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Mycobacterium leprae PowerPoint Presentation

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Description : Check out this medical PowerPoint presentation titled "Mycobacterium leprae" by Dr Puneet Kumar Gupta.

This medical PowerPoint presentation talks about mycobacterium leprae which is a type of bacteria that causes leprosy, also known as Hansens disease. It is an intracellular pathogen, which means that it lives inside cells of the immune system and can evade the bodys immune defenses.

Leprosy is a chronic infectious disease that primarily affects the skin, peripheral nerves, and mucous membranes of the upper respiratory tract. It can cause disfiguring skin lesions, nerve damage, and blindness if left untreated.

Mycobacterium leprae is slow-growing and has a unique cell wall structure that makes it difficult to culture in the laboratory. It is primarily transmitted through prolonged close contact with an infected person, although the exact mode of transmission is still not fully understood.

Fortunately, leprosy is curable with multidrug therapy, a combination of antibiotics that must be taken for several months to eliminate the bacteria. Early detection and treatment can prevent the development of complications and disability associated with the disease.

Tags : Mycobacterium leprae, leprosy, Hansens disease, Dermatology, Dermatology PowerPoint presentation

Published on : Mar 31, 2023 | Views : 1042 | Downloads : 2

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Mycobacterium leprae For MBBS (05-12-2017) By: Dr Puneet Kumar Gupta Assistant Professor, Microbiology 1
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Disease of Historical importance World's oldest recorded disease Stigmatized disease Gerhard Henrick Armauer Hansen (1873-Norway) 3
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The Bacterium 4
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Morphology :Straight rods. 1 - 8 x 0.2 - 0.5µmSingle / groups. Intracellular.Acid fast bacilli with 5% H2 SO4.As agglomerates, bacilli being bound together by a lipid like substance (Glia) – called GLOBI Armauer Hansen in 1868 5
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Parallel rows of bacilli in globi: CIGAR BUNDLE appearance – as in tissue section clumps of bacilli resemble cigarette ends GLOBI is seen in Virchow’s lepra cell or foamy cells (Large undifferentiated histiocytes) 6
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No artificial media / tissue culture available.Generation time: 12-13 daysMouse : Intradermally into Foot pads. Granulomatous lesions in 1- 6 months.Intact CMI : Limited replication.↓CMI : Generalized leprosy.Armadillo: Highly susceptible. Chimpanzees, Mangabey monkey. Cultivation 10
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Important Experimental Animal 11
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Most Important experimentalAnimal 12
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Adaptation in artificial media: ICRC, Bombay 1962. – AFB from leprosy patients were isolated in human fetal spinal ganglion cell culture= ICRC bacillus (LJ adapted) 13
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Warm humid environment 9 - 16 days. 46 days in Moist soil 2 hours in Sunlight 30 minutes U V rays Resistance 14
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LEPROSY 15
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Lepers are outcasts ? 16
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Exclusively Human disease & only source is a patientExact mode of transmission – not clear; probably via -Nasal secretions. (One nasal blow may release 8 x 108 bacilli)Entry via – respiratory tract or skinAsymptomatic infection not uncommon Epidemiology 17
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Not very communicable – 5% spouses suffer Incubation period is 3-5 years. (2to 40 yrs)Continuous close contact.Rare in children < 5 Years. Confined to underdeveloped tropical countries & southern hemisphere currently India Prevalence 0.68/10000 population in 2012 32 states/UT achieved target of elimination Chhattisgarh, Dadar & Nagar Haveli Prevalence >1/10000 18
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Annual Report 2015-16 from NLEP GOI (as on 1st April 2016) >1/10,000 Population (163 District out of 669) Total cases 86028 19
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Annual Report 2015-16 from NLEP GOI >1-Chattisgarh, Dadar Nagar Haveli, Delhi, Odisha, Chandigarh, Lakshadeep 20
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Classification of leprosy 21
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IV. WHO classification Based on bacterial load. 1. Paucibacillary I, T T, BT 2. Multibacillary BB, BL, LL. 22
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Clinically……………… 23
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Slow, chronic & progressive Granulomatous disease of Peripheral nerves,skin and Muco- cutaneous tissues (Nasal mucosa). It affects Skin, liver, testes ,bones. Leprosy 24
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Source : Nasal or Skin discharges from lesion. Portal of entry: Damaged skin -Inoculation. Nasal mucosa- Inhalation Pathogenesis 25
