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ATYPICAL MYCOBACTERIA
Dr. Aashish Thakur
Intern, Dept. of Dermatology
Date : 26/06/2077
Introduction
 Known by several terms-
 Non tuberculous mycobacteria (NTM)
 Atypical mycobacteria
 Mycobacteria other than tuberculosis ( MOTT )
Environmental mycobacteria –
 refer to mycobacteria other than Mycobacterium
tuberculosis,its close relatives (M. bovis, M. caprae, M.
africanum), and M. leprae.
 The number of known species currently exceeds 150.
NTM are highly adaptable and can adapt hostile
environments.
Epidemiology
 The true international epidemiology of infections due to NTM
is hard to determine.
 NTM are ubiquitous in soil and water.
 Most NTM cause disease in humans only rarely.
Epidemiology
 Human-to-human transmission of NTM is not known.
 Disseminated disease denotes significant immune dysfunction
(e.g., advanced HIV infection)
 Pulmonary disease
 more common
 highly associated with pulmonary epithelial defects.
Pathophysiology
 Normal host defenses against these organisms are strong.
 Healthy individuals in whom significant disease develops are
highly likely to have specific susceptibility factors that permit
NTM to become established, multiply, and cause disease.
HIV infection
CD4+ T lymphocytopenia.
Potent inhibitors of tumor necrosis factor (TNF), such as
infliximab, adalimumab, and etanercept
RUNYON CLASSIFICATION
GROUP PIGMENT GROWTH ORGANISMS
Group 1 Photochromogens M.Marinum
M.Kansassi
M.simiae
Group 2 Scotochromogens M.Scrofulaceum
M.szulgai
Group 3 Non-chromogens M.avium-intracellulare
M.ulcerans
Group 4 Rapidly-growing M.Fortuitum
M.Chelonae
M.abscessus
Group I - Photochromogens
 Non pigmented in the dark
 When young culture exposed to light for 1 hour and
reincubated for about 24-48 hours, a yellow orange pigment
is produced
 Slow growing are
 M kansasii
 M.marinum
 M simiae
 M asiacticum
Present in tap water
Group II Scotochromogens
 Pigmented colonies even in the dark
 M. scrofulaceium :
 causes scrofula ( cervical adenitis in children )
 M. gordonae
 Present in tap water
Group III- Non Photochromogens
 Do not form pigment even on exposure to light.
M.avium
M.xenopi
 Mostly occurs as opportunistic infection
 Called MAI(Mycobacterium avium-
intracellulare)complex
frequently affects AIDS patients
causes lung disease
Mycobacterium avium-intracellulare (x-ray findings)
Mycobacterium avium-intracellulare(skin lesions )
Skin lesions
multiple nodules
ulcerated nodules
abscesses
painless nodules
and plaques
Mycobacterium avium-intracellulare(skin lesions )
Figure showing ulcer and nodules
Type IV- Rapid growers
 Grows in < 7 days
 Grows at 25 – 37 degree celcius
 Few Species are :
 M fortuitum
 M flavescens
 M vaccae Fig : culture of M.
fortuitum in LJ media
Mycobacterium chelonae lesion
Figure showing ulcer on thigh
Mycobacterium Marinum
 Usually causes disease in fish
 Normally found in salt water, fresh water, or water sources, such
as swimming pools, rivers, lakes, oceans, and aquariums
 Cause human disease by penetration through impaired skin
barrier : Traumas, such as abrasions and puncture wounds
 It is not transmittable from person to person
 Swimming pool granuloma or Fish tank granuloma
Fig : lesions in the fish infected with M.marinum
Clinical features
Incubation period : 2 weeks
Sites :
 Extremities
 Fingers most common :
fish tank finger
 back of hands
 Elbows and knees of
swimmers.
Morphological variants
Nodule
Pustule
Ulcer or abscess
CLINICAL TYPES CLINICAL FEATURE
Fig : nodules in the hands of pt. infected Mycobacterium
Marinum
Fig : Plaque in hands of pt. infected with Mycobacterium Marinum
Fig : Ulcer and nodules in hands of pt. infected with Mycobacterium Marinum
Fig : Ulcer and nodules in hands of pt. infected with Mycobacterium Marinum
Diagnosis
 Sample: Tissue biopsy
 Culture media
 Solid media: Lowenstein Jensen medium
 Liquid media: Mycobacterial growth indicator tube
media
 Temperature for optimal growth: 30 – 32 °c
 Colonies
 smooth, shiny and creamy coloured
 turns yellow on exposure to light
(Photochromogenic)
Figure A : L J media with growth of M. marinum after exposing to sun light
Figure B : L J media with growth of M. marinum after 24-48 hours after re-
innoculation
Mycobacterium marinum
histopathology
 Mixed infiltrate including lymphocytes, neutrophils, and
histiocytes is seen
Treatment
Clinical types Treatment
Type 1 (limited 1-
3lesions)
Minocycline 100mg BD/
Clarithromycin 500mg BD/
Doxycycline 100mg BD/
Cotrimoxazole 800mg BD
(Monotherapy effective )
Type 2 / Type 3 / Type 4  Rifampicin 600mg/day +
ethambutol 15 -
25mg/kg/day OR
 Rifampicin +
minocycline
± surgical excision.
