# [Avian Cholera](/knowledge/bacteria/avian-bacteria/avian-cholera-fowl-cholera-poultry-wild-birds) ([Fowl Cholera](/knowledge/bacteria/avian-bacteria/avian-cholera-fowl-cholera)) in Poultry: Etiology, Clinical Signs, and Control

## Key Takeaways

- Avian cholera is caused by the Gram-negative bacterium *Pasteurella multocida*, with serogroup A being most common in poultry, and manifests in peracute, acute, and chronic forms, leading to high mortality in susceptible flocks.
- Transmission occurs through direct contact, inhalation of aerosols, or ingestion of contaminated feed/water, with outbreaks often triggered by stress factors like overcrowding or concurrent infections.
- Diagnosis relies on isolation and identification of *P. multocida* via culture and Gram staining, supplemented by rapid molecular methods like PCR targeting the *kmt1* gene and serological tests (ELISA) for antibody detection.
- Antimicrobial therapy is crucial for acute cases, but multidrug resistance is a growing concern, necessitating susceptibility testing; alternative treatments like phage therapy and probiotics show promise.
- Control strategies integrate stringent biosecurity measures, improved management practices, and vaccination using inactivated or live attenuated vaccines, with ongoing research into subunit and OMV vaccines for enhanced protection.
- Zoonotic transmission to humans is rare and typically results in localized wound infections, posing a low public health risk, primarily to immunocompromised individuals and poultry workers.

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## Introduction

[Avian cholera](/knowledge/bacteria/avian-bacteria/avian-cholera-pasteurella-multocida-poultry), also known as [fowl cholera](/knowledge/bacteria/avian-bacteria/fowl-cholera-avian-cholera-in-poultry), is a highly contagious bacterial disease of domestic and wild birds caused by *Pasteurella multocida* [<a href="#ref-1">1</a>, <a href="#ref-2">2</a>, <a href="#ref-3">3</a>]. The disease manifests in peracute, acute, and chronic forms and is responsible for significant economic losses in poultry production worldwide [<a href="#ref-3">3</a>, <a href="#ref-4">4</a>, <a href="#ref-5">5</a>]. Mortality can reach 100% in susceptible flocks, particularly in slow-growing broiler chickens and turkeys [<a href="#ref-3">3</a>, <a href="#ref-6">6</a>]. 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](/knowledge/bacteria/avian-bacteria/fowl-cholera-drug-choice), with emphasis on recent molecular and immunological advances.

## Etiology: [Fowl Cholera Is Caused by Which Bacteria](/knowledge/bacteria/avian-bacteria/fowl-cholera-etiology-clinical-manifestations-control-poultry)

[Fowl cholera](/knowledge/bacteria/avian-bacteria/fowl-cholera-avian-cholera-poultry) is caused by the Gram-negative, non-motile, facultative anaerobic coccobacillus *Pasteurella multocida* [<a href="#ref-1">1</a>, <a href="#ref-7">7</a>, <a href="#ref-8">8</a>]. The bacterium is classified into five capsular serogroups (A, B, D, E, F) and 16 lipopolysaccharide (LPS) genotypes based on the Heddleston scheme [<a href="#ref-8">8</a>, <a href="#ref-9">9</a>]. 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 [<a href="#ref-5">5</a>, <a href="#ref-10">10</a>, <a href="#ref-11">11</a>]. 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*) [<a href="#ref-8">8</a>, <a href="#ref-12">12</a>, <a href="#ref-13">13</a>, <a href="#ref-14">14</a>].

The bacterium produces a polysaccharide capsule that inhibits phagocytosis and a lipopolysaccharide that triggers a strong inflammatory response [<a href="#ref-1">1</a>, <a href="#ref-15">15</a>]. 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 [<a href="#ref-12">12</a>, <a href="#ref-13">13</a>]. The LPS outer core structure is critical for full virulence; truncation of the outer core attenuates the bacterium in ducks [<a href="#ref-14">14</a>, <a href="#ref-16">16</a>]. Phase variation in glycosyltransferase genes can alter LPS structure and contribute to immune evasion during outbreaks [<a href="#ref-9">9</a>].

