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25 Infalmmatory Lung Diseases Upper Respiratory Tract Notes

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   PATHOLOGY OF LUNG INFECTIONS   BACTERIAL PNEUMONIA  ã   Bacterial pneumonia is caused by bacterial invasion of the lung parenchyma →  exudative solidification (consolidation) of the pulmonary tissue. Pathogenesis of pneumonias Pneumonia can result whenever the defense mechanisms are impaired or the resistance of the host in general is lowered. Factors that interfere with the defense mechanisms: 1. factors that interfere with the clearing mechanisms ã    Loss of the cough reflex , as a result of coma, anesthesia, neuromuscular disorders, drugs, chest pain →  aspiration. ã    Injury to the mucociliary apparatus : tobacco smoke, inhalation of hot or corrosive gases, viral diseases genetic disturbances e.g. immotile cilia syndrome. ã    Interference with the phagocytic action of alveolar macrophages: alcohol, tobacco smoke, anoxia or oxygen intoxication. 2. pulmonary congestion and edema 3. accumulation of secretions (e.g. cystic fibrosis and bronchitis) Factors that affect the resistance of the host:  –    chronic diseases  –    immunologic deficiency  –    treatment with immunosuppressive agents  –    leukopenia  –    unusually virulent infections Features of pneumonia induced by bacteria 1.   Main features: alveolar inflammation, protein rich exudate, accumulation of PNGs later macrophages in the alveoli. 2.   Main types: ã    bronchopneumonia ã   lobar pneumonia Etiology of pneumonias ã   bronchopneumonia : the common agents are staphylococci, streptococci, pneumococci, haemophilus influenzae, pseudomonas aeruginosa, and the coliform bacteria ã   lobaris pneumonia : 90% is due to streptococcus pneumoniae Features of bronchopneumonia ã   usually in infancy and old age ã   usually secondary to pre-existing disease  Gross pathology: ã    patchy consolidation ã   frequently bilateral and basal ã   lesions are 3-4 cm in diameter, breakable, slightly elevated from the cut surface, dry, granular, gray-red to yellow Photo : Bronchopneumonia: gray-red patchy lesions, slightly elevated from the cut surface. Histology: ã   suppurative, neutrophil-rich exudate fills the lumen of bronchi, bronchioles and adjacent alveolar spaces Photo : Purulent bronchiolitis: exudate, rich in neutrophil granulocytes fills the lumen of the  bronchiole. Photo :   Bronchopneumonia: exudate, rich in neutrophil granulocytes fills the lumen of the alveoles focally. Features of lobar pneumonia ã   affects large part of or an entire lobe ã   90% is due to streptococcus pneumoniae ã   fibrinoso-suppurative consolidation is seen ã   It is associated with fibrinous pleuritis ã   relatively uncommon in infancy and childhood ã   affects males more than females ã   cough and fever with purulent or rusty sputum Morphology Stages of lobar pneumonia:   1. Congestion:  the affected lobe is heavy and red: LM:vascular engorgement, intraalveolar fluid, few neutrophils, bacteria. 2. Red hepatization:  red, airless lobe, with liver-like consistency. LM: vascular engorgement, the alveolar spaces are filled RBCs, neutrophils and fibrin. 3. Gray hepatization:  the lobe is grayish-brown and the cut surfaces are dry. LM: disintegration of RBCs, fibrinosopurulent exudate in the alveoli.  4. Yellow hepatization:  the gross appearance of the lobe is yellow. LM: high numbers of foamy, desintegrating macrophages. 5. Resolution:  the exudate undergoes progressive enzymatic digestion to produce granular, semifluid debris that is resorbed, ingested by macrophages, or coughed up. The average duration of the three hepatizations is two days each. Photo : Lobar pneumonia, red hepatization. The whole lobe is red, airless, with liver-like consistency. Photo : Lobar pneumonia, fibrinous pleuritis. Gray-red fibrin on the pleural surface. Photo : Lobar pneumonia, gray hepatization. The whole lobe is grayish and the cut surface is dry.  