Balantidium

Classification: Taxonomic ranks under review (cf. Illustrated Guide to Protozoa, 2000. Allen Press)

Protista (unicellular eukaryotes)
Ciliophora (with cilia, nuclear dualism, pellicular alveoli, reproductive conjugation)
Kinetofragminophorea (‘lower holotrichs’, little distinction between oral and body ciliature)
Rhabdophora (noncurved tubular cytopharyngeal apparatus = rhabdos)
Litostomatea (‘simple mouths’, special somatic kineties)
Trichostomatia (endosymbionts)
Vestibulifera (distict oral depression = vestibulum)

Family: Balantidiidae
These ciliates are monoxenous (one-host) endocommensals in vertebrates, some species of which can become histophagous parasites. The trophozoites have a uniform covering of somatic ciliary rows and a cytostome at the base of an anterior vestibulum.

Balantidium coli [this species causes balantidiasis in vertebrates, esp. pigs and humans]

Parasite morphology: Two developmental stages are formed: trophozoites and cysts. Trophozoites are variable in size ranging from 30-120µm in length. They are oblong-spherical in shape and are covered by longitudinal kineties (rows of cilia). At the anterior end there is a depression (vestibulum) leading to the cytostome (mouth). Internally, they contain a single large kidney-shaped macronucleus and single small micronucleus. The cysts appear as membrane-bound ovoid bodies ranging from 40-60µm in diameter.

Host range: Several Balantidium spp. have been recorded throughout the world in various species of crustacea, insects, fish, amphibia and mammals (including humans). Infections by B. coli are particularly prevalent in pigs, monkeys and humans, especially in the tropics, with zoonotic transmission frequently implicated by epidemiological studies.

Site of infection: Ciliates are found in the large intestines of their hosts. They are actively swimming organisms and they reproduce asexually (by transverse fission) and sexually (by conjugation).

Pathogenesis: Infections are usually not associated with any changes in the colonic mucosa. Healthy individuals often exhibit spontaneous recovery or become symptomless carriers. However, under certain conditions, the organisms produce proteolytic enzymes which digest away the epithelium producing flask-shaped ulcers. This stimulates inflammatory changes with lymphocytic infiltration and haemorrhage and secondary bacterial invasion may follow. Infections may cause a dysentery-like syndrome, involving diarrhoea, tenesmus, nausea, vomiting, anorexia, headache, insomnia and weakness. Colonic ulceration involves mucosal sloughing, necrosis, fluid loss, haemorrhage, occasional abscess formation and sometimes perforation of the bowel.

Mode of transmission: Infections are passed horizontally between hosts by faecal-oral transmission. Cysts passed in the faeces of infected hosts contaminate the environment. When ingested with contaminated food or water, the cysts excyst releasing trophozoites in the digestive tract.

Differential diagnosis: Infections are diagnosed by coprological examination and the detection of characteristic cysts in faecal material or trophozoites in colonic biopsy material.

Treatment and control: Clinical infections may be treated with metronidazole, di-iodohydroxyquin, tetracycline or carbarsone. Prevention and control depends on strict hygiene to prevent the contamination of food and water supplies, particularly by pig faeces. Effluent from intensive piggeries should not be used to fertilize vegetable gardens or edible crops. In developing countries, pigs should not be left to roam free in rural villages, but are best confined to pens and stys where proper waste disposal can be practiced.