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Case report: Fatal hematogenous gastrosplenic mucormycosis in an immunocompetent adult following sigmoid perforation, septic shock, and short-term stress glucocorticoids

Sep 2026 · Frontiers in Fungal Biology · 0 citations · 29 references

Abstract

Mucormycosis is an aggressive angioinvasive fungal infection that predominantly affects chronically immunosuppressed individuals. Hematogenous dissemination of Mucorales causing synchronous gastric full-thickness perforation and total splenic infarction is exceptionally rare, particularly in immunocompetent hosts without chronic comorbidities. To our knowledge, this presentation has not been reported in a patient with only three days of stress-dose glucocorticoid therapy following sigmoid perforation and septic shock. We report a fatal case of synchronous gastric perforation and total splenic infarction secondary to hematogenous Mucorales dissemination in a previously healthy adult who developed septic shock from spontaneous sigmoid perforation. The patient received only three days of guideline-recommended stress-dose hydrocortisone and had no pre-existing diabetes, malignancy, or organ transplantation. Routine serum 1,3-β-D-glucan testing and peritoneal fungal cultures were both negative. Empirical micafungin, an echinocandin, was administered for eight days before liposomal amphotericin B was initiated, during which time progressive fungal angioinvasion led to irreversible multi-organ failure and death. Histopathology confirmed broad, aseptate, right-angle branching hyphae invading gastric and splenic vessels, whereas no fungal elements were detected at the primary sigmoid lesion, supporting a predominantly hematogenous dissemination pathway without primary intestinal fungal colonization – an unprecedented finding that fundamentally distinguishes this case from classic primary gastrointestinal mucormycosis. These histopathological findings are biologically consistent with the CotH3 (CotH family protein 3) – GRP78 (glucose- regulated protein 78 kDa) host–fungal virulence axis, which represents a plausible mechanistic explanation for multi-organ angioinvasion observed in this patient. This case delivers three critical clinical takeaways. First, even brief stress-dose glucocorticoids may induce sufficient transient immune paralysis to permit life-threatening hematogenous mucormycosis in patients without chronic underlying immunosuppression, acting as one potential contributing factor alongside sepsis-related critical-illness immune dysfunction. Second, empirical carbapenem plus echinocandin regimens, commonly used in ICUs, lack activity against Mucorales ; prolonged reliance on this combination can result in irreversible fatal visceral injury. Third, negative peritoneal fungal cultures and serum 1,3-β-D-glucan do not exclude intra-abdominal mucormycosis; early re-laparotomy for histopathological biopsy is essential in refractory cases.

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