Leprosy - vikramuniv.ac.invikramuniv.ac.in/wp-content/uploads/M_Sc_II_-_Leprosy_PPT_-_Dr_S_… ·...

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1 Leprosy Hansen’s disease Prof. Shaleen Chandra

Transcript of Leprosy - vikramuniv.ac.invikramuniv.ac.in/wp-content/uploads/M_Sc_II_-_Leprosy_PPT_-_Dr_S_… ·...

Page 1: Leprosy - vikramuniv.ac.invikramuniv.ac.in/wp-content/uploads/M_Sc_II_-_Leprosy_PPT_-_Dr_S_… · Actinomycosis Prof. Shaleen Chandra. 13 Chronic granulomatous, suppurative and fibrosing

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Leprosy

Hansen’s disease

Prof. Shaleen Chandra

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Chronic granulomatous infection caused by Mycobacterium leprae

Mainly affects Skin

Peripheral nerves

Upper respiratory tract

Eyes

Testes

Seen mainly in developing countries 60% of total patients are in India

Bimodal age distribution First peak 10-14 years

Second peak 35-44 years

Prof. Shaleen Chandra

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Etiopathogenesis

Causitive organism M. leprae Obligate intracellular, acid fast bacillus

Only bacteria to infect peripheral nerves

Mode of infection nasal secretion

After infection bacteria is taken up by histiocytes in the skin and Schwann cells in the nerves

A component of the cell membrane of the bacteria (Lipoarabinomannan) induces immune suppression

Prof. Shaleen Chandra

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Clinical features

Classified into 4 types

Tuberculoid type (paucibacillary leprosy)

Lepromatous type (multibacillary leprosy)

Borderline type

Indeterminate type

Prof. Shaleen Chandra

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General features

Hypopigmented patches on the skin

Partial or total loss of cutaneous sensation

Thickening of nerves

Presence of acid fast bacilli in nasal smears

Prof. Shaleen Chandra

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Tuberculoid lesions

Single or multiple macular, erythematous

eruptions

Dermal and peripheral nerve trunk

involvement

Loss of sensation

Loss of sweating

Oral lesions are rare

Prof. Shaleen Chandra

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Lepromatous lesions

Early erythematous macules or papules

Progressive thickening of the skin

Formation of nodules on the skin

Sever disfigurement of the involved part

Facial paralysis

Loss of fingers

Plantar ulcers

“Leonine facies”

Prof. Shaleen Chandra

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8Prof. Shaleen Chandra

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Oral manifestations

Small tumor like masses (lepromas) develop on Tongue

Lips

Hard palate

Show tendency to break down and ulcerate

Gingival hyperplasia with loosening of teeth

Prof. Shaleen Chandra

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Histopathologic features

Granulomas containing epithelioid histiocytes and lymphocytes

Langhan’s giant cells

Sheets of vacoulated macrophages (lepra cells)

Prof. Shaleen Chandra

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Diagnosis

Demonstration of acid fast bacilli by modified Ziehl-Nielsen method in nasal smears or skin scrapings

Skin biopsy

Nerve biopsy

Culture Mouse footpad

Nine banded armadillo

ELISA

PCR

Prof. Shaleen Chandra

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Actinomycosis

Prof. Shaleen Chandra

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Chronic granulomatous, suppurative and fibrosing disease caused by Actinomyces species

Previously thought to be a fungal infection

Classified into

Cervicofacial

Abdominal

Pulmonary

Prof. Shaleen Chandra

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Etiopathogenesis

Causative organism Actinomyces species Anareobic, gram positive, non acid fast, branched, filamentous

bacteria

Normal saprophytic component of the oral cavity

Disruption of mucosal barrier causes invasion of bacteria

Initial acute inflammation followed by a chronic indolent phase

Associated with conditions that lead to immunosuppression

Prof. Shaleen Chandra

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Clinical features

Cervicofacial actinomycosis most common form (2/3rd of all cases)

Swelling and induration of the tissues

One or more abscesses that discharge through the skin surface liberating pus containing yellowish granules (“sulfur granules”)

