An unusual rare case report of colonic ameboma mimicking Crohn’s disease: A rare clinical masquerade

INTRODUCTION

Amebiasis, caused by Entamoeba histolytica, remains one of the most prevalent parasitic infections in developing countries. This infection is transmitted through the oral-fecal route through ingestion of cysts of E. histolytica. While most infections are asymptomatic, invasive amebiasis may present as colitis, liver abscess, or the rare formation of an ameboma. Ameboma is a localized granulomatous pseudotumors that mimic inflammatory or neoplastic colonic conditions on imaging. Diagnosis is challenging and often delayed due to their resemblance to Crohn’s disease or neoplastic bowel etiology. Here, we report a rare case of ameboma mimicking Crohn’s disease in a female patient.

CASE REPORT

A 52-year-old female, a known case of pancreatitis for which she was admitted to the hospital twice previously, is now presenting with a 4-month history of right-sided abdominal pain, weight loss, vomiting, loss of appetite, tenesmus, and constipation. On examination, her blood pressure was 130/92 mmHg, and pulse was 90/min, signifying mild tachycardia. Pallor was present, and right iliac fossa tenderness associated with a tender lump on palpation with restricted mobility and no hepato-splenomegaly. Laboratory tests revealed raised C-reactive protein (262 mg/dL), raised white blood cells, anemia (8 g/dL), mildly decreased albumin (3.16 g/dL), raised gamma-glutamyl transferase (182 U/L), raised alkaline phosphatase (239U/L), raised serum glutamic-oxaloacetic transaminase (69 U/L), serum glutamic pyruvic transaminase (91 U/L), however, normal bilirubin (0.7 mg/dL) and carcinoembryonic antigen, fecal occult blood was negative.

In our case, computed tomography (CT) enterography was done after bowel preparation, which was done using low-residue high fiber diet, ample fluids, laxative on the day before the examination, and by mouth on the day of the examination. Iso-osmotic mannitol at room temperature was used as a neutral enteral contrast agent. 20% of 450 mL mannitol was diluted with plain water to make 1500 mL total fluid to be consumed by the patient over a period of 40 min. An antispasmodic agent (injection buscopan 20 mg IV) was given before CT acquisition. Thereafter, the patient was taken up for CT scanning. 100 mL of non-ionic iso-osmolar iodinated contrast media was injected intravenously through a 20-gauge cannula at a rate of 4 mL/s, followed by 30 mL of saline flush. The Siemens 128 dual-source multi-detector CT scanner was used. Imaging was done in the enteric phase (50-s delay) to demonstrate bowel enhancement and to assess other abdominal findings. Images were obtained from the dome of the diaphragm to the lower margin of the symphysis pubis. Reformatted images were obtained in the coronal and sagittal planes with a software reconstruction technique. Images were interpreted on a Belgium American Radio Corporation workstation by an experienced gastrointestinal radiologist.

Contrast-enhanced CT enterography of abdomen [Figure 1a-f] revealed significant circumferential transmural wall thickening with hyperenhancement of terminal ileum, ileo-cecal (IC) junction , cecum and ascending colon, causing partial luminal narrowing with mild upsream dilatation of distal ileal loops. A locualted peripherally enhancing hypoattenuating collection was noted in the right iliac fossa, forming a fistulous communication with adjoining thickened terminal ileum loop, and cecum. Collection was seen involving right psoas muscle and right distal ureter causing upstream hydro-uretero-nephrosis. The crumpled appendix was ill-defined as effaced by the adjacent collection. There was no skip lesion seen. The rest of the colon showed no mural thickening and normal mural enhancement. Significant mesenteric fat stranding with prominent mesenteric vessels associated with congestion and near-centimetersized prominent heterogeneously enhancing loco-regional ileo-colic mesenteric lymph nodes were seen [Figure 1f]. As there was transmural inflammation of the bowel wall associated with fistulous communication of the collection with the involved terminal ileum and cecum, so, the imaging diagnosis of Crohn’s disease was kept; however, differential diagnoses of tuberculosis could not be dogmatically ruled out as India has a high disease load of tuberculosis.

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Figure 1:

CECT enterography (Coronal image-a): Circumferential transmural wall thickening in caecum (solid white arrow) and IC junction (black arrowhead) & terminal ileum (hollow white arrow) forming fistulisation (long black arrow) with collection (solid black arrow). (Sagittal images-b & c): Collection (black arrow; image b) involving the psoas muscle (transparent black arrow) with wall thickening in the ascending colon (white arrow; image c). (Axial image-d): Thickening in the caecum (white arrow) communicating (curved arrow) with the collection (black arrow). (Sagittal image-e): Collection (black arrow) obstructing the right ureter (curved arrow). (Coronal image-f): Lymph nodes and mesenteric fat stranding (long white arrow).