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Infiltration of bacilli in cooler body tissues like skin (nose, outer ear), testicles & superficial nerve endings→ (maculae) visible lesions. A non-specific or Indeterminate skin lesion is the First sign of disease. Schwann cell is target cell. Neuritis leads to Anesthesia & muscle paralysis. Pathogenesis contd….: 26
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Tuberculoid leprosy Lesions are large maculae on skin, superficial nerve endings. CMI is intact. Low infectivity Lepromatous leprosy Extensive maculae, papules or nodules; Extensive destruction of skin. CMI severely depressed High infectivity Regression Progression 27
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Generalized form with decreased CMI. “Lepromata” : Granulation tissue with plenty of vacuolated cells, from MN cells to Lepra cells. Ulceration Secondary infection & Mutilation of limbs. Skin lesions are extensive and bilaterally symmetrical. Lepromatous leprosy 28
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Sites: Commonly face, ear lobules, hands and feet. Symmetrical thickening of peripheral nerves & anesthesia Bacilli invade mucosa of Nose , Mouth and Respiratory tract → shed in secretions. Bacteremia present. RE system, Eyes, testes, kidney & bone involved 29
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Lepromin test is negative. CD8+ cells in plenty Antibodies / other Abs are seen (exaggerated humoral response) BFP= syphilis tests (STS) Infective form….more than other types – poor prognosis Lateral part of eyebrows are lost 30
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Lepromatous leprosy Lepromatous leprosy 31
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Complications : Acute exacerbations. Testicular atrophy, Gynaecomastia Diffuse thickening of face – (Leonine face). Necrosis of nasal bones, cartilage with loss of upper incisors. Corneal ulcers. 32
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Localized form in individuals with intact CMI.Skin lesions : Few hypo or hyper pigmented macular patches (anesthetic)Sharply demarcatedSeen on Face, trunk and limbs.Bacilli are scanty or absent. (paucibacillary)Infectivity is low. Tuberculoid leprosy 34
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Diagnosed with Clinical + Histological evidences.Nerves : Peripheral Nerves to bigger nerves involved.Thickened, hard and tender.Deformities in hand & feet Lepromin test is positive.Auto antibodies production is rare. CD4+ cells. 35
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Good prognosis 37
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Peripheral neuropathy. V & VII th cranial nerve : Corneal ulcers. Ulnar nerve : Claw hand. Lateral popliteal nerve : Foot drop. Posterior tibial & medial nerve: Trophic ulcers, Loss of digits. Complications 40
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Dimorphous/Borderline type : Lesions resembles both LL (bacteriology) & T T (Clinically). May turn to complete LL or T T type (depending on host resistance or chemo therpay) 41
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Borderline tuberculoid leprosy Borderline lepromatous Lesions are Slightly asymmetrical with or without anesthesia. Cirular, sharply demarcated lesions. Raised erythematous border with anesthesia. 43
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Indeterminate type: Early stages : Maculoanesthetic patches. Lesions are not like T T or LL Spontaneous healing. Turn to either LL or T T type. 44
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Indeterminate type 45
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Immunity : High degree of innate immunity. Induces both AMI & CMI. Antibodies are not effective. LL Pts : Large number of CD8 cells. TT Pts : Predominantly CD4 cells.Genetic relation: T T : HLA – DR2 L L : HLA MTI, DQ1 48
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Birth mark T. versicolor T.corporis Differential diagnosis of Leprosy 49
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Lichen planus Vitiligo Pytiriasis alba 50
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Fixed drug eruption Psoriasis Dermal leishmanoid Lupus vulgaris 51
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Sarcoidosis Kaposi’s sarcoma 52
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Lepra reactions:Acute inflammation of the disease due to Immunological reactions against bacilli.Medical emergency. Two types: 53
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Jopling type 1: CMI response against bacilli Synonym: Reversal reaction Occurrence: Spontaneous, Chemotherapy Seen in BT, BB, BL. Due to influx of lymphocytes into lesions changed to T T morphology Lesions are painful, tender Erythema and swelling. 54
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Jopling type 2 Synonym: Erythema Nodosum Leprosum (ENL) Due to vasculitis (Antigen – Antibody complex). Seen in LL & BL few months after starting the chemotherapy 57
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Characterised by: Tender, inflamed subcutaneous nodules Fever Lymphadenopathy, arthralgia. (Ag from dead bacilli – Arthus type response) IgG, neutrophil & C in lesions 58
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Lucio phenomenon: Cutaneous hemorrhagic infarct in LL cases. 60
