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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 - PowerPoint PPT Presentation
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Pathogenesis and pathology of porcine pneumonias
Dr. Biksi Imre
Structure of airways
Anatomy Histology
Conducting system
nasal passages, larynx, tracheabronchi
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 airwaysRhinitis, sinusitisLaryngitis, tracheitisPneumonia
BronchitisBronchiolitisAlveolitis
Bronchopneumonia
Pneumonias
BronchopneumoniaInterstitial pneumoniaFocal / multifocal pneumoniaGranulomatous pneumonia
Sequence of events in pneumonias
Forms of bronchopneumoniasPurulent bronchopneumonia („lobular”)Fibrinous bronchopneumonia („lobar”)Fibrinopurulent bronchopneumonia „Aspiration pneumonia”Necrotic bronchopneumonia (typhus)Haemorrhagic bronchopneumonia (CSF, anthrax)
Purulent bronchopneumoniaRoute of infection
AerogenousAgents
Mycoplasma hyopneumoniae, M. hyorhinisPCV-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 bronchopneumoniaLocation
cranioventralColour
purple to grayConsistency
firm, glandular (accelerated lobular pattern)Cut surface
purulent, mucopurulent to mucoid exsudatenormal fluid content (not dry)
Pleurausually intact
Lymphonodeslymphoid hyperplasia and/or proliferative changes
Chronic purulent bronchopneumonia
Purulent bronchopneumoniaResolution
starts in 7 days, ends in 2-4 weeksChronic suppurative bronchopneumonia
„fish flesh” macro appearancehyperplasia of goblet cellsbronchiectasisatelectasis, emphysemaperibronchiolar lymphoid hyperplasiapulmonary abscess („focal/multifocal pneumonia”)
Fibrinous bronchopneumoniaRoute of infection
AerogenousAgents
(M. hyopneumoniae, viruses as predisposing agents)Actinobacillus pleuropneumoniae, Actinobacillus suis, Pasteurella multocida, Streptococcus sp., Salmonella choleraesuis
Fibrinous bronchopneumonia
Bronchioloalveolar damage
Vascular damage Fibrin exsudation
Infiltration with PMNs, macrophages
Diffuse spread of the process
Fibrinous bronchopneumonia
Locationcaudodorsal (App), cranioventral
Colourdark red
Consistencyfirm, uniform („liverlike”)
Cut surfacefibrinous exsudate, focal areas of coagulative necrosisdry, haemorrhagicmarbling – fibrin and fluid in the interstitiummottled - lobuli in different stages of the process („hepatisation”)
Pleurafibrinous pleuritis („pleuropneumonia”)
Lymphonodesedema, acute purulent inflmmation, lesions caused by the primary agent
Acute-subacute fibrinopurulent bronchopneumoniaWeigert stain for fibrin
Subacute fibrinopurulent bronchopneumonia
Fibrinous bronchopneumoniaResolution
Complete regeneration rare, 2-4 weeksChronic fibrinous bronchopneumonia
bronchiolitis obliteranssequestrationgangreneabscessationpleural and pericardial adhesionsfibrosis
Forms of interstitial pneumoniasBronchointerstitial pneumonia Proliferative interstitial pneumoniaEosinophilic interstitial pneumonia
Interstitial pneumoniaRoute of infection
Aerogenous, haematogenous, migration of larvaeAgents
viruses PCV-2, PRRSV, SIV etc.
septicaemiaSalmonella sp., Streptococcus sp.
parasitesAscaris 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 pneumoniaLocation
diffuse, dorsocaudalColour
dark red to purpleConsistency
rubbery, elastic, „meaty” – like flaccid muscleCut surface
Exsudate not present, normal to increased fluid contentedema, emphysema!
Pleuraintact
Lymphonodeslymphoid 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 pneumoniaRestitution
can occur rapidlyChronic interstitial pneumonia
alveolar wall and interstitial fibrosispneumonocyte type II hyperplasiainterstitial infiltration with mononuclear cells
Focal / multifocal pneumoniaRoute of infection
haematogenous („embolic pneumonia”)aerogenous (sequel to bronchopneumonia)
Agents, source of infectionBacteriaemia / septicemia
ear biting, tail biting, thromboembolismArcanobacterium pyogenes, Streptococcus sp. etc.
Sequel to bronchopneumoniafibrinous bronchopneumonia
Apppurulent bronchopneumonia
Pasteurella multocida, Streptococcus sp. etc.
Focal / multifocal pneumoniaLocation
multifocal, random distribution (embolic pneumonia)cranioventral (chronic bronchopneumonia)
Coloursmall white foci with red perimeter, haemorrhagic fociabscesses
Consistencynodular, firm to flaccid
Cut surfacePurulent or necrotic exsudate
Pleurausually focal pleuritis
Lymphonodessimilar foci can occur
Wall of an abscess
Granulomatous pneumoniaRoute of infection
haematogenousaerogenouslarval migration
AgentsTuberculosis
Mycobacterium bovis, M. avium complexFungi
Aspergillus sp., Cryptococcus sp., Histoplasma sp.Parasites
dead Ascaris suum larvaeForeign bodies
feed (starch), desiccant powders
Granulomatous pneumoniaLocation
multifocal, random distribution (hematogenous spread)focal, solitary nodules (aspiration, larval migration)
Colourwhite to grey foci
Consistencynodular, firm, gritty when calcified
Cut surfaceusually no exsudate, necrotic (caseous, dry) or glistening
Pleurausually not affected
Lymphonodessimilar foci can occur
Morphologic types of pneumonias
Type of pneumonia Port of entry Distribution of
lesionsTexture of lung
Grossly visible exudate Example Pulmonary
sequelae
Suppurative broncho-
pneumonia (lobular)
Aerogenous Cranioventral consolidation
Firm, glandular
Purulent exudate in
bronchiMycoplasma-pneumonia
Abscesses, adhesions,
bronchiectasis, BALT hyperplasia
Fibrinous broncho-
pneumonia (lobar)
Aerogenous Craniodorsal consolidation Hard Fibrin in lung
and pleuraActinobacillus
pleuropneumoniaSequestra, adhesions, abscesses
Interstitial pneumonia
Aerogenous or haematogenous Diffuse
Elastic with rib imprints
Not visible PRRS
Edema, emphysema, pn.
type II hyperplasia,
fibrosis
Focal / multifocal pneumonia
Haematogenous Multifocal Nodular Purulent foci Ear bitingAbscesses with
random distribution
Granulo-matous
pneumoniaAerogenous or
haematogenous Multifocal NodularPyogranu-lomatous, caseous necrosis
TuberculosisDissemination lymphonodes and different
organs
Modified after Pathologic Basis of Veterinary Disease, 4th ed., p. 508.
Final hintsDevelop 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