Mycobacteria

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Chapter 16

Mycobacteria

Shared Mycobacterial Properties

• Mycobacteria are slow-growing, aerobic, facultative intracellular rods with a lipid-rich cell wall that makes them acid fast.

Cell wall components

Mycobacterial diseases (Table 16-1)

II Mycobacterium tuberculosis

Identification (Box 16-1)

1. Microscopic detection of acid-fast rods in sputum or biopsy specimen

2. Isolation by culturing on egg-based Löwenstein-Jensen medium or on special broth media

3. Serologic tests and DNA probes

4. Tuberculin skin test

• Intradermal injection of purified protein derivative (PPD) from cell wall induces a delayed-type hypersensitivity (DTH) response in those who have been previously exposed to M. tuberculosis or vaccinated.

• Positive reaction is indicated by an area of induration (>15 mm for healthy adults) 48 to 72 hours after PPD injection.

Transmission and incidence

Pathogenesis

1. Inhaled mycobacteria are engulfed by alveolar macrophages and replicate freely in these cells.

2. Sequence of formation of a tuberculous granuloma (type IV hypersensitivity reaction)

• Tubercle bacilli are phagocytosed by alveolar macrophages.

• Unactivated macrophages cannot kill mycobacteria.

• Other macrophages process and present antigen to CD4 T cells in association with class II antigen sites.

• Macrophages release interleukin-12 (IL-12), which stimulates naïve helper T cells to produce TH1 class memory cells, and IL-1, which causes fever and activates TH1 cells.

• TH1 cells release IL-2 (stimulates lymphocyte proliferation), interferon-γ (activates macrophages to kill tubercle bacillus, called epithelioid cells), and migration inhibitory factor (causes macrophages to accumulate).

• Lipids from killed tubercle bacillus lead to caseous necrosis.

• Activated macrophages fuse, become multinucleated giant cells, and wall off infection.

3. Lack of a host response (e.g., lack of CD4 T cells in acquired immunodeficiency syndrome [AIDS]) leads to dissemination of disease without the formation of granulomas.

Clinical course of TB (Fig. 16-2)

1. Primary pulmonary TB

• Overview

• Localized infection foci form within lung after inhalation of M. tuberculosis.

• Clinical manifestations of active TB (Box 16-2)

2. Secondary pulmonary tuberculosis

3. Extrapulmonary (miliary) TB

Prevention

Treatment of active TB

III “Atypical” Mycobacteria: Nontuberculosis Mycobacteria (NTB)

IV Mycobacterium leprae

• M. leprae causes leprosy (Hansen disease), which is characterized by skin lesions, nerve damage, and extensive tissue destruction in some cases.

Pathogenesis

Clinical presentations (Table 16-2)

TABLE 16-2

Clinical and Immunologic Manifestations of Leprosy

Property Tuberculoid Lepromatous
Appearance of skin lesions Few erythematous or hypopigmented and atrophic plaques with flat centers and raised demarcated borders Many erythematous macules, papules, or nodules accompanied by extensive tissue damage to nose cartilage, bone, testicles
Histopathology of skin lesions Granulomatous with Langerhans cells and epithelioid cells surrounded by lymphocytes Predominantly “foamy” macrophages with few lymphocytes and no Langerhans cells
Nerve involvement Early peripheral nerve damage with complete sensory loss; visible nerve enlargement (ulnar nerve, greater auricular nerve); autoamputation of the digits Late diffuse nerve damage with patchy sensory loss; no nerve enlargement
Acid-fast bacilli Few or none present in skin lesions or nerves Abundant in skin lesions, nerves, and internal organs
Infectivity Low High
Immune responses
DTH reaction to lepromin Yes No
Immunoglobulin levels Normal Hypergammaglobulinemia
Lepromin skin test Positive (intact cellular immunity) Negative (absent cellular immunity)

Transmission

Treatment