Duodenal Strongyloidiasis Mimicking Inflammatory Bowel Disease: A Case Report of a 52-Year-Old Immunocompetent Woman

Abstract

Background

Strongyloides stercoralis is an intestinal nematode with a unique autoinfective life cycle that enables decades-long persistence in the human host. Its gastrointestinal manifestations may resemble inflammatory bowel disease (IBD), creating a clinically important diagnostic pitfall. Misdiagnosis is particularly hazardous because corticosteroids or other immunosuppressive therapies may precipitate Strongyloides hyperinfection syndrome or disseminated disease.

Case Presentation

We report a 52-year-old immunocompetent woman from northern Iran who presented with a 20-day history of persistent watery inflammatory diarrhea, severe hypokalemia (2.4 mEq/L), leukocytosis, and thrombocytosis. Serial stool examinations for ova and parasites were repeatedly negative for larvae; however, fecal leukocytes and erythrocytes, together with erosive duodenopathy, initially raised concern for IBD. Duodenal biopsy established the diagnosis by demonstrating marked eosinophilic infiltration of the lamina propria, reaching 45–50 eosinophils per high-power field, and rhabditiform larvae within the mucosal crypts. The larvae showed morphologic features supporting Strongyloides stercoralis, including a short buccal cavity/canal and a characteristic rhabditiform esophagus. Molecular testing, serology, and independent expert parasitologist confirmation were not performed, which represents a diagnostic limitation. The patient was treated with oral ivermectin plus adjunctive albendazole. The addition of albendazole was an individualized, non-standard clinical decision rather than a routine evidence-based recommendation. Her symptoms improved rapidly, and she remained asymptomatic at one-month follow-up.

Conclusion

This case emphasizes the clinical and histopathological overlap between duodenal strongyloidiasis and IBD, particularly when stool parasitology is unrevealing. The novelty of this report lies primarily in its didactic value for clinicians in endemic regions: Strongyloides should remain in the differential diagnosis of IBD-like presentations with unexplained eosinophilic mucosal inflammation before immunosuppressive therapy is considered.

1. Introduction

Strongyloides stercoralis is a soil-transmitted intestinal nematode that infects an estimated 600 million people worldwide, primarily in tropical and subtropical regions where sanitation is suboptimal.^1,2 Unlike most helminths, Strongyloides possesses a unique autoinfective life cycle, enabling it to persist within the host for decades without further environmental exposure. ³ This capacity for autoinfection explains its potential to cause chronic infections or progress to life-threatening disseminated disease.

The clinical spectrum of strongyloidiasis is remarkably diverse, ranging from asymptomatic eosinophilia to severe gastrointestinal, pulmonary, and systemic involvement. Gastrointestinal manifestations are often non-specific and frequently mimic other gastrointestinal disorders, most notably inflammatory bowel disease (IBD).^4,5 This clinical mimicry represents a significant diagnostic hazard; misidentifying strongyloidiasis as ulcerative colitis or Crohn’s disease may lead to the administration of corticosteroids or other immunosuppressants. Such interventions can precipitate hyperinfection syndrome, characterized by a massive increase in larval burden and systemic dissemination, with mortality rates exceeding 80%.^6,7

Diagnosing Strongyloides remains challenging due to the intermittent and low larval output in stool samples. Standard stool microscopy often fails to detect the parasite, and more sensitive diagnostic tools, such as the Baermann concentration method or agar plate culture, are frequently unavailable in clinical settings. ⁸ Consequently, diagnosis may be made incidentally when larvae are identified in tissue biopsies obtained during endoscopic evaluation for unexplained gastrointestinal symptoms.

Strongyloides infection mimicking IBD has been reported previously. Therefore, the novelty of the present case is not that it represents an entirely unprecedented disease entity. Rather, its value lies in the specific convergence of features that created a compelling diagnostic facade of IBD in an immunocompetent patient from an endemic region: duodenal involvement, repeatedly negative stool examinations, inflammatory stool findings with leukocytes and erythrocytes, marked tissue eosinophilia, and concern for immune-mediated enteritis. This case is intended as a practical educational reminder that parasitic infection should be actively considered before immunosuppressive therapy is initiated in patients with IBD-like presentations.

