Juvenile (18.5 kg), female, pig (Sus scrofa).In a finishing herd there were some pigs with a decreased rate of body weight gain and a couple of pigs
had died during the previous week.
This pig was one of four growing pigs submitted for necropsy at the same time.Â The pig was in
poor nutritional condition.Â The main gross lesions were detected in the lungs.Â There were pneumonic lesions in the
cranial lung lobes and the caudal part of the left diaphragmatic lobe was covered with thick fibrinous exudate and
attached to the wall of the pleural cavity.Â The cranial part of the left diaphragmatic lobe contained also abscesses.
Lung: The lung parenchyma contains multifocal demarcated pale or basophilic areas
bordered by a thick band of degenerate neutrophils and macrophages, often with elongated, streaming or oat cell
nuclei, eosinophilic fibrillar material and nuclear dust, occasionally also fibroblasts.Â The alveolar walls inside are
pale and necrotic, congested or thickened with inflammatory cells.Â The alveolar space is often filled with variable
numbers of degenerate macrophages and neutrophils.Â The lobular septae are severely dilated and contain pale
edema fluid, eosinophilic fibrillar material, macrophages and few neutrophils.Â The pleura is severely thickened by
fibroblasts and covered by a thick eosinophilic fibrillar membrane with large numbers of degenerate macrophages
and neutrophils with streaming nuclei and occasional bacterial colonies.Â The bronchi are multifocally filled with
degenenerate neutrophils, macrophages and sloughing bronchial epithelial cells.Â Multifocally some arteriolar walls
are disrupted and infiltrated with degenerate neutrophils (vasculitis).
Severe, subacute, multifocal and locally extensive necrotizing and
fibrinosuppurative bronchopneumonia and pleuritis.
(clinical pathology, microbiology, PCR, ELISA, etc.): Bacteriology: Actinobacillus
pleuropneumoniae and Pasteurella multocida were cultured from the lungs.Â Salmonella bacteria were not detected.
Virology: Swine influenza was not detected (RT-PCR).
Immunohistochemistry: Porcine circovirus-2 antigen was demonstrated in lymph nodes.
Pleuropneumonia, caused by Actinobacillus pleuropneumoniae, is one of the most
important respiratory infections of swine.Â The disease is common worldwide and causes severe morbidity and
mortality especially in growing pigs, but pigs of all ages can be affected.Â The disease can be peracute, acute,
subacute or chronic.
In peracute cases, pigs can be found dead before clinical signs have been observed.Â In acute cases, pigs have high fever, apathy and anorexia, occasionally dyspnea and diarrhea or vomiting, cyanosis of skin and blood-tinged discharge from the nostrils is often seen.Â Gross lesions can be detected anywhere in the lungs, but often also one or both of the caudal lung lobes is affected.Â Blood stained froth fills the trachea.Â Fibrinous pleuritis and pleural adhesions are characteristic.Â Histologically there is a lobar fibrinosuppurative hemorrhagic and necrotizing pneumonia and fibrinous pleuritis.
Vasculitis with thrombosis is often seen.Â Differential diagnoses in acute cases include Salmonella Choleraesuis and Actinobacillus suis infections.
The disease is caused by a gram negative, encapsulated coccobacillus, Actinobacillus pleuropneumoniae.Â The bacterial agent is divided into two biovars according to the requirement of NAD (nicotinamide adenine dinucleotide).Â Biovar 1 strains are NAD- dependent and biovar 2 strains are NAD- independent.Â There are 15 serotypes based on capsular polysaccharides.
Clinical signs and pathological lesions are associated with several bacterial virulence factors combined with the host reaction.Â In addition to capsular components and cellular lipopolysaccharides, A.Â pleuropneumoniae produces several cytotoxins and proteolytic enzymes and can resist macrophage and complement killing.Â Acute disease is often followed by chronic encapsulated necrotic lung lesions and local pleuritis with adhesions.Â Chronic pleuritis seen at slaughter is common in herds with endemic infection.Â Asymptomatic carrier pigs spread the disease by direct contact or by aerosols.
A.Â pleuropneumoniae is capable of causing severe disease without predisposing factors, but the severity of the disease is affected by the immune status of the pigs and environmental factors such as crowding, ambient temperature or moving and mixing of animals.Â There are also differences in the virulence within and between the strains.Â Disease problems can be enhanced by other concurrent pathogens, for example Mycoplasma hyopneumoniae, swine influenza virus, PRRS (porcine respiratory and reproduction syndrome virus) or PMWS (porcine circovirus-2).
