Swine Bacterial Diseases: Colibacillosis, UTI, and Antimicrobial Resistance

Introduction

Swine production faces significant economic losses from bacterial diseases, with Escherichia coli being the most frequently isolated pathogen from clinical cases [80]. Among the diverse manifestations of E. coli infection in pigs, enteric colibacillosis and urinary tract infections (UTIs) represent two clinically and economically important syndromes. The emergence and dissemination of antimicrobial resistance (AMR) in swine E. coli populations have further complicated disease management and raised concerns about zoonotic transmission [72]. This article provides a detailed examination of the pathogenesis, diagnosis, and molecular epidemiology of swine colibacillosis and UTI, with a focus on the genetic mechanisms driving AMR.

Swine Colibacillosis

Etiology and Pathotypes

Swine colibacillosis is caused by pathogenic E. coli strains that colonize the intestinal tract and produce virulence factors. Four major pathotypes are recognized in pigs: enterotoxigenic E. coli (ETEC), Shiga toxin-producing E. coli (STEC, including edema disease E. coli [EDEC]), enteropathogenic E. coli (EPEC), and extraintestinal pathogenic E. coli (ExPEC) [72]. ETEC is the most prevalent pathotype, responsible for neonatal and post-weaning diarrhea (PWD) [77]. A systematic review and meta-analysis of virulence factor genes in swine isolates confirmed the dominance of ETEC-associated fimbrial and toxin genes [1].

Pathogenesis of ETEC Infection

ETEC strains adhere to porcine intestinal epithelial cells via fimbrial adhesins, primarily F4 (K88), F5 (K99), F6 (987P), F41, and F18 [77]. The fimbriae bind to specific receptors on enterocytes; for example, F18 fimbriae recognize receptors whose expression is influenced by the FUT1 gene polymorphism [2]. Following adhesion, ETEC produces enterotoxins: heat-labile toxin (LT), heat-stable toxin a (STa), and heat-stable toxin b (STb) [77]. LT activates adenylate cyclase, increasing intracellular cyclic AMP, while STa and STb activate guanylate cyclase or alter calcium signaling, leading to chloride secretion and water efflux into the intestinal lumen [73]. The resulting diarrhea causes dehydration, acidosis, and electrolyte imbalance.

Recent research has elucidated additional pathogenic mechanisms. ETEC-induced intestinal epithelial necroptosis drives lamina propria immune cell pyroptosis, contributing to mucosal injury in piglets [3]. The heat-labile enterotoxin also induces cell death and disrupts effector functions in porcine monocytes [64]. Co-infection with Cystoisospora suis synergistically increases pathogenicity in weaned piglets [4]. Furthermore, dietary factors such as high indigestible protein or soybean-derived trypsin inhibitor can exacerbate F18 ETEC disease [5, 6].

Shiga Toxin-Producing E. coli and Edema Disease

STEC strains produce Shiga toxin 2e (Stx2e), which causes edema disease in weaned piglets, characterized by neurological signs and subcutaneous edema [46]. The Stx2e toxin binds to globotetraosylceramide receptors on vascular endothelial cells, leading to vascular damage and increased permeability [78]. A recombinant Stx2e toxoid has been developed to enhance the efficacy of bacterin-inactivated vaccines against F18+ E. coli [43]. Phage therapy targeting STEC has shown promise in attenuating bacterial colonization and toxin production in piglets [7].

Diagnosis of Colibacillosis

Definitive diagnosis requires isolation of E. coli from intestinal contents or feces, quantification, and detection of virulence factor genes by PCR [77]. A diagnostic decision tree is presented in Figure 1.

