Resistance Mechanism of Chloramphenicol in <i>Streptococcus haemolyticus, Streptococcus pneumoniae</i> and <i>Streptococcus faecalis</i>

Miyamura, Sadao; Ochiai, Hiroshi; Nitahara, Yoshiyuki; Nakagawa, Yasuaki; Terao, Michinori

doi:10.1111/j.1348-0421.1977.tb02809.x

Cited by 31 publications

(12 citation statements)

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“…AGENTS CHEMOTHER. terminations and peptide maps of enzymatic digests of the two proteins and measurements of DNA-DNA hybridization between the plasmid of S. faecalis JH6 and its presumptive counterpart in strains of staphylococci that synthesize the type D variant of chloramphenicol acetyltransferase. Such studies will have to be extended to the chloramphenicol resistance systems that have been described in other streptococci (14,16).…”

Section: Resultsmentioning

confidence: 99%

Plasmid-Mediated Mechanisms of Resistance to Aminoglycoside-Aminocyclitol Antibiotics and to Chloramphenicol in Group D Streptococci

Courvalin

Shaw

Jacob

1978

Antimicrob Agents Chemother

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Genes conferring resistance to aminoglycoside-aminocyclitol antibiotics in three group D streptococcal strains, Streptococcus faecalis JH1 and JH6 and S. faecium JH7, and to chloramphenicol in JH6 are carried by plasmids that can transfer to other S faecalis celLs. The aminoglycoside resistance is mediated by constitutively synthesized phosphotransferase enzymes that have substrate profiles very similar to those of aminoglycoside phosphotransferases found in gram-negative bacteria. Phosphorylation probably occurs at the aminoglycoside 3'-hydroxyl group. Plasmid-borne streptomycin resistance is due to production of the enzyme streptomycin adenylyltransferase, which, as in staphylococci and in contrast to that detected in gram-negative bacteria, is less effective against spectinomycin as substrate. Resistance to chloramphenicol is by enzymatic acetylation. The chloramphenicol acetyltransferase is inducible and bears a close resemblance to the type D chloramphenicol acetyltransferase variant from staphylococci.In recent years it has become clear that many of the genes conferring resistance to antibiotics in group D streptococci are plasmid borne (4,5,13). The plaids can transfer between group D streptococcal strains; some plasmids are conjugative (13), and nonconjugative plasmids can be mobilized by conjugative plasmids (9).In gram-negative bacteria and Staphylococcus the mechanism of plasmid-mediated resistance involves the production of enzymes that inactivate the antibiotic by either modification or destruction of the antibiotic structure (8). This is in contrast to chromosomally detennined antibiotic resistance, which is more usually due either to prevention of entry of the antibiotic into the cell or to a specific alteration of the antibiotic target site (8). In this report it is shown that, like the plasmid-borne resistance in the gram-negative bacteria and staphylococci, plasmid-linked resistances to aminoglycoside-aminocyclitol antibiotics and chloramphenicol in group D streptococci are also mediated by enzymatic modification ofthe antibiotic. The properties of the Streptococcus faecalis enzymes are compared with the similar enzymes of staphylococci and the gram-negative bacteria. (12,13). Derivative strains were isolated by selection of spontaneous mutants (13).Media. Brain heart infusion broth and agar (Oxoid) were used, except where stated. All incubations were at 370C.MIC determinations. The method of Steers et al. (18) was used to determine antibiotic minimal inhibitory concentrations (MICs).Radiolabeling, isolation, and characterization of plasmid DNA. Plasmid DNA was isolated by cesium chloride-ethidium bromide density gradient ultracentrifugation and characterized by neutral sucrose gradient analysis as described previously (12, 13).Calculation of plasmid molecular weight. The empirical formulae of Barth and Grinter (1) were used to calculate plasmid molecular weights.Transfer of antibiotic resistance traits. The technique described by Jacob and Hobbs (13) was used in transferring antibiotic resist...

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Section: Resultsmentioning

confidence: 99%

Plasmid-Mediated Mechanisms of Resistance to Aminoglycoside-Aminocyclitol Antibiotics and to Chloramphenicol in Group D Streptococci

Courvalin

Shaw

Jacob

1978

Antimicrob Agents Chemother

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“…Chloramphenicol resistance in pneumococci is due to the production by resistant strains of inducible chloramphenicol acetyltransferase (188,225). Rifampin resistance may be based on an altered DNA-dependent RNA polymerase, as a result of a single amino acid substitution, and as this mutation may be present in low numbers in many populations of bacteria, use of rifampin alone rapidly selects resistant strains (202).…”

