Patient presentation
A 38-year-old African-American female presented to the George Washington University Hospital with odynophagia and a facial rash that had been worsening for 2 months. Her past medical history was significant for 22 years of HIV/AIDS for which she had not been treated nor had any regular follow-up. Her odynophagia secondary to candidiasis resolved with fluconazole (Diflucan) by day 3.
A dermatology consult was ordered for evaluation of the facial lesions. The facial lesions had worsened with increasing pruritus and tender bilateral cervical lymphadenopathy. She had been applying hydrocortisone cream and topical antibiotics without relief. The patient reported having tactile fevers and weight loss with a mild chronic non-productive cough. She reported a negative PPD test, which she had undergone in jail 6 months prior. She denied nausea, vomiting, diarrhea and abdominal pain.
Physical exam showed a thin woman in no acute distress with multiple 0.5- to 1-cm firm, flesh-colored to erythematous nodules with overlying crust located on her nose, cheeks and forehead and her posterior left arm, along with lichenified hyperpigmented plaques on her antecubital fossa. There was bilateral cervical lymphadenopathy with 1- to 2-cm hard mobile nodes, along with bilateral axillary and groin lymphadenopathy. Her Chem-7 and liver function tests were normal. Her CBC showed a hemoglobin count of 9.1, a white blood count of 3.9, a hematocrit of 30, and platelets of 153. Her lactate was 1.9 and her CD4 count was 4. A 4-mm skin punch biopsy was sent for histopathologic exam. A cervical lymph node was also excised and sent for histopathologic exam. A total body CT scan showed multiple neck lymphadenopathy with necrotic centers along with lymphadenopathy in the groin.
What is Your Diagnosis?
Diagnosis: Cryptococcal lymphadenitis
Cutaneous Cryptococcus may be the initial presenting sign of disseminated disease in 10% to 20% of cases of cryptococcal lymphadenitis.1 The usual mode of transmission is by inhalation; however, there have been a few reported cases of primary cutaneous infection without disseminated disease.2 Skin lesions are usually multiple and polymorphous in appearance. The majority of cryptococcal infections in immunocompromised patients are caused by Cryptococcus neoformans, while Cryptococcus gattii is the cause of 70% to 80% of cases in immunocompetent patients.3 In developed countries, the overall incidence of Cryptococcus in AIDS patients has decreased with the use of highly active anti-retroviral therapy (HAART) and prophylactic anti-fungal medications.4
CLINICAL PRESENTATION
Immunocompromised patients with disseminated cryptococcal infections commonly present with central nervous system (CNS) infections or, less commonly, pulmonary infections. CNS infections may be asymptomatic.
Cutaneous lesions develop in 10% to 15% of AIDS patients with disseminated Cryptococcus,5 with the majority of lesions occurring on the head and neck.6
Skin lesions present with a diverse morphology, although the most common presentation is umbilicated papules with a tiny central hemorrhagic crust.5
Other manifestations include pustules, ulcers, nodules, draining sinuses, abscesses or cellulitis. Papular lesions may be similar in
appearance to molluscum contagiosum. Large single lesions may resemble basal cell carcinomas or keratoacanthomas.5 Cryptococcal lymphadenitis is not commonly seen in AIDS patients, although when it is, the most common nodes involved are cervical and mediastinal.7
DIAGNOSIS
Even with systemic disease, routine blood work may produce normal results. A cerebrospinal fluid (CSF) examination is essential when diagnosing systemic disease. When India ink is used to stain the CSF, it will show cryptococcal meningitis 25% to 50% of the time.3 Anti-cryptococcal antibodies have no diagnostic significance since a large number of healthy individuals are exposed to Cryptococcus without apparent infection. However, cryptococcal antigen is positive in 90% of patients with systemic disease.3 Positive test results should always be followed up with cultures before diagnosing cryptococcosis.
In tissue specimens, Cryptococcus can be challenging to see with H&E stains. Methenamine silver or periodic acid-Schiff stain should be used. Fine needle aspiration can be diagnostic in cryptococcal nodal disease. However, it has been shown to miss the diagnosis in a case presented by Mohanty, et al; therefore, a lymph node excision and histo-pathological exam should be considered for obtaining an accurate diagnosis.8
TREATMENT
Disseminated cryptococcosis progressed from a fatal infection to a curable one with the advent of amphotericin B (AmBisome) 35 years ago.9 Amphotericin B has been successfully used to treat all forms of cryptococcal infections, although it is extremely nephrotoxic at therapeutic doses. Lipid formulations were later developed that allowed better delivery, decreased toxicity and higher doses; however, CNS penetration continued to be poor.
