Mixed Invasive Aspergillus–Mucorales Pulmonary Coinfection in a Diabetic Patient: An Uncommon Dual Fungal Pneumonia and Literature Review

ABSTRACT

Mixed pulmonary infection by Aspergillus and Mucorales is a rare condition but highly fatal in immunocompromised hosts. We report a 61‐year‐old diabetic man with diabetic kidney disease who presented with fever and cough. Bronchoscopy‐guided lung biopsy and lavage MUCOR 28S PCR assay confirmed dual invasive Aspergillus and Mucorales coinfection. He developed massive hemoptysis, septic shock, and eventually succumbed despite treatment with antibiotics, liposomal amphotericin B and posaconazole. This case underscores the importance of early diagnosis, antifungal therapy and vigilant monitoring in high‐risk patients.

Our case describes a rare lung co‐infection caused by Aspergillus and Mucorales in a 61‐year‐old man with uncontrolled diabetes and chronic kidney disease. The diagnosis was made by BAL PCR and biopsy. Despite antifungal treatment, the patient worsened and died. This displays that the infection is aggressive and needs early diagnosis and treatment.

1. Introduction

Fungal lung diseases have become more common over recent decades and pose a growing clinical challenge worldwide. Aspergillus species are common saprophytic fungi found widely in the environment, and the disease spans a broad range from hypersensitivity to invasive infection with high mortality [1]. Every year ~6.5 million people are affected by life‐threatening fungal infections, causing 3.75 million deaths of which 2.55 million are directly attributable to the fungal infection [2]. Invasive aspergillosis (IA) affects 2.1 million people globally with 85.2% mortality [2], and India reports about 46,490 cases annually [1]. India also has the highest mucormycosis burden with 140 cases per million [1], and coinfections or sequential infections with Mucorales and Aspergillus species are exceedingly uncommon [3]. We report a rare mixed invasive co‐infection of Aspergillus and mucormycosis in a poorly controlled diabetes mellitus patient.

2. Case Report

A 61‐year‐old man with Type 2 diabetes mellitus, hypertension and chronic kidney disease (CKD) presented with fever and cough for 1 week. He had no history of tuberculosis, pneumonia, hospitalisation, dialysis, antibiotic use or immunosuppressive therapy in the past. He had no history of substance use. On admission, his vitals included temperature 101°F, respiratory rate 26/min, heart rate 110/min and peripheral saturation 92% on room air requiring 2 L/min of O₂ via nasal prongs. Chest examination revealed bilateral coarse crepitations. The rest of the systemic examination was normal. Initial laboratory investigations showed haemoglobin of 12.9 g/dL, total leucocyte count of 48.16 x 10³/μL (N83%/L6%/M4%/E0) (normal range: 4000–11,000 cells/mm3), procalcitonin of 51 ng/mL (normal range: < 0.5 ng/mL), CRP of 132 mg/L (normal range: 0–5 mg/L), urea 63 mg/dL, creatinine 1.7 mg/dL and HbA1c 9%. Liver function tests were normal. His urine routine showed glucose 3+, protein 2+, negative ketone and nitrite; while the urine microscopy revealed pus cells 10/hpf, RBC 100–120/hpf and no bacteria/protozoa. Chest X‐ray (CXR) PA view revealed opacity in the right upper zone (Figure 1A). Blood, urine and sputum were sent for culture testing on Day 1. Sputum Gram stain showed mixed flora with Gram‐negative bacilli, Gram‐positive cocci and Gram‐negative cocci. The patient was initiated on anti‐diabetic measures (insulin) and dose‐modified empirical antibiotics.

FIGURE 1.

Chest X‐ray PA view (A) shows right upper/mid‐zone opacity. HRCT thorax (B—coronal view; C—axial view) reveals right upper‐lobe ground‐glass opacities with surrounding consolidation (reverse halo sign). Bronchoscopy shows erythematous, ulcerative mucosa with yellowish‐white plaques and necrotic slough in the right upper lobe bronchus (D).

