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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bacteremia due to Achromobacter xylosoxidans is rare, and little information on treatment is available. Between 1983 and 1988, A. xylosoxidans was recovered from 26 cultures of blood from 10 patients with cancer and clinical signs of infection, including one patient with septic shock and two with pneumonia. Neutropenia did not seem to be a predisposing factor. The infection may have been catheter related in four patients and associated with gastrointestinal pathology in four others. Probable cause was not determined in the remaining two. In vitro studies of susceptibility showed that the isolates were susceptible to trimethoprim-sulfamethoxazole (TMP-SMZ), the antipseudomonal penicillins, ceftazidime, cefoperazone, and imipenem; moderately susceptible to ciprofloxacin; and resistant to ceftriaxone, cefotaxime, cefoxitin, ceftizoxime, aztreonam, and amikacin. All patients receiving therapy recovered, including those six who received TMP-SMZ or a beta-lactam antibiotic as a single agent. A. xylosoxidans bacteremia is a significant infection and may be catheter related or associated with gastrointestinal pathology. The infection usually responds to therapy with TMP-SMZ or an appropriate beta-lactam antibiotic.
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PMID:Bacteremia due to Achromobacter xylosoxidans in patients with cancer. 835 82

Two clusters of Serratia marcescens in 14 adult cardiac surgical patients occurred over 10 months in an 876-bed teaching hospital. The 14 infections that were studied were as follows: one sternal and five leg incisions, five pneumonias, one bacteremia, one urinary tract infection, and one infected internal defibrillator site. The first cluster included four pneumonias, one urinary tract infection, and one bacteremia. Corrective actions were taken based on outbreak data through no source was identified. No further infections occurred during the following 2 months. The second cluster included one sternal and five leg incisions, an infected internal defibrillator incision site, and one pneumonia. Serratia marcescens was isolated from six electrocardiogram rubber welsh bulbs with sensitivities identical to patient isolates that indicated a common source outbreak in at least the second cluster of infections. Disposable electrocardiogram leads were introduced and the problem was resolved. We conclude that reusable electrocardiogram welsh bulbs are a vector for postoperative infections.
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PMID:An outbreak of Serratia marcescens in 14 adult cardiac surgical patients associated with 12-lead electrocardiogram bulbs. 155 44

Pneumococcal pneumonia and bacteremia are associated with appreciable mortality, most of which occurs very early in the course of infection. An initial step in the pathogenesis of pneumococcal pneumonia may include disruption of the pulmonary endothelial barrier with subsequent alveolar hemorrhage. We sought to determine whether soluble factors from Streptococcus pneumoniae can directly injure pulmonary endothelial cells in vitro and to identify pneumococcal toxins that may be involved in endothelial cell injury. Suspensions of S. pneumoniae (10(8) organisms per ml) caused significant injury to cultured bovine pulmonary artery endothelial cells in a time-dependent manner. The degree of endothelial cell cytotoxicity differed among S. pneumoniae strains; among the strains tested, a type 14 strain was the most cytotoxic and a type 3 strain was the least cytotoxic. During autolysis, type 14 S. pneumoniae released a soluble endothelial cell cytotoxin that was distinct from S. pneumoniae capsular and cell wall polysaccharides. The soluble cytotoxin was further characterized as a thiol-activated, heat-sensitive protein that coeluted with purified pneumolysin during gel filtration. The identity of the S. pneumoniae endothelial cell cytotoxin as pneumolysin was further supported by the ability of purified pneumolysin and the inability of S. pneumoniae mutants which lack pneumolysin to injure endothelial cells, as well as by the inhibition of the soluble S. pneumoniae cytotoxin by a neutralizing antibody to pneumolysin. Pneumolysin appears to be the major S. pneumoniae soluble cytotoxin for pulmonary endothelial cells in vitro and may be an important factor in the pathogenesis of alveolar hemorrhages in S. pneumoniae infections.
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PMID:Toxicity of pneumolysin to pulmonary endothelial cells in vitro. 156 59

