Infections of Oral

Mucosa
 INFECTIONS
• DEFINITION

“ Infection is the invasion of an

organism's body tissues by disease-
causing agents, their multiplication, and
the reaction of host tissues to these
organisms and the toxins they produce.”
Classification of Oral Infections
• Bacterial

• Viral

• Fungal

• Parasitic/protozoal
 Classification of Oral Infections
• Bacterial
Staphylococcal (abcess)
Streptococcal (cellulitis)
Mixed (ANUG)
Syphilis (Congenital, primary, secondary, tertiary)
TB (Lymphadenopathy, Ulcer)
Clostridia (tetanus)
Actinomycosis (Cervicofacial/abdominal)
• Fungal
• Viral
NORMAL FLORA: bacterias which can be found in or on our
bodies without causing any disease.

PATHOGENS: Microorganisms that causes disease or illness

to its host

OPPORTUNISTIC MICRORGANISMS: micro organisms that

is normally a commensal or does not harm its host but can
cause disease when the host immune resistance is low
 Normal flora
• All body surfaces possess a rich normal bacterial flora,
especially the mouth, nose, gingival crevice, large bowel,
skin, vagina
– This can be a nuisance in that
• it can contaminate specimens
• it can cause disease
– This is beneficial in that
• it can protect against infection by preventing
pathogens colonising epithelial surfaces
colonisation
( resistance )
• removal of the normal flora with antibiotics can
cause superinfection, usually with resistant microbes
 NORMAL FLORA OF ORAL
CAVITY
• Viridans Streptococci
• Lactobacilli
• Staphylococcus (Aureus,Epidermidis)
• Bacteroides
• Sterptococcus( Mutans,Sanguis)
• Actinomyces sp.
 PATHOGENECITY
Disease can come about in several overlapping ways

1. Some bacteria are entirely adapted to the pathogenic way of

life in humans. They are never part of the normal flora but
may cause subclinical infection, e.g.M . tuberculosis
2. Some bacteria which are part of the normal flora acquire
extra virulence factors making them pathogenic, e.g.E. coli
3. Some bacteria from the normal flora can cause disease if
they gain access to deep tissues by trauma, surgery, lines,
S.
especially if associated with a foreign body, e.g.
epidermidis
4. In immunocompromised patients many free-living bacteria
and components of the normal flora can cause disease,
Acinetobacter
especially if introduced into deep tissues, e.g.
 Bacterial Virulence
A simplistic view
• Some bacterial proteins (“exotoxins”) can elicit the
features of a bacterial infection when injected as pure
proteins, e.g.
– tetanus toxin, botulinum toxin
– diphtheria toxin, anthrax toxin
• Vaccination with inactivated toxins (“toxoids”) led to a
spectacular decline in the incidence of many bacterial
infections.
• Leading to the simplistic idea that all bacteria need to
cause disease is a single toxin…
 S teps in successful infection
• S ense environment • S tealth
– avoid immune system
• S witch virulence genes on and off
• S wim to site of infection • S trike-back
– damage host tissues
• S tick to site of infection
• S ubvert
• S cavenge nutrients – host cell cytoskeletal and signalling
– especially iron pathways

• S urvive stress • S pread

– through cells and organs

• S catter
 Damage host tissues

• Endotoxins:
heatstable toxin associated with the outer membrane
of certain gram-negative bacteria.
• Not secreted
• Less potent and less specific
• Do not form toxoids
• Examples: Toxins produced byE.coli, Salmonella
Typhi, Shigella, Vibrio cholera
• Exotoxins

potent toxin formed and excreted by the bacterial c

ell and found free in the surrounding medium.
Found in both Gram positive and Gram Negative
bacteria
- protein in nature
-heat labile
-highly toxic
-toxoids can be made
-Diseases: Tetanus, diphtheria, botulism
 Membrane-Damaging Exotoxins

