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Mycobacteria
- Atypical mycobacteria include nontuberculous mycobacteria found in the environment that can cause disease in humans under certain conditions. - Mycobacterium leprae causes leprosy (Hansen's disease), with a spectrum of clinical manifestations depending on immune response from tuberculoid to lepromatous leprosy. - Diagnosis involves skin smears and biopsy showing acid-fast bacilli. Treatment is multidrug therapy including dapsone, rifampin, and clofazimine.
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Mycobacteria
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- 3. Atypical mycobacteria • Nontuberculousmycobacteria (NTM) • occur as saprophytes of soil and water • No person to person transmission • Usually acquired in presence of immunodeficiency
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- 7. Photochromogens • M. kansasii •Pulmonary disease • Mycobacterium marinum, • Swimming pool granuloma • Fish tank granuloma • development of superficial granulomatous lesions in the skin • Mycobacterium simiae
- 8. Scotochromogens • Mycobacterium scrofulaceum, •lymphadenopathy • Mycobacterium gordonae, and • Mycobacterium szulga
- 9. Nonphotochromogens • These include •M. avium complex (MAC) • MAC includes mycobacterium intracellulare (battey bacillus)& mycobacterium avium • Highly resistant to ATT • Lymphadenopathy • Mycobacterium xenopi, and • Mycobacterium ulcerans
- 10. Rapid Growers • Amongthis group itself involve • photochromogens, • M phlei M smegmatis • scotochromogens, or • nonphotochromogens species • M fortuitum • M chelonie Post trauma/injection abscess
- 11. M ulcerans • burulis disease • Only mycobacteria producing toxin
- 12. • Saprophytic mycobacteriaare non pathogenic • M phlei • M smegmatis • M gordonae • M paratuberculosis
- 13. Pulmonary disease • MACis the commonest cause of pulmonary disease d/t non tuberculous mycobacteria in developed countries • M kansasii produces pulmonary ds indistinguishable from TB
- 14. Fish tank granuloma •M marinum
- 15. Disseminated ds • InAIDS related • Caused by MAC
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- 17. Mycobacterium leprae • Acidfast (5 % H2SO4) • Less acid fast than M tuberculosis (20 % H2S04)
- 18. M leprae • Lessacid fast than M tuberculae (hence 5 % H2SO4 or 1% HCl is used) • First bacillus to be associated with human disease • Modified fite stain • In tissue sections
- 20. • Phenolic glycolipoprotein1 plays important role in pathogenesis • LAM B1 external to cell wall in serodiagnosis
- 21. • Lepra bacillihas affinity for RE cells & schwann cells • Prefer cooler areas of body • Skin / peripheral N / anterior chamber of eye /URT/ testis • sparing warmer areas • Axila groin scalp midline of back
- 22. • Schwaan cellsare first cell to be involved in leprosy
- 23. • Virchows cellsare undifferentiated macrophages • Abundant in lepromatous leprosy
- 25. • Obligate intracellularbacillus • Can remain viable 1- 7 days • propagation is limited to • Armadillo • Also used for production of lepromin A • mouse foot pad • Sensitivity of antileprotic drug • nude mice • Generation time 12-13 days
- 26. Cardinal signs ofleprosy • Hypopigmented or erythematous skin lesions with definite loss of sensation • Involvement of peripheral nerves definite thickening • Skin smear AFB
- 27. • Highly infectiouswith low pathogenicity • Attack rate among house hold contacts is 4.4 -12 % • Clinical infection Source of infection • Active leprosy • Multibacillary >>sub • Portal of entry skin and respiratory tract • Chief mode of exit nasal mucosa of untreated LL patients • Modes of transmiision • Droplets >>contact>breast milk>transplacental>insect vectors
- 28. • The RidleyJopling classification • Indeterminate • Tuberculoid • Borderline: • borderline-tuberculoid, • borderline-borderline, • borderline-lepromatous • Lepromatous
- 29. Indian classification (byindian leprosy association)
- 30. • In TTis the most common form of leprosy
- 31. WHO Classification treatment Paucibacillary • 1-5 lesion • No nerve or only one nerve • Skin smears –ve at all sites • BI <2 • Involves IL BT TT Multibacillary • > 6 lesions • > 1 nerve irrespective of skin lesions • Skin smears + at all sites • BI > 2 • Involves BB BL LL
- 33. Diagnosis • Skin smears •7 in number • 4 from skin lesion • 2 from ear lobes • 1 from nasal swb • Nerve biopsy is taken from sural nerve
- 36. Morphological index responseto Rx/drug resistance/ disease activity/ • Percentage of solid staining bacilli in a stained smear to total no of bacilli Live bacilli solid stained Dead bacilli Fragmented
- 37. Bacteriological index density of bacilli in stained smear
- 38. • Bacilli areabsent in lungs , ovaries and CNS • Most common cranial nerve to get involve is VII • Goll & burdech tract proprioception • Not involved in leprosy • Other organs involved in leprosy are • Eyes • Iritis • Corneal beading • Testes • Muscles • Myopathy , wasting
- 39. Mouse foot padculture • Detect drug resistance • Evaluating potency of antileprosy treatment • Detecting viability of bacilli during Rx
- 40. Histamine test • Veryreliable method to detect at an early stage • Peripheral N damage d/t leprosy flare response is lost if peripheral N is damaged
