CDIs are the leading cause of healthcare-associated diarrhea worldwide and surpass all other healthcare-associated infections in some countries [5, 6]. The incidence rates of CDI dramatically increased early in the 2000s with the emergence of the epidemic ribotype 027 strain of C. difficile. In the United States, the CDI incidence increased from 4.5/1000 adult discharges in 2001 to 8.2/1000 discharges in 2010 [7]. The death numbers per million population in the United States also increased from 8.2 in 2001 to 23.7 in 2004 [8]. After the peak of CDI before 2010, the rates of CDI have declined remarkably in England and other parts of Europe, and those in the United States have plateaued [1].
In contrast to the prevalence of ribotype 027 in North America and Europe, there have been fewer reports of CDI by ribotype 027 in Asia, where ribotypes 001, 002, 014, 017, and 018 are prevalent [9]. In Japan, the first academic reports of ribotype 027 CDI were described in 2007 [10, 11], which were followed by a few sporadic reports [12]. There have been no reports on its outbreak in Japan. The actual prevalence of ribotype 027 in Japan is difficult to determine, as ribotyping has rarely been performed clinically. Mori et al. investigated 975 stool culture samples from inpatients in a university hospital in Japan, in which 177 C. difficile isolates were recovered and 127 isolates were toxigenic and 12 were positive for the binary toxin gene. However, clinically important ribotypes such as 027 and 078 were not identified [13]. Ribotyping is very crucial for understanding the epidemiology in Japan. However, it remains unknown whether there are clinical benefits in the treatment of each case since there have been few reports of ribotype 027.
Our case may be quite rare in terms of CA infection as well as disease severity and clinical settings. Severe complications of CDI, such as megacolon, perforation, colectomy, shock requiring vasopressor therapy, and death, were reported to be associated with an age of at least 65 years, nosocomial infection, high peripheral leukocyte count, high creatinine level, initial antibiotic treatment, immunosuppression, and tube feeding [14]. Reported colectomy rates in hospitalized patients with CDI range from 0.3 to 1.3% during endemic periods and 1.8% to 6.2% during epidemic periods [15]. It is uncertain whether C. difficile ribotype 027 in Asia has similar virulence to that in North America or Europe. In the whole genomic analysis, two ribotype 027 strains isolated from two Chinese patients with CDI were outside of two distinct epidemic lineages of C. difficile ribotype 027 that emerged in North America, suggesting different features among those strains [16]. Cheng et al. summarized 19 cases of ribotype 027 in Asia, which included only two cases of fulminant CDI [17].
Although CDI is classically considered a hospital-acquired infection, CA CDI has become an increasing public health threat. Previous reports suggested that substantial fractions of CDI cases were acquired in the community [5, 18, 19]. It was reported that 40% of patients with CA CDI required hospitalization, 20% had severe infection, 4.4% had severe complications, 20% ended up with treatment failure, and 28% had recurrent CDI [20]. The sources of and risk factors for CA CDI have not been well defined [1]. An analysis of 984 patients with CA CDI during 2009–2011 showed that a substantial proportion of patients did not have possible risk factors such as antibiotic exposure (18%) and proton pump inhibitors (31%) [21]. Moreover, related academic societies have reported that H. pylori triple-therapy is associated with CDI with an incidence of approximately 1% [22]. Our case had the risk of antibiotic exposure, the most important modifiable risk factor for CDI development [1, 22] 4 weeks before onset. The duration between drug administration and CDI onset seems to be reasonable, as the highest risk of CDI (seven- to tenfold increase) was observed during antibiotic therapy and in the first month after cessation of the therapy [23]. Another possible risk factor in our case was the use of stomach-acid suppressants although its role in CDI remains controversial [1, 19].
Emergency surgery is often required for fulminant CD colitis. The reasons are refractory cases, massive bleeding, paralytic ileus, sepsis, multiple organ failure, toxic megacolon and intestinal perforation [24]. Early surgical intervention is required in treatment-refractory cases because these complications increase the fatality rate. Lee et al. examined predictors of mortality after emergency colectomy for CD colitis and listed age > 80, preoperative septic shock, preoperative severe COPD, preoperative dialysis dependence, postoperative cardiac arrest, intraoperative wound infection, PLT count (× 103/mm3) < 150, INR > 2, and BUN (mg/dL) > 40 as risk factors [25]. Therefore, our case was at high risk of mortality because she was in septic shock before surgery. According to the Infectious Diseases Society of America (IDSA) guidelines, the first-line treatment for fulminant CD enteritis is vancomycin administered orally. Moreover, if the patients become severe, subtotal colectomy with preservation of the rectum is strongly recommended [26]. Indeed, it is very important to diagnose and treat CD enteritis at an early stage, but If the condition becomes severe, immediate surgical intervention should not be hesitated.