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Aspergillosis: A Literature Review

1. Introduction

Aspergillosis encompasses a broad and heterogeneous spectrum of diseases caused by filamentous fungi of the genus Aspergillus. These ubiquitous environmental molds reproduce by releasing vast numbers of airborne conidia (spores, approximately 3-5 µm in diameter) that are continuously inhaled by humans. Whether inhalation leads to disease depends far less on the virulence of the individual species than on the immunological competence of the host. The clinical outcomes range from benign hypersensitivity syndromes in atopic individuals to rapidly fatal disseminated infection in the severely immunocompromised. The World Health Organization's first priority list of fungal pathogens (FPPL), published in 2022, recognized Aspergillus fumigatus as a critical-priority pathogen, reflecting the growing global disease burden and the threat of emerging azole resistance - Goldman-Cecil Medicine, p. 3347.

2. Microbiology and Pathogen Biology

The genus Aspergillus comprises over 350 identified species, of which a small subset account for the vast majority of human infections. A. fumigatus is responsible for approximately 70-90% of cases, followed by A. flavus, A. niger, and A. terreus. Species identification historically relied on the characteristic microscopic morphology of hyphae and conidial-bearing structures; in the modern era, matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS) and molecular sequencing enable more precise identification, particularly for cryptic species within the A. fumigatus complex.
In tissue, Aspergillus species appear as dichotomously branched (Y-shaped) septate hyphae, a feature that differentiates them from the broad, aseptate or sparsely septate hyphae of the Mucorales. Scedosporium and Fusarium species also produce septate hyphae and must be distinguished by culture and molecular methods. Of clinical relevance, A. terreus is intrinsically resistant to amphotericin B, making species identification a prerequisite for appropriate antifungal selection - Goldman-Cecil Medicine, p. 3348.
The outer surface of conidia is coated with hydrophobin proteins that confer hydrophobicity and facilitate adherence to mammalian cell surfaces; dihydroxynaphtalene melanins further protect conidia from phagocytic killing. These virulence attributes, combined with thermotolerance (surviving temperatures up to 40-50°C), explain the particular fitness of A. fumigatus as a human pathogen - Goldman-Cecil Medicine, p. 3351.

3. Epidemiology

Aspergillus species are among the most widespread organisms in the natural environment, colonizing soil, decaying organic matter, and air worldwide. Within the healthcare setting, conidia can be isolated from air currents, unfiltered ventilation systems, showerheads, water storage tanks, potted plants, and building materials disturbed during renovation or construction. Nosocomial outbreaks linked to building construction or renovation have been well documented, and hospital water aerosolized during showering has been implicated as an underappreciated transmission route.
Globally, the annual incidence of invasive aspergillosis (IA) in patients with acute leukemia is estimated at approximately 5.84 per 100 patients. IA complicates the care of up to 13% of immunocompromised patients overall, and is associated with increased hospital mortality, excess hospitalization duration, 30-day readmission rates, and substantial costs - Goldman-Cecil Medicine, p. 3349.
A. flavus produces aflatoxin, one of the most potent known carcinogens, on stored grains, spices, and nuts, with foodborne ingestion linked to hepatic necrosis and hepatocellular carcinoma in animals and humans - Goldman-Cecil Medicine, p. 3348.

4. Classification and Clinical Syndromes

Aspergillosis is classically categorized into three broad groups: acute invasive, chronic, and allergic forms (Table 1).
Table 1: Classification of Aspergillosis (after Walsh & Patterson, Goldman-Cecil Medicine)
CategorySpecific Forms
Acute invasive aspergillosisInvasive pulmonary aspergillosis, tracheobronchial aspergillosis, acute sinusitis, cerebral/cerebellar infarction, endocarditis, osteomyelitis, cutaneous lesions
Chronic aspergillosisAspergilloma, chronic necrotizing pulmonary aspergillosis (CNPA), chronic cavitary pulmonary aspergillosis (CCPA)
Allergic formsAllergic bronchopulmonary aspergillosis (ABPA), extrinsic allergic alveolitis (hypersensitivity pneumonitis), allergic Aspergillus sinusitis

