Histoplasma capsulatum: Difference between revisions
From IDWiki
Histoplasma capsulatum
m (Text replacement - "Clinical Presentation" to "Clinical Manifestations") |
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− | == |
+ | ==Background== |
− | === |
+ | ===Microbiology=== |
− | * Dimorphic fungus; mold at room temperature, yeast at >37º C |
||
− | ** Mold: aerial hyphae with macroconidia |
||
− | *** Mold form is highly infectious, associated with lab-related outbreaks |
||
− | *** Mycelia have a typical appearance of spiked spherical conidia |
||
− | ** Yeast: |
||
− | *** Non-infectious, once hanging out in your body |
||
− | *** Narrow-based budding |
||
− | * ''H. capsulatum'' var. ''capsulatum'' most common worldwide, in various clades |
||
− | * ''H. capsulatum'' var. ''duboisii'' present in western Africa, has larger yeast forms |
||
− | ** Can take up to 7 days to grow |
||
+ | *Dimorphic fungus; mold at room temperature, yeast at >37º C |
||
− | === Epidemiology === |
||
+ | **Mold: aerial hyphae with macroconidia |
||
+ | ***Mold form is highly infectious, associated with lab-related outbreaks |
||
+ | ***Mycelia have a typical appearance of spiked spherical conidia |
||
+ | **Yeast: |
||
+ | ***Non-infectious, once hanging out in your body |
||
+ | ***Narrow-based budding |
||
+ | *''H. capsulatum'' var. ''capsulatum'' most common worldwide, in various clades |
||
+ | *''H. capsulatum'' var. ''duboisii'' present in western Africa, has larger yeast forms |
||
+ | **Can take up to 7 days to grow |
||
+ | |||
+ | ===Epidemiology=== |
||
[[File:Histoplasmosis_map.png|thumb|Distribution of histoplasmosis]] |
[[File:Histoplasmosis_map.png|thumb|Distribution of histoplasmosis]] |
||
− | * |
+ | *Endemic in many parts of the world |
− | ** |
+ | **Ohio and Mississippi River Valley systems (Central/Eastern US) |
− | ** |
+ | **Probably up through St. Lawrence River as well |
− | ** |
+ | **Probably more broadly distributed, including Central and South America, South and East Asia, and Australia |
− | ** |
+ | **''H. capsulatum'' var. ''duboisii'' in western Africa |
− | * |
+ | *Typically found in moist soil enriched with bat or bird droppings, which helps it to sporulate |
− | ** |
+ | **Disturbing the soil aerosolizes it, allowing the microconidia to be inhaled |
+ | **Microconidia can be transported for miles by air currents |
||
+ | |||
+ | ===Pathophysiology=== |
||
+ | *Inhaled microconidia reach the alveolii and are phagocytosed by alveolar macrophages |
||
− | === Pathophysiology === |
||
+ | **Innoculum size can be smaller with immunodeficiency |
||
+ | **Size of innoculation affects disease severity and progression |
||
+ | *Microconidia transform into budding yeasts, in a process that is dependent on macrophage calcium and iron |
||
+ | *They multiply inside macrophages, and translocate through the lymphatics |
||
+ | *Cellular immunity developed around 2 weeks later |
||
+ | **Response depends on IL-12 and TNF-alpha |
||
+ | **Organize to form granulomas to contain the infection |
||
+ | *Latent infection can reactivate, but rare |
||
+ | **Most common with infliximab |
||
+ | *In impaired cellular immunity, infection can become disseminated |
||
+ | ==Clinical Manifestations== |
||
− | * Inhaled microconidia reach the alveolii and are phagocytosed by alveolar macrophages |
||
− | ** Innoculum size can be smaller with immunodeficiency |
||
− | ** Size of innoculation affects disease severity and progression |
||
− | * Microconidia transform into budding yeasts, in a process that is dependent on macrophage calcium and iron |
||
− | * They multiply inside macrophages, and translocate through the lymphatics |
||
− | * Cellular immunity developed around 2 weeks later |
||
− | ** Response depends on IL-12 and TNF-alpha |
||
− | ** Organize to form granulomas to contain the infection |
||
− | * Latent infection can reactivate, but rare |
