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PubMed1996

Inherited prethrombotic disorders and infectious purpura.

Patients with severe meningococcal infection are characterized by extensive microvascular thrombosis, consumption coagulopathy and secondary hemorrhages. The contribution of the inherited prethrombotic disorders to the severity of the disease course is not established yet. Here, we report on the levels of protein C, protein S, antithrombin and the presence of the factor V Leiden mutation (R506Q) in 50 patients with meningococcal disease, as determined 6 to 58 months after hospital discharge. In addition, we recalled the parents of 16 deceased patients to screen for the mutation in factor V, an abnormality which results in resistance to activated protein C. Among the patients, the prevalence of the genetic risk factors for thrombosis was not higher than expected on the basis of their prevalence in the general population. Moreover, the prevalence of the factor V Leiden mutation was not increased among the parents of the deceased patients. The individual plasma levels of protein C, protein S, and antithrombin did not differ between the patients with or without severe purpura. The present data constitute circumstantial evidence that primary defects in the natural anticoagulant systems do not play a major role in the severity of the disease course. Screening of patients with infectious purpura for inherited thrombotic risk factors is therefore not indicated.

Adolescent↗

PubMed1992

Clusters of meningococcal disease in France (1987-1988).

We analyzed 814 cases of meningococcal disease notified in 1987 and 1988 to the Ministry of Health. Data were obtained by report forms including informations about possible additional cases among contacts. Coprimary cases (occurring within 24 hours after the index case) and secondary cases (occurring more than 24 hours after index case) were all reviewed. Twenty eight clusters of meningococcal disease were identified involving 65 cases (8% of total cases). Twelve of the 814 cases (1.5%) were coprimary cases of an index case and 25 (3%) were secondary cases. The secondary attack rate was 530/100,000 among household contacts and 31/100,000 among school contacts. Seventy two per cent of the secondary cases occurred in the first week after index case. Thirty-eight percent of the secondary cases occurred in the 15-20 age group as opposed to 15% of single cases. Serogroup A was more often found in coprimary (33%) and secondary cases (17%) than in single cases (6%). In France, prophylaxis of secondary cases is administered to the classroom contacts of a case of meningococcal infection but is not required for the entire school except under epidemic conditions.

Adolescent↗

PubMed1991

[The determination of antimeningococcal antibodies in the saliva of healthy people].

The determination of antibodies to the group-specific polysaccharide of group A meningococci (PS-A) in the saliva of 162 healthy persons at different seasons of the year revealed that antimeningococcal antibodies could be detected in all examines. The range of concentrations of antibodies to PS-A varied between 0.1 and 33.0 U/ml. The comparison of antibody content with the levels of morbidity in meningococcal infection and carriership made it possible to determine two threshold levels of antibody concentration: 9.0 U/ml and 18.0 U/ml.

Adolescent↗

PubMed1983

[Advances in the treatment of endotoxic shock].

Authors present their adopted measures, in the different clinical stages of endotoxic shock with a phisiological approach, paying special attention to those secondary to meningococcal infections.

Adrenal Cortex Hormones↗

PubMedDate not supplied

Serogroup Y meningococcal disease in Chicago, 1991-1997.

