Fowl Cholera: Etiology, Epidemiology, Clinical Signs, Pathology, Diagnostics, Treatment, and Control in Poultry

Introduction

Fowl cholera, also known as avian pasteurellosis or avian cholera, is a highly contagious bacterial disease of domestic and wild birds caused by the Gram-negative bacterium Pasteurella multocida [1, 2]. The disease is recognized globally as a significant cause of morbidity and mortality in poultry flocks, particularly in chickens, turkeys, ducks, and geese [3, 4]. Acute fowl cholera is characterized by septicemia with high morbidity and mortality, while chronic infections manifest as localized inflammatory lesions such as wattles, sinuses, and joints [5, 6]. The economic impact of fowl cholera on commercial poultry production is substantial, arising from direct mortality, reduced egg production, treatment costs, and trade restrictions [7, 8]. This article provides a detailed, publication-grade review of the etiology, epidemiology, clinical signs, pathology, diagnostics, treatment, and control of fowl cholera in poultry, with a focus on the molecular and biophysical mechanisms underlying the disease.

Etiology

The Causative Agent: Pasteurella multocida

Pasteurella multocida is a small, nonmotile, Gram-negative coccobacillus belonging to the family Pasteurellaceae [9, 10]. The bacterium is facultatively anaerobic and exhibits bipolar staining when treated with methylene blue or Giemsa stain [11]. On solid media, colonies are typically smooth, iridescent, and mucoid, reflecting the presence of a polysaccharide capsule [12]. The capsule is a critical virulence factor that mediates resistance to phagocytosis and complement-mediated killing [13, 12].

Serotyping and Genomic Diversity

P. multocida is classified into five capsular serogroups (A, B, D, E, F) and 16 somatic lipopolysaccharide (LPS) serotypes (1 through 16) based on the Heddleston scheme [14, 15]. Avian isolates most commonly belong to capsular serogroups A and F, with LPS serotypes 1, 3, and 4 being frequently associated with fowl cholera outbreaks [6, 15]. Genomic profiling has revealed substantial genetic diversity among avian P. multocida strains, with multilocus sequence typing (MLST) identifying sequence types (STs) such as ST20 as widespread in poultry populations [15, 16]. Whole-genome sequencing has further elucidated the presence of virulence-associated genes, including those encoding adhesins (e.g., filamentous hemagglutinin), toxins (e.g., Pasteurella multocida toxin, PMT), and iron acquisition systems [9, 17, 18].

Virulence Factors

The pathogenesis of fowl cholera is multifactorial, relying on a suite of virulence determinants. The hyaluronic acid capsule (encoded by the hya operon) is essential for evasion of host immune defenses [13, 12]. The LPS outer core locus exhibits phase variation, allowing the bacterium to alter its surface antigenicity and evade antibody-mediated clearance [19]. The Pasteurella multocida toxin (PMT) is a potent mitogen that activates intracellular signaling pathways, leading to cellular proliferation and immune dysregulation [18]. Filamentous hemagglutinin (FhaB) mediates adherence to host epithelial cells, although its role in avian pathogenesis may be strain-dependent [17]. The stringent response, mediated by the alarmone (p)ppGpp, negatively regulates capsule production, linking metabolic stress to virulence gene expression [12].

Epidemiology

Host Range and Susceptibility

Fowl cholera affects a wide range of avian species, with variable susceptibility among poultry types. Turkeys are highly susceptible and often experience acute, explosive outbreaks with high mortality [4, 6]. Chickens, particularly layers and broiler breeders, are also commonly affected, with mortality rates ranging from 10% to 100% depending on the strain and management conditions [5, 11]. Ducks and geese are susceptible, and outbreaks in waterfowl can result in significant losses [2, 3]. Wild birds, including waterfowl and passerines, serve as reservoirs and can introduce the pathogen into domestic poultry flocks [15, 20].

Transmission and Risk Factors

Transmission occurs primarily through direct contact with infected birds or indirect contact via contaminated fomites, feed, water, and equipment [7, 20]. The bacterium is shed in oral, nasal, and conjunctival secretions, as well as in feces. Ingestion or inhalation of contaminated material is the primary route of infection [7]. Environmental factors such as high stocking density, poor ventilation, and inadequate biosecurity increase the risk of transmission [20]. Land cover and proximity to water bodies have been associated with the occurrence of fowl cholera, likely due to the presence of wild bird reservoirs [20]. Coinfections with other pathogens, such as Mycoplasma gallisepticum, can exacerbate disease severity and mortality [4].