||
− | ** Most common with infliximab |
||
− | * In impaired cellular immunity, infection can become disseminated |
||
+ | *Often asymptomatic; in endemic areas, 50-80% of people skin-test positive or have radiographic evidence of previous infection |
||
− | == Clinical Manifestations == |
||
+ | *Can cross tissue planes |
||
+ | ===Acute pulmonary histoplasmosis=== |
||
− | * Often asymptomatic; in endemic areas, 50-80% of people skin-test positive or have radiographic evidence of previous infection |
||
− | * Can cross tissue planes |
||
+ | *Fever, chill, malaise, headaches, myalgias, anorexia, cough, dyspnea, and chest pain |
||
− | === Acute pulmonary histoplasmosis === |
||
+ | *Pneumonitis on chest x-ray, often with adenopathy |
||
+ | **"Buckshot" appearance? (Mandell) |
||
+ | *Can have rheumatologic sequelae in 5-10%, with arthralgias, arthritis, and erythema nodosum |
||
+ | *Can have pericarditis from the inflammatory response |
||
+ | *Hilar adenopathy can necrotize |
||
+ | *Usually self-limited, no need to treat unless longer than a month |
||
+ | ===Progressive disseminated histoplasmosis=== |
||
− | * Fever, chill, malaise, headaches, myalgias, anorexia, cough, dyspnea, and chest pain |
||
− | * Pneumonitis on chest x-ray, often with adenopathy |
||
− | ** "Buckshot" appearance? (Mandell) |
||
− | * Can have rheumatologic sequelae in 5-10%, with arthralgias, arthritis, and erythema nodosum |
||
− | * Can have pericarditis from the inflammatory response |
||
− | * Hilar adenopathy can necrotize |
||
− | * Usually self-limited, no need to treat unless longer than a month |
||
+ | *Usually, though not exclusively, in immunocompromised pations |
||
− | === Progressive disseminated histoplasmosis === |
||
+ | **Risk factors include CD4 <200, very old or very young, and therapeutic immunosuppression (pred, MMF, tac, MTX, TNF-alpha, other biologics |
||
+ | *Can be rapidly-progressing and acute, or more subacute |
||
+ | ===Acute progressive disseminated histoplasmosis=== |
||
− | * Usually, though not exclusively, in immunocompromised pations |
||
− | ** Risk factors include CD4 <200, very old or very young, and therapeutic immunosuppression (pred, MMF, tac, MTX, TNF-alpha, other biologics |
||
− | * Can be rapidly-progressing and acute, or more subacute |
||
+ | *Fever, weight loss, organomegaly, thrombocytopenia |
||
− | === Acute progressive disseminated histoplasmosis === |
||
+ | *Meningitis or focal brain lesions |
||
+ | *Oral and GI mucosal ulcerations |
||
+ | *Adrenal insufficiency |
||
+ | ===Chronic progressive disseminated histoplasmosis=== |
||
− | * Fever, weight loss, organomegaly, thrombocytopenia |
||
− | * Meningitis or focal brain lesions |
||
− | * Oral and GI mucosal ulcerations |
||
− | * Adrenal insufficiency |
||
+ | *In normal hosts |
||
− | === Chronic progressive disseminated histoplasmosis === |
||
+ | *Absent or low-grade fever |
||
+ | *Longer course |
||
+ | *Most common finding is oropharyngeal lesion: deep, well-circumscribed, unrated, and painless |
||
+ | **Mimics squamous cell carcinoma |
||
+ | *Can also have hepatosplenomegaly, chronic meningitis, or chronic granulomatous hepatitis |
||
+ | ===Chronic cavitary histoplasmosis=== |
||
− | * In normal hosts |
||
− | * Absent or low-grade fever |
||
− | * Longer course |
||
− | * Most common finding is oropharyngeal lesion: deep, well-circumscribed, unrated, and painless |
||
− | ** Mimics squamous cell carcinoma |
||
− | * Can also have hepatosplenomegaly, chronic meningitis, or chronic granulomatous hepatitis |
||
+ | *Typically seen in bullous emphysema |
||
− | === Chronic cavitary histoplasmosis === |
||
+ | *Productive cough, dyspnea, low-grade fever, night sweats, weight loss |
||
+ | **Hemoptysis is rare |
||
+ | **Progressive without treatment |
||
+ | *Chest x-ray shows upper-lobe infiltrations, vacitation, and pleural thickening, similar to tuberculosis |