Although AIDS was largely recognized and defined because of the increased presence of diseases that reflect deficiencies in cell-mediated immunity, susceptibility to common extracellular bacterial pathogens has also been shown to be increased. To our knowledge, adults with concurrent infection due to human immunodeficiency virus (HIV) and Streptococcus pneumoniae whose cases have been described to date have all had pneumococcal pneumonia and/or bacteremia. We describe five cases of HIV-infected patients who had unusual manifestations of pneumococcal infection, which include recurrent exudative pleural effusion, pyopneumothorax, purpura fulminans, mediastinitis with chest wall abscess, and multiple brain abscesses. Such complications of pneumococcal infection occurred more or less commonly in the preantibiotic era, but on the basis of our experience and an exhaustive literature search, these complications have been exceedingly rare in the past few decades. In four of our five patients, the unusual, complicated pneumococcal disease preceded and prompted a search for HIV infection. Because concurrent HIV infection increases the susceptibility to pneumococcal disease, other such cases are likely to be seen.
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PMID:Unusual manifestations of pneumococcal infection in human immunodeficiency virus-infected individuals: the past revisited. 157 28

This report reviews 45 episodes of group A streptococcal bacteremia during 1980-1989 in a large hospital; 24 episodes occurred in the first 5 years of study (1980-1984) and 21 in the last 5 years (1985-1989). Four episodes were nosocomial. The remaining 41 episodes were community acquired; of these episodes, 12 occurred in patients who were transferred from nursing homes. There was a definite seasonal predominance (84%) during November-June. All but three patients had chronic underlying conditions. The major portals of entry were the skin and lungs, and the main types of infection were primary septicemia, cellulitis and soft-tissue infection, pneumonia, and infective endocarditis. The overall mortality rate was 24%; 20% of the deaths were due to infection. Factors that adversely influenced mortality were septic shock (P less than .02), less than 10,000/mm3 leukocytes (P less than .05); less than 80% segmented polymorphonuclear leukocytes and band forms (P less than .02), and hyperbilirubinemia (P less than .01). Neither prevalence nor severity of group A streptococcal bacteremia increased during the last 5 years of study.
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PMID:Group A streptococcal bacteremia in a community teaching hospital--1980-1989. 157 44

Group-C beta-hemolytic streptococci (GCBHS) is an uncommon cause of bacteremia. In a 5-year period, GCBHS accounted for 0.28% of positive blood cultures and 0.35% of bacteremias documented at our hospital. The incidence of GCBHS bacteremia was 0.05 episodes per 1000 admissions. We were able to analyze clinical data of 10 of the 13 patients with GCBHS bacteremias. All but one were adults with significant underlying diseases, and seven episodes were community acquired. The skin was the portal of entry in only one case. Clinical syndromes included primary bacteremia (four cases), pneumonia (two cases), endocarditis (two cases), and meningitis, intraabdominal infection, and metastatic suppurative pericarditis (one episode each). Of 13 isolates, 12 were identified to species level: six, Streptococcus equisimilis; three S. equi; two S. dysgalactiae; and one S. zooepidemicus. Resistance to penicillin was detected in one isolate and none of our isolates displayed penicillin tolerance, Four patients died (40%) despite appropriate antimicrobial therapy.
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PMID:Group-C beta-hemolytic streptococcal bacteremia. 157 40

Actinomadura madurae is an aerobic actinomycete which is best known worldwide as the cause of actinomycotic mycetomas. It has not previously been reported to have caused invasive pulmonary or disseminated infection in humans. We describe an AIDS patient with opportunistic A. madurae-induced pneumonia and bacteremia. The isolate from the patient's blood was subjected to dilutional antimicrobial susceptibility tests with 12 antimicrobial agents and was found to have a wide spectrum of susceptibility. This unusual microorganism may be a cause of infections in severely immunosuppressed patients.
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PMID:Nonmycetomic Actinomadura madurae infection in a patient with AIDS. 157 56

