Gastrointestinal Mucormycosis: An Evolving Disease

Brad Spellberg, MD

Mucormycosis of the Intestine: A Rare Complication in Crohn’s Disease

Jordan Morton, MD1 
Vincent Nguyen, MD1
Tauseef Ali, MD2 

1Department of Internal Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma; 2Department of Internal Medicine, Section of Digestive Diseases and Nutrition, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 

Address correspondence to: Dr. Tauseef Ali, Section of Digestive Diseases and Nutrition, University of Oklahoma Health Sciences Center, 1345 WP. 920 SL Young Blvd., Oklahoma City, OK 73104; E-mail:

Mucormycosis is a rare fungal infection caused by fungi of the order Mucorales, with most cases caused by Rhizopus or Mucor species. The ubiquitous organisms responsible for infection can be found in decaying vegetation and soil.1 These rapidly growing fungi produce spores that can easily become airborne. Thus, most individuals have ample exposure to the fungi, with most cases of infection occurring in immunocompromised hosts. Risk factors for infection include diabetes mellitus, diabetic ketoacidosis, neutropenia, corticosteroid use, hematologic malignancies, bone marrow or solid organ transplantation, treatment with deferoxamine, iron overload, AIDS, intravenous drug use, and malnutrition.2 Infection can be rhinocerebral, pulmonary, cutaneous, gastrointestinal, renal, or disseminated; gastrointestinal infection comprises only 7% of reported cases.3 This report presents a rare case of gastrointestinal mucormycosis following treatment with corticosteroids in the setting of inflammatory bowel disease.

Case Report 

A 38-year-old white female was diagnosed with Crohn’s disease in February 2010 when she presented to a local hospital with a 9-month history of abdominal pain and diarrhea. A colonoscopy revealed moderately severe, ulcerative, ileocolonic Crohn’s disease. Her primary gastroenterologist placed her on 40 mg oral prednisone and mesalamine (1,600 mg twice daily). She had been smoking 1.5 packs of cigarettes daily for the past 19 years. Her mother also had Crohn’s disease. The patient was continued on prednisone at a dose of 40 mg for 2 months, after which she presented to our facility with worsening abdominal pain, hypotension, and sepsis. Her leukocyte count was 28,000/mm3 with 95% neutrophils, and her hemoglobin level was 8.5 g/dL. A computed tomography scan revealed dilated small bowel loops with oral contrast leaking into the peritoneum. An emergency laparotomy was performed, and the patient was found to have a perforated cecum at the level of the ileocecal valve, leading to a temporary cecostomy secondary to dense inflammation and adherent loops of bowel. One week later, she underwent repeat surgery for an end ileostomy with resection of the cecum and terminal ileum. The surgical specimen revealed chronic active inflammation, ulceration, and serositis with fibrinopurulent exudate. Grocott methenamine silver staining was positive for fungal organisms with ribbon-like morphology suggestive of mucormycosis (Figure 1). The glandular structures of the colon demonstrated architectural changes compatible with the patient’s history of inflammatory bowel disease. Results of acid-fast bacillus staining were negative. The patient was treated with liposomal amphotericin B at a dose of 500 mg daily for 1 month followed by posaconazole (Noxafil, Schering) at a dose of 400 mg twice daily for 1 month, with gradual improvement in her clinical condition.


The pathogenesis of mucormycosis is related to immunocompromised states or immune suppression. With mononuclear and polymorphonuclear phagocytes acting as the main host defense against the Mucorales order, individuals with hematologic malignancies, neutropenia, corticosteroid use, and/or diabetes are at increased risk for infection.2 In patients with diabetic ketoacidosis, the acidic, hyperglycemic environment leads to impaired chemotaxis of neutrophils and interferes with the ability of transferrin to bind iron, a necessary growth factor for fungi.1,2 Therefore, mucormycosis is most commonly identified in individuals with impaired host defenses or increased availability of serum iron.

