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Rhinocerebral Mucormycosis
Article Last Updated: Jun 26, 2006
AUTHOR AND EDITOR INFORMATION
Section 1 of 11  
Author: William P Baugh, MD, Assistant Clinical Professor of Dermatology, University of California Irvine School of Medicine and Western School of Medicine; Medical Director, Full Spectrum Dermatology; Consulting Staff, Department of Dermatology, St Jude Medical Center
William P Baugh is a member of the following medical societies: American Academy of Dermatology, American Society for Laser Medicine and Surgery, and Christian Medical & Dental Society
Coauthor(s):
Kenneth C Earhart, MD, FACP, Deputy Head, Disease Surveillance Program, United States Naval Medical Research Unit #3;
Cynthia L Chen, BA, Clinical Assistant, Full Spectrum Dermatology
Editors: John M Leedom, MD, Professor of Medicine, Keck School of Medicine, University of Southern California; Chief, Division of Infectious Diseases, Department of Internal Medicine, Los Angeles County, University of Southern California Medical Center; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Thomas M Kerkering, MD, Professor of Medicine and Microbiology, Department of Internal Medicine, Division of Infectious Disease, Brody School of Medicine at East Carolina University; Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital; Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Author and Editor Disclosure
Synonyms and related keywords:
phycomycosis, zygomycosis, rhinoorbital mucormycosis, Mucorales, Rhizopus, Absidia, Mucor, Rhizomucor, Saksenaea, Apophysomyces
Background
Rhinocerebral phycomycosis, commonly referred to as mucormycosis, is a rare but serious opportunistic infection of the sinuses and brain caused by saprophytic fungi. Other rare variants of mucormycosis include pulmonary, cutaneous, gastrointestinal, and disseminated forms. Rhinocerebral mucormycosis, the most common manifestation of mucormycosis, is a usually fatal fulminant infection.
Pathophysiology
Saprophytic aerobic fungi of the phycomycetes class, (order Mucorales) cause rhinocerebral mucormycosis (ie, phycomycosis). The 3 genera responsible for most cases are Rhizopus, Absidia, and Mucor. Researchers also report cases caused by Rhizomucor, Saksenaea, Apophysomyces, and Cunninghamella species.
Phycomycetes are common throughout the environment (eg, bread mold found in soil and vegetation) and are frequently found colonizing the oral mucosa, nose, paranasal sinuses, and throat. Mucor thrives in an acid pH and glucose-rich medium. Rhizopus species favor an iron-rich environment and are frequently observed in patients using deferoxamine. Rhizopus oryzae account for many cases of rhinocerebral mucormycosis. Hyperglycemia enhances fungal growth and impairs neutrophil chemotaxis, while lactic acidosis decreases phagocytosis. Mucor is highly resistant to itraconazole in vitro and reacts variably to amphotericin. Sensitivity testing is not standardized and does not necessarily correlate with disease.
These organisms do not generally cause disease in immunocompetent patients. In individuals who are at risk (ie, immunocompromised), the fungus can grow rapidly, invading the orbit and brain. In most patients, the typical port of entry is the sinuses. Transmission occurs through the inhalation of airborne spores.
Infection spreads along vascular and neuronal structures and infiltrates the walls of blood vessels. Infections cause erosion of bone through walls of the sinus and spread into the orbit and the retro-orbital area and may extend into the brain. Invasion of nerves, perineural spread, blood vessels, cartilage, bone, and meninges is common. Direct invasion by fungal elements results in thrombosis and nerve dysfunction. A case of rhinocerebral mucormycosis associated with renal failure has been reported. Advancing infection can result in cavernous sinus thrombosis, carotid artery thrombosis, and jugular vein thrombosis. Complications with carotid artery occlusion have also been reported. The term rhinocerebral indicates sinus involvement but does not always mean that CNS invasion has occurred.
