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Fig. 6.28. A The mucocutaneous form of entomophthoromycosis. Nasal obstruction and diffuse erythema and thickening of the skin of the nose. This form of infection can go on to develop into nasal polyps (B). In some patients skin of the cheek and lips is infiltrated (C), causing severe disfiguration. The eyelids may be involved, as in this patient. D Longstanding infections can spread into muscle and bones, as occurred when this palate was perforated.

Fig. 6.29 A-C. Mucormycosis can cause gross deformity in any part of the body. A The grossly deformed hand of a child and B the radiograph of the same hand. The bones are displaced and there is some periosteal reaction, but there is no invasion of any bone. C Usually saprophytic fungi can become very virulent and pathogenic in patients who are immunocompromised, such as this 60-year-old Indian man with diabetic ketoacidosis and chronic renal failure, being treated with dialysis. He suddenly became unconscious and delirious: there is consolidation in the right upper lobe.



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Imaging Diagnosis

In the facial form, the full extent of the facial soft tissue swelling can be demonstrated, and radiographs or CT scans of the sinuses are important to show the spread of the infection. Although sinus radiographs provide useful information, CT and MR scans are needed to demonstrate fully the extent of the ethmoid sinus or orbital spread and to show whether there is any intracerebral involvement. Rhinocerebral mucormycosis may be much more extensive than is expected from the clinical examination. All the causal organisms can be very destructive, although E. coronata does not usually involve bone.

Imaging can show when the subcutaneous form of zygomycosis involves the underlying bone, because there is usually a reactive periostitis adjacent to the soft tissue granuloma. Ultrasonography, soft tissue radiography, and MRI can demonstrate the superficial or deeper extension of the infection. In the foot or hand, deep infection may displace adjoining bones, shown as separation of the metatarsal or metacarpal heads.

Pulmonary mucormycosis may be very nonspecific. Chest imaging may show patchy or diffuse consolidation, often multifocal (Fig. 6.29 C). There may be cavitation, with or without consolidation and there may be small parenchymal nodules, often single. It is not always easy to distinguish consolidation from pulmonary infarction or to be sure whether the abscess is a direct result of the infection or is due to necrosis.

Pleural effusions are relatively uncommon, as is mediastinal involvement. Because mucormycetes invade the large blood vessels, there may be pseudoaneurysms. These may be multiple in the pulmonary artery, best shown by CT or MR scanning and, if necessary, confirmed by pulmonary arteriography. Both the central and the peripheral pulmonary arteries may be involved. When there is peripheral ischemia and infarction, some of the lung tissue may slough and become surrounded by air (pulmonary gangrene). This complication also occurs in aspergillosis, and if the volume of necrotic lung is sufficiently large, the circle of air could be mistaken for a hydatid cyst.

Mucormycotic infection of the bowel can be seen on plain radiographs as dilated bowel, or if there has been perforation, free intraperitoneal or subphrenic gas. Ascites may be recognized with ultrasonography or CT. Partial obstruction from a mucormycetoma can be demonstrated by contrast examination (if the patient is sufficiently well). Any part of the bowel may be involved, and pseudotumors have been reported around the duodenum, mid-ileum, ileocecal valve, and the splenic flexure of the colon. The patients may be too ill for gastrointestinal contrast examination, but ultrasonography or CT scanning may provide useful information. If the lesion can be seen by endoscopy, there is often a black or greenish area of central necrosis.

Cardiac mucormycosis is very uncommon, but has occurred, usually as a complication of disseminated infection.

Mucormycosis is often progressive, with fatal infections in which the diagnosis is only established as the disease progresses into its advanced stages, or not until autopsy. Spontaneous healing has occurred but, even if the underlying immunodeficiency can be rectified, the prognosis in most patients is poor.


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