Occurrence and associated lesions of Pasteurella multocida in porcine bronchopneumonia

Abstract

With the aim to extend the present knowledge on possible systemic spreading of Pasteurella multocida in pigs with bronchopneumonia, the occurrence and associated lesions of P. multocida were described by comparing cultural detection, pathological evaluation and in situ hybridization of P. multocida in lungs, hearts and kidneys from cases of porcine bronchopneumonia. P. multocida was cultivated from the lung lesions in 114 out of a total of 148 cases of porcine bronchopneumonia. Among the 114 cases, P. multocida was also cultivated from the pericardial sacs of 40 pigs and the kidneys of seven pigs. Gross lesions and histological findings included a variety of type and stages of bronchopneumonia in connection to the isolation of P. multocida. Furthermore, chronic fibrous pericarditis, interstitial nephritis and a high proportion of lympho-histocytic nephritis were observed. In situ hybridization identified P. multocida in the majority of the lungs, none of the hearts and in half of the kidneys examined. The results show a possible low rate of systemic spreading of P. multocida from lung lesions in pigs with bronchopneumonia.

Anatomopathological pneumonic aspects associated with highly pathogenic Pasteurella multocida in finishing pigs

“…In this study, the involvement of P. multocida with severe respiratory disease in finishing pigs was evaluated, confirming the co-infection of this agent with Influenza type A virus and M. hyopneumoniae but not with PCV2. Furthermore, cases with only P. multocida involvement were identified, reinforcing previous reports of the existence of pleurotropic highly pathogenic strains with a primary role in the induction of lesions in the respiratory tract (Cappuccio et al 2004, Kich et al 2007, Pors et al 2011, Pors et al 2016. Brazilian studies have reported the involvement of highly pathogenic P. multocida in respiratory infections in the mortality of finishing pigs in Santa Catarina (Morés 2006) and Rio Grande do Sul (Borowski et al 2002, Heres 2009 succeeded in experimentally reproducing the infection with a field isolate.…”

“…No samples showed bacteriological growth nor histological lesions that would suggest the involvement of A. pleuropneumoniae or A. suis infection, in addition to the remarkable presence of fibrin, or that would suggest the presence of other agents (Caswell & Williams 2007). These results corroborate the findings of Ono et al (2003), Kich et al (2007), Hansen et al (2010) and Pors et al (2011) who suggest the ability of P. multocida to induce fibrin exudation in the lung and pleura. Furthermore, bronchiectasis was observed in eleven samples, three with mixed infections of Mycoplasma hyopneumoniae, Influenza A virus and P. multocida, and two with Influenza A virus and P. multocida co-infection.…”

“…However, in twelve of these thirteen cases, the pulmonary alterations were still in an acute phase of inflammation, enhancing the probability of detecting other pathogens, such as Influenza A virus. Thus, the results of this study indicate that there is probably a difference inherent in this type of pathogenic strain that determines, for example, extended tissue damage, fibrin exudation, and systemic dissemination capacity, as reported by Pors et al (2011), and also by Kich et al (2007), Oliveira and Pors et al (2016) when experimentally succeeded in reproduce the clinical-pathological picture. Several researchers have used molecular techniques to compare isolates of P. multocida obtained from clinical cases and healthy animals.…”

“…Pasteurella multocida is an agent of major importance within the PRDC, and several Brazilian studies (Borowski 2001, Morés 2006, Borowski et al 2007, Kich et al 2007, Heres 2009 and international studies (Kim et al 2003, Ono et al 2003, Cappuccio et al 2004, Pijoan 2006, Hansen et al 2010, Wellenberg et al 2010, Pors et al 2011, 2016 have reported its role. In this study, the involvement of P. multocida with severe respiratory disease in finishing pigs was evaluated, confirming the co-infection of this agent with Influenza type A virus and M. hyopneumoniae but not with PCV2.…”

“…Historically, P. multocida is considered to be a secondary infection, aggravating pulmonary infections caused by M. hyopneumoniae and PCV2 (Kim et al 2003, Pijoan 2006, Hansen et al 2010, Wellenberg et al 2010, Fablet et al 2011, Pors et al 2011. However, researchers in southern Brazil (Borowski 2001, Morés 2006, Borowski et al 2007, Kich et al 2007 and Argentina (Cappuccio et al 2004) have suggested that P. multocida is a primary agent capable of causing severe respiratory disease, nevertheless its pathogenesis and invasiveness mechanisms are not clearly described yet.…”