Fowl Cholera in Chickens: Clinical Signs, Postmortem Lesions, Treatment, Vaccination, and Prevention

Introduction

Fowl cholera is a contagious bacterial disease of domestic and wild avian species caused by Pasteurella multocida, a Gram-negative, nonmotile, facultatively anaerobic coccobacillus belonging to the family Pasteurellaceae [1, 2]. In chickens, the disease manifests in peracute, acute, or chronic forms and constitutes a significant economic burden to commercial poultry operations worldwide due to mortality, reduced egg production, and treatment costs [3, 4]. P. multocida is also a zoonotic pathogen capable of causing localized infections in humans following bites or scratches, but this review restricts its focus to avian disease. The organism commonly colonizes the upper respiratory tract and oropharynx of apparently healthy carrier birds, and outbreaks are often precipitated by environmental or physiological stressors that compromise host immunity [5, 6, 4]. A 5-year retrospective study in Mississippi revealed that P. multocida isolates were recovered from chickens with respiratory signs, frequently in conjunction with Gallibacterium anatis, underscoring the polymicrobial nature of some outbreaks [3]. Genetic diversity among fowl cholera isolates has been demonstrated by ribotyping and comparative sequencing of 16S rRNA and atpD genes, with multiple capsular serotypes (A, D, F) and somatic serovars (1-16) identified in poultry populations [7]. Molecular detection via PCR targeting the kmt1 gene has become a cornerstone of rapid diagnosis, and recent work in Ethiopia confirmed that 14.3% of breeder chickens with suspected fowl cholera were positive for P. multocida by this method [1].

Clinical Signs

The clinical presentation of fowl cholera in chickens varies with the virulence of the infecting strain, host immune status, and route of exposure [5, 8]. Peracute disease is characterized by sudden death in apparently healthy birds, often without premonitory signs, especially in highly susceptible flocks or when highly virulent serovars are involved [8]. Acute cases exhibit fever, depression, anorexia, ruffled feathers, mucoid or foamy oral discharge, and pronounced respiratory distress including dyspnea and rales [1, 4]. Cyanosis of the comb and wattles is frequently observed, and birds may develop diarrhea, with feces ranging from watery to greenish or hemorrhagic [6, 8]. In chronic infections, localized manifestations predominate: wattles become edematous and swollen (wattle edema), joints may be distended due to fibrinous synovitis, and conjunctivitis or sinusitis can occur [5, 4]. Neurological signs such as torticollis or ataxia are occasionally reported when the infection extends to the central nervous system [9]. Concurrent infections with gastrointestinal nematodes such as Ascaridia galli have been shown to exacerbate clinical disease in free-range chickens, likely due to immune modulation and increased intestinal permeability [9]. A time-course investigation using a low-virulent strain in 12-week-old free-range chickens demonstrated that immunosuppression (induced by cyclophosphamide) significantly increased the severity and duration of clinical signs, highlighting the role of adaptive immunity in controlling infection [5]. Carrier birds, particularly those raised under scavenging conditions, may harbor P. multocida in the pharyngeal region without overt illness, serving as reservoirs for flock outbreaks [6].

Postmortem Lesions

Necropsy findings in fowl cholera correlate with the disease course and severity. In peracute cases, lesions may be minimal but often include petechial hemorrhages on the epicardium, serosal surfaces, and abdominal fat [10, 8]. Acute cases present with generalized congestion and hemorrhages in multiple organs. Petechiae and ecchymoses are prominent on the heart, liver (particularly the capsule), and kidneys [10]. The liver is frequently enlarged, friable, and exhibits focal to confluent areas of coagulative necrosis, giving a characteristic "nutmeg" appearance on cut section [10, 8]. Tang et al. (2017) demonstrated that liver injury in experimentally infected chickens involves both necroptosis and apoptosis, with upregulation of receptor-interacting protein kinase 3 (RIPK3) and caspase-3, accompanied by a robust inflammatory response dominated by heterophil infiltration and increased expression of interleukin-1β and tumor necrosis factor-α [10]. Pneumonia is common, with lungs showing consolidation and fibrinous exudate within the air sacs and thoracic cavity [3, 4]. Acute fibrinous polyserositis involving the pericardium and peritoneum is often present [8]. Chronic cases exhibit localized lesion: caseous wattle abscesses, fibrinous conjunctivitis, and purulent arthritis or tenosynovitis [5]. The spleen may be enlarged and mottled. Histologically, the hallmark is an acute, necrotizing heterophilic inflammation with abundant intra- and extracellular Gram-negative coccobacilli visible in impression smears or tissue sections [10, 11].

