Liposomal amphotericin B in the treatment of pediatric gastrointestinal basidiobolomycosis

Abstract

Background

Gastrointestinal basidiobolomycosis is a rare fungal infection caused by Basidiobolus ranarum, increasingly recognized as an intestinal pathogen in children. Its clinical features closely mimic malignancy or inflammatory bowel disease, leading to frequent diagnostic delays. Although endemic in regions such as Saudi Arabia, Iran, and Oman, sporadic cases occur worldwide. Amphotericin B-liposomal remains a cornerstone therapy for invasive fungal disease, but no standardized treatment protocol for pediatric gastrointestinal basidiobolomycosis has been established.

Case presentation

We report a 6-year-old Asian girl, born preterm with very low birth weight, who presented with persistent abdominal pain without organomegaly, alternating diarrhea and constipation, fever, and anorexia. Initial ultrasonography revealed colonic wall thickening with aneurysmal dilation at the splenic flexure. Colon biopsy confirmed Basidiobolus ranarum. The patient received intravenous liposomal amphotericin B (90 mg daily), with partial radiologic improvement but persistent symptoms, prompting exploratory laparotomy. Adhesiolysis, left hemicolectomy, and resection of jejunal and colonic masses were performed. Histopathology demonstrated dense eosinophil-rich granulomatous inflammation with multinucleated giant cells and a solitary fungal hypha, without classic Splendore–Hoeppli phenomenon, likely due to prior antifungal therapy. Postoperatively, the patient was discharged on oral itraconazole for 28 days with adjunctive cotrimoxazole. At 1-year follow-up, she remained asymptomatic with no evidence of recurrence.

Conclusion

This case highlights the diagnostic challenges of pediatric gastrointestinal basidiobolomycosis and demonstrates successful management with liposomal amphotericin B followed by itraconazole. It underscores the ongoing gap in establishing standardized treatment and supports further prospective studies to define optimal antifungal and surgical strategies for this rare entity.

Introduction

Gastrointestinal basidiobolomycosis (GIB) is a rare but increasingly recognized fungal infection caused by Basidiobolus ranarum, an environmental saprophyte classically associated with subcutaneous disease but now established as an emerging cause of intestinal involvement, particularly in children [1–3]. The clinical presentation is notoriously nonspecific, with abdominal pain, anorexia, altered bowel habits, and mass-like lesions that often mimic malignancy, tuberculosis, or inflammatory bowel disease, leading to frequent diagnostic delays [4–6].

Although the true incidence in children remains unknown, clusters have been reported in endemic regions such as Saudi Arabia, Iran, and Oman, where pediatric case series describe predominance in boys under 10 years old, with abdominal pain and colonic thickening as leading features [7–9]. Sporadic reports from the USA, Africa, and South Asia highlight its global but geographically restricted emergence [10–12]. Moreover, in endemic regions, intestinal basidiobolomycosis should be considered as a potential differential diagnosis in children, alongside other rare conditions such as Rapunzel syndrome, splenic, hepatic, and multi-organ hydatidosis [13–15].

Amphotericin B-liposomal (AmBisome®) is widely used as a cornerstone in the management of invasive fungal infections, including GIB. This lipid formulation enhances tissue distribution, minimizes renal toxicity, and improves tolerability compared to conventional amphotericin B, making it a preferred therapeutic option in pediatric populations [16]. Nevertheless, azoles such as itraconazole and voriconazole are also frequently employed, either as monotherapy or sequentially, with variable outcomes [17, 18].

Despite increasing case reports and regional series, the literature reveals a striking gap in consensus on definitive treatment. Outcomes remain heterogeneous, with some studies supporting antifungal monotherapy, while others emphasize combined surgical resection and antifungal therapy, particularly in cases with mass formation, obstruction, or perforation [3, 16, 19–22]. This uncertainty is especially pronounced in the pediatric population, where the rarity of disease and lack of controlled data hinder the establishment of standardized management protocols.

