COMPLEMENT DEFICIENCY STATES AND MENINGOCOCCAL DISEASE

Analysis of complement deficiency states has supported the role of com plement in host defense and elucidated diseases associated with defect ive complement function. Although neisserial infection plays a promine nt role in these deficiency states, examination of individuals with la te complement component deficiency (LCCD) reveals a particular propens ity for recurrent meningococcal disease and provides important clues t o the role of complement in neisserial infections. In response to meni ngococcal disease, LCCD individuals produce significantly greater amou nts of antilipooligosaccharide (LOS) antibody which can kill group B m eningococcus in a complement-sufficient in vitro system. Further studi es of antibody crossreactivity to other meningococci has led to a clea rer understanding of its epitopic specificity. Nevertheless, epidemiol ogic evidence is consistent with the relative absence of protective im munity in LCCD persons following an episode of infection and supported by quantitation of antibody to capsular polysaccharide. However, comp ared to anti-LOS antibodies, anticapsular antibodies can offer immune protection to LCCD individuals via complement-dependent opsonophagocyt osis the only form of complement-mediated killing available to these p ersons. Thus vaccination of LCCD persons with capsular antigens is con sidered an important means of protecting these high-risk individuals a gainst meningococcal disease.