Leprosy

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Presentation Transcript

Leprosy????????? : 

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Slide 2: 

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Background : 

Background meaning scales on a fish. Chronic granulamatous disease. Caused by Mycobacterium leprae. Anaesthetic skin lesions and peripheral nerve thickening. Stigmatization.

History : 

History Appears in an Egyptian Papyrus document written around 1550 B.C. Around 600 B.C. In Europe, leprosy first appeared in the records of ancient Greece after the army of Alexander the Great. For a long time leprosy was thought to be a hereditary disease, a curse, or a punishment from God.

1873: : 

1873: Dr.Armauer Hansen of Norway was the first person to identify the germ that causes leprosy under a microscope.

early 20th century: : 

early 20th century: Until the late 1940s, leprosy doctors all over the world treated patients by injecting them with oil from the chaulmoogra nut.

1941: : 

1941: Promin, a sulfone drug, was introduced as a treatment for leprosy.

1950s: : 

1950s: Dapsone pills, pioneered by Dr. R.G. Cochrane at Carville, became the treatment of choice for leprosy. Dapsone worked wonderfully at first, but unfortunately, M. leprae eventually began developing dapsone resistance.

1981: : 

1981: The World Health Organization began recommending MDT, a combination of three drugs: dapsone, rifampicin, and clofazimine.

Now : : 

Now : MDT with a combination of dapsone, rifampicin, and clofazimine is still the best treatment for preventing nerve damage, deformity, disability and further transmission.

Nigerian Mask: A representation of leprosy disfigurement : 

Nigerian Mask: A representation of leprosy disfigurement

MicrobiologyMycobacterium leprae : 

MicrobiologyMycobacterium leprae An obligatory intracellular parasite. Slow grosing acid fast bacillus. It has a highly resistant cell wall composed of lipids,carbohydrates and protiens. Phenolic glycolipid M.leprae is species-specific. Humans and armadillo are only the natural hosts.

Microbiology : 

Microbiology Kingdom: BacteriaPhylum: ActinobacteriaOrder: ActinomycetalesSuborder: CorynebacterineaeFamily: MycobacteriaceaeGenus: MycobacteriumSpecies: M. leprae

Immune response in leprosy : 

Immune response in leprosy The T cells and macrophages of the cell-mediated immunity. Several stages: Phagocytosis by macrophages. Presentation of antigens in association with human leucocyte antigen (HLA) class II. Binding of antigen specific T cells via the a/bT-cell receptor. Activation of T cells and production of interleukin 2 (IL-2) and T cell proliferation. IL-2 activates CD4, CD8, natural killer and macrophages. Interferon-? is produced and activates bactericidal mechanisms.

Immune responce : 

Immune responce Mycobacterium persistence causes granuloma formation and cytokine release. Leprosy granuloma ( macrophages,epitheloid cells and giant cells with lymphocytes). The immunological and clinical effects vary, Tuberculoid disease the CMI active and contains infection, so that few bacilli found in tissues, Lepromatous leprosy, the CMI is poor and there is many bacilli in tissues and responses include both CD4 and CD8.

Clinical features : 

Clinical features The cardinal Signs are : Skin lesions. Anaesthesia. Thickened peripheral nerves.

Factors determining clinical expression after infection : 

Factors determining clinical expression after infection Susceptibility: About 90% of the population is not susceptible to infection. Children are more susceptible than adults. Host immunity: If the individual has good immunity, organisms are contained and TT disease occurs. In subjects with moderate immunity, a battle occurs and results in borderline types of leprosy. In persons with poor immunity, LL occurs. Incubation period.

Skin lesions : 

Skin lesions Macules, plaques,papules and nodules. Lepromatous leprosy: diffuse infilteration of the skin. Tuberculoid leprosy: hypopigmented lesions.

Nerve damage : 

Nerve damage 16-56% of patients. Only peripheral nervous system. Motor weakness of the muscles and regional sensory loss. Principal sites are ulnar(elbow), median(wrist), radial cutaneous, common peroneal (knee), posteriar tibial and sural nerves (ankle) and the facial nerve (zygomatic arch)

Leprosy Classification : 

Leprosy Classification Ridley-jopling classification uses clinical and microbiological features. A simpler WHO field classification merely divides patients is thoso with few lesions (paucibacillary)or thoso with more (multibacillary)

Intermediate leprosy : 

Intermediate leprosy an incubation period of 2-15 years, No symptoms , only positive lepromin test. one or more grouped hypopigmented non-pruritic macules. Rarely, reduction of sensitivity (hypo-aesthesia).

Slide 23: 

Indeterminate leprosy, small lesion on left upper arm. The lesion was initially treated for suspected mycosis.

Tuberculoid leprosy : 

Tuberculoid leprosy asymmetrical skin spots on not more than two parts of the body. sharply delineated, elevated border and central healing. depigmented (hypopigmentation on dark skin) or erythematous (on white skin). loss of sensitivity:First the sensitivity to temperature decreases, then the sense of touch, then pain and finally deep sensitivity. hair loss and the skin is dry. Paralysis is common. thickening of the nerves.

Tuberculoid leprosy : 

Tuberculoid leprosy

Borderline leprosy : 

Borderline leprosy Fall between the tuberculoid and lepromatous forms. Multiple skin lesions exist and nerve lesions are common.

Lepromatous leprosy : 

Lepromatous leprosy countless disseminated macules and/or skin nodules, No tendency to central healing is seen and there is no hypopigmentation, "copper colour" is present. no anaesthesia, but numbness develops in the hands and feet. diffuse skin thickening, chiefly of the ears, lips and forehead ("lion’s face" in LLp). Mexico, the diffuse variety of leprosy is sometimes called "pretty leprosy" because it tends to iron out the wrinkles in the skin, restoring a youthfull appearance to the patient.

