Fowl Cholera (Avian Pasteurellosis): Comprehensive Veterinary Reference on Etiology, Epidemiology, Clinical Signs, Diagnosis, Treatment, and Control
1. Introduction
Fowl cholera, also known as avian pasteurellosis, is a highly contagious bacterial disease of domestic and wild birds caused by infection with Pasteurella multocida [1]. The condition is recognized globally as a major cause of economic loss in poultry production due to high morbidity and mortality, particularly in chickens, turkeys, and waterfowl [2, 3]. In the vernacular, the disease is referred to as fowl cholera in English, and in South Asian languages it is known as fowl cholera in hindi (मुर्गी हैजा) and fowl cholera meaning in bengali (পোল্ট্রি কলেরা), reflecting its widespread clinical recognition across diverse poultry-keeping communities [4]. The fundamental question fowl cholera is caused by which bacteria is answered definitively: it is caused by Pasteurella multocida, a Gram-negative coccobacillus [5]. Understanding the fowl cholera bacterial etiology is essential for implementing effective control measures, as the pathogen exhibits considerable genetic and serologic diversity [6, 7, 8]. This reference provides a comprehensive, evidence-based review of fowl cholera, integrating genomic, epidemiological, diagnostic, therapeutic, and vaccinological perspectives.
2. Etiology
2.1 The Causative Agent: Pasteurella multocida
Pasteurella multocida is a non-motile, facultatively anaerobic, Gram-negative coccobacillus belonging to the family Pasteurellaceae [9, 28]. The bacterium is characterized by a polysaccharide capsule and a lipopolysaccharide (LPS) outer core that together determine serotype specificity and contribute to virulence [10, 33]. Fowl cholera is caused by which bacteria? The answer is unequivocally P. multocida, although not all strains are equally pathogenic for avian hosts [5].
2.2 Capsular and LPS Serotypes
Isolates from poultry are traditionally classified into five capsular serogroups (A, B, D, E, F) and 16 LPS genotypes (1–16) [10, 34]. The majority of avian fowl cholera outbreaks are associated with capsular serogroup A and LPS genotypes 1 and 3 [11, 35]. However, untypable strains have been reported, as demonstrated in a draft genome sequence of a layer chicken isolate with an untypable capsular serotype in Japan [8]. The LPS outer core locus undergoes phase variation mediated by slipped-strand mispairing in glycosyltransferase genes, a mechanism linked to outbreak persistence on free-range layer farms [34].
2.3 Virulence Factors
Key virulence determinants include the polysaccharide capsule, which inhibits phagocytosis; LPS, which induces a pro-inflammatory host response; filamentous hemagglutinin (FhaB); and Pasteurella multocida toxin (PMT), a potent mitogenic toxin that activates intracellular signaling pathways [12, 13, 28]. The hyaluronic acid capsule is a critical virulence factor for avian strains, and its production is negatively regulated by the stringent response [33]. Genomic profiling of strains from Bangladesh in ISA Brown chickens and Jinding ducks has revealed conserved virulence gene repertoires, including ompH, ptfA, and toxA [6, 7]. The gene hyaD (involved in hyaluronic acid synthesis) contributes to virulence in avian P. multocida [13]. Conversely, the fhaB1 gene is not required for pathogenesis in turkey poults, indicating functional redundancy among adhesins [12].
2.4 Genomic Diversity and Antimicrobial Resistance Genes
Whole-genome sequencing has uncovered extensive genomic diversity among avian P. multocida isolates [9, 10]. Multidrug-resistant (MDR) strains carrying genes conferring resistance to tetracyclines, sulfonamides, and beta-lactams have been characterized from poultry in Egypt and Ethiopia [14, 5, 4]. A comprehensive genomic analysis of avian MDR P. multocida identified resistance-associated mutations and plasmid-borne resistance genes [9]. Sequence type 20 (ST20) is widespread in Australian poultry farms and has the capacity to infect wild waterbirds, highlighting a potential reservoir for spillover [15].
3. Epidemiology
3.1 Host Range and Geographic Distribution
Fowl cholera affects a broad range of avian species, including chickens, turkeys, ducks, geese, and many wild bird species [2, 16, 1]. The disease is reported worldwide, with endemic circulation in many commercial poultry operations [3]. In chickens, fowl cholera typically manifests as an acute or peracute septicemia, while turkeys are particularly susceptible to high mortality [17, 3]. Ducks and other waterfowl may serve as asymptomatic carriers and contribute to environmental contamination [15, 31].