Here, we present a pediatric case of intestinal basidiobolomycosis successfully managed with amphotericin B-liposomal, contributing further evidence toward defining effective treatment strategies for this rare and diagnostically challenging entity.

Case presentation

Case report

A 6-year-old Asian girl, born preterm at 34 weeks of gestation with very low birth weight of 1350 g, with no history of congenital anomalies, presented to the emergency department with persistent abdominal pain. Her symptoms were variable, alternating between diarrhea and constipation, and were accompanied by anorexia. No organomegaly was detected on initial assessment. She was admitted with a provisional diagnosis of acute abdominal pain, and further evaluation was carried out by the pediatric surgery department to determine the underlying cause. On physical examination at admission, the patient was lethargic and febrile (38 C) and exhibited tenderness localized to the left upper quadrant, radiating toward the umbilical region. There was no guarding or rebound tenderness, though anorexia was present. The patient denied nausea and vomiting. She also displayed symptoms consistent with coryza.

Patient evaluation prior to hospital admission

Before admission, the patient was evaluated by a pediatric gastroenterologist who recommended an abdominopelvic ultrasound (APUS). Initial imaging revealed dilated bowel loops with significant wall thickening of the descending colon, measuring approximately 7 × 7 mm, and absent peristalsis, indicative of inflammatory changes. A follow-up APUS was performed, demonstrating aneurysmal dilation of the splenic flexure of the left descending colon accompanied by adjacent fat stranding. These findings suggested a differential diagnosis that included fungal infection and lymphoma.

Patient evaluation during hospitalization

Upon admission to the pediatric infectious diseases ward, empirical antibiotic therapy was initiated, consisting of intravenous metronidazole (160 mg every 8 hours), cefotaxime (800 mg every 8 hours), and cotrimoxazole (80 mg twice daily). A colon biopsy was subsequently performed, confirming a diagnosis of Basidiobolomycosis affecting the large colon. Following this diagnosis, antifungal treatment with liposomal amphotericin B (90 mg intravenous (IV) once daily) was commenced. The patient was also monitored through serial abdominal ultrasound (APUS) examinations.

Chronological APUS findings included the identification of an accessory spleen measuring approximately 13 × 11 mm and multiple mesenteric lymph nodes. Notably, significant wall thickening of the splenic flexure of the large bowel was observed, with a maximum thickness of 10 mm and adjacent fat stranding, prompting further evaluation with abdominopelvic computed tomography (CT).

At 4 days after the biopsy and diagnosis, repeat abdominal point-of-care ultrasound (APUS) showed no evidence of fungal infection but revealed an iso-echoic structure measuring 11 × 11 mm adjacent to the splenic hilum, suggestive of an accessory spleen. Despite these findings, the patient’s symptoms, including abdominal pain and anorexia, persisted, necessitating further imaging. After 16 days, APUS demonstrated an ill-defined hypoechoic structure measuring 78 × 45 × 65 mm containing air bubbles, consistent with a fluid collection and associated mesenteric fat stranding. This finding prompted the initiation of broad-spectrum antibiotic therapy with meropenem.

After 23 days, while continuing antifungal treatment, a follow-up abdominal point-of-care ultrasound (APUS) was performed to assess disease progression or regression. The examination revealed mild hypoechoic circumferential thickening of the descending colon wall at the splenic flexure, with a maximum thickness of 6 mm, accompanied by mild, diffuse adjacent mesenteric fat edema. No definitive mass was detected in the left paracolic gutter, findings consistent with a favorable response to liposomal amphotericin B therapy. The final APUS, conducted 18 days later due to ongoing abdominal pain, anorexia, and fluctuating bowel habits, showed no evidence of bowel wall thickening or mesenteric lymphadenopathy.