Global Distribution and Economic Impact

Fowl cholera is distributed worldwide, with endemic presence in many regions with intensive poultry production [1, 9]. Outbreaks have been reported in Asia, Africa, Europe, North America, and Australia [1, 2, 15]. The economic impact includes direct losses from mortality, reduced egg production, and costs associated with treatment and vaccination [7, 8]. Mathematical modeling of transmission dynamics has highlighted the importance of rapid detection and control measures to mitigate flock-level losses [7].

Clinical Signs

Acute Form

The acute form of fowl cholera is characterized by sudden onset of septicemia with high morbidity and mortality [5, 11]. Affected birds may be found dead without premonitory signs. Clinical signs in surviving birds include fever, depression, anorexia, ruffled feathers, cyanosis of the comb and wattles, and increased respiratory rate [5, 11]. Mucoid to bloody diarrhea is frequently observed [11]. In layers, a sharp drop in egg production is a common presenting sign [8].

Chronic Form

Chronic fowl cholera results from localized infection following acute disease or exposure to less virulent strains [6, 11]. Clinical manifestations include swollen wattles (wattle edema), conjunctivitis, sinusitis, torticollis (due to otitis media or meningitis), and lameness from arthritis or synovitis [6, 11]. Chronic respiratory signs such as rales and dyspnea may also be present [4].

Peracute Form

In highly susceptible species such as turkeys, the peracute form is common, with birds dying within hours of infection without observable clinical signs [4, 5]. Mortality in such outbreaks can approach 100% [5].

Pathology

Gross Lesions

Gross pathological findings in acute fowl cholera reflect a systemic septicemic process. Petechial and ecchymotic hemorrhages are observed on the epicardium, serosal surfaces, and in the musculature [5, 11]. The liver is often enlarged, friable, and studded with multiple small, pale necrotic foci (miliary necrosis) [5, 11]. The spleen is enlarged and congested. The lungs may be congested and edematous, and fibrinous pneumonia can be present [4]. In chronic cases, localized lesions include caseous exudate in the wattles, sinuses, and joints [6, 11].

Histopathology

Histologically, acute fowl cholera is characterized by fibrinoid necrosis of blood vessels, leading to hemorrhage and thrombosis [5]. The liver shows multifocal coagulative necrosis with infiltration of heterophils and macrophages. Fibrinous exudate is present in the pericardium, air sacs, and peritoneum [4, 5]. In chronic cases, granulomatous inflammation with central caseous necrosis and peripheral fibroplasia is observed in affected tissues [6].

Diagnostics

Clinical and Gross Pathological Diagnosis

A presumptive diagnosis of fowl cholera is based on history, clinical signs, and gross lesions, particularly in acute outbreaks with high mortality and characteristic liver necrosis [5, 11]. However, definitive diagnosis requires laboratory confirmation due to clinical overlap with other septicemic diseases such as avian influenza and salmonellosis [8].

Bacteriological Culture and Isolation

P. multocida can be isolated from blood, liver, spleen, bone marrow, or localized lesions using standard bacteriological media such as blood agar or MacConkey agar [21, 11]. Colonies are typically small, gray, and mucoid after 24 to 48 hours of incubation at 37 degrees Celsius under microaerophilic conditions [11]. Identification is confirmed by Gram staining, biochemical tests (catalase positive, oxidase positive, indole positive), and specific antisera [21, 11].

Molecular Diagnostics

Molecular methods offer high sensitivity and specificity for the detection of P. multocida. Polymerase chain reaction (PCR) assays targeting the kmt1 gene (species-specific) and capsular typing genes are widely used for confirmation and serogroup determination [10, 22]. Loop-mediated isothermal amplification (LAMP) assays have been developed as rapid, field-deployable alternatives to PCR, with comparable sensitivity and specificity [22]. Whole-genome sequencing provides comprehensive genotypic information, including virulence gene profiles, antimicrobial resistance determinants, and phylogenetic relationships [1, 2, 9, 14].