Section: Other Infectionsmentioning

confidence: 99%

Pneumococcal resistance to antibiotics

1990

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The geographic distribution of pneumococci resistant to one or more of the antibiotics penicillin, erythromycin, trimethoprim-sulfamethoxazole, and tetracycline appears to be expanding, and there exist foci of resistance to chloramphenicol and rifampin. Multiply resistant pneumococci are being encountered more commonly and are more often community acquired. Factors associated with infection caused by resistant pneumococci include young age, duration of hospitalization, infection with a pneumococcus of serogroup 6, 19, or 23 or serotype 14, and exposure to antibiotics to which the strain is resistant. At present, the most useful drugs for the management of resistant pneumococcal infections are cefotaxime, ceftriaxone, vancomycin, and rifampin. If the strains are susceptible, chloramphenicol may be useful as an alternative, less expensive agent. Appropriate interventions for the control of resistant pneumococcal outbreaks include investigation of the prevalence of resistant strains, isolation of patients, possible treatment of carriers, and reduction of usage of antibiotics to which the strain is resistant. The molecular mechanisms of penicillin resistance are related to the structure and function of penicillin-binding proteins, and the mechanisms of resistance to other agents involved in multiple resistance are being elucidated. Recognition is increasing of the standard screening procedure for penicillin resistance, using a 1-microgram oxacillin disk.

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“…To date, linezolid-nonsusceptible pneumococcal strains are extremely rare. Chloramphenicol resistance in the pneumococcus occurs by acquisition of the cat gene encoding chloramphenicol acetyltransferase (3,18). Chloramphenicol acetyltransferase acetylates chloramphenicol, resulting in derivatives that are unable to bind the ribosome (22,23).…”

mentioning

confidence: 99%

Novel Mechanism of Resistance to Oxazolidinones, Macrolides, and Chloramphenicol in Ribosomal Protein L4 of the Pneumococcus

Wolter

Smith

Farrell

et al. 2005

Antimicrob Agents Chemother

139

104

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Two clinical Streptococcus pneumoniae isolates, identified as resistant to macrolides and chloramphenicol and nonsusceptible to linezolid, were found to contain 6-bp deletions in the gene encoding riboprotein L4. The gene transformed susceptible strain R6 so that it exhibited such resistance, with the transformants also showing a fitness cost. We demonstrate a novel bacterial mechanism of resistance to chloramphenicol and nonsusceptibility to linezolid.Macrolide resistance in Streptococcus pneumoniae is predominantly caused by acquisition of the erm(B) (target modification) (33) or mef(A) (drug efflux) (28) gene or a combination of these mechanisms (16). Mutations in 23S rRNA and riboproteins L4 and L22 have more recently been found to confer macrolide resistance (6,29,30). Nonsusceptibility to linezolid in laboratory-generated resistant Escherichia coli isolates (35) and enterococci (21) as well as in clinical isolates of methicillin-resistant Staphylococcus aureus (17, 32) and enterococci (4, 15) has been found to be conferred by mutations in domain V of 23S rRNA. To date, linezolid-nonsusceptible pneumococcal strains are extremely rare. Chloramphenicol resistance in the pneumococcus occurs by acquisition of the cat gene encoding chloramphenicol acetyltransferase (3,18). Chloramphenicol acetyltransferase acetylates chloramphenicol, resulting in derivatives that are unable to bind the ribosome (22,23). In this study, two clinical pneumococcal isolates with elevated macrolide, linezolid, and chloramphenicol MICs were identified and investigated for their resistance mechanisms.PU1071099 (PROTEKT surveillance study) (7) was isolated in Boston in 2001 from sputum of a 67-year-old, and TN33388 (ABCs program of the Centers for Disease Control) was isolated in Tennessee in 2003 from the blood of a 32-year-old who had been exposed to long-term azithromycin prophylaxis. Unencapsulated laboratory strain S. pneumoniae R6 was used in transformation studies. Pneumococci were routinely cultured at 37°C in 5% CO 2 on Mueller-Hinton agar supplemented with 5% horse blood. MICs were determined according to the CLSI

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Resistance Mechanism of Chloramphenicol in Streptococcus haemolyticus, Streptococcus pneumoniae and Streptococcus faecalis

Cited by 31 publications

References 5 publications

Plasmid-Mediated Mechanisms of Resistance to Aminoglycoside-Aminocyclitol Antibiotics and to Chloramphenicol in Group D Streptococci

Plasmid-Mediated Mechanisms of Resistance to Aminoglycoside-Aminocyclitol Antibiotics and to Chloramphenicol in Group D Streptococci

Pneumococcal resistance to antibiotics

Novel Mechanism of Resistance to Oxazolidinones, Macrolides, and Chloramphenicol in Ribosomal Protein L4 of the Pneumococcus

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