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A hypothesis is proposed, arguing that gentamicin administration in a single daily dose results in higher peak tissue concentration, marked bacteriolysis with endotoxin (ET) release and consequent ET-mediated febrile host responses, which resemble Jarisch-Herxheimer reactions.
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Genetic diversity and relationships among 108 isolates of the bacterium Streptococcus pyogenes recently recovered from patients in the United States with toxic-shock-like syndrome or other invasive diseases were estimated by multilocus enzyme electrophoresis. Thirty-three electrophoretic types (ETs), representing distinctive multilocus clonal genotypes, were identified, but nearly half the disease episodes, including more than two-thirds of the cases of toxic-shock-like syndrome, were caused by strains of two related clones (ET 1 and ET 2). These two clones were also represented by recent pathogenic European isolates. A previous report of a relatively high frequency of expression of exotoxin A among isolates recovered from toxic-shock-like syndrome patients in the United States was confirmed; and the demonstration of this association both within clones and among distantly related clones supports the hypothesis that exotoxin A is a causal factor in pathogenesis of this disease. Near identity of the nucleotide sequences of the exotoxin A structural gene of six isolates of five ETs in diverse phylogenetic lineages was interpreted as evidence that the gene has been horizontally distributed among clones, presumably by bacteriophage-mediated transfer.
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The typical febrile response of normal rabbits given bacterial endotoxin intravenously may be modified by prior administration of plasma or, less effectively, serum of endotoxin-tolerant donors. This altered response is characterized by disappearance of the second rise in fever and by a striking reduction in fever index. It thus resembles the course of fever shown by rabbits made tolerant to endotoxin by one or more previous daily doses. This transfer of tolerance by plasma or serum depends critically upon the manner in which tolerance is induced in the donors. The plasma of donor rabbits made tolerant, then given an RES-blocking dose of carbon, still confers tolerance upon normal recipient rabbits. Such donors have lost their tolerance and are highly sensitive to endotoxin at the time their blood is taken. The implications of these findings for endotoxin tolerance and for transfer of this phenomenon are discussed. The evidence is consistent with the hypothesis that both tolerance and its transfer are based upon RES function and are independent of antibody.
Analysis of 132 group A streptococcal (GAS) isolates from 151 invasive episodes, including streptococcal toxic shock syndrome (STSS), from 1983 to 1995 showed great genetic variation by use of T serotyping in combination with restriction fragment length polymorphism. In contrast, genetically homogenous T1M1 isolates appeared in epidemic patterns with significantly increased risk of STSS. The speA gene, with the allelic variants speA2 and speA3 carried by the T1M1 and T3M3 serotypes, respectively, was strongly associated with STSS. Infection with a GAS isolate carrying speA, alcohol abuse, and malignancy recently treated with cytostatic drugs were factors independently related to STSS. Neutralization of SpeA lymphocyte mitogenicity was totally absent in sera from patients with STSS and low in sera from persons with uncomplicated bacteremia compared with levels in sera from uncomplicated erysipelas. Neutralization of SpeB was significantly lower in sera of patients with STSS than in sera from persons with bacteremia or erysipelas.
OBJECTIVE: An epidemiological investigation was conducted to determine risk factors for adverse reactions among patients in hospitals and the possibility of extrinsic or intrinsic contamination of intravenous solutions. DESIGN: A retrospective cohort study was conducted to identify solutions associated with adverse reactions. Implicated lots were cultured for bacteria, and endotoxin concentrations were measured. SETTING: Five hospitals in the state of Pernambuco, Brazil, were investigated from February through March 2002. PATIENTS: Surgical inpatients or outpatients receiving intravenous solutions during the study period. RESULTS: Of 355 surgical patients or outpatients treated at hospitals, 28 (8%) developed illness within a mean of 2.5 hours after exposure to intravenous solutions implicated in adverse reactions; 5 (17.9%) of the case patients died. Laboratory testing of bottles from the lots of Ringer's lactate solution implicated in deaths demonstrated a high mean endotoxin concentration of 88.3 endotoxin units (EU)/mL (range, 9.7-298.0 EU/mL), compared with the permitted limit in Brazil of <0.5 EU/mL. Testing of metronidazole implicated in adverse reactions at another hospital and produced by the same company that manufactured the lots Ringer's lactate solution also showed high endotoxin concentrations (mean level, 8.3 EU/mL [range, 5.0-58.3 EU/mL]). The outbreak was controlled after a national recall of the implicated brand of intravenous solutions. CONCLUSIONS: Case patient status was associated with use of Ringer's lactate solution and metronidazole from large bottles, both of which were produced by the same company. High endotoxin concentrations were demonstrated in unopened bottles of implicated products, which is consistent with intrinsic contamination. The high mortality rate may have been compounded by the fact that clinicians administered additional volumes of contaminated 0.9% isotonic sodium chloride solution in response to hypotension or bleeding to some surgical patients. No additional case patients were identified after a national recall of products, inspection, closure of the implicated company's manufacturing facility, and establishment of random quality-control testing of intravenous solutions.
