Microbial Infections (Bacteria)

Presented byDr. Arun Singh

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Contents
Syphilis (Lues) Primary syphilis Secondary syphilis Tertiary or late stage syphilis Congenital syphilis Gonorrhea Tuberculosis

Contents

Leprosy Tuberculoid lesions Lepromatous lesions Actinomycosis Noma Bibliography

Syphilis (Lues)

A sexually transmitted disease Characterized by episodes of active disease altered with period of latency It may be Classified as acquired or congenital Acquired syphilis manifests three distinctive stages primary, secondary and tertiary
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Etiology
Syphilis is caused by Treponema pallidum A gram positive, motile, microaerophilic spirochete It can be best demonstrated by dark field microscope.

The infection can acquired by

Sexual contact with a partner with active lesions By transfusion of infected blood By transplacental inoculation of the fetus by an infected mother
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Pathogenesis - Primary syphilis

Direct contact Hard ulcer or chancre at the site of spirochete entry A painless , nonsuppurative regional lymphadenopathy Chancre heals spontaneously in 3-12 weeks without scarring
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Pathogenesis - Secondary syphilis

After a period of several (2-10) weeks secondary syphilis develops This is marked by Spirochetemia with wide dissemination Fewer, Mucocutaneous lesions and lymphadenopathy are typical The lesions are - multiple in number highly infectious Resolves spontaneously
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PathogenesisTertiary or late stage syphilis

It takes many years to appear

Develops in patients who have not been treated and undergo latency
The patients may have CNS and Cardiovascular

involvement

Focal necrotic inflammatory lesions gummas of any organ

Gumma formation is the result of hypersensitivity

reaction
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Pathogenesis

Congenital syphilis It occurs in the latter half of pregnancy T. pallidum crosses placenta from infected mother It may cause numerous inflammatory and destructive lesions in various fetal organs It may cause abortion or still birth
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Clinical features
Primary syphilis Painless indurated ulcer with is formed with rolled margins

At the site of inoculation

Lesion usually at genitalia

May occur at Lip, oral cavity and fingers

Lesions are generally covered by a grayish-white membrane and heals without therapy in 3-12 weeks with no scarring
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Clinical features

Secondary syphilis
It is characterized by a reddish brown

maculopapular cutaneous rash

Mucosal ulcers are - covered by a mucoid exudate (mucous patches)

Multiple, painless, grayish-white plaques Overlying an ulcerated surface
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Clinical features

Elevated broad based verrucal plaques condylomata lata May occur on skin and mucosal surface

Inflammatory lesions may also occur in any organ

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Clinical features

Tertiary syphilis It is non infectious stage The manifestations can be profound and that of neural syphilis include

General paresis(paralysis) Tabes dorsalis (locomotor ataxia)

Inflammatory involvement of CVS aneurysms Gummas of any organ

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Clinical features

Oral manifestations

Palatal perforation due to gumma There is development of generalized glossitis with mucosal atrophy.

Patients with syphilitis or luetic glossitis exhibit fissured tongue due to atrophy and fibrosis of tongue musculature hyperkeratosis exclusively occurs in males 15 about fourfold increased risk of OSCC

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Clinical features

Congenital syphilis Mucocutaneous rash seen early Variety of manifestations Frontal bossae Short maxilla High palatal arch A nasal deformity saddle nose due to involvement of vomar Excessive anterior bone growth in tibia due to periostitis saber shin
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Clinical features

Irregular

thickening of sternoclavicular portion of clavicle Relative protuberance of mandible

Hutchinsons triad Interstitial keratitis VIIIth nerve deafness Dental abnormalities notched screwdriver-shaped incisors and mulberry molars

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Histopathology

Basic tissue response to T. pallidum consists of a proliferative endarteritis and infiltration of plasma cells Narrowing of lumen of small arteries and arterioles Due to endothelial cell proliferation Plasma cells, lymphocytes and macrophages found in perivascular areas 20

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Histopathology

Gummas show - necrosis and greater number of macrophages Resulting in a granulomatous lesion Spirochetes can be demonstrated - using silver stains

