Bacteria relevant to dental hygiene

1. INFECTIONS RELEVANT TO
DENTISTRY
BOH I 2024

2. The oral environment
• Mouth is lined by stratified squamous epithelium
• May be modified in areas according to function, interrupted by other
structures such as teeth and salivary ducts
• The gingival tissues form a cuff around each tooth and there is a
continuous exudate of crevicular fluid from the gingival crevice
• A thin layer of saliva covers the surface of the oral mucosa
• The numerous microflora in the mouth exists in harmony with the
host, but disease occurs when this balance is disturbed
• Predominant dental diseases in humans: caries and periodontal
disease

3. MAJOR ORAL HABITATS
 Buccal mucosa
 Usually sparsely colonized
 Dorsum of tongue
 Papillae provides refuge for colonizers
 Low redox potential, thus promotes growth of anaerobes and may serve as
reservoir implicated in periodontal disease
 Tooth surfaces(both supragingival and subgingival)
 Only non-shedding area of the body that has a microbial population
 Large quantities of bacteria and their products accumulate on tooth surfaces
– produce dental plaque
 Plaque is a natural biofilm and plays a major role in initiating caries and
periodontal disease
 When caries and periodontal disease occurs it means that there is a shift in
the composition away from “healthy” plaque flora

4. MAJOR ORAL HABITATS
• Tooth surfaces
• Range of habitats associated with
the tooth surface
• Nature of bacterial communities
varies depending on the tooth
and environmental exposure
• Smooth surfaces are usually less
colonised than pits/fissures
• Subgingival surfaces are more
anaerobic than supragingival
surfaces

5. MAJOR ORAL HABITATS
 Crevicular epithelium and gingival crevice
 Colonizing bacteria play a critical role in the initiation and development of gingival
and periodontal disease
 There is a continuous flow of gingival crevicular fluid (increased during
inflammation)
 Function of crevicular fluid:
 Flushing of microbes
 Source of nutrients to bacteria in crevice
 Maintain pH
 Provides specific and non-specific defense factors: mainly IgG
 Phagocytosis of MOs – 95% of leucocytes in crevicular fluid are neutrophils
 Prosthodontic and orthodontic appliances if present
 May act as reservoir for bacteria and yeasts if not kept clean
 Yeasts on the fitting surface of dentures can lead to Candida-associated denture
stomatitis

6. SPECIFIC & NON SPECIFIC HOST
DEFENCE FACTORS OF MOUTH

7. DENTAL PLAQUE BIOFILM
 Microbial community which develops on soft and hard tissue surfaces of the
mouth
 Comprising of living, dead and dying bacteria and their extracellular products
 Plaque biofilm is found on dental surfaces and appliances (increased with poor
oral hygiene)
 Plaque samples are described in relation to their site of origin and are
categorized as:
 Supragingival
 Subgingival

8. DENTAL PLAQUE BIOFILM

9. ROLE OF ORAL FLORA IN
SYSTEMIC INFECTION
 Recently it has been recognized that plaque-related diseases, especially,
periodontitis may alter the course and pathogenesis of number of
systemic diseases. This is known as ‘focal infection theory’
 Cardiovascular disease
 Infective endocarditis
 Coronary heart disease: atherosclerosis and myocardial infection
 Stroke
 Bacterial pneumonia
 Diabetes mellitus
 Low birth weight in babies

10. ROLE OF ORAL FLORA IN
SYSTEMIC INFECTION
1. Metastatic infection: microbes gaining entry into the circulatory
system through breaches in the oral vascular barrier, as in the case of
bacteraemia produced during tooth extractions - infective
endocarditis.
2. Metastatic injury: products of bacteria, such as cytolytic enzymes,
exotoxins and endotoxins (i.e. LPSs) gaining access to the
cardiovascular system in individuals suffering from periodontitis.
3. Metastatic inflammation: caused by immunological injury due to
oral organisms. Thus, soluble antigens may enter the blood stream
from the oral route, react with circulating specific antibodies and form
macromolecular complexes, leading to immune- mediated diseases.