||
+ | ===Fibrosing mediastinitis=== |
||
− | * Typically seen in bullous emphysema |
||
− | * Productive cough, dyspnea, low-grade fever, night sweats, weight loss |
||
− | ** Hemoptysis is rare |
||
− | ** Progressive without treatment |
||
− | * Chest x-ray shows upper-lobe infiltrations, vacitation, and pleural thickening, similar to tuberculosis |
||
+ | *Rare but serious |
||
− | === Fibrosing mediastinitis === |
||
+ | *Progressive fibrosis around hilar/mediatinal lymphadenopathy, wither unilateral or bilateral |
||
+ | *Can present with a SVC syndrome, obstruction of pulmonary vessels, or airway obstruction |
||
+ | *Can also present with recurrent pneumonias, hemoptysis, or respiratory failure |
||
+ | *30% mortality |
||
+ | ===Other complications=== |
||
− | * Rare but serious |
||
− | * Progressive fibrosis around hilar/mediatinal lymphadenopathy, wither unilateral or bilateral |
||
− | * Can present with a SVC syndrome, obstruction of pulmonary vessels, or airway obstruction |
||
− | * Can also present with recurrent pneumonias, hemoptysis, or respiratory failure |
||
− | * 30% mortality |
||
+ | *Ophthalmic uveitis |
||
− | === Other complications === |
||
+ | *Meningitis |
||
+ | *Endocarditis |
||
+ | ==African histoplasmosis== |
||
− | * Ophthalmic uveitis |
||
− | * Meningitis |
||
− | * Endocarditis |
||
+ | *''H. capsulatum'' vars. ''capsulatum'' and ''duboisii'' coexist in Africa |
||
− | == African histoplasmosis == |
||
+ | *var. ''duboisii'' has more skin and skeletal manifestations |
||
+ | **Ulcers, nodules, or psoriaform lesions that can spontaneously resolve |
||
+ | ***Can cause a cold abscess, without inflammation |
||
+ | **Osteolytic bone lesions are common (50%) of cases |
||
+ | ***Skull and ribs most common |
||
+ | ***Can have sinus formation and cystic bone lesions |
||
+ | **May not have any evidence on CXR of prior pulmonary histoplasmosis |
||
+ | **Can also present with progressive disseminated disease, with fevers and multiorgan involvement |
||
+ | ***Combianation of granulomas and pus |
||
+ | ***Larger yeast is harder for macrophages to engulf |
||
+ | ==Diagnosis== |
||
− | * ''H. capsulatum'' vars. ''capsulatum'' and ''duboisii'' coexist in Africa |
||
− | * var. ''duboisii'' has more skin and skeletal manifestations |
||
− | ** Ulcers, nodules, or psoriaform lesions that can spontaneously resolve |
||
− | *** Can cause a cold abscess, without inflammation |
||
− | ** Osteolytic bone lesions are common (50%) of cases |
||
− | *** Skull and ribs most common |
||
− | *** Can have sinus formation and cystic bone lesions |
||
− | ** May not have any evidence on CXR of prior pulmonary histoplasmosis |
||
− | ** Can also present with progressive disseminated disease, with fevers and multiorgan involvement |
||
− | *** Combianation of granulomas and pus |
||
− | *** Larger yeast is harder for macrophages to engulf |
||
+ | *Fungal culture of sputum (chronic cavitary), or blood or bone marrow aspirate (disseminated), or CSF (CNS histo) |
||
− | == Diagnosis == |
||
+ | **Mold and yeast forms depending on the temperature |
||
+ | **Best stain is GMS (Giemsa m…. silver) |
||
+ | **Seen within the macrophages |
||
+ | *Serology can be done for antigen or antibody |
||
+ | **Serology may be negative in immunosuppressed patients |
||
+ | **Antigen of '''urine''' (best), BAL fluid, and serum if available |
||
+ | ***Urine is best, but only 40% sensitive in cavitary, up to 95% in AIDS patients |
||
+ | ***Cross-reacts with other endemic fungi; false-positives with antithymocyte globulin |
||
+ | *PCR is possible |
||
+ | **16S PCR |
||
+ | ==Management== |
||
− | * Fungal culture of sputum (chronic cavitary), or blood or bone marrow aspirate (disseminated), or CSF (CNS histo) |
||
− | ** Mold and yeast forms depending on the temperature |
||
− | ** Best stain is GMS (Giemsa m…. silver) |
||
− | ** Seen within the macrophages |
