Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004610 (bacteremia)
 13,199 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Liver changes and associated host responses were evaluated in four groups of male rats, weighing 300 +/- 20 gm., which received intravenous injection of 2.2 times 10(9) live Escherichia coli. This bolus was given either without additional treatment (group A) or prior to the following regimens: intramuscular injection of gentamicin sulfate, 5 mg. per kg. (group B); intravenous injection of methylprednisolone sodium succinate, 40 mg. per kg. (group C); and intramuscular injection of gentamicin immediately after methylprednisolone sodium succinate treatment (group D). Rats given injections of saline or methylprednisolone sodium succinate served as controls. Survival rates at 10 and 20 hours were 25 per cent and 4 per cent for group A; 44 per cent and 28 per cent for group B; 94 per cent and 70 per cent for group C; 98 per cent and 98 per cent for group D, respectively. In rats of groups A and B, killed at 1, 2, 4, and 6 hours, progressive liver changes included intravascular sequestration of rapidly degranulating leukocytes, fibrinous deposits, and platelet aggregates in sinusoids as well as in spaces of Disse adjacent to subendothelial collagen, and extensive Kupffer cell disruption in association with severe midzonal necrosis. These alterations were accompanied by progressive hypoglycemia and elevations of serum enzymes, glutamic pyruvic transaminase, lactate dehydrogenase, and glutamic oxaloacetic transaminase. Hematologic studies revealed that E. coli bacteremia results in rapid leukopenia and disseminated intravascular coagulation primarily due to activation of the intrinsic coagulation pathway. All above reactions were delayed and markedly reduced in rats treated with methylprednisolone sodium succinate. The results indicate that antibiotic treatment of lethal, Gram-negative bacteremia is effective only in conjunction with early steroid treatment. The protective effects of glucocorticoids on the liver microcirculation and polymorphonuclear leukocytes appear to play a basic role in preventing the early development of disseminated intravascular coagulation, hepatocellular necrosis, and associated major host responses, thereby attenuating lethality of gram-negative septic shock.
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PMID:Glucocorticoid and antibiotic effects on hepatic microcirculation and associated host responses in lethal gram-negative bacteremia. 36 36

One hundred and ninety-one triple lumen central venous catheters were placed into 107 sites in 81 surgical and trauma patients who were prospectively studied to determine the rate of catheter related infection using a subcutaneous cuff of biodegradable collagen containing bactericidal silver and a guide wire exchange protocol. Thirty-seven sites in 36 nonseptic patients (group 1) were compared with 70 sites in 45 septic patients (group 2). The data were also compared with data consecutively collected one year earlier, using the same exchange protocol without the cuff. Fourteen of 70 sites in group 2 had catheter related infections, with seven causing bloodstream infection. Five of 14 were the result of fungus, with three causing fungemia. Two of 37 sites in group 1 had catheter related infections (p = 0.044), with no associated bacteremia. The number of triple lumen catheter related infections and associated bacteremia or fungemia are higher in septic patients compared with nonseptic critically ill surgical and trauma patients. The cuff significantly prolongs time of catheter site use in patients who are nonseptic, but may be of no benefit in reducing infection rates or prolonging site use time in patients who are septic and may predispose to fungal colonization.
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PMID:The influence of an attachable subcutaneous cuff for preventing triple lumen catheter infections in critically ill surgical and trauma patients. 162 Nov 97

Collagen binding was examined in 90 strains of Staphylococcus aureus derived from patient samples. Slightly under one-half (39 of 90) of the S. aureus strains bound collagen. Collagen binding in S. aureus did not correlate with either immunoglobulin G or fibronectin binding by these organisms. Chi-square analysis of isolates obtained from patients with complicated bacteremia (bacteremia associated with deep tissue infection) compared with isolates from patients with uncomplicated bacteremia (bacteremia without other infection) showed that the former strains were significantly more likely to have collagen-binding ability. Subcloning of primary isolates from patients with bacteremia showed that all clones from individual patients were either all positive for collagen binding or all negative, suggesting a common clonal origin for this characteristic. The ability to bind collagen could not be induced in strains lacking collagen affinity by repeated subculture in media supplemented with collagen.
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PMID:Collagen binding in clinical isolates of Staphylococcus aureus. 342 18