• Many bacterial toxins form pores in

eukaryotic cell membranes,
producing oligomeric rings, e.g.
– streptolysin O of Streptococcus
pyogenes
– listeriolysin of Listeria
monocytogenes
– alpha-toxin ofS. aureus
• Other toxins, such as phospholipases,
degrade components of the
membrane
– e.g.Clostridium perfringens alpha
toxin
 Staphylococcal infection
• Staph. aureus (G+, Coag+)
• Skin infection
• GIT
• Deep infections
(endocarditis, meningitis,
pneumonia, wound
infection,
• Osteomyelitis
• Toxic shock synd.
Right buccal abcess
 Streptococcal infection
• Strep. viridans (anginous,
bovis, sanguis, mitis,
mutans) enterococci,
• > 90% diseases by Gr. A β
heamolytic strep.
• Cellulitis, Necrotising
facitis, Rheumatic fever,
Erythema nodosum,
glomerulonephritis.
• Tx: pen G
Cellulitis of lower lip
 ANUG
(Acute necrotizing ulcerative gingivitis)
• Common in smokers , HIVand
malnourished
• Fusospirocheatal(complex) infection
• C/F: Crater like punched out
ulceration(inter dental papilla), halitosis,
soreness, bleeding gums, increased
salivation
• Some pts develop fever, maliase and
Cervical lymphadenopathy
 ANUG
• Dx: Fusospirocheatal complex in deep
ging smear
• Organisms inc: Treponema vincentii,
denticola, Provetella intermedia,
Porphyromonas gingivalis, Fusobacterium
nucleatum.
• Mx: Supra/subgingival plaque control,
gentle deb. & syst.ABS ( Metronidazole is
the drug of choice)
ANUG
 “Noma”
• Also known as CANCRUM ORIS
• It is a rapidly progressive, polymicrobial, often gangrenous
infection of the mouth or genitals
• Primary organisms are Fusobacterium Necrophorum and
Prevotella intermedia
• Risk factors include Malnutrition,and immuno compromised
pt or intercurrent infections such as measles or malaria(esp
seen in childrens)
• Clinical features
rapid spread of Necrotic Gingival lesions
demarcated gangrene of oro facial tissues
• Micro biological features similar to Necrotizing Ulcerative
Gingivitis
YOUNG PATIENT SUFFERING FROM NOMA
 SYPHILIS

• Causative organism: Treponema Pallidum

• Etiology:
• Sexual contacts
• Blood products
• I/V drug abuse
• Vertically transmitted disease
 Primary syphilis
• Chancre(Small, firm, pink macule, papule, ulcer)
• Ulcer heals in 3-8 wks highly infectious
• Regional lymphadenopathy
• Common sites
 Lips
 Tongue
 Penis
 Vulva
 Secondary Syphilis
• Follows 6-8 wks of prim.
syphilis
• Highly infectious
• Symptoms inc, fever, headache,
maliase, rash, gen. Painless
lymphadenopathy & symetrical
coppery maculo papular rash
on hands & palms
• Oral lesions----- mucous
patches & snail track ulcers
SNAIL TRACK ULCERS
Skin lesions in secondary
syphilis
 Tertiary syphilis
• Untreated syphilis can progress to tert.
Syphilis after 3-10 years in aprox. 30 %
• Non infectious
• Cardiac & neural involvement in 10%
• Gumma is characteristic lesion
• Gumma can occur on skin, mucosa or
bone
• Palate perforation is common
Palatal perforation in tertiary
syphilis
 Congenital syphilis
• Exposure in 5th month of preg. can cause
congenital syphilis
• Early and late conginital syphilis
• Can cause deafness & blindness
• Depressed nasal bridge,promient frontal bone
and abnormal maxilla
• Hutchinson incisors and mulbury molars are imp
oral manifestations
 Mulberry molars

HUTCHISON’S INCISORS MULBERRY MOLARS

 HISTOLOGICAL FEATURES
Infiltration of lymphocytes, plasma
cells and macrophages

Organisms are readily distinguished

using Treponema Pallidum
immunoperoxidase staining

In tertiary syphilis Gumma consisting

of granulomatous inflammation with
central necrosis surrounded by large
no of mononuclear lymphocytes
•Drug of choice for Syphilis is Penicillin
• Procaine pen. IM, 600,000 u for 10 days
• Tetracycline/erythromycin for 14 days
 ACTINOMYCOSIS
• Actinomycosis is a chronic suppurative
polymicrobial infection caused mainly by
Actinomyces israelii.