Serological Assays

Enzyme-linked immunosorbent assays (ELISAs) are used for serological surveillance and vaccine response monitoring. In-house indirect ELISAs using whole-cell or recombinant antigens (e.g., lipoprotein E) have been developed for detecting antibodies against P. multocida in chickens [23, 24]. These assays are valuable for flock-level screening but are not typically used for individual diagnosis due to the acute nature of the disease [23].

Antimicrobial Susceptibility Testing

Antimicrobial susceptibility testing is critical for guiding treatment decisions, given the increasing prevalence of antimicrobial resistance (AMR) in P. multocida [9, 21, 10]. Disk diffusion and broth microdilution methods are used to determine minimum inhibitory concentrations (MICs) against a panel of antibiotics [21, 11]. Molecular detection of resistance genes, such as those encoding beta-lactamases and tetracycline resistance determinants, complements phenotypic testing [9, 10].

Diagnostic Workflow

The following Mermaid diagram illustrates a typical diagnostic workflow for suspected fowl cholera outbreaks.

flowchart TD
    A[Suspected Fowl Cholera Outbreak], > B{Clinical Signs & Gross Lesions}
    B, >|Acute mortality, liver necrosis| C[Collect Samples: Liver, Spleen, Bone Marrow]
    B, >|Chronic lesions| D[Collect Samples: Wattles, Joints, Sinuses]
    C, > E[Bacteriological Culture on Blood Agar]
    D, > E
    E, > F[Gram Stain & Biochemical Tests]
    F, > G[PCR for kmt1 & Capsular Typing]
    G, > H[Antimicrobial Susceptibility Testing]
    H, > I[Confirmatory Diagnosis & Treatment Plan]
    G, > J[Optional: Whole-Genome Sequencing]
    J, > K[Genomic Epidemiology & AMR Profiling]

Treatment

Antimicrobial Therapy

Treatment of fowl cholera relies on the prompt administration of effective antimicrobials. Commonly used antibiotics include tetracyclines (e.g., oxytetracycline, doxycycline), penicillins (e.g., amoxicillin), fluoroquinolones (e.g., enrofloxacin), and sulfonamides (e.g., sulfadimethoxine) [9, 21, 11]. However, the emergence of multidrug-resistant (MDR) strains is a growing concern, with resistance reported to tetracyclines, penicillins, and sulfonamides in many regions [9, 10]. Antimicrobial susceptibility testing is therefore essential to select an effective agent [21, 11]. Treatment is typically administered via drinking water or feed for 5 to 7 days [11].

Supportive Care

Supportive care includes improving ventilation, reducing stocking density, and ensuring access to clean water and feed [7]. Removal of dead and moribund birds reduces environmental contamination and transmission [7].

Alternative and Adjunctive Therapies

Research into alternative therapies is ongoing. Plant-derived compounds, such as wild Egyptian artichoke extract, have demonstrated in vitro antibacterial activity against P. multocida [25]. Immunomodulatory agents, including flagellin and other adjuvants, are being investigated to enhance vaccine efficacy [26, 27].

Control

Biosecurity

Strict biosecurity measures are the cornerstone of fowl cholera prevention. These include controlling access to poultry facilities, disinfecting equipment and vehicles, and preventing contact with wild birds and other potential reservoirs [7, 20]. All-in-all-out management practices and thorough cleaning and disinfection between flocks reduce pathogen load in the environment [7].

Vaccination

Vaccination is a key component of fowl cholera control programs. Both inactivated (killed) and live attenuated vaccines are available [28, 6]. Inactivated vaccines, often formulated with adjuvants such as oil emulsions or hydrogels, induce humoral immunity and are used in layers and breeders [29, 30]. Live attenuated vaccines, derived from serial passage or mutagenesis, provide broader protection including cell-mediated immunity [3, 28]. Next-generation vaccines, including recombinant subunit vaccines (e.g., lipoprotein E, OmpH) and vectored vaccines (e.g., recombinant turkey herpesvirus or duck enteritis virus expressing P. multocida antigens), are under development and offer improved safety and efficacy [28, 26, 31, 24, 32, 33]. Gamma-irradiated vaccines have also shown promise in inducing antibody responses and cytokine expression [30].

