Scand J Infect Dis 24: 323-332, 1992
DNA Fingerprinting in the Epidemiology of African Serogroup A Neisseria meningitidis
Scand J Infect Dis Downloaded from informahealthcare.com by University of Newcastle Upon Tyne on 12/20/14 For personal use only.
BJARNE BJORVATN', MUSA HASSAN-KING', BRIAN GREENWOOD', R E D D A TEKLE HAIMANOT', DANIEL FEKADE' and GUY SPERBER' From /he 'Centre for Interrzutional Health and Metlrcul l k p ~ ~ r t m e nB t, University of' Brrgrvi. Norwuji, the *Medical Research Council Ltihorcitor.ies, Fajara, The Garnhia, the 'Medrcd Depurtmetzt, Section of Neiudogy, Tikrrr Aiibe.ssu University Hospital. Addis Ahrrho. Elhiopiu, and 'lnstitut de Medecine fiopic.de ciu Service de Sun14 des Armkes, h.lur.cerlle. France
The restriction endonuclease (RE) technique was used to compare 172 meningococcal group A strains collected between 1969 and 1990, mainly from countries of the so-called African Meningitis Belt, the Gambia and Ethiopia. The 64 strains from various African countries (Niger, Chad, Burkina Faso, Cameroon, Morocco, Djibouti) were distributed within 3 main restriction enzyme patterns (REPs); the 77 Gambian strains fell into 5 REPs and the 24 Ethiopian strains into 2 such patterns. Several of the main REPs were formed by clusters of closely related clones. Clones, very similar to dominating REPs of the 1960s in Niger, Burkina Faso and Cameroon, were in the 1980s found to be strongly represented in the Gambia to the extreme west of the Meningitis Belt. One of the Gambian clones from 1983-86 was identical to an Indian clone recovered in New Delhi 1986-87. Another clone was detected in 1983 in the Gambia, in 1989 again in the Gambia as well as in Ethiopia, and in 1990 in Tanzania. Oiir results are largely in line with those of previous studies based on modern techniques of protein and isoenzyme electrophoresis. The RE method is useful mainly for the exact genotypic differentiation of closely related clones, and seems to be a valuable complement to phenotypic tools for epidemiological mapping of Group A meningococcal infection.
B . Bjorvatn, M D , PhD, Centre f o r International Health, Armauer Hansen Building, Haukeland University Hospital, N-5021 Bergen, Norway
INTRODUCTION At intervals of 8-12 years, meningococcal epidcniics reaching prevalence rates of up to 500-1 000/100 000 inhabitants have caused major public health problems in several countries of Sahelian Africa. Typically, the epidemics start well into the dry season and spread in the population with dramatic speed until ending abruptly with the onset of the rainy season (1-3). Apart from the fact that most epidemics of the so-called African Meningitis Belt seem to be caused by group A meningococci, little is known about the mechanisms triggering this particular epidemiological pattern. In fact. until recently it was quite unclear whether each epidemic wave is caused by a new and antigenically different bacterial clone, or represents outbreaks by the same virulent clone at intervals that are regulated mainly by the level of herd immunity. Over the last few years, accumulating evidence (3-6)suggests that a limited number of clonal populations, each consisting of one or several closely related clones, may circulate for decades between countries and even continents. Under favourable conditions such as international mass migration caused by the annual pilgrimage to Mecca, local outbreaks may within weeks spread to other countries and continents. According to OIyhoek et al. (6), at least 7 predominant clones have caused major epidemic waves since 1915. Insight into the epidemiology of group A meningococcal infection has recently been dramatically improved by the introduction of a number of modern research tools such as panels of monoclonal antibodies for serological testing (7). starch gel electrophoresis of cytoplasmic enzymes (5, 6, 8 ) , and sodium dodecyl sulphate-polyacrylamide gel electrophoresis of bacterial outer membrane proteins (6). In addition to such phenotypic technologies, a
324 B. Bjorvatn et al.
Scand J Infect Da 24
Table I. DNA restriction enzyme patterns of 64 meningococcal isolates from various African countries (1961-86) Clone designation
Type representative
No. ofisolates' Similarity ('YO) t o standard
Scand J Infect Dis Downloaded from informahealthcare.com by University of Newcastle Upon Tyne on 12/20/14 For personal use only.
