Section: Avian Bacteria

Avian Cholera (Fowl Cholera) in Poultry: Etiology, Clinical Signs, and Control

Introduction

Avian cholera, also known as fowl cholera, is a highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida [1, 2, 3]. The disease manifests in peracute, acute, and chronic forms and is responsible for significant economic losses in poultry production worldwide [4, 3, 5]. Mortality can reach 100% in susceptible flocks, particularly in slow-growing broiler chickens and turkeys [6, 3]. This article provides a detailed review of the etiology, epidemiology, clinical signs, pathology, diagnostic approaches, treatment options, and control measures for fowl cholera in poultry, with emphasis on recent molecular and immunological advances.

Etiology: Fowl Cholera Is Caused by Which Bacteria

Fowl cholera is caused by the Gram-negative, non-motile, facultative anaerobic coccobacillus Pasteurella multocida [1, 7, 8]. The bacterium is classified into five capsular serogroups (A, B, D, E, F) and 16 lipopolysaccharide (LPS) genotypes based on the Heddleston scheme [8, 9]. In poultry, serogroup A (especially A:1, A:3, and A:4) is most frequently isolated, although serogroups B and D have also been reported [5, 10, 11]. The complete genome sequences of multiple P. multocida isolates have been published, revealing extensive genomic diversity and the presence of virulence-associated genes such as kmt1, toxA, fhaB1, hyaD, and LPS outer core transferase genes (pcgD, hptE) [12, 8, 13, 14].

The bacterium produces a polysaccharide capsule that inhibits phagocytosis and a lipopolysaccharide that triggers a strong inflammatory response [1, 15]. Key virulence factors include filamentous hemagglutinin (FhaB1), which mediates adhesion to host epithelial cells, and the enzyme hyaluronidase (HyaD), which degrades hyaluronic acid in connective tissues and facilitates bacterial dissemination [12, 13]. The LPS outer core structure is critical for full virulence; truncation of the outer core attenuates the bacterium in ducks [16, 14]. Phase variation in glycosyltransferase genes can alter LPS structure and contribute to immune evasion during outbreaks [9].

Epidemiology

P. multocida is carried asymptomatically in the nasopharynx of many healthy birds and mammals, serving as a reservoir for transmission [17, 18]. Outbreaks often occur following stress factors such as overcrowding, poor ventilation, nutritional deficiencies, or concurrent infections (e.g., Mycoplasma gallisepticum) [6, 4]. Transmission occurs via direct contact with infected birds, inhalation of aerosolized respiratory droplets, or ingestion of contaminated feed and water [4, 17]. Fomites, equipment, and personnel can also mechanically spread the bacterium [4].

The disease has a global distribution and affects chickens, turkeys, ducks, geese, and numerous wild bird species [3, 5, 17, 11]. In Bangladesh, multidrug-resistant P. multocida type B:2 has been reported in fowl cholera outbreaks, highlighting the need for region-specific control strategies [10]. In Australia, sequence type ST20 is widespread in poultry farms and can infect wild waterbirds, indicating potential spillover events [17].

Avian Cholera Transmission to Humans

Pasteurella multocida is primarily an animal pathogen, but zoonotic transmission to humans can occur through bites, scratches, or direct contact with infected birds or their secretions [7, 18]. Human infections typically manifest as localized wound infections, cellulitis, or, rarely, respiratory disease [7]. However, avian cholera is not considered a major public health concern, and human cases are sporadic [18]. The risk is elevated for immunocompromised individuals and poultry workers [7].

Clinical Signs

The clinical presentation of fowl cholera varies with the virulence of the strain, host species, and route of infection [3, 19]. Three main forms are recognized:

  • Peracute form: Sudden death with no premonitory signs. Mortality can reach 100% within 24–48 hours [3, 19]. This form is common in highly susceptible flocks, such as slow-growing broilers and turkeys [6, 3].
  • Acute form: Fever (up to 44°C), depression, anorexia, ruffled feathers, mucoid or bloody diarrhea, increased respiratory rate, and cyanosis of the comb and wattles [3, 15, 20]. Swelling of the wattles and sinuses is characteristic [3]. Mortality peaks within 3–5 days [4].
  • Chronic form: Localized infections including swollen joints (arthritis), sternal bursitis, conjunctivitis, and torticollis due to otitis media [3, 20]. Chronic cases are more common in flocks with partial immunity or following subacute outbreaks [20].

In ducks, liver injury mediated by inflammatory, apoptotic, and autophagic pathways has been described [15]. In broilers, P. multocida induces liver pyroptosis through the MAPK-NLRP3-GSDMD signaling pathway [1].

Pathology

Gross lesions in acute fowl cholera include petechial hemorrhages on the heart, epicardium, and serosal surfaces; multifocal hepatic necrosis (small, pale foci); splenomegaly; and pulmonary congestion [1, 3, 15]. The liver may appear friable and mottled [1]. In chronic cases, caseous exudate is found in the wattles, joints, and sinuses [3].

Histopathological examination reveals hepatocellular necrosis, infiltration of heterophils and macrophages, and fibrin thrombi in hepatic sinusoids [1, 15]. In the lungs, interstitial pneumonia and congestion are common [6]. The MAPK-NLRP3-GSDMD pathway mediates pyroptosis in broiler hepatocytes, characterized by caspase-1 activation and gasdermin D cleavage [1]. In ducks, autophagy and apoptosis contribute to liver injury [15].

