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

Thirteen cases of group D streptococcal neonatal sepsis and/or meningitis were identified at the Cincinnati Children's Hospital from 1970 to 1976. Ages at onset of disease ranged from 1 to 25 days. The most frequent symptoms were fever (five cases), lethargy (five cases), and respiratory difficulty (four cases). Blood cultures for seven infants were positive; CSF cultures for five infants were positive; and CSF and blood cultures for one infant were both positive. In 12 patients, parenteral antibiotic therapy consisted of a penicillin and an aminoglycoside. One infant with a severe meningomyelocele died. The other 12 infants showed a rapid clinical response with seven patients improving within 48 hours of the start of therapy. Infection with group D streptococcus results in a low-grade systemic disease in both full-term and premature infants that responds favorably to appropriate therapy.
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PMID:Systemic group D streptococcal infection in newborn infants. 10 22

Nowadays, in severe infections during the neonatal period new bacteria--group B streptococci--have to be taken into account, since in some clinics they already predominate over gramnegative rods. Septicemia and meningitis may be caused by group B streptococci. The septicemia which especially threatents prematures starts with apnoeic spells in the very first hours after birth and may be easily misdiagnosed as an idiopathic respiratory distress syndrome. The mortality is very high (about 60%). Meningitis starts later, normally during the 3rd to 4th week. Seizures are typical at the onset. Group B streptococci may be identified in the CSF by counterimmunoelectrophoresis within one hour. The prognosis is more favourable in meningitis than in septicemia (mortality about 20%). Survivors have little neurological sequelae. Penicillin G or ampicillin combination with an aminoglycoside is recommended as chemotherapy. Exchange transfusion should be considered early. Group B streptococci causing the septic form may be transfered during labour since up to 25% of pregnant women are colonized. Nosocomial transmission of group B streptococci may be the reason for meningitis. Prophylactic penicillin does not seem to help in preventing the disease, but it is possible, that meningitis of the newborn may be prevented by immunizing the mother during pregnancy.
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PMID:[Group B streptococcus infections during the neonatal period (author's transl)]. 35 54

The conclusions from our studies to date may be summarized as follows. (1) Invasive E. coli strains causing neonatal meningitis are encapsulated. At least 80% of those strains inducing mengitis are K1 and approximately 40% of those strains isolated from infants with septicemia but without meningitis are also K1. Invasiveness is best related to the K1 antigen and not to E. coli O and H antigens. (2) The capsular content of CSF strains is not related to their invasiveness. In contrast to observations reporting higher K capsular polysaccharide content and molecular weight of E. coli invading the renal parenychma as compared with those E. coli confined to the bladder or in the stool, there were no differences among DSF K1 strains. Sepculation as to the mechanism of the invasive properties conferred by acidic capsular polysaccharides may be derived from the literature. Unencapsulated or "rough bacteria" are susceptible to the bactericidal action of agammaglobulinemice sera (15, 53). When injected into precolostral (agammaglobulinemic but complement containing), cesarian-delivered, and antigen-deprived piglets, unencapsulated bacteria are rapidly cleared from the circulation. In contrast, smooth bacteria injected into these same animals circulate without detectable splenic or hepatic clearance, multiply, and result in the death of these animals. The mechanism of the resistance of encapsulated bacteria has been postulated to be due to the inaccessibility of the deep somatic antigen structures capable of activating the alternate complement pathway system. Thus, opsoninization and other host complement-dependent activities may of necessity be antibody mediated for encapsulated bacteria. This complement resistance of encapsulated organisms may be quanititative and studies should be done to determine differences among various K1 E. coli strains. (3) K1 strains are widely prevalent among infants, children, and adults and are quickly transmitted to infants. In most cases the source of the infecting strain in diseased infants is the mother. However, transmission from attendants, demonstrable in our studies, is also a possible mechanism. (4) A protective role of serum anticapsular antibodies in animal models has been demonstrated. Our initial observations indicating low serum K1 antibodies in the general population and the finding that K1 antibodies are predominantly IgM in two animal species studied so far suggest that colostral K1 antibodies may be important in conferring immunity to this disease.
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PMID:A review: relation between invasiveness and the K1 capsular polysaccharide of Escherichia coli. 110 53

In a study of neonatal malaria at the University of Benin Teaching Hospital, we documented the features of six neonates in an effort to highlight that the manifestations of malaria in the newborn cannot be readily distinguished from those of neonatal sepsis. Maternal peripartum fever, an important identifiable risk factor for neonatal sepsis, also featured prominently in the mothers of these babies. These mothers ingested pyrimethamine weekly in the course of their pregnancy. All six neonates were critically ill. Their cultures of blood, CSF and urine for bacterial pathogens yielded no growth and they were unresponsive to conventional antibiotics. The diagnosis of malaria should be considered, in spite of regular maternal ingestion of antimalarial prophylaxis with pyrimethamine, in critically ill neonates in malarious areas. All six neonates responded satisfactorily to oral doses of chloroquine. We therefore suggest that a blood film for malaria parasites be included in screening for neonatal sepsis as part of the initial work-up.
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PMID:Malaria parasitaemia in neonates with predisposing risk factors for neonatal sepsis: report of six cases. 128 46