||
− | * Serology can be done for antigen or antibody |
||
− | ** Serology may be negative in immunosuppressed patients |
||
− | ** Antigen of '''urine''' (best), BAL fluid, and serum if available |
||
− | *** Urine is best, but only 40% sensitive in cavitary, up to 95% in AIDS patients |
||
− | *** Cross-reacts with other endemic fungi; false-positives with antithymocyte globulin |
||
− | * PCR is possible |
||
− | ** 16S PCR |
||
+ | *In general, mild infections are treated with [[Is treated by::itraconazole]] and severe infections with [[Is treated by::amphotericin B]] |
||
− | == Management == |
||
− | * In general, mild infections are treated with [[Is treated by::itraconazole]] and severe infections with [[Is treated by::amphotericin B]] |
||
{| class="wikitable" |
{| class="wikitable" |
||
− | ! |
+ | !Syndrome |
− | ! |
+ | !Treatment |
|- |
|- |
||
− | | |
+ | |Acute pulmonary histoplasmosis |
| |
| |
||
|- |
|- |
||
− | | |
+ | | Mild, self-resolving |
− | | |
+ | |If resolves within a month, no need to treat |
|- |
|- |
||
− | | |
+ | | Mild, ongoing symptoms |
− | | |
+ | |[[Itraconazole]] 200 mg po TID x3d then itra 200 mg po daily or BID for 6-12 weeks |
|- |
|- |
||
− | | |
+ | | Moderate to severe |
− | | |
+ | |[[Liposomal amphotericin B]] 3-5 mg/kg/d for 1-2 weeks, followed by [[itraconazole]] 200 mg TID x3d then [[itraconazole]] 200 mg BID x12wk<br />Methylpred 0.5-1 mg/kg IV daily for first 1-2 weeks if respiratory complications |
|- |
|- |
||
− | | |
+ | |Chronic cavitary pulmonary histoplasmosis |
− | | |
+ | |[[Itraconazole]] 200 mg TID x3d then daily or BID for at least 1 year (18-24 months may have lower relapse) |
|- |
|- |
||
− | | |
+ | |Complications |
| |
| |
||
|- |
|- |
||
− | | |
+ | | Pericarditis |
− | | |
+ | |NSAIDs if mild<br />Prednisone 0.5-1 mg/kg daily then taper over 1-2 weeks, plus itra (as above) for 6-12 weeks if hemodynamic compromise<br />May need therapeutic pericardiocentesis |
|- |
|- |
||
− | | |
+ | | Rheumatologic |
− | | |
+ | |NSAIDs if mild, prednisone and [[itraconazole]] (as for pericarditis) if severe |
|- |
|- |
||
− | | |
+ | | Mediastinal lymphadenitis |
− | | |
+ | |Usually no treatment. Follow guide for acute pulmonary histoplasmosis. |
|- |
|- |
||
− | | |
+ | | Mediastinal granuloma |
− | | |
+ | |Usually no treatment. Standard [[itraconazole]] protocol for 6-12 weeks if symptomatic. |
|- |
|- |
||
− | | |
+ | | Mediastinal fibrosis |
− | | |
+ | |Antifungals not recommended. Treat only if there is suspicion of mediastinal granuloma. May need stenting of obstructed pulmonary vessels. |
|- |
|- |
||
− | | |
+ | | Broncholithiasis |
− | | |
+ | |Antifungals not recommended. May need surgery. |
|- |
|- |
||
− | | |
+ | |Progressive disseminated histoplasmosis |
− | | |
+ | |Follow antigen levels during therapy and for 12 months after to monitor for relapse |
|- |
|- |
||
− | | |
+ | | Mild to moderate |
− | | |
+ | |[[Itraconazole]] for 12 months |
|- |
|- |
||
− | | |
+ | | Moderately severe to severe |
− | | |
+ | |[[Liposomal amphotericin B]] 3 mg/kg for 1-2 weeks then oral [[itraconazole]] for at least 12 months |
|- |
|- |
||
− | | |
+ | | Immunosuppressed |
− | | |
+ | |May need lifelong suppressive therapy with [[itraconazole]] 200 mg po daily |
|- |
|- |
||
− | | |
+ | |CNS histoplasmosis |
− | | |
+ | |[[Liposomal amphotericin B]] 5 mg/kg daily for 4-6 weeks (total 175 mg/kg) followed by itraconazole for at least 1 year, until resolution of CSF abnormalities |
|- |
|- |
||
− | | |
+ | |Pregnancy |
− | | |
+ | |[[Liposomal amphotericin B]] 3-5 mg/kg for 4-6 weeks |
|- |
|- |
||
− | | |
+ | |Children |
− | | |
+ | |As per above guidelines, with [[amphotericin B deoxycholate]] 1 mg/kg and [[itraconazole]] 2.5-5 mg/kg bid (max 400 mg daily) |
|- |
|- |
||
− | | |
+ | |Prophylaxis |
− | | |
+ | |[[Itraconazole]] 200 mg po daily recommended if HIV with CD4 <150 and more than 10 cases per 100 patient-years |
