Actinobacillus Infections in Pigs: Pleuropneumonia and Septicemia

Etiology and Taxonomy

The genus Actinobacillus belongs to the family Pasteurellaceae, a group of Gram-negative, facultatively anaerobic, non-motile coccobacilli. Two principal species cause significant disease in swine: Actinobacillus pleuropneumoniae and Actinobacillus suis. A. pleuropneumoniae is the primary etiological agent of porcine pleuropneumonia, a highly contagious and often fatal respiratory disease. A. suis is an opportunistic pathogen capable of causing septicemia and respiratory distress, particularly in young or immunologically naive pigs [1].

Actinobacillus pleuropneumoniae is classified into 19 serotypes based on capsular polysaccharide and lipopolysaccharide (LPS) antigens. Serotypes 1, 5, 7, and 9 are among the most prevalent in North America and Europe, though geographic distribution varies. The species is further divided into two biovars: biovar 1 (NAD-dependent) and biovar 2 (NAD-independent). Biovar 1 strains are more commonly associated with clinical disease. Actinobacillus suis is less serotypically diverse but possesses a range of virulence factors homologous to those found in A. pleuropneumoniae [2].

Epidemiology and Transmission

Porcine pleuropneumonia caused by A. pleuropneumoniae is endemic in most swine-producing regions worldwide. Transmission occurs primarily via direct contact between infected and susceptible pigs through respiratory droplets and aerosols. Subclinically infected carrier animals are the principal reservoir within a herd. Stressors such as crowding, poor ventilation, transportation, and commingling of pigs from different sources precipitate clinical outbreaks.

Actinobacillus suis is a commensal of the upper respiratory tract and tonsils of healthy pigs. Disease manifestation is typically sporadic and associated with immunosuppression, concurrent viral infections, or environmental stressors. The organism can cause septicemia with high mortality in neonatal and weanling pigs, whereas older animals may develop respiratory signs or localized abscesses [3].

Pathogenesis and Virulence Factors

The pathogenesis of A. pleuropneumoniae infection involves a multistep process of colonization, evasion of host defenses, and toxin-mediated tissue damage. The bacterium adheres to the respiratory epithelium via fimbriae and other putative adhesins. Once established, it produces a suite of exotoxins known as Apx toxins (ApxI, ApxII, ApxIII, and ApxIV), which are members of the repeats-in-toxin (RTX) family. These toxins are pore-forming cytolysins that lyse alveolar macrophages, neutrophils, and epithelial cells, leading to necrotic and hemorrhagic lung lesions [4].

The Apx toxin profile varies by serotype. For example, serotype 1 produces ApxI and ApxII and is highly virulent, whereas serotype 3 produces only ApxIII and is considered less virulent. In addition to RTX toxins, the bacterium expresses LPS, capsular polysaccharide, and outer membrane proteins that contribute to resistance to phagocytosis and complement-mediated killing. The host inflammatory response, driven by cytokines such as tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 (IL-1), exacerbates tissue damage and contributes to the systemic signs of septic shock [5].

Actinobacillus suis possesses homologues of the Apx toxins, designated ApxI/II and ApxII, as well as putative adhesins that facilitate colonization of the respiratory tract [2]. The organism can invade the bloodstream, leading to septicemia and dissemination to multiple organs. Colonization-deficient mutants of A. suis have been shown to lack the ability to establish infection in the upper respiratory tract, confirming the critical role of adhesins in pathogenesis [3].

Clinical Signs

Actinobacillus pleuropneumoniae

The clinical presentation of porcine pleuropneumonia ranges from peracute to chronic. In peracute cases, pigs are found dead without premonitory signs. Acute cases present with high fever (40.5 to 42.0 degrees Celsius), severe dyspnea, open-mouth breathing, cyanosis, and a characteristic frothy, blood-tinged nasal discharge. Affected animals often assume a dog-sitting posture to facilitate respiration. Mortality in acute outbreaks can reach 20 to 40 percent. Subacute and chronic infections are characterized by intermittent cough, reduced growth rates, and exercise intolerance. Chronically infected pigs may remain as asymptomatic carriers.

Actinobacillus suis

In neonatal and weanling pigs, A. suis septicemia presents with sudden death, fever, lethargy, and erythematous or cyanotic skin discoloration. Respiratory signs such as dyspnea and coughing are common. In older pigs, the disease may manifest as pneumonia, polyarthritis, or endocarditis. The clinical picture can be indistinguishable from other septicemic conditions such as erysipelas or salmonellosis.

Pathology

Gross Lesions

In A. pleuropneumoniae infection, the characteristic gross lesion is a fibrinous, necrotizing, and hemorrhagic pleuropneumonia. Lesions are typically bilateral and affect the caudal and diaphragmatic lung lobes. Affected lung tissue is firm, dark red to black, and covered with a layer of fibrin. A serosanguinous pleural effusion is often present. In chronic cases, pulmonary sequestra (encapsulated necrotic foci) are observed.

