Toxoplasma gondii
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A Microbial Biorealm page on the genus Toxoplasma gondii
Classification
Higher order taxa
Cellular organisms; Eukaryota; Alveolata; Apicomplexa; Coccidia; Eucoccidiorida; Eimeriorina; Sarcocystidae; Toxoplasma [1]
Species
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NCBI: Taxonomy |
Toxoplasma gondii [1]
Description and significance
Toxoplasma gondii is a single-celled eukaryotic protozoan parasite. The name Toxoplasma is derived from the shape of the organism, which is crescent-like (toxon is Greek for “arc”). T. gondii holds notoriety as the pathogen that causes the disease toxoplasmosis in humans. The microbe preferentially encysts itself within the tissues of the brain and the central nervous system of the host, causing encephalopathy, loss of normal cognitive brain function, impaired judgment, peripheral neuropathy, slowed reflexes, pathological lesions and other disorders classically associated with the invasion of brain tissue [4,5].Toxoplasmosis was discovered almost a century ago, in 1908, and the pathogen itself was identified in the North African rodent Ctenodactylus gundi as it was being used for research in the Pasteur Institute in Tunis.
The complete lifecycle of T. gondii was not examined in its entirety until 1970. It is shown that cats are definitive hosts to the pathogen, and are excreted as oocytes in their feces, while humans and other mammals, as well as birds, are intermediate hosts. When encysted, the pathogen is very tough and resistant to the low temperature extremes, sustaining viability at temperatures of 0, down to −12˚ C. Harsh agents (corrosives, such as bleach) also have minimal affect on it, as does direct sunlight. High temperatures (approximately 66˚C) can successfully destroy the protozoan, however. [5]
In 1923, the first case of human toxoplasmosis was reported, with the victim being an 11-month-old child[5]. It is universally accepted that this zoonosis occurred much farther back in time, however, and that the parasite originated from animal hosts that were in close contact with human, most notably cats (even though, as noted above, T. gondii can infect several mammals and birds) [2]. T. gondii mainly spreads via contaminated cat feces, consumption of undercooked meat, and vertical transmission[5].
Infants (especially via vertical transmission) and immuno-compromised hosts (including cats) are readily infected with the pathogen and show accelerated and concentrated symptoms mentioned in the first paragraph, but it is interesting to observe that the pathogen is generally docile and useless in healthy individuals with a competent immune system.[7,8]
Genome structure
The T. gondii haploid genome is approximately 80 Megabases in size, and consists of 11 circular [9] chromosomes, and currently serves as a basis of trying to understand and decipher more complicated areas in the related malarial pathogen, Plasmodium falciparum, among other protozoa. Research is still underway to decipher the functions of all the genes of this microbe, and a variety of techniques have been employed to gather data, notably among them are environmental shotgun sequencing (ESS), expressed sequence tags (EST) and bacterial artificial chromosome (BAC). As of late 2002, the genomic database for T. gondii consists of an excess of 70 million base pairs of nucleotide sequence. As mentioned above, though the function and underpinnings of every gene have yet to be resolved as data is received, the data obtained thus far represents the majority of the coding potential in the T. gondii genome[8]. The primary pool of data accumulation and analysis is neatly assembled into an extensive on-line database made specifically for Toxoplasma gondii [1], and is continually updated as new data is received.
Among the more important plasmids of the pathogen, ones that were associated with lactate dehydrogenase were found to be important to the organism. This dehydrogenase is expressed by genes LDH1 and LDH2 of T. gondii plasmids, and though the exact function is still under investigation, it was found that –LDH1 and –LDH2 mutants had substantially decreased viability and infectious ability, mostly brought upon by delayed stages of maturation. It was observed that tachyzoites of these mutants failed to form a stable number of tissue cysts in mice hosts, thereby severely diminishing their ability to inflict chronic infection, though this deficiency was not immediately fatal[10].
Like most apicomplexan microbes, Toxoplasma gondii contains a secondary internal symbiotic plastid, presumably incorporated by lateral gene transfer from a eukaryotic alga from its phylogenetic evolutionary past. The apicoplast is a potential target for chemotherapy, hence the interest surrounding it. T. gondii microbes die in the absence of this plastid, and is considered to be vital to the immediate viability of the parasite, since it affects replication of the microbe[11]. Though it is not completely understood how T. gondii crosses into the host cell, it is postulated that internal plasmids encode for organelles that provide adhesive protein expression, called micronemes[12] that play a central role in host cell-membrane breeching ability. It was discovered that “M2AP-MIC2” complex proteins were responsible for adhesive secretions, and mutants with the respective deficiency had a staggering 80% impairment of host cell entry, as well as severely stunted excretion of the adhesive protein itself that usually occurs when the parasite latches on to the cell in preparation for entry[12].
Cell structure and metabolism
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Ecology
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Pathology
How does this organism cause disease? Human, animal, plant hosts? Virulence factors, as well as patient symptoms.
Application to Biotechnology
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Current Research
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References
(1) NCBI: Toxoplasma gondii, Accessed August 15, 2007, <http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&id=5811&lvl=3&p=mapview&p=has_linkout&p=blast_url&p=genome_blast&lin=f&keep=1&srchmode=1&unlock>
Edited by Shumyyal Akhtar Malik
