# [Bacterial Poultry Diseases](/knowledge/bacteria/avian-bacteria/bacterial-poultry-diseases-overview): An Overview of Common Pathogens and Clinical Signs

## Key Takeaways

- Avian pathogenic *Escherichia coli* (APEC) causes colibacillosis, manifesting as septicemia or polyserositis (airsacculitis, pericarditis, perihepatitis), with common serogroups O1, O2, and O78 exhibiting high multidrug resistance, including to extended-spectrum cephalosporins and fluoroquinolones.
- *Salmonella* Gallinarum and *S. Pullorum* cause systemic fowl typhoid and pullorum disease, respectively, characterized by high mortality in young birds and potential carrier states in adults, while non-typhoidal serovars like *S. Enteritidis* contaminate carcasses and eggs.
- Thermophilic *Campylobacter* species (*C. jejuni*, *C. coli*) are primary reservoirs for human gastroenteritis, colonizing poultry ceca asymptomatically but spreading rapidly via the fecal-oral route, leading to carcass contamination.
- *Pasteurella multocida* causes highly contagious fowl cholera, presenting as peracute death or acute signs including cyanosis and mucoid discharge, with characteristic postmortem findings of petechial hemorrhages and hepatic necrosis.
- *Clostridium perfringens* is a major cause of necrotic enteritis, often secondary to coccidiosis or dietary factors, leading to intestinal necrosis and sudden mortality, while *Avibacterium paragallinarum* causes infectious coryza with characteristic nasal discharge and facial edema.
- Diagnostic approaches integrate clinical history, gross pathology, histopathology, and laboratory identification via culture (e.g., MacConkey agar for *E. coli*, selective media for *Campylobacter*), supplemented by rapid molecular methods like PCR and whole genome sequencing for resistance gene characterization.

---

## Introduction

Bacterial infections remain a primary cause of morbidity, mortality, and economic loss in commercial poultry operations worldwide [<a href="#ref-1">1</a>, <a href="#ref-2">2</a>]. The dense stocking conditions, high metabolic demands of modern broiler and layer breeds, and suboptimal biosecurity create environments conducive to the rapid spread of bacterial pathogens [<a href="#ref-3">3</a>]. These infections manifest as diverse clinical syndromes, including respiratory distress, enteritis, septicemia, lameness, and decreased egg production [<a href="#ref-1">1</a>, <a href="#ref-2">2</a>]. Additionally, many poultry bacterial pathogens represent significant zoonotic hazards, with ongoing implications for [food safety](/knowledge/bacteria/livestock-bacteria/cooking-chicken-bacteria-prevention) and public health [<a href="#ref-4">4</a>, <a href="#ref-5">5</a>, <a href="#ref-6">6</a>, <a href="#ref-7">7</a>]. This article provides a systematic overview of the most prevalent [bacterial pathogens in chickens](/knowledge/bacteria/avian-bacteria/bacterial-pathogens-chickens-salmonella-e-coli), turkeys, ducks, and other poultry, detailing their etiologic characteristics, pathogenesis, clinical presentations, and diagnostic considerations.

## Avian Pathogenic *Escherichia coli* (APEC) and Colibacillosis

*Escherichia coli* is a Gram-negative, facultatively anaerobic bacillus belonging to the Enterobacteriaceae family [<a href="#ref-3">3</a>, <a href="#ref-4">4</a>]. While many *E. coli* strains are commensal inhabitants of the avian intestinal tract, specific pathotypes termed avian pathogenic *E. coli* (APEC) possess an array of virulence factors that enable extraintestinal infection [<a href="#ref-4">4</a>]. APEC typically harbor genes encoding fimbriae (e.g., F1, P, and S fimbriae), aerobactin iron-sequestration systems, hemolysins, and the Iss protein (increased serum survival), which collectively facilitate adherence to respiratory epithelium, invasion of the bloodstream, and evasion of host immune defenses [<a href="#ref-3">3</a>, <a href="#ref-4">4</a>]. Colibacillosis, the disease syndrome caused by APEC, can present as an acute septicemia with rapid mortality, or as a subacute to chronic condition with polyserositis (airsacculitis, pericarditis, perihepatitis) [<a href="#ref-3">3</a>]. The classic lesions are fibrinous exudates on the liver capsule and pericardium, often referred to as "coligranuloma" or Hjarre's disease when localized to the liver [<a href="#ref-3">3</a>].