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Colonoscopy [Figure 2a-c] revealed extreme mucosal nodularity giving a cobble-stone appearance with few erosions and ulcerations in entire caecum and medial wall of ascending colon with deformed ileo cecal valve. The terminal ileum could not be assessed due to significant luminal narrowing, and a provisional diagnosis of Crohn’s disease/ tuberculosis was kept. One of the largest thickened cecal nodule was removed. On histopathology, it showed mild acute and chronic inflammatory infiltrates in the lamina propria, and a diagnosis of active colitis was made.

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Figure 2:

Endoscopy images (a-c) showing mucosal nodularity with cobble-stone appearance (a and b; black arrow) and large cecal nodule (c; black arrow). Gross specimen (d and e) showing right hemicolectomy specimen with terminal ileal perforation (black arrow; d) and cut section of specimen showing ulceration with perforation in cecum (white arrow; e).

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A multidisciplinary team discussion was held, and as there was localized ileal perforation and chronic duration of illness with partial terminal ileal stricture and poor response to conservative therapy, the patient was planned for ileo-cecal resection and anastomosis. However, intra-operatively, due to extensive inflammation and involvement of the terminal ileal loop, cecum, and ascending colon, the patient underwent right hemicolectomy with ileo-transverse anastomosis with covering ileostomy. Intra-operative findings included an 8 x 6 cm cecal and ascending colon mass with ulceration and perforation of the posterior cecal wall. Dense adhesions were seen between the omentum, cecum, ascending colon, distal ileal loops, and lateral abdominal wall, with a collection seen in vicinity of these loops communicating with the thickened cecum and perforated terminal ileal loop. Borderline-sized loco-regional lymphadenopathy was present.

Right hemicolectomy specimen [Figure 2d and e] revealed terminal ileal perforation and cut section showed ulceration with perforation in cecum.

The right hemicolectomy specimen histopathology [Figure 3a-c] revealed columnar epithelium-lined intestinal mucosa with focal surface ulceration and erosion. Patchy areas of crypt architectural distortion along with crypt abscesses were noted. Trans-mural intense and diffuse mixed inflammation composed of sheets of chronic lymphocytes, plasma cells, neutrophils along with lymphoid aggregates and occasional eosinophil’s reaching up to serosal surface is seen. No granulomas were noted. Fragments of fibrinous exudate with numerous scattered trophozoites having abundant pink vacuolated cytoplasm and erythrophagocytosis are noted. There was no evidence of dysplasia/malignancy.

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Figure 3:

Histopathology images (a-c): Hematoxylin and eosin staining showing trophozoites of Entamoeba histolytica (black arrow in a and white arrows in b) and periodic acid–schiff staining: showing periodic acid–schiff positive magenta-colored E. histolytica (black arrows in c).

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The post-operative period of the patient in the hospital was favorable with resolution of the chief complaints and normalization of the blood inflammatory parameters. She was discharged in stable condition with a covering ileostomy and suggested follow-up in the outpatient department (OPD) after a week in OPD with biopsy report and all the prescribed blood test investigations. The post-operative specimen on histopathological examination showed transmural intense, diffuse mixed inflammation and fragments of fibrinous exudate with numerous scattered trophozoites of E. histolytica, implying the diagnosis of ameboma. The patient was prescribed a proper dosage of the drug metronidazole, and after 6 weeks of follow-up, the patient was planned for ileostomy closure, for which a CT distal loopogram study was performed, which revealed no leak of contrast/no stricture segment in the distal loop. Stoma closure was done by the gastrointestinal surgery team with an uneventful post-operative period, and the patient was discharged in stable condition with prescribed medication and for follow-up in OPD.

DISCUSSION

Amebiasis is the most significant gastrointestinal parasitic infection in developing countries like India. Infections caused by E. histolytica are the second most common type of parasitosis in the world (malaria being the first), accounting for 40,000–100,000 deaths annually.^[1] Intestinal infection with E. histolytica can result in a range of clinical outcomes, from an asymptomatic carrier state to more severe manifestations such as colitis, abscess formation, and even colonic perforation. Intestinal perforation due to E. histolytica is rare and happens in only 1.9–9.1% of cases.^[2] Trophozoites of E. histolytica are responsible for the invasive disease. Amebomas or amebic granulomas are rare complications that can develop in patients with long-standing, partially treated, or untreated amebic infections. These amebomas are characterized by tumorous, cicatricial, exophytic, and inflammatory features.^[3] It is estimated that amebomas occur in approximately 1.5% of all cases of amebiasis.^[4] In decreasing order of frequency, amebomas develop in the cecum, the appendix, and the rectosigmoid region.^[1] Other sites include the hepatic flexure, transverse colon, and splenic flexure. Amebomas result from the formation of annular colonic granulation tissue at single or multiple sites, usually within the cecum or ascending colon.^[1] The tissue necrosis in amebic colitis is replaced by a marked inflammatory reaction and development of pseudotumors, potentially because of secondary bacterial infection. This can mimic colon carcinoma.^[4] Amebomas may cause obstructive symptoms. The differential diagnosis of ameboma includes conditions such as Crohn’s disease and appendiceal abscesses in younger patients, while in older individuals, it may be confused with colon cancer or diverticulitis.^[5,6] Contrast-enhanced tomography and colonoscopy are sensitive tools for the workup of differential diagnosis of a cecal mass.^[6] Endoscopic evaluation provides a definitive diagnosis in approximately 60% of cases. However, due to its rarity, ameboma is often identified incidentally during laparotomy.^[7]

