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BACTERIAL INFECTIONS OF
ORAL CAVITY
Presented by:
Monika
Post Graduate
Department of Public Health Dentistry
CONTENTS
• Introduction
• Bacterial infections
 Scarlet fever
 Diptheria
 Tuberculosis
 Leprosy
 Actinomycosis
 Tetanus
 Syphilis
 Gonorrhea
 Rhinoscleroma
 NOMA
 Pyogenic granuloma
 Pyostomatitis vegetans
Epidemiology
Clinical features
Oral manifestations
Public health significance
Conclusion
References
INTRODUCTION
• Certain bacteria produce disease which are
manifested in or about the oral cavity.
• This microbial specificity is characteristic of
infectious disease wherever they may occur in
the body and is necessarily confined to those
of oral cavity.
SCARLET FEVER
• It is a contagious systemic infection occurring
predominantly in children.
• Cause:β-hemolytic streptococci,
STREPTOCOCCUS PYOGENES.
• The rash occurs because of three exotoxins:
A,B,C.
EPIDEMIOLOGY
• Scarlet fever is similar in many respects to
acute tonsillitis and pharyngitis caused by
Streptococci paralleling the occurrence of
these conditions in its epidemiology.
Pharyngitis, tonsillitis,
headache, chills, fever,
abdominal pain, vomiting.
Enlargement and tenderness of
the regional cervical lymph
nodes.
Diagnosis: characteristic
diffused, bright, scarlet-skin
rash appears on 2nd or 3rd day
of illness.
Small papules of normal color
erupt through these rashes
giving characteristic sandpaper
feel to the skin: PASTIA
LINES
Clinical features
Oral manifestations: the chief oral manifestation is called
stomatitis scarlatina.
• FORCHHEIMER SPOTS:
Small punctate red macules may appear on the hard and soft
palate and uvula.
Oral manifestations: the chief oral manifestation is called
stomatitis scarlatina.
• FORCHHEIMER
SPOTS:
Small punctate red
macules may appear on
the hard and soft palate
and uvula.
• The tongue exhibits a white coating and
fungiform papillae are edematous and
hyperemic, projecting above the surface as
small red knobs :STRAWBERRY TONGUE.
• The coating of the tongue is soon lost
beginning at the tip and lateral margins and it
becomes red, glistening and smooth except for
the papillae: RASPBERRY TONGUE
• The tongue exhibits a white coating and
fungiform papillae are edematous and
hyperemic, projecting above the surface as
small red knobs :STRAWBERRY TONGUE.
• The coating of the tongue is soon lost
beginning at the tip and lateral margins and it
becomes red, glistening and smooth except for
the papillae: RASPBERRY TONGUE
TREATEMENT:
• The administration of antibiotics like
penicillin, dicloxacillin and cephalexin.
DIPTHERIA
• Acute life threatening, infectious and
communicable disease of the skin and mucous
membrane caused by toxaemic strains of
Cornebacterium diptheriae.
• Characterised by formation of a grayish adherent
pseudomembrane which bleeds on removal.
• Disease of children
• Humans are the principal reservoirs and
organisms may persist for two to six weeks.
• Transmitted mainly by respiratory droplet,
direct skin contact and from skin to the
respiratory tract through hands.
EPIDEMIOLOGY:
• Available data indicate a declining trend of diptheria in
India due to increasing coverage of child population by
immunization.
• Recent diptheria outbreaks in a number of countries have
demonstrated the shift in age distribution of cases to adults
and old age people.
• The outbreak warrants the need of booster immunization.
PATHOGENESIS:
Diptheria organism localises in
respiratory tract
Causes oedema, necrosis and acute
inflammation
Coagulation of fibrin, purulent
exudate produces grayish green
PSEUDOMEMBRANE.
PATHOGENESIS:
Diptheria organism localises in
respiratory tract
Causes oedema, necrosis and acute
inflammation
Coagulation of fibrin, purulent
exudate produces grayish green
PSEUDOMEMBRANE.
If pseudomembrane present
:diptheria cases.
If pseudomembrane absent:
diptheria carriers.
Incubation period: 2-5 days.
Clincal types according to
location of pseudomembrane:
tonsillar, pharyngeal,
laryngeal, tracheal, nasal,
conjunctival, cutaneous.
Fever, sore throat, weakness,
dysphagia, headache and
change of voice,restlessness,
pallor, tachycardia,
Hoarseness of voice,
respiratory stridor, dyspnea
which may progress to severe
respiratory obstruction and
death in young children.
Clinical features
ORAL MANIFESTATIONS:
• Patchy diptheritic membrane on the tonsils.
• This membrane covers soft palate, tongue, lips, gingiva,
buccal mucosa.
• Severly affected patients have bull neck appearance.
• Appears as non specific ulcers in oral cavity.
• Soft palate may become temporarily paralysed
• Peculiar twang and husky voice.
• Regurgitation of liquids
TREATMENT
• Administration of diptheria antitoxin and apart
from antibiotic administration done by
penicillin and erythromycin.
• Prevention by prophylactic active
immunisation with diptheria toxoid.
TUBERCULOSIS
• It is a specific infectious granulomatous
disease caused by MYCOBACTERIUM
TUBERCULOSIS.
• It commonly affects lung, intestine, meninges,
bones, joints, lymph glands, skin and other
tissues of body.
EPIDEMIOLOGY
• Among the world population, south east asian region
carries a disproportionate 88% of the world’s burden of
TB.