High‐resolution computed tomography (HRCT) thorax revealed right upper lobe ground‐glass opacities with surrounding consolidation suggestive of reverse halo sign (Figure 1B,C). Differentials of aspergillosis or mucormycosis were considered in view of uncontrolled diabetes with CKD. Microbiological evaluation showed no growth in the blood, urine and sputum culture. TLC decreased to 14 x 10³/μL after 5 days of antibiotic therapy. Bronchoscopy revealed erythematous, ulcerative mucosa with yellowish‐white plaques and necrotic slough in right upper lobe bronchus (Figure 1D). Bronchoalveolar lavage (BAL) and endobronchial forceps biopsy from lesion were obtained. BAL for acid‐fast bacilli (AFB), Grocott's methenamine silver stain (GMS), GeneXpert MTB and KOH mount were negative. BAL Galactomannan assay was 4.23 and Mucorales PCR (targeting 28S rRNA) came positive. Patient was started on liposomal amphotericin B (L‐AMB) at 5 mg/kg/day. Histopathological examination (HPE) of the biopsy specimen revealed granulation tissue and fibrinopurulent exudate along with fungal colonies composed of branching septate hyphae with conidia (Figure 2A–C) and a few broad, non‐septate fungal hyphae (Figure 2D) suggestive of Aspergillus spp. and Mucorales. The tissue was negative for AFB stain. Vasculitis panel including p‐ANCA and c‐ANCA returned negative. Non‐contrast CT of the head was normal. Kidney biopsy showed diabetic nephropathy changes. BAL and tissue fungal culture came back negative. Finally, the patient was diagnosed with IPA with mucormycosis on a background of uncontrolled diabetes and diabetic nephropathy.

FIGURE 2.

Histopathology (H&E) sections show septate hyphae with conidia consistent with Aspergillus species (A–C) and broad non‐septate hyphae (GMS stain) typical of Mucorales (D).

After 5 days of L‐AMB therapy, the patient developed fever with yellowish expectoration. Sputum culture grew Acinetobacter baumannii (sensitive only to colistin and tetracycline); IV polymyxin B and minocycline were initiated. After 14 days, L‐AMB therapy was switched to oral posaconazole (PCZ) as per our protocol. Patient developed an episode of haemoptysis (~150 mL) and underwent bronchial artery embolization (BAE). Pneumonectomy was planned; however, the patient had another episode of massive haemoptysis. He was immediately intubated. After 48 h, endotracheal (ET) aspirate culture grew A. baumannii (only sensitive to colistin). Culture‐directed antibiotics were continued along with other supportive measures (glycaemic control and blood transfusions for anaemia). However, his TLC rose to 72.51 × 10³/μL (neutrophils + bands—88%/L3%) and procalcitonin to 98 ng/mL. Despite aggressive antifungal and antibiotic therapy, the patient's condition deteriorated and succumbed to the invasive fungal infection and septic shock (Day 35).

3. Discussion

Aspergillus species are ubiquitous saprophytic fungi widely distributed in the environment and can cause pulmonary infection when their spores or hyphal fragments are inhaled, particularly in immunocompromised individuals [4]. Worldwide, the highest burden of IA is seen in patients with COPD (1.51 million cases per year) followed by ICU patients (519,000 cases), lung cancer (57,000 cases) and haematological malignancies (27,000 cases) [2]. The prevalence of IA and spectrum of causative fungi vary greatly between regions, even within the same country. These variations are influenced by factors such as the site of infection, patient age, climate, geography and local environmental or agricultural conditions [5]. Several categories of fungi are commonly encountered in critically ill patients, including moulds, Pneumocystis jirovecii and Candida species. Among them, invasive pulmonary aspergillosis (IPA) carries a high mortality rate, especially in individuals with severe immunosuppression [4].

While aspergillosis encompasses a broad clinical spectrum from hypersensitivity to invasive infection, mucormycosis is a distinctly angioinvasive infection characterised by extensive tissue necrosis. Clinical presentations of mucormycosis are classified based on the anatomic location. Among reported cases, the rhino‐orbital‐cerebral form accounts for 45%–74%, with cutaneous (10%–31%) and pulmonary (3%–22%) types occurring less frequently. Renal, gastrointestinal and disseminated variants are comparatively uncommon, each representing 0.5%–9% of cases [6]. Risk factors for both IPA and mucormycosis include neutropenia, poorly controlled diabetes, haematological malignancy, prolonged steroid use, iron overload and deferoxamine therapy, immunocompromised conditions like HIV, influenza, COVID‐19 and transplantation [1, 6]. In India, mucormycosis is most often seen in poorly controlled diabetes ~54%–76% of reported infections [6].

