[Relation between clinical manifestations and coagulation disorders in 31 cases of meningococcal infections. Evaluation of the efficacity of an early heparin therapy].
Explore the source record for details and available documents.
SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
It is shown that interrelationships between meningococci and positive symbionts can manifest themselves more often in the type of mutual or one-side regulatory reduction of intensity of the associates' growth and career they are displayed in stimulation of the development of pathogenic Neisseria populations. Representatives of three streptococci species (Streptococcus pyogenes, S. faecium and S. faecalis) are the most active antagonists in rate and strength of the suppressive effect in the simple and compound associations. The rest of the Corynebacteria and Staphylococci competitors in multicomponent associations show such properties career.
The red blood cell metabolic parameters ATP, ADP, sigma AN, ATP/ADP, ATP/ATP, energy charge, PAD, 2,3-DPH, Pn were studied in 106 patients with generalized meningococcus infection (GMI) and meningitis of other etiology over their natural history. There was a typical adaptative red blood cell response that featured glycolytic stimulation on hypoxia that ran with impaired red blood cell energy metabolism (RBCEM), negative energy balance. It was the most pronounced at the peak of disease. RBCEM changes occurred in the presence of antioxidative disorders of red blood cells as lowered PAD levels. When early complications, such as shock, brain edema, death developed, there was a high incidence of signs of erythrocytic biochemical disadaptation. The RBCEM changes were associated with the magnitude of cytolysis, i.e. serum AST and AST/ALT levels. The significance of the metabolic changes found in the red blood cells in the pathogenesis and clinical picture of GMI and purulent meningitis is discussed in the paper.
Explore the source record for details and available documents.
Household contacts of patients with group A meningococcal infection were vaccinated with either meningococcal vaccine or tetanus toxoid. Five of the 523 subjects who received tetanus toxoid developed meningococcal meningitis and another four probably had meningococcal disease. Only one possible case of meningococcal infection occurred among 520 contacts vaccinated with meningococcal vaccine. Vaccination had no effect on nasopharyngeal carriage of meningococci. Vaccination of household contacts of patients with group A meningococcal infections is an effective way of using limited supplies of meningococcal vaccine, though its value would be limited in an epidemic. Secondary cases of meningococcal infection often occur within a few days of the index case, and, although vaccine alone seemed to provide adequate prophylaxis in these Nigerian subjects, additional chemoprophylaxis may be needed to cover this critical period.
AIMS: To examine a number of simple clinical features and investigations in children with a non-blanching rash to see which predict meningococcal infection. METHODS: A total of 233 infants and children up to 15 years of age presenting with a non-blanching rash were studied over a period of 12 months. Clinical features and laboratory investigations were recorded at presentation. The ability of each to predict meningococcal infection was examined. RESULTS: Eleven per cent had proven meningococcal infection. Children with meningococcal infection were more likely to be ill, pyrexial (>38.5 degrees C), have purpura, and a capillary refill time of more than two seconds than non-meningococcal children. Five children with meningococcal disease had an axillary temperature below 37.5 degrees C. No child with a rash confined to the distribution of the superior vena cava had meningococcal infection. Investigations were less helpful, although children with meningococcal infection were more likely to have an abnormal neutrophil count and a prolonged international normalised ratio. No child with a C reactive protein of less than 6 mg/l had meningococcal infection. CONCLUSIONS: Most children with meningococcal infection are ill, have a purpuric rash, a fever, and delayed capillary refill. They should be admitted to hospital and treated without delay. Children with a non-blanching rash confined to the distribution of the superior vena cava are very unlikely to have meningococcal infection. Measurement of C reactive protein may be helpful-no child with a normal value had meningococcal infection. Lack of fever at the time of assessment does not exclude meningococcal disease.
4 patients with meningococcal infection and 141 meningococcal carriers were examined. The authors study heterogeneity of human population concerning susceptibility or stability of erythrocytes to adhesive influence of meningococci. In 17.4% of cases erythrocytes were highly susceptible to adhesion of meningococci, in 20.4% were stable to this influence, in 62.2% were moderately susceptible. The highest susceptibility of erythrocytes (out of statistics) was marked at the patients of Kirghiz and Tadjik nationalities. These indexes have the same statistic frequency for the persons with different blood groups (system ABO), independently of their rural or urban place of residence. The high susceptibility of erythrocytes (0.25 GAE or less) to adhesion of meningococci is three times more frequent among the persons with meningococcal infection and carriers of meningococcus. This connection may be regarded as a predisposition of the organism for the infection. Thus, the susceptibility of erythrocytes to adhesion of meningococci gives the possibility to determine the persons who need an urgent immunization at the forming collectives.
