Biomedical subjects
Publications and source records attributed to G A Jacoby.
Cloning the gene for gentamicin resistance from Pseudomonas aeruginosa plasmid pMG35 on the high-copy-number Escherichia coli cloning vehicle pMK20 allowed detection of 6'-N-acetyltransferase activity that was not readily detected when the parent plasmid was present either in P. aeruginosa or E. coli.
Eleven isolates including Escherichia coli, Salmonella enteritidis, and Shigella sonnei, obtained in Brazil, Hong Kong, Indonesia, Thailand, and the United States, were found to produce beta-lactamase of the PSE-1 type, which was previously considered to be Pseudomonas specific. The enterobacterial strains produced a beta-lactamase with the same isoelectric point, immunological reactions, and substrate profile as those of the prototype PSE-1 enzyme determined by Pseudomonas plasmid RPL11. The producer strains were resistant to multiple antibiotics, and all contained plasmids, ranging in size from 37 x 10(6) to 130 x 10(6), that belonged to at last six incompatibility groups. Plasmids of IncH2 and IncFIme were shown to contain 8 x 10(6)-molecular-weight transposons Tn1401 and Tn1402 that encoded PSE-1 beta-lactamase production, resistance to streptomycin and spectinomycin via AAD(3"), and resistance to sulfonamide. PSE-1 beta-lactamase was not Pseudomonas specific and appeared to have spread among plasmids found in enterobacteria by transposition.
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Azlocillin, carbenicillin, cefsulodin, mezlocillin, nocardicin A, piperacillin, pirbenicillin, sulbenicillin, and ticarcillin, but not HR756, showed reduced activity against Pseudomonas aeruginosa strains producing seven types of beta-lactamase.
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Plasmid-containing strains of Pseudomonas aeruginosa were screened for resistance to disinfectants. Two plasmids, pMG1 and pMG2, were found to determine hexachlorophene resistance.
Plasmids determining resistance to arsenic, mercury, silver, and tellurium compounds in Escherichia coli and Pseudomonas aeruginosa were tested for resistance to 40 other metal compounds. Resistance to trivalent boron and hexavalent chromium compounds was a property of certain P. aeruginosa plasmids.
Pseudomonas aeruginosa strain 9169 has been reported to contain a plasmid that expresses resistance to carbenicillin (Cb), kanamycin (Km), and tetracycline (Tc) in Escherichia coli but resistance only to Cb in certain Pseudomonas recipients. The triply resistant plasmid in E. coli belonged to incompatibility (Inc) group P or P-1, whereas the singly resistant plasmid in P. aeruginosa was compatible with IncP-1 plasmids and other plasmids of established Inc specificity but incompatible with plasmid pSR1 that is here used to define a new Pseudomonas Inc group P-10. Additional physical and genetic studies showed that strain 9169 contained not one but two plasmids: IncP-1 plasmid R91a, determining the Cb Km Tc phenotype, and IncP-10 plasmid R91, determining Cb that differed in molecular weight and in EcoRI and BamHI restriction endonuclease recognition sites. Plasmid multiplicity rather than host effects on plasmid gene expression can account for differences in the phenotype of strain 9169 transconjugants to E. coli and P. aeruginosa.
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The R factor pMG2 protects Pseudomonas aeruginosa against the lethal effects of ultraviolet (u.v.) and gamma irradiation, and methyl methanesulphonate and N-methyl-N'-nitro-N-nitrosoguanidine treatment. Enhanced survival occurs in strains of uvr+ rec+ (wild-type) genotype and a variety of uvr rec+ type mutants. No protection occurs in a rec A-type mutant. The plasmid also enhances u.v.-induced mutagenesis. These effects appear to be due to host-cell controlled plasmid-determined DNA repair function(s). Studies on P. aeruginosa strains deficient in DNA polymerase I (polyA) suggest that a plasmid-determined repair resynthesis function may be responsible for increased u.v.-survival and enhanced u.v.-mutability in pMG2-containing bacteria.
