Mucormycosis (phycomycosis) is caused by an infection with a saprophytic fungus that normally occurs in soil or as a mold on decaying food. The fungus is nonpathogenic for healthy individuals and can be cultured regularly from the human nose, throat, and oral cavity. (The organism represents an opportunistic rather than a true pathogen.) Infection occurs in individuals with decreased host resistance, such as those with poorly controlled diabetes or hematologic malignancies, or those undergoing cancer chemotherapy or immunosuppressive drug therapy.
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In the debilitated patient, mucormycosis may appear as a pulmonary, gastrointestinal, disseminated, or rhinocerebral infection.
The rhinomaxillary form of the disease, a subdivision of the rhinocerebral form, begins with the inhalation of the fungus by a susceptible individual. The fungus invades arteries and causes damage secondary to thrombosis and ischemia. The fungus may spread from the oral and nasal region to the brain, causing death in a high percentage of cases. Symptoms include nasal discharge caused by necrosis of the nasal turbinates, ptosis, proptosis secondary to invasion of the orbit, fever, swelling of the cheek, and paresthesia of the face.
ORAL MANIFESTATIONS
The most common oral sign of mucormycosis is ulceration of the palate, which results from necrosis due to invasion of a palatal vessel.The lesion is characteristically large and deep, causing denudation of underlying bone (Figure 4-45). Ulcers from mucormycosis have also been reported on the gingiva, lip, and alveolar ridge. The initial manifestation of the disease may be confused with dental pain or bacterial maxillary sinusitis caused by invasion of the maxillary sinus. The clinician must include mucormycosis in the differential diagnosis of large oral ulcers occurring in patients debilitated from diabetes, chemotherapy, or immunosuppressive drug therapy.
Early diagnosis is essential if the patient is to be cured of this infection. Negative cultures do not rule out mucormycosis because the fungus is frequently difficult to culture from infected tissue; instead, a biopsy must be performed when mucormycosis is suspected. The histopathologic specimen shows necrosis and nonseptate hyphae, which are best demonstrated by a periodic acid–Schiff stain.
TREATMENT
When diagnosed early, mucormycosis may be cured by a combination of surgical débridement of the infected area and systemic administration of amphotericin B for up to 3 months. Proper management of the underlying disorder is an important aspect affecting the final outcome of treatment. All patients given amphotericin B must be closely observed for renal toxicity by repeated measurements of the blood urea nitrogen and creatinine.
218,219
In the debilitated patient, mucormycosis may appear as a pulmonary, gastrointestinal, disseminated, or rhinocerebral infection.
The rhinomaxillary form of the disease, a subdivision of the rhinocerebral form, begins with the inhalation of the fungus by a susceptible individual. The fungus invades arteries and causes damage secondary to thrombosis and ischemia. The fungus may spread from the oral and nasal region to the brain, causing death in a high percentage of cases. Symptoms include nasal discharge caused by necrosis of the nasal turbinates, ptosis, proptosis secondary to invasion of the orbit, fever, swelling of the cheek, and paresthesia of the face.
ORAL MANIFESTATIONS
The most common oral sign of mucormycosis is ulceration of the palate, which results from necrosis due to invasion of a palatal vessel.The lesion is characteristically large and deep, causing denudation of underlying bone (Figure 4-45). Ulcers from mucormycosis have also been reported on the gingiva, lip, and alveolar ridge. The initial manifestation of the disease may be confused with dental pain or bacterial maxillary sinusitis caused by invasion of the maxillary sinus. The clinician must include mucormycosis in the differential diagnosis of large oral ulcers occurring in patients debilitated from diabetes, chemotherapy, or immunosuppressive drug therapy.
Early diagnosis is essential if the patient is to be cured of this infection. Negative cultures do not rule out mucormycosis because the fungus is frequently difficult to culture from infected tissue; instead, a biopsy must be performed when mucormycosis is suspected. The histopathologic specimen shows necrosis and nonseptate hyphae, which are best demonstrated by a periodic acid–Schiff stain.
TREATMENT
When diagnosed early, mucormycosis may be cured by a combination of surgical débridement of the infected area and systemic administration of amphotericin B for up to 3 months. Proper management of the underlying disorder is an important aspect affecting the final outcome of treatment. All patients given amphotericin B must be closely observed for renal toxicity by repeated measurements of the blood urea nitrogen and creatinine.
