Noncandidal Fungal Infections of the Mouth Medication

  • Author: Crispian Scully, MD, PhD, MDS, CBE, MRCS, FDSRCS, FDSRCPS, FFDRCSI, FDSRCSE, FRCPath, FMedSci, FHEA, FUCL, DSc, DChD, DMed(HC), Dr(HC), ; Chief Editor: William D James, MD   more...
 
Updated: Apr 10, 2012
 

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

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Antifungal Agents

Class Summary

The mechanism of action usually involves inhibiting pathways (enzymes, substrates, transport) necessary for sterol and/or cell membrane synthesis or altering the permeability of the fungal cell membrane (polyenes).

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Amphotericin B (Amphocin, Fungizone)

 

Polyene antibiotic produced by a strain of Streptomyces nodosus; can be fungistatic or fungicidal. Binds to sterols, (eg, ergosterol) in the fungal cell membrane, causing intracellular components to leak, with subsequent fungal cell death.

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Caspofungin (Cancidas)

 

Used to treat refractory invasive aspergillosis. First of a new class of antifungal drugs (glucan synthesis inhibitors). Inhibits synthesis of beta-(1,3)-D-glucan, an essential component of the fungal cell wall.

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Flucytosine (Ancobon)

 

Converted to fluorouracil after penetrating fungal cells. Inhibits RNA and protein synthesis. Active against Candida and Cryptococcus species and is generally used in combination with amphotericin B. Treats aspergillosis.

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Fluconazole (Diflucan)

 

Fungistatic activity. Synthetic oral antifungal (broad-spectrum bistriazole) that selectively inhibits fungal cytochrome P-450 and sterol C-14 alpha-demethylation, which prevents conversion of lanosterol to ergosterol, thereby disrupting cellular membranes.

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Ketoconazole (Nizoral)

 

Fungistatic activity. Imidazole broad-spectrum antifungal; inhibits synthesis of ergosterol, causing cellular components to leak and resulting in fungal cell death.

Miconazole (Monistat IV)

 

Damages fungal cell wall membrane by inhibiting biosynthesis of ergosterol. Membrane permeability is increased, causing nutrients to leak and resulting in fungal cell death. Interferes with mitochondrial enzymes.

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Itraconazole (Sporanox)

 

Fungistatic activity. Synthetic triazole antifungal agent that slows fungal cell growth by inhibiting cytochrome P-450 – dependent synthesis of ergosterol, a vital component of fungal cell membranes.

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Posaconazole (Noxafil)

 

Triazole antifungal agent. Blocks ergosterol synthesis by inhibiting the enzyme lanosterol 14-alpha-demethylase and sterol precursor accumulation. This action results in cell membrane disruption. Available as oral susp (200 mg/5 mL). Indicated for prophylaxis of invasive Aspergillus and Candida infections in patients at high risk because of severe immunosuppression.

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Voriconazole (Vfend)

 

Used for primary treatment of invasive aspergillosis and salvage treatment of Fusarium species or Scedosporium apiospermum infections. A triazole antifungal agent that inhibits fungal CYP450-mediated 14 alpha-lanosterol demethylation, which is essential in fungal ergosterol biosynthesis.

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Contributor Information and Disclosures
Author

Crispian Scully, MD, PhD, MDS, CBE, MRCS, FDSRCS, FDSRCPS, FFDRCSI, FDSRCSE, FRCPath, FMedSci, FHEA, FUCL, DSc, DChD, DMed(HC), Dr(HC),  Professor of Oral Medicine, Bristol University; Co-Director of World Health Organization Collaborating Centre for Oral Health-General Health; Emeritus Professor of Oral Medicine and Special Care Dentistry, University College London; Professor, Oral Medicine, Pathology, and Microbiology, University of London; Visiting Professor at Universities of Athens,Edinburgh, Granada, Helsinki and Plymouth

Crispian Scully, MD, PhD, MDS, CBE, MRCS, FDSRCS, FDSRCPS, FFDRCSI, FDSRCSE, FRCPath, FMedSci, FHEA, FUCL, DSc, DChD, DMed(HC), Dr(HC), is a member of the following medical societies: Academy of Medical Science, British Society for Oral Medicine, European Association for Oral Medicine, International Academy of Oral Oncology, International Association for Dental Research, and International Association for Oral and Maxillofacial Pathology

Disclosure: Nothing to disclose.

Coauthor(s)

Maria Regina Sposto, DDS, PhD, MDSc(Dental Science), PhD(Dentistry)  Associate Professor of Oral Diagnosis and Oral Medicine, Consulting Staff, Department of Oral Surgery and Diagnosis, Faculdade de Odontologia de Araraquara, UNESP-Universidade Estadual Paulista, Brazil

Disclosure: Nothing to disclose.

Specialty Editor Board

Shyam Verma  MBBS, DVD, FAAD, Clinical Associate Professor, Department of Dermatology, University of Virginia; Adjunct Associate Professor, Department of Dermatology, State University of New York at Stonybrook, Adjunct Associate Professor, Department of Dermatology, University of Pennsylvania

Shyam Verma is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

David F Butler, MD  Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic

David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Drore Eisen, MD, DDS  Consulting Staff, Department of Dermatology, Dermatology Research Associates of Cincinnati

Drore Eisen, MD, DDS is a member of the following medical societies: American Academy of Dermatology, American Academy of Oral Medicine, and American Dental Association

Disclosure: Nothing to disclose.

Catherine M Quirk, MD  Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania

Catherine M Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology

Disclosure: Nothing to disclose.

Chief Editor

William D James, MD  Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology and Society for Investigative Dermatology

Disclosure: Elsevier Royalty Other

Additional Contributors

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author, Oslei Paes de Almeida, MD, to the development and writing of this article.

References

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Cryptococcosis. Left image shows solitary, destructive lesion resulting in necrosis of alveolar bone and palatal mucosa; note the superficial pseudomembranous candidiasis of the palate. Right image shows nonspecific chronic ulceration of the buccal mucosa due to cryptococcosis; this is associated with submucosal induration and regional adenopathy. Courtesy of David Sirois, DMD, PhD.
Aspergillosis. Note deep mucosal ulceration and nodular expansion of the hard palate. Courtesy of David Sirois, DMD, PhD.
Blastomycosis. Top image shows nonspecific papillary nodular lesion on the hard palate. Bottom image shows extensive ulceration involving the skin of the face and neck. Courtesy of David Sirois, DMD, PhD.
Histoplasmosis. Top image shows periodontal recession and deep ulceration with exposed necrotic alveolar bone (arrow). Bottom image shows solitary, deep ulceration of the gingivae also associated with necrotic bone (arrow). Courtesy of David Sirois, DMD, PhD.
Mucormycosis. Top left image shows multiple, deep ulcerations (arrows) of the hard palate. Top right image shows destruction of the palate and the floor of the orbit (failed skin graft of the right eye after orbital enucleation); this infection originated in the maxillary sinus. Bottom image shows similar deep, destructive ulceration of the left posterior maxillary alveolar bone and mucosa due to mucormycosis of the maxillary sinus. Courtesy of David Sirois, DMD, PhD.
 
 
 
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