Given the persistence of the patient’s signs and symptoms and the recommendation from the abdominal ultrasound (APUS) to perform an abdominopelvic computed tomography (CT) scan with and without contrast, this imaging modality was utilized to further evaluate the presence of Basidiobolomycosis and to determine the need for exploratory laparotomy. The initial CT scan revealed a 15 × 12 mm accessory spleen adjacent to the lower pole of the spleen. In addition, there was notable circumferential wall thickening of the descending colon, measuring up to 130 mm in length and 23 mm in maximum thickness, accompanied by adjacent fat stranding and several mesenteric lymph nodes—findings suggestive of Basidiobolomycosis or lymphoma (Fig. 1).

Fig. 1.

Contrast-enhanced spiral computed tomography scan of the abdomen and pelvis with axial and coronal reconstructions. Multiple post-contrast axial and coronal reconstructed images demonstrate marked, circumferential wall thickening of the descending colon, measuring up to 130 mm in length and 23 mm in maximal thickness. The abnormal segment is associated with prominent pericolic fat stranding and the presence of enlarged mesenteric lymph nodes. These findings are radiologically suggestive of basidiobolomycosis-associated colonic lymphoma

The subsequent abdominopelvic CT scan revealed homogeneously hypodense, circumferential wall thickening in the proximal descending colon within the left upper quadrant, with a maximum thickness of approximately 17 mm (Fig. 2). Based on the patient’s clinical history, an infiltrative infectious process was considered the most likely diagnosis. Mild pericolic mesenteric fat stranding was also noted in the left upper quadrant. Several predominantly subcentimeter mesenteric and para-aortic lymph nodes were identified. Compared with the previous CT scan, there was a reduction in the thickening of the large bowel wall and a decrease in pericolic inflammation (Fig. 3).

Fig. 2.

There is homogeneous, circumferential wall thickening involving the proximal descending colon in the left upper quadrant, with a maximal thickness of approximately 17 mm. This is associated with mild pericolic fat stranding and several mesenteric and para-aortic lymph nodes, most of which are sub-centimeter in short-axis diameter. Small-volume free ascitic fluid is noted in the abdominopelvic cavity

Fig. 3.

Circumferential wall thickening is noted in the proximal descending colon within the left upper quadrant, measuring approximately 34 × 23 mm, and associated with adjacent pericolic fat stranding. In the context of the patient’s clinical history, an infiltrative infectious process remains a differential consideration. On comparison with the prior computed tomography study, there is interval decrease in the extent of colonic wall thickening and pericolic fat stranding, findings consistent with a partial response to treatment. Also, multiple subcentimeter mesenteric and para-aortic lymph nodes are also observed

The most recent abdominopelvic CT scan showed the spleen to be normal in size and density, with no evidence of space-occupying lesions. An accessory spleen measuring approximately 14 × 10 mm was identified at the splenic hilum. Both adrenal glands appeared normal. The kidneys were normal in size and density, with no signs of calculi, stasis, or abnormal densities; no hydronephrosis or ureteral dilatation was observed. There was no evidence of peripancreatic or para-aortic lymphadenopathy. Circumferential wall thickening was again noted in the proximal descending colon, measuring approximately 34 × 23 mm in the left upper quadrant, accompanied by adjacent fat stranding. Given the patient’s medical history, an infiltrative infectious process remained a consideration. Compared with the previous study, there was a decrease in the size of the bowel wall thickening and surrounding fat stranding, suggesting a partial response to treatment. Multiple subcentimeter mesenteric and para-aortic lymph nodes persisted (Figs. 3, 4).

Fig. 4.