Clinically, affected birds exhibit depression, ruffled feathers, anorexia, dyspnea, and a reduction in feed and water intake [<a href="#ref-3">3</a>]. In broilers, colibacillosis is a major contributor to first-week mortality, often linked to poor hatchery hygiene and vertical transmission from infected breeder flocks [<a href="#ref-3">3</a>]. Egg peritonitis and salpingitis are common in laying hens, leading to a drop in egg production and increased mortality from egg yolk peritonitis [<a href="#ref-3">3</a>]. A systematic review and meta-analysis of APEC serogroups identified O1, O2, and O78 as the most prevalent, and demonstrated a high prevalence of multidrug resistance, including to extended-spectrum cephalosporins and fluoroquinolones [<a href="#ref-4">4</a>]. Comparative plasmid analyses have shown that ESBL (extended-spectrum beta-lactamase) genes such as *bla*TEM-52, *bla*CTX-M-2, and *bla*CTX-M-15 are carried on conjugative plasmids of incompatibility groups I1 and HI2, which can transfer between *E. coli*, *Salmonella* enterica, and other Enterobacteriaceae from poultry, pigs, and humans, indicating a shared resistance gene pool [<a href="#ref-8">8</a>].

## *Salmonella* enterica in Poultry

*Salmonella* enterica subsp. *enterica* includes numerous serovars that cause disease in poultry and represent a major zoonotic threat [<a href="#ref-6">6</a>]. In chickens and turkeys, *Salmonella* Gallinarum and *Salmonella* Pullorum are host-adapted serovars that produce systemic disease: fowl typhoid and pullorum disease, respectively [<a href="#ref-6">6</a>]. Pullorum disease predominantly affects young chicks, causing acute septicemia with white fecal diarrhea (white diarrhea), anorexia, and high mortality [<a href="#ref-6">6</a>]. Older birds may survive but become asymptomatic carriers with ovarian localization, enabling transovarian transmission [<a href="#ref-6">6</a>]. Fowl typhoid, caused by *S.* Gallinarum, affects birds of all ages, with clinical signs including depression, drooping wings, greenish-yellow diarrhea, and a marked drop in egg production [<a href="#ref-6">6</a>]. Postmortem lesions often reveal an enlarged, friable liver with a bronze or greenish discoloration, splenomegaly, and hemorrhagic enteritis [<a href="#ref-6">6</a>].

Non-typhoidal serovars such as *S.* Enteritidis and *S.* Typhimurium are less pathogenic for adult poultry but can cause significant clinical disease in young birds, including enteritis and septicemia [<a href="#ref-6">6</a>]. More importantly, these serovars colonize the gastrointestinal tract without causing overt illness, leading to contamination of carcasses and eggs at slaughter and processing [<a href="#ref-5">5</a>, <a href="#ref-6">6</a>]. The prevalence of *Salmonella* in duck farms, for example, ranges from 0.5% to 20%, with *S.* Typhimurium being the most frequently isolated serovar [<a href="#ref-6">6</a>]. Antimicrobial resistance is extensive, with high rates of resistance to amoxicillin, ampicillin, tetracycline, and streptomycin [<a href="#ref-6">6</a>]. Control strategies include biosecurity, vaccination, bacteriophage therapy, and the use of probiotics, prebiotics, and organic acids as alternatives to antimicrobial growth promoters [<a href="#ref-3">3</a>, <a href="#ref-6">6</a>].