2. Case Presentation

A 52-year-old woman residing in northern Iran, with no known prior history of chronic illness or immunosuppression, presented to the emergency department with a 20-day history of persistent watery diarrhea. She reported six to eight large-volume bowel movements daily, associated with intermittent cramping abdominal pain, anorexia, generalized fatigue, and weakness. She reported no visible blood in the stool. Her only regular medication was pantoprazole 40 mg daily. One week before presentation, she had been hospitalized for four days at another facility, where supportive therapy was provided. She denied recent travel to high-endemicity regions, known contact with infected individuals, or use of untreated water. She reported attending a local gathering approximately 10 days before symptom onset, where homemade food was served. There was no known family history of gastrointestinal or inflammatory bowel disease. On admission, the patient appeared pale but was afebrile and hemodynamically stable. Her blood pressure was 110/70 mmHg, pulse rate was 92 beats/min, respiratory rate was 18 breaths/min, and temperature was 36.8 °C. Physical examination revealed diffuse abdominal tenderness without rebound tenderness, guarding, organomegaly, or peritoneal signs. Cardiopulmonary examination was unremarkable.

2.1. Laboratory Findings

Initial laboratory evaluation revealed leukocytosis with a white blood cell count of 14,000/µL and marked thrombocytosis with a platelet count of 563,000/µL. Serum electrolytes were remarkable for severe hypokalemia, with a potassium level of 2.4 mEq/L, necessitating urgent intravenous potassium replacement. Renal and hepatic function tests were not suggestive of organ failure. Inflammatory markers were unremarkable, with a negative C-reactive protein and an erythrocyte sedimentation rate of 8 mm/h. A major diagnostic challenge arose from stool evaluation. Serial stool examinations for ova and parasites were performed on three separate occasions and were consistently negative for Strongyloides larvae or other parasites. However, stool microscopy demonstrated an inflammatory pattern, with numerous white blood cells, approximately 10–15/HPF, and red blood cells, approximately 6–10/HPF. Stool cultures for Shigella and Salmonella were negative on two occasions. The combination of persistent inflammatory diarrhea, fecal leukocytes and erythrocytes, negative routine stool parasitology, and mucosal abnormalities initially raised concern for inflammatory bowel disease.

2.2. Hospital Course and Histopathological Diagnosis

The patient was admitted to the infectious diseases ward and managed with intravenous hydration, potassium supplementation, and empirical antibiotics with ciprofloxacin and metronidazole. Despite supportive care and empirical therapy, diarrhea and abdominal symptoms persisted. An upper gastrointestinal endoscopy was performed and revealed erosive duodenopathy and mild chronic gastritis. On hospital day 4, histopathological examination of the duodenal biopsy established the diagnosis. Sections of the duodenal mucosa demonstrated villous and crypt architectural changes with lymphocytic exocytosis, estimated at 9–10 intraepithelial lymphocytes per 100 enterocytes. The lamina propria showed intense and disproportionate eosinophilic infiltration, reaching 45–50 eosinophils per high-power field (Figure 1). Most importantly, rhabditiform larvae were identified within the duodenal mucosal crypts (Figure 2). The observed larvae showed morphologic features supporting Strongyloides stercoralis, including a short buccal cavity/canal and a characteristic rhabditiform esophagus. These features made other intestinal nematodes less likely. Capillaria philippinensis was considered in the differential diagnosis because it may also present with chronic diarrhea, malabsorption, and small intestinal involvement; however, the biopsy did not show characteristic Capillaria eggs, adult worms, or typical eggs with bipolar/polar prominences and a striated shell. Gastric biopsies showed only mild chronic gastritis and were negative for Helicobacter pylori.

Figure 1.

Duodenal mucosa section, H&E stain, showing marked chronic inflammation and intense eosinophilic infiltration in the lamina propria, reaching 45–50 eosinophils/HPF, mimicking eosinophilic enteritis or inflammatory bowel disease.]

Figure 2.

High-magnification histopathology of the duodenal crypts showing rhabditiform larvae morphologically compatible with Strongyloides stercoralis, indicated by white arrows, supporting the parasitic etiology

No molecular testing, Strongyloides serology, or independent expert parasitologist review was performed. Therefore, the diagnosis was based on histopathological identification and morphology of larvae in duodenal biopsy specimens. This limitation is acknowledged in the Discussion.

2.3. Outcome and Follow-Up

Following the histopathological diagnosis, empirical antibiotics were discontinued and antiparasitic therapy was initiated. Ivermectin monotherapy is considered the standard first-line treatment for uncomplicated strongyloidiasis. In this patient, the clinical team administered oral ivermectin at 200 µg/kg daily for two days, together with adjunctive albendazole 400 mg twice daily for seven days.

The addition of albendazole was an individualized and non-standard clinical decision rather than a recommendation for routine practice. This decision was made in the context of delayed diagnosis, severe hypokalemia at presentation, persistent symptoms, and visible mucosal larval burden on biopsy. The dual regimen was used as a pragmatic clinical approach to maximize parasite clearance in a metabolically unstable patient, but the favorable outcome in this case should not be interpreted as evidence that combination therapy is superior to standard ivermectin monotherapy in uncomplicated strongyloidiasis.

