ABSTRACT
Of 45 Russian patients with late complement component deficiency (LCCD) who experienced one to five meningococcal infections, 31 were immunised with a meningococcal A/C/W135/Y polysaccharide vaccine and were followed for 3-8 years. Total and immunoglobulin (Ig) class specific concentration of antibodies to meningococcal polysaccharides in sera of LCCD patients increased significantly 1 month after vaccination and remained elevated for 3 years. Revaccination of LCCD patients 3 years after the first dose restored the total Ig concentrations to those observed 1 year after the first vaccination. Six new episodes of meningococcal infection in four patients developed in the group of 31 vaccinees; six episodes in six patients developed in the same time in the group of 14 non-vaccinated LCCD persons. Survival analysis demonstrated the risk to contract meningococcal disease decreased significantly for vaccinees in comparison to non-vaccinees (P<0.05). Vaccination with of meningococcal tetravalent polysaccharide vaccine decreases the risk of meningococcal infection in LCCD patients.
Subject(s)
Complement System Proteins/deficiency , Lipopolysaccharides/immunology , Meningococcal Vaccines/immunology , Vaccination , Adult , Antibodies, Bacterial/biosynthesis , Female , Follow-Up Studies , Humans , Immunization, Secondary , Immunoglobulin A/biosynthesis , Immunoglobulin G/biosynthesis , Immunoglobulin M/biosynthesis , Kinetics , Lipopolysaccharides/adverse effects , Male , Meningitis, Meningococcal/cerebrospinal fluid , Meningitis, Meningococcal/immunology , Meningitis, Meningococcal/prevention & control , Meningococcal Vaccines/adverse effects , Reverse Transcriptase Polymerase Chain Reaction , SerotypingABSTRACT
BACKGROUND: Thirty-one Russian patients with late complement component deficiency (LCCD) who had experienced one to five meningococcal infections were immunized with meningococcal polysaccharide vaccine (A + C + W135 + Y) and were followed for 3-8 years. We investigated the potentially protective killing effect of human neutrophils (PMNL) on serogroup A and W135 meningococci. METHODS: Meningococci were incubated in LCCD vaccine sera in the absence or presence of PMNL, and the number of live bacteria (CFU) was determined by plating onto chocolate agar. RESULTS: When meningococci were incubated in the LCCD sera alone, exponential growth of meningococci occurred despite the presence of meningococcal antibodies. After the addition of PMNL, meningococci were inhibited in their growth or even eliminated. Group A or W135 meningococci were killed effectively by PMNL in 80% of the sera which were collected 1 month to 1 year after vaccination compared to only 40% in the prevaccination LCCD sera (p < 0.05). Three years after vaccination 67% of the LCCD sera were still capable of promoting killing (and even 90% after revaccination). The rate of killing correlated with the concentration of serogroup-specific immunoglobulins. In 83% of the 72 LCCD sera with more than 5 microg/ml anti-group A immunoglobulins the killing of group A meningococci was promoted. By contrast, only 21% of 19 samples with lower specific antibody levels showed a PMNL-mediated meningococcal killing (p < 0.05). The same effect was observed for group W135 meningococci. CONCLUSION: PMNL kill meningococci during incubation in LCCD serum; this effect increases after vaccination and depends on both specific antibody and complement. Protection by vaccination may therefore be caused by an increased killing capacity of PMNL.