CONTEXT: In 1994, surveillance by the Chicago Department of Public Health detected a growing trend in the proportion of invasive meningococcal infections caused by serogroup Y. OBJECTIVE: To examine the emergence of serogroup Y meningococcal disease and compare its clinical characteristics with those of other meningococcal serogroups. DESIGN: Population-based retrospective review of surveillance records; medical record review and cohort analysis of serogroup Y vs non-serogroup Y case patients. SETTING: Chicago, III. PARTICIPANTS: City residents with Neisseria meningitidis isolated from a normally sterile site from January 1, 1991, through December 31, 1997; cohort analysis included those identified through March 31, 1996. MAIN OUTCOME MEASURES: Serogroup-specific incidence, demographics, and clinical outcomes. RESULTS: We identified 214 case patients; 53 (25%) had serogroup Y. The attack rate of serogroup Y meningococcal disease increased from 0.04 cases per 100000 in 1991 to a peak of 0.82 cases per 100000 in 1995 and subsequently decreased to 0.26 cases per 100000 and 0.34 cases per 100000 in 1996 and 1997, respectively. Compared with patients infected by other serogroups, patients with serogroup Y were older (median age, 16 years vs 1 year; P = .001) and more likely to have a chronic underlying illness (prevalence ratio, 2.3; 95% confidence interval, 1.2-4.4). Outcome did not differ significantly between the 2 groups. Multilocus enzyme electrophoresis typing of isolates from 19 case patients identified 5 different types. We found no clustering among the enzyme types by age, race/ethnicity, community area, or time. CONCLUSIONS: Serogroup Y emerged as the most frequent cause of meningococcal disease in Chicago in 1995 and accounted for a substantial proportion of cases in 1996 and 1997. Current data suggest that the magnitude of serogroup Y meningococcal disease is sufficient for vaccine developers to incorporate serogroup Y into new vaccines.

Adolescent↗

PubMed2002

Molecular detection and characterization of Neisseria meningitidis.

Immediate management of meningococcal infections is a medical emergency that requires rapid identification and typing of bacterial strains. Isolation of Neisseria meningitidis is hindered by early antibiotic treatment. Molecular (nonculture) methods of diagnosis and characterization of N. meningitidis permit to overcome this failure. This bacterium is highly variable due to frequent horizontal DNA exchange between strains. Molecular approaches of typing allow a reliable tracking of meningococcal strains and a powerful epidemiological analysis.

DNA Fingerprinting↗

PubMed1999

PCR identification of the group A Neisseria meningitidis gene in cerebrospinal fluid.

The aim of this study was to develop a PCR method for direct identification of Neisseria meningitidis serogroup A in cerebrospinal fluid. The assay makes use of unique sites within the gene cassette responsible for expression of the (alpha1 --> 6)-linked N-acetyl-D-mannosamine-1-phosphate serogroup A capsule. A total of 67 different N. meningitidis strains and 12 clinical samples of CSF, culture positive for N. meningitidis, were examined. All the strains and samples of N. meningitidis serogroup A were correctly identified by an amplified PCR product of 519 bp. The PCR method for identification is specific for the group A gene of N. meningitidis. The assay may contribute to reducing recurrent, devastating epidemics of meningococcal infection by providing a diagnostic tool for grouping in developing countries where problems with false negative cultures are common and vaccination against serogroup A meningococci may be required.

Cells, Cultured↗

PubMed1990

Risk factors associated with a school-related outbreak of serogroup C meningococcal disease.

An outbreak of Neisseria meningitidis sero-group C disease occurred in four eighth grade students and in a younger sibling of another eighth grade student attending an intermediate school (seventh and eighth grades) in Santa Clara County, CA. Four cases had onset within 3 days in January, 1989, with the fifth case occurring approximately 10 days later. A case-control study was performed to determine risk factors associated with serogroup C meningococcal infection (disease or carriage) in this eighth grade class. Students were more likely to be infected if they had had a preceding viral-like respiratory illness characterized by fever (odds ratio (OR) 5.3, P = 0.03) or cough (OR 5.1, P = 0.048). A ski trip (OR 6.3, P = 0.01) and a poster-making session for a school dance (OR 3.7, P = 0.08) were identified as possible settings for a common exposure. Spending time with two specific students during lunchtime or outside of school was associated with an increased risk of infection (OR 7.0, P = 0.054; OR 5.8, P = 0.04).

Adolescent↗

PubMed1995

Meningococcal endocarditis presenting as cellulitis.

We report the case of a patient with mixed connective tissue disease who presented with two very unusual manifestations of meningococcal disease, cellulitis and endocarditis, concurrently. We also review the literature concerning Neisseria meningitidis as a causative agent of cellulitis or endocarditis. While meningococcal endocarditis or cellulitis is very rare, autoimmune disease predisposes patients to meningococcal infection. Therefore, unusual infections with this organism should be considered in the differential diagnosis of fever and rash in patients with connective tissue diseases.