Mild circumferential wall thickening is noted in the left colon, extending from the distal transverse colon and proximal splenic flexure to the mid-left colon, with a maximum wall thickness of approximately 4 mm. Minimal surrounding mesenteric fat stranding is present. A few subcentimeter, benign-appearing mesenteric lymph nodes are also observed. Compared with the previous computed tomography scan, there is a significant reduction in colonic wall thickening and mesenteric fat stranding, consistent with a favorable response to treatment. Additional few subcentimeter benign-appearing mesenteric lymph nodes are seen in the abdominopelvic cavity

The urinary bladder was semi-distended, showing no evidence of calculi or wall thickening. Other genitourinary structures within the pelvis exhibited normal density and anatomical configuration. No pelvic sidewall lymphadenopathy was observed. The visualized portions of the bony skeleton appeared normal in both density and morphology. Minimal ascitic fluid was also noted.

Exploratory laparotomy

Owing to the persistence of the patient’s symptoms and the incongruent findings observed across imaging modalities relative to the clinical presentation, the patient underwent an exploratory laparotomy. During the procedure, adhesionolysis, left hemicolectomy, colocolic end-to-end anastomosis, jejunojejunal anastomosis, resection of a 5-cm segment of the small bowel, mesorrhaphy, and insertion of a Nelaton drain were performed. Intraoperative exploration revealed a 20 × 30 mm mass located in the mid-portion of the left colon and a 10 × 10 mm mass in the jejunum approximately 100 cm distal to the ligament of Treitz, accompanied by severe adhesions between the jejunum, omentum, and left colon. All identified masses and adhesions were resected and released, respectively. Subsequently, a biopsy specimen from the resected masses were submitted to the attending pathologist for postoperative histopathological examination.

Histopathologic analysis results postoperatively

Pathologic examination of the surgical biopsy from the large colon revealed dense eosinophil-rich inflammatory infiltrates with granulomatous reaction and occasional multinucleated giant cells. Although an isolated fungal hypha was observed, there were no definitive histopathological hallmarks of basidiobolomycosis, such as the Splendore–Hoeppli phenomenon or well-formed fungal colonies (Fig. 5a–e). These findings most likely reflect the effect of prior medical therapy, as the patient had received liposomal Amphotericin-B, which appears to have markedly reduced the fungal burden and masked the classic features of gastrointestinal basidiobolomycosis.

Fig. 5.

A–E Histopathological examination of large colon biopsy from a patient with gastrointestinal basidiobolomycosis (H and E stain). Sections show dense transmural inflammatory infiltrates extending into the mucosa and submucosa, composed predominantly of eosinophils, lymphocytes, plasma cells, and histiocytes, with associated architectural distortion. Foci of granulomatous inflammation containing multinucleated giant cells are noted. An isolated fungal hypha is identified (arrow), while no definitive Splendore–Hoeppli phenomenon or well-formed fungal colonies are seen, likely reflecting the effect of prior antifungal therapy. Low-power views highlight the diffuse eosinophil-rich infiltrate and tissue disruption (A–C, H and E, ×4), whereas high-power views demonstrate eosinophil predominance, granulomatous reaction with giant cells, and a single fungal element (D–E, H and E, ×40)

Postoperative outcome

The patient was discharged in stable condition, having achieved complete clinical resolution of all symptoms. Upon discharge, she was prescribed an oral antifungal regimen consisting of itraconazole 200 mg administered every 12 hours for 28 consecutive days, along with cotrimoxazole 80 mg taken orally twice daily. A follow-up evaluation was recommended, including an APUS and laboratory assessments of C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR), to be seen by a pediatric infectious disease specialist 7 days post-discharge. At 1 year after discharge, a telephone interview was conducted with the patient’s legal guardians, during which no evidence of symptom recurrence or similar clinical manifestations was reported.

