1012 • JID 2009:200 (15 September) • CORRESPONDENCE 15 SEPTEMBER Correspondence Toxoplasma Strain Nomenclature To the Editor—I read the excellent work by Ajzenberg et al [1] about Toxoplasma strains in patients with immunodeficiency. In the article, the denominations type I, type II, type III, and nonarchetypal strains were used. Previous work with multilocus markers showed that global Toxoplasma populations could be grouped into 4 ma- jor populations (SA1, SA2, RW, and WW) [2] and that, by analyzing intron se- quences, Toxoplasma could be grouped into 11 haplogroups [3]. It is also impor- tant to point out that, for notation of re- sults for a single-marker locus such as SAG2, all results should be specifically in- dicated as SAG2 type I, SAG2 type II, or SAG2 type III. I think that the generalized use of the type I, II, and III nomenclature has been misleading. An early article that correlated the groups of parasites classified in this manner concluded that type I was found mainly in congenital toxoplasmosis, type II in reactivation forms, and type III in animals [4]. Subsequent work showed that this was a biased observation resulting from the geographical origin of the strains used in the study (Europe and North America). Multilocus analysis has been performed not only in Brazil and Guyana but also in Colombia in strains obtained from cats [5] and chickens [2]. Altogether, the results of haplotype analysis, multi- locus analysis, and serogenotyping [6, 7] are concordant and point to a predomi- nance of different parasite populations in South America, named SA1 and SA2 by multilocus markers or by the exclusive haplogroups that exist only in South America. The clinical relevance of this geo- graphical restriction of Toxoplasma strains was recently shown by a comparison of cohorts in South America and Europe [7, 8]. The risk of ocular lesions was much higher among Colombian and Brazilian children (47% [18/38]) than among chil- dren in Europe (14% [79/550]); the crude risk of intracranial lesions was also much higher among children in South America (53% [20/38]) than among those in Eu- rope (9% [49/550]) [8]. Additionally, a comparative prospective cohort study of congenitally infected children in Brazil and Europe found that Brazilian children had eye lesions that were larger, more nu- merous, and more likely to affect the part of the retina responsible for central vision, compared with their counterparts in Eu- rope [9]. The nomenclature for parasite popu- lations should reflect the discriminatory power of the genetic locus. Thus, the use of the type I, II, and III nomenclature for different techniques that use different ge- netic markers enhances confusion about what can be expected for the strain defi- nition; instead, nomenclature that indi- cates geographical origin should be pre- ferred. Of importance for clinicians is that the available genetic markers that have been studied in environmental and clinical samples, whether by single-locus marker, multilocus, or haplotype analysis, cannot predict clinical outcome. What we need now is a true and clinically relevant par- asite genotype classification system, and we need to evaluate the presence of ROP16 polymorphisms and of the insertion-de- letion polymorphism in the promoter re- gion of the gene ROP18 in Toxoplasma strains from clinical samples [10]. Jorge Enrique Go ´ mez-Marı ´n Grupo de Estudio en Parasitologı ´a Molecular, Universidad del Quindı ´o, Armenia, Colombia References 1. Ajzenberg D, Yera H, Marty P, et al. Genotype of 88 Toxoplasma gondii isolates associated with toxoplasmosis in immunocompromised patients and correlation with clinical findings. J Infect Dis 2009; 199:1155–67. 2. Lehmann T, Marcet PL, Graham DH, Dahl ER, Dubey JP. From the cover: globalization and the population structure of Toxoplasma gondii. Proc Natl Acad Sci U S A 2006; 103: 11423–8. 3. Sibley LD, Ajioka JW. Population structure of Toxoplasma gondii: clonal expansion driven by infrequent recombination and selective sweeps. Annu Rev Microbiol 2008; 62:329–51. 4. Howe DK, Sibley LD. Toxoplasma gondii comprises three clonal lineages: correlation of parasite genotype with human disease. J Infect Dis 1995; 172:1561–6. 5. Dubey JP, Su C, Cortes JA, et al. Prevalence of Toxoplasma gondii in cats from Colombia, South America and genetic characterization of T. gondii isolates. Vet Parasitol 2006; 141:42–7. 6. Morisset S, Peyron F, Lobry J, et al. Serotyping of Toxoplasma gondii: striking homogeneous pattern between acute and asymptomatic in- fections within Europe and South America. Microbes Infect 2008; 10:742–7. 7. Peyron F, Lobry JR, Musset K, et al. Serotyping of Toxoplasma gondii in chronically infected pregnant women: predominance of type II in Europe and types I and III in Colombia (South America). Microbes Infect 2006; 8:2333–40. 8. SYROCOT. Effectiveness of prenatal treat- ment for congenital toxoplasmosis: a meta- analysis of individual patients’ data. Lancet 2007; 369:115–22. 9. Gilbert RE, Freeman K, Lago EG, et al. Ocular sequelae of congenital toxoplasmosis in Brazil compared with Europe. The European Mul- ticentre Study on Congenital Toxoplasmosis (EMSCOT). PLoS Negl Trop Dis 2008; 2:e277. 10. Saeij JPJ, Boyle JP, Coller S, Taylor S, Sibley LD. Polymorphic secreted kinases are key vir- ulence factors in toxoplasmosis. Science 2006; 314:1780–3. Potential conflicts of interest: none reported. Financial support: none reported. Reprints or correspondence: Dr Jorge Go ´mez-Marı ´n, Grupo de Estudio en Parasitologı ´a Molecular, Universidad del Quindı ´o, Avenida Bolivar 12N, Armenia, Quindio 630004, Colombia (gepamol2@uniquindio.edu.co). The Journal of Infectious Diseases 2009; 200:1012  2009 by the Infectious Diseases Society of America. All rights reserved. 0022-1899/2009/20006-0022$15.00 DOI: 10.1086/605414 Reply to Go ´ mez-Marı´n To the Editor—Go ´mez-Marı´n raises some interesting issues in his letter [1]. We agree by guest on October 14, 2011 jid.oxfordjournals.org Downloaded from