Specific bacterial infections /prosthodontic courses

SPECIFIC BACTERIAL INFECTIONS
AFFECTING ORAL CAVITY
INDIAN DENTAL
ACADEMY
Leader in continuing Dental
Education
www.indiandentalacademy.com

• Tb
• Diphtheria
• Leprosy
• Syphilis
• Gonorrhea
• Noma
• Tetanus
• Scarlet Fever
• Cat Scratch Disease
• Actinomycosis
• Botryomycosis
• Melioidosis
• Granuloma Inguinale
• Rhinoscleroma
• Pyogenic Granuloma
• Tularemia
• Pyostomatitis Vegetans

CLASSIFICATION
A. Bacterial & Granulomatous infections:
1. Tuberculosis
2. Leprosy
3. Syphilis
4. Actinomycosis
5. Granuloma inguinale
6. Glander’s disease
7. Cat scratch disease
8. Tularaemia
9. Brucellosis

Tuberculosis
• well know phrase
• The more the things change, the more they remain
same
• This applies to tb which is a wide spread infectious
disease seen from centuries
• Chronic bacterial infection caused by
Mycobacterium tuberculi characterized by the
formation of granulomas in infected tissue by cell
mediated hypersensitivity

•M.tuberculosis is a rod
shaped
•Nonsporing
•Thin aerobic bacteria
• ACID FAST BACILLI
•acid fastness is due to high
content of mycolic acids ,
• long chain crosss linked
fatty acids and other cell
wall lipids
Causative org:
Myc. TB
Myc.Bovis
Myc.avium intercellulare
Causative org:
Myc. TB
Myc.Bovis
Myc.avium intercellulare

ETIOLOGY
• M.tb facultative intra cellular parasite
• Human strain is responsible for many cases
• bovine strain - illness through the ingestion of
unpasteurised cow’s milk .
• Rarely atypical or oppurtunistic mycobacteria -
pulmonary or generalised infection in
immunocompromised individuals

Mode of transmission :
1. Inhalation of organism
2. Ingestion of organism
3. Inoculation of organism
4. Transplacental route

Clinical features:
- Episodic fever, chills & night sweats
- Fatigue & malaise
- Loss of weight
- cough with or without hemoptysis
classification
Depending on extent of bacterial exposure &
resistance of the patient
- Asymptomatic primary TB
- Symptomatic primary TB
- Progressive primary TB &
- Reactivation TB

PRIMARY TB
 The infection of an individual who has not been
previously infected or immunized is called
Primary TB or Ghon’s complex.
 Tissue involved is lung & hilar lymph nodes,
tonsils, cervical lymph nodes.
 Ghon’s complex consists of 3 components:
1. Pulmonary component
2. Lymphatic vessel component
3. Lymph node component

GHON’S FOCUS

FATE OF PRIMARY TB
1. Fibrosis, calcification & ossification
1. Progressive primary tuberculosis
1. Primary miliary tuberculosis – seen in liver, spleen,
kidney, brain, bone marrow.

SECONDARY TB
 The infection of an individual who has been
previously infected and sensitized is called
secondary or post primary or reinfection or chronic
tuberculosis.
 Sec. TB occurs in lungs, tonsils, pharynx, larynx,
small intestine &skin.
 Infection acquired from
1. Endogenous source
2. Exogenous source

FATE OF SECONDARY TB
 Fibrosis & calcification
 Progressive pulmonary
TB.
1. Fibrocaseous TB
2. Tuberculous caseous
pneumonia
3. Miliary TB

EVOLUTION OF GRANULOMA
When Tubercle bacilli are injected into guinea pig- bacilli are
lodged in capillaries
Response of neutrophils
Infiltration of macrophages
After 2-3 days macrophages resemble - epitheloid cells
Aggregation of epitheloid cells
Granulomas

Macrophages
Dendritic cells
critical for induction
of t-h cells
IL-
12
IF
IF-Y
ACTIVATES
MACROPHAGES
CAUSE RELEASE
OF PDGF
FIBROSIS
MECHANISM OF TYPE IV HYPERSENSITIVITY IN FORMATION OF
GRANULOMA

CLINICAL PRESENTATION
Primary infection
Latent Active
Immunosuppression,
malnutrition
Pulmonary manifestations
(80-84%)
Extrapulmonary
manifestations
(16 -20%)