Gastrointestinal mucormycosis is rare and is thought to be secondary to ingestion of fungi.2,3 Within the gastrointestinal tract, the stomach is the most common site of infection, followed by the colon, ileum, duodenum, and jejunum.4 Symptoms vary by site of infection, with nonspecific abdominal pain, distention, nausea, and vomiting being the most common symptoms. Due to the high likelihood of bowel perforation, it is of utmost importance to begin empiric treatment with a polyene antifungal drug while diagnostic testing is being performed if clinical suspicion of mucormycosis is high.4

Because mucormycosis is generally limited to individuals with underlying defects in host immunity, specifically impaired phagocytic function, patients with Crohn’s disease are particularly vulnerable to this infection. This vulnerability is due to both the underlying physiology of Crohn’s disease itself, which has been proposed to result from impaired innate immunity, as well as the use of immunosuppressive agents in Crohn’s disease treatment, such as corticosteroids and agents that block tumor necrosis factor–a.5-8

Six case reports have described the development of mucormycosis in the setting of inflammatory bowel disease with immunosuppressant therapy (Table 1). One case reported mucormycosis of the sinus in a patient receiving infliximab (Remicade, Janssen Biotech) for ileocecal Crohn’s disease.9 This patient had been receiving both low-dose azathioprine and infliximab for treatment of Crohn’s disease when a sinus biopsy revealed mucormycosis. After administration of amphotericin B and posaconazole and discontinuation of all immunosuppressive agents, laboratory and imaging studies demonstrated clearance of the infection.

Similarly, gastrointestinal mucormycosis presenting as recurrent gastric perforation was reported in a patient with Crohn’s disease who was receiving glucocorticoids, 6-mercaptopurine, and infliximab.10 In this case, because the recurrent perforations were thought to be due to active Crohn’s disease, treatment with amphotericin B was delayed, and the patient suffered from multiorgan system failure and subsequent death.

The third case occurred following treatment of pyoderma gangrenosum in the setting of inflammatory bowel disease in a patient who developed a peristomal cutaneous rhizopus infection; this patient was successfully treated with sequential liposomal amphotericin B
and itraconazole.11

The fourth case occurred in a patient with Crohn’s disease who was being treated with corticosteroids and azathioprine; this patient was admitted due to peritonitis following an intestinal perforation. After initial treatment with voriconazole, resolution of the infection was complicated by recurring peritonitis resulting from necrosis and perforation of the left colon, which ultimately led to death. Microscopic examination of the peritoneal fluid revealed the presence of broad, irregular hyphae, and culture of this fluid yielded Rhizopus microsporus.12

The fifth case of mucormycosis in a patient with inflammatory bowel disease who was being treated with immunosuppressant therapy describes a case of mucormycosis endocarditis in an immunocompromised patient with ulcerative colitis whose condition was further complicated by multiple septic emboli to the lungs. The patient was managed with surgical excision of the right atrial endocarditic vegetation and antifungal treatment with high-dose liposomal amphotericin B.13

The last case occurred in a 60-year-old male who had recently been diagnosed with inflammatory bowel disease and was treated with total parenteral nutrition, oral sulfasalazine, intravenous methylprednisolone, and oral 6-mercaptopurine. Several weeks later, he developed abdominal pain and bloody diarrhea and subsequently underwent a laparotomy, which found invasion of the colon and kidney by Absidia corymbifera. The patient was treated with a low dose of amphotericin B; unfortunately, the case was complicated by multiorgan failure and eventually death.14

Diagnosis of mucormycosis can be based on either growth of the mold on culture or histopathologic demonstration on biopsy of aseptate, wide, ribbon-like hyphae that branch at right angles.1,2 However, due to the difficulty of growing organisms from tissue culture, biopsy with histologic identification remains the preferred mode of diagnosis.1

Treatment for mucormycosis consists of both surgical debridement of necrotic material and administration of liposomal or lipid-based formulations of amphotericin B.2 Depending on the site of infection, surgical debridement may not be possible or plausible, as in cases of disseminated disease. Adjunctive treatment options such as use of nonsiderophore iron chelators, hyperbaric oxygen, or cytokine therapy with either g interferon or colony-stimulating factor are being investigated, but these methods have not yet proven to be more beneficial than standard treatment with surgery and amphotericin B.4,15

Although the survival rate for patients with mucormycosis is approximately 50%, mortality can be as high as 100% in cases of disseminated disease.2 In patients with high clinical suspicion of mucormycosis, therefore, the importance of early diagnosis, correction of underlying risk factors, and treatment cannot
be overemphasized.


1. Kauffman CA, Malani AN. Zygomycosis: an emerging fungal infection with new options for management. Curr Infect Dis Rep. 2007;9:435-440.

2. Spellberg B, Edwards J Jr, Ibrahim A. Novel perspectives on mucormycosis: pathophysiology, presentation, and management. Clin Microbiol Rev. 2005;18:556-569.

3. Roden MM, Zaoutis TE, Buchanan WL, et al. Epidemiology and outcome of zygomycosis: a review of 929 reported cases. Clin Infect Dis. 2005;41:634-653.