In A. suis septicemia, gross findings include generalized congestion, petechial hemorrhages on serosal surfaces, and splenomegaly. Fibrinous polyserositis, pericarditis, and arthritis may be present. Pulmonary lesions, when present, resemble those of A. pleuropneumoniae but are generally less severe.

Histopathology

Histological examination of acute A. pleuropneumoniae lesions reveals coagulative necrosis of alveolar parenchyma, massive infiltration of neutrophils, and fibrin deposition. Thrombosis of pulmonary vessels is common. The presence of streaming leukocytes and "oat cells" (degenerate neutrophils with elongated nuclei) is a hallmark feature. In A. suis infections, histopathology shows multifocal necrosis and bacterial emboli in the lungs, liver, and spleen.

Diagnosis

Definitive diagnosis of Actinobacillus infections requires a combination of clinical observation, necropsy findings, and laboratory confirmation.

Sample Collection

For bacteriological culture, samples should be collected from affected lung tissue, pleural fluid, or systemic organs (liver, spleen) in septicemic cases. Swabs from the lower respiratory tract (bronchial or transtracheal washes) are suitable from live animals. Samples must be transported in appropriate transport media (e.g., Amies charcoal medium) and processed promptly.

Culture and Isolation

Actinobacillus species grow on chocolate agar or blood agar supplemented with nicotinamide adenine dinucleotide (NAD) for biovar 1 strains. Colonies appear as small, grayish, mucoid, and adherent after 24 to 48 hours of incubation at 37 degrees Celsius in 5 percent carbon dioxide. A satellite phenomenon may be observed around a nurse colony of Staphylococcus aureus on blood agar. Biochemical identification is based on urease positivity, fermentation of glucose and mannose, and lack of indole production.

Molecular Diagnostics

Polymerase chain reaction (PCR) assays targeting the apx toxin genes and the 16S rRNA gene are widely used for species identification and serotyping. Multiplex PCR panels can differentiate A. pleuropneumoniae from A. suis and other Pasteurellaceae. Real-time quantitative PCR (qPCR) offers higher sensitivity for detecting carrier animals with low bacterial loads. High-throughput sequencing approaches, including whole-genome sequencing, are increasingly employed for epidemiological surveillance and antimicrobial resistance profiling.

Serology

Commercial enzyme-linked immunosorbent assays (ELISA) based on ApxIV toxin or LPS antigens are available for detecting antibodies against A. pleuropneumoniae. Serological testing is useful for herd-level screening and monitoring vaccine responses but has limited utility for individual diagnosis due to the prevalence of subclinical infections.

Differential Diagnosis

The differential diagnosis for porcine pleuropneumonia includes other bacterial respiratory pathogens such as Pasteurella multocida, Bordetella bronchiseptica, Mycoplasma hyopneumoniae, and Streptococcus suis. Viral agents such as porcine reproductive and respiratory syndrome virus (PRRSV) and swine influenza virus can also cause similar clinical signs. Septicemic A. suis must be differentiated from Erysipelothrix rhusiopathiae, Salmonella spp., and Streptococcus suis.

The following table summarizes key diagnostic features for the two primary Actinobacillus species in swine.

| Feature | Actinobacillus pleuropneumoniae | Actinobacillus suis | |, - |, - |, - | | Primary disease | Fibrinous pleuropneumonia | Septicemia, respiratory disease | | Affected age groups | Grower-finisher pigs (8-16 weeks) | Neonatal to weanling pigs | | Key virulence factors | ApxI, ApxII, ApxIII, ApxIV | ApxI/II, ApxII, adhesins | | NAD dependence | Biovar 1: dependent; Biovar 2: independent | Independent | | Typical lung lesions | Necrotizing, hemorrhagic, fibrinous | Multifocal necrosis, less severe | | Diagnostic target genes | apxIV, apxII, apxIII | apxI/II, apxII |

Treatment

Antimicrobial therapy is most effective when initiated early in the course of disease. Selection of an antimicrobial agent should be guided by culture and susceptibility testing due to regional variations in resistance patterns. Commonly used antimicrobials include ceftiofur, florfenicol, tulathromycin, and enrofloxacin. Penicillins and tetracyclines may be effective against susceptible strains. Treatment is typically administered parenterally to acutely ill pigs, while in-feed or water medication may be used for mass medication during outbreaks.

