Continue Ntm

Continue NTM

(ATYPICAL MYCOBACTERIA (NTM  Acquired from the environment  World wide distribution  No evidence of case-to-case transmission  The organisms grow on the same media as MTB but usually more rapidly  NTM are usually more resistant than MTB to some of the antimicrobics.  Disseminated TB in AIDS patients and immunocompromised individuals.

DIFFERENCES OFATYPICAL FROM TYPICAL MYCOBACTERIA

 Colonial morphology  Niacin test – negative  Relatively more resistant to anti-TB drugs  Less acid fastness  Diseases less invasive

Non-Tuberculosis Mycobacteria (NTM) or Atypical Mycobacteria A- Slow –Growing •

Nonphotochromogens: colonies produce no pigments whether they are grown in dark or light e.g.,M. avium-intracellulare complex (MAC) M. Xenopi, M. ulcerans, M malmoens

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Photochromogens: colonies become pigmented when exposed to light eg M. marinum, M. kansasi

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Scotochromogenes: colonies are pigmentd when grown in the dark or the light e.g., M. scrofulaceum, M. szulgai

B- Rapid –Growing :colonies appear on solid media in 7 days or less. e.g., M. abscessus, M. fortuitum, M chelonae C- Non-cultiveable • M. leprae

Mycobacterium avium-Intracelluare Complex ))MAC :Nonphotochromogens  colonies produce no pigments whether they are grown in dark or light.  World wide distribution  Source – natural water Diseases  TB in birds  Cervical lymphadenitis in children  Disseminated TB in AIDS patients (CD4 ≤ 100 cell/µl )

Mycobacterium ulcerans Nonphotochromogens • The source of infection and transmission are unknown • Occurs in tropical areas • Grows at 300 -330 C • Severe progressive ulcerations involving the skin and subcutaneous tissue • Surgical excision and grafting are usually needed

Mycobacterium kansasii • Photochromogens • M. kansasii infection resemble tuberculosis • Cavitary pulmonary disease, cervical lymphadenitis, and skin infections. • Important cause of disease in patients with HIV infection. • Infection may cause PPD conversion

Mycobacterium marinum Photochromogens • Causes TB in fish • Typical presentation of a tender red subcutaneous nodule known as swimming pool granuloma • Usually occur on elbow, knee, toe, or finger with abscess formation at the site of inoculation with ascending spread along the lymphatics. • Treatment by surgical excision and antituberculosis drug therapy.

Mycobacteriumscrofulaceum Scotochromogenes • M. scrofulaceum is one of the common causes of granulomatous cervical lymphadenitis in young children

Mycobacterium fortuitum Mycobacterium chelonei • Rapid growing ,colonies appear on solid media in 3-5 days. • Infections of skin and soft tissues • Infections associated with long-term use of IV and catheters, injection sites • Surgical wounds following cardiac bypass procedures • M. chelonei exhibits more resistance to antimicrobial agents than M. fortuitum

MYCOBACTERIUM LEPRAE )Leprosy )Hansen's disease  Weak acid fast bacilli (AFB)  Multiply in the host cells to persist (Macrophages and Schwann cells)  Arranged as single, pairs or in masses  Do not grow on artificial culture media  Do not grow in tissue culture

Can be cultured in:  Foot pad of immuno-suppressed mice & armadillo  Optimal growth temp 30oC – lower than body temp  Grows preferably in skin and superficial nerves  Doubling time – 12 days

EPIDEMIOLOGY AND MODE OF TRANSMISSION  10-12 million patients worldwide  Source of infection: infected humans Disease is weakly infectious • Prolonged close contact with a patient of lepromatous • leprosy who discharges M. leprae in large numbers • In nasal secretions and skin lesions  Respiratory droplets transmission  Incubation period very long; may be years

