One rare cause of lower GI bleeding is GI mucormycosis. Mucormycosis is an opportunistic infection caused by fungi in the order of Mucorales(5). The low virulence of these organisms makes disease rare among immunocompetent individuals(6). However, prognosis among infected individuals are extremely poor, and mortality has been found to be associated with the site of infection(5). Most infected patients have underlying factors of compromised immunity, such as organ transplantation, malignancy, persistent neutropenia, poorly controlled diabetes mellitus and systemic corticosteroid therapy(7, 8).
Mucormycosis can manifest as different clinical syndromes: rhino-orbito-cerebral, pulmonary, cutaneous, gastrointestinal, disseminated, and uncommon presentations. Among these manifestations, gastrointestinal mucormoycosis is the rarest, making up only around 7% of all cases(6). Disease of the gastrointestinal tract is usually acquired through ingestion of contaminated food or device. Within the gastrointestinal tract, the stomach is the most common sight of infection, followed by the colon. Mortality of GI mucormyocosis has been reported to be as high as 85%(9). Patients often present with nonspecific symptoms such as abdominal pain, GI bleeding, change in bowel habits, and fever(5). It has been reported that the majority of patients presented with abdominal pain in the absence of fever(10). Nonspecific clinical presentation make diagnosis difficult and often delayed, and therefore contributes to the high mortality rate. It is estimated that less than half of the diagnosis of mucormycosis are made antepartum(8).
Definite diagnosis of mucormycosis is made by histopathological evidence of fungal invasion of tissue. Unlike aspergillosis, there is no reliable serological test for mucormycosis. In the case of GI mucormycosis, undergoing invasive endoscopy or even surgery is usually inevitable for diagnosis. A dark ulcer with sharp demarcated edges along with necrosis and thrombosis in the adjacent vessels is representative of a typical GI lesion(8). Endoscopic finding of a small, mushroom-like green mass with a small base attached to the colon wall has also been described in previous studies(11). Extended lesions can cause perforation, bleeding, and obstruction.
With the widespread availability of endoscopic techniques, early clinical suspicion and diagnosis as well as effective treatment are critical in reducing mortality. However, many patients with severe acute LGIB are unable to tolerate rapid colon preparation for diagnostic colonoscopy, making localization of lesions challenging due to poor visualization. Therefore, in immunocompromised patients such as those with DKA, organ transplantation, and malignancy, it is important to consider the possibility of GI mucormycosis. In cases with clinical suspicion but timely diagnosis cannot be made, prophylaxis antifungal treatment should not be delayed.
It is advised that treatment of mucormycosis include urgent surgical resection of infected area whenever feasible parallel to systemic antifungal therapy to prevent disease dissemination(7, 12). Liposomal amphotericin B is the recommended first line treatment for mucormycosis. Posaconazole has generally been recommended as maintenance and salvage therapy. However, Song et. al reported a higher survival rate in renal transplant patients with mucormycosis treated with Posaconazole compared to Amphotericin B(13). European Confederation of Medical Mycology 2019 guideline proposes the use of Posaconazole as first line treatment with moderate strength, especially in case of renal failure like our patient(14). Reversal of underlying problems is also fundamental to improve treatment outcome(7, 8). A study by Gebremariam et. al highlighted the importance of correcting acidemia in patients with ketoacidosis(15). For our patient, proper control of his diabetes mellitus and succession of alcohol drinking are of great importance.