Frequency
United States
The infectious agents are prevalent in nature but may be more prone to cause infection in moist temperate climates.
Mortality/Morbidity
No reports document survivors of mucormycosis before 1955. (Amphotericin became available in the 1950s.) Survival rates among groups of patients with invasive sinus disease without cerebral involvement may be as high as 50-80%. If infection spreads to the brain, case fatality ratios exceed 80%.
Prognosis may improve with rapid diagnosis, early management, and reversible underlying risk factors. Underlying disease is the most important determinant of survival.
Sex
Incidence does not appear to vary based on sex.
Age
Incidence does not appear to vary based on age.
History
Symptoms are often nonspecific, making early diagnosis difficult. The most common presentation is face or orbit pain, headache, lethargy, visual loss, proptosis, or palatal ulcer. Perinasal cellulitis or paresthesia is also a common early clinical sign of the disease. The incubation period is measured in days. The clinical course can progress from normal to symptomatic in a week and from sinus opacification to uncal herniation and death in just a few days.
- General symptoms
- Headache
- Nausea
- Fever
- Lethargy
- Nasal symptoms
- Purulent drainage
- Stuffiness and rhinorrhea
- Epistaxis
- Nasal hypoesthesia
- Eye symptoms
- Periorbital or retro-orbital pain
- Diplopia and blurred vision
- Amaurosis (unilateral or bilateral)
- May rapidly progress to blindness
- CNS symptoms: Convulsions can be the presenting sign. Alteration in mental status and lethargy may lead to paresis and death.
Physical
Most patients have diabetes mellitus, usually with acidosis and poor glycemic control. Patients with diabetic ketoacidosis (DKA) accompanied by mental status changes should improve within 24-48 hours; if they do not, consider CNS pathology.
- The palate or nasal turbinates may appear gray or erythematous and may progress to black necrotic masses or ulceration (ie, black eschar). A necrotic area to the alar crease or pain and swelling of the cheek may be observed. A rapid clinical course is standard.
- Eye findings
- Invasion of orbit
- Orbital cellulitis
- Proptosis
- Ophthalmoplegia
- Fixed pupil
- Orbital apex syndrome
- Blindness
- Visual loss secondary to thrombosis of retinal artery or direct fungal invasion
- Neurologic findings
- Palsies of cranial nerves II, III, IV, and VII (especially the abducens) are observed.
- Progression leads to coma and stroke from cerebral edema and vascular compromise.
Causes
Seventy percent of Mucor infections occur in patients with diabetes mellitus, although this percentage is declining with the use of chemotherapy and as the frequency of other immunocompromised states become more common. Fewer than 4% of cases occur without a recognized underlying condition.
- Risk factors
- Diabetes mellitus: This condition is a risk factor, particularly with poor glycemic control and acidosis as it relates to cellular immune dysfunction.
- Iron overload
- These states may be risk factors, as observed with hemochromatosis and deferoxamine treatment in patients receiving dialysis.
- Iron enhances fungal growth and leads to increased host susceptibility.
- Researchers report infection in patients with liver and renal failure.
- Burn patients: In burn patients, Mucor generally involves the skin and only rarely causes the rhinocerebral form.
- Leukemia: Researchers estimate that the incidence in hematologic malignancy is approximately 1%.
- Lymphoma
- Transplantation
- Infection may occur after solid organ (eg, liver, kidney) and bone marrow transplants and in association with graft versus host disease (GVHD), severe neutropenia, or steroid therapy.
- The incidence of Mucor in allogeneic bone marrow transplants is 1.9%; however, most cases do not involve the CNS.
- Immunosuppression
- Prolonged neutropenia
- Chemotherapy
- High-dose steroids
- Following donor leukocyte infusions
- Acquired immunodeficiency syndrome (AIDS)
- Intravenous drug use (embolic to brain)
Aspergillosis
Graves Disease
Other Problems to be Considered
Migraines
Chronic sinusitis
Dental abscess
Other causes of eye pain
Blepharitis
Preseptal cellulitis
Orbital cellulitis
Other causes of proptosis
Orbital tumor
Posttraumatic subperiosteal hematoma
Inflammatory pseudotumor
Cavernous sinus thrombosis
Infection may resemble sinusitis initially and mimic malignancy.
