MTB Flashcards
MTB - EPIDEMIOLOGY
Most common cause ID-related mortality in the world
Peak: 2003
WHO aims to eliminate by 2015
Humans: Only reservoir
Transmitted: Person - to - person (aerosols)
Morphological & structural characteristics
Obligate aerobe Bacillus, non-motile Heat sensitive Catalase + Nitrate reductase, niacin, pyrazinamidase test
Structural:
Cell wall - pep layer, MYCOLIC ACID (long chain FAs, hydrophobic acids/waxes)
Media
Middlebrooks
Lowenstein-jensen
Cord factor
combines w/mycolic acid
creates serpentine appearance
elicits granuloma formation
Catalase peroxidase
resists host cell’s oxidative response
Sulfatides
Glycolipid
Inhibits phagolysosome formation
Promotes IC growth
High mutation rate
requires multidrug therapy
Granuloma
macrophages
MGC
fibroblasts
collagen fibers
active primary
1) when granuloma breaks loose & disseminates
2) CASEOUS NECROSIS: internal lysis of macrophages/MTB cells in the granulomas
3) FEVER
4) radiography: hilar adenopathy, pulm infiltrates - looks like pneumonia
5) droplet nuclei infects middle/lower lobes
6) MTB gets phagocytosed by alveolar macro & multiplies….macro kills MTB and granuloma forms
7) MTB dies, macro presents to TH1 cell. IFN-g released, activated macro.
active secondary
UPPER LOBES
suppression of T cells - insidious onset of disease
normal symptoms + hemoptysis, dyspnea (SOB)
disseminated forms
ORAL MUCOSA: ulceration/pain
tongue & posterior mouth. osteomyelitis. salivary gland (parotid) infection
EYE: intraocular most common. anterior uveitis
TST/Mantoux test
depends on 2 factors: size & risk of infection
IGRA
measures TB sensitized t-cell IFN-G production
not affected by BCG
1 ov only, results in 24h
TX
3-4 drugs (ripe) rifampin isoniazid pyrazinamide ethambutol
rifampin
RNA synthesis
isoniazid
mycolic acid synthesis, hepatotoxic
pyrazinamide/ethambutol
hepatotoxic
dots
most effective form
directly observed treatment > short course
What species of Mycobacterium is the second leading cause of NTM infection in HIV-infected patients
Mycobacterium kansasii
MAC-> #1
MAC/MTB similarities
- Both consists of SLOW-GROWING ORGANISMS
- Strong ACID-FAST
- AEROBIC BACILLI
- Gram- POSITIVE
- Grows on MIDDLEBROOK agar
MAC/MTB differences
- Reservoirs
a. MAC → soil & water
b. MTB → Humans - MAC colonies
a. NO CORDING or CLUSTERING
b. Small, flat, translucent, smooth colony
c. Occasionally pale yellow pigment
d. LACK of GRANULOMA FORMATION
e. OVERGROWTH of microbe
treatment of MAC in HIV (-) vs HIV (+) pts
antibiotics for both (clarithromycin, azithromycin, ethambutol, rifampin)
(+): HAART
(+) W/MAC: lifelong antiretroviral; or antiretroviral for 2 wks then HAART (don’t begin both = IRIS…immune reconstitution inflamm syndrome)
(+) W/NO MAC: chemoprophylaxis until CD4TCELL>100cell/uL
(-): antibiotics until sputum is neg for a year
MAC=
M. avium
M. intracellulare
no person-to-person
opportunistic
MAC IN HIV (-)
PULMONARY
fibrocavity disease (men): COPD
fibronodulary disease (ladiez): BRONCHIECTASIS & lady windermere syndrome
lymphadenitis (kidsz): unilateral cervical nodes
MAC IN HIV (+)
PULMONARY
new infection, not latent reactivation
looks just like MTB, but GI component
DISSEMINATED (DMAC) lymphohematogenous dissemination of bact granulomas NOT EFFECTIVE enlarged organs, organ dysfxn can't develop CMI (no macrophage activation or granuloma formation)
> 5mm
hiv + pts
immunosuppresed
recnt contact w/TB pts
abnormal chest radiographs
> 10mm
immigrants
drug users
healthcare employees
kids <4 exposed
> 15mm
positive