4.1 Acute Invasive Aspergillosis

Acute IA develops almost exclusively in immunocompromised hosts. The major risk groups include patients with prolonged severe neutropenia (especially from acute leukemia or aplastic anemia), recipients of hematopoietic stem cell transplants (HSCT), solid organ transplant recipients (particularly heart, lung, and liver), and individuals receiving prolonged high-dose corticosteroids or other immunosuppressive agents. Graft-versus-host disease (GVHD) and concurrent cytomegalovirus infection are independent risk factors in the HSCT population. A genetic predisposition linked to homozygous PTX3 haplotype (h2/h2) in donor cells impairs neutrophilic antifungal capacity and raises IA risk in HSCT recipients.
Invasive pulmonary aspergillosis (IPA) is the most common form. Classic clinical manifestations include persistent fever unresponsive to antibacterials, focal pulmonary infiltrates, nodules, or wedge-shaped infarct-like densities. Cough, pleuritic chest pain, and hemoptysis may develop. In neutropenic patients recovering immunity, pulmonary infiltrates may cavitate. Tracheobronchial aspergillosis - presenting as ulcerative, pseudomembranous, or plaque-like airway disease - has been increasingly reported in mechanically ventilated patients, including those with COVID-19 - Goldman-Cecil Medicine, p. 3352.
Extrapulmonary and disseminated aspergillosis occurs by hematogenous spread due to the fungus's avid angioinvasion. Common extrapulmonary targets include the central nervous system (cerebral abscesses and infarcts), kidneys, liver, spleen, heart (myocarditis, endocarditis, pericarditis), gastrointestinal tract, and skin (nodules and ulcers). CNS involvement carries a particularly poor prognosis.
Acute Aspergillus sinusitis - predominantly caused by A. flavus - may occur alongside or independently of pulmonary disease. In severely immunocompromised patients the cardinal symptoms of fever, local pressure, and pain may be absent, and eschar of the nasal septum or turbinates may be the first sign. Extension to the cavernous sinus can compromise cranial nerves III, IV, V, and VI - Goldman-Cecil Medicine, p. 3352.

4.2 Virus-Associated Pulmonary Aspergillosis: Emerging Entities

Two newly characterized syndromes have attracted intense research attention over the past decade.
Influenza-associated pulmonary aspergillosis (IAPA): A 2024 systematic review and meta-analysis of 10 observational studies (1,720 critically ill influenza patients) reported an IAPA prevalence of 19.2%. Key risk factors included organ transplantation (OR 4.8), hematological malignancy (OR 2.5), general immunocompromise (OR 2.2), and prolonged pre-admission corticosteroid use (OR 2.4). IAPA was associated with a significantly elevated ICU mortality (OR 2.6, 95% CI 1.8-3.8), with higher complication rates and longer ICU stays compared to influenza without aspergillosis (Lu et al., Chest, 2024; PMID 37742914).
COVID-19-associated pulmonary aspergillosis (CAPA): A Lancet Respiratory Medicine systematic review and meta-analysis (27 studies, 6,848 COVID-19 patients) found CAPA in 19.3% of included patients. Eight independent risk factors were identified: haematological malignancy (OR 2.47), chronic liver disease (OR 2.70), COPD (OR 2.00), interleukin-6 inhibitors (OR 2.88), invasive mechanical ventilation (OR 2.83), renal replacement therapy (OR 2.26), corticosteroids (OR 1.88), and cerebrovascular disease (OR 1.31). Patients with CAPA were older and had significantly longer mechanical ventilation durations (Gioia et al., Lancet Respir Med, 2024; PMID 38185135).

