Volume 1, Number 2—April 1995
Epidemic-Associated Neisseria meningitidis Detected by Multilocus Enzyme Electrophoresis
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|EID||Reeves MW, Perkins BA, Diermayer M, Wenger JD. Epidemic-Associated Neisseria meningitidis Detected by Multilocus Enzyme Electrophoresis. Emerg Infect Dis. 1995;1(2):53-54. https://dx.doi.org/10.3201/eid0102.950203|
|AMA||Reeves MW, Perkins BA, Diermayer M, et al. Epidemic-Associated Neisseria meningitidis Detected by Multilocus Enzyme Electrophoresis. Emerging Infectious Diseases. 1995;1(2):53-54. doi:10.3201/eid0102.950203.|
|APA||Reeves, M. W., Perkins, B. A., Diermayer, M., & Wenger, J. D. (1995). Epidemic-Associated Neisseria meningitidis Detected by Multilocus Enzyme Electrophoresis. Emerging Infectious Diseases, 1(2), 53-54. https://dx.doi.org/10.3201/eid0102.950203.|
In Oregon and parts of Washington State, the incidence of serogroup B meningococcal disease increased substantially in 1994 (1). Multilocus enzyme electrophoresis (MEE) subtyping of N. meningitidis serogroup B strains collected in these areas during 1993 and 1994 suggested that these increases were due to a group of genetically related strains of the enzyme type-5 (ET-5) complex. ET-5 N. meningitidis serogroup B were first recognized in Norway in 1974 as the cause of a meningococcal disease epidemic that persisted through 1991. Since 1974, serogroup B meningococci of the ET-5 complex have caused epidemics in Europe, Cuba, and South America; these epidemics elevated disease rates for many years in the affected areas (2,3) and led to sustained efforts for vaccine development. This report describes the use of MEE to compare invasive N. meningitidis serogroup B meningococcal strains from Oregon and Washington with epidemic serogroup B strains from other countries and with serogroup B strains that have caused endemic disease in other parts of the United States.
MEE, first described in 1966 as a molecular approach to the study of genetic variation in eukaryotic systems, has only gradually been adopted by microbiologists and epidemiologists. The fundamental concept underlying MEE is that differences in the electrophoretic mobility of constitutive enzymes (resulting from amino acid substitutions) reflect the chromosomal genotype of strains and thereby allow the calculation of a genetic-relatedness index (Figure. [cannot be viewed in ASCII]). As recently as 1984, only one bacterial species, Escherichia coli, had been studied by MEE. Since then, however, MEE has been used to characterize genetic variation among populations of Legionella spp., Bordetella spp., Haemophilus influenzae, Streptococcus spp., Listeria monocytogenes, Neisseria meningitidis, and other bacteria (4).
To carry out MEE, crude aqueous extracts of bacteria are electrophoresed in a block of 11% to 12% starch in the presence of a dilute buffer (pH 8.0). The block is then cut into thin slices, which are stained to detect specific enzymes. The distance traveled by each enzyme is used to create a series of numbers representing the set of enzyme mobilities characteristic of individual strains. The number of enzymes used is somewhat arbitrary and varies between organisms; 15 to 24 enzymes have usually been adequate to characterize genetic diversity among bacterial populations. For this investigation, electrophoretic variations in 24 enzymes were used to describe genetic variability among isolates of N. meningitidis serogroup B. N. meningitidis strains used for this analysis were collected from Oregon (1993-1994, n=64) and part of Washington State (1993-1994, n=17; 1992, n=2; 1990, n=1; unknown, n=2); serogroup B meningococcal epidemics outside the United States (1976-1993; Norway n=1; Cuba n=1; Brazil n=1; and Chile n=2); and active population-based surveillance for meningococcal disease in selected areas of the United States (1991-1994, from the San Francisco Bay area, Georgia, Maryland, Oklahoma, and Tennessee, n=57). The epidemic strains tested from Norway and Cuba are the type used for the outer membrane protein vaccines developed and tested in these countries.
The MEE data analyzed here (PubMedcannot be viewed in ASCII) suggest that the increased rates of disease in Oregon and part of Washington are caused by highly genetically related N. meningitidis serogroup B strains of the ET-5 complex. These strains have been relatively rare in the United States. Oregon and Washington strains match a strain isolated in Santiago, Chile, during 1993. The prolonged duration of some ET-5 serogroup B meningococcal epidemics in large regions (e.g., Brazil, Argentina, and Chile) demands careful monitoring of this organism in the United States. Efforts to identify potentially modifiable risk factors for the disease and develop a vaccine have been intensified. MEE will continue to be the primary means for epidemiologic tracking and surveillance of ET-5 complex N. meningitidis serogroup B in the United States.
(Bacteria strains were provided by K. Steingart, Southwest Washington Health Dist., and M. Goldoft, Washington Dept. of Health.)
- Centers for Disease Control and Prevention. Serogroup B meningococcal disease--Oregon, 1994. MMWR. 1995;44:121–4.
- Caugant DA, Froholm LO, Bovre K, Holten E, Frasch CE, Mocca LF, Intercontinental spread of a genetically distinctive complex of clones of Neisseria meningitidis causing epidemic disease. Proc Natl Acad Sci U S A. 1986;83:4927–31.
- Sacchi CT, Pessoa LL, Ramos SR, Milagres LG, Camargo MCC, Hidalgo NTR, Ongoing group B Neisseria meningitidis epidemic in São Paulo, Brazil, due to increased prevalence of a single clone of the ET-5 complex. J Clin Microbiol. 1992;30:1734–8.
- Selander RK, Caugant DA, Ochman H, Musser JM, Gilmour MN, Whittam TS. Methods of multilocus enzyme electrophoresis for bacterial population genetics and systematics. Appl Environ Microbiol. 1986;51:873–84.
- Figure. Genetic relatedness of serogroup B strains of Neisseria meningitidis from Oregon, Washington, other countries, and endemic-disease cases in the United States. A. Computer-generated dendrogram for all isolates; 68 enzyme types...
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