amebiasis, amebic colitis, metronidazole
C Gideon. Amebic Colitis. The Internet Journal of Advanced Nursing Practice. 2007 Volume 9 Number 2.
Amebic colitis, also known as amebiasis, is a gastrointestinal disorder caused by invasion of the intestine by the protozoan parasite,
Definition and Epidemiology
Amebic colitis, also known as amebiasis, is a protozoal disease affecting the large intestine caused by
Amebiasis affects both adults and children equally (2). In the U.S., most cases are found in people who have recently traveled to developing countries where food and water sanitation are less sophisticated (2). Once infected, an individual can easily pass the protozoan on to other family members in the household (2).
Trophozoites begin to attach to the epithelial cells of the colon by releasing D-galactose/N-acetyl-Dglactosamine (Gal/GalNAc), which allows adherence to the epithelial surface of the colon (7). Cysteine proteinases from the trophozoite causes the mucus lining of the colon to disperse and the affected epithelial cells quickly begin to lose their structure (7). The trophozoite uses structures called amebapores to puncture the epithelial cell's phospholipid bilayer, causing cytolysis (2). Lysed cells release pre-Interleukin 1ß, which is degraded by amebic cysteine protease to form Interleukin-1ß (IL-1ß), a cytokine (8). IL-1ß then attaches to adjacent epithelial cells, causing them to release the cytokines cycloexegenase-2 (COX-2) and Interleukin-8 (IL-8) (2). These substances attract neutrophils, which squeeze into the intestinal lumen from the mucosa by creating a passage between the epithelial cells, providing an entryway for the amebae to enter the colonic mucosa. Neutrophils, killed when exposed to
Trophozoites are also able to cause host cell death by causing the cell to enter apoptosis, or programmed cell death. This process adds to the ability of the ameba to invade the mucosa via channels created by macrophages called to destroy the dying epithelial cell (6). Once in the host's mucosa, the trophozoite is able to continue its tissue destruction in a lateral direction. This destruction results in an ulcer that is characteristically “flask-shaped,” with a wide base and a thin neck that extends to the intestinal lumen (6). This ulcer produces bloody stools that are a hallmark of amebic colitis (2). The host is at risk of developing paralytic ileus, sloughing of colonic mucosa, and perforation of the GI tract, causing fulminant amebic colitis, which has a mortality rate of greater than 40% (2). Toxic megacolon may also develop, particularly if the patient has been treated with corticosteroids, which inhibit the inflammatory process and allow
Brain abscesses due to amebic invasion are rare, with death occurring in about half of patients developing this complication (2). Trophozoites are able to encase themselves in cysts, which are then excreted in the feces. An individual coming into contact with the infected feces is then at risk for developing amebiasis (4).
Signs and Symptoms Often Encountered in the Emergency Department
The typical amebic colitis patient presents to the emergency department (ED) with a chief complaint of abdominal cramping. History of the present illness usually presents as a sudden onset of fever, abdominal pain, and diarrhea that may be bloody (5). Social history should include questions about any recent travel outside the U.S., particularly to underdeveloped countries, as well sexual practices, particularly anal-oral intercourse (4,5). Review of systems may reveal a recent bout of nausea and vomiting, fever, weakness, and unintentional weight loss. An accurate past medical should be obtained, as comorbidities such as acquired immune deficiency syndrome (AIDS) can severely impair the patient's ability to fight the infection (5). Physical exam of the patient may reveal a person in mild to severe distress with profuse diarrhea that is guiac positive and sometimes containing frank blood. Cramping abdominal pain with distension and rebound tenderness may also be present (3). Orthostatic hypotension may also be present due to fluid loss from diarrhea (3).
Differential diagnoses for this type of patient may include
Giardiasis is caused by the protozoan
Shigellosis can be found worldwide, particularly in countries with poor water sanitation. Seventy-five percent of U.S. cases are caused by the bacterium
Ulcerative colitis, a type of inflammatory bowel disease (IBD), typically presents with bloody diarrhea. The patient usually does not complain of abdominal pain, but is often anemic, leading to fatigue. The lack of abdominal pain helps to rule out this disease process (12).
Crohn's disease, another form of IBD, usually presents with abdominal pain, bloody diarrhea, anemia, and weight loss. Contrast radiography using barium enemas has been useful in identifying the characteristic “skip lesions” and cobblestone-like appearance found in the colon. Normal findings from the barium enema studies help to rule out both ulcerative colitis and amebiasis (12).