Rhinocerebral phycomycoses may be confused with allergic fungal sinusitis, which is caused by phaeohyphomycoses in patients with histories of allergic rhinitis, elevated immunoglobulin E, nasal polyps, and recurrent or chronic sinusitis. Infection slowly progresses over months to years, and, although it causes proptosis and a large rhinocerebral mass, it does not invade tissue or meninges.
Aspergillosis can cause a similar disease with CNS invasion and poor prognosis; an important difference is that itraconazole may play a role in treatment.
Lab Studies
- Diagnosis depends on the demonstration of tissue invasion using biopsy. The aggressive clinical features of the disease suggest the diagnosis. Laboratory study results are generally nonspecific but may show metabolic acidosis and hyperglycemia.
- Blood culture findings are negative.
- Sinus culture findings may be positive, although this may only reflect colonization. Culture identifies the species, while evidence of tissue invasion in histology samples confirms the diagnosis.
- Cerebrospinal fluid (CSF), if inadvertently examined, may show an increased opening pressure, modest neutrophilic pleocytosis, normal or slightly elevated protein levels, or low glucose. In most cases, CSF study findings were normal.
- Direct microscopic examination can be performed to identify the hyphae of infectious agents.
- Scrape smears stained with hematoxylin-eosin (H&E) and Papanicolaou stains
- Air-dried smears stained with May-Grunwald-Giemsa and periodic acid-Schiff (PAS) stains
- Paraffin sections of surgical material stained with H&E and PAS stains
Imaging Studies
- Imaging helps to support the diagnosis and to precisely determine the extent of disease.
- Sinus radiographs reveal mucosal thickening with or without air-fluid levels. Sinus opacification, especially ethmoid or sphenoid, may be observed.
- CT scanning demonstrates mucosal thickening, opacification of sinuses, and bony destruction of the sinuses and orbit. A CT scan may also demonstrate cavernous sinus thrombosis, enhancement of vessels, and CNS lesions (eg, cerebritis, cerebral edema).
- MRI shows findings similar to those on a CT scan. MRI additionally helps to define early vascular intracranial invasion before clinical signs develop.
Procedures
- Fine-needle aspiration can yield a diagnosis but should not preclude definitive therapy.
Histologic Findings
Frozen tissue biopsy at the time of surgery should demonstrate tissue invasion by nonseptate hyphae with right- or obtuse-angle branching. The tissue culture result is positive for the fungus. Histology demonstrates invasion along the elastic lamina of blood vessels with subsequent thrombosis and tissue necrosis.
Medical Care
Clinicians treat rhinocerebral mucormycosis by (1) reversing underlying immunocompromised states, (2) administering systemic antifungals, and (3) performing urgent surgical debridement. No studies address the appropriate dose or formulation of antifungal therapy; therefore, clinicians use a wide range of doses and formulations. Antifungal therapy alone or surgical therapy alone is not effective.
- Aggressively control hyperglycemia and acidosis.
- Discontinue or maximally reduce chemotherapy and immunosuppressive therapy.
- Promptly initiate antifungal therapy. Amphotericin B is the only reliable systemic antifungal agent approved for the treatment of mucormycoses.
- Growth colony-stimulating factor (GCSF) can be administered to reconstitute host defenses and enhance leukocytosis.
- If disease is limited to the sinus and orbit (ie, sino-orbital), debridement and systemic antifungals combined with local amphotericin irrigation may control the process.
- Physicians have used hyperbaric oxygen (HBO) to attempt control of the infection. Experts suggest that HBO may have fungistatic activity by reducing tissue hypoxia and acidosis. No studies address its efficacy.
