Clostridium difficile infection in patients with inflammatory bowel disease

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ACHAIKI IATRIKI | 2020; 39(2): 60–62

Editorial

Nicoletta T. Karavasili1, Konstantinos H. Katsanos2, Dimitrios K. Christodoulou3

1 Infection Control Committee, University Hospital of Ioannina, Ioannina, Greece
2 Division of Gastroenterology, Faculty of Medicine, School of Health Sciences, University of Ioannina, Ioannina, Greece
3 Division of Gastroenterology, Faculty of Medicine, School of Health Sciences, University of Ioannina, Ioannina, Greece

Received: 7 March 2020; Accepted: 28 March 2020

Corresponding author: Nicoletta Karavasili, Infection Control Nurse, Infection Control Committee,University Hospital of Ioannina, Greece, Ionias Ave., 12 Ioannina, Greece. PC. 45221. mob.tel. +30 6945251997 fax: +30 2651099272, E- mail: nicolekaravasili@gmail.com

Key words: Clostridium difficile, inflammatory bowel disease, infections

 

Inflammatory boweldisease (IBD) includes two types of idiopathic intestinal disease, ulcerative colitis (UC) and Crohn’s disease (CD) that are distinguished by their location and depth of involvement in the bowel wall [1, 2]. The North American incidence of IBD ranges from 2.2 to 19.2 cases per 100,000 person-years for UC and 3.1 to 20.2 cases per 200,000 person-years for CD. IBD is much more prevalent in North America and Europe compared to Asia or Africa [3].

Clostridium difficile (C. difficile), a gram-positive anaerobic bacterium, constitutes the main cause of pseudomembranous colitis [4]. C. difficile infection (CDI) is a significant threat to the health of immunocompromised and hospitalized patients. UC patients are at high risk for CDI (3.7%), as well as patients with CD (1.1%). Most clinical trials for CDI have excluded patients with underlying diarrheal disorders such as IBD, creating an evidence gap in the management of IBD patients. The impact of CDI on these populations can be notable [5]. The diagnosis of CDI is based on the detection of toxin A/B on stool or detection of toxin A/B producing C. difficile on stool by polymerase chain reac­tion (PCR) or culture and pseudomembrane visualiza­tion at endoscopy [6].

Chronic use of antibiotics, corticosteroids and immunomodulators has been shown to increase the risk of CDI in patients with IBD [7, 8]. CDI can alter the natural course of IBD, leading to symptom worsening and longer disease duration. It is neces­sary for patients with IBD, hospitalized for flare signs and symptoms, to detect opportunistic agents such as C. difficile or pro­gression of the underlying IBD as causative agent of flare [9, 10]. The incidence of CDI in patients with IBD is relatively high considering the incidence rate of Healthcare Associated CDI in non-IBD population (67%) [11]. Recent studies report a CDI incidence of 7% among hospitalized adult inpatients with IBD [12]. Furthermore, the incidence of CDI in mixed IBD populations (inpatient and outpatient) ranges between 5.1%-16.7% [13].

There is significant uncertainty among clinicians regarding the initiation of corticosteroid therapy in the setting of suspected IBD flare in a patient with known CDI. Some previous studies have reported that CDI in patients with IBD may be associated with the use of steroids describing worse outcomes among IBD patients [14, 15]. A US study reported no association between the operative management and current steroids use among hospitalized patients with CDI, as well as no potential role of steroids in the treatment of CDI, although corticosteroids are a mainstay in the treatment of IBD [16]. A European study of 155 IBD patients hospitalized with CDI estimated the effects of combination antibiotic and immunomodulator therapy compared to antibiotics alone. Antibiotics and immunomodulators were associated with worse outcomes among IBD patients, with higher morbidity and mortality compared to antibiotic monotherapy [17].

In the setting of acute CDI in IBD patients, most recent AGA practice guidelines suggest postponing corticosteroids dose escalation for 72 to 96 hrs after the initiation of appropriate antibiotic regimen [18]. Additionally, in IBD patients with concomitant CDI, recent CDI guidelines suggest maintaining, but not escalating the dosage of current immunosuppressive therapy, including immunomodulators such as methotrexate, azathioprine and biologic agents [19]. In addition, CD4 T cells in general and Th17 cells in particular during CDI have emerged as potential therapeutic targets for IBD patients who are at risk for severe disease [20].

Conclusions

Clinicians should consider CDI with every flare of symptoms in patients with IBD. Surveillance and aggressive management including early detection and fast treatment of the infection, faecal transplant or colectomy will improve IBD outcome and preserve quality of life in such vulnerable patients. More data is needed on the impact that increased pathogenic Th17 responses will have on IBD patients; targeting these cells may ameliorate IBD symptoms and reduce the risk of developing severe CDI. Prediction tools will be gradually important in helping to identify at-risk patients, so that management can be tailored to individual patients as further preventive and treatment choices become available.

Conflict of interest disclosure

The authors have no conflict of interest to declare regarding this paper.

Declaration of funding sources

None to declare

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