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[Results of intensive therapy of meningococcal sepsis in children].

The authors report on the method, course and results of treatment of patients with meningococcal septicaemia. The two most common forms of meningococcal disease are meningococcal septicaemia (MS) and meningitis. Severe MS is a fulminant form of sepsis characterized by a rapidly spreading purpuric rash, haemodynamic instability and rapid progression to shock or death. The diganosis of MS was confirmed by isolation of NM in blood or cerebrospinal fluid, and/or positive solubile bacterial antigenes. However, in some children whose symptoms were consistent in MS (temperature and extensive purpura), no bacterial or soluble antigens were detected, particularly when they had been previours antibiotic treatment. Several scoring systems have been used to predict morbidity and mortility from MS. We selected the prognostic scor developed by Malley et al. Absolute neutrophil count less than 3 x 10(3)/mm3, platelet count less than 150 x 10(3)/mm3 and poor perfusion are indicators of poor prognosis. The presence of at least two of these indicators was associated with an 82% of risk of death. We reviewed the hospital records of 36 paediatric patients with acute meningococcal infection during a 5-year period. The age of our patients ranged from 2 months to 15 years (mean 4.4 yrs). Twenty seven (70%) of 36 children had MS and 11 (40.7%) had both MS and meningitis. Based on Malley scor, 13 (48.1%) patients had at least two predictors with > 82% of risk of lethal outcome. Four children (30.7%) died. Severe MS was diagnosed in 16 (59.2%) patients, who required mechanical ventilation (16; 59.2%), or continuous inotropic support and invasive measures of circulatory parametars (15; 55.5%). Shock treatment consisted of large volumes of crystalloid or colloid infusions thad ranged from 140 to 500 ml/kg/24 hrs (mean 215 ml/kg) Our results indicate that early controlled mechanical ventilations increase safety of large volume infusion with continuous invasive monitoring and inotropic stimulation, and may contribute to a greater survival of children with severe MS.

Adolescent↗

PubMed2005

[Reversible autonomic dysfunction in a young woman with septic multiple organ dysfunction syndrome].

HISTORY: A 24-year-old woman was admitted for treatment of a meningococcal infection accompanied by fulminant autonomic dysfunction. INVESTIGATIONS: Laboratory tests indicated acute renal failure and disseminated intravascular coagulopathy (creatinine 183 mmol, D-dimer 1.52 mg/l). The initial central venous oxygen saturation was 60-65%. The diagnosis of severe septic shock was supported by a high procalcitonin level of 66.7 ng/ml, CRP of 79.8 mg/l, and a WBC count of 12.2 Gpt/l. TREATMENT AND COURSE: Treatment of sepsis with antibiotics (ciprofloxacin, penicillin G, ceftriaxon and erythromycin in standard dosages), activated protein-C, hydrocortisone and GMA-embedded immunoglobulin led to complete cure and restoration of normal autonomic function. CONCLUSIONS: This case shows that even in multiple organ dysfunction syndrome autonomic dysfunction can occur which is improved by adequate treatment.

Adult↗

PubMed2002

The class A macrophage scavenger receptor is a major pattern recognition receptor for Neisseria meningitidis which is independent of lipopolysaccharide and not required for secretory responses.

