This document provides information on the morphology, properties, classification, and pathogenicity of mycobacteria. It discusses Mycobacterium tuberculosis and Mycobacterium leprae, the causative agents of tuberculosis and leprosy, respectively. It also covers atypical (nontuberculous) mycobacteria (MOTT). Mycobacteria are acid-fast, aerobic bacteria that are often slow-growing and can survive intracellularly. M. tuberculosis causes tuberculosis through airborne transmission, while M. leprae causes leprosy via prolonged skin contact. Both can have varied clinical presentations depending on host immunity. MOTT are opportunistic pathogens typically found in the environment that can cause disease in immunocomp

2. MYCOBACTERIUM
Morphology
Slender,
Straight or
Slightly curved
 Non capsulate
 Non- spore forming
 Non motile
 aerobic bacteria

3. Properties
Acid fastness
Obligate aerobe
Slow growers
Intracellular survival and replication
killed by ultraviolet light and heat
Resistant to dryness and corrosive
action of alkalis and acids

4. Classification of the
Mycobacteria
genus
 >200 species, most are
saprophytes.
Mycobacteria
Pathogenic
Mycobacteria
Mycobacterium
tuberculosis
complex (MTC
M.
leprae
Potentially pathogenic
(Atypical )Mycobacteria
- Mycobacterium
avium complex (MAC)
- Mycobacterium
kansaii
- Others

5. Causative agent of
TUBERCULOSIS
“A chronic granulomatous disease
which affects any organ in the body,
particularly the lungs”
“About one third of the world’s population
is infected”
Mycobacterium tuberculosis

6. Routes of infection
 Airborne.(Humans are the only reservoir for
M. tuberculosis)
 Ingestion in milk. (M bovis)
 Occupational. (skin lesion in
Lab)
 NB: Skin lesion in milliary TB

7. Virulence factors:
(M. tuberculosis has neither exotoxin nor
endotoxin)
Tissue Invasion
 Intracellular survival and replication
Glycolipids on the outer surface.
 Enhance granuloma formation.
 Inhibit migration of polymorph-
nuclear leucocytes (PMNs).
 Help in surviving inside macrophages.

8. Factors determining The
risk of acquiring infection
I. Microorganism: Dose of infecting
Mycobacteria, duration of contact
II. Host: Innate and cell mediated
immunity.

9. 2 Host Responses
Immunity and Hypersensitivity
 2 – 4 weeks after primary infection.
Cell mediated immunity (CMI):
• sensitized T- lymphocytes secrete cytokines to
activate macrophages to kill Mycobacteria.
Delayed- type hypersensitivity(DTH) =
immunologically mediated tissue injury
• First DTH inhibit growth inside macrophage later
persistent inflammation with destruction of
macrophages and damage of lung tissue.
• Tuberculin test becomes positive.

10. M.
Presentations of
infection:
tuberculosis
Presentation
of TB
Active tuberculosis
*Symptoms + signs are present
depending on site of infection
*Radiological findings+Laboratory
evidence may be found
Pulmonary
Extra-
pulmonary
Milliary
Latent TB infection
(LTBI)
- asymptomatic
state
- living inactive TB
bacilli within
tissue
- non-infectious
- May reactivate
.
Heals

11. Cutaneous TB
 is a relatively uncommon form of
extrapulmonary TB (Occuptional in Lab)
 2-4 weeks after mycobacteria enter
through broken skin,
or mucous membranes from an outside
source of mycobacteria
 initial lesion called the tuberculous
chancre(firm shallow ulcers with a
granular base).
 The immune response of the patient and
the virulence of the mycobacteria
determine the type and severity
of cutaneous TB
 several different types of cutaneous TB
exist

12. TB verrucosa cutis
 direct inoculation of TB
into the skin in someone
who has been previously
infected with Mycobacteria
 purplish or brownish-red warty growth
 on the knees, elbows, hands,
feet,buttocks
 Lesions may persist for years but can
clear up even without treatment

13. Lupus vulgaris
Persistent and progressive form
of cutaneous TB
Small sharply defined reddish-brown
lesions with a gelatinous consistency
(called apple-jelly nodules)
Lesions persist for years, leading to
disfigurement and sometimes
skin cancer

14. Scrofuloderma
Result from direct extension of
underlying TB infection of lymph
nodes, bone or joints
Often associated with lung TB
Firm, painless lesions that eventually
ulcerate with a granular base
May heal even without treatment but
this takes years and leaves
unsightly scars