4.3 Chronic Aspergillosis

Chronic aspergillosis encompasses a group of overlapping syndromes that develop in patients with structural lung disease (tuberculosis sequelae, COPD, bronchiectasis, fibrocystic sarcoidosis, prior Pneumocystis infection) rather than severe immune deficiency.
  • Aspergilloma (simple fungal ball): A mass of matted hyphae and debris colonizing a preformed cavity - most often a residual TB cavity. Patients are frequently asymptomatic, but hemoptysis is the main complication and may be life-threatening.
  • Chronic cavitary pulmonary aspergillosis (CCPA): Multiple Aspergillus-related cavities, with or without an aspergilloma, progressing over months to years with weight loss, fatigue, and productive cough.
  • Chronic necrotizing pulmonary aspergillosis (CNPA) / Subacute invasive aspergillosis: A slowly progressive inflammatory destruction of lung tissue superimposed on mild-to-moderate immunosuppression (diabetes, malnutrition, low-dose steroids).
A landmark 2025 individual patient data meta-analysis in Lancet Infectious Diseases (79 studies, 8,778 patients) reported pooled CPA mortality of 27% overall, 15% at 1 year, and 32% at 5 years. Mortality hazard increased 25% with each decade of age. Among predisposing conditions, underlying malignancy and COPD conferred the worst outcomes, while prior pulmonary tuberculosis was associated with comparatively lower mortality. Subacute invasive and CCPA subtypes carried significantly higher mortality than simple aspergilloma (Sengupta et al., Lancet Infect Dis, 2025; PMID 39617023).

4.4 Allergic Bronchopulmonary Aspergillosis (ABPA)

ABPA represents a hypersensitivity response to Aspergillus colonization of the airways in susceptible hosts - primarily those with asthma or cystic fibrosis. Immunologically, it is driven by a combined type I (IgE-mediated, mast cell degranulation, bronchoconstriction) and type III (immune complex-mediated) hypersensitivity, resulting in elevated total and Aspergillus-specific IgE, peripheral eosinophilia, elevated IL-4 and IL-5, mucus plugging, and ultimately bronchiectasis if untreated. Diagnostic criteria typically require asthma or cystic fibrosis as a background diagnosis, skin-test or IgE reactivity to Aspergillus antigens, elevated total serum IgE (>1000 IU/mL), peripheral eosinophilia, and characteristic radiological findings (central bronchiectasis, mucoid impaction, fleeting pulmonary infiltrates).
A 2025 systematic review highlighted an association between ABPA/Aspergillus sensitization and tuberculosis - 607 pooled cases showed Aspergillus sensitization in patients with TB can complicate diagnosis and management (Ajayababu et al., J Infect Chemother, 2025; PMID 40812722).

5. Pathobiology and Immune Evasion

After inhalation, conidia that elude mucociliary clearance encounter pulmonary alveolar macrophages. These macrophages recognize (1→3)-β-D-glucan on swollen conidia via dectin-1, triggering cytokine and chemokine release. Normally, conidia are destroyed within phagolysosomes by non-oxidative mechanisms. Conidia that survive germinate into hyphae, which are then targeted by neutrophils using oxidative burst (reactive oxygen species). This neutrophil-dependent hyphal damage is the key defense mechanism, explaining why neutropenia is the single most important risk factor for IPA.
When host defenses are overwhelmed, hyphae invade and penetrate blood vessel walls - a process called angioinvasion - producing hemorrhagic infarction and necrosis. This pathological process generates the characteristic radiological "halo sign": a nodular density surrounded by a ring of ground-glass opacity (hemorrhage and edema) on computed tomography (CT). Release of galactomannan, a heteropolysaccharide of the Aspergillus cell wall, and (1→3)-β-D-glucan into the circulation during active invasion forms the basis of serum biomarker detection - Goldman-Cecil Medicine, p. 3351.
In the ABPA spectrum, hyphal colonization without true invasion drives the hypersensitivity response. Genetic susceptibility (HLA-DR and HLA-DQ alleles) and Th2-polarized immune responses underlie the predisposition in asthmatic and cystic fibrosis patients.

6. Diagnosis

Definitive diagnosis of aspergillosis relies on a combination of clinical, radiological, microbiological, histopathological, and biomarker-based evidence - Medical Microbiology 9e, p. (block 7).

6.1 Imaging

CT of the chest is the most sensitive imaging modality for IPA. The halo sign (a nodule or mass surrounded by a ground-glass halo) is highly suggestive of angioinvasive disease in neutropenic patients, though it is neither pathognomonic nor persistent. As neutropenia resolves, lesions may cavitate, producing the "air-crescent sign." In ABPA, chest CT shows central bronchiectasis, mucoid impaction ("finger-in-glove" pattern), and fleeting infiltrates.