• India accounts for nearly one fifth(20%) of the global
burden of TB.
• The vulnerability to TB in developing countries results
from poverty, economic recession and malnutrition.
Episodic fever, chills,
fatigability, malaise, gradual
loss of weight accompanied
by a persistent cough.
TB can be pulmonary or
extrapulmonary.
Pulmonary TB: primary,
secondary or miliary.
Extrapulmonary sites: lymph
nodes, pleura, genitourinary
tract, bones , joint e.t.c
Primary pulmonary TB: seen
in children and majority
asymptomatic.
Secondary TB: fever, cough,
chest pain.
Tuberculous infection of
submandibular and cervical
lymph nodes.
Primary tuberculosis of the
skin or lupus vulgaris
appears papular nodules.
Clinical
features
ORAL MANIFESTATIONS
• Lesions of secodary tuberculosis may occur at any site
on the oral mucous membrane i.e. tongue, palate, lips,
buccal mucosa, gingiva and frenula.
• The usual presentation is an irregular, superficial or
deep, painful ulcer which tends to increase in size.
• Diffuse involvement of the maxilla or mandible may
also occur by hematogenous spread.
• Tuberculosis lesions in the mouth do not differ
microscopically from tuberculosis lesions in
other organs of the body.
• The characteristic appearance is due to the cell
mediated hypersensitvity reaction.
DIAGNOSIS
• The presence of acid-fast bacilli in sputum smear
is the gold standard for the diagnosis.
• Microscopical smears: Z-N staining, Kinyoun’s
cold staining method.
• A minimum of five acid –fast bacilli on
fluorescent microscopy and three on Z-N staining
is reported as positive.
TUBERCULIN TEST OR MANTOUX TEST
• Subcutaneous injection of 0.1 ml of 5
tuberculin units of purified protein derivative
into the forearm.
• If positive induration is seen after 48-72 hours.
TUBERCULIN TEST OR MANTOUX TEST
• Subcutaneous injection of 0.1 ml of 5
tuberculin units of purified protein derivative
into the forearm.
• If positive induration is seen after 48-72 hours.
Diameter of induration Interpretation
> 15 mm Strongly positive
>10 mm positive
5-9 mm indeterminate
< 5 mm negative
LEPROSY (HANSEN’S DISEASE)
• Leprosy is a chronic granulomatous infection
caused by MYCOBACTERIUM LEPRAE.
• It multiplies very slowly and incubation period is
about five years.
• It mainly affects skin, peripheral nerves, upper
respiratory tract, eyes, testes, muscles, bones and
joints.
EPIDEMIOLOGY
• It is almost exclusively a disease of developing
countries.
• It is common in Asia, Africa, Latin America .
• Africa has the highest disease prevalence and
Asia has the most cases.
• India accounts for 80%of the detection of
leprosy cases in the world.
• The annual case detection rate in India is
among the highest in the world (53 per
100,000).
• Prevalence is high in Bihar, Uttar-Pradesh,
Tamil Nadu, West Bengal e.t.c.
PATHOPHYSIOLOGY
Once infected both cell mediated and
humoral response are elicited by bacterial
antigen DNA, glycolipids.
Lipoarabinomannan, component of the cell
membrane, induces immune response
Bacteria are taken by histiocytes in the
skin and schwann cells in the nerves.
• TUBERCULOID TYPE: cell mediated immune
response and low bacillary load.
• LEPROMATOUS TYPE: low cell mediated
immune response and high bacillary load.
Oral lesion consist of
small tumor like masses
called lepromas which
develop on the tongue,
lips or hard palate.
Gingival hyperplasia with
loosening of the teeth.
Paralysis of facial and
maxillary division of
trigeminal nerve.
Dental manifestations are
described as
odontodysplasia leprosa.
Premaxilla is affected in
childhood, circumferential
hypoplasia, shortening of
roots involving maxillary
anterior teeth.
Oral
manifestations
Treatment :
ACTINOMYCOSIS
• It is a chronic granulomatous suppurative and fibrosing
disease caused by anaerobic or microaerophilic gram
positive filamentous bacteria.
• Characterised chiefly by the formation of abscesses that
tend to drain by the formation of sinus tracts.
• Pus from the abscesses shows typical ‘sulfur granules.’
• Actinomycosis is classified anatomically
according to the location of lesions:
• Cervicofacial
• Abdominal
• Pulmonary forms.
EPIDEMIOLOGY
• Infection occurs throughout the lifetime with
peak incidence in the middle age.
• Males are more commonly affected than
females.
PATHOGENESIS
• It appears to be endogenous infection.
• The disruption of the mucosal barrier is the
main step in the invasion of bacteria.
• Initial acute inflammation is followed by a
chronic indolent phase.
CERVICOFACIAL ACTINOMYCOSIS
• It is the most common form of this disease.
• The organisms may enter the tissues through the
oral mucous membrane and may either remain
localised in the subjacent soft tissues or spread to
involve the salivary glands, tongue, bone
producing swelling and induration of tissue.
• The skin overlying the abscess is purplish red,
indurated and has feel of wood or often fluctuant.
• The patient over a period of time may show a
great deal of scarring and disfigurement of the
skin.
• The infection of the soft tissues may extend to
involve the mandible or less commonly maxilla
results in actinomycotic osteomyelitis.
ABDOMINAL ACTINOMYCOSIS
• It carries a high mortality rate.
• Generalized signs and symptoms of fever,
chills, nausea and vomiting, intestinal
manifestations develop followed by symptoms
of the involvement of liver and spleen.
