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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A direct antimicrobial susceptibility test and a direct identification of positive blood culture broths for gram-negative rods confirmed with Gram stain by using a new instrument, Cobas-Bact, were compared with the conventional Kirby-Bauer agar diffusion disk method and with the in-house set of identification or API 20E, respectively. The bacterial pellet of centrifuged positive blood culture broth was used to inoculate a Cobas-Bact susceptibility and identification rotor. Bacteria from 206 cases of monomicrobial septicemia due to members of the family Enterobacteriaceae were tested. In 198 episodes (96%), direct identification and antimicrobial susceptibility testing results were obtained for the same bacterial pathogen within 5 h of detection. Of 204 direct identifications obtained, 177 (86.6%) were "high-confidence" correct identifications (percentage of likelihood [P] greater than or equal to 80%) and 25 (12.5%) "low-confidence" correct identifications (P less than 80%), whereas only 2 misidentifications occurred (1 Escherichia coli and 1 Proteus mirabilis). Direct susceptibility testing was performed in 199 episodes (96%), providing 1,885 antibiotic-microorganism combinations. Full agreement reached 86.3%, and essential agreement reached 92.8%. Minor discrepancies were found in 120 (6.5%) of the tests, major discrepancies were found in 127 (6.8%) tests, and very major discrepancies were found in only 7 (0.4%) tests. Subsequent MIC determinations in cases of major or very major discrepancies reduced the number of major discrepancies involving cephalosporins from 60 to 16, whereas all those involving aminoglycosides remained. Overall, this direct and rapid Cobas-Bact identification and susceptibility testing procedure offered accurate information with 5 to 6 h after the laboratory detection of bacteremia and septicemia due to members of the Enterobacteriacease.
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PMID:Evaluation of the Cobas-Bact system for direct and rapid identification and antimicrobial susceptibility testing of gram-negative rods from positive blood culture broths. 264 13

Burn wound sepsis can be due to exogenous or endogenous bacteria. When rare organisms cause infection, exogenous sources are implicated. This sets into motion hospital infection control team searches, which are both exhausting and harassing to patients and staff. This study examines the skin bacteria present at admission and the frequency of endogenous infection in burn patients. Sixty-two patients with burns up to 92% of the total body surface area underwent unburned skin bacterial surveillance on admission and at weekly intervals using RODAC contact plates. Burn wounds were biopsied for quantitative and qualitative analyses. Morphologically dissimilar colonies were isolated and identified using standard gram-positive and gram-negative identification strips (Analytab Products, Inc. [API]). On admission, the patients harbored Staphylococcus species, many of which were burn wound sepsis were infected with the same organisms cultured from their unburned skin on admission. A subset of patients (14) grew methicillin-resistant Staphylococcus aureus from their wounds or other sites. A comparison with admission isolates showed identical susceptibilities. These data suggest skin is an endogenous source of infection in the burned patient.
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PMID:The effect of endogenous skin bacteria on burn wound infection. 276 60

Production of cytotoxin and enterotoxin by Aeromonas strains obtained from stools of 50 children in Mexico and Texas and from blood of 9 children with sepsis was determined. Results were correlated with clinical features of infected children as well as with biochemical traits of Aeromonas strains. Cytotoxin was produced by 40 of 42 Aeromonas strains (95%) isolated from stools of children with diarrhea, by all 8 isolates from stools of well children, and by all 9 isolates from children with sepsis. There was no difference in the quantities (amount of cytotoxin per milligram of protein required to kill 50% of the cells) of cytotoxin produced and in clinical manifestations among the groups. None of the isolates produced a toxin that could be neutralized by antiserum raised against Shiga toxin produced by Shigella dysenteriae 1 60R. Heat-labile-like enterotoxin (LT) was produced by 26 of 42 stool isolates (62%), while only 1 of the 42 isolates (2%) produced enterotoxinlike activity in suckling mice; 65% of the cytotoxin-producing strains also produced an LT-like material. All strains from blood produced LT-like material, and 2 of 6 (33%) produced activity in suckling mice. All strains produced hemolysin; 37 of 57 (65%) were Voges-Proskauer positive; 27 of 57 (47%) were lysine decarboxylase positive by API 20E strips, none were positive for lysine decarboxylose production by lysin-iron agar slants at 24 h, but 17 of 54 (31%) were positive at 48 h. There was no correlation between biochemical reactions and enterotoxin or cytotoxin production. There appears to be no correlation between toxin production by Aeromonas spp. and gastroenteritis.
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PMID:Clinical and biochemical significance of toxin production by Aeromonas hydrophila. 358 26