Although viral respiratory tract infections may predispose to meningococcal disease, strong evidence that they do so exists only for influenza. Data on laboratory reported cases of respiratory syncytial virus (RSV) infections and meningococcal disease in England and Wales from mid-1989 to mid-1994 were analysed. Although the rise in RSV cases preceded the rise in meningococcal disease cases each winter, the interval between the rise and fall of the two diseases was inconsistent, no association was found between time series after removal of the seasonal component, and there was no evidence that more cases of meningococcal disease occurred in winters with more RSV disease. RSV may have less effect on the two most likely mechanisms whereby influenza predisposes to meningococcal disease, namely lowered immunity and impaired pharyngeal defences.
OBJECTIVE: To determine the length of time cases of meningococcal disease wait before receiving parenteral antibiotic therapy in hospital. METHOD: The hospital case notes of residents of Birmingham who were admitted to local hospitals in 1993 and discharged with a diagnosis of meningitis or meningococcal disease were reviewed. This information was combined with that held by the West Midlands Ambulance Service. RESULTS: Forty out of the 82 patients (49%) who met the case definition had meningococcal infection. Twenty one patients (26%) were admitted by ambulance, 11 of whom had meningococcal infection. The mean time from a request for an ambulance to the patient reaching hospital was 52 min for those with meningococcal infection compared to 55 min for those without. Nineteen patients (47.5%) with meningococcal infection waited more than one hour after admission for antibiotic treatment. Seven had an initial diagnosis of meningitis or meningococcal infection. Ten out of 27 patients with a meningococcal rash (37%), 13 out of 22 patients aged under five years (59%) and 13 out of 24 patients with microbiologically confirmed meningococcal infection (54%) waited more than one hour for treatment. Seven patients with meningococcal infection received benzyl penicillin before admission. Six received hospital antibiotic treatment within the hour. CONCLUSION: The assumption that patients suspected of having meningitis or meningococcal disease are treated promptly once in hospital is not always correct. The results of this study reinforce the need for all doctors to give benzyl penicillin promptly to patients they suspect have meningococcal disease.
Patients whose blood is deficient in the terminal component of complement have an increased susceptibility to meningococcal infection. However, mortality from meningococcal infection is lower in these patients than in immunocompetent subjects. We studied a C6-deficient patient with meningococcal sepsis who received fresh frozen plasma (FFP). The patient's initial plasma endotoxin, C6, and terminal-complement-complex concentrations were low, but rose sharply after treatment with FFP. Samples of the patient's serum taken shortly after admission did not cause endotoxin release from Escherichia coli J5 in vitro, but endotoxin-releasing activity was restored in serum samples taken after infusion of FFP. It is possible that C6-deficient patients have reduced mortality from meningococcal infection because their serum cannot cause acute release of endotoxin from the invading organism and extensive tissue damage is thus avoided.
BACKGROUND: In vitro studies have shown that the neutrophil Fc gamma receptor IIA (FcgammaRIIA) polymorphism influences the phagocytic capacity of neutrophils and the removal of encapsulated bacteria from the bloodstream. In particular, the R/R131 allotype is associated with less phagocytic activity. SUBJECTS AND METHODS: We performed a case-control study to determine the influence of the FcgammaRIIA polymorphism (R/R131, R/H131, H/H131) on the risk and outcome of meningococcal disease. The polymorphisms were measured in 130 patients with microbiologically proven meningococcal disease diagnosed from 1987 to 1998 (cases) and 260 asymptomatic sex-matched blood donors (controls). Clinical manifestations and complications of meningococcal disease were recorded, and a prognostic score (based on age, hemorrhagic diathesis, neurologic signs, and the absence of preadmission antibiotic) therapy was calculated. RESULTS: The distributions of FcgammaRIIA allotypes were similar in cases and controls. However, among patients with meningococcal infection, fulminant meningococcal disease (odds ratio [OR] = 3.9; 95% confidence interval [CI]: 1.0 to 16; P = 0.04) and meningococcemia without meningitis (OR = 3.0; 95% CI: 1.4 to 7.8; P = 0.004) were more common in those with the FcgammaRIIA-R/R131 allotype. Complications were also significantly more frequent in these patients. Of the 42 patients with the R/R131 allotype, 31 (74%) had an adverse prognostic score, compared with 7% (4 of 59) of those with the R/H131 allotype and 3% (1 of 29) of those with the H/H131 allotype (P <0.0001). CONCLUSION: The FcgammaRIIA-R/R131 allotype is associated with more severe forms of meningococcal disease.
