Erythromycin resistance determinants include Erm methylases, efflux pumps, and inactivating enzymes. To distinguish the different mechanisms of resistance in clinical isolates, PCR primers were designed so that amplification of the partial gene products could be detected in multiplex PCRs. This methodology enables the direct sequencing of amplified PCR products that can be used to compare resistance determinants in clinical strains. Further, this methodology could be useful in surveillance studies of erythromycin-resistant determinants.

Detection of erythromycin-resistant determinants by PCR.

Macrolide-resistant Streptococcus pyogenes isolates from Finland, Australia, and the United Kingdom and, more recently, Streptococcus pneumoniae and S. pyogenes strains from the United States were shown to have an unusual resistance pattern to macrolides, lincosamides, and streptogramin B antibiotics. This pattern, referred to as M resistance, consists of susceptibility to clindamycin and streptogramin B antibiotics but resistance to 14- and 15-membered macrolides. An evaluation of the macrolide-lincosamide-streptogramin B resistance phenotypes among our streptococcal strains collected from 1993 to 1995 suggested that this unusual resistance pattern is not rare. Eighty-five percent (n = 66) of the S. pneumoniae and 75% (n = 28) of the S. pyogenes strains in our collection had an M phenotype. The mechanism of M resistance was not mediated by target modification, as isolated ribosomes from a pneumococcal strain bearing the M phenotype were fully sensitive to erythromycin. Further, the presence of an erm methylase was excluded with primers specific for an erm consensus sequence. However, results of studies that determined the uptake and incorporation of radiolabeled erythromycin into cells were consistent with the presence of a macrolide efflux determinant. The putative efflux determinant in streptococci seems to be distinct from the multicomponent macrolide efflux system in coagulase-negative staphylococci. The recognition of the prevalence of the M phenotype in streptococci has implications for sensitivity testing and may have an impact on the choice of antibiotic therapy in clinical practice.

Streptococcus pneumoniae and Streptococcus pyogenes resistant to macrolides but sensitive to clindamycin: a common resistance pattern mediated by an efflux system.

The resistance of Streptococcus pneumoniae to penicillin and other antimicrobial agents is increasing in many parts of the world. The frequency of erythromycin resistance in parts of Europe1 and, to a lesser extent, in the United States2 limits the usefulness of macrolide antibiotics for the treatment of pneumonia, and resistance to trimethoprim-sulfamethoxazole, chloramphenicol, and tetracycline is an important problem in some other countries3,4. Recently, resistance to and clinical failure of the extended-spectrum cephalosporins ceftriaxone and cefotaxime in the treatment of pneumococcal meningitis have been noted in Spain5,6 and the United States7,8. In addition, there have . . .

Management of infections caused by antibiotic-resistant streptococcus pneumoniae

Background Streptococcus pneumoniae is a major cause of illness, and the emergence of drug-resistant strains threatens to complicate the management of pneumococcal infections. We conducted a laboratory-based surveillance for drug-resistant S. pneumoniae among patients with invasive pneumococcal infections in Atlanta. Methods From January through October 1994, pneumococcal isolates from 431 patients with invasive disease in metropolitan Atlanta were serotyped and tested to determine their susceptibility to various antimicrobial agents. Susceptibility to the antimicrobial agents was defined according to guidelines established by the National Committee for Clinical Laboratory Standards. Results The annual incidence of invasive pneumococcal infection was 30 cases per 100,000 population. Isolates from 25 percent of the patients were resistant to penicillin (7 percent were highly resistant), and isolates from 26 percent were resistant to trimethoprim–sulfamethoxazole (7 percent highly resistant). Fifteen percen...

https://www.nejm.org/doi/pdf/10.1056/NEJM199508243330803

The prevalence of drug-resistant Streptococcus pneumoniae in Atlanta.

Children 12-18 months old were randomized to receive one dose of a conjugate heptavalent pneumococcal vaccine, two doses of the same vaccine, or one dose of a 23-valent native polysaccharide vaccine. Before immunization, pneumococci included in the conjugate vaccine were isolated from 24% of the children, and an antibiotic-resistant pneumococcus was isolated from 22% of the children. The vaccines had no effect on carriage of non-vaccine-type pneumococci. In contrast, there was a significant reduction in carriage of vaccine-type pneumococci 3 months after one dose and 1 month after a second dose of conjugate vaccine (from 25% to 9% and 7%, respectively; P < .001). No effect was seen after vaccination with the nonconjugate vaccine. One year after immunization, carriage of antibiotic-resistant vaccine-type pneumococci in children receiving conjugate vaccine was lower than that in children receiving the nonconjugate vaccine (4% vs. 14%, P = .042). Conjugate pneumococcal vaccines may reduce spread of pneumococci in the community.

Reduction of Nasopharyngeal Carriage of Pneumococci during the Second Year of Life by a Heptavalent Conjugate Pneumococcal Vaccine

During a 12-month period we tested all isolates of Streptococcus pneumoniae recovered from patients at St. Louis Children's Hospital for resistance to penicillin and other antibiotics. Twenty-seven (20%) of 136 had relative penicillin resistance (minimum inhibitory concentration 0.1 to 1.0 μg/ml) an

Deborah S. Keller

Papers

Resistance to penicillin and non-beta-lactam antibiotics of Streptococcus pneumoniae at a children's hospital.