Similarity of bacteriocins of Streptococcus mutans from mother and infant

Berkowitz, Robert J.; Jordan, H.V.

doi:10.1016/0003-9969(75)90042-4

Cited by 138 publications

(88 citation statements)

References 27 publications

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“…MS seems to be an important part of the total bacteria counts as the results show, though other studies suggest that MS acquisition happens later and other kinds of streptococci are dominant [11][12][13] . The results of this study, might lead to a better prevention plan among newborn and children.…”

Section: Discussionmentioning

confidence: 58%

Acquired Oral Microflora of Newborns During the First 48 Hours of Life

Rosenblatt¹,

Steinberg²,

Mankuta³

et al. 2015

Journal of Clinical Pediatric Dentistry

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Section: Discussionmentioning

confidence: 58%

Acquired Oral Microflora of Newborns During the First 48 Hours of Life

Rosenblatt¹,

Steinberg²,

Mankuta³

et al. 2015

Journal of Clinical Pediatric Dentistry

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“…Mutacins are peptide or protein antibiotics that are mainly bactericidal for other bacteria of the same or closely related species, as well as for other Gram-positive micro-organisms, and are likely to confer an ecological advantage in diverse bacterial communities such as the dental biofilm (Parrot et al, 1990; Balakrishnan et al, 2002). Some studies have demonstrated that the mutacin activity of S. mutans could be related to the prevalence of this species in the dental biofilm, saliva and dental caries (Berkowitz and Jordan, 1975;Hillman et al, 1987).Classification of mutacin-producer strains based on their bactericidal activity divides mutacins into four types, I, II, III and IV. The antimicrobial spectrum of mutacin IV is specifically against members of the mitis group of oral streptococci, while that of mutacins I, II and III is broader (Qi et al, 1999a(Qi et al, , b, 2001.…”

mentioning

confidence: 99%

Frequency of four different mutacin genes in Streptococcus mutans genotypes isolated from caries-free and caries-active individuals

Kamiya

Napimoga

Höfling

et al. 2005

Journal of Medical Microbiology

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The ability of Streptococcus mutans to produce mutacins, combined with the production of other virulence factors such as lactic acid, may contribute to the pathogenesis of this bacterium. In the present study, the detection of genes encoding mutacin types I/III, II and IV was performed by PCR with specific primers to each type in a total of 63 S. mutans genotypes isolated from caries-active and caries-free individuals. In the caries-free group, PCR screening for mutacin IV revealed that 31 . 8 % of strains were positive for this mutacin. PCR for the other three mutacins tested (I/III and II) did not yield amplicons in any S. mutans strains in this group. The PCR with primers of mutacin IV showed 68 . 3 % positive genotypes in the caries-active group, on the other hand, the amplicons of mutacins I/III revealed 41 . 5 % positive strains that carried these genes. The chi square test showed significant differences in the number of positive strains to mutacin IV when comparing the caries-free and caries-active genotypes of S. mutans (P ¼ 0 . 01). All tested S. mutans strains were negative by PCR for mutacin II. The low frequencies of detection of some mutacin genes suggest the existence of high diversity and polymorphism in the production of genetic determinants of mutacin-like substances. In addition, the production of a wide spectrum of mutacins can play an important biological role in colonization by S. mutans strains, mainly in the niche of high-complexity microbial communities. INTRODUCTIONMutans streptococci are generally accepted as one of the principal aetiological agents of dental caries (Loesche, 1986;Becker et al., 2002). The dental biofilm consists of a complex bacterial community, and the ability of specific strains of Streptococcus mutans to compete with other strains may be essential for colonization. Alaluusua et al. (1996) suggested that some strains of S. mutans might be able to colonize the host and induce dental caries better than other strains. Alternatively, dietary patterns of the host may be an important factor, since a high salivary mutans streptococci count does not necessarily exert a cariogenic challenge (van Palenstein Helderman et al., 1996).Numerous factors affect the equilibrium among oral populations of micro-organisms, and several inhibitory substances have been identified, including mutacins (Fukushima et al., 1985;Caufield et al., 1985;Delisle, 1976). Mutacins are peptide or protein antibiotics that are mainly bactericidal for other bacteria of the same or closely related species, as well as for other Gram-positive micro-organisms, and are likely to confer an ecological advantage in diverse bacterial communities such as the dental biofilm (Parrot et al., 1990; Balakrishnan et al., 2002). Some studies have demonstrated that the mutacin activity of S. mutans could be related to the prevalence of this species in the dental biofilm, saliva and dental caries (Berkowitz and Jordan, 1975;Hillman et al., 1987).Classification of mutacin-producer strains based on their bactericidal activity...

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“…In recent decades the process has been much better defined from several aspects including microbiology, saliva, tooth mineral composition, tooth ultrastructure, diffusion processes, kinetics of demineralization, the reversal of demineralization that is known as remineralization, and factors that contribute to the reversal of the process. [1][2][3][4][5][6][7][8][9][10][11][12] Now, we have a rather deep understanding of what goes on in the mouth, but this knowledge is far from being effectively utilized in dental practice.…”

Section: What Is Dental Caries and What Do We Know About It?mentioning

confidence: 99%

Dental caries: a dynamic disease process

Featherstone

2008

Australian Dental Journal

542

357

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Dental caries is a transmissible bacterial disease process caused by acids from bacterial metabolism diffusing into enamel and dentine and dissolving the mineral. The bacteria responsible produce organic acids as a by-product of their metabolism of fermentable carbohydrates. The caries process is a continuum resulting from many cycles of demineralization and remineralization. Demineralization begins at the atomic level at the crystal surface inside the enamel or dentine and can continue unless halted with the end-point being cavitation. There are many possibilities to intervene in this continuing process to arrest or reverse the progress of the lesion. Remineralization is the natural repair process for non-cavitated lesions, and relies on calcium and phosphate ions assisted by fluoride to rebuild a new surface on existing crystal remnants in subsurface lesions remaining after demineralization. These remineralized crystals are acid resistant, being much less soluble than the original mineral.

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Similarity of bacteriocins of Streptococcus mutans from mother and infant

Cited by 138 publications

References 27 publications

Acquired Oral Microflora of Newborns During the First 48 Hours of Life

Acquired Oral Microflora of Newborns During the First 48 Hours of Life

Frequency of four different mutacin genes in Streptococcus mutans genotypes isolated from caries-free and caries-active individuals

Dental caries: a dynamic disease process

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