Colibacillosis in Poultry: Avian Pathogenic Escherichia coli (APEC) Infections

Etiology of Avian Pathogenic Escherichia coli

Avian pathogenic Escherichia coli (APEC) constitutes a pathotype of extraintestinal pathogenic E. coli (ExPEC) responsible for colibacillosis, one of the most economically significant bacterial diseases of poultry worldwide [1, 2, 3]. APEC strains are characterized by a distinct repertoire of virulence-associated genes (VAGs) that distinguish them from commensal E. coli isolates [4, 5, 6]. Key VAGs include those encoding adhesins (e.g., type 1 fimbriae, P fimbriae), iron acquisition systems (e.g., aerobactin, salmochelin, the iroN gene), protectins (e.g., lipopolysaccharide O antigens, K1 capsule), and toxins (e.g., hemolysin HlyE, colicins) [7, 8, 9, 10, 11]. The presence of the iroN gene, for instance, has been used as a marker for APEC detection in multidrug-resistant isolates from quail [9]. The O78 serogroup remains among the most prevalent APEC serotypes globally [12, 13].

Genomic characterization of APEC isolates has revealed extensive diversity and the presence of plasmids harboring multiple resistance and virulence determinants [3, 14, 15, 4]. Complete genome sequencing of APEC from colibacillosis cases in Georgia (USA) demonstrated considerable genomic plasticity [14]. Comparative genomic studies have identified regions shared between APEC and other ExPEC strains, including uropathogenic E. coli, indicating potential zoonotic gene pools [16, 17]. The species tropism of certain fimbrial adhesins, such as P-like fimbriae (PLF), influences host range and zoonotic potential [16]. Emergence of extensively drug-resistant (XDR) and multidrug-resistant (MDR) APEC strains has been documented in numerous poultry-producing regions, complicating therapeutic management [3, 18, 4, 19, 20].

Pathogenesis: Molecular and Cellular Mechanisms

APEC infection typically begins with colonization of the upper respiratory tract or the gastrointestinal epithelium, followed by translocation into the bloodstream and systemic dissemination [7, 21, 22]. The initial adhesion is mediated by fimbrial and afimbrial adhesins, including type 1 fimbriae and the autotransporter eYadA of the type V secretion system, which promote bacterial attachment to host epithelial cells and extracellular matrix components [11]. Direct interaction between APEC and respiratory viruses, such as H9N2 avian influenza virus, has been shown to enhance bacterial adhesion through viral neuraminidase activity, thereby predisposing poultry to secondary colibacillosis [7].

Once internalized or translocated, APEC must withstand host oxidative stress and phagocytic killing. The quorum-sensing regulator LsrR modulates resistance to oxidative stress by interfering with sulfate assimilation, thereby enhancing bacterial survival within macrophages [23]. Two-component systems and small regulatory RNAs (sRNAs) such as RyfA and TimR orchestrate stress resistance and virulence gene expression during infection [21]. The toxin-antitoxin system ecnAB regulates capsular sialic acid biosynthesis, modulating capsule thickness and virulence [8]. APEC hemolysin HlyE, delivered via outer membrane vesicles, induces mitochondria-dependent apoptosis in avian HD11 macrophages, contributing to immunosuppression [10].

Biofilm formation is a critical virulence mechanism enabling APEC persistence on both biotic and abiotic surfaces. MDR APEC strains exhibit robust biofilm formation on various surfaces, including poultry meat contact surfaces, which contributes to cross-contamination during processing [24, 19, 25]. Biofilm-associated gene expression differs between planktonic and sessile states, with upregulation of curli and cellulose biosynthesis genes observed in biofilm cells [25]. Biofilm formation on stored chicken meat is a key factor in the persistence of APEC in the food chain, directly relating to the question of "raw chicken breast bacteria" contamination and the risk posed by "undercooked chicken e coli" for human exposure (though this article focuses on poultry health) [24].

Clinical Signs

Colibacillosis manifests in several clinical forms depending on the age of the bird, the route of infection, and the virulence of the APEC strain [1, 4, 26]. In broiler chickens, the most common presentations include yolk sac infection (omphalitis) in neonates, respiratory colibacillosis (airsacculitis), and systemic colibacillosis (colisepticemia) [22, 6, 27]. Clinical signs are non-specific and include depression, ruffled feathers, reduced feed and water intake, drooping wings, and respiratory distress [1, 28]. In laying hens, colibacillosis often presents as salpingitis and peritonitis, leading to decreased egg production [29]. Embryonic infection can result in high mortality during incubation [22].

