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At least 253 records · Page 14Linked to original sources
PubMed1981

Disseminated intravascular coagulation, antithrombin III, and complement in meningococcal infections.

Serial assessments of some blood coagulation factors, antithrombin III (AT III), and complement were made in 18 patients with meningococcal (mgc) infection. All patients displayed laboratory evidence of activation of the blood clotting system. Two patients showed clinical signs of disseminated intravascular coagulation. Only AT III differed significantly between patients with and without complications. There was no correlation between changes in blood clotting, activation of the complement system and the course or duration of the disease. These results do not enable one t identify patients who need specific prophylactic therapy. Controlled clinical trials, including administration of heparin, dextran, aprotinin, and others, are still required to ensure optimal treatment in fulminant mgc infections.

Adolescent↗
PubMed1977

Protective effect of polymyxin B sulfate in experimental meningococcal infection in mice.

The mouse model of intraperitoneal meningococcal sepsis was used to evaluate the antiendotoxic activity of polymyxin B sulfate independent of its antibiotic effects. Administered either before or after the infective challenge therapeutic doses of polymyxin B sulfate produced small but significant increases in survival over unprotected animals. These results also suggest that endotoxin contributes to the outcome in this variety of Gram-negative infection.

Animals↗
PubMed1991

[Renal function in meningococcal infection. Analysis of 116 cases].

We study the renal function in meningococcal sepsis in other to get prognostic data in disease evolution. We include 116 patients of whom we take data of anamnesis; physical examination; blood, urine and cerebrospinal fluid biochemical and microbiologic studies and TISS and APS score. We analyze qualitative and quantitative data of renal function statistical and we compare with another prognostic data of disease. We find that renal failure in meningococcal sepsis gets worse the prognostic of the disease.

Acute Kidney Injury↗
PubMed1985

[Current therapy of meningococcal infection in childhood].

The article discusses the present therapy of acute meningococcal septicemia. Besides adequate antibiotic treatment, the importance of early and aggressive shock and respiratory therapy, i.e. endotracheal intubation and mechanical ventilation, is stressed. The role of corticosteroids is discussed. The use of anticoagulants, fibrinolytic agents and inhibitors of fibrinolysis is discouraged.

Adrenal Cortex Hormones↗
PubMed1990

Prevalence of hereditary properdin, C7 and C8 deficiencies in patients with meningococcal infections.

High incidence of hereditary complement (C) deficiencies was found among 101 patients who had a meningococcal disease. This study revealed 11 non-related patients with complete C deficiency: five deficient in C7, three in C8, two in properdin and one in C2. Additional C-deficient individuals, most of them with no history of severe bacterial infections, were detected in family studies. The C8-deficient patients were found to have a selective deficiency of the C8-beta subunit and a reduced expression of the alpha/gamma subunit. Only a few families with properdin deficiency have been described so far. However, it is likely that frequent analysis of the activity of the alternative C pathway in survivors of severe bacterial infections will disclose numerous properdin-deficient patients. All our C7-, C8- and properdin-deficient patients are Sephardic Jews whose families originated from Morocco, Yemen (C7 and C8 deficient) or Tunisia (properdin deficient). This and other findings indicate that the type of complement abnormality found in association with meningococcal infections varies with the ethnic origin of the patient.

Adolescent↗
PubMed1981

[Survey of gonococcal and meningococcal infections. Results from a systematic study of patients from an urban dispensary and sexual partners (author's transl)].

Over a period of 28 months, 605 strains of gonococci and 302 strains of meningococci have been isolated in an urban dispensary. The study was particularly concerned with the identification of gonococcal and meningococcal strains isolated from the patients sexual partners and with epidemiological distribution of the two species. There was only little seasonal variations in the occurrence of gonococcal infections. The frequency of meningococcal infections (which are only poorly transmitted, by the nasopharyngeal route) varied inconsistently during the period covered.

Female↗
PubMed2000

Seroconversion and duration of immunity after vaccination against group C meningococcal infection in young children.

An increase in the incidence of group C meningococcal disease was observed in the Murcia Region (Spain) during 1996-1997. In September 1997, a massive vaccination campaign was implemented among the population aged 18 months to 19 years. The aim of this study was to assess the seroconversion rate of children aged 18-59 months and the persistence of immune response 1 year after vaccination. A total of 296 children were included. Blood samples were obtained before vaccination and 1 month and 1 year after vaccination. Three point seven percent of the children had bactericidal antibody titres of >/=1:8 before vaccination. One month after vaccination seroconversion was 63.7%, with a growing trend related to age at vaccination (p<0.0001). The increase in antibody titres was shown to be quantitatively greater above the age of 36 months (p<0.0001). One year after vaccination only 4.3% of the children who initially seroconverted still had bactericidal activity. Seroconversion in children under 5 increases with age but antibodies decline rapidly in the year following vaccination.

Antigens, Bacterial↗
PubMed2006

Deficient alternative complement pathway activation due to factor D deficiency by 2 novel mutations in the complement factor D gene in a family with meningococcal infections.

The complement system is an essential element in our innate defense against infections with Neisseria meningitidis. We describe 2 cases of meningococcal septic shock, 1 of them fatal, in 2 children of a Turkish family. In the surviving patient, alternative pathway activation was absent and factor D plasma concentrations were undetectable. Concentrations of mannose-binding lectin (MBL), C1q, C4 and C3, factor B, properdin, factor H, and factor I were normal. Mutation analysis of the factor D gene revealed a T638 > G (Val213 > Gly) and a T640 > C (Cys214 > Arg) mutation in the genomic DNA from the patient, both in homozygous form. The consanguineous parents and an unaffected sister had these mutations in heterozygous form. In vitro incubation of factor-D-deficient plasma of the boy with serogroup B N meningitidis showed normal MBL-mediated complement activation but no formation of the alternative pathway C3-convertase C3bBbP, and severely decreased C3bc formation and terminal complement activation. The defect was restored after supplementation with factor D. In conclusion, this is the second report of a factor D gene mutation leading to factor D deficiency in a family with meningococcal disease. This deficiency abolishes alternative-pathway dependent complement activation by N meningitidis, and leads to an increased susceptibility to invasive meningococcal disease.

Amino Acid Substitution↗
PubMed2000

Hypocalcaemia in severe meningococcal infections.

AIM: To determine the incidence of hypocalcaemia in critically ill children with meningococcal disease. METHODS: In a prospective cohort study, 70 of 80 patients admitted consecutively with a clinical diagnosis of meningococcal disease to intensive care had measurements of total and ionised calcium on admission. Parathormone and calcitonin were measured in a proportion of the children. RESULTS: Total and ionised calcium concentrations were low in 70% of the children. There was a weak relation of calcium concentration to the volume of blood derived colloid which had been given, but a good relation to disease severity, where sicker children had lower calcium concentrations. Although the parathormone concentration was higher in children with lower calcium concentrations, some children had low ionised calcium concentrations, without an increase of parathormone concentration. Serum calcitonin concentration was not related to calcium concentrations. CONCLUSION: Hypocalcaemia is common in meningococcal disease.

Calcitonin↗