Pathogenesis and Virulence Factors

P. multocida employs a repertoire of virulence determinants to colonize the respiratory epithelium, evade host defenses, and cause systemic infection. The polysaccharide capsule is a critical antiphagocytic factor, and serotype-specific capsular antigens (A, D, F) are associated with differing pathogenic potentials [2, 11]. Lipopolysaccharide (LPS) contributes to endotoxic shock and tissue damage through activation of the inflammatory cascade [2, 10]. Outer membrane proteins, including OmpH and OmpA, mediate adhesion to host cells and are targets of the immune response [11]. Iron acquisition systems, such as the Fur-regulated receptor, enable survival within the iron-limited environment of the host [2]. Molecular characterization of multidrug-resistant isolates from poultry and rabbits in Egypt revealed a high prevalence of virulence-associated genes including toxA (encoding a dermonecrotic toxin), pfhA (filamentous hemagglutinin), hgbA (hemoglobin-binding protein), and oma87 (outer membrane protein) [2]. The kmt1 gene, a species-specific marker, is widely used for molecular detection and is conserved across strains [1, 2]. Recent genomic studies have also identified antibiotic resistance genes such as tetH, blaROB-1, floR, and sul2 in isolates from chickens and rabbits, correlating with phenotypic resistance to tetracyclines, beta-lactams, phenicols, and sulfonamides [2].

Diagnosis

Definitive diagnosis of fowl cholera requires isolation and identification of P. multocida from affected tissues (liver, spleen, lung, bone marrow) or oropharyngeal swabs of symptomatic or carrier birds [1, 6]. Samples are cultured on blood agar or selective media (e.g., MacConkey agar with enrichment) under 5-10% CO₂ at 37°C for 24-48 hours. Colonies are small, grayish, mucoid, and non-hemolytic on sheep blood agar [11]. Presumptive identification is based on Gram stain (negative coccobacilli), oxidase and catalase positivity, and characteristic biochemical profiles (indole positive, urease negative, lactose negative) [11]. Confirmatory identification relies on PCR amplification of kmt1 and capsular typing genes [1, 2]. Antibiogram profiling is critical for guiding therapy, given the increasing prevalence of multidrug resistance [1, 2, 12]. In a study of Ethiopian breeder chickens, 78.6% of P. multocida isolates exhibited resistance to at least three antibiotic classes, with high resistance to tetracycline and ampicillin [1]. A Mermaid diagram summarizing the diagnostic workflow is presented below.

flowchart TD
 A[Clinical suspicion of fowl cholera] --> B[Necropsy and sample collection]
 B --> C[Impression smears for Gram stain]
 C --> D{Presence of Gram-negative coccobacilli?}
 D -->|Yes| E[Isolation on blood agar / selective media]
 D -->|No| F["Consider alternative diagnoses: infectious coryza, colibacillosis, mycoplasmosis"]
 E --> G["Biochemical identification: oxidase+, catalase+, indole+"]
 G --> H[PCR for kmt1 and capsular typing]
 H --> I[Confirmed P. multocida]
 I --> J["'Antimicrobial susceptibility testing (disk diffusion or microdilution')"]
 J --> K[Report and treatment selection based on antibiogram]

Differential diagnoses include Infectious Coryza in Poultry caused by Avibacterium paragallinarum, Escherichia coli in Chickens (colibacillosis), Mycoplasma synoviae infection, and Highly Pathogenic Avian Influenza. Clinical and pathological overlap necessitates laboratory confirmation.

