Alexandre Leite de Souza

Two centuries of meningococcal infection: from Vieusseux to the cellular and molecular basis of disease.

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.

Compartmentalization of Interleukin-6 Response in a Patient with Septic Meningococcal Peritonitis

ABSTRACT 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.

Purulent pericarditis caused by Neisseria meningitidis serogroup C and confirmed through polymerase chain reaction

We here report the case of a previously healthy 20-y-old male with disseminated meningococcal disease and purulent pericarditis. Polymerase chain reaction was used to identify Neisseria meningitidis serogroup C as the causative agent in the pericardial fluid.

Gram Staining: An Unexplored Diagnostic Tool for Diagnosis of Meningococcal Infection in the Developing World

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Cerebellar hemorrhage as an atypical complication of meningococcal meningitis.

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The Fundamental Nature of Meningococcal Disease

To the Editor: The excellent review by Pelton of meningococcal disease highlights clinical and epidemiological factors affecting prevention and management in the United States [1]. I would like to draw attention to a key point made in this review. The author has stated that, ‘‘Primary meningococcal bacteremia is the presenting syndrome in 30%–40% of patients with meningococcal disease.’’ Historically, at the dawn of the twentieth century, the pioneer Herrick, in his classic article entitled ‘‘Extrameningeal meningococcus infections,’’ appropriately stated: ‘‘For a satisfactory understanding of the complications of epidemic cerebrospinal meningitis a proper knowledge of the fundamental nature of disease is necessary’’ [2]. Astutely, he also stated that ‘‘the result of the study of epidemic cerebrospinal meningitis in the camps has been the quite definitive establishment of the disease as primarily a meningococcic sepsis, a blood-stream invasion from the initial focus in the upper air-passages with usual but not constant localization in various susceptible parts of the body’’ [2]. In fact, meningococcal pathogenesis involves multiple links that interconnect in a complex web of phenomena from Neisseria meningitidis attachment to meningococcal sepsis or meningitis [3]. As the first step in the chain of events, meningococci attach to the microvillous surface of nonciliated columnar mucosal cells of the human nasopharynx, where they multiply (colonization process) [4]. Subsequently, N meningitidis penetrates the mucosa and gains access to the bloodstream, causing bacteremia, which is a critical step in the pathophysiology of neisserial disease [4, 5]. Therefore, colonization and invasion of the nasopharyngeal mucosa with subsequent bacteremia are primary events in the genesis of meningococcal infection [3–5]. However, meningococcal sepsis occurs in only 5%–20% of patients [4]. In fact, bacteremia without sepsis is one of four major clinical syndromes of neisserial infection [6]. Meningococcal sepsis is a N meningitidis bacteremia associated with a systemic inflammatory response syndrome (SIRS), including leukocytosis, cutaneous manifestations as petechial or purpuric lesions, myalgia, weakness, fever, and high levels of cytokines [6, 7].