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The aims of this study were to investigate the possible effects of new antimicrobial agents, the conventional antituberculosis drugs and several combinations of these agents against 190 clinical isolates of Mycobacterium tuberculosis and 30 of M. avium.
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Activity of ticarcillin combined with clavulanic acid against 203 P. aeruginosa strains was studied. 159 strains produced a constitutive beta-lactamase with resistance to ticarcillin (MIC less than 128 mg/l) as a result. Minimal inhibitory concentrations (MICs) were determined using the agar dilution method for ticarcillin alone and combined with 4 and 8 mg/l clavulanic acid. Addition of clavulanic acid failed to change the activity of ticarcillin on ticarcillin-susceptible stains and on strains producing a constitutive cephalosporinase. A synergic effect was demonstrated for PSE and TEM type beta-lactamase producers and for OXA type beta-lactamase producers (4 halving dilutions and 1 to 2 halving dilutions respectively). However, because of the levels of baseline MICs, the combination brought the MIC of ticarcillin below the cutoff level for a small percentage of PSE strains (6%), moderate percentage of OXA strains (17 to 50%) and significant percentage of TEM strains. These percentages were slightly higher with 8 mg than 4 mg clavulanic acid. Given current data on the prevalence of the various beta-lactamases among resistant strains now being isolated in France, the ticarcillin + clavulanic acid combination will enable to achieve an MIC less than 128 mg/l for 11% (with 4 mg) or 16% (with 8 mg) of resistant strains.
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The authors investigated the antibacterial activity of some cysteine sulphonamides substituted in the sulphonamide group as well as that of some peptides containing cysteine sulphonamide. They found that the antibacterial activity of these compounds was in part considerably stronger than that of cysteine sulphonamide.
A method for determination of specificity and activity of the inflammatory process is described. The method is based on the reaction of immunocytoadherence between granulocytes with the round nucleus (nuclei) and microorganisms. The method is sensitive, as the phagocytic reaction is inhibited and the patient's blood cells interact with microbial cells due to the presence of immunoglobulins or receptors of the immunoglobulin nature, active against the causative agent of the disease, on the blood cell surface. The values of immunocytoadherence in tuberculosis, brucellosis and pneumonia are presented.
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With the checkerboard-technique, it was found in vitro, that methyl-[7-chloro-6,7,8-tridesoxy-6-trans-(1-methyl-4-propyl-L-2-pyrrolidincarboxamido)-1-thio-L-threo-alpha-D-galacto-octopyranoside] (clindamycin) in combination with cefoxitin, cefotaxim, mezlocillin, azlocillin, gentamicin and amikacin has no antagonistic effects against common infective microorganisms such as staphylococci, enterococci and E. coli. In most cases the combination was found to be synergistic. If the results of the in vitro experiments are calculated with the FIC-indices (fractional inhibitory concentration), only the combination of clindamycin with cefoxitin and clindamycin with cefotaxime showed no synergistic efficacy against Staphylococcus aureus. Only 20% of the enterococci strains were inhibited synergistically with the combination clindamycin and gentamicin or with amikacin, respectively. All the other strains tested were inhibited synergistically by the combinations of clindamycin with the antibiotics mentioned above. In clinical use clindamycin can be administered in combination with cefoxitin, cefotaxime, mezlocillin, gentamicin and amikacin, respectively, without any loss in its activity against the microorganisms tested in this study.
The interaction of a microbial pathogen with its host is a highly dynamic process shaped by evolution. Understanding cellular responses to microbial products is essential for a complete understanding of virulence. Similarly, studies aimed at determining how a particular virulence factor functions have helped unravel molecular mechanisms that govern eukaryotic cellular events. These two seemingly diverse areas were brought together on the beautiful Spanish Costa Brava in a recent meeting (October 13-17, 2002) sponsored by European Research Conferences (EURESCO) and the European Molecular Biology Organization (EMBO).
A stepwise and interactive identification procedure for foodborne microbial hazards has been developed in which use is made of several levels of detail ranging from rough hazard identification to comprehensive hazard identification. This approach allows one to tackle the most obvious hazards first, before focusing on less obvious hazards. The interactive character of the identification procedure is based on the use of several knowledge sources. Combination of knowledge sources, expressed in the use of knowledge rules, supports the user in systematically selecting hazards which may pose a real risk to the consumer. Due to the structured method and the clear definitions of the knowledge rules, the procedure is transparent and may be changed if necessary. The hazard identification procedure has been implemented as a computer program, resulting in a decision-supporting identification system. It provides a way to efficiently assess those hazards which may cause harm if not brought under control during processing. The procedure forms a basis for quantitative risk assessments.
Two-hundred-and-thirty-three asymptomatic couples with a mean duration of infertility of 5 years were submitted to postcoital testing (PT) and to sperm penetration meter test (SPMT) and simultaneous microbial screening. Cervical swabs and semen specimens were collected for culture of Mycoplasma hominis, Ureaplasma urealyticum, Chlamydia trachomatis, Neisseria gonorrhoeae, other potentially pathogenic and commensal aerobic and anaerobic bacteria, herpes simplex virus, vaginal swabs for Trichomonas vaginalis and yeasts. Results of microbial screening were analysed with regard to sperm penetration ability into wives' cervical mucus in vivo and in vitro, but no marked influence was revealed for most microorganisms. Samples of only one of the 233 couples proved to be completely sterile. The findings suggest that in asymptomatic patients microbial colonization is of minor importance for sperm-mucus interaction.
