have always been antibiotic-resistant. 

Acquired resistance. This occurs when bacteria which were previously susceptible become resistant, usually, but not always, after exposure to the antibiotic concerned. Intrirrsic resistance is always chromosomally mediated, whereas acquired resistance may occirr by mutations in the chromosome or by the acquisition of genes coding for resistance ftom an external source normally via a plasmid or transposon. Both types are clinically important and can result in treatment failure, although acquired resistance is more of a threat in the spread of antibiotic resistance (Russell Chopra 1996). 

The clinical relevance of biocide resistance of antibiotic-resistant staphylococci is, however, unclear. It has been claimed that the resistance of these organisms to cationic-type biocides confers a selective advantage, i.e. survival, when such disinfectants are employed clinically. However, the in-use concentrations are several times higher than those to which the organisms are resistant. 

Antibiotic resistance plays a smaller role in pharyngitis therapy compared with other URIs. O Penicillin resistance has not yet been documented in group A streptococci, but resistance and clinical failures occur more frequently with tetracyclines, trimethoprim-sulfamethoxazole, and to a lesser degree macrolides. 

Bergeron, M. G. Ouellette, M. Preventing antibiotic resistance through rapid genotypic identification of bacteria and of their antibiotic resistance genes in the clinical microbiology laboratory. J. Clin. Microbiol. 1998, 36, 2169-2172. 

The preceding protocol can be successfully applied, essentially without modifications, to prepare active cell-free extracts from bacteria other than Escherichia coli (e.g., Bacillus stearothermophilus and clinical isolates of Pseudomonas aeruginosa bearing multiple antibiotic resistance). 

Despite much effort, antibiotic resistance continues to increase [61]. Looking back, it is clear that this was an inevitable consequence of antibiotic use [62], Antibiotic resistance, which has been recognized to be an important clinical problem, varies in prevalence from one country to another and among the pathogens themselves. This has great clinical, economic, political and environmental implications worldwide [63]. Strict adherence to the ongoing measures of infection control, education and antibiotic policy should minimize antibiotic resistance [64],... 

Essentially, three major lines of evidence contribute to demonstrate the gradual increase of antibiotic resistance - (1) annual reports on antibiotic resistance prevalence values of clinically relevant antibiotics for human pathogens [27, 28] (2) the comparison of antibiotic resistance prevalence values in samples or bacterial cultures of our days with others archived from the pre-antibiotic era (e.g. [29, 30]) and (3) the establishment of significant correlations between antibiotics consumption and resistance increase [28, 31]. 

Antibiotic resistance testing was developed by and for clinical microbiologists aiming the therapy of bacterial infections. These methods, highly standardized worldwide, enable laboratories to assist the clinicians in the selection of the appropriate agent and the adequate doses to administrate in each particular simation [63-65]. Additionally, the use of standardized methods supports different... 

Culture-dependent methods to characterize antibiotic resistance in the environment are essentially based on the guidelines developed for clinical and veterinary microbiology (e.g. [20, 66-69]). Nevertheless, several adaptations have been introduced. 

Over the last years, a renewed interest on the antibiotic resistance phenotypes in municipal waste water treatment plants became apparent in the scientific literature. The underlying hypothesis of these smdies is that urban sewage treatment plants are potential reservoirs of antibiotic resistance, and, in general, it is aimed at contributing to assess the risks of dissemination, posed by the treated effluents discharged into natural water courses. As a general trend, these studies focus on human/animal commensal and environmental bacteria, frequently disseminated via faecal contamination, and which can survive in waters. The relevance of these bacteria, which may exhibit clinically relevant resistance phenotypes, as possible nosocomial agents seems also to be a motivation behind these smdies. 

Table 3 Examples of antibiotic resistance genes of clinical relevance distributed worldwide in aquatic environments and illustration of some methodological approaches commonly used to detect resistance determinants in the environment... 

The dramatic increase of severe or lethal infections caused by antibiotic-resistant bacteria triggered numerous studies on antibiotic resistance, not only from clinical but also from environmental sources. Nowadays it is clear that environment, and water in particular, plays a central role on antibiotic resistance dispersion to and from clinical settings. However, the current state of the art clearly suggests that only a small fraction of the environmental resistome is known. The modes and mechanisms of emergence, evolution and transmission of resistance determinants are still not very well understood. Although environmental pollution is recognized to play an important role on antibiotic resistance evolution and spreading, it is still very difficult to draw cause-effect relationships, which sometimes seems to be strain/species dependent. 

Szczepanowski R, Linke B, Krahn I et al (2009) Detection of 140 clinically relevant antibiotic-resistance genes in the plasmid metagenome of waste water treatment plant bacteria showing reduced susceptibility to selected antibiotics. Microbiology 155 (Pt 7) 2306-2319... 

Canton R (2009) Antibiotic resistance genes from the environment a perspective through newly identified antibiotic resistance mechanisms in the clinical setting. Clin Microbiol Infect 15(Suppl l) 20-25... 

Volkmann H, Schwartz T, Bischoff P et al (2004) Detection of clinically relevant antibiotic-resistance genes in municipal waste water using real-time PCR (TaqMan). J Microbiol Methods 56(2) 277-286... 

Wright GD (2010) Antibiotic resistance in the environment a link to the clinic Curr Opin Microbiol 13(5) 589-594... 

Smith, W. (1974). Clinical Problems of Preventive Medicine Antibiotic-Resistant Bacteria in Animals The Dagers to Human Health. British Veterinary Journal 130 ly. 110-119. 

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