BAGIAN ILMU KESEHATAN KULIT DAN KELAMIN FAKULTAS KEDOKTERAN UNIVERSITAS HASANUDDIN

DEPARTMENT OF DERMATOVENEROLOGY JUNE 2014MEDICAL FACULTYHASANUDDIN UNIVERSITYPRESENTING AS A TASK ON CLERKSHIPDEPARTMENT OF DERMATOVENEROLOGYMOSLEM UNIVERSITY OF INDONESIAMAKASSAR2014LEPROSY

BY :Muhlis Yusuf 110 207 0031Haerul Anwar110 209 0040Uni Insyirah110 2100107

ADVISOR :dr. Putu Marcelina

SUPERVISOR :dr.Widyawati Djamaluddin sp.KK

DEFINITION Leprosy (also known as Hansens Disease) is a chronic granulomatous infection caused by Mycobacterium Leprae.

The primary affinity is peripheral nerves, skin and mucosa of the upper respiratory system.

EPIDEMIOLOGY Incidence : Approximately 250,000-500,000 new cases yearly, worldwide. In 2012, 211,903 cases of leprosy were notified by World Health Organization (WHO) in 141 countries. More common in men than in women by a 2:1 ratio.

ETIOLOGY Mycobacterium LepraeNon-cultivable, Gram-positive, obligate intracellular, acid-facid bacillus

PATHOGENESIS

CLINICAL FINDINGSClinical features of Leprosy by Ridley and Jopling : Clinical findingsINDETERMINATETT(TUBERCULOID POLAR)BT (BORDERLINE TUBERCULOIDType of lesionsMacules, often hypopigmentedInfiltrated plaques, often hypopigmentedInfiltrated plaquesNumberOne or fewOne or few (up to 5) lesionsSingle, usually with satellite lesions, or more than 5 lesionsDistributionVariableLocalized, asymmetricAsymmetric SensationImpairedAbsentAbsentBacilli in skin lesions Usually non detectedNone detectedFew (1+), if any, detectedClinical findingsBB(MID BORDERLINE)BL (BORDERLINE LEPROMATOUS)

LL (POLAR LEPROMATOUS)Type of lesionsPlaques and domeshaped, punched-out lesions

Macules, papules, plaques, infiltrationMacules, papules, nodules, diffuse infiltrationNumberManyManyNumerousDistributionEvident asymmetryTendency to symmetrySymmetric SensationDiminishedDiminishedNot affectedBacilli in skin lesionsManyManyMany (globi)1. LESIONS Tuberculoid Polar

The primary skin lesion of TT :PlaqueCentral clearingBorder is sharply marginatedElevatedErythematousScalyDryHairlessHypopigmented

2. Borderline tuberculoid (BT)

One of several lesions of borderline tuberculoid leprosy (BT), which had an incompletely annular configuration with satellite papules.

less erythema, no evident scales, but the sharp margination, and the footprints of absent pinprick perception are well developed. 3. Borderline lepromatous (BL)

Multiple lesions (BL)

The annular lesions vary in size asymmetrically distributed.

Poorly defined papular and nodular lesions are roughly symmetric.

Impaired sensation was present in most lesions.4. Lepromatous Leprosy

The skin between such nodules is diffusely infiltrated.

WHO CLASSIFICATION PBMBSkin lesion ( flat macule, papule, nodule )1-5 lesionsHypopigmentation/ erythema Unsymmetrical distributionClear lost of sensation> 5 lesionsThe distribution is more symmetricalUnclear lost of sensation.

Nerve damage ( caused lost of sensation/ weakness of the muscles that being innervated by damaged nerves)Only 1 peripheral nerve.A lot of peripheral nerves

DIAGNOSTICDiagnosis can be made based on the clinical feature, bacterioscopic and histopathology. There are 3 Cardinal Signs in leprosy :Hyposthesia or anesthesia of skin lesionThickened and tender peripheral nerveAcid-fast bacilli in slit skin smears (SSS) or BTA (+).If one of the cardinal sign is founded, then the patient is diagnosted with leprosy.

SUPPORTING EXAMINATION1. BACTERIOSCOPIC Preparations were made from skin scrapings were stained with acid-fast bacilli "Ziehl-Neelsen staining. Bacterioscopic negative in a patient does not mean the person does not contain basil M. Leprae or leprosy.

If someone has a Cellular Immunity System is high then the macrophages capable of phagocytizing M. leprae.In patients who have a low immunity, macrophages cannot phagocyte M. Leprae and even become the breeding ground.It is called Virchow cells or leprosy cells.