Lepromatous leprosy : 

Lepromatous leprosy Infiltration of the mucosa leads to chronic rhinitis with epistaxis, septum perforation and destruction of the nasal cartilages. The tongue is thickened and there may be hoarseness. The upper incisors become loose and often drop out. Loss of the eyebrows (madarosis) and eyelashes. Testicular atrophy leads to gynaecomastia. The nerves are not severely thickened, but involvement of the nerves is extensive, generalised, gradual and symmetrical.

Lepromatous leprosy : 

Lepromatous leprosy

Other forms of leprosyBlindness : 

Other forms of leprosyBlindness occurs more often in tuberculoid than in lepromatous leprosy. Involvement of the facial nerve ?The eye can no longer close (lagophthalmia)?drying out of the cornea. Involvement of the trigeminal nerve leads to an insensitive cornea. Infiltration of the eye by countless bacilli with possible formation of lepromas (nodules full of bacteria). Iridocyclitis, Glaucoma.

Mutilations : 

Mutilations Paralysis with muscular atrophy and contractures. Loss of sensitivity leads to not noticing wounds or burns and maintaining postures which would otherwise be painful. Failure of autonomous nerves resulting in trophic skin disturbances. Untended wounds with secondary infections may lead to chronic ulceration. Direct destruction of tissues,

Diagnosis : 

Diagnosis General : based on clinical and microscopic examination. Acid fast bacilli in smear: Ziehl-Neelsen stain, scoring is performed on a logarithmic scale, Biopsy:If the smears are negative, a skin biopsy is performed, which must penetrate into the subcutaneous tissue.

Diagnosis : 

Diagnosis Lepromine: not used as a diagnostic Lymphocyte transformation tests have been developed. Serology:phenolic glycolipid-I antibody (PGL-I), ELISA or dipstick assay. PCR.

Management : 

Management Education. Chemotherapy :WHO proposed a multidrug regimen for treatment of leprosy. The 1st line antileprotic drugs : Rifampicin, Dapson, Clofazimine.

Chemotherapy : 

Chemotherapy Rifampicin: Potent bactericidal. Inhibits DNA dependent RNA polymerase. Well absorbed orally. Hepatotoxic. Dapsone:(diamino-diphenyl sulfone) Blocking folic acid synthesis. Weakly bactericidal. Well absorbed orally, long half life. Hemolytic anaemia, DDS syndrome (LN, hepatosplenomegaly, fever and hebatities)

Chemotherapy : 

Chemotherapy Clofazimine: Dye, weakly bactercidal action, anti-inflammatory action. Skin discoloration, icothyosis on shins and forearms. GIT upset.

WHO Multidrug therapy (MDT) : 

WHO Multidrug therapy (MDT) Since 1995, WHO has supplied MDT free of cost to leprosy patients in all endemic countries. According to the classification for field:

WHO Multidrug therapy (MDT) : 

WHO Multidrug therapy (MDT) Multibacillary (MB) leprosy : Rifampicin: 600 mg once a month Dapsone: 100 mg daily Clofazimine: 300 mg once a month and 50 mg daily Duration= 12 months. Paucibacillary (PB) leprosy : Rifampicin: 600 mg once a month Dapsone: 100 mg daily Duration= six months. Single Skin Lesion Paucibacillary leprosy : a single dose of: Rifampicin: 600 mg Ofloxacin: 400 mg Minocycline: 100 mg.

Leprosy reactions : 

Leprosy reactions Type 1 or reversal reactions Lesions caused by a change in the immunologic defence of the patient. may triggered by treatment. 30% in borderline leprosy. May cause damage to the body itself. Erythema, swelling, and tenderness of skin lesions and tenderness of peripheral nerves. Treated with 40mg/day prednisolone,reducing by 5mg/day every month.

Leprosy reactions : 

Leprosy reactions Type 2 reactions: Erythema nodosum leprosum reaction Immune complex deposition,T-cell dysregulation and overproduction of TNF. 20% of LL and 10%of BL patients. Systemic illness with fever and malaise, Widespread erythema nodosum,neurities, irities, arthrities, orchities, lymphoadenopathy and renal disease. Second year of chemotherapy. May relapse Prednisolone 60-80 mg/day. Thalidomide,

Epidemiology : 

Epidemiology Spread from human to human by droplets. There is long clinical incubation period 2-5 years for tuberculoid disease and 8-11 years for lepromatous disease. Patchy geographical distribution, 70 % in india. Steady global incidence 650 000 per year. In 2000, there were an estimated 1.3 million cases worldwide, mainly in India, Brazil and countries of South-East Asia and Africa.

Epidemiology : 

Epidemiology In 1985, 122 countries were identified in which Leprosy was a major public health concern; at the end of 2002 there were only 14. Approximately 775,000 new cases of Leprosy were detected during 2001. Cases of Leprosy are highly concentrated in six countries. Brazil, India, Mozambique, Myanmar, Nepal, and Madagascar accounted for 90% of the prevalence of the disease in 2002.

Epidemiology : 

Epidemiology At the beginning of 2008, the registered prevalence of leprosy globally was 212 802; the number of new cases detected during 2007 was 254525. Number of cases in Sudan in 2007 is 1 706.

The Global Prevalence of Leprosy by Region : 

The Global Prevalence of Leprosy by Region

Leprosy control programe : 

Leprosy control programe Case detection, treatment with WHO regimen and contact examination. Prevention of disability and population education about leprosy.

Care of Hands and feet : 

Care of Hands and feet Self-care training Inspect for injury,exercise, treat injury promptly. Hands, problems with heat,pressure and sharp objects. Feet, planter ulcer.(Clean wounds, bed rest, check the cause) Footwear.

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