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Transcript
College of Medicine
Microbiology
Adv. Bacteriology
Mycobacterium:
Dr.Jawad Kadhim Tarrad
----------------------------------------------------------------------------------------Mycobacterium tuberculosis (Koch bacillus):
Important properties :
 It is acid-fast bacillus(AFB).
 It is non-capsulated.
 It is non-motile.
 Strict aerobe.
 Facultative intracellular.
Source and Transmission:
 Humans are only natural host of M.tuberculosis (strict human pathogen).
 M.tuberculosis transmitted direct from infected person to person by respiratory
aerosol(droplet nuclei) during coughing and sneezing or by saliva exchange
during mouth kissing. The organism also can be transmitted by fomite of
patients. Latent cases can not contagious.
Virulence factors :
1. Virulence of the organism depends on several toxic compounds of cell wall,
such Lipoarabinomannan(LAM) acts as endotoxin. The bacterium does not
produce toxin.
2. Facultative intracellular survival: ability of organism to multiply inside
macrophages, and escape of immune response mechanisms.
Pathogenesis:
 The pathogenicity is dependent on presence of organism and immune response
of host.
 When the mycobacteria inhale and establish themselves in tissues, they
engulfed by alveolar macrophage. The organisms can be survive and
proliferate inside macrophages (intracellular survive) especially in
monocytes, reticuloendothelial cells, and giant cells. This phagocytic cell may
act as vehicle transporting the infection to other organs.
 Two types of lesion: Exudative lesion, when a host has first contact with
tubercle bacilli, the immune response represent with acute inflammatory
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reaction and edema fluid; polymorphonuclear leukocytes; and, later,
monocytes accumulate around the tubercle bacilli. Productive phase; Tubercle
formed by cell-mediated immunity (CMI) response during 2-6wk after
infection. A caseous (cheesy) tubercle may erode into bronchus or blood,
empty its contents and form acavity (open tubercle) result in progression of
active disease, or it progresses into healing by fibrosis or calcification. It
becomes calcified and enclosed in dense connected tissue capsule (enclosed
tubercle).


Miliary disease : Miliary distribution can results from tubercle erosion and
dissemination via blood stream or lymphatics with subsequent involvement of
any organs especially in well-oxygenated tissues. If a caseating lesion
discharges its contents into a bronchus, they are aspirated and distributed to
other parts of the lungs, or they are swallowed and passed into the stomach
and intestines.
Because the bacteria can survive for many years inside tubercles and therefore
can become reactivated in patients with immunosuppression and cause
secondary infection.
Immunology:
 Cellular immunity : two major mechanisms of host cellular response against
T.B infection :(CMI and DTH).
 CMI refers to activate alveolar macrophages and release TNF-α to kill T.B by
phagocytosis. The activated macrophages are aggregated to form granuloma,
which has anoxic and acidic center, leading to tissue necrosis. This
environment does not favour for growth of the organism, most T.B die.
 DTH functions to kill intracellular T.B by lysing infected macrophage(T.Bcontaining macrophage) by cytotoxic T-cells.
 Humoral immunity: Abs are formed but not play important role in resistance
of host.
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Diseases and clinical features:
1. Pulmonary tuberculosis: After 1-2 months following exposure, two types of
lesion are developed:
Primary pulmonary tuberculosis; usually occur in highly oxygenated tissues
of lungs, when a host has first contact with tubercle bacilli. The primary
infection type occurred usually in childhood, and involved any part of the lung
but most often the mid-lung fields or the base such as lower lobes. The
primary site of infection in lung which located in either upper part of lower
lobe or in lower part of upper lobe.
There are two lesions of primary infection: (i) Exudative lesion, it consists of
an acute inflammatory reaction with edema fluid; polymorphonuclear
leukocytes; and, later, monocytes accumulate around the tubercle bacilli. (ii)
Productive lesion (granuloma and tubercle formation). It is consists of three
zones: (1) a central area of large, multinucleated giant cells containing tubercle
bacilli; (2) a mid-zone of pale epithelioid cells, often arranged radially; and (3)
a peripheral zone of fibroblasts, lymphocytes, and monocytes. Finally it is
surrounded by fibrous tissue , and the central area undergoes caseation
necrosis (liquefaction), such lesion is called a tubercle. Tubercle formed by
cell-mediated immunity (CMI) response during 2-6wk after infection.
 Secondary pulmonary tuberculosis (re-infection, reactivation): is primarily
occur in immunocompromised persons, or lower immunity (adult persons over
50 years old). Reactivation tuberculosis is characterized by chronic tissue
lesions, formation of tubercles, caseation, and fibrosis. Regional lymph nodes
are slightly involved, and they do not caseate. The reactivation type almost
always begins at the apex of the lung, where the oxygen tension is highest.