The common question "does chicken have e coli or salmonella" reflects public awareness of poultry as a reservoir of bacterial pathogens. While both APEC and Salmonella spp. are found in poultry, APEC is primarily a cause of disease in the birds themselves, whereas Salmonella is more frequently linked to human foodborne illness. However, APEC strains possess zoonotic potential due to shared ExPEC virulence genes, so their presence in poultry flocks has implications beyond avian health [16, 20, 17]. Asymptomatic carriage of fluoroquinolone-resistant APEC has been documented in broiler chickens at slaughter, highlighting the risk of "raw chicken breast bacteria" entering the food chain [20].

Pathology

Gross pathological lesions vary by disease form. In acute colisepticemia, birds exhibit fibrinous pericarditis, perihepatitis, and airsacculitis, often described as a "polyserositis" [2, 6, 27]. The liver and spleen may be enlarged and congested [27]. In yolk sac infection, unabsorbed yolk contents are caseous and discolored [22]. Salpingitis in layers is characterized by a distended oviduct filled with fibrino-caseous exudate [29]. Histopathological examination reveals fibrinoheterophilic inflammation, bacterial emboli in capillaries, and necrotic foci in the liver and spleen [6]. Transcriptomic analysis of chicken liver and spleen during APEC infection has shown dynamic expression of immune-related genes, including upregulation of acute phase proteins and toll-like receptors [27].

Diagnostics

Definitive diagnosis of colibacillosis requires isolation and identification of E. coli from affected tissues (e.g., liver, spleen, pericardium, yolk sac) in pure culture [4, 5, 6]. Conventional microbiology involves culture on MacConkey agar and subsequent biochemical confirmation. Molecular detection of APEC-specific VAGs, such as iroN, iss, and ompT, is widely used for pathotyping [9, 6, 11]. PCR-based assays targeting these genes allow differentiation of APEC from commensal E. coli [5]. Genomic approaches, including whole-genome sequencing and comparative genomics, provide high-resolution typing for epidemiological surveillance and antimicrobial resistance profiling [3, 14, 15, 17]. For field surveillance, multiplex PCR panels and commercial ELISA kits can detect APEC antigens or antibodies, though culture confirmation remains the gold standard [6].

A typical diagnostic workflow for suspected colibacillosis is illustrated below.

graph TD
    A[Clinical signs: respiratory distress, depression, mortality], > B[Post-mortem examination: fibrinous polyserositis, omphalitis]
    B, > C1[Collect tissues: liver, spleen, pericardium, yolk sac]
    B, > C2[Collect swabs: cloacal, tracheal]
    C1, > D[Aerobic culture on MacConkey agar]
    D, > E[Biochemical identification: E. coli]
    E, > F1[Serotyping: O78, O2, O1]
    E, > F2[Molecular pathotyping: PCR for iroN, iss, ompT]
    E, > F3[Antimicrobial susceptibility testing: disk diffusion / broth microdilution]
    F2, > G{APEC virulence gene profile positive?}
    G, > H[Confirm APEC pathotype]
    F3, > I[Guide treatment selection]
    I, > J[Implement control measures]
    H, > J

Treatment

Treatment of colibacillosis relies primarily on antimicrobial therapy, but the emergence of MDR and XDR APEC strains has severely compromised the efficacy of many commonly used agents [3, 18, 4, 19, 20]. Fluoroquinolones, tetracyclines, and beta-lactams are frequently ineffective due to plasmid-mediated resistance genes [3, 20, 18]. Extended-spectrum beta-lactamase (ESBL)-producing APEC have been reported in Egypt and other regions [3, 18]. Antimicrobial susceptibility testing is therefore essential for rational therapy selection [4].

Alternative therapeutic strategies are under active investigation. Bacteriophage therapy has shown promise in controlling APEC infections, with phages administered via drinking water reducing systemic infection and pathology in laying hens [29, 13]. Phage cocktails and phage antibiotic synergism can also disrupt preformed biofilms [19, 30, 12]. Probiotic metabolites and plant-derived compounds, such as Ilex rotunda–Cyperus rotundus herb pair extract, Myrmecodia sp. extract, and deep eutectic solvent emulsions containing Piper betle L. extract, have demonstrated antimicrobial and anti-biofilm activity against APEC [1, 2, 24, 31, 26]. Epitope-based and peptide-based vaccines, designed with machine learning, represent a novel immunoprophylactic approach [32, 33]. In ovo delivery of trivalent inactivated nanovaccines has shown safety and immunogenicity under commercial hatchery conditions [34]. However, vaccine development remains challenging due to APEC serotype diversity.

Control

Control of colibacillosis requires an integrated approach combining biosecurity, management practices, and vaccination. Strict hygiene in hatcheries and poultry houses reduces early exposure to APEC [34, 22]. Embryonic thermal manipulation has been shown to enhance splenic immunity and regulate inflammatory responses to E. coli in broilers, suggesting a potential management tool for improving disease resistance [28]. Probiotics, such as Lactobacillus plantarum ZG-7, can improve intestinal barrier function and modulate gut microbiota to reduce APEC colonization [35].