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Differential diagnosis
Chancre OSCC Chronic traumatic lesions Tuberculosis Histoplamosis Secondary Infections marked by mucocutaneous eruption Palatal gumma T- cell lymphoma
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Laboratory diagnosis
1. Dark field examination of scrapings or exudate
False

positive results by salivary contamination due to T. microdontium, T. macrodontium and T. mucosum

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Laboratory diagnosis

2. Silver stains or immunologic preparations of biopsy tissue 3. Serologic tests for antibodies to T pallidum VDRL RPR ELISA
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Treatment
Drug of choice Penicillin

Other antibiotics Erythromycin Tetracycline

Surgical correction of facial defects

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Gonorrhea

Primarily a venereal disease Affecting male and female genitourinary tract One of the most prevalent bacterial disease In India, 80% of infected women asymptomatic carriers Affected age group 15-29 years
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Etiology

It is caused by gram ve, non-motile, nonspore forming dipplococci - Neisseria gonorrhoeae Which infects columnar epithelium of lower genital tract, rectum, pharynx and eyes Transmitted by direct sexual contact with an infected partner Incubation period less than 7 days
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Etiology

The organism - very sensitive to drying Requires break in the skin or mucosa to establish infection

Oral and pharyngeal mucosa may be infected through orogenital contact

Or inoculation through infected hands Pharyngeal mucosa has more chances of infection
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Clinical features

In males acute urethritis, prostatitis, balanitis In females cervicitis with candidal or trichomonal vaginitis

In pharyngeal infection Sore throat Generalized erythema Ulcers with a gray or white pseudomembrane Cervical lymphadenopathy

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Oral manifestations

Accompanied by - fever and regional lymphadenopathy Orally - multiple ulcerations and generalized erythema

Lips- acute painful ulceration, limiting motion

Gingiva- erythematous with or without necrosis Tongue- red dry ulcerations or glazed or swollen with painful erosions
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Differential diagnosis

Conditions that cause generalized erythema or multiple ulcers

Aphthous

ulcers Herpetic ulcers Erythema multiforme Pemphigus Pemphigoid Drug eruptions Streptococcal infections
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Diagnosis
Traditionally Demonstration of organism with Grams stain Culture on Thayer Martin medium or Stuart or Armies media

Newer techniques Immunofluorescent antibody technique for rapid identification of N. gonorrhoeae

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Treatment

Uncomplicated gonorrhea dose of 2- 3.5 gm of Ampicillin

Single

For penicillin resistant cases

Single

dose of 500 mg of Ciprofloxacin

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TUBERCULOSIS

Systemic infection disease Worldwide prevalence & of varying clinical manifestation

Infectious granulomatous disease

Acid fast bacilli mycobacterium tuberculosis Mycobacterium bovis

Infects - about one third population of world Kills - approximately 3 million people per year A major health problem in most developing countries India nearly one-third of global burden of TB
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Tuberculosis

In developed countries a significant decrease in incidence Reemergence of cases - in association with HIV and AIDS in Europe and Africa Multidrug resistance - an increasing problem in managing disease
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Prevalence - low income group with low socioeconomic and unhygienic condition.

Direct person to person spread through airbone droplet from patient with active

disease

Entry of the bacillus in body is by inhalation.

Etiology

Caused by aerobic, non spore forming bacillus Mycobacterium tuberculosis A facultative intracellular parasite Surrounded by - a thick waxy coat

Which retains red dyes (Ziehl Neelsen)

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Etiology

Organism do not decolour with acid-alcohol Acid-fast bacilli Due to

High

content of mycolic acids Long chain cross-linked fatty acids Other cell wall lipids

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Etiology

Types of Mycobacterium Two major types M tuberculosis in humans M bovis primarily in cows Two other closely related forms M avium M intracellulare Both are nonvirulent in healthy individuals
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Constitutional factor

Low income group Low and unhygienic living condition Malnutrition Overcrowding are constitute for tuberculosis infection

Pathogenesis

Spread of M tuberculosis through small airborne droplets Carry organism to pulmonary air spaces Pathogenecity of organism due to

Ability

to resist degradation by macrophages Development of type IV hypersensitivity reaction

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Pathogenesis

After 2 - 4 weeks

A granulomatous inflammatory response hard tubercle Central part show caseous necrosis

May undergo -

Dystrophic

calcification ( Ranne complex ) ~ Latent organisms in calcification foci -may become reactivated later
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Pathogenesis

Liquefaction

and discharge into lung

~ Leads to formation of cavity ~ May never heal / enlarge / shrink or remain stable In few cases hematogenous or lymphatic spread - Miliary TB

Found in childhood with poor immunity

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Type
1. 2. 3. 4. 5.

