COVID-19 and Fulminant Clostridium difficile Colitis Co-Infection

The development of Clostridium difficile infection in COVID-19 patients is an understudied complication of the disease. Herein, we present the case of a 46-year-old man who developed severe healthcare-associated C. difficile infection leading to toxic megacolon and perforation in the setting of COVID-19 infection. It is important to continue to follow guidelines regarding antibiotics in healthcare settings to prevent such complications.

Severe Constipation in a Wheelchair-Bound, Elderly Woman

Constipation is a common household word. Effective remedies in most cases are also simple household remedies such as over-the-counter medicines, lifestyle modification, and a high fiber diet. In the hospital setting, constipation is multifactorial, with multiple etiologies explained in this case study. Complications can lead to abdominal pain and more serious complications like ischemic bowel, toxic megacolon, perforation, and even death. Causes of serious complications include diabetic gastroparesis, paralytic ileus, or surgical adhesions. These are explored in the paper and gives the reader a deeper realistic medical insight into the seriousness of the situation. Osteopathic techniques to treat constipation are discussed and demonstrated to the caregiver with great response.

Clostridioides difficile exploits toxin-mediated inflammation to alter the host nutritional landscape and exclude competitors from the gut microbiota

Clostridioides difficile is a bacterial pathogen that causes a range of clinical disease from mild to moderate diarrhea, pseudomembranous colitis, and toxic megacolon. Typically, C. difficile infections (CDIs) occur after antibiotic treatment, which alters the gut microbiota, decreasing colonization resistance against C. difficile. Disease is mediated by two large toxins and the expression of their genes is induced upon nutrient depletion via the alternative sigma factor TcdR. Here, we use tcdR mutants in two strains of C. difficile and omics to investigate how toxin-induced inflammation alters C. difficile metabolism, tissue gene expression and the gut microbiota, and to determine how inflammation by the host may be beneficial to C. difficile. We show that C. difficile metabolism is significantly different in the face of inflammation, with changes in many carbohydrate and amino acid uptake and utilization pathways. Host gene expression signatures suggest that degradation of collagen and other components of the extracellular matrix by matrix metalloproteinases is a major source of peptides and amino acids that supports C. difficile growth in vivo. Lastly, the inflammation induced by C. difficile toxin activity alters the gut microbiota, excluding members from the genus Bacteroides that are able to utilize the same essential nutrients released from collagen degradation.