- Physicians have used dexamethasone for brain edema.
Surgical Care
The mainstay of therapy is extensive debridement of all infected and necrotic tissue with drainage of all sinus and abscess fluid collections.
- Immediately obtain a surgical consultation. Conservative attempts to spare tissue may result in retention of the organism and subsequent failure of treatment.
- Intraoperative frozen sections help determine involved tissues and margins.
- Treatment may require orbital debridement and exenteration.
- Decreased survival with delay in surgery may result in all forms of invasive mucormycosis.
- Wide excision should ideally occur before CNS invasion.
- The role of endoscopic sinus surgery is unclear, although it may provide some initial diagnostic role.
Consultations
- Infectious diseases
- Neurosurgery
- Ophthalmology
- Otolaryngology
Unlike the phaeohyphomycoses that cause fungal sinusitis, the currently approved azoles have no activity against Mucor molds. Amphotericin B is fungistatic for Mucor molds but is the only reliable systemic antifungal agent. Amphotericin is a highly toxic agent that is administered intravenously in its conventional form or in 1 of 3 new lipid-complex formulations. Physicians have also administered amphotericin by intracavitary (ie, via catheter into the space), interstitial, and intrathecal methods. Reports document use of nebulized amphotericin B for sinonasal disease. Large doses are required for cure.
Only conventional amphotericin B is approved by the US Food and Drug Administration (FDA) as initial therapy; thus, it is considered the standard therapy for invasive mucormycosis. Lipid formulations are approved if creatinine rises to greater than 2.5 mg/dL, if adverse events are severe and persistent, or if disease progresses despite a total dose greater than 500 mg. Experience with the lipid formulations is growing, but no head-to-head studies exist. Many experts initiate therapy with a lipid-complex formulation if there is preexisting renal impairment. Some experts argue that lipid-formulation amphotericin offers better penetration across the blood-brain barrier and into the sinus.
Use amphotericin at the maximum dose tolerated for this life-threatening infection. Experimental antifungal agents have demonstrated in vitro activity against the Mucor molds and may offer additional treatment options in the future.
Drug Category: Antifungal agents
Their mechanism of action may involve inhibition of fungal cell membrane formation and impairing the integrity of fungal cell membrane.
| Drug Name | Amphotericin B (Fungizone) |
|---|
| Description | Polyene antibiotic with poor oral availability. Produced by a strain of Streptomyces nodosus; can be fungistatic or fungicidal. Binds to sterols (eg, ergosterol) in the fungal cell membrane, causing leakage of intracellular components and fungal cell death. Toxicity to human cells may occur via this same mechanism. |
|---|
| Adult Dose | 0.25-1 mg IV test dose infused over 30-60 min; observe for severe fever, chills, hypotension
1-1.5 mg/kg/d IV infusion over 4-6 h |
|---|
| Pediatric Dose | 0.5-1 mg/kg/d IV recommended test dose infusion over 4-6 h
Alternatively: 0.25 mg/kg IV on day 1, 0.5 mg/kg IV on day 2, then 1 mg/kg/d IV |
|---|
| Contraindications | Documented hypersensitivity |
|---|
| Interactions | Antineoplastic agents may enhance the potential of amphotericin B for renal toxicity, bronchospasm, and hypotension; corticosteroids, digitalis, and thiazides may potentiate hypokalemia; the risk of renal toxicity is increased with cyclosporine |
|---|
| Pregnancy | B - Usually safe but benefits must outweigh the risks.