flowchart TD
    A[Piglet with diarrhea or edema] --> B{Clinical signs}
    B -->|Watery diarrhea, dehydration| C[Suspect ETEC]
    B -->|Neurologic signs, eyelid edema| D[Suspect STEC/EDEC]
    C --> E[Collect fecal or intestinal sample]
    D --> E
    E --> F[Quantitative culture on MacConkey agar]
    F --> G[Isolate E. coli colonies]
    G --> H["PCR for virulence genes: fimbriae, toxins"]
    H --> I{Results}
    I -->|F4/F18 + LT/ST| J[ETEC confirmed]
    I -->|Stx2e +| K[STEC/EDEC confirmed]
    I -->|Negative for major pathotypes| L[Consider other enteric pathogens]
    J --> M[Antimicrobial susceptibility testing]
    K --> M
    M --> N[Select targeted therapy or alternative control]

Figure 1. Diagnostic algorithm for swine colibacillosis. PCR targets include fimbrial genes (F4, F18, F5, F6, F41) and toxin genes (LT, STa, STb, Stx2e) [77, 1].

Immunochromatographic test strips have been developed for sensitive detection of heat-labile enterotoxin in field settings [48]. Histopathological examination reveals villous atrophy and crypt hyperplasia in the ileum of infected piglets [71].

Urinary Tract Infection in Swine

UTI in swine is less frequently studied than colibacillosis but represents an important cause of reproductive disorders in sows and reduced productivity. A recently established E. coli UTI model in Göttingen minipigs allows for strain recovery and characterization, providing a platform for studying pathogenesis and treatment [8]. The model involves transurethral inoculation of uropathogenic E. coli (UPEC) strains, followed by quantitative urine culture and histopathology. UPEC strains typically express type 1 fimbriae and P fimbriae, which mediate adherence to uroepithelial cells. Although the literature on swine UTI is limited, the pathophysiological mechanisms are analogous to those in other mammals, with ascending infection from the lower urinary tract being the primary route.

Antimicrobial Resistance in Swine E. coli

Mechanisms of Resistance

Swine E. coli isolates exhibit resistance to multiple antimicrobial classes through a variety of genetic mechanisms. Table 1 summarizes key resistance genes and their associated phenotypes.

Table 1. Major antimicrobial resistance genes identified in swine E. coli isolates.

Epidemiology of AMR in Swine Populations

Surveillance studies across multiple countries have documented high prevalence of multidrug resistance (MDR) in swine E. coli. In Spanish pig farms, 87.1% of diarrheagenic E. coli isolates were MDR, with high rates of resistance to nalidixic acid (82%), colistin (77%), and ampicillin (76%) [76]. Similarly, in Hungarian pig farms, antimicrobial use patterns correlated with resistance profiles, enabling data-driven farm-level analysis [17]. In German fattening pigs, AMR prevalence differed at subnational levels, indicating regional variation in selective pressure [47]. Dutch livestock showed flattening patterns of AMR levels in indicator E. coli, suggesting that interventions may be having an effect [18].

The emergence of carbapenemase-producing E. coli in farm animals is particularly concerning. OXA-244-producing E. coli was detected in Dutch farm animals in 2024 [10]. Carbapenem-resistant E. coli from pigs can disseminate blaNDM-5 via membrane vesicles, a process enhanced by elevated temperature and the rpoE/degP pathway [11]. Sub-inhibitory concentrations of gentamicin and tilmicosin promote extracellular vesicle biogenesis and horizontal transfer of blaNDM through the mrdA/mrdB and zraS/zraR systems, respectively [55, 19].

Colistin Resistance and mcr Genes

Colistin is a last-resort antibiotic for treating MDR infections in humans, and the emergence of plasmid-mediated colistin resistance (mcr genes) in swine E. coli is a major One Health concern. In Spain, mcr-1, mcr-4, and mcr-5 variants were identified in ETEC and STEC isolates from swine colibacillosis [67]. In China, mcr-1-positive E. coli from livestock showed high prevalence and genomic diversity over a five-year period [12]. Co-existence of mcr-1 and blaCTX-M in porcine isolates has been documented, and cephalosporin pressure can select for mcr-1 [54]. The flexible cotransfer of plasmids drives the dissemination of tet(X4) in swine E. coli [14]. Novel sequence types such as ST3871 carrying tet(X4) exhibit diverse transmission modes [16].

