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Review
. 2013 Oct;1(5):167-78.
doi: 10.1177/2049936113504754.

Blastocystis, an unrecognized parasite: an overview of pathogenesis and diagnosis

Affiliations
Review

Blastocystis, an unrecognized parasite: an overview of pathogenesis and diagnosis

Ivan Wawrzyniak et al. Ther Adv Infect Dis. 2013 Oct.

Abstract

Blastocystis sp. is among the few enteric parasites with a prevalence that often exceeds 5% in the general population of industrialized countries and can reach 30-60% in developing countries. This parasite is frequently found in people who are immunocompromised (patients with human immunodeficiency virus/acquired immunodeficiency syndrome or cancer) and a higher risk of Blastocystis sp. infection has been found in people with close animal contact. Such prevalence in the human population and the zoonotic potential naturally raise questions about the impact of these parasites on public health and has increased interest in this area. Recent in vitro and in vivo studies have shed new light on the pathogenic power of this parasite, suggesting that Blastocystis sp. infection is associated with a variety of gastrointestinal disorders, may play a significant role in irritable bowel syndrome, and may be linked with cutaneous lesions (urticaria). Despite recent significant advances in the knowledge of the extensive genetic diversity of this species, the identification of extracellular proteases as virulence factors and the publication of one isolate genome, many aspects of the biology of Blastocystis sp. remain poorly investigated. In this review, we investigate several biological aspects of Blastocystis sp. (diversity and epidemiology, diagnosis tools and pathophysiology). These data pave the way for the following challenges concerning Blastocystis sp. research: deciphering key biological mechanisms and pathways of this parasite and clarification of its clinical impact in humans.

Keywords: Blastocystis; diagnosis; gut; pathogenesis; subtypes.

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Figures

Figure 1.
Figure 1.
Vacuolar form of in vitro cultivated Blastocystis sp. viewed under transmission electron microscopy (a). This form is spherical with a large central vacuole (v) and a thin peripheral band of cytoplasm (c) around the vacuole. (b) The cytoplasm contains the nucleus (n) and mitochondrion-like organelles (m). (c) Blastocystis sp. cell is surrounded by a surface coat (sc). Bars, 2 µm for (a) and 500 nm for (b) and (c).
Figure 2.
Figure 2.
Blastocystis sp. subtypes (STs 1–9) with various host specificities. Humans can be infected by nine STs, some being mainly found in humans (ST3 and ST9). ST1, 2, 5 and 8 are found both in human and mammalian isolates (primate, pig, human, cattle and pig), while ST4 is also present among rodent isolates, and ST6, 7 and 8 among avian isolates. Some STs are exclusively found in animals (ST10–17). ST10 and 15 are present among Artiodactyla and nonhuman primates, ST11 among Proboscidea, ST12 among Artiodactyla and marsupials, ST13 among nonhuman primates and marsupials, ST14 among Artiodactyla, ST16 among marsupials and ST17 among rodents.
Figure 3.
Figure 3.
Mechanisms of blastocystosis physiopathology. Blastocystis sp. may release cysteine protease that may participate in the attack of intestinal epithelium with other hydrolases and may cause the increase in paracellular permeability that is observed in several digestive pathologies such as irritable bowel syndrome (IBS). Blastocystis sp. is able to induce physiological disturbances linked to IBS: host cell apoptosis, the modulation of host immune response and a microinflammation. Some as yet uncharacterized secondary metabolites produced by the polyketide synthase or nonribosomal peptide synthases could participate in host intestinal symptoms by inducing changes in the host microbiota, another feature of IBS. Finally, drug-resistant isolates of the parasite could be explained by the presence of multidrug resistance proteins that could eject active drugs. GM-CSF, granulocyte–macrophage colony-stimulating factor; Ig, immunoglobulin; IL, interleukin; INF, interferon; TNF, tumour necrosis factor.

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