Mortality in severe meningococcal disease.

AIM: To evaluate mortality of critically ill children admitted with meningococcal disease. METHODS: Prospective study of all children admitted to a regional paediatric intensive care unit (PICU) between January 1995 and March 1998 with meningococcal disease. Outcome measures were actual overall mortality, predicted mortality (by PRISM), and standardised mortality ratio. RESULTS: A total of 123 children were admitted with meningococcal disease. There was an overall PICU mortality of 11 children (8.9%). The total mortality predicted by PRISM was 24.9. The standardised mortality ratio (SMR) was 0.44. Results were compared with those from four previously published meningococcal PICU studies (USA, Australia, UK, Netherlands) in which PRISM scores were calculated. The overall PICU mortality and SMR were lower than those in the previously published studies. CONCLUSION: Compared with older studies and calibrating for disease severity, this study found a decrease in the mortality of critically ill children with meningococcal disease.     

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.     

Long-term psychological distress in parents of child survivors of severe meningococcal disease

OBJECTIVE: To study psychological distress in parents of child survivors of Severe Meningococcal Disease (SMD) after discharge of their child from the Paediatric Intensive Care Unit (PICU). METHODS: This study approached parents of child survivors of SMD treated on the PICU between 1993-2001. Five cross-sectional groups were created for mothers and fathers separately. The five groups differed from each other by the period after discharge they entered the project (ranging from 3 months to 7 years after discharge). For research purposes, mothers and fathers (n = 192) individually completed the Goldberg General Health Questionnaire-30 (GHQ), measuring their level of psychological distress. STATISTICS: Mean group scores were examined and a one-way-analysis of variance (ANOVA) performed to study differences between groups for mothers and fathers separately. In addition, percentages of parents with GHQ scores above cut-off were calculated and it was determined whether it differed from norm data. RESULTS: Data reveal that both mothers and fathers experience high mean levels of psychological distress after discharge, showing no significant differences in group means over time. High percentages of parents experience psychological distress after discharge, if compared with the normal population. CONCLUSIONS: Parents of child survivors of SMD experience profound and prolonged psychological distress after discharge. Future interventions should focus on follow-up care for this population to help them re-adjust after this stressful event.     

Mortality from group C meningococcal disease: a case for a conjugate vaccine?

This 17-year retrospective review of children with meningococcal disease (MCD) has determined the mortality due to serogroup C, in order to assess the potential impact of a group C conjugate vaccine. Four hundred and forty-nine cases of MCD were admitted to our hospitals during 1977–1993; 78 due to group C, 11 of whom died. There was a significant increase in the proportion of cases due to group C from 1986 onwards (10% vs 21%), and an increase in the total number of cases of MCD (151 vs 298). The currently available group C polysaccharide vaccine has low efficacy below 2 years of age and could not have prevented 54 cases of group C disease. A conjugate group C vaccine administered between 2 and 4 months of age could have prevented 68 cases, including all fatal cases. The recent increase in MCD is partly due to an increase in group C disease. A meningococcal group C conjugate vaccine could prevent most cases of infection due to group C, and decrease the mortality from MCD by up to 30%.     

Ophthalmitis in meningococcal disease.

We report an infant with meningococcal septicaemia and meningitis who had panophthalmitis at presentation that was unresponsive to standard systemic antibiotic treatment but which responded to topical steroid and mydriatic treatment. The pathogenesis may have been immune mediated.     

Management of meningococcal disease

In recent years remarkable progress has been made in the development of vaccines against the different disease-causing serotypes of Neisseria meningitidis. Despite this, invasive meningococcal disease (IMD) remains a life-threatening illness with significant mortality, morbidity and long term sequelae. Prompt recognition and early treatment with antibiotics are the first steps in its management. Professionals looking after children with suspected IMD should be familiar with its clinical course, so that progression of the disease can be identified early, and its complications including septic shock, coagulopathy and raised intracranial pressure managed aggressively. This article summarizes the clinical features, presentation, pathophysiology and management of IMD focusing on its two common clinical presentations: septicaemia with associated shock and meningitis.     

