Skip to content
Download PDF

Blastomycosis

Chapter 220 | Harrison's 22e · Part 5 – Infectious Diseases: Fungal · Chapter 220

Key Clinical Points

  1. Pyogranulomatous disease caused by inhalation of Blastomyces conidia or hyphal fragments.
  2. Dimorphic fungus: grows as hyphae in soil (22–25°C) and as broad-based budding yeast in tissue (37°C).
  3. Characteristic morphology: Broad-based budding yeast cells, 4–29 μm in size.
  4. Clinical presentation varies by stage: pulmonary (mimics pneumonia/TB/malignancy), disseminated (skin, bone, GU), or meningitis.
  5. Diagnosis relies on microscopy (broad-based budding), culture (Sabouraud agar at 37°C), serology, and PCR.
  6. Initial treatment for severe/disseminated disease: Amphotericin B formulation + oral triazole.
  7. Maintenance therapy: Oral triazoles for 6 months to 1 year; ≥1 year for chronic or disseminated cases.
  8. High relapse rates: 80% in meningitis and 15–30% in disseminated disease after stopping treatment.
  9. Surgical extirpation indicated for pulmonary cavities >4 cm.
  10. Prophylaxis: 6–12 months for solid-organ transplant (SOT) recipients; lifelong for lung transplant recipients.

1. DEFINITION & OVERVIEW

• Definition (Harrison's 22e): Blastomycosis is a pyogranulomatous disease that follows the inhalation of Blastomyces conidia or hyphal fragments.

• Clinical Scope: Primary fungal infection in patients with intact or impaired immune systems. ◦ Pulmonary: Most common site of infection. ◦ Disseminated: Occurs in a subset of patients; involves skin, bone, brain, or genitourinary system.

2. ETIOLOGY

• Species Complex: Includes B. dermatitidis, B. gilchristii, B. helicus, B. percursus, B. emzantsi, B. silverae, and B. parvus. ◦ Note: B. silverae and B. parvus are not known to commonly infect humans.

• Thermal Dimorphism: Conversion between hyphal and yeast morphologies based on temperature: → In soil (22–25°C) → growth as septate hyphae producing infectious conidia. → In organs/tissues (37°C) → growth as pathogenic yeast eliciting pyogranulomatous inflammation.

• Morphology: All species grow as broad-based budding yeast cells. ◦ Size: 4–29 μm. ◦ B. helicus unique feature: Hyphae grow in a coiled pattern and do not sporulate under in vitro conditions.

3. EPIDEMIOLOGY

• Global Distribution: Majority of cases in North America; also reported in Africa and Asia.

• United States Regions: Mississippi and Ohio River basins, St. Lawrence River basin, states bordering the Great Lakes, and southeastern states.

• Risk Factors/Settings: Rural and urban settings. → Associated activities: construction, excavation of dirt, water sports, exposure to compost piles or beaver dams.

• Canada Regions: Saskatchewan, Manitoba, Ontario, and Quebec.

• Transmission Route: Inhalation of particles from disturbed soil.

4. CLINICAL MANIFESTATIONS

• Pulmonary Stage: Initial symptoms may mimic bacterial pneumonia, tuberculosis, or malignancy.

• Disseminated Stage: ◦ Skin lesions (papules, nodules). ◦ Bone involvement (painful osteolytic lesions). ◦ Genitourinary tract infections.

• Meningitis: Symptoms: headache, fever, and altered mental status. ◦ Risk: 80% of patients experience relapse after discontinuation of therapy.

5. DIAGNOSTIC APPROACH

  1. Direct microscopy: Identification of broad-based budding yeast in clinical specimens.
  2. Culture: Growth on Sabouraud agar at 37°C.
  3. Serologic testing: Detection of Blastomyces-specific antibodies.
  4. Molecular methods: PCR for Blastomyces DNA.

• Differential Diagnosis: Bacterial pneumonia, tuberculosis, and malignancy. → Note: Pulmonary nodules may require biopsy to distinguish from malignancies.

6. MANAGEMENT & TREATMENT

  1. Initial therapy (severe or disseminated): Amphotericin B formulation combined with oral triazole antifungal.
  2. Maintenance therapy (after clinical improvement): ◦ Oral triazole antifungal continued for 6 months to 1 year.
  3. Extended maintenance: ◦ Required for chronic pulmonary or disseminated disease: ≥1 year. ◦ Monitoring includes: symptoms, radiographic changes, sputum cultures, and serologic titers.
  4. Surgical intervention: ◦ Pulmonary cavities >4 cm → surgical extirpation.
  5. Special cases (Coccidioidal meningitis): ◦ Lifelong therapy with oral triazoles. ◦ Refractory cases → intrathecal amphotericin B.
  6. Relapse Risk: ◦ Disseminated disease: 15–30% relapse after discontinuation of therapy. ◦ Meningitis: 80% relapse rate.

7. PREVENTION STRATEGIES

  1. General Population: No proven methods to reduce risk in endemic regions; recommendation is avoidance of inhalation of disturbed soil/dust.

  2. High-Risk Populations: ◦ Solid-organ transplant recipients: Universal antifungal prophylaxis for 6–12 months post-transplantation. ◦ Lung transplant recipients: Lifelong universal prophylaxis. ◦ Donors from endemic regions: → Serologic screening before transplantation. → Organ donation deferred if active infection detected.

8. FURTHER READING

Galgiani JN et al: 2016 Infectious Diseases Society of America (IDSA) clinical practice guideline for the treatment of coccidioidomycosis. Clin Infect Dis 63:e112, 2016. Gorris ME et al: Expansion of coccidioidomycosis endemic regions in the United States in response to climate change. Geohealth 3:308, 2019. Shubitz LF et al: Δcps1 vaccine protects dogs against experimentally induced coccidioidomycosis. Vaccine 39:6894, 2021. Taylor JW, Barker BM: The endozoan, small-mammal reservoir hypothesis and the life cycle of Coccidioides species. Med Mycol 57:S16, 2019. Troung CN et al: Universal lifelong fungal prophylaxis and risk of coccidioidomycosis in lung transplant recipients living in an endemic area. Clin Infect Dis 74:1966, 2021.