Macrophages (Mphi) play a key role in the pathogenesis of invasive meningococcal infections. The roles of two pattern recognition molecules, the Mphi scavenger receptor (SR-A) and Toll-like receptor 4 (TLR-4), have been investigated using bone marrow culture-derived Mphi (BMMphi). Surprisingly, a comparison of BMMphi from wild-type and SR-A knockout (SR-A(-/-)) mice showed that nonopsonic phagocytosis of meningococci was mediated almost exclusively via SR-A. Previous studies have demonstrated only a partial involvement of the receptor in the uptake of other bacteria, such as Escherichia coli. Interestingly, we also show that lipopolysaccharide (LPS) was not the ligand for the receptor on these organisms. Further study of the downstream events of SR-A-mediated ingestion of Neisseria meningitidis demonstrated that SR-A was not required for cytokine production. To determine the bacterial and host factors required to stimulate Mphi activation, we examined TLR-4-deficient Mphi from C3H/HeJ mice and LPS-deficient meningococci. TLR-4-deficient cells elaborated reduced amounts of tumor necrosis factor alpha, interleukin-12 (IL-12), and IL-10, even though ingestion via SR-A was unaffected in these cells. Similarly, although there was no change in SR-A-mediated ingestion of LPS-deficient meningococci, the mutant failed to stimulate a Mphi-dependent cytokine response. Thus, we show that Mphi SR-A mediates opsonin-independent uptake of N. meningitidis independently of lipid A and that this activity is uncoupled from the Mphi secretion of proinflammatory cytokines, which provides a basis for further investigation of the role of this receptor in meningococcal disease in humans.

Animals↗

PubMed2003

Admission plasma vasopressin levels in children with meningococcal septic shock.

OBJECTIVE: Vasopressin (AVP) response has been reported to be inappropriately low in adult established septic shock. We studied admission AVP levels in children with meningococcal septic shock (MSS). PATIENTS AND METHODS: All children with meningococcal infection admitted to our PICU between May 2001 and August 2002 were classified as MSS (persistent hypotension despite fluid therapy, with perfusion abnormalities and the need for vasoactive drug infusion for at least 24 h or until death), or meningococal infection without shock (fever and purpura, with or without meningitis). Blood samples were collected at admission and AVP levels were subsequently determined using Nichols Institute Diagnostics vasopressin assay. Eighteen of 19 children with MSS (7 deaths) and 15 without shock (no death) were included. RESULTS: In children with MSS median admission AVP level was 41.6 pg/ml (1.4-498.9) and in those without 3.3 pg/ml (1.6-63.8). In children with MSS the AVP level was not correlated with duration of shock and fluid expansion prior to AVP sampling, or with age-adjusted blood pressure and natremia at the time of blood sampling. AVP levels were higher in nonsurvivors, but not significantly so. Only one nonsurvivor had an admission AVP level below 30 pg/ml. CONCLUSIONS: In our children with established MSS who died the admission AVP level Delta were not inappropriately low. Further studies including serial AVP level assessments are needed before concluding that AVP administration is of little interest in children with MSS.

Child, Preschool↗

PubMed1997

Functional characterization of an isogenic meningococcal alpha-2,3-sialyltransferase mutant: the role of lipooligosaccharide sialylation for serum resistance in serogroup B meningococci.

The neisserial alpha-2,3-sialyltransferase, which is encoded by the lst gene, terminally links sialic acid to the lacto-N-neotetraose residue of neisserial lipooligosaccharide (LOS). We used the recently published nucleotide sequence of the neisserial lst gene to construct an isogenic serogroup B meningococcal lst mutant by insertion of a kanamycin resistance gene. The resulting lst mutant expressed the unsialylated lacto-N-neotetraose structure. Using bactericidal assays and an infant rat model of meningococcal infection, we were able to demonstrate that lst mutation, in contrast to galE mutation, which results in a truncated LOS, or to siaD mutation, which results in loss of the capsule, neither had an effect on resistance to normal human serum, nor did it impair the ability of meningococci to spread systemically in the non-immune host. The lst mutant was serum resistant despite of the fact that the central factor of complement activation, C3b, was deposited on the lst mutant as efficiently as it was on the galE mutant. Thus, the terminal sialic acid residue linked to the wild-type LOS inhibited C3b deposition on the meningocuccus. However, in contrast to the galE mutant, where C3b deposition is promoted by IgM binding, the lst mutant's surface is not a target for IgM molecules. Thus, the lacto-N-neotetraose residue of neisserial LOS alone, without the presence of terminal sialic acid, is sufficient to block IgM epitopes either on the LOS itself, or on other surface molecules. Our data provide further insight into the complex interplay of capsular and LOS sialic acids in serogroup B meningococci with host effector mechanisms, and suggest that LOS sialylation in meningococci is of a less central importance as it is in gonococci.

