Abstract

Avian pathogenic Escherichia coli (APEC) causes colibacillosis in avian species, and recent reports have suggested APEC as a potential foodborne zoonotic pathogen. Herein, we discuss the virulence and pathogenesis factors of APEC, review the zoonotic potential, provide the current status of antibiotic resistance and progress in vaccine development, and summarize the alternative control measures being investigated. In addition to the known virulence factors, several other factors including quorum sensing system, secretion systems, two-component systems, transcriptional regulators, and genes associated with metabolism also contribute to APEC pathogenesis. The clear understanding of these factors will help in developing new effective treatments. The APEC isolates (particularly belonging to ST95 and ST131 or O1, O2, and O18) have genetic similarities and commonalities in virulence genes with human uropathogenic E. coli (UPEC) and neonatal meningitis E. coli (NMEC) and abilities to cause urinary tract infections and meningitis in humans. Therefore, the zoonotic potential of APEC cannot be undervalued. APEC resistance to almost all classes of antibiotics, including carbapenems, has been already reported. There is a need for an effective APEC vaccine that can provide protection against diverse APEC serotypes. Alternative therapies, especially the virulence inhibitors, can provide a novel solution with less likelihood of developing resistance.

Highlights

  • B) [57], iaL, cjrC [108], and mig-14p [41] have been reported in Avian pathogenic Escherichia coli (APEC). capU is putative hexosyltransferase with uncharacterized function, whereas cif belongs to bacterial toxins that arrest host cell division. tir and tccp are involved in bacterial adherence to host cells, whereas nleB is a component of a type III secretion system. iaL is involved in cell penetration, whereas cjrC is a putative siderophore receptor. mig-14p plays a role in resistance to antimicrobial peptides in host cells

  • ST95 and ST131 or O1, O2, and O18 serogroups might serve as a source of human extraintestinal infections

  • There is a need for an ideal APEC vaccine that can provide cross-protection against multiple APEC serotypes

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Summary

Introduction

Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Broiler chickens between the ages of 4 and 6 weeks are more susceptible [1], whereas layer chickens can be affected throughout the grow and lay periods, the peak egg by APEC. Studies have shown that APEC can studies have shown that APEC can colonize the gastrointestinal and respiratory tracts of colonize the gastrointestinal and respiratory tracts of chickens without causing disease and chickens without causing disease and only translocate to extra‐intestinal sites in the only translocate to extra-intestinal sites in the presence of stressors (production-related presence of stressors (production‐related stress, immunosuppression, and concurrent stress, immunosuppression, and concurrent infections) as an opportunistic pathogen [2,9]. Schematic diagram showing overview of Avian pathogenic Escherichia coli (APEC) infection in chickens along

Schematic diagram showing of Avian
Virulence and Pathogenesis Factors
Adhesins
Invasins
Iron Acquisition Systems
Protectins
Toxins
Other Virulence and Pathogenesis Factors
Secretion Systems
Two-Component Systems
Transcriptional Regulators
Metabolism-Associated Genes
Miscellaneous
Genes Essential for Systemic Infections and Adaptation in Chickens
Zoonotic Potential
Genetic Similarity and Commonality in Virulence Genes
Ability to Cause Disease with Similar Clinical Manifestations
Control Strategies
Management and Biosecurity Measures
Antibiotics
Vaccines
Main Findings
Probiotics
Bacteriophages
New Alternative Approaches
Innate Immune Stimulants
APEC Virulence and Growth Inhibitors
Antimicrobial Peptides
Conclusions and Future Perspectives
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