Diagnostics

Definitive diagnosis of fowl cholera requires isolation and identification of P. multocida from affected tissues (liver, spleen, bone marrow, or exudate) [3, 21, 19]. The bacterium grows on blood agar or MacConkey agar (weak growth) as small, gray, mucoid colonies [19]. Gram staining reveals Gram-negative coccobacilli with bipolar staining (safety pin appearance) [19].

Molecular methods offer rapid and specific detection. Conventional PCR targeting the kmt1 gene is widely used [7, 21]. Loop-mediated isothermal amplification (LAMP) assays provide a field-deployable alternative with sensitivity comparable to PCR [21]. Real-time PCR and whole-genome sequencing are employed for epidemiological typing and antimicrobial resistance gene profiling [2, 8, 18].

Serological diagnosis using indirect ELISA kits has been developed for detecting antibodies against P. multocida in chickens [22]. These assays are useful for monitoring vaccine responses and herd immunity [22, 23, 24].

The following diagnostic workflow summarizes the recommended approach:

flowchart TD
    A[Clinical suspicion: sudden death, fever, cyanosis], > B[Postmortem examination: petechiae, liver necrosis]
    B, > C[Sample collection: liver, spleen, bone marrow, wattle exudate]
    C, > D[Gram stain: bipolar coccobacilli]
    D, > E[Culture on blood agar: mucoid colonies]
    E, > F[Biochemical identification: oxidase+, catalase+]
    F, > G[PCR: kmt1 gene detection]
    G, > H[Serotyping: capsular and LPS typing]
    H, > I[Antimicrobial susceptibility testing]
    I, > J[Confirm outbreak and guide treatment]

Treatment

Antimicrobial therapy is the mainstay of treatment for acute fowl cholera. Historically, tetracyclines, sulfonamides, and penicillin derivatives have been used [2, 7]. However, multidrug resistance is increasingly reported, particularly against tetracycline, sulfonamides, and aminoglycosides [2, 7, 10]. Resistance genes such as tet(H), blaROB-1, and strA-strB have been identified in avian isolates [2, 7].

Antimicrobial susceptibility testing is essential to guide therapy [2]. In cases of confirmed resistance, alternative agents such as fluoroquinolones or florfenicol may be considered, although resistance to these has also emerged [2, 7]. Phage therapy using lytic bacteriophages (e.g., vB_PmuM_CFP3) has shown promise as an alternative or adjunct to antibiotics [25]. Probiotic formulations containing multiple Lactobacillus and Bacillus strains have reduced mortality in broilers experimentally infected with P. multocida [26]. Plant extracts, such as wild Egyptian artichoke extract, have demonstrated in vitro antibacterial activity against P. multocida [27].

Control and Prevention

Control of fowl cholera relies on biosecurity, management practices, and vaccination [4, 28, 5]. Biosecurity measures include all-in-all-out production, cleaning and disinfection of facilities, control of rodents and wild birds, and quarantine of new stock [4, 17].

Vaccination

Both inactivated (bacterin) and live attenuated vaccines are available [29, 28, 5, 30]. Inactivated vaccines are commonly used in commercial poultry and are often adjuvanted with aluminum hydroxide or oil emulsions [28, 23, 30]. Novel vaccine approaches include:

  • Subunit vaccines: Recombinant lipoproteins such as PlpE and VacJ, and outer membrane protein H, have shown immunoprotective effects in chickens and ducks [23, 31, 32, 33, 34]. Multi-epitope proteins incorporating PlpE epitopes enhance immunogenicity [23].
  • Outer membrane vesicle (OMV) vaccines: E. coli-derived OMVs displaying PlpE protein induce strong antibody responses [31].
  • Gamma-irradiated vaccines: Irradiated whole-cell vaccines formulated with various adjuvants elicit both humoral and cell-mediated immunity [24, 35].
  • Hydrogel-based vaccines: Gel 01 hydrogel inactivated vaccine provides sustained antigen release and improved protection [28].
  • Live attenuated vaccines: Serial passage-derived strains (e.g., PMZ8 in ducks) show reduced virulence and good immunogenicity [29].

Vaccination strategies should be tailored to the prevalent serotypes and local epidemiological conditions [5, 10]. In Bangladesh, for example, type B:2 is common, and vaccines should include this serotype [10].

Fowl Cholera Meaning in Bengali

In Bengali, fowl cholera is commonly referred to as "মুরগির কলেরা" (murgir cholera), reflecting the disease's clinical similarity to human cholera (diarrhea and rapid death) [10]. The term is used in veterinary extension materials and outbreak reports in Bangladesh [10].

Conclusion

Avian cholera remains a major threat to poultry health worldwide. Advances in genomics, immunology, and vaccine technology have improved our understanding of P. multocida pathogenesis and host responses [1, 2, 15, 18]. Integrated control programs combining biosecurity, antimicrobial stewardship, and effective vaccination are essential to reduce the impact of this disease [4, 5, 30]. Continued surveillance of antimicrobial resistance and genomic diversity will inform future control strategies [2, 7, 10].

References

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