Other uncommon lesions associated with A.Â pleuropneumoniae include endocarditis, pericarditis, arthritis, osteomyelitis, meningitis, otitis media, granulomatous hepatitis and granulomatous pneumonia.(3) A.Â pleuropneumoniae was cultured from lung lesions of all the four examined pigs.
In this case, Pasteurella multocida was also isolated from the lungs.Â Pasteurella multocida can cause suppurative pneumonia in pigs, but it is often a secondary invader.Â The lymph nodes exhibited depletion of lymphocytes and loss of the follicular architecture.Â Porcine circovirus-2 antigen was also detected by immunohistochemistry in lymph nodes of this pig.Â These lesions were indicative of PMWS (postweaning multisystemic wasting syndrome). However, in this pig the lesions associated with PCV2 were considered to be an additional finding.
Lung: Pleuropneumonia, fibrinosuppurative and necrotizing, multifocal to coalescing, subacute,
severe, with oat cell formation, fibrinonecrotizing vasculitis, and colonies of coccobacilli.
The moderator focused the discussion on recognizing patterns of pneumonia and lung
injury.Â Participants classified patterns of pneumonia as bronchopneumonia, interstitial, bronchointerstitial, embolic
and granulomatous.Â The authors of McGavin and Zacharys Pathologic Basis of Veterinary Disease provide an
excellent overview of pneumonia.Â The following table summarizes key points of each pattern:(1,2)
|Pneumonia||Route of exposure||Anatomic Distribution||Lung Texture||Anatomic Location of Injury||Example||Common Pulmonary Sequelae|
|Broncho-pneumonia||Aerogenous||Cranioventral||Firm, hard||Bronchiolar-alveolar junction||Enzootic pneumonia;|
|Abscesses, pleural adhesions|
|Interstitial||Aerogenous or hematogenous||Diffuse||Elastic, rubbery||Alveolar or interlobular septae||PRRS, PCV2||Edema, type II pneumocyte hypertrophy, alveolar fibrosis|
|Bronchointerstitial||Aerogenous||Multifocal||Firm to rubbery||Bronchioloar and alveolar epithelium||BRSV, swine influenza||Mix of bronchoand interstitialpneumonias|
|Granulomatous||Aerogenous or hematogenous||Multifocal||Nodular||Non-specific||Tuberculosis, blastomycosis||Dissemination of infection|
|Embolic||Hematogenous||Multifocal||Nodular||Pulmonary vasculature||Vegetative endocarditis||Random abscesses|
The moderator discussed additional patterns of lung injury.Â Bronchitis and bronchiolitis result from direct damage to and subsequent necrosis of airway epithelium leading to airway inflammation.Â Potential etiologic agents or disease syndromes resulting in this pattern include feline asthma, viral infection, inhalation of toxic gases, toxins metabolized by P450 cytochrome oxidase of Clara cells, and inhaled irritants.(1)
As noted by the contributor, Actinobacillus pleuropneumoniaehas several virulence factors which play a unique role in the pathogenesis of porcine pleuropneumonia.Â The organism produces three RTX toxins: Apx I, II, and III which are cytolytic for neutrophils, erythrocytes, alveolar macrophages, and epithelial cells - once lysed, the contents of neutrophils and macrophages damage host tissue.Â Macrophages activated by lipopolysaccharide secrete neutrophil chemoattractants, activate complement, and promote coagulation.Â In addition to resisting macrophage phagocytosis, the bacterial capsule prevents complement activation.Â In order to survive in the milieu of cytotoxins and reactive oxygen species from lysed leukocytes, Actinobacillus pleuropneumoniae produces a variety of antioxidant enzymes including superoxide dismutase, catalase and hydrogen peroxide reductase.(1)
1.Â Caswell JL, Williams KJ.Â Respiratory system.Â In: Maxie MG, ed.Â Jubb, Kennedy and Palmers Pathology of
Domestic Animals. 5th ed., vol.Â 3.Â Philadelphia, PA: Elsevier Ltd; 2007:555-575,587-588.
2.Â Lopez A.Â Respiratory system.Â In: McGavin MD, Zachary JF, eds.Â Pathologic Basis of Veterinary Disease. 4th ed. St.Â Louis, MO: Elsevier; 2007:508-517.
3.Â Ohba T, Shibahara T, Kobayashi H,et al.Â Prevalence of granulomatous pleuropneumonia associated with Actinobacillus pleuropneumoniae serotype 2 in slaughter pigs.Â J Vet Med Sci. 2009;71:1089-1092.