# [Fowl Cholera in Poultry](/knowledge/bacteria/avian-bacteria/fowl-cholera-drug-choice): Etiology, Diagnosis, and Control

## Key Takeaways

- Fowl cholera is caused by the Gram-negative coccobacillus *Pasteurella multocida*, with capsular serogroup A being the most prevalent in poultry. Virulence is mediated by factors such as the hyaluronic acid capsule, lipopolysaccharide (LPS), adhesins, and the *P. multocida* toxin (PMT).
- Transmission occurs primarily through direct contact with carrier birds, contaminated feed and water, and inhalation of aerosolized droplets, with environmental and management factors significantly influencing outbreak risk.
- Diagnosis relies on isolation and identification of *P. multocida* via bacteriological culture, supplemented by rapid molecular methods like PCR and LAMP assays for species-specific detection and capsular typing.
- Clinical signs range from peracute death without premonitory signs to acute septicemia characterized by fever, depression, and diarrhea, or chronic localized infections such as arthritis and sinusitis.
- Antimicrobial resistance in *P. multocida* is a growing concern, necessitating susceptibility testing for effective treatment; fluoroquinolones and ceftiofur often show good in vitro activity, but resistance to tetracyclines and sulfonamides is common.
- Control strategies integrate stringent biosecurity measures, vaccination with inactivated bacterins or live attenuated vaccines, and in severe cases, depopulation and thorough disinfection to eliminate carrier states.

---

## Introduction

[Fowl cholera](/knowledge/bacteria/avian-bacteria/avian-cholera-fowl-cholera-in-poultry), also known as avian pasteurellosis, is a highly contagious bacterial disease affecting domestic poultry, wild birds, and waterfowl worldwide [<a href="#ref-1">1</a>, <a href="#ref-2">2</a>]. The disease is caused by the Gram-negative coccobacillus *Pasteurella multocida* [<a href="#ref-3">3</a>, <a href="#ref-4">4</a>]. Outbreaks of [fowl cholera](/knowledge/bacteria/avian-bacteria/avian-cholera-fowl-cholera) result in significant economic losses due to high morbidity and mortality, decreased egg production, and the costs associated with treatment and control measures [<a href="#ref-5">5</a>, <a href="#ref-6">6</a>]. The disease can manifest in peracute, acute, or chronic forms depending on host susceptibility, strain virulence, and environmental stressors [<a href="#ref-2">2</a>, <a href="#ref-7">7</a>].

## Etiology

### The Causative Agent: *Pasteurella multocida*

The [fowl cholera bacterial](/knowledge/bacteria/avian-bacteria/avian-cholera-fowl-cholera-comprehensive-veterinary-reference) agent, *P. multocida*, is a nonmotile, facultatively anaerobic, bipolar-staining Gram-negative rod belonging to the family Pasteurellaceae [<a href="#ref-8">8</a>, <a href="#ref-9">9</a>]. Capsular serogroups A, B, D, E, and F are recognized based on capsular antigens, with serogroup A being the most common cause of [fowl cholera in poultry](/knowledge/bacteria/avian-bacteria/fowl-cholera-in-poultry-etiology-clinical-signs-diagnosis-and-control) [<a href="#ref-9">9</a>, <a href="#ref-10">10</a>]. The lipopolysaccharide (LPS) outer core of the bacterium is a critical virulence determinant, and isolates are further classified into eight LPS genotypes (L1 through L8) based on outer core biosynthesis loci [<a href="#ref-9">9</a>, <a href="#ref-11">11</a>, <a href="#ref-12">12</a>].

The genome of *P. multocida* is approximately 2.3 to 2.5 Mb in size and encodes a range of virulence factors, including adhesins, toxins, iron acquisition systems, and a polysaccharide capsule [<a href="#ref-13">13</a>, <a href="#ref-14">14</a>, <a href="#ref-15">15</a>]. The hyaluronic acid capsule, encoded by the *hyaD* gene cluster, is a key antiphagocytic component [<a href="#ref-14">14</a>, <a href="#ref-15">15</a>]. Strains deficient in capsule production exhibit reduced virulence in avian models [<a href="#ref-15">15</a>].