|
|---|
| Precautions | Monitor renal function, serum electrolytes (eg, magnesium, potassium), liver function, CBC, and hemoglobin concentrations; resume therapy at the lowest level (eg, 0.25 mg/kg) when therapy is interrupted for more than 7 d; hypoxemia, acute dyspnea, and interstitial infiltrates may occur in neutropenic patients receiving leukocyte transfusions (separate time of amphotericin infusion from time of leukocyte transfusion) |
|---|
| Drug Name | Amphotericin B lipid complex (ABLC, Abelcet) |
|---|
| Description | Amphotericin B in phospholipid complexed form. Polyene antibiotic with poor oral availability. Produced by a strain of Streptomyces nodosus; can be fungistatic or fungicidal. Binds to sterols (eg, ergosterol) in the fungal cell membrane, causing leakage of intracellular components and fungal cell death. Toxicity to human cells may occur via this same mechanism. |
|---|
| Adult Dose | 5 mg/kg/d IV infusion over 2 h |
|---|
| Pediatric Dose | Administer as in adults |
|---|
| Contraindications | Documented hypersensitivity |
|---|
| Interactions | Antineoplastic agents may enhance the potential of amphotericin B for renal toxicity, bronchospasm, and hypotension; corticosteroids, digitalis, and thiazides may potentiate hypokalemia; the risk of renal toxicity is increased with cyclosporine |
|---|
| Pregnancy | B - Usually safe but benefits must outweigh the risks.
|
|---|
| Precautions | Acute infusional toxicities per conventional amphotericin B occur at a somewhat lower rate; nephrotoxicity is less frequent and less severe, but can still occur; monitoring of electrolytes, BUN, and creatinine is still required, and potassium and magnesium should be replaced as needed |
|---|
| Drug Name | Amphotericin B (AmBisome) |
|---|
| Description | A lipid preparation consisting of amphotericin B within unilamellar liposomes. Delivers higher concentrations of the drug, with a theoretical increase in therapeutic potential and decreased nephrotoxicity.
Polyene antibiotic with poor oral availability. Produced by a strain of Streptomyces nodosus; can be fungistatic or fungicidal. Binds to sterols (eg, ergosterol) in the fungal cell membrane, causing leakage of intracellular components and fungal cell death. Toxicity to human cells may occur via this same mechanism. |
|---|
| Adult Dose | 5-7.5 mg/kg/d IV infused over 2 h |
|---|
| Pediatric Dose | 5 mg/kg/d IV infused over 2 h |
|---|
| Contraindications | Documented hypersensitivity |
|---|
| Interactions | Antineoplastic agents may enhance the potential of amphotericin B for renal toxicity, bronchospasm, and hypotension; corticosteroids, digitalis, and thiazides may potentiate hypokalemia; the risk of renal toxicity is increased with cyclosporine |
|---|
| Pregnancy | B - Usually safe but benefits must outweigh the risks.
|
|---|
| Precautions | Acute infusional toxicities per conventional amphotericin B occur at a somewhat lower rate; nephrotoxicity is less frequent and less severe, but can still occur; monitoring of electrolytes, BUN, and creatinine is still required, and potassium and magnesium should be replaced as needed |
|---|
| Drug Name | Amphotericin B colloidal dispersion (Amphocil, ABCD) |
|---|
| Description | A lipid preparation consisting of amphotericin B attached to lipid discoid structures.
Polyene antibiotic with poor oral availability. Produced by a strain of Streptomyces nodosus; can be fungistatic or fungicidal. Binds to sterols (eg, ergosterol) in the fungal cell membrane, causing leakage of intracellular components and fungal cell death. Toxicity to human cells may occur via this same mechanism. |
|---|
| Adult Dose | 2-7.5 mg/kg/d IV infused over 2 h |
|---|
| Pediatric Dose | Administer as in adults |
|---|
| Contraindications | Documented hypersensitivity |
|---|
| Interactions | Antineoplastic agents may enhance the potential of amphotericin B for renal toxicity, bronchospasm, and hypotension; corticosteroids, digitalis, and thiazides may potentiate hypokalemia; the risk of renal toxicity is increased with cyclosporine |
|---|
| Pregnancy | B - Usually safe but benefits must outweigh the risks.
