pneumonia n.
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  1. Pneumonia: Inflammation of alveoli, alveolar ducts, bronchioles, and interstitial tissue of lung that induced by microbial invasion of natural barriers. (Inflammation of lung parenchyma). Barriers to infection: 1-Epiglottis; protects airway from aspiration. 2-Cough Reflex. 3-Mucociliary escalator; Mucus viscosity and cilia motion. 4-Alveolar Macrophage.

  2. Classification of pneumonia: Traditionally, clinicians have classified pneumonia by clinical characteristicsinto "acute" (less than three weeks duration) and "chronic" pneumonias. Acute pneumonia is classified according to etiology, mode of transmission, and place where it was acquired into: 1-Community-acquired acute pneumonia: A-Person-to-Person: 1-Classic bacterial pneumonia: Streptococcuspneumoniae, Haemophilus , Klebsiella pneumoniae, Moraxella catarrhalis, and Aspiration pneumonia (Mixture of bacteria or Staphylococcus aureus).

  3. N A-Person-to-Person: 2-Atypical bacterial pneumonia: Chlamydophila pneumoniae, and Mycoplasma pneumoniae. 3-Viral pneumonia: Influenza virus type A, B, andC, Coronavirus, and others (RSV, Measles , CMV). B-Animal, or Environmental Exposure: -Tularemia. -Legionella pneumophila. -Plague. -Q fever. -Anthrax. 2-Nosocomial Hospital-acquired Pneumonia:

  4. Streptococcus pneumoniae : Transmission: -Reservoir: Human Nasopharynx; Children and adults. (Asymptomatic carrier state) -Droplets inhalation. Pathogenesis and microbial virulence: -Colonization of bronchi and alveoli. -Pneumolysin: Cholesterol-binding toxin; epithelial cell-damage -Production of hydrogen peroxide; cell damage, and inhibition of other bacteria. -Engulfment of microbe by alveolar macrophage; Polysaccharide capsule resist phagocytosis.

  5. N Production of Cytokines; TNF-alpa,IL-1, IL-8 by alveolar macrophage: 1-Filling of alveoli by fluids, bacteria, and few inflammatory cell. 2-Early Consolidation stage; infiltration of alveoli by neutrophils, activation of complement-C3b Pathway CRP-interacts with bacterial teichoic acid. 3-Late Consolidation stage: -Killing of microbe. -Neutrophils heavy infiltration (Hepatization). 4-Infection eradication: -Replacement of neutrophils by alveolar macrophages. Clinical presentation: Acute Lobar pneumonia.

  6. Classic bacterial pathogenesis: R

  7. N Complications of Streptococcus pneumonia: 1-Local: Pleural effusion; Outpouring of fluid into pleural space in 25% of cases. Empyema: in 1% of cases require drainage of fluid. 2-Systemic: The microbe transmitted to lymphatic vessels that drain the infected area of lung; thoracic duct; Bloodstream; bacteremia(Pneumococcemia). -In 25% of cases; blood culture give positive results -Depending on Lympho-Reticular system humoral function; Meningitis. (Splenectomy, Sickle cell pat)

  8. Diagnosis of Classic bacterial pneumonia: Clinical specimens: Sputum, trantrachealaspirate, Broncheoalveolar Lavage, and lung biopsy. Direct: Microscopy: Streptococcus pneumoniae: All species are Gram’s positive lanceolate shaped cocciarranged in pairs or chains, and capsulated.

  9. N Cultural characteristics: -Facultative anaerobic bacteria. -All species show alpha hemolytic activity on blood agar. -All species are Optochin sensitive.

  10. N Haemophilus influenzaeinfection: -Tracheobronchitis and Pneumonia. -Gram’s negative Coccobacilli, rod-shaped pleomorphic bac.

  11. N Isolation of Haemophilus influenzae: -Aerobic or facultative anaerobic bacteria that isolated on chocolate agar (factorX (haemin) and factorV (NAD). -Satellitism phenomenon. Satellitism around Staph. aureus.

  12. N Treatment and prevention: -Beta-Lactam for Streptococcus pneumoniae. -Penicillin-resistant Streptococcus; Mutation in penicillin- binding protein due to transformation. -Macrolide or Fluoroquinolones. -Vaccine: -Capsular antigen active vaccine for Streptococcus and Haemophilus species.

