eMedicine Specialties > Dermatology > Fungal Infections

Sporotrichosis: Treatment & Medication

Author: Scott D Miller, MD, Dermatologist and Dermatologic Surgeon, Department of Dermatology, Carolinas Dermatology Group, PA
Contributor Information and Disclosures

Updated: Mar 19, 2009

Treatment

Medical Care

Systemic antifungal agents are the mainstay of treatment. An increase in cutaneous induration, redness, and local lymphadenopathy may be expected after treatment is started, resulting from an increased immune response to the antigenic challenge of the killed fungus. Thermal adjuvant therapy to systemic antifungals may be beneficial, as S schenckii does not survive above 39°C.19,20  Passive immunization with monoclonal antibody against a 70-kd putative adhesin of S schenckii induces protection in murine sporotrichosis, giving promise for future therapies for this and similar deep-space fungal infections.16

Infectious Disease Society of America Clinical Practice Guidelines for the Management of Sporotrichosis20

  • Lymphocutaneous/cutaneous sporotrichosis
    • Administer itraconazole at 200 mg/d.
    • In patients who do not respond, administer itraconazole at 200 mg twice daily, 500 mg twice daily, or add potassium iodide (see below).
    • In patients intolerant of itraconazole, administer fluconazole at 400-800 mg/d or local hyperthermia.
  • Osteoarticular sporotrichosis
    • Administer amphotericin B and switch to itraconazole after therapeutic response.
    • Administer amphotericin B lipid formulation at  3-5 mg/kg/d.
    • Administer amphotericin B deoxycholate at 0.7-1.0 mg/kg/d.
    • Administer itraconazole at 200 mg twice daily for at least 12 months.
    • Confirm serum therapeutic levels after 2 weeks.
  • Pulmonary sporotrichosis
    • Antifungals are administered for localized disease after surgery, and this is also for initial therapy for severe infections.
    • Administer amphotericin B and switch to itraconazole after therapeutic response.
    • Administer amphotericin B lipid formulation at  3-5 mg/kg/d.
    • Administer amphotericin B deoxycholate at 0.7-1.0 mg/kg/d.
    • Administer itraconazole at 200 mg twice daily for at least 12 months.
    • Confirm serum therapeutic levels after 2 weeks.
  • Meningeal and disseminated (systemic) sporotrichosis
    • Administer amphotericin B and switch to itraconazole after therapeutic response.
    • Administer amphotericin B lipid formulation at 3-5 mg/kg/d.
    • Administer amphotericin B deoxycholate at 0.7-1.0 mg/kg/d.
    • Administer itraconazole at 200 mg twice daily for at least 12 months.
    • Confirm serum therapeutic levels after 2 weeks.
  • Pregnancy
    • Administer amphotericin B lipid formulation at  3-5 mg/kg/d.
    • Administer amphotericin B deoxycholate at 0.7-1.0 mg/kg/d.
    • Avoid azoles.
  • Pediatric cutaneous sporotrichosis: Administer potassium iodide, 1 drop 3 times daily, increasing as tolerated to a maximum of 1 drop/kg or 40-50 drops 3 times daily, which ever is lowest.
  • Pediatric disseminated sporotrichosis: Administer amphotericin B deoxycholate at 0.7 mg/kg/d, followed by itraconazole at 6-10 mg/kg, not to exceed 400 mg/d.

Surgical Care

Surgery combined with antifungals for localized pulmonary disease has proven beneficial.20

Consultations

  • Infectious disease specialist
  • Internist and subspecialists as indicated by organ system involvement

Medication

The goals of pharmacotherapy are to reduce morbidity and prevent complications.  Continue systemic therapy until clinical resolution is achieved, typically 4-6 months.

Antifungal agents

Fungicidal or fungistatic eradication of the infective organism S schenkii.19,20


Amphotericin B (AmBisome)

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. DOC for systemic disease, although more recent literature indicates itraconazole or terbinafine may replace amphotericin B as the DOC for systemic sporotrichosis.
Adult dosages below are for (1) osteoarticular sporotrichosis, (2) pulmonary sporotrichosis, and (3) meningeal and disseminated (systemic) sporotrichosis

Adult

Amphotericin B lipid formulation: 3-5 mg/kg/d
Amphotericin B deoxycholate: 0.7-1 mg/kg/d
Switch to itraconazole after response

Pediatric

Disseminated sporotrichosis: (deoxycholate): 0.7 mg/kg/d; switch to itraconazole after response

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

Monitor renal function, serum electrolytes (eg, magnesium and potassium), liver function, CBC count, and hemoglobin concentrations; resume the therapy at the lowest level (eg, 0.25 mg/kg) when the therapy is interrupted for >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)


Itraconazole (Sporanox)

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. DOC for cutaneous disease and second DOC (likely to soon be first DOC) for systemic disease. Available as 100-mg cap.