Flucytosine (Ancobon), an anti-fungal with excellent CNS penetration, has been successfully used for cryptococcal infections; however, resistance has developed limiting its use as a monotherapy.
Subsequently, flucytosine and amphotericin B have been successfully combined due to their differing pharmacokinetics and synergistic mechanisms of action.8,9 The standard treatment recommendations call for combining amphotericin B (0.5 to 1 mg/kg/day) and oral flucytosine (150 mg/kg/day) for 2 weeks followed by oral fluconazole (Diflucan) (400 mg/day) for 10 weeks.10 Fluconazole increases the clearance of cryptococci from the CNS. Cutaneous lesions will heal completely within 1 to 2 months after starting therapy.
Treating Patients with AIDS
Cryptococcus in AIDS patients may not be cured, only put into remission. Thus, life-long suppressive chemotherapy may be required after the treatment for active disease has ended.5 Positive cultures may continue to persist, or recur, despite adequate treatment. There has been no clear answer as to the use of primary prophylactic therapy for Cryptococcus.
It is not clear from current data which anti-fungal (fluconazole vs. itraconazole [Sporanox]) is superior for the primary prevention of Cryptococcus or what the optimal dose and frequency of intervention should be. Patient population characteristics may be an important consideration in choosing the best treatment since itraconazole is more effective against certain endemic fungal infections such as histoplasmosis and penicilliosis. The incidence of Cryptococcus disease was shown to be decreased in patients taking primary prophylaxis compared to those taking placebo.11 Itraconazole and fluconazole appear to be equally effective in patients with a CD4 counts less than 100, although neither show any decrease in overall mortality.11
Prophylactic therapy will vary according to pathogens wished to cover, and avoiding of drug interactions.
DISCUSSION
Cryptococcus neoformans is a polysaccharide encapsulated yeast that is ubiquitous in nature, found especially in pigeon droppings and nests.12 It was first described in 1894 by a pathologist named Busse when he isolated it from a tibial lesion of a patient in Germany.13
Its pathogenicity is very diverse, anywhere from harmless colonization of the airway to meningitis and systemic disease. It gains access by inhalation and spreads hematogenously from the lungs to the meninges, skin and kidneys.
Cryptococcal infections in immunocompetent individuals are relatively rare; however, these infections occur in 6% to 13% of AIDS patients5 due to their defective cell-mediated immunity. There appears to be a relationship to the amount of inoculum8 and whether an immunocompromised patient will become symptomatic during primary infection. There is no significant difference in incidence in regard to sex, age, race or occupation.
Cutaneous manifestations are found in 10% to 15% of patients with disseminated cryptococcosis. There have been reports of primary cutaneous infections, but these are rare and controversial.14 The most common sites of cutaneous lesions are the head and neck regions.
In 10% to 20% of patients,14 this may be the first presenting sign of disseminated cryptococcosis. These lesions may present similar in appearance to molluscum contagiosum, pyoderma gangrenosum and Kaposi’s sarcoma.
Diagnostic and Treatment Tips
Cryptococcus neoformans is a common pathogen in immunocompromised patients that causes disseminated disease. It often presents with a wide variety of manifestations. Cutaneous Cryptococcus are the first sign of systemic disease 10% to 20% of the time.1
Cutaneous lesions can often mimic other skin disorders such as molluscum contagiosum, basal cell cancers or keratoacanthomas.5 In both immunocompromised and immunocompetent patients, cutaneous cryptococcal lesions most commonly present on the head or neck.6
A useful tool for diagnosing cryptococcosis is serum cryptococcal antigen, as it will be positive in 90% of patients with systemic disease,3 but should always be followed with a lumbar puncture and cultures. The treatment of choice is 2 weeks of amphotericin B at 0.5 to 1 mg/kg/day and oral flucytosine at 150 mg/kg/day followed by 10 weeks of oral fluconazole at 400 mg/day.10
In AIDS patients it is important to consider suppressive treatment after active disease has ended to prevent recurrence.3 Prophylactic therapy with fluconazole or itraconazole has been shown to be effective, but has not been shown to decrease mortality.