Miliary tuberculosis Potts disease Scroful Primary tuberculosis Secondary tuberculosis

Pathogenesis

OMM may become infected implantation of organism found in

Through

sputum
Or

by secondary or miliary TB

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Clinical features

TB pulmonary or extrapulmonary Extrapulmonary

lymph nodes pleura genitourinary tract oral cavity bones joints meninges peritonium

Pulmonary may be primary, secondary or miliary

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Clinical features

No symptoms of primary infection unless becomes progressive

In progressive or secondary TB - low-grade signs and symptoms fever night sweats malaise gradual weight loss

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Clinical features

With progression cough hemoptysis chest pain (pleural involvement)

In miliary TB anorexia loss of weight hepatosplenomegaly lymphadenopathy

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Clinical features

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Oral manifestations

Lesions seldom primary but secondary to pulmonary disease May appear on any mucosal surface Tongue and palate - favored locations

Typical lesion - an irregular, superficial or deep indurated, chronic, nonhealing ulcer

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Oral manifestations

Usually painful and tend to increase slowly in size Bony involvement of - maxilla and mandible By direct extension - through root canal or even after tooth extraction

But most likely - hematogenous spread of organism

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Oral manifestations

May produce periapical granuloma or tuberculoma

Tuberculous

Tuberculous

osteomyelitis ( in later stage )

Pharyngeal involvement - painful ulcers

Laryngeal lesions may cause - dysphagia and voice changes

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Histopathology

Basic microscopic lesion of TB granulomatous inflammation Focal zones of activated macrophages surrounded by lymphocytes, plasma cells and fibroblasts Macrophages may develop an abundant eosinophilic cytoplasm Resembling epithelial cells -- Epithelioid cells
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Histopathology

Fusion of macrophages -- Langhans giant cells Nuclei - distributed around the periphery of cytoplasm

As granulomas age - central necrosis occurs Referred to as - caseous necrosis Because of- gross cheesy texture of these
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Diagnosis

Presence of acid fast bacilli (AFB) in sputum smear gold standard -

Ziehl-

Neelsen Kinyouns cold staining method Rhodamine stain for fluorescent microscopy

Chest X-ray and tuberculin test supplement

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Diagnosis

CT scan to diagnose mediastinal or hilar lymphadenopathy, cavities and intralesional calcification MRI for extrapulmonary TB

Mycobacterial culture ( 4-6 weeks ) Lowenstein Jensen medium Middle brook medium
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Diagnosis

Mantoux or Tuberculin test Use tubercle bacillus antigen

Called - purified protein derivative (PPD) A positive inflammatory skin reaction (induration) seen after 48-72 hrs

Indicates that individual's cell-mediated immune system has been sensitized

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Diagnosis

Signifies previous exposure and subclinical infection Not necessarily imply active disease
Greater value in excluding TB

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Differential diagnosis

Chronic indurated ulcer may be present in -

primary

syphilis oral manifestations of deep fungal diseases squamous cell carcinoma chronic traumatic ulcer major aphthae

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Differential diagnosis

Microscopically, no AFB in -

syphilis cat-

scratch disease tularemia histoplasmosis blastomycosis coccidioidomycosis sarcoidosis some foreign body reactions
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Treatment

First-line drugs for TB include-

isoniazid rifampin pyrazinamide ethambutol

streptomycin - rarely used for first-line treatment

except in multidrug-resistant cases

Drug combinations - used in 6, 9, or l2 month regimens But may be extended - as long as 2 years

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Treatment

Patients with positive tuberculin test Benefit from prophylactic chemotherapy

Typically using isoniazid for l year

Oral lesions resolve with treatment of patient's systemic disease

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Leprosy

Also known as Hensons disease Moderately contagious

Caused by acid fast bacilli Mycobacterium leprae It is an obligate intracellular, gram-positive bacilli Most common cause of peripheral neuritis
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Etiology