Histological examination of lung tissue remains the gold standard for diagnosing invasive fungal diseases (IFDs), but it is invasive and carries risks such as pneumothorax and pulmonary haemorrhage [7]. Because of these complications, lung biopsy is not routinely recommended. In day‐to‐day practice, less invasive approaches like bronchoalveolar lavage fluid (BALF) analysis and repeated sputum cultures are used more often to detect fungal pathogens and aid early diagnosis [8]. A meta‐analysis of Aspergillus PCR in blood reported pooled sensitivity 79% and specificity 80%, comparable to the galactomannan assay. PCR testing on BAL fluid showed similar sensitivity (76%–80%) and higher specificity (93%–95%), supporting its reliability for confirming IA. Recent advances in molecular diagnostics have also improved detection of Mucorales DNA, overcoming the low sensitivity of culture and lack of serological tests. Conventional and quantitative PCR assays targeting ribosomal DNA can detect Mucorales in tissue, BAL fluid or serum, markedly improving the diagnosis of mucormycosis. BAL Mucorales PCR has sensitivity of almost 100%, while serum Mucorales PCR has a sensitivity of 85.2% and specificity of 89.8% [9].

We conducted a comprehensive literature search in PubMed, Scopus and Web of Science database for pulmonary Aspergillus–Mucorales co‐infection excluding COVID‐19 infection using the terms (‘mucormycosis’ OR ‘Mucorales’ OR ‘zygomycosis’) AND (‘aspergillosis’ OR ‘Aspergillus’) AND (‘pulmonary’ OR ‘lung’) AND (‘co‐infection’ OR ‘mixed infection’ OR ‘dual infection’) from 1990 to 2025. Our search yielded 26 reports describing 34 patients (Table 1). Most patients were men (58.8%). The mean age was 47.2 ± 16.6 years, and the median duration of illness was 60 days (range 15–365). The most common risk factors were diabetes mellitus (50%) and haematological malignancy or HSCT (23.5%). Less common risk factors included trauma or accident (8.8%), post‐tubercular cavity (5.8%), organ transplantation (2.9%), liver cirrhosis (2.9%), ARDS (2.9%), sarcoidosis on steroids (2.9%) and solid cancer on chemotherapy (2.9%). Most diagnoses were made on histopathology, which showed both septate hyphae (Aspergillus) and broad aseptate hyphae (Mucorales). Diagnosis was based on histopathology alone in 55.9%, culture alone in 11.8% and a combination of methods or molecular tests (PCR, tNGS or mNGS together with histology or culture) in 32.4%, with next‐generation sequencing used more often in recent reports. The common CT findings were cavitation (50%), consolidation (47.1%), nodules (17.6%), the air‐crescent sign (14.7%) and halo or reverse‐halo signs (8.8%).

TABLE 1.

Reported cases of pulmonary Aspergillus and Mucor co‐infection.