Cultured endothelial cells phagocytize Staphylococcus aureus, but the resultant effects are unknown. Monolayers of cultured bovine endothelial cells with or without [3H]adenine label were exposed to 100, 10, or 1 S. aureus organism per endothelial cell for 3.5 h. Lysostaphin was then applied to all cultures to destroy extracellular but not phagocytized S. aureus. In cultures treated for only 20 min with lysostaphin, S. aureus multiplied exponentially after a 9- to 12-h lag period. In cultures treated continuously with lysostaphin, numbers of S. aureus remained constant or decreased. These results indicate that S. aureus became extracellular and multiplied but did not multiply intracellularly. In parallel experiments, the release of 3H-adenine from prelabeled endothelial cell monolayers was assayed to indicate cytotoxicity. Results indicated that the loss of 3H-adenine from endothelial cell monolayers depended on the following: (i) the size of the S. aureus inoculum, (ii) the strain of S. aureus, and (iii) the length of time after exposure to S. aureus. S. aureus endocarditis and persistent septicemia could arise, at least in part, from ingestion of S. aureus by host endothelium. The intracellular location would afford S. aureus protection from host defenses and antibiotics. Eventual damage to endothelial cells could expose collagen, thus resulting in platelet adherence and vegetation formation. Intracellular S. aureus would be continuously released into the circulation, possibly accounting for the persistent bacteremia that is found in S. aureus endovascular infections.
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PMID:Ingestion of Staphylococcus aureus by bovine endothelial cells results in time- and inoculum-dependent damage to endothelial cell monolayers. 362 96

Intravenous infusion of live. E. coli bacteria in cats did not induce microscopic damage to the gastric mucosa within 3 hours. However, if the cats before the induction of bacteremia were given 80 mM HCl and 0.6 ml gallbladder bile/kg b.w. microscopic mucosal damage developed regularly in the corpus-fundus area of the stomach. The gastric mucosal damage was not associated with significant decrease of total gastric blood flow as measured continuously electromagnetically or decreased gastric mucosal blood flow measured early and late during sepsis using radioactively labelled microspheres. Neither was the development of gastric mucosal damage associated with reduced gastric wall collagen concentration nor in RNA, DNA concentrations or RNA/DNA ratio in the gastric mucosa.
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PMID:Acute gastric mucosal ulceration in septic shock. An experimental study on pathogenic mechanisms. 608 89

Human C1q displayed a dose-dependent protection of gonococcal cells (GC) from the bactericidal effect of newborn rat serum. All rat pups injected with C1q-preincubated GC developed bacteremia, while none of the animals injected with GC only were infected. After clearance of bacteremia at day 6, live GC could still be recovered from tested organs, including the liver. Preincubation of GC with higher concentrations of C1q was associated with increased morbidity. In contrast to human serum as a source of C1q, rat, rabbit, and mouse sera did not increase the in vivo virulence of Neisseria gonorrhoeae. C1q-deficient human serum, heat-inactivated C1q or human serum, type IV collagen, and complement C3 were inefficient in inducing infection. Experimental infection by C1q-preincubated GC was inhibited by anti-C1q antibodies in a dose-dependent fashion, demonstrating a causal effect of C1q function. This report demonstrates the novel finding that human C1q, a component of the human immune system with a general function for elimination of infection, may increase GC virulence and result in the development of disseminated infection in a nonhuman host.
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PMID:Gonococcal infection in a nonhuman host is determined by human complement C1q. 759 Nov 37

The present study explored in adults suffering from recurrent tonsillitis the association between macroscopic oropharyngeal signs of recurrent inflammation, immunomorphology of palatine tonsils (counts of neutrophils by CD4 and macrophages by CD68 monoclonal antibodies in tonsillar microcompartments) and the occurrence of post-tonsillectomy bacteremia. The study involved 50 adults (31 females and 19 males) with recurrent tonsillitis. According to predominance of either inflammatory changes or evidence of sclerotic process in palatine tonsils and surrounding tissue macroscopic at oropharyngeal examination, the patients were divided into groups with 'inflammatory-type' and 'sclerotic-type' tonsils. Biochemically detected mean collagen content was significantly higher in 'sclerotic-type' tonsils than in 'inflammatory-type' tonsils (p=0.001). Post-tonsillectomy bacteremia was found in 22 patients (44%). A noteworthy finding was the higher recovery of anaerobes from blood cultures than in previous studies. A logistic regression analysis revealed that the post-tonsillectomy bacteremia was strongly associated with 'sclerotic-type' tonsils (p=0.0015) and with low counts of neutrophils in tonsillar tissue (p=0.047). We conclude that macroscopic oropharyngeal signs of sclerotic process in palatine tonsils indicate impaired tonsillar defense, in terms of lowered counts of neutrophils, increasing the risk of post-tonsillectomy bacteremia.
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PMID:Macroscopic oropharyngeal signs indicating impaired defensive function of palatine tonsils in adults suffering from recurrent tonsillitis. 1523 39