|
|---|
| Precautions | Acute infusional toxicities per conventional amphotericin B occur at a somewhat lower rate; nephrotoxicity is less frequent and less severe, but can still occur; monitoring of electrolytes, BUN, and creatinine is still required, and potassium and magnesium should be replaced as needed |
|---|
| Drug Name | Fluconazole (Diflucan) |
|---|
| Description | Bis-triazole antifungal agent. Fluconazole binds to the fungal p450 enzymes and stops the cells that make ergosterol, the main component of the cell wall. |
|---|
| Adult Dose | Individualize; 200 mg PO on day 1, then 100 mg/d PO for at least 2 wk |
|---|
| Pediatric Dose | Individualize; 6 mg/kg on day 1, then 3 mg/kg/d for at least 3 wk; treat for at least 2 wk after symptoms resolve; max 12 mg/kg/d |
|---|
| Contraindications | Documented hypersensitivity |
|---|
| Interactions | Fluconazole may increase the concentration and enhance the effects of warfarin, antidiabetic sulfonylurea medication (tolbutamide, glibenclamide, gliclazide, glipizide), phenytoin, theophylline, ciclosporin, and celecoxib |
|---|
| Pregnancy | C - Safety for use during pregnancy has not been established.
|
|---|
| Precautions | Side effects include vomiting, diarrhea, abdominal pain, and skin rashes; may cause hepatoxicity |
|---|
Further Inpatient Care
- If the patient survives the initial presentation, the extent of disease dictates additional inpatient care. Further surgical debridement, surgical repair, and wound care may be required. Continue medical therapy with close monitoring for drug toxicity or recurrence of disease.
Further Outpatient Care
- Once the patient is stable, continue amphotericin in the outpatient setting, administered either as a home infusion or in an ambulatory infusion center. At this point, the frequency of amphotericin infusion is often reduced to every other day or more, depending on renal function.
- Follow-up MRI or CT scans at the end of therapy should demonstrate significant improvement and lack of inflammation.
- Treatment may require 7 months of therapy or more.
- Physicians have observed chronic presentations and late sequelae after successful therapy; therefore, patients require long-term monitoring to detect recurrence or signs of indolent residual infection.
Complications
- Rhinocerebral mucormycosis progresses rapidly, resulting in carotid artery occlusion, cavernous sinus thrombosis, CNS infarction secondary to fungal thrombosis leading to hemiparesis, hemiplegia, coma, and death.
- Other complications include CNS hemorrhage, abscess, and cerebritis.
- Postsurgical disfigurement is likely.
- Patients can recover neurologic function if no irreversible damage has occurred, but morbidity is very common.
Prognosis
- Prognosis involves high morbidity and mortality; survival depends on reversibility of underlying risk factors and early surgical intervention.
Patient Education
Medical/Legal Pitfalls
- The only medicolegal information in the literature is the discussion by Bullock and Warwar (1999). Bullock relates his personal experience and discusses the controversy of exenteration. The authors aptly state that patients, family members, and all involved health care personnel must understand that the physical and psychological morbidity of disfiguring wide surgical debridement must be weighed against the life-threatening nature of the disease.
| Media file 1:
Clinical view of the face of a patient with rhinocerebral mucormycosis. |
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| Media file 3:
A tissue hematoxylin and eosin stain of Rhizopus species. |
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| Media file 4:
The appearance of a culture slant of Rhizopus species. |
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| Media file 6:
Low-power photomicrograph of a Gomori methenamine silver stain of Rhizopus species. |
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| Media file 7:
High-power photomicrograph of a Gomori methenamine silver stain of Rhizopus species. |
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| Media file 8:
CT brain scan illustrating the appearance of cavernous sinus thrombosis. |
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| Media file 9:
CT brain scan showing the appearance of a cerebral infarct. |
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Rhinocerebral Mucormycosis excerpt Article Last Updated: Jun 26, 2006
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