Disseminated mucormycosis: report of a successfully treated immunosuppressed child with clinical, radiographic and pathological findings

Celgow, L.; Cohn, Richard J.; Sacks, Ashleigh

doi:10.1007/bf01372092

Cited by 7 publications

(1 citation statement)

References 5 publications

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“…Disseminated mucormycosis involves more than two contiguous organs. In 23–62% of the cases, it occurs in patients with haematological disease [13,47,64,86, 110,206,207,303–324] and, in most cases, the patient is deeply immunodepressed and suffering from neutropenia. Other risk‐factors for dissemination are the use of corticosteroids, immunodepression after solid‐organ transplant, chemotherapy and the use of deferoxamine.…”

Section: Disseminated Diseasementioning

confidence: 99%

Mucormycosis: an emerging disease?

Bouza

Muñóz

Guinea

2006

Clinical Microbiology and Infection

137

127

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A B S T R A C TMucormycosis is the third invasive mycosis in order of importance after candidiasis and aspergillosis and is caused by fungi of the class Zygomycetes. The most important species in order of frequency is Rhizopus arrhizus (oryzae). Identification of the agents responsible for mucormycosis is based on macroscopic and microscopic morphological criteria, carbohydrate assimilation and the maximum temperature compatible with its growth. The incidence of mucormycosis is approximately 1.7 cases per 1000 000 inhabitants per year, and the main risk-factors for the development of mucormycosis are ketoacidosis (diabetic or other), iatrogenic immunosuppression, use of corticosteroids or deferoxamine, disruption of mucocutaneous barriers by catheters and other devices, and exposure to bandages contaminated by these fungi. Mucorales invade deep tissues via inhalation of airborne spores, percutaneous inoculation or ingestion. They colonise a high number of patients but do not cause invasion. Mucormycosis most commonly manifests in the sinuses (39%), lungs (24%), skin (19%), brain (9%), and gastrointestinal tract (7%), in the form of disseminated disease (6%), and in other sites (6%). Clinical diagnosis of mucormycosis is difficult, and is often made at a late stage of the disease or post-mortem. Confirmation of the clinical form requires the combination of symptoms compatible with histological invasion of tissues. The probable diagnosis of mucormycosis requires the combination of various clinical data and the isolation in culture of the fungus from clinical samples. Treatment of mucormycosis requires a rapid diagnosis, correction of predisposing factors, surgical resection, debridement and appropriate antifungal therapy. Liposomal amphotericin B is the therapy of choice for this condition. Itraconazole is considered to be inappropriate and there is evidence of its failure in patients suffering from mucormycosis. Voriconazole is not active in vitro against Mucorales, and failed when used in vivo. Posaconazole and ravuconazole have good activity in vitro. The overall rate of mortality of mucormycosis is approximately 40%.

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Section: Disseminated Diseasementioning

confidence: 99%

Mucormycosis: an emerging disease?

Bouza

Muñóz

Guinea

2006

Clinical Microbiology and Infection

137

127

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Two Cases of Disseminated Mucormycosis in Patients with Hematological Malignancies and Literature Review

Cuvelier

Vogelaers

Peleman

et al. 1998

European Journal of Clinical Microbiology & Infectious Dise

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Two cases of disseminated mucormycosis in patients with underlying hematological disease are described. Both patients presented with fever and pulmonary infiltrates which did not respond to empirical treatment with broad-spectrum antibiotics and antifungal agents, and in both patients there was rapid progression with a fatal outcome. All cultures were negative and the diagnosis was made postmortem. A review of the literature revealed only three recent reports of successful treatment of disseminated mucormycosis. Survival correlated with control of the underlying disease and early diagnosis based on histological examination of biopsy specimens from suspected lesions. Therapy consisted of surgical debridement and amphotericin B. Standard therapeutic schedules need to be defined for this infection.

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