PULMONARY ACTINOMYCOSIS
• The organisms may spread beyond the lungs to
involve adjacent structure.
• Fever and chills accompanied by a productive
cough and pleural pain.
TREATMENT
• Long term high dose penicillin, tetracycline,
and erythromycin have been used frequently.
• In addition to this surgical drainage of the
abscess and excision of sinus tract is necessary
to accelerate healing.
TETANUS (LOCK JAW)
• It is an acute infection of nervous system
characterized by intense activity of motor
neurons and results in severe spasms.
• Anaerobic gram positive bacillus:
CLOSTRIDIUM TETANI.
EPIDEMIOLOGY
• Tetanus is now a comparatively rare disease in
developed countries.
• Neonatal tetanus is fatal with a mortality rate of 80-
90%.
• However in asia, especially in china, myanmar,
indonesia and India, the death rate due to
neonatal tetanus is greately reduced due to
immunisation coverage of pregnant women.
PATHOGENESIS
In suitable anaerobic conditions potential
spores of the Cl. Tetani produce potent
neurotoxin( tetanospasmin)
It binds to the peripheral motor nerve
terminal and followed by retrograde
intraneuronal transport.
The toxin migrate across synapse and blocks
the release of glycine and GABA.
Incubation period ranges
from : 3days to 4 weeks.
Generalised tetanus:
characterised by lock jaw or
trismus due to spasm of
masseter, dysphagia,
stiffness in the neck or back
muscle.
Sustained contraction of
facial muscle results in
Grimace-risus sardonicus.
Arched back- opisthotonus.
Local tetanus manifests as
spasm of muscle near
wound.
Clinical
features
TREATMENT
• Sedation, airway and nutrition should be
maintained.
• Penicillin 10-12 million units IV for 10 days.
• Prophylaxis: wound debridement and booster
doses of TT.
SYPHILIS (LUES )
• It is caused by TREPONEMA PALLIDUM
and is characterised by episodes of active
disease interrupted by the period of latency.
• Route of transmission: sexual contact,
transmission from mother to child in utero.
EPIDEMIOLOGY
• Syphilis specifically congenital syphilis continues
to be a major problem in many countries.
• It is recognised that if treatment with antibiotics
begins in infected pregnant women before fourth
month of pregnancy approximately 95% of the
offspring of these mothers will be free of the
disease.
ACQUIRED SYPHILIS
• It is contracted primarily as a venereal disease
as well as dentists working on infected patients
can acquire it.
• Three distinctive stages: primary, secondary
and tertiary.
PRIMARY STAGE:
• Lesion known as CHANCRE develops at the
site of inoculation approximately 3-90 days
after contact with infection.
• About 95% of it occur on genitalia but they are
also found in other areas.
• Of particular interest are those lesions occuring on
the lips, tongue, palate, gingiva and tonsils.
• Such a primary lesion on the lip may have a
brownish, crusted appearance.
• The intraoral chancre is an ulcerated lesion
covered by a grayish white membrane which may
be painful.
SECONDARY OR METASTATIC STAGE
• Commences about six weeks after the primary
lesion, is characterized by diffuse eruptions of
the skin and mucous membrane.
• The oral lesion are called mucous patches,
usually multiple, painless, grayish-white
plaques overlying an ulcerated surface.
• They occur frequently on the tongue, gingiva, or
buccal mucosa.
• Mucous patches are highly infectious since they
contain vast numbers of microorganisms.
• Secondary syphilis can be present as an explosive
and widespread form known as lues maligna.
• Secondary stage is characterised by fever,
headache and muscle pain followed by necrotic
ulcerations involving the face and scalp.
• After second stage they enter a latent stage which
may last for 1-30 years till the next stage tertiary
syphilis.
TERTIARY SYPHILIS
• It involves chiefly the CVS, CNS and certain
other tissues and organs.
• It is non infectious.
• Classic lesion is GUMMA : consist of a focal,
granulomatous, inflammatory process with
central necrosis.
• The intraoral gumma commonly involves the
tongue and palate.
• In either situation the lesion appears as a firm
nodular mass in the tissue, which may ulcerate
to form a deep painless ulcer.
• Lesion of palate cause perforating by
sloughing of the necrotic mass of tissue.
• Atrophic glossitis is the most common and is
due to endarteritis obliterans.
• Surface of tongue gets broken by fissures due
to atrophy of tongue .
Syphlitic
gumma
CONGENITAL (PRENATAL) SYPHILIS
• It is transmitted to the offspring only by an
infected mother.
• Pathognomic of disease: hypoplasia of the
incisor and molar teeth, eighth nerve deafness
and interstitial keratitis.
TREATMENT
• Penicillin is the drug of choice.
• Surgical correction of the facial defects gives
good esthetic results.
GONORRHEA
• It is primarily a venereal disease affecting the
genitourinary tract and is transmitted by sexual
intercourse.
• Commonly manifests as: cervicitis, urethritis,
prostratitis and conjuntivitis.
• Cause by: Neisseria gonorrhoeae.
EPIDEMIOLOGY
• It is a significant cause of morbidity in developing
countries but exact incidence is difficult to
ascertain because of limited surveillance.
• In India gonorrhea is more widely prevalent than
syphilis and 80% of women report to be
significant carriers.
Acute
urethritis,
dysuria, and
urethral
discharge:
MALE
Cervicitis
with candidal
or
trichonomal
vaginitis:
Female
Clinical
feature
Lips : develop acute
painful ulcerations.
