Toxoplasma gondii

Determinants of tachyzoite to bradyzoite conversion

Sini Skariah, Matthew Karmen McIntyre, Dana G. Mordue

Research output: Contribution to journalReview article

64 Citations (Scopus)

Abstract

Apicomplexa are primarily obligate intracellular protozoa that have evolved complex developmental stages important for pathogenesis and transmission. Toxoplasma gondii, responsible for the disease toxoplasmosis, has the broadest host range of the Apicomplexa as it infects virtually any warm-blooded vertebrate host. Key to T. gondii's pathogenesis is its ability to differentiate from a rapidly replicating tachyzoite stage during acute infection to a relatively non-immunogenic, dormant bradyzoite stage contained in tissue cysts. These bradyzoite cysts can reconvert back to tachyzoites years later causing serious pathology and death if a person becomes immune-compromised. Like the sexual stage sporozoites, bradyzoites are also orally infectious and a major contributor to transmission. Because of the critical role of stage conversion to pathogenesis and transmission, a major research focus is aimed at identifying molecular mediators and pathways that regulate differentiation. Tachyzoite to bradyzoite development can occur spontaneously in vitro and be induced in response to exogenous stress including but not limited to host immunity. The purpose of this review is to explore the potential contributors to stage differentiation in infection and how a determination is made by the parasite to differentiate from tachyzoites to bradyzoites.

Original languageEnglish
Pages (from-to)253-260
Number of pages8
JournalParasitology Research
Volume107
Issue number2
DOIs
Publication statusPublished - 1 Jul 2010
Externally publishedYes

Fingerprint

Apicomplexa
tachyzoites
Toxoplasma
Toxoplasma gondii
Cysts
bradyzoites
Sporozoites
pathogenesis
Host Specificity
Toxoplasmosis
Infection
Vertebrates
Immunity
Parasites
Pathology
sporozoites
toxoplasmosis
Research
host range
infection

ASJC Scopus subject areas

  • Parasitology
  • Infectious Diseases
  • Medicine(all)

Cite this

Toxoplasma gondii : Determinants of tachyzoite to bradyzoite conversion. / Skariah, Sini; McIntyre, Matthew Karmen; Mordue, Dana G.

In: Parasitology Research, Vol. 107, No. 2, 01.07.2010, p. 253-260.

Research output: Contribution to journalReview article

Skariah, Sini ; McIntyre, Matthew Karmen ; Mordue, Dana G. / Toxoplasma gondii : Determinants of tachyzoite to bradyzoite conversion. In: Parasitology Research. 2010 ; Vol. 107, No. 2. pp. 253-260.
@article{3f60c2e02b3d433e888fdcf6cd218670,
title = "Toxoplasma gondii: Determinants of tachyzoite to bradyzoite conversion",
abstract = "Apicomplexa are primarily obligate intracellular protozoa that have evolved complex developmental stages important for pathogenesis and transmission. Toxoplasma gondii, responsible for the disease toxoplasmosis, has the broadest host range of the Apicomplexa as it infects virtually any warm-blooded vertebrate host. Key to T. gondii's pathogenesis is its ability to differentiate from a rapidly replicating tachyzoite stage during acute infection to a relatively non-immunogenic, dormant bradyzoite stage contained in tissue cysts. These bradyzoite cysts can reconvert back to tachyzoites years later causing serious pathology and death if a person becomes immune-compromised. Like the sexual stage sporozoites, bradyzoites are also orally infectious and a major contributor to transmission. Because of the critical role of stage conversion to pathogenesis and transmission, a major research focus is aimed at identifying molecular mediators and pathways that regulate differentiation. Tachyzoite to bradyzoite development can occur spontaneously in vitro and be induced in response to exogenous stress including but not limited to host immunity. The purpose of this review is to explore the potential contributors to stage differentiation in infection and how a determination is made by the parasite to differentiate from tachyzoites to bradyzoites.",
author = "Sini Skariah and McIntyre, {Matthew Karmen} and Mordue, {Dana G.}",
year = "2010",
month = "7",
day = "1",
doi = "10.1007/s00436-010-1899-6",
language = "English",
volume = "107",
pages = "253--260",
journal = "Parasitology Research",
issn = "0932-0113",
publisher = "Springer Verlag",
number = "2",

}

TY - JOUR

T1 - Toxoplasma gondii

T2 - Determinants of tachyzoite to bradyzoite conversion

AU - Skariah, Sini

AU - McIntyre, Matthew Karmen

AU - Mordue, Dana G.

PY - 2010/7/1

Y1 - 2010/7/1

N2 - Apicomplexa are primarily obligate intracellular protozoa that have evolved complex developmental stages important for pathogenesis and transmission. Toxoplasma gondii, responsible for the disease toxoplasmosis, has the broadest host range of the Apicomplexa as it infects virtually any warm-blooded vertebrate host. Key to T. gondii's pathogenesis is its ability to differentiate from a rapidly replicating tachyzoite stage during acute infection to a relatively non-immunogenic, dormant bradyzoite stage contained in tissue cysts. These bradyzoite cysts can reconvert back to tachyzoites years later causing serious pathology and death if a person becomes immune-compromised. Like the sexual stage sporozoites, bradyzoites are also orally infectious and a major contributor to transmission. Because of the critical role of stage conversion to pathogenesis and transmission, a major research focus is aimed at identifying molecular mediators and pathways that regulate differentiation. Tachyzoite to bradyzoite development can occur spontaneously in vitro and be induced in response to exogenous stress including but not limited to host immunity. The purpose of this review is to explore the potential contributors to stage differentiation in infection and how a determination is made by the parasite to differentiate from tachyzoites to bradyzoites.

AB - Apicomplexa are primarily obligate intracellular protozoa that have evolved complex developmental stages important for pathogenesis and transmission. Toxoplasma gondii, responsible for the disease toxoplasmosis, has the broadest host range of the Apicomplexa as it infects virtually any warm-blooded vertebrate host. Key to T. gondii's pathogenesis is its ability to differentiate from a rapidly replicating tachyzoite stage during acute infection to a relatively non-immunogenic, dormant bradyzoite stage contained in tissue cysts. These bradyzoite cysts can reconvert back to tachyzoites years later causing serious pathology and death if a person becomes immune-compromised. Like the sexual stage sporozoites, bradyzoites are also orally infectious and a major contributor to transmission. Because of the critical role of stage conversion to pathogenesis and transmission, a major research focus is aimed at identifying molecular mediators and pathways that regulate differentiation. Tachyzoite to bradyzoite development can occur spontaneously in vitro and be induced in response to exogenous stress including but not limited to host immunity. The purpose of this review is to explore the potential contributors to stage differentiation in infection and how a determination is made by the parasite to differentiate from tachyzoites to bradyzoites.

UR - http://www.scopus.com/inward/record.url?scp=77955467410&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=77955467410&partnerID=8YFLogxK

U2 - 10.1007/s00436-010-1899-6

DO - 10.1007/s00436-010-1899-6

M3 - Review article

VL - 107

SP - 253

EP - 260

JO - Parasitology Research

JF - Parasitology Research

SN - 0932-0113

IS - 2

ER -