Ulcerative colitis (UC) demonstrates a bimodal incidence distribution, with a significant second peak and the highest prevalence observed in individuals aged ≥60 years. The pathogenesis of elderly UC involves immunosenescence-manifested by Th17/Treg imbalance and the accumulation of cells with a pro-inflammatory senescence-associated secretory phenotype (SASP)-alongside age-related dysbiosis, increased intestinal permeability, and mitochondrial dysfunction that impairs mucosal regeneration. Clinically, older patients more frequently present with left-sided colitis, characterized by anemia and weight loss, while abdominal pain is less common. Managing geriatric UC is challenging due to inadequate colonoscopy preparation and complex differential diagnosis (e.g., colorectal cancer, ischemic colitis). Furthermore, older adults face a fivefold increased risk of Clostridioides difficile infection and a sharply rising risk of colorectal cancer if diagnosed after 70 years of age. While 5-aminosalicylic acid remains the first-line therapy, it requires renal monitoring. Conversely, steroids increase infection and osteoporosis risks, thiopurines are restricted due to myelotoxicity and malignancy risks, and among biologics, vedolizumab offers better safety than anti-TNF agents. Ultimately, managing UC in older adults requires a comprehensive, multidisciplinary approach that accounts for multimorbidity, polypharmacy, nutritional status, and mental health to optimize pharmacotherapy and mitigate high-risk surgical interventions.

Clostridioides difficile infection (CDI) remains a major cause of antibiotic-associated colitis and is characterized by excessive intestinal inflammation, epithelial barrier disruption and impaired mucosal repair. Although sodium butyrate (NaB), a microbiota-derived short-chain fatty acid, has demonstrated anti-inflammatory and barrier-protective properties, the immunological mechanisms underlying its protective effects during CDI remain incompletely understood. In this study, we investigated the role of NaB in regulating macrophage polarization and epithelial repair using murine CDI models, primary bone marrow-derived macrophages, THP-1-derived macrophages, Caco-2 epithelial cells and macrophage-epithelial co-culture systems. NaB treatment significantly alleviated CDI-associated weight loss, colonic shortening, histopathological injury and inflammatory cytokine production while restoring epithelial barrier integrity and tight junction protein expression. Mechanistically, NaB promoted macrophage polarization towards an anti-inflammatory M2 phenotype, characterized by increased CD206 and IL-10 expression and reduced CD86 and IL-1β expression. These immunomodulatory effects were accompanied by suppression of PI3K/Akt/mTOR signalling in both colonic tissues and macrophages. Pharmacological inhibition and activation studies further supported the involvement of this pathway in NaB-mediated macrophage reprogramming. Importantly, conditioned medium from NaB-treated macrophages enhanced epithelial viability, migration and barrier-associated protein expression, whereas IL-10 neutralization partially abolished these protective effects, highlighting a critical role for macrophage-epithelial crosstalk. Collectively, our findings demonstrate that low-dose NaB protects against CDI-induced intestinal injury through coordinated regulation of macrophage polarization and epithelial barrier repair, at least in part via modulation of PI3K/Akt/mTOR signalling. These results identify NaB as a promising host-directed therapeutic strategy for CDI and provide new insights into microbiota-derived metabolite-immune interactions during intestinal inflammation.

Clostridioides difficile is an important opportunistic pathogen mainly linked to healthcare-associated infections, which arise when the intestinal microbiota is disrupted - most often due to antibiotic treatment. In recent years, however, its presence in the community has been reported more frequently. The incidence of C. difficile infection reflects both the quality of antibiotic policies and the rigor of infection control, while mortality remains substantial, especially among the elderly and patients with multiple comorbidities. The pathogenesis of the disease is based on the production of toxins A and B, which damage the intestinal epithelium and lead to the development of manifestations ranging from mild diarrhea to fulminant colitis. Diagnosis requires correlation of the clinical presentation with evidence of a toxigenic strain or its toxins while colonization alone, without clinical symptoms, is not an indication for treatment. The high rate of recurrence remains a significant problem. A rational antibiotic policy and strict hygiene measures play a crucial role in prevention. The treatment of C. difficile infection has undergone a significant shift in recent years. Current recommendations favor fidaxomicin as the first-line treatment for the initial episode due to a lower risk of recurrence; oral vancomycin is an alternative. For recurrent forms, an individualized approach is necessary, including the possibility of using fecal microbiota transplant or monoclonal antibodies. In the Czech Republic, oral vancomycin is still widely used; it is now also available in a standardized capsule form, which improves pharmaceutical safety and facilitates dosing. Keywords: Clostridioides difficile, fidaxomicin, oral vancomycin, antimicrobial stewardship.

Clostridioides difficile is a gram-positive, anaerobic bacteria that is ubiquitous. Oral-fecal transmission of the organism and its spores leads to C difficile colonization and infection (CDI) within the human gastrointestinal tract. Patients with inflammatory bowel disease (IBD) are more likely to be colonized with C difficile, develop CDI, and experience recurrence when compared to the general population. The biggest challenge of managing CDI in IBD remains diagnostic uncertainty and relies on clinicians' judgment.

Severe and fulminant Clostridioides difficile infection (CDI) represent distinct clinical entities that portend poor outcomes and require close monitoring and multidisciplinary management. Early recognition is key, and CDI-directed antimicrobials are the mainstay of therapy. If patients fail to improve despite maximal medical therapy, fecal microbiota transplantation (FMT) or surgical intervention should be considered. If FMT is performed, repeated dosing is often required. Surgical interventions such as colectomy or loop ileostomy are necessary in FMT nonresponders or those who have developed a complication such as perforation.

Clostridioides difficile is a gram-positive bacterium and major cause of infectious colitis, in hospital and health care settings, where it remains a significant public health threat. Accurate diagnosis of C difficile infection (CDI) is challenging and requires a clinical assessment supported by laboratory stool testing. Reliance on laboratory tests can lead to both overdiagnosis and underdiagnosis. This article outlines the pathophysiology of C difficile, with emphasis on aspects related to diagnostic testing, and discusses the clinical approach to clinical diagnosis. New therapies for the treatment and prevention of CDI all rely on accurate clinical and laboratory identification of true infection.

The rising incidence of pediatric Clostridioides difficile infection (CDI), particularly in medically complex patients, calls for novel, individualized treatments. While fecal microbiota transplantation (FMT) is well-described for recurrent CDI, this report describes the first pediatric case of fulminant CDI with toxic megacolon successfully treated with FMT. This critically ill patient experienced failure of standard-of-care antibiotics and was a poor surgical candidate due to neutropenia and abdominal radiation for rhabdomyosarcoma. Ultimately, FMT rapidly resolved the patient's symptoms without adverse events. FMT should be considered for pediatric fulminant CDI.