4. Agha FP, Lee HH, Boland CR, Bradley SF. Mucormycoma of the colon: early diagnosis and successful management. Am J Roentgenol. 1985;145:739-741.

5. Lawrence IC, Radford-Smith GL, Bampton PA, et al. Serious infections in patients with inflammatory bowel disease receiving anti-tumor-necrosis-factor-alpha therapy: an Australian and New Zealand experience. J Gastroenterol Hepatol. 2010;25:1732-1738.

6. D’Haens G, Colombel JF, Hommes DW, et al. Corticosteroids pose an increased risk for serious infection: an interim safety analysis of the ENCORE registry. Gastroenterology. 2008;34(suppl):A-140.

7. Korzenik JR. Is Crohn’s disease due to defective immunity? Gut. 2007;56:2-5.

8. Vavricka SR, Rogler G. New insights into the pathogenesis of Crohn’s disease: are they relevant for therapeutic options? Swiss Med Wkly. 2009;139:527-534.

9. Wall GC, Leman BI. Mucormycosis in a Crohn’s disease patient treated with infliximab. Digestion. 2009;80:182-184.

10. Devlin SM, Hu B, Ippoliti A. Mucormycosis presenting as recurrent gastric perforation in a patient with Crohn’s disease on glucocorticoid, 6-mercaptopurine, and infliximab therapy. Dig Dis Sci. 2007;52:2078-2081.

11. Hunter AJ, Bryant RE. Abdominal wall mucormycosis successfully treated with amphotericin and intraconazole. J Infect. 2002;44:203-204.

12. Hyvernat H, Dunais B, Burel-Vandenbos F, Guidicelli S, Bernardin G, Gari-Toussaint M. Fatal peritonitis caused by Rhizopus microsporus. Med Mycol. 2010;48:1096-1098.

13. Gubarev N, Separovic J, Gasparovic V, Jelic I. Successful treatment of mucormycosis endocarditis complicated by pulmonary involvement. Thorac Cardiovasc Surg. 2007;55:257-258.

14. Ibañez R, Serrano-Heranz R, Sánchez-Zaballos I, Carbonero P, López G. Disseminated mucormycosis due to Absidia corymbifera in a patient with inflammatory bowel disease. Clin Microbiol Infect. 1997;3:268-270.

15. Boelaert JR, Van Cutsem J, de Locht M, Schneider YJ, Crichton RR. Deferoxamine augments growth and pathogenicity of Rhizopus, while hydroxypyridinone chelators have no effect. Kidney Int. 1994;45:667-671.


Gastrointestinal Mucormycosis: An Evolving Disease

Brad Spellberg, MD

Division of General Internal Medicine, Los Angeles Biomedical Institute at Harbor-UCLA Medical Center, Torrance, California; David Geffen School of Medicine at UCLA, Los Angeles, California 

Address correspondence to: Dr. Brad Spellberg, 1124 W. Carson St. RB3, Torrance, CA 90502; Tel: 310-781-3680; E-mail:

Mucormycosis is a life-threatening infection caused by fungi of the subphylum Mucoromycotina, order Mucorales.1 Traditional risk factors for the development of invasive mucormycosis include diabetes, defects in host phagocytes, corticosteroid use, organ or stem cell transplantation, and increased levels of available serum iron as a result of acidosis or administration of deferoxamine.2-4 In recent years, the disease has also increasingly been described in patients without traditional risk factors.2

Mucormycosis can affect any organ system, but the most common presentations involve either the nasal sinuses, orbit, and brain (rhino-orbital-cerebral) or the lung. For many years, gastrointestinal mucormycosis was quite rare, especially in industrialized nations. However, there has been a substantial increase in the number of cases of gastric and gastrointestinal mucormycosis indexed on PubMed over the past 2 decades, particularly over the past decade. For example, a PubMed search for the title words “gastric” or “gastrointestinal” and “mucormycosis” or “zygomycosis” revealed 8 publications from 1959–1989 (31 years), 23 publications from 1990–1999 (10 years), and 50 publications from 2000–2011 (12 years).

The stomach is the most common site of gastrointestinal mucormycosis, followed by the colon and ileum. In the past, gastrointestinal mucormycosis was seen primarily in premature neonates, often in association with widespread disseminated disease.5-12 For example, necrotizing enterocolitis has been described largely in premature neonates and, more rarely, in neutropenic adults.8,9,13-20 Other rare cases of gastrointestinal mucormycosis were previously described in association with other immuno-compromising conditions, including AIDS, systemic lupus erythematosus, and organ transplantation.21-26 Cases of hepatic mucormycosis have also been associated with ingestion of herbal medications.27 Because this infection is acute and rapidly fatal, it is often diagnosed postmortem.