### Virulence Factors

*P. multocida* possesses multiple molecular determinants of pathogenicity. The polysaccharide capsule inhibits phagocytosis and complement-mediated killing [<a href="#ref-14">14</a>]. Lipopolysaccharide contributes to serum resistance and induces a strong inflammatory response [<a href="#ref-12">12</a>]. The filamentous hemagglutinin (FhaB) and other adhesins facilitate attachment to host respiratory epithelial cells [<a href="#ref-16">16</a>]. The *P. multocida* toxin (PMT), encoded by the *toxA* gene, is a potent mitogen that activates intracellular signaling cascades, leading to cellular proliferation and immune modulation [<a href="#ref-17">17</a>]. While PMT is classically associated with atrophic rhinitis in swine, its role in avian [fowl cholera](/knowledge/bacteria/avian-bacteria/fowl-cholera-avian-cholera-in-poultry) pathogenesis remains variable depending on the host species and strain [<a href="#ref-17">17</a>]. Iron acquisition systems, including receptors for hemin and transferrin, are essential for bacterial survival within the avian host [<a href="#ref-8">8</a>, <a href="#ref-14">14</a>].

Phase variation in LPS glycosyltransferase genes is a documented mechanism of immune evasion in *P. multocida* strains associated with outbreaks on free-range layer farms [<a href="#ref-11">11</a>]. This reversible, high-frequency switching of surface carbohydrate structures allows the bacterium to evade host antibody responses and persist in carrier birds [<a href="#ref-11">11</a>].

## Epidemiology

[Fowl cholera](/knowledge/bacteria/avian-bacteria/fowl-cholera-avian-cholera-poultry) occurs in all poultry-producing regions of the world [<a href="#ref-3">3</a>, <a href="#ref-4">4</a>]. Domestic chickens, turkeys, ducks, and geese are all susceptible [<a href="#ref-10">10</a>, <a href="#ref-18">18</a>, <a href="#ref-19">19</a>]. Turkeys and waterfowl are generally more susceptible to acute disease than chickens [<a href="#ref-2">2</a>, <a href="#ref-19">19</a>]. A 100% mortality rate has been documented in commercial slow-growing broiler chickens during acute [fowl cholera](/knowledge/bacteria/avian-bacteria/fowl-cholera-avian-cholera) outbreaks [<a href="#ref-2">2</a>].

The primary source of infection is carrier birds that harbor *P. multocida* in their upper respiratory tracts or oropharyngeal tonsils [<a href="#ref-4">4</a>, <a href="#ref-20">20</a>]. Transmission occurs via direct contact between infected and susceptible birds, through contaminated feed and water, and by inhalation of aerosolized droplets [<a href="#ref-3">3</a>, <a href="#ref-4">4</a>]. Fomites, contaminated equipment, and footwear can also spread the organism between flocks [<a href="#ref-1">1</a>, <a href="#ref-5">5</a>].

Environmental and management factors influence the occurrence of [fowl cholera](/knowledge/bacteria/avian-bacteria/fowl-cholera-avian-pasteurellosis-comprehensive-reference). Brucellosis coinfection and interactions with mycoplasmas can exacerbate disease severity [<a href="#ref-18">18</a>]. Land cover and farm location may influence outbreak risk through exposure to wild bird reservoirs [<a href="#ref-20">20</a>]. A compartmental model of [fowl cholera](/knowledge/bacteria/avian-bacteria/fowl-cholera-avian-pasteurellosis-comprehensive-veterinary-reference) transmission in poultry farms demonstrated that biosecurity measures and early detection are critical for controlling disease spread [<a href="#ref-1">1</a>].

