Furoxone

Protozoa, a diverse group of single-celled primitive organisms, may cause gastrointestinal illness that is spread by poor sanitation. Although such illnesses have traditionally occurred in underdeveloped countries, they are becoming more common in the United States. Protozoal intestinal illness is usually diagnosed by examination of the stool for ova and parasites. In practice, however, the diagnosis is often missed or delayed because of intermittent cyst passage and false-negative stool examinations. In other cases, the responsible organism may simply be overlooked. Symptoms often resolve spontaneously, but even when an organism is identified, confusion often arises regarding the need for treatment and treatment alternatives.

Currently, the three most important causes of protozoal intestinal illness in the United States are Giardia lamblia, Entamoeba histolytica and Cryptosporidium parvum, but other protozoa may become increasingly significant pathogens as the epidemic of human immunodeficiency virus (HIV) infection and acquired immunodeficiency syndrome progresses (Table 1).

[TABULAR DATA 1 OMITTED]

Giardiasis

Giardia lamblia is the most clinically significant protozoal pathogen in the United States. Outbreaks have been associated with improper food handling, day care centers and compromised municipal water supplies, and have also been associated with contaminated beaver ponds and springs.[1] In all of these situations, cysts from animal or human feces are transferred to the mouth via contaminated hands, food or water. Travelers are also vulnerable to this infection, and some urban water supplies, such as that in St. Petersburg, Russia, are known as a source of giardia infection.[2] Patients with immunoglobulin deficiencies are particularly susceptible to infection. Sexual activity, usually homosexual, has also been associated with transmission.[3]

Once cysts are ingested, the trophozoite, or active motile form of the parasite,. emerges in the small intestine (Figure 1). The trophozoites rapidly multiply and attach themselves to the intestinal villi. Symptoms begin within one to two weeks. While the oval, refractile cysts contain four nuclei, the tear-drop-shaped, flagellated trophozoites have two eye-like nuclei and transverse median bodies, so that they look like tiny faces.[4]

Both Giardia trophozoites and nomnotile cysts may be found in stools, although the trophozoites soon perish. Living trophozoites are best seen in fresh duodenal fluid aspirate. Formed stools usually contain only cysts, which are highly infectious and environmentally stable, persisting for at least five weeks when stored in water at 8[degrees]C (46.4[degrees]F).[2]

CLINICAL FEATURES

Symptoms of giardiasis usually include cramping and diarrheal stools, often with excessive flatus with an odor of hydrogen sulfide (rotten eggs). Abdominal bloating with sulfur-odor eructation, nausea and anorexia are more common symptoms of giardiasis than diarrhea. It is very unusual for Giardia infection alone to cause severe abdominal pain, fever or dysentery.[5,6] Symptoms may persist for months, then resolve spontaneously. Conversely, some asymptomatic hosts persistently excrete cysts.

DIAGNOSIS

The diagnosis of giardiasis is usually confirmed by stool examination. Since cyst passage may be intermittent, a single negative stool examination for ova and parasites never rules out infection.[6] If Giardia infection is suspected, at least three examinations should be performed over a one-to two-week period. An enzyme-linked immunosorbent assay (ELISA) for Giardia antigen in the stool is a more accurate method of identifying Giardia but cannot diagnose other parasitic infections. Both a stool examination for ova and parasites and an ELISA for Giardia antigen are recommended to investigate possible parasitic gastrointestinal infections.[6]

In diagnostic dilemmas, duodenal aspiration or the Enterotest may demonstrate Giardia. In the latter test, the patient swallows a gelatin capsule containing a nylon string, with one end of the string attached to the patient's cheek. After about six to eight hours, the string is removed, and any adherent fluid is placed on a slide for microscopic examination. The Enterotest is an accurate, inexpensive option for the diagnosis of giardiasis in a cooperative patient.[6]

Some physicians resort to presumptive treatment of giardiasis in high-risk symptomatic patients before confirmation. Although this approach can be effective, giardiasis can be confused with irritable bowel syndrome, traveler's diarrhea caused by enterotoxigenic Escherichia coli, disaccharidase deficiency, malabsorption, pancreatic insufficiency and other diarrheas of parasitic origin.

TREATMENT

Giardiasis may be treated with oral metronidazole (Flagyl), 250 mg three times daily for five to 10 days (pediatric dose: 15 mg per kg per day in three doses), or, until recently, quinacrine (Atabrine), 100 mg three times per day after meals for five days (pediatric dose: 7 mg per kg per day in three doses, with a maximum dose of 300 mg per day).[7] Both treatments are usually well tolerated in adults and are over 90 percent effective. Quinacrine, however, is no longer available in the United States.

