AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Background

Zygomycosis is an infection caused by fungi in the orders Mucorales and Entomophthorales. The Mucorales order contains 2 families exist—Mucoraceae and Cunninghamellaceae.¹ Mucormycosis is another common name applied to this same group of diseases. This designation reflected the predominance of the Mucorales in causing disease in humans. However, this term ignored the role of the Entomophthorales (Conidiobolus species and Basidiobolus species).² The currently accepted designation is zygomycosis, reflecting all disease processes caused by the members of the class Zygomycetes. During the past decade, the Zygomycetes have emerged as common causes of invasive fungal infections.^{3, 4, 5}

The pathogens that cause zygomycosis are commonly found in the environment on fruit, on bread, and in soil and are common components of decaying organic debris.² These organisms are ubiquitous and generally saprophytic, rarely causing disease in immunocompetent hosts, but they are the third-most-common cause of invasive fungal infection in immunocompromised patients, especially stem cell transplant recipients and patients with underlying hematologic malignancies.^{6, 7, 8, 9}

Fungi are ubiquitous in the natural world, often found in association with plants, mammals, and insects. Accordingly, humans are continually exposed to multiple genera of fungi via various routes, including the respiratory and gastrointestinal routes, which allow the possibility of colonization. Depending on the interaction between host mucosal defense mechanisms and fungal virulence factors, colonization may be transient or persistent, or local disease may ensue.

Pathophysiology

Overall, Rhizopus species from the Mucoraceae family are the most commonly identified etiologic agents of zygomycosis in humans. Of the Rhizopus species, the most common agent associated with zygomycosis is Rhizopus arrhizus (Rhizopus oryzae), followed by Rhizopus rhizopodiformis. Other causes include Mucor species, Cunninghamella bertholletiae, Apophysomyces elegans, Absidia species, Saksenaea species, Rhizomucor pusillus, Entomophthora species, Conidiobolus species, and Basidiobolus species.^{2, 9} 

Zygomycosis caused by R arrhizus is acute and rapidly fatal despite early diagnosis and treatment. These organisms have a particular predilection for invading major blood vessels, with ensuing ischemia, necrosis, and infarction of adjacent tissues, resulting in the production of black pus. Persons at particular risk include those with granulocytopenia and acidosis. For unknown reasons, the Zygomycetes have a propensity to affect patients with acidosis, particularly those with diabetes. They also infect patients with acidosis secondary to renal insufficiency, diarrhea, and aspirin intake. Patients who are receiving glucocorticoids or deferoxamine and those who have undergone splenectomy also are at risk.^{10, 9}

Frequency

International

The distribution of the various forms of zygomycosis is uniform regardless of age, geography, or race.

Mortality/Morbidity

The overall mortality rate associated with zygomycosis is approximately 50% and has remained at this level for the past 50 years. Rhinocerebral zygomycosis carries a mortality rate of approximately 85%. Mortality rates are very high because, by the time zygomycosis is suspected and diagnosed, it has frequently spread diffusely and caused extensive tissue destruction. However, the risk of mortality varies depending on the characteristics of the host, the type of infection, the site of infection, and the use of surgical intervention. In general, antifungal therapy and surgical management independently decrease the likelihood of death.^{10, 9}

Sex

According to the latest epidemiologic surveys, approximately two thirds of all zygomycosis cases occur in males. The reason for this discrepancy is poorly understood.

CLINICAL

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

History

Zygomycosis manifests as a spectrum of diseases, depending on the portal of entry and the predisposing risk factors of the patient. The 5 major clinical forms include rhinocerebral zygomycosis, pulmonary zygomycosis, abdominopelvic and gastric (gastrointestinal) zygomycosis, primary cutaneous zygomycosis, and disseminated zygomycosis.^{10, 3}