Treatment

Antimicrobial therapy is the mainstay for managing active fowl cholera outbreaks, but the emergence of multidrug-resistant (MDR) strains complicates treatment decisions [2, 12, 13]. Commonly used antibiotics include tetracyclines (doxycycline, oxytetracycline), beta-lactams (amoxicillin, ampicillin), fluoroquinolones (enrofloxacin), sulfonamides, and phenicols (florfenicol) [2, 12, 13]. In a controlled study comparing oral treatment regimens in broilers and turkeys experimentally infected with P. multocida, enrofloxacin and amoxicillin both significantly reduced mortality, with enrofloxacin demonstrating superior efficacy in clearing infection from tissues [12]. Doxycycline administered at 20 mg/kg body weight per day for five days in feed provided high therapeutic efficacy in broilers, with recovery of clinical signs and reduction of bacterial load in the liver [13]. However, the same study noted that doxycycline-resistant strains required alternative therapy [13]. The increasing prevalence of MDR isolates, particularly those carrying tetH and blaROB-1, underscores the need for antibiogram-guided therapy [1, 2]. Probiotic interventions have also been explored: a multi-strain probiotic comprising Lactobacillus and Bacillus species given orally for 21 days prior to challenge with P. multocida significantly reduced mortality (from 50% to 12.5%) in broilers and modulated the gut microbiome and immune response [14]. Concurrent infections with Ascaridia galli can impair drug efficacy due to immune modulation, highlighting the value of integrated parasite control [9]. Treatment protocols should comply with local regulations regarding withdrawal times, especially for egg-laying flocks.

Vaccination

Vaccination remains a central component of fowl cholera prevention, particularly in endemic regions. Commercial bacterins (inactivated whole-cell vaccines) are widely used but often confer serovar-specific protection and require periodic booster administration [15]. Live attenuated vaccines have been developed to induce broader and more durable immunity. Scott et al. (1999) evaluated two aroA auxotrophic mutants of P. multocida administered via drinking water to chickens; both mutants were safe (no reversion to virulence) and elicited significant protection against homologous challenge, although cross-protection against heterologous serovars was limited [15]. Autogenous vaccines prepared from local isolates are sometimes used in flocks experiencing persistent outbreaks [3, 4]. Subunit vaccines targeting immunogenic proteins such as OmpH, OmpA, and iron-regulated outer membrane proteins (IROMPs) are under investigation, but none have yet replaced conventional bacterins or live vaccines in commercial practice [11]. The genetic diversity of field strains, as shown by ribotyping and sequence analysis, presents a major challenge for vaccine development; successful immunization strategies must account for the prevalent serovars in a given region [7].

Prevention and Control

Effective prevention of fowl cholera hinges on biosecurity, management practices, and monitoring of carrier status. P. multocida is transmitted horizontally via direct contact, aerosol droplets, and contaminated feed, water, or equipment [6, 4]. Introduction of carrier birds from external sources is a primary risk factor; therefore, strict quarantine and testing of new additions are recommended [6]. Rodents, wild birds, and fomites can disseminate the organism [4]. In scavenging chicken populations, age-related susceptibility has been noted, with younger birds more likely to become carriers, and transmission between chickens and ducks occurs under free-range conditions [6]. Stress reduction through optimal nutrition, ventilation, stocking density, and parasite control is essential, as immunosuppression increases susceptibility and severity [5, 9]. A comprehensive control protocol includes:

• All-in/all-out flock management with thorough cleaning and disinfection between cycles.
• Routine bacteriological or PCR surveillance of breeder and layer flocks to detect carriers.
• Water chlorination at 3-5 ppm to reduce oral transmission.
• Rodent and wild bird exclusion via netting and bait stations.
• Integrated parasite management addressing ectoparasites and nematodes that can exacerbate disease.

