Chapter 136. Meningococcal Infections (Part 2)

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In the United States, the attack rate for sporadic meningococcal disease is ~1 case per 100,000 persons per year. Disease attack rates are highest among infants 3–9 months of age (10–15 cases per 100,000 infants per year). Attack rates are higher among children than among adults, and there is a second peak of incidence among teenagers, in whom outbreaks have often been tied to residence in barracks, dormitories, or other crowded conditions. This observation has prompted the recommendation that meningococcal polysaccharide-based vaccines (see below) be administered to incoming college freshmen to prevent outbreaks at colleges. Although the age-specific incidence...

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Chapter 136. Meningococcal Infections (Part 2) In the United States, the attack rate for sporadic meningococcal disease is ~1 case per 100,000 persons per year. Disease attack rates are highest among infants 3–9 months of age (10–15 cases per 100,000 infants per year). Attack rates are higher among children than among adults, and there is a second peak of incidence among teenagers, in whom outbreaks have often been tied to residence in barracks, dormitories, or other crowded conditions. This observation has prompted the recommendation that meningococcal polysaccharide-based vaccines (see below) be administered to incoming college freshmen to prevent outbreaks at colleges. Although the age-specific incidence is much lower among adults (
young adults. In sub-Saharan Africa, epidemic outbreaks occur with the dry season and the coming of the dry dusty winds of the harmattan. Meningococcal disease occurs more commonly among the household contacts of primary cases than in the general population. The secondary attack rate is 400–1000 per 100,000 household members. School-based clusters of cases have also been described; the attack rate among school contacts of cases has been estimated at 2–4 cases per 100,000 exposed individuals. In outbreaks on college campuses, attack rates have been highest among students living in dormitories. Most secondary cases occur within 2 weeks of the primary case, although some cases may develop as long as several months later. Secondary cases account for
Pathogenesis (Fig. 136-1) Meningococci that colonize the upper respiratory tract are internalized by nonciliated mucosal cells and may traverse them to enter the submucosa, from which they can make their way into the bloodstream. While meningococcal colonization of healthy humans is common, bloodstream infection is an infrequent event that is not essential for the organisms' survival and spread. The production of human disease has no obvious evolutionary advantage for either pathogen or host. Although some strains of N. meningitidis are thought to cause more severe disease in humans than do other strains, the basis for this difference is not understood. Meningococci may undergo important phenotypic changes when they adapt to growth in vivo; presumed virulence traits include the antiphagocytic capsular polysaccharide, an ability to sialylate LOS so that it mimics host-cell carbohydrate moieties and inhibits complement deposition, the secretion of IgA protease, and mechanisms for iron acquisition. However, there is little evidence that alteration in meningococcal components, putative toxins, or other secreted substances affects virulence. Moreover, the ET-5 strain of serogroup B N. meningitidis has been associated with high case-fatality rates in some populations but not in others. These points suggest that host factors, as opposed to bacterial components, are the main mediators of immune resistance and disease pathogenesis.
Figure 136-1 Meningococcal disease pathogenesis, susceptibility, and severity. After human-to-human transmission, environmental factors (smoking, co-infections), polymorphisms in innate immunity or other genes, and absence of mucosal antibodies may confer susceptibility to meningococcal invasion from the nasopharynx into the bloodstream. In individuals who lack bactericidal antibodies, terminal or alternative pathway complement-deficiency states and other genetic polymorphisms may influence the severity of the ensuing host response and the clinical presentation. Although each of these gene associations has been reported, most of them require confirmation in different ethnic groups. MBL, mannose-
binding lectin; TNF, tumor necrosis factor; FcγRIIA, FCγRIIA R131 allele; PAI- 1, plasminogen activator inhibitor 1; ACE-1, angiotensin-converting enzyme 1; IL, interleukin; IL-1Ra, interleukin 1 receptor antagonist. A meningococcal organism that enters the bloodstream from the nasopharynx and survives host defenses generally has one of two fates. If multiplication occurs slowly, the bacteria eventually may seed local sites, such as the meninges and/or (rarely) the joints or the pericardium. More rapid multiplication in the bloodstream is associated with the clinical features of meningococcemia [i.e., petechiae, purpura, disseminated intravascular coagulation (DIC), and shock], which usually causes symptoms before local sites become infected. Thus, compartmentalization of bacterial growth and host inflammation either in the blood or at a local site (usually the meninges) can occur.