Patient presentation
A 38-year-old African-American female presented to the George Washington University Hospital with odynophagia and a facial rash that had been worsening for 2 months. Her past medical history was significant for 22 years of HIV/AIDS for which she had not been treated nor had any regular follow-up. Her odynophagia secondary to candidiasis resolved with fluconazole (Diflucan) by day 3.
A dermatology consult was ordered for evaluation of the facial lesions. The facial lesions had worsened with increasing pruritus and tender bilateral cervical lymphadenopathy. She had been applying hydrocortisone cream and topical antibiotics without relief. The patient reported having tactile fevers and weight loss with a mild chronic non-productive cough. She reported a negative PPD test, which she had undergone in jail 6 months prior. She denied nausea, vomiting, diarrhea and abdominal pain.
Physical exam showed a thin woman in no acute distress with multiple 0.5- to 1-cm firm, flesh-colored to erythematous nodules with overlying crust located on her nose, cheeks and forehead and her posterior left arm, along with lichenified hyperpigmented plaques on her antecubital fossa. There was bilateral cervical lymphadenopathy with 1- to 2-cm hard mobile nodes, along with bilateral axillary and groin lymphadenopathy. Her Chem-7 and liver function tests were normal. Her CBC showed a hemoglobin count of 9.1, a white blood count of 3.9, a hematocrit of 30, and platelets of 153. Her lactate was 1.9 and her CD4 count was 4. A 4-mm skin punch biopsy was sent for histopathologic exam. A cervical lymph node was also excised and sent for histopathologic exam. A total body CT scan showed multiple neck lymphadenopathy with necrotic centers along with lymphadenopathy in the groin.
What is Your Diagnosis?
Diagnosis: Cryptococcal lymphadenitis
Cutaneous Cryptococcus may be the initial presenting sign of disseminated disease in 10% to 20% of cases of cryptococcal lymphadenitis.1 The usual mode of transmission is by inhalation; however, there have been a few reported cases of primary cutaneous infection without disseminated disease.2 Skin lesions are usually multiple and polymorphous in appearance. The majority of cryptococcal infections in immunocompromised patients are caused by Cryptococcus neoformans, while Cryptococcus gattii is the cause of 70% to 80% of cases in immunocompetent patients.3 In developed countries, the overall incidence of Cryptococcus in AIDS patients has decreased with the use of highly active anti-retroviral therapy (HAART) and prophylactic anti-fungal medications.4
CLINICAL PRESENTATION
Immunocompromised patients with disseminated cryptococcal infections commonly present with central nervous system (CNS) infections or, less commonly, pulmonary infections. CNS infections may be asymptomatic.
Cutaneous lesions develop in 10% to 15% of AIDS patients with disseminated Cryptococcus,5 with the majority of lesions occurring on the head and neck.6
Skin lesions present with a diverse morphology, although the most common presentation is umbilicated papules with a tiny central hemorrhagic crust.5
Other manifestations include pustules, ulcers, nodules, draining sinuses, abscesses or cellulitis. Papular lesions may be similar in
appearance to molluscum contagiosum. Large single lesions may resemble basal cell carcinomas or keratoacanthomas.5 Cryptococcal lymphadenitis is not commonly seen in AIDS patients, although when it is, the most common nodes involved are cervical and mediastinal.7
DIAGNOSIS
Even with systemic disease, routine blood work may produce normal results. A cerebrospinal fluid (CSF) examination is essential when diagnosing systemic disease. When India ink is used to stain the CSF, it will show cryptococcal meningitis 25% to 50% of the time.3 Anti-cryptococcal antibodies have no diagnostic significance since a large number of healthy individuals are exposed to Cryptococcus without apparent infection. However, cryptococcal antigen is positive in 90% of patients with systemic disease.3 Positive test results should always be followed up with cultures before diagnosing cryptococcosis.
In tissue specimens, Cryptococcus can be challenging to see with H&E stains. Methenamine silver or periodic acid-Schiff stain should be used. Fine needle aspiration can be diagnostic in cryptococcal nodal disease. However, it has been shown to miss the diagnosis in a case presented by Mohanty, et al; therefore, a lymph node excision and histo-pathological exam should be considered for obtaining an accurate diagnosis.8
TREATMENT
Disseminated cryptococcosis progressed from a fatal infection to a curable one with the advent of amphotericin B (AmBisome) 35 years ago.9 Amphotericin B has been successfully used to treat all forms of cryptococcal infections, although it is extremely nephrotoxic at therapeutic doses. Lipid formulations were later developed that allowed better delivery, decreased toxicity and higher doses; however, CNS penetration continued to be poor.
