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)

Pseudomonas aeruginosa is thought to be one of the main species of bacteria producing infection in leukemic patients, especially in those with neutropenia. Although bacteremia is frequent, hematogenous spread causing secondary meningitis is rarely seen. The mortality rate is extremely high. This is believed to be the first report of a successfully treated secondary meningitis caused by Pseudomonas aeruginosa in an adult leukemic patient with a decreased neutrophil count. The patient was treated with intravenous Carbenicillin and gentamicin, and intrathecal gentamicin. The good clinical response was supported by a prompt return of the CSF to normal and by appropriate CSF antimicrobial concentration and bacteriostatic activity.
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PMID:Successful treatment of Pseudomonas meningitis and septicemia in a leukemic neutropenic adult. 80 43

We review the clinical and laboratory features of 79 children with 83 episodes of pneumococcal meningitis over a 26-year period. The onset of illness was often severe, with convulsions occurring in 31% of the patients. The mortality was 10.8% and all deaths occurred in patients younger than 1 year of age; the death rate has dropped from 19% in the 1948 to 1962 era to 3% from 1963 to 1973. The association of pneumonia with meningitis, the presence of hypoglycorrhachia, and an increased CSF protein concentration were associated with a poor prognosis; bacteremia and convulsions were also more common in the fetal cases. Neurologic sequelae including recurrent meningitis, deafness, hydrocephalus, convulsions, and retardation were present in 56% of the patients observed. Findings from EEGs did not correlate well with the clinical picture during the acute or convalescent stage of the illness. Despite accurate diagnosis, prompt therapy, and a decrease in the mortality in the past decade, pneumococcal meningitis in children is still often associated with a serious outcome.
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PMID:Pneumococcal meningitis in children. 88 97

Peripheral blood cells (PBC) can hasten hematopoietic recovery after high-dose chemotherapy. To determine if PBC apheresed after mobilization further enhance hematopoietic recovery over that achieved with autologous bone marrow (ABM) and recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF), 14 patients with metastatic solid tumors were supported by ABM and rhGM-CSF during the first course of high doses of cyclophosphamide, etoposide, and cisplatin (CVP) and 11 of these 14 patients by mobilized PBC with ABM and rhGM-CSF during the second CVP. Each patient served as his or her own control. Identical doses of CVP were administered in both courses: cyclophosphamide 5.25 g/m2, etoposide 1,200 mg/m2, and cisplatin 165 to 180 mg/m2. PBC were collected on day 10 after mobilization with cyclophosphamide (3 g/m2) intravenously (IV) on day 1, doxorubicin (50 mg/m2) as a continuous IV infusion over 48 hours starting day 2, and rhGM-CSF as a daily 4-hour IV infusion starting day 4 at 0.6 mg/m2 for 14 days. Comparing recovery in the 11 patients to receive two cycles of therapy, the median days to an absolute neutrophil count of 0.1 x 10(9)/L and 0.5 x 10(9)/L were not statistically significant between the two courses; neither was there a difference in the incidence of fever and bacteremia. The median number of days to platelet count of 0.02 x 10(12)/L unmaintained by platelet transfusion was 20 from marrow infusion for course 1 and 16 for course 2 (P = .059). The median number of days to a platelet count of 0.05 x 10(12)/L was significantly shortened: 24 and 19 days for courses 1 and 2, respectively (P = .045). Patients who received PBC required fewer number of platelet transfusions. Extramedullary toxicities were not different between the groups. Our finding of enhanced early recovery of platelets and reduced platelet transfusion requirement is in concordance with other studies.
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PMID:Influence of mobilized peripheral blood cells on the hematopoietic recovery by autologous marrow and recombinant human granulocyte-macrophage colony-stimulating factor after high-dose cyclophosphamide, etoposide, and cisplatin. 159 78

Modulation of the host's inflammatory response in bacterial meningitis may be beneficial. In this study, the effects of dexamethasone and HWA-138, an analog of pentoxifylline, on CSF cultures and cochlear inflammation in an infant rat model of Haemophilus influenzae type b were studied. Five-day-old infant rats were inoculated once intraperitoneally with 1 x 10(4) to 10 x 10(4) CFU of H. influenzae type b (strain 1406). Twenty-four hours later, infant rats were treated intraperitoneally with one dose of ampicillin (0.1 mg/g of body weight), cefotaxime (0.05 mg/g), or cefuroxime (0.05 mg/g) alone or in combination with one dose of dexamethasone (0.00015 mg/g) or HWA-138 (0.005 mg/g). Twenty-four hours after treatment with cefuroxime plus dexamethasone, animals had a significantly (P less than or equal to 0.04) greater incidence of bacteremia and meningitis (eight of nine animals) than that in animals of the other treatment groups. Overall, dexamethasone was associated with less inflammation (P less than 0.04) of the cochlear nerve compared with that from antibiotic treatment alone. In this model, when suboptimal antimicrobial therapy is administered, anti-inflammatory agents may be beneficial with respect to reducing cochlear inflammation. However, dexamethasone and cefuroxime lead to a higher rate of positive blood and cerebral spinal fluid cultures than cefuroxime alone.
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PMID:Effect of dexamethasone or HWA-138 in combination with antibiotics in experimental Haemophilus influenzae type b infection. 175 17

