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

The clinical features of 27 patients with early onset group B beta hemolytic streptococcus sepsis were reviewed. Fifteen presented with a clinical pattern indistinguishable from the idiopathic respiratory distress syndrome and were compared with 15 patients with IRDS. Rupture of membranes for greater than 12 hours prior to delivery occurred more often in patients with GBS (33%) than in the patients with IRDS (16%). Hypotension was more commonly seen in the patients with GBS (56%) than in the patients with IRDS (36%). There was no difference in the incidence of apnea or the respirator peak inspiratory pressure requirements between the two groups of patients, but there was a tendency for a decline in the total white blood cell count in the first 24 hours of life in those patients with GBS sepsis.
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PMID:Group B beta hemolytic streptococcal sepsis and the idiopathic respiratory distress syndrome: a comparison. 37 Mar 55

The pneumonia, sepsis and meningitis are common diseases of GBS infection in infants. There are early-onset and late-onset types in this disease, the result of the infection is unknown. M. Sugiyama reported that M9 is a new type of GBS in Japan in 1989. Analysis of GBS typing and serum specific antibody concentrations of the type are simple with new technics. By studying the infants' contamination we discovered that GBS appeared to originate from mother-infant sources. The infants were followed for a year. 52% of the infants had GBS contamination in their throat or stool. The most common type was Ia, followed by III, JM9 and NT6. Those types without III type had been present for more than 9 months in the infant. The contamination term of Ia or III type in infants correlated with the blood specific antibody concentration of the type.
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PMID:[Maternal carriage and vertical transmission of group B Streptococcus (GBS)]. 129 21

The authors describe the advantages of a new method to determinate the erythrocyte sedimentation rate (micro-ESR) during neonatal GBS infections. They utilize a capillary tube placed at a 45 degrees angle and have the results of this test only after 15 minutes. The micro-ESR is proposed as a simple and quick method of sepsis screen in term and preterm newborns.
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PMID:[The micro-ESR with the capillary tube inclined to 45 degrees in the "sepsis screen" of neonatal infection due to beta-hemolytic B-group Streptococcus]. 148 6

The use of recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF) as therapy in neonatal sepsis has been proposed because of observed defects in polymorphonuclear leukocyte (PMNL) production and function in infected neonates. Newborn rats were infected intraperitoneally (ip) with type III group B streptococcus (III-GBS) and effects of treatment with rhGM-CSF given ip 7-19 h after infection were studied. Overall mortality was 67% in controls and 37% in animals treated with rhGM-CSF (P = .003). No changes in peripheral blood PMNL number or oxidative metabolic function were found in infected or uninfected animals given rhGM-CSF compared with controls. In uninfected animals, there was an increase in the oxidative burst of peritoneal cells at 3.5 h (P = .043) and in the numbers of peritoneal cells at 3 h (P = .001) in animals receiving ip rhGM-CSF compared with controls. Phagocyte priming, cellular influx into the peritoneum, or both appear to contribute to the decreased mortality observed in this model of rhGM-CSF therapy of III-GBS disease in neonates.
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PMID:Therapeutic use of recombinant human granulocyte-macrophage colony-stimulating factor in neonatal rats with type III group B streptococcal sepsis. 153 38

Streptococcus agalactiae (group B streptococci [GBS]) is the leading cause of neonatal sepsis and meningitis in the United States. The surface-associated C proteins of GBS play a role in immunity, but their number, size, structure, function, and virulence properties have not been well characterized. A recombinant library of DNA fragments from GBS strain A909 (type Ia/C) was prepared in the plasmid pUX12, a specially constructed Escherichia coli expression vector. The library was screened with a rabbit antiserum shown to be protective for passive immunity to GBS infection in a mouse lethality model. Clones were divided into two distinct groups on the basis of DNA-DNA cross-hybridization, restriction enzyme analysis, and the expression of antigenic proteins in E. coli. A characteristic clone from each group was chosen for further study. Clone pJMS23 expresses gene products that biochemically and immunologically correspond to the trypsin-resistant, C-protein alpha antigen. Clone pJMS1 expresses a gene product that binds to immunoglobulin A and is similar to the trypsin-sensitive, C-protein beta antigen. Antisera raised in rabbits against E. coli containing each of the plasmid clones were able to elicit protective immunity in mice challenged by GBS strains carrying the C proteins but not by non-C-protein-bearing strains. Southern blot analysis shows no DNA homology between the clones, and there is no immunological cross-reactivity between the antigens they express. Therefore, pJMS23 and pJMS1 encode two different C proteins that define unique protective epitopes.
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PMID:Cloned alpha and beta C-protein antigens of group B streptococci elicit protective immunity. 167 38