Discussion

Gastrointestinal basidiobolomycosis (GIB) is a rare opportunistic fungal infection caused by the zygomycete Basidiobolus ranarum, predominantly affecting immunocompetent individuals in tropical and subtropical regions. Transmission occurs via ingestion of contaminated soil, decaying vegetation, or insects, resulting in gastrointestinal manifestations that mimic inflammatory bowel disease, lymphoma, or malignancy [1, 2, 4]. In the present case, a 6-year-old Asian female, born preterm at 34 weeks gestation with a birth weight of 1350 g, presented with persistent abdominal pain, alternating diarrhea and constipation, anorexia, and fever (38 °C). Initial abdominopelvic ultrasonography revealed dilated bowel loops and descending colon wall thickening (7 × 7 mm), progressing to aneurysmal dilation at the splenic flexure with adjacent fat stranding. Colon biopsy confirmed GIB, initiating treatment with liposomal amphotericin B and empirical antibiotics. Serial imaging demonstrated partial response, with wall thickness reducing from 23 to 17 mm; however, persistent symptoms necessitated exploratory laparotomy, including resection of colonic and jejunal masses with adhesions. Postoperative histopathology showed dense eosinophil-rich granulomatous inflammation with multinucleated giant cells and an isolated fungal hypha, without the Splendore–Hoeppli phenomenon, likely attributable to prior antifungal therapy. The patient was discharged on oral itraconazole and cotrimoxazole, achieving complete symptom resolution with no recurrence at 1-year follow-up.

The pediatric impact of GIB is notable despite its rarity, particularly in endemic areas such as Saudi Arabia, Iran, and Togo, where environmental exposures (e.g., insects or household geckos) contribute to incidence [2, 4, 23]. It primarily affects children aged 2–6 years, with a male predominance (60–91%) and frequent involvement of the bowel (69–72%), occasionally complicated by hepatic dissemination (10–19%) or perforation (< 5%) [2, 23]. Peripheral eosinophilia is observed in 60–80% of cases but is absent in up to 40%, including certain resistant variants [1, 6]. Untreated, GIB can progress to obstruction or perforation, associated with a historical pediatric mortality rate of 25% [2].

The literature, comprising over 100 reported cases since 1964, lacks a definitive consensus on medical, surgical, or combined management strategies, which are often determined by diagnostic delay and disease extent [1, 4]. Surgical intervention is required in 33–55% of pediatric cases for debulking or diagnostic purposes but carries risks such as fistula formation or stoma creation [2, 4]. In this case, liposomal amphotericin B monotherapy during hospitalization induced a partial radiographic response, followed by 28 days of oral itraconazole postdischarge, resulting in sustained remission without recurrence. This outcome aligns with antifungal monotherapy success in 67% of recent pediatric series [1, 2, 23]; However, our patient developed periodic hypokalemia following liposomal amphotericin B therapy, a well-recognized and literature-supported adverse effect of this medication (Table 1) [24].

Table 1.

Serum potassium level fluctuation trend

Although voriconazole is increasingly recommended in contemporary reports (83% utilization, cure rates > 90%) [2, 4, 5], liposomal amphotericin B was selected here owing to its superior cost-effectiveness and accessibility in resource-limited settings, eliminating the need for therapeutic drug monitoring required with voriconazole to prevent toxicity [2, 4, 5]. Administered at 90 mg intravenously daily, it achieved regression without the resistance observed in voriconazole-refractory cases (minimum inhibitory concentration > 16 µg/mL) [6, 25]. Adjunctive oral cotrimoxazole postdischarge provided additional support, consistent with its role in synergistic multidrug regimens [4, 25].

Serial abdominopelvic ultrasonography and computed tomography in this patient documented progressive reduction in descending colon wall thickness (from 23 to 17 mm) and resolution of fat stranding and lymphadenopathy, serving as noninvasive indicators of therapeutic response [1, 5]. These findings, comparable to mean lesion reductions of 55–69 mm reported in series [4, 23], suggest that such monitoring could facilitate treatment de-escalation and prevent surgical intervention in up to 67% of cases. Also, this case underscores the necessity for prospective pharmaceutical studies to establish optimized regimens for GIB, given its variable antifungal susceptibility and diagnostic challenges, thereby informing standardized protocols for pediatric management.