Metronidazole may cause nausea, vomiting, a metallic taste in the mouth or a reaction with alcohol similar to the reaction with disulfiram (Antabuse). It is also contraindicated in at least the first trimester of pregnancy. Quinacrine, on the other hand, may produce dizziness, psychosis, gastrointestinal side effects (especially in children) and a temporary yellow discoloration of the skin. In the case of treatment failure, use of the alternative drug is an option or a longer course may be used.

Furazolidone (Furoxone), 100 mg four times daily for 10 days (pediatric dosage: 6 mg per kg per day, in four doses, for seven to 10 days), is also effective, and its suspension form is especially useful for treatment of children under the age of five.[8] Tinidazole (Fasigyn), a single dose of 2 g (not available in the United States), and paromomycin (Humatin, Aminosidine) are alternative treatments. Paromomycin is less effective but, because it is nonabsorbable, it may be useful to control Giardia populations in very symptomatic pregnant women in the first trimester.[9] Metronidazole may be considered for use later in pregnancy only if symptoms warrant but the other agents are contraindicated. Asymptomatic persons usually do not clinically require treatment, but prompt intervention reduces cyst passage and possible transmission, particularly when food handlers, homosexual persons, institutionalized patients and children attending day care and day-care workers are involved.

OTHER FLAGELLATES

Other flagellate intestinal pr-otozoa such as Chilomastix mesnili, Trichomonas hominis and Retortamonas intestinalis are less well known than Giardia, but they can also occasionally be found in the human intestine, although they usually do not cause disease.[4]

Dientamoeba fragilis is a cosmopolitan ameba-like organism, recently reclassified as an atypical flagellate. Infection with D. fragilis is now known to be much more common than was previously thought, even in the U.S. population. Since it disappears very rapidly after stool passage, it is easily missed on routine stool examinations but can be detected in fresh or immediately preserved specimens. Its mode of transmission is uncertain since it is not known to form cysts, but an association with pinworms exists in many patients. D. fragilis is now generally considered to be a potential pathogen, especially in children, producing mild diarrhea, nausea, abdominal discomfort, weight loss and eosinophilia.[10] No well-accepted treatment is available for symptomatic cases, but paromomycin, 25 to 30 mg per kg per day in three doses for seven days, or iodoquinol (Yodoxin), 650 mg three times per day for 20 days, may be useful.[7] Tetracycline, 500 mg four times per day for 10 days, appears effective and may become the treatment of choice, with erythromycin being substituted in the treatment of pregnant women and younger children.[8]

Amebiasis

Entamoeba histolytica is now less common in the United States but is still common in most tropical regions. This organism may cause either a simple colitis or severe amebic dysentery, an invasive ulceration of the lower large intestine. Amebic dysentery is a life-threatening illness if untreated or misdiagnosed. In the United States, overseas travelers, recent immigrants, institutionalized populations and male homosexuals are considered to be at higher risk.[3]

Like giardiasis, amebiasis is a protozoal disease easily spread by contaminated water or other fecal-oral means (Figure 2). Also like Giardia, there is a motile trophozoite phase in the intestine and a durable infectious cyst that survives passage in the stool, remaining viable for at least three months in cold water.[3] Trophozoites do not survive outside the body and usually disappear from the stool within 30 minutes of passage. The E. histolytica trophozoite measures 25 to 50 [mu]m and has a single nucleus with a centrally placed endosome. With its mobile pseudopods, rapid movement and ability to engulf food, it closely resembles the familiar free-living ameba commonly studied in biology classes. Pathogenic amebas, however, are capable of invading tissue and often contain host red blood cells. Their cysts measure an average of 12 [mu] in diameter and are best distinguished from the cysts of nonpathogenic ameba species by evaluation after iodine staining.

