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 ¼ 10), subacute (n ¼ 24) or chronic (n ¼ 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.

No abstract

No abstract

No abstract

No abstract

No abstract

No abstract

Genetic studies have demonstrated profound differences between the 'porcine' genotype of Cryptosporidium parvum, versus 'human' and 'bovine' genotypes. The study analysed infectivity and pathogenicity of the 'porcine' genotype (CPP-13 isolate) of C. parvum, and compared the results with published data on the 'bovine' genotype (CPB-0 isolate). This was investigated in calves and piglets from commercial herds. Piglets were mildly affected by the CPP-13 isolate, contrary to piglets infected with the CPB-0 isolate, which caused diarrhoea of a mean duration of 3.5 days. CPP-13 produced no or very mild clinical signs in piglets despite the excretion of high numbers of oocysts. Concomitant infection with rotavirus, however, caused a dramatic aggravation of the clinical signs, and 5 of 6 experimentally infected piglets died. CPP-13 appeared to be adapted to porcine hosts as illustrated by the lack of infectivity to 1 experimentally inoculated calf, and the absence of clinical signs, the long pre-patent period (15 days), and the excretion of very low numbers of oocysts following experimental infection of another calf. Thus, in accordance with other molecular studies, our results support the genetic evidence for the existence of a new species of Cryptosporidium adapted to pigs.