1. What is tuberculosis caused by?
Mycobacterium tuberculosis, a bacterium that grows slowly like a fungus (‘myco’)
2. What does it mean if TB is multidrug resistant?
INH and rifampin
3. What are the symptoms of TB?
a. Weight loss / anorexia
b. Low fevers / night sweats
c. Fatigue
d. Bloody sputum
4. Which pneumocytes does TB adhere to?
Type two (the kind that produces surfactant and can split into type 1) – for there it can travel
to central lung tissue
5. What are the methods of transmission?
a. Saliva and body fluids
b. Living in close proximity (close contact) – less common
c. Coughing and sneezing – most common
6. What are the 5 main LRT defense mechanisms?
a. Alveolar macrophages
b. Complement
c. Lining fluid (Surfactant, IgG, IgE and IgA, factor B (for alternative pathway) )
d. B and T cells
e. Lymphoid tissue
7. How is primary infection caused?
The smaller particles access the distal alveoli and macrophages attack, the bacteria infect
the macrophages and a granuloma forms from macrophages/inflammatory cells in a ball. If
it is large enough to see, it is a Gohn focus.
The infection then spreads to the regional lymph nodes (Gohn complex). This is the latent
stage and does not cause a real problem. If this progresses or the Gohn complex gets larger
and pneumonia occurs (pulmonary disease) or many bacteria spread through the lymph
nodes to the liver, brain and other organs. Milirary TB occurs when the millits (small spots of
bacteria) spread over an organ, such as the lungs.
8. What else causes secondary infection?
Reactivation can occur after the latent stage many years later if the host is
immunocompromised, smokes or is malnourished. Another way is to be re-exposed to TB
and either experience more latent infection or it can become primary infection.
9. What are the normal bacterial evasion mechanisms?
a. Proteases (Nessieria)
b. Antigenic structures (Gonorrhea)
c. Capsules and M proteins
d. Living inside macrophages (e.g. Chlamydia)
e. Causing apoptosis (e.g. Shigella)
f. Cell walls (gram positive cells)
g. LPS on gram negative cells
h. Elastase acting on C3a and C5a (Pseudomonas)
i. Hyluronidase