Dr.Goswami,

Did you perform a biopsy from the ulcer edge? Any clinical manifestation? History?

Can be TB, Crohn's or malignancy.

How was the terminal ileum?

What is the histopathology and culture results for TB?

The two main hypotheses of malignancy or Crohn's find a full agreement. And it is obvious that a diagnosis needs absolutely histological examination. But the case is coming from tropical area. And you, @Amitava, mentioned many other possible causes. Could you let us know the most frequent?

I am agreed completely with Prof.Enzo.

Guessing attempts about the nature of this disease without the histopathological conclusion (and other laboratoral data) are unthankful and fruitless business. IMHO, the ulcer given at the picture above might not look like a malignancy or Crohn's, and might resembe to me that one after an X-ray therapy against the right kidney/ureter tumor. But this suggestion is very vague and is not worth anything without aforementioned investigations performed.

On the other hand, if Dr.Goswani possesses certain visual experience related to diagnostics of tropical or tuberbulosis caecal ulcers, why not to share it here with us?

Thank you in advance.

I agree that biopsies, laboratory and fecal culture data are very important to direct diagnosis.

I think that an imaging technique such as MRI or CT could help us to better understand the case.

Thanks everyone for wonderful participation.

I just  submitted this image to share that  Colonic involvement occurs in amoebic liver abscess. Colonic lesions are the primary sites of invasion for amoebic trophozoites. The penetrating trophozoites either invade superior mesentric vein or inferior mesentric vein and finally reaching liver through portal vein (streamline flow concept).

I have shown in my article  colonic involvement commonly in caecum and ascending colon and when it extends beyond hepatic flexure; multiple or bilobar liver abscess results. 

Dr.Goswami,

It is a brilliant study and pictures. Thank you very much. I have never seen amoebic lesions either in the colon, or in the liver. Now I know how they look like.

From that a simple conclusion follows that any patient with a liver abscess which is not evidently gallstone-related should have had the intestine examined including fibrocolonoscopy.

By the way, have you any idea why these amoebic lesions presented as local ulcers? Do they (the ulcers) develop on the lymphoid follicles like thypoid ulcers, or are there another mechanisms to take place?

Dr Andrey

Yes some work have been published on invasive mechanisms of entamoeba histolytica. The trophozoites secretes a N-Gal - lechitin to penetrate the colonic mucosa. Finally trophozoites make their way to vessels/ venules and later SMV/IMVPortal vein. Other cystenase or proteinase are also secreted by the active trophozoites. Lymphoid hyperplasia or ulcerations over payer patches has not been found till date. Amoebic trophozoites possibly has special tropism for colonic epithelium and mucosa. 

I see. Tropism, etc...

However, is there any idea to explain the patchy distribution of the amoebial lesion in the colon, and the sharp border of the ulcers along with visually unaltered mucosa?

Dr Andrey

Very true, amoebic ulcers are punched out with sharp borders and normal intervening area. Patchy nature of colonic ulcers is probably due multiple trophozoites acts adhere to colonic mucosa in patches. 

Are you sure about the trophozoite patches (a colony) in the colon, or is it just a speculation? As far as I can see, there are a pathc of the fibronoid necrosis (yellowish colour) and the left is the granulational tissue (pink colour). Where the amoebas live there, in the necrosis or on the gran.tissue?

Dr Andrew

Nice observation. Classically colonic histology shows necrotic epithelium with amoebic trohozoites at edges of ulcer and a variable inflammatory infiltrates. Throphozotes have an unique property of erythrophagocytosis (ingested RBC). 

So, the throphozoites move like a circular front of fire, and only the necrosis is left behind, do they? In that case, this may resemble the Streptococcian lesions of the skin and soft tissues in the necrotizing cellulitis/fasciitis (what used to be called 'severe forms of the erysipelas').

How many colony-forming units (or how throphosoids can be counted) are in the edge of the colon ulcer?

In histology trophozoites may be seen clusters (10-20 /hpf) depending on the biopsy sample. So biopsy from edges of ulcer are more diagnostic than other areas. Erythrophagocyosis is the hallmark for entamoeba hystolitica. Sometimes trophozoites are missed completely and are confused with inflammatory bowel disease, but cryptic architecture is not altered

Interestingly, taking in mind that hemoglobin is rather toxic a substance with properties of mineral acid. How they do protect from that vulnerable effect? Do they not have a kind of NADPH or bilirubinsinthaze in the way of the splenic residual macrophages?

So pathogenesis of colonic ulcers in entamoeba histolytica with special reference to erythrophagocytosis may be an open area for future research. I may go for it in near future. Thanks for sharing your views.

As commonly known, the acetic ulcer model was been developed by Susume Okabe in the 60th [PMID: 16079471]. Perhaps, the entamoeba may produce some acid metabolytes those can destroy the colon wall layers for the ulcers to occur there.  Unfortunately, I do know nothing about this tropical creature metabolic ways: what it eats, what it excretes?

And one more thing: Have you experience of the colon stricture lead to the obturation and subsequent surgery due to the amoebial colitis?

Solitary caecal (better paravalvular) ulcer is well known.

In metropolitan France, it is usually idiopathic,sometimes to slow-release NSAID tablets rarely and  due to Behçet's disease.

It is very frequently asymptomatic and, when idiopathic, disappears within 2 months.

When NSAID induced, cicatrization occurs with 1 month after withdrawal.

In the my case of Behçet's, it has disappeard within 2 weeks after starting amiodarone for arrythmia, in parrallel with aphtous buccal ulcers.