Mycobacterium tuberculosis by Sikandar Ali sumalani email sikanderalisumalani11@gmail.com

1. Mycobacterium Tuberculosis
BS 3rd semester presentation
By
SikandarAli
Submittedto: Sir Musawir khan
Department Of Microbiology

2. introduction
The mycobacteria are rod-shaped, aerobic bacteria .
Mycobacterium is a genus of Actinobacteria, given
its own family, the Mycobacteriaceae.
Over 190 species are recognized in this genus
This genus includes pathogens known to cause
serious diseases in mammals,
including tuberculosis (Mycobacterium tuberculosis)
and leprosy (Mycobacterium leprae) in humans.
They are Facultative intracellular pathogens usually
infecting mononuclear phagocytes (e.g.
macrophages).

3. MORPHOLOGY
SHAPE - long, slender, straight, curved rod.
 SIZE - 2-4 micrometers in length and 0.2-0.5 um
in width.
 Mycolic acid, waxes & lipids are present in cell
wall
 The high lipid content (approximately 60%) of
their cell wall makes mycobacteria acid-fast and
hydrophobic.
 Neither gram-positive nor gram-negative.

4. CULTURE:
 Mycobacteria are aerobes.
 substances are either solid substances on culture
plates, or bottles of liquid known as culture broths.
 Grow slowly: 14-15 hours
 Optimum temperature: 37degree C. Do not grow
below 25degree C.
 pH between 6.4 to 7.0
 Grow only in specially enriched media containing
egg, potatoes.
 Colonies appear in 2-6 weeks

5. ACID FAST BACILLI:
 Mycobateria are virtually the only bacteria that
are acid-fast because of the presence of mycolic
acid and their lipid-rich cell walls, which are
relatively impermeable to various basic dyes
unless the dyes are combined with phenol.
 Once stained, the cells resist decolourization
with acidified organic solvents and are therefore
called "acid-fast". Carbol Fuchsin Stain (Ziehl-
Neelsen).

6. Species
Growth on Bacteriologic
Media
Temperature (˚C)
Source or Mode of
Transmission
M. tuberculosis Slow (weeks) 37 Respiratory droplets
M. bovis Slow (weeks) 37 Milk from infected animals
M. leprae None 32 Prolonged close contact
Atypical mycobacteria (ex.
M. kansasii)
Slow (weeks) 37 Soil and water
M. marinum Slow (weeks) 32 Water
M. avium- intracellulare
complex
Slow (weeks) 37 Soil and water
M. fortuitum-chelonae
complex
Rapid (days) 37
Soil and water

7. Mycobacterium Tuberculosis
 It causes TUBERCULOSIS which is the most
common cause of death due to bacterial infection
worldwide.
 Tuberculosis (TB) is a potentially serious infectious
disease that mainly affects our lungs.
 Tuberculosis (TB) stays one of the major worldwide
wellbeing dangers prompting dismalness and
mortality.
 Mycobacterium Tuberculosis, is transmitted through
the air as it does not thrive on surfaces
 M. tuberculosis is resistant to dehydration and so
survives in dried expectorated sputum; this property
may be important in its transmission by aerosol.

8. Types

9. History
 On March 24, 1882, Dr. Robert Koch announced
the discovery of Mycobacterium tuberculosis, the
bacteria that causes tuberculosis (TB). at a time
when one of every seven deaths in Europe was
caused by TB
 Isolated the mammalian tubercle bacillus on Heat
Coagulated Bovine Serum and proved its causative
role in Tuberculosis.
 He received the Nobel Prize in physiology and
medicine in 1905 for this discovery.

10. Cases of Pakistan
323,255
355,502
358,886
275,279
0 50,000 100,000 150,000 200,000 250,000 300,000 350,000 400,000
2015
2016
2017
2018
case
(NTP) National TB control program
(WHO) the world health Organization

11. TRANSMISSION
 Tuberculosis (TB) bacteria get into the air when
a person with TB speaks, coughs or sings
 Tuberculosis is not easily transmitted. Family
members living together are at highest risk. Risk
of transmission is very small in casual contacts.
Only one third of exposed persons become
infected.
 TB is not transmitted through dishes, drinks,
food, clothes or surfaces.