• Rhinocerebral zygomycosis
• • Rhinocerebral zygomycosis is the most frequently encountered form of the disease. Approximately 50% of zygomycosis cases in persons with diabetes are of the rhinocerebral type. Rhinocerebral zygomycosis is frequently observed in patients presenting with diabetic ketoacidosis. The typical presentation of rhinocerebral zygomycosis generally involves the nose, followed by the eyes, brain, and, occasionally, the meninges.
  • Patients with rhinocerebral zygomycosis typically present with a history of fever, unilateral facial pain or headaches, nasal congestion, epistaxis, visual disturbances, and lethargy.
  • Physical examination may reveal periorbital cellulitis, proptosis, and loss of extraocular muscle movement (see Image 1). These lesions are frequently accompanied by cranial nerve palsy of the II, III, IV, and VI nerves.
  • Black necrotic lesions are generally observed on the hard palate or nasal mucosa of these extremely ill patients.
• Pulmonary zygomycosis
• • Patients with pulmonary zygomycosis typically present with a history of fever, cough, hemoptysis, chest pain, and increasing shortness of breath.
  • Physical examination may reveal pleuritic rub and rhonchi over the affected area.
  • Primary pulmonary zygomycosis is the second-most-common form of zygomycosis and tends to occur in patients with hematological malignancy, those with profound neutropenia, stem cell transplant recipients, and in those who have been receiving high-dose steroid therapy.
• Gastrointestinal zygomycosis
• • Patients with gastrointestinal zygomycosis typically present with a history of abdominal pain or distention, dyspepsia, nausea and vomiting, diarrhea, and hematochezia.
  • Physical examination may reveal decreased bowel sounds, guarding or rebound tenderness, and localized-to-diffuse abdominal tenderness.
  • Gastrointestinal zygomycosis is the least common form of the infection, accounting for less than 10% of all cases of zygomycosis.⁹
  • Gastrointestinal zygomycosis tends to develop in malnourished individuals, low birth weight infants, or in patients with renal failure who are on peritoneal dialysis. Infection is caused by ingestion of the organism and results in necrotic ulcerations, with ischemia and gangrene of the stomach and colon. Gastrointestinal zygomycosis carries an extremely high mortality rate because of the high incidence of bowel perforation and the difficulty in establishing the diagnosis.¹¹
• Cutaneous zygomycosis
• • Cutaneous zygomycosis accounts for approximately 20% of all zygomycosis cases.
  • Primary cutaneous zygomycosis is generally due to local trauma or inoculation, while secondary infection is due to hematogenous dissemination of the organisms to the skin.
  • Patients with cutaneous zygomycosis typically present with a history of previous local trauma, with pain around the trauma site.
  • Physical examination may reveal single skin lesions that begin with induration and erythema and gradually develop into a necrotic ulcer with a characteristic dark central area. The margins of the ulcer are sharply demarcated.
  • Cutaneous zygomycosis may be primary, resulting from direct inoculation of the organism into disrupted integument. It also has been associated with the use of Elastoplast bandages over biopsy sites and in burn patients with prior colonization. Secondary cutaneous zygomycosis is generally observed with widely disseminated zygomycosis because of hematogenous seeding.
• Disseminated zygomycosis
• • Disseminated zygomycosis generally arises from the lungs and spreads hematogenously to the central nervous system.
  • Patients with disseminated zygomycosis typically present with a history of headaches, fever, visual disturbances, and changes in mental status.
  • Physical examination may reveal lethargy, obtundation, coma, sudden onset of focal neurologic deficits, and necrotic ulcerations on the respiratory-tract mucosa or the skin.
  • Deferoxamine therapy appears to be the most significant risk factor for disseminated zygomycosis. This underscores the importance of iron availability as a virulence factor for these infections.
  • Disseminated zygomycosis in individuals with hematological malignancies begins in the lungs and spreads to the CNS, producing infarction and abscess. It also can spread to the liver, spleen, kidney, heart, and skin.

Physical

See History.

