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Lineage and Virulence of Streptococcus suis Serotype 2 Isolates from North America - Vol. 17 No. 12 - December 2011 - Emerging Infectious Disease journal - CDC

Lineage and Virulence of Streptococcus suis Serotype 2 Isolates from North America - Vol. 17 No. 12 - December 2011 - Emerging Infectious Disease journal - CDC

Volume 17, Number 12—December 2011


Lineage and Virulence of Streptococcus suis Serotype 2 Isolates from North America

Nahuel Fittipaldi, Jiangu Xu, Sonia Lacouture, Prasit Tharavichitkul, Makoto Osaki, Tsutomu Sekizaki, Daisuke Takamatsu, and Marcelo GottschalkComments to Author 
Author affiliations: Université de Montréal, St-Hyacinthe, Quebec, Canada (N. Fittipaldi, S. Lacouture, M. Gottschalk); National Institute for Communicable Disease Control and Prevention, Beijing, People’s Republic of China (J. Xu); Chiang Mai University, Chiang Mai, Thailand (P. Tharavichitkul); Agriculture, Forestry and Fisheries Research Council, Tokyo, Japan (M. Osaki); The University of Tokyo, Tokyo (T. Sekizaki); National Institute of Animal Health, Tsukuba, Japan (D. Takamatsu)
Suggested citation for this article


We performed multilocus sequence typing of 64 North American Streptococcus suis serotype 2 porcine isolates. Strains were sequence type (ST) 28 (51%), ST25 (44%), and ST1 (5%). We identified nonrandom associations between STs and expression of the virulence markers suilysin (SLY), muramidase-relased protein (MRP), and extracellular factor (EF). Expression of pili encoded by the srtF and srtG pilus clusters was also nonrandomly associated with STs. ST1 strains were SLY+ EF+ MRP+ srtF pilus+ srtG pilus−. ST25 strains were SLY− EF− MRP− srtF pilus− srtG pilus+, and most ST28 strains were SLY− MRP+ EF− srtF pilus+ srtG pilus+. ST28 isolates proved essentially nonvirulent in a mouse infection model; ST25 strains showed moderate virulence and ST1 isolates were highly virulent. ST1 is responsible for a high proportion of S. suis disease in humans worldwide. Its presence in North America indicates that potential zoonotic S. suis outbreaks in this continent cannot be disregarded.

Streptococcus suis causes meningitis and septicemia in pigs and is a zoonotic agent (1). In the Western hemisphere, human S. suis disease is infrequent and usually affects workers in the swine industry. However, S. suis is the most commonly reported cause of streptococcal meningitis in adults in Vietnam and the second in Thailand (2,3). Two outbreaks of human S. suis disease have occurred in People’s Republic of China, affecting hundreds of persons and causing 39 deaths (4). Most cases of animal and human S. suis infection have been caused by serotype 2 strains (5). The percentage of S. suis serotype 2 strains recovered from diseased pigs and the number of cases of human disease is lower in North America than in other parts of the world (6,7).

Multilocus sequence typing (MLST) has shown that S. suis serotype 2 strains can be divided into at least 16 sequence types (STs). Closely related STs are grouped in the so-called ST complexes. Although ST complexes 1, 27, and 87 dominate the S. suis population, most invasive isolates belong to the ST1 complex (8). For example, most strains isolated from human patients in Japan were ST1 (9), whereas those causing the human outbreaks in People’s Republic of China were ST7, included in the ST1 complex (10,11). However, Takamatsu et al. showed that 80% of the isolates recovered from blood or cerebrospinal fluid of humans in Thailand belonged to STs grouped in the ST27 complex (12).

Most of the S. suis serotype 2 strains genotyped so far by MLST originated in Europe and Asia (812). Isolates from Canada and the United States have received less attention. In this study, we used MLST to genotype a relatively large collection of US and Canadian S. suis serotype 2 strains.

Suggested citation for this article: Fittipaldi N, Xu J, Lacouture S, Tharavichitkul P, Osaki M, Sekizaki T, et al. Lineage and virulence of Streptococcus suis serotype 2 isolates from North America. Emerg Infect Dis [serial on the Internet]. 2011 Dec [date cited]. http://dx.doi.org/10.3201/eid1712.110609External Web Site Icon
DOI: 10.3201/eid1712.110609

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