DEPARTMENT OF ORAL

PATHOLOGY
SEMINAR ON,
ACTINOMYCOSIS
TETANUS
SYPHILIS

SUBMITTED BY,
ANANDHU SUDHAKARAN
THIRD YEAR - B D S
 CONTENTS
 Introduction  Tetanus
 Actinomycosis  Epidemiology
• Etiology  Pathogenesis
• Epidemiology  Clinical Features
• Pathogenesis  Generalised Tetanus
• Clinical Features  Localized Tetanus
• Diagnosis  Diagnosis
• Differential Diagnosis  Treatment
• Treatment And Prognosis  Syphilis
 Tetanus  Acquired Syphilis
• Epidemiology  Congenital Syphilis
• Pathogenesis  Diagnosis And Treatment
• Clinical Features  Case History
 INTRODUCTION

 Certain bacteria, viruses and fungi produce diseases, which

are manifested in or about the oral cavity.

 Actinomycosis, Tetanus and Syphilis are some among the

diseases which are caused by bacteria.

 In this seminar we will be discussing about them.

 Actinomycosis is a chronic granulomatous
suppurative and fibrosing disease.
 It is caused by aerobic or micro-aerophilic,
Gram-positive, nonacid-fast and branched
filamentous bacteria.
 ETIOLOGY
 Actinomyces species are classified as anaerobic, Gram-
positive and filamentous bacteria. • A . israelii
 Among the 30 differrent species, Actinomyces israelii is
• A . viscous
found in most of the clinical forms of actinomycosis.
 Actinomyces meyeri is responsible for dissemination. • A . odontolyticus

• A . naeslundii

• A . meyeri

• A . gerencseriae

Actinomyces israelii Actinomyces meyeri

 The usual pattern of this disease is
charachterized chiefly by the formation of
abcesses.
 The pus from the abcesses when examined
shows the typical ‘sulfur granules’ or colonies
of organisms. Abcess in Actinomycosis
 Actinomycete is a common inhabitant of the
oral cavity even in the absence of any specific
infection.
 Thus, they can be cultured from carious tooth,
dental plaques, calculus and periodontal
pockets.
 Cervicofacial

Actinomycosis Abdominal
(According to the location
of the lesions)
Pulmonary
 EPIDEMIOLOGY

 Infection occurs throughout the lifetime with peak incidence in the

middle age.

 Males are more commonly affected than females.

 Incidence has decreased presently due to improved oral hygiene and

antibiotics.
 PATHOGENESIS
 Predisposing factors include trauma or dental extraction in case of
cervicofacial actinomycosis.

 Lesions usually appear as single or multiple indurations.

 Central fluctuance with pus-containing neutrophils and sulphur

granules is diagnostic of the disease.

 It occurs in association with HIV infection, transplantation,

chemotherapy, herpes and cytomegaloviral ulcerative mucosal lesions.
 CLINICAL FEATURES
 Cervicofacial actinomycosis is the most common form.
 It forms 2/3rd s of all cases and produces ‘lumpy jaw
syndrome’.
 The organisms may enter the tissues producing swelling
of the tissue.
 These soft tissue swellings eventually develop into one or
more abcesses.
 The skin overlying the abcesses will be purplish red,
indurated and has the feel of wood or fluctuant.
 The infection of the soft tissues may extend to involve the
mandible or maxilla which results in actinomycotic
osteomyletis.
 DIAGNOSIS
 It should be differentiated from Osteomyelitis caused by other bacterial
and fungal organisms and soft tissue infections caused by
Staphylococcus.
 The diagnosis of actinomycosis depends not only on clinical findings but
also on their culture.
 Most actinomycosis is poly-microbial.
Actinobacillus actinomycetemcomitans
Eikenella corrodens
Fusobacterium
A molecular diagnostic approach from And species of:
bone biopsies is used in diagnosis of Staphylococcus
Actinomycosis osteomyelitis. Streptococcus
 `

 Most pathogens will grow on chocolate blood agar at 37 °C within 5 days

 Acid fast stains include Kinyoun and Ziehl-Neelsen

Atinomycotic colonies in a smear of a pus

 DIFFERENTIAL DIAGNOSIS
 Nocardiosis

 Botryomycosis

 Tuberculosis

 Mold infection
 TREATMENT AND PROGNOSIS
 Treatment is difficult for this disease.

 Long standing fibrosis cases are treated by draining the abcess, excising
the sinus tract with high doses of antibiotics.

 Long-term high dose penicillin, tetracycline and erythromycin have

been used most frequently.