PULMONARY TB
• Symptoms : fever, fatigue,
malaise, weakness,
anorexia, wt loss.
• Temp.rise in afternoon or
evening and fall at night.
Night sweats, cough with
blood streaked sputum.
• Chest pain wheezing, chills,
rales.
• Tracheal deviation, apical
dullness and bronchial
breath sounds

EXTRAPULMONARY TB
• Involvement of cervical and hilar nodes.- “Scrofula”
• Scrofula in latin means “ glandular swelling”, in French
means “female high with a full neck”.
 Spread is usually hematogenous.
 Pericardium : Dyspnea, cough, ankle swelling, cardiac
enlargement.
 Peritoneum: fever, abdominal pain, ascitis, wt loss, night
sweats.
 Kidneys: dysuria, nocturnal urgency, hematuria
 Bones & joints : Pott’s disease
 Male genitalia: Tenderness & swelling of other genital
organs

Lupus vulgaris ( tb of skin)

Cervical lymphadenopathy seen in
lung tb

Tb showing scarring from cold abscess

SCROFULA

 Female genitalia : Abdominal pain, vaginal disorders,
menstrual disorders.
 Meningitis : cranial nerve palsies, hydrocephalus,
blindness, optic atrophy.
 Skin : Lupus vulgaris

ORAL MANIFESTATIONS
 Oral mucosa has rarely been reported
 Age :Children and adolescents
 Sex : Male :female :: 5:1

• Primary TB : gingiva, tooth extraction sockets,
buccal folds
• Sec. TB : tongue, palate, lips, alveolar mucosa &
jaw bones
• Lesions present as ulcers or less commonly as
nodules, vesicles, fissures,, plaques, granulomas
and verrucous proliferations.
• Lesion may be single or multiple, painful or
painless

• Mucosa :Ulcer – irregular, ragged, undermined
edges, minimal induration , with yellowish
granular base
• Tongue
 Site : lateral border, ant. Dorsum, base of tongue
 Painful, grayish-yellow, firm well demarcated
• Palate : Small granulomas or ulcerations
• Gingiva
• Lips : shallow granulating ulcers

TUBERCULOSIS - ULCERS

• Tooth apex & socket involvement: Brodsky &
Klattel - 1943
• Jaw bone involvement: Tuberculous
osteomyelitis
 TB of mandible : difficulty in eating, trismus,
paraesthesia of lower lip, lymphadenopathy
 Loosening of teeth.
 TB of maxilla
• Involvement of major salivary glands:
 Parotid gland followed by submandibular and
sublingual glands
(Zheng &Zhang –1995, Mignogna et al – 2000)

INVESTIGATIONS
• Examination of sputum
• Bacterial culture
• Radiographs
• Mantoux test
 False negatives : Severe TB, AIDS, recent
infection,malnutrition, malignancy, sarcoidosis.
 False positive : infection by related bacteria

CALCIFIED CERVICAL LYMPH NODES

• Culture of Mycobacterium tuberculosis
remains the gold standard for both diagnosis
and drug sensitivity testing.
• Conventional culture methods using
Lowenstein-Jensen (LJ) or 7H11 medium,
• disadvantage of being very slow. take 20 – 56
days for diagnosis
• four to six weeks after initial culture for drug
sensitivity testing.
• .

• 7H11- medium slightly accelerates the
process, but requires antibiotics in the
medium to prevent contamination and a CO2
incubator.
• Diagnosis with 7H11 medium takes 17 –21
days,
• DST information is available three to six
weeks later

MEDICAL MANAGEMENT
First line of drugs Second line of
drugs
Rifampin Cycloserine
Rifapentine Ethinomide
Ethambutol Streptomycin
Pirazinamide Amikacin
Isoniazid Capreomycin
Rifabutin Para amino salicylic
acid
Levofloxacin
Moxifloxacin
Gatefloxacinwww.indiandentalacademy.com

Treatment
Medical: 4 drug regimen for 2 months
-Isoniazid Hydrazide 300mg/day (after food)
-Rifampin 400-600mg/day (on empty stomach)
-Ethambutol 800mg/day
-Pyrazinamide 1200-1500mg/day
3 drug regimen for 4 months
Surgical:
- Sequestrectomy
- abscess drainage
- curettage of granulation tissue
- if pathological fracture - immobilization

