Streptococcus suis and Porcine Reproductive and Respiratory Syndrome, Vietnam

To the Editor: Streptococcus suis, an opportunistic pathogen of swine, is an emerging zoonotic pathogen among humans (1). In Vietnam, S. suis is the leading cause of human acute bacterial meningitis (2). Infection in humans is associated with direct exposure to infected pigs or infected raw or undercooked pork products (3). Of the 35 S. suis serotypes, only a limited number are pathogenic for pigs, and clinical cases in humans have most frequently been attributed to serotype 2 (SS2) (1). In Vietnam during September 2006–November 2007, the carrier rate of S. suis among slaughterhouse pigs was 41% (222/542); SS2 was the most frequently identified serotype in 14% (45/317) of S. suis isolations (4). 
 
Porcine respiratory and reproductive syndrome (PRRS) is a major disease affecting the swine industry globally; the severity of PRRS in pigs can be increased by co-infection with S. suis (5). In 2010, PRRS outbreaks in swine were reported in 49 of 63 Vietnamese provinces (Technical Appendix Figure) (6). To understand the potential implications of swine PRRS outbreaks for human S. suis disease, we investigated co-infections of S. suis and PRRS virus (PRRSV) in sick pigs in 3 provinces of Vietnam during the PRRS outbreaks in 2010 (Technical Appendix Figure). 
 
We sampled 108 farms reporting pigs that had a clinical syndrome consistent with PRRSV infections in the provinces of Thai Binh (May), Tien Giang (July), and Soc Trang (July). Samples were blood from sick febrile pigs and postmortem tissue from freshly culled pigs. To confirm swine PRRS outbreaks, we performed reverse transcription real-time PCR on 1 randomly selected plasma sample from each farm (7). A total of 103 (95%) plasma samples from 103 farms tested positive for PRRSV (Chinese genotype). We additionally selected 3 PRRSV-positive farms per province for comprehensive PRRSV screening of all 42 sampled pigs; 100% of samples from the 9 farms were PRRSV positive. After swine outbreaks ended, blood samples from 52 healthy pigs from 10 farms that had no recent history of PRRS were collected from Tien Giang Province (March 2011). None of the 52 plasma samples from the 10 control farms tested positive for PRRSV. 
 
We investigated the presence of SS2 in blood and tissue samples from pigs on PRRS- and non-PRRS–affected farms by bacterial culture (Technical Appendix Table). A total of 534 specimens from sick pigs yielded 9 (1.7%) SS2 isolates. One (2%) of 52 specimens from the healthy control pigs yielded a non-SS2 S. suis isolate. S. suis has been proposed to contribute to the spread of antimicrobial resistance genes to other human pathogenic streptococci (8). The antimicrobial susceptibility results of 9 SS2 isolates by disk diffusion (9) revealed a high prevalence (6/9, 66%) of resistance to tetracycline, tobramycin, enrofloxacin, and either marbofloxacin or chloramphenicol. 
 
PCR amplification of the 16SrDNA gene (10) and the cps2J gene (2) was performed on all blood samples to detect S. suis and SS2, respectively. Ninety-two (18%) of 521 sick pigs from PRRSV outbreak farms were systemically infected with S. suis. In contrast, no healthy pigs from control farms were positive for S. suis by PCR (Technical Appendix Table). The SS2-cps2J–specific PCR was positive for 58 (11%) of 521 samples, and the S. suis-16SrDNA PCR was positive for 55 (11%). Twenty-one of the 16SrDNA-positive samples also were positive for cps2J-PCR, which indicated that 34 (7%) sick pigs were infected with non-SS2 strains. Therefore, SS2 accounted for most (58 [63%] of 92) S. suis–positive detections. The bacterial load of SS2 in blood ranged from 1 × 103 CFU/mL–1 to 8.3 × 106 CFU/mL–1 (median 9.2 × 103 CFU/mL–1). Overall, SS2 was found in 58 (11%) sick pigs and on 33 (32%) PRRS outbreak farms. The higher prevalence (92 [18%]) of systemic infections of S. suis and SS2 with high bacterial load in pigs from PRRS outbreak farms compared with prevalence on nonoutbreak farms (1 [2%] of 52) suggests increased systemic S. suis infections during swine PRRS outbreaks (p = 0.001, Fisher exact test). 
 
We investigated the possible association between swine PRRS outbreaks and human S. suis infection. Case reports of confirmed human infections during 2007–2010 at the 2 tertiary referral hospitals in Hanoi and Ho Chi Minh City were reviewed. The number of human S. suis infection cases increased in August 2010 in southern Vietnam and doubled in northern Vietnam during May–August and October–November 2010 (Figure). Swine PRRS outbreaks were reported during June–September and March–December 2010 in southern and northern provinces, respectively (6) (Technical Appendix Figure). Most patients with S. suis infection during these periods resided in provinces reporting swine PRRS outbreaks. Our data suggest a possible temporal association between swine PRRS outbreaks and human S. suis infections. 
 
 
 
Figure 
 
Monthly distribution of human Streptococcus suis infections in 2 referral hospitals, Vietnam, 2007–2010. Humans infected with S. suis during 2007–2009 are presented as mean total cases per month. Dark gray and black bars represent the ... 
 