Only bacteria to infect peripheral nerves It is unique in exhibiting dopa oxidase activity and acid fastness

Grows best in cooler tissue Skin Peripheral nerves Upper Reparatory Tract (URT) Anterior chamber of eye Testes
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Etiology

Living leprosy bacillus is solid pink rod Non living granular or fragmented

It is grown well in mouse footpad and in armadillo Transmission occurs either by direct contact for a long time or nasal secretion
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Leprosy

Exclusively a disease of developing countries 60% of leprosy patients in India Rare in infants

Bimodal age peak at 10-14 and 35-44 years

It is a disease which runs a chronic course
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Pathogenesis

Once infected, both cell mediated and humoral responses elicited by bacterial antigen DNA Bacteria taken by histiocytes in skin and Schwann cells in nerves
This usually results in an inflammatory response involving macrophages and lymphocytes
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Clinical features

Range of clinical spectrumleprosy(limited form) to lepromatous leprosy (generalized

Tuberculoid

form) In between indeterminate form (borderline)

Usually skin and peripheral nerves are affected

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Clinical features

Tuberculoid lesions single or multiple macular, erythematous plaque or nodules with dermal nerve involvement loss of sensation and loss of sweating

Lepromatous lesions Progressive thickening of skin Characteristic nodules Produces severe disfigurement

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Oral manifestations

Similer lesions may occur intraorally and intranasally similer lesions On tongue lips and hard palate small tumor like masses lepromas These nodules show a tendency to break down and ulcerate
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Clinical features

In advance stage Facial paralysis Lump in skin of face and ears Loss of fingers and toes Nasal depression Foot drop Claw toe Facies leprosa a classical destruction of anterior maxilla

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Histopathology

Microscopically, a granulomatous inflammatory response Epithelioid macrophages and multinucleated giant cells predominate In tuberculoid leprosy - well-formed granulomas, like in TB

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Histopathology

Lapromatous leprosy Poorly formed granulomas Sheets of lymphocytes Vacuolated macrophages (lepra cells) More numerous organisms

Acid-fast bacilli - found within macrophages

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Diagnosis

History of direct contact or living in endemic area Signs & symptoms of skin and nerve involvement Appearance of oral lesions without skin lesions- highly improbable

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Diagnosis

Staining of skin and nasal smears Modified Ziehl-Neelsen method A biopsy must be performed to confirm diagnosis

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Differential diagnosis

Other disorders with hypo-pigmentation

Sarcoidosis Leishmaniasis

Lupus

vulgaris Lymphomas Syphilis

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Treatment
Several drugs used dapsone Rifampin minocycline

Thalidomide - to manage complications of leprosy therapy

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Actinomycosis

Chronic granulomatous suppurative and fibrosing disease Exhibits some clinical and microscopic features -that are fungus like Caused by Actinomyces israelii Anaerobic or microaerophilic, gram-positive, non acid fast, branched filamentous bacterium

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Actinomycosis

Normal inhabitant of the oral cavity in healthy individuals Saprophytic in nature

Usually found in tonsillar crypts gingival crevices carious lesions non vital root canals plaque & calculus periodontal pocket
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Actinomycosis

Other Actinomyces species may be involved A. naeslundi A. viscosus A. odontolyticus

Nocardia asteroides, a related aerobic bacterium Responsible for a similar clinical picture
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Actinomycosis

Actinomycosis - not regarded as a contagious disease Infections usually appear - after trauma, surgery or previous infection Predisposing factors- tooth extraction, gingival surgery and oral infections Disruption of mucosal barrier main step in invasion
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Actinomycosis

May be found in osteoradionecrosis of jaws with serious systemic illness Peak incidence middle age Males more affected

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Clinical features
Classified anatomically Cervicofacial - In head and Abdominal Pulmonary

neck

Cervicofacial actinomycosis

According to Norman 2/3 of all cases M/C Site soft tissue in angle of jaw - as a swelling of mandible May simulate a pyogenic infection
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Clinical features

Lesion become indurated Eventually form one or more abscesses with draining sinuses

From medullary spaces of mandible to the skin Draining pus contain small yellow granules sulfur granules
Represent colonies of organisms
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Clinical features