2. HISTOPATHOLOGIC

LEPROMATOUS LEPROSY TUBERCULOID

GranulomaShowing tuberculoid granulomas around nerve and skin. Around the granulomas there is a dense lymphocytic infi ltrate.showing thin epidermis, a clear subepidermal zone and a dense, uniform macrophage infiltrate inthe dermis. Examination is based on the formation of specific antibodies against the body of anti-phenolic glicolipid-1 M.Leprae (GPL-1).

The test is to aid in the diagnosis of leprosy is doubtful if clinical signs and bacterioscopic test is unclear3. SEROLOGIC TEST17DIFFERENTIAL DIAGNOSIS

PITYRIASIS VERSIKOLORis a common fungal infection of the skinScaly patches of fine white to dark brown body mainly include and itch. VITILIGOMacula depigmentation Round or oval with firm boundaries without other changes in epidermal

PITYRIASIS ALBA

Macular pink or according to skin color with smooth scaling

LEPROSY REACTIONSFifty percent of patients will experience a reaction after the institution of multidrug- therapy.Reactional states of leprosy are distinctive, tissue destructive,inflammatory processes, putatively immunologically driven, that greatly increase the morbidity of the disease.Reactional states are divided into two forms, called type 1 and type 2 reactionsType I Reactions (Reversal Reactions)Type 2 Reactions (Erythema Nodosum Leprosum)

TYPE 1- REVERSAL REACTION (UPGRADING)TYPE 2-ERYTHEMA NODUSUM LEPROSUMCLINICAL CHARACTERISTIC

Type 1 reactions occur in borderline disease and are characterized by acute neuritis and/or acutely inflamed skin lesions.Acute nerve pain or tenderness (neuritis) and loss of function.Existing skin lesions become erythematous or oedematous and may desquamate or rarely ulcerate.1. Type 2 (ENL) reactions occur in patients with multibacillarydisease (LL and BL).2. fever, anorexia, andMalaise3. ENL manifests most commonly as painful red nodules on the face and extensor surfaces of limbs.4.Iridocyclitis,orchitis/epididymitis

TREATMENTThere are five main principles of treatment:Stop the infection with chemotherapyTreat reactions and reduce the risk of nerve damageEducate the patient to cope with existing nerve damage, in particular anesthesiaTreat the complications of nerve damageRehabilitate the patient socially and psychologically

WHO MDT REGIMENT

PROGNOSISWith the combination of drugs, treatment becomes simpler and shorter, and the better the prognosis. If there contracture and chronic ulcers, the prognosis is not goodREFERENSIKosasih A, Wisnu I M, Sjamsoe-Daili E. Kusta In: Djuanda A, Hamzah M, Aisah S editors. Ilmu Penyakit Kulit Dan Kelamin.5th Ed.Jakarta: Balai Penerbit FKUI. p. 73-88.Lockwood DNJ. Leprosy, In: Burns T, Breathnach S, Cox N, Griffiths C editors. Rooks Textbook of Dermatology. 8th Ed.Willey-Blackwell;2010. p. 32.1-32.19Girao R J dkk. Leprosy treatment dropout: a systematic review.Int J Med Abbreviation. 2013.6 :34.Ramos, Marcia, Castro M. Mycobacterial Infections.In: Bolognia JL, Jorizzo JL, Rapini RP, editors. Bolognia Dermatology. 2nd ed. USA: Mosby Elsevier; 2008. Chapter 74. James DW, Berger GT, Elston MD. Hansens Disease. In: Andrews Disease of The Skin. 3rd Ed. Elsvier Saunders;2006. p. 343-352.

Lee Delpine J, Rea Thomas H..Leprosy, In: Wolff K, Goldsmith AL, Katz IS, Gilchrest AB, Paller SA, Leffel JD editors. Fitzpatricks Dermatology In General Medecine. 8th Ed. New York: Mc Grew Hill Medical;2012.p. 3206-3219..Romero, E. Leprosy : An Overview of Pathophysiology. Rev Art Med Karnataka. Vol 2012. Article ID 181089.Ramos, Jose M. Gender differential on characteristics and outcome of leprosy patients admitted to a long-term carerural hospital in South-Eastern Ethiopia. Int J Equ In Health.2012.11:56Mathur, Ghimire, Shrestha. Clinicohistopathological Correlation in Leprosy. Kathamdu Univ Medical J 2011;36(4):248-51.Naik, Vaishali , Usha B. Evaluation of significance of skin smears in leprosy for diagnosis, follow-up, assessment of treatment outcome and relapse. Asiatic J Biotech Res.2011:2(5)547-552THANK YOU