pathogenesis and pathology of porcine pneumonias

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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

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