The Apo-1/Fas antigen (CD95) mediates programmed cell death of lymphocytes when bound by Fas ligand or anti-Apo-1/Fas antibody. In contrast, the CD40 antigen provides a potent activation and survival signal to B lymphocytes when it is engaged by its T cell ligand (CD40L, gp39) or cross-linked by anti-CD40 antibody. In this study, we use human tonsillar B cells and the Ramos Burkitt's lymphoma B cell line, which serves as a model for human germinal center B lymphocytes, to study the effectors of Apo-1/Fas expression and apoptosis of human B cells. We found that Apo-1/Fas expression was upregulated on both malignant and normal human B lymphocytes after CD40 ligation induced by (a) cognate T helper-B cell interaction mediated by microbial superantigen (SAg); (b) contact-dependent interaction with CD40L+, but not CD40L- Jurkat mutant T cell clones; and (c) monoclonal anti-CD40, but not any of a panel of control antibodies. Enhanced B cell Fas/Apo-1 expression is functionally significant. Coculture of Ramos Burkitt's lymphoma line cells with irradiated SAg-reactive CD4+ T cells with SAg or CD40L+ Jurkat T cells results in B cell apoptosis, evidenced by reduced cell viability and DNA laddering. This process is augmented by the addition of anti-Apo-1/Fas monoclonal antibody, consistent with an acquired susceptibility to Apo-1/Fas-mediated apoptosis. These data support an immunoregulatory pathway in which seemingly contradictory signals involving the B cell proliferation/survival antigen CD40, as well as the Apo-1/Fas molecule, which mediates programmed cell death of lymphocytes, are linked in the process of human B cell activation.
Gut microbiota often undergo metabolic cross-feeding and resource competition. However, our understanding of global variations in these interactions and their implications for host health remain elusive. By analyzing a microbial genome catalog from 841 fecal metagenomes across 53 primate species worldwide, we identified key microbiota assigned to two taxa, i.e., Bacillota_A and Pseudomonadota, which well predicted the trade-off of community-level interaction types between metabolic competition and cooperation. Specifically, Bacillota_A species were inherently competitive and amino acid auxotrophic and typically found in anaerobic habitats. In contrast, members of Pseudomonadota were inherently cooperative, siderophore producers, and more abundant in aerobic conditions. Random forest models successfully distinguished unhealthy gut samples from healthy samples through the key competitive and cooperative microbiota, suggesting potential links between community metabolic interactions and host health. Together, this study enhances our mechanistic understanding of microbial interaction dynamism within complex gut ecosystems, offering new targets for understanding host health.
The interactions among Spartina patens and sediment microbial populations and the interactions among Phragmites australis and sediment microbial populations were studied at monotypic sites in Piermont Marsh, a salt marsh of the Hudson River north of New York, N.Y., at key times during the growing season. Arbuscular mycorrhizal fungi (AMF) effectively colonized S. patens but not P. australis, and there were seasonal increases and decreases that coincided with plant growth and senescence (17 and 6% of the S. patens root length were colonized, respectively). In sediment samples from the Spartina site, the microbial community and specific bacterial populations were at least twice as large in terms of number and biomass as the microbial community and specific bacterial populations in sediment samples from the Phragmites site, and peak values occurred during reproduction. Members of the domain Bacteria, especially members of the alpha-, gamma-, and delta-subdivisions of the Proteobacteria, were the most abundant organisms at both sites throughout the growing season. The populations were generally more dynamic in samples from the Spartina site than in samples from the Phragmites site. No differences between the two sites and no differences during the growing season were observed when restriction fragment length polymorphism analyses of nifH amplicons were performed in an attempt to detect shifts in the diversity of nitrogen-fixing bacteria. Differences were observed only in the patterns generated by PCR or reverse transcription-PCR for samples from the Spartina site, suggesting that there were differences in the overall and active populations of nitrogen-fixing bacteria. Regression analyses indicated that there was a positive interaction between members of the delta-subdivision of the Proteobacteria and root biomass but not between members of the delta-subdivision of the Proteobacteria and macroorganic matter at both sites. In samples from the Spartina site, there were indications that there were bacterium-fungus interactions since populations of members of the alpha-subdivision of the Proteobacteria were negatively associated with AMF colonization and populations of members of the gamma-subdivision of the Proteobacteria were positively associated with AMF colonization.
A novel extension of traditional growth models for exposure assessment of food-borne microbial pathogens was developed to address the complex interactions of competing microbial populations in foods. Scenarios were designed for baseline refrigeration and mild abuse of servings of chicken broiler and ground beef Our approach employed high-quality data for microbiology of foods at production, refrigerated storage temperatures, and growth kinetics of microbial populations in culture media. Simple parallel models were developed for exponential growth of multiple pathogens and the abundant and ubiquitous nonpathogenic indigenous microbiota. Monte Carlo simulations were run for unconstrained growth and growth with the density-dependent constraint based on the "Jameson effect," inhibition of pathogen growth when the indigenous microbiota reached 10(9) counts per serving. The modes for unconstrained growth of the indigenous microbiota were 10(8), 10(10), and 10(11) counts per serving for chicken broilers, and 10(7), 10(9) and 10(11) counts per serving for ground beef at respective sites for backroom, meat case, and home refrigeration. Contamination rates and likelihoods of reaching temperatures supporting growth of the pathogens in the baseline refrigeration scenario were rare events. The unconstrained exponential growth models appeared to overestimate L. monocytogenes growth maxima for the baseline refrigeration scenario by 1500-7233% (10(6)-10(7) counts/serving) when the inhibitory effects of the indigenous microbiota are ignored. The extreme tails of the distributions for the constrained models appeared to overestimate growth maxima 110% (10(4)-10(5) counts/serving) for Salmonella spp. and 108% (6 x 10(3) counts/serving) for E. coli O157:H7 relative to the extremes of the unconstrained models. The approach of incorporating parallel models for pathogens and the indigenous microbiota into exposure assessment modeling motivates the design of validation studies to test the modeling assumptions, consistent with the analytical-deliberative process of risk analysis.