Genetic Recombination and Cryptosporidium hominis Virulent Subtype IbA10G2 - Vol. 19 No. 10 - October 2013 - Emerging Infectious Disease journal - CDC

full-text ►
Genetic Recombination and Cryptosporidium hominis Virulent Subtype IbA10G2 - Vol. 19 No. 10 - October 2013 - Emerging Infectious Disease journal - CDC


Table of Contents
Volume 19, Number 10–October 2013

Volume 19, Number 10—October 2013

Research

Genetic Recombination and Cryptosporidium hominis Virulent Subtype IbA10G2

Article Contents

• Materials and Methods
• Results
• Discussion
• Acknowledgments
• References
• Figure 1
• Figure 2
• Figure 3
• Figure 4
• Table 1
• Table 2
• Table 3
• Table 4
• Suggested Citation

Na Li, Lihua Xiao, Vitaliano A. Cama, Ynes Ortega, Robert H. Gilman, Meijin Guo, and Yaoyu Feng 

Author affiliations: East China University of Science and Technology, Shanghai, China (N. Li, M. Guo, Y. Feng); Centers for Disease Control and Prevention, Atlanta, Georgia, USA (N. Li, L. Xiao, V.A. Cama); University of Georgia, Griffin, Georgia, USA (Y. Ortega); Johns Hopkins University, Baltimore, Maryland, USA (R.H. Gilman)

Suggested citation for this article

Abstract

Little is known about the emergence and spread of virulent subtypes of Cryptosporidium hominis, the predominant species responsible for human cryptosporidiosis. We conducted sequence analyses of 32 genetic loci of 53 C. hominis specimens isolated from a longitudinally followed cohort of children living in a small community. We identified by linkage disequilibrium and recombination analyses only limited genetic recombination, which occurred exclusively within the 60-kDa glycoprotein gene subtype IbA10G2, a predominant subtype for outbreaks in industrialized nations and a virulent subtype in the study community. Intensive transmission of virulent subtype IbA10G2 in the study area might have resulted in genetic recombination with other subtypes. Moreover, we identified selection for IbA10G2 at a 129-kb region around the 60-kDa glycoprotein gene in chromosome 6. These findings improve our understanding of the origin and evolution of C. hominis subtypes and the spread of virulent subtypes.

Cryptosporidium spp. are emerging pathogens of humans and a variety of vertebrates, and cause severe diarrhea in immunocompetent and immunocompromised persons (1). Cryptosporidium hominis is responsible for > 70% of human infections in most areas, especially North America and developing countries (2). C. hominis is primarily transmitted anthroponotically, has several transmission routes, and causes numerous waterborne outbreaks of diarrheal illness each year in the United States and other industrialized nations.
Among several C. hominis subtype groups (e.g., Ia, Ib, Id, Ie, If, Ig) identified by sequence analysis of the 60-kDa glycoprotein (gp60) gene, the Ib subtype is the major subtype responsible for waterborne and foodborne outbreaks of cryptosporidiosis in many countries. Subtype IbA10G2 has been found in ≈50% of C. hominis–associated outbreaks in the United States, including the massive outbreak in Milwaukee, Wisconsin, USA, in 1993 (2,3). It is the only subtype identified in cryptosporidiosis outbreaks by C. hominis in countries in Europe and in Australia (4–11). In a longitudinal birth-cohort study of cryptosporidiosis in a periubran shantytown in Lima, Peru, IbA10G2 was more virulent than other C. hominis subtypes (12). Genetic determinants for virulence of Cryptosporidium spp. and reasons for emergence of virulent subtypes are poorly understood because of availability of only limited genomic sequence data and lack of robust cultivation systems and genetic manipulation tools (13).
We conducted a comparative population genetic analysis of virulent C. hominis subtype IbA10G2 in children living in a periurban community in Lima, Peru, by multilocus sequence typing (MLST) of 32 genetic markers. Data obtained should be useful in understanding emergence and spread of virulent C. hominis subtypes.