Sixteen patients with relapsed non-Hodgkin's lymphoma underwent autologous bone marrow transplantation and infusion of recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF). Treatment consisted of involved-field radiotherapy, cyclophosphamide 60 mg/kg/d intravenously (IV) for 2 days, and fractionated total body irradiation (1,200 cGy). Autologous bone marrow was thawed and infused IV, followed 3 hours later by the first infusion of IV rhGM-CSF 11 micrograms/kg/d over 4 hours. Infusions of rhGM-CSF were continued daily until either both neutrophil count exceeded 1,500/microL and platelet count exceeded 50,000/microL, or until 30 days after marrow re-infusion. Toxicities encountered were mild and included fever, chills, hypertension, alopecia, rash, diarrhea, stomatitis, myalgias, and synovial (knee) effusions. Neutrophil recovery greater than 500/microL occurred a median of 14 days (range, 9 to 30 days) after marrow infusion, significantly earlier than in a comparable group of historic controls who recovered counts at a median time of 20 days (range, 12 to 51 days) (P = .00002). Median time to self-sustaining platelet counts greater than 20,000/microL was 23.5 days (range, 12 to 100 days), comparable with the historic group (P = .38). One bacteremia (central venous catheter exit site infection with Staphylococcus epidermidis) and one local infection (Giardia lamblia in stool) occurred. Patients received a median of 11.4 (range, 4.4 to 20.2) x 10(4) colony-forming unit granulocyte-macrophage (CFU-GM) progenitors per kg. Stem cell progenitors CFU-GM, CFU-granulocyte, erythroid, monocyte, megakaryocyte (CFU-GEMM), and burst-forming unit-erythroid (BFU-E) were detected in the bone marrow as early as 7 days after marrow re-infusion, and increased in proportion to peripheral blood counts, but by 30 to 60 days still remained much lower than before transplant. Neutrophils transiently decreased in 13 of 16 patients (median decrease, 42%) within 24 to 72 hours of discontinuing rhGM-CSF infusions. These data suggest that rhGM-CSF therapy enhances neutrophil recovery by forcing stem cells to produce mature elements at an enhanced rate but may not affect marrow stem cell and early progenitor population sizes.
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PMID:Recombinant granulocyte-macrophage colony-stimulating factor after autologous bone marrow transplantation for relapsed non-Hodgkin's lymphoma: blood and bone marrow progenitor growth studies. A phase II Eastern Cooperative Oncology Group Trial. 185 94

Organisms belonging to the Mycobacterium avium complex (MAC) are associated with life-threatening bacteremia in patients with the acquired immunodeficiency syndrome (AIDS). As these organisms survive within macrophages, we examined the ability of recombinant human granulocyte-monocyte colony-stimulating factor (GM-CSF) to activate human monocyte-derived macrophages to inhibit the intracellular growth or kill the most mouse-virulent MAC strain in our collection that belongs to serotype 1. While unstimulated cells did not inhibit intracellular growth of MAC, macrophages activated by GM-CSF (10-10(4) U/ml) inhibited or killed up to 58 +/- 5% of the initial inoculum. This activation was dose-dependent, with maximal change occurring with a dose of 100 U/ml after 72 hr exposure. Inhibition or killing was demonstrated if GM-CSF was given both before or after establishment of infection. The combination of GM-CSF (10(2) U/ml) plus TNF (10(2) U/ml) augmented macrophage killing (range, 31 +/- 4%) compared with GM-CSF (10(2) U/ml) alone, but the combination of recombinant human interferon-gamma (IFN gamma) plus GM-CSF resulted in a significant decrease in intracellular inhibition of growth or killing (13.3 +/- 2%) compared with 57.7 +/- 5% obtained with GM-CSF alone. These results indicate that: 1) GM-CSF can activate macrophages to inhibit intracellular growth or kill MAC; 2) killing may be augmented by TNF; and 3) IFN gamma may impair GM-CSF-dependent macrophage activation.
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PMID:Recombinant granulocyte-macrophage colony-stimulating factor activates human macrophages to inhibit growth or kill Mycobacterium avium complex. 211 63

