Excerpt from MeningococcemiaSynonyms, Key Words, and Related Terms: meningococcal sepsis, meningococcal disease, Neisseria meningitidis, N meningitidis, meningococcal infection, meningitis, bacteremia, meningococcemia, acute meningococcal septicemia, adrenal hemorrhage, Waterhouse-Friderichsen syndrome, meningococcal septicemia Please click here to view the full topic text: MeningococcemiaBackgroundMeningococcal disease is a communicable infection caused by Neisseria meningitidis. It is transmitted from person to person via respiratory secretions. N meningitidis infection can be clinically polymorphic. The most common disease presentation is meningitis. Rarely, N meningitidis infection may manifest as chronic meningococcemia that resembles the arthritis-dermatitis syndrome of gonococcemia; however, acute meningococcal septicemia (also called meningococcemia) is the most devastating form of the disease. Meningococcemia can kill more rapidly than any other infectious disease. Early recognition is critical to implement prompt antibiotic therapy and supportive care. Treatment must be instituted rapidly because irreversible shock and death may occur within hours of the onset of symptoms. Cutaneous manifestations in meningococcemia may be important clues to the diagnosis. Skin involvement can be the most dramatic aspect of the disease and is often the first sign that leads to the clinical consideration of meningococcemia. PathophysiologyN meningitidis is an obligate, nonmotile, aerobic, encapsulated, gram-negative diplococcus that can only be cultured on blood-enriched media in a 5-10% carbon dioxide–enriched environment. The outer polysaccharide capsule of N meningitidis serves as the basis of serologic grouping. To date, at least 13 different serogroups have been identified; however, groups A, B, C, Y, and W-135 are the major pathogens involved in human disease. Transmission of N meningitidis occurs from person to person through respiratory secretions. The human upper respiratory tract is the only known reservoir. Carrier rates depend on age. Approximately 2% of children younger than 2 years, 5% of children up to 17 years, and 20-40% of young adults are carriers of N meningitidis. Overcrowded conditions (eg, schools, military camps) can significantly increase the carrier rate. Screening of military recruits performed during recent epidemics demonstrated that although as many as 95% of recruits were oropharyngeal carriers, only 1% developed systemic disease. Because very few recruits with meningococcal disease had ever been in contact with another such patient, asymptomatic carriers are thought to be the major source of transmission of pathogenic strains. A complex interaction between host factors and the organism determines the outcome of exposure to N meningitidis. Colonization and invasion of meningococci are facilitated by pili that attach to mucosal epithelial cells. A concomitant viral infection may facilitate the invasion of N meningitidis into the bloodstream or lower respiratory tract. Once in the bloodstream, N meningitidis causes profound effects on small blood vessels, related to both direct invasion of endothelial cells and indirect damage from endotoxin release. Endotoxin from the lipopolysaccharide of meningococci causes endothelial cells, monocytes, and macrophages to release tumor necrosis factor-alpha, interleukin 1, interleukin 6, and interferon-gamma. The deleterious effects of these cytokines play a major role in the pathogenesis of meningococcemia by causing severe hypotension, reduced cardiac output, and increased endothelial permeability. Multiple organ failure, shock, and death may ensue as a result of anoxia in vital organs and massive disseminated intravascular coagulation (DIC). FrequencyUnited StatesAn estimated 2600 cases of meningococcemia occur each year. Mortality/MorbidityThe mortality rate is approximately 5% in children and 5-10% in adults; however, meningococcemia associated with DIC has a mortality rate of higher than 90%. AgeChildren younger than 4 years have the highest risk of developing meningococcal disease. Neonates are often resistant to disease because passively acquired maternal immunoglobulin G antibodies are present until approximately age 6 months. As the child grows older, asymptomatic exposure to a variety of encapsulated and nonencapsulated N meningitidis strains increases protective bacterial immunity. Protective immunoglobulin M and immunoglobulin G are found in up to 95% of young adults. Please click here to view the full topic text: Meningococcemia |
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