In the context of regional nomenclature, the [fowl cholera bacterial](/knowledge/bacteria/avian-bacteria/avian-cholera-fowl-cholera-etiology-pathogenesis-and-control) disease is referred to as मुर्गी हैजा (murgi haiza) in Hindi ([fowl cholera](/knowledge/bacteria/avian-bacteria/fowl-cholera-avian-pasteurellosis-poultry) in hindi), reflecting its clinical similarity to classic cholera in terms of rapid-onset diarrhea and septicemia.

## Clinical Signs

The clinical presentation of [fowl cholera](/knowledge/bacteria/avian-bacteria/fowl-cholera-causal-agent) varies with the course of disease [<a href="#ref-4">4</a>]. In the peracute form, birds are found dead without premonitory signs [<a href="#ref-2">2</a>]. Mortality can spike rapidly, with no observed illness before death [<a href="#ref-2">2</a>].

Acute [fowl cholera](/knowledge/bacteria/avian-bacteria/fowl-cholera-causative-agent) is characterized by fever (elevated body temperature), depression, anorexia, ruffled feathers, cyanosis of the comb and wattles, and mucoid or bloody diarrhea [<a href="#ref-4">4</a>, <a href="#ref-7">7</a>]. Respiratory signs, including cough, dyspnea, and rales, are common due to the involvement of the respiratory tract [<a href="#ref-18">18</a>]. In chickens, oral discharge and swelling of the wattles (wattle edema) are frequently observed [<a href="#ref-2">2</a>, <a href="#ref-4">4</a>].

Chronic [fowl cholera](/knowledge/bacteria/avian-bacteria/fowl-cholera-etiology-clinical-manifestations-control-poultry) typically develops after an acute outbreak or in flocks with partial immunity [<a href="#ref-4">4</a>]. Clinical signs include localized infections such as swollen joints (arthritis), sternal bursitis, torticollis from otitis media, and chronic respiratory disease [<a href="#ref-4">4</a>, <a href="#ref-5">5</a>]. Conjunctivitis and sinusitis are also reported, particularly in turkeys [<a href="#ref-10">10</a>, <a href="#ref-18">18</a>].

## Pathology

### Gross Lesions

Peracute cases may lack gross lesions [<a href="#ref-2">2</a>]. In acute [fowl cholera](/knowledge/bacteria/avian-bacteria/fowl-cholera-etiology-clinical-signs-post-mortem-lesions-poultry), gross lesions are those of a fulminant septicemia. Petechial and ecchymotic hemorrhages are found on the epicardium, serosal membranes, and abdominal fat [<a href="#ref-2">2</a>, <a href="#ref-7">7</a>]. The liver is friable with multifocal pinpoint necrotic foci of a pale yellow color [<a href="#ref-4">4</a>, <a href="#ref-7">7</a>]. The spleen is enlarged and congested. The lungs may be congested or edematous, with fibrinous pneumonia in some cases [<a href="#ref-18">18</a>, <a href="#ref-19">19</a>].

In chronic [fowl cholera](/knowledge/bacteria/avian-bacteria/fowl-cholera-etiology-epidemiology-clinical-signs-pathology-diagnostics-treatment-control-poultry), lesions are localized. Caseous exudate is present in the infraorbital sinuses, wattles, joints, and tympanic cavities [<a href="#ref-4">4</a>]. Fibrinous pericarditis and airsacculitis are common findings in turkeys [<a href="#ref-10">10</a>].

### Histopathology

Histologically, acute cases demonstrate acute fibrinous pneumonia, multifocal hepatic necrosis with heterophilic infiltration, and splenic lymphoid depletion [<a href="#ref-7">7</a>]. Fibrin thrombi are present in small vessels [<a href="#ref-19">19</a>]. In chronic cases, pyogranulomatous inflammation with central caseous necrosis and peripheral fibroplasia is observed in affected joints and sinuses [<a href="#ref-4">4</a>].

