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Mucormycosis Medication

  • Author: Nancy F Crum-Cianflone, MD, MPH; Chief Editor: Pranatharthi Haran Chandrasekar, MBBS, MD  more...
 
Updated: Apr 03, 2015
 

Medication Summary

Antifungal treatment consists of lipid formulations of amphotericin (eg, liposomal amphotericin), amphotericin B deoxycholate, or posaconazole. Although most clinical experience has focused on amphotericin agents, data on the efficacy of posaconazole are promising. This agent may eventually become the drug of choice, but more evaluation is needed.[45]

Amphotericin agents

Amphotericin B has proven efficacy in the treatment of mucormycosis, and the conventional form (deoxycholate) is typically administered at 1-1.5 mg/kg/d (the total dose given over the course of therapy is usually 2.5-3 g). High doses of this drug are required, and nephrotoxicity may result.

A lipid formulation of amphotericin B has now replaced amphotericin B deoxycholate as the drug of choice, owing to improved efficacy and safety of these formulations (eg, AmBisome).[46] Lipid preparations of amphotericin B are typically used at 5 mg/kg/d. Some have used doses of up to 15 mg/kg/d to treat mucormycosis, although the clinical advantages of higher doses are unknown.

Posaconazole

Posaconazole, a triazole, is currently considered a second-line drug for treatment of mucormycosis, and the typical dose is 400 mg orally twice daily (total of 800 mg/d). Since achieving steady-state plasma concentrations of this drug takes approximately 1 week, most experts would not recommend using this agent for initial treatment, but rather initially administering intravenous liposomal amphotericin B. Sequential therapy by first using liposomal amphotericin followed later by posaconazole has been used.[40, 41] Since posaconazole is only available in an oral formulation, absorption is an important consideration; administration with high-fat food or acidic beverage and the avoidance of antacids is advised.

Studies have reported that posaconazole yielded a 50-70% success rate, whereas the comparator (typically amphotericin B or lipid-based amphotericin, in many cases used as salvage therapy) yielded a success rate of only 25%, which suggests that posaconazole may become the preferred drug for mucormycosis. A recent review of 96 cases treated between 2003 and 2011 with posaconazole found that complete response was achieved in 62 (64.6%), partial response in 7 (7.3%) patients, and stable disease in 1 (1%), with an overall mortality of 24% (no data for 3 patients).[38] However, further studies are needed.[53, 54]

Posaconazole has also been studied in several case reports,[28] including as salvage therapy after failure of amphotericin B therapy.[37] Rickerts et al reported that liposomal amphotericin B plus posaconazole was successful in the treatment of disseminated mucormycosis in a patient who could not undergo surgery; however, the benefit of dual antifungal therapy is unclear.[39]

Most commonly, posaconazole is used as sequential therapy after the initial administration and control of the disease with liposomal amphotericin B.[40, 41]

Isavuconazole

Isavuconazole (Cresemba) is a triazole antifungal agent. Isavuconazole is the active moiety of the prodrug isavuconazonium sulfate. It is indicated for invasive mucormycosis infection caused by Mucorales fungi (eg, R oryzae, Mucormycetes species).

Isavuconazole’s approval in March 2015 was based on an open-label noncomparative study in adult patients with invasive aspergillosis and renal impairment or in patients with invasive fungal disease caused by other rare fungi. A subpopulation of 37 patients with invasive mucormycosis treated with isavuconazole showed all-cause mortality was 38%. The efficacy of isavuconazole in the treatment of invasive mucormycosis has not been evaluated in concurrent, controlled clinical trials.[42]

Other medications

Other azoles (eg, fluconazole, voriconazole) have not shown significant activity against these fungi. Of note, despite the use of voriconazole prophylaxis in high-risk patients (eg, transplant recipients), breakthrough zygomycosis has been reported.[43, 44, 45]

Animal and limited clinical data suggest that combination therapy with lipid formulations of amphotericin and an echinocandin (eg, micafungin, caspofungin) may improve survival; however, more clinical trial data are needed before this strategy can be definitively recommended.[46, 33, 47]

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Antifungals

Class Summary

Antifungal agents are used to treat Mucorales infection. The mechanism of action may involve an alteration of RNA and DNA metabolism or an intracellular accumulation of peroxide that is toxic to the fungal cell.

