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

Usually, presenting infections in children with agammaglobulinemia include pneumonia and otitis media caused by pyogenic bacteria. We report here two cases of Pseudomonas aeruginosa septicemia with ecthyma gangrenosum, in previously healthy boys, leading to the diagnosis of X-linked agammaglobulinemia.
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PMID:X-linked agammaglobulinemia presenting as pseudomonas aeruginosa septicemia. 889 10

The surveillance of pneumococcal resistance in nasopharyngeal isolates is a practical way to determine the prevalence of resistant strains and is a reasonable predictor of resistance in systemic isolates. The increasing prevalence of resistance is shifting the distribution of invasive pneumococcal serotypes toward those included in conjugate vaccines. If these vaccines reduce carriage, they may eliminate or greatly reduce the prevalence of resistant strains. Meningitis is the most important infection caused by PRP for which penicillin or ampicillin therapy is inappropriate. Although the extended spectrum cephalosporins will be effective for most cases of PRP meningitis, it is clear that such therapy is not foolproof. It is important for the laboratory to test CSF isolates not only for penicillin resistance but also for resistance to the cephalosporins. beta-Lactam antibiotics can still be considered appropriate empiric therapy for otitis media, pneumonia, or sepsis. However, occasional treatment failures with these agents may necessitate use of alternative therapeutic strategies.
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PMID:Antibiotic-resistant pneumococci in pediatric disease. 915 79

A 74-year-old man with multiple myeloma developed facial and cervical cellulitis and severe sepsis as a complication of surgery (alar region basal cell carcinoma). The etiological agent was, surprisingly, penicillin-resistant Streptococcus pneumoniae (PRSP). The patient successfully received 16 days of antibiotics. Amoxicillin was given as monotherapy during the last 14 days of treatment. PRSP can be responsible not only for otitis media, pneumonia or meningitis, but also for various other types of infection in patients with predisposing factors.
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PMID:Cellulitis due to Streptococcus pneumoniae with diminished susceptibility to penicillin in an immunocompromised patient. 943 45

Pasteurella multocida is a bacterial pathogen that causes rhinitis (snuffles), pneumonia, otitis media, septicemia, metritis, and death in domestic rabbits. Currently, there are no effective vaccines to prevent infection by this organism. Subcutaneous (s.c.) immunization with either exotoxin or thiocyanate extracts of P. multocida induces partial protection in rabbits. Since disease begins at mucosal sites, induction of local immunity may be important in preventing systemic disease. Little is known concerning the efficacy of intranasal (i.n. ) administration of these antigens in inducing protective mucosal immunity to P. multocida in rabbits. The purpose of this study was twofold: (i) to investigate the effectiveness of vaccination with purified P. multocida toxin (PMT) and a potassium thiocyanate extract of P. multocida (CN) in combination and (ii) to evaluate the efficacy of administration of these antigens i.n. versus s.c. Forty-eight rabbits were randomly divided into eight different treatment groups. Rabbits received either one or both antigens by either s.c. or i.n. administration. Following vaccination, each group received an i.n. challenge of P. multocida. Rabbits vaccinated with both antigens i.n. or s.c. had a 100% survival rate, few or no bacteria in the liver and lungs, high serum immunoglobulin G (IgG) and IgM antibody titers, and significant numbers of IgG antibody-secreting cells (ASC) in the spleen and tracheobronchial lymph node. Rabbits vaccinated i.n. had significant nasal and bronchoalveolar lavage IgA antibody levels. Rabbits vaccinated with only one antigen, either PMT or CN, had lower antibody titers, moderate to severe liver and lung infections, and fewer ASC compared to rabbits receiving both antigens. Rabbits in the control groups had moderate to severe liver and lung infections. This study indicates that i.n. immunization with both PMT and CN induces an effective response against homologous P. multocida challenge.
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PMID:Induction of protective immunity in rabbits by coadministration of inactivated Pasteurella multocida toxin and potassium thiocyanate extract. 967 63

Clinical and pathological data on 10 children who died of pneumococcal infection were analyzed. The disease started as primary pneumococcal meningitis in 4 cases, secondary to otitis media meningitis in 1 and pneumococcal pneumonia in 5 cases. The latter complicated with secondary pneumococcal meningitis in 3 cases, pneumococcemia with hemolytico-uremic syndrome in 1 case. 9 patients died of infectious-toxic shock and 1 patient of massive bleeding from acute gastric and duodenal ulcers. The results suggest that a grave course of pneumococcal infection is due to development of the infectious-toxic shock. Emergence of metastatic suppurative focuses was indicative of sepsis. A fulminant form of pneumococcal sepsis--pneumococcemia--has no large or evident primary focus. Neuraminidase produced by pneumococci is responsible for development of hemolytico-uremic syndrome.
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PMID:[Pathomorphology of pneumococcal infection in children]. 970 99