CLINICAL FEATURES

Symptoms of infection with E. histolytica begin about two to four weeks after cyst ingestion, although the majority of patients are believed to remain asymptomatic. Those who do become ill usually have a noninvasive colitis characterized by diarrhea, cramping and fatigue, perhaps with mild tenderness of the right lower quadrant. Amebic dysentery, on the other hand, is often of sudden onset one to three weeks after exposure, with severe cramping, tenesmus, fever, bloody stools with mucus, and generalized abdominal discomfort. Physical findings may include a tender mass in the right lower abdomen, called an ameboma, which is believed to be related to granulation tissue. Symptoms resemble those of ulcerative colitis and, on sigmoidoscopy, the openings of flask-shaped ulcerations may be visualized in the proctosigmoid colon.[3] Tender hepatomegaly may also be noted, but actual amebic liver abscesses are unusual in this country. Although fever, elevated erythrocyte sedimentation rate, elevated alkaline phosphatase level and abdominal tenderness may be found in association with both dysentery and amebic liver abscess, the latter condition is distinguished by more severe pain, a significant mass effect and a positive hepatic ultrasound or computed tomographic scan. The abscess usually develops in the right lobe of the liver, often without a previous history of colitis or dysentery.[11]

Amebiasis can mimic many conditions besides inflammatory bowel disease; occasionally, it may present as a sexually transmitted infection with painful genital ulcerations that may resemble squamous cell cancer.[3] Amebomas of the intestine may often resemble colon cancer on radiography or colonoscopy and, very rarely, the amebas may metastasize to the lung, pericardium or brain, mimicking diseases of these sites.[12] Diagnosis is made microscopically by testing for stool ova and parasites (in the case of diarrhea) or by anal swabs, ulcer fluid aspiration or tissue biopsy during sigmoidoscopy. Serologic testing is available at specialized laboratories.[11]

TREATMENT

Treatment of amebiasis depends on whether the infection is believed to be limited to the intestinal lumen or invasive in nature. Iodoquinol, 650 mg three times per day for 20 days (pediatric dosage: 30 to 40 mg per kg per day in three doses for 20 days), is recommended for noninvasive intestinal disease. Side effects may include gastrointestinal distress and, rarely, optic neuritis. Metronidazole, 750 mg three times per day for 10 days (pediatric dose: 35 to 50 mg per kg per day in three doses for 10 days), is effective for invasive disease or hepatic abscess.[7] Such high doses of metronidazole frequently precipitate gastrointestinal distress. Since metronidazole is contraindicated in at least the first trimester of pregnancy and the effects of iodoquinol in pregnancy are unknown, treatment of amebiasis, in early pregnancy is often problematic and entails weighing fetal-maternal risk in invasive disease. However, paromomycin appears to be a safe, nonabsorbed alternative for noninvasive intestinal disease in the first trimester.[9]

In practice, metronidazole and iodoquinol are usually administered together to the nonpregnant patient with symptomatic intestinal disease, since metronidazole alone fails to eliminate the luminal phase. Right lobe liver abscesses may require treatment with percutaneous aspiration if they are very large and tender or if no response to medical therapy is achieved in 72 hours.[3] Aspiration yields a characteristic anchovy sauce" brown sludge, which is odorless and usually negative for organisms except at the abscess periphery. A course of metronidazole or, alternatively, dehydroemetine (not available in the United States), followed by chloroquine can be used in the treatment of amebic liver abscess.[7]

It has long been known that nonpathogenic strains of E. histolytica exist that are morphologically indistinguishable from the pathogenic types and, therefore, treatment of asymptomatic patients has been controversial. Those who suggest that such treatment is indicated are concerned that nonpathogenic strains may be transformed into pathogens by unknown host factors.[3]

OTHER ENTAMOEBA

Nonpathogenic E. hartmanni is identical to E. histolytica in everything but size, with trophozoites measuring 8 to 10 [mu]m and cysts 6 to 10 [mu]m.[12] Another nonpathogenic ameba, Entamoeba coli, is a fairly common intestinal commensal, and infection also requires no treatment. Entamoeba coli is usually slightly larger than E. histolytica and may be distinguished, when alive, by its short pseudopods and sluggish motility. In addition, fixed specimens have a coarser cytoplasm and an eccentrically placed endosome, and ingested host red blood cells are absent. Cysts are also usually larger than those of E. histolytica (15 to 20 [mu]m) and contain one to eight nuclei. Within the cyst nucleus, the endosome is eccentric rather than centrally placed as in E. histolytica.[12] Three other nonpathogenic amebas may be found in the human intestine: Endolimax nana, Iodamoeba butschlii and Entamoeba polecki. E. nana is a slug-like ameba, 8 to 12 [mu]m long, with a single nucleus containing a large, blot-like endosome. Cysts are round, measuring 7 to 10 [mu]m, with one to four nuclei.