Individuals deficient in C3 or a late complement component are susceptible to recurrent meningococcal infections. Since they experience meningococcal episodes mostly with uncommon meningococcal serogroups, vaccination with a tetravalent vaccine containing A, C, Y and W135 polysaccharides has been suggested. We vaccinated a cohort of two C3 and 17 late complement component-deficient (LCCD) patients, revaccinated them 7 years later and investigated the development of their IgG antibodies to the capsular polysaccharides of the meningococcal vaccine. Seven years after the first vaccination levels of IgG antibodies declined compared with the levels present at 6 months after the first vaccination, but were still at least four times higher than before vaccination. Levels of antibodies to Y polysaccharide in serum of complement-deficient patients were rather low but they did not differ significantly from those in serum of healthy non-related controls (P = 0.07). Three months after the second vaccination IgG antibodies against all polysaccharides increased, exceeding those measured at 6 months after the first vaccination. In the 8 years of observation after the first vaccination two new meningococcal infections with strains related to the vaccine (serogroup Y strains) occurred in two patients, 3.5 and 5 years after the first vaccination. Our findings show that high IgG antibody levels against the tetravalent meningococcal polysaccharide vaccine were reached after revaccination of two C3 and 17 LCCD individuals 7 years after the first vaccination. Whether revaccination should be required within a period shorter than 7 years is discussed, since two vaccinees developed meningococcal disease to vaccine serogroup Y.
Meningococcal lipooligosaccharide (LOS) induces a strong proinflammatory response in humans during meningococcal infection. We analyzed the role of LOS in the inflammatory response and virulence during the early infectious process in a mouse model of meningococcal respiratory challenge. An lpxA mutant strain (serogroup B) devoid of LOS (strain Z0204) could not persist in the lungs and did not invade the blood. The persistence in the lungs and invasion of the bloodstream by a rfaD mutant expressing truncated LOS with only lipid A and 3-deoxy-d-manno-2-octulosonic acid molecules (strain Z0401) was intermediate between those of the wild-type and Z0204 strains. Both LOS mutants induced acute pneumonia with the presence of infiltrating polymorphonuclear leukocytes in lungs. Although tumor necrosis factor alpha production was reduced in mice infected with the mutant of devoid LOS, both LOS mutants induced production of other proinflammatory cytokines, such as interleukin-1beta (IL-1beta), IL-6, and the murine IL-8 homolog KC. Together, these results suggest that meningococcal LOS plays a role during the early infectious and invasive process, and they further confirm that other, nonlipopolysaccharide components of Neisseria meningitidis may significantly contribute to the inflammatory reaction of the host.
BACKGROUND: Meningococcal infections associated with late complement component deficiency are rarely severe and usually occur during adolescence and adulthood. We report severe manifestations in a boy in whom the first episode appeared early. CASE REPORT: A 14 year-old gypsy boy was admitted because of a febrile meningococcal meningitis that was complicated by a rapidly extensive and necrotic purpura, obnubilation and clotting abnormalities without hemodynamic anomalies. The patient was given symptomatic therapy and a 12-day course of antibiotics that resulted in rapid and complete recovery. Medical history of this patient showed that he had been admitted at the age of 3 years for a severe febrile purpura with septic shock and clotting abnormalities followed by rapid and complete recovery after symptomatic and antibiotic therapy. No germ had been then isolated. The complement system was studied 3 weeks after the second hospitalization: total hemolytic complement activity could not be detected and C2, C3 and C4 were normal. Examination of the terminal pathway-revealed total C8 deficiency. The patient received meningococcal vaccine and was discharged on oral penicillin prophylaxis. He remained healthy during the ensuing 4 years. CONCLUSIONS: Meningococcal infections associated with late complement component deficiency are generally uncomplicated but they remain potentially severe. Early screening for this late complement component deficiency should be considered after severe clinical manifestations.
