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Pathogenesis and pathology of porcine pneumonias. Dr. Biksi Imre. Structure of airways. alveolar macrophages. macrophages. Respiratory system defense mechanisms. Inflammatory conditions in the airways. Rhinitis, sinusitis Laryngitis, tracheitis Pneumonia Bronchitis Bronchiolitis
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Pathogenesis and pathology of porcine pneumonias Dr. Biksi Imre
alveolar macrophages macrophages
Inflammatory conditions in the airways Rhinitis, sinusitis Laryngitis, tracheitis Pneumonia Bronchitis Bronchiolitis Alveolitis Bronchopneumonia
Pneumonias Bronchopneumonia Interstitial pneumonia Focal / multifocal pneumonia Granulomatous pneumonia
Forms of bronchopneumonias Purulent bronchopneumonia („lobular”) Fibrinous bronchopneumonia („lobar”) Fibrinopurulent bronchopneumonia „Aspiration pneumonia” Necrotic bronchopneumonia (typhus) Haemorrhagic bronchopneumonia (CSF, anthrax)
Purulent bronchopneumonia Route of infection Aerogenous Agents Mycoplasma hyopneumoniae, M. hyorhinis PCV-2, PRRSV etc. Secondary bacterial invaders Pasteurella multocida, Arcanobacterium pyogenes, Streptococcus sp.
Purulent bronchopneumonia Bronchioloalveolar damage, mild vascular involvement, congestion, edema • Infiltration with leukocytes (48h) • Intraductal spread of the process
Purulent bronchopneumonia Location cranioventral Colour purple to gray Consistency firm, glandular (accelerated lobular pattern) Cut surface purulent, mucopurulent to mucoid exsudate normal fluid content (not dry) Pleura usually intact Lymphonodes lymphoid hyperplasia and/or proliferative changes
Purulent bronchopneumonia Resolution starts in 7 days, ends in 2-4 weeks Chronic suppurative bronchopneumonia „fish flesh” macro appearance hyperplasia of goblet cells bronchiectasis atelectasis, emphysema peribronchiolar lymphoid hyperplasia pulmonary abscess („focal/multifocal pneumonia”)
Fibrinous bronchopneumonia Route of infection Aerogenous Agents (M. hyopneumoniae, viruses as predisposing agents) Actinobacillus pleuropneumoniae, Actinobacillus suis, Pasteurella multocida, Streptococcus sp., Salmonella choleraesuis
Bronchioloalveolar damage • Vascular damage • Fibrin exsudation • Infiltration with PMNs, macrophages • Diffuse spread of the process Fibrinous bronchopneumonia
Fibrinous bronchopneumonia Location caudodorsal (App), cranioventral Colour dark red Consistency firm, uniform („liverlike”) Cut surface fibrinous exsudate, focal areas of coagulative necrosis dry, haemorrhagic marbling – fibrin and fluid in the interstitium mottled - lobuli in different stages of the process („hepatisation”) Pleura fibrinous pleuritis („pleuropneumonia”) Lymphonodes edema, acute purulent inflmmation, lesions caused by the primary agent
Acute-subacute fibrinopurulent bronchopneumonia Weigert stain for fibrin
Fibrinous bronchopneumonia Resolution Complete regeneration rare, 2-4 weeks Chronic fibrinous bronchopneumonia bronchiolitis obliterans sequestration gangrene abscessation pleural and pericardial adhesions fibrosis
Forms of interstitial pneumonias Bronchointerstitial pneumonia Proliferative interstitial pneumonia Eosinophilic interstitial pneumonia
Interstitial pneumonia Route of infection Aerogenous, haematogenous, migration of larvae Agents viruses PCV-2, PRRSV, SIV etc. septicaemia Salmonella sp., Streptococcus sp. parasites Ascaris suum larvae, Metastrongylus sp. noxious gases, allergens (hypersensitivity reaction), fumes (cattle!)
Interstitial pneumonia Vascular / alveolar damage • Pneumocyte I. necrosis, pneumocyte II. proliferation, hyaline membrane formation • Infiltration of the interstitium (+ alveoli) with leukocytes
Interstitial pneumonia Location diffuse, dorsocaudal Colour dark red to purple Consistency rubbery, elastic, „meaty” – like flaccid muscle Cut surface Exsudate not present, normal to increased fluid content edema, emphysema! Pleura intact Lymphonodes lymphoid hyperplasia and/or proliferative or degenerative changes Heavy wet lungs which fail to collapse, difficult macro diagnosis!
Chronic eosinophilic interstitial pneumonia, Ascaris larval migration
Interstitial pneumonia Restitution can occur rapidly Chronic interstitial pneumonia alveolar wall and interstitial fibrosis pneumonocyte type II hyperplasia interstitial infiltration with mononuclear cells
Focal / multifocal pneumonia Route of infection haematogenous („embolic pneumonia”) aerogenous (sequel to bronchopneumonia) Agents, source of infection Bacteriaemia / septicemia ear biting, tail biting, thromboembolism Arcanobacterium pyogenes, Streptococcus sp. etc. Sequel to bronchopneumonia fibrinous bronchopneumonia App purulent bronchopneumonia Pasteurella multocida, Streptococcus sp. etc.
Focal / multifocal pneumonia Location multifocal, random distribution (embolic pneumonia) cranioventral (chronic bronchopneumonia) Colour small white foci with red perimeter, haemorrhagic foci abscesses Consistency nodular, firm to flaccid Cut surface Purulent or necrotic exsudate Pleura usually focal pleuritis Lymphonodes similar foci can occur
Granulomatous pneumonia Route of infection haematogenous aerogenous larval migration Agents Tuberculosis Mycobacterium bovis, M. avium complex Fungi Aspergillus sp., Cryptococcus sp., Histoplasma sp. Parasites dead Ascaris suum larvae Foreign bodies feed (starch), desiccant powders
Granulomatous pneumonia Location multifocal, random distribution (hematogenous spread) focal, solitary nodules (aspiration, larval migration) Colour white to grey foci Consistency nodular, firm, gritty when calcified Cut surface usually no exsudate, necrotic (caseous, dry) or glistening Pleura usually not affected Lymphonodes similar foci can occur
Morphologic types of pneumonias Modified after Pathologic Basis of Veterinary Disease, 4th ed., p. 508.
Final hints Develop a system of evaluation for both macro and microscopic diagnosis Do not forget to check the rest of the carcass! More than one form of pneumonia can be present in the same specimen e.g. interstitial pneumonia + fibrinous / purulent bronchopneumonia + focal pneumonia