Salmonella and Escherichia coli Infections in Poultry: Food Safety and Veterinary Perspectives
Introduction
Salmonella and Escherichia coli are the two most significant bacterial pathogens of poultry in terms of clinical disease, economic impact, and food safety concerns [1]. Salmonella enterica subsp. enterica comprises over 2,600 serovars, many of which cause either systemic disease in birds (e.g., S. Gallinarum, S. Pullorum) or asymptomatic intestinal carriage that leads to carcass contamination [2]. Avian pathogenic Escherichia coli (APEC) causes colibacillosis, a complex disease syndrome including respiratory infection, septicemia, and polyserositis [3]. Both pathogens are transmitted horizontally via the fecal-oral route and vertically through eggs, leading to widespread dissemination in commercial flocks [4]. The emergence of antimicrobial resistance (AMR) further complicates control and amplifies the zoonotic risk [5, 6]. This article provides a detailed review of the etiology, epidemiology, clinical presentations, diagnostic approaches, treatment strategies, and food safety implications of Salmonella and E. coli infections in poultry.
Etiology
Salmonella
Salmonella is a Gram-negative, facultative anaerobic bacillus belonging to the family Enterobacteriaceae [2]. The species Salmonella enterica is subdivided into six subspecies, with subspecies enterica responsible for virtually all infections in warm-blooded animals [7]. Host-restricted serovars such as S. Gallinarum and S. Pullorum cause fowl typhoid and pullorum disease respectively, while broad-host-range serovars like S. Enteritidis and S. Typhimurium colonize the gastrointestinal tract of poultry without causing clinical signs but represent a major public health risk [1, 2]. The lipopolysaccharide (LPS) O-antigen and flagellar H-antigens define serovar identity, and phase variation of flagellin genes influences host immune evasion [8]. Salmonella uses a type III secretion system (T3SS) encoded on pathogenicity islands to inject effector proteins into host cells, facilitating invasion of intestinal epithelium and survival within macrophages [8, 9].
Escherichia coli
E. coli is also a Gram-negative, facultative anaerobic rod and a normal inhabitant of the avian intestinal microbiota [9]. Pathogenic strains possess additional virulence genes that distinguish them from commensals. APEC harbor large virulence plasmids (ColV or ColBM plasmids) encoding genes such as iss (increased serum survival), iucC/iutA (aerobactin siderophore system), and hlyF (hemolysin) [3]. Other pathotypes relevant to poultry include enterotoxigenic E. coli (ETEC) and attaching/effacing E. coli (AEEC), though APEC is the predominant cause of clinical disease [10]. Extended-spectrum beta-lactamase (ESBL)-producing E. coli, which carry resistance genes such as blaCTX-M, are increasingly reported in poultry populations worldwide [11, 12]. The O77 serogroup has been associated with hemolytic uremic syndrome in humans, though such strains are rare in chickens [13].
Epidemiology
The prevalence of Salmonella and E. coli in poultry varies by region, production system, and biosecurity level. A 2023-2024 surveillance study in Jiangxi, China, found Salmonella contamination in 14.2% of poultry samples and E. coli in 68.5%, with high rates of multidrug resistance (MDR) [6]. In Uganda, broiler farms showed a 22% prevalence of Salmonella and 45% prevalence of pathogenic E. coli [3]. The European Union One Health 2024 Zoonoses Report identified Salmonella Enteritidis as the most common serovar in laying hens, while broiler flocks are more frequently colonized by S. Infantis and S. Typhimurium [7]. Addressing the common query "does chicken have e coli or salmonella", it is established that both organisms are routinely isolated from raw poultry carcasses, with E. coli present in >90% of samples and Salmonella in 10-40% depending on geographic and seasonal factors [1, 6]. The concept of producing "chicken without salmonella" has become a major industry goal, achieved through integrated control programs including vaccination, competitive exclusion, and strict biosecurity [14, 15].
Transmission occurs horizontally through contaminated feed, water, litter, and equipment, and vertically via transovarian infection (particularly with S. Enteritidis and S. Pullorum) [2]. APEC is primarily horizontally transmitted through respiratory aerosols or fecal contamination of eggshells leading to yolk sac infections in chicks [3]. Free-living birds such as pigeons can act as reservoirs for both pathogens, contributing to environmental contamination [16]. In rabbit farms, E. coli carrying the mcr-1.1 colistin resistance gene have been identified, underscoring the interconnectedness of livestock reservoirs [17].