Biosecurity measures that prevent co-infections with respiratory viruses (e.g., H9N2 avian influenza) are critical, as viral co-infection potentiates APEC adhesion and severity [7]. Monitoring of antimicrobial resistance patterns in APEC isolates is essential for guiding empirical therapy and detecting emerging XDR clones [3, 15, 18, 4]. The use of APEC as a marker organism for antimicrobial resistance surveillance in poultry production systems has been proposed [15]. Ultimately, a One Health framework that addresses APEC in the context of food safety (including risks from "raw chicken breast bacteria" and "undercooked chicken e coli") and zoonotic potential is necessary for sustainable poultry production [2, 16].

This article provides a comprehensive overview of colibacillosis in poultry caused by APEC. For further reading on specific aspects, readers are directed to related resources on this portal: Avian Colibacillosis: Etiology, Clinical Signs, and Control of Escherichia coli Infections in Poultry, Chicken Blood Bacteria: Understanding Avian Pathogenic Escherichia coli (APEC) and Colibacillosis, and E. coli and Salmonella on Raw Chicken: Comparative Pathogenesis and Food Safety.

References

[1] Liu H, Yang A, Wei X et al. Preventive effects and underlying mechanisms of Ilex rotunda Thunb.-Cyperus rotundus L. herb pair extract on avian colibacillosis in chickens. Poult Sci. 2026.

[2] Lisnanti EF, Lokapirnasari WP, Arif MAA et al. Comparative effects of Myrmecodia sp. extract and infusion on organ function biomarkers, lipid metabolism, and meat lipid profile in avian pathogenic Escherichia coli-infected broiler chickens: Implications for sustainable poultry production within a One Health framework. Vet World. 2026.

[3] Ni W, Chen L, Chen H et al. Genomic and Pathogenic Characterization of an Extensively Drug-Resistant Avian Pathogenic Escherichia coli Strain. Transbound Emerg Dis. 2026.

[4] ELTarabili RM, Abo Hashem ME, Ahmed MA et al. Emergence of multidrug-resistant and virulent Escherichia coli with APEC-associated traits in broiler chickens from Ismailia, Egypt. Sci Rep. 2026.

[5] da Silva AL, Luna FS, Nogueira JF et al. Phenotypical-genetic virulence and resistance in atypical avian pathogenic Escherichia coli. Int Microbiol. 2026.

[6] Freshinta JW, Adhitya YRC, Arief M et al. Histopathological Diagnosis and Detection of Avian Pathogenic Escherichia Coli Virulence Genes in Broiler Chickens in Indonesia. Arch Razi Inst. 2025.

[7] Li Y, Xue Y, Quan Y et al. Direct interaction between avian pathogenic Escherichia coli and H9N2 avian influenza virus promotes bacterial adhesion during their infections. Microbiol Spectr. 2026.

[8] Jing Y, Shen X, Yin D et al. The ecnAB toxin-antitoxin system modulates avian pathogenic Escherichia coli virulence through regulating the capsular sialic acid biosynthesis pathway. Vet Microbiol. 2026.

[9] Keytimu MO, Rahayu U, Wibisono FJ et al. Detection of the iroN virulence gene in multidrug-resistant Escherichia coli isolated from quails in traditional markets of Surabaya, Indonesia. Vet World. 2026.

[10] Mou Y, Liang Y, Zhu D et al. Extracellular vesicles (EVs) carrying hemolysin HlyE variant (HlyE-V) from avian pathogenic Escherichia coli (APEC) induce mitochondria-dependent apoptosis in HD11 macrophages. Microb Pathog. 2026.

[11] Xia P, Chen Z, Luo Y et al. Effects of the type V secretion system eYadA on the biological properties and pathogenicity of avian pathogenic Escherichia coli. Vet Res. 2026.

[12] Xu T, Yang W, Cao J et al. Isolation and therapeutic potential of phage vB_EcoM_GXW16 against a drug-resistant avian pathogenic Escherichia coli strain. Poult Sci. 2026.

[13] Lu Q, Jin X, Wang Z et al. Genomic characterization of APEC phages and evaluation of the efficacy in reducing the loads of APEC O78 infections in chickens. Front Microbiol. 2026.

[14] Runcharoon K, Ienes-Lima J, Logue CM. Complete genomes of 21 avian pathogenic Escherichia coli isolated from colibacillosis cases in Georgia poultry. Microbiol Resour Announc. 2026.

[15] Gaonkar PP, Golden R, Santana-Pereira ALR et al. Genomic characterization of avian pathogenic Escherichia coli and its potential as a marker organism for antimicrobial resistance. Appl Environ Microbiol. 2026.

[16] Akrami F, Jamali H, Houle S et al. Host range and zoonotic potential linked to P-like fimbrial (PLF) adhesin specificity in avian pathogenic Escherichia coli. PLoS Pathog. 2026.

