Microbiology: Mycobacteria

Rod-shaped, aerobic bacteria that do not form spores

Acid-fast bacilli
Species:
Mycobacterium tuberculosis tuberculosis
Mycobacterium leprae leprosy.
Other nontuberculous (NTM) mycobacteria infect patients with AIDS, are opportunistic
pathogens in other immunocompromised persons
Mycobacteirum Tuberculosis
1. Morphology & Identification
A. Organisms
In tissue, tubercle bacilli are thin, straight rods
On artificial media, coccoid and filamentous forms are seen with variable morphology
from one species to another
In smears of sputum or sections of tissue, mycobacteria can be demonstrated by
yellow orange fluorescence after staining with fluorochrome stains
Acid fastness depends on integrity of the waxy envelope Ziehl Neelsen technique
B. Culture
i.
Selective media
Contain antibiotics to prevent the overgrowth of contaminating bacteria and fungi
ii.
Nonselective media
Semisynthetic agar media
The media which composition contain both natural and chemical substances
FUNCTION: observing colony morphology, for susceptibility testing & with added
antibiotics, as selective media
Inspissated egg media Lwenstein Jensen)
FUNCTION: with added antibiotics are used as selective media
Broth media
Ordinarily, mycobacteria grow in clumps or masses because of the hydrophobic
character of the cell surface
If tweens (water-soluble esters of fatty acids) are added, they wet the surface and
thus permit dispersed growth in liquid media
C. Growth characteristics
Obligate aerobes
Derive energy from the oxidation of many simple carbon compounds
The doubling time of tubercle bacilli is about 18 hours
Saprophytic forms tend to grow more rapidly, to proliferate well at 2233 oC, to produce
more pigment, and to be less acid fast than pathogenic forms
D. Reaction to Physical & Chemical agents
Mycobacteria tend to be more resistant to chemical agents than other bacteria
because of the hydrophobic nature of the cell surface and their clumped growth
Tubercle bacilli are resistant to drying and survive for long periods in dried sputum
E. Pathogenicity of mycobacteria
The route of infection (respiratory vs. intestinal) determines the pattern of lesions
2. Constituents of Tubercle Bacilli
Cell walls can induce delayed hypersensitivity and some resistance to infection
A. Lipids
Rich in lipids some extent responsible for acid fastness
Acid fastness can lost after sonication
Phospholipids induce caseous necrosis
B. Protein
Can elicit the tuberculin reaction

Can elicit the formation of a variety of antibodies

C. Polysaccharides
Can induce the immediate type of hypersensitivity
Can serve as antigens in reactions with sera of infected persons
3. Pathogenesis

Emitted in droplets
(cough,
sneeze,speak)

Inhaled &
deposited in
alveoli

Host immune
responds releaseing
meditors that
stimulates
mcrophage

1 - 2 months after
exposure, lesions
associated with
infection apear in
lung

Mycobacteria
multiply in
macrophage. some
macrophage
enhanced ability to
kill bacteria but
some are kiiled by
bacteria

4. Pathology
Production & development of lesion & healing or progression determines by:
i.
Number of mycobacteria in inoculum & multiplication
ii.
Type of host
A. Two principal lesions
i.
Exudative type acute inflammatory reaction with edema fluid, polymorphonuclear
leukocytes, & monocytes around tubercle bacilli
Seen in lung tissue may lead to massive necrosis of tissue or may develop into
productive lesion
Tuberculin test positive
ii.
Productive type fully develop, chronic granuloma, consists of zones:
Central area of large, multinucleated giant cells containing tubercle bacilli
Mid zone of pale epithelioid cells, often arranged radially
Peripheral zone of fibroblast, lymphocytes & monocytes
B. Spread of organisms in host
Tubercle bacilli spread in the host by direct extension, through the lymphatic channels
and bloodstream, and via the bronchi and gastrointestinal tract
C. Intracellular site of growth
When mycobacteria establish themselves in tissue, they reside principally
intracellularly in monocytes, reticuloendothelial cells, and giant cells
5. Primary infection & Reactivation types of Tuberculosis
Host has first contact with tubercle bacilli, following features are observed:
i.
Acute exudative lesion develops and rapidly spreads to the lymphatic and regional
lymph nodes
ii.
Lymph node undergoes massive caseation, which usually calcifies
iii.
Tuberculin test result becomes positive
Primary infection
Occurred in the past, usually in childhood
Involvement may be in any part of the lung but is most often at the base
Reactivation
Caused by tubercle bacilli that have survived in the primary lesion
Characterized by chronic tissue lesions, the formation of tubercles, caseation, and
fibrosis
Almost always begins at the apex of the lung, where the oxygen tension (PO2) is
highest

6. Immunity & Hypersensitivity

Immunity there is an increased capacity to localize tubercle bacilli, retard their
multiplication, limit their spread, and reduce lymphatic dissemination
Hypersensitivity development of a positive tuberculin reaction