Actinomyces israelii and Eikenella corrodens isolation from a pleural effusion case.
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Biomedical subjects
Publications and source records attributed to Y Chong.
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A plasmid-encoded beta-lactamase conferring extended broad spectrum resistance including cephamycins was identified in a Klebsiella pneumoniae strain isolated from a patient's wound. Strains harbouring the plasmid pMVP-1 were resistant to penicillins, cephalosporins of all generations (parenteral and new oral compounds) cephamycins, aztreonam, tetracycline, chloramphenicol, sulfonamides and to all aminoglycosides modified by AAC-(6)-I-transferase. beta-lactams still active against these strains were temocillin, ceftazidime, cefpirome, carumonam and the carbapenems imipenem and meropenem. The new cephamycinase (CMY-1) was more strongly inhibited by sulbactam in the majority of combinations than by clavulanic acid or tazobactam. MICs of ceftazidime and carumonam were not reduced by inhibitors in the wild type and the transconjugant. A transferable plasmid (pMVP-1) of about 9.6 x 10(7) dalton was demonstrated by gel-electrophoresis. In the wild type and the transconjugant a beta-lactamase with an isoelectric point of 8.0 was identified. This enzyme CMY-1 is different from the other extended broad spectrum beta-lactamases (TEM-3 to TEM-10, SHV-2 to SHV-5). The incidence of this enzyme may be underestimated, since resistance to cephamycins in Klebsiella and Escherichia coli has so far been regarded as almost exclusively chromosomally encoded and sensitivity of CMY-1 to clavulanic acid is low. Therefore, screening for CMY-1 beta-lactamases by the usual double disk test including clavulanic acid is not sensitive enough to detect CMY-1 producers. Sulbactam (e.g. in combination with ampicillin) disks and a cephamycin should therefore be used as well when screening for super extended broad spectrum (SEBS-) beta-lactamases.
The in-vitro activity of fluconazole against 46,831 yeast isolates collected over a two-year period from 57 laboratories in 33 countries worldwide was assessed using a disc diffusion method. Candida albicans was the organism isolated most frequently, accounting for 68.6% of the total number of isolates. C. glabrata, C. tropicalis, C parapsilosis and C. krusei and Cryptococcus neoformans represented 9.9, 4.7, 4.3, 1.9, and 1.4% of isolates respectively during the 2 year period and rates varied markedly between countries. In 1999 data blood isolates represented 4.9% of all isolates and intensive care unit isolates represented 9.9%. In both the 1998 and 1999 data, 99% of C. albicans were fully susceptible (S) to fluconazole, and 95.6% of all species of yeasts tested were S or susceptible-dose dependent (S-DD) to fluconazole. No emerging trends of resistance were noted with any of the Candida spp. tested as 96% of all isolates retained susceptibility (S or S-DD) to this agent.
Computer modeling studies have been performed on the several pairs of D- and L-nucleoside inhibitors with the HIV-1 RT model. Additionally, clinically important M184V mutation, which confers the viral resistance against 3TC and FTC, were studied by the same modeling system.
The effect of combination anti-retroviral therapy regimens on HIV-1 proviral DNA levels in peripheral blood mononuclear cells was examined in 12 HIV-1-positive patients, using endpoint dilution polymerase chain reaction and serial cloning, and sequencing of the gag region of HIV-1. The major clone was defined as the most numerous of 10 analysed clones, and observation periods ranged from 8 months to 32 months (mean 19.7 +/- 10.2 months). In five patients (one with primary-stage HIV-1 infection) receiving three anti-retroviral drugs, HIV-1 RNA reduced to undetectable levels (i.e. < or = 100 copies/ml). HIV-1 proviral DNA and the number of major clones reduced in four of these patients. HIV-1 RNA levels reduced, but remained detectable, in five other patients. In the two remaining patients (both receiving two rather than three anti-retroviral drugs), HIV-1 RNA levels increased. These results suggest that the population of major clones may be affected when HIV-1 RNA levels reduce following combination regimens of anti-retroviral therapy.