 In addition to this, surgical drainage of the abcesses and excision of

sinus tract is necessary to accelerate healing.
 Tetanus is an acute potentially fatal infection of the
nervous system characterized by intense activity of
motor neurons and results in severe muscle spasms.

 It is caused by the exotoxin of the anaerobic Gram-

positive bacillus Clostridium tetani that is commensal in
human and animal GIT and soil.

 It acts as the synapse of the interneurons of inhibitory

pathways and motor neurons to produce blockade of
spinal inhibition.
 EPIDEMIOLOGY

 It occurs sporadically and almost always affects non-

immunized persons, partially immunized and even,
less often, fully immunized individuals.
 It is more common in males than in females.
 It usually occurs after acute injuries such as laceration Neonatal Tetanus
or abrasion.
 It is associated with burns, frostbite, middle ear
infection, surgery, abortion and childbirth.
 Neonatal tetanus is fatal with a mortality rate of 80-
90%.
 PATHOGENESIS

 Under suitable anaerobic conditions spores of C. tetani produce a

potent neurotoxin in the wounds.
 It binds to the peripheral motor nerve terminal, enters the axon and to
the nerve cell body in the brainstem and spinal cord by retrograde
intraneural transport.
 The toxin migrates to the presynaptic terminal, where it blocks the
release of glycine and gamma-amino butyric acid (GABA).
 Once the inhibitory action is diminished, the resting-fixing rate of
locomotor neuron increases, producing rigidity.
 CLINICAL FEATURES
 The incubation period ranges from 3 days to 4 weeks.

 However, it may be as short as one day or as long as

months due to dormant spores in the wound.

 The prophylaxis against tetanus can also prolong the

incubation period.

 Tetanus occurs in generalized form, neonatal, local and

cephalic form.
 GENERALISED TETANUS
 Characterized by lock-jaw or trismus.
 Dysphagia, stiffness or pain in the neck,
shoulder or back muscles appear
concurrently.
 Laryngeal spasms may lead to asphyxia. 1 2
 Contraction of facial muscles results in a
grimace or sneer called as ‘risus
sardonicus’.
 The contraction of muscles of the back
produces an arched back called
‘opisthotonus’
3
 LOCALIZED TETANUS
 It manifests as spasm of muscles near the wound and is uncommon.
 The acute trismus which develops in these patients may stimulate acute oral
infection, pterygomandibular space or masticator space infection, trauma and even
hysteria.
 It should be differentiated from other inflammatory conditions of oral cavity,
strychnine poisoning, drug induced reactions and hypocalcemic tetany.
 DIAGNOSIS

 Diagnosis of tetanus is by asking about the history of cuts, scrapes,

punctures and trauma and examining for certain signs and symptoms.
 There are no lab tests that can confirm tetanus.
 TREATMENT
 The aim is to remove spores at the site of the wound, prevent toxin
production, neutralize unbound toxins and prevent muscular spasms.
 Sedation, airway and nutrition should be maintained.
 Penicillin 10-12 million units i.v for 10 days.
 Metronidazole 1gm every 12 hours should be administered.
 Anti-toxin like Human tetanus immunoglobulin(TIG) 3000-6000 units
i.m as individual doses.
 Wound debridement and booster doses of TT is given.
 For unimmunized patients, Antitetanus serum 1500 units or TIG 250
units should be given.
 Syphilis is caused by Treponema pallidum, a spirochete.
 It is characterized by episodes of active disease interrupted
by the period of latency.

Electron microscopic view of

Treponema pallidum

 It is a Gram-positive, motile and micro-aerophilic spirochete

pathogenic to humans.
 The route of transmission of syphilis is usually by sexual
contact, although there are examples of congenital syphilis
via transmission from mother to child.
 ACQUIRED SYPHILIS
 The acquired form of Syphilis is contracted primarily as a venereal
disease, after sexual intercourse with an infected person.

 Although persons such as dentists, working on infected patients in a

contagious stage, have innocently acquired syphilis.