11. PERIODONTAL DISEASE
 Definition: disorders of supporting structures of the teeth, such as the
gingivae, periodontal ligaments and supporting alveolar bone
 Categorized into gingivitis (inflammation of gum tissue) and periodontitis (a
serious gum infection that damages the soft tissue and destroys the bone
that supports your teeth)
 The main aetiological agent is microflora inhabiting subgingival plaque
biofilm
 There is no universally acknowledged classification of periodontal
disease and the clinical descriptors used relate to:
 the rate of disease progress (e.g. chronic, aggressive) lesion distribution (e.g.
localized, generalized)
 age group of the person (e.g. prepubertal, juvenile, adult)
 association with systemic or developmental disorders.

12. Classification of periodontal disease

14. STREPTOCOCCUS
■Gram-positive spherical or oval cocci in chains, Catalase -ve
■Haemolyic reactions on blood agar medium
■ α haemolysis – narrow zone of partial haemolysis and green discolouration
around colonies. e.g.. viridans streptococci
■ β haemolysis – clear zone of complete haemolysis around colonies. e.g. S.
pyogenes
■ γ no haemolysis – e.g..non-haemolytic streptococci
■ Lancefield Grouping
■ 20 beta - haemolytic groups (A-H and K-V)
■ Group A - S. pyogenes (tonsillitis, scarlet fever,
otitis media, impetigo sinusitis)
■ Group B – S. agalactiae (infection in neonates)
■ Group D – Enterococci – E. faecalis
■ Streptococcus pneumoniae (pneumonia, septicaemia)

16. ORAL STREPTOCOCCI
Four Groups
■ Mutans group
■ Salivarius group
■ Anginosus group
■ Mitis group
■ Each group comprises of number of species
■ Make up large proportion of oral flora
■ Infective endocarditis (IE) – viridans streptococci enters blood during intraoral surgical procedures (tooth
extraction)
■ Mutans Group
■ Major agents of dental caries
■ Infective endocarditis (bacteria settle on damaged heart valves, causing infective endocarditis-
prophylactic antibiotic should always be given to patients at risk of IE before dental procedure)
■ Produce extracellular polysaccharide in the presence of dietary carbohydrates which helps the organism to
bind to enamel and to each other
■ Gram positive Anaerobic Streptococci (GPAC) - isolated from dental plaque -pathogenic role unclear

17. STAPHYLOCOCCUS
■Gram positive in grape-like clusters
■Medical importance: S. aureus and S. epidermidis
■Abscesses and toxic shock syndrome
■S. aureus: human skin, anterior nares and the perineum
■High carriage in hospital patients.
■Transmission is via contact
■Toxins: coagulase and enterotoxin
■Not considered part of oral flora. Frequently isolated from children and the
elderly and those with systemic disease
■Diseases:
■ superficial (boils, pustules, abscesses and wound infections)
■ Food poisoning (enterotoxin)
■ Toxic shock syndrome (enterotoxin)
■ Deep infections (septacaemia, pneumonia, endocarditis)
Rx: Flucloxacillin, vancomycin, cephalosporins.
Mehicillin resistant S.aureus (MRSA) huge problem in hospital setting and
community

18. LACTOBACILLUS
■ Commensals inhabiting the oral cavity (less than 1% of total flora), gastrointestinal
tract and female genital tract
■ Gram positive rod shaped bacilli. Species: Lactobacillus casei,
Lactobacillus fermentum and Lactobacillus oris
■ Ferment carbohydrate to form acids
■ Ability to tolerate acidic environments and hence
associated with carious process
■ Frequently isolated from deep carious lesions where pH is acidic
■ Lactobacillus count in saliva taken as indicator
of caries activity as it can be an indicator of dietary carbohydrate intake