Skin overlying the abscesses is purplish red, indurated (feel of wood), or fluctuant

Prof. Shaleen Chandra

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16Prof. Shaleen Chandra

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May extend to mandible or maxilla to cause actinomycotic osteomyelitis

May eventually involve cranium, meninges, or the brain

May occur in a localized area at the apex of teeth to simulate pulp related infections

Prof. Shaleen Chandra

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Abdominal actinomycosis

Extremely serious with high mortality rate

Fever, chills, nausea, vomiting, and intestinal

manifestation

Pulmonary actinomycosis

Fever and chills

Cough

Pleural pain

Prof. Shaleen Chandra

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Histopathologic features

Granulomas showing

central abscess

formation and containing

colonies of

microorganisms

Multinucleated giant cells

and macrophages

around the periphery

Prof. Shaleen Chandra

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Colonies appear to

float in a sea of

polymorphonuclear

leukocytes

Prof. Shaleen Chandra

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Individual colonies

Rounded or lobulated

Made up of meshwork of filaments that stains

with hematoxylin

Eosinophilia of peripheral club shaped ends

(“Splendor-Hepoelli phenomenon”)

Surrounded by a rim of inflammatory cells

Called as “Ray fungus”Prof. Shaleen Chandra

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Diagnosis

Demonstration of organisms in tissue

sections and smears

Culture

Prof. Shaleen Chandra

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Cat scratch disease

Cat scratch fever

Benign lymphoreteculosis

Benign nonbacterial regional lymphadenitis

Prof. Shaleen Chandra

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Causative organism Bartonella henselae (Rochalimaea henselae)

Gram negative bacillus

Previously thought to be a viral infection

Thought to arise after a traumatic break in the skin due to scratch or bite of a cat or other house hold animals

Prof. Shaleen Chandra

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Clinical features

Seen predominantly in children or young adults

Primary lesion Papule, pustule, or vesicle at

the site of injury

Prof. Shaleen Chandra

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Followed by regional lymphadenitis

Nodes are painful, several centimeters in

diameter

Overlying skin may be inflamed

May persist for one to six months

Prof. Shaleen Chandra

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Low grade fever

Headache

Chills

Abdiminal pain

Nonpruritic maculopalular rashes

Parotid swelling

Oculoglandular syndrome of Parinaud Conjunctival granuloma

Periauricular lymphadenopathy

Primary lesion adjacent to the eye

Prof. Shaleen Chandra

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Histopathologic features

Lymph nodes Reticuloendothelial hyperplasia

Destruction of node architecture

Focal granulomas

Supuration and necrosis

Epitheliod cells and multinucleated giant cells

Prof. Shaleen Chandra

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Stains for the organism

Warthin Starry silver stain

Brown-Hopps gram stain

Prof. Shaleen Chandra

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Diagnosis

Indirect immunofluorescent antibody assay

ELISA

Demonstration of antigen in the skin

Prof. Shaleen Chandra

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Noma

Cancrum oris

Gangrenous stomatitis

Prof. Shaleen Chandra

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Rapidly spreading, mutilating, gangrenous stomatitis that occurs usually in debilitated or nutritionally deficient persons

Seen chiefly in children and is more common in underdeveloped countries

Predisposing factors Undernourished

Debilitated due to infections Diphtheria

Dysentery

Measles

Blood dysacrasias

Prof. Shaleen Chandra

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Causative organism Borrelia vincentii

(Vincent’s organism)

Other organisms

Staphylococcus aurius

Streptococcus species

Prof. Shaleen Chandra

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Clinical features

Usually begins as a small ulcer on gingiva

Spreads and involves the surrounding tissues by gangrenous necrosis

Overlying skin becomes inflamed, edematous, and finally necrotic Sharp line of demarcation present between the

affected and nonaffected tissues

Prof. Shaleen Chandra

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Sloughing out of tissues with exposure of the jaws

Blackening of skin

Necrosis of subcutaneous fat pad and buccal pad of fat

Extremely foul odor

High temperature

Secondary infections

Toxemia

Prof. Shaleen Chandra

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