1-30 Mycobacteria

Question 1

What is the bacteriology of M. tuberculosis?

Answer 1

• Very successful pathogen: 1/3 of Earth’s pop. is infected
• Multidrug resistance is becoming a global health emergency
• Resistance is chromosomal; no known plasmids
• Grows in vitro, but very slowly, and requires special nutrients
• Obligate aerobe: colonization is restricted to oxygen-rich parts of the body (CNS, kidney, lung, lymph nodes, ends of long bones)
• Produce no toxins
• Gram stain very poorly, but are almost uniquely acid-fast

Question 2

What is the pathogenesis of M. tuberculosis?

Answer 2

• Transmission is almost always to lung by inhalation, to lymph nodes, kidney, bones, CNS by hematogenous spread, to GI by swallowing infected sputum
• Immunocompetent host raises strong CMI response, can hold infection latent for decades; immunosenescence or -suppression reactivates
• Hematogenous spread by intracellular infection of naive macrophages (Trojan Horse); activated ones clear it, CD8 cells kill infected macrophages and establish caseating granulomas in which infection is contained
• Extrapulmonary manifestations are usually reactivations: scrofula in neck, genitourinary, CNS (meningitis or abscess), skeletal (long bone or spine), GI (very rare for now)
• Pediatric: must have been recently acquired (trace source), watch for miliary and meningitis (lethal primary infections)

Question 3

What are the classic symptoms of M. tuberculosis, and what is the basic diagnostic procedure?

Answer 3

The classic symptoms of Tb can be seen in ~75% of patients:

• Cough
• Weight loss (“consumption”)
• Fever
• Night sweats
• Hemoptysis
• Chest pain

Check sputum and chest x-ray.

Question 4

What are some risk factors for M. tuberculosis?

Answer 4

• Crowded at-risk environments (prisons, hospitals, homeless shelters)
• HIV

Additionally, a risk factor for poor outcomes is any immunosuppressive factor:

• Uncontrolled HIV (inadequate HAART)
• Steroids
• IFNɣ deficiency
• TNF-alpha antagonists (Remicade)
• Age <5yrs, >65yrs

Question 5

What is the procedure for microscopic acid-fast differential staining?

Answer 5

Acid-fastness is an uncommon characteristic shared by Mycobacteria and Nocardia, which makes this stain extremely helpful in identification of these bacteria. Since their cell walls are very impermeable, a special stain is needed; carbolfuchsin is lipid-soluble and contains phenol, and can penetrate the cell wall with heat. Non-acid-fast cells are then decolorized and counterstained.

Question 6

What are atypical mycobacteria?

Answer 6

Atypical mycobacteria are environmentally-acquired infections that cause neither TB nor leprosy.

• Infection in an immunocompetent adult is usu. cutaneous; scrofula in children; immunosuppressed hosts may have systemic symptoms that mimic TB, particularly from M. kansasii or MAI/C
• Infections may be difficult to treat once established; require multiple antibiotics

Question 7

What is the bacteriology and pathogenesis of M. leprae?

Answer 7

• NO IN VITRO CULTURE SYSTEM
• Extremely long incubation period
• Transmits through nasal secretions and skin lesions, but not easily (only 5-10% of humans believed susceptible to disease)
• Hansen’s Disease (leprosy) presents on a range from Tuberculoid (paucibacillary, vigorous CMI both contains infection and damages nerves, PPD+) to Lepromatous (multibacillary, weak CMI, extensive cutaneous symptoms, PPD-)