## Diagnosis

A definitive diagnosis of [fowl cholera](/knowledge/bacteria/avian-bacteria/fowl-cholera-in-poultry-etiology-pathogenesis-diagnostic-methods-and-control-strategies) requires isolation and identification of *P. multocida* from clinical specimens [<a href="#ref-3">3</a>, <a href="#ref-4">4</a>]. Samples from acutely affected birds include heart blood, liver, spleen, and bone marrow. In chronic cases, swabs of exudate from wattles, sinuses, or joints are appropriate [<a href="#ref-4">4</a>].

### Conventional Diagnostic Methods

Bacteriological culture is the gold standard [<a href="#ref-3">3</a>, <a href="#ref-4">4</a>]. Tissue samples are streaked onto blood agar or [MacConkey agar](/knowledge/diagnostics/microbiology/macconkey-agar-selective-differential-enteric) and incubated at 37 degrees C under 5% CO2 for 18 to 24 hours [<a href="#ref-8">8</a>]. *P. multocida* appears as small, gray, mucoid colonies with a characteristic musty odor. Gram staining reveals Gram-negative coccobacilli with bipolar staining after methylene blue staining [<a href="#ref-3">3</a>, <a href="#ref-7">7</a>].

Biochemical profiling is used for confirmation. *P. multocida* is positive for oxidase, catalase, and indole, and ferments glucose, sucrose, and mannitol without gas production [<a href="#ref-10">10</a>]. Capsular serotyping using the passive hemagglutination test distinguishes serogroups [<a href="#ref-9">9</a>, <a href="#ref-10">10</a>].

### Molecular Diagnostics

Molecular methods offer rapid and sensitive detection of *P. multocida* [<a href="#ref-21">21</a>]. Polymerase chain reaction (PCR) assays targeting the *kmt1* gene (species-specific) and capsular typing genes are widely used [<a href="#ref-3">3</a>, <a href="#ref-8">8</a>, <a href="#ref-21">21</a>]. [Loop-mediated isothermal amplification](/knowledge/diagnostics/molecular/lamp-assay-rapid-detection-african-swine-fever-virus-oral-fluids) (LAMP) assays provide a field-deployable alternative to PCR, with comparable sensitivity and specificity [<a href="#ref-21">21</a>]. Comparative evaluation of PCR and LAMP for detecting *P. multocida* in poultry shows both methods are reliable, but LAMP does not require thermocycling equipment [<a href="#ref-21">21</a>].

Genomic characterization is increasingly employed for outbreak investigations and antimicrobial resistance profiling [<a href="#ref-9">9</a>, <a href="#ref-13">13</a>, <a href="#ref-22">22</a>]. Whole-genome sequencing (WGS) enables the assignment of sequence types (e.g., ST20) and detection of resistance genes [<a href="#ref-22">22</a>, <a href="#ref-23">23</a>]. [Pulsed-field gel electrophoresis](/knowledge/diagnostics/molecular/pulsed-field-gel-electrophoresis) (PFGE) remains a useful tool for genotypic evaluation and epidemiological linkage of isolates [<a href="#ref-24">24</a>].

### Serological Assays

Enzyme-linked immunosorbent assays (ELISAs) are used to detect antibodies against *P. multocida* in chicken sera [<a href="#ref-25">25</a>]. In-house indirect ELISAs have been developed and optimized for serosurveillance in unvaccinated and vaccinated flocks [<a href="#ref-25">25</a>]. These assays are valuable for monitoring vaccine-induced immune responses [<a href="#ref-25">25</a>, <a href="#ref-26">26</a>].

