Tuberculosis 

(TB) and Anti TB drugs

Dr. Haji Bahadar PharmD, PhD

Assistant Professor KMU-IPMS
Lecture outlines
What is TB?
Types of TB
Signs and symptoms of TB
Diagnosis
Treatment of TB
What is TB?

Tuberculosis (TB) is an infectious diseases disease

caused by bacteria called Mycobacterium tuberculosis.
Tuberculosis (TB) is a serious infectious disease
mainly affecting the lungs. Other organs(kidney,
meninges) may also be affected
Tuberculosis is a public health problem worldwide,
including in the United States—particularly among
immunocompromised patients 
Types of TB based on organ involved

Pulmonary TB: It means when the bacterium

Mycobacterium tuberculosis  infection involves the
lungs. Pulmonary  TB  occurs by breathing in air
droplets from a cough or sneeze of an infected person.
Abdominal TB: It is a type of TB that affects the gut,
the peritoneum abdominal lymph nodes , and, more
rarely, the solid organs in the abdomen (liver, pancreas,
and spleen
Tubercular meningitis or TB meningitis: When the
membranes surrounding the brain and spinal cord are
Infected by bacteria
Transmission

 Mycobacterium tuberculosis is spread by small

airborne droplets generated by the coughing, sneezing,
talking, or singing of a person with pulmonary or
laryngeal tuberculosis
 Bovine tuberculosis (TB) is a chronic disease of
animals caused by a bacteria called Mycobacterium
bovis.
Latent TB. In this type TB the bacteria remain the
body in an inactive state and cause no symptoms.
Latent TB, also called inactive TB or TB infection,
isn't contagious. It can turn into active TB, so
treatment is important for the person with latent TB
and to help control the spread of TB. An estimated 2
billion people have latent TB.
Active TB. This condition causes symptoms and can
spread to others. It can occur in the first few weeks
after infection with the TB bacteria, or it might occur
years later.
RISK FACTORS
HIV infection (the virus that causes AIDS)
Organ transplants
Severe kidney disease
Close contacts of a person with infectious TB disease
Pathophysiology

Goblet cells: column-shaped cells found in the

respiratory and intestinal tracts, which secretes the
main component of mucus
Once inhaled, the infectious droplets settle throughout
the airways. The majority of the bacilli are trapped in
the upper parts of the airways where the mucus-
secreting goblet cells exist
Classic clinical features
Cough (chronic)
Weight loss/anorexia
Fever
Night sweats
Hemoptysis
Chest pain (can also result from tuberculous acute
pericarditis)
Fatigue
 Diagnosis
Diagnosis of tuberculosis requires the identification of M
tuberculosis in a culture of a diagnostic specimen. The
most frequent sample used from a patient with a persistent
and productive cough is sputum
Mantoux test or The tuberculin skin test: it is
performed by intradermally injecting 0.1 mL of
intermediate-strength purified protein derivative (PPD)
that contains 5 tuberculin units. After 48 to 72 hours, the
injection site is examined for induration but not redness 
Mycobacteria
Mycobacteria are rod-shaped aerobic bacilli that
multiple slowly, every 18 to 24 hours in vitro.
Their cell walls contain mycolic acids. Mycolic acids
are very long-chain fatty acids.
Mycobacteria produce highly lipophilic cell walls that
stain poorly with Gram stain. Once stained, the bacilli
are not decolorized easily by acidified organic
solvents. Hence, the organisms are called “acid-fast
bacilli.”
 Treatment
Mycobacterium tuberculosis is an aerobic, acid-fast
microorganism. Acid-fast organisms like Mycobacterium
contain large amounts of lipid substances within their cell
walls called mycolic acids. These acids resist staining by
ordinary methods such as a Gram stain
Treatment
Isolate patients with possible tuberculosis (TB)
infection in a private room. Medical staff must wear
high-efficiency disposable masks sufficient to filter the
tubercle bacillus. Continue isolation until sputum
smears are negative 
Isoniazid (INH)
Isoniazid is mycolic acid synthesis inhibitor
Isoniazid penetrates into macrophages and is active
against both extracellular and intracellular organisms.
 It is metabolized in the liver via acetylation into
acetylhydrazine
Rapid acetylators  have a higher risk of INH-induced
liver injury than slow acetylators
Slow acetylators have an increased risk of peripheral
neuropathy during therapy with INH
Hepatitis is the most serious adverse effect associated with
isoniazid
 The typical dosage of isoniazid is 5 mg/kg/d; a typical
adult dose is 300 mg given once daily
 Pyridoxine, 25–50 mg/d, is recommended for those
with conditions predisposing to neuropathy, an adverse
effect of isoniazid
Rifampin
 Rifampin binds to the β subunit of bacterial DNA-
dependent RNA polymerase and thereby inhibits RNA
synthesis
Rifampin is well absorbed after oral administration
and excreted mainly through the liver into bile. It then
undergoes enterohepatic recirculation
rifampin may cause a flu-like syndrome characterized
by fever, chills, myalgias, anemia, and
thrombocytopenia
Mechanism of action.
Isoniazid and ethambutol: They   inhibit the
synthesis of mycolic acids, which are required
components of the mycobacterial cell wall
Rifampicin inhibits bacterial protein synthesis
Pyrazinamide: Pyrazinamide stops the growth
of Mycobacterium tuberculosis.
DOSES SELF STUDY