 
 
We demonstrated increased prevalence of systemic S. suis and SS2 infection in pigs co-infected with PRRSV during the 2010 swine outbreaks in Vietnam. The results indicate an increased risk for potential zoonotic transmission of S. suis to humans during outbreaks of PRRS in swine. 
 
Technical Appendix: 
Systemic Streptococcus suis infections in sick pigs from farms with confirmed porcine reproductive and respiratory syndrome and temporal distribution of outbreaks of porcine reproductive and respiratory syndrome in swine, 3 provinces, Vietnam, 2010. 
 
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Streptococcus suis and Porcine Reproductive and Respiratory Syndrome, Vietnam
To the Editor: Streptococcus suis, an opportunistic pathogen of swine, is an emerging zoonotic pathogen among humans (1). In Vietnam, S. suis is the leading cause of human acute bacterial meningitis (2). Infection in humans is associated with direct exposure to infected pigs or infected raw or undercooked pork products (3). Of the 35 S. suis serotypes, only a limited number are pathogenic for pigs, and clinical cases in humans have most frequently been attributed to serotype 2 (SS2) (1). In Vietnam during September 2006-November 2007, the carrier rate of S. suis among slaughterhouse pigs was 41% (222/542); SS2 was the most frequently identified serotype in 14% (45/317) of S. suis isolations (4).
Porcine respiratory and reproductive syndrome (PRRS) is a major disease affecting the swine industry globally; the severity of PRRS in pigs can be increased by co-infection with S. suis (5). In 2010, PRRS outbreaks in swine were reported in 49 of 63 Vietnamese provinces (online Technical Appendix Figure, wwwnc.cdc.gov/ EID/article/19/2/12-0470-Techapp1. pdf) (6). To understand the potential implications of swine PRRS out-breaks for human S. suis disease, we investigated co-infections of S. suis and PRRS virus (PRRSV) in sick pigs in 3 provinces of Vietnam during the PRRS outbreaks in 2010 (online Technical Appendix Figure).
We sampled 108 farms reporting pigs that had a clinical syndrome consistent with PRRSV infections in the provinces of Thai Binh (May), Tien Giang (July), and Soc Trang (July). Samples were blood from sick febrile pigs and postmortem tissue from freshly culled pigs. To confirm swine PRRS outbreaks, we performed reverse transcription real-time PCR on 1 randomly selected plasma sample from each farm (7). A total of 103 (95%) plasma samples from 103 farms tested positive for PRRSV (Chinese genotype). We additionally selected 3 PRRSV-positive farms per province for comprehensive PRRSV screening of all 42 sampled pigs; 100% of samples from the 9 farms were PRRSV positive. After swine outbreaks ended, blood samples from 52 healthy pigs from 10 farms that had no recent history of PRRS were collected from Tien Giang Province (March 2011). None of the 52 plasma samples from the 10 control farms tested positive for PRRSV.
We investigated the presence of SS2 in blood and tissue samples from pigs on PRRS-and non-PRRS-affected farms by bacterial culture (online Technical Appendix Table). A total of 534 specimens from sick pigs yielded 9 (1.7%) SS2 isolates. One (2%) of 52 specimens from the healthy control pigs yielded a non-SS2 S. suis isolate. S. suis has been proposed to contribute to the spread of antimicrobial resistance genes to other human pathogenic streptococci (8). The antimicrobial susceptibility results of 9 SS2 isolates by disk diffusion (9) revealed a high prevalence (6/9, 66%) of resistance to tetracycline, tobramycin, enrofloxacin, and either marbofloxacin or chloramphenicol.
PCR amplification of the 16SrD-NA gene (10) and the cps2J gene (2) LETTERS was performed on all blood samples to detect S. suis and SS2, respectively. Ninety-two (18%) of 521 sick pigs from PRRSV outbreak farms were systemically infected with S. suis. In contrast, no healthy pigs from control farms were positive for S. suis by PCR (online Technical Appendix Table). The SS2-cps2J-specific PCR was positive for 58 (11%) of 521 samples, and the S. suis-16SrD-NA PCR was positive for 55 (11%). Twenty-one of the 16SrDNA-positive samples also were positive for cps2J-PCR, which indicated that 34 (7%) sick pigs were infected with non-SS2 strains. Therefore, SS2 accounted for most (58 [63%] of 92) S. suis-positive detections. The bacterial load of SS2 in blood ranged from 1 × 10 3 CFU/ mL -1 to 8.3 × 10 6 CFU/mL -1 (median 9.2 × 10 3 CFU/mL -1 ). Overall, SS2 was found in 58 (11%) sick pigs and on 33 (32%) PRRS outbreak farms.  Figure). Most patients with S. suis infection during these periods resided in provinces reporting swine PRRS outbreaks. Our data suggest a possible temporal association between swine PRRS outbreaks and human S. suis infections.
We demonstrated increased prevalence of systemic S. suis and SS2 infection in pigs co-infected with PRRSV during the 2010 swine outbreaks in Vietnam. The results indicate an increased risk for potential zoonotic transmission of S. suis to humans during outbreaks of PRRS in swine.