SYPHYLIS ( LUES)
Treponema pallidum( spirochete)
• Microaerophilic , Gram +ve, Motile
Acquired
• Primary
• Secondary
• Teritiary
congenital

PRIMARY
• Incubation period is 3-4 weeks
• Ulcerated lesion called CHANCRE develops at site of
entry.
• Male and female genitalia
• Solitary , painless, indurated , elevated, ulcerated
• with serous exudates
• Highly infectious
• Regional lymphadenopathy
• Firm , painless, discrete with rubbery consistency
• Chancre Disappears within 3-8 weeks

Oral consideration
• Orogenital or oroanal contact
• Solitary ulcer on lip
• Upper lips in male, lower lip in females
• Ulceration-deep, red purple or brown base and
irregular raised border
• Tongue-lateral surface, anterior two third
• Enlargement of foliate papillae
• Palate, gingiva, tonsil

• Tonsil- red, edematous
• Uvula-swollen and red
• Fresh extraction wound may infected
• Submaxillary, submental, cervical lymph node
enlarged, rubbery
• Chancre painful when secondarily infected
• Dd of io primary: ruptured vesicles of hsv, traumatic
ulcer, carcinoma.

SECONDARY/metastatic
• After 2 months
• Haematogenous spread of T.P.
• Diffuse eruptions of skin & mucous membrane
• Skin : Macular /papular patches which are painless
• Nodular appearance-condyloma lata
• Circinate or coin like lesions-face
• Serological test is always positive

Oral manifestations
Macular
• Hard palate
• Flat to slightly raised firm red lesion
Papular
• Round nodules with grey center
• Red firm and raised lesions
• Buccal mucosa or commissures

Mucous patches
• Tongue,gingiva, buccal mucosa, tonsil,larynx,pharynx
• Multiple, painless, greyish white glistening plaques overlying
an ulcerated surfaces
• Ovoid/irregular in shape surrounded with erythematous halo
• Surface is covered by greyish pseudomembrane which can be
easily removed.
• Highly infectious.
• Commissures -split papules
• Coalesce-snail track ulcers
• Tongue-fissured

• Oral condyloma lata
– round
– Pale and white
– Velvety raised lesions
• Heal 2-6 weeks after they appear

Lues maligna
• explosive & wide spread form of secondary
• Fever,headache,myalgia
• Necrotic ulcerations on face, scalp with brown crusts
organized in rupoid layer
• Crater form or shallow ulcers with multiple erosions
– Hard and soft palate, Tongue
– lower lip, gingiva

Latent
• After second stage pts are symptom free
• Enter latent stage
• Lasts for 1-30yrs
• Pts demonstrate reactive serological tests for
syphilis

Tertiary/ late
• Non infectious as tissue damage is due to
delayed type of hypersenstivity reaction
between host & treponemes/their break
down products

Gumma – classical lesion
• Painless, Non infective, Localized
• single or multiple
• varying in size from pin head to several cms
• Sites : skin, mm, bone, liver, testes
• Focal granulomatory inflammation with central
necrosis
• ulcer- punched out edges with vertical walls
• red Granulomatous base with irregular outline

Introrally :
• involves tongue, palate
• Intially firm, pale, nodular mass
• Later forms deep painful ulcer
• Palatal perforation occurs due to sloughing of necroti
mass
• Following vigorous antibiotic therapy…hexheimer
reaction.

Oral manifestations
• Tongue, hard and soft palate, lips
• Ulcer with central necrosis and punched out
edges with wash leathery floor
• Progressive necrosis and sloughing
– Perforation of palate
• Destruction of soft palate
• Obstruction of nasopharyngeal airway

Syphilitic glossitis/ luetic glossitis
• Almost exclsively in males
• Due to endarteritis obliterans of lingual vasculature leading
to circulatory deficiency
• Surface of tongue gets broken up by fissures , wrinkled
lingual surface
• atrophy of filliform, fugiform papilla
• fibrosis of tongue musculature
• Hyperkeratosis frequently occurs
• May undergo carcinomatous transformation.