No.	Author	Age	Sex	Underlying disease	Disease duration (days)	CT finding	Diagnostic specimen	Laboratory evidence	Antifungal drugs	Surgery	Outcome	Course (days)	Year
1.	Mölle et al. [10]	40	F	Acute myeloid leukaemia	30	Bilateral GGOs	BALF	Hyphae of both species (and culture positive post‐mortem)	AmB (11 days)	No	Died	30	1996
2.	Blin et al. [11]	52	F	Renal PTLD/NHL	90	Diffuse lung nodules	Biopsy	Hyphae of both species on HPE + culture positive	VCZ → L‐AmB	No	Died	NA	2004
3.	Weng et al. [12]	10	M	Aplastic anaemia/HSCT	180	Consolidation	Biopsy	Aspergillus flavus on culture and Mucor hyphae on HPE	L‐AmB → PCZ	Yes	Survival	100	2010
4.	Radowsky et al. [13]	22	M	Trauma	16	Consolidation	BALF	Culture positive (A. niger/terreus/flavus + Cunninghamella species)	L‐AmB + PCZ + VCZ	No	Died	NA	2011
5.	Alvarez et al. [14]	43	M	Fall from height (work‐related accident)	17	Scattered nodular and patchy consolidations	BALF	Aspergillus and Mucor on culture	L‐AmB (8‐15th), VCZ (13‐27th)	No	Survival	33	2011
6.	Pacheco et al. [15]	34	F	HIV/plasmablastic lymphoma	60	GGOs, focal consolidations, typical cavitation	BALF, biopsy/RUL lobectomy	Aspergillus and Mucor hyphae on HPE	L‐AmB → PCZ	Yes	Survival	60	2013
7.	Webb et al. [16]	52	M	Diabetes/cardiac transplant/renal failure	365	Nodular opacities/mass	Biopsy/left lower lobectomy	Aspergillus fumigatus and septate hyphae on HPE	VCZ + CSP → PCZ + L‐AmB	Yes	Died	88	2013
8.	Bergantim et al. [17]	58	F	Acute myeloid leukaemia	270	Pleural effusion, consolidation, cavitation	Biopsy/lobectomy	Aspergillus and Mucor hyphae on HPE	PCZ (3rd‐15th); VCZ (18th–60th); L‐AmB (18th–391st)	Yes	Survival	111	2013
9.	Mahadevaiah et al. [18]	27	F	DM	18	Consolidation, cavitation	BALF, biopsy	Broad aseptate hyphae in BAL and A. fumigatus on culture	L‐AmB → VCZ	No	Died	18	2013
10.	Henn et al. [19]	42	M	Chronic lymphocytic leukaemia	270	Multiple nodules with cavitation	BALF, biopsy/right middle lobectomy	Aspergillus positive PCR and histopathology confirming Mucor	VCZ → L‐AmB + PCZ	Yes	Died	270	2014
11.	Davoudi et al. [20]	24	F	Acute myeloid leukaemia/HSCT	180	Anti‐halo sign	BALF/biopsy	Rhizomucor spp. culture, Aspergillus morphology on histopathology	L‐AmB + VCZ + CSP → VCZ + L‐AmB + PCZ	Yes	Survival	540	2014
12.	Persichino et al. [21]	58	M	Liver cirrhosis	25	Patchy infiltration	BALF, biopsy	Rhizopus arrhizus + Aspergillus spp. on culture	MCF → VCZ + L‐AmB	No	Died	25	2018
13.	Zhang et al. [22]	44	M	Renal transplantation	42	GGOs, mass opacity, patchy shadows	BALF	Culture + ITS sequencing	VCZ → L‐AmB + PCZ	No	Survival	60	2019
14.	Lin et al. [23]	52	M	DM	180	Cavity with wall thickening	BALF, biopsy/RUL lobectomy	Aspergillus and Mucor hyphae on HPE	VCZ → PCZ	Yes	Survival	180	2019
15.	Leelawattanachai et al. [24]	44	M	Car accident	120	Multifocal consolidation	Tracheal aspirate	A. flavus, A. fumigatus, Rhizopus microsporus and Lichtheimia corymbifera on culture	L‐AmB → PCZ	No	Survival	120	2019
16.	Prohaska et al. [25]	67	M	ARDS/High dose dexamethasone	21	Massive right upper lobe infarct, extensive necrosis	BALF, biopsy	Aspergillus and Mucor hyphae on HPE	L‐AmB + ANF	No	Died	42	2020
17.	Hu et al. [26]	51	F	Acute B‐lymphoblastic leukaemia/DM	180	Miliary nodules	BALF, jejunal/Ileal resection	Aspergillus and Mucor hyphae A. flavus + Cunninghamella bertholletiae on culture and ITS sequencing	VCZ → AmB deoxycholate → L‐AMB + VCZ → PCZ	Yes	Survival	130	2021