A review of the literature shows persistent diagnostic challenges and diverse therapeutic approaches, with both parallels and divergences compared with the present case. The clinical features of abdominal pain, anorexia, and altered bowel habits reflect reported prevalence rates of 76–100% [1, 6, 23]. However, the absence of peripheral eosinophilia in this patient contrasts with the 60–80% rates typically reported, though this has also been described in early or resistant presentations [1, 6, 23]. As a result, routine eosinophil counts should be interpreted with caution, as their absence does not exclude GIB.

Geramizadeh et al. [1] documented gastrointestinal involvement across 17 Iranian cases, predominantly stomach, small bowel, colon, and liver, mirroring the colonic involvement here. Unlike their largely immunocompetent cohort, this case involved a preterm background without congenital anomalies. The amphotericin-based regimen contrasts with their surgical emphasis, which historically carried higher mortality. Similarly, Mirmoosavi et al. [2] described a pediatric case responsive to antifungals without surgery, unlike the laparotomy required here for jejunal masses. Dodington et al. [4] emphasized the frequent mimicry of malignancy, tuberculosis, or cytomegalovirus colitis, resonating with the lymphoma differential in this case, while eosinophilic infiltrates paralleled the granulomatous pathology reported. Seemingly, early antifungal initiation may reduce the need for extensive surgical intervention in suspected cases.

In a bicentric Saudi review, Dhayhi et al. [7] found abdominal pain (70.8%) and colonic thickening (69%) as common findings, with voriconazole used in most and surgery in 33%. While demographics and presentation overlap, amphotericin was favored here for cost-effectiveness, with outcomes comparable to their 92% cure rate despite surgical adhesiolysis. Similarly, Pouladfar et al. [8] observed comparable lesion dimensions, eosinophilia, and antifungal regimens, though most of their patient’s avoided surgery. Geramizadeh et al. [1] underscored underdiagnosis and the centrality of histopathology, consistent with the fungal confirmation in this biopsy, though the patient’s prematurity diverges from their immunocompetent population. Combining imaging with early biopsy confirmation may optimize treatment pathways and minimize morbidity.

Kurteva et al. [17] described an infant with colonic GIB presenting with abdominal pain, bloody stools, and marked eosinophilia, with Splendore–Hoeppli phenomenon present—unlike its absence here. Their patient required colectomy and prolonged combination antifungals, while this case avoided such radical intervention despite jejunal extension. Abbag et al. [18] and Karimi et al. [25] similarly documented colonic mimicry with imaging parallels, though with limited outcome details. Al Yazidi et al. [23] highlighted a fatal disseminated case in an immunocompromised child, emphasizing the contrast with the favorable response in this immunocompetent patient. Therefore, prognosis may improve substantially with immunocompetence and timely antifungal escalation.

Ghazwani et al. [9] reported universal voriconazole success across 25 pediatric cases, with overlapping demographics, clinical features, and biopsy confirmation. However, amphotericin provided accessibility in this setting where azoles were limited, though surgical resection for jejunal masses contrasted with their biopsy-based diagnosis. Takrouni et al. [26] similarly noted obstructive colonic masses mimicking cancer, but their patient succumbed to septic complications, unlike the survival and partial medical response here. Ravindranath et al. [5] and Rizk et al. [6] both underscored lymphoma mimicry, with histopathology confirming fungal hyphae and eosinophilia, though treatment specifics varied. Tailored antifungal regimens must balance drug accessibility with disease severity, especially in resource-limited contexts.

Golestani Eraghi et al. [27] reported itraconazole–amphotericin–voriconazole resistance leading to shock, underscoring the contrast with therapeutic success here despite absent Splendore–Hoeppli phenomenon. Darré et al. [10] highlighted African cases with granulomatous inflammation and ketoconazole therapy, while Meeralam et al. [19] emphasized the need for prospective pediatric studies. Vikram et al. [11] confirmed success with amphotericin–itraconazole in USA cases, though predominantly in adults. AlSaleem et al. [28] reported Crohn’s-like pediatric cases managed with potassium iodide rather than amphotericin, while Saeed et al. [29] described hepatic dissemination successfully managed postresection. Resistance patterns highlight the importance of antifungal susceptibility monitoring in guiding therapy.

