Bacteria constitute a large domain or kingdom of
prokaryotic microorganisms. Typically a few
micrometres in length, bacteria have a wide range of
shapes, ranging from spheres to rods and spirals
Scarlet Fever (Scarlatina)
Systemic infection produced commonly by group A, β –
Organisms elaborate an erythrogenic toxin
Attacks blood vessels, produces characteristic skin rash
• The microorganism enters the body usually through pharynx
• Incubation period: 3-5 days
• Headache, chills, fever (102 -104 ), vomiting.
• Enlargement & tenderness of cervical lymph nodes
• Characteristic diffuse, bright scarlet skin rash which appears on
the 3rd day– “sun burn” with “goose pimples”
• When the rash is prominent in areas of skin folds – “Pastia
• Rash clears in 1 week followed by period of desquamation for
3 – 8 weeks.
Scattered petechiae on soft palate.
First 2 days – white coating on dorsal surface of tongue
through which only fungiform papillae seen (white strawberry
By 4th or 5th day – white coating desquamates, reveals
erythematous dorsal surface with hyperplastic fungiform
papillae – (red strawberry tongue or raspberry tongue)
Acute infection of the nervous system
Causative organism: exotoxin of anaerobic gram +ve bacilli
Its is characterized by intense activity of motor neurons & results
in the severe muscle spasm.
Incubation period: there is wide range of incubation period but the
clinical manifestations starts with in 14 days of onset
Pain, stiffness in jaws & neck muscles
Muscle rigidity producing trismus & dysphagia
Facial muscle rigidity also occur producing a typical “Risus
Some times the muscles of entire body are affected leading to
the condition called as “Opisthotonus”
“Cephalic Tetanus” is a condition which occurs in association
with 7th cranial nerve palsy
Incubation period: 1-10 days
Listlessness, malaise, headache, fever & vomiting
Mild redness & edema of pharynx
Cervical lymphadenopathy – involvement of tonsils
Edema of neck, submandibular region & anterior part of the
neck giving “bull neck” appearance
Involvement of nasal cavity – prolonged mucoid or hemorrhagic
Oropharyngeal exudate – begins on one or both tonsils as
patchy, yellow white, thin film.(diphtheritic membrane)
Thickens to form adherent grayish green covering.
May develop patches of green or black necrosis.
Involve entire soft palate, uvula, larynx or trachea.
DIRECT MICROSCOPY:smear stained with albert
stain show “CHINESE LETTER” or “CUNEIFORM
ARRANGEMENT”. The bacilli look green and
metacromatic granules appear bluish black
Anti diphtheritic toxins combined with antibiotics.
Erythromycin, procaine penicillin or i.v. penicillin
Prevention : By immunization of “diphtheria toxoid”
Tuberculosis (Koch's disease)
It is an chronic granulomatous inflammation.
Causative organism: Mycobacterium tuberculosis (acid fast
Incidence: more common in poor countries of Africa, Latin
• Mode of transmission: inhalation, ingestion, inoculation &
• Pulmonary TB is the chief form of the disease although it may
also occur in any part of the body including major organs such as
kidney, liver, bone etc..
• Pathogenesis: in open case of TB, bacilli is shed in respiratory
Pathogenesis of Primary tuberculosis
Droplet spread & inhalation
Goes in to the lung alveoli
Engulfed by alveolar macrophages
Multiply within macrophages
Either host cells overcome bacteria, or vice versa
Reactivation of organisms in previously infected person –
Diffuse dissemination through vascular system producing
multiple small foci of infection – Miliary TB
• Episodic fever, chills, fatigability, malaise.
• Gradual loss of weight
• Persistent cough with or with out hemoptysis.
• Night sweating, dyspnea.
Extra – pulmonary TB
• May involve lymph nodes, skin, skeletal system, CNS, kidneys
• Scrofula: TB infection of oropharyngeal & cervical lymph
• Swelling, tenderness of lymph nodes.
• Involved nodes may develop significant caseous necrosis
• Cold Abscess
• Lupus vulgaris – involvement of the skin
Do occur but are relatively uncommon (0.1%)
Lesions of oral mucosa are seldom primary, but they are
secondary to pulmonary diseases.
Organisms are carried in the sputum & enter the mucosal tissues
only if there is a break or a breach in the mucosal surface.
Organisms may be carried to the oral tissues by the
hematogenous route, deposited in the submucosa & subsequently
proliferate & ulcerate the overlying mucosa.
Lesions may occur at any site in oral mucosa, but the tongue is the
most common site followed by palate, lips, buccal
mucosa, gingiva & frenum.
Usually the TB lesion is irregular, superficial or deep, painful ulcer
which tends to increase in size.
Less frequent –nodular, granular or firm leukoplakic areas
TB gingivitis – manifests as diffuse, hyperemic, nodular or
papillary proliferation of gingival tissues.
Staining of the smear prepared from sputum by Ziehl-Neelsen
Bacterial culture in Lowenstein-Jensen media
Ten tuberculin units of purified derivative in 0.1 ml normal
saline intradermally in flexor aspect of the forearm.