Cryptosporidiosis

Cryptosporidium parvum, although little known until recently, is now recognized as the agent responsible for significant but self-limited diarrheal disease in the United States. hi the presence of acquired immunodeficiency syndrome, however, this normally restrained pathogen becomes intractable and life-threatening.[3] Cryptosporidium is a non-host-specific, intracellular coccidian measuring 2 to 6 [mu]m that infects the epithelial cells lining the entire digestive tract, especially those of the small intestine. It is readily spread by oocysts which, after being passed in the feces, are extremely resistant to chlorination and other methods of water purification. The spherical, refractile oocysts measure 4 to 8 [mu]m and contain four slender sporozoites. They are best identified in modified Kinyoun acid-fast stains of the stool specimen since they do not stain with iodine. They are often missed or confused with harmless yeast (which are not acid fast and which do stain with iodine) and, indeed, were not recognized as an important cause of gastroenteritis until 1976.[8]

Cryptosporidium outbreaks have been associated with contaminated municipal water supplies,[13] day care centers,[8] Swimming pools[14] and animal contact.[8] Cryptosporidium is a common cause of "scours" in farm animals (especially calves) and can be spread as a zoonosis.[15] It is one of many causative agents of traveler's diarrhea overseas and is increasingly being recognized as a troublesome persistent contaminant of our domestic water supply.

CLINICAL FEATURES

When infected, healthy individuals may have watery diarrhea lasting up to 14 days, often accompanied by vomiting, cramps and flu-like symptoms. This is followed by spontaneous resolution, although cysts may be passed for another two weeks. Nearly all cases go undiagnosed, but no treatment is usually required. Peak incidence is in the late summer and early fall.[16] In the immunocompromised patient, cryptosporidiosis is a far different problem. The hallmark symptom is profuse watery diarrhea that lasts for months and leads to emaciation and,,at times, pulmonary involvement as wen. Cryptosporidium clearly appears to be associated with the "slim disease" of African patients with AM.16

TREATMENT

Cryptosporidium is resistant to drugs usually used in antidiarrheal therapy since there is no proven treatment for Cryptosporidium in patients with AIDS. Spiramycin (Rovamycine), 1 to 3 g per day for two weeks or longer, has been used with some success, as has octreotide (Sandostatin), 300 to 500 mg three times per day subcutaneously, but only in the control of Symptoms.[7] Paromomycin, 500 mg orally every six hours for 14 days, is perhaps the most promising agent for control.[20] Azithromycin (Zithromax), 1,250 mg daily for two weeks followed by 500 mg per day, has also been reported as effective.[7]

OTHER COCCIDIA

Isospora. Isospora belli is an uncommon coccidial intestinal pathogen that, like Cryptosporidium, has gained a certain notoriety with the advent of AIDS. Isosporiasis may rarely occur in healthy travelers or immigrants from Africa, tropical South America and Haiti, but its presence should always arouse suspicion of AIDS or immunodeficiency. Like Cryptosporidium, Isospora causes a self-limited diarrhea in healthy hosts. Oocysts spread the infection in contaminated food or water, but no animal reservoir is yet known. Isospora cysts are occasionally mistaken for the far more familiar Giardia cysts; however, when mature, they contain two sporocysts, each of which contains four elongated sporozoites.[8] In immunocompromised patients, infection with Isospora may result in serious, persistent watery diarrhea. The treatment of choice is frimethoprim-sulfamethoxazole DS (Bactrim, Septra), 160 mg/800 mg four times daily for 10 days, then twice daffy for three weeks.[7]

Sarcocystis. Sarcocystis spicies are coccidian parasites that are occasionally found in human intestine or muscle. Their life cycle involves a definitive, carnivorous host (in which the sexual/intestinal phase takes place) and an intermediate herbivorous host, such as cattle. Humans may serve as either definitive or intermediate hosts. Infection occurs when sporocysts in undercooked meat are consumed. Immunocompetent hosts may have self-limited diarrhea and shedding of sporocysts (measuring 11 x 16 [mu]m) in the stool. Like Isospora, this obscure infection may become more significant with the AIDS epidemic. Trimethoprim-sulfamethoxazole has been used to treat the intestinal disease.[8,18]

Microspora. Microsporidiosis describes various Aids-related intracellular coccidian protozoa such as Enterocytozoon bieneusi and Septata intestinalis, which infect the intestine, causing significant diarrhea and weight loss.[8] Therapy with albendazole (Zentel), 400 mg twice daily, is helpful but may not eradicate infection.[19] New intestinal coccidian pathogens such as Cyclospora (previously identified as cyanobacteria-like bodies) appear to be continually emerging from the tropics, and it is likely that even more will be described in the near future.[20]

