The population genetic structure of Toxoplasma gondii was determined by multilocus restriction fragment length polymorphism analysis at 6 loci in 106 independent isolates from humans and animals. Phylogenetic and statistical analyses indicated a highly unusual population structure consisting of 3 widespread clonal lineages. Extensively mixed genotypes were only apparent in 4 strains, which indicated that, while not separate species, sexual recombination between the 3 lineages is exceedingly rare in natural populations. T. gondii is a major cause of subclinical human infection and an important opportunistic pathogen that causes severe disease in immunocompromised patients. While strains from all 3 lineages were isolated from humans, the majority of human toxoplasmosis cases were associated with strains of a type II genotype. The correlation of specific clonal lineages with human toxoplasmosis has important implications for development of vaccines, drug treatments, and diagnostic protocols.

Toxoplasma gondii is among the most prevalent parasites worldwide, infecting many wild and domestic animals and causing zoonotic infections in humans. T. gondii differs substantially in its broad distribution from closely related parasites that typically have narrow, specialized host ranges. To elucidate the genetic basis for these differences, we compared the genomes of 62 globally distributed T. gondii isolates to several closely related coccidian parasites. Our findings reveal that tandem amplification and diversification of secretory pathogenesis determinants is the primary feature that distinguishes the closely related genomes of these biologically diverse parasites. We further show that the unusual population structure of T. gondii is characterized by clade-specific inheritance of large conserved haploblocks that are significantly enriched in tandemly clustered secretory pathogenesis determinants. The shared inheritance of these conserved haploblocks, which show a different ancestry than the genome as a whole, may thus influence transmission, host range and pathogenicity.

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Objective To estimate the effect of playing Pokémon GO on the number of steps taken daily up to six weeks after installation of the game.Design Cohort study using online survey data.Participants Survey participants of Amazon Mechanical Turk (n=1182) residing in the United States, aged 18 to 35 years and using iPhone 6 series smartphones.Main outcome measures Number of daily steps taken each of the four weeks before and six weeks after installation of Pokémon GO, automatically recorded in the “Health” application of the iPhone 6 series smartphones and reported by the participants. A difference in difference regression model was used to estimate the change in daily steps in players of Pokémon GO compared with non-players.Results 560 (47.4%) of the survey participants reported playing Pokémon GO and walked on average 4256 steps (SD 2697) each day in the four weeks before installation of the game. The difference in difference analysis showed that the daily average steps for Pokémon GO players during the first week of installation increased by 955 additional steps (95% confidence interval 697 to 1213), and then this increase gradually attenuated over the subsequent five weeks. By the sixth week after installation, the number of daily steps had gone back to pre-installation levels. No significant effect modification of Pokémon GO was found by sex, age, race group, bodyweight status, urbanity, or walkability of the area of residence.Conclusions Pokémon GO was associated with an increase in the daily number of steps after installation of the game. The association was, however, moderate and no longer observed after six weeks.