Antimicrobial Stewardship

Given the rise of AMR, antimicrobial stewardship is critical. This involves using antimicrobials only when necessary, based on susceptibility testing, and avoiding prophylactic use [9, 10]. Rotation of antimicrobial classes and adherence to withdrawal periods are recommended to minimize resistance development [9].

Eradication and Depopulation

In severe outbreaks, particularly in high-value breeder flocks, depopulation of affected flocks may be implemented to eliminate the pathogen and prevent spread to other farms [7]. This is followed by thorough cleaning, disinfection, and a fallow period before restocking.

Fowl Cholera in Hindi: A Brief Translation Note

For readers seeking information in Hindi, the term "fowl cholera" is translated as "मुर्गी हैजा" (Murghi Haiza) or "एवियन हैजा" (Avian Haiza). The causative agent, Pasteurella multocida, is referred to as "पाश्चरेला मल्टोसिडा" (Pasteurella Multosida). The following table provides translations of key terms.

| English Term | Hindi Translation | | :-, | :-, | | Fowl Cholera | मुर्गी हैजा (Murghi Haiza) | | Pasteurella multocida | पाश्चरेला मल्टोसिडा (Pasteurella Multosida) | | Poultry | मुर्गीपालन (Murghipalan) | | Vaccination | टीकाकरण (Tikakaran) | | Antibiotic | एंटीबायोटिक (Antibiotic) |

Conclusion

Fowl cholera remains a major infectious disease threat to global poultry production. The causative agent, Pasteurella multocida, exhibits significant genomic and serotypic diversity, with virulence mediated by a complex interplay of capsular polysaccharides, LPS, toxins, and adhesins. Accurate diagnosis relies on a combination of clinical observation, bacteriological culture, and molecular methods such as PCR and whole-genome sequencing. Treatment is increasingly challenged by antimicrobial resistance, underscoring the need for susceptibility-guided therapy and robust biosecurity. Vaccination, using both conventional and next-generation platforms, remains a cornerstone of sustainable control. Continued research into the molecular pathogenesis, epidemiology, and vaccine development of P. multocida is essential to mitigate the impact of fowl cholera on poultry health and productivity.

References

[1] Islam MA, Haque ME, Iftehimul M, et al. Genomic profiling of Pasteurella multocida strains isolated from ISA Brown (Gallus gallus domesticus) in Bangladesh. Microbiol Resour Announc. 2026. URL: https://pubmed.ncbi.nlm.nih.gov/41920836/

[2] Islam MA, Haque ME, Iftehimul M, et al. Genome sequencing of Pasteurella multocida strains isolated from Jinding duck (Anas platyrhynchos) in Bangladesh. Microbiol Resour Announc. 2026. URL: https://pubmed.ncbi.nlm.nih.gov/41758112/

[3] Ji X, Meng Y, Yang H, et al. Attenuation mechanisms and vaccine potential of the serial passage-derived Pasteurella multocida strain PMZ8 in ducks. Poult Sci. 2026. URL: https://pubmed.ncbi.nlm.nih.gov/41747463/

[4] Gornatti-Churria CD, Jerry C, Ramsubeik S, et al. High mortality in a commercial turkey flock associated with coinfection by Pasteurella multocida and Mycoplasmoides (Mycoplasma) gallisepticum. J Vet Diagn Invest. 2026. URL: https://pubmed.ncbi.nlm.nih.gov/40996859/

[5] Miller I, Jerry C, Nguyen V, et al. 100% Mortality in Commercial Slow-Growing Broiler Chickens with Acute Fowl Cholera. Avian Dis. 2025. URL: https://pubmed.ncbi.nlm.nih.gov/40643942/

[6] Semmate N, Bamouh Z, Elkarhat Z, et al. Isolation and Characterization of Pasteurella multocida A from an Outbreak in Turkeys in Morocco and Vaccine Preparation and Evaluation. Avian Dis. 2025. URL: https://pubmed.ncbi.nlm.nih.gov/40643939/

[7] Malek A. Dynamics of cholera transmission in poultry farm: insights from a compartmental model and control strategies. Br Poult Sci. 2026. URL: https://pubmed.ncbi.nlm.nih.gov/40960429/