Causes

Most persons who develop zygomycosis are immunocompromised, although 15-20% of patients have no evidence of any underlying condition at the time of the diagnosis.^{10, 5, 9} Thus, sporadic cases in immunocompetent hosts are not uncommon. The most common risk factors include the following:

• Stem cell transplantation
• Poorly controlled diabetes mellitus, either type 1 or type 2
• Hematologic malignancy (eg, leukemias, lymphomas)
• Solid organ transplants
• Steroid use
• Metabolic acidosis
• Deferoxamine therapy
• Severe and prolonged neutropenia
• Intravenous drug use
• Renal failure
• Peritoneal dialysis
• Burns
• Penetrating trauma (rare)

DIFFERENTIALS

Section 4 of 11  

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Other Problems to be Considered

Rhinocerebral zygomycosis

Aspergillosis of the nasal cavity
Infection due to Pseudallescheria boydii and other filamentous molds
Cavernous sinus thrombosis
Bacterial sinusitis
Periorbital cellulitis

Pulmonary zygomycosis

Pulmonary aspergillosis
Pulmonary infection with Pseudallescheria boydii and other filamentous molds
Pulmonary infection with Pseudomonas aeruginosa

Gastrointestinal zygomycosis

Peptic ulcer disease
Gastrointestinal carcinoma
Gastrointestinal infection with Aspergillus or other filamentous molds
Mesenteric ischemia

Cutaneous zygomycosis

Ecthyma gangrenosum
Cutaneous aspergillosis
Cutaneous infections with other molds

Disseminated zygomycosis

Disseminated aspergillosis
Nocardiosis
Cryptococcosis
Toxoplasmosis
CNS lymphoma or other CNS malignancies
Bacterial brain abscess

WORKUP

Section 5 of 11  

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• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab Studies

Unfortunately, findings from laboratory studies are nonspecific for zygomycosis.^{7, 10} Diagnosis requires a high index of suspicion, a host with appropriate risk factors, and evidence of tissue invasion with the characteristic appearance of broad nonseptate hyphae with right-angle branches. No serologic tests are available, and blood cultures are of no benefit.¹

• Rhinocerebral zygomycosis
• • Discharge scrapings may be examined with potassium hydroxide (KOH) to reveal broad irregularly shaped hyphae with right-angle branching (see Image 2).
  • Fungal stains of biopsy material obtained from affected tissue remains the mainstay for a definitive diagnosis.
  • Fungal culture of biopsy tissue also may be helpful, but results frequently are negative despite positive histopathology. In fact, fungal culture results are only positive in 15-25% of cases.
• Pulmonary zygomycosis
• • Sputum smear and cultures are rarely helpful.
  • Lung tissue biopsy is generally needed for diagnosis.
• Gastrointestinal zygomycosis
• • Most cases of gastrointestinal zygomycosis are diagnosed at surgery or postmortem.
  • Fungal stains and cultures of biopsy material are needed for definitive diagnosis.
• Cutaneous zygomycosis: Diagnosis of this type requires fungal stains and cultures of a skin biopsy.
• Disseminated zygomycosis
• • Blood cultures are of no benefit.
  • Fungal stains and cultures of affected tissue and histopathologic identification of the fungus are needed.
  • Brain biopsy may be helpful.
  • Cerebrospinal fluid analysis is generally nonspecific, even in the presence of brain involvement.
  • Cerebrospinal fluid abnormalities include slightly increased pressure, modest pleocytosis with predominant polymorphonuclear cells, and slightly elevated protein levels. Hypoglycorrhachia is unusual. Erythrocytosis is occasionally observed. Fungal stains and culture results are rarely positive.

Imaging Studies

• Rhinocerebral zygomycosis
• • Plain radiographs of sinuses and orbits may demonstrate sinus mucosal thickening, with or without air-fluid levels, but this is nonspecific.
  • CT scans with contrast or MRI may demonstrate erosion or destruction of bone or sinuses and delineate the extent of disease (see Image 3).
• Pulmonary zygomycosis
• • Chest radiographs may demonstrate single or multiple large masslike infiltrates, pulmonary nodules, and cavitary lesions. These lesions, however, are indistinguishable from those caused by aspergillosis.
  • CT scan with contrast may help delineate the extent of disease.
• Gastrointestinal zygomycosis
• • Abdominal radiographs may demonstrate air under the diaphragm in patients with perforation.
  • Barium studies of the upper GI tract or colon may demonstrate a filling defect or a masslike effect that suggests zygomycosis.
• Disseminated zygomycosis
• • CT scan of the chest and head may demonstrate invasive disease and delineate the extent of disease.
  • CT scan of the abdomen and pelvis may demonstrate lesions in the liver, spleen, kidney, pancreas, stomach, and omentum.

