###### Abstract
Given the absence of specific treatment protocols for PI-IBS, typically symptoms are addressed based on the subtype of IBS present [16]. Although certain treatment approaches like mesalamine, corticosteroids and glutamine have been explored directly in the context of PI-IBS, the prevailing guidelines for management are derived from general strategies employed in treating IBS [10]. This approach emphasizes the need for symptom-based treatment plans, highlighting the gap in targeted therapies for PI-IBS. IBS affects 10-20% of the population, with around 10% of individuals developing PI-IBS following a _C. jejuni_ infection [1; 17]. Delineating the specific pathmechanisms underlying PI-IBS is challenging, especially due to the combinations of its various forms [1; 17]. In 2019, due to the absence of sensitive and specific markers for diagnosis, the Rome Foundation Working Group introduced symptomatic diagnostic criteria for PI-IBS, leveraging the Rome IV guidelines [7]. They characterized PI-IBS as an intricate and multifactorial condition underpinned by various potential mechanisms, including altered visceral motility, increased visceral sensitivity, microbiome variations, changes in intestinal permeability, immune system dysregulation, chronic low-grade inflammation, enteroendocrine pathway alterations, affected neuromuscular function, post-infectious dyspepsia and genetic factors [18; 19]. Persistent inflammation underpins many IBS symptoms, with mucosal inflammation affecting the enteric nervous system's function [20]. This initiates a series of reactions within the mucosa and submuc, including the activation of visceral hypersensitivity, disrupted motor functions and a reduction in phase III inter-digestive waves, all contributing to the development of small intestinal bacterial overgrowth [20]. The reported incidence of PI-IBS stands at \(\approx\)20% under the Rome III criteria, whereas the Rome IV criteria suggest a slightly lower incidence rate of between 10% and 12.8% [18]. Based on the predominant bowel pattern, as measured by the Bristol stool scale, PI-IBS classificationswere proposed, including most common mixed (IBS-M), diarrhea-dominant (IBS-D) and constipation-dominant (IBS-C) [1,7,17]. Beyond the three primary clinical forms, additional research has identified three distinct variants of IBS: pain-predominant IBS (P-IBS), PI-IBS and post-diverticulitis (IBS-PD). Any other gastrointestinal symptoms fitting the IBS profile are classified as unclassified (IBS-U) under the ROME III diagnostic criteria [21]. A bowel pattern qualifies as predominant if it accounts for \(\geq\)25% of bowel movements and is categorized as hard/lumpy (indicative of IBS-C), loose/watery (suggestive of IBS-D) or a combination of both (referred to as IBS-M) [7]. Patients with PI-IBS are more inclined to exhibit a diarrhea-predominant pattern compared to those with sporadic IBS. Identifying the specific PI-IBS subtype associated with each patient is critical in guiding disease management and therapeutic interventions. The impact of chronic gastrointestinal symptoms following an infection may surpass the scope of what the Rome criteria define [10]. Recently, [PERSON] et al., 2021 highlighted that, beyond a 21% prevalence of PI-IBS post-_Campylobacter_ enteritis, an additional 9% of individuals experienced new-onset abdominal pain and bowel irregularities yet did not fulfill the Rome criteria for IBS diagnosis [14]. Furthermore, GI infections not only prompt the onset of new IBS cases but can also alter the phenotype of preexisting IBS conditions. Notably, about half of the individuals with IBS-C transitioned to either IBS-M or IBS-D following an episode of _Campylobacter_ enteritis [14]. In a cohort study, researchers found that IBS developed in 301 out of 1418 patients with culture-confirmed _Campylobacter_ infections [14]. This finding is significant because it relies on culture-confirmed cases, offering a more accurate representation of the prevalence of PPI-IBS following a _Campylobacter_ infection.