19. ACTINOMYCETES
■ Commensals of mouth in humans and
animals
■ Major component of dental plaque
■ Association between root surface caries of
teeth
■ Most important human pathogen is
A.israelii
■ Enamel demineralization associated with
A. odontolyticus
Characteristics
■ Gram positive filamentous branching rods.
■ Grow anaerobically.
■ Pus contains yellowish “sulphur granules”
(clumps of organisms)
■ Molar tooth shaped colonies on blood
agar
■ Slow growing

20. ACTINOMYCETES
Pathogenicity
■ Endogenous infection of orofacial region
■ Lesions present as chronic abscess, commonly at the angle
of the jaw with multiple draining sinuses
■Abscess often preceded by tooth extraction or blow to the
jaw
Treatment and Prevention
■Penicillin/amoxicillin for prolonged course
■Tetracycline for recalcitrant lesions (good bone penetration)
■Surgical intervention for chronic lesions
■ Prevention difficult as it an endogenous infection

22. Aggregatibacter actinomycetemcomitans
• Latin aggregare: to come together, aggregate; bacter: bacterial rod;
Aggregatibacter: rod-shaped bacterium that aggregates with others
• This species is routinely isolated from the oral cavity and is frequently
isolated with Actinomyces spp from actinomycotic lesions
• Found in the subgingival sites in humans and animals and is
associated with aggressive periodontal disease

23. Bacteroides, Tannerella, Porphyromonas and
Prevotella
• Obligate anaerobes
• Short Gram-negative
rods/coccobacilli
• Comprise a substantial
proportion of the microflora of
dental plaque (also found in the
intestine and female genital
tract)

24. Bacteroides fragilis
• Most predominant flora in the
intestine
• Can lead to serious anaerobic
infections – intra abdominal sepsis,
peritonitis, liver and brain
abscesses
• Polysaccharide capsule is an
important virulence factor
• Pathogenicity is related to
endotoxin and protease production
• Facultative anaerobes utilize
oxygen in the infective focus and
facilitate the growth of anaerobic
Bacteroides strains, thus many
infections are polymicrobial
Prevotella intermedia
• Found in the human oral cavity and
is associated with periodontal
disease
• Prevotella nigrescens is associated
with healthy gingiva

25. Tannerella forsythia
• Mostly found in subgingival
sites
• Spindle-shaped Gram-negative
rods
• Associated with periodontal
disease :
• Induces apoptotic cell death
• Invades epithelial cells
Porphyromonas gingivalis
• Found in subgingival sites
• Gram-negative coccobacillus
• Aggressive periodontal
pathogen:
• Fimbriae for adhesion
• Capsule for immune evasion
• Produces collagenase, endotoxin,
fibrinolysin and phospholipase A

26. FUSOBACTERIUM
■Inhabitants of oral cavity, colon and
female genital tract.
■Several subspecies found in healthy
gingival crevice
■F. nucleatum from periodontal
pockets - endogenous infection
■Gram-negative, anaerobic organism
■Pathogenicity mediated by:
■Fusobacterium adhesin A (FadA) for
adherence
■Endotoxin production

27. SPIROCHAETES
■Spiral, motile organisms with number of coils. Cork-screw motility
■Gram negative cell wall.
■Strictly anaerobic
■Treponema: causes syphilis bejel, yaws, pinta and in the oral
cavity, acute necrotizing ulcerative gingivitis (together with
Fusobacterium)
■ Oral treponemes of note includes: Treponema denticola,
Treponema pectinovarum, Treponema vincentii and Treponema
socranskii
■Predominantly found at gingival margin and crevice

28. Fusospirochaetal infections
■Fusobacterium nucleatum and Treponema vincentii produce:
■Acute (necrotizing) ulcerative gingivitis or trench mouth
■Vincent’s angina- an ulcerative tonsillitis causing tissue necrosis
■Cancrum oris/Noma- sequel of acute ulcerative gingivitis – gross tissue loss
of facial region

29. NECROTISING ULCERATIVE
GINGIVITIS
 Acute necrotizing ulcerative gingivitis is a painful infection of
the gums.
 Associated with poor oral hygiene, malnutrition and systemic
diseases
 Characterized by inflamed, red and bleeding gingivae, with
irregularly shaped ulcers
 Extremely painful and covered with a pseudo membrane
 Foul smelling breath
 Specific anaerobic polymicrobial infection due to combined
activity of
F. nucleatum and oral spirochaetes;
(Treponema spp): fusospirochaetalcomplex