[17] Martins TW, Trotereau A, Lahnig-Jacques S et al. Sequencing of the invasive E. coli strain BEN2908 isolated from poultry: A comparative investigation of genomic regions shared with intestinal and extraintestinal model E. coli strains. PLoS One. 2026.

[18] El-Shazly DA, Nasef SA, Mahmoud FF et al. Corrigendum to "Expanded spectrum β-lactamase producing Escherichia coli isolated from chickens with colibacillosis in Egypt". Poult Sci. 2026.

[19] Bhutada P, Joshi N, Saroj SD et al. Dynamics of multidrug-resistant avian pathogenic E. coli biofilm formation on various surfaces and its dispersion with phage antibiotic synergism. BMC Microbiol. 2026.

[20] Yongyod R, Eiamsam-Ang T, Kamolrat N et al. Fluoroquinolone-Resistant Avian Pathogenic Escherichia coli Isolated from Asymptomatic Broiler Chickens in a Slaughterhouse in Northern Thailand. Pathogens. 2026.

[21] Anamalé C, Bessaiah H, Ng Kwan Lim E et al. Orchestrating infection: the impact of RyfA and TimR sRNAs on stress resistance and virulence in avian pathogenic Escherichia coli in chickens. Appl Environ Microbiol. 2026.

[22] Wang J, Bajagai YS, Sajid GA et al. Transcriptomic analysis reveals a crucial role of the yolk sac during Avian Pathogenic Escherichia coli infection in chicken embryos. Poult Sci. 2026.

[23] Kong L, Tu C, Song X et al. Quorum-sensing regulator LsrR modulates resistance to oxidative stress by interfering with sulfate assimilation in avian pathogenic Escherichia coli. J Bacteriol. 2026.

[24] Ratchasong K, Saengsawang P, Yusakul G et al. Deep Eutectic Solvent-Based Emulsion Containing Piper betle L. Extract and Hydroxychavicol Prevent Biofilm Development and Surface Adhesion of Avian Pathogenic Escherichia coli on Stored Chicken Meat. Antibiotics (Basel). 2026.

[25] He Y, Kuang N, Chang Z et al. Biofilm Formation in Chicken-Derived Extraintestinal Pathogenic Escherichia coli Alters the Expression of Biofilm- and Virulence-Associated Genes. Antibiotics (Basel). 2026.

[26] Lisnanti EF, Lokapirnasari WP, Al-Arif MA et al. The ameliorative effects of Myrmecodia sp. as an antibiotic growth promoter in broiler chicken with avian pathogenic Escherichia coli infection. Open Vet J. 2025.

[27] Wang T, He Y, Zhang T et al. Transcription profiles of chicken liver and spleen in response to infection with avian pathogenic Escherichia coli at different stages. Poult Sci. 2026.

[28] Al-Zghoul MB, Okour R, Alghizzawi D et al. Embryonic thermal manipulation enhances splenic immunity and regulates inflammatory responses to Escherichia coli in broiler chickens. Front Vet Sci. 2026.

[29] Gohar M, Hyun JE, Smith KR et al. Bacteriophage cocktail in drinking water suppresses systemic avian pathogenic Escherichia coli infection and pathology in laying hens. Curr Res Microb Sci. 2026.

[30] Rashid MU, Ahmed S, Muhammad J et al. Screening of bacteriophages for subsequent treatment of resistant Escherichia coli infections transmitted through poultry. Braz J Microbiol. 2026.

[31] Thapa K, Phan A, Tung CW et al. Evaluation of Probiotic Metabolites Mediated Antimicrobial Activity and Inhibition of Virulence Factors in Avian Pathogenic Escherichia Coli. Probiotics Antimicrob Proteins. 2026.

[32] Waseem M, Kamran Z, Ali A. Advancing poultry health: A meta-analysis of epitope-based and peptide-based vaccines against Avian Pathogenic E. coli with machine learning insights. PLoS One. 2026.

[33] Li Y, Quan Y, Quan K et al. Construction and immunogenicity evaluation of avian Escherichia coli-derived bacterial biomimetic vesicles displaying H9 subtype avian influenza virus HA1 protein. Vet Microbiol. 2026.

[34] Scuotto A, Ogonczyk-Makowska D, Magnez R et al. Safety, Immunogenicity, and Vaccine Compatibility of a Trivalent Inactivated In Ovo Nanovaccine Against Avian Colibacillosis in Broilers Under Commercial Hatchery Conditions. Animals (Basel). 2026.

[35] Peng S, Xie B, Mei G et al. Effects of Lactobacillus plantarum ZG-7 on the intestinal barrier and intestinal flora of Muscovy ducks infected with avian pathogenic Escherichia coli. Front Immunol. 2025. *** 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.