## Epidemiology

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

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

### [Avian Cholera](/knowledge/bacteria/avian-bacteria/avian-cholera-pasteurella-multocida) 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 [<a href="#ref-7">7</a>, <a href="#ref-18">18</a>]. Human infections typically manifest as localized wound infections, cellulitis, or, rarely, respiratory disease [<a href="#ref-7">7</a>]. However, [avian cholera](/knowledge/bacteria/avian-bacteria/avian-cholera-fowl-cholera-poultry-wild-birds) is not considered a major public health concern, and human cases are sporadic [<a href="#ref-18">18</a>]. The risk is elevated for immunocompromised individuals and poultry workers [<a href="#ref-7">7</a>].

## Clinical Signs

The clinical presentation of [fowl cholera](/knowledge/bacteria/avian-bacteria/fowl-cholera-avian-pasteurellosis-comprehensive-reference) varies with the virulence of the strain, host species, and route of infection [<a href="#ref-3">3</a>, <a href="#ref-19">19</a>]. Three main forms are recognized:

- **Peracute form**: Sudden death with no premonitory signs. Mortality can reach 100% within 24-48 hours [<a href="#ref-3">3</a>, <a href="#ref-19">19</a>]. This form is common in highly susceptible flocks, such as slow-growing broilers and turkeys [<a href="#ref-3">3</a>, <a href="#ref-6">6</a>].
- **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 [<a href="#ref-3">3</a>, <a href="#ref-15">15</a>, <a href="#ref-20">20</a>]. Swelling of the wattles and sinuses is characteristic [<a href="#ref-3">3</a>]. Mortality peaks within 3-5 days [<a href="#ref-4">4</a>].
- **Chronic form**: Localized infections including swollen joints (arthritis), sternal bursitis, conjunctivitis, and torticollis due to otitis media [<a href="#ref-3">3</a>, <a href="#ref-20">20</a>]. Chronic cases are more common in flocks with partial immunity or following subacute outbreaks [<a href="#ref-20">20</a>].

In ducks, liver injury mediated by inflammatory, apoptotic, and autophagic pathways has been described [<a href="#ref-15">15</a>]. In broilers, *P. multocida* induces liver pyroptosis through the MAPK-NLRP3-GSDMD signaling pathway [<a href="#ref-1">1</a>].

## Pathology

Gross lesions in acute [fowl cholera](/knowledge/bacteria/avian-bacteria/fowl-cholera-avian-pasteurellosis-comprehensive-veterinary-reference) include petechial hemorrhages on the heart, epicardium, and serosal surfaces; multifocal hepatic necrosis (small, pale foci); splenomegaly; and pulmonary congestion [<a href="#ref-1">1</a>, <a href="#ref-3">3</a>, <a href="#ref-15">15</a>]. The liver may appear friable and mottled [<a href="#ref-1">1</a>]. In chronic cases, caseous exudate is found in the wattles, joints, and sinuses [<a href="#ref-3">3</a>].

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

## Diagnostics

Definitive diagnosis of [fowl cholera](/knowledge/bacteria/avian-bacteria/fowl-cholera-avian-pasteurellosis-poultry) requires isolation and identification of *P. multocida* from affected tissues (liver, spleen, bone marrow, or exudate) [<a href="#ref-3">3</a>, <a href="#ref-19">19</a>, <a href="#ref-21">21</a>]. The bacterium grows on blood agar or [MacConkey agar](/knowledge/diagnostics/microbiology/macconkey-agar-selective-differential-enteric) (weak growth) as small, gray, mucoid colonies [<a href="#ref-19">19</a>]. Gram staining reveals Gram-negative coccobacilli with bipolar staining (safety pin appearance) [<a href="#ref-19">19</a>].

Molecular methods offer rapid and specific detection. Conventional PCR targeting the *kmt1* gene is widely used [<a href="#ref-7">7</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 with sensitivity comparable to PCR [<a href="#ref-21">21</a>]. Real-time PCR and whole-genome sequencing are employed for epidemiological typing and antimicrobial resistance gene profiling [<a href="#ref-2">2</a>, <a href="#ref-8">8</a>, <a href="#ref-18">18</a>].

Serological diagnosis using indirect ELISA kits has been developed for detecting antibodies against *P. multocida* in chickens [<a href="#ref-22">22</a>]. These assays are useful for monitoring vaccine responses and herd immunity [<a href="#ref-22">22</a>, <a href="#ref-23">23</a>, <a href="#ref-24">24</a>].