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Main features of lepra reactions. Type 1 Type 2 1.Immunological basis : CMI Vasculitis with Ag – Ab deposits. 2. Type of patient : BT,BB, BL BL, LL. 3. Systemic disturbances : Not seen . Present. 4. Hematological Not present Present disturbances: 5. T Helper response TH1 predominate TH2 6. Proteinuria Not seen. Frequently present. 6.Relation to therapy Seen in first Rare in first 6 months. 6 months 61
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Lab diagnosis Microscopy Culture Serology (Ab detection) Molecular method Demonstration of CMI 62
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Lab diagnosis Bacteriological Diagnosis is easy in LL types but difficult in TT. Specimen: smears collected from Nasal mucosa, Lesion, Skin (slit smear of ear lobule, forehead, Cheek, Chin, buttock) = 5-6 sites Sample from thickened nerve or Nodular lesion are collected for H/P 63
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Nasal mucosa (nasal Blow or Nasal Scrapping) A blunt, narrow scalpel is introduced into the nose and internal septum Scraped sufficiently to remove a piece of mucous membrane, which is transferred to a slide and teased out into a uniform smear. 64
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Slit Skin smear: Taken from Edge of lesion Skin is pinched up tight to minimize bleeding a cut about 5 mm long made with a scalpel, deep enough to get into the infiltrated layers. Wipe off blood or lymph that may have exuded Scalpel blade is turned transversely to scrape the sides and bottom of the cut for tissue pulp smeared uniformly on a slide. About 5-6 different areas of the skin buttocks, forehead, chin, cheek and ears. Collection of skin smears 65
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Smears are stained by the Ziehl-Neelsen technique using 5% sulphuric acid. Biopsy Nodular lesions and thickened nerves, and lymph node puncture may be necessary 66
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Z-N staining: Decolorizer =5% H2SO4 Acid fast bacilli within the undifferentiated macrophages: L L Live bacilli : Solid, uniformly stained, parallel side, rounded ends, length five times width Dead bacilli :Fragmented and granular 67
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Grading 1-10 / 100 oil immersion fields : 1+ 1 -10/10 “ “ : 2+ 1 -10 / 1 “ “ : 3+ 10-100/ field : 4+ 100-1000 /field : 5+ >1000, clumps/globi in every field: 6+ 69
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Load of bacilli: 1. Bacteriological index (BI): total no of pluses (+) scored in all the smears divided by no of smears; Minimum 4 skin lesion, nasal scrap & both ear lobule must 2. Morphological index(% of uniformly stained bacilli) = Uniformly stained bacilli X 100 Total number of bacilli (= SFGB/Total x100) 70
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Skin & Nerve biopsy. 71
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Lymphohistiocytic infiltrate surrounding a nerve fiber 72
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Culture: No Culture media Animal inoculation: Mouse foot pad: 9 banded Armadillo Advantage: 10 times more sensitive Drug resistance detection Evaluation of drug potency Check Viability Disadvantage: Time consuming (6-9 months) Ethical issue: animals used 74
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LESIONS DEVELOPING FOLLOWING INOCULATION IN FOOT PAD OF MICE 75
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Serological test : Antibodies against phenolic glycolipid Ag -ELISA (Antibody against PGL-I) Sensitivity LL: 95% TT: 60% -FLA-Abs-Fluorescent leprosy Ab Absorption Test Detect specific Ab irrespective of duration and stage of disease 92% sensitive & 100% specific Molecular diagnosis: 76
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Detection of CMI (Lepromin test) : Skin test for delayed hypersensitivity to lepra bacilli. Antigens: 1. Boiled extract of Lepromatous tissue in isotonic saline. 2. Leprosins : Ultrasonicates of tissue – free bacilli from lesions. a). leprosins – H b). leprosins – A 3.Dharmender’s antigen. 4.Soluble antigen. 77
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Two types of reactions on Intradermal injection1. Early reaction of Fernandez : Erythema & Induration within 1 - 2 days Remains for 3 - 5 days. Poorly defined with little significance.2. Late reaction of Mistuda. Erythematous, indurated , granulomatous nodular skin lesion. Seen in 1 - 2 weeks reaches to peak in 4 weeks. Indicates CMI status in leprosy patients. 78
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Significance : 1. To classify the lesions of leprosy. T T ( + ) L L ( - ) Borderline (+/-)2. To assess prognosis & response to treatment. Positive: Good prognosis Negative: Bad prognosis3. To assess the resistance of individuals to leprosy.4. Identify candidate lepra bacilli 79
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Treatment : Until 1982 : Dapsone only. Now MDT being given because of resistant strains. WHO recommended Multi drug therapy Paucibacillary case. (I, TT, BT) Rifampicin 600 mg/ month annually Dapsone 100mg / day till 2year 80
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Multi bacillary case: (BB, BL, LL) Rifampicin 600mg / month Dapsone 100 mg / day annually Clofazimine 300 mg / month till 5 years + 50 mg / day (Ethionamide/prothionamide) 81
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Vaccines: BCG, MAI complex vaccine. Mycobacterium w vaccine. Chemoprophylaxis: Dapsone ; in TT variety only 82
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THANKS 83