Clinical presentations of zygomycosis in immunocompromised patients are almost indistinguishable from those of invasive mycotic infections caused by other types of moulds. The spectrum of disease includes rhinocerebral disease, organ infection, and disseminated disease.
A retrospective review that evaluated whether criteria could be developed to help distinguish pulmonary zygomycosis from invasive pulmonary aspergillosis found that fever was the most common presenting sign in each group.38 In logistic regression analysis of clinical characteristics, concomitant sinus involvement (P = .003), voriconazole(Drug information on voriconazole) prophylaxis (P = .005), and diabetes mellitus (P = .03) were significantly associated with pulmonary zygomycosis. A review of CT scans revealed that the number of nodules (10 or more) was highly indicative of pulmonary zygomycosis versus invasive pulmonary aspergillosis (64% vs 18%; P = .02). Prospective validation of this study is needed.
In SOT recipients, the most common presentation is pulmonary disease, especially in diabetic renal allograft recipients. Extrapulmonary sites include rhinocerebral, genitourinary, CNS, musculoskeletal, and cutaneous sites. GI zygomycosis has been reported as a rare infection in the early posttransplant period in heart transplant and other allograft recipients and is associated with high mortality.34
Regarding laboratory findings, Mucorales moulds grow well on both nonselective and fungal-selective media. Recovery of Zygomycetes organisms from tissue is difficult. Indeed, numerous reports of negative cultures from premortem and autopsy specimens have been published. Blood cultures are rarely positive34; neither are cultures from CSF, sputum, urine, or swabs of infected areas.
Definitive diagnosis of zygomycosis almost always requires histopathological evidence of fungal invasion of tissue. Zygomycetes organisms can be distinguished from Aspergillus species in tissue by their broad (3 to 25 μm in diameter), thin walled, mostly aseptate hyphae that are best seen with H&E stain. Identification of Zygomycetes fungi at the genus and species level requires culture studies, because all members of this group are morphologically similar in tissue.33
Successful treatment of zygomycosis depends on timely diagnosis, reversal of underlying risk factors, surgical debridement, and effective systemic antifungal therapy. There have been no prospective studies of primary treatment of zygomycosis and most evidence comes from small case series; therefore, optimal therapy is not known. A multivariate analysis of data from 59 patients with hematological cancers and proven or probable zygomycosis revealed that the only factor that significantly correlated with recovery from infection was treatment with liposomal amphotericin B(Drug information on amphotericin b).39
Currently, the recommended antifungal therapy for zygomycosis includes amphotericin B deoxycholate 1 to 1.5 mg/kg/d. Lipid formulations of amphotericin B have been used to treat zygomycosis. Less renal toxicity may be associated with their use than with other formulations of amphotericin B.33
Zygomycetes fungi are resistant in vitro to the echinocandins and most triazoles, including fluconazole(Drug information on fluconazole) and voriconazole. Posaconazole, however, may be useful as salvage therapy for zygomycosis. In a retrospective review of 91 patients with zygomycosis who were refractory or intolerant to other antifungal therapies and received posaconazole on a compassionate-use basis, complete or partial response was seen in 60% after 12 weeks of treatment.40