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Biomedical subjects

N Datta

Publications and source records attributed to N Datta.

At least 55 records · Page 3Linked to original sources
PubMed1982

pHH502, a plasmid with IncP and IncI alpha characters, loses the latter by a specific recA-independent deletion event.

Plasmid pHH502, of molecular weight 70 X 10(6), determined resistance to tetracycline, chloramphenicol, trimethoprim, sulphonamides and mercuric chloride and was incompatible with members of IncP and IncI alpha. It resembled other plasmids of IncI alpha in the following properties: it determined pili that were morphologically and serologically I alpha pili, whose production was repressed in established plasmid-carrying (R+) cultures; its transfer was equally efficient in liquid or on solid medium; it exerted surface exclusion against other IncI alpha plasmids; it was non-transferable to Proteus. In a reproducible, recA-independent event, pHH502 gave rise to pHH502-1, a plasmid of molecular weight 40 X 10(6), lacking determinants for resistance to tetracycline and chloramphenicol and all detectable IncI alpha characteristics. pHH502-1 was incompatible only with IncP plasmids and resembled other IncP plasmids in determining constitutive production of rigid pili, in its surface exclusion, in transferring at greater frequency on solid than in liquid medium and in being transmissible to Proteus mirabilis. It differed from other IncP plasmids in the morphology and serological type of its pili and in failing to transfer to Pseudomonas aeruginosa or Acinetobacter calcoaceticus. Small numbers of pHH502-1 rigid pili were present on bacteria carrying pHH502. Possible mechanisms for the generation of pHH502 and pHH502-1 are discussed.

Bacteria↗
PubMed1981

Salmonella typhi in vivo acquires resistance to both chloramphenicol and co-trimoxazole.

Salmonella typhi in the bowel of a patient with enteric fever treated with chloramphenicol and later co-trimoxazole acquired resistance to these drugs. Chloramphenicol and sulphonamide resistances were determined by one plasmid, of IncH, whose carriage also changed the Vi phage type. Trimethoprim resistance was determined by a transposon, Tn7, carried in another plasmid, of IncI. The same resistance genes were identified in a strain of klebsiella isolated from the patient.

Adult↗
PubMed1981

Discrimination between multiply-resistant klebsiella strains during a hospital outbreak: use of klebecin-typing and a screening test for plasmids.

During an outbreak of hospital infection, 71 multiply-resistant klebsiella strains were classified by two extra tests in addition to biotyping, serotyping and sensitivity testing. These were klebecin sensitivity tests (Edmondson & Cooke, 1979) and screening for plasmid DNA molecules by agarose gel electrophoresis of single colony lysates (Eckhardt, 1978). There were 56 examples of an epidemic strain of serotype K21; ten of these differed from 46 identical strains in some minor character. The other 15, although resembling the epidemic strain in biotype and antibiotic resistance differed from it sufficiently to be considered as unrelated.

Cross Infection↗
PubMed1981

Diversity of plasmids responsible for multiple resistance in Klebsiella serotype K2.

Klebsiella of capsular type K2 were investigated to find out whether a single epidemic clone was the source of many outbreaks of infection in different hospitals, in different areas over a period of five years. The klebsiellas studied were found to be very similar; they were of the same biotype, had similar klebecin sensitivity patterns and carried multiple drug-resistance plasmids; however, characterization of these plasmids showed that they were heterogeneous. Thus there was not a single epidemic bacterial clone.

Cross Infection↗
PubMed1981

Characterisation of an epidemic strain of Klebsiella and its variants by computer analysis.

An outbreak of hospital-acquired klebsiella infection was investigated by means of six different typing schemes. Interpretation of the information generated by these schemes proved difficult and allowed only tentative conclusions to be reached concerning the origin of some strains. Consequently, the results were subjected to computer analysis by means of a numerical taxonomic programme adapted for the purpose. A dendrogram was constructed giving the percentage similarity between strains. It established the source of four atypical strains and showed that three of them were derived from the original clone. This form of numerical epidemiological analysis could have useful applications in the investigation of hospital-acquired infection.

Anti-Bacterial Agents↗
PubMed1980

Anticholinergic substances: A single consistent conformation.

An interactive computer-graphics analysis of 24 antagonists of acetylcholine at peripheral autonomic post-ganglionic (muscarinic) nervous junctions and at similar junctions in the central nervous system, the crystal structures of which are known, has led to the determination of a single, consistent, energetically favorable conformation for all 24 substances, although their observed crystal structure conformations vary widely. The absolute configuration and the single, consistent (ideal) conformation of the chemical groups required for maximum anticholinergic activity are described quantitatively.

Journal Article↗
PubMed1980

Distribution of genes for trimethoprim and gentamicin resistance in bacteria and their plasmids in a general hospital.

The incidence of trimethoprim resistance in enterobacteria causing infection in a London hospital increased from 5.6% in 1970 to 16% in 1979. The proportion of gentamicin-resistant aerobic Gram-negative bacilli had risen to 6.5% by 1979. During a 5-month period in 1977, during which no epidemic was recognized, all isolates resistant to either trimethoprim, gentamicin, tobramycin or amikacin were studied. The proportion of enterobacteria resistant to both trimethoprim and gentamicin (3.8% of the total) was significantly higher than expected assuming no correlation between acquisition of resistance characters. The resistance was transferable in 23% of trimethoprim-resistant and 76% of gentamicin-resistant strains. Trimethoprim resistance was carried by plasmids of seven different incompatibility groups and in at least four instances was part of a transposon. Gentamicin resistance was determined by plasmids of three groups - IncC, IncFII and IncW. Transposition of gentamicin resistance was not shown, though this may have been the means of evolution of the gentamicin R plasmids of InW, which determined aminoglycoside acetyltransferase, AAC(3). Some bacterial strains with their plasmids were endemic. There was evidence for these plasmids (i) acquiring new resistance genes by transposition, (ii) losing resistance genes by deletion and (iii) being transferred between bacterial species in the hospital.

Amikacin↗
PubMed1980

Transposable gentamicin resistance in IncW plasmids from Hammersmith Hospital.

A transposon, Tn733, encoding the gentamicin acetyltransferase AAC(3) was found on two gentamicin R plasmids of IncW at Hammersmith Hospital. Transposon TN733 has a molecular mass of 5.8 megadaltons and gives a characteristic 2.4 megadalton fragment on digestion with EcoRI. The appearance of gentamicin resistance on a transposon will increase the chances of spread of this gene.

Conjugation, Genetic↗
PubMed1979

A transposon, Tn732, encoding gentamicin/tobramycin resistance.

Gentamicin and tobramycin are important antibiotics in the treatment of hospital infections because of their activity against a wide range of bacterial genera. With their increasing use, bacteria resistant to these drugs have appeared, the resistance being frequently plasmid determined. The resistance genes determine various enzymes that modify and inactivate the drugs and there is association between particular gentamicin/tobramycin resistance genes and plasmids of particular groups, implying that acquisition of such a gene by any plasmid is a rare event. We now report the identification of a transposon or 'jumping gene' encoding the gentamicin/tobramycin adenylylating enzyme, ANT(2"), on a plasmid of incompatiblity group FII (IncFII).

Anti-Bacterial Agents↗