Extended-Spectrum β-Lactamase (ESBL) and Carbapenemase Producers

ESBL-producing E. coli are widespread in pig farms. In Korea, prevalence and molecular epidemiology of ESBL-producing E. coli were linked to antimicrobial use across multiple industry sectors [9]. In China, blaCTX-M-55-carrying E. coli were found in both ceftiofur-use and non-use farms, indicating environmental persistence [61]. Whole-genome sequencing of isolates from pig slaughterhouses in Indonesia revealed diverse AMR genes, including ESBL genes [20]. A One Health perspective integrating genomic data from human and swine E. coli showed temporal trends in AMR and zoonotic transmission risks [40].

Biofilm Formation and AMR

Biofilm production is an important virulence factor that also contributes to antimicrobial tolerance. In E. coli isolated from slaughtered pigs, 46% of strains produced biofilm, and 99% exhibited multi-resistance [70]. Biofilm formation is associated with increased resistance to disinfectants and antibiotics, complicating farm hygiene measures. Phage therapy has been explored for biofilm disruption in swine farm environments [21].

Control Strategies

Antimicrobial Stewardship

Rational use of antimicrobials is critical to slow the spread of AMR. Farm-level analysis of antimicrobial use and resistance patterns can guide stewardship programs [17, 60]. In Japan, association between farm-level antimicrobial usage and AMR in E. coli from healthy swine was demonstrated [60]. In China, factors such as season, pig type, and medication type influenced resistance levels [75].

Vaccination

Vaccines against ETEC and STEC are available, but their efficacy is limited by serotype diversity. The dominant clones in Spanish swine colibacillosis include O157:HNM-A-ST10 (F4ac) and O108:HNM-A-ST10 (F18) [76]. The H39 antigen is associated with prevalent O antigens and may be a valuable subunit vaccine component [67]. Recombinant Stx2e toxoid has been used to enhance bacterin-inactivated vaccines against F18+ E. coli [43]. The B subunit of Stx2e bundled by a five-stranded α-helical coiled coil protects piglets from edema disease [65].

Phage Therapy

Bacteriophages offer a targeted alternative to antibiotics. Several phages have been isolated and characterized against MDR swine E. coli. A Kayfunavirus phage targeting MDR E. coli from swine feces showed lytic activity [22]. Another phage, vB_EcoS_P78, was effective against MDR strains [44]. Phage therapy in post-weaning piglets challenged with ETEC reduced clinical signs in a controlled minitrial [23]. However, bacterial regrowth was observed, indicating the need for phage cocktails or combination therapy [74]. A novel Escherichia phage against hybrid IPEC/ExPEC E. coli has also been described [24].

Alternative Approaches

Probiotics, prebiotics, organic acids, phytogenic substances, and zinc oxide have been investigated as alternatives to antibiotics [73]. Immunomodulatory probiotics can alleviate bacterial diarrhea by regulating gut function and immune responses [79]. Enterococcus hirae from Ningxiang pigs protected against E. coli-induced gut dysbiosis and inflammation via acetate/propionate-MyD88-NF-κB axis [25]. Dietary lysophospholipid alleviated diarrhea and improved intestinal health in ETEC-challenged piglets [26]. Nano-porous zinc oxide effectively alleviated ETEC-induced diarrhea and intestinal inflammation [27]. Plant-derived compounds such as linarin, baicalin-aluminum complexes, and isoliquiritigenin have shown anti-adhesive or anti-virulence effects [28, 42, 52]. Tannic acid and berberine also modulate gut microbiota to enhance immunity [50, 45].

Conclusion

Swine colibacillosis and UTI caused by E. coli remain major challenges for the pig industry. The high prevalence of MDR, including resistance to critically important antibiotics such as colistin and carbapenems, underscores the urgent need for improved surveillance, stewardship, and alternative control strategies. Genomic epidemiology, as demonstrated by numerous studies using whole-genome sequencing, provides essential data for tracking resistance determinants and informing vaccine development. Phage therapy, probiotics, and phytogenic compounds represent promising avenues for reducing reliance on conventional antimicrobials.

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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.