Streptococcus mutans & other streptococci

1. STREPTOCOCCUS MUTANS
Dr. Ali Yaldrum
Faculty of Dentistry, SEGi University.

2. LEARNING OBJECTIVES
At the end of this session, the student should be able to:
1.Describe what are Streptococci Organisms
2.Classification of Streptococci Organisms
3.Describe role played by Streptococcus mutans in health and disease

3. 1. GENERAL PROPERTIES
•Catalase negative
•Gram +ve
•Spherical or Oval Cocci
•Appears in pairs or chains
•0.7 to 0.9 um in diameter
•causes a wide variety of diseases (fig. 1)

4. 2. PATHOGENICITY
Pathogenic Streptococcus produces several extra cellular
substances that contribute to their pathogenicity

5. 2. PATHOGENICITY
1.products that destroy the phagocytic cells & ingest them
2.produces enzymes that digest the connective tissue resulting in
extensive tissue destruction
3.can also lyse “Fibrin”

6. caries
pneumonia
endocarditis
necrotizing fasciitis
meningitis
(see fig 2&3)
(fig 1)

7. facial cellulitis which progressed relentlessly with necrosis
(fig 2)

8. (fig 3)

9. 4. CULTURE
•Grow well on blood agar
•There are 3 types of hemolytic reactions produced on blood agar
(fig 4 & 5)
1.α -hemolysis
2.β-hemolysis
3.γ-hemolysis

10. TYPES OF HEMOLYTIC REACTIONS
(FIG 4)
β-hemolysis
wide clear translucent zone
of complete hemolysis around
the colony
α -hemolysis
narrow zone of partial
hemolysis
γ-hemolysis:
no hemolysis occurs

11. TYPES OF HEMOLYTIC REACTIONS
(FIG 5)
shorter arrow: α hemolysis longer arrow: β-hemolysis

12. 3. SEROLOGY
•Surface Carbohydrate antigens are related to their virulence
•Hence serogrouping termed Lancefield grouping is useful in
identification of the more virulent β-hemolytic species
•20 Lancefield groups are recognized

13. MUTANS GROUP

14. •originally isolated from human teeth by Clark in 1924
•in 1960 caries were induced experimentally in animals, artificially
infected with strains resembling S.mutans
•cells can loose their coccal morphology and appear as cocco-bacilli

15. •9 serotypes have been identified (a-h & k)
•Human isolates are : c,e f and k
•S.mutans have been implicated as the primary pathogen in :
1.enamel caries in children & young adults
2.root surface caries in elderly

16. •occupy hard non-shedding surfaces i.e teeth or dentures
•Regularly isolated from dental plaque at carious site, but low
prevalence on sound enamel
•opportunistic pathogens (isolated from cases of infective endocarditis)
•communicate with other mutans

17. •cell wall carbohydrate antigen (I/II)
•lipoteichoic acid
•lipoproteins
•cell wall associated protein

18. Streptococcus mutans
Extracellular Polysaccharides
(glucan, mutan, fructan)
Intracellular Polysaccharides
(glucan, mutan, fructan)
excess sugar
glucosyl and fructosyltransferase
contribute to characteristic colonial morphology
act as carbohydrate reserve, used to produce
acid in absence of available sugar

19. Salivarius group

20. This group consists of two bacterias
1. S. salivarius
2. S. vestibularis

21. •salivarius prefer mucosal surface especially the tongue
•produce unusual quantity of extracellular fructan
•rarely isolated from diseased sites

22. •S. vestibularis prefers the vestibular mucosa
•no extracellular polysaccharide production
•produces ‘urease’ leading to rise in local pH and hydrogen peroxide

23. Anginosus group

24. The group is differentiated into
•S. constellatus
•S. intermedius
•S. anginosus

25. •readily isolated from dental plaque & from mucosal surface
•cause serious, purulent diseases
•commonly found in abscess of internal organs
•no strain produces polysaccharide from sucrose

26. Mitis group

27. This group consists of
•S. sanguinis
•S. gordonii
•S. mitis
•S. oralis

28. •Early colonizers of tooth
•produce soluble and insoluble glucans from sucrose
•contribute to plaque formation
•ammonia generation from arginine

29. •S. sanguinis produces a protease that can cleave sIgA
•S. gordonii can bind with salivary amylase enabling the breakdown
of starch

30. 1. Philip D. Marsh, Michael V Martin, “The Resident Oral Microflora” in Oral Microbiology, 5
th
Edition,
Churchil Livingstone, 2009, pp 25-35
References