Clinical Signs and Pathology
Salmonella
Clinical manifestations depend on serovar and host age. In young chicks infected with S. Pullorum or S. Gallinarum, signs include anorexia, huddling, white diarrhea, and high mortality (pullorum disease and fowl typhoid respectively) [18]. Necropsy findings reveal enlarged, congested liver and spleen, caseous cecal cores, and hemorrhagic ovaries in adult hens [16]. Infection with broad-host-range serovars usually results in subclinical carrier states, but stress can precipitate clinical enteritis [9]. Salmonella infection triggers an inflammatory response characterized by heterophil infiltration and upregulation of pro-inflammatory cytokines [8].
Escherichia coli (Colibacillosis)
APEC causes colibacillosis, which presents in several forms: airsacculitis, pericarditis, perihepatitis, salpingitis, and omphalitis (yolk sac infection) [3]. Gross pathology shows fibrinous exudates on serosal surfaces, thickened air sacs, and purulent joint exudates in chronic cases [16]. In laying hens, E. coli can cause egg peritonitis and salpingitis, reducing egg production [14]. The bacterium adheres to respiratory epithelium and subsequently invades the bloodstream, causing septicemia [19]. Systemic infection leads to polyserositis with characteristic fibrinous polyserositis (coligranuloma) [3].
Diagnostics
Accurate diagnosis of Salmonella and E. coli infections relies on culture, molecular detection, and serological methods.
Bacteriological Culture
Traditional isolation involves pre-enrichment in buffered peptone water, selective enrichment (Rappaport-Vassiliadis for Salmonella, MacConkey agar for E. coli), and plating on selective agar (XLD, HE, or CHROMagar for Salmonella; MacConkey or EMB for E. coli) [5, 6]. Suspect colonies are identified by biochemical tests (triple sugar iron, urease, indole) and serotyping using O and H antisera [2].
Molecular Diagnostics
PCR-based methods offer rapid and specific detection. Multiplex PCR panels targeting invasion genes (e.g., invA for Salmonella, iss for APEC) allow simultaneous screening of multiple pathogens [20]. Real-time quantitative PCR (qPCR) provides quantitation and has been applied to detect calf diarrhea pathogens but is equally valid for avian enteric agents [20]. Droplet digital PCR (ddPCR) offers absolute quantification without standard curves and has been used to detect Brucella abortus vaccine strains, but its principles are transferable to bacterial quantification in poultry [21]. For strain typing, whole genome sequencing (WGS) and multilocus sequence typing (MLST) are increasingly used to track transmission and AMR determinants [11, 13, 10].
Serology
Enzyme-linked immunosorbent assays (ELISAs) detect antibodies against Salmonella LPS or flagellar antigens and are used for flock screening in vaccination programs [19]. For E. coli, serotyping remains important for epidemiological studies [13].
Antimicrobial Susceptibility Testing
Disk diffusion and broth microdilution are standard [5]. Results are interpreted against clinical breakpoints. MDR is defined as non-susceptibility to three or more antimicrobial classes [6, 12].
The diagnostic workflow is summarized in Figure 1.
flowchart TD
A[Clinical sample: feces, organs, carcass swab], > B{Pre-enrichment}
B, >|Buffered peptone water| C{Selective enrichment}
C, >|Rappaport-Vassiliadis| D[Salmonella selective agar]
C, >|MacConkey broth| E[E. coli selective agar]
D, > F[Biochemical & serological ID]
E, > F
F, > G{Confirmatory PCR}
G, > H[invA, iss, virulence genes]
G, > I[Whole genome sequencing]
I, > J[Serovar / ST / AMR profile]
H, > J
Figure 1. Diagnostic workflow for Salmonella and Escherichia coli in poultry.
Treatment and Control
Antimicrobial Therapy
Therapeutic use of antimicrobials in poultry is restricted in many jurisdictions to minimize AMR development. Fluoroquinolones (enrofloxacin), tetracyclines, and sulfonamides have been used historically, but resistance is now widespread [4, 5]. In Ethiopia, conventional poultry farms showed 72.5% of Salmonella isolates and 81.3% of E. coli isolates were MDR [5]. Similarly, Chinese poultry isolates exhibited resistance to cefotaxime, ciprofloxacin, and colistin [10, 6]. The plasmid-borne tet(X4) resistance gene, which confers tigecycline resistance, has been identified in E. coli ST3871 from poultry, representing a novel transmission mode [10].
