Enteroinvasive E. coli (EIEC)

EIEC Introduction

Enteroinvasive E. coli (EIEC) are etiological agents of bacillary dysentery closely similar to that induced by Shigella spp., especially in low-income countries. The pathogenesis is characterized by the ability of the pathogen to invade the human colonic mucosa. Following penetration, EIEC replicate in macrophages, spread to adjacent IECs, causing inflammatory destruction of the intestinal epithelial barrier. The virulence genes have been acquired in a large F-type plasmid (pINV), but no molecular marker has been yet defined to discriminate EIEC and Shigella. Notwithstanding the similarities in the invasion mechanisms, the infectious dose of EIEC has been observed to be much higher than that of Shigella and the diseases caused by EIEC appear in some cases to be milder. Symptoms are self-limiting and characterized by the presence of blood, mucus and leukocytes in stools.

Serotypes of EIEC

It comprises 21 serotypes with patterns of O antigen and fewer with H antigens like O28:NM, O29:NM, O112:NM, O115:NM, 0121:NM, O124:NM, O124:H7, O124:H30, O124:H32, O135:NM, O136:NM, O143:NM, O144:NM, O144:H25, O152:NM, O159:H2, O164:NM, O167:NM, O167:H4, O167:H5, and O173:NM.

Pathogenesis of EIEC

Enteroinvasive E. coli (EIEC) shares many pathogenic features with Shigella, including possession of the pINV plasmid and the ability to invade intestinal epithelial cells via M cells, escape from macrophages through T3SS-mediated pyroptosis, and spread intracellularly using actin-based motility. EIEC produces a less severe illness than Shigella but needs a greater number of bacteria to cause infection. The virulence genes ipaC of EIEC show reduced expression while the pathogen demonstrates poor macrophage escape and cell-to-cell spread and produces smaller epithelial cell plaques. The inflammatory cytokines IL-8 and TNF-α show similar responses to both pathogens but EIEC activates ERK1/2 more strongly while producing weaker NF-κB signaling. The reduced virulence of EIEC stems from its weak expression of invasion-related genes and its limited capacity to affect host immune responses and signaling mechanisms.

Figure 1. Adherence mechanism of EIEC. (Govindarajan, 2020)

Core Virulence Factor of EIEC: pINV

It is widely acknowledged that, as in Shigella, in EIEC the critical event in the transition toward a pathogenic lifestyle has been the acquisition of a large F-type plasmid (pINV) which encodes the molecular machinery required for invasion, survival, and diffusion of the bacterium within the host. The genetic organization of the pINV is very complex. As a matter of fact these plasmids are made up of a mosaic of genes of various origins and harbor traces of four different plasmids. pINV isolated from EIEC share wide regions of high structural and functional homology and are interchangeable with those isolated from Shigella strains. In the pINV there is only one large (31 kb) region, which does not host any IS elements. This is the so-called entry region, which displays a PAI-like structure. It is composed by two large, divergently transcribed gene clusters coding for a T3SS apparatus (Mxi and Spa), for most of its effectors (IpaB, IpaC, and IpaD) with their chaperons (IpgA, IpgC, IpgE, and Spa15), and for two transcriptional regulators (VirB and MxiE), both required for the activation of most virulence genes. The entry region is extremely conserved among Shigella and EIEC pINV plasmids.

Figure 2. Genetic map of the pINV of Shigella and EIEC strains. (Pasqua, 2017)

Clinical Presentation

The stool shows signs of blood and mucoid appearance with leukocytes in abundance (dysentery) but some patients begin with watery diarrhea. The patient experiences fever and chills and malaise and abdominal cramps and occasional vomiting. The condition typically heals on its own within a few days but patients need oral or IV rehydration therapy for dehydration and electrolyte imbalances. The main complications of this disease include dehydration and electrolyte disturbances which can lead to shock in severe cases particularly among young children and elderly patients.

Laboratory Diagnosis

Practical diagnostic algorithm (commonly used in clinical labs)

Stool culture → confirm E. coli‑like colonies.

Real‑time PCR for ipaH (and optionally lacY to separate Shigella from EIEC) → rapid confirmation of invasive strain.

If ipaH‑positive → perform serotyping or multiplex PCR for additional virulence markers to characterize the isolate.

For outbreak or research → proceed to WGS for high‑resolution typing.

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Target	Cat. No.	Product Name	Host
E. coli	DAG-ZL0480	Inactivated Escherichia coli EIEC Culture Fluid	N/A	Inquiry