SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Studies were made on nonselective culture medium and the method of culture for the investigation of the bacterial flora in the digestive tract of cattle. With their results, further studies were done to clarify changes in the fecal bacterial flora in eight calves less than 6 months of age with the lapse of time. Three roll-tube media were used in the gas jet method. They were modified VL agar (VL medium), rumen fluid glucose cellobiose agar (RGCA medium), and Medium 10 (M 10). Moreover, glucose liver blood agar (BL medium) was used in the anaerobic jar method. In this method the steel wool method was applied after the substitution of carbon dioxide. Of the four media used, VL medium was proved to be the most efficient. It was followed by RGCA medium and M 10. BL medium was much less efficient than any other medium. When the fecal bacterial flora was examined in calves for changes with the advance in age, the total bacterial count and the enteric bacterial count decreased in the second half of the experimental period. The lactobacillary group count remained almost at a constant level of 7 approximately 9 (logarithmic value) per gram in breast-fed calves, but decreased to a level of 5 (logarithmic value) per gram in bottle-fed calves at about 2 months of age or later. The streptococcal group count showed no particular tendency to change. When the organic acid contents of the feces were estimated in calves in every stage of growth, the amount of total organic acids and that of propionic acid were larger in bottle-fed than in breast-fed calves.
Novel bacterial structures have been demonstrated in lysed blood filtrates placed in special culture media from patients with idiopathic hematuria. These structures converted rapidly to gram-positive coccal (streptococcal and staphylococcal-like), coccobacillary and filamentous, bacterial forms in vitro from 96 per cent of the patients studied. Blood cultured conventionally yielded negative findings. Although structures (dense bodies) were demonstrated in normal control blood specimens (albeit in lesser numbers) few converted to classical bacteria in vitro (7 per cent). Erythromycin therapy appeared to correlate with disappearance of hematuria and inability to revert rapidly the variant forms to classical bacteria in vitro. It is suggested that continual bombardment of the blood by bacteria entering from the mouth or other sites may lead to the development of variant bacterial parasitism. In an effort to survive the deleterious host effects the organisms may convert to persisting osmotically stable variant bacterial forms (dense bodies). Development of a disease state may be conditioned by some existing or developing abnormality in the host (immunologic, physiologic and/or biochemical). Furthermore, changes (genetic?) that might take place in the organisms per se during their transition to variant forms and adaptation to life in vivo may not allow certain host environments to adapt to these new forms, possibly leading to a pathogenetic role in renal diseases whose etiologies have long been enigmas.
Novel bacterial structures have been demonstrated in lysed blood filtrates placed in special culture media from patients with idiopathic hematuria. These structures converted rapidly to gram-positive coccal (streptococcal and staphylococcal-like) coccobacillary and filamentous, bacterial forms in vitro from 96 per cent of the patients studied. Blood cultured conventionally yielded negative findings. Although structures (dense bodies) were demonstrated in normal control blood specimens (albeit in lesser numbers) few converted to classical bacteria in vitro (7 per cent). Erythromycin therapy appeared to correlate with disappearance of hematuria and inability to revert rapidly the variant froms to classical bacteria in vitro. It is suggested that continual bombardment of the blood by bacteria entering from the mouth or other sites may lead to the development of variant bacterial parasitism. In an effort to survive the deleterious host effects the organisms may convert to persisting osmotically stable variant bacterial forms (dense bodies). Development of a disease state may be conditioned by some existing or developing abnormality in the host (immunologic, physiologic and/or biochemical). Furthermore, changes (genetic?) that might take place in the organisms per se during their transition to variant forms and adaptation to life in vivo may not allow certain host environments to adapt to these new forms, possibly leading to a pathogenetic role in renal diseases whose etiologies have long been enigmas.
A micrococcal and a diplocaccal strain isolated from the nasal space of a clinically intact nursed calf were used for artificial bacterial invasion in the first phase of the experiment. Application of bacterial suspension prepared from those strains had no effect upon the rise of coli counts in the nasal secretion of nursed calves during their first days of age nor upon the morbidity or mortality of all 677 test animals in comparison to 665 controls. Therefore, an avirulent E.-coli strain was used in subsequent bacterial invasion experiments. The strain was retrievable up to the seventh day of age, the count having been about 10(5) bacteria per gram nasal secretion. Application of a bacterial suspension prepared from that E.-coli strain did not reduce morbidity and mortality among 820 test animals that were compared to 809 controls. Results are discussed in this paper with reference to literature.
