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Staphylococcus aureus erythromycin resistance

Outbreaks of bacterial infections in pork processing factories have shown that cuts on the skin made with bone were the most common port of entry of infection (Barnham and Kerby 1981). Streptococcus pyogenes and Staphylococcus aureus were the causative organisms. Nail-biting was suspected as one important cause of transmission of Staphylococcus aureus. Erythromycin-resistant Streptococcus pyogenes affected 46 of 194 workers in an outbreak that lasted 7 months (Sims and Riordan 1996). [Pg.851]

Staphylococcus aureus Abscesses bacteremia cellulitis endocarditis osteomyelitis pneumonia others If methicillin-sensitive nafcillin or oxacillin If methicillin-resistant vancomycin gentamicin or rifampin 1 st-generation cephalosporin clindamycin erythromycin trimethoprim-sulfamethoxazole a penicillin + a penicillinase inhibitor... [Pg.516]

C Lai, B Weisblum. Altered methylation of ribosomal RNA in an erythromycin-resistant strain of Staphylococcus aureus. Proc Natl Acad Sci (USA) 68 856-860, 1971. [Pg.260]

H Westh, DM Hougaard, J Vuust, VT Rosdahl. Prevalence of erm gene classes in erythromycin-resistant Staphylococcus aureus strains isolated between 1959 and 1988. Antimicrob Agents Chemother 39 369-373, 1995. [Pg.260]

Infections in cystic fibrosis are often due to Staphylococcus aureus, Haemophilus influenzae or Pseudomonas aeruginosa. Infecting organisms need to be identified so that the most appropriate antibiotics can be used. Antibiotics used to treat respiratory infections in cystic fibrosis commonly include ciprofloxacin, erythromycin, flu-cloxacillin and amoxicillin. However, specialist individual therapy is essential for maximum benefit to the patient and avoidance of the development of resistant strains of bacteria. [Pg.93]

It is widely accepted that MLS antibiotics inhibit protein synthesis by binding to closely related sites on the 508 subunit of the 70S ribosome of bacteria [4], despite being structurally different from each other (see Figs. 1 and 2 in a later section). That is the reason why, when inducible resistant Staphylococcus aureus cells are exposed to a low concentration of the drug (0.05 tg erythromycin/ml - 6.8 x 10 M), they show resistance against not only erythromycin but also other macrolide antibiotics as well as lincosamide and type B streptogramin antibiotics. Erythromycin has been widely used and has been the object of extensive molecular and biological studies. [Pg.454]

Saito, T., Hashimoto, H., and Mitsuhashi, S. (1968). Drug resistance of staphylococci, formation of erythromycin-ribosome complex, decrease in the formation of erythromycin-ribosome complex in erythromycin-resistant strains of Staphylococcus aureus. Jpn. J. Microbiol. 13, 119-121. [Pg.490]

Hachler, H., Berger-Bachi, B., and Kayser, F. H. (1987). Genetic characterization of a Clostridium difficile erythromycin-clindamycin resistance determinant that is transferable to Staphylococcus aureus. Antimicrob. Agents Chemother. 31, 1039-1045. [Pg.491]

Ross, J. I., Eady, E. A., Cove, J. H., and Baumberg, S. (1996). Minimal functional system required for expression of erythromycin resistance by msrA in Staphylococcus aureus RN4220. Gene 183, 143-148. [Pg.498]

The importance of the serial route in transmission of antibiotic-resistant staphylococci can be indirectly illustrated by findings in the environment, patients and the nursing personnel of a surgical clinic in Bratislava (Czechoslovakia) [8j. The results were obtained during corroborative studies on the distribution of resistant staphylococci from different environments in Slovakia [11]. The strains of coagulase-positive strains of Staphylococcus aureus from the clinic were tested for their sensitivity to six common antibiotics of that time. With staphylococci isolated from the environment, patients and the personnel, the percentages of resistance to benzylpeni-cillin, streptomycin, chlorotetracycline, erythromycin, chloramphenicol and vancomycin are shown in Fig. 6.1. The percentages of resistance to the individual antibiotics were positively correlated with the consumption of their preparations at the clinic. [Pg.609]

However, the mixture of the two components has an activity of 0.1 mg L" on 97 to 98% of the strains, including those strains of Staphylococcus aureus that are resistant to other commonly used antibiotics (for example erythromycin and lincomycin). The synergistic behavior between pristinamycin I and pristinamycin II not only results in increased potency and greatly improves the spectrum of activity, but in addition also renders the mixture bactericidal [8]. [Pg.188]

A related kind of resistance, target withdrawal , falls somewhere in between Type 2 and Type 3. In an example, the clinical resistance Staphylococcus aureus to erythromycin, the 505 ribosome subunits were found to have been methylated by an enzyme peculiar to the resistant strain (Lai and Weisblum, 1971). Also, in some examples of clinical resistance of pneumococci to sulfonamides, the target enzyme, dihydrofolate synthetase, has been found chemically altered (Ortiz, 1970). [Pg.261]

Sad to say, there are also strains of Staphylococcus aureus which owe their resistance to another factor, possibly a change in cell-wall composition. Such strains, which are becoming increasingly common in hospitals, are also resistant to cephalosporins, erythromycin, the aminoglycosides, and the tetracyclines. For them, the only effective antibiotic is a rather unselective one, vancomycin (p. 565), but the synthetic anti-bacterials, such as nitrofurantoin and trimethoprim are usually effective. [Pg.560]


See other pages where Staphylococcus aureus erythromycin resistance is mentioned: [Pg.270]    [Pg.2]    [Pg.2066]    [Pg.2573]    [Pg.71]    [Pg.43]    [Pg.251]    [Pg.367]    [Pg.166]    [Pg.50]    [Pg.139]    [Pg.69]    [Pg.251]    [Pg.170]    [Pg.224]    [Pg.26]    [Pg.384]    [Pg.243]   
See also in sourсe #XX -- [ Pg.109 ]




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