MYCOBACTERIA AND ATYPICAL PNEUMONIA Flashcards
MYCOBACTERIA
rod-shaped, obligate aerobic bacteria
derive energy from the oxidation of many simple carbon compounds
growth rate is slower than other bacteria
do not stain readily
cannot be classified as gram-positive or gram-negative
acid-fast – resist decolorization by acid or alcohol
MYCOBACTERIA
Mycobacterium tuberculosis
Mycobacterium leprae
Mycobacterium avium complex (M. avium-intracellulare)
Mycobacterium bovis
Mycobacterium tuberculosis
Koch’s Bacillus
Culture Medium:
Inspissated Egg Media (e.g.
Löwenstein-Jensen) – contain salts, glycerol, complex organic substances (eg, fresh eggs or egg yolks, potato
flour, malachite green)
Mycobacterium tuberculosis
Virulence Factors
Lipids (in cell wall) – responsible for
acid fastness
Mycolic acid (long chain fatty acids C78- C90) – can cause granuloma formation; resists drying
Cord factor - inhibits migration ofleukocytes, causes chronic granulomas
Waxes
Phosphatides – induce caseous necrosis
Proteins
elicit tuberculin reaction and antibody
production
Mycobacterium tuberculosis
Pathogenesis
Primary Complex
* granuloma (tubercle) formation due to migration of macrophages (cell-mediated immunity)
* caseous necrosis at the center of the granuloma
* formation of Ghon lesion/focus – calcified granuloma; visible under X-ray Mycobacterium tuberculosis
* formation of Ghon complex – Ghon lesion/focus
+ regional lymphadenopathy
Latent TB
* dormancy of bacilli in the granuloma
Reactivation/Secondary Tb
* reactivation of dormant bacilli due to depressed cell-mediated immunity or reinfection
Mycobacterium tuberculosis
Pathogenesis
Spread in the host via 3 ways:
1- Direct Extension
2- Lymphatic Spread – through regional lymph nodes
3- Hematogenous Spread – to all organs (miliary distribution)
Intracellular Growth
reside principally intracellularly
in monocytes, reticuloendothelial cells, and giant cells
Mycobacterium tuberculosis
Clinical Findings: Primary
Complex
occurs usually in childhood
usually involves the base of the lungs
Features:
CXR: Ghon complex
Positive TST
Mycobacterium tuberculosis
Clinical Findings: Latent TB
no clinical manifestations
Host is noninfectious
Mycobacterium tuberculosis
Clinical Findings: Reactivation/Secondary TB
Causes:
Endogenous – dormant bacilli in the primary lesion (more common)
Exogenous – reinfection
tubercle bacilli that have survived in the primary lesion
Mycobacterium tuberculosis
Clinical Findings: Reactivation/Secondary TB
usually involves the apex of the lung,
where O2 tension is highest
Features:
chronic tissue lesions, formation of
tubercles, caseation, and fibrosis
regional lymph nodes are only slightly
involved, w/o caseation
CXR: infiltrate and cavity w/ air-fluid level
Mycobacterium tuberculosis Clinical
Findings:
Tuberculosis (Koch’s Disease)
fatigue, weakness, weight loss, fever, and night sweats
Pulmonary TB: chronic cough, hemoptysis
Spinal/ TB (Pott’s disease) – involves ≥2 adjacent vertebral bodies
Miliary TB: bloodstream dissemination, infection of many organs
Mycobacterium tuberculosis
Diagnosis
TST: Latent TB, Past Infection
Culture (Löwenstein-Jensen Medium): gold standard
Acid Fast Smear (Ziehl-Neelsen method)
Chest X Ray
Gene Xpert MTB/RIF
Tuberculin Skin Test (TST)
a.k.a. Mantoux test
Purified Protein Derivative (PPD)
obtained by chemical fractionation of old tuberculin (a
concentrated filtrate of broth in which tubercle bacilli have grown for 6 weeks)
injected on the inner surface of the forearm
examined within 48-72 hrs after injection
(+) result: induration/wheal formation
due to type IV hypersensitivity
Tuberculin Skin Test (TST)
may be negative upon isoniazid treatment
may become positive after bacillus Calmette-Guérin (BCG) vaccination
Acid Fast Smear/AFB Microscopy
low sensitivity (40–60%)
Ziehl-Neelsen method
2 sputum specimens
collected early in the morning
Positive = ≥1 positive sputum smear
Negative = both sputum smears are negative