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.