15. Miliary TB
 Chronic TB infection spread from the
primary infection(usually in lungs) to other
organs and tissues via the bloodstream
 Skin lesions are small (millet-sized) red spots
that develop into ulcers and abscesses
 in immunocompromised patients, eg HIV,
AIDS, cancer
 Prognosis is poor (many patients die even if
diagnosed and treated)

16. diagnosis
 Usually by characteristic histobathological
features on skin biopsy.
 Typical tubercles are caseating epithelioid
granulomas that contain acid-fast bacilli.
These are detected by
tissue staining,
 culture and
polymerase chain reaction (PCR).

17. Other tests that may be
necessary include:
 Tuberculin skin test (Mantoux or PPD
test)
 Interferon gamma release assay blood
test
 Sputum culture (it may take a month
or longer for results to be reported)
 Chest X-ray and other radiological
tests for extrapulmonary infection.

18. Direct smear:
-
2
 Ziehl- Neelsen (Z.N.) stain
Acid fast bacilli
(red bacilli and blue background)

19. TB on LJ medium
Automated TB culture
system

20. Laboratory diagnosis of latent
TB
(T-cell based assays)
1. Tuberculin skin test (TST):
(Invivo)
2. Interferon-gamma release
assays (IGRAs):
(In tube)

21. Tuberculin skin test (TST)
 Type: Delayed hypersensitivity skin test,
 Time :+ve 3-8 weeks after infection or BCG
vaccination.
 Procedure: 0.1 ml of PPD (5TU) is injected
ID in the volar aspect of the forearm
 Reading :The diameter of induration (not
erythema) – (48-72) hours at the site of
injection.

22. √√ ××

23. Interpretation of TST result
Is considered +ve if
Is considered +ve if
Is considered +ve if

24. Prevention
• Eradication of T.B. from infected
cattle and pasteurization of milk
to reduce infection with M. bovis.
• Improvement of socio-economic
states (e.g. poverty, malnutrition
and bad aeration).
• Treatment of cases (active, and
latent T.B).
• Follow up of contact by (Chest X
ray &TST).
A-General
measures

25. • -INH for 6-9 months for:
• 1-Recent tuberculin converters
• 2-Children contact with TB
patients.
• 3-Tuberculin positive individuals
on immunosuppresive therapy
B-
Chemo
-
prophy
laxis
•BCG “Bacillus Calmette Guerin”.
•live attenuated bovine strain.
•ID. In Deltoid region single dose;
•Gives partial immunity against
both M. tuberculosis and M. bovis.
C-Immuno-
prophylaxis
(Vaccine):

26. BCG

27. Mycobacterium leprae
Caustive organism of
Leprosy “Hansen’s disease”
 Acid fast bacilli
 Less acid fast than MTB (only resists
decolorization by 5% H2SO4).

28. (Hansen's disease)
Leprosy
 A chronic slowly developing * (from
six months to 40 years) progressive
disease that damages the skin and
peripheral nervous system
 caused by M. Leprae.
 results in skin lesions and
deformities, most often affecting the
cooler places on the body (eg. eyes,
nose, earlobes, hands, feet, and
testicles)

29. Mode of infection
 can affect people of all races all around the world.
However, it is most common in warm, wet areas in
tropics and subtropics.
 Worldwide prevalence is around 5.5 million, with most cases
found in 5 countries:India,Indonesia, Myanmar,
Brazil and Nigeria.
 most often during two different periods of life, between 10-14 and in 35-44 years old.
“Airborne”via inhalation of
contaminated nasal secretions and
shedding skin lesions.
Prolonged contact with patients is
necessary.
Susceptibility to getting leprosy may be

30. Leprosy
 a chronic granulomatous
disease, similar to tuberculosis,
because it produces inflammatory
nodules (granulomas) in the skin,
MM and nerves
 Early symptoms begin in cooler
areas of the body and include
loss of sensation.
 If it isn’t treated, it can cause
severe disfigurement and

31. Classification

32. Lepromatous leprosy Tuberculoid
Lesion Numerous lesions
( plaques, macules, papules a
nd nodules)
Leonine facies (Multiple skin
nodules
Early symptoms : nasal
stuffiness, discharge and
bleeding, and swelling of the
legs and ankles
Few flat lesions
(hypopigmented
asymmetric macular
skin lesions)
Superficial
nerves
Intact sensation Thickened
&significant
anesthesia
Number of
bacilli in lesion
large number of bacilli Small number
Infection Highly infectious, sever form Less infective, mild
Cell mediated Reduced (lepromin test -ve) Maintained

33. lepromatous
leprosy
active,
neglected
nodules .