Transferable plasmids in gram-negative bacteria that confer resistance to potassium tellurite or tellurate were found. This re-istance was distinct from resistance to mercury, silver, or arsenic compounds and was unrelated to antibiotic resistance. In Escherichia coli, plasmids determine a 100-fold increase in the minimal inhibitory concentration for tellurite and a 10-fold increase in tellurate resistance. Many, but not all, of the plasmids belong to incompatibility group S. In Pseudomonas aeruginosa, tellurium resistance is specifically associated with incompatibility group P-2 and involves a 5- to 10-fold increase in tellurite or tellurate resistance.
An outbreak of gentamicin- and tobramycin-resistant Pseudomonas aeruginosa infection occurred in a surgical ward over a three-month period. Resistant Ps. aeruginosa strains with the same serological, phage, and pyocin type were cultured from the urine of six patients. Identical organisms were found on urine bottles, bedpans, and the hands of attendant staff. Inadequate disinfection played a major role in cross-infection. Isolates of the epidemic strain from each of the patients and of an unrelated but similarly resistant Ps. aeruginosa from one of them could transfer resistance to a recipient strain of Ps. aeruginosa. Resistance to gentamicin, kanamycin, tobramycin, sulphonamides, and mercuric chloride was determined by R factors belonging to Pseudomonas incompatibility group P-3. Aminoglycoside resistance was due to acetylation.
R plasmids of incompatibility group P-2 are readily transmissible between Pseudomonas strains, but not to Escherichia coli or other enterobacteria, whereas those of group P-1 have a broad host range. Pseudomonas aeruginosa donor strains carrying both a P-1 plasmid (RP1, RP4, or R751) and a P-2 plasmid (pMG1, pMG2, pMG5, or RPL11) were mated with E. coli K-12, and selection was imposed for resistance markers on the P-2 plasmids. Transconjugants were obtained at a low frequency, in which P-2 markers were expressed and were serially transmissible in E. coli together with P-1 markers. These plasmids had P-1 incompatibility properties, conferred susceptibility to phages active on P-1 carrying strains, and behaved on sucrose gradient centrifugation as unimolecular species of higher molecular weights than the P-1 parent. Recombinant plasmid formation was independent of a functional Rec gene in both donor and recipient and, with R751, had a preferred site leading to loss of trimethoprim resistance. Interaction between insertion sequences may be involved. Thus, plasmids of group P-2 can recombine with R factors of another group quite separate in compatibility properties, host range, and pilus type. Formation of such recombinants provides one pathway by which the genetic diversity of plasmids may have evolved.
Two clinical isolates of Pseudomonas aeruginosa, one a pyocin type 5 strain from Atlanta, could transfer gentamicin resistance by conjugation. Donor and recipient strains inactivated gentamicin by acetylation. The R plasmids, pMG1 and pMG2, also determined resistance to sisomicin, another substrate of gentamicin acetyltransferase I, sulfonamides, and streptomycin, but not resistance to kanamycin, neomycin, tobramycin, butirosin, or BB-K 8. They were transmissible to many strains of P. aeruginosa, including a Rec(-) strain, but not to Escherichia coli or other enterobacteriaceae. These R plasmids were compatible with R plasmids transmissible to P. aeruginosa from E. coli, including members of C, N, P, and W incompatibility groups. From a strain carrying pMG1 and a compatible plasmid, pMG1 was transferred independently but transfer of the second plasmid often resulted in cotransfer of pMG1. In contrast, pMG1 and pMG2 were incompatible with pseudomonas R plasmids R931 and R3108, and with R931 they readily formed recombinant plasmids. The four plasmids in this incompatibility group determine additional biological properties, including resistance to inorganic and organic mercury compounds, to ultraviolet light, and to certain deoxyribonucleic acid phages. pMG1 and pMG2 also phenotypically inhibited pyocin production. Consequently such R plasmids alter the phage and pyocin types of their host strains.