30. NECROTISING ULCERATIVE
GINGIVITIS
Diagnosis
 based on clinical appearance and offensive smell
 Confirmatory evidence is based on microscopy of a Gram-stained, deep
gingival smear. The following three components should be present:
 Fusobacteria
 Spirochaetes
 Leukocytes
Management
• Initial local debridement (with ultrasonic scaling, if possible) is essential.
• Oral hygiene advice should be given, and mouthwashes, e.g. chlorhexidine,
should be prescribed.
• Metronidazole (200 mg three times daily for 4 days) is the drug of choice.

31. SPIROCHAETES
Treponema pallidum (syphilis)
■ Transmission
■ Acquired - occurs via direct contact with lesions/body
secretions/saliva/blood/semen
■ Congenital - Mother to child
■ Acquired syphilis can be classified as primary, secondary, latent or tertiary,
depending on the time elapsed since exposure

32. Oral manifestations of syphilis
Primary syphilis
• Initial lesion is called a chancre
and appears 1-2 weeks post
exposure at the site of
inoculation
• Chancre is usually ulcerated,
singular, painless, indurated,
hard base
• The chancre usually heals
spontaneously

33. Oral manifestations of syphilis
Secondary syphilis
• Systemic component of the disease
– lesions contain highly infectious
spirochaetes
• Occurs 4-8 weeks after chancre
emergence
• Oral lesions are usually painful,
multiple and accompanied by other
systemic symptoms
• Macular/popular eruption can
occur or mucous patches
• Mucous patches: oval or
serpiginous, raised erosions/ulcers
with a erythematous border
• Overlying greyish white
membranous exudates

34. Oral manifestations of syphilis
Tertiary
• Occurs in patients who didn’t
receive treatment in earlier
stages
• Gumma can be seen on the hard
palate as a chronic, progressive
granulomatous lesion that can
perforate through the palate
into the nasal septum
• Tongue may appear atrophic,
fissured and with leukoplakic
plaque dorsally
• This stage is not infectious

35. Oral manifestations of syphilis
Congenital syphilis
• Dental abnormalities are caused
by infection of the enamel organ
that leads to screwdriver shaped
incisors (Hutchinson’s incisors
and Mulberry molars

36. ORAL PROTOZOA
Genus Trichomonas
 Flagellated protozoa
 Main species: Trichomonas tenax
 Strict anaeobe
 Difficult to grow in pure culture
 Its role in disease is unclear

37. ORAL PROTOZOA
Genus Entamoeba
 Large motile amoeba
 Main species: Entamoeba gingivalis
 Strict anaerobe. Cannot be easily cultures
 Infection of periodontal tissues, especially in patients who have
received radiotherapy and are on metronidazole
 Its role in periodontal disease is unclear

38. DENTOALVEOLAR
INFECTIONS
 Definition: Pus-producing (pyogenic) infections associated with the teeth
and surrounding supporting structures such as the periodontnium and the
alveolar bone
 A dentoalveolar abscess develops by extension of oral commensals from an
initial carious lesion
 infection is usually polymicrobial (endogenous), with a mixture of three or
four different species
 monomicrobial (endogenous) infection (i.e. with a single organism) is
unusual
 strict anaerobes are the predominant organisms, and the viridans group
streptococci are less common
 The common species isolated from dentoalveolar abscesses are Prevotella,
Porphyromonas and Fusobacterium spp., and anaerobic streptococci;
facultative anaerobes are the second largest group, e.g. Streptococcus milleri

40. DENTOALVEOLAR INFECTIONS
Clinical features:
 a non-viable tooth with or without a carious lesion
 evidence of trauma
 swelling, pain
 Redness
 Trismus (inability to open the mouth)
 local lymph node enlargement
 sinus formation
 Fever and malaise

