eMedicine Specialties > Pediatrics: General Medicine > Infectious Disease

Sporotrichosis: Treatment & Medication

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): Brad S Graham, MD, Consulting Staff, Dermatology Associates of Tyler; Cynthia L Chen, Western University of Health Sciences College of Osteopathic Medicine of the Pacific
Contributor Information and Disclosures

Updated: Aug 28, 2009

Treatment

Medical Care

Medical therapy is the standard of care for sporotrichosis. Patients are commonly treated with an oral antifungal agent on an outpatient basis. Surgical therapy, other than to perform a biopsy from a lesion for establishing the diagnosis, is rarely used as a form of treatment. Aggressive treatments are seldom necessary. This fungus does not grow well in temperatures higher than 38.5°C, so warm compresses are often used as adjunctive therapy. See the Medication section for a suggested pharmaceutical approach to treating sporotrichosis.

Consultations

Consult with a dermatologist.

Activity

Activity limitations, determined on a case-by-case basis, may be necessary for optimal care. Wearing long sleeves and gloves is recommended when gardening or handling plant matter that may cause sporotrichosis.

Medication

Approach the treatment of sporotrichosis based upon each patient's clinical presentation and severity of illness. Most patients are treated with some form of antifungal therapy. Many agents are reported to be successful. For simple cutaneous forms, a saturated solution of potassium iodide is often used and is the least expensive form of treatment.

Systemic antifungal medications, such as amphotericin B, itraconazole,9 terbinafine, or fluconazole, may be used to treat more severe forms of sporotrichosis (eg, lymphonodular, pulmonary, osteoarticular, disseminated). For all clinical types of sporotrichosis, continue the treatment course for at least 1 week after clinical cure.

Antifungal agents

The mechanism of action may involve an alteration of RNA and DNA metabolism or an intracellular accumulation of peroxide that is toxic to the fungal cell.


Potassium iodide (SSKI)

For simple cutaneous lesions, the least expensive medication for treatment is a saturated solution of potassium iodide. This approach is commonly used in developing countries because of its low cost. SSKI can be administered on average for approximately 4-6 wk, but as long as 6 months. However, prolonged use should be undertaken with caution (see interactions below). The mechanism of action is unknown. Ineffective for systemic disease.

Adult

5 drops (approximately 0.5 mL when using standard eye-dropper) PO tid; may increase as tolerated not to exceed 40-50 drops tid

Pediatric

1 drop (using a standard eye-dropper) PO tid, may increase as tolerated, not to exceed 1 drop/kg or 40-50 drops tid (whichever is lowest)

Reported to interact with a number of different medications; because of potential for inducing elevated serum potassium levels, use cautiously with other medications that may cause hyperkalemia (eg, potassium-sparing diuretics, ACE inhibitors, potassium supplements) because these may result in very high levels of serum potassium, causing cardiac dysrhythmias and/or cardiac arrest; use with caution when prescribing with other antithyroid drugs because its ability to inhibit thyroid hormone secretion may result in significant hypothyroid states; coadministration with lithium may cause additive hypothyroid effects
Use of SSKI for more than 1 mo can lead to interruption of thyroid hormone production, called Wolff-Chaikoff effect, because of excess iodide; patients with defective or absent autoregulatory mechanisms can become hypothyroid; with prolonged therapy, evaluation of TSH and T3 is advised

Documented hypersensitivity; renal failure; hyperkalemia; pulmonary edema; tuberculosis; goiter; hypothyroidism

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in hyperkalemic states, cardiac disease, and acute bronchitis; prior to treatment, explain potential consequences of nausea, salivary gland swelling and salivation, fever, rash, and metallic taste


Itraconazole (Sporanox)

DOC for cutaneous sporotrichosis. A fungistatic azole with broad spectrum of activity because of its inhibition of enzyme 14-alpha-demethylase, which is needed by the fungus for cell wall synthesis. Particularly effective for lymphocutaneous forms of sporotrichosis but may be used for fixed cutaneous and systemic forms. The caps and PO solution are not interchangeable (PO solution exhibits higher bioavailability).

Adult

Lymphocutaneous: Average dose is 200 mg/d PO for 2-4 wk after all lesions have resolved, usually administered for a total of 3-6 mo
Meningeal and disseminated: 200 mg PO bid; recommended as step-down therapy after the patient responds to initial treatment with amphotericin B and should be given to complete at least 12 months of therapy; measure serum levels after receiving itraconazole for at least 2 wk
AIDS and other immunosuppressed patients may require lifelong suppressive therapy (200 mg daily) to prevent relapse

Pediatric

Cutaneous of lymphocutaneous sporotrichosis: 6-10 mg/kg PO qd; not to exceed 400 mg daily

Potent inhibitor or CYP450 3A4, thus, other medications metabolized via this system may accumulate, resulting in elevated levels and adverse effects (eg, alprazolam, midazolam, cisapride, terfenadine, astemizole, simvastatin, cyclosporine, tacrolimus); medications known to induce cytochrome P450 system (eg, rifampin) may lower levels of itraconazole, making drug ineffective; antacids may reduce absorption of itraconazole; conversely, acidic or carbonated beverage consumption may facilitate absorption; may increase digoxin levels

Documented hypersensitivity; concomitant use with cisapride, terfenadine, and astemizole because of a drug-drug metabolism interaction causing potentially lethal cardiac effects

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 with hepatitis or liver failure history (regularly monitor LFT results, although elevated LFT results are uncommon); other typical adverse effects include headache, pruritus, nausea, rhinitis, rash, and dyspepsia; PO solution contains hydroxypropyl-beta-cyclodextrin (solubilizing agent), which causes pancreatic hyperplasia and neoplasia at high doses in rats


Amphotericin B (Fungizone)

DOC for disseminated or meningeal forms of systemic sporotrichosis. Some providers even consider this DOC for lymphocutaneous forms of sporotrichosis.
Polyene antibiotic produced by a strain of Streptomyces nodosus; can be fungistatic or fungicidal. Binds to sterols, such as ergosterol, in the fungal cell membrane, causing intracellular components to leak with subsequent fungal cell death.