|} |
|} |
||
Revision as of 05:57, 14 August 2020
Background
Microbiology
- Dimorphic fungus; mold at room temperature, yeast at >37º C
- Mold: aerial hyphae with macroconidia
- Mold form is highly infectious, associated with lab-related outbreaks
- Mycelia have a typical appearance of spiked spherical conidia
- Yeast:
- Non-infectious, once hanging out in your body
- Narrow-based budding
- Mold: aerial hyphae with macroconidia
- H. capsulatum var. capsulatum most common worldwide, in various clades
- H. capsulatum var. duboisii present in western Africa, has larger yeast forms
- Can take up to 7 days to grow
Epidemiology
- Endemic in many parts of the world
- Ohio and Mississippi River Valley systems (Central/Eastern US)
- Probably up through St. Lawrence River as well
- Probably more broadly distributed, including Central and South America, South and East Asia, and Australia
- H. capsulatum var. duboisii in western Africa
- Typically found in moist soil enriched with bat or bird droppings, which helps it to sporulate
- Disturbing the soil aerosolizes it, allowing the microconidia to be inhaled
- Microconidia can be transported for miles by air currents
Pathophysiology
- Inhaled microconidia reach the alveolii and are phagocytosed by alveolar macrophages
- Innoculum size can be smaller with immunodeficiency
- Size of innoculation affects disease severity and progression
- Microconidia transform into budding yeasts, in a process that is dependent on macrophage calcium and iron
- They multiply inside macrophages, and translocate through the lymphatics
- Cellular immunity developed around 2 weeks later
- Response depends on IL-12 and TNF-alpha
- Organize to form granulomas to contain the infection
- Latent infection can reactivate, but rare
- Most common with infliximab
- In impaired cellular immunity, infection can become disseminated
Clinical Manifestations
- Often asymptomatic; in endemic areas, 50-80% of people skin-test positive or have radiographic evidence of previous infection
- Can cross tissue planes
Acute pulmonary histoplasmosis
- Fever, chill, malaise, headaches, myalgias, anorexia, cough, dyspnea, and chest pain
- Pneumonitis on chest x-ray, often with adenopathy
- "Buckshot" appearance? (Mandell)
- Can have rheumatologic sequelae in 5-10%, with arthralgias, arthritis, and erythema nodosum
- Can have pericarditis from the inflammatory response
- Hilar adenopathy can necrotize
- Usually self-limited, no need to treat unless longer than a month
Progressive disseminated histoplasmosis
- Usually, though not exclusively, in immunocompromised pations
- Risk factors include CD4 <200, very old or very young, and therapeutic immunosuppression (pred, MMF, tac, MTX, TNF-alpha, other biologics
- Can be rapidly-progressing and acute, or more subacute
Acute progressive disseminated histoplasmosis
- Fever, weight loss, organomegaly, thrombocytopenia
- Meningitis or focal brain lesions
- Oral and GI mucosal ulcerations
- Adrenal insufficiency
Chronic progressive disseminated histoplasmosis
- In normal hosts
- Absent or low-grade fever
- Longer course
- Most common finding is oropharyngeal lesion: deep, well-circumscribed, unrated, and painless
- Mimics squamous cell carcinoma
- Can also have hepatosplenomegaly, chronic meningitis, or chronic granulomatous hepatitis
Chronic cavitary histoplasmosis
- Typically seen in bullous emphysema
- Productive cough, dyspnea, low-grade fever, night sweats, weight loss
- Hemoptysis is rare
- Progressive without treatment
- Chest x-ray shows upper-lobe infiltrations, vacitation, and pleural thickening, similar to tuberculosis
Fibrosing mediastinitis
- Rare but serious
- Progressive fibrosis around hilar/mediatinal lymphadenopathy, wither unilateral or bilateral
- Can present with a SVC syndrome, obstruction of pulmonary vessels, or airway obstruction