Procedures

• Bronchoscopy with bronchoalveolar lavage and transbronchial biopsy provides adequate tissue to diagnose pulmonary zygomycosis.
• CT-guided percutaneous lung biopsy may also be beneficial.¹²
• Open lung biopsy may be required if bronchoscopy findings are negative.
• Endoscopy provides direct examination of the esophagus and stomach, the most commonly affected organs in patients with gastrointestinal zygomycosis.
• Brain biopsy may be required to establish a diagnosis.

Histologic Findings

Fixed tissue can be stained with hematoxylin and eosin (H&E). Fungal hyphae may be demonstrated with Grocott methenamine-silver stain or periodic acid-Schiff (PAS) staining. The typical appearance demonstrates the fungus as broad, nonseptate hyphae with acute right-angle branching.

TREATMENT

Section 6 of 11  

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Medical Care

• Take aggressive surgical measures to débride affected tissue. Without early and aggressive therapy, zygomycosis is almost always fatal.
• Take aggressive measures to control the underlying condition.
• • Correct hyperglycemia and ketoacidosis to improve outcome.
  • Correct neutropenia with granulocyte colony-stimulating factor (G-CSF) or granulocyte-macrophage colony-stimulating factor (GM-CSF) to improve outcome.
• Institute early and appropriate antifungal administration.
• If possible, discontinue steroids or deferoxamine.

Surgical Care

• The mainstay of treatment for any form of zygomycosis is early and aggressive surgical removal of all infected tissue.
• Remove as much devitalized tissue as possible and consider wide surgical debridement, if feasible.
• Patients with zygomycosis frequently require numerous surgical procedures to eradicate all infected and necrotic material.

Consultations

• Infectious disease specialist
• Surgeon
• Otorhinolaryngologist
• Gastroenterologist
• Pulmonologist
• Ophthalmologist
• Neurosurgeon

MEDICATION

Section 7 of 11  

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Start antifungal therapy as early as possible. Amphotericin B is the only available antifungal that has some proven efficacy against the Zygomycetes. Because of drug toxicity, monitor for adverse effects and toxicity. Lipid preparations of amphotericin B are the current mainstay of therapy for all forms of zygomycosis.^{10, 4} The lipid preparations of amphotericin B are used more frequently because they allow the delivery of higher doses of the parent compound, amphotericin B. In addition, lipid preparations cause milder renal insufficiency typically associated with amphotericin B. Although still investigational, combination therapy with lipid preparations of amphotericin B and G-CSF have been successful in several studies.

In addition, a new triazole, posaconazole, was recently approved by the US Food and Drug Administration (FDA). Posaconazole has proven efficacy against most Zygomycetes in vitro and in vivo.^{13, 14, 15} Posaconazole was approved with an indication for prophylaxis of invasive Aspergillus and Candida infections in patients at high risk because of severe immunosuppression.¹⁵ Eventually, posaconazole may replace amphotericin B compounds as the drug of choice for zygomycosis. Posaconazole is available only in an oral suspension and must be administered 2-4 times per day. It has shown encouraging results in open-labeled clinical trials involving complicated Zygomycetes infections.¹⁶ Posaconazole is frequently used as oral de-escalation therapy in patients in whom amphotericin B has elicited an initial response.

Drug Category: Antifungals

These agents are polyene antifungals. They represent the only antifungal class with known activity against Zygomycetes.