Diagnostic Test for Amebiasis
Historically, testing for amebiasis was done using visualization with the presence of the characteristic ameboid protozoan in the patient's stool confirming the diagnosis. This method has since become non-diagnostic in the U.S. with the discovery of
Picture used with permission from DPDx: CDC's Web site for parasite identification http://www.dpd.cdc.gov/dpdx
Link to DPDx Amebiasis webpages:
Conclusive diagnosis of
Colonoscopy may be helpful if stool tests for
Many areas where amebic colitis is endemic do not have the resources to afford the ELISA test, and may not have access to equipment needed for a colonoscopy. In these situations, accurate microscopy coupled with the clinical presentation for acute amebic colitis may provide enough evidence to treat the patient for the disease. If microscopy were not available, the clinical signs and symptoms of amebic colitis may be the only information available to diagnose the patient, and treatment for amebic colitis should be initiated.
Standardized Treatment Plan for Amebic Colitis
Maintenance of the airway, breathing, and circulation must be monitored at all times while in the ED. Treatment of amebic colitis involves the prescription or administration of several drugs. Patients with mild colitis (not needing intravenous [IV] fluid therapy) may be treated on an outpatient basis with metronidazole (Flagyl) 750 mg orally three times daily for 10 days (3). This treatment should be a followed by luminal agent such as the aminoglycoside paromomycin (Humatin) to destroy the cysts in the intralumen. Dosing of paromomycin is 25-35 mg/kg orally three times daily for seven days (3). Taking these two medicines at the same time is not recommended, as paromomycin may cause diarrhea and may become difficult distinguish from the signs of amebic colitis (11).
The use of loperamide (Imodium) is discouraged. Loperamide slows the ability of the intestinal smooth muscles to move, allowing increased water uptake in the colon for the typical diarrhea case (14). However, decreased smooth muscle activity increases the time the luminal wall is exposed to
Patients with severe colitis should be admitted to the hospital and given intravenous (IV) hydration (3). Normal saline with 5% dextrose may be useful for severe volume depletion as well as providing glucose lost to diarrhea. Potassium should be replaced if the patient is found to be hypokalemic because of the diarrhea. Admitted patients should receive metronidazole 500 mg IV every six hours for ten days (11). In the case of fulminant amebic colitis, broad-spectrum antibiotics should be given in addition to metronidazole, particularly if intestinal perforation is suspected (16). Ciprofloxacin (Cipro) may be given IV at 400 mg every eight hours (17).
Metronidazole is the most effective medication for treating amebic colitis. This agent is effective only against obligate anaerobic organisms. The trophozoite phase absorbs the inactive form of the drug, transforming this agent to the active form. The active form then causes degradation of the anaerobe's DNA, eventually causing death of the organism. Death of
Side effects of metronidazole include nausea, headache, and dry mouth. Consumption of alcoholic beverages can cause severe and intractable vomiting (16). Use of cimetidine (Tagamet) may increase plasma levels of metronidazole due to cimetidine's ability to inhibit enzyme activity (3). Metronidazole may also synergistically act on warfarin, resulting in prolonged bleeding times (11).
Paromomycin is an aminoglycoside antibiotic. Aminoglycosides disrupt protein synthesis in aerobic bacteria, causing cell death. Although
Paromomycin's primary side effect is diarrhea, but this drug may also cause nausea and abdominal pain (20). Nephrotoxicity may result if paromomycin is used with other aminoglycosides, penicillins, or loop diuretics (11). Paromomycin may decrease plasma levels of digoxin (3).
Ciprofloxacin is a fluoroquinolone, a class of broad-spectrum antibiotics. This class inhibits bacterial DNA gyrase, preventing DNA from uncoiling from its normal supercoiled state. Unable to uncoil, DNA is incapable of replicating and producing new strands for daughter cells (18).
The side effects of ciprofloxacin side effects include nausea, vomiting, and diarrhea (18).
Non-Medical Treatment Methods
An herbal remedy used in Mexico for amebiasis is chaparro amargo, scientific name
Health Promotion and Lifestyle Considerations
Patients with amebic colitis must take care to prevent passing the
Any person traveling to a developing foreign country should be counseled about prevention of amebic colitis. All unbottled water should be boiled prior to consumption or other use (3). Typical chlorine treatment alone is ineffective at destroying amebic cysts (11). Eating raw vegetables should be discouraged (11). Vegetable preparation includes washing with soap and water, then placing them in vinegar for 10-15 minutes prior to cooking (3).
Amebic colitis can present a true medical emergency for the advanced practice nurse (APN). Accurate history taking, including questions of recent travel to underdeveloped countries, is essential (4). Microscopy of stool samples for evidence of
The author would like to thank the following individuals for their encouragement and assistance in editing this manuscript: Elda G. Ramirez, PhD, RN, APRN,BC, CEN, FAANP and Susan D. Ruppert, PhD, RN, APRN,BC, NP-C, FCCM.