eMedicine Specialties > Dermatology > Parasitic Infections

Protothecosis, Cutaneous: Treatment & Medication

Author: Sarah K Taylor, MD, Staff Physician, Department of Dermatology, Walter Reed Army Medical Center and National Naval Medical Center
Coauthor(s): Jon H Meyerle, MD, Assistant Professor, Department of Dermatology, Johns Hopkins University School of Medicine; Consulting Staff, Laboratory Director, Department of Dermatology, Walter Reed Army Medical Center and National Naval Medical Center; Earl J Glusac, MD, Professor, Departments of Pathology and Dermatology, Yale University School of Medicine
Contributor Information and Disclosures

Updated: Dec 11, 2008

Treatment

Medical Care

Protothecosis is difficult to eradicate once infection takes hold. Given that the infection is rare, no defined pharmacologic protocol is available. All reported patients with disseminated disease have been treated with intravenous amphotericin B. Isolated reports describe successful treatment of localized disease with ketoconazole, itraconazole, and fluconazole. Sensitivity in vitro has not been shown to be correlated with in vivo efficacy. Surgical removal of isolated lesions in combination with antifungal therapy (eg, with azoles) is effective in immunocompetent individuals.

Surgical Care

Surgical excision is the treatment of choice in all cases amenable to excision.

Medication

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

Antifungal agents

These agents exert a fungicidal effect by altering the permeability of the fungal cell membrane. The mechanism of action may also involve an alteration of RNA and DNA metabolism or an intracellular accumulation of peroxide that is toxic to the fungal cell.


Amphotericin B (AmBisome)

For use in disseminated disease. Produced by a strain of Streptomyces nodosus; can be fungistatic or fungicidal. Binds to sterols (eg, ergosterol) in fungal cell membrane, causing intracellular components to leak with subsequent fungal cell death.

Adult

3-5 mg/kg/d IV of liposomal amphotericin B over approximately 120 min

Pediatric

Administer as in adults

Antineoplastic agents may enhance the potential for renal toxicity, bronchospasm, and hypotension; corticosteroids, digitalis, and thiazides may potentiate hypokalemia; risk of renal toxicity increased with cyclosporine

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Monitor renal function, serum electrolyte levels (eg, magnesium, potassium), liver function, CBC, and hemoglobin concentrations; resume therapy at lowest level (eg, 0.25 mg/kg) when therapy is interrupted for > 7 d; hypoxemia, acute dyspnea, and interstitial infiltrates may occur in patients with neutropenia receiving leukocyte transfusions (separate time of amphotericin infusion from time of leukocyte transfusion)


Fluconazole (Diflucan)

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. Has little affinity for mammalian cytochromes, which is believed to explain its low toxicity. Available as tabs for oral administration, as a powder for oral suspension, and as a sterile solution for IV use. Has fewer adverse effects and better tissue distribution than older systemic imidazoles.
Can be used in severe or life-threatening infections in patients intolerant of amphotericin B and may be used for maintenance after a course of amphotericin B in coccidioidal meningitis. Penetrates well into CSF. Metabolic clearance is prolonged in patients with renal dysfunction.

Adult

400 mg/d PO/IV; in certain circumstances dosages of 800 mg/d or higher have been administered

Pediatric

Not established

Levels may increase with hydrochlorothiazides; levels may decrease with chronic coadministration of rifampin; may increase concentrations of theophylline, phenytoin, tolbutamide, cyclosporine, glyburide, and glipizide; effects of anticoagulants may increase with coadministration

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Adjust dose for renal insufficiency; closely monitor if rashes develop, and discontinue drug if lesions progress; may cause clinical hepatitis, cholestasis, and fulminant hepatic failure (including death) when taken with underlying medical conditions (eg, AIDS, malignancy) or while taking multiple concomitant medications; not recommended for breastfeeding mothers
Convenience and efficacy of single-dose regimen for treatment of vaginal yeast infections should be weighed against difficulties resulting from higher incidence of adverse reactions reported with oral fluconazole versus intravaginal agents


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.

