Immune response, ciprofloxacin activity, and gender differences after human experimental challenge by two strains of enterotoxigenic Escherichia coli.

In order to test vaccines against enterotoxigenic Escherichia coli (ETEC)-induced diarrhea, challenge models are needed. In this study we compared clinical and immunological responses after North American volunteers were orally challenged by two ETEC strains. Groups of approximately eight volunteers received 10(9) or 10(10) CFU of E. coli B7A (LT+ ST+ CS6+) or 10(8) or 10(9) CFU of E. coli H10407 (LT+ ST+ CFA/I+). About 75% of the volunteers developed diarrhea after challenge with 10(10) CFU B7A or either dose of H10407. B7A had a shorter incubation period than H10407 (P = 0.001) and caused milder illness; the mean diarrheal output after H10407 challenge was nearly twice that after B7A challenge (P = 0.01). Females had more abdominal complaints, and males had a higher incidence of fever. Ciprofloxacin generally diminished or stopped symptoms and shedding by the second day of antibiotic treatment, but four subjects shed for one to four additional days. The immune responses to colonization factors CS6 and colonization factor antigen I (CFA/I) and to heat-labile toxin (LT) were measured. The responses to CFA/I were the most robust responses; all volunteers who received H10407 had serum immunoglobulin A (IgA) and IgG responses, and all but one volunteer had antibody-secreting cell (ASC) responses. One-half the volunteers who received B7A had an ASC response to CS6, and about one-third had serum IgA or IgG responses. Despite the differences in clinical illness and immune responses to colonization factors, the immune responses to LT were similar in all groups and were intermediate between the CFA/I and CS6 responses. These results provide standards for immune responses after ETEC vaccination.

Characterization of fouled membranes from a membrane enhanced biological phosphorus removal system.

Characterization of fouled membranes is the first step towards a good understanding of membrane fouling nature and thus formulating effective engineering measures for fouling prevention and control. In this study, fouled membrane fibres collected from a pilot scale membrane enhanced biological phosphorus removal (MEBPR) process were systematically examined. Several analytical tools, including scanning electron microscopy (SEM), conventional optical microscopy (COM), energy dispersive X-ray (EDX) microanalysis, matrix assisted laser desorption/ionization--mass spectrometry (MALDI-MS) analysis, and conventional chemical analysis techniques were used. The results indicated that membrane fouling in the MEBPR process was mainly of an organic nature, and most extractable foulants were carbohydrates and humic or humic-like substances. Unlike in other wastewater treatment membrane bioreactors, microbial growth on fouled membranes was not substantial, probably due to the vigorous aeration applied and the strong hydrodynamic conditions within the membrane pore structure. After a period of sludge filtration, membrane surfaces became more hydrophobic and the resultant hydrophobic interactions between the fouled membranes and mixed liquor constituents might have accelerated the fouling process.

The effect of smokeless-tobacco extracts on the growth of oral bacteria of the genus Streptococcus.

Aqueous tobacco extracts were used to supplement a basic salts solution (BSS) and a microbial medium. Thin-layer chromatography revealed sucrose in only one of four extracts. Discs saturated with extracts (0.1-50 mg/ml) failed to inhibit growth of any of the micro-organisms. Supplementation (10 mg/ml) of BSS with the tobaccos lacking sucrose resulted in augmented growth of Streptococcus mutans, Streptococcus salivarius and Streptococcus sanguis whereas the sucrose-containing brand augmented only Strep. sanguis growth. Thus extracts of these smokeless tobaccos would serve as a growth substrate for three species of oral streptococci which are frequently associated with human dental caries.

Modulation of vascular thrombosis by products of arachidonic acid metabolism.

It has been postulated that metabolites of the arachidonic acid pathway exert an important influence on hemostasis and thrombosis. This notion is based on in vitro experiments. We have utilized two experimental models to elucidate the physiologic roles of thromboxane A2 (TxA2) and prostacyclin (PGI2) in the modulation of thrombus formation. The role of TxA2 in promoting thrombus formation was evaluated in a rabbit model where the aorta was deendothelialized by a balloon catheter technique and indium-111-labeled platelets were used as a marker for quantifying platelet deposition. Both 1-benzylimidazole, a thromboxane synthase inhibitor, and 13-azaprostanoic acid, an antagonist of thromboxane/endoperoxide receptors significantly reduced the platelet deposition onto the damaged vessel wall. The data indicate the TxA2 plays an important role in thrombosis and hemostasis. The influence of PGI2 insufficiency due to accelerated PGI2 degradation on microvascular thrombosis was evaluated in a unique clinical disease, i.e. thrombotic thrombocytopenic purpura (TTP). Accelerated PGI2 degradation was observed in several patients with chronic TTP. The degradation abnormalities were corrected by plasma infusion in vivo or serum supplement in vitro. To test the hypothesis that PGI2 must be bound to serum macromolecules to prevent rapid hydrolysis, serum binding capacity for PGI2 was measured by Sephadex G-25 gel filtration. The binding capacity was significantly reduced in the patients and was corrected by serum supplement. Abnormalities of PGI2 binding were also noted in a group of patients with ischemic stroke. Our findings suggest that there exist in the serum certain constituents which bind and stabilize PGI2.(ABSTRACT TRUNCATED AT 250 WORDS)