The symptoms of gastrointestinal mucormycosis are varied and depend on the affected site. Nonspecific abdominal pain and distention associated with nausea and vomiting are the most common symptoms. Fever and hematochezia may also occur. The patient is often thought to have an intra-abdominal abscess. The diagnosis may be made by biopsy of the suspected area during surgery or endoscopy. Recently, an iatrogenic outbreak of gastric mucormycosis occurred due to contamination of wooden applicators that were used to mix drugs for patients with nasogastric feeding tubes.28 These patients presented with massive gastric bleeds. The diagnosis was made by culturing gastric aspirates and the wooden tongue depressors.  This experience further underscores the alarming trend of increasing iatrogenic/nosocomial onset of mucormycosis.

As mentioned previously, older clinical literature (prior to 1990) primarily describes cases of mucormycosis in neonates and premature infants.15-18 During the 1990s, cases were predominantly described in patients receiving immunosuppressant medications due to solid organ transplantation.23,24,29,30 While such cases continue to be described in the 21st century, a substantial proportion of the cases described since 2000 have occurred in more widely disparate patient populations; these patients may have risk factors such as diabetes mellitus or corticosteroid use, a gastric or peptic ulcer that apparently became infected with the fungi, or no predisposing risk factors.4,31-37

The case reported by Morton and colleagues is typical of the increasing experience with this illness in the 21st century.38 This patient had preexisting gastrointestinal mucosal ulcerations due to her underlying Crohn’s disease, and she was immunosuppressed due to her corticosteroid therapy. When she presented with her perforation, there was no specific reason to suspect mucormycosis; indeed, the disease was much less likely than more typical causes of colonic perforations in such patients. Only the appearance of the fungi on histopathology caused the diagnosis to be made and appropriate therapy to be initiated. Thus, this case highlights the need to maintain a high index of suspicion for invasive fungal infections, including mucormycosis, in patients who are being treated with corticosteroids and who present with disease that crosses tissue planes.

The need to make a rapid diagnosis is underscored by recent data from the oncology setting, in which initiation of polyene antifungal therapy within 6 days of presentation was strongly associated with improved survival.39 There have been no prospective randomized trials to define the optimal antifungal therapy for mucormycosis. Nevertheless, primary antifungal therapy for mucormycosis should be based on a polyene antifungal agent, as this drug class is by far the most active against the relevant pathogens. Most experts prefer to use lipid formulations of amphotericin B, which can be administered at higher doses and with less toxicity than amphotericin B deoxycholate.3 The role of combination therapy in mucormycosis remains unclear, although data from mouse studies and concordant retrospective data in humans suggest that combining lipid polyenes with echinocandins may improve outcomes.3 Additional research is needed to confirm this hypothesis in prospective trials.

Antifungal therapy alone is typically inadequate to control mucormycosis, and surgery to debulk the fungal infection and/or resect all infected tissue is often required to effect cure. Aside from the resistance of some fungal strains to amphotericin B, several hallmark features of mucormycosis—including angioinvasion, thrombosis, and tissue necrosis—result in poor penetration of anti-infective agents to the site of infection. Therefore, even if the causative organism is susceptible to the antifungal agent in vitro, the antifungal agent may be ineffective in vivo. In a logistic regression model, surgery was found to be an independent variable for favorable outcomes in patients with mucormycosis.2 Furthermore, in multiple case series, patients who did not undergo surgical debridement of mucormycosis had a far higher mortality rate than patients who underwent surgery.40-48 While there is potential selection bias in these case series—patients who did not undergo surgery likely differed in disease severity and/or comorbidities from those who did undergo surgery—these data support the concept that surgical debridement is necessary to optimize cure rates. Finally, immunosuppressive medications, particularly corticosteroids, should be dose-reduced or stopped if at all possible.

Given the increasing incidence of cancer in the aging US population, an ongoing epidemic of obesity and diabetes, and the increasing population of patients receiving corticosteroid therapy for inflammatory diseases and/or solid organ or stem cell transplantation, it is not surprising that recent studies have reported alarming increases in the incidence of mucormycosis.49-51 Clinicians will likely continue to encounter this disease more frequently in the coming years, especially in the nosocomial setting. Further research is needed regarding new diagnostic and therapeutic modalities for these devastating infections. In the meantime, improvement in patient outcomes will require a high index of suspicion and emergent diagnostic evaluation to allow early initiation of antifungal and surgical therapy.


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