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Since the introduction of antibiotics in the 1940s, antibiotic resistance has become an increasing problem. Today, multiple-antibiotic resistance is commonly associated with a number of clinically important pathogens and is therefore an important issue in clinical nursing practice. Epidemiological studies identify a number of important factors associated with increases in antimicrobial resistance. These include patterns of antimicrobial use, changes in medical and veterinary care and social practices affecting the transmission of microbes. Bacterial mechanisms of antibiotic resistance and the genetics of resistance-gene transfer are explored, with the intention of developing nurses\' knowledge and understanding of control measures.

The rapid spread of antibiotic resistances in a wide variety of bacteria is mainly due to the location of antibiotic resistance genes on mobile genetic elements such as plasmids and transposons. Principal ways of transfer of plasmid- and transposon-encoded resistance genes are presented using examples of the predominant genes mediating resistances to protein biosynthesis inhibitors such as tetracyclines, aminoglycosides, macrolide-lincosamide-streptogramin B antibiotics, and chloramphenicol in staphylococci. Transfer between different staphylococcal cells is substantially based on transduction, transformation, conjugation and mobilization while transfer of resistance genes within the same bacterial cell often includes interplasmidic recombination events and chromosomal integration of resistance plasmids or transposons. The abilities of the transferred resistance plasmids or transposons to integrate or to be integrated into DNA molecules, plasmids or chromosomal DNA, of the new host cell are of major importance to circumvent strain-, species- or genusspecific barriers such as restriction/modification systems, plasmid incompatibilities or deficiencies of plasmid replication which may limit efficient resistance gene transfer.

The increasing prevalence of infections due to ampicillin-resistant strains of Haemophilus influenzae type b requires that suspected H. influenzae meningitis in children be initially treated with both ampicillin and chloramphenicol. Previously, the recognition of strains resistant to chloramphenicol but susceptible to ampicillin supported combination chemotherapy. In this study one case of meningitis due to a strain of H. influenzae resistant to ampicillin, chloramphenicol, and tetracycline was analyzed. The patient involved received intravenous trimethoprim-sulfamethoxazole, but putative resistance to this combination prompted the additional administration of intravenous moxalactam. The resistance of this organism was mediated by a conjugative 43-megadalton R plasmid; the determinants of ampicillin and chloramphenicol resistance were transferred as a single unit. However, not all of the multiply resistant transconjugants contained a detectable plasmid; DNA homology studies with R plasmids of H. influenzae confirmed that these extrachromosomal DNA sequences were associated with chromosomal DNA and that an extrachromosomal location was rare.

Epidemic aminoglycoside resistance may be caused by the spread of a species with distinctive chromosomal genes (e.g., Pseudomonas aeruginosa), or it may be due to the dissemination of plasmids or transposons between genera. Although strains of P. aeruginosa resistant to aminoglycosides because of impermeability may cause nosocomial outbreaks, most of the acute increases in aminoglycoside resistance are due to the spread of inactivating enzymes by plasmids. The index species for intergeneric outbreaks is usually Klebsiella pneumoniae carrying the ANT(2\") or AAC(3) gene; however, the distribution of resistance varies greatly by location and species. The AAC(6\')-I gene is most common in Serratia marcescens and in East Asian isolates of other species, whereas the AAC(3) gene is common in Chile. In the United States, the ANT(2\") and AAC(3) genes are particularly common among Enterobacteriaceae, except for Proteus and Providencia, which often carry the AAC(2\') gene. The most common patterns of epidemic resistance lead to the inactivation of gentamicin and, less frequently, tobramycin, but only rarely affect amikacin.

The plasmid pBR322 was one of the first EK2 multipurpose cloning vectors to be designed and constructed (ten years ago) for the efficient cloning and selection of recombinant DNA molecules in Escherichia coli. This 4363-bp DNA molecule has been extensively used as a cloning vehicle because of its simplicity and the availability of its nucleotide sequence. The widespread use of pBR322 has prompted numerous studies into its molecular structure and function. These studies revealed two features that detract from the plasmid\'s effectiveness as a cloning vector: plasmid instability in the absence of selection and, the lack of a direct selection scheme for recombinant DNA molecules. Several vectors based on pBR322 have been constructed to overcome these limitations and to extend the vector\'s versatility to accommodate special cloning purposes. The objective of this review is to provide a survey of these derivative vectors and to summarize information currently available on pBR322.

From 1972 to 1984, all Enterobacteriaceae isolated from clinical specimens at St. Joseph Hospital in Paris were tested for susceptibility to trimethoprim. During this period, resistance to trimethoprim increased from 17.9% to 25.5%; the increase was due mainly to strains with high-level resistance. Genetic studies, including transferability, incompatibility grouping, determination of the molecular mass of plasmids, and hybridization with dihydrofolate reductase I and II genes, were performed with randomly selected strains, and the results were compared with those of similar studies in other countries. The most striking phenomenon in trimethoprim-resistant strains was the presence of various resistance mechanisms and of different plasmids, transposons, and genetic determinants.

We describe a case of septic arthritis in a child with no apparent predisposing conditions. Salmonella virchow was isolated from her knee and faeces, both isolates being identical except for the latter\'s resistance to ampicillin. Evidence is presented for the acquisition of ampicillin resistance in vivo, including the demonstration of the R plasmid and its ready transferability to Escherichia coli. The recent literature on the subject is reviewed and the role of group CI salmonellae in invasive disease is examined.

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