Adult

Osteoarticular, pulmonary, and systemic (initial therapy) with lipid formulation): 3-5 mg/kg IV daily
Meningeal (lipid formulation): 5 mg/kg IV daily for 4-6 wk

Pediatric

Initial therapy: 0.7 mg/kg IV daily

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

Precautions

Nephrotoxicity manifests as hypokalemia and renal tubular acidosis; regular renal function monitoring is recommended; fever and chills are not uncommon after first few administrations of drug; rare acute reactions may include hypotension, bronchospasm, arrhythmias, and shock


Terbinafine (Daskil, Lamisil)

A fungicidal allylamine antifungal agent. Considered a third-line agent against sporotrichosis. Blocks ergosterol synthesis by inhibiting squalene epoxidase. Effective against S schenckii and other fungi and fungal infections, including most dermatophytes, Aspergillus species, blastomycosis, histoplasmosis, and Scopulariopsis brevicaulis. Terbinafine is well absorbed PO and has a long half-life.
No elixir form is available; 250-mg tab is not scored and cannot be easily pulverized for use in children and is not palatable.

Adult

250 mg PO qd

Pediatric

20-40 kg: 125 mg PO qd/qod
>40 kg: Administer as in adults

May decrease cyclosporine effects; toxicity of terbinafine may increase with rifampin and cimetidine

Pregnancy

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

Precautions

Pancytopenia, neutropenia, erythema multiforme, Steven-Johnson syndrome, acute generalized exanthematous pustulosis, taste disturbances, dyspepsia, and cholestatic liver disease; use with caution in patients with liver and/or renal dysfunction; LFT results should be monitored q6wk if long-term therapy is anticipated; monitor CBC count in patients with known or suspected immunodeficiency who are treated >6 wk


Fluconazole (Diflucan)

A broad-spectrum azole antifungal agent. Considered a third-line agent for sporotrichosis treatment. Effective for various fungi, including dermatophytes, candidal species, S schenckii, and some molds. It inhibits the enzyme 14-alpha-demethylase, preventing fungal cell wall formation.

Adult

800 mg PO qd for 4-6 wk

Pediatric

5-6 mg/kg/d PO for approximately 4-6 wk

Levels may increase with hydrochlorothiazide; fluconazole levels may decrease with long-term coadministration of rifampin; coadministration of fluconazole may decrease phenytoin clearance; may increase concentrations of theophylline, tolbutamide, glyburide, and glipizide; effects of anticoagulants may increase with fluconazole coadministration; increases in cyclosporine concentrations may occur when administered concurrently; moderately inhibits CYP450 3A3/4 isoenzymes

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

May cause GI upset, headache, rash, exfoliative dermatitis, and drug-induced hepatitis; discontinue if patient develops rash, elevated LFT results, or cholestasis

More on Sporotrichosis

Overview: Sporotrichosis
Differential Diagnoses & Workup: Sporotrichosis
Treatment & Medication: Sporotrichosis
Follow-up: Sporotrichosis
Multimedia: Sporotrichosis
References

References

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Further Reading

Keywords

Sporothrix schenckii, S schenckii, dimorphic fungal infection, lymphocutaneous sporotrichosis, fixed cutaneous sporotrichosis, disseminated sporotrichosis, Schenck disease, laryngeal and respiratory tract sporotrichosis, cutaneous sporotrichosis, lymphangitic cutaneous sporotrichosis, cellulitic sporotrichosis, mycetomalike sporotrichosis, systemic sporotrichosis, acquired immunodeficiency syndrome, AIDS, erythema nodosum, polyarteritis nodosum, treatment, diagnosis

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)

Brad S Graham, MD, Consulting Staff, Dermatology Associates of Tyler
Brad S Graham, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society of Dermatopathology, and Texas Dermatological Society
Disclosure: Nothing to disclose.

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

Medical Editor

Gary J Noel, MD, Department of Pediatrics, Clinical Associate Professor, Weill Medical College of Cornell University
Gary J Noel, MD is a member of the following medical societies: Pediatric Infectious Diseases Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Larry I Lutwick, MD, Professor of Medicine, State University of New York, Downstate Medical School; Director, Infectious Diseases, Veterans Affairs New York Harbor Health Care System, Brooklyn Campus
Larry I Lutwick, MD is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

CME Editor

Daniel Rauch, MD, FAAP, Director, Pediatric Hospitalist Program, Associate Professor, Department of Pediatrics, New York University School of Medicine
Daniel Rauch, MD, FAAP is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, and Society of Hospital Medicine
Disclosure: Baxter Honoraria Consulting

Chief Editor

Russell W Steele, MD, Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine
Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association
Disclosure: None None None

 
 
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