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

Nine patients with bacteremia Escherichia coli pneumonia were studied, and 22 cases from the literature of the bacteremic and nonbacteremic variety were reviewed. The findings of this study indicate that E coli pneumonia most often occurs in persons who are elderly and have associated conditions that impair host defenses. Escherichia coli pneumonia is usually nosocomially acquired. The organism may reach the respiratory tract by aspiration of oropharyngeal secretions due to colonization or by hematogenous dissemination from a primary source in the gastrointestinal tract or the genitourinary tract. The clinical manifestation most often is that of pneumonia in the lower lobe, but the process can be roentgenographically variable. Sputum culture is usually positive in the bacteremic form of E coli pneumonia. The high morbidity found in this study, despite appropriate antimicrobial therapy, emphasizes the need for earlier recognition and infection prevention in predisposed groups.
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PMID:Bacteremic Escherichia coli pneumonia. 675 79

Pneumonia due to Escherichia coli (E. coli) has a reported mortality of up to 70 per cent. Most infections are associated with underlying disease, and follow bacteraemia from a genitourinary or gastrointestinal source. This report describes two patients with bacteraemic E. coli pneumonia, presumed secondary to aspiration of E. coli from the oropharynx. Both patients presented a rapidly progressive illness with hypotension. Response of the pneumonia to early, appropriate antimicrobial therapy, was complete. Our cases are discussed with particular reference to clinical features of the infection and choice of antimicrobial therapy.
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PMID:Pneumonia with bacteraemia due to Escherichia coli. 703 72

Escherichia coli pneumonia occurred in 17 elderly patients over a two-year period. All cases were documented by transtracheal aspiration. Six of the 17 E. coli organisms causing pneumonia contained K1 capsular polysaccharide. E. coli K1 organisms did not appear to be more virulent than non-K1 strains as measured by incidence of bacteremia, shock and death. E. coli K1 pneumonia was usually community- acquired (five of six cases) and occurred in patients with a prior history of urinary infection. Non-K1 E. coli pneumonia occurred in the hospital setting in eight of 11 patients, and a gastrointestinal source of infection was likely in five patients. All patients were treated with appropriate initial antibiotic therapy, and 71 percent of patients survived.
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PMID:Escherichia coli pneumonia in the elderly with reference to the role of E. coli K1 capsular polysaccharide antigen. 704 33

To determine the role of CD11/CD18 complexes in neutrophil emigration, inflammation was induced in the skin, lungs, or peritoneum of mutant mice deficient in CD18 (CD18-/- mutants). Peripheral blood of CD18-/- mutants contained 11-fold more neutrophils than did blood of wild-type (WT) mice. During irritant dermatitis induced by topical application of croton oil, the number of emigrated neutrophils in histological sections of dermis was 98% less in CD18-/- mutants than in WT mice. During Streptococcus pneumoniae pneumonia, neutrophil emigration in CD18-/- mutants was not reduced. These data are consistent with expectations based on studies using blocking antibodies to inhibit CD11/CD18 complexes, and on observations of humans lacking CD11/CD18 complexes. The number of emigrated neutrophils in lung sections during Escherichia coli pneumonia, or in peritoneal lavage fluid after 4 h of S. pneumoniae peritonitis, was not reduced in CD18-/- mutants, but rather was greater than the WT values (240 +/- 30 and 220 +/- 30% WT, respectively). Also, there was no inhibition of neutrophil emigration during sterile peritonitis induced by intraperitoneal injection of thioglycollate (90 +/- 20% WT). These data contrast with expectations. Whereas CD11/CD18 complexes are essential to the dermal emigration of neutrophils during acute dermatitis, CD18-/- mutant mice demonstrate surprising alternative pathways for neutrophil emigration during pneumonia or peritonitis.
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PMID:Neutrophil emigration in the skin, lungs, and peritoneum: different requirements for CD11/CD18 revealed by CD18-deficient mice. 933 75

A two year old girl with chronic neurologic convulsive disease was admitted with a six day history of pneumonia and, despite treatment, died on hospital day 3. The X-ray revealed right upper lobar pneumonia. The results of pleural effusion and blood cultures drawn on admission yielded a non-typable Escherichia coli. No other source of infection was identified. The authors discuss the clinical and pathophysiological aspects of Escherichia coli pneumonia.
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PMID:Primary community-acquired pneumonia by Escherichia coli. Case report and review of the literature. 933 70

We hypothesized that tumor necrosis factor (TNF)-alpha signaling is essential to inflammation and host defense during Escherichia coli pneumonia. We tested this hypothesis by instilling E. coli into the lungs of wild-type (WT) mice and gene-targeted mice that lack both p55 and p75 receptors for TNF-alpha. The emigration of neutrophils 6 h after instillation of E. coli was not decreased, but rather was significantly increased (167% of WT), in TNF receptor (TNFR)-deficient mice. This increased neutrophil emigration did not result from peripheral blood neutrophilia or enhanced neutrophil sequestration, inasmuch as the numbers of neutrophils in the circulating blood and in the pulmonary capillaries did not differ between TNFR-deficient and WT mice. The accumulation of pulmonary edema fluid was not inhibited in TNFR-deficient compared with WT mice. Nuclear factor-kappaB (NF-kappaB) translocation in the lungs was not prevented in TNFR-deficient mice. Thus, signaling pathways independent of TNFRs can mediate the acute inflammatory response during E. coli pneumonia. However, despite this inflammatory response, bacterial clearance was impaired in TNFR-deficient mice (109 +/- 8% versus 51 +/- 14% of the original inoculum viable after 6 h in TNFR-deficient and WT mice, respectively). Increased neutrophil emigration during E. coli pneumonia in TNFR-deficient mice may thus result from an increased bacterial burden in the lungs. During acute E. coli pneumonia, the absence of TNFR signaling compromised bacterial killing, but did not prevent inflammation, as measured by the accumulation of edema fluid and neutrophils.
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PMID:Roles of tumor necrosis factor receptor signaling during murine Escherichia coli pneumonia. 1061 69