Gingiva: become
erythematous with or
without necrosis.
Tongue: may present
red and dry
ulcerations.
Oral
manife
stations
Sore throat
TREATMENT
• Antibiotics and other preventive measures
should be followed.
NOMA (cancrum oris, gangrenous stomatitis)
• Noma, which means to devour ( a spreading
sore) is rapidly mutilating, gangrenous
stomatitis.
• Predisposing factors: undernourished,
deblitated from infections such as diptheria,
dysentary, measles, pneumonia, scarlet fever.
EPIDEMIOLOGY
• Most cases occur in Africa, south east Asia and
south east America.
• One of the last reports, 69 cases of noma in
miserably malnourished nigerian children
between the ages of two and seven years.
• The palate and occasionally tongue may
become involved.
• Patients have a high temperature during the
course of disease, suffer secondary infection
and may die from toxaemia.
TREATMENT
• The prognosis is considerably better if
antibiotics are administered before patient
reaches a final stage.
• Immediate treatment of any existing
malnutrition further improves the probability
of saving the patient.
PYOGENIC GRANULOMA
• It is a tumor like growth that is considered as
an exaggerated, conditioned response to minor
trauma.
• It is of particular significance because of its
common intraoral occurrence .
• Cause: staphylococci or streptococci.
CLINICAL FEATURES
• Most frequently on gingiva.
• Also occurs on the lips, tongue and buccal
mucosa.
• The lesions are more common in the facial
aspects of gingiva and can occur involving
both sides including interdental papilla.
TREATMENT
• Treated by surgical excision.
• When excising the granuloma of the gingiva it
is extreme certain to make the tooth free of
calculus.
PYOSTOMATITIS VEGETANS
• It is an uncommon inflammatory disease of the
oral cavity.
ORAL MANIFESTATIONS
• Most frequently affected area: buccal mucosa
which presented a cobblestone appearance.
• Vestibular lesions appears as folds and ulcer.
• Lips : diffusely swollen
• Gingival and alveolar mucosal lesions were
granular.
• Palatal lesions appear as multiple apthous
ulcer.
TREATMENT
• It’s treatment is not specific since the oral
lesions are refractory to antibiotic therapy.
GRANULOMA INGUINALE
• This disease is a progressive, chronic,
infectious granulomatous disease caused by
Calymmatobacterium granulomatis.
• Clinical feature:
It chiefly affects adult
blacks of either gender.
Primary lesions appear
as papules, or nodules.
• Oral manifestations:
 oral lesions appear to
be the most common
extragenital form.
Lesions can occur on
lips, buccal mucosa, or
palate.
Treatment
• Tetracycline, chloramphenicol, streptomycin,
garamycin e.t.c are effective in treatement.
Rhinoscleroma( Scleroma)
• It is a chronic, slowly progressive, localised
infectious, granulomatous disease caused by the
bacillus Klebsiella rhinoscleromatis.
• ORAL MANIFESTATIONS:
• Appears as proliferative granulomas, impairment of
the sensation of taste, anesthesia of soft palate.
Treatement
• Administration of tetracycline or
ciprofloxacin.
PUBLIC HEALTH SIGNIFICANCE
In 1974, the WHO launched it’s “expanded
programme on immunization” (EPI) against
most common preventable childhood disease i.e.
diptheria, tetanus, tuberculosis e.t.c
The GOI launched its EPI in 1978.
• MISSION INDRADHANUSH: The GOI
launched this mission on 25th december 2014.
• The goal is to vaccinate all under five years by
the year 2020.
• Introduction of pentavalent vaccine in India,
consist of DPT, hepatitis B and Hib .
• National Leprosy “ERADICATION”
PROGRAMME:
• It has been in operation since 1955, as a
centrally aided programme to achieve control
of leprosy through early detection of cases and
dapsone monotherapy.
• Leprosy diagnosis and treatment services are
available at all PHCs.
• The End TB Strategy: 2016 is the first year
of implementation of the WHO End TB
Strategy in the context of the United Nations
Sustainable Development Goals Agenda, both
of which include the aim of ending the TB
epidemic.
• Revised National Tuberculosis Control
Program (RNTCP) is the state-
run tuberculosis (TB) control initiative of
the Government of India.
• DOTS (directly observed treatment, short-
course), also known as TB-DOTS, is the name
given to the tuberculosis control strategy
recommended by the World Health Organization.
• The National Leprosy Eradication Programme
is a centrally sponsored Health Scheme of the
Ministry of Health and Family Welfare, Govt.
of India.
• In 2016 WHO launched the Global Leprosy
Strategy 2016–2020: Accelerating towards a
leprosy-free world.
CONCLUSION
• There are various BACTERIAL infections which
produce oral manifestation prior to any other
symptoms and as a public health dentist we
should be able to identify the symptoms so that
we can alert the authorities as well treat the
patient accordingly and refer the patient to
required authority.
REFRENCES:
• Rajendran R, Sivapathasundharam B, editor.
Shafer’s Textbook of Oral Pathology.7th ed.
New Delhi: Elsevier; 2012. p.317-338.
• Neville BW, Damm DD. Oral and
Maxillofacial Pathology. 1st South Asia ed.
New Delhi: Elsevier; 2016. p.167-188.
• Park K. Park’s Textbook of Preventive And
Social Medicine. 23rd ed. Jabalpur: M/s
Banarsidas Bhanot; 2015.