### Differential Diagnosis

[Fowl cholera](/knowledge/bacteria/avian-bacteria/fowl-cholera-poultry-clinical-diagnostics-control) must be differentiated from other bacterial septicemic diseases affecting poultry. Key differentials include [avian influenza](/knowledge/bacteria/avian-bacteria/avian-influenza-cdc-global-surveillance) (highly pathogenic), Newcastle disease, *Salmonella* Gallinarum infection (fowl typhoid), *Gallibacterium anatis* infection, and *[Mycoplasma gallisepticum](/knowledge/bacteria/avian-bacteria/mycoplasma-gallisepticum-poultry-chronic-respiratory-disease-control)* infection [<a href="#ref-5">5</a>, <a href="#ref-18">18</a>, <a href="#ref-27">27</a>]. The 100% mortality pattern in acute outbreaks can clinically mimic exotic viral infections, necessitating rapid laboratory confirmation [<a href="#ref-2">2</a>].

The following decision tree summarizes the diagnostic workflow for [fowl cholera](/knowledge/bacteria/avian-bacteria/fowl-cholera-poultry-etiology-clinical-signs-control).

```mermaid
flowchart TD
 A["Clinical signs of acute septicemia or chronic localized lesions"] --> B["Post-mortem examination"]
 B --> C{"Sample collection"}
 C --> D["Heart blood, liver, spleen, bone marrow"]
 C --> E["Swabs from wattles, sinuses, joints"]
 D --> F["Bacteriological culture on blood agar"]
 E --> F
 F --> G{"Colony morphology: gray, mucoid, musty odor"}
 G --> H["Gram stain: Gram-negative coccobacilli, bipolar staining"]
 H --> I["Biochemical confirmation: oxidase+, catalase+, indole+"]
 I --> J{"Advanced identification"}
 J --> K["Species-specific PCR (kmt1)"]
 J --> L["Capsular serotyping PCR or passive hemagglutination"]
 J --> M["LAMP assay for field detection"]
 J --> N["Whole-genome sequencing for typing and AMR genes"]
 K --> O["Definitive diagnosis: Fowl cholera"]
 L --> O
 M --> O
 N --> P["Epidemiological assignment: ST type, resistance profile"]
```

## Antimicrobial Resistance

Antimicrobial resistance in avian *P. multocida* is a growing global concern [<a href="#ref-3">3</a>, <a href="#ref-8">8</a>, <a href="#ref-22">22</a>]. Comprehensive genomic characterization of isolates has revealed the acquisition of resistance genes via mobile genetic elements [<a href="#ref-6">6</a>, <a href="#ref-22">22</a>]. Multidrug-resistant (MDR) strains have been reported from poultry and rabbits, showing resistance to tetracyclines, sulfonamides, beta-lactams, and aminoglycosides [<a href="#ref-6">6</a>, <a href="#ref-8">8</a>].

An antibiogram profiling study in Ethiopia found that most *P. multocida* isolates from breeder chickens were susceptible to fluoroquinolones and ceftiofur, but resistant to penicillin and tetracycline [<a href="#ref-3">3</a>]. Another study highlighted that the stringency of the antimicrobial policy and careful selection of antimicrobials are critical to mitigate resistance development [<a href="#ref-4">4</a>, <a href="#ref-22">22</a>]. The presence of multiple resistance genes in the same isolate, such as tetH, blaROB-1, and sul2, has been documented in MDR strains [<a href="#ref-6">6</a>, <a href="#ref-8">8</a>].

## Treatment

Antimicrobial therapy should be based on in vitro susceptibility testing [<a href="#ref-3">3</a>, <a href="#ref-4">4</a>]. Enrofloxacin, norfloxacin, and ceftiofur have demonstrated good in vitro activity against *P. multocida* isolates from poultry [<a href="#ref-3">3</a>]. Tetracyclines (e.g., oxytetracycline, doxycycline) and sulfonamide-trimethoprim combinations are also used, though resistance is increasingly reported [<a href="#ref-6">6</a>, <a href="#ref-8">8</a>].

