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  Table of Contents    
ORIGINAL ARTICLE  
Year : 2015  |  Volume : 58  |  Issue : 4  |  Page : 427-432
The differentiation of amebic colitis from inflammatory bowel disease on endoscopic mucosal biopsies


1 Department of Pathology, Christian Medical College and Hospital, Vellore, Tamil Nadu, India
2 Department of Gastrointestinal Sciences, Christian Medical College and Hospital, Vellore, Tamil Nadu, India
3 Department of Pathology, Christian Medical College and Hospital, Vellore, Tamil Nadu; Department of Gastrointestinal Sciences, Christian Medical College and Hospital, Vellore, Tamil Nadu, India

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Date of Web Publication4-Nov-2015
 

   Abstract 

Background: Intestinal amebiasis is one of the important differential diagnoses of Inflammatory Bowel Disorders in areas where it is highly prevalent. Aim: Studies comparing the clinical, endoscopic and histological features of these disorders have never been done, so we undertook this study. Materials and Methods: A retrospective study comparing mucosal biopsies of 14 consecutive cases of intestinal amebiasis with 14 cases of Ulcerative colitis and 12 cases of Crohn's disease. A total of 65 biopsies from patients with amebiasis, 56 biopsies from patients with Crohn's disease and 65 biopsies of patients with Ulcerative colitis were reviewed. Results and Conclusions: Discrete small ulcers less than 2 cm in diameter in the cecum or rectosigmoid, with intervening normal mucosa, were the most common finding on endoscopy in patients with amebiasis. On histology, necrotic material admixed with mucin, proteinaceous exudate and blood clot lining ulcers, significant surface epithelial changes such as shortening and tufting adjacent to sites of ulceration, mild chronic inflammation extending into the deep mucosa and mild architectural alteration were features of amebiasis. Trophozoite forms of ameba were seen in the necrotic material lining sites of ulceration or lying separately, as well as over intact mucosa. Necrotic material lining ulcers was less common in IBD, but chronic inflammation, crypt abscess formation and architectural alteration were more severe.

Keywords: Amebic colitis, inflammatory bowel disease, mucosal biopsy

How to cite this article:
Singh R, Balekuduru A, Simon EG, Alexander M, Pulimood A. The differentiation of amebic colitis from inflammatory bowel disease on endoscopic mucosal biopsies. Indian J Pathol Microbiol 2015;58:427-32

How to cite this URL:
Singh R, Balekuduru A, Simon EG, Alexander M, Pulimood A. The differentiation of amebic colitis from inflammatory bowel disease on endoscopic mucosal biopsies. Indian J Pathol Microbiol [serial online] 2015 [cited 2019 Oct 15];58:427-32. Available from: http://www.ijpmonline.org/text.asp?2015/58/4/427/168880



   Introduction Top


Amebiasis due to invasive infection with Entamoeba histolytica is said to affect up to 50 million individuals worldwide.[1] Undiagnosed amebiasis can lead to fulminant intestinal infection and liver abscesses that are associated with a high mortality rate and cause about 100,000 deaths every year. Amebiasis is most prevalent in developing countries, but a high incidence is also encountered in Western countries, among Human Immunodeficiency Virus-infected individuals and travelers returning from endemic areas. Amebiasis classically presents with chronic dysentery [2] and is one of the important differential diagnoses of inflammatory bowel disorders in areas where it is highly prevalent.[2],[3] The rising incidence of inflammatory bowel disease (IBD) in many of these countries has increased the importance of being able to differentiate them from amebiasis. This is particularly important because amebiasis can be cured by antibiotics, whereas IBD requires long-term anti-inflammatory therapy. The use of immunosuppressants for IBD could precipitate fulminant disease or dissemination of infection in individuals with amebiasis.

