Mycoplasma pnemoneia.pptx

Mycoplasma pnemoneia.pptx

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  Mycoplasma pneumoniae Presented to: Dr.P. Saranraj Head, Department of microbiology Sacred heart college (Autonomous) Tirupattur Presented by: M. Monisha (BP211522) I M.Sc. Applied microbiology Department of microbiology Sacred heart college (Autonomous) Tirupattur
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  Content  Introduction  Morphology Pathogenicity of Mycoplasma pneumoniae  Pathogenesis of Mycoplasma pneumoniae  Clinical Diseases by Mycoplasma pneumoniae  Laboratory Diagnosis of Mycoplasma pneumoniae  Treatment  Prevention  Reference
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  Introduction  Pneumonia isan infection of one or both lungs caused by bacteria, viruses and fungi.  It is an endogenous infection because causative agents are contacted from normal flora of respiratory tract.  An infection of lung that involves the small air sacs or alveoli and the tissue around is called pneumonia.
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  Morphology  Mycoplasma pneumoniaeare the smallest free-living bacteria.  Mycoplasma pneumoniae are unique among bacteria because they do not have cell wall and their cell membrane contains sterols.  Pleomorphic  Non-motile, non-capsulated, non-sporing.  Aerobic respiration  Optimum temperature is 37 ͦ C.  Optimum pH is 7.8 – 8.0, Mycoplasma pneumoniae may die if the pH is below 7.  Mycoplasma pneumoniae are found in the mucosa of upper respiratory tract (UTR) and Urogenital tract of humans. Also found in oval cavity.
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  Pathogenicity of Mycoplasmapneumoniae  Disease transmission Mycoplasma pneumoniae causes Respiratory infection that spreads easily through contact with respiratory fluids.  Incubation period is about 1 to 3 Weeks.  Virulence factors of Mycoplasma pneumoniae Adhesin Proteins (P1 Adhesins) Lipoproteins (evades host Immune system)
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  Pathogenesis of Mycoplasmapneumoniae  Mycoplasma pneumoniae is an extracellular pathogen that adheres to the Respiratory epithelium by means of a complex of Adhesions proteins (P1 Adhesin).  The adhesions interact specifically with Isolated Glycoprotein Receptors at the base of Cilia on the epithelial cell surface (and on the surface of erythrocytes).  Ciliostasis then occurs, after which first the cilia, then the ciliated epithelial cells, are destroyed.  The loss of these Cilia cells interferes with the normal clearance of the upper airways and permits the Lower respiratory tract to become contaminated with microbes and mechanically irritated. This process is responsible for the Persistent cough present in patients with symptomatic disease.  Mycoplasma pneumoniae functions as a Superantigen ( antigens that result in excessive activation of the immune system), stimulating inflammatory cells to migrate to the site of infection and release Cytokines, initially Tumor Necrosis Factor-α and Interleukin-1 (IL-1) and later, IL-6. This process contributes to both the clearance of the bacteria and the observed disease.  A number of Mycoplasma pneumoniae are able to rapidly change expression of surface lipoproteins, which is believed to be important for evading the host immune response and establishing persistent or chronic infections.
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  Clinical diseases byMycoplasma pneumoniae  Exposure to Mycoplasma pneumoniae typically results in asymptomatic carriage.  The most common clinical presentation of Mycoplasma pneumoniae infection is Tracheobronchitis (Lower respiratory tract infection particularly in Windpipe and Bronchi).  Low grade fever, Malaise, Headache, and a dry, non-productive cough develop 2 to 3 weeks after exposure.  Acute Pharyngitis (Inflammation of the pharynx) may also be present.  Symptoms gradually worsen over the next few days and can persist for 2 weeks or longer.  The Bronchial passages primarily become infiltrated with Lymphocytes and Plasma cells.  Pneumonia (referred to as Primary Atypical Pneumonia or Walking Pneumonia) can also develop, with a patchy Bronchopneumonia.  Myalgias and Gastrointestinal tract symptoms are uncommon.  Secondary complications include Neurologic abnormalities (e.g., Meningoencephalitis, Paralysis and Myelitis), Pericarditis, Hemolytic anemia, Arthritis and Mucocutaneous lesions.
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  Clinical Manifestation  Symptomsof pneumonia include,  Shortness of breath  Fever  Chills  Cough  Chest pain  Pain during inhalation  Fluid around lungs – pleural effusion.  Abscess  Emphyema  Rust-coloured sputum.
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  Complications  Complications ofpneumonia are  Local destruction of lung tissue  Frank cavitation  Respiratory failure  Respiratory distress syndrome  Bronchiectasis  Ventilator dependence  Pulmonary abscess  Emphyema  Superinfection  Death.
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  Laboratory diagnosis ofmycoplasma pneumoniae  Microscopy is of no diagnostic value because Mycoplasma pneumoniae have no cell wall.  The colony morphology on Eaton’s agar  Unlike other Mycoplasmas, Mycoplasma pneumoniae is a strict aerobe.  The Mycoplasma pneumoniae grow slowly in culture, with a generation time of 6 hours.  Colonies of Mycoplasma pneumoniae are small and have a homogeneous granular appearance (“Mulberry shaped”), unlike the fried-egg morphology of other Mycoplasmas.  Serology (Antibody detection) like Enzyme Immunoassay (EIA), Complement fixation test (CFT) and Cold Agglutination test  Molecular diagnosis like 16S rRNA Sequencing and Polymerase Chain Reaction (PCR).
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  Treatment and prevention Drug of choice is Erythromycin, Doxycycline or Fluoroquinolones  Immunity to reinfection is not lifelong, and vaccines have proved ineffective
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  Reference  Medical Microbiologyby S. Rajan Pg. No: 155 – 159.  Medical Bacteriology (Chapter-42 Mycoplasma pneumoniae) by Dr. P. Saranraj Pg. No: 205
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