SYPHILITIC OSTEOMYELITIS
• Mandible > maxilla
• Gummatous involvement of bone
• Extensive necrosis
• Characterised by pain, swelling,
suppuration,sequestration
• Clinically & radiographically resembles pyogenic
osteomyelitis
• If lesion ossifies radiographic appearance is similar to
osteogenic sarcoma

C.V.S.
• Aortitis is key feature
Destruction of large blood vessels
Aneurysm, aortic incompetence, angina
Cardiac insufficiency
Neurosyphilis
Csf abnormalities in absence of clinical signs
Paresis, tabes dorsalis
Dementia
stroke

Ptosis seen in neuro syphilis

Portrait of Gerard de
Lairesse ( 1665–67). De
Lairesse, himself a painter
and art theorist, suffered
from congenital syphilis
that severely deformed his
face and eventually blinded
him.
Congenital syphilis

• T.p – has ability to cross placental barrier
• Fetus infected during 2nd,3rd trimester
Disease manifest as
• Latent : no symptoms but +ve serology
Early :
• Frontal bossing, Saddle nose
• short maxilla, relative protruberance of mandible
• Higoumenakis’s Sign : irregular thickening of
sternoclavicular portion of clavicle

• Rhagades
• Saber shin
Hutchinsons triad: late manifestations
Occurs 2 yrs after birth
• notching of incisor,
• Mulberry molars
• Interstitial keratitis of cornea
• 8th nerve deafness/ sensorineural hearing loss

HUTCHINSONS INCISOR

Saber shin

Actinomycosis
• Actinomycosis is a suppurative and granulomatous
chronic infectious disease
• usually spreads into adjacent soft tissues without
regard for tissue planes or lymphatic drainage
• may also be associated with a draining sinus tract
• Caused by ray fungus a.israelli, a.nalesundi,
a.viscosus, a.odontolyticus, a.propionica
• A.bovis produce lumpy jaw

• Actinomyces are Gram-positive, non-acid fast, anaerobic or
microaerophilic filamentous branched bacteria
• living as commensal organisms in the human oral cavity and
respiratory and digestive tracts,
• Becoming invasive when, through a mucosal lesion, they
gain access to the subcutaneous tissue.
• Infection is always endogenous. Doesnot occur by person
to person contact.
• Thus, dental caries, dental manipulations and
oromaxillofacial traumas are the most common triggering
events

• Presents as a chronic, fluctuant mass
• Located at the border of the mandible
• pain is rare, slight fever
• sensation of superficial tension around the mass.
• Initially, the mass may be surrounded by induration
or erythema; later, it may become tender to
palpation, on account of a central necrosis process
• Becoming progressively larger within weeks or
months

• Mass breaks down and abscess, sinuses are formed
• Discharging pus contain typical yellow sulphur
granules
• Skin overlying abscess is purplish,red indurated has
appearance of wood.
• Infection may extend into adjoining soft tissue as
well as bone
• Leads actinomycotic osteomyelitis

CERVICO FACIAL ACTINOMYCOSIS

• Definitive diagnosis may be established only by a
positive culture, however, Actinomyces growth is
very difficult even on appropriate anaerobic media
• The macroscopic presence of the classic sulfur
granules in tissue specimens or drainage may be of
some help when making diagnosis, even if these
features are not pathognomic, since nocardiosis,
botryomycosis may also present with sulfur granules

• Surgery plays an important role both in the diagnosis
and treatment of actinomycosis,
• recurrence following surgery alone is very common
• 2-4 weeks of high-dose intravenous antibiotics
followed by 3-6 months of oral antibiotics.
• Penicillin is the drug of choice
• Tetracycline and erythromycin are employed in
patients allergic to penicillin.

SCARLET FEVER
• Highly contagious, systemic infection
Causative agent :
• ß hemolytic streptococci
• S. pyogenes
• Produces pyrogenic / erythrogenic/ scarlet fever
toxin

CLINICAL FEATURES
• Common in children
• Mo enters into body through pharynx
• Incubation period is 3- 5days
• Cause severe pharyngitis, tonsilitis
• Headache, fever, chills, vomiting
• Cervical lymphadenopathy

• 2nd/3rd day - diffuse, bright red scarlet skin rash appears
• Rash first appears on upper trunk
• Spreads to extremities
• Spares palms & soles
• Colour of rash varies from scarlet to dusky red
• Small papules of normal colour erupt through
rash….sand paper feel to skin
• Rash is prominent in areas of skin folds… PASTA LINES
• Rash subsides after 6 to 7 days followed by
desquamation of palms & soles

