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MYCOBACTERIUM
TUBERCULOSIS
MYCOBACTERIUM-INTRODUCTION
• Mycobacterium is a genus within the orderActinomycetales that
comprises a large number of well characterised species, several of
which are associated with human and animal disease such as
tuberculosis and leprosy.
• Aerobic bacilli –non spore forming
• non motile,rod shaped.
• Cell wall –rich in lipids
• Acid-fast bacilli
• Very slow growing
CULTURE-m.tuberculosis
• It includes non-selective and a selective media.
• There are three general formulation that can be
used for both the media
they are:
– Semisynthetic agar media
– Inspissated egg media
– Broth media
Mycobacterium tuberculosis
• The bacterium that causes tuberculosis.
• M. tuberculosis has unusually waxy walls, is slow-growing and
among the most recalcitrant bacteria to treatment.
• Thin straight rods-0.4x 3m.
• On artificial media, coccoid and filamentous forms are seen with
variable morphology from one species to another.
• cannot be classified as either gram-positive or gram-negative
• The Ziehl-Neelsen technique of staining is employed for
identification of acid-fast bacteria.
CONSTITUENTSOF TUBERCLE BACILLI
⦿The constituents listed below are found mainly in cell walls.
⦿ Mycobacterial cell walls can induce delayed
hypersensitivity and some
resistance to infection.
– Lipids-mycolicacid,waxes,phosphatides
– Proteins-induce tuberculin sensitivity
– Polysaccharides
PATHOGENSIS
• Inhaledaerosols
Engulfedbyalveolarmacrophages
Bacillireplicate
Macrophagesdie
locallymphnodes
Primarycomplex
• Infectedmacrophagesmigrate
• DevelopGhon’sfocus
• Cellmediatedimmuneresponse
stopscycleofdestructionandspread
• Viablebutnonreplicatingbacillipresentinmacrophages
CLINICAL PRESENTATION
• Pulmonary tuberculosis
Primary complex
Asymptomatic
HEALS
REACTIV
A
TION
Post-primary
tuberculosis
Acutepulmonary disease
Systemic spread
Aymptomatic /symptomatic
LATER DISEASE
Renal / CNSetc
MILIARYTUBERCULOSIS
Pulmonary
meningitis
PRIMARY INFECTION TYPE OF TB
⦿When a host has first contact with tubercle bacilli, the following
features are usually observed:
(1)An acute exudative lesion develops and rapidly spreads to the
lymphatics and regional lymph nodes. The exudative lesion in tissue
often heals rapidly.
(2)The lymph node undergoes massive caseation, which usually
calcifies.
(3)The tuberculin test becomes positive.
⦿This primary infection type occurred in the past, usually in childhood
but now frequently in adults who have remained free from infection
and therefore tuberculin-negative in early life.
⦿In primary infections, the involvement may be in any part of the lung
but is most often at the base.
REACTIVATION TYPE OF TB
⦿The reactivation type is usually caused by tubercle bacilli that
have survived in the primary lesion.
⦿Reactivation tuberculosis is characterized by chronic tissue lesions,
the
formation of tubercles, caseation, and fibrosis.
⦿Regional lymph nodes are only slightly involved, and they do not
caseate.
⦿The reactivation type almost always begins at the apex of the lung,
where the oxygen tension (PO2) is highest.
⦿These differences between primary infection and reinfection
or reactivation are attributed to
(1)resistance and
(2)hypersensitivity induced by the first infection.
DIAGNOSIS
⦿Specimens
fresh sputum, gastric washings, urine, pleural fluid, cerebrospinal
fluid, joint fluid, biopsy material, blood, or other suspected material.
⦿Smears
Sputum, exudates, or other material is examined for acid-fast bacilli by
Ziehl-Neelsen staining.
Stains of gastric washings and urine generally are not recommended,
because saprophytic mycobacteria may be present and yield a
positive stain.
Fluorescence microscopy with auramine-rhodamine stain is more
sensitive than acid-fast stain.
If acid-fast organisms are found in an appropriate specimen, this is
presumptive evidence of mycobacterial infection.
TUBERCULIN TESTS
⦿In an individual who has not had contact with mycobacteria, there is no reaction.
⦿An individual who has had a primary infection with tubercle bacilli develops
induration, edema, erythema in 24–48 hours, and, with very intense reactions,
even central necrosis.
⦿The skin test should be read in 48 or 72 hours.
⦿It is considered positive if the injection of 5 TU[Tuberculin units] is followed
by induration 10 mm or more in diameter.
⦿Positive tests tend to persist for several days. Weak reactions may disappear more
rapidly.
Interpretation of TuberculinTest
• A positive tuberculin test indicates that an individual has been infected
in the past.
• It does not imply that active disease or immunity to disease is present.
• Tuberculin-positive persons are at risk of developing disease from
reactivation of the primary infection, whereas tuberculin-negative
persons who have never been infected are not subject to that risk,
though they may become infected from an external source.
