Pathogenesis and pathology of porcine pneumonias Dr. Biksi Imre

Structure of airways AnatomyHistology Conducting system nasal passages, larynx, trachea bronchi pseudostratified ciliated columnar epithelium, goblet cells Transitional system bronchioli, terminal bronchioli low columnar to cuboidal epithelium, Clara cells Gas exchange system alveolar ducts, alveoli pneumonocyte I. pneumonocyte II., alv. macrophages

alveolar macrophages macrophages

Respiratory system defense mechanisms Main defense mechanisms Conducting system Mucociliary clearance, antibodies, lysozyme, mucus Transitional system Clara cells, antioxidants, lysozyme, antibodies Gas exchange system Alveolar macrophages (inhaled pathogens), intravascular macrophages (circulating pathogens), opsonizing antibodies, surfactant, antioxidants

Inflammatory conditions in the airways Rhinitis, sinusitis Laryngitis, tracheitis Pneumonia ◦ Bronchitis ◦ Bronchiolitis ◦ Alveolitis Bronchopneumonia

Pneumonias Bronchopneumonia Interstitial pneumonia Focal / multifocal pneumonia Granulomatous pneumonia

Sequence of events in pneumonias Bronchiolar / vascular injury Proliferative changes leukocytes pneumonocyte II Airway/vessel damage pneumoncyte I., basement membrane Pneumonia Resolution complete regeneration Death Chronic pneumonia fibrosis, abscessation etc. Exsudative changes fluid & fibrinogen leakage

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. ◦ S econdary bacterial invaders  P asteurella 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

Chronic purulent bronchopneumonia

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, P asteurella multocida, Streptococcus sp., Salmonella choleraesuis

Fibrinous bronchopneumonia Bronchioloalveolar damage Vascular damage Fibrin exsudation Infiltration with PMNs, macrophages Diffuse spread of the process

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

Subacute fibrinopurulent bronchopneumonia

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 Infiltration of the interstitium (+ alveoli) with leukocytes Pneumocyte I. necrosis, pneumocyte II. proliferation, hyaline membrane formation

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!

Interstitial pneumonia, PRRSV infection, IHC

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

Wall of an abscess

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 Type of pneumonia Port of entry Distribution of lesions Texture of lung Grossly visible exudate Example Pulmonary sequelae Suppurative broncho- pneumonia (lobular) Aerogenous Cranioventral consolidation Firm, glandular Purulent exudate in bronchi Mycoplasma- pneumonia Abscesses, adhesions, bronchiectasis, BALT hyperplasia Fibrinous broncho- pneumonia (lobar) Aerogenous Craniodorsal consolidation Hard Fibrin in lung and pleura Actinobacillus pleuropneumonia Sequestra, adhesions, abscesses Interstitial pneumonia Aerogenous or haematogenous Diffuse Elastic with rib imprints Not visiblePRRS Edema, emphysema, pn. type II hyperplasia, fibrosis Focal / multifocal pneumonia HaematogenousMultifocalNodularPurulent fociEar biting Abscesses with random distribution Granulo- matous pneumonia Aerogenous or haematogenous MultifocalNodular Pyogranu- lomatous, caseous necrosis Tuberculosis Dissemination lymphonodes and different organs 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