Balantidiasis

Balantidium coli, the largest protozoan affecting humans, is a ciliated organism often associated with pigs. The greenish-yellow trophozoites may measure up to 120 x 150 [mu]m and are capable of attacking the intestinal epithelium, creating ulcers and causing bloody diarrhea similar to that of amebic dysentery. A variety of gastrointestinal symptoms, including cramping, abdominal pain, nausea and foul breath, also occur. Encystment usually occurs in the intestinal lumen or stool (human or swine), and the large round cysts (40 to 60 [mu]m) transmit the infection when ingested in food or water. Pigs act as carriers and are not often adversely affected by this organism.[21]

Fortunately, balantidiasis is uncommon in temperate climates. It is found in association with pigs throughout the tropics, especially the Philippines.[21] Evidence indicates that some infected humans may become asymptomatic cyst passers, whereas others clear the infection spontaneously. As with amebiasis, this condition probably runs the gamut between mild colitis and severe, potentially fatal dysentery. Treatment in adults and older children is usually accomplished with tetracycline, 500 mg four times daffy for 10 days, but potential treatment alternatives include iodoquinol, 650 mg three times daily for 20 days and metronidazole, 750 mg three times daily for five days.[7]

Other Commensals

Several nonpathogenic protozoa may be found m human stool specimens. Although most of these or-ganisms are probably har-mless, their presence should arouse concern regarding poor sanitation and an increased likelihood of other parasitic exposure.

One of the most common stool commensals in the United States is Blastocystis hominis,,which was originally thought to be a stool yeast rather than a protozoa. Its size is quite variable, ranging from 7 to 40 [mu]m and, like yeast, it stains with iodine.[8] Although most Blastocystis infections are asymptomatic and require no treatment, this organism's pathogenicity is now controversial, since large numbers are sometimes noted in diarrheal stools in the absence of any other pathogen.[10,22]

[Figure 1 ILLUSTRATION OMITTED]

RELATED ARTICLE: Giardiasis

What is giardiasis?

Giardia (say gee-ar-dee-ah) is the name of a microscopic parasite that can live in the human bowel. The sickness that this parasite causes is called giardiasis (gee-ar-dye-asis). Some symptoms of giardiasis are diarrhea, belching, gas and cramps. Although these problems are very unpleasant, the illness isn't usually dangerous.

How does a person get this disease?

Giardiasis is easy to catch if you drink spring water or stream water. Many animals carry Giardia in their feces and may introduce this parasite into rivers, streams and springs in rural areas. Infected stream water may look clean and safe when it really isn't. City water may also be infected if sewer lines flood or leak. If you travel overseas, you may get giardiasis by drinking water (even tap water) that hasn't been boiled or treated.

Some people who get giardiasis don't become ill, but they may spread the parasite to other people. Giardiasis may be spread in day care centers if workers aren't careful to wash their hands each time after changing diapers.

How can this disease be prevented?

You should be very careful about the water you drink. If you go camping, take bottled water or boil water before you use it. Wash your hands carefully several times a day (with an antibacterial soap, if possible). If you are traveling, don't brush your teeth or wash dishes with water that hasn't been boiled. Peel raw fruits and vegetables before you eat them, and don't eat undercooked food. If someone in your family gets giardiasis, it's likely that this problem will spread to everyone in your home--especially to the children.

How can my doctor tell if I have this disease?

Your doctor usually diagnoses giardiasis by looking at stool samples under a microscope, although several samples may have to be checked before the diagnosis can be made. Sometimes other tests may be necessary.

How is this disease treated? Can medicine help?

Giardiasis is usually treated with a medicine called metronidazole (Flagyl). It's usually taken three times a day for five to 10 days. Side effects may include a metallic taste in the mouth or nausea. If you take Flagyl, you should not drink any alcohol. This medicine shouldn't be taken in the early stages of pregnancy.

Young children (under five years old) may be treated with furazolidone (Furoxone). This medicine has fewer side effects and comes in a liquid form, but it shouldn't be given to babies younger than one month old.

It's usually best if a whole family is treated at the same time, because,giardiasis is so easily spread. In most cases, your doctor will want to check a stool sample after the treatment, to be sure the medicine worked. Sometimes you may need to take medicine for a longer time, or your doctor may want you to take another medicine for a complete cure.

