Myco Leprae

Mycobacterium Leprae : 

Mycobacterium Leprae Arif Talpur Physiotherapist

Introduction to Mycobactarium : 

Introduction to Mycobactarium Grow slowly Acid fast bacteria Have Mycolic acids Virulence factor  complex, lipid-rich cell wall Is responsible for many of the characteristic properties of the bacteria (e.g. acid fastness, slow growth, resistance to detergents, resistance to common antibacterial antibiotics and antigenecity)

Some Types of Mycobacterium Pathogenesis : 

Some Types of Mycobacterium Pathogenesis M. Tuberculosis: Pulmonary and disseminated TB M. Leprae: Leprosy or “Hansen’s disease” M. Bovis: GI T.B in humans (from Cow’s mild) M. Avium Intracellular complex: Pulmonary or disseminated infections and usually the mose common oppertunistic bacterial pathogen in AIDS. Patient has no specific symptoms M. Kansasii: TB like pulmonary infections M. Scrofulceum: Cervical Lymphadinitis M. Ulcerans: Subcutaneous nodules and ulcers

Mycobacterium Leprae : 

Mycobacterium Leprae Causes leprosy (also called Hansen’s disease) derived from a Greek term “lepi” meaning scales on a fish. Endemic disease found in armadillos Clinical manifestations of leprosy (similar to infection with M. tuberculosis) depend on the patient’s immune reaction to bacilli

Mycobacterium Leprae : 

Mycobacterium Leprae Tuberculoid leprosy Low infectivity Strong cellular immune response but a weak humoral antibody reponse Infected tissues typically have many lymphocytes and granulomas but relatively few bacilli Lepromatous leprosy Most infectious form Strong antibody response but a specific defect in their cellular response to M. leprae antigens An abundance of bacilli are typically observed in dermal macrophages and the Schwann cells of peripheral nerves

Epidemiology : 

Epidemiology Rare in Europe Countries, While common in Asia and Africa. Humans are primary reservoirs but also found in some animals E.g. Armadillo, Chimpanzee, and Mangabey Monkeys. Person-person spread by direct contact or inhalation of infectious aerosols.

Incubation Period : 

Incubation Period Ranges from few months to 20-50 years but the mean incubation period has been estimated to be 4-10 years. The incubation period of tuberculoid cases tend to be shorter than that for lepromatous cases Diagnostic: The diagnosis of leprosy is primarily clinical In 1 Ethiopian study, the following criteria have a sensitivity of 97% with a positive predictive value of 98% in diagnosing leprosy. Diagnosis will base on 1 or more of 3 signs: Hypopigmented or reddish patches with definite loss of sensation Thickened peripheral nerves Acid-fast bacilli on skin smears or biopsy material

Laboratory Diagnosis : 

Laboratory Diagnosis Immunologic tests: PGL-1: This is A specific serologic test based on the detection of antibodies to phenolic glycolipid-1 (PGL-1). This test has a sensitivity of 95% for the detection of lepromatous disease but only 30% for tuberculoid disease. Lymphocyte migration inhibition test (LMIT): Cell-mediated immunity to M leprae is absent in the lepromatous form of disease but present in the tuberculoid form of disease. Acid Fast Stained Bacilli Stained with carbol-fuschin and decolorized with acid-alcohol and counterstained

Treatment : 

Treatment Multi-Drug Treatment is recommended for prevention of resistance Main Therapeutics Dapsone Rifampin Clofazimine The length of treatment ranges from 6 months to 2 years. Patients are considered noninfectious within 1-2 weeks of treatment (usually after the first dose).

Prognosis : 

Prognosis Early diagnosis and effective antimicrobial treatment can arrest and even cure the disease. The prognosis also depends on the patient's access to therapy, the patient's compliance, and the early initiation of treatment. The prognosis depends on the stage of disease. BT usually involves rapid and severe nerve damage. Reversal reactions are uncommon with lepromatous disease; therefore, LL is a chronic state with long-term complications. Even with MDT, patients have long-term nerve damage and disability.