Administration of antimicrobials via drinking water is the most practical route for flock treatment during an outbreak [<a href="#ref-4">4</a>]. Early treatment during the acute phase can reduce mortality [<a href="#ref-3">3</a>]. However, treatment may not eliminate the carrier state, and chronic infections often respond poorly [<a href="#ref-4">4</a>]. The selection of antimicrobials must consider withdrawal periods to prevent drug residues in poultry meat and eggs [<a href="#ref-5">5</a>].

Research into alternative therapeutic approaches includes the use of plant extracts. Wild Egyptian artichoke extract has shown in vitro antibacterial activity against *P. multocida*, suggesting potential for development as a natural control agent [<a href="#ref-28">28</a>].

## Control and Prevention

### Biosecurity

Strict biosecurity is the cornerstone of [fowl cholera](/knowledge/bacteria/avian-bacteria/fowl-cholera-poultry-etiology-clinical-signs-zoonotic-implications) control [<a href="#ref-1">1</a>, <a href="#ref-5">5</a>]. All-in/all-out production systems, rodent and wild bird control, disinfection of facilities and equipment, and restricted visitor access are essential measures [<a href="#ref-1">1</a>, <a href="#ref-20">20</a>]. Monitoring land cover and waterfowl activity near farms may help identify farms at elevated risk for outbreaks [<a href="#ref-20">20</a>].

### Vaccination

Vaccination is a critical component of [fowl cholera](/knowledge/bacteria/avian-bacteria/fowl-cholera-poultry-etiology-epidemiology-control) control programs [<a href="#ref-10">10</a>, <a href="#ref-26">26</a>, <a href="#ref-29">29</a>, <a href="#ref-30">30</a>]. Both inactivated (bacterin) and live attenuated vaccines are available [<a href="#ref-29">29</a>, <a href="#ref-31">31</a>, <a href="#ref-32">32</a>].

Inactivated vaccines (bacterins) contain whole killed *P. multocida* cells and are often adjuvanted to enhance immunogenicity [<a href="#ref-30">30</a>, <a href="#ref-31">31</a>]. Water-in-oil and aluminum hydroxide-adjuvanted bacterins induce strong humoral immune responses and protection [<a href="#ref-26">26</a>, <a href="#ref-30">30</a>, <a href="#ref-32">32</a>]. Gel 01 hydrogel-adjuvanted inactivated vaccines have been shown to provide immunoprotection in chickens [<a href="#ref-30">30</a>]. Gamma-irradiated inactivated vaccines formulated with various adjuvants induce antibody production and cytokine expression in chickens [<a href="#ref-26">26</a>, <a href="#ref-32">32</a>].

Live attenuated vaccines are derived from serial passage of virulent strains and can provide broader immunity, including mucosal and cell-mediated responses [<a href="#ref-29">29</a>]. The strain PMZ8, attenuated through serial passage in ducks, demonstrates reduced virulence while retaining immunogenicity [<a href="#ref-29">29</a>]. Flagellin-based subunit vaccines targeting lipoprotein E (PlpE) have also been investigated [<a href="#ref-33">33</a>, <a href="#ref-34">34</a>]. The inclusion of the native signal sequence of PlpE improves its immunogenicity when used as a recombinant subunit vaccine [<a href="#ref-34">34</a>]. A trivalent outer membrane vesicle (OMV) vaccine approach, while primarily developed against Salmonella, demonstrates the expanding field of poultry vaccinology [<a href="#ref-27">27</a>]. Vaccine efficacy is influenced by the LPS outer core composition and the presence of specific capsular antigens [<a href="#ref-10">10</a>, <a href="#ref-12">12</a>].