18.	Ravindra et al. [27]	70	M	Post‐tubercular cavity	21	Air crescent sign, right middle lobe fibrosis, traction bronchiectasis	Biopsy/RUL + RML lobectomy	Aspergillus and Mucor hyphae on HPE	L‐AmB (21 days)	Yes	Survival	60	2021
		65	M	DM/smoker	21	Reverse halo sign, cavitating consolidation	Biopsy	Aspergillus and Mucor hyphae on HPE	L‐AmB	No	Survival	NA	2021
19.	Teng et al. [28]	54	F	DM/DKA	78	Multiple nodules, air crescent signs, bilateral pleural effusion	BALF, biopsy/right middle + lower lobectomy	Aspergillus and Mucor hyphae on HPE	VCZ (23rd–30th) → AmB (30th–44th) → L‐AmB (45‐55th), PCZ (50th–end)	Yes	Survival	78	2022
20.	Zhan et al. [29]	66	F	DM	NA	Lesions + cavity	Biopsy	Aspergillus and Mucor hyphae on HPE	VCZ → AMB+ PCZ	No	Survival	NA	2022
		57	M	DM, smoker	NA	Consolidation + cavity	Biopsy	Aspergillus and Mucor hyphae on HPE	L‐AMB	No	Survival	NA
		61	F	DM	NA	Consolidation + cavity	BALF, biopsy	A. fumigatus cultured; histology consistent with Aspergillus + Mucor	L‐AMB	No	Died	NA
		76	F	DM	NA	Lesions, consolidation, cavity	Biopsy	Aspergillus and Mucor hyphae on HPE	AMB + PCZ; VCZ	No	Survival	NA
		48	M	DM & DN	NA	Lesions, consolidation	Biopsy	Aspergillus and Mucor hyphae on HPE	AMB + PCZ later VCZ	No	Survival	NA
		66	M	DM & HTN	NA	Lesions and cavity	Biopsy	Aspergillus and Mucor hyphae on HPE	AMB + PCZ	No	Survival	NA
		46	M	DM	NA	Lesions, consolidation, cavity	Biopsy	Aspergillus and Mucor hyphae on HPE	L‐AMB	No	Survival	NA
		25	M	DM	NA	Lesions, consolidation, cavity	Biopsy	Aspergillus and Mucor hyphae on HPE	L‐AMB	No	Survival	NA
21.	Wang et al. [3]	11	F	DM	20	Air crescent and halo signs, consolidation in right lower lobe	BALF, biopsy, mNGS	A. fumigatus & R. microsporus confirmed on mNGS and histopathology	VCZ → ISZ + L‐AmB	Yes	Survival	49	2024
22.	Ling et al. [8]	60	M	DM	15	Patchy, crescent‐shaped, low‐density gas shadows	BALF, biopsy	mNGS and histopathology confirmed A. flavus and Mucor microsporus	Itraconazole → L‐AmB → VCZ → Intrabronchial AmB	Yes	Survival	73	2024
23.	Sagawa et al. [30]	54	F	Sarcoidosis on glucocorticoids	120	Multiple pulmonary nodules, posterior mediastinal mas	Autopsy/biopsy	A. fumigatus (ITS, D1/D2, β‐tubulin sequencing) and Mucorales (18S rDNA sequencing)	L‐AmB	No	Died	120	2024
24.	Devalla et al. [31]	48	M	Metastatic prostate carcinoma on docetaxel	38	Bird's nest sign, cavitation, GGO, pleural effusion	BALF, TBLB	Septate hyphae (Aspergillus) on BAL; broad aseptate hyphae (Mucor) on HPE	VCZ → L‐AmB	Yes	Survival	NA	2024
25.	Zhao et al. [32]	52	M	DM	30	Multiple cavities, consolidation, pleural effusion	BALF (tNGS), biopsy	Azole‐resistant A. fumigatus and R. microsporus on tNGS/culture; Mucor on HPE	VCZ → ISZ + L‐AmB + CSP → HD‐POS + L‐AmB	Yes	Survival	137	2025
26.	Ahmed et al. [33]	27	F	Post‐tubercular cavity	180	Air crescent sign, cavity (fungal ball), right upper lobe	Biopsy/RUL lobectomy	Septate (Aspergillus) and broad aseptate (Mucor) hyphae on HPE	L‐AmB → PCZ	Yes	Survival	NA	2025
27.	Present case	61	M	Diabetes mellitus, DKD and HTN	7	Bilateral cavitary consolidations with halo sign	BALF, biopsy	Aspergillus and Mucor hyphae on HPE BAL Mucor 28S PCR positive	L‐AmB [1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14] → PCZ (16–35)	No	Died	35	2025