REFERENCES

[1.] Hill DR. Giardiasis. Issues in diagnosis and management. Infect Dis Clin North Am 1993;7: 503-25. [2.] Wright SG. Giardiasis. In: Strickland GT, ed. Hunter's Tropical medicine. 7th ed. Philadelphia: Saunders, 1991:565-70. [3.] Levine GI. Sexually transmitted parasitic diseases. Prim Care 1991;18:101-28. [4.] Schmidt GD, Roberts LS. Other flagellate protozoans. In: Schmidt GD, Roberts LS. Foundations of parasitology. 4th ed. St. Louis: Times Mirror/ Mosby College Publication, 1989. [5.] Jones JE. Giardiasis. Prim Care 1991;18:43-52 [Published erratum appears in Prim Care 1991;18: following xii]. [6.] Babb RR. Giardiasis. Taming this pervasive parasitic infection. Postgrad Med 1995;98(2):155-8. [7.] Drugs for parasitic infections. Med Lett Drugs Ther 1995;37:99-108. [8.] Croft JC. Nonamebic protozoal enteridites. In: Hoeprich PD, Jordan MC, Ronald AR, eds. Infectious diseases: a treatise of infectious processes. 5th ed. Philadelphia: Lippincott, 1994:769-74. [9.] Tietze PE, Jones JE. Parasites during pregnancy. Prim Care 1991;18:75-99. [10.] Wolfe MS. Miscellaneous intestinal protozoa. In: Strickland GT, ed. Hunter's Tropical medicine. 7th ed. Philadelphia: Saunders, 1991:575-82. [11.] Wolfe MS. Amebiasis. In: Strickland GT, ed. Hunter's Tropical medicine. 7th ed. Philadelphia: Saunders, 1991:550-65. [12.] Schmidt GD, Roberts LS. Subphylum sarcodina amebas. In: Schmidt GD, Roberts LS. Foundations of parasitology. 4th ed. St. Louis: Times Mirror/ Mosby College Publication, 1989:99-113. [13.] Newman RD, Wuhib T, Lima AA, Guerrant RL, Sears CL. Environmental sources of Cryptosporidium in an urban slum in northeastern Brazil. Am J Trop Med Hyg 1993;49:270-5. [14.] Cryptosporidium infections associated with swimming pools-dane county, Wisconsin, 1993. MMWR Morb Mortal Wkly Rep 1994;43:561-3. [15.] Schmidt GD, Roberts LS. Phylum apicomplexa. In: Schmidt GD, Roberts LS. Foundations of parasitology. 4th ed. St. Louis: Times Mirror/mosby College Publication, 1989:114-37. [16.] Cook G.C. Cryptosporidiosis. hi: Strickland GT, ed. Hunter's Tropical medicine. 7th ed. Philadelphia: Saunders, 1991:570-4. [17.] Danziger LH, Kanyok TP, Novak RM. Treatment of cryptosporidial diarrhea in an AIDS patient with paromomycin. Ann Pharmacother 1993;27:1460-2. [18.] Kan SP, Pathmanathan R. Review of sarcocystosis in Malaysia. Southeast Asian J Trop Med Public Health 1991;22(Suppl):129-34. [19.] Oldfield EC 3d. Albendazole: new hope for treatment of microsporidiosis in AIDS. Am J Gastroenterol 1995;90:159-60. [20.] Chiodini PL. A 'new' parasite: human infection with Cyclospora cayetanensis. Trans R Soc Trop Med Hyg 1994;88:369-71. [21.] Schmidt GD, Roberts LS. Phylum coli. hi: Schmidt GD, Roberts LS. Foundation of parasitology. 4th ed. St. Louis: Times Mirror/mosby College Publication, 1989:175-80. [22.] Carrascosa M, Martinez J, Perez-Castrillon JL. Hemorrhagic proctosigmoiditis and Blastocystis hominis infection [Letter]. Ann Intern Med 1996; 124:278-9.

The Author

GREGORY JUCKETT, M.D. is an assistant professor in the department of Family Medicine at West Virginia University School of Medicine, Morgantown. He is a graduate of Pennsylvania State University College of Medicine, Hershey, and completed a three-year residency in family medicine at the Medical University of South Carolina College of Medicine, Charleston.

Address correspondence to Gregory Juckett, M.D., Box 9247, Robert C. Byrd Health Sciences Center, West Virginia University School of Medicine, Morgantown, WV 26506.

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