OBJECTIVE: To describe the features of community-acquired Escherichia coli pneumonia and to compare these patients with patients with pneumonia caused by other etiologic agents. PATIENTS AND METHODS: This prospective study was carried out at five medical institutions in three geographic locations---Pittsburgh, PA, Boston, MA and Halifax, NS. Pneumonia etiology was assigned, based on results of microbiological investigations, by a committee consisting of five investigators using rules established prior to the study. Demographic and clinical features and outcomes of patients with E. coli pneumonia were compared with those of pneumonia due to other microorganisms. RESULTS: Nineteen patients (9 (47.4%) blood culture positive) had pneumonia due to E. coli and 430 (69 (16.0%) blood culture positive) had pneumonia caused by other etiologic agents. E. coli was the second most common cause of bacteremic pneumonia. The E. coli patients were older, and more likely to be female, from a nursing home and confused compared with patients with pneumonia due to other microbial agents. They were more severely ill as measured by a validated pneumonia specific severity of illness scoring measure. Although there was no in-hospital mortality for the patients with E. coli pneumonia, the 90-day mortality was 21%. Thirty-two (7.4%) of the patients with pneumonia due to other agents died in hospital and the 90-day mortality rate was 13.5% (p NS). Eight of the 19 patients with E. coli pneumonia were admitted from a nursing home and an additional four patients (63.2%) were discharged to such a facility. In contrast, only 44 (10.2%) of the patients with pneumonia due to other agents were discharged to a nursing home (p<0.001). CONCLUSIONS: Patients diagnosed with E. coli pneumonia are frequently bacteremic. They are older than patients with pneumonia due to other etiologies, and more likely to be female, from a nursing home and severely ill. Despite the absence of in-hospital mortality, 21% of these patients died within 90 days of presentation.
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PMID:Community-acquired pneumonia due to Escherichia coli. 1186 80

We examined the relationship between neutrophil [polymorphonuclear leukocyte (PMN)] influx and lung vascular injury in response to Escherichia coli pneumonia. We assessed lung tissue PMN uptake by measuring myeloperoxidase and transvascular PMN migration by determining PMN counts in lung interstitium and bronchoalveolar lavage fluid (BALF) in mice challenged intratracheally with E. coli. Lung vascular injury was quantified by determining microvessel filtration coefficient (Kf,c), a measure of vascular permeability. We addressed the role of CD18 integrin in the mechanism of PMN migration and lung vascular injury by inducing the expression of neutrophil inhibitory factor, a CD11/CD18 antagonist. In control animals, we observed a time-dependent sixfold increase in PMN uptake, a fivefold increase in airway PMN migration, and a 20-fold increase in interstitial PMN uptake at 6 h after challenge. Interestingly, Kf,c increased minimally during this period of PMN extravasation. CD11/CD18 blockade reduced lung tissue PMN uptake consistent with the role of CD18 in mediating PMN adhesion to the endothelium but failed to alter PMN migration in the tissue. Moreover, CD11/CD18 blockade did not affect Kf,c. Analysis of BALF leukocytes demonstrated diminished oxidative burst compared with leukocytes from bacteremic mice, suggesting a basis for lack of vascular injury. The massive CD11/CD18-independent airway PMN influx occurring in the absence of lung vascular injury is indicative of an efficient host-defense response elicited by E. coli pneumonia.
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PMID:E. coli pneumonia induces CD18-independent airway neutrophil migration in the absence of increased lung vascular permeability. 1281 90

During infection, inflammation is essential for host defense, but it can injure tissues and compromise organ function. TNF-alpha and IL-1 (alpha and beta) are early response cytokines that facilitate inflammation. To determine the roles of these cytokines with overlapping functions, we generated mice deficient in all of the three receptors mediating their effects (TNFR1, TNFR2, and IL-1RI). During Escherichia coli pneumonia, receptor deficiency decreased neutrophil recruitment and edema accumulation to half of the levels observed in wild-type mice. Thus these receptors contributed to maximal responses, but substantial inflammation progressed independently of them. Receptor deficiency compromised antibacterial efficacy for some infectious doses. Decreased ventilation during E. coli pneumonia was not affected by receptor deficiency. However, the loss of lung compliance during pneumonia was substantially attenuated by receptor deficiency. Thus during E. coli pneumonia in mice, the lack of signaling from TNF-alpha and IL-1 decreases inflammation and preserves lung compliance.
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PMID:Roles for early response cytokines during Escherichia coli pneumonia revealed by mice with combined deficiencies of all signaling receptors for TNF and IL-1. 1496 82

Pulmonary pneumatoceles are a rare complication of nosocomial pneumonia. They occur most often in staphylococcal infections and are hence more frequent in children. We report the case of an immunocompromised adult who shortly after digestive surgery developed Escherichia coli pneumonia which evolved rapidly towards pneumatocele formation revealed by pneumothorax.
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PMID:Pneumatocele formation in adult Escherichia coli pneumonia revealed by pneumothorax. 1623 Jan 86


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