Adult

Lymphocutaneous/cutaneous sporotrichosis: 200 mg/d; if no response, 200 mg or 500 mg bid or add potassium iodide
Osteoarticular sporotrichosis: 200 mg bid for at least 12 mo; confirm serum therapeutic levels after 2 wk
Pulmonary sporotrichosis, less severe cases: 200 mg bid for at least 12 mo; confirm serum therapeutic levels after 2 wk
Meningeal and disseminated (systemic) sporotrichosis and after response to amphotericin B: 200 mg bid for at least 12 mo; confirm serum therapeutic levels after 2 wk

Pediatric

Disseminated sporotrichosis and after response to amphotericin B deoxycholate: 6-10 mg/kg, not to exceed 400 mg/d

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 (eg, 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 itraconazole levels (phenytoin metabolism may be altered)

Documented hypersensitivity; coadministration with cisapride may cause adverse cardiovascular effects (possibly death)

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

Monitor hepatic enzyme tests in pre-existing hepatic function abnormalities; absorption is impaired by low stomach acidity and enhanced when administered with an acidic beverage (eg, cola)


Potassium iodide (SSKI, Pima)

Saturated solution containing approximately 142 g potassium iodide in 100 mL water. Inhibits thyroid hormone secretion. Mechanism of action against Sporothrix unknown. Third DOC for cutaneous disease. Not effective for systemic disease. Contains 8 mg of iodide per drop. May be mixed with juice or water for intake.

Adult

Cutaneous sporotrichosis only: 5 drops tid; titrate up to tolerance, not to exceed 40-50 drops tid

Pediatric

Cutaneous sporotrichosis only: 1 drop tid, increasing as tolerated, not to exceed 1 drop/kg or 40-50 drops tid, which ever is lowest

Coadministration with lithium and other antithyroid drugs may potentiate hypothyroid and goitrogenic effects; concurrent use with potassium-containing or potassium-sparing medications and ACE inhibitors may result in hyperkalemia and cardiac arrhythmias or cardiac arrest

Documented hypersensitivity; pulmonary edema, bronchitis, tuberculosis, and hyperkalemia

Pregnancy

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

Precautions

Prolonged use of iodides can lead to hypothyroidism; caution in patients with Addison disease, cardiac disease, hyperthyroidism, myotonia congenita, tuberculosis, acute bronchitis, or renal function impairment


Fluconazole (Diflucan)

Synthetic oral antifungal (broad-spectrum bistriazole) that selectively inhibits fungal cytochrome P-450 and sterol C-14 alpha-demethylation. Fourth DOC for systemic disease, modestly effective and thus reserved for itraconazole-intolerant patients.

Adult

Lymphocutaneous or cutaneous patients intolerant of itraconazole: 400-800 mg/d

Pediatric

Not established

Levels may increase with hydrochlorothiazide; fluconazole levels may decrease with chronic 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

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

Monitor closely if rashes develop and discontinue drug if lesions progress; may cause clinical hepatitis, cholestasis, and fulminant hepatic failure (including death) with underlying medical conditions such as AIDS or a malignancy and while taking multiple concomitant medications; not recommended in breastfeeding


Terbinafine (Lamisil)

Synthetic allylamine hypothesized to act by inhibiting squalene epoxidase, thus blocking synthesis of ergosterol, a vital component of fungal cell membranes. An alternative DOC for cutaneous disease, with promise for systemic disease.

Adult

250-500 mg PO bid

Pediatric

Not established

Inhibitor of CYP450 2D6 isozyme; carefully monitor with coadministration of drugs predominantly metabolized by isozyme (TCAs, SSRIs, beta-blockers, and type B MAOIs); clearance is increased 100% by rifampin and decreased 33% by cimetidine

Pregnancy

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

Precautions

Not recommended for patients with liver disease; hepatotoxicity may occur in patients with and without history of liver disease (pretreatment serum transaminase levels [AST, ALT] recommended); patients should report symptoms of persistent nausea, anorexia, fatigue, vomiting, right upper abdominal pain or jaundice, dark urine, or pale stools; not recommended in patients with renal impairment; may exacerbate or precipitate lupus erythematous; isolated cases of several neutropenia reported

More on Sporotrichosis

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

References

  1. Schenck RB. On refractory subcutaneous abscesses caused by a fungus possibly related to the sporotricha. Bull John Hopkins Hospital. 1898;9:286-90.

  2. Davis BA. Sporotrichosis. Dermatol Clin. Jan 1996;14(1):69-76. [Medline].

  3. Lopes-Bezerra LM, Schubach A, Costa RO. Sporothrix schenckii and sporotrichosis. An Acad Bras Cienc. Jun 2006;78(2):293-308. [Medline].

