Study of the in vitro activity of amoxicillin/clavulanic acid and other beta-lactam antibiotics against Escherichia coli isolated from urine specimens

A total of 205 serial, unduplicated urinary isolates of Escherichia coli was collected from June through August 1998 in 2 community and 3 hospital laboratories. By using the NCCLS broth microdilution technique, their in vitro susceptibility to ampicillin, amoxicillin/clavulanic acid, cefuroxime, cefuroxime axetil, ticarcillin/clavulanic acid and piperacillin/tazobactam was determined. One hundred and twenty isolates were from hospitalised patients, 85 from ambulatory, 129 community acquired and 76 nosocomial. Half of the nosocomial isolates were obtained from naturally produced and half from alternatively produced urine specimens. In general, the highest susceptibility rates, following NCCLS criteria, were found for piperacillin/tazobactam (93.2%) followed by cefuroxime (92.2%) and amoxicillin/clavulanic acid (82.9%). Ampicillin showed a clear bimodal distribution with a clear peak for the resistant population. The highest degree of ampicillin resistance was found in nosocomial isolates. Overall, ampicillin showed the lowest degree of susceptibility. Most of the ampicillin resistant isolates remained susceptible to piperacillin/tazobactam, cefuroxime and amoxicillin/clavulanic acid. In general, the community acquired isolates had higher susceptibility rates than the nosocomial isolates.     

Abnormal erythroid progenitor cells in human preleukemia

Ten patients with preleukemia were studied by the erythroid cell clonal culture technique. In nine of these patients, erythroid colonies derived from peripheral blood BFU-E were not observed, while the other patient had markedly decreased peripheral blood BFU-E-derived erythroid colonies in vitro. In three patients, marrow cells were also cultured and no BFU-E-derived erythroid colonies were detected. These studies indicate that immature erythroid progenitor cells, BFU-E, in patients with preleukemia are either markedly decreased in number or grossly defective in their proliferative or differentiative capacities.     

Serological confirmation of human T-lymphotropic virus type I infection in healthy blood and plasma donors

We wished to develop criteria for serological confirmation of human T- lymphotropic virus type I (HTLV-I) infection in healthy donors. Selected serum or plasma samples reactive by HTLV-I enzyme immunosorbent assay or gel-agglutination assays with at least one viral- specific band on Western immunoblot (WIB) were tested in six laboratories by four WIBs and four radioimmunoprecipitation assays (RIPAs) for antibodies to HTLV-I proteins encoded by gag (p19 and p24), env (gp46 and/or gp61), and tax (p40x) genes. One hundred forty-two donor sera were obtained from 38 Japanese, 69 American, and 35 Caribbean blood or plasma donors. Among these samples, WIB assays appeared more sensitive to p24 antibodies, whereas RIPAs were significantly more sensitive to gp61 antibodies. All sera (137) with gp61 antibodies had p24 antibodies. Of the 137 sera positive for p24 and gp61 antibodies, p19 antibodies were detected in 129 sera, and p40x antibodies were detected in 108. In sera with p19 antibodies and antibodies to env- or tax-encoded proteins, p24 antibodies were always present. Antibodies to p40x were not found in the absence of gp61 antibodies. Virological evidence of infection was found in seven American donors by lymphocyte coculture (one HTLV-I, one HTLV-II) or by polymerase chain reaction (three HTLV-I, two HTLV-II). Sera from all seven donors showed p24 and gp46 and/or gp61 antibodies. We suggest that seroreactivity to both p24 and gp46 and/or gp61 by WIB or RIPA or both are suitable criteria to confirm but not to distinguish HTLV-I and HTLV-II infections.     

Autologous versus homologous donors. Evaluation of markers for infectious disease

Autologous blood donations may provide a new source of blood when components not used by the donors are deemed suitable for homologous use. However, the risk of transfusion-transmitted diseases form such donors has not been evaluated. We compared the prevalence of infectious markers and rate of abnormal responses to a confidential donor ballot in autologous donors from two blood collection programs, one blood center and one hospital-based, to corresponding homologous blood programs. The incidence of abnormal test results in autologous donors for HIV antibodies (either Western blot confirmed or repeatedly reactive, unconfirmed), HBsAg, ALT, and anti-HBc were not statistically different from homologous rates. The incidence of STS abnormalities in autologous donors was statistically significant, although all positive results were biologic false positives. The rate of abnormal responses to the confidential ballot was statistically significant only in autologous donors whose collections were already determined to be unsuitable for homologous use due to medical history problems. Although the data do not address infectious complications in transfusion recipients, this study offers no evidence that autologous blood components are less safe than their homologous equivalents.