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La resistenza agli antibiotici B-lattamici nelle Enterobacteriaceae e in Pseudomonas aeruginosa
Prevalence and distribution of R plasmid mediated beta-lactamases in Enterobacteriaceae.
290 ampicillin - resistant clinical isolates of various genera of Enterobacteriaceae were collected. 223 our of 290 isolates produced beta-lactamases: 95 of these resulted R plasmid mediated. The predominant R plasmid beta-lactamase was the TEM-1 enzyme. TEM-2 and SHV-1 enzymes were also produced
[The role of beta-lactamases and the permeability barrier in resistance to beta-lactam antibiotics].
The role played by beta-lactamases and by permeability barrier in resistance to beta-lactam antibiotics was investigated in 250 clinical isolates of Enterobacteriaceae. The data obtained showed that in 73 strains (52.9\%) was a significant correlation between the specific enzyme activity and resistance, however in 38 strains (27.5\%) an essential role was played by permeability barrier because the addition of subinhibitory levels of EDTA produced markedly reduction in the MIC
"In vitro" studies on susceptibility and resistance of clinical Chlamydia tracomathis strains
Emergenza di ceppi resistenti al cefotaxime (HR 756) in stipiti di Enterobacteriaceae di isolamento clinico.
A plasmid-linked caseinolytic activity in Enterobacteriaceae.
We have tested for production of caseinolytic activity the strain of E. coli K12 J62 carrying different R factors from various Enterobacteriaceae of clinical isolates. The results obtained showed the presence of a caseinolytic activity in 7 out of 139 R factors tested. All of these positive (cas+) R factors derived from strains of Klebsiella pneumoniae and all were able to transfer a strong lac+ phenotype as well as multiple antibiotic resistances (R-lac factors). Another strain of E. coli K12, J53, which is plasmid-free, produced levels of caseinolytic activity comparable to those of the Klebsiella R factors; J62, on the contrary, appeared to possess an inhibitor specific for the caseinolytic activities of J53 and of the R factors but not of other cas+ Gram+ and Gram- organisms. The hypothesis that the expression of the cas+ phenotype in E. coli K12 may be due to the presence of plasmid-linked regulatory genes is discussed
Emergence of cross-resistance to imipenem and other beta-lactam antibiotics in Pseudomonas aeruginosa during therapy.
The emergence of resistance to imipenem and other beta-lactams by Pseudomonas aeruginosa was investigated with two pairs of isolates. Two of these isolates were susceptible to imipenem and other beta-lactam antibiotics, such as moxalactam, ceftriaxone and cefotaxime, while the other two had developed resistance to those antibiotics during imipenem therapy. So far imipenem-resistant isolates have not demonstrated cross-resistance to other beta-lactam agents. We examined in these clinical isolates the possible mechanisms of resistance due to permeability modifications, either in outer membrane proteins (porins) or to LPS (lipopolysaccharides) complex. Particularly we analysed possible modification of physico-chemical properties of outer membrane proteins, such as changes in their hydrophobicity and electrical charge. beta-lactamase production was also studied. Results showed that resistance to imipenem may be related to loss or modifications in hydrophobicity of an outer membrane protein of about 46 Kdal; other modifications concerned hydrophobicity of the porin OMP F and, in one strain, the LPS complex appears to be responsible for resistance to other beta-lactam antibiotics together in combination with the production of beta-lactamases
R factor-mediated adhesiveness to mammalian cells in E. coli K12.
We checked the possible effects of the standard plasmids of known compatibility groups on the ability of three strains of E. coli K12, J62, J53 and C600, to agglutinate human and guinea pig erythrocytes and to adhere to cultures of human epithelial cells. The results obtained showed that under defined experimental conditions one plasmid, R478, from a clinical isolate of Serratia marcescens is able to modulate the adhesive properties of the strain J62 which lacks adhesiveness. On the contrary, the same factor did not alter the ability of strains J53 and C600 to agglutinate erythrocytes and to adhere to human epithelial cells in culture, nor did it induce adhesive properties in wild-type strains of E. coli from clinical isolates that lacked them. This would suggest a possible plasmidic control of chromosomally encoded surface structures that mediated adhesiveness of E. coli to mammalian cells
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