Exam2 Respiratory

Question 0

MTB virulence factors

Answer 0

M.Acid - ONLY in AFB (prevent dehydration, resist H2O2)
CORD/glycolipid - MYCOSIDE (glycolipid) = M. Acid + disach.:
- produce serpertine cords of cells: cells stick to each other (parallel growht of bug)
- responsible for formation of GRANULOMAS
SULFATIDES: Mycoside (cord factor/glycolipid) + Sulfate :
- inh. phagosome from fusing with lysosome (inh phagolysosome) inside marcophage
LipoArabinoMannan (LAM): inh cell mediated imm(CMI), inh IFNy (released/made by T cells) from activating marcoph’s

Question 1

Mycoplasma TB

Answer 1

Acid Fast (AF) bacillus (rod), curved
Responds to heat
INTRACELLULAR growth - use macrophages to divide
Colonies Ruff Buff Tuff
Cell envelope: cell membrane, cell wall (peptidoglycan (thick like G+), Mycolic Acid 60%:long chain FAs, clump in broth cultures, LipoARABINOmannan (LAM): FA in cell memr and long ch of sugars (like LPS)
CORD factor (glycolipids) attached to M.Acid
ArabinoGalactan - connects peptidog to m.acid

Question 2

MTB epi

Answer 2

Cuases CASEOUS NECROSIS: Host Antibacterial Immunogenesis (bodys rxn) -> form granulomas -> casous necrosis within granulomas ->CAVITIES in lungs
Humans ONLY
young adults
p t p by
aerosol droplets, MDR, SDR
crowded and prolonged exposure
1-10 microbes or droplets? (needed?)
bimodal: infants and olds (by blood to other tissues)
Long double time - long tx
risks: DM, alc, low imm, HIV - 10% yr, healthy 10% in life

Question 3

PRIMARY TB

Answer 3

low fever 39C, 14-21d, PE normal (25% CP and pleuritic CP)
CXR: hilar LAD
inspire (MID LOW lung) -> pneumonitis with neutrophils and edema -> enter macrophages in alveoli and mult -> INTRACELL GROWTH (LAM:deactivae INFy and keep macroph’s deactivated) -> divide in phagosome (SULFATIDE inh from fusing with lysosome) ->shit happens

ESAT 6 and CFP 10 are MTB antigens presented on macrophage to Th cell: stim T cells to
1) release cytokines (IFNy, TNFa) to attract and ACTIVATE Macroph’s
2) produce ABs but not effective bc they can’t bind to MTB due to Mycoild Acid layer and most are inside macrophages anyway (INTRACELLULAR GROWTH)
Activated macroph’s destroy MTB -> local tissue destroyed -> increase GRANULOMA FORMATION (after T cell activate Macroph’s):
bc bacteria are inside Mph - body seals it off and form GRANULOMAS

Question 4

Granuloma formation

Answer 4

-area of viable MTB
-surrounded by Mph’s, epith histocytes, MULTI NUCLEAR LANGERHANS giant cells: granuloma structure becomes evident 2-6 wks later
-do 2 tests, TB sensitiivty test 2-6 wks
-can become fibrotic, calcifies: LESIONS on CXR
Activated macroph’s destroy MTB -> local tissue destroyed -> increase GRANULOMA FORMATION (after T cell activate Macroph’s):
bc bacteria are inside Mph - body seals it off and form GRANULOMAS

Question 5

Dx of MTB (primary TB? only?)

Answer 5

use ESAT6 and CFP10 antigens to stim T cell to produce INFy <- measure IFNy
(eg QuantiFERONgold Elisa
spot TB - Elispot)
-CXR: cavities, calcified leasions from calc granulomas
- Acid fast stain
-Ziehl/Kihgoun stains
- FLOURESCENT stain - fast
Media:
Middlebrooks (+others)
Lowenstein - Jensen (MTB only)
Ruff Tuff Buff