Avibacterium volantium Infection in Chickens and Turkeys: Upper Respiratory Disease

Avibacterium volantium is a gram-negative, pleomorphic rod belonging to the family Pasteurellaceae. Within the genus Avibacterium, the recognized species include Av. paragallinarum, Av. avium, Av. gallinarum, Av. endocarditidis, and Av. volantium [1]. Av. paragallinarum is the well-established primary pathogen causing infectious coryza in chickens, a disease characterized by acute upper respiratory signs [1]. By contrast, Av. volantium has been historically regarded as either a commensal organism of the upper respiratory tract or a low-grade opportunistic pathogen. However, accumulating field and experimental evidence indicates that under appropriate predisposing conditions, Av. volantium can contribute to upper respiratory disease in both chickens and turkeys, particularly when co-infections or environmental stressors are present [1]. This article provides a detailed reference on the etiology, epidemiology, clinical presentation, pathology, diagnostic methods, treatment, and control of Av. volantium infection in poultry.

Etiology

Avibacterium volantium shares the general phenotypic characteristics of the genus: it is a nonmotile, facultatively anaerobic, catalase-positive, oxidase-positive, and urease-negative coccobacillus. On solid media, colonies appear small, translucent, and nonhemolytic on sheep blood agar. Growth requires nicotinamide adenine dinucleotide (NAD, factor V) but not hemin (factor X), distinguishing it from some other Pasteurellaceae members. The species is distinguished from Av. paragallinarum by its inability to produce acid from galactose and its lack of β-galactosidase activity, among other biochemical tests [1]. Molecular identification relies on 16S rRNA gene sequencing or species-specific polymerase chain reaction (PCR) assays targeting housekeeping genes.

Av. volantium is most frequently isolated from the nasal cavity, infraorbital sinuses, and trachea of clinically healthy poultry, indicating a carrier state. Its transition to pathogenicity is believed to require mucosal damage, immunosuppression, or concurrent infections (e.g., with Mycoplasma spp., infectious bronchitis virus, or avian metapneumovirus). The organism adheres to respiratory epithelium but lacks the robust capsular antigens that drive the acute inflammatory response seen with Av. paragallinarum.

Epidemiology

Av. volantium has a worldwide distribution in commercial and backyard poultry flocks. Prevalence studies in chickens report isolation rates from apparently healthy birds ranging from 10% to 40%, with higher rates in flocks with concurrent respiratory disease [1]. In turkeys, Av. volantium is recovered less frequently but has been associated with sinusitis and airsacculitis, especially in young poults under poor ventilation conditions.

Transmission occurs horizontally via aerosolized respiratory droplets, direct contact between birds, and potentially contaminated fomites. Vertical transmission has not been documented. Stressors such as high stocking density, poor litter quality, ammonia exposure, vaccination reactions, and intercurrent parasitic infections (e.g., the poultry ectoparasites Dermanyssus gallinae or Knemidocoptes mutans; see Ectoparasites of Poultry) can precipitate clinical disease.

The economic impact of Av. volantium is generally considered lower than that of Av. paragallinarum, infectious coryza (see Infectious Coryza in Chickens and Quail), or other upper respiratory pathogens such as Ornithobacterium rhinotracheale (see Ornithobacterium rhinotracheale (ORT)). However, when Av. volantium contributes to multifactorial respiratory disease, it can cause reduced feed conversion, increased condemnations at slaughter, and heightened susceptibility to secondary bacterial invaders.

Clinical Signs

The clinical presentation of Av. volantium upper respiratory infection is typically mild and indistinguishable from mild forms of infectious coryza or other bacterial upper respiratory infections. In chickens and turkeys, the following signs may be observed:

• Serous to mucoid nasal discharge
• Sneezing and snicking
• Submandibular or infraorbital sinus swelling (less pronounced than in infectious coryza)
• Conjunctivitis with mild ocular discharge
• Reduction in feed and water intake in severe cases
• Occasional frothy ocular exudate in advanced stages

In turkeys, sinusitis may be more prominent, and the disease can progress to airsacculitis if left untreated, particularly when exacerbated by concurrent infection with Mycoplasma meleagridis (see Mycoplasma meleagridis).

Clinical signs typically appear within 3 to 7 days after exposure and may persist for 1 to 2 weeks. In uncomplicated cases, recovery is spontaneous, but chronic carrier states are common.

Pathology

Gross lesions are confined to the upper respiratory tract. The nasal passages and infraorbital sinuses contain variable amounts of catarrhal to mucopurulent exudate. The mucosal lining is congested and edematous. In turkeys, the caudal thoracic and abdominal air sacs may show mild cloudiness and thickening when airsacculitis develops.

Histopathological examination reveals:

• Loss of ciliated epithelial cells in the nasal turbinates and trachea
• Infiltration of heterophils, macrophages, and lymphocytes in the lamina propria
• Hyperplasia of mucous glands
• Mild hyperplasia of lymphoid aggregates (mucosa-associated lymphoid tissue)

Unlike Av. paragallinarum, which can cause severe fibrinopurulent inflammation and caseous sinus exudate, Av. volantium lesions are less severe and rarely result in caseous plugs [1].

Diagnostics

Definitive diagnosis of Av. volantium infection requires isolation and identification of the organism from affected tissues, supported by molecular methods to differentiate it from other Avibacterium species. The diagnostic workflow is summarized in Figure 1.