Duration of treatment Atleast 2 months after
definite clinical resolution
Mycobacterium ulcerans
 Also known as Buruli ulcers
 Infection most common in Central and West Africa ,
Australia.
 Solitary, painless and sometimes itchy nodule of 1-2 cm
develops about 7-14 days after infection through broken skin.
 Over one to two months the nodule may break down to form a
shallow ulcer that spreads rapidly and may involve up to 15%
of the patient's skin surface
 Severe infections may destroy blood vessels, nerves and
invade bone
Buruli ulcer
 Buruli ulcer is a chronic ulcerative skin disease, caused by
M .ulcerans, that mostly affects the limbs.
 The lack of acute inflammatory response is typical and is
likely due to an immunosuppressive toxin called
Mycolactone, which is produced by mycobacteria.
 Buruli ulcer mainly affects children living in humid areas
of the tropical rain forest..
Fig. showing ulcer in hand
Figure A to D showing ulcers in hands
Figure showing ulcers in foot
Management of Buruli ulcer
 Treatment of Buruli ulcers relies on timely and accurate
diagnoses.
 When treated early, antibiotics alone are adequate.
 If treatment is delayed, surgical debridement, skin grafts,
extensive wound care, and physical therapy may be needed
M scrofulaceum
Cervical
lymphadenitis in
children
Subcutaneous
abscess.
Disseminated
infection in
immunocompromised
state
Figure showing subcutaneous abscess
M.peregrinum
Fig. showing ulcer in
hand
Differential Diagnosis
 Cat Scratch Disease ( Cat Scratch Fever )
 Cutaneous Fungal Infections
 Cellulitis
 Cutaneous Tuberculosis
 Pyoderma Gangrenosum
Refrences
 Andrew’s Disease Of Skin , 13th Edition
 Illustrated synopsis of Dermatology and Sexually Transmitted
Diseases by Neena Khanna, 5th edition
 Robins and Cotran Pathological Basis Of disease, 10th edition.
 Research Article by Daniel Marks ( Univesity College London )
 WHO epidemiological data (on Buruli Ulcer)
L

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Atypical mycobacteria

  • 1. ATYPICAL MYCOBACTERIA Dr. Aashish Thakur Intern, Dept. of Dermatology Date : 26/06/2077
  • 2. Introduction  Known by several terms-  Non tuberculous mycobacteria (NTM)  Atypical mycobacteria  Mycobacteria other than tuberculosis ( MOTT ) Environmental mycobacteria –  refer to mycobacteria other than Mycobacterium tuberculosis,its close relatives (M. bovis, M. caprae, M. africanum), and M. leprae.  The number of known species currently exceeds 150. NTM are highly adaptable and can adapt hostile environments.
  • 3. Epidemiology  The true international epidemiology of infections due to NTM is hard to determine.  NTM are ubiquitous in soil and water.  Most NTM cause disease in humans only rarely.
  • 4. Epidemiology  Human-to-human transmission of NTM is not known.  Disseminated disease denotes significant immune dysfunction (e.g., advanced HIV infection)  Pulmonary disease  more common  highly associated with pulmonary epithelial defects.
