The Role of Pathology in the Diagnosis of Swine Respiratory Disease

Abstract

The definition "porcine respiratory disease complex" (PRDC) is used to indicate the current approach for presenting respiratory pathology in modern pig farming. PRDC includes pneumonias with variable pictures, mixed with both aerogenous and hematogenous forms with variable etiology, often multimicrobial, and influenced by environmental and management factors. The notion that many etiological agents of swine respiratory pathology are ubiquitous in the airways is commonly understood; however, their isolation or identification is not always associable with the current pathology. In this complex context, lung lesions registered at slaughterhouse or during necropsy, and supplemented by histological investigations, must be considered as powerful tools for assigning a prominent role to etiologic agents. In recent years, the goal of colocalizing causative agents with the lesions they produce has been frequently applied, and valid examples in routine diagnostics are those that indicate pulmonary involvement during porcine reproductive and respiratory syndrome virus (PRRSV) and porcine circovirus type 2 (PCV2) infections.

Keywords: PRDC; diagnosis; histopathology; respiratory disease; swine.

Figure 2

Aerogenous lung involvement. Cranioventral distribution (A) of coalescing, slightly depressed dark-red lobules (C) with consolidation and mucus in airways (E) in an acute, moderate, aerogenous non-complicated pneumonia. These features are indicative of enzootic pneumonia. Cranioventral distribution of consolidated dark-red lung parenchyma (B) with multifocal yellowish foci of suppuration (D) with pleural ulceration and fibrosis (G). These features are indicative of complicated enzootic pneumonia or of bronchopneumonia. In (F), cuffing of small airways, usually present in enzootic pneumonia, but also found in complicated pneumonias.

Figure 1

Progressive atrophic rhinitis (PAR): (A) control non-affected; (B) bilateral symmetric complete atrophy of turbinates; (C) discontinuous mural bone in the turbinate; (D) hyperplasia of osteoclasts facing bone trabeculae. (C) hematoxylin–eosin (H–E) stain. (D): Masson’s trichrome stain.

Figure 3

Acute (A) and chronic (B) pleuropneumonia by Actinobacillus pleuropneumoniae: in (A), an acute, locally extensive, and protruding nodule coexists with associated pleuritis localized in the craniodorsal side of the left lung lobe, referable to A. pleuropneumoniae and cranioventral pneumonia. In (B), multifocal nodules of the chronic form.

Figure 4

Hematogenous lung spread: in (A), together with a cranioventral pneumonia, the right basal lobe shows multiple acute and recent red foci of hyperemia/hemorrhage referable to bacteremia often of intestinal origin. In (B), multiple foci of suppuration surrounded by normal lung parenchyma, due to lung arrest of microthrombi originating from septic phlebitis outside the lungs.

Figure 5

Interstitial pneumonia: non-collapsed lungs, with rib impressions (A), in acute (A) and chronic (B) interstitial pneumonia. Acute changes include diffuse hyperemia and edema of perilobular connective tissue (C). In chronic stages, the lung is slightly increased in consistency and colored whitish due to fibrosis (D).

Figure 6

For histological examination, the lesions should never be collected in the center, since they often contain a complicated or necrotic lesion. A sample at the margin with the surrounding normal parenchyma (yellow box) allows one to identify the pathological process at its onset (in the peripheral part of the lesion) and its evolution (progressing in observation towards the center). If the lesions are small (1–2 cm), they can be sampled entirely; if they are larger, it is appropriate to take them from the margin, with some surrounding normal tissue.

Figure 7

Pneumonia with alveolar macrophages (A) and lymphocytic peribronchial cuffing (B); when associated with gross changes in cranioventral non-complicated pneumonia, these histological findings are indicative of EP. Increase in airway and alveolar neutrophils (C) indicates complication. Necrosis of lung parenchyma (D) and of alveolar cell exudate (E), fibrin alveolar collection (F) associated with vessel fibrinoid necrosis (G), thrombosis (H), and fibrinous pneumonia (I) are a histologic indication of porcine pleuropneumonia, for which etiologic indication is imperative, as similar gross and histologic changes are also due to bacteria different from Actinobacillus pleuropneumoniae. (A–E,G–I): H–E stain. (F): PTAH stain.

Figure 8

Interstitial pneumonia in PRRSV (A–C) and PCV2 (D–F) infections share similarities that need etiologic validation. A granulomatous pattern of inflammation (D) is suggestive of PCV2 pneumonia, whereas it is lacking in PRRSV pneumonia. This latter infection is characterized by macrophage alveolar exudation and necrosis (B) and type II pneumocyte hyperplasia (C) in alveolar walls. In PCV2 pneumonia, both alveolar septa and peribronchial space are thickened (E), and bronchiolar necrosis (F) can be recognized. H–E stain.

Figure 9

Airways epithelium necrosis (A) is a hallmark of SIV infection, but the lesion is shared with other pathogens and the acquisition of etiologic indication is imperative. The opportunity to have positive results by IHC (B) is contingent on time, because the lungs can rapidly clear the virus. In this case, sampling on animals with very recent and acute symptoms, in association with other investigations (PCR, serology), provides useful data ((A): H–E stain; (B): IHC with monoclonal anti-SIV antibody clone 1331. Meridian Life Science, Inc.).

Figure 10

(A) Immunohistochemical stain to PCV2 (monoclonal antibody anti-PCV2, clone F217) with positive macrophages in alveolar septa. (B) Immunohistochemical stain to PRRSV (monoclonal antibody anti-PRRSV, clone SDOW17-A) with positive hyperplastic type II pneumocytes and rare interstitial machrophages.

Figure 11

(A) Acute serofibrinous pleuritis and pericarditis: fibrinous exudate forms loosely adherent strands of material on the pleural surface. (B) Layers of fibrin covering the thoracic wall in acute serofibrinous pleuritis. (C) Chronic fibrous pleuritis with strongly adherent fibrous strands between the lung and thoracic wall.