## *Campylobacter* Species (Thermophilic Campylobacters)

*Campylobacter jejuni* and *Campylobacter coli* are Gram-negative, microaerophilic, spiral-shaped bacteria that are the leading bacterial cause of human gastroenteritis worldwide, with poultry and poultry products being the primary reservoir and source of infection [<a href="#ref-5">5</a>, <a href="#ref-7">7</a>, <a href="#ref-9">9</a>]. In poultry, thermophilic *Campylobacter* species are commensal inhabitants of the ceca and colon, typically causing no clinical signs in birds under commercial conditions [<a href="#ref-5">5</a>, <a href="#ref-9">9</a>]. However, in some experimental models or under stress conditions, *C. jejuni* can induce mild enteritis, characterized by watery diarrhea, increased fecal moisture, and reduced weight gain [<a href="#ref-5">5</a>]. The organism is highly motile via polar flagella and possesses multiple adhesins (e.g., CadF, FlpA) and capsular polysaccharides that facilitate colonization of the intestinal mucus layer [<a href="#ref-9">9</a>].

Transmission within a flock is rapid: once a single bird becomes colonized (often from environmental sources such as contaminated water or litter), the organism spreads horizontally through the fecal-oral route, and within days a majority of birds may be colonized [<a href="#ref-5">5</a>, <a href="#ref-9">9</a>]. At slaughter, fecal contamination of carcasses leads to widespread dissemination of *Campylobacter* into the food chain [<a href="#ref-5">5</a>]. Passive immunization using hyperimmune egg yolk (IgY) derived from hens immunized with *C. jejuni* whole-cell lysates or hydrophobic protein fractions significantly reduced cecal colonization in seeder birds and dramatically decreased transmission to naive pennates in experimental settings [<a href="#ref-9">9</a>]. The immunodominant antigens identified included AtpA, EF-Tu, GroEL, and CtpA, which represent conserved proteins with potential as subunit vaccine targets [<a href="#ref-9">9</a>].

## *Pasteurella multocida*: [Fowl Cholera](/knowledge/bacteria/avian-bacteria/avian-cholera-fowl-cholera-in-poultry)

[Fowl cholera](/knowledge/bacteria/avian-bacteria/avian-cholera-fowl-cholera) is a highly contagious disease of domestic and wild birds caused by *Pasteurella multocida*, a Gram-negative, bipolar-staining coccobacillus [<a href="#ref-1">1</a>]. Capsular serogroups A and D are most commonly associated with avian disease, with multiple somatic serotypes (e.g., 1, 3, 4) implicated [<a href="#ref-1">1</a>]. The organism produces a polysaccharide capsule and lipopolysaccharide that contribute to serum resistance and induction of a severe inflammatory response [<a href="#ref-1">1</a>]. In peracute cases, birds die suddenly without premonitory signs, often with good body condition and a full gastrointestinal tract [<a href="#ref-1">1</a>]. Acute [fowl cholera](/knowledge/bacteria/avian-bacteria/fowl-cholera-avian-cholera-in-poultry) presents with fever, depression, mucoid discharge from the beak and eyes, cyanosis of the comb and wattles, and diarrhea [<a href="#ref-1">1</a>]. Postmortem findings include petechial hemorrhages on the epicardium and serosal surfaces, multifocal hepatic necrosis (characteristic small, pale foci), and fibrinous pneumonia [<a href="#ref-1">1</a>]. Chronic infections manifest as localized swellings (joints, wattles, sinuses) and torticollis due to meningeal involvement [<a href="#ref-1">1</a>].

## *Clostridium perfringens*: [Necrotic Enteritis](/knowledge/bacteria/avian-bacteria/necrotic-enteritis-poultry) and Gangrenous Dermatitis

