Mycobacterium Study PDF

MYCOBACTERIA  GENUS MYCOBACTERIA GENERAL CHARACTERISTICS The Genus Mycobacteria has approximately more CELL WALL than 100 species and the two familiar ones are the Very unique , has...

MYCOBACTERIA  GENUS MYCOBACTERIA GENERAL CHARACTERISTICS The Genus Mycobacteria has approximately more CELL WALL than 100 species and the two familiar ones are the Very unique , has an extremely high lipid M. tuberculosis and M. leprae. content. 2 major groups: MTB Complex and NTMs lipid content has N-glycolylmuramic MTB Complex acid NTMs “Acid-fastness” Mycobacteria belongs to the Family Strictly aerobic Mycobacteriaceae An increase in the carbon dioxide They are slender, slightly curved or straight, and rod- concentration will hasten or pop-up shaped organisms. glycemia or will enhance the growth of some species. Nonmotile and non-spore formers  Mycobacterium tuberculosis COMPLEX The term complex is often used in microbiology to describe two or more species whose distinction is complicated, that’s why it is complex. The MTB complex is composed of the following organisms: M. tuberculosis M. bovis M. africanum M. microti M. canetii These organisms are slow growers as they grow more slowly than other bacteria. They possess non-pigmented colonies. These organisms cause tuberculosis.  MOTT Mycobacteria other than the tubercle bacillus RUNYON’S CLASSIFICATION (4 GROUPS) Based on pigment production (usually of yellow pigment) and rate of growth, and whether the pigment was produced in the dark or only after exposure to light. Pigment groups are helpful in the presumptive identification of Mycobacteria. The Runyon’s Classification was designed to classify the species within the genus. Not transmissible Group I: Photochromogens Group II: Scotochromogens Group III: Non-photochoromogens Group IV: Rapid growers (*group I, II, III: based on photosensitivity and are classified as slow growing mycobacteria) GROUP I: PHOTOCHROMOGENS ❖ Slow growers: >7 days to appear on solid media ❖ Develop yellow pigment when exposed to light ❖ No pigment production in the dark  GROUP II: SCOTOCHROMOGENS Slow growers: >7 days to appear on solid media Produce pigment in the light or dark Yellow to orange in the dark Intensifies to orange or red upon exposure to light  GROUP III: NON-PHOTOCHROMOGENS No pigment whether they are grown in the dark or the light White to tan  GROUP IV: RAPID GROWERS Growth >7 days (3-5 days) Do not produce pigments Potentially pathogenic  CLINICALLY SIGNIFICANT SPP Under the genus Mycobacteria we have (2) two clinically significant species. M. tuberculosis M. Leprae Mycobacterium tuberculosis Robert Koch (1882) Oldest communicable disease and leading cause of morbidity and mortality. It causes tuberculosis which usually attacks the lungs but can also attack other parts of the body. Can be transmitted through direct contact: Sneezing, coughing or talking. (3) Three types of Tuberculosis Primary TB Reactivation TB Extrapulmonary TB  PRIMARY TUBERCULOSIS Also called Primary complex Disease of the respiratory tract. Infection in a patient who has never been treated with TB. It is the patient’s first exposure to bacteria. Usually occurs in children and young adults After being exposed to bacteria, the possibility of whether or not you will develop TB will be determined by (3) three factors. Cellular immune response Amount of exposure Virulence of the strain TRANSMISSION Person-to-person contact through air by droplet nuclei with MTB Meaning, from an infected person to another through coughing, sneezing or coughing Airborne droplets from an infected person can enter the respiratory tract of an exposed individual and may reach the alveoli of the lungs  PRIMARY TB PATHOGENICITY Droplet nuclei reaches the alveoli The airborne droplets which contain the bacteria (1-5 micrometers in size) may enter the respiratory tract of individuals reaching the alveoli. Large droplets: reach upper RT Small droplets: go through alveoli (this is where the infection begins)  REACTIVATION TUBERCULOSIS A.k.a. Secondary TB Happens after initial exposure, this is when the infection progressed. This may occur if the individual immune system becomes weakened and can no longer contain the latent bacteria in your body; the bacteria become active and can make the person sick. Latent bacteria means that there is a bacteria in your body but it does not make you sick which happens during primary TB. There is alteration or suppression of the cellular immune response in the infected host which makes the bacteria replicate and progress to disease.  