6.2 Microbiological Culture and Histopathology

Recovery of Aspergillus from bronchoalveolar lavage (BAL) or tissue biopsy remains the gold standard for proven infection. However, sensitivity of BAL culture for IPA is low (~50%), and false-positive results can occur due to airway colonization. Histopathology demonstrating septate branching hyphae invading tissue - optimally combined with culture - establishes a "proven" diagnosis according to EORTC/MSGERC criteria. Special stains include Gomori methenamine silver (GMS) and periodic acid-Schiff (PAS).

6.3 Serological and Molecular Biomarkers

Galactomannan (GM): Detected in serum or BAL by enzyme immunoassay (EIA). Serum GM has good sensitivity in neutropenic and HSCT patients (~70-80%), but sensitivity is lower in non-neutropenic patients (including solid organ transplant recipients) and in those on mold-active prophylaxis. BAL GM has higher sensitivity than serum GM in many populations.
Beta-D-glucan (BDG): A panfungal marker, not specific for Aspergillus, but useful as part of a diagnostic algorithm. False positives occur with other fungi, some antibiotics, and dialysis membranes.
Lateral flow assay (LFA) for Aspergillus: A point-of-care GM detection method with comparable performance to EIA that can be performed directly on BAL fluid without laboratory processing.
PCR: Molecular detection of Aspergillus DNA in blood, BAL, or tissue has increasing validation, though standardization across platforms and thresholds remains an active area.
IgG precipitins: Particularly useful in ABPA and CPA, where elevated Aspergillus-specific IgG supports the diagnosis. A 2022 meta-analysis comparing immunoprecipitation versus immunoassay methods found immunoassay (ELISA) was non-inferior to immunoprecipitation for detecting A. fumigatus-specific IgG in ABPA (Sehgal et al., Mycoses, 2022; PMID 35757847).

6.4 Azole Resistance Surveillance

Emerging azole resistance in A. fumigatus - driven predominantly by the TR34/L98H and TR46/Y121F/T289A mutations in the cyp51A gene following environmental exposure to fungicide azoles - is a growing diagnostic concern. The 2024 WHO FPPL systematic review reported voriconazole susceptibility rates as low as 22.2% in some Netherlands isolates, while rates in Brazil, India, Korea, and the UK remained above 76%. Cross-resistance across triazoles is common: 85%, 92.8%, and 100% of voriconazole-resistant isolates were also resistant to itraconazole, posaconazole, and isavuconazole, respectively. Twelve-week mortality was significantly higher in voriconazole-resistant versus voriconazole-susceptible IA (54.5% vs. 30.7%, p=0.035) (Morrissey et al., Med Mycol, 2024; PMID 38935907).

7. Treatment

7.1 Invasive Aspergillosis

Voriconazole remains the established first-line agent for primary treatment of IA based on a pivotal 2002 RCT showing superiority over amphotericin B deoxycholate (Herbrecht et al., NEJM 2002). A 2026 Bayesian network meta-analysis published in Drugs (5 RCTs, 1,293 patients, 6 treatment regimens) found no statistically significant mortality differences between voriconazole, isavuconazole, posaconazole, or the combination of voriconazole plus anidulafungin. Integrated efficacy-safety analysis, however, demonstrated a favorable balance for isavuconazole (SUCRA ranking 79.4% for mortality), given its superior tolerability profile. The combination of voriconazole plus anidulafungin may benefit a subset of severe cases (SUCRA 84.3%, though non-significant vs. voriconazole alone) (Gu et al., Drugs, 2026; PMID 42012594).
A separate 2024 network meta-analysis in BMC Infectious Diseases comparing antifungal agents in primary therapy of IA largely confirmed these findings, concluding isavuconazole and voriconazole have equivalent efficacy but isavuconazole has a better safety profile (Liu et al., BMC Infect Dis, 2024; PMID 38867163).
Lipid formulations of amphotericin B (liposomal amphotericin B, amphotericin B lipid complex) are the primary alternatives when triazoles are not tolerated or when azole resistance is documented. Amphotericin B deoxycholate should generally be avoided due to nephrotoxicity. A. terreus is intrinsically resistant to all amphotericin B formulations.
Echinocandins (caspofungin, micafungin, anidulafungin) are not recommended as monotherapy but may be combined with triazoles in refractory cases.
Prophylaxis in high-risk (neutropenic, HSCT) patients is typically achieved with mold-active azoles: posaconazole, voriconazole, or itraconazole. A 2024 systematic review in Clinical Infectious Diseases found breakthrough IA rates of 2.4% and 1.6% in patients on voriconazole and posaconazole prophylaxis, respectively, highlighting that prophylaxis does not eliminate risk (Boutin et al., Clin Infect Dis, 2024; PMID 38752732).
Therapeutic drug monitoring (TDM) of voriconazole is recommended given wide pharmacokinetic variability and its CYP2C19-dependent metabolism; target trough concentrations of 1-5.5 mg/L are recommended, with Asian patients generally requiring lower doses. A 2022 clinical practice guideline meta-analysis provided consensus TDM targets across ethnic groups (Takesue et al., Clin Ther, 2022; PMID 36424314).
Surgical resection is considered in cases with localized disease invading adjacent structures (ribs, pericardium, great vessels), in single lesions with impending hemoptysis, or to reduce fungal burden before further immunosuppression.
The 2025 German national guideline executive summary for IPA in critically ill ICU patients emphasizes early CT, BAL GM testing, and prompt antifungal initiation as cornerstones of management (Wichmann et al., Infection, 2025; PMID 40465080).