Cellulitis↗

PubMed1983

[Diagnostic test-system for the immunoenzymatic detection of meningococcal antigen].

To detect meningococcal antigen, the use of the enzyme-labeled immunosorbent assay (ELISA), a new variant of the immunoenzymatic method, permitting one to carry out quantitative analysis, is proposed. The optimum conditions for the test to detect group A meningococcal antigen, as well as the procedure for the approbation of the test on patients with meningococcal infection and on healthy persons, have been worked out. The method is shown to be highly specific and sensitive.

Animals↗

PubMed1982

Shift in the age-distribution of meningococcal disease as predictor of an epidemic?

Demographic data for several years before, during, and after an epidemic of meningococcal meningitis show that the age-distribution of the disease shifts considerably during an epidemic--although the highest incidence of meningococcal infections was still that among children under 5 years old, the proportion of patients aged greater than 4 years increased significantly. The ratio of the number of cases aged over 4 years to that aged up to 4 years was 0.833 and 0.775 in two non-epidemic periods, but 2.95 and 2.29 in two epidemic years. Careful demographic surveillance may reveal the approach of a meningococcal epidemic sooner than do the present surveillance methods.

Adolescent↗

PubMed1988

BK virus infection in children with cancer: serological response studied by haemagglutination inhibition, neutralization, and IgG- and IgM-class specific ELISA tests.

We recently developed enzyme-linked immunosorbent assays (ELISAs) for the detection of anti-BK virus IgG- and IgM-antibodies, and also a convenient and rapid serum neutralization test. Complemented by a traditional haemagglutination inhibition test (HAI) these methods were used to investigate the longitudinal response to BKV infection in sequentially taken sera from 29 children under treatment for cancer. In separate experiments it was shown that the results were not at any extent influenced by antibodies against other polyomaviruses. At the time of diagnosis the prevalence of specific IgG- and IgM-antibodies and the geometric mean IgG levels were not significantly different for the patients compared with a group of healthy children. The primary infections seemed to occur at the same age for the two groups of children. Seven of the patients had a primary infection with BKV. The results indicate that the host response in moderately immunosuppressed children during primary infection is the same as expected for healthy individuals with the development of specific IgG, HAI, and NT antibodies, and, usually, production of BKV-IgM for several months. The results indicated that whether specific IgM was demonstrated in the first sample or appeared later during a reactivation episode, this parameter was correlated with profound immunosuppression. Significant titre changes, detectable IgM antibodies and/or seroconversions were demonstrated in 69% (20/29) of the cancer patients. Such indications of recent viral activity was recorded in 42% (8/19) of children with meningococcal infections. The observation periods for the two groups of patients are, however, not directly comparable.

Antibodies, Viral↗

PubMed1986

Meningococcal serotypes and serogroup B disease in north-west Europe.

Examination of the trends of meningococcal infection in Norway, Iceland, Faroe Islands, Denmark, England and Wales, and the Netherlands, has shown that Neisseria meningitidis B:2b:P1.2 and/or B:2a:P1.2 phenotypes were associated with peaks of infection in the Netherlands in 1966, in Iceland 1976-77, and in England and Wales in 1973-75. These strains were present in all six countries in the decade 1970-80 but their prevalence is now practically negligible. In contrast the prevalence of the B:15:P1.16 phenotype has risen. In the Faroe Islands and northern Norway this change in serotype prevalence has been followed by rises in incidence of meningococcal disease; the same is happening in England and Wales but not yet in the other countries.

Adult↗

PubMed1986

An outbreak of meningococcal disease in Gloucestershire.

Between October, 1981, and March, 1986, there were 65 cases of meningococcal infection, about five times the expected number, in Gloucester Health District. The cases, mainly in teenagers and young adults, were clustered in the Stroud district and in the southern part of Gloucester City, and most were caused by a sulphonamide-resistant group B type 15 meningococcus. 2 patients died. Only 57% of meningitis cases were formally notified. 7 (11%) patients had septicaemia without meningitis, not a notifiable disease. All meningococcal disease should be made notifiable and meningococci should be serotyped routinely so that the epidemiology of the disease can be monitored before the introduction of suitable vaccines.