Because rates of morbidity and mortality due to newborn sepsis are unacceptably high, adjunctive therapies must be investigated. In the current studies, after healthy adults were immunized with type III group B streptococcal (III-GBS) capsular polysaccharide vaccine, serum was obtained from "vaccine-responders" from which a pooled human IgG preparation hyperimmune for III-GBS was prepared by ion-exchange column chromatography. This preparation, containing 549 micrograms/ml III-GBS antibody was very active functionally when evaluated against multiple III-GBS strains both in vitro in an opsonophagocytic assay using newborn sera and in a newborn rat model of III-GBS disease. The level of functional activity was dramatically higher than that of commercially available human IgG preparations for intravenous use demonstrated previously in identical assays. Human IgG preparations hyperimmune for GBS offer promise for use as adjunctive therapy of sepsis in newborns.
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PMID:Pooled human IgG hyperimmune for type III group B streptococci: evaluation against multiple strains in vitro and in experimental disease. 201 63

GBS (Group B Hemolytic Streptococci) cause pulmonary hypertension with associated neutropenia. We investigated whether there is a correlation between the neutropenia of sepsis and GBS-induced pulmonary vasoconstriction, through study of the effects of inhibiting pulmonary vasoconstriction on the neutropenia of GBS in newborn piglets. Fifteen piglets were infused with GBS. After one hour, animals were given either a thromboxane inhibitor (DAZ), a combined cyclooxygenase/lipoxygenase inhibitor, BW755C, or placebo. With GBS infusion, WBC and PMN counts dropped steadily, from similar baselines, to 2250 +/- 570, 3300 +/- 500 and 5400 +/- 1100 cells/mm3 respectively (p less than 0.05; DAZ and BW vs. placebo). PMN's dropped similarly to 710 +/- 320, 2390 + 1240 and 3130 +/- 1050 cells/mm3 respectively (p less than 0.05; DAZ vs. BW and placebo). The drop in WBC's predominantly resulted from proportional decreases in PMN's (DAZ: r = 0.98; BW: r = 0.88; placebo r = 0.93). Compared to GBS alone, DAZ reduced pulmonary vasoconstriction, but exacerbated the granulocytopenia. BW755C similarly reduced pulmonary hypertension: however, it ameliorated the exacerbation of GBS induced neutropenia described above. These data imply that there is no direct correlation between GBS induced granulocytopenia and pulmonary hypertension.
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PMID:Prostanoid inhibition and group B hemolytic streptococci (GBS) induced neutropenia in newborn piglets. 212 31

Molecular biology has provided new technology for evaluating the traits of bacterial pathogens that are important in the pathogenesis of infections. The ability to derive isogenic strains that differ by a single trait provides a powerful tool for investigating the interaction of a putative virulence factor with the host at any of the various steps in pathogenesis. Recombinant DNA techniques afford the opportunity to clone the genes involved in the biosynthesis of a particular virulence factor. Once the gene(s) are cloned, a vast amount of information can be learned about their composition, structure, and regulation, and similarity with genes in other organisms. Understanding the molecular biology of a virulence factor also provides information about potential targets for future therapies and preventive modalities. The molecular analysis of two virulence factors from the type III group B streptococcus has been reviewed to provide specific examples of how these techniques can be used. The data has shown that the capsular polysaccharide is an essential factor in GBS virulence. The structural influence of sialic acid on the capsule plays a major role in its virulence properties. The importance of the capsule has been tested in several assays to identify its role in pathogenesis. Its primary role appears to be evading host phagocytic mechanisms, but it does not appear to be essential in the vascular response observed during GBS sepsis. Using the isogenic strains, we have also learned that the capsule does not mask a fibronectin receptor on GBS. In contrast to the capsule, the beta-hemolysin of GBS does not appear to be essential for systemic disease once the organism has invaded. Its role in the initial invasive steps in GBS pathogenesis has not been tested, but the availability of isogenic mutants in beta-hemolysin production will allow this question to be answered once the model systems are available.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Molecular analysis of two group B streptococcal virulence factors. 217 47