The patient’s gastrointestinal symptoms improved rapidly within 48 hours after initiation of antiparasitic therapy. Follow-up stool examinations on days 5 and 7 showed a reduction in inflammatory cells and remained negative for larvae. Serum potassium levels normalized prior to discharge. At the one-month follow-up visit, the patient remained asymptomatic, with complete resolution of diarrhea and abdominal pain and no evidence of clinical recurrence. A chronological overview of the clinical course is summarized in Table 1.

Table 1.

Timeline of Clinical Events, Diagnostic Evaluation, and Therapeutic Interventions

Time	Clinical event
Day −20	Onset of persistent watery diarrhea and abdominal discomfort
Day 0	Hospital admission with severe hypokalemia and leukocytosis
Days 1–3	Stool examinations negative for parasites; inflammatory stool findings raised suspicion of IBD
Day 4	Upper endoscopy and duodenal biopsy performed
Day 4	Histopathology revealed Strongyloides stercoralis larvae in duodenal mucosa
Days 4–10	Treatment with ivermectin (200 µg/kg/day for 2 days) and albendazole (400 mg twice daily for 7 days)
Days 5–7	Stool examination negative for larvae; clinical symptoms improved
1 Month	Complete recovery with no recurrence of symptoms

2.4. Patient Perspective

The patient reported that persistent diarrhea and weakness had substantially affected her daily activities and caused significant anxiety before hospitalization. She expressed relief once the diagnosis was established and treatment was started. Following therapy with ivermectin and albendazole, she noted rapid improvement and was able to return to normal daily activities within a short period. At the one-month follow-up visit, she reported complete recovery and satisfaction with the care she received.

3. Discussion

This case highlights a clinically important diagnostic dilemma: differentiating chronic Strongyloides stercoralis infection from inflammatory bowel disease (IBD), particularly in regions where exposure to soil-transmitted helminths remains possible. Strongyloides infection has been repeatedly reported as a harmful mimic of IBD, including ulcerative colitis and Crohn’s disease, with overlapping clinical, endoscopic, and histopathological features. This distinction is not merely academic; misclassification of strongyloidiasis as IBD may lead to corticosteroid or other immunosuppressive therapy, which can precipitate hyperinfection syndrome, disseminated disease, sepsis, multiorgan failure, and death.^7,9-11

The main educational value of the present case lies not in claiming an entirely novel disease entity, but in highlighting a specific and clinically misleading convergence of findings. Previous case reports and case series have already described Strongyloides colitis or enteritis mimicking IBD.^7,9-11 However, in our patient, several features together created a strong diagnostic facade of IBD: immunocompetent status, duodenal involvement, persistent inflammatory diarrhea, fecal leukocytes and erythrocytes, repeatedly negative stool examinations for parasites, erosive duodenopathy, and marked tissue eosinophilia. This combination is particularly relevant for clinicians practicing in endemic or potentially endemic settings, where parasitic infection should remain in the differential diagnosis before immunosuppressive therapy is considered.

A major diagnostic pitfall in this case was the repeated negativity of routine stool examinations. Negative stool microscopy does not exclude strongyloidiasis, because larval output in chronic infection may be low and intermittent, and conventional stool ova-and-parasite examination has limited sensitivity for S. stercoralis. More sensitive diagnostic approaches, including the Baermann concentration method, agar plate culture, serology, and molecular assays, may improve diagnostic yield, although these tests are not always routinely available or may not be requested when IBD becomes the leading clinical suspicion.^8,12-14 In the present case, the inflammatory stool pattern strengthened the initial impression of immune-mediated intestinal disease, whereas repeated negative stool parasitology falsely lowered suspicion for parasitic infection.