Risk Factors that contributes to the progression from infection to an active disease: Malnutrition Alcoholism Old age Immunosuppression AIDS EXTRAPULMONARY TUBERCULOSIS (EPTB) Infection outside the lungs, this less commonly occur compared to pulmonary TB HIV infection contributes to the increase of EPTB cases. EPTB is a common presentation among HIV patients.  MILIARY TB Life-threatening form of TB that results from massive lymphohematogenous dissemination of the tubercle bacilli. The common sites of the spread of M. TB are the following: Miliary tuberculosis in a Spleen → Liver → Lungs → patient with end-stage liver Bone marrow → Kidney → disease Adrenal gland  EPTB OTHER FORMS Pleural (Tuberculosis Pleural Effusion (TPE)) Meningeal TB/Meningitis One of the most common forms which AsciteRarely; base of the brain where it is usually represented as an acute may develop a very thick gelatinous illness with fever, cough, and pleuritic mass-like lesions chest pain After pulmonary infections The organism M. tuberculosis is Peritoneal TB detected in the pleural fluid or in Manifested by a slow progressive pleural biopsy specimens abdominal swelling from ascites Lymphadenitis s - condition where there is Disease of the children wherein there is accumulation of fluid within the spaces painless swelling of the head and neck of abdomen GI Tuberculosis Genitourinary TB Manifested by abdominal symptoms Involve kidneys and genital organs (pains, obstruction) Skeletal TB Renal TB - Typical UTI and pyuria Manifested by a skeletal of the spine - Male genital TB which appears as a Pott’s Disease/TB spondylitis mass on the scrotum and often occurs Back pain alongside TB  CLINICAL MANIFESTATIONS MTB Fever Hemoptysis - coughing of blood which indicate Night sweats and chills cavitation and necrosis Dyspnea - shortness of breath/fatigue Weight loss Leukocytosis - increased leukocytes because of Positive PPD Test (Purified Protein Derivative) - the increased PMNs and macrophages as part of skin the immune response test that determines if person has TB Anemia - highly prevalent and may indicate the Chest X-ray - presence of cavitations which severity of the TB dse result from tissue necrosis and abscess formation Cough (productive/wet) - typically brings up TB bacilli destroys lung tissues in a cave mucus or sputum formation  TREATMENT TB TB disease can be treated by taking several drugs for at least 6-9 months; the duration of treatment will depend on the physician Currently, there are 10 drugs that are approved by the U.S. Food and Drug Administration for treating TB  It is very important that TB patients are treated and should finish the medicine and take the drugs exactly as prescribed by the physician. If they stop taking the drugs too soon, they can become sick again. If they do not take the drugs correctly, the TB bacteria that are still alive may become resistant to these drugs. TB that is resistant to drugs is harder and more expensive to treat. The more it becomes antibiotic resistant, the more complicated and difficult to treat, and the drugs becomes more expensive as well  MDR-TB Multi-drug Resistant Mycobacterium tuberculosis Resistance to isoniazid and rifampin (rifampicin) - first-line of anti- TB drugs Usually happens when: Only 1 TB drug is used the patient fails to complete the course of medication Requires an extended treatment period: more resistant → more complicated treatment → longer treatment period (+ second-line drugs) → more expensive.  XDR-TB Extensively Drug-resistant Mycobacterium tuberculosis Resistance to isoniazid and rifampin + any fluoroquinolone, and at least one of the injectable second-line anti-TB drugs (referring to: Amikacin, Kanamycin, Capreomycin).  Mycobacterium leprae Rod-shaped CA of Hansen’s disease (leprosy or ketong) Cannot be cultured in vitro but can be cultivated in: Armadillos Footpads of the mice Optimal growth: 30 deg C  LEPROSY Characterized by the Infection of the skin, mucous membranes, and peripheral nerves. TRANSMISSION Direct contact with infected respiratory droplets  LEPROMIN TEST Skin test A small sample of inactivated M.leprae is injected into the forearm. The ability of the host to mount a delayed hypersensitivity reaction against M. leprae. A small lump will form at the injection site which indicates that the correct amount of bacterium has been injected at the correct depth of the skin for the test to be effective. (+): Tuberculoid leprosy Positive: Redness, Swelling, or Other Skin Changes (-): Lepromatous leprosy Negative: No Skin Reaction TREATMENT Dapsone Clofazimine Rifampin THANK YOU!