An investigation of the pathology and pathogens associated with porcine respiratory disease complex in Denmark

Abstract

Respiratory infections are among the most important diseases of growing pigs. In order to elucidate the multifactorial aetiology of porcine respiratory disease complex (PRDC) in Denmark, lungs from 148 finishing pigs with cranioventral bronchopneumonia (case group) and 60 pigs without lung lesions (control group) were collected from abattoirs. The pathogens involved in PRDC and their interactions were identified and linked to the histopathological diagnosis. The lung samples were cultured for bacteria and tested by multiplex polymerase chain reaction for presence of swine influenza virus (type A), porcine reproductive and respiratory syndrome virus (both European and US type), porcine circovirus type 2 (PCV2), porcine respiratory coronavirus, porcine cytomegalovirus, Mycoplasma hyopneumoniae and Mycoplasma hyorhinis. All cases had cranioventral lobular bronchopneumonia consistent with PRDC. There was a broad range of microscopical lesions and the cases were characterized as acute (n=10), subacute (n=24) or chronic (n=114) bronchopneumonia. Five bacterial species, five viruses and two Mycoplasma spp. were detected in different combinations. PCV2, M. hyopneumoniae, M. hyorhinis and Pasteurella multocida were detected most frequently among the PRDC affected swine and the diversity and number of pathogens were higher in these animals compared with controls. No clear-cut associations were detected between pathogens and histological lesions or histopathological diagnoses. PRDC occurs more frequently than enzootic pneumonia among Danish finishing pigs and has complex and varied histopathology.

Fig. 1

Porcine lung tissue with different histological lesions found in cases of CBP. (a) Mild BALT hyperplasia (+) showing diffuse infiltration of lymphocytes (arrows) into the peribronchial, peribronchiolar and perivascular tissues including the lamina propria of the airways. B, bronchiole; V, blood vessel. HE. Bar, 250 μm. (b) Moderate BALT hyperplasia (++) showing greater diffuse infiltration of lymphocytes and/or the presence of a few lymphoid nodules (N). B, bronchiole. HE. Bar, 250 μm. (c) Marked BALT hyperplasia (+++) showing a considerable number of lymphoid nodules (N). B, bronchiole. HE. Bar, 250 μm. (d) Extensive BALT hyperplasia (++++) showing an extensive number of lymphoid nodules (N) affecting most of the lung section. A compressed bronchiole (B) can be seen. HE. Bar, 250 μm. (e) Suppurative alveolar exudates showing a cellular infiltrate dominated by neutrophils in acute suppurative bronchopneumonia (ASBP). HE. Bar, 25 μm. (f) Non-suppurative exudates showing a cellular infiltrate dominated by mononuclear inflammatory cells in chronic non-suppurative bronchopneumonia (CNBP). HE. Bar, 25 μm. (g) Mixed exudates showing cellular infiltrate with both neutrophils and mononuclear cells in subacute mixed bronchopneumonia (SMBP). HE. Bar, 25 μm. (h) Marked hyperplasia of type II pneumocytes. More than 50% of the alveolar surface is lined by type II pneumocytes. IHC. Bar, 25 μm.

Fig. 2

Porcine lung tissue with different lesions. (a) Gross appearance of chronic CBP. Inset shows lung tissue with a bronchial pattern of pulmonary consolidation. (b) Suppurative bronchiolitis and concurrent epithelial hyperplasia (E). HE. Bar, 25 μm. (c) Oedematous flooding of alveoli. HE. Bar, 50 μm. (d) Thickening of alveolar septa by collagenous (blue) tissue. Masson's trichrome. Bar, 50 μm. (e) Alveolar polyp-like structures, P1 with a fibrinous core and P2 with cellular infiltrate. Both are covered by type I and type II pneumocytes as shown by immunohistochemical labelling for cytokeratin expression. Bar, 25 μm. (f) Alveolar polyp-like structure (P) with a collagenous core (blue). Masson's trichrome. Bar, 15 μm. (g) Focal necrotic encapsulated tissue with central mineralization (M). HE. Bar, 100 μm. (h) Mild thickening of alveolar septa from a pig in the control group. HE. Bar, 50 μm.

Fig. 3

The frequency of pathogen count detected in control animals (n = 60) and in animals with CBP of acute (n = 10), subacute (n = 24) or chronic (n = 114) type.