During an 18-month period we identified two cases of septicemia and 24 examples of colonization of humans by Klebsiella trevisanii. Organisms were identified using the API 20EC and API 147 assimilation galleries. Of 147 clinical isolates initially identified as K. oxytoca, 18% were found to be K. trevisanii. Tracheal aspirate was the most common source of the organism. An extensive environmental sampling survey in the rooms of 12 colonized patients revealed a possible reservoir of the organism only once (a face cloth).
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PMID:Nosocomial infection and colonization by Klebsiella trevisanii. 371 Dec 81

On occasion, a patient may have two or more clinical cultures yielding a coagulase-negative staphylococcus If these multiple isolates have the same phenotype, one might conclude that the same strain was reisolated from the patient, indicating its persistent and pathological presence. We examined the validity of this conclusion when we applied a number of characterizing systems to a collection of 143 isolates of coagulase-negative staphylococci collected during an outbreak of intravascular catheter-associated sepsis. The probability of classifying two random isolates as the same phenotype or species was as follows: P = 0.356 for phage typing, P = 0.348 for Baird-Parker biotyping, P = 0.346 for the API STAPH-IDENT (Analytab Products) system, P = 0.327 for Bentley et al. biotyping, and P = 0.077 for antimicrobial susceptibility patterns. Although antimicrobial susceptibility patterns had the lowest probability, a variability in test results of 7.7% and a tendency for strains to have similar antibiograms effectively raised the probability to P = 0.897. The combination of the API STAPH-IDENT with antibiograms resulted in a probability of P = 0.037 to P = 0.147. When all of the above methods were used together a probability of P = 0.014 was achieved. Five patients had isolates from two or more blood cultures spaced more than 1 day apart that were identical by all of the above criteria, thus confirming prolonged bacteremia. The collection was also examined for the incidence of slime production. Slime production was not associated with any of the above groups, but was associated with symptomatic infections (P less than 0.05) and gentamicin resistance (P less than 0.01). Slime production was strain stable and was of assistance in typing strains of coagulase-negative staphylococci.
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PMID:Characterization of clinically significant strains of coagulase-negative staphylococci. 631 70

We first noted the appearance of thymidine-requiring, gram-negative bacilli in clinical specimens 2 years ago. Since then we have seen 10 patients colonized or infected with these organisms. These strains do not grow on Mueller-Hinton media, growth on MacConkey agar is variable, and growth in API 20E (Analytab Products) and Enterobacteriaceae-Plus Cards (AutoMicrobic system; Vitek Systems Inc.) is inadequate for reliable identifications. Thymidine-requiring organisms are routinely resistant to sulfonamides and trimethoprim. Infection or colonization is associated with previous sulfamethoxazole-trimethoprim therapy in most cases. Of 10 patients, 1 had septicemia of urinary tract origin, 5 had urinary tract colonization or infection, 2 had wound colonization, and two had colonization of respiratory secretions. Thymidine-requiring, gram-negative bacilli can be pathogens and present potential problems in diagnosis, identification, and susceptibility testing.
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PMID:Infection caused by thymidine-requiring, trimethoprim-resistant bacteria. 660 70

Corynebacterium species that are normally abundant on the skin and mucous membranes rarely cause infections and are susceptible to most antibiotics. The report in 1976 of four cases of sepsis at the National Institutes of Health caused by a hitherto undescribed corynebacterium that is highly antibiotic resistant, but uniformly susceptible to vancomycin, alerted the medically oriented scientific community to the emergence of these organisms as a possible new cause of nosocomial infections. Although we have always performed antibiotic susceptibility tests on all microorganisms recovered from normally sterile body fluids, our first recovery of these organisms was in August 1977. Since then we have recovered 52 such strains from 39 patients, most frequently from the rectum, followed by the groin, blood, lesions and urine in order of predominance. Characterization by API 50 L strips revealed that most, but not all strains resemble the JK group of Riley et al. [1]. Cell wall studies and DNA base ratios further confirmed their status as corynebacteria. Hospital acquisition has been proved; cross infection between patients is the most likely mode of spread. Their recognition is necessary for optimal preventive and therapeutic care of patients with compromised host defenses.
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PMID:The emergence of coryneform bacteria as a cause of nosocomial infections in compromised hosts. 721 98

