Article about Blastocystis hominis infection.
- Aetiology and biology of the parasite
- Clinical features and treatment
- Evidence for pathogenicity
- Further reading
Blastocystis hominis is an anaerobic unicellular colonic parasite of animals and humans. It is transmitted faeco-orally, with human infection associated with travel, institutions, animal handlers and immunodeficiency. Case reports strongly suggest that it causes a self-limited diarrhoeal illness. Diagnosis is by microscopic examination of faecal smears or concentrates. A trial of treatment with metronidazole is justified in patients who are immunocompromised, also when symptoms are prolonged.
Aetiology and biology of the parasite
Molecular and ribosomal RNA studies now indicate that Blastocystis hominis is a stramenopile belonging to the kingdom Chromista; other stramenopiles include slime nets, water moulds, and brown algae. The form commonly described in faeces and also in cultures is spherical, from 4 to 15 μm in diameter, with one prominent central vacuole surrounded by peripheral cytoplasm that electron microscopy shows to contain a nucleus, a Golgi complex, and mitochondrion-like organelles. It grows readily in cultures with mixed bacteria but axenic cultures can also be established; division is by binary fission.
Transmission is by small, resistant, faecal cysts, from 6 to 8 μm in diameter. The basic life cycle alternates between the univacuolar and cystic stages. However electron microscopy of faeces and cultures may also show multivacuolar, granular, and amoeboid forms of uncertain significance. Bizarre environmentally induced forms with huge vacuoles may develop in cultures. The common ‘univacuolar’ form was named Blastocystis by Brumpt in 1912 as a yeast, although it was first described by Alexieff in 1911 as a protozoan cyst.
Prevalence is high in many human populations associated with high faeco–oral transmission. This infection is associated with travel, institutions, animal handlers, and immunodeficiency. Blastocystis is genetically diverse and occurs in a wide range of domesticated and wild animals including invertebrates. Currently only one species, Blastocystis hominis, is recognized. There is now good evidence that this infection can be zoonotic. The resistant cysts can occur in both sewage influents and effluents.
Blastocystis hominis is usually recognized as univacuolar forms in direct wet faecal smears or formol ether concentrates. Wet mounts can be stained with iodine, giving a brownish central body, or with toluidine blue. The organism is often numerous in symptomatic subjects. Permanent mounts stain well with trichrome. Blastocystis can resemble amoebic cysts but lack their characteristic nuclei. In fixed smears stained specifically for Cryptosporidium, there is no oocyst wall. Special techniques are used to concentrate and identify cysts in environmental samples.
Clinical features and treatment
A diarrhoeal illness lasting from 3 to 10 days is attributed to this organism, sometimes symptoms continue for weeks or months. Associated features are abdominal bloating, flatulence, and anorexia. Symptoms are more prolonged in immunocompromised subjects. There is no definite association with irritable bowel syndrome. Illnesses are self limiting in most persons but infection and symptoms can usually be eliminated with metronidazole or tinidazole; the organism is also sensitive to furazolidine and hydroxyquinoline.
Evidence for pathogenicity
Definite histopathology in humans is still lacking, although serum antibody has been reported in symptomatic subjects. Experimental infections in mice produce mucosal inflammation, but a good laboratory model remains elusive; mice are not normal hosts for this parasite and pathology is not reported in any of its normal hosts. A convincing in vitro cytopathic model awaits discovery although cultured colonic epithelial cells release cytokines in the presence of Blastocystis.
The genetic heterogeneity between Blastocystis isolates correlates weakly with host species. In a recent human study, genotype determined by PCR, correlated with symptoms. Clinical response to metronidazole is hardly compelling evidence for pathogenicity since concurrent infection with other enteropathogens is common and this drug has a wide spectrum of activity including an effect upon small bowel bacterial overgrowth. More well-documented outbreaks and cytopathic evidence are needed.
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