The microbiologists use the term corynebacteria to describe aerobically growing, asporogenous, irregularly sharped gram-positive rods. They comprise strictly aerobic bacteria isolated from environment as well as preferentially anaerobic bacteria found in clinical specimens. A large part of these bacteria is considered as commensal of skin and mucous membranes. This group of organisms has recently been subjected to considerable taxonomic revisions, which have resulted in the proposal of several new species, many of them representing previous Centers for Diseases Control coryneform groups. Moreover, recent investigations demonstrated the existence of a pathogenic role for some of them. These bacteria comprise well-known pathogens such as C. diphtheriae responsible for diphtheria, Actinomyces spp. responsible for actinomycosis and Arcanobacterium haemolyticum recovered from pharyngitis, but other corynebacteria were related to particular infections. For example, the lipophilic and antibiotics multiresistant species Corynebacterium urealyticum and C. jeikeium were found to be responsible for urinary tract infections and septicemias, respectively. The recently described species Turicella otitidis was found to be implicated in otitis media and C. seminale were recovered from genital specimens of male patients. Implantation of material devices, use of broad-spectrum antibiotics led to an increase of sepsis due to the species C. jeikeium and C. amycolatum. Many of the new Actinomyces species grow well under aerobic conditions and are often implicated in various abscesses. Moreover an increase of immunocompromised patients led to the development of infections due to the aerobic actinomycete Rhodococcus equi. The association of some corynebacteria with particular diseases should prompt the microbiologist to identify these bacteria when they are encountered in a pathogenic situation. Identification of the major part of corynebacteria isolated from clinical specimens can now be achieved by using recent schemes.
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PMID:[Bacteriological and clinical aspects of corynebacterium]. 975 61

Streptococcus pneumoniae is the major cause of bacterial pneumonia, and it is also responsible for otitis media and meningitis in children. Apart from the capsule, the virulence factors of this pathogen are not completely understood. Recent technical advances in the field of bacterial pathogenesis (in vivo expression technology and signature-tagged mutagenesis [STM]) have allowed a large-scale identification of virulence genes. We have adapted to S. pneumoniae the STM technique, originally used for the discovery of Salmonella genes involved in pathogenicity. A library of pneumococcal chromosomal fragments (400 to 600 bp) was constructed in a suicide plasmid vector carrying unique DNA sequence tags and a chloramphenicol resistance marker. The recent clinical isolate G54 was transformed with this library. Chloramphenicol-resistant mutants were obtained by homologous recombination, resulting in genes inactivated by insertion of the suicide vector carrying a unique tag. In a mouse pneumonia model, 1.250 candidate clones were screened; 200 of these were not recovered from the lungs were therefore considered virulence-attenuated mutants. The regions flanking the chloramphenicol gene of the attenuated mutants were amplified by inverse PCR and sequenced. The sequence analysis showed that the 200 mutants had insertions in 126 different genes that could be grouped in six classes: (i) known pneumococcal virulence genes; (ii) genes involved in metabolic pathways; (iii) genes encoding proteases; (iv) genes coding for ATP binding cassette transporters; (v) genes encoding proteins involved in DNA recombination/repair; and (vi) DNA sequences that showed similarity to hypothetical genes with unknown function. To evaluate the virulence attenuation for each mutant, all 126 clones were individually analyzed in a mouse septicemia model. Not all mutants selected in the pneumonia model were confirmed in septicemia, thus indicating the existence of virulence factors specific for pneumonia.
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PMID:Large-scale identification of virulence genes from Streptococcus pneumoniae. 982 34