004 Afr 1.1
004
16
100
Afr 1.2
006
23
96
256 86088 250 023 29s
I 2 S 7 10
98 96 4 0
DNA Fingerprinting in the Epidemiology of African Serogroup A Neisseria meningitidis
Scand J Infect Dis Downloaded from informahealthcare.com by University of Newcastle Upon Tyne on 12/20/14 For personal use only.
BJARNE BJORVATN', MUSA HASSAN-KING', BRIAN GREENWOOD', R E D D A TEKLE HAIMANOT', DANIEL FEKADE' and GUY SPERBER' From /he 'Centre for Interrzutional Health and Metlrcul l k p ~ ~ r t m e nB t, University of' Brrgrvi. Norwuji, the *Medical Research Council Ltihorcitor.ies, Fajara, The Garnhia, the 'Medrcd Depurtmetzt, Section of Neiudogy, Tikrrr Aiibe.ssu University Hospital. Addis Ahrrho. Elhiopiu, and 'lnstitut de Medecine fiopic.de ciu Service de Sun14 des Armkes, h.lur.cerlle. France
The restriction endonuclease (RE) technique was used to compare 172 meningococcal group A strains collected between 1969 and 1990, mainly from countries of the so-called African Meningitis Belt, the Gambia and Ethiopia. The 64 strains from various African countries (Niger, Chad, Burkina Faso, Cameroon, Morocco, Djibouti) were distributed within 3 main restriction enzyme patterns (REPs); the 77 Gambian strains fell into 5 REPs and the 24 Ethiopian strains into 2 such patterns. Several of the main REPs were formed by clusters of closely related clones. Clones, very similar to dominating REPs of the 1960s in Niger, Burkina Faso and Cameroon, were in the 1980s found to be strongly represented in the Gambia to the extreme west of the Meningitis Belt. One of the Gambian clones from 1983-86 was identical to an Indian clone recovered in New Delhi 1986-87. Another clone was detected in 1983 in the Gambia, in 1989 again in the Gambia as well as in Ethiopia, and in 1990 in Tanzania. Oiir results are largely in line with those of previous studies based on modern techniques of protein and isoenzyme electrophoresis. The RE method is useful mainly for the exact genotypic differentiation of closely related clones, and seems to be a valuable complement to phenotypic tools for epidemiological mapping of Group A meningococcal infection.
B . Bjorvatn, M D , PhD, Centre f o r International Health, Armauer Hansen Building, Haukeland University Hospital, N-5021 Bergen, Norway
INTRODUCTION At intervals of 8-12 years, meningococcal epidcniics reaching prevalence rates of up to 500-1 000/100 000 inhabitants have caused major public health problems in several countries of Sahelian Africa. Typically, the epidemics start well into the dry season and spread in the population with dramatic speed until ending abruptly with the onset of the rainy season (1-3). Apart from the fact that most epidemics of the so-called African Meningitis Belt seem to be caused by group A meningococci, little is known about the mechanisms triggering this particular epidemiological pattern. In fact. until recently it was quite unclear whether each epidemic wave is caused by a new and antigenically different bacterial clone, or represents outbreaks by the same virulent clone at intervals that are regulated mainly by the level of herd immunity. Over the last few years, accumulating evidence (3-6)suggests that a limited number of clonal populations, each consisting of one or several closely related clones, may circulate for decades between countries and even continents. Under favourable conditions such as international mass migration caused by the annual pilgrimage to Mecca, local outbreaks may within weeks spread to other countries and continents. According to OIyhoek et al. (6), at least 7 predominant clones have caused major epidemic waves since 1915. Insight into the epidemiology of group A meningococcal infection has recently been dramatically improved by the introduction of a number of modern research tools such as panels of monoclonal antibodies for serological testing (7). starch gel electrophoresis of cytoplasmic enzymes (5, 6, 8 ) , and sodium dodecyl sulphate-polyacrylamide gel electrophoresis of bacterial outer membrane proteins (6). In addition to such phenotypic technologies, a
324 B. Bjorvatn et al.
Scand J Infect Da 24
Table I. DNA restriction enzyme patterns of 64 meningococcal isolates from various African countries (1961-86) Clone designation
Type representative
No. ofisolates' Similarity ('YO) t o standard
Scand J Infect Dis Downloaded from informahealthcare.com by University of Newcastle Upon Tyne on 12/20/14 For personal use only.
004 Afr 1.1
004
16
100
Afr 1.2
006
23
96
256 86088 250 023 29s
I 2 S 7 10
98 96 4 0