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bacterial infection

  • 1. BACTERIAL INFECTIONS OF ORAL CAVITY Presented by: Monika Post Graduate Department of Public Health Dentistry
  • 2. CONTENTS • Introduction • Bacterial infections  Scarlet fever  Diptheria  Tuberculosis  Leprosy  Actinomycosis  Tetanus  Syphilis
  • 3.  Gonorrhea  Rhinoscleroma  NOMA  Pyogenic granuloma  Pyostomatitis vegetans Epidemiology Clinical features Oral manifestations Public health significance Conclusion References
  • 4. INTRODUCTION • Certain bacteria produce disease which are manifested in or about the oral cavity. • This microbial specificity is characteristic of infectious disease wherever they may occur in the body and is necessarily confined to those of oral cavity.
  • 5. SCARLET FEVER • It is a contagious systemic infection occurring predominantly in children. • Cause:β-hemolytic streptococci, STREPTOCOCCUS PYOGENES. • The rash occurs because of three exotoxins: A,B,C.
  • 6. EPIDEMIOLOGY • Scarlet fever is similar in many respects to acute tonsillitis and pharyngitis caused by Streptococci paralleling the occurrence of these conditions in its epidemiology.
  • 7. Pharyngitis, tonsillitis, headache, chills, fever, abdominal pain, vomiting. Enlargement and tenderness of the regional cervical lymph nodes. Diagnosis: characteristic diffused, bright, scarlet-skin rash appears on 2nd or 3rd day of illness. Small papules of normal color erupt through these rashes giving characteristic sandpaper feel to the skin: PASTIA LINES Clinical features
  • 8.
  • 9. Oral manifestations: the chief oral manifestation is called stomatitis scarlatina. • FORCHHEIMER SPOTS: Small punctate red macules may appear on the hard and soft palate and uvula.
  • 10. Oral manifestations: the chief oral manifestation is called stomatitis scarlatina. • FORCHHEIMER SPOTS: Small punctate red macules may appear on the hard and soft palate and uvula.
  • 11. • The tongue exhibits a white coating and fungiform papillae are edematous and hyperemic, projecting above the surface as small red knobs :STRAWBERRY TONGUE. • The coating of the tongue is soon lost beginning at the tip and lateral margins and it becomes red, glistening and smooth except for the papillae: RASPBERRY TONGUE
  • 12. • The tongue exhibits a white coating and fungiform papillae are edematous and hyperemic, projecting above the surface as small red knobs :STRAWBERRY TONGUE. • The coating of the tongue is soon lost beginning at the tip and lateral margins and it becomes red, glistening and smooth except for the papillae: RASPBERRY TONGUE
  • 13. TREATEMENT: • The administration of antibiotics like penicillin, dicloxacillin and cephalexin.
  • 14. DIPTHERIA • Acute life threatening, infectious and communicable disease of the skin and mucous membrane caused by toxaemic strains of Cornebacterium diptheriae. • Characterised by formation of a grayish adherent pseudomembrane which bleeds on removal.
  • 15. • Disease of children • Humans are the principal reservoirs and organisms may persist for two to six weeks. • Transmitted mainly by respiratory droplet, direct skin contact and from skin to the respiratory tract through hands.
  • 16. EPIDEMIOLOGY: • Available data indicate a declining trend of diptheria in India due to increasing coverage of child population by immunization. • Recent diptheria outbreaks in a number of countries have demonstrated the shift in age distribution of cases to adults and old age people. • The outbreak warrants the need of booster immunization.
  • 17. PATHOGENESIS: Diptheria organism localises in respiratory tract Causes oedema, necrosis and acute inflammation Coagulation of fibrin, purulent exudate produces grayish green PSEUDOMEMBRANE.
  • 18. PATHOGENESIS: Diptheria organism localises in respiratory tract Causes oedema, necrosis and acute inflammation Coagulation of fibrin, purulent exudate produces grayish green PSEUDOMEMBRANE.
  • 19. If pseudomembrane present :diptheria cases. If pseudomembrane absent: diptheria carriers. Incubation period: 2-5 days. Clincal types according to location of pseudomembrane: tonsillar, pharyngeal, laryngeal, tracheal, nasal, conjunctival, cutaneous. Fever, sore throat, weakness, dysphagia, headache and change of voice,restlessness, pallor, tachycardia, Hoarseness of voice, respiratory stridor, dyspnea which may progress to severe respiratory obstruction and death in young children. Clinical features
  • 20. ORAL MANIFESTATIONS: • Patchy diptheritic membrane on the tonsils. • This membrane covers soft palate, tongue, lips, gingiva, buccal mucosa. • Severly affected patients have bull neck appearance.
  • 21. • Appears as non specific ulcers in oral cavity. • Soft palate may become temporarily paralysed • Peculiar twang and husky voice. • Regurgitation of liquids
  • 22. TREATMENT • Administration of diptheria antitoxin and apart from antibiotic administration done by penicillin and erythromycin. • Prevention by prophylactic active immunisation with diptheria toxoid.
  • 23. TUBERCULOSIS • It is a specific infectious granulomatous disease caused by MYCOBACTERIUM TUBERCULOSIS. • It commonly affects lung, intestine, meninges, bones, joints, lymph glands, skin and other tissues of body.
  • 24. EPIDEMIOLOGY • Among the world population, south east asian region carries a disproportionate 88% of the world’s burden of TB. • India accounts for nearly one fifth(20%) of the global burden of TB. • The vulnerability to TB in developing countries results from poverty, economic recession and malnutrition.