Streptococcus pneumoniae infection and disease have been modeled in several animal species including infant and adult mice, infant and adult rats, infant Rhesus monkeys, and adolescent and adult chinchillas. Most are models of sepsis arising from intravenous or intraperitoneal inoculation of bacteria, and a few were designed to study disease arising from intranasal infection. Chinchillas provide the only animal model of middle ear pneumococcal infection in which the disease can be produced by very small inocula injected into the middle ear (ME) or intranasally, and in which the disease remains localized to the ME in most cases. This model, developed at the University of Minnesota in 1975, has been used to study pneumococcal pathogenesis at a mucosal site, immunogenicity and efficacy of pneumococcal capsular polysaccharide (PS) vaccine antigens, and the kinetics and efficacy of antimicrobial drugs. Pathogenesis experiments in the chinchilla model have revealed variation in ME virulence among different pneumococcal serotypes, enhancement of ME infection during concurrent intranasal influenza A virus infections, and natural resolution of pneumococcal otitis media (OM) without intervention. Research has explored the relative contribution of pneumococcal and host products to ME inflammation. Pneumococcal cell wall components and pneumolysin have been studied in the model. Host inflammatory responses studied in the chinchilla ME include polymorphonuclear leukocyte oxidative products, hydrolytic enzymes, cytokine and eicosanoid metabolites, and ME epithelial cell adhesion and mucous glycoprotein production. Both clinical (tympanic membrane appearance) and histopathology (ME, Eustachian tube, inner ear) endpoints can be quantified. Immunologic and inflammatory studies have been facilitated by the production of affinity-purified antichinchilla immunoglobulin G (IgG), IgM, and secretory IgA polyclonal antibody reagents, and the identification of cross-reactivity between human and chinchilla cytokines, and between guinea pig and chinchilla C3. Alteration of ME mucosa by pneumococcal neuraminidase and alteration of ME epithelial cell (MEEC) surface carbohydrates during intranasal pneumococcal infection have been demonstrated. Pathogenesis studies have been aided by cultured chinchilla MEEC systems, in which the ability of platelet activating factor and interleukin (IL)-1 beta to stimulate epithelial mucous glycoprotein synthesis has recently been demonstrated. Because chronic OM with effusion is characterized by presence of large amounts of mucous glycoprotein in the ME, pneumococcus may have an important role in both acute and chronic ME disease. Both unconjugated PS and PS-protein-conjugated vaccines are immunogenic after intramuscular administration without adjuvant in chinchillas. Passive protection studies with human hyperimmune immunoglobulin demonstrated that anti-PS IgG alone is capable of protecting the chinchilla ME from direct ME challenge with pneumococci. Active PS immunization studies demonstrated protection following direct ME and intranasal pneumococcal challenge with and without concurrent influenza A virus infection. An attenuated influenza A virus vaccine also showed protection for pneumococcal OM. Antimicrobial treatment of acute OM has been based almost exclusively on empirical drug use and clinical trials without a foundation of ME pharmacokinetics. Studies in the chinchilla model have started to bring a rational basis to drug selection and dosing. Microassays have been developed using high-pressure liquid chromatography for many relevant drugs. Studies have explored the in vivo ME response in pneumococcal OM to antimicrobial drugs at supra- and sub-minimum inhibitory concentration (MIC), the effect of concurrent influenza A virus infection on ME drug penetration, and the effect of treatment on sensorineural hearing loss produced by pneumococcal OM.
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PMID:Otitis media: the chinchilla model. 1033 23

Blocking the primary stages of infection, namely bacterial attachment to host cell receptors and colonization of the mucosal surface, may be the most effective strategy to prevent bacterial infections. Bacterial attachment usually involves an interaction between a bacterial surface protein called an adhesin and the host cell receptor. Recent preclinical vaccine studies with the FimH adhesin (derived from uropathogenic Escherichia coli) have confirmed that antibodies elicited against an adhesin can impede colonization, block infection, and prevent disease. The studies indicate that prophylactic vaccination with adhesins can block bacterial infections. With recent advances in the identification, characterization, and isolation of other adhesins, similar approaches are being explored to prevent infections, from otitis media and dental caries to pneumonia and sepsis.
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PMID:Adhesins as targets for vaccine development. 1034 Nov 76

Increasingly, Streptococcus pneumoniae with reduced susceptibility to penicillin is becoming a healthcare concern, not only because of the high prevalence of infections caused by this pathogen but also because of the rate at which resistance has progressed. The incidence of penicillin resistance in strains of S. pneumoniae approaches 40% in some areas of the United States, and the incidence of high-level resistance has increased by 60-fold during the past 10 years. With the exception of meningitis and otitis media, there is no conclusive evidence that the acquisition of resistance by S. pneumoniae to beta-lactam antibiotics incurs greater morbidity and mortality in infections caused by this pathogen. However, if the current trends of resistance patterns continue, one can expect the morbidity and mortality to increase. The mechanism of beta-lactam resistance of S. pneumoniae involves genetic mutations which alter penicillin-binding protein structure, resulting in a decreased affinity for all beta-lactam antibiotics. In the treatment of infections caused by S. pneumoniae, it should not be assumed that nonsusceptibility to beta-lactam antibiotics correlates with clinical ineffectiveness of these agents. On the contrary, the recommended therapy for nonmeningeal pneumococcal infections (e.g., pneumonia, sepsis, acute otitis media) includes a beta-lactam antibiotic: penicillin G, amoxicillin, amoxicillin/clavulanate, cefuroxime, cefotaxime, or ceftriaxone. Recommended therapy for meningitis is cefotaxime or ceftriaxone, with the addition of vancomycin until susceptibility is known. These agents are recommended because of their ability to achieve serum/tissue concentrations greater than the minimum inhibitory concentrations (MICs) of these agents against penicillin-susceptible, penicillin-intermediate, and most penicillin-resistant strains (e.g., penicillin G, cefotaxime, ceftriaxone, amoxicillin, amoxicillin/clavulanate, and cefuroxime), or their ability to provide adequate concentrations in cerebrospinal fluid (e.g., cefotaxime, ceftriaxone).
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PMID:Drug-resistant Streptococcus pneumoniae: rational antibiotic choices. 1034 60


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