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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 1 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. 2 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. 3 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 4 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 5