Adult

200 mg PO qd; not to exceed 400 mg/d; increase in 100-mg increments if no improvement (administer >200 mg/d in divided doses)
200 mg IV bid for 4 doses, followed by 200 mg/d
Nail infections: 200 mg/d PO for 3-4 mo or pulse dosing of 400 mg/d for 1 wk each mo for 3-4 mo

Pediatric

Not established; 100 mg/d PO suggested for systemic fungal infections

Antacids may reduce absorption; edema may occur with coadministration of calcium channel blockers (eg, amlodipine, nifedipine); hypoglycemia may occur with sulfonylureas; may increase tacrolimus and cyclosporine plasma concentrations when high doses are used; rhabdomyolysis may occur with coadministration of HMG-CoA reductase inhibitors (lovastatin or simvastatin); coadministration with cisapride can cause cardiac rhythm abnormalities and death
May increase digoxin levels; coadministration may increase plasma levels of midazolam or triazolam; phenytoin and rifampin may reduce levels (phenytoin metabolism may be altered)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in hepatic insufficiencies

More on Protothecosis, Cutaneous

Overview: Protothecosis, Cutaneous
Differential Diagnoses & Workup: Protothecosis, Cutaneous
Treatment & Medication: Protothecosis, Cutaneous
Follow-up: Protothecosis, Cutaneous
Multimedia: Protothecosis, Cutaneous
References
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References

  1. Walsh SV, Johnson RA, Tahan SR. Protothecosis: an unusual cause of chronic subcutaneous and soft tissue infection. Am J Dermatopathol. Aug 1998;20(4):379-82. [Medline].

  2. Lass-Florl C, Mayr A. Human protothecosis. Clin Microbiol Rev. Apr 2007;20(2):230-42. [Medline].

  3. Lee JS, Moon GH, Lee NY, Peck KR. Case report: Protothecal tenosynovitis. Clin Orthop Relat Res. Dec 2008;466(12):3143-6. [Medline].

  4. Khoury JA, Dubberke ER, Devine SM. Fatal case of protothecosis in a hematopoietic stem cell transplant recipient after infliximab treatment for graft-versus-host disease. Blood. Nov 15 2004;104(10):3414-5. [Medline].

  5. Torres HA, Bodey GP, Tarrand JJ, Kontoyiannis DP. Protothecosis in patients with cancer: case series and literature review. Clin Microbiol Infect. Aug 2003;9(8):786-92. [Medline].

  6. Carey WP, Kaykova Y, Bandres JC, Sidhu GS, Brau N. Cutaneous protothecosis in a patient with AIDS and a severe functional neutrophil defect: successful therapy with amphotericin B. Clin Infect Dis. Nov 1997;25(5):1265-6. [Medline].

  7. Polk P, Sanders DY. Cutaneous protothecosis in association with the acquired immunodeficiency syndrome. South Med J. Aug 1997;90(8):831-2. [Medline].

  8. Boyd AS, Langley M, King LE Jr. Cutaneous manifestations of Prototheca infections. J Am Acad Dermatol. May 1995;32(5 Pt 1):758-64. [Medline].

  9. Kantrow SM, Boyd AS. Protothecosis. Dermatol Clin. Apr 2003;21(2):249-55. [Medline].

  10. Zaitz C, Godoy AM, Colucci FM, de Sousa VM, Ruiz LR, Masada AS, et al. Cutaneous protothecosis: report of a third Brazilian case. Int J Dermatol. Feb 2006;45(2):124-6. [Medline].

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Further Reading

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Keywords

Prototheca, Prototheca wickerhamii, P wickerhamii, Prototheca zopfii, P zopfii, cutaneous protothecosis

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Contributor Information and Disclosures

Author

Sarah K Taylor, MD, Staff Physician, Department of Dermatology, Walter Reed Army Medical Center and National Naval Medical Center
Disclosure: Nothing to disclose.

Coauthor(s)

Jon H Meyerle, MD, Assistant Professor, Department of Dermatology, Johns Hopkins University School of Medicine; Consulting Staff, Laboratory Director, Department of Dermatology, Walter Reed Army Medical Center and National Naval Medical Center
Jon H Meyerle, MD is a member of the following medical societies: American Academy of Dermatology and Sigma Xi
Disclosure: Nothing to disclose.

Earl J Glusac, MD, Professor, Departments of Pathology and Dermatology, Yale University School of Medicine
Earl J Glusac, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

Medical Editor

Barbara R Reed, MD, Clinical Professor, Department of Dermatology, Dermatology Service, Denver Veterans Affairs Medical Center, University of Colorado Health Sciences Center; Consulting Staff, Denver Skin Clinic
Disclosure: Nothing to disclose.

Pharmacy Editor

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
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: 3M Pharmaceutical Grant/research funds Other; Graceway Pharmaceuticals Grant/research funds Other

Managing Editor

Christen M Mowad, MD, Associate Professor, Department of Dermatology, Geisinger Medical Center
Christen M Mowad, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, and Phi Beta Kappa
Disclosure: Nothing to disclose.

CME Editor

Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University
Catherine Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology
Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

 
 
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