[8] Fasina YO, Suarez DL, Ritter GD, et al. Unraveling frontiers in poultry health (part 1) - Mitigating economically important viral and bacterial diseases in commercial Chicken and Turkey production. Poult Sci. 2024. URL: https://pubmed.ncbi.nlm.nih.gov/38417326/

[9] Miao F, Dai B, Li Z, et al. Antimicrobial resistance and genomic characteristics of avian Pasteurella multocida. Poult Sci. 2026. URL: https://pubmed.ncbi.nlm.nih.gov/41637789/

[10] El-Tarabili RM, Enany ME, Alenzi AM, et al. Unveiling resistance patterns, kmt1 sequence analyses, virulence traits, and antibiotic resistance genes of multidrug-resistant Pasteurella multocida retrieved from poultry and rabbits. Sci Rep. 2025. URL: https://pubmed.ncbi.nlm.nih.gov/39948418/

[11] Geda AM. Fowl Cholera in Chickens: Current Trends in Diagnosis and Phenotypic Drug Resistance in Gondar City, Ethiopia. Vet Med Int. 2024. URL: https://pubmed.ncbi.nlm.nih.gov/39669206/

[12] Smallman TR, Williams GC, Harper M, et al. Genome-Wide Investigation of Pasteurella multocida Identifies the Stringent Response as a Negative Regulator of Hyaluronic Acid Capsule Production. Microbiol Spectr. 2022. URL: https://pubmed.ncbi.nlm.nih.gov/35404102/

[13] Gao P, Wang L, Wang S, et al. The activity of hyaD contributed to the virulence of avian Pasteurella multocida. Microb Pathog. 2024. URL: https://pubmed.ncbi.nlm.nih.gov/38960217/

[14] Hashish A, Johnson TJ, Ghanem M, et al. Complete genome sequences of eight Pasteurella multocida isolates representing all lipopolysaccharide outer core loci. Microbiol Resour Announc. 2024. URL: https://pubmed.ncbi.nlm.nih.gov/39365089/

[15] Allen JL, Bushell RN, Noormohammadi AH, et al. Pasteurella multocida ST20 is widespread in Australian poultry farms and may infect wild waterbirds. Vet Microbiol. 2024. URL: https://pubmed.ncbi.nlm.nih.gov/38228079/

[16] Hamada K, Kawashima S, Hoshinoo K, et al. Draft genome sequence of Pasteurella multocida strain BD1769 with untypable capsular serotype isolated from a layer chicken. Microbiol Resour Announc. 2023. URL: https://pubmed.ncbi.nlm.nih.gov/37877706/

[17] Dassanayake RP, Briggs RE, Kaplan BS, et al. Pasteurella multocida filamentous hemagglutinin B1 (fhaB1) gene is not involved with avian fowl cholera pathogenesis in turkey poults. BMC Vet Res. 2025. URL: https://pubmed.ncbi.nlm.nih.gov/40140814/

[18] Kubatzky KF. Pasteurella multocida toxin - lessons learned from a mitogenic toxin. Front Immunol. 2022. URL: https://pubmed.ncbi.nlm.nih.gov/36591313/

[19] Omaleki L, Blackall PJ, Cuddihy T, et al. Phase variation in the glycosyltransferase genes of Pasteurella multocida associated with outbreaks of fowl cholera on free-range layer farms. Microb Genom. 2022. URL: https://pubmed.ncbi.nlm.nih.gov/35266868/ *** Disclaimer: This article is for educational and informational purposes only. It is not intended to substitute for professional veterinary advice, diagnosis, treatment, or regulatory guidance. Always consult a licensed veterinarian or qualified specialist regarding animal health, disease diagnosis, and therapeutic decisions.

