Ontology for Parasite Life Cycle

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What is the Ontology for Parasite Lifecycle (OPL)?

OPL models the life cycle stage details of T.cruzi and two related kinetoplastids, Trypanosoma brucei and Leishmania major. In addition, the ontology also models necessary contextual details such as host information, vector information, strain and anatomical location. All the entities in the ontology are linked to each other by explicitly modeled named relationships that will enable software applications to accurately interpret data annotated with this ontology. For example, “Trypanosoma_cruzi→has_vector_organism→triatominae”. The PLO is modeled in the W3C Web Ontology Language (OWL) standard and currently has 41 classes and 5 properties with a description logic expressivity of ALU. OPL(ver 0.1), which was called Parasite Lifecycle Ontology is released through NCBO’s BioPortal repository for public use.

Snapshot of class hierarchy of the parasite life cycle ontology using Protege toolkit. Detail of this ontology is available at NCBO BioPortal
List of ontology classes


Organisms in OPL

Here is brief description and life-cycles of the organisms that are covered in OPL.

Trypanosoma cruzi
T. cruzi Lifecycle

The life cycle of Trypanosoma cruzi involves both vertebrate and invertebrate hosts (see figure below). Metacyclic trypomastigotes are deposited on the mammalian (vertebrate host's) skin through the faeces of the triatomine bug vector. They have the capacity to penetrate skin through wounds, such as the bite from the bug, and across the mucosal membranes surrounding the eyes and mouth.

Inside the mammalian host, the trypomastigotes penetrate either phagocytic or non-phagocytic cells, in a manner distinct from phagocytosis. Parasites subvert the host cell Ca2+ -regulated lysosomal exocytic pathway, literally ‘hijacking’ lysosomes to enable them to invade effectively (Sibley and Andrews, 2000; Tan and Andrews, 2002). Within the host cell, trypomastigotes are initially held within a membrane bound vacuole. They subsequently enter the host cell cytoplasm directly, transforming into amastigotes (the intracellular replicative forms) (Tan and Andrews, 2002). Around five days post invasion, the amastigotes transform back into C- shaped trypomastigotes, and the host cell ruptures, releasing the parasites into the bloodstream. These bloodstream trypomastigotes can then either infect further cells, or can be taken up by a reduviid bug. Within the insect vector, epimastigotes develop in the alimentary tract, taking 10 – 15 days to replicate and transform into infective stages in the rectum (Kollien and Schaub, 2000). T. cruzi can also be transmitted via contaminated blood and infected organs used in transplant operations, or congenitally from mother to child.

Trypanosoma brucei
T. brucei Lifecyle

Trypanosoma brucei is also transmitted by an insect vector, in this case the tsetse fly, one of the Glossina sp. Blood stream trypomastigotes are ingested by the tsetse from an infected patient during the insect blood meal. In the midgut of the tsetse, the trypanosomes develop into procyclic forms that divide by binary fission. Some of these then migrate to the salivary glands where they differentiate into infectious metacyclic trypomastigotes. These are transmitted into new hosts during further blood feeds (Barrett et al, 2003).

Leishmania sp.
Leishmania sp. Lifecycle

Leishmania species are also transmitted by insect vectors, in this case metacyclic promastigotes are introduced into the skin by the bite of various species of sand fly. These are taken up by macrophages and transform into intracellular amastigotes (reviewed by Handman and Bullen, 2002), remaining in this form for the duration of the life cycle in the mammalian host. Development within the sand fly vector varies from species to species, but is thought to involve 2 distinct growth phases (Gossage et al, 2003).


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