*Clostridium perfringens* is a Gram-positive, spore-forming, anaerobic rod [<a href="#ref-2">2</a>]. Type A and type C strains produce a range of toxins, with alpha-toxin (phospholipase C) and NetB ([necrotic enteritis](/knowledge/bacteria/avian-bacteria/poultry-necrotic-enteritis-pathogenesis-control) toxin B) being key virulence factors in the pathogenesis of [necrotic enteritis in broiler chickens](/knowledge/bacteria/avian-bacteria/necrotic-enteritis-broiler-clostridium-perfringens-virulence-microbiome-probiotics) [<a href="#ref-2">2</a>]. [Necrotic enteritis](/knowledge/bacteria/avian-bacteria/necrotic-enteritis-poultry) typically occurs secondary to predisposing factors such as coccidiosis (e.g., *[Eimeria maxima](/knowledge/parasites/avian-parasites/eimeria-maxima-midgut-coccidiosis-chickens-lesion-scoring)*), dietary changes (high levels of non-starch polysaccharides), or immunosuppression [<a href="#ref-2">2</a>]. The disease is characterized by sudden mortality, depression, and diarrhea, often with intestinal shedding of necrotic mucosal casts [<a href="#ref-2">2</a>]. At necropsy, the small intestine, particularly the jejunum and ileum, is distended, friable, and filled with a "Turkish towel" appearance of the mucosa, with a diphtheritic membrane overlying necrotic villi [<a href="#ref-2">2</a>]. Gaseous distension and a foul odor are common [<a href="#ref-2">2</a>]. Gangrenous dermatitis, caused by *C. perfringens* (often in combination with other clostridia), produces subcutaneous emphysema, edema, and necrosis of the skin over the breast, thighs, and wings [<a href="#ref-2">2</a>].

## *Avibacterium paragallinarum*: [Infectious Coryza](/knowledge/bacteria/avian-bacteria/avian-infectious-coryza)

*Avibacterium paragallinarum* (formerly *Haemophilus paragallinarum*) is a Gram-negative, pleomorphic rod that requires nicotinamide adenine dinucleotide (V factor) for growth [<a href="#ref-1">1</a>]. It is the etiologic agent of [infectious coryza](/knowledge/bacteria/avian-bacteria/infectious-coryza-chickens-quail), an acute respiratory disease of chickens, turkeys, and quail [<a href="#ref-1">1</a>]. The bacterium produces a polysaccharide capsule that confers serovar specificity (A, B, C) and is associated with virulence [<a href="#ref-1">1</a>]. Clinical signs include serous to mucoid nasal discharge, sneezing, facial edema (especially around the wattles), conjunctivitis, and dyspnea [<a href="#ref-1">1</a>]. In laying flocks, egg production drops significantly (10-40%), and morbidity can reach 100% [<a href="#ref-1">1</a>]. Mortality is low unless complicated by secondary infections (e.g., *E. coli*, *[Mycoplasma gallisepticum](/knowledge/bacteria/avian-bacteria/mycoplasma-gallisepticum-poultry-chronic-respiratory-disease-control)*) [<a href="#ref-1">1</a>]. Diagnosis is based on isolation of the organism on chocolate agar or selective media supplemented with V factor, or by PCR targeting the *HMTp210* gene [<a href="#ref-1">1</a>].

## Other Significant Bacterial Pathogens

### *[Mycoplasma gallisepticum](/knowledge/bacteria/avian-bacteria/mycoplasma-gallisepticum-poultry-chronic-respiratory-disease-control)* and *[Mycoplasma synoviae](/knowledge/bacteria/avian-bacteria/mycoplasma-synoviae-infectious-synovitis-chickens-turkeys-eggshell-apex-abnormalities)*

Mycoplasmas are cell wall-deficient bacteria belonging to the class Mollicutes [<a href="#ref-1">1</a>]. *[Mycoplasma gallisepticum](/knowledge/bacteria/avian-bacteria/mycoplasma-gallisepticum-poultry-chronic-respiratory-disease-control)* is the primary cause of chronic respiratory disease (CRD) in chickens and infectious sinusitis in turkeys [<a href="#ref-1">1</a>]. The organism adheres to ciliated respiratory epithelium via specialized attachment organelles, leading to ciliostasis, inflammation, and exudation [<a href="#ref-1">1</a>]. Clinical signs include rales, coughing, nasal discharge, and airsacculitis, often exacerbated by concurrent infections or environmental stressors [<a href="#ref-1">1</a>]. *[Mycoplasma synoviae](/knowledge/bacteria/avian-bacteria/mycoplasma-synoviae-infectious-synovitis-chickens-turkeys-eggshell-apex-abnormalities)* causes infectious synovitis (tenosynovitis) and respiratory disease in chickens and turkeys, characterized by lameness, joint swelling, and breast blisters [<a href="#ref-1">1</a>]. In layers, *M. synoviae* is associated with eggshell apex abnormalities [<a href="#ref-1">1</a>].

