Pathophysiology

Mucormycosis is the most common form of acute invasive fungal infection and is caused by pathogens within the order Mucorales. Rizopus oryzae is the most virulent and common species within the order. Other members, in decreasing frequency, include Absidia, Cunninghamella, Rhizomucor, Syncephalastrum, Saksenaea, Apophysomyces, and Mucor. Mucormycosis is discussed in detail in Chapter 14.

Rhinocerebral infection is the most common manifestation of mucormycosis. Infection begins with inhalation of spores that usually land on the nasal turbinates. Fungal hyphae grow and invade the mucosa of the paranasal sinuses. As the infection continues, hyphae grow along and into blood vessels, resulting in vascular infarction. Invasion progresses through soft tissue, muscle, cartilage, and bone. The infection spreads to the hard palate and nose where it can result in septal and palatal necrosis. These areas of infarction appear black on gross inspection and are surrounded by a rim of yellow, dying tissue. If allowed to continue, it can breach the orbits and cribriform plate. Death occurs following direct infection of the brain or by invasion of the carotid vessels, with resulting cerebral infarction (Fig. 2).

R. oryzae has an enzyme, ketone reductase, which promotes survival in high glucose, acidic conditions. It is no surprise that patients with diabetic ketoacidosis are especially vulnerable to infection. Iron overload and deferoxamine also increase the risk of mucormycosis. Increased iron uptake by the fungus seems to stimulate growth.

Aspergillus infection can also become invasive in immunocompromised hosts, with extension into the mucosa and bone. This fulminant necrotizing form is seen in AIDS patients with CD4 counts below 50 and in the setting of persistent neutropenia. A. fumigatus is the most common pathogen, and the infection can be fatal within days, due to hematogenous dissemination (5).

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