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Circulating and ex vivo production of interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha, IL-6, and IL-1 receptor antagonist (ra) and the diagnostic utility of these cytokines were studied in 123 patients with fever of unknown origin (FUO). Diagnoses were infections, 28; neoplasms, 14; noninfectious inflammatory diseases (NIID), 32; miscellaneous diseases, 10; and none made, 39. IL-1beta, IL-6, and IL-1ra concentrations were higher in patients with infections, neoplasms, and NIID than in healthy controls. Patients with infections had higher concentrations of TNF-alpha than controls. The ex vivo production of IL-1beta and IL-1ra in all patients with FUO did not differ from that in controls; however, production of TNF-alpha was lower in patients with neoplasms and NIID, and IL-6 production was lower in patients with neoplasms. Thirty-five patients with fever did not have elevated cytokines. Although some significant differences were found among the diagnostic subgroups, there was wide variation. Thus, measurement of these cytokines does not aid in the diagnosis of FUO.
BACKGROUND: General anesthetics increase the sweating-to-vasoconstriction interthreshold range (temperatures not triggering thermoregulatory defenses), whereas fever is believed to only increase the setpoint (target core temperature). However, no data characterize thresholds (temperatures triggering thermoregulatory defenses) during combined anesthesia and fever. Most likely, the combination produces an expanded interthreshold range around an elevated setpoint. The authors therefore tested the hypothesis that thermoregulatory response thresholds during the combination of fever and anesthesia are simply the linear combination of the thresholds resulting from each intervention alone. METHODS: The authors studied eight healthy male volunteers. Fever was induced on the appropriate days by intravenous injection of 30 IU/g human recombinant interleukin 2 (IL-2), followed 2 h later by an additional 70 IU/g. General anesthesia consisted of desflurane 0.6 minimum alveolar concentration (MAC). The volunteers were randomly assigned to the following groups: (1) control (no desflurane, no IL-2); (2) IL-2 alone; (3) desflurane alone; and (4) desflurane plus IL-2. During the fever plateau, volunteers were warmed until sweating was observed and then cooled to vasoconstriction. Sweating was evaluated from a ventilated capsule and vasoconstriction was quantified by volume plethysmography. The tympanic membrane temperatures triggering significant sweating and vasoconstriction identified the respective response thresholds. Data are presented as the mean +/- SD; P < 0.05 was considered significant. RESULTS: The interthreshold range was near 0.40 degrees C on both the control day and during IL-2 administration alone. On the IL-2 alone day, however, the interthreshold range was shifted to higher temperatures. The interthreshold range increased significantly during desflurane anesthesia to 1.9+/-0.6 degrees C. The interthreshold range during the combination of desflurane and IL-2 was 1.2+/-0.6 degrees C, which was significantly greater than on the control and IL-2 alone days. However, it was also significantly less than during desflurane alone. CONCLUSION: The combination of desflurane and IL-2 caused less thermoregulatory inhibition than would be expected based on the effects of either treatment alone. Fever-induced activation of the sympathetic nervous system may contribute by compensating for a fraction of the anesthetic-induced thermoregulatory impairment.
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BACKGROUND: Acute glomerulonephritis can follow infection by group A streptococci. An immune-complex pathogenesis is accepted, but the causative antigen(s) is still controversial. In recent years, 2 streptococcal antigens, the cationic cysteine proteinase exotoxin B (SPE B) and the plasmin receptor, a glyceraldehyde phosphate dehydrogenase (Plr, GAPDH) have attracted attention because: (1) they were localized in glomeruli in patients with acute post-streptococcal glomerulonephritis (APSGN); and (2) serum antibody to these antigens was associated with nephritogenic streptococcal infections. To date, putative nephritogens were always tested independently. Here, the relevance of SPE B and GAPDH was evaluated in the same renal biopsies and serum samples of well-defined APSGN patients. METHODS: Renal biopsies (17 patients) and serum samples (53 patients) with APSGN and appropriate controls were examined. Immunofluorescent staining of frozen sections was performed using specific antibodies to SPE B and GAPDH. Serum antibodies were investigated by both enzyme-linked immunosorbent assay (ELISA) and Western blot methodology. RESULTS: Glomerular deposits of SPE B were demonstrated in 12/17 APSGN biopsies, and 2 cases were borderline; circulating antibodies were found in all instances (53/53 patients). Glomerular deposition of GAPDH was detected in 1/17 biopsies, and 2 cases were borderline; circulating antibodies were found in 5/47 patients. In 31 control biopsies, only weak staining for each antigen was found in 2 cases. CONCLUSION: In this study, glomerular deposits of and antibody response to zymogen/SPE B are more consistently present in APSGN than deposits and antibody response to GAPDH. Zymogen/SPE B is likely to be the major antigen involved in the pathogenesis of most cases of APSGN.
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