MB 5223 Immunology and Medical Microbiology 2024 PDF
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2024
Debalina Chaudhuri, PhD
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Summary
These lecture notes cover Immunology and Medical Microbiology, focusing on pathogenic microorganisms, particularly Mycobacterium tuberculosis. The document details morphology, staining properties, and various aspects of the bacteria, including diagnostic and treatment methods. It also delves into factors affecting the spread of the disease.
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MB 5223 IMMUNOLOGY AND MEDICAL MICROBIOLOGY Debalina Chaudhuri, PhD 2024 IMPORTANT GROUPS OF PATHOGENIC MICROORGANISMS: (SIGNS, SYMPTOMS, ANTIGENIC STRUCTURE, PATHOGENESIS, DIAGNOSIS, EPIDEMIOLOGY, PROPHYLAXIS AND CHEMOTHERAPY). Mycobacterium t...
MB 5223 IMMUNOLOGY AND MEDICAL MICROBIOLOGY Debalina Chaudhuri, PhD 2024 IMPORTANT GROUPS OF PATHOGENIC MICROORGANISMS: (SIGNS, SYMPTOMS, ANTIGENIC STRUCTURE, PATHOGENESIS, DIAGNOSIS, EPIDEMIOLOGY, PROPHYLAXIS AND CHEMOTHERAPY). Mycobacterium tuberculosis MYCOBACTERIA In liquid cultures, they form a mould -like pellicle (hence, the name mycobacteria, meaning fungus-like bacteria). Do not stain readily, but once stained, resist decolourisation with dilute mineral acids, due to the presence of mycolic acid in their cell wall. They are called acid fast bacilli (AFB). Slow-growing (generation time of 14-15 hours; colonies appear between two weeks to eight weeks), aerobic, non- motile, non-capsulated and non-sporing. The genus Mycobacteria contains three groups: 1. Obligate parasites: Mycobacterium tuberculosis 2. Opportunistic pathogens and 3. Saprophytes. Mycobacterium tuberculosis Morphology Straight or slightly curved rod, about 3 µm x 0.3 µmin size, occurring singly, in pairs or as small clumps. Acid fast staining: They differ in their staining property from other bacteria. ACID FAST: ZN STAINING When stained with carbol fuchsin by the Ziehl-Neelsen method, they resist decolorization by 20% sulphuric acid and therefore called acid fast. Acid fastness has been ascribed to the presence of an unsaponifiable lipid- rich (mycolic acid) material in the Carbol-fuschin, which is basic, strongly binds to the negative components of the bacteria which include the mycolic acid and the lipid cell wall. cell wall or to a semipermeable Addition of acid alcohol along with the application of heat forms a strong complex that can not be easily washed off with solvents. membrane around the cell. MEDIA Liquid Solid Lowenstein-Jensen ( LJ) media Dubo’s - coagulated hen eggs Middlebrook’s - mineral salt solution Proskauer and Beck’s - asparagine - malachite green (acts as a selective agent inhibiting other bacteria) Other solid media: - egg containing (Petragnini, Dorset), - blood (Tarshis), - serum (Loeffler) or - potato (Pawlowsky) MEDIA Automated culture methods: BACTEC MGIT This is an automated mycobacteria growth indicator tube (MGIT). It is a rapid growth detection method, which uses 7H9 Middlebrook medium with fluorometric detection technology via oxygen consumption. An added advantage is that the incorporation of Pyrazinamide (PZA) in the medium detects resistance to this drug. *The enzyme pyrazinamidase hydrolyses pyrazinamide to ammonia and pyrazinoic acid which is detected by adding ferric ammonium sulphate. This is positive in M.tuberculosis ANTIGENIC PROPERTIES Lipids: The mycobacterial cell wall is rich in mycolic acid. Mycolic acids play a role in pathogenesis and, when complexed with peptidoglycan, are responsible for granuloma formation. Another factor called cord factor is also responsible for the virulence of bacteria. Proteins: These induce delayed type hypersensitivity and elicit tuberculin reaction. Polysaccharides: Can induce immediate type of hypersensitivity. TUBERCULOSIS Tuberculosis is a potentially fatal infection, caused mainly by M.tuberculosis, that can affect any part of the body, with lungs being the most common organ involved. Source: An open case of tuberculosis in India may infect, on an average, 25 contacts before death or cure. Direct inhalation of aerosolised bacilli contained in the droplet nuclei of expectorated sputum. Infection also occurs infrequently by ingestion, for example, through infected milk, and rarely by inoaculation. INFECTION The inhaled bacilli are arrested by the natural defences of the upper respiratory tract. Those that escape reach the lungs and are phagocytosed by the alveolar macrophages. Several factors including the number and virulence of the infecting bacilli, host factors including genetic susceptibility, age, immunocompetence, stress, nutrition and co- existing illness influence the outcome of the infection. INFECTION AND IMMUNITY Cell-mediated immunity is the specific immune mechanism that plays a major role in tuberculosis. Humoral immunity has little or no role in protection or pathogenesis. Key cell is the activated CD4+ helper T cell. Allergy and immunity: Infection with the tubercle bacillus induces cell-mediated immunity which manifests as delayed type hypersensitivity and resistance to infection (immunity). The resultant of these two processes determines the course of the infection. PATHOLOGY The essential pathology in tuberculosis is the production of a characteristic lesion, the tubercle, in infected tissues. This is an avascular granuloma composed of a central zone containing giant cells, with or without caseation(necrotic cells), and a peripheral zone of lymphocytes and fibroblasts. PATHOLOGY Tuberculous lesions are primarily of two types: exudative and productive. Exudative type: Acute inflammatory reaction with accumulation of edema fluid, polymorphonuclear leucocytes, and later of lymphocytes and mononuclear cells. This is typically seen when there are plenty of virulent bacilli and the host response is DTH than of protective immunity. Productive type: Predominantly cellular, associated with protective immunity. PATHOLOGY Primary tuberculosis is the initial Post-primary (secondary or adult) infection by the mycobacteria in a tuberculosis is due to reactivation of host. In endemic countries like India, latent infection (post-primary young children usually are more progression, endogenous reactivation) susceptible. or exogenous re-infection. Lower lobe or the lower art of the upp upper lobes of the lungs affected er lobe affected In the immunodeficient, there is widespread dissemination of lesions in the lungs and other organs FACTORS OF SPREAD Poverty HIV-AIDS Multiple Drug resistance among tubercle bacilli. Sputum, laryngeal aspirates DIAGNOSIS or bronchial washings may be collected. In small children who tend to swallow the sputum, gastric lavage. Demonstrating the bacilli in the lesion, by microscopy. ZN Isolating the bacilli in culture. LJ Using molecular diagnostic methods to detect DNA or RNA of the bacilli from clinical specimen. PCR Demonstrating hypersensitivity to tuberculoprotein. SYMPTOMS AND TREATMENT Hemoptysis: Cough with blood PREVENTION