Figure 1. Diagnostic workflow for Av. volantium upper respiratory infection in chickens and turkeys.

flowchart TD
    A["Suspected bacterial upper respiratory infection"], > B["Collect samples: nasal swabs, sinus exudate, tracheal swabs"]
    B, > C["Gram stain: pleomorphic Gram-negative rods"]
    C, > D["Culture on chocolate agar or sheep blood agar with nurse colony (NAD-dependent)"]
    D, > E["Colony morphology: small, translucent, nonhemolytic"]
    E, > F["Biochemical characterization: catalase+, oxidase+, urease-, galactose-"]
    F, > G["Molecular identification: 16S rRNA or species-specific PCR"]
    G, > H{"Av. volantium detected?"}
    H, >|Yes| I["Consider significance: evaluate predisposing factors, co-infections"]
    H, >|No| J["Rule out Av. paragallinarum, Av. gallinarum, Ornithobacterium rhinotracheale, Mycoplasma spp."]
    I, > K["Antimicrobial susceptibility testing (disc diffusion or MIC)"]

Sample collection. Acceptable specimens include deep nasal swabs (from both nares), infraorbital sinus aspirates, and tracheal swabs from live birds. At necropsy, sections of nasal turbinate, sinus mucosa, and proximal trachea are collected. Transport media (e.g., Amies charcoal medium) preserve viability for up to 48 hours if refrigeration is maintained.

Culture and isolation. Samples are inoculated onto chocolate agar or sheep blood agar with a nurse colony of Staphylococcus epidermidis to supply NAD. Plates are incubated at 37°C in a 5% CO2 atmosphere for 24 to 48 hours. Suspect colonies are subcultured for purity and subjected to Gram stain and biochemical testing.

Biochemical differentiation. Key tests to distinguish Av. volantium from other avian Avibacterium species are provided in Table 1.

Table 1. Biochemical differentiation of selected Avibacterium species [1].

Molecular diagnostics. Amplification and sequencing of the 16S rRNA gene or PCR targeting the pgi (glucose-6-phosphate isomerase) gene can provide species-level identification. Real-time PCR assays that differentiate Avibacterium species are available in reference laboratories and are preferred for their sensitivity and speed. These methods are especially useful when cultures are negative due to prior antimicrobial therapy.

Serology. No commercial serological tests exist for Av. volantium. The detection of antibodies by ELISA is not routinely performed because the low antigenic stimulus produced by this opportunistic pathogen yields variable and often cross-reactive results.

Treatment

Antimicrobial therapy should be guided by in vitro susceptibility testing, as resistance patterns vary among isolates. Commonly used antimicrobial classes include:

• β-lactams (amoxicillin, ampicillin)
• Macrolides (tylosin, tilmicosin)
• Tetracyclines (oxytetracycline, doxycycline)
• Quinolones (enrofloxacin, danofloxacin)
• Potentiated sulfonamides (trimethoprim-sulfamethoxazole)

Administration is typically via drinking water for 3 to 5 days for flock treatment. In severe sinusitis cases, individual injection of a long-acting tetracycline or amoxicillin may be warranted. Although clinical response is often rapid, elimination of the carrier state is difficult to achieve; therefore, recurrence may occur if predisposing factors are not corrected.

Control

Control of Av. volantium upper respiratory infection relies on reducing predisposing stress and preventing co-infections. Specific measures include:

• Biosecurity. All-in/all-out management, sanitation of feeders and waterers, and quarantine of new stock reduce introduction and spread of the organism.

• Environmental management. Optimal ventilation, control of ammonia levels (<20 ppm), appropriate litter moisture (20% to 30%), and maintenance of stocking density as per national guidelines minimize respiratory mucosal damage.

• Vaccination. No commercial vaccines are available for Av. volantium. Vaccines targeting primary respiratory pathogens (e.g., infectious bronchitis virus, Mycoplasma gallisepticum, and Av. paragallinarum) indirectly reduce the frequency of opportunistic Av. volantium disease.

• Monitoring and surveillance. Periodic culture or PCR of nasal swabs from sentinel or sick birds can identify early infection. Treatment of only clinically affected lots, with targeted antimicrobials, helps preserve overall flock health.

• Integrated parasite and disease control. Managing ectoparasites (e.g., Argas persicus; see Ectoparasites of Poultry), and enteric nematodes (e.g., Heterakis gallinarum; see Heterakis gallinarum) reduces overall flock immunosuppression.

Conclusion

Avibacterium volantium is a facultative pathogen of the upper respiratory tract in chickens and turkeys. While generally mild and self-limiting, its clinical significance increases in the presence of environmental stress, immunosuppression, or concurrent infections. Accurate diagnosis requires culture and molecular methods to differentiate it from other Avibacterium species, particularly the primary pathogen Av. paragallinarum. Treatment with appropriate antimicrobials is effective, but long-term control depends on comprehensive flock management that addresses predisposing factors. Continued surveillance and characterization of Av. volantium isolates from respiratory disease outbreaks will refine our understanding of its pathogenic role and inform future prevention strategies.

References

[1] Blackall P, Soriano-Vargas E. Infectious Coryza and Related Bacterial Infections. In: Diseases of Poultry. 2019. URL: https://www.semanticscholar.org/paper/0fd29ccddec044f18fdd546049d249255fec6bf2