Liposomal amphotericin B (AmBisome)

 

Liposomal amphotericin B is amphotericin B encapsulated in a bilayer of liposomes. This antifungal agent is considered first-line therapy for mucormycosis. It should also be used in the setting of preexisting renal dysfunction, when renal toxicity develops during amphotericin B deoxycholate therapy, or when amphotericin B deoxycholate therapy is failing. Nephrotoxicity and infusion-related toxicity are reduced compared with conventional amphotericin B deoxycholate.

Amphotericin B deoxycholate

 

Amphotericin B is the drug of choice (DOC) to treat most fungal infections. Amphotericin B deoxycholate is produced by a strain of Streptomyces nodosus and can be fungistatic or fungicidal. Amphotericin B binds to sterols (eg, ergosterol) in the fungal cell membrane, causing intracellular components to leak, with subsequent fungal cell death. This agent is active against mucormycosis, Cryptococcus neoformans, Histoplasma capsulatum, Coccidioides immitis, Candida species, and Aspergillus species.

Amphotericin B lipid complex (Abelcet)

 

Amphotericin B lipid complex is amphotericin B in phospholipid complexed form. This is an alternate therapy to liposomal amphotericin B.

Posaconazole (Noxafil)

 

Posaconazole is a triazole antifungal agent that blocks ergosterol synthesis by inhibiting the enzyme lanosterol 14-alpha-demethylase and sterol precursor accumulation. This action results in cell membrane disruption. Posaconazole is available as an oral suspension (200 mg/5 mL).

Posaconazole is indicated for prophylaxis of invasive Aspergillus and Candida infections in patients at high risk because of severe immunosuppression. This agent has also been used for serious fungal infections (eg, mucormycosis, invasive aspergillosis, Fusarium infection, Scedosporium apiospermum infection, candidemia, candidiasis).

Isavuconazole (Cresemba)

 

Triazole antifungal agent. Isavuconazole is the active moiety of the prodrug isavuconazonium sulfate. It is indicated for invasive mucormycosis infection caused by Mucorales fungi (eg, R oryzae, Mucormycetes species).

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Contributor Information and Disclosures
Author

Nancy F Crum-Cianflone, MD, MPH Consulting Staff, Department of Internal Medicine, Division of Infectious Diseases, Naval Medical Center at San Diego

Nancy F Crum-Cianflone, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Chief Editor

Pranatharthi Haran Chandrasekar, MBBS, MD Professor, Chief of Infectious Disease, Program Director of Infectious Disease Fellowship, Department of Internal Medicine, Wayne State University School of Medicine

Pranatharthi Haran Chandrasekar, MBBS, MD is a member of the following medical societies: American College of Physicians, American Society for Microbiology, International Immunocompromised Host Society, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Acknowledgements

Mark T Duffy, MD, PhD Consulting Staff, Division of Oculoplastic, Orbito-facial, Lacrimal and Reconstructive Surgery, Green Bay Eye Clinic, BayCare Clinic; Medical Director, Advanced Cosmetic Solutions, A BayCare Clinic

Mark T Duffy, MD, PhD is a member of the following medical societies: American Academy of Ophthalmology, American Medical Association, American Society of Ophthalmic Plastic and Reconstructive Surgery, Sigma Xi, and Society for Neuroscience

Disclosure: Allergan - Botox Cosmetic Honoraria Speaking and teaching

Ronald A Greenfield, MD Professor, Department of Internal Medicine, University of Oklahoma College of Medicine

Ronald A Greenfield, MD is a member of the following medical societies: American College of Physicians, American Federation for Medical Research, American Society for Microbiology, Central Society for Clinical Research, Infectious Diseases Society of America, Medical Mycology Society of the Americas, Phi Beta Kappa, Southern Society for Clinical Investigation, and Southwestern Association of Clinical Microbiology

Disclosure: Pfizer Honoraria Speaking and teaching; Gilead Honoraria Speaking and teaching; Ortho McNeil Honoraria Speaking and teaching; Abbott Honoraria Speaking and teaching; Astellas Honoraria Speaking and teaching; Cubist Honoraria Speaking and teaching; Forest Pharmaceuticals Speaking and teaching

Simon K Law, MD, PharmD Clinical Professor of Health Sciences, Department of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine

Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology

Disclosure: Nothing to disclose.

