Rhino-orbital-cerebral mucormycosis: etiopathogenesis, diagnosis and treatment

Abstract

Introduсtion. Rhino-orbito-cerebral mucormycosis (ROCM) is a severe invasive fungal infection caused by fungi of the order Mucorales. The disease primarily develops in immunocompromised patients, particularly those with uncontrolled diabetes mellitus, hematological malignancies, or longterm corticosteroid therapy. The aggressive course of mucormycosis is largely determined by the ability of fungal hyphae to penetrate host tissues and blood vessels. A better understanding of the cellular mechanisms involved in fungal invasion and host immune response is essential for early diagnosis and the development of effective therapeutic strategies. Therefore, studying the etiopathogenesis of ROCM at the cellular level remains an important objective in modern medical research. Materials and Methods. This study is based on a review and analysis of recent literature on the pathogenesis, cellular mechanisms, and clinical manifestations of rhino-orbito-cerebral mucormycosis. Particular attention is given to the interactions between fungal elements and host cells, including endothelial cells, phagocytic immune cells, and affected tissues. Results. Infection in rhino-orbito-cerebral mucormycosis begins with the inhalation of fungal spores that settle on the mucosa of the nasal cavity and paranasal sinuses. In healthy individuals, the immune system—primarily macrophages and neutrophils—rapidly eliminates these spores through phagocytosis and oxidative mechanisms. In immunocompromised patients, these defense mechanisms are weakened, allowing the spores to germinate and develop into invasive fungal hyphae. The hyphae have the ability to actively adhere to endothelial cells and penetrate them. An important molecular mechanism of this process is the interaction between fungal surface proteins and endothelial receptors, including GRP78, which facilitates angioinvasion. Damage to endothelial cells leads to vascular thrombosis, impaired blood flow, and progressive tissue ischemia. Vascular occlusion subsequently results in extensive necrosis of surrounding tissues, which is a characteristic feature of mucormycosis. In addition, metabolic factors such as hyperglycemia and increased levels of free iron stimulate fungal growth and contribute to further cellular damage. These mechanisms explain the rapid progression of the infection, which may involve the nasal cavity, orbit, and sometimes intracranial structures. Conclusions. Rhino-orbito-cerebral mucormycosis is a serious invasive infection, the development of which is largely determined by the interaction of fungal pathogens with host cells and tissues. Understanding the processes of endothelial invasion, immune cell dysfunction, and subsequent tissue necrosis contributes to improved diagnostic approaches and increased treatment effectiveness. Timely initiation of antifungal therapy in combination with surgical intervention remains the primary and most effective treatment for this disease.