A combination of procedures was employed to develop a radioimmunoassay which quantified the binding of antibodies to antigens of either intact Propionibacterium acnes or to antigens of insoluble extracts derived from the bacteria. Reactive antibody populations were purified by use of bacterial immunoadsorbents which were prepared by coupling P. acnes to diethylaminoethyl cellulose. Binding of antibodies was detected with [125I]staphylococcal protein A ([125I]SpA) and optimal conditions for the assay defined by varying the amounts of antibodies, bacterial antigenic targets and [125I]SpA. In antibody excess, 100% of available [125I]SpA was bound by the target-antibody complexes. However, when antibody concentration was limiting, a linear relationship was demonstrated between per cent specific binding of [125I]SpA and antibodies bound to bacterial targets. These results were achieved only with immunoadsorbent-purified antibody populations and not with hyperimmune sera or IgG. The radioimmunoassay detected subtle antigenic differences and similarities between P. acnes, P. acnes extracts and a variety of unrelated microorganisms.
Bacterial aneurysms are aneurysms which develop on a vascular wall weakened as a result of a bacterial infection. They can develop anywhere. This paper describes a female patient with subacute bacterial endocarditis and multiple cerebral aneurysms. Conservative treatment followed.
SUMMARY: Pan-genome analysis is a fundamental tool for studying bacterial genome evolution; however, the variety in methods used to define and measure the pan-genome poses challenges to the interpretation and reliability of results. Using Mycobacterium tuberculosis, a clonally evolving bacterium with a small accessory genome, as a model system, we systematically evaluated sources of variability in pan-genome estimates. Our analysis revealed that differences in assembly type (short-read versus hybrid), annotation pipeline, and pan-genome software, significantly impact predictions of core and accessory genome size. Extending our analysis to two additional bacterial species, Escherichia coli and Staphylococcus aureus, we observed consistent tool-dependent biases but species-specific patterns in pan-genome variability. Our findings highlight the importance of integrating nucleotide- and protein-level analyses to improve the reliability and reproducibility of pan-genome studies across diverse bacterial populations. AVAILABILITY AND IMPLEMENTATION: Panqc is freely available under an MIT license at https://github.com/maxgmarin/panqc.
The role of dextran in the pathogenesis of bacterial endocarditis was investigated by studying the adherence of dextran producing oral streptococci to the constituents of nonbacterial thrombotic endocarditis (NBTE) in vitro and in vivo. The adherence of Streptococcus sanguis to fibrin and platelets was determined in an in vitro assay system simulating nonbacterial thrombotic endocarditis. Adherence was increased when the organisms were grown in sucrose-supplemented media (adherence ratio X 10(4), 177 +/- 6 in 5% sucrose vs. 140 +/- 7 in 0.5% sucrose, P less than 0.001), and decreased by incubating the organisms in dextranase (adherence ratio X 10(4), 117 +/- 16, P less than 0.001), an effect which was nullified by heat inactivating this enzyme (adherence ratio X 10(4), 192 +/- 7, P less than 0.001). The amount of dextran produced in broth by three different oral streptococci correlated directly with the adherence observed to fibrin and a fibrin-platelet matrix in vitro (P less than 0.001). These organisms adhered more readily to a fibrin-platelet matrix than to fibrin alone (adherence ratio X 10(4), 455 +/- 30 vs. 177 +/- 6, respectively, P less than 0.001). The role of dextran formation was also examined in vivo in rabbits with preexisting NBTE. After injection of 10(7) S. sanguis, 12 of 17 animals developed endocarditis. In contrast, when the organisms were pretreated with dextranase (an enzyme that removes dextran from the bacterial cell surface), the same inoculum resulted in endocarditis in only 5 of 19 animals (P less than 0.05). In addition, a fresh strain of S. sanguis that produced high levels of dextran (1,220 +/- 50 microgram/ml) and adhered avidly to fibrin (adherence ratio X 10(4), 220 +/- 11) produced endocarditis in 12 of 18 rabbits after injection of 10(7) organisms. Another isolate of the same strain that had been passed repeatedly in the laboratory produced less dextran (400 +/- 30 microgram/ml), adhered poorly to fibrin (adherence ratio X 10(4), 140 +/- 7), and produced endocarditis in only 3 of 14 rabbits under identical conditions (P less than 0.05). This study demonstrates that dextran production is important in the adherence of oral streptococci to the constituents of NBTE and may play a role in the pathogenesis of bacterial endocarditis by oral streptococci.
