mycobacteriamycobacteriamycobacteriamycobacteriamycobacteriamycobacteriamycobacteria

mycobacteriamycobacteriamycobacteriamycobacteriamycobacteriamycobacteriamycobacteriamycobacteria

2. MYCOBACTERIA
Dr. Abid HussainChang (M.Phil)
Associate professor

3. Mycobacteria
Are thin, aerobic,rods, 0.4-3 micron.
They are stained with ZEIHL NEELSEN (Z.N)
staining.
Once stained, they resist decolorization by acid
or alcohol even.
Also calledAcid Fast Bacilli (A.F.B)
Nocardiaasteroides.

4. Major pathogens
M.Tuberculosis causes
Tuberculosis
M.leprae–causesLeprosy

5. M.tuberculosis
Causes Tuberculosis
Causes more deathsworldwide than any
other single microorganism.
1/3
rd
population of world
3 m deaths each year
8 m new cases

6. Importantproperties;
Obligate aerobes
Growth rate much slower

7. Mycobacterialcellwall;
Can induce delayed hypersensitivity and
some resistance to infection.
Delayed hypersensitivity only in sensitized
individuals

8. Cell wall contents
Lipids-(remain bound to proteins and
polysaccharides)
include,
Mycolicacids,
waxes and phosphatides.
Are responsible for acid fastness;

9. Cellwallcontents
Proteins;
Polysaccharides;
a variety of polysaccharides-role in
pathogenesis uncertain.

10. Transmission
From person to person by
respiratory aerosol.
In the body, it resides within R.E cells
(macrophages).
M.boviscan cause intestinal T.B if infected cow`s
milk is ingested.
Risk of infection & disease highest,
socioeconomically disadvantaged people
having poor housing, hygiene and
nutrition.

11. Pathogenesis
Exported repetitive protein;
a protein produced by the organism that prevents
the fusion of phagosomewith lysosome

12. Pathogenesis;
Lesions;are of 2 types;
1.Exudative type;
acute inflammatory reactions and resembles
bacterial pneumonia.

13. Pathogenesis;
2.Productivetype-Granulomatous
3 zones,
1-a central zoneof large multinucleated giant
cells containing tubercle bacilli,
2-a mid zoneof epithellioidcells
3-a peripheral zoneof fibroblasts,
lymphocytes and monocytes .
Latter fibrous tissue develops,

14. Central area undergoes caseation necrosis,
This is called tubercle.
It may lead to cavitation, and healing by
fibrosis or calcification
Primarylesion;
Gohncomplex.

15. Spreadof organism
Erode into a bronchus, empty its contents
and spread the organism to other parts of
lung.
To G I T if swallowed,
To other persons if expectorated.
Can disseminate via bloodstreamto other
body organs.

16. Clinical Features
About 90% infections are asymptomatic.
Fatigue, weakness, weight loss, fever with night sweats
Pulmonary; Cough and hemoptysis
Scrofula
Dissemination; lesions in many organs,
T.B meningitis & T.B Osteomylitis(esppott’sdiseas)
Renal T.B—
Intestinal T.B—caused by M.tuberculosiswhen swallowed
or, M.boviswhen ingested in unpasturizedmilk-

17. lab diagnosis
Specimens; Sputum ,gastric washings,
pleural fluid, CSF, joint fluid, biopsy material,
blood & other suspected material
Staining; Z.N staining;
AFB appear thin red rods against background.
Auraminestain
Culture; 6—8 weakson Lowenstein
Jensen (L.J) medium.

18. Tuberculin test;
A skin test which detects any prior infection due
to tubercle bacilli.
PPD (5 TU) is used as antigen
0.1ml
Evaluation and interpretation;

19. Tuberculintest;
A positive test
.Indurationof 10 mm or more in diameter +
erythema.
. A positive test indicates that the person has
been infected in the past,
active disease is not necessarily present.
+veare at increased risk
-veare not

20. lab diagnosis-Rapid diagnosis
Molecular probes;Provide more rapid
identification of mycobacteria i.e as early as
within 24 hrs.
sensitive and specific.
DNA detectionby PCR;
H P L C (high performance liquid
chromatography)
Based on development of profiles of mycolic
acids and vary from one species to another.

23. Treatment
Pulmonary TB with 3 drugs
INH for 6 months
Rifampin for 6 months
Pyrazinamide stopped after 2
months
4th drug Ethambutolis added
.Immunocompromised(AIDS)
.Suspected INH resistance
.Disseminated disease
And all 4 drugs are given for 9-12 months
Drug resistance is a worldwide problem.

24. Prevention and control
BCG vaccine;
.Provides partial resistance to T.B
.It contains a strain of live attenuated M.bovis
called Bacillus CalmetteGuerin.
.It is effective in preventing the appearance of
clinical disease.

25. M.LEPRAE
Causes leprosy.
Discovered by Hansen in 1873 i.e9 years
before discovery of tubercle bacilli
Found in endothelial cellsof blood vessels or
mononuclear cells
Does not growon artificial media but can be
grown in the mouse footpad or the armadillo

26. Thetemperaturefor growth is lower (30c)
than body temp
Slowest growing bacterialpathogen
i.ea doubling time of 14 days.-----Prolong
treatment

27. Transmission;
By contact, with pt: suffering from ,
lepromatousleprosy through,
nasal secretions and skin lesions.
Most cases occur in tropical areas of Asia and
Africa

28. Pathogenesis;
Organism infects and xxx I/C typically
within .Skin histiocytes,
.Endothelial cells,
.Shwanncells of nerves.
Two forms of leprosy:
1.Tuberculoid Goodimmune response
Leprominskin test+ve
2.lepromatous-Poorimmune response

29. Nerve damage-
Direct damage by organism
Attack by cell mediated immune
response

30. CLINICAL FEATURES
Tuberculoid;
.Hypopigmentedmacular skin lesions
.Thickened superficial nerves
.Anesthesia of skin lesions
Lepromatous;
.Multiple nodular skin lesions (leonine
facies-lion like)-Disfiguring

31. Lepromatous vs. Tuberculoid Leprosy

32. lab diagnosis
Specimens—skin or nasal scrapings
Tuberculoid—few AFB seen
typical granulomas+ve
lepromatous.
Many AFB in macrophages (Foam cells)
No granulomas
*Culture---vein both*
*Are weak A.F.B*

33. TREATMENT
Dapsone
is main drug but combination is recommended
Tuberculoid:
dapsone, rifampin
Lepromatous:
dapsone,rifampin,clofazimine
.Treated for atleast2 years

34. ATYPICAL MYCO BACTERIA
Are so called because,
They differ in certain respects from
the prototype M. tuberculosis.

35. ATYPICAL MYCO BACTERIA
Group-1.Photochromogens;
Yellow orange colony only in the presence of
light
e.gM.kansasii-causes tuberculosis-like disease
M.marinum-causes swimming pool
granuloma.
Group-2.Scotochromogens;
Pigment in the dark not in light
e.g.M.scrofulaceum-causes scrofula
(granulomatous cervical adenitis)

36. ATYPICAL MYCO BACTERIA
Group-3. Nonchromogens;
No Pigment produced neither in light nor
in dark
e.g.M.aviumintracellularecomplex-cause
tuberculosis like disease in
immunocompromisedpts(AIDS)
Group-4.Rapidly growing.
Growth within 7 days
e.g.M.fortuitumcheloneicomplex-cause
disease in immunocomromisedpt.& pt. with
implanted prosthetics.

37. THANKS