TREATMENT
• Anti-tuberculous drugs
– INAH
– Rifampicin
– Ethambutol
– Pyrazinamide
• Multi-drug resistant tuberculosis
mycobacterium tuberculosis
mycobacterium tuberculosis

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mycobacterium tuberculosis

  • 2. MYCOBACTERIUM-INTRODUCTION • Mycobacterium is a genus within the orderActinomycetales that comprises a large number of well characterised species, several of which are associated with human and animal disease such as tuberculosis and leprosy. • Aerobic bacilli –non spore forming • non motile,rod shaped. • Cell wall –rich in lipids • Acid-fast bacilli • Very slow growing
  • 3. CULTURE-m.tuberculosis • It includes non-selective and a selective media. • There are three general formulation that can be used for both the media they are: – Semisynthetic agar media – Inspissated egg media – Broth media
  • 4. Mycobacterium tuberculosis • The bacterium that causes tuberculosis. • M. tuberculosis has unusually waxy walls, is slow-growing and among the most recalcitrant bacteria to treatment. • Thin straight rods-0.4x 3m. • On artificial media, coccoid and filamentous forms are seen with variable morphology from one species to another. • cannot be classified as either gram-positive or gram-negative • The Ziehl-Neelsen technique of staining is employed for identification of acid-fast bacteria.
  • 5.
  • 6. CONSTITUENTSOF TUBERCLE BACILLI ⦿The constituents listed below are found mainly in cell walls. ⦿ Mycobacterial cell walls can induce delayed hypersensitivity and some resistance to infection. – Lipids-mycolicacid,waxes,phosphatides – Proteins-induce tuberculin sensitivity – Polysaccharides
  • 7. PATHOGENSIS • Inhaledaerosols Engulfedbyalveolarmacrophages Bacillireplicate Macrophagesdie locallymphnodes Primarycomplex • Infectedmacrophagesmigrate • DevelopGhon’sfocus • Cellmediatedimmuneresponse stopscycleofdestructionandspread • Viablebutnonreplicatingbacillipresentinmacrophages
  • 8. CLINICAL PRESENTATION • Pulmonary tuberculosis Primary complex Asymptomatic HEALS REACTIV A TION Post-primary tuberculosis Acutepulmonary disease Systemic spread Aymptomatic /symptomatic LATER DISEASE Renal / CNSetc MILIARYTUBERCULOSIS Pulmonary meningitis
  • 9. PRIMARY INFECTION TYPE OF TB ⦿When a host has first contact with tubercle bacilli, the following features are usually observed: (1)An acute exudative lesion develops and rapidly spreads to the lymphatics and regional lymph nodes. The exudative lesion in tissue often heals rapidly. (2)The lymph node undergoes massive caseation, which usually calcifies. (3)The tuberculin test becomes positive. ⦿This primary infection type occurred in the past, usually in childhood but now frequently in adults who have remained free from infection and therefore tuberculin-negative in early life. ⦿In primary infections, the involvement may be in any part of the lung but is most often at the base.
  • 10. REACTIVATION TYPE OF TB ⦿The reactivation type is usually caused by tubercle bacilli that have survived in the primary lesion. ⦿Reactivation tuberculosis is characterized by chronic tissue lesions, the formation of tubercles, caseation, and fibrosis. ⦿Regional lymph nodes are only slightly involved, and they do not caseate. ⦿The reactivation type almost always begins at the apex of the lung, where the oxygen tension (PO2) is highest. ⦿These differences between primary infection and reinfection or reactivation are attributed to (1)resistance and (2)hypersensitivity induced by the first infection.
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  • 13. DIAGNOSIS ⦿Specimens fresh sputum, gastric washings, urine, pleural fluid, cerebrospinal fluid, joint fluid, biopsy material, blood, or other suspected material. ⦿Smears Sputum, exudates, or other material is examined for acid-fast bacilli by Ziehl-Neelsen staining. Stains of gastric washings and urine generally are not recommended, because saprophytic mycobacteria may be present and yield a positive stain. Fluorescence microscopy with auramine-rhodamine stain is more sensitive than acid-fast stain. If acid-fast organisms are found in an appropriate specimen, this is presumptive evidence of mycobacterial infection.
  • 14. TUBERCULIN TESTS ⦿In an individual who has not had contact with mycobacteria, there is no reaction. ⦿An individual who has had a primary infection with tubercle bacilli develops induration, edema, erythema in 24–48 hours, and, with very intense reactions, even central necrosis. ⦿The skin test should be read in 48 or 72 hours. ⦿It is considered positive if the injection of 5 TU[Tuberculin units] is followed by induration 10 mm or more in diameter. ⦿Positive tests tend to persist for several days. Weak reactions may disappear more rapidly.
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  • 16. Interpretation of TuberculinTest • A positive tuberculin test indicates that an individual has been infected in the past. • It does not imply that active disease or immunity to disease is present. • Tuberculin-positive persons are at risk of developing disease from reactivation of the primary infection, whereas tuberculin-negative persons who have never been infected are not subject to that risk, though they may become infected from an external source.
  • 17. TREATMENT • Anti-tuberculous drugs – INAH – Rifampicin – Ethambutol – Pyrazinamide • Multi-drug resistant tuberculosis