This study assessed the hepatic acute phase response and cellular Ca2+ regulation in septic animals and in hepatoma cell lines in vitro. Sepsis was induced in male Sprague-Dawley rats by implanting in their abdominal cavities fecal pellets impregnated with live Escherichia coli and Bacteroides fragilis. 8 h after implantations, rats were treated with diltiazem (1.2 mg/kg) or superoxide dismutase (SOD) (5 x 10(3) units/kg). After 24 h, plasma acute phase proteins (APP) were determined by immunoelectrophoresis, and hepatic APP-mRNAs by Northern blot hybridization. Effects of diltiazem, verapamil, or SOD on hepatic cells were determined in rat Reuber H-35 and human HepG2 hepatoma cells. Sepsis induced a significant increase in plasma APP and their hepatic mRNAs. Diltiazem and SOD reduced the sepsis-induced elevations in plasma lactate, the febrile response and mortality. APP expression in H-35 and HepG2 cells, stimulated by interleukin 1 (IL-1), IL-6, and dexamethasone, was inhibited by diltiazem or verapamil but not SOD. The results suggest that a heightened hepatic APP response in septic animals accompanies systemic/metabolic derangements and a significant animal mortality. Because diltiazem was previously shown to prevent sepsis-related disturbances in hepatic cellular Ca2+ regulation, its mediation of decrease in APP, systemic/metabolic response, and mortality may be effected through modifications in cellular Ca2+ regulation. The data from hepatoma cells show an attenuation of the AAP can result from direct effects of a calcium blocker. However, whether the blocker primarily modifies cellular Ca2+ regulation and secondarily effects APP gene expression, or directly effects gene expression remains unknown.
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PMID:Diltiazem and superoxide dismutase modulate hepatic acute phase response in gram-negative sepsis. 753 32

Bacterial translocation and the development of sepsis after small bowel transplantation may be promoted by immunological damage to the intestinal mucosa or by quantitative and qualitative changes in intestinal microflora. This study assessed the effects of rejection, graft-versus-host disease (GVHD) and immunosuppression on intestinal microflora and bacterial translocation after heterotopic rat small bowel transplantation. Isografts, allografts with and without CsA immunosuppression, and the semi-allogeneic parent to the F1 hybrid GVHD model were studied. Intestinal microflora in graft and host loops and bacterial translocation to host organs and the graft mesenteric lymph node were determined. Bacterial colonies were counted and individual colonies identified using API 20E nutrient and fermentation indicator techniques. Colony counts in isografts and allografts were significantly higher than in the native intestine, whereas there was a massive overgrowth in the native intestine in the GVHD group. The species profile for the host and graft loops was similar in animals that had received isografts, allografted animals receiving CsA, and animals undergoing GVHD. However, there was a large increase in Staphylococcus epidermidis in animals with rejection. Bacterial translocation was not detected in isografted animals, but was observed in all other animal groups, with S. epidermidis being the most prevalent organism. These findings demonstrate that rejection and GVHD are associated with shifts in intestinal microflora toward potentially pathogenic organisms and that bacterial translocation into recipient tissues poses a major threat for the development of sepsis.
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PMID:The effect of rejection and graft-versus-host disease on small intestinal microflora and bacterial translocation after rat small bowel transplantation. 824 2

Septicaemia caused by Acinetobacter occurred in six infants in the neonatal unit. A total of 18 acinetobacters were isolated from blood cultures, cultures of intravascular catheters, and surveillance cultures. Twelve isolates from the six affected infants were identified as Acinetobacter junii by the use of a novel method, amplified ribosomal DNA restriction analysis (ARDRA). Typing of the organisms using the biochemical profiles of the API 20NE system, antibiogram typing, cell envelope protein electrophoresis, and PCR fingerprinting with two primer sets, ERIC1/ERIC2 and ERIC2/ 1026, showed that these 12 isolates were indistinguishable, whereas the remaining six isolates were different. The six infants recovered after therapy with ciprofloxacin alone in five cases and with a combination of ciprofloxacin and gentamicin in one case. This study showed that A. junii is capable of causing a serious, though non-fatal infection in neonates. The combined use of genotypic and phenotypic methods allowed the rapid separation of epidemic from non-epidemic isolates. It is concluded that for a better understanding of the role of the various Acinetobacter genomic species in human pathology, identification of acinetobacters according to the recent taxonomy is imperative.
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PMID:Outbreak of septicaemia in neonates caused by Acinetobacter junii investigated by amplified ribosomal DNA restriction analysis (ARDRA) and four typing methods. 904 17


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