Comparative genomics were used to assess genetic differences between Staphylococcus aureus strains derived from infected animals versus colonized or infected humans. A total of 77 veterinary isolates were genetically characterized by high-throughput amplified fragment length polymorphism (AFLP). Bacterial genotypes were introduced in a large AFLP database containing similar information for 1,056 human S. aureus strains. All S. aureus strains isolated from animals in close contact with humans (e.g., pet animals) were predominantly classified in one of the five main clusters of the AFLP database (cluster I). In essence, mastitis-associated strains from animals were categorized separately (cluster IVa) and cosegregated with bacteremia-associated strains from humans. Distribution of only 2 out of 10 different virulence genes differed across the clusters. The gene encoding the toxic shock syndrome protein (tst) was more often encountered among veterinary strains (P < 0.0001) and even more in the mastitis-related strains (P<0.0001) compared to human isolate results. The gene encoding the collagen binding protein (cna) was rarely detected among invasive human strains. The virulence potential, as indicated by the number of virulence genes per strain, did not differ significantly between the human- and animal-related strains. Our data show that invasive infections in pets and humans are usually due to S. aureus strains with the same genetic background. Mastitis-associated S. aureus isolated in diverse farm animal species form a distinct genetic cluster, characterized by an overrepresentation of the toxic shock syndrome toxin superantigen-encoding gene.
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PMID:Host- and tissue-specific pathogenic traits of Staphylococcus aureus. 1596 69

Streptococcus mutans is generally known as a pathogen of dental caries, and it is also considered to cause bacteremia and infective endocarditis (IE). S. mutans was previously classified into 3 serotypes, c, e, and f, due to the different chemical compositions of the serotype-specific polysaccharides, which are composed of a rhamnose backbone and glucose side chains. We recently designated non-c/e/f serotype S. mutans strains as novel serotype k, which is characterized by a drastic reduction in the amount of the glucose side chain. A common biological feature of novel serotype-k strains is a lower level of cariogenicity due to alterations of several major cell surface protein antigens. As for virulence in blood, these strains survive in blood for a longer duration due to lower antigenicity, while the detection rate of all strains carrying the gene encoding collagen-binding adhesin has been shown to be high. Furthermore, molecular biological analyses of infected heart valve specimens obtained from IE patients revealed a high detection rate of serotype-k S. mutans. Together, these findings suggest that serotype-k S. mutans strains show low cariogenicity but high virulence in blood as compared to the other serotypes, due to alterations of several cell surface structures.
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PMID:Roles of oral bacteria in cardiovascular diseases--from molecular mechanisms to clinical cases: Cell-surface structures of novel serotype k Streptococcus mutans strains and their correlation to virulence. 2050 65

Bacterial pathogens commonly show intra-species variation in virulence factor expression and often this correlates with pathogenic potential. The group A Streptococcus (GAS) produces a small regulatory RNA (sRNA), FasX, which regulates the expression of pili and the thrombolytic agent streptokinase. As GAS serotypes are polymorphic regarding (a) FasX abundance, (b) the fibronectin, collagen, T-antigen (FCT) region of the genome, which contains the pilus genes (nine different FCT-types), and (c) the streptokinase-encoding gene (ska) sequence (two different alleles), we sought to test whether FasX regulates pilus and streptokinase expression in a serotype-specific manner. Parental, fasX mutant and complemented derivatives of serotype M1 (ska-2, FCT-2), M2 (ska-1, FCT-6), M6 (ska-2, FCT-1) and M28 (ska-1, FCT-4) isolates were compared. While FasX reduced pilus expression in each serotype, the molecular basis differed, as FasX bound, and inhibited the translation of, different FCT-region mRNAs. FasX enhanced streptokinase expression in each serotype, although the degree of regulation varied. Finally, we established that the regulation afforded by FasX enhances GAS virulence, assessed by a model of bacteremia using human plasminogen-expressing mice. Our data are the first to identify and characterize serotype-specific regulation by an sRNA in GAS, and to show an sRNA directly contributes to GAS virulence.
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PMID:The small regulatory RNA FasX enhances group A Streptococcus virulence and inhibits pilus expression via serotype-specific targets. 2558 84


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