It was shown that 3-amino-3-deoxy-D-glucose, one of the constituents of the kanamycin molecule and a metabolite of Bacillus sp., inhibits the bacterial synthesis of cell wall. The antibiotic (100 microgram/ml) significantly inhibits the growth of Staphylococcus aureus FDA 209P as well as the incorporation of DL-[14C]alanine into the acid-insoluble macromolecular fraction of its growing cells in the presence of chloramphenicol (100 microgram/ml). In contrast, the antibiotic does not affect the incorporation of [3H]thymidine, [3H]uridine and L-[14C]leucine. The other constituents of kanamycin, 6-amino-6-deoxy-D-glucose and deoxystreptamine do not inhibit the synthesis of bacterial cell wall peptidoglycan.
Humic-like substances obtained from cells of Pseudomonas acidovorans were separated on Sephadex G-25 into two groups of substances of different molecular weight. The substances of the molecular weight greater than 5000 were successively separated on Sephadex gels G-50, G-75, G-100. Five fractions of different molecular weight were obtained, the percentage of which varied depending on the media used and time of incubation of the bacteria. Most (38%--46%) of the compounds contained in the bacterial humic acids were of approximate molecular weight of 40 000--50 000. The distribution of the fractions in the bacterial "humic-acids" was compared with those of the humic acid made by Fluka A. G. The synthetic humic acid contained most (approximately 40%) of the compounds of approximate molecular weight of 8000--10 000. In the bacterial and synthetic material the content of the compounds with the molecular weight above 100 000 was very similar (8%--12%).
Twenty human amniotic fluids obtained from gestations of 20 weeks' duration supported bacterial growth. Nine of the 20 fluids could be made inhibitory by adjusting the phosphate to zinc ratios of the fluids to less than 200 mug per milliliter. These fluids contained the phosphate-sensitive bacterial inhibitor previously, but the fluids contained sufficient phosphate to inactivate the antibacterial system. The remaining 11 amniotic fluids did not contain the peptide component of the phosphate-sensitive bacterial inhibitor and could not be made inhibitory by adjusting the phosphate to zinc ratio to less than 200 mug per milliliter. The data obtained suggested synthesis of the peptide component may occur at a gestational age of approximately 20 weeks. The peptide may indirectly be detected in fluids by determining whether antibacterial activity is obtained when the phosphate to zinc ratio of the fluids is adjusted to less than 200 mug per milliliter.
MDCK cells (a line of stable canine kidney cells) infected with influenza A/NWS/33 virus (a neurotropic variant of the Wilson Smith strain) were tested with 18 selected bacterial species to determine whether mammalian cells become susceptible to bacterial adherence as a result of virus infection. Cell monolayers were washed and examined microscopically for adherence. Bacteria of only two of 18 species were seen to adhere to the infected cells: a group B Streptococcus and Streptococcus sanguis. Control monolayers were negative for adherence. Pretreatment of virus-infected cultures with mouse ascitic fluid containing antibody to influenza A virus completely blocked adherence of the bacteria. Further testing with the strains representative of the five serotypes of group B Streptococcus disclosed that adherence occurred with types Ia, Ic, and II, but not with types Ib and III.