7.2 Chronic Pulmonary Aspergillosis

Long-term oral azole therapy - principally itraconazole or voriconazole - is the mainstay of treatment for CPA. Given the high 5-year mortality of ~32% noted by Sengupta et al. (2025), sustained treatment and monitoring are required. Surgical resection carries low mortality (~3%) in selected patients and is considered for refractory or localized CPA, especially when complicated by severe hemoptysis - Goldman-Cecil Medicine, p. 3352; Medical Microbiology 9e (block 7). Treatment duration is typically at least 6 months; many patients require indefinite therapy.

7.3 Allergic Bronchopulmonary Aspergillosis

First-line treatment of ABPA is oral corticosteroids, which suppress the hypersensitivity response and prevent progressive bronchiectasis. Itraconazole is used as a steroid-sparing agent, reducing Aspergillus airway burden. Biologics have emerged as promising alternatives and adjuncts. A 2024 systematic review and meta-analysis (86 studies, 346 patients) found:
  • Omalizumab (anti-IgE) significantly reduced exacerbation rates (-2.29/year), OCS dose (-10.91 mg/day), and total IgE (-273 IU/mL), while improving FEV1 (+10%).
  • Dupilumab (anti-IL-4Rα) and mepolizumab (anti-IL-5) significantly reduced exacerbations, steroid use, and IgE.
  • Benralizumab (anti-IL-5Rα) showed a favorable trend without reaching statistical significance. (Chen et al., Lung, 2024; PMID 38898129).

8. Special Populations

Pediatric patients: A 2023 systematic review of pulmonary aspergillosis in children noted that IPA occurs in the same high-risk immunocompromised groups as adults; voriconazole dosing requires weight-based adjustments, and younger children metabolize voriconazole faster due to greater CYP2C19 activity (Terlizzi et al., Ital J Pediatr, 2023; PMID 36978151).
Patients on BTK inhibitors: A 2025 systematic review reported that patients with B-cell malignancies receiving Bruton tyrosine kinase (BTK) inhibitors (ibrutinib, acalabrutinib) have elevated risk of Aspergillus infection, mediated by impaired B-cell and macrophage function (Gibert et al., Clin Microbiol Infect, 2025; PMID 39742965).
Hematopoietic stem cell transplantation: A 2024 systematic review and meta-analysis confirmed IA as the leading invasive fungal infection after HSCT, with the highest incidence in recipients of mismatched or unrelated donor grafts and in those with severe GVHD requiring high-dose steroids (Biyun et al., Clin Microbiol Infect, 2024; PMID 38280518).

9. Prevention and Infection Control

Prevention of nosocomial aspergillosis centers on environmental controls: high-efficiency particulate air (HEPA) filtration in HSCT units, positive-pressure rooms, avoidance of building renovation near immunocompromised wards, and regular inspection of water systems. Patient-level strategies include antifungal prophylaxis with mold-active azoles in high-risk neutropenic and HSCT populations. Early granulocyte colony-stimulating factor (G-CSF) administration to shorten neutropenia duration is also beneficial. Reduction of immunosuppression whenever clinically feasible remains a fundamental principle.