Flucytosine (Ancobon), an anti-fungal with excellent CNS penetration, has been successfully used for cryptococcal infections; however, resistance has developed limiting its use as a monotherapy.
Subsequently, flucytosine and amphotericin B have been successfully combined due to their differing pharmacokinetics and synergistic mechanisms of action.8,9 The standard treatment recommendations call for combining amphotericin B (0.5 to 1 mg/kg/day) and oral flucytosine (150 mg/kg/day) for 2 weeks followed by oral fluconazole (Diflucan) (400 mg/day) for 10 weeks.10 Fluconazole increases the clearance of cryptococci from the CNS. Cutaneous lesions will heal completely within 1 to 2 months after starting therapy.
Treating Patients with AIDS
Cryptococcus in AIDS patients may not be cured, only put into remission. Thus, life-long suppressive chemotherapy may be required after the treatment for active disease has ended.5 Positive cultures may continue to persist, or recur, despite adequate treatment. There has been no clear answer as to the use of primary prophylactic therapy for Cryptococcus.
It is not clear from current data which anti-fungal (fluconazole vs. itraconazole [Sporanox]) is superior for the primary prevention of Cryptococcus or what the optimal dose and frequency of intervention should be. Patient population characteristics may be an important consideration in choosing the best treatment since itraconazole is more effective against certain endemic fungal infections such as histoplasmosis and penicilliosis. The incidence of Cryptococcus disease was shown to be decreased in patients taking primary prophylaxis compared to those taking placebo.11 Itraconazole and fluconazole appear to be equally effective in patients with a CD4 counts less than 100, although neither show any decrease in overall mortality.11
Prophylactic therapy will vary according to pathogens wished to cover, and avoiding of drug interactions.
DISCUSSION
Cryptococcus neoformans is a polysaccharide encapsulated yeast that is ubiquitous in nature, found especially in pigeon droppings and nests.12 It was first described in 1894 by a pathologist named Busse when he isolated it from a tibial lesion of a patient in Germany.13
Its pathogenicity is very diverse, anywhere from harmless colonization of the airway to meningitis and systemic disease. It gains access by inhalation and spreads hematogenously from the lungs to the meninges, skin and kidneys.
Cryptococcal infections in immunocompetent individuals are relatively rare; however, these infections occur in 6% to 13% of AIDS patients5 due to their defective cell-mediated immunity. There appears to be a relationship to the amount of inoculum8 and whether an immunocompromised patient will become symptomatic during primary infection. There is no significant difference in incidence in regard to sex, age, race or occupation.
Cutaneous manifestations are found in 10% to 15% of patients with disseminated cryptococcosis. There have been reports of primary cutaneous infections, but these are rare and controversial.14 The most common sites of cutaneous lesions are the head and neck regions.
In 10% to 20% of patients,14 this may be the first presenting sign of disseminated cryptococcosis. These lesions may present similar in appearance to molluscum contagiosum, pyoderma gangrenosum and Kaposi’s sarcoma.
Diagnostic and Treatment Tips
Cryptococcus neoformans is a common pathogen in immunocompromised patients that causes disseminated disease. It often presents with a wide variety of manifestations. Cutaneous Cryptococcus are the first sign of systemic disease 10% to 20% of the time.1
Cutaneous lesions can often mimic other skin disorders such as molluscum contagiosum, basal cell cancers or keratoacanthomas.5 In both immunocompromised and immunocompetent patients, cutaneous cryptococcal lesions most commonly present on the head or neck.6
A useful tool for diagnosing cryptococcosis is serum cryptococcal antigen, as it will be positive in 90% of patients with systemic disease,3 but should always be followed with a lumbar puncture and cultures. The treatment of choice is 2 weeks of amphotericin B at 0.5 to 1 mg/kg/day and oral flucytosine at 150 mg/kg/day followed by 10 weeks of oral fluconazole at 400 mg/day.10
In AIDS patients it is important to consider suppressive treatment after active disease has ended to prevent recurrence.3 Prophylactic therapy with fluconazole or itraconazole has been shown to be effective, but has not been shown to decrease mortality.