Amebiasis is classically associated with discrete, flask-shaped mucosal ulcers, commonly located in the cecum and the rectum, but irregular ulcers surrounded by edema and erythema, resembling those seen in IBD, have also been described.[4] The prolonged nature of the infection and the intense mucosal damage that are often associated with amebiasis are factors that could contribute to distortion of the mucosal architecture and induce significant chronic inflammation, both of which are classical features of IBD. Studies comparing the clinical, endoscopic, and histological features of these disorders are not available. We therefore undertook a retrospective pilot study on 14 cases each of amebic colitis and ulcerative colitis (UC) and 12 cases of Crohn's disease (CD) in order to identify features that could be used to differentiate them.


   Materials and Methods Top


Fourteen consecutive cases of amebiasis were retrieved from the histology records of the Department of Pathology over 9 years (2001–2009). All cases had been diagnosed on the basis of the presence of amebic trophozoites in mucosal biopsies. Fourteen cases of UC and 12 cases of CD were also selected from the files of the Department of Gastrointestinal Sciences. The available clinical data were reviewed by a gastroenterologist, and the final clinical diagnosis made on the basis of a combination of clinical findings, laboratory data, radiological, and follow-up.

A total of 65 biopsies from patients with amebiasis, 56 biopsies from patients with CD, and 65 biopsies of patients with UC were reviewed. All slides were reviewed by 2 pathologists. A minimum of 2 serial sections were studied for each mucosal biopsy. The following histological features were evaluated in each case:

  1. Presence of ulceration (whether superficial - involving only part of the mucosal thickness, or deep)
  2. Nature of tissue lining ulcers (acute inflammatory exudate, mucus, blood, necrotic material, or inflammatory granulation tissue)
  3. Surface epithelial change (mucin depletion, shortening of the epithelial cells, tufting, infiltration by neutrophils, and lymphocytes): graded as mild, moderate, or severe
  4. Architectural alteration (whether crypt branching, disarray, dilatation, rupture, or loss): graded as mild, moderate, or severe
  5. Activity (cryptitis or crypt abscesses): graded as mild, moderate, or severe for cryptitis and few or many for crypt abscesses
  6. Chronic inflammation in the superficial and deep lamina propria (mild, moderate, or severe) and submucosa
  7. Presence of edema, fibrosis, eosinophilia, and other changes in the lamina propria
  8. Presence of trophozoite forms of E. histolytica (over intact mucosa, in exudates lining ulcers or invading tissue) and their number.


Ethical clearance

Clearance for the study was obtained from the Institutional Review Board.

Statistical analysis

Data entry and analysis were done using statistical software SPSS for Windows Version 16.0 (SPSS Inc., Chicago, IL, USA)" The Chi-square test was used.


   Results Top


Clinical features

Clinical data were available for 10 of the 14 cases of amebiasis, and the salient features are shown in [Table 1]. (Mild-1, moderate to severe)
Table 1: Salient clinical features of patients with amebiasis

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Endoscopy

All patients had undergone colonoscopy, and the segments involved are shown in [Table 2]. The colonoscopic findings in patients with amebiasis and the tentative clinical diagnosis at the time of endoscopy are shown in [Table 3]. Endoscopic findings were available in 13 cases of amebic colitis. Eleven had discrete ulcers that were 2 cm or less in diameter in 7 and aphthoid in 1. The size of the ulcers was not documented in the remaining cases. Ulcers were located in the cecum in 7, rectosigmoid in 2, transverse colon in 1, and in all colonic segments in 2. No other changes were noted in the surrounding mucosa in any of the patients.
Table 2: Segmental distribution of sites involved by amebiasis, CD, and UC on colonoscopy

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Table 3: Clinical diagnosis at colonoscopy and salient endoscopic findings of patients with amebiasis

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Endoscopic findings were available in all 14 cases of UC and 11 cases of CD. One or more mucosal changes such as nodularity, friability, edema, erythema, loss of vascularity, and cobblestoning were seen adjacent to all ulcers in patients with IBD except for 1 case of CD. Other changes noted in UC included erythema (2), edema (6), attenuation of haustra (1), loss of vascularity (6), granularity and friability (11), pseudopolyp (1), and nodularity (1). In CD, other changes noted included erythema (1), edema (3), loss of vascularity (1), strictures (3), pseudopolyps (3), cobblestoning (1), and nodularity (2) (data not shown).