 Typical clinical features of tuberculosis are chest pain, persist cough,
breathlessness, night sweat, weight loss, hemoptysis, lethargy, fever and
others. T.B causes tuberculosis which mean (loss of body weight). Most Tb
infections are asymptomatic cases 90% (latent infection).
2. Extra-pulmonary tuberculosis:
Military tuberculosis (disseminated lesion) occur when necrotic tubercle
erode into blood vessels or into lymphatic fluid and lead to fulminating
infection in any organ system. 5-20 % of active TB spread outside lungs, in
other well-oxygenated tissues such as kidney, CNS and bone, Skin ….etc. Tb
causes Tuberculous meningitis, tuberculous osteomyelitis , urinary
tuberculosis… and so on.
Epidemiology:
 Tuberculosis occurs worldwide, approximately one-third of world population
is infected (latently infection) with this bacteria, 10% active TB and 90%
Latent TB. Each year from this pool, 8-10 millions, new active cases occur.
New infection take at rate one per second.
 Mortality rate is 2-3 million persons die annually therefore the disease is
called king of disease.
Lab. Dx:
 Staining with Ziehl-Nelseen stain display typical AFB.
 Lowenstein-Jenson agar is selective medium for isolation of T.B human type.
The culture must be incubated at 37C for 4-8wk.
 Tuberculin skin test(Mantoux test): this test widely used in diagnosis of TB.
 Serologic tests are little helpful in diagnosis.
 PCR is used for detection of DNA.
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 Radiography examination: X-ray for chest ,bone, kidney.
Control and therapy:
 Rifampicin and Isoniazid are first line of therapy. Streptomycin and
Kanamycin are second line. The treatment should be given for long time
(6-12months).
 BCG vaccine(Bacillus Calmette-Guerin) is conferring for up to 5-7 years
protection. It is not given for immunocompromised individuals.
 Enhance conditions of housing and nutrition.
 The use masks and other respiratory isolation procedures to prevent spread to
medical personnel are important.
Mycobacterium bovis (bovine type)
It is found in cattle. It is transmitted from animal to human by ingestion of unpasteurized milk and cause gastrointestinal tuberculosis in rare cases. The GI
tuberculosis also can be caused by M.tuberculosis when it swallowed after being
coughed up from a lung lesion.
Mycobacterium leprae :
Important properties:
 It is acid-fast rod.
 It is non-capsulated.
 It is non-motile.
 Obligated aerobes.
 Facultative intracellular.
Source and transmission:
 Humans are only natural host for M.leprae.
 It is transmitted via direct contact ,prolonged exposure to infected sources.
Pathogenesis:
 The optimal temperature for growth of M.leprae is (30Ċ) lower than body
temperature , it therefore grows preferentially in cooler tissues of the body:
skin , superficial nerves, nose, pharynx , larynx ,eyes and testicles .
 The organism replicate inside (intracellular) macrophages, typically within
skin histocytes, endothelial cells and Schwann cells of nerves, it induces
CMI, T-helper cell, epitheloid and giant cells causing large patches with
elevated red edges on skin at site of entry. These patches have dry , pale,
hairless center with loss of sensation.
Pathogenicity and clinical features:
 It strict human pathogen and causes leprosy (Hansen disease) that uncommon.
 The incubation period average several years, probably 2-10 years or more..
 The leprosy lesions are divided into two major types; Tuberculoid and
lepromatous. The leprosy causes tissue and nerve damage.
 Tuberculoid leprosy(TL) the course is nonprogressive and benign , with a
small number of macular skin lesions containing few bacilli, severe
asymmetric nerve involvement of sudden onset. The hypopigmented macular
or plaque lesions are displayed on trunk, face, and limbs. These lesions have
raised erythromatous edge and dry, pale, hairless center that may be
hypopigmented. It invades sensory nerves, causing thickened superficial
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nerves and significant anesthesia (loss of sensation) of skin lesions. Systemic
manifestations of eye infection, anemia and lymphadenopathy may also occur.
 Lepromatous leprosy(LL) the course is progressive and malignant, with
nodular skin lesions; slow, symmetric nerve involvement. It is characterized
by formation of large granulomatous lesion, multiple nodular skin lesions
occur, such as facial disfigurement, anesthesia (sensory loss). Thickening of
skin of forehead, ear lobes, and lips, results in leonine face(lion-like face).
Control:
 LL is treated by triple therapy with dapsone, rifampin, clofzimine. It is given
for minimum of 2 years or longer for lifelong. TT is tread by combination of
dapsone and rifampin for 6 months.
 Hospitalized isolation of all patients in special rooms.
 Vaccine is not available.
Fig. Early and late stages of lepromatous leprosy
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