Patient presentation
A 38-year-old African-American female presented to the George Washington University Hospital with odynophagia and a facial rash that had been worsening for 2 months. Her past medical history was significant for 22 years of HIV/AIDS for which she had not been treated nor had any regular follow-up. Her odynophagia secondary to candidiasis resolved with fluconazole (Diflucan) by day 3.
A dermatology consult was ordered for evaluation of the facial lesions. The facial lesions had worsened with increasing pruritus and tender bilateral cervical lymphadenopathy. She had been applying hydrocortisone cream and topical antibiotics without relief. The patient reported having tactile fevers and weight loss with a mild chronic non-productive cough. She reported a negative PPD test, which she had undergone in jail 6 months prior. She denied nausea, vomiting, diarrhea and abdominal pain.
Physical exam showed a thin woman in no acute distress with multiple 0.5- to 1-cm firm, flesh-colored to erythematous nodules with overlying crust located on her nose, cheeks and forehead and her posterior left arm, along with lichenified hyperpigmented plaques on her antecubital fossa. There was bilateral cervical lymphadenopathy with 1- to 2-cm hard mobile nodes, along with bilateral axillary and groin lymphadenopathy. Her Chem-7 and liver function tests were normal. Her CBC showed a hemoglobin count of 9.1, a white blood count of 3.9, a hematocrit of 30, and platelets of 153. Her lactate was 1.9 and her CD4 count was 4. A 4-mm skin punch biopsy was sent for histopathologic exam. A cervical lymph node was also excised and sent for histopathologic exam. A total body CT scan showed multiple neck lymphadenopathy with necrotic centers along with lymphadenopathy in the groin.
What is Your Diagnosis?
Diagnosis: Cryptococcal lymphadenitis
Cutaneous Cryptococcus may be the initial presenting sign of disseminated disease in 10% to 20% of cases of cryptococcal lymphadenitis.1 The usual mode of transmission is by inhalation; however, there have been a few reported cases of primary cutaneous infection without disseminated disease.2 Skin lesions are usually multiple and polymorphous in appearance. The majority of cryptococcal infections in immunocompromised patients are caused by Cryptococcus neoformans, while Cryptococcus gattii is the cause of 70% to 80% of cases in immunocompetent patients.3 In developed countries, the overall incidence of Cryptococcus in AIDS patients has decreased with the use of highly active anti-retroviral therapy (HAART) and prophylactic anti-fungal medications.4
CLINICAL PRESENTATION
Immunocompromised patients with disseminated cryptococcal infections commonly present with central nervous system (CNS) infections or, less commonly, pulmonary infections. CNS infections may be asymptomatic.
Cutaneous lesions develop in 10% to 15% of AIDS patients with disseminated Cryptococcus,5 with the majority of lesions occurring on the head and neck.6
Skin lesions present with a diverse morphology, although the most common presentation is umbilicated papules with a tiny central hemorrhagic crust.5
Other manifestations include pustules, ulcers, nodules, draining sinuses, abscesses or cellulitis. Papular lesions may be similar in
appearance to molluscum contagiosum. Large single lesions may resemble basal cell carcinomas or keratoacanthomas.5 Cryptococcal lymphadenitis is not commonly seen in AIDS patients, although when it is, the most common nodes involved are cervical and mediastinal.7
DIAGNOSIS
Even with systemic disease, routine blood work may produce normal results. A cerebrospinal fluid (CSF) examination is essential when diagnosing systemic disease. When India ink is used to stain the CSF, it will show cryptococcal meningitis 25% to 50% of the time.3 Anti-cryptococcal antibodies have no diagnostic significance since a large number of healthy individuals are exposed to Cryptococcus without apparent infection. However, cryptococcal antigen is positive in 90% of patients with systemic disease.3 Positive test results should always be followed up with cultures before diagnosing cryptococcosis.
In tissue specimens, Cryptococcus can be challenging to see with H&E stains. Methenamine silver or periodic acid-Schiff stain should be used. Fine needle aspiration can be diagnostic in cryptococcal nodal disease. However, it has been shown to miss the diagnosis in a case presented by Mohanty, et al; therefore, a lymph node excision and histo-pathological exam should be considered for obtaining an accurate diagnosis.8
TREATMENT
Disseminated cryptococcosis progressed from a fatal infection to a curable one with the advent of amphotericin B (AmBisome) 35 years ago.9 Amphotericin B has been successfully used to treat all forms of cryptococcal infections, although it is extremely nephrotoxic at therapeutic doses. Lipid formulations were later developed that allowed better delivery, decreased toxicity and higher doses; however, CNS penetration continued to be poor.
