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UNIVERSITY OF CAPE COASST

MLS303A: MICROBIOLOGY III

PRESENTATION ON THE TOPIC: MYCOBACTERIUM


TUBERCULOSIS

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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

• The diagram above illustrate colony of


Mycobacterium tuberculosis in a culture media

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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

• lipoarabinomannan (LAM) is structurally and


functionally analogous to the lipopolysaccharide of
Gram-negative bacteria
• Transport proteins and porins are interspersed
throughout the cell wall
 antigenic
 Extracted and partially purified preparations of
these protein derivatives (PPDs) are used for
tuberculin test.
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A DIAGRAM OF THE CELL STRUCTURE

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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

• Infections begun around the 18th and 19th centuries in


urban areas,
• The disease flourish with ignorance, poverty, overcrowding
and poor ventilation
• Attack rates still high in developing countries
• The majority of tuberculosis infection is contracted through
respiratory route by inhalation of droplet nuclei carrying
the causative organism
• Repeated coughing, sneezing by infectious person
generate infectious dose into the air which is inhaled by
other people.
• It can also be contracted through ingestion of milk from
tuberculos cow

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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

• Pulmonary tuberculosis− sputum


• Renal tuberculosis − urine
• Tuberculos meningitis −CSF

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LABORATORY DIAGNOSIS

• Tuberculin Skin Test


• Infection with M. tuberculosis typically leads to the
development of delayed hypersensitivity to MTB antigens,
which can be detected by the tuberculin (Mantoux) test.
• About 2 to 4 weeks after infection, intracutaneous injection
of purified protein derivative of M. tuberculosis (PPD)
induces a visible and palpable induration that peaks in 48
to 72 hours
• A positive tuberculin test result signifies cell-mediated
hypersensitivity to tubercular antigens
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TUBERCULIN TEST RESULTS

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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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