A Rare Case of Pseudomembranous Colitis Presenting with Pleural Effusion and Ascites with Literature Review

Clostridium difficile infection usually results from long-term and irregular antibiotic intake. The high-risk individuals for this infection include the patients undergoing chemotherapy due to malignancy, immunocompromised patients, and hospitalized patients receiving broad-spectrum antibiotics. The most common clinical manifestation of Clostridium difficile infection is diarrhea. However, pleural effusion and ascites have rarely been observed. As mentioned, these manifestations can be developed in a patient being treated with broad-spectrum antibiotics. Therefore, the present study reports a rare case of Clostridium difficile infection manifesting with these rare manifestations who was a 78-year-old female patient with a history of COVID-19, orthopedic surgery, and antibiotic treatment with cefixime and gentamicin.

Production of p-cresol by Decarboxylation of p-HPA by All Five Lineages of Clostridioides difficile Provides a Growth Advantage

Clostridioides difficile is the leading cause of antibiotic-associated diarrhea and is capable of causing severe symptoms, such as pseudomembranous colitis and toxic megacolon. An unusual feature of C. difficile is the distinctive production of high levels of the antimicrobial compound para-cresol. p-Cresol production provides C. difficile with a competitive colonization advantage over gut commensal species, in particular, Gram-negative species. p-Cresol is produced by the conversion of para-hydroxyphenylacetic acid (p-HPA) via the actions of HpdBCA decarboxylase coded by the hpdBCA operon. Host cells and certain bacterial species produce p-HPA; however, the effects of p-HPA on the viability of C. difficile and other gut microbiota are unknown. Here we show that representative strains from all five C. difficile clades are able to produce p-cresol by two distinct mechanisms: (i) via fermentation of p-tyrosine and (ii) via uptake and turnover of exogenous p-HPA. We observed strain-specific differences in p-cresol production, resulting from differential efficiency of p-tyrosine fermentation; representatives of clade 3 (CD305) and clade 5 (M120) produced the highest levels of p-cresol via tyrosine metabolism, whereas the toxin A-/B+ isolate from clade 4 (M68) produced the lowest level of p-cresol. All five lineages share at least 97.3% homology across the hpdBCA operon, responsible for decarboxylation of p-HPA to p-cresol, suggesting that the limiting step in p-cresol production may result from tyrosine to p-HPA conversion. We identified that elevated intracellular p-HPA, modulated indirectly via CodY, controls p-cresol production via inducing the expression of HpdBCA decarboxylase ubiquitously in C. difficile populations. Efficient turnover of p-HPA is advantageous to C. difficile as p-HPA has a deleterious effect on the growth of C. difficile and other representative Gram-negative gut bacteria, transduced potentially by the disruption of membrane permeability and release of intracellular phosphate. This study provides insights into the importance of HpdBCA decarboxylase in C. difficile pathogenesis, both in terms of p-cresol production and detoxification of p-HPA, highlighting its importance to cell survival and as a highly specific therapeutic target for the inhibition of p-cresol production across C. difficile species.

Bacteremia after Bacillus clausii administration for the treatment of acute diarrhea: A case report

Bacillus clausii is a gram-positive rod used as a probiotic to treat diarrhea and the side effects of antibiotics such as pseudomembranous colitis. We report a case of B. clausii bacteremia in a non-immunocompromised patient with active peptic ulcer disease and acute diarrhea. The probiotic was administered during the patient´s hospitalization due to diarrhea of infectious origin. B. clausii was identified in the bloodstream of the patient through Matrix-Assisted Laser Desorption Ionization-Time of Flight (MALDI-TOF) days after her discharge.Given the wide use of probiotics, we alert clinicians to consider this microorganism as a causative agent when signs of systemic infection, metabolic compromise, and hemodynamic instability establish after its administration and no pathogens have been identified that could explain the clinical course.

Pseudomembranous colitis after COVID-19 antibacterial therapy

A new coronavirus infection poses a challenge to infectious disease specialists, health care administrators, and subspecialty physicians in the search for the most eff ective treatment options. The past year has allowed us to clarify the main aspects of pathogenesis with a focus on the most severe versions of the COVID-19 course. Most signifi cant is to understand that the severe course is associated with prolonged viremia and T-cell lymphocyte defi ciency leading to activation of innate immunity, manifested by a burst of macrophage activity known as the “cytokine storm”. This inadequate response is a major factor in both pulmonary and multiple organ failure. Fever, pulmonary infi ltrates with leukocytosis and neutrophilia are traditionally perceived by doctors as indications for antibiotic therapy, which is nevertheless erroneous in the absence of signs of bacterial infection. We present a case that illustrates the severe course of pseudomembranous colitis and secondary myocarditis in an elderly woman with comorbid pathology and massive antibiotic therapy received during hospitalization for COVID-19.