Oral manifestations
• Stomatitis scarlatina
• Palatal mucosa: congested
• Petechiae scattered on
soft palate
• Palate, throat – fiery red
• Tonsils , faucial pillars
swollen
• Often covered by pseudomembrane

• Tongue : white coating
• Fungiform papilla becomes edematous, hyperemic
• Projects above the surface – white strawberry
tongue

• Tongue coating is lost
• Deep red, glistening, smooth except for swollen,
hyperemic papillae
• Raspberry tongue/ red strawberry tongue

TREATMENT
• Drug of choice is PENICILLIN.
• 250 mg (400,000 Units)
2-3tyms x 10 days 27 kg (60 lb)
• 500 mg (800,000 Units) for > 27kgs
• ERYTHROMYCIN ESTOLATE (20-40 mg/kg/day orally in 2-
4 div doses) /
• ERYTHROMYCIN ETHYLSUCCINATE (40 mg/kg/day orally
in 2-4 div doses) x 10 days.
• Clarithromycin x 10 days
• Azithromycin x 5days also may be considered -www.indiandentalacademy.com

DIPHTHERIA
• Acute life threatening infectious
• communicable disease of skin & mucous
membrane
characterized by involvement of the
• respiratory system
• local production of membrane
• general symptoms caused by absorption of toxin

• Historically described as Egyptian/ Syrian Ulcer
• 1826 – BRETONNEAU first described the disease
Host factors :
• Affects children of 1-5 years of age
• It effects both sexes.
Environmental factors
• Occurs in winter months in temperate countries
• Through out year in tropical countries

CORYNEBACTERIUM DIPHTHERIA
• 1883 – klebs described d.bacillus
• 1884 – cultivated by loeffler
KLEBS LOEFFLER’S BACILLUS
• 1888 – yersin discovered exotoxin
• He established its pathogenic effect
• 1890 – von behring discovered antitoxin

• Gram +ve, Non AFB
• Non Motile, Non Sporing, Non Capsulated
• Arrangement of bacillus is chinese letter/ cuneiform
arrangement
• At poles poly metaphosphate granules are
present(polar bodies)
• In loeffler methylene blue medium they take bluish,
purpule colour
• Metachromatic granules / volutin/babes ernst

• Transmission is by droplet infection
Portal of entry :
• RESPIRATORY ROUTE : Localises in mucous
membrane
• CUTANEOUS ROUTE : Invades open skin lesions due
to insect bite/trauma
• Bacillus at site of entry liberates toxin
• DIPHTHERIAL EXOTOXIN

Types of diphtheria
• Pharyngotonsillar diphtheria
• Laryngotracheal diphtheria
• Nasal diphtheria
• Cutaneous diphtheria

Clinical features
• Gradual in onset
Incubation period:
• Respiratory – 2 to 5 days
• Cutaneous – 7 days
• Sites:
• Tonsil, pharynx, trachea
• Nose, cutaneous
• Conjuctiva
• Genital

• Manifest as fever, sore throat, dysphagia,
headache, change of voice
• Pts without toxicity exhibit discomfort,
associated with local infection, malaise
• Toxic patients exhibit restlessness, pallor,
tachycardia

• Hoarseness of voice
• Respiratory stridor
• Dyspnoea, respiratory obstruction
• Cutaneous: deep punched out ulcers with a
leathery discharge.

ORAL MANIFESTATIONS
• Patchy diphtheric membrane
• Often begins on tonsils
• Enlarges & becomes confluent over surfaces
• Pseudomembrane is seen on
• Tonsil, tongue, gingiva, site of erupting teeth,
soft palate, lips, buccal mucosa

Erythema
of
posterior
pharyngeal
wall
white/gray
spots
Coalesce to
form veil
like
membrane
Thickens
and
becomes
gray

• Toxin induces initial edema & hyperemia
• Followed by Epithelial Necrosis &
Acute Inflammation
• Coagulation of fibrin & purulent exudate produce
PSEUDOMEMBRANE
• Vascular congestion extends into underlying tissues
• This toxin has special affinity for myocardium, adrenals,
n.endings
• Systemically toxin produce myocarditis, neuritis, focal
necrosis

