Signalment:  

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.

Gross Description:  

This pig was one of four growing pigs submitted for necropsy at the same time. The pig was in poor nutritional condition. The main gross lesions were detected in the lungs. 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. The cranial part of the left diaphragmatic lobe contained also abscesses.

Histopathologic Description:

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. The alveolar walls inside are pale and necrotic, congested or thickened with inflammatory cells. The alveolar space is often filled with variable numbers of degenerate macrophages and neutrophils. The lobular septae are severely dilated and contain pale edema fluid, eosinophilic fibrillar material, macrophages and few neutrophils. 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. The bronchi are multifocally filled with degenenerate neutrophils, macrophages and sloughing bronchial epithelial cells. Multifocally some arteriolar walls are disrupted and infiltrated with degenerate neutrophils (vasculitis).

Morphologic Diagnosis:  

Severe, subacute, multifocal and locally extensive necrotizing and fibrinosuppurative bronchopneumonia and pleuritis.

Lab Results:  

(clinical pathology, microbiology, PCR, ELISA, etc.): Bacteriology: Actinobacillus pleuropneumoniae and Pasteurella multocida were cultured from the lungs. Salmonella bacteria were not detected.

Virology: Swine influenza was not detected (RT-PCR).

Immunohistochemistry: Porcine circovirus-2 antigen was demonstrated in lymph nodes.

Condition:  

Actinobacillus pleuropneumoniae

Contributor Comment:  

Pleuropneumonia, caused by Actinobacillus pleuropneumoniae, is one of the most important respiratory infections of swine. The disease is common worldwide and causes severe morbidity and mortality especially in growing pigs, but pigs of all ages can be affected. The disease can be peracute, acute, subacute or chronic.

In peracute cases, pigs can be found dead before clinical signs have been observed. 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. Gross lesions can be detected anywhere in the lungs, but often also one or both of the caudal lung lobes is affected. Blood stained froth fills the trachea. Fibrinous pleuritis and pleural adhesions are characteristic. Histologically there is a lobar fibrinosuppurative hemorrhagic and necrotizing pneumonia and fibrinous pleuritis.

Vasculitis with thrombosis is often seen. Differential diagnoses in acute cases include Salmonella Choleraesuis and Actinobacillus suis infections.

The disease is caused by a gram negative, encapsulated coccobacillus, Actinobacillus pleuropneumoniae. The bacterial agent is divided into two biovars according to the requirement of NAD (nicotinamide adenine dinucleotide). Biovar 1 strains are NAD- dependent and biovar 2 strains are NAD- independent. 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. In addition to capsular components and cellular lipopolysaccharides, A. pleuropneumoniae produces several cytotoxins and proteolytic enzymes and can resist macrophage and complement killing. Acute disease is often followed by chronic encapsulated necrotic lung lesions and local pleuritis with adhesions. Chronic pleuritis seen at slaughter is common in herds with endemic infection. Asymptomatic carrier pigs spread the disease by direct contact or by aerosols.

A. 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. There are also differences in the virulence within and between the strains. 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. pleuropneumoniae include endocarditis, pericarditis, arthritis, osteomyelitis, meningitis, otitis media, granulomatous hepatitis and granulomatous pneumonia.(3) A. pleuropneumoniae was cultured from lung lesions of all the four examined pigs.

In this case, Pasteurella multocida was also isolated from the lungs. Pasteurella multocida can cause suppurative pneumonia in pigs, but it is often a secondary invader. The lymph nodes exhibited depletion of lymphocytes and loss of the follicular architecture. Porcine circovirus-2 antigen was also detected by immunohistochemistry in lymph nodes of this pig. 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.

JPC Diagnosis:  

Lung: Pleuropneumonia, fibrinosuppurative and necrotizing, multifocal to coalescing, subacute, severe, with oat cell formation, fibrinonecrotizing vasculitis, and colonies of coccobacilli.

Conference Comment:  

The moderator focused the discussion on recognizing patterns of pneumonia and lung injury. Participants classified patterns of pneumonia as bronchopneumonia, interstitial, bronchointerstitial, embolic and granulomatous. The authors of McGavin and Zacharys Pathologic Basis of Veterinary Disease provide an excellent overview of pneumonia. 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; Pneumonic mannheimiosis	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

Adapted from Table 9-4, McGavin and Zacharys Pathologic Basis of Veterinary Disease(2)

The moderator discussed additional patterns of lung injury. Bronchitis and bronchiolitis result from direct damage to and subsequent necrosis of airway epithelium leading to airway inflammation. 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. 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. Macrophages activated by lipopolysaccharide secrete neutrophil chemoattractants, activate complement, and promote coagulation. In addition to resisting macrophage phagocytosis, the bacterial capsule prevents complement activation. 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)

References:

1. Caswell JL, Williams KJ. Respiratory system. In: Maxie MG, ed. Jubb, Kennedy and Palmers Pathology of Domestic Animals. 5th ed., vol. 3. Philadelphia, PA: Elsevier Ltd; 2007:555-575,587-588.
2. Lopez A. Respiratory system. In: McGavin MD, Zachary JF, eds. Pathologic Basis of Veterinary Disease. 4th ed. St. Louis, MO: Elsevier; 2007:508-517.
3. Ohba T, Shibahara T, Kobayashi H,et al. Prevalence of granulomatous pleuropneumonia associated with Actinobacillus pleuropneumoniae serotype 2 in slaughter pigs. J Vet Med Sci. 2009;71:1089-1092.

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4-1. Lung

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