### *Gallibacterium anatis*

*Gallibacterium anatis* is a Gram-negative, facultatively anaerobic rod that is part of the normal flora of the avian upper respiratory and lower genital tracts but can act as an opportunistic pathogen [<a href="#ref-2">2</a>]. It is isolated frequently from laying hens with salpingitis and peritonitis, often in mixed infection with *E. coli* [<a href="#ref-2">2</a>]. The bacterium produces hemolysins (GtxA) and a capsular polysaccharide that contribute to virulence [<a href="#ref-2">2</a>]. Clinical signs are nonspecific: decreased egg production, increased mortality due to egg yolk peritonitis, and occasionally respiratory signs [<a href="#ref-2">2</a>].

### *Streptococcus zooepidemicus* and *Staphylococcus aureus*

*Streptococcus zooepidemicus* (Lancefield group C) is an emerging pathogen in poultry, causing septicemia, arthritis, and endocarditis, particularly in adult breeders and layers [<a href="#ref-2">2</a>]. Transmission is often through skin wounds or the respiratory route [<a href="#ref-2">2</a>]. *Staphylococcus aureus* is the primary cause of bumblefoot (pododermatitis), osteomyelitis, and arthritis in broilers [<a href="#ref-2">2</a>]. The organism invades through abrasions on the feet or legs, leading to abscess formation, lameness, and in severe cases, bacterial chondronecrosis with osteomyelitis (BCO) [<a href="#ref-2">2</a>].

## Diagnostic Approaches

Definitive diagnosis of [bacterial poultry diseases](/knowledge/bacteria/avian-bacteria/bacterial-poultry-diseases-overview) relies on a combination of clinical history, gross pathology, histopathology, and laboratory identification of the causative agent [<a href="#ref-1">1</a>, <a href="#ref-4">4</a>]. Culture and isolation remain the gold standard for most bacterial pathogens, with selective media and incubation conditions tailored to the suspected organism (e.g., [MacConkey agar](/knowledge/diagnostics/microbiology/macconkey-agar-selective-differential-enteric) for Enterobacteriaceae, blood agar for *Pasteurella* and *Streptococcus*, modified charcoal-cefoperazone-deoxycholate agar for *Campylobacter*) [<a href="#ref-1">1</a>, <a href="#ref-5">5</a>]. Biochemical profiling, serotyping, and antimicrobial susceptibility testing (disk diffusion or broth microdilution) are performed for epidemiological surveillance and therapeutic guidance [<a href="#ref-4">4</a>, <a href="#ref-6">6</a>].

Molecular diagnostic methods, particularly PCR and quantitative PCR (qPCR), offer rapid, sensitive, and specific detection of bacterial DNA from tissue samples, swabs, or environmental samples [<a href="#ref-1">1</a>, <a href="#ref-5">5</a>]. Multiplex PCR panels targeting multiple virulence genes or species-specific sequences (e.g., *iss* for APEC, *invA* for *Salmonella*, *hipO* for *C. jejuni*) are widely used in diagnostic laboratories [<a href="#ref-1">1</a>, <a href="#ref-5">5</a>]. Whole genome sequencing (WGS) has become increasingly important for characterizing strain relatedness, identifying virulence and antimicrobial resistance genes, and conducting source attribution during outbreaks [<a href="#ref-4">4</a>, <a href="#ref-8">8</a>].

