Prospective study of potential sources of Streptococcus mutans transmission in nursery school children

Abstract

Transmission of Streptococcus mutans, a major dental caries pathogen, occurs mainly during the first 2.5 years of age. Children appear to acquire S. mutans mostly from their mothers, but few studies have investigated non-familial sources of S. mutans transmission. This study prospectively analysed initial S. mutans oral colonization in 119 children from nursery schools during a 1.5-year period and tracked the transmission from child to child, day-care caregiver to child and mother to child. Children were examined at baseline, when they were 5-13 months of age, and at 6-month intervals for determination of oral levels of S. mutans and development of caries lesions. Levels of S. mutans were also determined in caregivers and mothers. A total of 1392 S. mutans isolates (obtained from children, caregivers and mothers) were genotyped by arbitrarily primed PCR and chromosomal RFLP. Overall, 40.3 % of children were detectably colonized during the study, and levels of S. mutans were significantly associated with the development of caries lesions. Identical S. mutans genotypes were found in four nursery cohorts. No familial relationship existed in three of these cohorts, indicating horizontal transmission. Despite high oral levels of S. mutans identified in most of the caregivers, none of their genotypes matched those identified in the respective children. Only 50 % of children with high levels of S. mutans carried genotypes identified in their mothers. The results support previous evidence indicating that non-familial sources of S. mutans transmission exist, and indicate that this bacterium may be transmitted horizontally between children during the initial phases of S. mutans colonization in nursery environments.

Genetic Diversity and Evidence for Transmission of Streptococcus mutans by DiversiLab rep-PCR

“…Mother-to-child transmission is widely accepted as the primary route of infection with S. mutans , although other sources of shared genotypes have been reported (i.e., father, nursery and school classmates) (Alves et al, 2009, Binks and Duane, 2015, Domejean, Zhan, DenBesten Stamper, Boyce and Featherstone, 2010, Kozai et al, 1999, Liu, Zou, Shang and Zhou, 2007, Redmo Emanuelsson and Wang, 1998, Tedjosasongko and Kozai, 2002). There are several missing pieces in the current literature.…”

Comparisons of IgA response in saliva and colostrum against oral streptococci species

“…3 However, these species may also be detected in predentate children highly exposed to S. mutans. 4 Some major antigens expressed in the S. mutans cell surface, such as antigen I/II (Ag I/II), glucosyltransferase (Gtf) and glucan-binding protein B (GbpB), are involved in the ability of these microorganisms to adhere and accumulate in the oral biofilm, promoting the development of dental caries. 5,6,7 Several studies have shown that the induction of specific antibodies against these antigens can confer protection against the development of dental caries in animal models.…”

Fatores de virulência de Streptococcus mutans e sua relação com a persistência e transmissão de genótipos entre membros de famílias brasileiras

“…Estudos realizados com diferentes técnicas de tipagem bacteriana apontam a transmissão vertical intrafamiliar dos pais para os filhos como via primária de infecção por S. mutans, ao mesmo tempo que indicam a mãe como principal, mas não exclusiva, fonte de contaminação precoce (BERKOWITZ; JORDAN, 1975;ROGERS, 1981;DAVEY;ROGERS, 1984;BERKOWITZ;JONES, 1985;WALKER, 1989;KULKARNI;CHAN;SANDHAM, 1989;AZEVEDO;ZELANTE, 1994;CAUFIELD, 1995;ALALUUSUA et al, 1996;GRÖNROOS et al, 1998 TEDJOSASONGKO; KOZAI, 2002;KÖHLER et al, 2003;SPOLIDORIO et al, 2003;ERSIN et al, 2004;KLEIN et al, 2004;LINDQUIST;EMILSON, 2004;FIGUEIREDO;CRUZ;LI,S et al, 2005;LI,Y et al, 2005;RUBIRA, 2007;HAMEŞ-KOCABAŞ et al, 2008;LAPIRATTANAKULL et al, 2008;ALVES et al, 2009;MITCHELL et al, 2009;CARLETTO-KÖRBER et al, 2010;TEANPAISAN et al, 2012;ZHAN et al, 2012). No decorrer dos anos, também tem sido relatada uma rota adicional de aquisição desses patógenos.…”

“…No decorrer dos anos, também tem sido relatada uma rota adicional de aquisição desses patógenos. O compartilhamento de genótipos idênticos de S. mutans suporta evidências de transmissão horizontal entre cônjuges (ROGERS, 1981;DAVEY;ROGERS, 1984;KULKARNI;CHAN;SANDHAM, 1989;SAARELA et al, 1993;AZEVEDO;ZELANTE, 1994;WANG, 1998;KOZAI et al, 1999;VAN LOVEREN;BUIJS;TEN CATE, 2000;BIAN, 2002;KÖHLER et al, 2003;ERSIN et al, 2004;RUBIRA, 2007), entre irmãos (KULKARNI; CHAN; SANDHAM, 1989;AZEVEDO;ZELANTE, 1994;KOZAI et al, 1999;KÖHLER et al, 2003;SPOLIDORIO et al, 2003;MITCHELL et al, 2009) e entre crianças não relacionadas geneticamente (MATTOS-GRANER et al, 2001a;KOZAI, 2002;LIU et al, 2007;ALVES et al, 2009;DOMÉJEAN et al, 2010;BACA et al, 2012 (ROGERS, 1975;DAVEY;ROGERS, 1984;KULKARNI;CHAN;SANDHAM, 1989;KOZAI et al, 1991;ALALUUSUA et al, 1994;THORNQVIST, 2000;KÖHLER et al, 2003;REDMO EM...…”

“…A comparação entre as cepas bacterianas adquiridas pela criança e as de seus conviventes tem sido realizada com base nas características fenotípicas, usando métodos como a mutacinotipagem (BERKOWITZ; JORDAN, 1975;ROGERS, 1975ROGERS, , 1981DAVEY;ROGERS, 1984;BERKOWITZ;JORDAN, 1985;AZEVEDO;ZELANTE, 1994 (SAARELA et al, 1993;ALALUUSUA et al, 1994ALALUUSUA et al, , 1996GRÖNROOS et al, 1998) e a AP-PCR (LI; WANG; MATTOS-GRANER et al, 2001a;SPOLIDORIO et al, 2003;ERSIN et al, 2004;KLEIN et al, 2004;FIGUEIREDO;CRUZ;LI,S et al, 2005;LI,Y et al, 2005;LIU et al, 2007;RUBIRA, 2007;HAMEŞ-KOCABAŞ et al, 2008;ALVES et al, 2009;MITCHELL et al, 2009;CARLETTO-KÖRBER et al, 2010;DOMÉJEAN et al, 2010;BACA et al, 2012;TEANPAISAN et al, 2012;ZHAN et al, 2012).…”