Eduardo Ortega-Barria and Elidia Dominguez
Balantidium coli is the largest protozoan parasite and the only ciliate known to cause infection in humans. B. coli is a zoonosis and has been found in pigs, rodents, cattle, reptiles, birds, fishes, annelids, arthropods, and many simian hosts. Pigs are typically the source of human infections, although species-to-species transmission requires adaptation of the parasite. The host’s health can be a factor, since individuals who are malnourished or suffering from concurrent infections are at greater risk of developing balantidiasis. Once a porcine strain becomes established in the human intestine, the infection may spread from human-to-human, and this may account for the occasional reported epidemics.
The genus Balantidium belongs to the phylum Ciliophora, class Litostomatea, order Vestibuliferida, and family Balantidiidae.1 Many species have been described on the basis of morphological features or the host in which they were identified; however, the validity of these species is unconfirmed. The parasite has two stages in its life cycle: the trophozoite and the cyst. The cyst is the resting, resistant stage and is essential for transmission, since the trophozoite cannot survive passage through the stomach’s low pH. The cysts are spherical or ovoid with a diameter of 40 to 60 μm and remain viable at room temperature for at least 2 weeks, particularly if kept moist and away from direct sunlight.2
Cysts are formed in the lumen of the colon or in freshly evacuated stools. Nuclear division does not occur in the cyst; therefore, only one parasite is obtained on excystation. The motile trophozoite is the form for division. Its shape and size vary with the amount of ingested food, from 30 to 300 μm in length and 30 to 100 μm in width. The surface is covered by longitudinal rows of cilia that function as the organs of locomotion and give the trophozoite its characteristic morphology.2 The anterior end contains the cell mouth (cytostome) through which debris, bacteria, and other particulate material are ingested and pass into food vacuoles. The cytoplasm contains a large macronucleus, a micronucleus, several digestive vacuoles, and two contractile vacuoles that serve as osmoregulatory organelles. The macronucleus is bean shaped, and the micronucleus is spherical and generally lies in the concavity of the macronucleus. The posterior end is rounded and contains the anal pore (cytopyge), through which the residual contents of food vacuoles empty. Reproduction occurs by transverse binary fission or, less commonly, by budding.2 In addition, a sexual event (ie, conjugation) has been observed in cultures. The parasite can be grown in vitro in xenic cultures, at reference or research laboratories.1
Balantidiasis is a disease of tropical and subtropical regions and is a reflection of poor sanitation and inadequate protection of the water supply from sewage contamination. Domestic and wild swine represent a reservoir for human infections. Several studies report high incidence rates (47%) in intensive pig farms3 and up to 100% in research farms.4 Infections occur when fecal material from swine contaminates drinking water or food. A relatively high prevalence has been found in New Guinea, southern Iran, South and Central America, central Asia, the Philippines, and some Pacific Islands.5 Interestingly, a cross-sectional survey of gastrointestinal parasites in nonhuman primates in four zoological gardens in Belgium reported a 13% prevalence of B. coli.6
Several cofactors are involved in the pathogenesis of this disease, including the intrinsic virulence of the strain and the host’s susceptibility. Symptomatic infection may be observed in cases of malnutrition, alcoholism, hypochlorhydria, and immunodeficiency7,8.
Once the parasite is ingested, excystation occurs in the small intestine, and the trophozoites pass to the colon, where they may establish themselves in the lumen; they usually fail to cause any signs or symptoms. The parasite feeds upon bacteria and debris in the gut, but also releases enzymes (hyaluronidase) that attack the mucosal surface.
In some patients, the trophozoites invade the mucosa and cause large ulcerative lesions similar to those produced by Entamoeba histolytica; however, balantidial lesions usually are larger. As the trophozoites multiply by binary fission in the mucosa and submucosa, adjacent lesions may anastomose with one another, and the ulcers often extend deeply into the muscularis. Fortunately, perforation or extraintestinal invasion rarely ensues.
With invasive disease, patients may have mild to severe diarrhea that contains mucus and blood, abdominal pain, nausea, vomiting, and often tenesmus. Secondary infection of the colonic lesions by bacteria can worsen the clinical picture. The disease may be self-limiting, with spontaneous eradication and healing, or it can become chronic, with constipation alternating with diarrhea. Occasionally, cecal swelling can lead to typhlitis, and rarely the organisms will perforate the large intestine and affect the small intestine, the appendix, the vagina, the uterus, and the bladder, and on very rare occasions may disseminate to the liver and lungs.7,8
History of contact with pigs (eg, farmers, veterinarians, slaughterhouse personnel) may be indicative of infection. The diagnosis of balantidiasis rests on finding active ciliates or cysts in the patient’s feces. It is relatively easy to recognize in clinical specimens due to its large size, an outer membrane covered by short cilia, and a single, large kidney-bean-shaped nucleus.
Trophozoites are short-lived; they will disintegrate unless stool specimens are examined promptly. Diagnosis is also made by visualizing the organisms in scrapings taken from the periphery of ulcers; by irrigating over an ulcer at colonoscopy and examining aspirated irrigate; or by endoscopic biopsy of an ulcer. Cysts sometimes are found in formed stools. Autofluorescence after excitation with UV light provides a convenient technique for detecting the protozoa when direct smears are examined.9
Treatment in adults involves tetracycline, 500 mg qid for 10 days; in children (≥ 8 years of age), treatment is 10 mg/kg qid for 10 days (maximum 2 g/d). Metronidazole has been used successfully in children and adults (35 to 50 mg/kg per day in three doses for 5 to 10 days).7,8,10,11 Alternatively, iodoquinol may be used, at 650 mg tid for 20 days in adults and 40 mg/kg per day in three divided doses for 20 days (maximum 2 g/d) in children.12