Outbreaks of fowl cholera in commercial flocks have been documented worldwide, with mortality rates ranging from 10% to 50% in acute cases [4, 8]. Early detection, rapid laboratory confirmation, and targeted antimicrobial therapy based on susceptibility profiles are critical to minimizing losses. Vaccination, combined with stringent biosecurity, offers the most sustainable path to long-term control. The role of molecular diagnostics and genomic surveillance is increasingly recognized for tracking resistance genes and informing vaccine composition [2, 7]. Adherence to WOAH guidelines for notification may apply in some jurisdictions, although fowl cholera is not classified as a notifiable disease in all regions.

References

[1] 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. https://pubmed.ncbi.nlm.nih.gov/40297765/

[2] 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. https://pubmed.ncbi.nlm.nih.gov/39948418/

[3] Jones KH, Thornton JK, Zhang Y, et al. A 5-year retrospective report of Gallibacterium anatis and Pasteurella multocida isolates from chickens in Mississippi. Poult Sci. 2013. https://pubmed.ncbi.nlm.nih.gov/24235226/

[4] Hinz KH, Lüders H. Pasteurella multocida as the cause of disease outbreaks in commercial poultry flocks. Berl Munch Tierarztl Wochenschr. 1991. https://pubmed.ncbi.nlm.nih.gov/1953629/

[5] Mbuthia PG, Njagi LW, Nyaga PN, et al. Time-course investigation of infection with a low virulent Pasteurella multocida strain in normal and immune-suppressed 12-week-old free-range chickens. Avian Pathol. 2011. https://pubmed.ncbi.nlm.nih.gov/22107097/

[6] Mbuthia PG, Njagi LW, Nyaga PN, et al. Pasteurella multocida in scavenging family chickens and ducks: carrier status, age susceptibility and transmission between species. Avian Pathol. 2008. https://pubmed.ncbi.nlm.nih.gov/18202950/

[7] Petersen KD, Christensen H, Bisgaard M, et al. Genetic diversity of Pasteurella multocida fowl cholera isolates as demonstrated by ribotyping and 16S rRNA and partial atpD sequence comparisons. Microbiology (Reading). 2001. https://pubmed.ncbi.nlm.nih.gov/11577153/

[8] Sander JE, Glisson JR. Fowl cholera in broilers. Avian Dis. 1989. https://pubmed.ncbi.nlm.nih.gov/2619670/ *** 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.

[9] Dahl C, Permin A, Christensen JP, et al. The effect of concurrent infections with Pasteurella multocida and Ascaridia galli on free range chickens. Vet Microbiol. 2002. https://pubmed.ncbi.nlm.nih.gov/11955781/

[10] Tang Q, Li W, Dai N, et al. The Role of Necroptosis, Apoptosis, and Inflammation in Fowl Cholera-Associated Liver Injury in a Chicken Model. Avian Dis. 2017. https://pubmed.ncbi.nlm.nih.gov/29337619/

[11] Ireland L, Adler B, Milner AR. Proteins and antigens of Pasteurella multocida serotype 1 from fowl cholera. Vet Microbiol. 1991. https://pubmed.ncbi.nlm.nih.gov/1829560/

[12] Sarközy G, Semjén G, Laczay P, et al. Treatment of experimentally induced Pasteurella multocida infections in broilers and turkeys: comparative studies of different oral treatment regimens. J Vet Med B Infect Dis Vet Public Health. 2002. https://pubmed.ncbi.nlm.nih.gov/12019943/

[13] Semjén G, Magyar T, Laczay P. Therapeutic efficacy of doxycycline against experimental Pasteurella multocida infection in broiler chickens. Acta Vet Hung. 1998. https://pubmed.ncbi.nlm.nih.gov/9704513/

[14] Reuben RC, Sarkar SL, Ibnat H, et al. Novel multi-strain probiotics reduces Pasteurella multocida induced fowl cholera mortality in broilers. Sci Rep. 2021. https://pubmed.ncbi.nlm.nih.gov/33903662/

[15] Scott PC, Markham JF, Whithear KG. Safety and efficacy of two live Pasteurella multocida aro-A mutant vaccines in chickens. Avian Dis. 1999. https://pubmed.ncbi.nlm.nih.gov/10216763/