The etiology of purulent meningitis was investigated in 109 newborn infants admitted in a neonatal intensive care unit throughout a ten year period. Bacterial pathogens were isolated from the CSF in 57 (52.2%) neonates. There was a predominance of Gram-negative bacilli isolated in 38 (34.9%) neonates. Gram-positive cocci were isolated from CSF in only 12 (11.0%) neonates. Microorganisms associated with nosocomial septicemia and meningitis in neonates--Klebsiella sp, Salmonella sp. Enterobacter sp, Pseudomonas sp, Flavobacterium meningosepticum and Serratia marcescens--were responsible for presumptive etiology in 38 (49.3%) among 77 patients with positive cultures in "closed sites". They were isolated from 22 (57.0%) neonates with prior hospitalization but only from 12 (34.3%) neonates coming directly from their households (chi 2 = 4.08; p < 0.05). The mortality rate was significantly higher in patients with positive CSF cultures (47.4%) in comparison to patients with negative cultures (18.4%) (X2 = 5.01; p < 0.05). It is possible to conclude that Gram-negative bacilli, many of them of hospital origin, are the major pathogens in this study. An improvement on neonatal health care and a scrupulous control of neonatal nosocomial infections are recommended.
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PMID:[Neonatal bacterial meningitis: etiological agents in 109 cases during a 10 year period]. 130 5

Neonatal hematopoiesis and host defense are developmentally immature and under states of increased demand predispose the newborn to peripheral cytopenias and depletion of bone marrow storage pool reserves. We have previously demonstrated that recombinant human granulocyte colony-stimulating factor (rhG-CSF) can significantly modulate neonatal rat granulopoiesis and act synergistically with antibiotic therapy to reduce the mortality rate during experimental group B streptococcal sepsis. Stem cell factor (SCF) has been shown to stimulate early hematopoietic progenitor cells and, in the presence of lineage-specific CSFs, enhance committed progenitor cell proliferation. In the present study we examined the in vivo neonatal hematologic effects of recombinant rat (rr) SCF (14 days), simultaneous rrSCF + rhG-CSF (14 days), and sequential combination of rrSCF (7 days) + rhG-CSF (7 days). Sprague-Dawley newborn rats (less than or equal to 24 hours) were injected intraperitoneal (IP) x 14 days with the above combinations. rrSCF (0 to 200 micrograms/kg/d) had a negligible effect on the peripheral platelet count and absolute neutrophil count (ANC) but the diminution in the hematocrit during the first 10 days of treatment was less pronounced (P = .0001). However, the simultaneous use of rrSCF + rhG-CSF synergistically increased the circulating day 6 to 13 ANC (P = .001). Similarly, sequential rrSCF + rhG-SCF also had a synergistic significant effect during the second week of therapy on the circulating ANC (P = .01). The bone marrow neutrophil storage and proliferative pools were also significantly increased in newborn rats treated with rrSCF + rhG-CSF versus rhG-CSF (P = .02). The bone marrow and liver/spleen CFU-GM pool was unchanged; however, the CFU-GM proliferative rates were significantly increased in the rrSCF + rhG-CSF group (P = .04). rrSCF also induced a significant increase in the bone marrow and liver/spleen mast cell pool (P = .002). Lastly, rrSCF x 14 days +/- rhG-CSF significantly reduced the mortality rate at 48 and 120 hours after experimental group B streptococcus sepsis (P = .03 and .05, respectively). These data suggest that combination SCF + G-CSF therapy compared with G-CSF alone significantly increases the neonatal rat peripheral neutrophil count, bone marrow myeloid pools and proliferative rates, and induces a reduction in the mortality rate during experimental bacterial sepsis. SCF therapy may have future potential applications in the modulation of human neonatal hematopoiesis and host defense.
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PMID:Effect of stem cell factor with and without granulocyte colony-stimulating factor on neonatal hematopoiesis: in vivo induction of newborn myelopoiesis and reduction of mortality during experimental group B streptococcal sepsis. 137 57