PSEUDOMEMBRANE
• wash leather greyish green membrane
• Asymmetrical membrane
• Thick fibrinous, gelatinous exudate
• with a well defined edge
• surrounded by acute inflammation
• Advancing end is reddend
• If stripped off leaves bleeding surface

• Non specific ulcers are seen in oral cavity
• Temporary paralysis of soft palate during 3rd to 5th
week of disease
• paralysis disappears in few weeks/ months
• Peculiar nasal twang
• Exhibits nasal regurgitation of liquids during drinking
• Sub mandibular & anterior cervical nodes are
enlarged
BULL NECK APPEARANCE

• If infection spreads unchecked
• Larynx becomes edematous covered by
pseudomembrane
• Leading to mechanical obstruction
• Typical cough, diphtheric croup
• If airway not cleared suffocation may result

• INVESTIGATIONS : collecton of swab collection
• Followed by smear/ culture
• PROPHYLAXIS : can be controlled by
immunisation
• Diphtheroid toxoid is a trivalent prep( DPT)
• 3 doses for atleast 4 weeks
• 4th dose – after 1yr…..
• booster dose at school entry

Treatment
• Diphtheria antitoxins ranging 10,000 to 80,000 units
or more are administered iv or im depending on
severity of care

TETANUS ( tetanos – to contract)
• Described by Hippocrates & Susruta
• A Neurological disease characterised by increased
muscle tone & spasms.

• Cause: CLOSTRIDIUM TETANI
• Anaerobic , motile, gram +ve rod
• forms oval, colourless, terminal spores –
Tennis Racket Or Drumstick Shape

• Reservoir:
• found in the soil
• in inanimate environment
• in animal faeces & occasionally human faeces
• Mode of Transmission:
• contaminated wounds
• Tissue injury( surgery, burns, deep puncture wounds
,crush wounds,Otitis media ,dental infection, animal
bites)

PATHOGENESIS
• Contamination of wounds with spores of C.tetani.
• Germination & toxin production –
• In wounds with low red- ox potential ( devitalized
tissues, active infection )
• Tetanospasmin ( neurotoxin )
• Tetanolysin ( hemolysin )

Tetanospasmin
Binds To
Peripheral
Motor Neuron
Terminals &
N.Cells Of Ant
Horn Of Sc
Transpoted
To N.Cell
Body
Presynaptic
Terminals
Blocks
Release Of
Glycine &
Gaba
TETANOSPASMIN
Retrograde intraneuronal transport
Migrate
to
synapseFrom
axon
Released
into blood

• With diminished inhibition
• Lessened activity of reflexes which limit
polysynaptic spread of impulses, agonists &
antagonists recruited – SPASMS
• Resting firing rate of alpha motor neurons
increases – RIGIDITY

Clinical features
• Age : 5-40 years
• New born baby
• female during delivery or abortion
• Sex : males > females
• Occupation : Agricultural workers are at high risk
• Incidence is > in rural areas
• Environmental and social factors: Unhygienic custom
habits, Unhygienic delivery practices

GENERALIZED TETANUS
• Most common
• Increased muscle tone
• Generalized spasms
• Incubation period : few days to 3 weeks

• Stiffness / pain in neck, shoulder, back
muscles appear concurrently / soon thereafter
• Rigid abdomen & stiff proximal limb muscles
• Hands, feet spared.
• Laryngeal spasm may leads to asphyxia

• Opisthotonus : Painful spasms of neck, trunk
and extremity.
• producing characteristic bowing and arching
of back

Oral considerations
• Tonic rigidity of muscles of mastication – 1ST manifestation
• Stiffness of face
• Difficulty in chewing, Dysphagia
• Edentulous pts- inability to insert dentures
• Pt 1st notices increased tone in masseter
Trismus, lock jaw
• Risus Sardonicus : Spasm of facial muscles
( frontalis & angle of mouth muscles ) producing grinning
facies

RISUS SARDONICUS
Corners of mouth are drawn back, lips protruded,
forehead is wrinkledwww.indiandentalacademy.com

Treatment – general measures
• Goal is to eliminate the source of toxin
• neutralize the unbound toxin
• prevent muscle spasm
• providing support - resp support
• Admit in a quiet room in ICU
• Continuous careful observation & cardiopulmonary
monitoring
• Minimize stimulation
• Protect airway
• Explore wounds – debridement