The following table summarizes key [fowl cholera vaccine](/knowledge/bacteria/avian-bacteria/fowl-cholera-vaccine) types and their characteristics.

| Vaccine Type | Platform | Advantages | Limitations | Sources |
|-------|-----|------|-------|-----|
| Inactivated bacterin | Whole killed cells + adjuvant | Safe; induces humoral immunity; oil-adjuvant formulations provide long protection | Requires injection; may not protect against heterologous serotypes; less effective cell-mediated response | [<a href="#ref-30">30</a>, <a href="#ref-31">31</a>, <a href="#ref-32">32</a>] |
| Live attenuated | Passaged strain (e.g., PMZ8) | Induces mucosal and cell-mediated immunity; potentially broader protection | Residual virulence risk; requires careful cold chain; not recommended for immunocompromised flocks | [<a href="#ref-29">29</a>] |
| Subunit (PlpE) | Recombinant lipoprotein E + flagellin adjuvant | Defined antigen; no risk of reversion; excellent safety profile | Requires multiple doses for optimal protection; cost per dose may be higher | [<a href="#ref-33">33</a>, <a href="#ref-34">34</a>] |
| Gamma-irradiated | Whole cell inactivated by gamma rays | Preserves surface epitopes better than formalin inactivation; strong immune responses | Requires specialized irradiation facilities; regulatory approval may be complex | [<a href="#ref-26">26</a>, <a href="#ref-32">32</a>] |

### Eradication

On farms with recurrent [fowl cholera](/knowledge/bacteria/avian-bacteria/fowl-cholera-poultry-game-birds-pasteurella-multocida-pathogenesis-management) outbreaks, depopulation, thorough cleaning and disinfection, followed by a rest period, may be necessary to eliminate the carrier state [<a href="#ref-1">1</a>, <a href="#ref-5">5</a>]. Replacement stock should be sourced from *P. multocida*-free suppliers [<a href="#ref-5">5</a>].

## Conclusion

[Fowl cholera](/knowledge/bacteria/avian-bacteria/fowl-cholera-poultry-pasteurella-multocida-outbreak-management) remains a major threat to poultry production systems worldwide [<a href="#ref-1">1</a>, <a href="#ref-5">5</a>]. Successful management requires integration of accurate and rapid molecular diagnostics, targeted antimicrobial therapy guided by susceptibility testing, rigorous biosecurity, and effective vaccination programs [<a href="#ref-3">3</a>, <a href="#ref-4">4</a>, <a href="#ref-29">29</a>]. The emergence of multidrug-resistant *P. multocida* strains underscores the urgency of developing alternative control strategies, including novel vaccine platforms and plant-derived antimicrobials [<a href="#ref-6">6</a>, <a href="#ref-8">8</a>, <a href="#ref-22">22</a>, <a href="#ref-28">28</a>].

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<a id="ref-2"></a>[<a href="#ref-2">2</a>] Miller I, Jerry C, Nguyen V, et al. 100% Mortality in Commercial Slow-Growing Broiler Chickens with Acute [Fowl Cholera](/knowledge/bacteria/avian-bacteria/fowl-cholera-poultry-pasteurella-multocida). Avian Dis. 2025. URL: https://pubmed.ncbi.nlm.nih.gov/40643942/

<a id="ref-3"></a>[<a href="#ref-3">3</a>] Geda AM, Wendimu A, Lulie S, et al. Molecular Detection and Antibiogram Profiling of Pasteurella multocida Isolated From Breeder Chickens Suspected of [Fowl Cholera](/knowledge/bacteria/avian-bacteria/fowl-cholera) in Gondar City, Ethiopia. Int J Microbiol. 2025. URL: https://pubmed.ncbi.nlm.nih.gov/40297765/

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<a id="ref-10"></a>[<a href="#ref-10">10</a>] 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/

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<a id="ref-12"></a>[<a href="#ref-12">12</a>] Zhao X, Yang F, Shen H, et al. Immunogenicity and protection of a Pasteurella multocida strain with a truncated lipopolysaccharide outer core in ducks. Vet Res. 2022. URL: https://pubmed.ncbi.nlm.nih.gov/35236414/

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