What Is Amebic Colitis?
Amebic colitis is the invasion of the mucosa of the colon by Entamoeba histolytica. Amebic colitis differs from bacterial dysentery in that it manifests symptoms gradually throughout one to two weeks. The most typical symptom is diarrhea. In addition, patients with amebic colitis often experience stomach cramps, pain, bloody or watery diarrhea, and weight loss. A few patients present with fever as well. Rectal cancer and acute appendicitis can both be mistaken for intestinal amebiasis. However, rectal bleeding can happen without diarrhea, especially in young children.
One of the rare complications of amebic colitis is fulminant amebic colitis. It quickly develops into severe bloody diarrhea and abdominal discomfort. Fever is also present. Poor nutrition, pregnancy, corticosteroid usage, and young age (less than two years) are risk factors for fulminant colitis. Intestinal perforation is commonly seen. A risk factor for the occurrence of fulminant forms of amebic colitis is corticosteroid medication. Sometimes, diarrhea is absent, which makes diagnosis more challenging. It has a high mortality rate.
Clinically, chronic amebic colitis resembles inflammatory bowel disease (IBD). People with chronic amebic colitis with antibodies to Entamoeba histolytica experience recurrent episodes of bloody diarrhea and vague stomach discomfort. Before treating suspected inflammatory bowel disease, amebic colitis should be ruled out because corticosteroid therapy worsens amebic colitis.
What Is the Pathophysiology of Amebic Colitis?
Entamoeba histolytica causes amebic colitis. It is a protozoal parasite. It is a pseudopod-forming and non-flagellated protozoan that can cause host cell apoptosis, tissue lysis, and proteolysis. A replicative trophozoite stage and a dormant cyst stage are both present in Entamoeba histolytica. The activated feeding stage of protozoa's life cycle is known as a trophozoite. After being ingested from the environment, Entamoeba histolytica cysts undergo excystation (stage present in a newly infected host where the sporozoites are released from the sporocytes) in the terminal ileum or colon to create extremely mobile trophozoites. The trophozoite may infiltrate the intestinal mucosal barrier and obtain access to the bloodstream. It subsequently spreads to the liver, lung, and other locations, or it may encyst and be expelled in the feces after colonizing the colon. Finally, the cysts that have been excreted reach the environment to finish the cycle. The interaction between the host's protective mechanisms and the parasite's virulence is assumed to be the cause of developing an invasive amebic infection in a few people. The following three main virulence factors are known to affect pathogenicity:
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N-Acetylgalactosamine Inhibitable Lectin - A galactose/N-acetylgalactosamine inhibitable lectin (a protein that binds to carbohydrates) appears to mediate trophozoite adhesion to colonic epithelial cells. Mucosal immunoglobulin A (IgA) response against the lectin can result in less recurrent infection.
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Amebapore - These tiny peptides make it easier to kill host cells. They exhibit cytolysis and create pores in the lipid bilayer.
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Cysteine Proteases - These proteases cause disintegration and rupture of the extracellular matrix of the host cell membrane. The invasion and inflammation of the gut have been directly linked to cysteine proteinases, which may also increase interleukin-1-mediated inflammation by imitating human interleukin activity-converting enzymes. In addition, the anaphylatoxins C3a and C5a, as well as IgA and immunoglobulin G, are also broken down and rendered inactive by the cysteine proteinases.
As the disease progresses, the infected mucosa becomes inflamed, edematous, and necrotic. Sometimes it may cause perforation of the wall of the intestines. Other changes seen in the pathogenesis of amebic colitis include:
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Epithelial cells produce inflammatory mediators like interleukin1, interleukin-8, and cyclooxygenase (COX)-2 that attract neutrophils and macrophages. The corticosteroid medication suppresses the innate immune response and worsens the clinical outcome.
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The disease also affects the other host defense system of the body, like the complement system. It has been proven that trophozoites directly inhibit these defense mechanisms.
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In response to the disease, serum antibodies can develop in 7 days and last up to 10 years. In addition, when invasive amebiasis is present, a mucosal IgA response to Entamoeba histolytica occurs.
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Cell-mediated immunity is crucial for controlling the illness and avoiding recurrences. Antigen-specific blastogenic responses occur, resulting in the synthesis of lymphokines, including interferon-delta, which activates the macrophages' ability to destroy Entamoeba histolytica trophozoites. Contact, oxidative pathways, nonoxidative pathways, and nitric oxide (NO) all play a role in this death.
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Lymphokines like TNF-alpha activate the neutrophilic activity of killing amoeba.
What Is the Histopathology of Amoebic Colitis?
Amoebic colitis can affect any part of the bowel, but the most common sites are the cecum and ascending colon. Few cases may see the involvement of the large bowel extending into the terminal ileum. Ulcers caused due to the amoeba appear flask-shaped, and inflammatory cells can be seen below the ulcer.
Usually, the parasites are round or oval-shaped and measure from 1.9 to 1.31 feet. They have many vacuolated cytoplasms, small nuclei, and a conspicuous nuclear membrane. The organism's cytoplasm appears clear and devoid of ingested bacteria and vacuoles in a trichrome stain. The small central karyosome and the finely granular nuclear chromatin, which show even distribution across the nuclear membrane, stain a dark purple-red. Ingested red blood cells can be detected in Entamoeba histolytica trophozoites but are typically absent. Furthermore, periodic acid-Schiff (PAS) and immunoperoxidase stains can be used to identify the organisms.
How Does Entamoeba Histolytica Enter the Body and Harm Its Cells?
Entamoeba histolytica is toxic to certain cells like neutrophils (in the early stage of invasion), T-lymphocytes, and macrophages (in the later stages of invasion). The organism attaches to the intestinal mucosa, crosses the mucosal barrier, causes contact-dependent death, and incites intestinal cell apoptosis. The cell is lysed and phagocytosed by the organism. The invasion of the deeper layers of the intestinal wall is mediated by cysteine proteases, which break down fibronectin and collagen. Proinflammatory cytokines are secreted by the host, which causes an immediate inflammatory response and the migration of neutrophils and macrophages into the tissue. Moreover, the organism is capable of secreting chemoattractants for neutrophils. The intestinal mucosa is further harmed due to the release of lysozymes, superoxides, and collagenases from the neutrophil granules after it kills these cells by contact-dependent lysis.
What Is the Treatment of Amebic Colitis?
Combination therapy is necessary to treat amebic colitis. The available therapies include luminal medicines mixed with tissue amebicides. A few luminal amebicides are Iodoquinol, Diloxanide Furoate, and Paromomycin. Some tissue amebicides are Nitroimidazole (Metronidazole), Nitazoxanide, Erythromycin, and Chloroquine. Surgery is recommended for the patient with a liver abscess requiring drainage. It is also an emergency with toxic megacolon.
Conclusion
Given the great danger of developing an invasive infection and the risk of spreading the infection to other family members, all symptomatic and asymptomatic cases of Entamoeba histolytica infection should be treated. Amebic colitis may cause necrotizing colitis, peritonitis, bleeding, bowel perforation, and stricture formation, which can be fatal if not treated timely. In most patients, a cure is feasible with drug therapy. However, the mortality rate is high without proper treatment with medication. With drug treatment, recovery could take a few weeks or months.