  • 25.
  • 26.
  • 27. Episodic fever, chills, fatigability, malaise, gradual loss of weight accompanied by a persistent cough. TB can be pulmonary or extrapulmonary. Pulmonary TB: primary, secondary or miliary. Extrapulmonary sites: lymph nodes, pleura, genitourinary tract, bones , joint e.t.c Primary pulmonary TB: seen in children and majority asymptomatic. Secondary TB: fever, cough, chest pain. Tuberculous infection of submandibular and cervical lymph nodes. Primary tuberculosis of the skin or lupus vulgaris appears papular nodules. Clinical features
  • 28. ORAL MANIFESTATIONS • Lesions of secodary tuberculosis may occur at any site on the oral mucous membrane i.e. tongue, palate, lips, buccal mucosa, gingiva and frenula. • The usual presentation is an irregular, superficial or deep, painful ulcer which tends to increase in size. • Diffuse involvement of the maxilla or mandible may also occur by hematogenous spread.
  • 29.
  • 30. • Tuberculosis lesions in the mouth do not differ microscopically from tuberculosis lesions in other organs of the body. • The characteristic appearance is due to the cell mediated hypersensitvity reaction.
  • 31. DIAGNOSIS • The presence of acid-fast bacilli in sputum smear is the gold standard for the diagnosis. • Microscopical smears: Z-N staining, Kinyoun’s cold staining method. • A minimum of five acid –fast bacilli on fluorescent microscopy and three on Z-N staining is reported as positive.
  • 32. TUBERCULIN TEST OR MANTOUX TEST • Subcutaneous injection of 0.1 ml of 5 tuberculin units of purified protein derivative into the forearm. • If positive induration is seen after 48-72 hours.
  • 33. TUBERCULIN TEST OR MANTOUX TEST • Subcutaneous injection of 0.1 ml of 5 tuberculin units of purified protein derivative into the forearm. • If positive induration is seen after 48-72 hours. Diameter of induration Interpretation > 15 mm Strongly positive >10 mm positive 5-9 mm indeterminate < 5 mm negative
  • 34.
  • 35.
  • 36. LEPROSY (HANSEN’S DISEASE) • Leprosy is a chronic granulomatous infection caused by MYCOBACTERIUM LEPRAE. • It multiplies very slowly and incubation period is about five years. • It mainly affects skin, peripheral nerves, upper respiratory tract, eyes, testes, muscles, bones and joints.
  • 37. EPIDEMIOLOGY • It is almost exclusively a disease of developing countries. • It is common in Asia, Africa, Latin America . • Africa has the highest disease prevalence and Asia has the most cases.
  • 38. • India accounts for 80%of the detection of leprosy cases in the world. • The annual case detection rate in India is among the highest in the world (53 per 100,000). • Prevalence is high in Bihar, Uttar-Pradesh, Tamil Nadu, West Bengal e.t.c.
  • 39. PATHOPHYSIOLOGY Once infected both cell mediated and humoral response are elicited by bacterial antigen DNA, glycolipids. Lipoarabinomannan, component of the cell membrane, induces immune response Bacteria are taken by histiocytes in the skin and schwann cells in the nerves.
  • 40. • TUBERCULOID TYPE: cell mediated immune response and low bacillary load. • LEPROMATOUS TYPE: low cell mediated immune response and high bacillary load.
  • 41.
  • 42.
  • 43. Oral lesion consist of small tumor like masses called lepromas which develop on the tongue, lips or hard palate. Gingival hyperplasia with loosening of the teeth. Paralysis of facial and maxillary division of trigeminal nerve. Dental manifestations are described as odontodysplasia leprosa. Premaxilla is affected in childhood, circumferential hypoplasia, shortening of roots involving maxillary anterior teeth. Oral manifestations
  • 45. ACTINOMYCOSIS • It is a chronic granulomatous suppurative and fibrosing disease caused by anaerobic or microaerophilic gram positive filamentous bacteria. • Characterised chiefly by the formation of abscesses that tend to drain by the formation of sinus tracts. • Pus from the abscesses shows typical ‘sulfur granules.’
  • 46.
  • 47.
  • 48. • Actinomycosis is classified anatomically according to the location of lesions: • Cervicofacial • Abdominal • Pulmonary forms.
  • 49. EPIDEMIOLOGY • Infection occurs throughout the lifetime with peak incidence in the middle age. • Males are more commonly affected than females.
  • 50. PATHOGENESIS • It appears to be endogenous infection. • The disruption of the mucosal barrier is the main step in the invasion of bacteria. • Initial acute inflammation is followed by a chronic indolent phase.
  • 51. CERVICOFACIAL ACTINOMYCOSIS • It is the most common form of this disease. • The organisms may enter the tissues through the oral mucous membrane and may either remain localised in the subjacent soft tissues or spread to involve the salivary glands, tongue, bone producing swelling and induration of tissue.
  • 52. • The skin overlying the abscess is purplish red, indurated and has feel of wood or often fluctuant. • The patient over a period of time may show a great deal of scarring and disfigurement of the skin. • The infection of the soft tissues may extend to involve the mandible or less commonly maxilla results in actinomycotic osteomyelitis.
  • 53. ABDOMINAL ACTINOMYCOSIS • It carries a high mortality rate. • Generalized signs and symptoms of fever, chills, nausea and vomiting, intestinal manifestations develop followed by symptoms of the involvement of liver and spleen.