The following table summarizes key bacterial pathogens, their primary clinical presentations, and typical transmission routes in poultry.

| Pathogen | Primary Disease(s) | Key Clinical Signs | Transmission |
|-----|----------|----------|-------|
| *Escherichia coli* (APEC) | Colibacillosis (airsacculitis, pericarditis, perihepatitis, salpingitis) | Depression, dyspnea, fibrinous exudates on viscera, egg peritonitis | Respiratory, fecal-oral, vertical via egg |
| *Salmonella* Gallinarum / Pullorum | Fowl typhoid / Pullorum disease | White diarrhea (chicks), greenish diarrhea, hepatomegaly, anemia, high mortality | Fecal-oral, transovarian |
| *Salmonella* Enteritidis / Typhimurium | Subclinical enteritis, septicemia in young birds | Usually asymptomatic in adults; diarrhea, mortality in chicks | Fecal-oral, horizontal |
| *Campylobacter jejuni* | Commensal colonization (occasional enteritis) | Usually asymptomatic; watery diarrhea under stress | Fecal-oral, water, litter |
| *Pasteurella multocida* | [Fowl cholera](/knowledge/bacteria/avian-bacteria/fowl-cholera-avian-cholera-poultry) | Sudden death, cyanosis, mucoid discharge, hepatic necrosis | Respiratory, direct contact |
| *Clostridium perfringens* | [Necrotic enteritis](/knowledge/bacteria/avian-bacteria/poultry-necrotic-enteritis-pathogenesis-control), gangrenous dermatitis | Depression, diarrhea, intestinal necrosis, sudden death | Fecal-oral, predisposed by coccidiosis |
| *Avibacterium paragallinarum* | [Infectious coryza](/knowledge/bacteria/avian-bacteria/infectious-coryza-poultry-diagnosis-symptoms) | Nasal discharge, facial edema, sneezing, drop in egg production | Respiratory, direct contact |
| *[Mycoplasma gallisepticum](/knowledge/bacteria/avian-bacteria/mycoplasma-gallisepticum-poultry-chronic-respiratory-disease-control)* | Chronic respiratory disease | Rales, coughing, airsacculitis, sinusitis | Respiratory, egg-borne (transovarian) |
| *Gallibacterium anatis* | Salpingitis, peritonitis | Drop in egg production, increased mortality | Ascending from cloaca |
| *Staphylococcus aureus* | Bumblefoot, osteomyelitis, arthritis | Lameness, footpad abscesses, swollen joints | Skin wounds, environmental |

The decision tree (Mermaid diagram) below outlines a simplified diagnostic workflow for a poultry flock presenting with increased mortality or respiratory signs.

```mermaid
flowchart TD
 A["Flock presenting with mortality or respiratory signs"] --> B{"Clinical history & necropsy"}
 B --> C["Respiratory signs: nasal discharge, sneezing, facial edema"]
 B --> D["Septicemia: sudden death, cyanosis, hemorrhages"]
 B --> E["Enteric signs: diarrhea, reduced growth"]
 B --> F["Lameness, joint swelling, footpad lesions"]

 C --> G["Suspect infectious coryza or CRD"]
 G --> H["PCR or culture for A. paragallinarum / Mycoplasma spp."]
 
 D --> I["Suspect fowl cholera or colibacillosis"]
 I --> J["Blood culture, liver swab on MacConkey/blood agar"]
 J --> K{"Gram-negative rods?"}
 K -->|"Pasteurella multocida"| L["Fowl cholera confirmed"]
 K -->|"Escherichia coli"| M["Colibacillosis confirmed"]

 E --> N["Suspect Salmonella or necrotic enteritis"]
 N --> O["Intestinal contents culture + selective enrichment"]
 O --> P["Salmonella isolated?"]
 P -->|"Yes"| Q["Salmonellosis"]
 P -->|"No"| R["Consider Clostridium perfringens toxins / histopathology"]

 F --> S["Suspect Staphylococcus aureus or Mycoplasma synoviae"]
 S --> T["Aspirate joint/bumblefoot for culture & PCR"]
 
 L --> U["Antimicrobial susceptibility testing & vaccine review"]
 M --> U
 Q --> U
 R --> U
 T --> U
```