NEUTRALIZE TOXIN :
• Inj.Human Tetanus Immunoglobulin 3000 – 6000
units IM, usually in divided doses as volume is large.
ANTIBIOTIC THERAPY :
• IV Penicillin 10 -12 million units daily for 10 days
• IV Metronidazole 500mg Q 6 hrly / 1gm Q 12 hrly
• Allergic to Penicillin : consider Clindamycin &
Erythromycin

Passive immunization
• ATS
• 1500 IUcafter sensitivity testing for 7 – 10 days
• High risk of serum sickness
• Active immunization:
• 3doses dpt in 1st yr of life
• Booster dose at school entry of tt
• 5 to 10yr intervals

Gonorrhea
• Primarily veneral infection affecting male & female
Genitourinary tract
• Cause : Neisseria Gonorrhea( gr –ve, non motile,
non sporing)
• Clinically asymptomatic:
• 15- 20% males
• 75 – 80% females
• Age : 15-29 years

Clinical features
Males
– Acute Urethritis
– Dysuria
– Discharge of purulent material
– Itching and burning sensation in urethra
• Epididymitis
• Chronic prostatis
• Balanitis
• Posterior urethritis

• Females
–Cervicitis
–Vaginal discharge
–Discomfort
–Dysuria
–Candidial or trichomonal vaginitis

Oral manifestations
Gonorrheal stomatitis
• Burning / itching sensation
• Dry hot feeling in mouth which in 24-48 hrs turns
to acute pain
• Foul oral taste, fetid breath
• Enlarged, tender sub mandibular lymphnodes
• Severe infection – fever occurs

• Gingiva : erythematous with/without necrosis
• Lips : acute painful ulcers leading to limitation of
movement
• Tongue : red, dry , ulcerations/
• Become glazed, swollen/painful
• Similar lesions on BM AND PALATE

• Speech, swallowing,mouth opening
– Painful
• Pseudomembrane
– White,yellow,gray in colour
– Easily scrappable
– Bleeding surfaces
• Pharyngitis and tonsillitis
– Vesicles and ulcers with pseudomembrane
• Gonococcal parotitis
– Ascending infection from duct to gland

Disseminated Gonococcal infection
• Septic embolic phenomenon
– Erythematous,purpuric,vesiculopustular,hemor
rhagic ulcerative lesions
• Gingiva
• Tongue
• Hard and soft palate
• Hypersensitivity reaction
– Erythematous lesions
• Gingiva
• Buccal mucosa
• Hard and soft palate

Gonococcal Arthritis
• Rapid onset fever
• Swollen joints, Migrating polyarthritis
• Fluid aspirate - P.M.N.leucocytes, Gram-ve diplococci
• TMJ LOCAL MANIFESTATIONS
• Trismus due to masseter muscle spasm
• Swelling & edema
• Perforation of tympanic plate, extension of infection into
EAM
• Destruction of articular cartilage
• Fibrous ankylosis of joint

Dd
• Streptococcal Stomatitis
• Herpetic Infection
• Candidiasis
DIAGNOSIS:
• Gram staining
• E.I.A.
• D.N.A. probes

Fluorescent antibody stained
micrograph

Treatment
• Inj ceftriaxone-I.M. 400mg
• Uncomplicated gonococcal pharyngitis
– 125mg-ceftriaxone-I.M.
– Ciprofloxacin 500mg orally
– Ofloxacin 400mg

Noma
• Means to devour
• A spreading sore
• Cancrum oris
• gangrenous stomatitis occuring in debilitated/
nutritionally deficient persons
• Occurs mostly as a secondary complication of
systemic disease rather than a primary disease

• Appears to originate from vincents organism
Clinical features
• Begins as small ulcer on gingival mucosa
• Rapidly spreads & involves surrounding tissues
• Jaws, lips, cheeks
• Initial site is commonly an area of stagnation around
fixed bridge or crown
• Overlying skin becomes inflammed, edematous, necrotic
• Line of demarcation develops between healthy and dead
tissue

• The commencement of gangrene is denoted by
appearance of blackening of skin
• Large masses of tissue may slough, leaving jaw
exposed
• Foul odour arise from these tissue
• Pts have high temp
• Suffer secondary infection
• May die from toxemia or pneumonia

Gangrenous stomatitis of buccal
mucosa in debilitated person

Thank you !!

Specific bacterial infections /prosthodontic courses

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