We reported two HIV infected patients with bacteremia and pneumonia due to Rhodococcus equi. None of them had suffer any opportunistic infection before this episode. Clinical presentation includes respiratory tract symptoms of subacute onset and fever. The X-ray examination in both cases revealed pneumonia and lung abscess in upper lobes as well as lung infiltrates in other lobes. The microorganism was isolated in lung fine needle aspiration, bronchoalveolar lavage and blood cultures in both cases. One patient died and the other was under antibiotic treatment 5 months after discharge. The therapeutic options in this infection must include the use of at least two different antibiotics to which the microorganism is sensitive, and for a prolonged period of time. Surgical treatment should be considered if the evolution is poor.
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PMID:[Rhodococcus equi in HIV infected patients: 2 new cases]. 160 24

A multicenter, prospective randomized trial was conducted to determine if the addition of rifampin to a combination therapy of an antipseudomonal beta-lactam agent and aminoglycoside improves the outcome of patients with Pseudomonas aeruginosa bacteremia. The Zelen protocol for randomized-consent design was used. Consent was sought only from patients randomized to the experimental therapy (rifampin+). If the experimental therapy was refused, the patient would then receive the standard combination therapy (control); however, when outcome was evaluated, all patients randomized to the rifampin+ group, including those that declined rifampin, were compared with the control group. One hundred twenty-one consecutive hospitalized patients with positive blood cultures for P. aeruginosa were enrolled. Entry was stratified for prior use of empiric antipseudomonal antibiotics, neutropenia, severity of illness, and presence of pneumonia. Fifty-eight patients were randomized to receive rifampin (600 mg orally every 8 h for the first 72 h and then every 12 h for a total of 10 days) plus a beta-lactam agent plus an aminoglycoside. Sixty-three received the standard therapy of a beta-lactam plus an aminoglycoside agent (control). Bacteriologic cure occurred significantly more frequently in patients randomized to the rifampin+ regimen. Breakthrough or relapsing bacteremias occurred in 2% of the three-drug (rifampin+) group, compared with 14% for the two-drug (standard therapy) group. Despite this favorable trend in bacteriological response, no significant differences in survival were seen for the two treatment groups. Rifamycin derivatives warrant further clinical study as antipseudomonal agents. The Zelen protocol appears well suited for comparative trials of antimicrobial agents.
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PMID:Addition of rifampin to combination antibiotic therapy for Pseudomonas aeruginosa bacteremia: prospective trial using the Zelen protocol. 162 73

This study was performed to demonstrate the characteristic findings in pneumonia under neutropenic condition. The results were as follows. 1) After nebulizing Klebsiella pneumonia DT-S strains, the survival rate in the neutropenic mouse group rapidly decreased compared with that of the control group. 2) In the neutropenic state, a rapid decline of survival rate was demonstrated during the initial stage of infection. Bacteremia and endotoxemia developed earlier than in the healthy control group. 3) In neutropenic pneumonia, the neutrophil cell count in BALF was significantly lower than that in usual pneumonia. Consequently, a large number of bacteria grew in the alveolar spaces during the early period after inhalation. Neither inflammatory cell infiltration nor thickening of the alveolar wall was present; however, structural destruction of alveolar and vascular walls was found. 4) These pathological changes were also seen following intratracheal inoculation of some extracellular enzymes of Klebsiella pneumoniae DT-S into rabbit lung. However, no destruction of alveolar walls was observed after nebulizing the killed Klebsiella pneumoniae DT-S. It was suggested that the significant amount of enzymes produced by the bacteria growing in the alveoli caused tissue damage, especially in the neutropenic state. 5) Thus the typical inflammatory changes that occurred in the usual state, were not seen in neutropenic pneumonia, and a large number of bacteria grew in the alveoli. Marked tissue damage was caused by extracellular enzymes produced by bacteria. Consequently, bacteria entered the blood stream and bacteremia and endotoxemia developed. These processes observed in neutropenic pneumonia readily progressed to bacteremia of endotoxemia, which are more severe in this state.
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PMID:[Experimental study on development and lung injury in pneumonia under neutropenic condition]. 162 94


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