[20] Ouyang L, Campler MR, Wong S, et al. Exploring the Impact of Land Cover on the Occurrence of Ornithobacteriosis and Fowl Cholera: A Case-Case Study. Animals (Basel). 2025. URL: https://pubmed.ncbi.nlm.nih.gov/39943166/

[21] Geda AM, Wendimu A, Lulie S, et al. Molecular Detection and Antibiogram Profiling of Pasteurella multocida Isolated From Breeder Chickens Suspected of Fowl Cholera in Gondar City, Ethiopia. Int J Microbiol. 2025. URL: https://pubmed.ncbi.nlm.nih.gov/40297765/

[22] Poussard M, Pant SD, Huang J, et al. Comparative evaluation of PCR and loop-mediated isothermal amplification (LAMP) assays for detecting Pasteurella multocida in poultry. N Z Vet J. 2025. URL: https://pubmed.ncbi.nlm.nih.gov/39448061/

[23] Beyene D, Shite A, Getachew B. Development and optimization of in-house made indirect ELISA kit for the detection of antibodies against Pasteurella multocida in chicken. BMC Immunol. 2026. URL: https://pubmed.ncbi.nlm.nih.gov/41724974/

[24] Cheng LT, Chu CY, Vu-Khac H, et al. Signal sequence contributes to the immunogenicity of Pasteurella multocida lipoprotein E. Poult Sci. 2023. URL: https://pubmed.ncbi.nlm.nih.gov/36423524/

[25] Wahdan A, Elsebai MF, Elhaig MM, et al. Innovative use of wild Egyptian artichoke extract to control fowl cholera in vitro. Vet World. 2025. URL: https://pubmed.ncbi.nlm.nih.gov/40182829/

[26] Chung YC, Cheng LT, Chu CY, et al. Flagellin Enhances the Immunogenicity of Pasteurella multocida Lipoprotein E Subunit Vaccine. Avian Dis. 2024. URL: https://pubmed.ncbi.nlm.nih.gov/39400212/

[27] Manohar MM, Campbell BE, Walduck AK, et al. Enhancement of live vaccines by co-delivery of immune modulating proteins. Vaccine. 2022. URL: https://pubmed.ncbi.nlm.nih.gov/36064671/

[28] Tesfaye AB, Werid GM, Tao Z, et al. Advances in Pasteurella multocida Vaccine Development: From Conventional to Next-Generation Strategies. Vaccines (Basel). 2025. URL: https://pubmed.ncbi.nlm.nih.gov/41150422/

[29] Chen J, Sun Y, Hu Y, et al. Evaluation of the immunoprotective effect of gel 01 hydrogel inactivated vaccine against Pasteurella multocida infection in chickens. Microb Pathog. 2025. URL: https://pubmed.ncbi.nlm.nih.gov/40934985/

[30] Belay E, Bitew M, Ibrahim SM, et al. Gamma-irradiated fowl cholera vaccines formulated with different adjuvants induced antibody response and cytokine expression in chickens. Front Immunol. 2025. URL: https://pubmed.ncbi.nlm.nih.gov/40103817/

[31] Apinda N, Yao Y, Zhang Y, et al. Efficiency of NHEJ-CRISPR/Cas9 and Cre-LoxP Engineered Recombinant Turkey Herpesvirus Expressing Pasteurella multocida OmpH Protein for Fowl Cholera Prevention in Ducks. Vaccines (Basel). 2023. URL: https://pubmed.ncbi.nlm.nih.gov/37766174/

[32] Apinda N, Muenthaisong A, Chomjit P, et al. Simultaneous Protective Immune Responses of Ducks against Duck Plague and Fowl Cholera by Recombinant Duck Enteritis Virus Vector Expressing Pasteurella multocida OmpH Gene. Vaccines (Basel). 2022. URL: https://pubmed.ncbi.nlm.nih.gov/36016245/

[33] Apinda N, Yao Y, Zhang Y, et al. CRISPR/Cas9 Editing of Duck Enteritis Virus Genome for the Construction of a Recombinant Vaccine Vector Expressing ompH Gene of Pasteurella multocida in Two Novel Insertion Sites. Vaccines (Basel). 2022. URL: https://pubmed.ncbi.nlm.nih.gov/35632442/

[34] Tabatabaei M, Janparvar A, Motamedifar M. Genotypic evaluation of Pasteurella multocida isolated from cattle and sheep by pulsed-field gel electrophoresis. Vet Res Forum. 2023. URL: https://pubmed.ncbi.nlm.nih.gov/37181852/

[35] Cavaillon JM, Legout S. Louis Pasteur: Between Myth and Reality. Biomolecules. 2022. URL: https://pubmed.ncbi.nlm.nih.gov/35454184/