 The disease if untreated, manifests three different stages ;

 Primary stage
 Secondary stage
 Tertiary stage
 In the primary stage, a lesion known as chancre
develops at the site of inoculation.
 The intraoral chancre is an ulcerated lesion covered
by a grayish-white membrane, which may be
painful.
 The chancre abounds with spirochetes, easily demonstrable by dark-
field examination of a smear.
 The secondary stage usually commences about 6 weeks
after the primary lesion.
 Characterized by diffuse eruptions of the skin and mucous
membranes.
 The oral lesions called ‘mucous patches’ are usually
multiple, painless, grayish-white plaques overlying an
ulcerated surface.
 They occur most frequently on tongue, gingiva or buccal
mucosa.
 Secondary syphilis can be present as an explosive and
widespread form known as ‘lues maligna’.
 The tertiary stage, also called late syphilis, does not
usually appear for several years.
 Classic lesion of the tertiary syphilis is Gumma.
 Gumma occurs most frequently in the skin, and mucous
membranes, liver, testes and bone.
 The intraoral gumma mostly involves the tongue and
palate.
 Atrophic or interstitial glossitis, is the most
characteristic and important lesion of syphilis and is
due to ‘endarteritis obliterans’.
•In syphilitic glossitis,
the surface of the
tongue gets broken
up by fissures due to
atrophy and fibrosis
of tongue
musculature.
•Syphilitic glossitis is
found almost
exclusively in males. SYPHILITIC GLOSSITIS
 CONGENITAL SYPHILIS
 It is transmitted to the offspring only by an infected
mother and is not inherited.
 Treatment with antibiotics should begin before the
fourth month of pregnancy, in which case the offspring
might become free of the disease.
 Reportedly, pathognomic of the disease is Hutchinson
triad ;
 Hypoplasia of the incisor and molar teeth
 Eighth nerve deafness
 Interstitial keratitis
 DIAGNOSIS AND TREATMENT
 The diagnosis can be made by examining the exudates of the active lesion
under a dark-field microscope for spirochetes.
 Care should be taken to avoid contamination by saliva since false positive
results are possible due to presence of T .microdentium, T
.macrodentium and T .mucosum.

 Penicillin is the drug of choice.

 Erythromycin or tetracycline is used if the patient is allergic to penicillin.
 Surgical correction of the facial defects gives good esthetic results.
CASE REPORT
 Name : Shruthi
 Age : 32
 Sex : Female
 Address : Kannur

 Chief Complaint : Patient complaints pain on the lower left posterior

teeth region since 6 days.
 History Of Present Illness : Patients c/o pain on the lower left
posterior teeth region since 6 days. Pain is sudden on onset, sharp
shooting type, continous and severe in intensity without any sensitivity
or radiating pain.

 Past Medical History : No relevant history

 Past Dental History : Patient had undergone tooth removal and

filling, which was uneventful.
 Drug History : Patient is under medication for pain for 3 days.

 Personal History :
 Diet : Mixed
 Apetite : Normal

 Bowel and Bladder : Normal

 Sleep : Adequate

 Delecterious Habit : Not reported

 Oral Hygiene Status : Brush twice using soft bristle brush and
toothpaste.
 Intraoral Examination :
1. Soft Tissue Examination :
• Tongue : Pigmentation present on lateral aspect of tongue bilaterally.
2. Gingiva :
• Colour : Coral pink
• Consistency : Firm and resilient
• Contour : Scalloped
• Texture : Stippled
 Hard Tissue Examination :
• Partially eruption irt 38
• 18 missing
• Restoration on 36
 Local Examination irt 38 :
• Operculum present
• Edematous and Erythematous
• Ovoid shape
• Margins : Well defined
• Colour : Pinkish red
• Palpation : Tenderness present
• Consistency : Soft and freely movable
• No pus discharge

 Case Summary
 Provisional Diagnosis : Pericoronitis irt partially erupted 38.
 Investigation : IOPAR irt 38
 WHAT IS PERICORONITIS ?

 It is an inflammation or infection of the soft tissue around the crown of

partially impacted tooth especially mandibular and third molar and is
usually caused by normal oral flora.
 It is either acute, sub acute or chronic pericoronitis.
 Radiographic Diagnosis : Long axis of 37 irt 38 is vertical in nature,
therefore suggesting of vertical impaction.

 Final Diagnosis : Pericoronitis irt vertically impacted 38.

 DIAGNOSIS OF PERICORONITIS
 Pericoronitis is diagnosed based on symptoms and appearance during a
clinical evaluation.
 An X-ray is also used to asses the
situation.
 HISTOLOGIC FEATURES
 There is an evidence of presence of hyperplastic epithelial lining of
pericoronal flap along with intercellular edema and infiltration of
leukocytes.
 DIFFERENTIAL DIAGNOSIS

 Trismus

 Tonsilitis

 Dentigerous cyst

 Odontogenic cyst

 Peridontitis
 Treatment Plan : Surgical extraction irt 38
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