[PHYSIOLOGY LECTURE DR.

REVILLA]
TUBERCULOSIS: Physiologic consideration

Non-immunologic defenses
Cell Mediated Immunity
2 Major types:
1. Primary TB (Primary complex)- due to
underdeveloped immune system; usually
not infectious in nature (children)
2. Post-primary/Secondary TB/ Adult TB

INTRODUCTION:
Problem with management of TBdiscovery to
development (notorious for causing death)past (drug for 12
mos but poor compliance); present (6 mos for TB/made
available to people for FREE)yet people still develop TB due
to culture (when signs and symptoms are reduced, they stop
taking the medication)development of DOTS (Directly
observed treatment shortcourse) where in the patient will take
the drug in front of the health care giver and monitored
weekly.

INFECTION AND MACROPHAGE INVASION:

Once it is not cleared by the mucociliary
system, Mtb reaches the alveoli
Alveolar macrophages phagocytize the bacilli
called PHAGOSOMES (alveolar
macrophage with Mtb inside)
Lipoarabinomannan prevents the killing
*some are killed, some are not
Not killed Replication begins and
macrophage eventually rupturesgoes to
other area of lungs
Since they are AEROBICwant more oxygen
live in area with high oxygen tension (APEX of
the lungs because alveoli in this area is always
distended)

TUBERCULOSIS:
Scourge of mankind for thousand of years
Remains one of the largest problem in the world
Estimated 9 million cases a year
At least 2 million deaths a year
Philippines: 9th among 22 high burden countries
#6th among causes of morbidity and mortality
75 Filipinos die daily
Estimated 240,000 new cases annually
Approximately 15M Filipinos have TB
60% of Filipinos are exposed to TB

HOST RESPONSE & GRANULOMA FORMATION:

Mycobacterial CHONMMP9 (matrix
metalloproteinases 9)stimulate nave macrophage
granuloma formation/TB granuloma
2-4 weeks after infection, 2 host responses to Mtb
development:
1. CMI (Cell Mediated Immunity) response
-activated macrophage neutralizes tubercle
bacilli
-2 things happen:
a) early solid necrosis in the center of tubercle
CASEATION NECROSIS (cheese-like)
b) other viable bacilli may remain DORMANT
**if exposed = only 10-15% develop into disease
(unless: smokers,drinking ROH, sleeping less,
DM, HIV due to less CMI and t-cells CD4, CD8)
**if IMMUNOCOMPROMISEdormant to active
Mtb RELAPSE
2. Delayed-type Hypersensitivity (DTH)
-tissue damaging effect lesion enlarges and
tissue is progressively damage
-caseous material liquefiescavity ( bacilli in
center)
-cavitary Tb: most deadly
-single cavity lesion= 3,000 bacilli
-serves as the basis for TST (Tubercle skin test)
positive due to T cell present in that area of the
skin)

GLOBAL EMERGENCY :needs other people to combat TB

Mycobacterium TB
Rod-shaped, non-spore forming
Importantt:
a. Thin; aerobic loves lung tissue
b. measuring 0.5microns by 3 microns (able to deposit
to alveoli)
acid-fast bacilli- due to failure to decolorized with acid
ROH; cell wall contains mycolic acid
cell wall contains:
a. arabinogalactan and peptidoglycan- makes cell wall
impermeable difficult to treat need more drugs
to destroy bacilli
*** Drugs
Rifampicin, Isoniazid, Pyrazinamide,
Ethambutol
b. Lipoarabinomannan- prevents destruction of bacilli
once engulfed by alveolar macrophages
bacillialveolimacrophage will phagocytize but
due to lipoarabinomannannot immediately killed
and can remain DORMANT/develop own mutation)
An INFECTIOUS DISEASE

Droplet Nuclei
In saliva
Coughing /Speaking
<5 10 microns
If it breaks <5
microns
*bacilli can enter
MODERATELY INFECTIOUS DSE
(+) smear may infect 10-15 persons a year = exponential

TB

***Extensively drug-resistant TB: 95% mortality rate (South

Africa) in 56 pts55 died
**PATIENT should be the one wearing the mask degree of
decrease in infectiousness is greater
***TB great mimicker of all diseases can be found in all
body parts; mimics cancer
CLINICAL MANIFESTATIONS :
I.
Pulmonary TB
Primary Disease
a. Middle and lower lung zones
b. Ghon complex
Post-primary (adult type)
a. Apex and post segment of upper lobes
b. Rasmussens aneurysm
II.
Extra-pulmonary TB
a. Lymph nodes TB
b. Pleural TB
c. TB of the upper airways
d. GU TB

From exposure to infectionnot all infected with

TBEXOGENOUS FACTORS
a. Exposure to a TB patient
b. Virulence of case
c. Closeness to patient
d. If living/sleeping together in the same room
From infection to disease ENGENOUS FACTORS: Immunity
a. Good immune system
b. Low immune system
**the risk of developing depend on:
Innate immunologic defenses

[PHYSIOLOGY LECTURE DR. REVILLA]

e.
f.
g.
h.
i.

Skeletal TB
Tuberculous meningitis
Peritoneal TB
Pericardial TB
Miliary TB

Early 2005 = Bill Gates GFATM (Global Funding against AIDS,

TB and Malaria)
*provide funds only for 5 years
*should be self sustainable after
Private initiated PPMD Unit: SLU PPMD (Public Private Mixed
DOTS) Unit

DIAGNOSIS:
AFB SMEAR: most important due to accessibility
Chest X-ray
TB culture

Follow up meeting:
Other problems: educational lapses: pharmacy and
medical school
*Mandated lecture on TB from 1st to 4th year

National CDR 2005: target of 70% case detection rate (met by

Region 3,4,5,6,8,10,12,ARMM)
CAR: lowest rate - only37%
Baguio: lowest - 12% in 2005; 17% in 2006
Together with Mt. Province, Benguet

Note taker: DONATO, MK//DION, Carol//CENIL, Ella