Clinical course of pneumonias  ã   Major symptoms: malaise, fever, and cough productive sputum. ã   When pleuritis is present: pleuritic pain and pleural friction rub. ã   The identification of the organisms and the determination of its antibiotic sensitivity are the keys to appropriate therapy. ã   Fewer than 10% of hospitalized cases of pneumonia die, death may be attributed either to a complication or to some predisposing disease. VIRAL AND MYCOPLASMAL PNEUMONIA (PRIMARY ATYPICAL PNEUMONIA - PAP)  ã   It is atypical  because there is a lack of alveolar exudates, the inflammation involves the interstitium. Better term: interstitial pneumonitis . ã   Causes:  –    Mycoplasma pneumoniae (commonest)  –    Viruses: ã   Influenza virus types A and B ã   Respiratory syncytial viruses ã   Adenovirus ã   Rhinoviruses ã   Rubella virus ã   Varicella virus  –    Chlamydia (psittacosis)  –    Coxiella burnetti (Q fever) Morphology of PAP 1. patchy or lobar areas of congestion, without consolidation 2. mononuclear inflammatory cell infiltrate, lymphocytes in the widened, edematous alveolar walls (interstitial pneumonitis) 3. formation of hyaline membranes 4. frequent superimposed bacterial infection 5. characteristic cytopathic changes are seen with some viruses Clinical course of PAP ã   extremely varied ã   fever, headache, and muscle aches ã   sporadic is usually mild with low mortality rate, below 1% ã   in viral influenza epidemics greater mortality is often due to fulminating pneumonia with pulmonary haemorrhage and to secondary bacterial infection Photo: Hemorrhagic tracheitis, influenza. Hyperaemic mucosa with hemorrhage. Photo: Rs virus pneumonia in an infant, (influenza sy.). The lung is heavy and red. Photo: Pneumonia, influenza. Interstitial round cell infiltrate, alveoli are lined by homogenous eosinophil material, hyaline membranes.   TUBERCULOSIS (TBC)   Etiology of tuberculosis  ã   Mycobacteria are aerobic, non-spore-forming, nonmotile bacilli. Their waxy coat is responsible for the characteristic acid fast staining properties. ã    M tuberculosis(M tbc) hominis  is transmitted by inhalation of infective droplets coughed into the air by a tuberculosis patient. ã   M bovis is transmitted by milk from diseased cows and first produces intestinal or tonsillar lesions. ã   M avium and M intracellulare (MAI), two closely related species have no virulence in normal hosts, but cause disseminated infections in 15 to 25% of patients with AIDS. Pathogenesis of tuberculosis  ã   At initial infection with M tbc nonspecific inflammatory response ensues, resembling the reaction to any form of bacterial invasion. ã   In 2 to 4 weeks after initial infection delayed hypersensitivity (type IV) develops to the tubercle bacillus, that controls 95% of infections. Tissue reactions to M. tbc  ã   High resistance: productive (proliferative) lesions →  specific caseating epitheloid cell granuloma i.e. tubercle formation ã   Low resistance: exudative lesions Productive tuberculosis: tubercle formation  Components of tubercle: ã   central caseation: total tissue necrosis containing nuclear debris only ã   caseation is surrounded by modified macrophages, epithelioid cells ã   amongst the epithelioid cells: Langhans type giant cells, their nuclei are arranged at the peripheri of cytoplasm in a horseshoe pattern ã   outermost layer: lymphocytes, fibroblasts, in time: scarring ã   number of M. tbc: low Photo: Tubercle in lung. Central caseation, Langhans type giant cells (arrows). Photo: Langhans cell. Nuclei are arranged in a horseshoe pattern at the periphery of the cytoplasm. Photo:  Acid fast mycobacteria in caseous pneumonia. Pathogenesis of tuberculosis The pattern of host response depends on whether the infection represents a  primary first exposure to the organism or a secondary  reaction in an already sensitized host. Morphology of primary tuberculosis Ranke-Ghon primary complex in the lung  ã   subpleural focus (upper part of the lower lobe, buttom part of the upper lobe) ã   lymphangitis ã   hilar lymphadenitis Photo: Morphology of primary tuberculosis. Ranke-Ghon primary complex.
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