eMedicine Specialties > Infectious Diseases > HEENT Infections

Rhinocerebral Mucormycosis

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
Coauthor(s): Cynthia L Chen, BA, Western University of Health Sciences College of Osteopathic Medicine of the Pacific
Contributor Information and Disclosures

Updated: Feb 11, 2009

Introduction

Background

Rhinocerebral mucormycosis (RCM) is a rare opportunistic infection of the sinuses and brain caused by saprophytic fungi. The infection can rapidly result in death. Rhinocerebral mucormycosis commonly affects individuals with diabetes and those in immunocompromised states. Other rare variants of mucormycosis include lingual, pulmonary, cutaneous, gastrointestinal, and disseminated forms. For additional information on other types of mucormycosis, see the article Mucormycosis in eMedicine’s Infectious Diseases volume.

Pathophysiology

Saprophytic aerobic fungi of the Phycomycetes class (order Mucorales) cause rhinocerebral mucormycosis, also known as phycomycosis. The three genera responsible for most cases include Rhizopus, Absidia, and Mucor. Researchers have also reported cases of rhinocerebral mucormycosis caused by Rhizomucor, Saksenaea, Apophysomyces, and Cunninghamella species.

Phycomycetes are ubiquitous in nature, commonly found in decaying vegetation, soil, and bread mold. They grow rapidly and can release large numbers of airborne spores. Thus, they are frequently found colonizing the oral mucosa, nose, paranasal sinuses, and throat. Phycomycetes do not generally cause disease in immunocompetent individuals who are able to generate phagocytic containment of the organisms. Persons at risk for infection (ie, immunocompromised) typically also have decreased phagocytic activity because of an impaired glutathione pathway.

Rhizopus species have an active ketone reductase system that enables them to thrive in an acidic pH and glucose-rich medium. Hyperglycemia enhances fungal growth and impairs neutrophil chemotaxis; therefore, individuals with diabetic ketoacidosis are commonly affected. Rhizopus species also favor an iron-rich environment and are frequently isolated in patients receiving deferoxamine therapy (an iron-chelating agent).

In most cases, the fungi gain entry to the body via inhalation of airborne spores through the sinuses. It has been postulated that the most common reservoir for organisms is the pterygopalatine fossa. Infection spreads along vascular and neuronal structures and infiltrates the walls of blood vessels. Infections can erode bone through walls of the sinus and can spread into the orbit and the retro-orbital area, thereby extending into the brain.

Invasion of nerves, blood vessels, cartilage, bone, and meninges and perineural spread1,2 are common. Direct invasion by fungal elements results in thrombosis and nerve dysfunction. Advancing infection can result in thromboses arising in the cavernous sinus, carotid arteries, and jugular vein. Carotid artery occlusion has also been reported as a complication.3,4,5

Frequency

United States

The pathogens that cause rhinocerebral mucormycosis are prevalent in nature but may be more prone to cause infection in moist temperate climates.

Mortality/Morbidity

No survivors of mucormycosis had been reported before 1955. (Amphotericin became available in the 1950s.)

Mucormycosis has a fulminantly fatal clinical pattern. The survival rates among patients with invasive sinus disease without cerebral involvement may be as high as 50-80%. If infection spreads to the brain, the case fatality rate can exceed 80%.

The prognosis of mucormycosis may improve with rapid diagnosis, early management including combined antifungal and surgical interventions, and reversal of underlying risk factors. One case series reported that the survival rate is approximately 80% when both medical and surgical interventions are administered. The cause of death in many patients is mucormycosis itself rather than the progression of the underlying disease.

Sex

Rhinocerebral mucormycosis does not appear to have a sexual predilection.

Age

Rhinocerebral mucormycosis does not appear to have an age predilection. For additional information on pediatric mucormycosis, see the article Mucormycosis in eMedicine’s Pediatrics: General Medicine volume.

Clinical

History

Symptoms of rhinocerebral mucormycosis (RCM) are often nonspecific, complicating early diagnosis. The most common presentation includes facial pain, headache, lethargy, visual loss, proptosis, and/or palatal ulcer. Perinasal cellulitis and paresthesia are also common early clinical signs of rhinocerebral mucormycosis. 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
  • Facial symptoms
    • Weakness
    • Numbness
    • Pain
  • Nasal symptoms
    • Purulent drainage
    • Stuffiness and rhinorrhea
    • Epistaxis
    • Nasal hypoesthesia
  • Ocular symptoms (For additional information on ocular manifestations of mucormycosis, see the article Mucormycosis in eMedicine’s Ophthalmology volume.)
    • Periorbital or retro-orbital pain
    • Diplopia and blurred vision
    • Amaurosis (unilateral or bilateral)
    • May rapidly progress to blindness
  • CNS symptoms
    • Convulsions
    • Altered mental status
    • Dizziness
    • Unsteady gait

Physical

Many individuals with rhinocerebral mucormycosis have underlying diabetes mellitus, usually with acidosis and poor glycemic control. Patients with diabetic ketoacidosis accompanied by mental status changes should improve within 24-48 hours; if they do not, consider CNS pathology.