Animals↗

PubMed2002

New therapies and vaccines for bacterial meningitis.

Acute bacterial meningitis remains an important cause of morbidity and mortality worldwide. There have recently been major advances in the prevention of the major causes of bacterial meningitis following improvements in vaccinology. The success of immunisation against Haemophilus influenzae type b infection is being mirrored with serogroup C conjugated meningococcal vaccine and pneumococcal conjugate vaccine. However, there remain major challenges, notably, serogroup B meningococcal infection and shifts in epidemiology caused by vaccine introduction. In addition, much of the world's population is unvaccinated. Therefore, improvements in management of acute bacterial meningitis are vital. In this review we attempt to summarise important advances in both prevention and treatment of acute bacterial meningitis.

Adult↗

PubMed1976

Protection against group B meningococcal disease. I. Comparison of group-specific and type-specific protection in the chick embryo model.

Protection against group B meningococcal infection was examined using the chick embryo. 12-day-old embryos were challenged intravenously with various meningococcal strains. The chick embryo has an active reticuloendothelial system but lacks functional complement. In this model we found that protection against group B infection was primarily group specific. The group B polysaccharide antibody is an effective opsonin, but is a very poor bactericidal antibody. In contrast, the serotype antibody was bactericidal but only slightly protective in the chick embryo where protection is primarily phagocytic in nature. The group-specific and type-specific antibodies are strongly synergistic. Minute amounts of group B polysaccharide antibody caused a very significant increase in the protective effects of the serotype antibody.

Animals↗

PubMed1998

[Association of class I HLA antigens with invasive meningococcal disease].

BACKGROUND: The majority of meningococcal infections are characterized by nasopharyngeal carriership. In some patients invasive disease with a mild course develops, while some cases have a lethal outcome. The reasons of this wide variation range are not clear. The objective of the present work was to assess whether the development of invasive meningococcal disease or its prognosis are associated with HLA class I. METHODS AND RESULTS: The group of patients was formed by 40 patients (29 females, 11 males, mean age 16 years, range 8 months to 52 years). In 28 patients the disease was caused by N. meningitidis group C, in 9 cases group B, in three cases the serotype was not assessed. The etiology was confirmed by cultivation or latex agglutination. Twenty-three patients had a mild course of the disease, 8 a medium severe one, 9 patients a severe clinical course (score according to Stiehme, Damrosch and Rosenblat). The patients were compared with 227 non-related blood donors (114 women, 113 men, 18 to 50 years old). In patients and controls 24 lymphocytic HLA antigens class I were identified as to type. Typing was done using the standard microlymphocytotoxic test in the NIH modification. The results were processed by statistical methods using Fisher's exact test and the 2 x 2 test with Yates correction. In patients with a mild course HLA antigens B7 and B12 predominate (p = 0.03; p = 0.02), in medium severe cases antigen A11 (p = 0.03), in patients with the most severe course antigen A9 (p = 0.04). In invasive infections caused by N. meningitidis serotype B antigen B17 predominates (p = 0.05). CONCLUSIONS: The severity of meningococcal invasive infections is associated with HLA class I. Invasive disease caused by N. meningitidis serotype B are more likely to occur in carriers of HLA B17. No relationship was found between HLA class I and invasive disease caused by N. meningitidis regardless of serotype and with serotype C.

Adolescent↗

PubMed2001

[Role of host response during severe bacterial infection].

