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Scientific knowledge of meningococcal infection has increased greatly since the epidemic nature of the illness was first described by Vieusseux at the dawn of the nineteenth century. In fact, revolutionary advances have been made in public-health measures, antimicrobial therapy, diagnostic procedures, anti-inflammatory drugs and supportive care facilities. Based on the knowledge accumulated to date, it is generally accepted that the pathogenesis of meningococcal infection involves multiple links that interconnect in a complex web of phenomena from Neisseria meningitidis attachment to meningococcal sepsis or meningitis. In fact, a myriad of strongly interacting inflammatory molecules and cells have been implicated in neisserial infection, illustrating the complexity of meningococcal pathogenesis. In addition, many of these signallers are critically involved in outcomes in the human host. Deciphering the pathogenesis of meningococcal infection could expand our knowledge and provide important clues to the host–pathogen interaction, as well as leading to the development of new therapeutic tools. Herein, we review the history of the discovery and characterization of meningococcal disease, epidemiological features of the disease with an emphasis on recent developments in Brazil, the cellular and molecular basis of disease, and discuss diagnosis and therapy.

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An unusual case of leptospirosis is described in a 19-month-old male child presenting with meningitis and acute renal failure without jaundice. Some aspects concerning the pathogenesis and treatment of this potentially life-threatening disease are also discussed. Leptospirosis was diagnosed on the basis of history and serological tests.

We report the first case of Neisseria meningitidis-induced septic peritonitis diagnosed by PCR assay of peritoneal fluid. Concentrations of interleukin-6 were notably higher in the peritoneal fluid than in the blood. PCR diagnosis of septic meningococcal peritonitis and the pathogenesis of the disease are discussed.Case report. A previously healthy 6-year-old girl presented with a 24-h history of fever, headache, and intense myalgia. In the 2 h preceding her examination, she had developed petechiae on her abdomen, arms, face, and legs, accompanied by a deteriorating level of consciousness. Upon examination, petechial lesions were noted on both palpebral conjunctivae, and a dramatic progression from petechiae to confluent ecchymoses was observed on her skin, apparently fitting the clinical profile of disseminated intravascular coagulation. Her vital signs were as follows: axillary temperature, 38°C; pulse, 160 beats/min; respiration, 40 breaths/min; and blood pressure, 80/60 mm Hg. She was positive for Kernig's sign and Brudzinski's sign, and her Glasgow coma scale score was 13. The rest of the examination was unremarkable. The white blood cell (WBC) count was 28,000 WBCs/mm 3 (93% polymorphonuclear neutrophils, 3% lymphocytes, 4% monocytes). The hemoglobin concentration was 9.3 g/dl, and the platelet count was 58,000 cells/mm 3 . Coagulation studies demonstrated an international normalized ratio of 2.12 and an activated partial-thromboplastin time of 55 s. Abnormal laboratory values included the following serum levels: creatine kinase, 784 U/liter; albumin, 2.7 g/dl; aspartate aminotransferase, 106 U/liter; and alanine aminotransferase, 63 U/liter. The acid/base response to this clinical profile was consistent with acidemia, metabolic acidosis, and respiratory alkalosis (arterial pH, 7.28; partial O 2 pressure, 96 mm Hg; bicarbonate, 15 mmol/liter; base deficit, Ϫ3 mmol/liter; partial CO 2 pressure, 26 mmol/liter). A computed tomography scan of the brain was normal, and a lumbar puncture was performed. The cerebrospinal fluid (CSF) was cloudy and contained 1,680 WBCs/mm 3 (80% polymorphonuclear neutrophils, 15% lymphocytes, 5% monocytes), 104 mg/dl of protein, and 27 mg/dl of glucose. Gram staining of the CSF showed gram-negative diplococci, and Neisseria meningitidis serogroup C was detected by using a latex agglutination test. Blood samples and CSF samples were collected for culture. Counterimmunoelectrophoresis results for Neisseria meningitidis serogroup C in the serum were positive. The preliminary diagnosis was meningitis accompanied by meningococcemia. Therefore, antibiotic treatment was initiated with ceftriaxone (100 mg/kg of body weight/ day) and dexamethasone (0.6 mg/kg/day for 4 days). In addition, supportive measures to maintain homeostasis, including electrolyte replacement, fluid reposition, vitamin K administration, and transfusion of fresh-frozen plasma, were implemented. The patient's close contacts received chemoprophylaxis.Initially, the general status of the patient improved. However, 48 h a...