Maria D Mileno, MD Associate Professor of Medicine, Division of Infectious Diseases, The Warren Alpert Medical School of Brown University

Maria D Mileno, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, International Society of Travel Medicine, and Sigma Xi

Disclosure: Nothing to disclose.

Ron W Pelton, MD, PhD Private Practice, Colorado Springs, Colorado

Ron W Pelton, MD, PhD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, American Society of Ophthalmic Plastic and Reconstructive Surgery, AO Foundation, and Colorado Medical Society

Disclosure: Nothing to disclose.

Hampton Roy Sr, MD Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Kimberly G Yen, MD Associate Professor of Ophthalmology, Department of Ophthalmology, Cullen Eye Institute, Baylor College of Medicine

Kimberly G Yen, MD is a member of the following medical societies: American Academy of Ophthalmology and American Association of Pediatric Ophthalmology & Strabismus (AAPOS)

Disclosure: Nothing to disclose.

Michael T Yen, MD Associate Professor of Ophthalmology, Division of Ophthalmic Plastic, Lacrimal, and Orbital Surgery, Cullen Eye Institute, Medical Director, BCM Ambulatory Surgery Center, Program Director, ASOPRS Fellowship, Baylor College of Medicine

Michael T Yen, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Ophthalmic Plastic and Reconstructive Surgery, and Association for Research in Vision and Ophthalmology

Disclosure: Nothing to disclose.

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Postmortem photograph of a woman with diabetes and left rhinocerebral mucormycosis complicating ketoacidosis. Rhizopus oryzae was the causative organism. Note the orbital and facial cellulitis and the black nasal discharge. (Courtesy of A. Allworth, MD, Brisbane, Australia.)
The right eye of an immunocompetent man who sustained a high-pressure water jet injury, resulting in rhinocerebral mucormycosis. Traumatic inoculation of Apophysomyces elegans was the pathogenetic mechanism. Note the proptosis. (Courtesy of A. Allworth, MD, Brisbane, Australia.)
The right eye of an immunocompetent man who sustained a high-pressure water jet injury, resulting in rhinocerebral mucormycosis. Traumatic inoculation of Apophysomyces elegans was the pathogenetic mechanism. Chemosis is shown in this photograph. Internal and external ophthalmoplegia, no light perception, and afferent pupil defect were present, which is consistent with orbital apex syndrome. (Courtesy of A. Allworth, MD, Brisbane, Australia.)
An immunocompetent man who sustained a high-pressure water jet injury, resulting in rhinocerebral mucormycosis. Traumatic inoculation of Apophysomyces elegans was the pathogenetic mechanism. A surgical field of this patient is shown. Excision of the right orbit, maxillary antrum, nasal cavity, sphenoid sinus, and infratemporal fossa has taken place. The tissue was infarcted. (Courtesy of A. Allworth, MD, Brisbane, Australia.)
An immunocompetent man who sustained a high-pressure water jet injury, resulting in rhinocerebral mucormycosis. Traumatic inoculation of Apophysomyces elegans was the pathogenetic mechanism. Picture of the patient after successful treatment with repeated surgical debridement and high-dose liposomal amphotericin B. (Courtesy of A. Allworth, MD, Brisbane, Australia.)
Histologic findings from an immunocompetent man who sustained a high-pressure water jet injury, resulting in rhinocerebral mucormycosis. Traumatic inoculation of Apophysomyces elegans was the pathogenetic mechanism. Findings show the typical Mucorales hyphae on Grocott methenamine-silver staining. The hyphae are the dark structures with budlike, right-angle hyphae. (Courtesy of A. Allworth, MD, Brisbane, Australia.)
Chest computed tomography (CT) scan showing pulmonary mucormycosis with left basal consolidation and widespread nodules due to Rhizopus oryzae infection. The patient was receiving cytotoxic chemotherapy for myelodysplastic syndrome and had iron overload from numerous blood transfusions.
Chest computed tomography (CT) scan showing pulmonary mucormycosis with left basal consolidation and widespread nodules due to Rhizopus oryzae infection. The patient was receiving cytotoxic chemotherapy for myelodysplastic syndrome and had iron overload from numerous blood transfusions. This CT scan of the patient shows resolution of pulmonary mucormycosis after 5 months of antifungal treatment.
 
 
 
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