The following diagnostic workflow summarizes the recommended approach:

```mermaid
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](/knowledge/bacteria/avian-bacteria/fowl-cholera-causal-agent). Historically, tetracyclines, sulfonamides, and penicillin derivatives have been used [<a href="#ref-2">2</a>, <a href="#ref-7">7</a>]. However, multidrug resistance is increasingly reported, particularly against tetracycline, sulfonamides, and aminoglycosides [<a href="#ref-2">2</a>, <a href="#ref-7">7</a>, <a href="#ref-10">10</a>]. Resistance genes such as *tet*(H), *bla*ROB-1, and *strA-strB* have been identified in avian isolates [<a href="#ref-2">2</a>, <a href="#ref-7">7</a>].

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

## Control and Prevention

Control of [fowl cholera](/knowledge/bacteria/avian-bacteria/fowl-cholera-causative-agent) relies on biosecurity, management practices, and vaccination [<a href="#ref-4">4</a>, <a href="#ref-5">5</a>, <a href="#ref-28">28</a>]. Biosecurity measures include all-in-all-out production, cleaning and disinfection of facilities, control of rodents and wild birds, and quarantine of new stock [<a href="#ref-4">4</a>, <a href="#ref-17">17</a>].

### Vaccination

Both inactivated (bacterin) and live attenuated vaccines are available [<a href="#ref-5">5</a>, <a href="#ref-28">28</a>, <a href="#ref-29">29</a>, <a href="#ref-30">30</a>]. Inactivated vaccines are commonly used in commercial poultry and are often adjuvanted with aluminum hydroxide or oil emulsions [<a href="#ref-23">23</a>, <a href="#ref-28">28</a>, <a href="#ref-30">30</a>]. 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 [<a href="#ref-23">23</a>, <a href="#ref-31">31</a>, <a href="#ref-32">32</a>, <a href="#ref-33">33</a>, <a href="#ref-34">34</a>]. Multi-epitope proteins incorporating PlpE epitopes enhance immunogenicity [<a href="#ref-23">23</a>].
- **Outer membrane vesicle (OMV) vaccines**: *E. coli*-derived OMVs displaying PlpE protein induce strong antibody responses [<a href="#ref-31">31</a>].
- **Gamma-irradiated vaccines**: Irradiated whole-cell vaccines formulated with various adjuvants elicit both humoral and cell-mediated immunity [<a href="#ref-24">24</a>, <a href="#ref-35">35</a>].
- **Hydrogel-based vaccines**: Gel 01 hydrogel inactivated vaccine provides sustained antigen release and improved protection [<a href="#ref-28">28</a>].
- **Live attenuated vaccines**: Serial passage-derived strains (e.g., PMZ8 in ducks) show reduced virulence and good immunogenicity [<a href="#ref-29">29</a>].

Vaccination strategies should be tailored to the prevalent serotypes and local epidemiological conditions [<a href="#ref-5">5</a>, <a href="#ref-10">10</a>]. In Bangladesh, for example, type B:2 is common, and vaccines should include this serotype [<a href="#ref-10">10</a>].

### [Fowl Cholera](/knowledge/bacteria/avian-bacteria/fowl-cholera-etiology-clinical-manifestations-control-poultry) Meaning in Bengali

In Bengali, [fowl cholera](/knowledge/bacteria/avian-bacteria/fowl-cholera-etiology-clinical-signs-post-mortem-lesions-poultry) is commonly referred to as "মুরগির কলেরা" (murgir cholera), reflecting the disease's clinical similarity to human cholera (diarrhea and rapid death) [<a href="#ref-10">10</a>]. The term is used in veterinary extension materials and outbreak reports in Bangladesh [<a href="#ref-10">10</a>].

## Conclusion

[Avian cholera](/knowledge/bacteria/avian-bacteria/avian-cholera-pasteurella-multocida-poultry) 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 [<a href="#ref-1">1</a>, <a href="#ref-2">2</a>, <a href="#ref-15">15</a>, <a href="#ref-18">18</a>]. Integrated control programs combining biosecurity, antimicrobial stewardship, and effective vaccination are essential to reduce the impact of this disease [<a href="#ref-4">4</a>, <a href="#ref-5">5</a>, <a href="#ref-30">30</a>]. Continued surveillance of antimicrobial resistance and genomic diversity will inform future control strategies [<a href="#ref-2">2</a>, <a href="#ref-7">7</a>, <a href="#ref-10">10</a>].

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