34. Tuberculoid leprosy:
well- defined, annular, anesthetic plaque.

35. Borderline tuberculoid
leprosy

36. How to diagnose leprosy
 Examine skin
 Check for patches
 Test for sensation
 Count the number of patches
 Look for damage to nerves

NB: Early diagnosis and early
adequate drug treatment is very
important

37. Laboratory Diagnosis:
 Specimen :scrapping or biopsy from
nasal mucosa, earlobe and skin lesions.
 Direct microscopy:
”Modified Z-N technique”
(decolorization with 5% H2SO4).
o Bacilli are abundant in lepromatous type
and few in tuberculoid type)

38. M Leprae (intracellular acid-fast bacilli)
Found in macrophages and nerves

39. Lab diagnosis
 Histopathological examination
for characteristic lesion
 No culture is available
 Lepromin test : (like tuberculin test)
- positive in tuberculoid but not in
lepromatous type.

40. Complications of Leprosy?
Due to delayed diagnosis and treatment
I. disfigurement
II. hair loss, mainly eyebrows,eyelashes
III. muscle weakness
IV. permanent nerve damage in the arms
and legs
V. inability to use the hands and feet
VI. chronic nasal congestion, nosebleeds,
and collapse of the nasal septum

41. I. iritis (inflammation of the iris of
the eye)
II. glaucoma (an eye disease that
causes damage to the optic
nerve)
III. blindness
IV. erectile dysfunction and
infertility
V. kidney failure

42. Treatment
Sulphones (e.g. dapsone) are the main
therapeutic agents.
Combinations (e.g., dapsone , rifampicin
and clofazimine ) to stop emergence of resistance.
 Should be continued for up to 2 years or until
lesions are organisms-free.
 The disease is completely curable and nodules
can be reversed by treatment.
 Long course of Oral
corticosteroids and thalidomide preventing
nerve damage by reducing swelling.

43. Lepromatous vs. Tuberculoid Leprosy

44. Prevention and control
 The best way to prevent leprosy
is to avoid long-term, close
contact with an untreated,
infected person.
 Infection control measures
 Chemoprophylaxis for contacts

45. Leprosy - one of the few diseases
which can be eliminated
 Leprosy meets the demanding criteria for
elimination
opractical and simple diagnostic tools: can
be diagnosed on clinical signs alone;
oan effective multidrug therapy
oa single reservoir of infection: humans.

46. Mycobacterium leprae (Summary)
 Acid fast bacilli
 Strict human pathogens
 Cannot be cultivated in-vitro
 Armadillo’s used for obtaining M leprae
 Transmission - ? Air borne
 Low infectivity - prolonged contact required
 Spectrum of clinical presentations
◦ dependent on host –parasite interactions
Tuberculoid
Borderline
Tuberculoid
Borderline
lepromatous
Lepromatous

47. ATYPICAL
(MOTT)
MYCOBACTERIA

48. ATYPICAL
)
(MOTT
MYCOBACTERIA
 Refers to Mycobacteria other
than tubercle bacilli the typical
representative of the genus
Mycobacterium.
 opportunistic pathogens
 Habitat:
- Environment (e.g. water and soil)
- Commensals in human secretions

49. Examples of MOTT
M KANSASII
 Infection of respiratory compromised hosts
Present like pulmonary tuberculosis
M SCROFULACEUM
Chronic cervical lymphadenitis in children
(scrofula)
M fortuitum
 Injection related abscesses
Associated with sternal wound infections following
cardo-thoracic surgery

50. M avium intracellulare
Presents as cervical lymphadenopathy
in immunocompetent host
 Tuberculosis-like disease, especially in
in immunocompromised patients (e.g. AIDS):
M. chelonae
Skin, soft tissue
Bone infections and infections of prosthetic
joints

51. Non tuberculous mycobacteria
Diagnosis:
•Like diagnosis of T.B.
•Differentiated by their rate of growth,
pigment production and biochemical
reactions.
•Molecular techniques .

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