Professional Documents
Culture Documents
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GROUP 13
• PS/MLB/16/0072
• PS/MLB/16/0073
• Ps/MLB/16/0074
• PS/MLB/16/0075
• PS/MLB/16/0076
• PS/MLB/16/0077
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CONTENT
• INTRODCTION
• GENERAL CHARACTERISTICS
• MORHOLOGY
• TAXONOMY
• DISEASE CAUSED
• PATHOGENESIS
• VIRULENCE
• EPIDERMIOLOGY
• SIGNS AND SYMTOMS
• LABORATORY DIAGNOSIS
• REFERENCES
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INTRODUCTION
• Mycobacterium tuberculosis is a pathogenic
bacteria that demonstrate the staining
characteristics of acid fastness.
• It was discovered by Robert Koch in the year 1892
while working in Berlin and the means of
culturing the organism.
• He cultured them on Lowenstein Jensen medium
which contain nutrient required for their growth.
However their growth was very slow.
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GENERAL CHARACTERISTICS
• They are obligate aerobes
• They are non −motile and do not form spores
• Slow rate of growth and require s rich medium
as well as carbon dioxide for growth
• They are acid− fastness
• They are sensitive to heat but resistant to
drying
• They are rod in shape
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COLONY CHARACTRISTICS
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CONTINUATION
• Pale yellow, rough surface are typical
morphological characteristics seen in M
tuberculosis
• they grow best at 37◦C
• Habitat : found in soil, water, dust, and can
live in the body
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MORPHOLOGY
• Shape −long, slender, straight or slightly curved bacilli(rod)
• Mycolic acid, waxes, and lipid are present in cell.
• High lipid content approximately 60% of the total cell wall
mass .
• They have hydrophobic core and tend to clump together.
• The cell wall contains peptidoglycan similar to that of gram
positive organism , except that it contain N
−glycolymuramic instead of N− acetylmuramic acid
• Size − 0.4×0.3µm
• non−capsulated.
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CONTINUATION
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TAXONOMY
• Domain: Bacteria
• phylum: Actinobacteria
• class: Actinobacteria
• Order: Actinomycetales
• Suborder: Corynebacterineae
• Family: Mycobacteriacea
• Genus : Mycobacterium
• Species : Mycobacterium tuberculosis
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DISEASE THEY CAUSED
Extrapulmonary tuberculosis occuring
outside the respiratory tract.
Potts's disease —paralysis, Spine TB
Lupus vulgaris -skin
Scrofula —characterized by swellings of the
lymphatic glands
TB synovitis —hips, bone, wrist, elbow
Renal TB —dysuria, hematuria,
Genital TB —affects reproductive function
TB meningitis —mental deterioration,
retardation, blindness,
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SOME TUBERCULOSIS PATIENTS
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CONTINUATION
They can also caused pulmonary tuberculosis
which affect the lungs. Below are TB patients
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PATHOGENESIS
• Individuals immunological response
determines the outcome of exposure
• Inhaled organisms are deposited in the
peripheral respiratory alveoli and are engulf
by activated macrophages.
• They multiply in the macrophages if the
macrophages fails to destroy them
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PRIMARY INFECTION
• 6-12 weeks after initial infection
• alveolar macrophage infected with M. tuberculosis releases
interleukins 12 and 18
• These attract and stimulate T lymphocytes (mainly CD4)
• CD4 cell meets mycobacterial antigen presented by
macrophage and becomes activated= transformed
• CD4 cells release interferon gamma
• interferon gamma stimulates macrophage to secrete
regulatory factors including tumor necrosis factor alpha
(TNF alpha).
• TNF alpha increases macrophages ability to kill M
tuberculosis and is required for granuloma formation 16
POST PRIMARY INFECTION
.
• When the defenses fail, a mature tubercle may
form whereby the caseous center will enlarge
and liquefy to form a tuberculous cavity where
the bacilli multiply outside the macrophages.
• The tubercle eventually ruptures, releasing
tubercle bacilli that can disseminate throughout
the lungs and then to the circulatory and
lymphatic systems (MiliaryTb).
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A GRANULOMA OF TUBERCULOSIS
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VIRULENCE
• Ability to multiply in macrophage is central
virulence
• Mycolic acid, lipids, lipoarabinomanna(LAM)
help to disrupt phagosome− lysosome
interaction and interfere with oxidative killing
• They also modulate cytokines and inhibit
killing.
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EPIDERMIOLOGY
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CONTINUATION
• It can be prevented through vaccination with
Bacillus Calmette Guerin(BCG) . It is an
attenuated strain of M tuberculosis that does
not cause disease but can stimulate the
immune response.
• Antimicrobial agent used for treatment
include isoniazid, rifampin, streptomycin etc.
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RISK FACTORS
• Weak immune system especially in children
and disease conditions that weaken the
immune system e.g. HIV, cancer etc
• Smoking. This destroys the cilia in the
respiratory tract and also weakens the
alveolar macrophages.
• Health care workers .
• People who live with individuals with active TB
infection.
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SIGNS AND SYMPTOMS
• Coughing
• Chest pain
• Blood present in sputum(hemoptysis)
• Weight loss
• Loss of appetite
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SPECIMEN REQUIRED FOR DIAGNOSIS
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LABORATORY DIAGNOSIS
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DIAGNOSIS
• Auramine-Rhodamine Fluorochrome Staining
• Auramine-Rhodamine, forms a complex with
mycolic acids in cell wall
• esist decolorization by acid-alcohol.
• The counterstain, potassium permanganate,
renders tissue and its debris non-fluorescent,
thus reducing the possibility of artifacts.
• The cells visualized under ultraviolet light
appear bright yellow or reddish orange.
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M TUBERCULOSIS IN AURAMINE STAIN
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CONTINUATION
• Other techniques include Ziehl Nelseen stain.
• The bacteria resist decolorization by acid
alcohol after forming complex with carbol
fuschine.
• They appear red when observing the smear
under the microscope while the background
and other cells appear blue.
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A FIGURE SHOWING M TUBERCULOSIS
IN ZIEHL NELSEEN STAIN
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REFERENCES
• Ryan, Kenneth J, Ray, C. George (2004).”Mycobacteria”
Sherris Medical Microbiology. “An introduction to
infectious disease”(4th edition). New york: McGraw-
Hill. page 439−455.
• Gordon, S.V. Parish, T. (2018) .Microbe profile.
Mycobacteria tuberculosis: Humanity deadly
microbial foe. 437−439
• Keane J, Balcewicz−Sablinska MK, Remold HG, (1997).
Infection by “ Mycobacteria tuberculosis promotes
human alveolar macrophages apoptosis” Infection and
immunity. 298−304 .
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