ETIOLOGY
Dental caries
Poor oral hygiene
Periodontal disease
Infected root canal
 ACTINOMYCOSIS
• Three forms

Abdominal form

Cervicofacial form

Generalised
 Cervicofacial Actinomycosis
• Begins as small, flat, hard, sometimes
painful swellings in the mouth, on the skin
of the neck, or below the jaw. These
swellings may soften and multiple pus
draining sinuses that contains small,
round, yellowish sulphur granules.
• Reddish /bluish discoloration of over lying
skin
• Difficulty in chewing
Actinomyosis infection assocated with multiple draing
sinuses
Actinomycosis (Diagnosis & Treatment)

• Isolation of organism (Actinomycosis

israelii) from discharge.

• Treatment involves drainage of abscesses

and high doses of broad spectrum
antibiotics such as penicillin or
tetracycline.

• To prevent relapse, antibiotics shld. be

prescribed for as long as 6 to 12 months.
 TUBERCLOSIS
• infection caused by Mycobacterium
Tuberculosis
• Primary Oral T.B lesion is un common
• Secondary, due to hematogenous or lymphatic
dissemination and extensions of nearby
structures
• Chronic ,painless ulcer covered with grayish –
yellow slough on the tongue
• Tongue ,palate, lips, buccal mucosa, gingiva,
palatine tonsil, and floor of the mouth
• Persistent cervical lymphadenopathy.
LATERAL BORDER HARD PALATE
OF TONGUE
 Diagnostic Criteria
• . If there is no systemic involvement, one
should go for excisional biopsy for tissue
diagnosis and bacteriologic examination
with culture for a definitive diagnosis
• The efficiency of demonstration of acid
fast bacilli in histological specimen
• A radiological examination of chest and a
Mantoux skin test are mandatory to rule
out systemic TB
Classical presentation ,formation
of Granuloma
Circumscribed collection of
epitheloid macrophages,
lymphocytes, langhan’s Giant cell
along with Central caseous
necrosis
Acid Fast Staining
Also known as Ziehl Neelson
staining
Performed for acid fast bacilli
 Treatment
• the most effective regimens require a
combination of four drugs (Isoniazid, Rifampicin,
Pyrazinamide, and Ethambutol) administered
daily for the first two months.
• followed by an additional four months with only
two drugs (Isoniazid and Rifampicin) .
 “LEPROSY”
“ A contagious disease that affects the skin,
mucous membranes, and nerves, causing
discoloration and lumps on the skin and, in
severe cases, disfigurement and deformities”
• Causative organism is Myocobacterium Leprae
• The route of transmission is thru aerosol spread
of nasal secretions.
• 2 types are present:
i)tubercloid
ii)lepromatous
Patient with extensive nodular growth on scalp ,face
and exposed body parts
 Tubercloid Type
• Individuals who have a vigorous cellular
immune response toM leprae have the
tuberculoid form of the disease.
• Skin lesions are few. One erythematous
large plaque is usually present, with well-
defined borders that are elevated and that
slope down into an atrophic center.The
number of skin lesions is limited, and they
tend to be dry and hypoesthetic.
• Nerve involvement is usually asymmetric.
 Lepromatous Type
• Individuals with minimal cellular immune
response have the lepromatous form of
the disease
• characterized by extensive skin
involvement along with oral lesions
• Skin lesions are often described as
infiltrated nodules and plaques, and nerve
involvement tends to be symmetric in
distribution.
• Oral lesion are sec. to nasal involvement
•Oral lepromas, usually located on the hard
and soft palate, uvula, tongue ("
cobblestoning"), lips, and gums, can
progress to necrosis and ulceration. Tissue
destruction may result.
 Sign and Symptoms
• Painless skin patch accompanied by loss of
sensation but not itchiness (Loss of sensation is
a feature of tuberculoid leprosy, unlike
lepromatous leprosy, in which sensation is
preserved.
• Wasting and muscle weakness
• Foot drop or clawed hands
• corneal ulceration or secondary cataract due to
nerve damage
• The leonine facies(face that resembles that of
a lion) associated with progressive disease,
 DIAGNOSTIC CRITERIA
• Skin biopsy, nasal smears, or both are
used to assess for acid-fast bacilli
• Polymerase chain reaction (PCR)
• Lepromin skin test
• Contact or family screening for history of
leprosy
 TREATMENT
• WHO recommends the use of the long-
term multidrug regimens.
• Rifampin, Minocycline, or Ofloxacin .
• To be used over a period of 12-24 months.