Compartmentalization of the inflammatory response in meningococcal peritonitis

Abstract

To the Editor: The excellent review of "The innate immune response to secondary peritonitis" by van Till et al. (1) failed to explore a potential and relevant cause of secondary peritonitis linked to compartmentalization of the inflammatory response: meningococcal disease. Meningococcal disease is an infection caused by Neisseria meningitidis and is of an epidemic and overpowering nature (2). This infection remains a critical public health burden worldwide, presenting high rates of morbidity and mortality, principally in poorer countries (3, 4). The bacterial pathogen N. meningitidis is typically a commensal of the human nasopharynx. Factors that lead to invasion of the bloodstream, often followed by the crossing of the blood-brain barrier and meningitis, may be partly host and partly bacterium-dependent, but are ill-understood (3). In patients with meningococcal infection, atypical presentations such as complications involving abdominal organs, which may converge to acute abdomen, have been well documented (2). In fact, N. meningitidis has been linked to several abdominal disturbances: peritonitis, cholecystitis, mesenteric adenitis, splenic rupture, and pelvic inflammatory disease (2). We recently published a case of septic meningococcal peritonitis diagnosed by PCR analysis of peritoneal fluid (2). The case highlights the importance of considering peritonitis within the constellation of the clinical profiles of neisserial disease. In addition, the concentration of interleukin-6 (IL-6) was higher in the peritoneal fluid than in the serum. This cytokine pattern suggests a compartmentalized inflammatory response in which IL-6 is probably synthesized by activated resident cells, such as reticuloendothelial and mesothelial cells (1), and/or inflammatory cells that have migrated from the blood to the peritoneal compartment (2). Therefore, we would like to emphasize the importance of considering meningococcal peritonitis in patients who present with drastic abdominal pain during meningococcal sepsis. In addition, meningococcal organisms have been shown to penetrate a wide range of compartments other than the leptomeninges and can evoke a compartmentalization of the inflammatory response (2, 5). Notably, the pioneer Herrick stated in 1919: "The meningeal picture resulting from meningococcus infection has so fixed the attention of clinicians and pathologists that possibilities of extrameningeal infections by the organism have had scant notice" (6). Now, at the dawn of the third millennium, this challenging insight still holds true. Alexandre Leite de Souza Antonio Carlos Seguro Emílio Ribas Institute of Infectology, São Paulo, Brazil University of São Paulo School of Medicine, São Paulo, Brazil