- Can also present with recurrent pneumonias, hemoptysis, or respiratory failure
- 30% mortality
Other complications
- Ophthalmic uveitis
- Meningitis
- Endocarditis
African histoplasmosis
- H. capsulatum vars. capsulatum and duboisii coexist in Africa
- var. duboisii has more skin and skeletal manifestations
- Ulcers, nodules, or psoriaform lesions that can spontaneously resolve
- Can cause a cold abscess, without inflammation
- Osteolytic bone lesions are common (50%) of cases
- Skull and ribs most common
- Can have sinus formation and cystic bone lesions
- May not have any evidence on CXR of prior pulmonary histoplasmosis
- Can also present with progressive disseminated disease, with fevers and multiorgan involvement
- Combianation of granulomas and pus
- Larger yeast is harder for macrophages to engulf
- Ulcers, nodules, or psoriaform lesions that can spontaneously resolve
Diagnosis
- Fungal culture of sputum (chronic cavitary), or blood or bone marrow aspirate (disseminated), or CSF (CNS histo)
- Mold and yeast forms depending on the temperature
- Best stain is GMS (Giemsa m…. silver)
- Seen within the macrophages
- Serology can be done for antigen or antibody
- Serology may be negative in immunosuppressed patients
- Antigen of urine (best), BAL fluid, and serum if available
- Urine is best, but only 40% sensitive in cavitary, up to 95% in AIDS patients
- Cross-reacts with other endemic fungi; false-positives with antithymocyte globulin
- PCR is possible
- 16S PCR
Management
- In general, mild infections are treated with itraconazole and severe infections with amphotericin B
Syndrome | Treatment |
---|---|
Acute pulmonary histoplasmosis | |
Mild, self-resolving | If resolves within a month, no need to treat |
Mild, ongoing symptoms | Itraconazole 200 mg po TID x3d then itra 200 mg po daily or BID for 6-12 weeks |
Moderate to severe | Liposomal amphotericin B 3-5 mg/kg/d for 1-2 weeks, followed by itraconazole 200 mg TID x3d then itraconazole 200 mg BID x12wk Methylpred 0.5-1 mg/kg IV daily for first 1-2 weeks if respiratory complications |
Chronic cavitary pulmonary histoplasmosis | Itraconazole 200 mg TID x3d then daily or BID for at least 1 year (18-24 months may have lower relapse) |
Complications | |
Pericarditis | NSAIDs if mild Prednisone 0.5-1 mg/kg daily then taper over 1-2 weeks, plus itra (as above) for 6-12 weeks if hemodynamic compromise May need therapeutic pericardiocentesis |
Rheumatologic | NSAIDs if mild, prednisone and itraconazole (as for pericarditis) if severe |
Mediastinal lymphadenitis | Usually no treatment. Follow guide for acute pulmonary histoplasmosis. |
Mediastinal granuloma | Usually no treatment. Standard itraconazole protocol for 6-12 weeks if symptomatic. |
Mediastinal fibrosis | Antifungals not recommended. Treat only if there is suspicion of mediastinal granuloma. May need stenting of obstructed pulmonary vessels. |
Broncholithiasis | Antifungals not recommended. May need surgery. |
Progressive disseminated histoplasmosis | Follow antigen levels during therapy and for 12 months after to monitor for relapse |
Mild to moderate | Itraconazole for 12 months |
Moderately severe to severe | Liposomal amphotericin B 3 mg/kg for 1-2 weeks then oral itraconazole for at least 12 months |
Immunosuppressed | May need lifelong suppressive therapy with itraconazole 200 mg po daily |
CNS histoplasmosis | Liposomal amphotericin B 5 mg/kg daily for 4-6 weeks (total 175 mg/kg) followed by itraconazole for at least 1 year, until resolution of CSF abnormalities |
Pregnancy | Liposomal amphotericin B 3-5 mg/kg for 4-6 weeks |
Children | As per above guidelines, with amphotericin B deoxycholate 1 mg/kg and itraconazole 2.5-5 mg/kg bid (max 400 mg daily) |
Prophylaxis | Itraconazole 200 mg po daily recommended if HIV with CD4 <150 and more than 10 cases per 100 patient-years |
Note: therapeutic drug level monitoring is recommended for itraconazole
Source: IDSA guidelines 2007