Histology

Segmental mucosal biopsies were available in 11 of the 14 cases of amebiasis and all cases of IBD. Distribution of histological changes in the different segments is shown in [Table 4] and a summary of the salient mucosal changes in [Table 5]. The biopsy with the most severe change in each patient was used to compile the latter table.
Table 4: Segmental distribution of sites involved by amebiasis, CD, and UC on histology

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Table 5: Salient histological changes in patients with amebiasis, CD, and UC

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Superficial ulceration involving only part of the mucosal thickness was seen in all the cases of amebiasis. Deep ulceration lined by granulation tissue was present in 6. In 12 cases of amebiasis, parasites were located within necrotic material admixed with mucin, proteinaceous exudate, and blood clot overlying ulcerated mucosa or lying separately. This material was scanty in 4 and moderate to abundant in 8 [Figure 1]. The material was deeply basophilic in 2 cases. Trophozoites were also seen over intact mucosa in all cases. Tissue invasion was seen in only one case [Figure 2] and [Table 6].
Figure 1: Amebic parasites located within eosinophilic and basophilic necrotic material lining an ulcer (H and E stain. Original magnification ×100)

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Figure 2: Colonic mucosa showing tissue invasion by amebic trophozoites (H and E stain. Original magnification ×200)

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Table 6: Number and location of trophozoite forms of entamoeba in cases of amebiasis

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Necrotic materials lining ulcer was seen in only 3 cases of UC and 2 cases of CD and was scanty. It was never associated with mucin, proteinaceous exudate, or blood clot.

Surface epithelial changes such as shortening and tufting adjacent to sites of ulceration were more common in amebiasis [Figure 3] than in UC and CD. Epithelial shortening was moderate to severe in 11 cases of amebiasis and mild in 3 cases. In UC, on the other hand, shortening was more commonly mild (in 10) and moderate to severe in 4. In CD, it was mild in 6 and moderate to severe in 6. Mild epithelial tufting was seen in 7 cases of amebiasis and moderate to severe tufting in 6. In UC, this feature was mild in 6 and moderate to severe only in 1. CD had mild tufting in 5 and moderate to severe in 1. Intraepithelial neutrophils were common in amebiasis and UC (10 of 14 cases of amebiasis, 11 of 14 cases in UC, and 6 of 12 cases in CD). Intraepithelial lymphocytes were rarely increased.
Figure 3: Mucosa adjacent to a site of amebic ulceration with severe surface epithelial shortening and tufting (H and E stain. Original magnification ×400)

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Cryptitis and crypt abscess formation were seen in most cases. The prevalence of cryptitis was similar in all three groups. Crypt abscesses were rare in amebiasis and CD (a few seen in 5 cases each), but common in UC (many crypt abscesses in 6 cases and a few in 7).

In all cases of amebiasis and IBD, chronic inflammation was seen to involve the superficial and deep zones of the lamina propria. The inflammation in the deep lamina propria was only mild in 13 of 14 cases of amebiasis, whereas in the IBD cases, it was moderate to severe in 14 of 26 cases (3 cases of UC and 11 cases of CD).

Architectural alteration was seen in 5 cases of amebiasis and was always mild. In IBD, on the other hand, architectural alteration was mild in 3 cases of UC and 3 cases of CD, but moderate to severe in 11 cases of UC and 7 cases of CD.


   Discussion Top


Our study has identified some endoscopic and histologic features that could be useful in differentiating amebiasis from IBD. Discrete small ulcers, 2 cm or less in diameter, in the cecum or rectosigmoid, were the most common finding on endoscopy in patients with amebiasis in our series. Their presence in the absence of other findings should alert clinicians and pathologists to the possibility of amebiasis.