Abbreviations: ARDS, acute respiratory distress syndrome; BAL, bronchoalveolar lavage; BALF, bronchoalveolar lavage fluid; biopsy, tissue biopsy; CT, computed tomography; DKA, diabetic ketoacidosis; DM, diabetes mellitus; DN, diabetic nephropathy; GGOs, ground‐glass opacities; HM, hematologic malignancy; HPE, histopathological examination; HSCT, haematopoietic stem cell transplantation; HTN, hypertension; ISZ, Isavuconazole; L‐AmB, liposomal amphotericin B; MALDI‐TOF, matrix‐assisted laser desorption/ionization‐time of flight; mNGS, metagenomic next‐generation sequencing; NA, not available; PCR, polymerase chain reaction; PCZ, posaconazole; PTLD, post‐transplant lymphoproliferative disorder; RML, right middle lobe; RUL, right upper lobe; VCZ, voriconazole.

The most frequently isolated species were Aspergillus fumigatus , Aspergillus flavus and Rhizopus microsporus, followed by Mucor, Cunninghamella and Lichtheimia species. Amphotericin B ([AMB] liposomal form) was used in 97.1% of patients. It was given alone in 23.5%, in combination with voriconazole (VCZ) in 20.6% and PCZ in 14.7%, while a triple or step‐wise regimen of AMB, VCZ and PCZ was used in 35.3%. The overall survival was 70.6% (24 of 34 patients). Surgery was performed in 44.1% (15 patients) and was linked to better survival (86.7%, 13 of 15) than medical treatment alone. Death occurred in 29.4% of patients. Haematological malignancy and diabetes (30% each) were the most common risk factors for death. Till date, all the available data remain retrospective and lack randomised evidence.

Mixed pulmonary infection with Aspergillus and Mucorales tends to progress quickly with poor outcomes. Survival depends on early recognition and right antifungal therapy. VCZ and itraconazole (ITZ) are commonly used for pulmonary aspergillosis; while VCZ has no activity against Mucor spp., and its overuse in Aspergillus infection may inadvertently prone to mucormycosis [4, 8]. AMB is considered the first‐line therapy followed by PCZ and isavuconazole (ISZ) for mucormycosis [6]. All three agents are effective against aspergillosis. Intrabronchial AMB instillation has also been tried successfully [8]. Treatment comprising L‐AMB in combination with VCZ or PCZ and surgery remains the cornerstone for mixed Aspergillus–Mucorales pulmonary infection.

In our patient, combination therapy was not initiated initially because both liposomal amphotericin B and PCZ possess activity against Aspergillus and Mucorales; added nephrotoxicity was unfavourable due to diabetic nephropathy and concurrent polymyxin B therapy. Surgical resection was planned but delayed due to renal dysfunction initially; later it was abandoned due to sepsis and haemodynamic instability. Patient's rapid progression despite therapy underscores that early surgical referral is needed before the disease erodes the adjacent bronchial circulation and may offer survival advantage.

This report has several limitations. Fungal culture was negative, so specific Mucorales and Aspergillus species could not be determined and susceptibility testing was not available. Serum galactomannan, β‐D‐glucan and serum Mucorales PCR were not performed for comparison with BAL results. An autopsy was not obtained, so the extent of angioinvasion and dissemination remains unknown. Conclusions regarding management cannot be drawn from a single case. Our literature synthesis was narrative rather than systematic, restricted to published reports which are subject to publication bias; pooled survival of 70.6% may overestimate the real‐world survival. Reporting across included studies was heterogeneous and all the data are retrospective.

In conclusion, pulmonary coinfection with Aspergillus and Mucorales carries high mortality and remains difficult to manage. Prompt suspicion, early diagnosis and timely intervention are critical for improving the patient's outcome. The increasing incidence of such mixed infections needs clear treatment protocols to reduce mortality.

Author Contributions

S.K. and V.V.: planning and supervision; V.V., A.R.W., G.K.S., A.G., V.K., S.M.: involved in patient's care, bronchoscopic procedure and follow‐up; A.S.: histopathology and IHC interpretation; V.V. and A.G.: drafted the manuscript; while all authors reviewed, refined and approved the final version together.

Funding

The authors have nothing to report.

Consent

The authors declare that written informed consent was obtained from the patient's next of kin for the publication of this manuscript and accompanying images and attest that the form used to obtain consent complies with the Journal requirements as outlined in the author guidelines.

Conflicts of Interest

The authors declare no conflicts of interest.

Venugopal V., Karmakar S., Wani A. R., et al., “Mixed Invasive Aspergillus–Mucorales Pulmonary Coinfection in a Diabetic Patient: An Uncommon Dual Fungal Pneumonia and Literature Review,” Respirology Case Reports 14, no. 10 (2026): e70765, 10.1002/rcr2.70765.

Data Availability Statement

The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.