Strains of Toxoplasma gondii can be grouped into three predominant clonal lineages with members of the type I group being uniformly lethal in mice. To elucidate the basis of this extreme virulence, a genetic cross was performed between a highly virulent type I strain (GT-1) and a less-virulent type III strain (CTG), and the phenotypes of resulting progeny were analyzed by genetic linkage mapping. Analysis of independent recombinant progeny identified several quantitative trait loci that contributed to acute virulence. A major quantitative trait locus located on chromosome VII accounted for Ϸ50% of the virulence phenotype, whereas a minor locus on chromosome IV, linked to the ROP1 gene, accounted for Ϸ10%. These loci are conserved in other type I strains, indicating that acute virulence is controlled by discrete genes common to the type I lineage.QTL mapping ͉ genetics ͉ parasite ͉ linkage analysis T oxoplasma gondii is a widespread protozoan parasite that infects most types of warm-blooded mammals and causes opportunistic disease in humans (1). The vast majority of T. gondii strains that have been studied fall into one of three highly clonal, yet closely related, lineages (2-5). These clonal types do not show strong geographic or host boundaries, and each is distributed worldwide and found in a variety of different hosts. However, there are strong phenotypic differences between the lineages, the most notable of which is virulence in the mouse model. Archetypal type I strains share the trait of being uniformly lethal in outbred mice (LD 100 ϭ 1); by contrast, types II and III are considerably less virulent (LD 100 Ն 10 3 ) (5). By nature, virulent type I strains do not readily give rise to chronic infections in mice, whereas such long-term infections are characteristic of types II and III strains (5). Several studies have observed an increased frequency of type I strains in severe congenital toxoplasmosis in humans, suggesting the type I lineage may be more pathogenic for humans as well (4, 6).T. gondii is readily propagated in a variety of cultured cell types and is equipped with efficient techniques for molecular genetic analyses that facilitate the introduction of foreign genes and the disruption of endogenous genes (7). Classical genetic crosses can be performed in cats, the definitive host in the life cycle, where a complex developmental program leads to the production of an oocyst that undergoes meiosis after being shed into the environment (8, 9). The genome is haploid and relatively stable, and a molecular karyotype has been developed by hybridization of markers to specific chromosomes separated by pulse-field gel electrophoresis (10). The segregation of restriction fragment length polymorphism (RFLP) markers has previously been used to build a rudimentary genetic linkage map (10, 11). Equipped with both forward and reverse genetics, T. gondii provides an ideal model for genetic analysis of complex biological traits such as virulence (12).The three lineages of T. gondii differ by only 1-2% at the DNA sequ...

Equine protozoal myeloencephalitis (EPM) is a serious disease of horses, and its management continues to be a challenge for veterinarians. The protozoan Sarcocystis neurona is most commonly associated with EPM. S. neurona has emerged as a common cause of mortality in marine mammals, especially sea otters (Enhydra lutris). EPM-like illness has also been recorded in several other mammals, including domestic dogs and cats. This paper updates S. neurona and EPM information from the last 15 years on the advances regarding life cycle, molecular biology, epidemiology, clinical signs, diagnosis, treatment and control.

Equine protozoal myeloencephalitis (EPM) remains an important neurologic disease of horses. There are no pathognomonic clinical signs for the disease. Affected horses can have focal or multifocal central nervous system (CNS) disease. EPM can be difficult to diagnose antemortem. It is caused by either of 2 parasites, Sarcocystis neurona and Neospora hughesi, with much less known about N. hughesi. Although risk factors such as transport stress and breed and age correlations have been identified, biologic factors such as genetic predispositions of individual animals, and parasite‐specific factors such as strain differences in virulence, remain largely undetermined. This consensus statement update presents current published knowledge of the parasite biology, host immune response, disease pathogenesis, epidemiology, and risk factors. Importantly, the statement provides recommendations for EPM diagnosis, treatment, and prevention.

Large-scale EST sequencing projects for several important parasites within the phylum Apicomplexa were undertaken for the purpose of gene discovery. Included were several parasites of medical importance (Plasmodium falciparum, Toxoplasma gondii) and others of veterinary importance (Eimeria tenella, Sarcocystis neurona, and Neospora caninum). A total of 55,192 ESTs, deposited into dbEST/GenBank, were included in the analyses. The resulting sequences have been clustered into nonredundant gene assemblies and deposited into a relational database that supports a variety of sequence and text searches. This database has been used to compare the gene assemblies using BLAST similarity comparisons to the public protein databases to identify putative genes. Of these new entries, ∼15%-20% represent putative homologs with a conservative cutoff of p < 10 −9 , thus identifying many conserved genes that are likely to share common functions with other well-studied organisms. Gene assemblies were also used to identify strain polymorphisms, examine stage-specific expression, and identify gene families. An interesting class of genes that are confined to members of this phylum and not shared by plants, animals, or fungi, was identified. These genes likely mediate the novel biological features of members of the Apicomplexa and hence offer great potential for biological investigation and as possible therapeutic targets.