Ulcers with undermining edges and hemorrhagic material in their bases separated by normal mucosa are classically described as the mucosal change associated with amebiasis.[5],[6] It is possible that the lesions seen in our study were identified at an earlier stage than those described in previous studies. UC and CD, unlike amebiasis, show ulceration in association with other mucosal changes such as edema, erythema, loss of vascularity, friability, and nodularity.[7],[8] Amebiasis is also known to produce mass lesions called amebomas,[9] and malignancy was suspected in 3 of 14 cases in this series. Amebiasis can rarely present with perforation or toxic dilatation of the colon,[10],[11] but these forms of clinical presentation were not seen in our patients.

Amebic trophozoites invade the mucosa and digest the tissue.[12] This was evident in the mucosal biopsies as necrotic material admixed with mucin, proteinaceous exudate, and blood clot lining ulcers and was seen in all the cases of amebiasis reviewed. The necrotic material was seen in only in 3 cases of UC and in 2 cases of CD and was never abundant or associated with mucin, proteinaceous exudate, or blood clot in these cases. Trophozoite forms of ameba were seen in the necrotic material lining sites of ulceration, in separate fragments of necrotic material as well as over intact mucosa. Tissue invasion was seen only in one case.

Chronic inflammation and architectural alteration are the histological hallmarks of IBD. In infectious colitis, chronic inflammation is confined to the superficial part of the mucosa, unlike IBD that shows basal plasmacytosis.[13] All our cases of amebic colitis showed evidence of extension of chronic inflammation into the deep part of the mucosa, although the inflammation was mild in 13 cases and moderate only in one. In the IBD cases, on the other hand, inflammation in the deep mucosa was moderate to severe in 14 of 26 cases (3 cases of UC and 11 cases of CD).

The cases of IBD in our series frequently showed moderate architectural alteration. Architectural alteration was seen in all 14 cases of UC, 10 of 12 cases of CD, and 5 of 14 cases of amebiasis. In the latter patients, it was always only mild.

Significant surface epithelial changes such as shortening and tufting adjacent to sites of ulceration are known to be associated with infective colitis and were more common in amebiasis than in UC and CD in our series.[14]

Crypt abscesses were seen in both amebiasis and IBD, but were more likely to be present and were more frequent in the latter. In a study by Prathap and Gilman, crypt abscesses were not seen in any of the 53 rectal biopsies in acute amebic colitis.[15] But, in our study, a few crypt abscesses were seen in 5 cases of amebiasis. None of the cases of amebiasis in our study had numerous crypt abscesses. Crypt abscesses were seen in 13 of 14 cases of UC, of which 6 had many crypt abscesses. Of the 12 CD cases in our study, 5 had few, and 2 had many crypt abscesses.

A part of the failure to suspect amebiasis at the time of endoscopy could be attributed to the absence of the classical clinical features at the time of presentation. Detailed clinical records were available in 10 of the 14 cases of amebiasis. The classical history of chronic diarrhea with blood in the stools was seen in only 4 cases of amebiasis in our study. Two cases had diarrhea without blood in stool, and 2 cases had blood in the stools without diarrhea. One case had Ascaris on routine stool examination, and another had Entamoeba cyst, while the rest 7 cases checked were negative for 3 consecutive day routine samples. In 1 case, stool examination was not done. Examination of the stool for occult blood was not done in any of the cases. The diagnosis of amebic colitis in the majority of these patients was therefore determined by the endoscopic and biopsy findings.