10. Emerging Challenges and Future Directions

Several pressing challenges define the current research agenda:
  1. Azole resistance: The spread of environmentally acquired azole-resistant A. fumigatus (driven by TR34/L98H mutations from agricultural fungicide use) threatens current first-line therapy, particularly in the Netherlands and parts of South Asia. Routine susceptibility testing at diagnosis is becoming essential.
  2. New at-risk populations: The emergence of IAPA, CAPA, and aspergillosis in BTK inhibitor recipients has substantially expanded the population requiring vigilance beyond classical neutropenic hosts.
  3. Biomarker optimization: Point-of-care lateral flow assay for galactomannan, BAL metagenomics, and multiplex PCR panels are under active evaluation to improve the speed and sensitivity of diagnosis.
  4. Novel therapeutics: Olorofim, the first member of the orotomide class targeting dihydroorotate dehydrogenase, has shown activity against azole-resistant A. fumigatus and was granted breakthrough therapy designation. Ibrexafungerp (triterpenoid glucan synthase inhibitor) and manogepix are in clinical development.
  5. Biologics for ABPA: The meta-analytic evidence for omalizumab, dupilumab, and mepolizumab is encouraging but based largely on observational data; randomized controlled trials with standardized endpoints are needed.
  6. CPA mortality: The high and persistent mortality of CPA underscores the need for tailored treatment strategies based on subtype, age, and underlying comorbidity, as highlighted by the 2025 individual patient data meta-analysis.

11. Conclusion

Aspergillosis is a disease of growing clinical and public health importance. Its clinical spectrum - from benign hypersensitivity syndromes to devastating invasive infection - requires a nuanced, host-directed diagnostic and therapeutic approach. The paradigm has expanded significantly: once primarily a concern in neutropenic patients, IA now threatens populations with viral infections (influenza, COVID-19), those receiving novel immunotherapies, and patients with structural lung disease over the chronic spectrum. Diagnostic advances in galactomannan testing, point-of-care assays, and molecular methods have improved early identification, but azole resistance is an escalating threat that demands surveillance and may require rethinking first-line choices. Isavuconazole increasingly appears as a viable, better-tolerated alternative to voriconazole. For ABPA, biologic therapies are reshaping steroid-sparing management. Future research should prioritize resistant strains, underserved CPA populations, and well-designed trials of the rapidly evolving biological and antifungal armamentarium.

Key References

  1. Walsh TJ, Patterson TF. "Aspergillosis." Goldman-Cecil Medicine, 27th ed. (ISBN 9780323930345), pp. 3347-3355.
  2. Medical Microbiology, 9th ed. Murray PR et al. (ISBN 9780323673228), block 7.
  3. Murray & Nadel's Textbook of Respiratory Medicine (ISBN 9780323655873), Chapter on opportunistic mycoses.
  4. Morrissey CO et al. Med Mycol 2024 - WHO FPPL systematic review on A. fumigatus (PMID 38935907).
  5. Sengupta A et al. Lancet Infect Dis 2025 - Mortality in CPA: individual patient data meta-analysis (PMID 39617023).
  6. Gioia F et al. Lancet Respir Med 2024 - Risk factors for CAPA (PMID 38185135).
  7. Lu LY et al. Chest 2024 - IAPA systematic review and meta-analysis (PMID 37742914).
  8. Gu Q et al. Drugs 2026 - Network meta-analysis of antifungal primary therapy for IA (PMID 42012594).
  9. Chen X et al. Lung 2024 - Biologics in ABPA meta-analysis (PMID 38898129).
  10. Boutin CA et al. Clin Infect Dis 2024 - Breakthrough IFI on voriconazole/posaconazole prophylaxis (PMID 38752732).
  11. Wichmann D et al. Infection 2025 - German national guideline for IPA in ICU (PMID 40465080).
  12. Sehgal IS et al. Mycoses 2022 - Aspergillus-specific IgG detection in ABPA (PMID 35757847).
  13. Gibert C et al. Clin Microbiol Infect 2025 - Fungal infection in BTK inhibitor-treated patients (PMID 39742965).
  14. Biyun L et al. Clin Microbiol Infect 2024 - Risk factors for IFI after HSCT (PMID 38280518).
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