  13. Atypical bacterial pneumonia: 1-Chlamydophilapneumoniae: -Infective stage: Elementary bodies. -Receptor-mediated endocytosis (Intracellular infection) -Infection of Columnar epithelial cells, endothelial cells , macrophages. -Lymphocytic infiltration; Interferon-Gamma; creates persistence infection. -Diagnostic stage: Reticulate bodies. -Clinical presentation: 1-Acute tracheobronchitis. 2-Bronchopneumonia (Patchy infiltrates by Radiography)

  14. N Chlamydophilapneumoniae is associated with Coronary artery disease: 1-Adults with CAD have a high antibodies titer for this bacterium. 2-The microbe is isolated from atherosclerotic lesions. 3-The microbe establish CAD in animal model studies. Diagnosis: Immunofluorescent Microscopy and PCR. Treatment: -Macrolide: Long-term Cmaxof azithromycin. -Multiple doses of Doxycycline over 7 days. -Pregnant women: Erythromycin.

  15. N 2-Mycoplasmapneumoniae: -Infection mainly in individuals aged 5-20 years old. -Smallest prokaryotes that lack cell-wall. -Tip-mediated attachment to columnar epithelial cells- carbohydrate receptor; intracellular invasion. -Exotoxins: 1-ADP-ribosyltransferase: split ADP-ribose from NAD; attach it to G-Protein; inhibition of neutrophils chemotaxis and phagocytosis. 2-Vacuolatingtoxin: apoptosis. -Destruction of epithelial cells with monocytic infiltration.

  16. N Clinical presentation: -Tracheobronchitis (Persistent Cough). -Bronchopneumonia; ( Perivascular and Peribronchial infiltration of monocytes with few neutrophils); Patchy infiltrate by Radiography. -In 50% of severe Mycoplasma infections; mild-hemolytic anemia is detectable due to Cold hemagglutininformation. -Complications: -Encephalitis, Renal disease and arthritis (antibody complex) -Autoimmune thrombocytopenic purpura.

  17. N Erythema multiforme skin rash due to Mycoplasma pneumoniae. Diagnosis: -Direct: PCR or Immunofluorescent Microscopy. -Indirect: serology: Complement fixation or cold agglutinin. Treatment: 1-Macrolide. 2-Resistance strains; Tetracycline or Fluoroquinolones.

  18. Acute Viral Pneumonia: 1-Influenza virus infection: -Enveloped, 8-segments RNA virus. -Orthomyxoviridae. -Type A :infects Man, and animals (birds, pigs) -Type B, C: infects Man only. -Hemagglutinin (HA), and Neuraminidase (NA) are major surface antigens. -Antigenic drift: accumulated chemical changes in HA. -Antigenic shift: Genetic re-assortment between two viruses results in production of new virus with different NA-HA combinations.

  19. N Before 1968; H2N2 (Asian flu ; human). Since 1968; H3N2 (Hong Kong flu; Avian), H5N1 In the last years: H1N1 (Swine flu; Animal-Human). (five genes from swine, two from avian, one from human) Transmission of H1N1: -Respiratory droplets infects upper and lower R.S. Pathogenesis: -Tropism: Specific interaction of viral HA with Columnar epithelial cell Sialic acid containing glycoprotein or glycolipids. -Up-take of virus into endocytic vesicle.

  20. N Tissue Damage: -Replication of viral RNA into nucleus. -Interferon-alpha produced by Columnar epithelial of Large bronchioles; monocytic infiltration in lamina propria ; Lymphocytic infiltration-INF-γ. -Primary infection: Hemorrhagic and necrotizing bronchitis and Tracheobronchitis. -Later infection: Bronchiopneumonia and alveolar damage with extensive fibrosis.

  21. N Treatment and Prevention: Anti-viral drugs: 1-Amantadine or rimantadine; inhibition of viral uncoating process. 2-NA inhibitors: Zanamivir, and peramivir. Vaccines: 1-Inactivated living vaccine. 2-Attenuated vaccine. Both could be given by intramuscular injection or as a Nasal spray.

  22. N 2-Coronaviruses: Greek word; crowndue to crown like appearance of the surface projections. Virology: -Helical, enveloped, single stranded RNA viruses. -Coronaviridae(Co-Vs). Pathogenesis: -Upper respiratory infection in 30% of common cold cases. -Lower respiratory infection: Due to new virus known as SARS-CoV; and MERS-CoV. -SARS-CoV interacts with lungs-cellular receptor (angiotensin-converting enzyme 2).