Flucytosine (Ancobon), an anti-fungal with excellent CNS penetration, has been successfully used for cryptococcal infections; however, resistance has developed limiting its use as a monotherapy.
Subsequently, flucytosine and amphotericin B have been successfully combined due to their differing pharmacokinetics and synergistic mechanisms of action.8,9 The standard treatment recommendations call for combining amphotericin B (0.5 to 1 mg/kg/day) and oral flucytosine (150 mg/kg/day) for 2 weeks followed by oral fluconazole (Diflucan) (400 mg/day) for 10 weeks.10 Fluconazole increases the clearance of cryptococci from the CNS. Cutaneous lesions will heal completely within 1 to 2 months after starting therapy.
Treating Patients with AIDS
Cryptococcus in AIDS patients may not be cured, only put into remission. Thus, life-long suppressive chemotherapy may be required after the treatment for active disease has ended.5 Positive cultures may continue to persist, or recur, despite adequate treatment. There has been no clear answer as to the use of primary prophylactic therapy for Cryptococcus.
It is not clear from current data which anti-fungal (fluconazole vs. itraconazole [Sporanox]) is superior for the primary prevention of Cryptococcus or what the optimal dose and frequency of intervention should be. Patient population characteristics may be an important consideration in choosing the best treatment since itraconazole is more effective against certain endemic fungal infections such as histoplasmosis and penicilliosis. The incidence of Cryptococcus disease was shown to be decreased in patients taking primary prophylaxis compared to those taking placebo.11 Itraconazole and fluconazole appear to be equally effective in patients with a CD4 counts less than 100, although neither show any decrease in overall mortality.11
Prophylactic therapy will vary according to pathogens wished to cover, and avoiding of drug interactions.
DISCUSSION
Cryptococcus neoformans is a polysaccharide encapsulated yeast that is ubiquitous in nature, found especially in pigeon droppings and nests.12 It was first described in 1894 by a pathologist named Busse when he isolated it from a tibial lesion of a patient in Germany.13
Its pathogenicity is very diverse, anywhere from harmless colonization of the airway to meningitis and systemic disease. It gains access by inhalation and spreads hematogenously from the lungs to the meninges, skin and kidneys.
Cryptococcal infections in immunocompetent individuals are relatively rare; however, these infections occur in 6% to 13% of AIDS patients5 due to their defective cell-mediated immunity. There appears to be a relationship to the amount of inoculum8 and whether an immunocompromised patient will become symptomatic during primary infection. There is no significant difference in incidence in regard to sex, age, race or occupation.
Cutaneous manifestations are found in 10% to 15% of patients with disseminated cryptococcosis. There have been reports of primary cutaneous infections, but these are rare and controversial.14 The most common sites of cutaneous lesions are the head and neck regions.
In 10% to 20% of patients,14 this may be the first presenting sign of disseminated cryptococcosis. These lesions may present similar in appearance to molluscum contagiosum, pyoderma gangrenosum and Kaposi’s sarcoma.
Diagnostic and Treatment Tips
Cryptococcus neoformans is a common pathogen in immunocompromised patients that causes disseminated disease. It often presents with a wide variety of manifestations. Cutaneous Cryptococcus are the first sign of systemic disease 10% to 20% of the time.1
Cutaneous lesions can often mimic other skin disorders such as molluscum contagiosum, basal cell cancers or keratoacanthomas.5 In both immunocompromised and immunocompetent patients, cutaneous cryptococcal lesions most commonly present on the head or neck.6
A useful tool for diagnosing cryptococcosis is serum cryptococcal antigen, as it will be positive in 90% of patients with systemic disease,3 but should always be followed with a lumbar puncture and cultures. The treatment of choice is 2 weeks of amphotericin B at 0.5 to 1 mg/kg/day and oral flucytosine at 150 mg/kg/day followed by 10 weeks of oral fluconazole at 400 mg/day.10
In AIDS patients it is important to consider suppressive treatment after active disease has ended to prevent recurrence.3 Prophylactic therapy with fluconazole or itraconazole has been shown to be effective, but has not been shown to decrease mortality.