A study was made of the cytotoxic effect of antibacterial antibody and complement reacting with bacterial antigens firmly adsorbed to epidermal cells. It is believed that this phenomenon enhances the severity of the lesions and their spread in some cases of disseminated eczema. In this first part of the study it is confirmed that Staphylococcus aureus and micrococci are frequently present on lesions and 'unaffected' skin of patients with disseminated eczema. Intradermal skin tests with antigens of staphylococci and micrococci on 122 eczematous patients elicited immediate, or combined immediate and 4 h (Arthus-like) responses, in a large proportion, but few showed uncombined 4 h responses or delayed hypersensitivity, in contrast to findings reported by others. Immunofluorescence tests on skin of thirty patients showed that IgG and IgM diffused into the epidermis, sometimes to the skin surface, of lesional skin, and more immunoglobulin was found in skin of 'unaffected' areas than in skin of normal healthy persons, indicating that clinically unaffected skin in patients with disseminated eczema is abnormal. IgD was present in three of eight samples of unfixed, and six of eight samples of fixed eczematous skin. Staphylococcal and micrococcal antigen was shown on the skin surface and also diffusely in the cytoplasm of cells in the dermis beneath the surface deposits, indicating percutaneous absorption. Further small amounts of antigen were adsorbed to some epidermal cells. These results show that the predisposing conditions for a cytotoxic reaction mediated by hypersensitivity to bacteria do occur. Increased growth of staphylococci and micrococci on eczematous skin would result in increased deposits of antigen. Bacterial antigens are absorbed into the skin and bind with epidermal cells, and immunoglobulins diffuse into the epidermis. Furthermore, skin tests showed that many eczematous patients were hypersensitive to bacteria. Studies on the nature of the antibacterial antibody will be published in the succeeding reports.
The deposition of fibrin on infected vegetations and the presence of mononuclear phagocytes that have phagocytized bacteria are remarkabe features in experimental bacterial endocarditis. In a study in vitro, we show that phagocytosis of bacteria by human monocytes enhances thromboplastin generation by these cells. Maximal enhancement of the generation of thromboplastin by monocytes was about six times compared with that in the control experiment without bacteria, and it was obtained by preincubation of the monocytes with 5 to 10 bacteria per monocyte. No quantitative difference was observed between Staphylococcus epidermidis and Streptococcus sanguis as to the enhancement of the monocyte thromboplastin generation. An enhancement of the procoagulant activity generation was also observed after addition of bacteria to human or rabbit whole blood. Probably, this generation was also due to synthesis of thromboplastin by monocytes. It is conceivable that fibrin deposition on infected vegetations during bacterial endocarditis is mediated by thromboplastin synthesis by monocytes.
An outbreak of watery diarrhea occurred in 14 of 15 infants in a special care unit over a four-day period. Using the CHO cell assay for enterotoxin, we found that 11 of these patients had toxigenic bacteria in their stools. These bacteria comprised nine different serotypes of three species of organisms: Escherichia coli, Klebsiella, and Citrobacter. None of the three serotypes of E. coli were classic enteropathogenic serotypes. Rectal swab specimens from all 15 infants were examined for the presence of viruses by electron microscopic and cell culture techniques as well as by studies in suckling mice. None had parvovirus- or reovirus-like agents and two had adenoviruses. No other viral agents were detected. Of 38 bacterial strains isolated from ten control infants without diarrhea, three Klebsiella strains from two individuals were found to be toxigenic. Analysis of a total of 136 enteric isolates showed that toxigenicity as measured by the CHO assay was strongly associated with strains isolated during acute diarrheal illness when compared with strains isolated in convalescence (p less than 10(-5)) or with strains from control infants without diarrhea (p less than 10(-5)). This study raises the possibility of an outbreak of disease caused by a transmissible plasmid responsible for a cholera-like enterotoxin production in several enteric bacterial strains.
The ability of 50 human amniotic fluid samples to inhibit the growth of Escherichia coli was measured with a new semimicro plate-count technique. A range from bacterial growth-sustaining fluid to bactericidal fluid was observed. When the inhibitory capacities of the fluid samples were correlated with gestational age, a progressive increase was obtained with maximum inhibitory capacity at 36 to 40 weeks. All fluid samples obtained before 20 weeks' gestation were capable of supporting bacterial growth. Fluid samples of 36 to 40 weeks' gestation were all bactericidal or bacteriostatic. More variability in inhibitory capacity was seen after 40 weeks, with an over-all loss of inhibition observed.
Bacterial growth inhibition in amniotic fluid is associated with a compound or class of compounds which resembles antibacterial cationic peptides. The inhibitor studied in amniotic fluid is sensitive to treatment with monobasic and dibasic potassium phosphate, and the inhibitory activity of amniotic fluid is lost following adsorption onto bentomite. The inhibitory component in amniotic fluid interacts with bacterial cells by adsorption or is internalized by viable cells only. The inhibitory quality of amniotic fluid is not destroyed by heating to 100 degrees C. for 15 minutes, and this heat-stable inhibitory activity is associated with the compound or compounds which are phosphate sensitive. A possible mode of antibacterial action which is consistent with the data presented is discussed.