Avian pathogenic Escherichia coli (APEC): current insights and future challenges

Abstract

Avian pathogenic Escherichia coli (APEC) causes colibacillosis in avian species, and new investigations have implicated APEC as a possible foodborne zoonotic pathogen. This review analyzes APEC's pathogenic and virulence features, assesses the zoonotic potential, provides an update on antibiotic resistance and vaccine research efforts, and outlines alternate management approaches. Aside from established virulence factors, various additional components, including 2-component systems (TCS), adhesins, secretion systems (SS), invasions, iron acquisition systems, quorum sensing systems (QS), transcriptional regulators (TR), toxins, and genes linked with metabolism, contribute to APEC pathogenesis. APEC may spread to diverse species of birds in all business sectors and can infect birds of varying ages. However, younger birds experience more severe sickness than mature ones, probably due to their developing immune systems, and stress factors such as vaccination, Mycoplasma Infections, poor housing circumstances, respiratory viruses, and other risk factors for secondary infections can all make APEC both primary and secondary pathogens. Understanding these factors will help in generating new and effective treatments. Moreover, APEC O145 was the most prevalent serotype recently reported in all of China. Thus, the APEC's zoonotic potential should not be underrated. Furthermore, it has already been noted that APEC is resistant to almost all antibiotic classes, including carbapenems. A robust vaccine capable of protecting against multiple APEC serotypes is urgently needed. Alternative medications, particularly virulence inhibitors, can provide a special method with a decreased likelihood of acquiring resistance.

Keywords: avian pathogenic Escherichia coli; foodborne; virulence; zoonotic.

Figure 1

Schematic representation of pathogenic and virulence factors of APEC. Adhesins (Top-left) found on the surface of APEC cells may be classified as fimbrial, nonfimbrial, and atypical. The fimbrial facilitates chaperone proteins whereas the curli fimbriae is assembled in nucleation and precipitation. Nonfimbrial adhesins comprise afimbrial adhesins and autotransporters. Invasin (Top-right) contains cellulose, LPS, and K-capsule which can cause local and systemic disease. Toxins (Bottom-left) enable bacteria to enter and damage tissues APEC acquire iron acquisition (Bottom-right) which helps in the production and secretion of siderophores- small molecules that bind iron with high affinity and facilitate its uptake into bacterial cells.

Figure 2

World map illustrating the continents with APEC serotypes.

Figure 3

A schematic representation of avian pathogenic E. coli (APEC) infection in chickens, highlights how APEC colonizes the mucosal areas of the gastrointestinal, respiratory, and reproductive tracts after entering through oral, nasal, or cloacal routes.