Several additional reports reinforce the diagnostic mimicry of GIB, its frequent overlap with malignancy or inflammatory bowel disease, and variable reliance on surgery. For example, Bering et al. [30] and Mirmoosavi et al. [2] stressed antifungals as primary therapy, Abduh et al. [31] noted survival even with perforation after combined therapy, and Pasha et al. [32] confirmed amphotericin–itraconazole responsiveness. Soleimani et al. [33] showed rare absence of Splendore–Hoeppli phenomenon with successful outcomes, while Zabolinejad et al. [34] validated itraconazole monotherapy. Shaker et al. [35] and Lyon et al. [36] further confirmed surgical variability and antifungal efficacy. The authors suggest that a combined diagnostic algorithm including imaging, histopathology, and early antifungal initiation should be standardized.

In addition, Mobarki et al. [37], Rabie et al. [38], Alsharidah et al. [39], Gupta et al. [12], Balkhair et al. [40], and Al Asmi et al. [41] all reiterated the mimicry of malignancy and Crohn’s disease, with amphotericin and itraconazole forming the backbone of therapy, while adjunctive cotrimoxazole, as used here, offers potential synergy. Reviews by El-Shabrawi et al. [42], Al-Shanafey et al. [20], and Awadh et al. [21] confirmed that histopathology remains the diagnostic cornerstone and that hybrid surgical–medical strategies are common when masses or obstruction develop. Therefore, adjunctive antifungal combinations (e.g., amphotericin plus azole or cotrimoxazole) may enhance outcomes and reduce relapse risk. Lastly, the antibiotic of choice should always align with the community’s overall antimicrobial resistance patterns in conjunction with appropriate bowel management tools [43–45].

Conclusion

Gastrointestinal basidiobolomycosis exerts a significant, underrecognized burden on pediatric populations in endemic areas, posing a diagnostic challenge that mimics malignancy or inflammatory bowel disease and risks obstruction, perforation, and mortality over 25% if untreated. Here, intravenous liposomal amphotericin B during hospitalization, followed by 28 days of oral itraconazole postdischarge, yielded complete clinical and radiographic resolution without recurrence at 1 year. Postlaparotomy biopsy confirmed the regimen’s sufficiency, showing reduced fungal burden and obscured histopathological features due to prior therapy, avoiding extended surgical needs. Nonetheless, the prolonged treatment duration highlights the need for prospective, randomized trials to optimize antifungal choices, define surgical indications, and identify predictive biomarkers for this rare infection.

Abbreviations

APUS

Abdominopelvic ultrasound

CT

Computed tomography

CRP

C-reactive protein

ESR

Erythrocyte sedimentation rate

GIB

Gastrointestinal basidiobolomycosis

IV

Intravenous

Author contributions

M.F conceptualized the study and performed surgical excision of the mass; B.G contributed in the histopathologic examination of the mass; S. H. contributed in the medical management of the case; Sh. Y contributed in the initial draft, review of the literature, revision, and submission of the manuscript; S. Sh contributed in curation of data and visualization; S.N contributed in administration of the project, data collection, patient’s legal guardian long term follow-up via telephone interview.

Funding

This study did not receive funds.

Availability of data and materials

Data is available within the manuscript.

Declarations

Ethics approval and consent to participate

Informed written consent was obtained from the patient and her legal guardians for participation in this study. This study was exempted from the ethical approval due to its retrospective nature and according to the regulations set forth by Shiraz university of medical sciences’ ethics committee.

Consent for publication

Written informed consent was obtained from the patient’s legal guardian for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

Competing interests

The authors declare no conflicts of interest.