Prevention of meningococcal disease

Neisseria meningitidis is the most common cause of meningitis in children aged 2-18 with a mortality rate ranging from 4-40% and substantial morbidity in 11-19% of survivors. Of the four serogroups ofNeisseria meningitidis, serogroups B and C are the most common causes in the United States, with serogroup C causing most disease among adolescents, a population at risk for invasive meningococcal disease. The meningococcal polysaccharide vaccine was developed in response to increasing rates of bacterial meningitis among military recruits. With widespread use of the vaccine in the military, there was a dramatic decreased incidence in invasive meningococcal disease. However, there may be limitations to the polysaccharide vaccine including lack of durable protection, lack of induction of T-cell-dependent immune response, and lack of immunogenicity in children less than 2 years of age. Based on the success of other conjugate vaccines in pediatrics, a new conjugate polysaccharide vaccine, Menactra, has been approved by the Food and Drug Administration and recommended for routine vaccination in adolescents by the Advisory Committee on Immunization Practices.     

Vaccines against meningococcal disease

The meningococcal disease has been a source of preoccupation all over the world. Epidemics have been registered periodically in developed or developing countries. The most frequent meningococci are those concerned with serogroups A, B and C. Researches to develop effective vaccines against the disease have been taking place since the 40's. Presently, only vaccines against the meningococci from the serogroups A, C, Y and W-135 are available. These vaccines have important limitations both due to the age range that they protect and the period of time that the protection lasts. They are not routinely used in vaccination programs and are indicated only in risky situations. This demands a strict epidemiological surveillance of the disease. There are no vaccines against the serogroup B meningococci with recognized effectiveness, although, in the last decades, many have been tested. There are perspectives of important advances in this area, mainly with the development of conjugated vaccines, like the Haemophilus influenzae type B vaccine. Until the present, the chemoprophylaxis of the intimate communicants of a case is the best way to avoid secondary cases.     

Plasma fibronectin levels in meningococcal disease

Fibronectin (a glycoprotein which modulates inflammation) may decrease mortality in systemic infection. Children with meningococcal disease (MCD) may have low fibronectin levels. We aimed to compare plasma fibronectin levels in children with MCD and controls, correlate fibronectin levels with interleukin-6 (IL-6), shock and death, and assess fibronectin as an aid to early diagnosis in MCD. Samples were taken on admission from 99 children with MCD and 49 controls. Plasma fibronectin was measured using a turbidimetric immunoassay. Plasma fibronectin was significantly lower in MCD compared to controls (57 μg/ml vs 105 μg/ml; P < 0.005). Children who died had significantly lower levels than survivors (29 μg/ml vs 62 μg/ml; P = 0.01). Fibronectin levels were negatively correlated with IL-6 levels. Fibronectin was a poor predictor of MCD. Conclusion Plasma fibronectin levels are decreased in children with MCD, especially in shock and death. This decrease is associated with high IL-6 levels. Fibronectin could be a novel therapy in severe MCD. Received: 6 June 1996 / Accepted: 16 October 1996     

Epidemiology of meningococcal disease in Australia

A review of the epidemiology of meningococcal disease (MD) in Australia was undertaken, with particular emphasis on the 1990s, when national strain differentiation data became available. The data included a review of clinical and laboratory notification data and published reports on clusters and outbreaks. There have been considerable changes in the patterns of MD in the 1990s. In some cases, these changes can be related to the dominance of a particular phenotype. In the early 1990s, widely scattered urban and rural clusters were associated with the phenotype C:2b:P1.2 and strains were closely genetically related. Larger urban clusters and increased numbers of cases in adolescents and young adults were most obvious in New South Wales in the mid-1990s and were associated with a phenotype C:2a:P1.5. This ET-15 clone of the ET-37 complex caused similar patterns of MD to those seen in other countries as part of the global spread of the clone. In contrast, the B:4:P1.4 phenotype, with close genetic similarities to New Zealand strains, did not cause the hyperendemic disease seen in New Zealand this decade. The epidemiology of MD will continue to exhibit considerable variation due, at least in part, to the genetic flexibility of meningococci. Information about strain variation expands our understanding of changing patterns of disease.