3.2 Transmission and Outbreak Dynamics
Transmission occurs horizontally via direct contact with infected birds or indirectly through contaminated feed, water, and fomites [2]. The bacterium can survive for weeks in moist organic matter. Chickens in a chicken bacteria outbreak often show a sudden spike in mortality without prior clinical signs [3]. Epidemiological compartmental models have been developed to simulate the dynamics of cholera transmission within poultry farms and to evaluate the effectiveness of control strategies such as culling and vaccination [2]. Land cover and environmental factors, including proximity to wetlands, influence the occurrence of fowl cholera, as shown in a case-case study comparing ornithobacteriosis and fowl cholera in Ohio, USA [16].
3.3 Zoonotic Considerations
Avian cholera transmission to humans is exceptionally rare but documented. Pasteurella multocida can cause localized wound infections or bacteremia following scratches or bites from infected birds. A case report described bacteremia in a patient scratched by an adopted Pekin duck, underscoring the potential for zoonotic transmission in close-contact settings [18]. However, poultry-to-human transmission is not a significant public health concern, and human infections are primarily opportunistic rather than epidemic.
3.4 Risk Factors and Coinfections
High stocking density, poor biosecurity, and concurrent viral or bacterial infections exacerbate fowl cholera severity. A case of high mortality in a commercial turkey flock was associated with coinfection by P. multocida and Mycoplasmoides gallisepticum, demonstrating the potentiating effect of mycoplasmosis on pasteurellosis [17]. Stress factors such as transport, overcrowding, and poor ventilation predispose birds to clinical disease.
4. Clinical Signs
The clinical presentation of fowl cholera varies with host species, strain virulence, and immune status. In peracute cases, birds are found dead with no premonitory signs, especially in layers and turkeys [3]. Acute fowl cholera is characterized by fever, depression, anorexia, ruffled feathers, oral and nasal mucus discharge, cyanosis of combs and wattles, and greenish watery diarrhea [4]. Respiratory signs, including dyspnea and rales, may predominate in some outbreaks. Chronic infections manifest as localized swelling of the wattles, conjunctivitis, and arthritis, leading to lameness [5]. In slow-growing broiler chickens, acute outbreaks can reach 100% mortality if untreated [3].
5. Pathology
Gross pathologic findings in acute fowl cholera include generalized congestion, petechial hemorrhages on the heart (epicardium) and serosal surfaces, hepatic necrosis (miliary necrotic foci), splenomegaly, and fibrinous pericarditis or airsacculitis [17, 3]. Turkeys often exhibit severe hemorrhagic enteritis. Chronic cases show caseous abscesses in the wattles and joint exudates. Histologically, acute disease presents with fibrinoid necrosis of blood vessels and multifocal coagulative necrosis in the liver and spleen. Intracellular bacteria are visible in macrophages and Kupffer cells.
6. Diagnosis
Accurate and timely diagnosis is essential for implementing control measures. A stepwise diagnostic workflow is presented in Figure 1.
6.1 Diagnostic Workflow
flowchart TD
A[Clinical suspicion: high mortality, cyanosis, hepatic necrosis], > B{Specimen collection}
B, > C[Tissue swabs (liver, spleen, bone marrow)]
B, > D[Blood smears from acutely ill birds]
C, > E[Culture on blood agar or MacConkey agar]
D, > F[Gram stain: bipolar Gram-negative coccobacilli]
E, > G[Biochemical identification: oxidase +, catalase +, no hemolysis]
G, > H{PCR or LAMP confirmation}
H, > I[kmt1 gene amplification]
H, > J[Capsular typing PCR (hyaD-hyaC, etc.)]
H, > K[Ames strain-specific assays]
I, > L[Positive: P. multocida confirmed]
L, > M[Antimicrobial susceptibility testing]
M, > N[Treatment recommendation]
J, > O[Serotype determination for vaccine selection]
Figure 1. Diagnostic workflow for fowl cholera in poultry.
6.2 Bacteriological and Molecular Methods
Presumptive diagnosis is based on isolation of P. multocida from liver, spleen, or bone marrow of freshly dead birds on blood agar (non-hemolytic, dewdrop-like colonies) [4]. Confirmatory identification is achieved through biochemical tests and molecular assays. The kmt1 gene (species-specific) is a common target for PCR and loop-mediated isothermal amplification (LAMP) [19]. A comparative evaluation of PCR and LAMP for detecting P. multocida in poultry showed that LAMP is more rapid and does not require thermal cycling, making it suitable for field diagnosis [19]. Capsular serotyping is performed using multiplex PCR targeting capsule biosynthesis genes [14, 10].
6.3 Serological Assays
Enzyme-linked immunosorbent assays (ELISAs) are used for serosurveillance. An in-house indirect ELISA kit for detection of anti-P. multocida antibodies in chickens has been developed and optimized, demonstrating high sensitivity and specificity [20]. Antibiotic resistance profiling is essential for treatment guidance; disk diffusion and broth microdilution methods are applied according to CLSI guidelines [9, 14].