The use of anti-inflammatory drugs, such as flunixin meglumine or meloxicam, can reduce fever and inflammation and improve survival rates. The effects of pentoxifylline, a phosphodiesterase inhibitor, on inflammatory cytokine expression have been investigated in experimental models of pleuropneumonia. Pentoxifylline reduced TNF-alpha and IL-1 expression in lung tissue, suggesting a potential adjunctive role in modulating the inflammatory response [5].

Control and Prevention

Control of Actinobacillus infections relies on a combination of biosecurity, management practices, and vaccination.

Biosecurity

Strict all-in/all-out production systems, adequate ventilation, and reduction of stocking density minimize the risk of transmission. Quarantine of incoming stock and segregation of age groups prevent introduction and spread of the pathogen. Eradication of A. pleuropneumoniae from a herd is possible through depopulation and repopulation or through medicated early weaning protocols.

Vaccination

Commercial bacterins and subunit vaccines containing Apx toxins and outer membrane proteins are available. Vaccination reduces the severity of clinical disease and mortality but does not prevent colonization or the establishment of carrier states. Autogenous vaccines may be used for herds infected with serotypes not covered by commercial products.

Antimicrobial Prophylaxis

In-feed or in-water antimicrobials may be used during high-risk periods, such as after weaning or during transport. However, this practice is increasingly discouraged due to concerns about antimicrobial resistance. The emergence of multidrug-resistant Actinobacillus strains has been documented, underscoring the need for judicious antimicrobial use.

The following Mermaid diagram outlines a decision tree for the diagnostic and management workflow in a suspected outbreak of porcine pleuropneumonia.

flowchart TD
    A[Clinical suspicion of pleuropneumonia], > B[Necropsy and gross examination]
    B, > C{Characteristic lesions present?}
    C, >|Yes| D[Collect lung tissue, pleural fluid]
    C, >|No| E[Consider differential diagnoses]
    D, > F[Bacteriological culture on chocolate agar + NAD]
    F, > G[Gram-negative coccobacilli isolated?]
    G, >|Yes| H[PCR for apx genes and 16S rRNA]
    G, >|No| I[Re-evaluate culture conditions]
    H, > J{apxIV positive?}
    J, >|Yes| K[Confirm A. pleuropneumoniae]
    J, >|No| L[Test for A. suis and other Pasteurellaceae]
    K, > M[Serotyping and antimicrobial susceptibility testing]
    M, > N[Implement treatment and control measures]
    L, > O[Identify species and treat accordingly]

Prognosis and Economic Impact

The prognosis for individual pigs with acute A. pleuropneumoniae infection is guarded to poor, especially if treatment is delayed. Chronic infections result in reduced weight gain, increased feed conversion ratios, and increased susceptibility to secondary infections. The economic impact of pleuropneumonia includes mortality, treatment costs, reduced carcass quality, and lost productivity. A. suis septicemia in neonatal pigs can cause significant mortality in affected litters, with economic losses proportional to the number of piglets lost.

Zoonotic Considerations

Actinobacillus pleuropneumoniae and Actinobacillus suis are not considered significant zoonotic pathogens. Human infections with these species are exceedingly rare and typically occur only in immunocompromised individuals with direct occupational exposure to swine or swine products. The primary public health concern associated with swine production is the potential for antimicrobial resistance genes to transfer from porcine Actinobacillus strains to human pathogens, a phenomenon that warrants ongoing surveillance.

References

[1] Rycroft AN, Garside LH. Actinobacillus species and their role in animal disease. Vet J. 2000. URL: https://pubmed.ncbi.nlm.nih.gov/10640409/

[2] Bujold AR, MacInnes JI. Identification of putative adhesins of Actinobacillus suis and their homologues in other members of the family Pasteurellaceae. BMC Res Notes. 2015. URL: https://pubmed.ncbi.nlm.nih.gov/26567540/

[3] Ojha S, Lacouture S, Gottschalk M et al. Characterization of colonization-deficient mutants of Actinobacillus suis. Vet Microbiol. 2010. URL: https://pubmed.ncbi.nlm.nih.gov/19664889/

[4] Elvira SM, Perez JT, Ortega MET et al. Septic shock in pigs infected, vaccinated and challenged with Actinobacillus pleuropneumoniae: A clinicopathological study. Vet J. 2025. URL: https://pubmed.ncbi.nlm.nih.gov/41248799/

[5] Myers MJ, Baarsch MJ, Murtaugh MP. Effects of pentoxifylline on inflammatory cytokine expression and acute pleuropneumonia in swine. Immunobiology. 2002. URL: https://pubmed.ncbi.nlm.nih.gov/11999342/

[6] Komal JP, Mittal KR. Grouping of Actinobacillus pleuropneumoniae strains of serotypes 1 through 12 on the basis of their virulence in mice. Vet Microbiol. 1990. URL: https://pubmed.ncbi.nlm.nih.gov/2281607/