Vaccination
Vaccination against Salmonella is common in layer flocks. Live attenuated vaccines (e.g., S. Enteritidis ΔaroA mutants) and inactivated bacterins induce both humoral and cellular immunity [19]. Flagellin proteins have been explored as vaccine adjuvants to enhance immune responses [22]. For APEC, bacterins are available but autogenous vaccines are often preferred due to serovar diversity [19]. In ovo delivery of CpG oligodeoxynucleotides combined with intrapulmonary vaccination against Clostridium perfringens was shown to induce trained immunity that protects against E. coli septicemia later in life [19].
Alternative Control Strategies: Phage Therapy and Probiotics
Bacteriophage therapy is a promising alternative to antibiotics. Phage vB_SalS_KY05 significantly reduced Salmonella colonization in broilers without disrupting the cecal microbiota [23]. Holins from Salmonella Pullorum phages have been characterized and show therapeutic efficacy against pullorum disease in chickens [18]. A phage cocktail (SalmoFree) improved health and productivity in laying hens [24]. For E. coli, phage BECP15 demonstrated strong lytic activity against MDR strains [25].
Probiotics and feed additives are widely used. Chicken-derived Lactobacillus rhamnosus CIQ249 protected broilers against enteropathogens by regulating intestinal homeostasis [26]. Enterococcus faecium with probiotic characteristics reduced APEC and Salmonella burdens in laying hens [14]. Bacillus subtilis GX15 showed in vitro antibacterial activity against S. Typhimurium and protective effects in mice [27]. Plant-based alternatives such as fermented purple onion and chive extracts have also shown efficacy in reducing toxin-carrying bacteria [28]. Dietary supplementation with fenugreek-based antibiotic alternatives improved health in chicks with mixed bacterial infections [29]. Butyrate enhances antimicrobial defense in chicken macrophages by inducing reactive oxygen species and autophagy [30]. Saccharomyces cerevisiae fermentation products combined with phytogenic feed additives mitigated pathogens and improved immunomodulation in commercial broilers [31]. A safe formulation that induces biofilm formation in probiotics has been developed to control Salmonella and APEC in wood shavings litter [15].
Food Safety Perspectives
Poultry meat and eggs are major vehicles for human salmonellosis and colibacillosis. The public health question "does chicken have e coli or salmonella" is answered affirmatively: both are common contaminants of raw poultry [1, 32]. The term "chicken without salmonella" refers to flocks that have been raised under strict biosecurity and vaccination programs to achieve Salmonella-free status at the farm level, a goal that is increasingly realized in high-income countries but remains challenging in low-resource settings [4, 3]. However, even with on-farm control, cross-contamination during slaughter and processing is common [32].
"Undercooked chicken e coli" poses a direct food safety risk because APEC strains can cause human urinary tract infections and sepsis, though the primary foodborne E. coli pathotype is O157:H7 of bovine origin [1]. APEC strains share virulence genes with human extraintestinal pathogenic E. coli (ExPEC), suggesting a zoonotic potential [13]. Proper cooking to an internal temperature of 74°C eliminates both Salmonella and E. coli, but consumer education on handling and cross-contamination prevention remains critical [1].
Control of AMR in poultry is a One Health priority. The spread of ESBL-producing E. coli and MDR Salmonella from poultry to humans via the food chain is well documented [4, 12]. International surveillance programs monitor AMR trends, and biosecurity measures such as all-in/all-out management, litter management, and rodent control reduce pathogen load [7, 2].
Conclusion
Salmonella and E. coli remain formidable challenges in poultry production, affecting animal health and generating food safety risks. Advances in molecular diagnostics, vaccination, phage therapy, and probiotics provide a growing arsenal for control, but antimicrobial resistance continues to erode therapeutic options. Integrated control programs incorporating biosecurity, vaccination, and alternative interventions are essential to reduce pathogen prevalence in flocks and minimize contamination of poultry products. Sustained research and surveillance are needed to address the evolving epidemiology of these pathogens in the context of global food production.
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.
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