Gómez-López D, Martínez-Manzo KA, Hernández-Reyes TI, Rodríguez-Kirwan S, Rivera-García MÁ, Gutiérrez-Ramírez JL

Language: Spanish
References: 16
Page: 98-105
PDF size: 1273.32 Kb.

ABSTRACT

Mucormycosis is a rare, highly destructive, and rapidly progressive invasive fungal infection caused by filamentous fungi of the order Mucorales, with Rhizopus arrhizus being the most prevalent species. It features an aggressive angioinvasive nature associated with severe morbidity and high mortality rates, particularly in immunocompromised individuals or those with uncontrolled diabetes mellitus. In vulnerable hosts, environmental sporangiospores evade immune clearance and adhere to epithelial cells via the interactions of fungal CotH surface proteins with host receptors (such as GRP78 and integrin α3β1). The hyphae then invade endothelial cells, secreting proteases and the toxin mucoricin, which induce vascular thrombosis, tissue infarction, and extensive necrosis. A critical driver of this pathogenesis is metabolic acidosis and hyperglycemia, which disrupt iron-binding proteins (transferrin and ferritin), markedly increasing free serum iron—a vital nutrient that upregulates fungal virulence and replication via specific ferroxidase systems. This clinical case of a 54-year-old male with a 20-year history of type 2 diabetes mellitus. The patient presented with rhino-orbital-facial mucormycosis triggered by severe euglycemic diabetic ketoacidosis and refractory metabolic acidemia. Diagnostic confirmation was obtained through a periorbital KOH mount showing characteristic thick, non-septate hyphae. The clinical course rapidly deteriorated into necrotizing fasciitis, septic shock, and severe acute kidney injury, requiring mechanical ventilation, vasopressor support, and continuous renal replacement therapy in the Intensive Care Unit. The aggressive progression observed in this patient underscores the necessity of a multidisciplinary approach based on five therapeutic pillars: early clinical suspicion, prompt administration of liposomal Amphotericin B (5 mg/kg/day), aggressive surgical debridement of necrotic tissues, reversal of immunosuppression, and aggressive correction of underlying metabolic derangements.

REFERENCES

1. Patel A, A. R. (2021 Sep). MucoCovi Network. Multicenter EpidemiologicStudy of Coronavirus Disease-Associated Mucormycosis,India. Emerg Infect Dis, 27(9):2349-2359.

2. Skiada A, P. I.-A. (2020 Nov 2). Epidemiology and Diagnosis ofMucormycosis: An Update. . J Fungi (Basel), 6(4):265.

3. Jeong W, K. C. (2019 Jan). The epidemiology and clinical manifestationsof mucormycosis: a systematic review and meta-analysisof case reports. Clin Microbiol Infect, 25(1):26-34.

4. Nucci M, E. M. (2019 Sep). Mucormycosis in South America: Areview of 143 reported cases. Mycoses, 62(9):730-738.

5. Cornely OA, A.-I. A. (2019 Dec). Global guideline for the diagnosisand management of mucormycosis: an initiative of the EuropeanConfederation of Medical Mycology in cooperation with the MycosesStudy Group Education and Research Consortium. LancetInfect Dis, 19(12):e405-e421.

6. Millon L, S. E. (2019 Mar 20). Molecular Strategies to DiagnoseMucormycosis. J Fungi (Basel), 5(1):24.

7. Gebremariam T, L. M. (2014). CotH3 mediates fungal invasion ofhost cells during mucormycosis. J Clin Invest, 124:237-50.

8. Ibrahim A, S. B. (2012). Pathogenesis of mucormycosis. Clin InfectDis, 54 Suppl 1:516-22.

9. Lanternier F, D. E.-H. (2012). A global analysis of mucormycosisin France: The RetroZygo Study (2005-2007). Clin Infect Dis, 54Suppl 1:535-43.

10. Liu M, S. B. (2010). El receptor de células endoteliales GRP78es necesario para la patogénesis de la mucormicosis en ratonesdiabéticos. J Clin Invest, 120:1914-24.

11. Chamilos G, L. R. (2008). Zygomycetes hyphae trigger an early, robustproinflammatory response in human polymorphonuclear neutrophilsthrough Toll-like receptor 2 induction but display relative resistanceto oxidative damage. Antimicrob Agents Chemother, 52:722-4

12. Spellberg B, E. J. (2005 Jul). Novel perspectives on mucormycosis:pathophysiology, presentation, and management. Clin MicrobiolRev, 18(3):556-69.

13. Boelaert JR, d. L. (1993). La mucormicosis durante la terapia condeferoxamina es una infección mediada por sideróforos: estudiosin vitro y en animales in vivo. J Clin Invest, 91:1979-86.

14. Artis WM, F. J. (1982). n mecanismo de susceptibilidad a la mucormicosisen la cetoacidosis diabética: transferrina y disponibilidadde hierro. Diabetes, 31:1109-14.

15. Gartenberg G, B. E. (1978). Hospital-acquired mucormycosis(Rhizopus rhizopodiformis) of skin and subcutaneous tissue: Epidemiology,mycology and treatment. N Engl J Med, 299:1115-8.

16. Martin G, M.T., Salavert L, M. (2021 Abril). Mucormicosis: perspectivade manejo actual y de futuro, 38(2): 39-104.