12. Pathogenesis
 TB pathogenesis can be divided in four well-defined events
 1st
 Inhalation of the mycobacteria:is followed by its interaction with
resident macrophages through cellular receptors and its
internalization.
 Macrophage bactericidal mechanisms are then activated,
 The efficient killing of mycobacteria depends on pathogen and host
factors.
 2nd step
 Inflammatory cell recruitment: survived mycobacteria proliferate
within macrophages inducing the production of pro inflammatory
cytokines.
 The local inflammatory environment induces the recruitment of
several cell types including monocytes, neutrophils, and dendritic
cells to the site of infection.

13. Pathogenesis
 3rd
 High levels of TNF-α contribute to control Mycobacterium tb growth and granuloma formation.
 Control of mycobacteria proliferation: arrival of immune cells to the site of infection including T
cells, which become organized in characteristic structures called granulomas efficiently stop
mycobacteria proliferation and contain the mycobacteria within the granuloma walls preventing its
spread.
 Characteristic of this structure is the presence of foam cells resulting from the differentiation of
chronically activated macrophages.
 Mycobacteria containment eventually becomes stable (latent) infection.
 4th
 Post primary TB: mycobacteria persistence associated with a failure in the immunosurveillance
system increases the risk that latent disease becomes reactivated, inducing the damage of nearby
bronchi and conditioning the spreading of the Mycobacterium tb to other areas of the lung and the
transmission of the disease.

14. Signs and symptoms
 symptoms of active TB include:
• Coughing that lasts three or
more weeks.
• Coughing up blood.
• Chest pain, or pain with breathing
or coughing.
• Unintentional weight loss.
• Fatigue.
• Fever.
• Night sweats.
• Chills.

15. Risk Factors
 contact with a known TB case, e.g. family
member or friend
 migration from a country with a high incidence
of TB
 history of travel to an area with a high incidence
of TB
 smoking
 alcohol and/or drug abuse
 malnutrition
 homelessness

16. Preventions
 There are several other TB prevention
activities. This includes preventing people
with latent TB from developing active, and
infectious, TB disease.
 TB infection control which means
preventing the transmission of TB in such
settings as hospitals & prisons.
 The pasteurization of milk also helps to
prevent humans from getting bovine TB.
 It does little to interrupt the transmission of
TB among adults.

17. Diagnosis
 During the physical exam, your doctor will check your lymph
nodes for swelling and use a stethoscope to listen carefully to
the sounds your lungs make while you breathe.
 PPD tuberculin:
 just below the skin of your inside forearm. You should feel
only a slight needle prick.
 Within 48 to 72 hours, a health care professional will check
your arm for swelling at the injection site. A hard, raised red
bump means you're likely to have TB infection.
 Blood test
 Blood tests may be used to confirm or rule out latent or active
tuberculosis. These tests use sophisticated technology to
measure your immune system's reaction to TB bacteria.

18. Diagnosis
 Imaging tests
 If you've had a positive skin test, your doctor is likely to order a
chest X-ray or a CT scan. This may show white spots in your
lungs where your immune system has walled off TB bacteria, or
it may reveal changes in your lungs caused by active
tuberculosis.
 Sputum tests
 If your chest X-ray shows signs of tuberculosis, your doctor may
take samples of your sputum — the mucus that comes up when
you cough. The samples are tested for TB bacteria.
 Sputum samples can also be used to test for drug-resistant strains
of TB. This helps your doctor choose the medications that are
most likely to work

19. Treatment
For initial empiric treatment of TB, start patients on a 4-
drug regimen:
Isoniazid, (Myrin Fort)
Pifampin, (Myrin Fort)
pyrazinamide (Pyrazid)
streptomycin
2nd line
Kanamycin (KM); (kanacyn)
capreomycin, (Capreomycin)
Ciprofloxacin (CIP), (ciproxin)
Ethionamide, (Ethomid)
Terizidone, (Terizidone)

20. 3rd line
 Third-line drugs (WHO group 5) include drugs that may be
useful, but have doubtful or unproven efficacy:
 Rifabutin (RIFABUTIN)
 Clarithromycin (CLR); (Klaricid)
 Linezolid (LZD); (ZOLREST)
 Thioacetazone (T); (isoniazid)
 Thioridazine; (Diagesic-P)
 Arginine; (Permen)
 Vitamin D; (Osnate-D)
 Bedaquiline; (Sirturo)

21. Thank you
s