   Conclusion Top


Discrete mucosal ulcers with intervening normal mucosa should raise a suspicion of colonic amebiasis, whereas the presence of mucosal changes around ulcers is suggestive of IBD. On histology, necrotic material admixed with mucin, proteinaceous exudate, and blood clot lining ulcers, significant surface epithelial changes such as shortening and tufting adjacent to ulcers, mild chronic inflammation extending into the deep mucosa, and mild architectural alteration are characteristic features of amebiasis. In countries where amebiasis is highly prevalent, cases with mild mucosal architectural alteration and mild chronic inflammation extending into the deep mucosa in the absence of other features of IBD should be screened thoroughly for amebic trophozoites, especially if ulceration is also present. Amebic trophozoites are most frequently located within the necrotic material, mucin, proteinaceous material, and blood clot lining ulcers.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
   References Top

1.
World Health Organization (WHO). Amoebiasis. WHO Wkly Epidemiol Rec 1997;72:97-100.  Back to cited text no. 1
    
2.
Petri WA Jr, Singh U. Diagnosis and management of amebiasis. Clin Infect Dis 1999;29:1117-25.  Back to cited text no. 2
    
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Pai SA. Amebic colitis can mimic tuberculosis and inflammatory bowel disease on endoscopy and biopsy. Int J Surg Pathol 2009;17:116-21.  Back to cited text no. 3
    
4.
Yoon JH, Ryu JG, Lee JK, Yoon SJ, Jung HC, Song IS, et al. Atypical clinical manifestations of amebic colitis. J Korean Med Sci 1991;6:260-6.  Back to cited text no. 4
    
5.
Pittman FE, el-Hashimi WK, Pittman JC. Studies of human amebiasis. II. Light and electron-microscopic observations of colonic mucosa and exudate in acute amebic colitis. Gastroenterology 1973;65:588-603.  Back to cited text no. 5
    
6.
Pittman FE, Hennigar GR. Sigmoidoscopic and colonic mucosal biopsy findings in amebic colitis. Arch Pathol 1974;97:155-8.  Back to cited text no. 6
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Powell-Tuck J, Day DW, Buckell NA, Wadsworth J, Lennard-Jones JE. Correlations between defined sigmoidoscopic appearances and other measures of disease activity in ulcerative colitis. Dig Dis Sci 1982;27:533-7.  Back to cited text no. 7
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Holdstock G, DuBoulay CE, Smith CL. Survey of the use of colonoscopy in inflammatory bowel disease. Dig Dis Sci 1984;29:731-4.  Back to cited text no. 8
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Hardin RE, Ferzli GS, Zenilman ME, Gadangi PK, Bowne WB. Invasive amebiasis and ameboma formation presenting as a rectal mass: An uncommon case of malignant masquerade at a western medical center. World J Gastroenterol 2007;13:5659-61.  Back to cited text no. 9
    
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Eggleston FC, Verghese M, Handa AK. Amoebic perforation of the bowel: experiences with 26 cases. Br J Surg 1978;65:748-51.  Back to cited text no. 10
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Wig JD, Talwar BL, Bushnurmath SR. Toxic dilatation complicating fulminant amoebic colitis. Br J Surg 1981;68:135-6.  Back to cited text no. 11
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12.
Ravdin JI. Pathogenesis of disease caused by Entamoeba histolytica: studies of adherence, secreted toxins, and contact-dependent cytolysis. Rev Infect Dis 1986;8:247-60.  Back to cited text no. 12
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13.
Schumacher G, Sandstedt B, Kollberg B. A prospective study offirst attacks of inflammatory bowel disease and infectious colitis. Clinical findings and early diagnosis. Scand J Gastroenterol 1994;29:265-74.  Back to cited text no. 13
    
14.
Talbot I, Price A, Salto-Tellez M. Assessment of abnormailities: diagnostic signposts. In: Biopsy Pathology in Colorectal Disease. 2nd ed., Ch. 3. London, England: Hodder Arnold; 2007. p. 14-53.  Back to cited text no. 14
    
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Prathap K, Gilman R. The histopathology of acute intestinal amebiasis. A rectal biopsy study. Am J Pathol 1970;60:229-46.  Back to cited text no. 15
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Correspondence Address:
Dr. Reecha Singh
Department of Pathology, Christian Medical College and Hospital, Vellore, Tamil Nadu
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0377-4929.168880

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    Figures

  [Figure 1], [Figure 2], [Figure 3]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]

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