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Therapeutic Strategies

Deep Fungal Infections

Timothy Berger Bruce Wintroub

Saturday, January 01, 2011

Sporotrichosis

Sporotrichosis is acquired from decaying vegetation or sphagnum moss or from infected felines. Disease follows accidental inoculation of the organism by thorns or splinters or scratches. The guidelines provided are for the treatment of the chronic lymphocutaneous form of the disease. Joint or pulmonary involvement requires treatments of longer duration and higher dosage.

First Steps

Itraconazole 200 mg daily until all lesions have resolved, then an additional 4 weeks of treatment. (Total duration of treatment is usually 3-6 months.)

Alternative Steps

  1. Terbinafine 250 mg daily until complete resolution, then 4 more weeks.
  2. Saturated solution of potassium iodide (SSKI). Begin with 5-10 drops 3 times daily and increase over several weeks to 15 drops 3 times daily until the disease is cleared and then 4 more weeks.
  3. In refractory cases, the dose of itraconazole may be increased to 200 mg twice daily. The duration of therapy may be quite prolonged in refractory cases.

Pitfalls

  1. The lymphangitic lesions of sporotrichosis must be differentiated from some types of atypical mycobacterial and nocardial infection. Tularemia and staphylococcal lymphangitis can present with clinically similar lesions, but patients are usually febrile.
  2. As with all systemic mycoses, erythema nodosum may occur.
  3. Iodism is a universal, dose-related concomitant condition of SSKI therapy. Symptoms include coryza, rhinorrhea, nausea, salivary gland swelling, metallic taste, and a toxic iododerma. Therapy should be adjusted according to drug tolerance.
  4. Amphotericin B may be used in cases refractory to the above treatments. Once the disease is improving, change the patient to itraconazole therapy.
  5. For AIDS patients with sporotrichosis, lifelong prophylaxis with itraconazole 200 mg once daily is recommended.

Coccidioidomycosis

For practical purposes, coccidioidomycosis occurs only in residents or visitors to the Southwestern United States. Black (14-fold increase) and Filipino populations (75-fold increase) have a much higher rate of dissemination than white populations. Primary pulmonary infection may be asymptomatic or mildly symptomatic and does not require treatment. Erythema nodosum may appear during this period. Extrapulmonary disease is serious and should be treated aggressively. Specific cutaneous lesions containing the spherules on biopsy may be the presenting sign of dissemination. Dissemination is far more likely to occur in Filipino and black populations and in the immunosuppressed. The therapeutic strategy is to eliminate the causative microorganism.

First Steps

Itraconazole or fluconazole at a dose of at least 400 mg daily. Fluconazole is preferred if there is evidence of coccidioidal meningitis. Azole therapy may not be effective in eradicating CNS involvement.

Subsequent Steps

Intravenous amphotericin B is used in cases failing azole therapy. The daily dose ranges from 0.4 to 1.0 mg/kg. Cumulative doses range is from 0.5 g to 3.0 g. Liposomal amphotericin may be used in patients intolerant of amphotericin side effects. Note: For patients with meningeal involvement, amphotericin must be given intrathecally as well.

Ancillary Steps

Surgical drainage and/or debridement may be required for encapsulated abscesses or avascular necrotic lesions.

Pitfalls

  1. Coccidioidomycosis may become a chronic disease, and patients may require lifelong maintenance therapy.
  2. Relapses may occur after cessation of azole or amphotericin B therapy.
  3. Pregnancy is a risk factor for dissemination.
  4. Disseminated coccidioidomycosis results from hematogenous spread of the fungus. Subcutaneous abscesses, cellulitis, and draining sinuses are the cutaneous hallmarks, although bone and meninges are frequently involved. A negative skin test to coccidioidin with rising antibody titers suggests impending dissemination.
  5. Amphotericin B can produce toxicity especially if infused too rapidly. Reactions, including chills, fever, nausea, malaise, and anorexia, although reversible, can be severe. These symptoms can be aborted by premedication regimens. Kidney function must be monitored closely (e.g., twice-weekly BUN and creatinine). Other side effects include hypokalemia, hypomagnesemia, and anemia.

Mycetoma

Mycetoma, a disease primarily of tropical climatic zones, is a chronic, slowly progressive infection of the subcutaneous tissue and deeper structures including bone. It is characterized by scarring, tumefaction, and sinus tracts exuding "grains." The therapeutic strategy is to identify the infectious agent and attempt to eradicate it. Mycetoma is divided into two groups for therapeutic purposes: Actinomycetoma, caused by filamentous aerobic actinomycetes; and eumycetoma, caused by true fungi.

Actinomycetoma

The expected response rate should be about 90%, and surgery is rarely a primary treatment modality.

First Steps

The treatment is directed at the infectious agent, and its documented susceptibilities: Trimethoprim sulfamethoxazole 1 to 2 double-strength tablets twice daily with or without rifampin 600 mg daily.

Subsequent Steps

  1. If there is an initial response after 1 month, continue treatment for 9-12 months, or 2 months beyond any evidence of grains and drainage.
  2. Surgery is of limited benefit in most cases, but may help manage some small refractory areas once antibiotics have been used for 6-9 months.
  3. In unresponsive cases, streptomycin up to 2 g daily plus dapsone 100-200 mg daily.
  4. Refractory Norcardia infections may respond to daily amikacin treatment

Eumycetoma

Response rates are poor (about 50%), and amputation more often occurs. It should be reserved for advanced and refractory cases.

First Steps

Ketoconazole 200 mg twice daily for 9-12 months.

Subsequent Steps

  1. Itraconazole 200 mg twice daily or terbinafine up to 500 mg twice daily for 9-12 months may be attempted.

Amphotericin may be used as rescue therapy, but many of the fungi causing eumycetoma are amphotericin resistant.

Chromoblastomycosis

Chromoblastomycosis (chromomycosis) is a chronic infection of the dermis and epidermis caused by dematiaceous fungi from the soil and decaying plant matter. Lesions present as vegetative, verrucous plaques. The treatment strategy is to eradicate the infectious agent.

First Steps

  1. Itraconazole 200 mg twice daily until the lesion is resolved (often up to 6 months), then for an additional 1 month.
  2. Voriconazole 200 mg twice daily as above.

Ancillary Steps

Limited lesions may be approached surgically, if antibiotic therapy is given appropriately before, during, and after the surgery.

Subsequent Steps

In refractory cases, terbinafine 500 mg twice daily may be considered

Blastomycosis

All patients with cutaneous lesions of blastomycosis are considered to have disseminated infection and require treatment.

First Steps

  1. Itraconazole 200-400 mg daily for at least 6 months.
  2. Fluconazole up to 200-400 mg twice daily is an alternative.

Subsequent Steps

Amphotericin B up to 1 mg/ kg to a total of 1-2 g. After clinical improvement, patient may be switched back to Itraconazole oral therapy.

Histoplasmosis

Cutaneous lesions of histoplasmosis often indicate immunosuppression, and appropriate evaluation of the immune system is indicated. All patients with symptomatic disseminated infection or skin lesions should receive systemic antifungal treatment.

First Steps

Itraconazole 200 mg twice daily for 12 months.

Subsequent Steps

  1. Continue treatment until all signs and symptoms have resolved, which may be longer than 12 months.
  2. Chronic suppressive therapy of itraconazole 200 mg once daily is required for immunosuppressed patients and may be started after the patient has received 3 months of twice daily itraconazole therapy.
  3. In severe disseminated histoplasmosis, give amphotericin B 0.7-1.0 mg/kg daily to a total dosage of 35 mg/kg. Lipid formulations are appropriate for patients with renal compromise.

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