PATHOGENESIS OF LEPROSY • Intracellular replication within skin histiocytes & Schwann cells of nerves. SEVERITY OF LESIONS depends on : The cell-mediated immune response (CMI) by the person. A. Good CMI response Lesions have numerous lymphocytes with few organisms as in“Tuberculoid leprosy”. B. Poor CMI response Lesions have numerous bacilli as in “Lepromatous leprosy”. C. Intermediate CMI response lesions in between A & B as in “Borderline leprosy”

CLINICAL PICTURE OF LEPROSY M. leprae mainly affects skin and superficial nerves. Three types of leprosy 

Tuberculoid Leprosy (TL)

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Few macular depigmented lesions with loss of sensation on arms, face and trunk

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Thickened superficial nerves

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CMI

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No. of AFB in lesion

+++ ±

CLINICAL PICTURE OF LEPROSY

2. Borderline Leprosy (BL) Features intermediate between TL and LL CMI No. of AFB in lesion

++ +

CLINICAL PICTURE OF LEPROSY .3(Lepromatous Leprosy (LL • Erythromatous and granulomatous skin lesion • Nose congested – discharging AFB • Collapsed nasal septum • Leonine (lion-like) faces - thick skin • Eye blindness ° CMI +++ ° No. of AFB in lesion ° (as many as 105 / ml may be present in blood)

CLINICAL PICTURE OF LEPROSY Disfiguring in LL is due to : 1. Skin anaesthesia – burns and trauma often get infected 2. Resorption of bones – loss of features of nose and fingertips 3. Infiltration of skin and nerves – thickening and folding

LAB DIAGNOSIS OF LEPROSY SPECIMENS • Discharge or scrapings from:

° ear lobes, ° skin lesions or ° nasal septum for ZN staining.

• Skin biopsy for histopathology

DIRECT ZN SMEAR (ZN method II) • AFB in groups • Some bacilli inside mononuclear cells “Leprae cells”. HISTOPATHOLOGY Characteristic lymphocytic infiltration in TL and changes in LL.

LAB DIAGNOSIS OF LEPROSY BACTERIAL INDEX Number of bacilli inside macrophages MORPHOLOGICAL INDEX Ratio of viable AFB (long, evenly stained) to non-viable (abnormal, uneven staining). Monitoring of treatment  Morphological index gradually decreases  The bacterial index may remain same for many months.

LAB DIAGNOSIS OF LEPROSY LEPROMIN TEST I/D inj of lepromin; two reactions: 1. Erythema and induration after 48 hours • Person infected at one time 2. A nodule may ulcerate after 3-4 weeks – immunity – Tuberculoid leprosy.

TREATMENT OF LEPROSY FIRST LINE DRUGS  Dapsone (a bacteriostatic drug) Bacilli may become non-viable after 6 months  Rifampicin (a bactericidal drug) Bacilli may become non-viable after few weeks.  COMBINATION THERAPY Dapsone + Rifampicin (first 6 months) SECOND LINE DRUGS ° Ofloxacin ° Mnocycline ° Clarythromycin

Clinical Case A 58 year-old woman with a slowly progressive skin lesion on her left leg. She otherwise felt well and reported no systemic symptoms (including no fevers or night sweats). She is a gardner, but other than kneeling during garden work, could recall no specific local trauma at the site. Skin lesion samples were sent to microbiology laboratory, where the organism was detected in the specimen with a Ziel-Neelsen stain, colonies appear on solid media in 5 days

Questions • What is your differential diagnosis? • What is the possible source of infection? • Who would you manage the case?

Clinical assessment • A patient who had AIDS was readmitted to hospital, following treatment for pnemocystis pneumonia, with retinitis caused by CMV, the patient was treated with ganciclovir. The patient previous history included an attack of pneumocystis Pneumonia 1 year before his current episode, and Kaposi’s sarcoma, for which he had received radiotherapy. His current CD4 count was 50 mm3. During his course treatment for CMV retinitis, he became pyrexial and anaemic and complained of diarrhea. Blood culture and faeces were sent to microbiology laboratory, where the organism was detected in both specimens with ZNS

Questions • What is likely identity of the organism? • Wow would you manage this patient?