Test is positive if 2-4 days later there is at least induration
with surrounding erythema.
Through BCG (Bacille Calmette Guerin)
Strain of bovine TB
Intradermal vaccination (0.1 ml)
Protection for up to 7 years
Chronic granulomatous infection.
Causative organism: Mycobacterium leprae (AFB)
Slightly contagious disease.
Mostly documented in Brazil, India, Indonesia, Myanmar
Tuberculoid lesions: (paucibacillary)
Small number of well circumscribed, hypopigmented skin lesions
Nerve involvement results in anesthesia of affected skin
Accompanied by loss of sweating.
Oral lesions rare
Lepromatous lesions: (multibacillary)
Begins slowly with numerous, ill defined, hypopigmented
macules or papules.
With time, lesions become thickened
Hair, eyebrows & eyelashes often lost.
Nerve involvement – leads to loss of sweating
Decreased sensation of light touch, pain & temperature.
Begins in extremities & spreads to most of body.
Facial involvement common
Skin enlargement leads to distorted facial features (leonine facies)
Nasal involvement – nose bleeds, stuffiness, loss of smell
Collapse of bridge of nose – pathognomonic
Paucibacillary type – granulomatous inflammation with well formed
clusters of epitheloid histiocytes, lymphocytes & giant cells.
Paucity of organisms – can be demonstrated only with acid fast
Multibacillary type – no well formed granulomas.
Sheets of lymphocytes mixed with vacuolated histiocytes called as
Noma (Cancrum Oris, Gangrenous
It is a rapidly spreading gangrene of the oral & facial tissues.
Seen commonly in debilitated or nutritionally deficient children.
Occurs chiefly in persons who are undernourished or debilitated
Considered a 2o complication of systemic disease rather
then a primary disease.
Appears to originate as a specific infection by the Vincent’s
Fusobacterium, Prevotella intermedia, Borrelia
vincentii, Porphyromonas gingivalis
Begins as a small ulcer of the gingival mucosa.(NUG)
Rapidly spreads and involve the surrounding tissues of the
jaws, lips & cheeks by gangrenous necrosis.(NUS)
The over lying skin becomes inflamed, edematous & finally
Line of demarcation develops between healthy & dead tissue.
Large masses of tissue may slough out, leaving the jaw exposed
Commencement of the gangrene is denoted by the appearance
of blacking of the skin.
Subcutaneous fat pad & buccal fat pad undergo necrosis in
advance of other adjoining tissues.
Odor arises from the gangrenous tissue which is extremely
Occasionally the tongue & palate are involved.
Lesion not restricted by tissue planes, spreads through
Patients have high temperature during the course of the
They usually suffer from 2o infections and may die from
toxemia or pneumonia
Antibiotics (penicillin & metronidazole)
Correction of nutrition, hydration & electrolyte imbalance
Chronic granulomatous, suppurative & fibrosing disease.
Caused by anaerobic, gram+ve, non-acid
fast, branched, filamentous bacteria.
Actinomyces israelii most common causative agent, A. viscosus
It is characterized chiefly by the formation of abscesses which
tends to drain by the formation of sinus tracts.
Classified anatomically according to the location of the lesion
1) Cervico-facial Actinomycosis
May either be an acute, rapidly progressing infection, or
slow, chronic lesion.
Organism enters the tissue though the oral mucous
May either remain localized in the mucous membrane itself
or might spread to involve the salivary glands, bones or skin
Swelling & induration of the tissues
Develop into one or more abscesses which later rupture to
liberate pus which contain “sulphur granules”.
o Skin over these abscesses is purplish red in color.
o These abscess areas after rupturing do heal but due to
chronicity of the disease , by the time one abscess heal the
other abscess is ready to rupture & perforate the skin
o Thus the patient over a period of time shows scars and
disfigurement of skin.
o The induration of soft tissues my get extended to the
underlying bones (maxilla & mandible)
o Mandible is more commonly involved than maxilla, if at all
maxilla is involved it may also involve cranium, meninges
or the brain itself.
Granulomatous inflammation showing central abscess
formation, which shows typical bacterial colonies.
Colonies appear to be floating in a sea of PMNL’s with
giant cells & macrophages around the lesional periphery.
The individual colony appear round or lobulated, made up
of a meshwork of filaments in a rosette pattern.
Filaments stain with hematoxylin, but shows eosinophilia
of the peripheral club shaped end of the filaments (ray
The colonies are surrounded by a fibrous tissue wall at the
The treatment of the disease is difficult & has not been
Penicillin & Tetracycline have been used more frequently.
Syphilis is a sexually transmitted chronic infection caused by
Characterized by an incubation period of about 2 to 6 weeks.
Infection goes through a classic evolution characterized by 3 stages
- Primary syphilis
- Secondary syphilis
- Tertiary syphilis
The usual mode of transmission is through
- sexual intercourse
- secretions by intimate contacts
- transplacental transmissions
T. pallidum gains entry through the intact mucosa or through
microscopic abrasions in the skin.