## Conclusions

Bacterial diseases of poultry encompass a wide spectrum of pathogens, each with distinct virulence mechanisms, epidemiological features, and clinical manifestations. The emergence of antimicrobial resistance, especially in APEC, *Salmonella*, and *Campylobacter*, underscores the urgent need for integrated control strategies that include enhanced biosecurity, vaccination, alternative interventions (probiotics, prebiotics, organic acids, bacteriophages), and prudent antimicrobial use [<a href="#ref-3">3</a>, <a href="#ref-5">5</a>, <a href="#ref-6">6</a>, <a href="#ref-8">8</a>]. Molecular diagnostics and genomic surveillance are essential tools for early detection, monitoring of resistance trends, and informing evidence-based management decisions [<a href="#ref-4">4</a>, <a href="#ref-8">8</a>]. As the global poultry industry continues to expand, understanding these bacterial pathogens and their clinical presentations remains fundamental to maintaining flock health, productivity, and [food safety](/knowledge/bacteria/livestock-bacteria/cooking-chicken-bacteria-prevention).

## References

<a id="ref-1"></a>[<a href="#ref-1">1</a>] Liu H, Pan S, Wang C, et al. Review of respiratory syndromes in poultry: pathogens, prevention, and control measures. Vet Res. 2025. URL: https://pubmed.ncbi.nlm.nih.gov/40382667/

<a id="ref-2"></a>[<a href="#ref-2">2</a>] Mor-Mur M, Yuste J. Emerging bacterial pathogens in meat and poultry: an overview. 2009. URL: https://www.semanticscholar.org/paper/6dd7333be21ba4f59ae8c13e47f30ae80b816188

<a id="ref-3"></a>[<a href="#ref-3">3</a>] Swelum AA, Elbestawy AR, El-Saadony MT, et al. Ways to minimize bacterial infections, with special reference to *Escherichia coli*, to cope with the first-week mortality in chicks: an updated overview. Poult Sci. 2021. URL: https://pubmed.ncbi.nlm.nih.gov/33752065/

<a id="ref-4"></a>[<a href="#ref-4">4</a>] Jamali H, Akrami F, Bouakkaz S, et al. Prevalence of specific serogroups, antibiotic resistance and virulence factors of avian pathogenic *Escherichia coli* (APEC) isolated from clinical cases: A systematic review and meta-analysis. Microb Pathog. 2024. URL: https://pubmed.ncbi.nlm.nih.gov/39117015/

<a id="ref-5"></a>[<a href="#ref-5">5</a>] Soro AB, Whyte P, Bolton DJ, et al. Strategies and novel technologies to control *Campylobacter* in the poultry chain: A review. Compr Rev Food Sci Food Saf. 2020. URL: https://pubmed.ncbi.nlm.nih.gov/33337085/

<a id="ref-6"></a>[<a href="#ref-6">6</a>] Hamed RI, Nabil NM, Tawakol M, et al. An overview of current status of salmonellosis in duck farms in Egypt. Egypt J Anim Health. 2024. URL: https://www.semanticscholar.org/paper/8093c7b00376828e38685276ef0f1b77f7c83348

<a id="ref-7"></a>[<a href="#ref-7">7</a>] Nguyen NH, Nguyen TM, Hotzel H, et al. Thermophilic *Campylobacter* - neglected foodborne pathogens in Cambodia, Laos and Vietnam. Gastroenterol Hepatol. 2017. URL: https://www.semanticscholar.org/paper/3681b712d7e18deb75396154af36d7a977ad3d18

<a id="ref-8"></a>[<a href="#ref-8">8</a>] Smet A, Martel A, Persoons D, et al. Comparative analysis of extended-spectrum-beta-lactamase-carrying plasmids from different members of Enterobacteriaceae isolated from poultry, pigs and humans: evidence for a shared beta-lactam resistance gene pool? J Antimicrob Chemother. 2009. URL: https://www.semanticscholar.org/paper/a3cf839b2827dd8d1ce75d2a990a3c26bceee949

<a id="ref-9"></a>[<a href="#ref-9">9</a>] Hermans D, van Steendam K, Verbrugghe E, et al. Passive immunization to reduce *Campylobacter jejuni* colonization and transmission in broiler chickens. Vet Res. 2014. URL: https://www.semanticscholar.org/paper/b0859e6cb7fe2a2465ef78a7d669a364f8a6e477

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