  • 5. Pathophysiology  Normal host defenses against these organisms are strong.  Healthy individuals in whom significant disease develops are highly likely to have specific susceptibility factors that permit NTM to become established, multiply, and cause disease. HIV infection CD4+ T lymphocytopenia. Potent inhibitors of tumor necrosis factor (TNF), such as infliximab, adalimumab, and etanercept
  • 6. RUNYON CLASSIFICATION GROUP PIGMENT GROWTH ORGANISMS Group 1 Photochromogens M.Marinum M.Kansassi M.simiae Group 2 Scotochromogens M.Scrofulaceum M.szulgai Group 3 Non-chromogens M.avium-intracellulare M.ulcerans Group 4 Rapidly-growing M.Fortuitum M.Chelonae M.abscessus
  • 7. Group I - Photochromogens  Non pigmented in the dark  When young culture exposed to light for 1 hour and reincubated for about 24-48 hours, a yellow orange pigment is produced  Slow growing are  M kansasii  M.marinum  M simiae  M asiacticum Present in tap water
  • 8. Group II Scotochromogens  Pigmented colonies even in the dark  M. scrofulaceium :  causes scrofula ( cervical adenitis in children )  M. gordonae  Present in tap water
  • 9. Group III- Non Photochromogens  Do not form pigment even on exposure to light. M.avium M.xenopi  Mostly occurs as opportunistic infection  Called MAI(Mycobacterium avium- intracellulare)complex frequently affects AIDS patients causes lung disease
  • 11. Mycobacterium avium-intracellulare(skin lesions ) Skin lesions multiple nodules ulcerated nodules abscesses painless nodules and plaques
  • 12. Mycobacterium avium-intracellulare(skin lesions ) Figure showing ulcer and nodules
  • 13. Type IV- Rapid growers  Grows in < 7 days  Grows at 25 – 37 degree celcius  Few Species are :  M fortuitum  M flavescens  M vaccae Fig : culture of M. fortuitum in LJ media
  • 14. Mycobacterium chelonae lesion Figure showing ulcer on thigh
  • 15. Mycobacterium Marinum  Usually causes disease in fish  Normally found in salt water, fresh water, or water sources, such as swimming pools, rivers, lakes, oceans, and aquariums  Cause human disease by penetration through impaired skin barrier : Traumas, such as abrasions and puncture wounds  It is not transmittable from person to person  Swimming pool granuloma or Fish tank granuloma
  • 16. Fig : lesions in the fish infected with M.marinum
  • 17. Clinical features Incubation period : 2 weeks Sites :  Extremities  Fingers most common : fish tank finger  back of hands  Elbows and knees of swimmers. Morphological variants Nodule Pustule Ulcer or abscess
  • 19. Fig : nodules in the hands of pt. infected Mycobacterium Marinum
  • 20. Fig : Plaque in hands of pt. infected with Mycobacterium Marinum
  • 21. Fig : Ulcer and nodules in hands of pt. infected with Mycobacterium Marinum
  • 22. Fig : Ulcer and nodules in hands of pt. infected with Mycobacterium Marinum
  • 23. Diagnosis  Sample: Tissue biopsy  Culture media  Solid media: Lowenstein Jensen medium  Liquid media: Mycobacterial growth indicator tube media  Temperature for optimal growth: 30 – 32 °c  Colonies  smooth, shiny and creamy coloured  turns yellow on exposure to light (Photochromogenic)
  • 24. Figure A : L J media with growth of M. marinum after exposing to sun light Figure B : L J media with growth of M. marinum after 24-48 hours after re- innoculation
  • 25. Mycobacterium marinum histopathology  Mixed infiltrate including lymphocytes, neutrophils, and histiocytes is seen
  • 26. Treatment Clinical types Treatment Type 1 (limited 1- 3lesions) Minocycline 100mg BD/ Clarithromycin 500mg BD/ Doxycycline 100mg BD/ Cotrimoxazole 800mg BD (Monotherapy effective ) Type 2 / Type 3 / Type 4  Rifampicin 600mg/day + ethambutol 15 - 25mg/kg/day OR  Rifampicin + minocycline ± surgical excision. Duration of treatment Atleast 2 months after definite clinical resolution
  • 27. Mycobacterium ulcerans  Also known as Buruli ulcers  Infection most common in Central and West Africa , Australia.  Solitary, painless and sometimes itchy nodule of 1-2 cm develops about 7-14 days after infection through broken skin.  Over one to two months the nodule may break down to form a shallow ulcer that spreads rapidly and may involve up to 15% of the patient's skin surface  Severe infections may destroy blood vessels, nerves and invade bone
  • 28. Buruli ulcer  Buruli ulcer is a chronic ulcerative skin disease, caused by M .ulcerans, that mostly affects the limbs.  The lack of acute inflammatory response is typical and is likely due to an immunosuppressive toxin called Mycolactone, which is produced by mycobacteria.  Buruli ulcer mainly affects children living in humid areas of the tropical rain forest..
  • 30. Figure A to D showing ulcers in hands
  • 32. Management of Buruli ulcer  Treatment of Buruli ulcers relies on timely and accurate diagnoses.  When treated early, antibiotics alone are adequate.  If treatment is delayed, surgical debridement, skin grafts, extensive wound care, and physical therapy may be needed
  • 35. Differential Diagnosis  Cat Scratch Disease ( Cat Scratch Fever )  Cutaneous Fungal Infections  Cellulitis  Cutaneous Tuberculosis  Pyoderma Gangrenosum
  • 36. Refrences  Andrew’s Disease Of Skin , 13th Edition  Illustrated synopsis of Dermatology and Sexually Transmitted Diseases by Neena Khanna, 5th edition  Robins and Cotran Pathological Basis Of disease, 10th edition.  Research Article by Daniel Marks ( Univesity College London )  WHO epidemiological data (on Buruli Ulcer)
  • 37. L