Movable genetic elements and antibiotic resistance in enterococci

The enterococci possess genetic elements able to move from one strain to another via conjugation. Certain enterococcal plasmids exhibit a broad host range among gram-positive bacteria, but only when matings are performed on solid surfaces. Other plasmids are more specific to enterococci, transfer efficiently in broth, and encode a response to recipient-produced sex phermones. Transmissible non-plasmid elements, the conjugative transposons, are widespread among the enterococci and determine their own fertility properties. Drug resistance, hemolysin, and bacteriocin determinants are commonly found on the various transmissible enterococcal elements. Examples of the different systems are discussed in this review.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47900/1/10096_2005_Article_BF01963632.pd

The epidemiology of enterococci

The enterococci are emerging as a significant cause of nosocomial infections, accounting for approximately 10 % of hospital acquired infections. They are found as normal inhabitants of the human gastrointestinal tract, but may also colonize the oropharynx, vagina, perineal region and soft tissue wounds of asymtomatic patients. Until recently, evidence indicated that most enterococcal infections arose from patients' own endogenous flora. Recent studies, however, suggest that exogeneous acquisition may occur and that person-to-person spread, probably on the hands of medical personnel, may be a significant mode of transmission of resistant enterococci within the hospital. The use of broad-spectrum antibiotics, especially cephalosporins, is another major factor in the increasing incidence of enterococcal infections. These findings suggest that barrier precautions, as applied with other resistant nosocomial pathogens, along with more judicial use of antibiotics may be beneficial in preventing nosocomial spread of resistant enterococci.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47899/1/10096_2005_Article_BF01963631.pd

Metabolically deficient dwarf-colony mutants of Escherichia coli: deficiency and resistance to antibiotics of strains isolated from urine culture

Sixteen metabolically deficient dwarf-colony mutants of Escherichia coli were isolated from urine culture and represented about 2% of all E. coli isolated during the same period. In 14 cases, mutants were isolated from debilitated patients: elderly persons or patients in the terminal stages of a chronic disease. In 15 of these subjects, deficient dwarf-colony mutants appeared to be the true cause of urinary tract infection, since there was leukocyturia and important bacteriuria, and organisms were obtained in pure culture. Study of metabolic deficiencies on Davis synthetic medium and nutritive agar resulted in the identification of eleven deficiencies in cysteine, two in thiamine, two in thymidine, and one in glutamine. Study of resistance to antibiotics revealed that nine were susceptible to all antibiotics, three were resistant to tetracycline alone, two were resistant to two antibiotics (chloramphenicol-tetracycline, streptomycin-tetracycline), and two were resistant to three antibiotics (ampicillin-chloramphenicol-tetracycline, ampicillin-streptomycin-tetracycline). Resistance was coded for by conjugative plasmids in five strains.</jats:p

Conjugative transfer of multiple antibiotic resistance markers in Streptococcus pneumoniae

Two antibiotic-resistant isolates of Streptococcus pneumoniae were investigated for conjugative transfer of their drug resistance markers into streptococcal (groups B and D) and pneumococcal (encapsulated and non-encapsulataed) recipients. Of these, 7 wild-type donor pneumococci transferred all their resistance markers (except Pc [penicillin], Su [sulfonamide], and Tp [trimethoprim]) into group D Streptococcus and non-encapsulated S. pneumoniae recipients at a low frequency (10(-5) to 10(-6)). The resistance markers transferred were Tc (tetracycline); Tc and Cm (chloramphenicol); Tc and MLS (macrolides, lincosamides, and streptogramin B); Tc, MLS, Km (kanamycin), and Cm. The transconjugants obtained retransferred their resistance markers into appropriate streptococcal or pneumococcal recipients or both. The resistance markers of streptococcal transconjugants could not be cured by chemical agents. All attempts to detect extra-chromosomal deoxyribonucleic acid from pneumococcal or streptococcal transconjugants were unsuccessful. The molecular weight of a streptococcal conjugative R plasmid (pIP501) was investigated after transfer into the non-encapsulated S. pneumoniae recipient and was found to be similar to that of the wild-type group B Streptococcus host (20 x 10(6)).</jats:p

Genetic and physical studies of recombinant plasmids formed between an R plasmid of compatibility group FI and sex factor F of HfrH

Recombinant plasmids between an R plasmid of the FI group (R162/3) and the sex factor F or HfrH were produced after the conjugal transfer of this R plasmid into HfrH. Three types of recombinant plasmids were identified after the mating of HfrH (R162/3) with recA and rec+ recipients. One specimen of each type (pIP218, pIP222, pIP226) was studied in this report. All three recombinant plasmids carry the same genetic information for resistance to antibiotics (CSSuT) retained from R162/3. pIP218 retained all the other properties from F of HfrH: derepression for pilus synthesis, mobilization of the chromosome for the proximally transferred HfrH genes (thr, leu, proA), interference with T7 propagation, and ability to be cured by acridine orange. pIP222 retained from F of HfrH the derepression for pilus synthesis and the same polarity of chromosome transfer (thr, leu, proA), while pIP226 retained the interference with T7 propagation and acridine orange curing. Physical studies revealed that replication control and/or recovery of F and pIP218 as covalent circles of deoxyribonucleic acid are similar, and are different from R162/3. The new plasmids are more likely the result of a substitutive recombination event than a fusion. We propose genetic maps of these recombinant plasmids, showing the unequal participation of the parental plasmids in their formation.</jats:p