Pretreatment with recombinant human granulocyte CSF (G-CSF) protected mice in two different models of septic shock. Intravenous injection of 250 micrograms/kg G-CSF to mice prevented lethality induced by 5 mg/kg LPS. Injection of 50 micrograms/kg G-CSF protected galactosamine-sensitized mice against LPS-induced hepatitis. In either case, this protection was accompanied by a suppression of LPS-induced serum TNF activity. In contrast, when galactosamine-sensitized mice were pretreated with 50 micrograms/kg murine recombinant granulocyte/macrophage CSF instead of G-CSF and subsequently challenged with LPS, serum TNF activity was significantly enhanced and mortality was increased. The suppressive effect of G-CSF on LPS-induced TNF production was also demonstrated in rats. In vivo, no TNF was detectable in the blood of LPS-treated rats, which had been pretreated with G-CSF. Ex vivo, alveolar macrophages, bone marrow macrophages, Kupffer cells, or peritoneal macrophages prepared from G-CSF-treated rats produced significantly less TNF upon stimulation with LPS than corresponding populations from control rats. However, when these macrophage populations were incubated with G-CSF in vitro, LPS-induced TNF production was unaffected. These data suggest that the G-CSF-mediated suppression of TNF production is not a direct effect of G-CSF on macrophages. To examine whether, independent of the protection against LPS, G-CSF treatment still activated neutrophils, it was demonstrated that granulocytes from G-CSF-treated rats were primed for PMA-induced oxidative burst and for ionophore/arachidonic acid-stimulated lipoxygenase product formation. The experiments of this study support the notion that G-CSF is a negative feedback signal for macrophage-derived TNF-alpha production during Gram-negative sepsis.
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PMID:Granulocyte colony-stimulating factor treatment protects rodents against lipopolysaccharide-induced toxicity via suppression of systemic tumor necrosis factor-alpha. 137 68

Newborns are predisposed to neutropenia and thrombocytopenia during bacterial sepsis. The presence of peripheral cytopenias during overwhelming infection may be secondary to decreased hematopoietic growth factor production during states of increased demand. We therefore examined circulating levels of granulocyte-colony stimulating factor (G-CSF) and IL-3, production of G-CSF and IL-3 from unstimulated and stimulated mononuclear cells (MNC), expression of G-CSF and IL-3 genes during unstimulated and stimulated conditions, and equilibrium and binding of G-CSF receptors on mature effector peripheral blood cells of adults and neonates. Serum from cord and adult peripheral blood contained negligible amounts of both G-CSF (less than or equal to 50 pg/mL) and IL-3 (less than or equal to 5 pg/mL). Constitutive supernatant levels of G-CSF and IL-3 from cord and adult unstimulated MNC were also undetectable. However, there was a significant difference in G-CSF and IL-3 production from stimulated cord and adult MNC. Supernatants from stimulated adult MNC had significantly more G-CSF (p less than 0.007) and IL-3 (p less than 0.02). Additionally, Northern blot hybridization and densitometry of autoradiographs demonstrated significantly more G-CSF and IL-3 mRNA transcripts from adult than from cord MNC. Lastly, affinity, binding, and number of G-CSF receptors on cord and adult peripheral effector cells were equal. These data suggest that, during states of increased demand, cord MNC produce less G-CSF and IL-3 than do adult MNC and have an associated reduction in their respective mRNA transcripts. These findings may have implications in the pathogenesis of neonatal cytopenias during states of increased demand, such as sepsis.
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PMID:Decreased G-CSF and IL-3 production and gene expression from mononuclear cells of newborn infants. 137 59

A previously healthy breast-fed baby was admitted at 10 days of age to a hospital in the north of Pakistan with diarrhoea and fever. He was treated for suspected sepsis with intravenous cefotaxime and tobramycin. Cultures of blood and faeces at that time proved negative. At 12 days of age, seizures began and examination of CSF revealed evidence of pyogenic meningitis but bacteria were neither seen microscopically nor isolated in culture. Ceftazidime was substituted for cefotaxime and carbenicillin was given also. Since the baby's condition continued to deteriorate with persistent fever, vomiting and recurrent seizures, he was transferred to the Aga Khan University Hospital, Karachi. Examination of CSF there confirmed the diagnosis of pyogenic meningitis and revealed Gram-negative bacteria. Cultures of CSF and faeces yielded Salmonella paratyphi A but the blood culture was negative. The isolate was found to be multiple antimicrobially resistant but sensitive to ciprofloxacin. Treatment with this drug was therefore started 3 days after the baby's admission to the Aga Khan Hospital. Within 36 h, improvement was observed. From then onwards, the baby made a progressive recovery and was healthy when seen at 7 months of age.
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PMID:Eradication of a multiple drug resistant Salmonella paratyphi A causing meningitis with ciprofloxacin. 143 Nov 77

Hypereosinophilia has been detected in the CSF of 22 patients in a series of 81 cases of shunt infection. It was related with the evolution of the sepsis. Its persistence at the end of treatment appeared to predict later complications, septic or obstructive, and it could be the sign of latent infection. HE might be the result of a specific reaction directed against the infected material, but a non-specific process cannot be eliminated.
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PMID:Cerebro-spinal fluid eosinophilia in shunt infections. 145 41


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