The FDA has approved 3 novel lipid formulations of amphotericin B. The advantage of the lipid preparation over standard amphotericin B deoxycholate is that it delivers higher concentrations of amphotericin B, resulting in a theoretical increase in therapeutic potential and causes decreased nephrotoxicity (25%). The 3 lipid formulations include amphotericin B lipid complex (ABLC; Abelcet), amphotericin B colloidal dispersion (ABCD; Amphotec), and liposomal amphotericin B (L-AMB; AmBisome).

Drug Category: Antifungal agents, triazoles

Posaconazole has shown encouraging results in clinical trials for complicated Zygomycetes infections.

FOLLOW-UP

Section 8 of 11  

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Further Inpatient Care

• Inpatient care of zygomycosis is frequently prolonged because of the severe nature of the illness.
• Patients with zygomycosis frequently undergo multiple surgical procedures in an attempt to eradicate devitalized tissue.
• Antifungals are generally provided parenterally for a period of several months to achieve cure.

Further Outpatient Care

• Once the patient is stabilized and no further surgical procedures are planned, discharge the patient home on antifungal therapy with follow-up visits every 2-4 weeks.
• Monitor patients on amphotericin B products at least biweekly for adverse effects and toxicity (eg, CBC counts, electrolytes, BUN, serum creatinine).

In/Out Patient Meds

• Because of the severity of the infection, most patients with zygomycosis undergo inpatient care for most of their treatment. If patient is clinically stable, the infection appears controlled, and the gastrointestinal tract is functional, he or she may be switched to oral posaconazole and discharged home with close monitoring for efficacy and toxicity.

Transfer

• Transfer patients to the service that can care for serious infections (eg, neurosurgery, otorhinolaryngology, infectious diseases, ophthalmology).
• Transfer patients with altered mental status to an appropriate critical care unit.

Deterrence/Prevention

• Control blood sugar in patients with diabetes mellitus.
• Control metabolic acidosis.
• Eliminate risk factors such as neutropenia and immune modulators.
• Closely monitor patients on deferoxamine therapy.

Complications

• Invasive zygomycosis generally spreads to adjacent organ systems (ie, osteomyelitis), including sinuses and adjacent bones.
• The ocular globe is frequently affected, which may cause blindness.
• Cavernous sinus thrombosis with cranial nerve palsies and extension of infection into the brain and meningitis is a possibility.
• Brain abscess and CNS infarction with ischemia and necrosis may occur.
• Pulmonary infiltrates, cavitary lesions, and life-threatening pulmonary hemorrhages are possible.
• Gastrointestinal hemorrhages may result from gastrointestinal perforation and may lead to peritonitis and sepsis.

Prognosis

• The prognosis of zygomycosis depends on several factors, including the infection site, rapidity of diagnosis, and type and severity of immunosuppression.
• The overall mortality rate among patients with zygomycosis is approximately 50%, although rhinocerebral and gastrointestinal forms of the infection carry a mortality rate of approximately 85%. Mortality rates are high because of the difficulty in establishing the diagnosis and the lack of adequate antifungal therapy. By the time a diagnosis of zygomycosis is confirmed, it has frequently spread via either local invasion with extensive tissue destruction or widely disseminated infection.

Patient Education

• Inform patients and family members that this is an extremely serious condition with a poor prognosis (high morbidity and mortality rate) unless aggressive action is taken early.

MISCELLANEOUS

Section 9 of 11  

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• Miscellaneous
• Multimedia
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Medical/Legal Pitfalls

• The major pitfall in treating zygomycosis is differentiating it from more common bacterial infections, which may delay diagnosis, surgical resection, and appropriate antifungal therapy.
• Rule out invasive zygomycosis early in patients with appropriate risk factors with fungal stains and cultures of affected tissues.

