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MYCOBACTERIUM
Group IV M. fortuitum Rapid (-)
- rod-shaped aerobic bacilli M. chelonei (4)
- neither Gram-positive or negative M. smegmatis
- acid fast due to mycolic acid M. flavescens
- do not stain readily once stained resistant to
(1) Pigment formed in the presence of light only
decolorization with acid or alcohol ACID FAST
(2) Pigment formed in the presence or absence of light
- decolorizer is acid alcohol (95% ethyl alcohol + 3% HCl)
(3) Non-pigmented
- Cell wall: waxy, hydrophobic and high lipid contents
(4) Growth < 1 week
60% of dry weight
- Adjuvant properties responsible for development of
delayed type hypersensitivity The Global Emergency
- ALL mycobacterial pathogens are intracellular
8-12M new infections per year
pathogens
2-3M people die from TB per year
major pathogens:
Emergence of MDR M. Tuberculosis
o M. tuberculosis (Kochs bacillus)
th
Philippines is the 9 out of the 22 highly burdened
o M. leprae (Hansens bacillus) countries
th
o M. bovis Philippines is the 8 out of the 25 high MDRTB cases
Potentially pathogenic:
o M. avium complex
Mycobacterium tuberculosis
o M. kasasii
o M. fortuitum Morphology
MOTT (Mycobacterium Other Than Tuberculosis) - acid fast bacilli
- Anonymous, atypical, unclassified Mycobacteria, - non-motile, non-sporogenous, non-encapsulated
NMT (Non-tuberculose Mycobacteria) - arranged singly or in groups
- long, slender rods, beaded
Ranyoun Classification
- much granules in grams staining
Representative Growth Pigment Niacin
Species - easily destroyed by pasteurization
TB M. tuberculosis slow Pigmented (+) - Cord formation when obtained in liquid culture
Complex M. africanum medium
M. bovis - Requires glycerolated agar or potato medium
- Stained by acid-fast stains (Ziehl-Neelsen, Kinyoun) or
Group I M. asiaticum Slow Photo- (-) flourochrome stain
M. kasasii chromogens
- Culture: Non-pigmented, rough, irregular, wrinkled,
M. simiae (1)
M. marinum may show cauliflower-like appearance
Staining
1. Acid Fast Stain Drug-Resistant Tuberculosis
Two Methods - in the 1900s, multi-drug resistant tuberculosis (MDR-
a. Ziehl Neelsen method TB), defined as resistant to Isoniazid & Rifampicin
hot method began to emerge both in the US & worldwide
conterstain methylene blue - today 400,000 cases of MDR-TB globally
b. Kinyoun method - outbreak of extensively drug-resistant tuberculosis
(XDR-TB) MDR-TB with additional resistance of
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Fluroquinolones & at least one of the following - discrete erythematous, infiltrated nodules
injectibles: Capreomycin, Amikacin, or Kanamycin in 1 5 cm in diameter
South Africa & in over 40 countries - diffuse skin infiltration
- estimated nearly 30,000 XDR-TB cases globally
Neurologic Disturbances
Why is there so much drug-resistant tuberculosis? - nerve infiltration and thickening anesthesia,
Drug resistance is created when patients with neuritis, paresthesia, trophic ulcers, bone
tuberculosis are not treated adequately either because: - resorption and shortening of digits
a. The patient does not take the drug treatment - disfigurement (leonine facies) due to skin infiltration
regimen as prescribed (nonadherent) and nerve involvement
b. The treating physician or program does not treat - saddle nose due to bone resorption
the patient with the appropriate drug regimen
Appearance of Disease
- acid-fast bacilli
- singly, parallel bundles, or globular masses Lepromatous Tuberculoid
- regularly found in scrapings from skin or mucous Deficient CMI Intact CMI
membranes (nasal septum) of leper Progressive disease Non-progressive disease
Nodular skin lesions Macular skin lesions
LEPROSY (Hansens disease)
Abundant bacilli in Few bacilli in lesions
- incubation period is short (few days) up to 40 years lesions
- onset is insidious Symmetric nerve Severe asymmetric nerve
- involves the cooler tissue of the body: involvement involvement
o skin Slow onset Sudden onset
o superficial nerves IL-4 and IL-10 IL2 IFN gamma and IL12
o nose Skin is infiltrated with Skin infiltrated with Th1
o pharynx suppressor T cells cells
Ab levels are high
o larynx
Malignant Benign
o eyes
Continuous
o testicles bacteremia
- mode of transmission is through prolonged contact Negative lepromin, Positive lepromin skin test
and exposure extract of
lepromatous tissue,
Skin Lesions skin test
- pale, anesthetic macular lesions (1 10 cm in
diameter)
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Diagnosis / Clinical Findings
- acid fast staining of skin lesions or nasal scrapings
- Leromin test for tuberculoid leprosy
o Fernandez reaction early reaction
o Mitsuda reaction late reaction
- no serologic test is useful
- cannot be grown in any artificial laboratory medium
Treatment
- Dapsone (Diaminophenylsulfone)
o mainstay of therapy
- Dapsone + Rifampicin + Clofazimine
o drug combination is used in case of an
emerging drug resistance
- 2 years duration
Prevention
- isolation of patients
- for exposed children and household members
chemoprophylaxis Dapsone
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