From here it enter the blood and lymphatics to eventually produce
The disease is generally classified into two:
Is acquired from an infected person
It can be either through
▫ Sexual contact with an infected partner
▫ Careless handling of the infected patients by the health
Manifests in three stages:
1. Primary syphilis
2. Secondary syphilis
3. Tertiary (late) syphilis
Develops at the site of inoculation approximately 3 weeks after
Clinical symptoms appear at the site of inoculation
▫ male and female genitalia
▫ extra genital site like-fingers, oral region, perianal region &
(at these sites the spirochetes undergo rapid replication and
enter into the lymphatics or blood stream)
Characteristic primary lesion of syphilis is called “Chancre”
It is a solitary, painless, indurated, nontender, non -
hemorrhagic, ulcerated or eroded lesion.
Chancre starts as a dull red macule or papule, which later on becomes
eroded or ulcerated and produces Regional lymphadenopathy
Resolves within 3 - 8 weeks
Chancre occurs on the lips, tongue, palate, gingiva, uvula and tonsils
May be painful due to secondary infection and are highly contagious
Chancres are ulcerated, indurated lesions covered by a grayish white
Often mistaken for an early carcinoma
Also called Metastatic Stage
Appears in about 6-8 weeks after the appearance of the primary
Occurs due to the generalized hematogenous dissemination of the
infection in the body
Characterized by skin lesions, mucosal lesions, few constitutional
symptoms and generalized lymphadenopathy
Skin lesions may also occur in the form of nodular, flat-
papillary (condyloma lata) or pustular lesions.
Circinate (coin-like) lesions on the face & skin are
characteristic of secondary syphilis.
Areas of hyperpigmentations may be seen on the palms and
The secondary lesions are mucocutaneous in nature and they
usually occur 6 to 8 weeks after the primary infection.
The oral lesions in this stage are called "mucous patches”;
commonly seen over the tongue, gingiva, tonsils, larynx, pharynx
and cheek, etc.
These patches are characterized by multiple, flat, irregular or
circular, slightly raised, painless, round erosions.
Covered by a thin yellowish-grey (glistening) slough; surrounded
by a painful erythematous halo
Multiple mucous patches in the oral cavity coalesce together and
from “snail track” like ulcers.
Called the Hidden Stage
Begins when the Secondary symptoms disappear
The bacteria begins to infest the bone marrow, lymph glands, vital
organs, and the central nervous system
It may last up to a month or a lifetime
1/3 of the cases left untreated will proceed to tertiary stage
Tertiary (Late) Syphilis
Occurs about 5-10 years after the primary infections and it affects
nearly every organs of the body
It mainly affects skin, mucous membrane, CNS & CVS
Typical lesions of tertiary syphilis is called " Gumma",
Localized, chronic granulomatous lesion having either nodular or
Often appears as a "punched-out" ulcer, having vertical walls and a
dull red granulomatous base with an irregular outline.
Tertiary Syphilis :Oral manifestations
Gumma are commonly seen on the hard and soft palate, lips and
This stage is not contagious.
Lesions begin as firm, small, pale, nodular masses in the midline
of the palate.
They frequently ulcerate by central necrosis and have a punched-
out edge with a wash-leather floor.
The ulcers are either single or multiple and are mostly painless.
Congenital syphilis is a rare entity that occurs in children born of an
The condition occurs due to transplacental infection with
Treponema pallidum during fetal development
Congenital infection is associated with several adverse
Low birth weight
Clinical manifestations after birth are divided
- Early Congenital syphilis (<=2 years of age)
- Late Congenital syphilis ( >2 years of age)
Clinical Manifestations of Early Congenital
Jaundice due to the hepatitis
Clinical Manifestations of Late Congenital
High -arched palate
Enlargement of clavicle adjacent to the sternum
Relative prognathism of mandible
Premature perioral fissuring
Anterior bowing of tibia as a result of periostitis
Eighth nerve deafness
Concavity of vertebral border of the scapulae
Painless synovitis and enlargement of joints, usually the knee
Described by Sir Jonathan Hutchinson in 1858.
Defined the following three pathognomonic diagnostic features
Ocular interstitial keratitis
Eighth nerve deafness
The infection alters the formation of both the anterior teeth
(Hutchinson's incisors) and the posterior dentition (Mulberry
molars, Fournier's molars, Moon's molars).
Hutchinson's incisors - exhibit their greatest mesiodistal width in
the middle third of the crown.
The incisal third tapers to the incisal edge
Resulting tooth resembles a straight - edge screwdriver.
The incisal edge often exhibits a central hypoplastic notch.
Mulberry molars - taper toward the occlusal surface with a
constricted grinding surface.
The occlusal anatomy is abnormal
Numerous disorganized globular projections that resemble the
surface of a mulberry
Detection of bacteria in smear by dark ground illumination
Bacterial culture in artificial media.
Wasserman reaction, Khan test, Venereal disease research laboratory
Penicillin will cure a person that has had syphilis for less than a
Blood tests should check to make sure the infection has been
Tertiary syphilis is incurable as it has damaged body organs.