In our case, the patient presented with right-sided abdominal pain, weight loss, vomiting, loss of appetite, tenesmus, and constipation. Clinical examination showed right iliac fossa tenderness with a palpable lump with restricted mobility, and findings on radiological imaging, mentioned earlier, were suggesting the possibility of inflammatory bowel disease, likely Crohn’s disease due to transmural involvement of the bowel and significant surrounding inflammatory changes. Colonoscopy revealed extreme nodularity with cobblestone appearance and a few erosions and ulcerations noted in the entire cecum and medial wall of the ascending colon. Provisional diagnosis of Crohn’s disease and the differential diagnosis of tuberculosis were kept. As there was a chronic illness with poor response to conservative treatment, after multi-disciplinary team discussion, consensus was reached to approach the case surgically, given localized ileal perforation and partial terminal ileal stricture causing vomiting and intestinal obstruction. The patient underwent a right hemicolectomy with ileo-transverse anastomosis and a covering ileostomy.

This case underscores the diagnostic challenges associated with amebic colitis, as it can closely resemble inflammatory bowel disease or colonic carcinoma, especially in the absence of a recent travel history to an endemic region. Colonic resection may be necessary when malignancy cannot be ruled out or in emergencies involving complications such as perforation, abscess, obstruction, or intussusception^[8] or in refractory cases not responding to conservative treatment. Inflammatory bowel disease is commonly treated with steroids and immunosuppressive drugs. However, administering steroids to patients with amebiasis can cause severe, rapidly worsening illness and may be life-threatening, so diagnosis is crucial.^[9] The mortality rate of amebiasis significantly increases when complications such as acute necrotizing colitis, toxic megacolon, perforation, and peritonitis arise, often necessitating surgical intervention.^[10] To date, only six cases of ameboma have been reported, all located in the right colon. These cases presented with symptoms of acute abdomen or intestinal obstruction and were diagnosed only after surgery through histopathological examination.^[11]

For evaluation of bowel pathologies on imaging, CT/magnetic resonance enterography is the modality of choice. Ameboma shows heterogeneously enhancing wall thickenings involving the cecum and adjacent ascending colon with or without involvement of the terminal ileum. Associated collections can be there with extensive surrounding mesenteric fat stranding and borderline to enlarged heterogeneously enhancing loco-regional lymph nodes. There is no evidence of skip lesions. The presence of PAS-positive trophozoites having abundant pink vacuolated cytoplasm and erythrophagocytosis on histopathology favors ameboma.

The imaging findings on cross-sectional imaging, along with their differentiating points from other differential diagnoses, are discussed in detail in Table 1.

CONCLUSION

Amebiasis, one of the most prevalent infections in India, typically presents as colitis, with a rare formation of an ameboma, which can mimic inflammatory bowel disease, such as Crohn’s ileitis or neoplastic bowel disease on imaging. Although the diagnosis is challenging, optimal image interpretation by a dedicated gastrointestinal (GI) radiologist and clinical correlation help differentiate these close imaging differentials, leading to optimal patient care.

TEACHING POINTS

1. Ameboma, though rare, should be considered in the differential diagnosis of colonic masses, especially in tropical regions

2. Misdiagnosis as Crohn’s disease can lead to wrong and harmful treatment; colonoscopy correlation and biopsy are crucial for definitive diagnosis.

MCQs

1. Which of the following features is diagnostic of ameboma on histopathology?

   1. Caseating granulomas

   2. Crypt abscesses

   3. Trophozoites with ingested RBCs

   4. Malignant epithelial cells

   Answer Key: c

2. What is the most appropriate initial treatment for ameboma?

   1. Corticosteroids

   2. Surgery

   3. Anti-amebic agents like ornidazole

   4. Immunosuppressants

   Answer Key: c

3. Why is it critical to distinguish ameboma from Crohn’s disease before treatment?

   1. Ameboma never requires treatment

   2. Crohn’s disease is self-limiting

   3. Steroid use in ameboma can cause fulminant colitis

   4. Both conditions are treated with the same drugs

   Answer Key: c