Explosion of knowledge both in human genomics and in host inflammatory response explains the increasing interest in infectious disease genetics over the last 5 years. However, twin and adoptee studies have suggested more than 15 years ago, that host genetic factors are major determinants of susceptibility to infectious diseases in humans. Recently, candidate gene studies (association studies) and human genomewide analysis have been used to identify infectious diseases susceptibility and resistance genes. Rarely, a single gene defect has been directly related to devastating consequences such as interferon-gamma receptor mutations leading to fatal infections with ubiquitous mycobacteria. For clinical practice, gene polymorphisms of specific host immune defence elements appear to be of major importance. These genetic variants, which modify the regulation or function of the mediators, have been associated with susceptibility and/or outcome of severe sepsis and septic shock. All steps of the host response to bacteria may be affected by genetic factors. For example, Fc gamma receptor, Toll like receptor or mannose binding protein mutations have been shown to modify the detection of pathogens leading to pneumococcal severe infections, Gram-negative bacteria septic shock, and meningococcal disease, respectively. Polymorphisms of cytokine genes (TNF-alpha, TNF-beta, IL-1-ra) have been reported to influence the level of secreted mediators and to unbalance the inflammatory cascade. Coagulation response to sepsis may also be affected by gene variants such as the plaminogen activator inhibitor 1 (PAI-1) common functional polymorphism which increases the risk of death from meningococcal infection or severe trauma. The impact of these findings on the understanding of infectious disease pathogenesis and on the design of future preventive and therapeutic strategies should be considerable.

Bacterial Infections↗

PubMed2006

Immunogenicity of meningococcal PBP2 during natural infection and protective activity of anti-PBP2 antibodies against meningococcal bacteraemia in mice.

OBJECTIVE: To evaluate the immunogenicity of the meningococcal penicillin-binding protein 2 (PBP2) and its potential as a vaccine candidate. METHODS: The immunogenicity of meningococcal PBP2 was investigated using acute and convalescent sera from patients who recovered from meningococcal disease. Sera were tested against purified recombinant PBP2s corresponding to meningococcal isolates of different genetic lineages, of different serogroups and with various susceptibility levels to penicillin G. Mice were vaccinated with recombinant PBP2 and challenged with Neisseria meningitidis. A purified anti-PBP2 rabbit IgG was also used for passive protection experiments in mice. RESULTS: Convalescent patients' sera recognized PBP2s from different strains, showing that this protein is immunogenic in meningococcal disease. Vaccination with purified recombinant PBP2 and purified anti-PBP2 rabbit IgG antibody conferred protection against experimental meningococcaemia in mice. CONCLUSION: These data argue for considering meningococcal PBP2 as a vaccine candidate.

Animals↗

PubMed1983

Turnover in the transferrin iron pool during the hypoferremic phase of experimental Neisseria meningitidis infection in mice.

Mouse transferrin was used to specifically label the plasma transferrin iron pool for studies of iron kinetics in normal mice and infected mice during the hypoferremic phase of experimental meningococcal infection. The plasma transferrin iron pool of normal mice was found to be very dynamic, with a half-life of iron in the pool of 0.7 h. Iron left the plasma pool, entered the bone marrow, and was released into the blood in erythrocytes. Iron from the transferrin pool also entered the liver and spleen and was presumably in the reticuloendothelial system components of these organs. Most of the iron that had been supplied as transferrin iron was found in erythrocytes by 48 h after injection. Studies with mice infected with Neisseria meningitidis strain M1011 revealed similar kinetics for transferrin iron. There was no redistribution of iron within the various iron pools as a result of infection. Iron turnover in the plasma transferrin pool during the hypoferremic phase was similar to control rates, and iron leaving the pool entered its normal erythroid compartments. The lack of accelerated turnover of plasma iron and the finding that plasma iron was not rerouted to storage compartments during the hypoferremic phase provided good evidence that lactoferrin and leukocytic endogenous mediator were not directly involved in redirecting transferrin iron. Our evidence has implicated an impaired return of reticuloendothelial system-processed iron to the transferrin pool during the hypoferremic response. This appears to be a logical point in the erythroid iron cycle for host-mediated iron sequestration, as the reticuloendothelial system is involved in iron storage and may regulate iron levels in the plasma transferrin pool under normal conditions.

Animals↗

PubMed1953