Another important feature was the intense eosinophilic infiltration of the duodenal lamina propria, reaching 45–50 eosinophils per high-power field. Strongyloides infection can produce a broad clinical spectrum, ranging from asymptomatic infection to gastrointestinal, pulmonary, and disseminated disease, and may trigger both local and systemic immune responses. Peripheral eosinophilia is a useful clue in many helminthic infections, but it may be absent, intermittent, or clinically inconspicuous in some patients; therefore, its absence should not exclude strongyloidiasis.^15,16 In tissue, localized eosinophil-rich and lymphoplasmacytic inflammation may be misinterpreted as eosinophilic gastroenteritis or IBD if larvae are overlooked or absent in the examined sections. Histopathological studies have shown that Strongyloides may involve the gastric and duodenal mucosa and may be identified in biopsy specimens obtained during endoscopic evaluation.^17,18 Histopathological identification was central to the diagnosis in this patient. The presence of rhabditiform larvae within duodenal mucosal crypts, together with supportive morphologic features, favored S. stercoralis. Distinguishing features of Strongyloides larvae include a very short buccal cavity/canal and a rhabditiform esophagus, with larval forms detectable in stool, duodenal fluid, and biopsy specimens.^12,19 Capillaria philippinensis was specifically considered in the differential diagnosis because it can also cause chronic diarrhea, malabsorption, and electrolyte disturbances. However, Capillaria infection is typically supported by the identification of characteristic eggs or adult worms; C. philippinensis eggs are classically described as peanut-shaped or barrel-shaped, with flattened bipolar/polar plugs and a striated shell.^20,21 These findings were not identified in the present biopsy specimens, making Capillaria less likely. Nevertheless, because molecular testing, serology, agar plate culture, and independent expert parasitologist confirmation were not performed, the diagnosis in this report should be understood as histopathology-based rather than molecularly confirmed. The treatment strategy also requires careful interpretation. Ivermectin is generally considered the preferred first-line therapy for uncomplicated strongyloidiasis, and comparative trials and systematic reviews have shown ivermectin to be more effective than albendazole for parasitological cure.^22-25 In a randomized trial, ivermectin achieved higher cure rates than albendazole in children with S. stercoralis infection, and a Cochrane review concluded that ivermectin results in more parasitological cures than albendazole and is at least as well tolerated.^24,25 Therefore, the use of ivermectin plus albendazole in the present patient should not be interpreted as a routine evidence-based recommendation for uncomplicated strongyloidiasis.

In this case, the addition of albendazole was an individualized, non-standard clinical decision made by the treating team. The rationale was the patient’s severe metabolic disturbance, delayed diagnosis, persistent symptoms, and visible mucosal larval burden on biopsy. However, robust evidence supporting routine ivermectin–albendazole combination therapy for individual uncomplicated Strongyloides infection is lacking. Existing discussions of ivermectin–albendazole coadministration mainly relate to soil-transmitted helminth control, preventive chemotherapy, and public health strategies rather than routine management of single uncomplicated clinical cases.^26,27 Accordingly, the favorable clinical outcome in this patient should not be used to infer superiority of combination therapy over standard ivermectin-based treatment.

The patient’s pantoprazole exposure should also be interpreted with caution. Proton pump inhibitors have been associated with increased susceptibility to some enteric infections and with alterations in gut microbial ecology in systematic reviews and mechanistic discussions.^28,29 However, these data do not establish a causal relationship between pantoprazole use and strongyloidiasis, and they should not be overextended to this single case. Therefore, pantoprazole use in this patient can only be mentioned as a speculative and unproven contextual factor, not as an established risk factor for Strongyloides infection, autoinfection, or disease severity.

This case has several limitations. First, diagnosis was based on histopathological morphology without molecular confirmation, serology, agar plate culture, or independent expert parasitologist review. Second, stool examinations remained negative, so parasitological confirmation from stool was not obtained. Third, follow-up was limited to one month; longer-term clinical and parasitological monitoring would have been preferable, because relapse or persistent infection can occur in strongyloidiasis, particularly when diagnostic follow-up relies on methods with limited sensitivity. Fourth, because this is a single case report, no general conclusion can be drawn regarding the superiority of combination therapy or any causal association between pantoprazole use and strongyloidiasis.

Despite these limitations, the case provides a practical warning. In patients with chronic diarrhea, inflammatory stool findings, mucosal eosinophilia, and suspected IBD, Strongyloides should remain in the differential diagnosis even when routine stool examinations are negative. This is particularly important before initiating corticosteroids, biologic agents, or other immunosuppressive therapies. Screening and careful histopathological review are essential in at-risk patients, because timely recognition of strongyloidiasis can prevent potentially fatal iatrogenic complications.

4. Conclusion

Strongyloides stercoralis can closely mimic inflammatory bowel disease, particularly when stool parasitology is repeatedly negative and fecal inflammatory findings are present. This case is best understood as a didactic reminder rather than as a claim of an entirely novel disease presentation. In endemic regions, duodenal strongyloidiasis should be considered in patients with unexplained eosinophilic mucosal inflammation and IBD-like symptoms before immunosuppressive therapy is started. Histopathological recognition of larval morphology is essential, but the absence of molecular or expert parasitological confirmation should be acknowledged as a limitation. Ivermectin remains the standard first-line therapy for uncomplicated strongyloidiasis; adjunctive albendazole in this case was an individualized, non-standard decision and should not be generalized as a routine treatment recommendation.

ORCID iD

Alireza Davoodi https://orcid.org/0009-0008-0125-587X

Consent to Participate

Written informed consent was obtained from the patient for publication of this case report and the accompanying clinical data and images. A copy of the written consent is available for review by the Editor-in-Chief of this journal upon request.