6.4 Advanced Molecular Tools
Whole-genome sequencing provides detailed insights into virulence gene content, LPS genotype, and antimicrobial resistance determinants [6, 7, 10, 8]. The availability of complete genome sequences for all LPS outer core loci facilitates precise serotyping and molecular epidemiology [10]. Real-time PCR assays targeting the ompH gene have been employed in vaccine development studies [27,32].
7. Treatment
7.1 Antimicrobial Therapy
The question what kills chicken bacteria in the context of fowl cholera is addressed through antimicrobial chemotherapy. Antibiotics commonly used include tetracyclines, sulfonamides, penicillin, and fluoroquinolones [4]. However, widespread antimicrobial resistance (AMR) compromises treatment efficacy [5]. Antibiogram profiling of P. multocida from breeder chickens in Ethiopia revealed high resistance to tetracycline and sulfamethoxazole-trimethoprim but susceptibility to enrofloxacin [14, 4]. Similarly, MDR strains from poultry and rabbits in Egypt carried multiple resistance genes, including blaTEM, tetA, and sul1 [5].
7.2 Alternative and Adjunctive Therapies
Innovative approaches to control fowl cholera include the use of natural products. Wild Egyptian artichoke extract demonstrated in vitro bactericidal activity against P. multocida, offering a potential alternative to synthetic antibiotics [21]. However, clinical validation in vivo is lacking.
8. Control and Prevention
8.1 Biosecurity and Management
Strict biosecurity measures are the cornerstone of fowl cholera prevention. These include all-in/all-out production, disinfection of facilities between flocks, control of rodents and wild birds, and quarantine of newly introduced birds [1, 15]. Early detection and removal of sick or dead birds reduce environmental contamination. Vaccination is the most effective long-term control strategy.
8.2 Fowl Cholera Vaccine Development
The fowl cholera vaccine landscape encompasses killed bacterins, live attenuated vaccines, and next-generation recombinant vaccines [22]. Traditional inactivated vaccines (bacterins) are widely used but provide serotype-specific protection and require annual revaccination [23, 11]. Advanced formulation with gel 01 hydrogel adjuvant enhanced the immune response and protection in chickens [23]. Gamma-irradiated vaccines combined with adjuvants induced strong antibody and cytokine responses in chickens [24].
Live attenuated vaccines, such as strain PMZ8 generated by serial passage, show promise in ducks by eliciting robust mucosal immunity [25]. Subunit vaccines targeting immunogenic proteins like OmpH and lipoprotein E (PlpE) have been evaluated. Lipoprotein E with its native signal sequence enhanced immunogenicity in chickens [29]. Flagellin fusion with PlpE further improved vaccine efficacy in chickens [26].
Recombinant vector vaccines represent the cutting edge. The NHEJ-CRISPR/Cas9 system and Cre-LoxP recombination have been used to engineer recombinant turkey herpesvirus expressing P. multocida OmpH for protection in ducks [27]. Similarly, recombinant duck enteritis virus (DEV) vectors expressing OmpH provided simultaneous protection against both duck plague and fowl cholera [31,32]. Immune modulating proteins co-delivered with live vaccines can enhance protective responses [30].
Another promising strategy involves LPS truncation. A P. multocida strain with a truncated LPS outer core conferred immunogenicity and protection against homologous challenge in ducks [35].
8.3 Vaccination Recommendations
Vaccination programs should be tailored to farm-specific serotypes. Multivalent bacterins containing the predominant capsular and LPS types in the region are recommended. For long-lived birds such as layers and breeders, revaccination every 3–6 months is essential to maintain protective antibody levels.
9. Conclusion
Fowl cholera remains a significant threat to global poultry production. The causative agent, Pasteurella multocida, exhibits substantial genomic diversity and a broad host range, complicating control efforts. Advances in whole-genome sequencing have illuminated virulence mechanisms and resistance patterns, informing both treatment and vaccine design. Rapid molecular diagnostics, including LAMP and PCR, facilitate early detection and typing. Antimicrobial stewardship is critical in the face of rising MDR prevalence. Next-generation vaccines, particularly recombinant viral vectors and rationally attenuated strains, offer the potential for broad, durable protection. Integrated biosecurity and vaccination programs remain the most effective strategies for reducing the impact of fowl cholera in poultry flocks.
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.
References
[1] 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/
[2] 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/
[3] 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/
[4] 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/
[5] 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/
[6] 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/
[7] 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/
[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] 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/
[11] 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/
[12] 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/
[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] 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/
[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] 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/
[17] 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/
[18] Bathobakae L, Cho H, Philip S, et al. Friend turned foe: Pasteurella multocida bacteremia following a scratch by an adopted Pekin duck. J Investig Med High Impact Case Rep. 2025. URL: https://pubmed.ncbi.nlm.nih.gov/40110910/
[19] 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/
[20] 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/
[21] 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/
[22] 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/
[23] 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/
[24] 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/
[25] 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/
[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/