  4. Saravanakumar PS, Eslami P, Zar FA. Lymphocutaneous sporotrichosis associated with a squirrel bite: case report and review. Clin Infect Dis. Sep 1996;23(3):647-8. [Medline].

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  6. Barros MB, Schubach Ade O, do Valle AC, et al. Cat-transmitted sporotrichosis epidemic in Rio de Janeiro, Brazil: description of a series of cases. Clin Infect Dis. Feb 15 2004;38(4):529-35. [Medline].

  7. Dooley DP, Bostic PS, Beckius ML. Spook house sporotrichosis. A point-source outbreak of sporotrichosis associated with hay bale props in a Halloween haunted-house. Arch Intern Med. Sep 8 1997;157(16):1885-7. [Medline].

  8. Hajjeh R, McDonnell S, Reef S, et al. Outbreak of sporotrichosis among tree nursery workers. J Infect Dis. Aug 1997;176(2):499-504. [Medline].

  9. Ticoras CJ, Schroeter AL, Hornbeck KL. Disseminated ulcerated papules and nodules. Cutaneous disseminated sporotrichosis. Arch Dermatol. Aug 1996;132(8):963-4, 966-7. [Medline].

  10. Howell SJ, Toohey JS. Sporotrichal arthritis in south central Kansas. Clin Orthop Relat Res. Jan 1998;207-14. [Medline].

  11. Sanz J, Andreu JL, Martinez-Garcia G, Suarez D, Mulero J, Larrea A. Sporotrichial bursitis. Br J Rheumatol. Apr 1998;37(4):461-2. [Medline].

  12. Kim S, Rusk MH, James WD. Erysipeloid sporotrichosis in a woman with Cushing's disease. J Am Acad Dermatol. Feb 1999;40(2 Pt 1):272-4. [Medline].

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  14. Ware AJ, Cockerell CJ, Skiest DJ, Kussman HM. Disseminated sporotrichosis with extensive cutaneous involvement in a patient with AIDS. J Am Acad Dermatol. Feb 1999;40(2 Pt 2):350-5. [Medline].

  15. Ruiz-Baca E, Toriello C, Perez-Torres A, Sabanero-Lopez M, Villagomez-Castro JC, Lopez-Romero E. Isolation and some properties of a glycoprotein of 70 kDa (Gp70) from the cell wall of Sporothrix schenckii involved in fungal adherence to dermal extracellular matrix. Med Mycol. July 2008;4:1-13. [Medline].

  16. Nascimento RC, Espindola NM, Castro RA, et al. Passive immunization with monoclonal antibody against a 70-kDa putative adhesin of Sporothrix schenckii induces protection in murine sporotrichosis. Eur J Immunol. Nov 2008;38(11):3080-9. [Medline].

  17. Meffert JJ. Cutaneous sporotrichosis presenting as a keratoacanthoma. Cutis. Jul 1998;62(1):37-9. [Medline].

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  19. Anonymous. Systemic antifungal drugs. Med Lett Drugs Ther. Sep 12 1997;39(1009):86-8. [Medline].

  20. Kauffman C, Bustamante B, Chapman S, Pappas P. Clinical Practice Guidelines for the Management of Sporotrichosis: 2007 Update by the Infectious Disease Society of America. Clin Infect Dis. November 2007;45(10):1255-65. [Medline][Full Text].

Further Reading

Keywords

Contributor Information and Disclosures

Author

Scott D Miller, MD, Dermatologist and Dermatologic Surgeon, Department of Dermatology, Carolinas Dermatology Group, PA
Scott D Miller, MD is a member of the following medical societies: American Academy of Dermatology and American Society for Dermatologic Surgery
Disclosure: Nothing to disclose.

Medical Editor

Kathryn Schwarzenberger, MD, Associate Professor of Medicine, Division of Dermatology, University of Vermont College of Medicine; Consulting Staff, Division of Dermatology, Fletcher Allen Health Care
Kathryn Schwarzenberger, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Contact Dermatitis Society, American Dermatological Association, Dermatology Foundation, Medical Dermatology Society, and Women's Dermatologic Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University School of Medicine; Consulting Staff, Mountain View Dermatology, PA
Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association
Disclosure: Nothing to disclose.

Managing Editor

Lester F Libow, MD, Dermatopathologist, South Texas Dermatopathology Laboratory
Lester F Libow, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, and Texas Medical Association
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

William D James, MD, Paul R Gross Professor of Dermatology, University of Pennsylvania School of Medicine; Vice-Chair, Program Director, Department of Dermatology, University of Pennsylvania Health System
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; american college of physicians Honoraria Other

 
 
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