  • 54. PULMONARY ACTINOMYCOSIS • The organisms may spread beyond the lungs to involve adjacent structure. • Fever and chills accompanied by a productive cough and pleural pain.
  • 55. TREATMENT • Long term high dose penicillin, tetracycline, and erythromycin have been used frequently. • In addition to this surgical drainage of the abscess and excision of sinus tract is necessary to accelerate healing.
  • 56. TETANUS (LOCK JAW) • It is an acute infection of nervous system characterized by intense activity of motor neurons and results in severe spasms. • Anaerobic gram positive bacillus: CLOSTRIDIUM TETANI.
  • 57. EPIDEMIOLOGY • Tetanus is now a comparatively rare disease in developed countries. • Neonatal tetanus is fatal with a mortality rate of 80- 90%.
  • 58. • However in asia, especially in china, myanmar, indonesia and India, the death rate due to neonatal tetanus is greately reduced due to immunisation coverage of pregnant women.
  • 59. PATHOGENESIS In suitable anaerobic conditions potential spores of the Cl. Tetani produce potent neurotoxin( tetanospasmin) It binds to the peripheral motor nerve terminal and followed by retrograde intraneuronal transport. The toxin migrate across synapse and blocks the release of glycine and GABA.
  • 60. Incubation period ranges from : 3days to 4 weeks. Generalised tetanus: characterised by lock jaw or trismus due to spasm of masseter, dysphagia, stiffness in the neck or back muscle. Sustained contraction of facial muscle results in Grimace-risus sardonicus. Arched back- opisthotonus. Local tetanus manifests as spasm of muscle near wound. Clinical features
  • 61.
  • 62. TREATMENT • Sedation, airway and nutrition should be maintained. • Penicillin 10-12 million units IV for 10 days. • Prophylaxis: wound debridement and booster doses of TT.
  • 63. SYPHILIS (LUES ) • It is caused by TREPONEMA PALLIDUM and is characterised by episodes of active disease interrupted by the period of latency. • Route of transmission: sexual contact, transmission from mother to child in utero.
  • 64. EPIDEMIOLOGY • Syphilis specifically congenital syphilis continues to be a major problem in many countries. • It is recognised that if treatment with antibiotics begins in infected pregnant women before fourth month of pregnancy approximately 95% of the offspring of these mothers will be free of the disease.
  • 65. ACQUIRED SYPHILIS • It is contracted primarily as a venereal disease as well as dentists working on infected patients can acquire it. • Three distinctive stages: primary, secondary and tertiary.
  • 66. PRIMARY STAGE: • Lesion known as CHANCRE develops at the site of inoculation approximately 3-90 days after contact with infection. • About 95% of it occur on genitalia but they are also found in other areas.
  • 67. • Of particular interest are those lesions occuring on the lips, tongue, palate, gingiva and tonsils. • Such a primary lesion on the lip may have a brownish, crusted appearance. • The intraoral chancre is an ulcerated lesion covered by a grayish white membrane which may be painful.
  • 68.
  • 69.
  • 70. SECONDARY OR METASTATIC STAGE • Commences about six weeks after the primary lesion, is characterized by diffuse eruptions of the skin and mucous membrane. • The oral lesion are called mucous patches, usually multiple, painless, grayish-white plaques overlying an ulcerated surface.
  • 71. • They occur frequently on the tongue, gingiva, or buccal mucosa. • Mucous patches are highly infectious since they contain vast numbers of microorganisms. • Secondary syphilis can be present as an explosive and widespread form known as lues maligna.
  • 72. • Secondary stage is characterised by fever, headache and muscle pain followed by necrotic ulcerations involving the face and scalp. • After second stage they enter a latent stage which may last for 1-30 years till the next stage tertiary syphilis.
  • 73. TERTIARY SYPHILIS • It involves chiefly the CVS, CNS and certain other tissues and organs. • It is non infectious. • Classic lesion is GUMMA : consist of a focal, granulomatous, inflammatory process with central necrosis.
  • 74. • The intraoral gumma commonly involves the tongue and palate. • In either situation the lesion appears as a firm nodular mass in the tissue, which may ulcerate to form a deep painless ulcer.
  • 75. • Lesion of palate cause perforating by sloughing of the necrotic mass of tissue. • Atrophic glossitis is the most common and is due to endarteritis obliterans. • Surface of tongue gets broken by fissures due to atrophy of tongue .
  • 77. CONGENITAL (PRENATAL) SYPHILIS • It is transmitted to the offspring only by an infected mother. • Pathognomic of disease: hypoplasia of the incisor and molar teeth, eighth nerve deafness and interstitial keratitis.
  • 78.
  • 79.
  • 80. TREATMENT • Penicillin is the drug of choice. • Surgical correction of the facial defects gives good esthetic results.
  • 81. GONORRHEA • It is primarily a venereal disease affecting the genitourinary tract and is transmitted by sexual intercourse. • Commonly manifests as: cervicitis, urethritis, prostratitis and conjuntivitis. • Cause by: Neisseria gonorrhoeae.
  • 82. EPIDEMIOLOGY • It is a significant cause of morbidity in developing countries but exact incidence is difficult to ascertain because of limited surveillance. • In India gonorrhea is more widely prevalent than syphilis and 80% of women report to be significant carriers.