41. DENTOALVEOLAR
INFECTIONS
Specimen collection:
 Aspirated pus sample should be
collected and place in sterile
container
 Swabs should be avoided due to
high contamination rate with
oral flora
Management:
 Drain the pus
 Remove source of infection
 Antibiotics indicated when:
 Drainage cannot be done
 Any spread to superficial soft
tissues
 Febrile patient
 Penicillin or amoxicillin are
drugs of choice

42. DENTOALVEOLAR INFECTIONS
Complications of dentoalveolar infections:
Local spread: soft tissue abscess/cellulitis/sinus formation
Ludwig’s angina: spreading, bilateral infection of the
sublingual and submandibular spaces. It is a life threatening
infection: may occlude the airways due to oedema
Osteomyelitis (Infection of bone)
Maxillary sinusitis
Haematogenous spread – brain abscesses (Rare)

43. MICROBIOLOGY OF DENTAL
CARIES
 Dental caries is a chronic endogenous infection caused by
the normal oral commensal flora
 The carious lesion is the result of demineralization of
enamel – and later of dentine – by acids produced by
plaque microorganisms as they metabolize dietary
carbohydrates.
 Microorganisms in the form of dental plaque are a pre-
requisite for the development of dental caries.
 Some bacteria (mutans streptococci, Lactobacillus spp.
and Actinomyces spp.) may be more important than
others in the initial as well as subsequent events leading
to both enamel and root surface caries.

44. ORAL MUCOSAL & SALIVARY
GLAND INFECTIONS
 Oral candidiasis
 Hyperplastic candidiasis (Candida/hairy leukoplakia)
 Candida associated denture stomatitis
 Angular stomatitis
 Oral viral
 Herpetic stomatitis
 Herpes labialis
 Herpetic whitlow
 Oral bacterial
 Syphilis
 Tuberculosis
Salivary gland infections
 Viral (majority) - mumps
 Bacterial
 Xerostomia and enlargement of major salivary glands are in HIV infection
Please refer to
virology and
mycology lectures

45. GRAM-NEGATIVE COCCI
■Neisseria meningitides
■causes septicaemia, bacterial meningitis
■Neisseria gonorrhoeae
■causes sexually transmitted infections

46.  Aerobic Gram-negative cocci often arranged in pairs
(diplococci) with adjacent sides flattened (like kidney or
bean shaped)
 Oxidase positive
 Non-motile
 Acid from oxidation of carbohydrates
GENERAL CHARACTERISTICS

47. ORGANISM
Neisseria meningitidis
(meningococcus)
DISEASES
 Meningitis
 Septicemia with or without meningitis
 Meningoencephalitis

48. ■ Humans only natural hosts
■ Person-to-person transmission by aerosolization of respiratory
tract secretions in crowded conditions
■ Close contact with infectious person (e.g.family members, day
care centers, military barracks, prisons, and other institutional
settings)
EPIDEMIOLOGY OF
MENINGOCOCCAL DISEASE

49. ORGANISM
Neisseria gonorrhoeae
(gonococcus)
DISEASE
GONORRHOEA

50. ■ Readily transmitted by sexual contact
■ Gram-negative diplococci flattened
along the adjoining side
■ Fastidious, susceptible to cool temperatures,
drying
EPIDEMIOLOGY
■ Found only in humans with strikingly different presentations in
females and males
■ Asymptomatic carriage is important as serves as reservoir
■ Transmission primarily by sexual contact
■ Lack of protective immunity and therefore re-infection, partly due to
antigenic diversity of strains
CHARACTERISTICS

51. Pharyngeal gonorrhoea
• Acquired by oral sexual
exposure
• Majority of oropharyngeal
infections – asymptomatic
• Sore throat, pharyngeal
exudates, and/or cervical
lymphadenitis can be present
• Bacterial concentrations in the
pharynx are generally lower
than in the rectum and genitals
• The pharynx is thought to be
the site where horizontal
transfer of gonococcal
antimicrobial resistance genes
commonly occurs