MULTIMEDIA

Section 10 of 11  

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Media file 1:  A 45-year-old woman with poorly controlled diabetes mellitus with facial and periorbital swelling due to zygomycosis. She was unable to open her right eye upon admission.
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Media type:  Photo

Media file 2:  Material from the periorbital tissue of a woman with poorly controlled diabetes mellitus with facial and periorbital swelling due to zygomycosis (see Image 1) is stained with periodic acid-Schiff stain (X 560). The material demonstrates the classic appearance of irregularly shaped broad hyphae with right-angle branching (arrow).
	View Full Size Image
Media type:  Photo

Media file 3:  A CT scan of the head of a patient with zygomycosis shows involvement of the paranasal sinuses and periorbital soft tissues.
	View Full Size Image
Media type:  CT

REFERENCES

Section 11 of 11

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1. Kwon-Chung KJ, Bennett JE. Mucormycosis. In: Cann C, ed. Medical Mycology. Lea & Febiger; 1992:524-59.
2. Rippon JW. Zygomycosis. In: Wonsiewicz M, ed. Medical Mycology. The Pathogenic Fungi and the Pathogenic Actinomycetes. 3^rd ed. Philadelphia, Pa: W.B. Saunders; 1998:681-713.
3. Kontoyiannis DP, Wessel VC, Bodey GP, et al. Zygomycosis in the 1990s in a tertiary-care cancer center. Clin Infect Dis. Jun 2000;30(6):851-6. [Medline].
4. Greenberg RN, Scott LJ, Vaughn HH, et al. Zygomycosis (mucormycosis): emerging clinical importance and new treatments. Curr Opin Infect Dis. Dec 2004;17(6):517-25. [Medline].
5. Kauffman CA. Zygomycosis: reemergence of an old pathogen. Clin Infect Dis. Aug 15 2004;39(4):588-90. [Medline].
6. Ribes JA, Vanover-Sams CL, Baker DJ. Zygomycetes in human disease. Clin Microbiol Rev. Apr 2000;13(2):236-301. [Medline].
7. Gonzalez CE, Rinaldi MG, Sugar AM. Zygomycosis. Infect Dis Clin North Am. Dec 2002;16(4):895-914, vi. [Medline].
8. Petrikkos G, Skiada A, Sambatakou H, et al. Mucormycosis: ten-year experience at a tertiary-care center in Greece. Eur J Clin Microbiol Infect Dis. Dec 2003;22(12):753-6. [Medline].
9. Roden MM, Zaoutis TE, Buchanan WL, et al. Epidemiology and outcome of zygomycosis: a review of 929 reported cases. Clin Infect Dis. Sep 1 2005;41(5):634-53. [Medline].
10. Ibrahim AS, Edwards JE, Filler SG. Zygomycosis. In: Dismukes WE, Pappas PG, Sobel JD, eds. Clinical Mycology. First ed. New York: Oxford University Press; 2003:241-251.
11. Thomson SR, Bade PG, Taams M, et al. Gastrointestinal mucormycosis. Br J Surg. Aug 1991;78(8):952-4. [Medline].
12. Lass-Flörl C, Resch G, Nachbaur D, Mayr A, Gastl G, Auberger J, et al. The value of computed tomography-guided percutaneous lung biopsy for diagnosis of invasive fungal infection in immunocompromised patients. Clin Infect Dis. Oct 1 2007;45(7):e101-4. [Medline].
13. Sun QN, Fothergill AW, McCarthy DI, et al. In vitro activities of posaconazole, itraconazole, voriconazole, amphotericin B, and fluconazole against 37 clinical isolates of zygomycetes. Antimicrob Agents Chemother. May 2002;46(5):1581-2. [Medline].
14. Dannaoui E, Meletiadis J, Mouton JW, et al. In vitro susceptibilities of zygomycetes to conventional and new antifungals. J Antimicrob Chemother. Jan 2003;51(1):45-52. [Medline].
15. Herbrecht R. Posaconazole: a potent, extended-spectrum triazole anti-fungal for the treatment of serious fungal infections. Int J Clin Pract. Jun 2004;58(6):612-24. [Medline].
16. van Burik JA, Hare RS, Solomon HF, Corrado ML, Kontoyiannis DP. Posaconazole is effective as salvage therapy in zygomycosis: a retrospective summary of 91 cases. Clin Infect Dis. Apr 1 2006;42(7):e61-5. [Medline].

Article Last Updated: Aug 18, 2008