Of 45 Russian patients with late complement component deficiency (LCCD) who experienced one to five meningococcal infections, 31 were immunised with a meningococcal A/C/W135/Y polysaccharide vaccine and were followed for 3-8 years. Total and immunoglobulin (Ig) class specific concentration of antibodies to meningococcal polysaccharides in sera of LCCD patients increased significantly 1 month after vaccination and remained elevated for 3 years. Revaccination of LCCD patients 3 years after the first dose restored the total Ig concentrations to those observed 1 year after the first vaccination. Six new episodes of meningococcal infection in four patients developed in the group of 31 vaccinees; six episodes in six patients developed in the same time in the group of 14 non-vaccinated LCCD persons. Survival analysis demonstrated the risk to contract meningococcal disease decreased significantly for vaccinees in comparison to non-vaccinees (P<0.05). Vaccination with of meningococcal tetravalent polysaccharide vaccine decreases the risk of meningococcal infection in LCCD patients.
CONTEXT: Incidence of invasive meningococcal disease has increased recently in persons aged 15 through 24 years. OBJECTIVE: To characterize meningococcal infection in adolescents and young adults in Maryland during the 1990s. DESIGN AND SETTING: Population-based surveillance study for meningococcal disease from January 1, 1990, through December 31, 1999, in Maryland. PATIENTS: Maryland residents diagnosed as having invasive meningococcal disease. MAIN OUTCOME MEASURE: Invasive meningococcal infection. RESULTS: Of 295 total cases, 71 (24.1%) occurred among persons aged 15 through 24 years. Sixteen (22.5%) of these cases were fatal. The annual incidence rate increased from 0.9 to 2.1 cases per 100 000 among 15 through 24 year olds (P =.01). The proportion of all disease increased from 16.0% to 28.9% (P =.03). The incidence and proportion of cases subsequently decreased to 1.0 and 16.4% in 1998 through 1999, respectively. Infection in 15 through 24 year olds was more likely to be fatal than infection in those younger than age 15 years (22.5% vs 4.6%; P =.001). Infection in 15 through 24 year olds, compared with those aged 25 years or older, was more likely to be associated with male sex (66.2% vs 34.8%; P<.001) and serogroup C infection (46.9% vs 20.2%; P<.001), respectively. Infections were potentially preventable with the licensed meningococcal vaccine in 82.8% of 15 through 24 year olds, 68.1% of those younger than 15 years, and 76.8% of adults aged 25 years or older. CONCLUSIONS: Incidence of meningococcal infection in 15 through 24 year olds in Maryland increased and then declined during the 1990s. Infection in this age group was associated with an unusually high case-fatality ratio, and the vast majority of cases were potentially vaccine preventable.
In four recently formed military units pharyngeal meningococcal carrier state and dynamics of nasopharyngeal meningococcal infections have been examined. Carrier state found in at least 50% of recruits at their entering the army has been increased during the first two months for 10-26.4% and it was associated with very significant dynamics of meningococcal infection: changes in carrier state during the first two months have been found in 61.3% of soldiers with very marked changes in distribution of some meningococcal serologic groups among isolated species. Two months later stagnation and lower percentage of the carrier state was observed together with reducing dynamics of meningococcal infection. Meningococcal disease did not occur in the examined environment and this was explained by the absence of virulent meningococcal serotypes. It was concluded that in the risk for meningococcal disease evaluation final identification of meningococcal species isolated from patients and their contacts should be made aiming to timely detection of species known to have significant degree of virulence.
A 15-year-old woman with a history of recurrent episodes of meningococcal infections was admitted to our hospital with signs and symptoms indicating a meningeal inflammation. Since in the last few years some of the patients affected by recurrent meningococcal infections have been recognized to have selective complement deficiencies, the patient's serum was studied for determining the complement function. C8 was found to be present only in traces, with a pattern of partial identity as compared with that of the normal human serum. Moreover, total hemolytic complement was undetectable and could be completely restored with purified C8, but not with other complement components; thus, we concluded for the presence of a C8 deficiency state. Further reconstitution experiments carried out with sera having selective deficiencies of either C8 beta or C8 alpha-gamma subunits allowed us to recognize the presence of a dysfunctional C8 molecule lacking the beta chain, but possessing the alpha-gamma subunit. The clinical history of the patient, characterized by recurrent meningococcal infections, further supports the current concept of an increased susceptibility of the C8 beta-deficient patients to Neisseria meningitidis infections.