Overlying skin purplish red, indurated and having a woody hard consistency Healing leads to a large fibrotic mass Over the time a great deal of scarring and disfigurement of skin Radiographically radiolucent lesion with irregular and ill-defined margins
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Clinical features

Less commonly - maxilla may be involved

Resulting in an actinomycotic osteomyelitis - may drain through gingiva Or may involve cranium, meninges or brain

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Histopathology

A granulomatous inflammatory response With central abscess formation In the center of abscesses - distinctive colonies of gram-positive organisms Appear to float - on the sea of neutrophils Associated with multinucleated giant cells and macrophages
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Histopathology

Individual colony round or lobulated Radiating from center of coloniesnumerous filaments with clubbed ends Ray fungus Surrounding tissue exhibit fibrosis

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Diagnosis

Dependent on identification of organism -

through

direct examination of exudate microscopic evaluation of tissue sections microbiologic culture of pathologic material

Methinamine silver stain demonstrate organism better

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Differential Diagnosis

Clinically -

Osteomyelitis

Infections

of soft tissue of neck- scrofula Staphylococcus infections - botryomycosis

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Treatment

Long-term, high-dose penicillin

For severe cases i v penicillin followed by oral penicillin Tetracycline Erythromycin

Drainage of abscesses and surgical excision of scar and sinus tracts

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Noma

Noma - - - to devour ( a spreading sore )

Also known as cancrum oris or gangrenous stomatitis A devastating disease of malnourished childrenEnwonwu Described as a severe scourge of mankind
Characterized by a destructive process of orofacial tissues

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Etiology and Pathogenesis

Considered a secondary complication of systemic disease Predisposing factors -

malnutrition
ANUG debilitating

conditions

trauma
other

oral mucosal ulcers systemic disease - pneumonia or sepsis

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Etiology and Pathogenesis

In person, whose systemic health significantly compromised Necrosis of oral tissue occurs Results from heavy infestation of Fusobacterium necrophorum An anaerobic bacteria and commensal in gut of herbivores
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Etiology and Pathogenesis

Secondary invasion of other microorganisms include-

Borrelia

vincentii Staphylococcus aureus Prevotella intermedia

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Clinical features

Initial lesion - a painful ulceration Usually of gingiva or buccal mucosa Spreads rapidly and involve surrounding tissue
Overlying skin inflammed, edematous and finally necrotic A line of demarcation - develops between healthy and dead tissue
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Clinical features

Large masses of tissue - may slough out leaving jaw exposed Leading to necrosis and sequestration of bone Slough cone shaped, apex superficially Underlying destruction more extensive Teeth in affected area - may become loose and may exfoliate
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Clinical features

Commencement of Gangrene blackening of skin Resulting in necrotic lesions - with oedema of face, fatid odour and profused salivation Penetration of organisms into cheek, lip, or palate may occur

Patient - suffer from secondary infection

May die from toxemia or pneumonia
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Treatment

Fluids electrolytes and general nutrition

Antibiotics Clindamycin Piperacillin Gentamicin

In extensive lesions debridement of necrotic tissue

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Bibliography

Oral pathology : clinical pathologic correlations : Regezi, Sciubba, Jordan ; 4th edition Shafer, Hine, Levy : Textbook of Oral Pathology ; editors - Rajendran, Shivapathasundharam 5th edition Oral and Maxillofacial Pathology : Neville, Damm , Allen, Bouquot ; 2nd edition
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Bibliography

Contemporary oral and maxillofacial pathology : Sapp, Eversole, Wysocki ; 2nd edition Robbins : Pathologic basis of disease; Kumar, Abbas, Fausto ; 7th edition Differential diagnosis of oral & maxillofacial lesions : Wood & Gauz ; 5th edition Burkets Oral Medicine : Greenberg, Glick, Ship ; 11th edition
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Bibliography

Cawsons : Essentials of oral pathology and oral medicine : Cawson, Odell ; 7th edition Color atlas of clinical oral pathology : Neville, Damm, White ; 2nd edition A manual on clinical surgery : S Das ; 5th edition Compilato D et al : Long standing oral ulcers : proposal for a new S-C-D Classification system ; J Oral Pathol Med (2009) 38 : 241115

Thank you
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