- 41. Lepromin test to detect CMI / Test for prognosis Early or Fernandez reaction • after 48 hours of injection • Erythema & induration >10 mm is +ve • Delayed hypersensitivity reaction to soluble constituents Late or Mitsuda reaction • After 3 weeks • Nodule > 5 mm is +ve • indicates CMI to bacillary component of Ag of lepra bacilli Mitsuda lepromin / Dharmendra lepromin antigen intradermally BCG vaccination can covert it from negative to positive
- 42. Uses of lepromintest • To classify lesions into tuberculoid or lepromatous • To assess prognosis • If positive good prognosis • Not used for diagnosis • In the first 6 mth of life most children are lepromin negative
- 43. Nerve commonly involved •Ulnar N elbow (posteriorly) • Median N at wrist • Dorsal cutaneous N of ulnar @ wrist • Common peroneal around fibular neck • Superficial peroneal in front of ankle • Posterior tibial below medial malleoli
- 44. Great auricular Ninvolvement
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- 49. Indeterminate leprosy • Bacteriologicallynegative • One or two vague hypopigmented macules • Definite sensory impairement
- 50. Tuberculoid leprosy (mostcommon type of leprosy in INDIA and Africa • CMI ↑↑ • Lepromin +ve • Bacillary load ↓↓ • Skin lesions anaesthetic early • One or few sharply defined annular asymmetric macules or plaques with a tendency towards central clearing , elevated border
- 51. Tuberculoid leprosy histopathology •Noncaseating granuloma with epitheliod and giant cells
- 52. Grenz zone isinvolved in TL
- 53. Borderline Tuberculoid • SATellitelesions • Nerve Abscess (mainly ulnar nerve abscess) • Rx with I & D • SANTA BanTa SATellite lesions
- 54. Borderline leprosy (BL) •Inverted saucer shaped ulcers • All kinds of bizzare lesions in single patient distributed asymmetrically • Epitheliod cells +
- 55. Lepromatous leprosy • CMI↓↓ • lepromin test negative • Bacillary load ↑↑ • Temperature and pain lost first >> Hypoaesthesia is a late sign • Ulnar N most common >>low median >posterior tibial> • Radial N is involved last serious • Acral,distal,symmetric anaesthesia common • M.leprae PGL-1(phenolic glycolipid) ab +
- 56. Lion with outteeth • Leonine facies • Atrophy of anterior nasal spine collapse of nose • Alveolar resorption Loosening of teeth • Diffuse dermal infiltration of face • Loss of eye brow
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- 59. Lepromatous leprosy • Clearsub epidermal free grenz zone • Virchow or lepra cells • Foamy macrophages laden with acid fast bacilli • Intracellular bacilli in spheroidal masses (globi) • Epitheliod and giant cells are not seen (absence of CMI)
- 61. Globi in LL/AFB forming spherical cluster
- 62. Lucio phenomenon • Onlower extremities • High parasitism in endothelial cell endothelial proliferation thrombus formation • Characterised by arteritis and ulcers on legs is limited to patients with diffuse non nodular lepromatous leprosy • Untreated patients • Mexico and carribean only
- 63. Histoid leprosy • Typeof LL • Shiny cutaneous and subcutaneous nodules • Caused by drug resistant lepra bacilli • In b/w skin appears normal
- 64. • Pure neuritic(indian classification) • Asymmetric nerve involvement with no skin lesion and usually of tuberculoid origin • Painless trophic ulcers
- 65. Treatment • Chaulmoogra oil •First effective antileprosy Rx • Form Myanmar • MDT is used since 1982 • Not C/I in HIV infected patients and is safe in pregnancy • Rifampicin highly bactericidal and most effective against M leprae • Dapsone is bacteriostatic
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- 67. • Paucibacillary • Undersurveillance for atleast 2years • Multibacillary • Under surveillance for 5vyeras
- 68. Treatment of singlelesion leprosy • ROM regimen • Rmp • Ofloxacin • Minocycline • ROM -6 (Monthly for 6 months) - Paucibacillary • ROM -12 (Monthly for 12 months) – Multibacillary
- 69. Follow up Annually for2 years Annually for 5 years
- 70. • Rifampicin isthe most active (bactericidal & rapidly acting) for leprosy
- 71. • In pureneuritic type • Corticosteroids are also given along with multi drug therapy
- 72. Lepra reactions Type 1(reversal) • Borderline type of leprosy (BT,BB,BL) • In 1st month or yr after Rx initiation • Sudden increase in effective CMI in reponse to rapid killing of bacilli • Type IV • a/c tenderness and swelling at the site of skin or nerve lesion • a/c neuritis wrist drop • Rx • Mild NSAIDS • Severe high dose glucocorticoid Type 2 (erythema nodosum leprosum) • In lepromatoum leprosy and also in BL • With in 2 years of RX • d/t activation of t helper cells • Type III HS (arthus reaction) • Tender inflamed subcutaneous nodules • Rx • Glucocorticoids • Thalidomide (DOC) • Cloazimine • Aspirin
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- 75. Erythema nodosum leprosum •Thalidomide DOC
- 76. Downgrading reaction • Inuntreated patients and in 3rd trimester of pregnancy • Clinically mimic reversal reaction
- 77. Dapsone • Bacteriostatic • 1-2mg/kg • Half life >24 hours • s/e • Hemolutic anemia • Methaemoglobinemia • c./I • Hb <7 • G6PD deficiency
- 78. clofazimine • Dye withleprostatic and anti inflammatory property • s/e • Reddish brown discolourarion of exposed parts • Hair and body secretions • Dry & itchy skin
- 79. New drugs • Rifapentine •Most effective