Adolescent↗

PubMed1984

The latency of serum acute phase proteins in meningococcal septicemia, with special emphasis on lactoferrin.

Serum lactoferrin concentrations were elevated in almost all children with meningococcal septicemia, in whom the disease had been clinically apparent for less than 18 hours, while the concentrations were normal or only moderately elevated in patients who had had the disease longer before being admitted. Concentrations of C-reactive protein (CRP) were markedly elevated, even with a time lapse of less than six hours, making this the most suitable parameter for the early diagnosis of severe meningococcal infection. Following an operative injury on children the lactoferrin concentrations changed very little. More than six hours after an operation, however, a marked increase in CRP-values was observed, possibly indicating differentiation of this response from that of bacterial infection. The concomitant study of serum alpha 1-antitrypsin, alpha 1-antichymotrypsin, orosomucoid and haptoglobin did not uncover results of great significance with regard to early changes.

Acute Disease↗

PubMed2004

Role of interleukin 6 in myocardial dysfunction of meningococcal septic shock.

BACKGROUND: Myocardial failure has a central role in the complex pathophysiology of septic shock and contributes to organ failure and death. During the sepsis-induced inflammatory process, specific factors are released that depress myocardial contractile function. We aimed to identify these mediators of myocardial depression in meningococcal septic shock. METHODS: We combined gene-expression profiling with protein and cellular methods to identify a serum factor causing cardiac dysfunction in meningococcal septic shock. We identified genes that were significantly upregulated in blood after exposure to meningococci. We then selected for further analysis those genes whose protein products had properties of a myocardial depressant factor--specifically a 12-25 kDa heat-stable protein that is released into serum shortly after onset of meningococcal infection. FINDINGS: We identified 174 significantly upregulated genes in meningococcus-infected blood: six encoded proteins that were of the predicted size and had characteristics of a myocardial depressant factor. Of these, interleukin 6 caused significant myocardial depression in vitro. Removal of interleukin 6 from serum samples of patients with meningococcaemia and from supernatants of inflammatory cells stimulated by meningococci in vitro abolished the negative inotropic activity. Furthermore, concentrations in serum of interleukin 6 strongly predicted degree of myocardial dysfunction and severity of disease in children with meningococcal septic shock. INTERPRETATION: Interleukin 6 is a mediator of myocardial depression in meningococcal disease. This cytokine and its downstream mediators could be a target for future treatment strategies.

Adult↗

PubMed2000

Survey of the prescribing of chemoprophylaxis to index cases of invasive meningococcal disease.

Chemoprophylaxis is given to contacts of cases of invasive meningococcal disease to reduce the risk of secondary cases by eradicating carriage. In the United Kingdom index cases are also recommended to receive chemoprophylaxis. This is usually undertaken by the clinical team managing the case. One hundred and fifty cases of probable meningococcal infection notified to the consultants in communicable disease control in a local health authority were reviewed to identify the proportion receiving chemoprophylaxis and to examine the final clinical outcome, in terms of diagnosis, of each case. Twenty-five per cent of notified cases (37) did not receive chemoprophylaxis and this proportion varied significantly between three local hospitals. We estimate that 15 of the 37 index cases who did not receive chemoprophylaxis were likely to have had invasive meningococcal disease.

Antibiotic Prophylaxis↗

PubMed1996

Meningococcemia.

Meningococcal infection is a contagious disease that is spread via the respiratory route through pharyngeal secretions. Clinical manifestations range from occult bacteremia to overwhelming septicemia or meningitis. Skin manifestations often develop and may be the first sign that leads to clinical suspicion of meningococcemia. Treatment consists of antibiotic therapy and supportive care, which may include aggressive fluid resuscitation, oxygen, ventilatory support, and inotropic support. The use of chemoprophylaxis and in certain circumstances vaccination are important in preventing secondary cases of meningococcal disease.

Bacteremia↗