Population structure of group B streptococcus from a low-incidence region for invasive neonatal disease

Abstract

The population structure of group B streptococcus (GBS) from a low-incidence region for invasive neonatal disease (Israel) was investigated using multilocus genotype data. The strain collection consisted of isolates from maternal carriage (n=104) and invasive neonatal disease (n=50), resolving into 46 sequence types. The most prevalent sequence types were ST-1 (17?5 %), , , and . Serotype III was the most common, accounting for 29?2 % of the isolates. None of the serotypes was significantly associated with invasive neonatal disease. BURST analysis resolved the 46 sequence types into seven lineages (clonal complexes), from which only lineage ST-17, expressing serotype III only, was significantly associated with invasive neonatal disease. Lineage ST-22 expressed mainly serotype II, and was significantly associated with carriage. The distribution of the various sequence types and lineages, and the association of lineage ST-17 with invasive disease, are consistent with the results of analyses from a global GBS isolate collection. These findings could imply that the global variation in disease incidence is independent of the circulating GBS populations, and may be more affected by other risk factors for invasive GBS disease, or by different prevention strategies. INTRODUCTIONOver the last three decades, group B streptococcus (GBS) has become the leading cause of neonatal meningitis and septicaemia in North America, western Europe and Australia, causing considerable rates of morbidity and mortality (Baker, 2001; Isaacs et al., 1995;Schrag et al., 2000). The increasing incidence of invasive neonatal GBS disease has prompted measures to reduce its prevalence in the USA (American Academy of Pediatrics Committee on Infectious Diseases and Committee on Fetus and Newborn, 1997), Australia (Isaacs & Royle, 1999), and recently in the UK (www.hpa.org.uk/infections/). Interestingly, reports from many developing countries and some developed countries show rates of invasive neonatal GBS disease that are much lower than those reported from North America (Chong et al., 1993;Mayon-White, 1985;Schuchat, 1995;Stan et al., 2001;Stoll, 1997;Tsolia et al., 2003). An explanation for such variation is not apparent, and has not been systematically investigated. Low rates of GBS carriage among pregnant women have been suggested as a possible explanation, yet reports from developing countries have shown that, despite significant geographical variation in the proportion of GBS carriage, the range of colonization is similar to that identified in North America (Stoll & A possible explanation for such a low incidence of invasive neonatal GBS disease, despite the substantial carriage rate, is that invasive disease may be caused by a few virulent lineages (clones) within the total GBS population, such that measurement of the total GBS colonization rates may be misleading as to the true size of the population at risk. Secondly, virulent lineages may account for a different proportion of the vaginal GBS population in different geographical location...

Population Structure of Invasive and Colonizing Strains of Streptococcus agalactiae from Neonates of Six U.S. Academic Centers from 1995 to 1999

“…Thirty-nine percent of the serotype II GBS in this study were from CC 17, an unusual finding since serotype II GBS from CC 17 have only rarely been identified among sam- (4,15,16,23). Similar to findings for serotype III GBS, the invasive serotype II GBS in this study were found more frequently to be from CC 17: 67% (6/9 isolates) of invasive type II GBS were in CC 17, compared to only 34% (16/47 isolates) of colonizing type II GBS.…”

“…GBS from these CCs have been shown to cause the majority of neonatal GBS infections in Sweden, the United Kingdom, and Israel (4,15,23 Serotype V GBS emerged in the 1990s and have become established globally as an important cause of GBS infection in both neonates and adults. This study, along with previous studies, indicates that these serotype V GBS are clonal and are from CC 1 (4,5,15,16,23). While colonizing serotype V strains in this study were also occasionally found in a variety of other lineages, the only other invasive serotype V strain in this study was ST-26, an ST related to a bovine serotype V ST-256 strain isolated from a bovine udder in Brazil (27).…”

“…Investigators using a variety of techniques have demonstrated that the population of GBS that colonizes and infects humans is comprised of a relatively small number of lineages (4, 12-16, 23, 26, 28, 31, 32). Each serotype is usually distributed among several different lineages, and each lineage may contain several different serotypes, indicating that serotype alone is not a sufficient marker to identify a phylogenetic lineage and suggesting that serotype switching occurs within lineages, presumably by horizontal transfer of cps genes (4,16,23).Multilocus sequence typing (MLST) has become the standard method for determining the population structure of GBS and has been applied to the molecular epidemiology of GBS infections by several investigators (4,9,15,16,22,23). We recently reported the relationship between the phylogenetic lineages that comprise serotype III GBS isolates and the occurrence of neonatal early-onset disease in a NICHD multicenter prospective study of GBS disease and colonization in the newborns.…”

“…Multilocus sequence typing (MLST) has become the standard method for determining the population structure of GBS and has been applied to the molecular epidemiology of GBS infections by several investigators (4,9,15,16,22,23). We recently reported the relationship between the phylogenetic lineages that comprise serotype III GBS isolates and the occurrence of neonatal early-onset disease in a NICHD multicenter prospective study of GBS disease and colonization in the newborns.…”

“…Investigators using a variety of techniques have demonstrated that the population of GBS that colonizes and infects humans is comprised of a relatively small number of lineages (4, 12-16, 23, 26, 28, 31, 32). Each serotype is usually distributed among several different lineages, and each lineage may contain several different serotypes, indicating that serotype alone is not a sufficient marker to identify a phylogenetic lineage and suggesting that serotype switching occurs within lineages, presumably by horizontal transfer of cps genes (4,16,23).…”