  • 83. Acute urethritis, dysuria, and urethral discharge: MALE Cervicitis with candidal or trichonomal vaginitis: Female Clinical feature Lips : develop acute painful ulcerations. Gingiva: become erythematous with or without necrosis. Tongue: may present red and dry ulcerations. Oral manife stations
  • 85. TREATMENT • Antibiotics and other preventive measures should be followed.
  • 86. NOMA (cancrum oris, gangrenous stomatitis) • Noma, which means to devour ( a spreading sore) is rapidly mutilating, gangrenous stomatitis. • Predisposing factors: undernourished, deblitated from infections such as diptheria, dysentary, measles, pneumonia, scarlet fever.
  • 87.
  • 88. EPIDEMIOLOGY • Most cases occur in Africa, south east Asia and south east America. • One of the last reports, 69 cases of noma in miserably malnourished nigerian children between the ages of two and seven years.
  • 89. • The palate and occasionally tongue may become involved. • Patients have a high temperature during the course of disease, suffer secondary infection and may die from toxaemia.
  • 90. TREATMENT • The prognosis is considerably better if antibiotics are administered before patient reaches a final stage. • Immediate treatment of any existing malnutrition further improves the probability of saving the patient.
  • 91. PYOGENIC GRANULOMA • It is a tumor like growth that is considered as an exaggerated, conditioned response to minor trauma. • It is of particular significance because of its common intraoral occurrence . • Cause: staphylococci or streptococci.
  • 92. CLINICAL FEATURES • Most frequently on gingiva. • Also occurs on the lips, tongue and buccal mucosa. • The lesions are more common in the facial aspects of gingiva and can occur involving both sides including interdental papilla.
  • 93.
  • 94. TREATMENT • Treated by surgical excision. • When excising the granuloma of the gingiva it is extreme certain to make the tooth free of calculus.
  • 95. PYOSTOMATITIS VEGETANS • It is an uncommon inflammatory disease of the oral cavity.
  • 96. ORAL MANIFESTATIONS • Most frequently affected area: buccal mucosa which presented a cobblestone appearance. • Vestibular lesions appears as folds and ulcer. • Lips : diffusely swollen
  • 97. • Gingival and alveolar mucosal lesions were granular. • Palatal lesions appear as multiple apthous ulcer.
  • 98.
  • 99. TREATMENT • It’s treatment is not specific since the oral lesions are refractory to antibiotic therapy.
  • 100. GRANULOMA INGUINALE • This disease is a progressive, chronic, infectious granulomatous disease caused by Calymmatobacterium granulomatis.
  • 101. • Clinical feature: It chiefly affects adult blacks of either gender. Primary lesions appear as papules, or nodules. • Oral manifestations:  oral lesions appear to be the most common extragenital form. Lesions can occur on lips, buccal mucosa, or palate.
  • 102. Treatment • Tetracycline, chloramphenicol, streptomycin, garamycin e.t.c are effective in treatement.
  • 103. Rhinoscleroma( Scleroma) • It is a chronic, slowly progressive, localised infectious, granulomatous disease caused by the bacillus Klebsiella rhinoscleromatis. • ORAL MANIFESTATIONS: • Appears as proliferative granulomas, impairment of the sensation of taste, anesthesia of soft palate.
  • 104. Treatement • Administration of tetracycline or ciprofloxacin.
  • 105. PUBLIC HEALTH SIGNIFICANCE In 1974, the WHO launched it’s “expanded programme on immunization” (EPI) against most common preventable childhood disease i.e. diptheria, tetanus, tuberculosis e.t.c The GOI launched its EPI in 1978.
  • 106. • MISSION INDRADHANUSH: The GOI launched this mission on 25th december 2014. • The goal is to vaccinate all under five years by the year 2020. • Introduction of pentavalent vaccine in India, consist of DPT, hepatitis B and Hib .
  • 107. • National Leprosy “ERADICATION” PROGRAMME: • It has been in operation since 1955, as a centrally aided programme to achieve control of leprosy through early detection of cases and dapsone monotherapy. • Leprosy diagnosis and treatment services are available at all PHCs.
  • 108. • The End TB Strategy: 2016 is the first year of implementation of the WHO End TB Strategy in the context of the United Nations Sustainable Development Goals Agenda, both of which include the aim of ending the TB epidemic.
  • 109. • Revised National Tuberculosis Control Program (RNTCP) is the state- run tuberculosis (TB) control initiative of the Government of India. • DOTS (directly observed treatment, short- course), also known as TB-DOTS, is the name given to the tuberculosis control strategy recommended by the World Health Organization.
  • 110. • The National Leprosy Eradication Programme is a centrally sponsored Health Scheme of the Ministry of Health and Family Welfare, Govt. of India. • In 2016 WHO launched the Global Leprosy Strategy 2016–2020: Accelerating towards a leprosy-free world.
  • 111. CONCLUSION • There are various BACTERIAL infections which produce oral manifestation prior to any other symptoms and as a public health dentist we should be able to identify the symptoms so that we can alert the authorities as well treat the patient accordingly and refer the patient to required authority.
  • 112. REFRENCES: • Rajendran R, Sivapathasundharam B, editor. Shafer’s Textbook of Oral Pathology.7th ed. New Delhi: Elsevier; 2012. p.317-338. • Neville BW, Damm DD. Oral and Maxillofacial Pathology. 1st South Asia ed. New Delhi: Elsevier; 2016. p.167-188.
  • 113. • Park K. Park’s Textbook of Preventive And Social Medicine. 23rd ed. Jabalpur: M/s Banarsidas Bhanot; 2015.