In the former report, the bacterial portal of entry in experimental mice with bacteremia were analysed in detail. And it was clarified that almost all of the isolates from blood of cyclophosphamide (CY) and antibiotics treated mice were entered by their own flora, especially by their faecal flora. From this point of view, great care must be taken when using antibiotics for immunosuppressed patients, because it easily causes a super-infection, that is one of the most important factors of endogenous infections. In order to potentiate host immunity, we examined the preventative effect of biological response modifiers (BRM) to experimental endogenous septicemia. MDP-Lys (L18), rhG-CSF, and rhIL-1 were effective on experimental Pseudomonas aeruginosa endogenous septicemia of mice. The effect did not depend on the increased number of total leukocytes and PMN. Further experiments using nude mice suggested that the host defence mechanism inhibiting Pseudomonas endogenous infection might not depend on T-cell mediated immunity.
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PMID:[Etiology of sepsis occurring in the immunocompromised host and its prevention. 2. Preventive effect of BRM to experimental Pseudomonas endogenous septicemia and analysis of its immunological etiology]. 261 93

We evaluated fever in 342 hospitalized infants less than 8 weeks of age. Sixteen infants (5%) had bacteremia or bacterial meningitis. Fifty-two percent of the infants were admitted during the months of July through September. We found no significant relationship between season, sex, height of fever, or erythrocyte sedimentation rate and the recovery of bacteria from the blood or CSF. A WBC less than or equal to 5,000/cu mm or a ratio of immature to total neutrophils greater than or equal to 20% correlated significantly with bacteremia or bacterial meningitis, though the sensitivities of these tests were unacceptably low. Prospectively, of 61 infants whose clinical appearance did not suggest sepsis, none had bacterial pathogens in the blood or CSF, whereas four of 36 infants with a septic appearance did have pathogens. Recent investigations support the initial clinical impression as important in assessing these febrile infants. We found that bacteremia is more likely to occur in infants less than 4 weeks of age (8%) than in the older infants (2.9%).
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PMID:Evaluation of fever in infants less than 8 weeks old. 330 62

Two children in a day care facility developed Haemophilus influenzae type b meningitis. The second child was enrolled in the facility after rifampin had been administered to the other attendees. The isolate from the first child was susceptible to rifampin, but the isolate from the second was resistant. Both isolates had identical outer membrane protein PAGE profiles. To investigate the virulence of these isolates, we inoculated infant rats intranasally with either the rifampin-resistant or rifampin-susceptible CSF isolate. The rates of nasal colonization (14 of 20 and eight of eight animals inoculated with the rifampin-resistant and rifampin-susceptible isolates, respectively) did not differ significantly. However, bacteremia occurred less frequently in pups inoculated with the rifampin-resistant strain than in animals inoculated with the susceptible strain (four of 20 vs eight of eight, P less than 0.0001). Nasal washings, blood, and CSF obtained from animals inoculated with the rifampin-resistant isolate were divided and plated on media containing rifampin (1 microgram/ml) or without rifampin. Except for those from one animal, organisms isolated from blood and CSF grew only on medium lacking rifampin, whereas H. influenzae type b growing from nasal washings was frequently found on both media. We conclude that mutation of H. influenzae to rifampin resistance is a hazard of rifampin chemoprophylaxis. Rifampin-resistant isolates have the potential to cause disease in patients and experimental animals, although they may be relatively less pathogenic than the parent, susceptible organism.
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PMID:Pathogenicity of a rifampin-resistant cerebrospinal fluid isolate of Haemophilus influenzae type b. 348 83

In a multicenter randomized trial, 107 children with bacterial meningitis were initially given either cefuroxime or ampicillin plus chloramphenicol. Patients were alternately assigned to 7- or 10-day courses of the designated antimicrobial regimen. CSF isolates included Haemophilus influenzae type b (89, of which 25% were beta-lactamase positive), Streptococcus pneumoniae, and Neisseria meningitidis. Although mean CSF bactericidal titers against Haemophilus isolates were 1:6 in each treatment group, H. influenzae was cultured from CSF in four of 39 patients receiving cefuroxime, 24 to 48 hours after initiation of therapy, compared with none of 40 patients given ampicillin plus chloramphenicol (P = 0.11). Clinical cure rates were similar (95%); one death occurred in each group. One child given cefuroxime had persistent meningitis after 5 days of therapy, and mastoiditis with secondary bacteremia developed in one on day 10. Three patients had relapse or reinfection. One patient who received cefuroxime for 10 days had a relapse of epiglottitis 17 days later, and of the patients given ampicillin plus chloramphenicol, one had a relapse of meningitis 1 week after 7 days of therapy, and bacteremia developed in one 42 days after completion of 10 days of therapy. No increase in either in-hospital complications or relapses occurred with a 7-day treatment course. Proof of the equivalence of the antibiotic regimens and the efficacy of 7-day courses of treatment, as well as the consequences of delayed CSF sterilization, will require additional investigation.
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PMID:Cefuroxime versus ampicillin plus chloramphenicol in childhood bacterial meningitis: a multicenter randomized controlled trial. 352 32


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