GBS have attracted increasing attention in recent years as a major cause of serious neonatal sepsis. The maternal genital tract is the principal source of organism for babies with the most serious early onset form of disease. Reported rates of GBS carriage in the genital and anorectal tract of pregnant women vary widely: much of the variations is undoubtedly associated with differences in laboratory technique, sampling site and number of samples taken. The key bacteriological factor is the use of enrichment culture technique. We have studied GBS colonization in 274 pregnant women during labor and in their newborns (275). Carriage was documented in 25.91% women by vaginal (low portion) and anorectal swabs, and in 6.14% newborns by auricolar, pharyngeal and rectal swabs taken at birth and before leaving nursery. The higher rectal colonization rate in pregnant women suggests that the gastrointestinal tract is the primary site of GBS carriage. Colonized newborns have no obstetrics risk factors, except for maternal GBS carriage. Our data confirms that limiting antimicrobial intrapartum prophylaxis to premature infants leaves term infants (who account for 60% of the fetal cases of early onset disease) unprotected, unless membrane rupture is prolonged. Prevention of early onset infections among low-risk term infants will require additional investigations.
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PMID:[Epidemiology of beta-hemolytic streptococcus group B colonization in perinatology. Methodology considerations and personal data]. 268 54

Certain infections, such as UTI, may have an increased incidence during pregnancy owing to physiological changes. Between 2 and 10% of pregnant women have covert or asymptomatic bacteriuria which is associated with an increased incidence of acute symptomatic UTI in later pregnancy if left untreated. Thus antenatal screening to detect the presence of bacteriuria is justified. Most women will remain abacteriuric throughout the remainder of pregnancy after a single course of antibiotic therapy but a small percentage will fail to respond or have recurrent UTIs. Maternal infection with certain organisms, namely those which resist phagocytosis, may result in transplacental infection of the fetus in utero. Congenital syphilis is preventable and antenatal serological screening is usually routinely performed. Listeriosis following maternal infection in pregnancy is less predictable and the epidemiology of L. monocytogenes remains unclear. Genital tract carriage of sexually transmitted organisms, such as N. gonorrhoeae or C. trachomatis, may also be detected during pregnancy and antibiotic therapy will be indicated to eradicate such organisms and prevent maternal and neonatal morbidity. Antibiotic therapy during pregnancy will not, however, eradicate carriage of GBS from the genital tract, although carriage status at term can now be reliably predicted by using enriched culture techniques and swabbing multiple sites on more than one occasion. Where carriage is confirmed, the administration of intrapartum antibiotics to the mother appears a useful approach in the prevention of early onset neonatal GBS disease. Broad spectrum intrapartum antibiotics may also be indicated when there are complications, such as prolonged labour or premature rupture of membranes, which are associated with a higher incidence of maternal postpartum endometritis and morbidity than in women following uncomplicated vaginal delivery. Serious postnatal sepsis and shock is fortunately now rare. The pharmacokinetics of antibiotics in late pregnancy and the puerperium are altered and maternal serum levels may be reduced by 10-50%. Most antibiotics cross the placenta and are excreted in breast milk. Some agents, such as the beta-lactams, are considered safe in pregnancy and breast-feeding women while other antibiotics are contraindicated owing to risk of toxicity (often rare) or teratogenicity (often theoretical). Caution is necessary with many agents which may cause side effects or toxicity although this does not necessarily contraindicate their use in pregnancy.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Prescribing in pregnancy. Bacterial infections in pregnancy. 352 53


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