  • Nasal and palatal findings
    • Gray or erythematous appearance
    • Can progress to black necrotic masses (ie, black eschar)
    • Inflammation
  • Ocular findings
    • Orbital invasion
    • Orbital cellulitis
    • Proptosis
    • Ophthalmoplegia
    • Fixed pupil
    • Orbital apex syndrome6
    • Blindness
    • Nystagmus
    • Visual loss secondary to retinal artery thrombosis or direct fungal invasion
  • Neurologic findings
    • Palsies of cranial nerves II, III, IV, V, VI, and VII are commonly observed, prompting a thorough neurologic workup.
    • Cerebral edema and vascular compromise may lead to coma and stroke.

Causes

Seventy percent of mucormycosis cases occur in patients with diabetes mellitus, although this percentage is declining with the use of chemotherapy and as increasing frequency of other types of immunocompromised state. An underlying risk factor is recognized in more than 96% of mucormycosis cases.

  • Risk factors for rhinocerebral mucormycosis include the following:
    • Diabetes mellitus: This condition is a risk factor, particularly in association with poor glycemic control and acidosis as it relates to cellular immune dysfunction.
    • Iron overload
      • Iron overload states, as observed with hemochromatosis and deferoxamine treatment in patients receiving dialysis, may be risk factors.
      • Iron enhances fungal growth and increases susceptibility.
      • Researchers have reported infection in patients with liver and renal failure.7
    • Burns: In individuals with burns, mucormycosis generally involves only the skin and rarely results in rhinocerebral infection.8
    • HIV infection
    • AIDS
    • Blood dyscrasias
      • Leukemia: Researchers estimate that the incidence of mucormycosis in persons with hematologic malignancy is approximately 1%.
      • Lymphoma
      • Prolonged neutropenia
    • Transplantation
      • Solid organ (eg, liver,9 kidney10 ) and bone marrow transplantation: Maertens et al (1999) found that the incidence of mucormycosis in recipients of allogeneic bone marrow transplants was 1.9%.11 However, most cases do not involve the CNS.
      • Graft versus host disease (GVHD)
      • Donor leukocyte infusions12
    • Immunosuppression (ie, prednisone therapy)13
    • Chemotherapy
    • Disease states treated with high-dose steroids: One case report described mucormycosis in a patient with an adrenal corticotropic hormone (ACTH)–producing pulmonary tumor, associated with Cushing syndrome.14
    • Intravenous drug use (embolic to brain)

More on Rhinocerebral Mucormycosis

Overview: Rhinocerebral Mucormycosis
Differential Diagnoses & Workup: Rhinocerebral Mucormycosis
Treatment & Medication: Rhinocerebral Mucormycosis
Follow-up: Rhinocerebral Mucormycosis
Multimedia: Rhinocerebral Mucormycosis
References
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Further Reading

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Keywords

rhinocerebral mucormycosis, RCM, phycomycosis, zygomycosis, rhinoorbital mucormycosis, rhino-orbital mucormycosis, Mucorales, Rhizopus, Absidia, Mucor, Rhizomucor, Saksenaea, Apophysomyces

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Contributor Information and Disclosures

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, MD is a member of the following medical societies: American Academy of Dermatology, American Society for Laser Medicine and Surgery, and Christian Medical & Dental Society
Disclosure: Nothing to disclose.

Coauthor(s)

Cynthia L Chen, BA, Western University of Health Sciences College of Osteopathic Medicine of the Pacific
Disclosure: Nothing to disclose.

Medical Editor

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
John M Leedom, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, American Society for Microbiology, Infectious Diseases Society of America, International AIDS Society, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Thomas M Kerkering, MD, Chief of Infectious Diseases, Virginia Tech, Carilion School of Medicine, Roanoke, Virginia
Thomas M Kerkering, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Public Health Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Medical Society of Virginia, and Wilderness Medical Society
Disclosure: Nothing to disclose.

CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Chief Editor

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
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

 
 
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