Kotaro Suzuki Kotaro Suzuki

Additional information is available at the end of the chapter Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/66936

#### **Abstract**

This chapter focuses on *Staphylococcus aureus* (SA) infections in athletes. Previous SA infection studies performed starting in the 1980s examined close physical contact athletes, with a focus primarily on injured skin. However, more recent studies of skin SA transmission in athletes were conducted using molecular epidemiology. When participants in sports having a greater duration of competition were examined, results indicated that there was prolonged contact between athletes on the same team and athletes from other teams. These findings demonstrate that effective measures for preventing SA infections are urgently needed. Factors that can affect skin SA infections include high rates of SA nasal colonization, the type of "position on a team," repeated skin-to-skin contact, and perspiration that occurs during exercise in SA nasal carriers. Thus, it should be possible to utilize molecular typing methods to assess skin-to-skin contact in athletes. This study summarizes the current understanding of SA infections in athletes. In order to develop preventive strategies, it will be necessary to further elucidate the predisposing factors and mechanisms behind SA infections and the subsequent transmission in athletes.

**Keywords:** athletes, transmission, physical contact, genotyping

### **1. Introduction**

*Staphylococcus aureus* (SA) infections and its transmission among athletes have long been of interest to sports medicine scientists. SA is very well adapted to colonize the human skin, as the human body provides major ecological niches for the species. Although originally thought to be a nosocomial pathogen, it has become a rapidly emerging, problematic infection in athletes [1]. When outbreaks occur, the infection is spread through repeated skin-to-skin contact, especially due to physical contact between the broken skin of players during games and practices. In addition, sharing contaminated equipment [2], turf burns, and shaving [3]

© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2017 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

also contribute to the high incidence of infection among athletes. A review of past studies of SA infections in athletes suggested that the risk factors associated with the outbreaks could be classified into three categories (**Figure 1**). These include direct contact (which refers to "contact sports" where physical contact between players is an acceptable part of the sport), nosocomial infections, and skin wounds. The infections that occur during these outbreaks can also disrupt or potentially eliminate the opportunity for a team to compete at the highest level of their sport. Furthermore, outbreaks of infectious diseases can additionally spread to the player's social contacts and propagate within their communities [4, 5]. However, the association between direct physical contact and the SA transmission has yet to be fully understood.

The primary goal of the review presented in this chapter is to provide a better understanding of SA infections and the potential relationship with the associated sports activity. This chapter is divided into four parts, with the first section summarizing the latest insights into the sports activity related to SA infections and risk factors. In the second part, we focus on the latest insights into the determinants of SA nasal carriage and skin infections. As nasal carriers may be the reservoir responsible for the transmission in athletes and teams, this section describes the first high-throughput SA nasal carriage effort for large numbers of SA from athletes. As nasal carriers may be the reservoir responsible for the transmission in athletes and teams, this section describes the first high-throughput SA nasal carriage genotyping effort that has been used to examine the SA transmission in athletes. Previous reports have shown that nasal carriage may play a key role in the epidemiology and pathogenesis of SA infections [6, 7]. The third part presents information on our current understanding on how SA can thrive on the skin and be easily transmitted from person to person via sweat. Thus, when a sport involves physical contact, this route is likely to be the major mode of transmission between the athletes. In the final section, we discuss the high-throughput genotyping effort that has been undertaken in order to investigate SA transmission in athletes.

**Figure 1.** A hypothetical example of a *Staphylococcus aureus* infection resulting in an outbreak within an athletic setting. *Staphylococcus aureus* outbreaks are classified into three categories, which include "direct contact," "nosocomial infection," and "skin wound." These hypothetical schemes will need to be further examined in future experiments.

The discovery of SA outbreaks in athletes taking part in physical contact sports is not new. In 1982, Bartlett et al. published the first scientific paper on SA infections in athletes [8]. This study examined 26 players of a high school football team and reported finding a total of 55 lesions, with two players found to have Methicillin-Susceptible Staphylococcus Aureus (MSSA), while 24 had methicillin-resistant SA (MRSA). There was no pathogen growth observed for any of the players. There were three essential findings observed and confirmed by the authors in subsequent studies. First, the majority of the lesions observed were located on the extremities and in areas not usually covered by a football uniform or other apparels. Second, 61% of the affected players reported the development of a furuncle at the site of a previously open wound, while 27% reported the development of a furuncle at the site of a previous bruise. Third, cultures obtained from the lesions of two players grew SA that was sensitive to nafcillin, clindamycin, erythromycin, cephalosporin, tetracycline, and sulfa and resistant to penicillin and ampicillin. This is of importance, as infections with drug-resistant bacteria may lead to longer and more costly hospital care, in addition to an increase in the risk of dying from the infection.

also contribute to the high incidence of infection among athletes. A review of past studies of SA infections in athletes suggested that the risk factors associated with the outbreaks could be classified into three categories (**Figure 1**). These include direct contact (which refers to "contact sports" where physical contact between players is an acceptable part of the sport), nosocomial infections, and skin wounds. The infections that occur during these outbreaks can also disrupt or potentially eliminate the opportunity for a team to compete at the highest level of their sport. Furthermore, outbreaks of infectious diseases can additionally spread to the player's social contacts and propagate within their communities [4, 5]. However, the association between direct physical contact and the SA transmission has yet to be fully

The primary goal of the review presented in this chapter is to provide a better understanding of SA infections and the potential relationship with the associated sports activity. This chapter is divided into four parts, with the first section summarizing the latest insights into the sports activity related to SA infections and risk factors. In the second part, we focus on the latest insights into the determinants of SA nasal carriage and skin infections. As nasal carriers may be the reservoir responsible for the transmission in athletes and teams, this section describes the first high-throughput SA nasal carriage effort for large numbers of SA from athletes. As nasal carriers may be the reservoir responsible for the transmission in athletes and teams, this section describes the first high-throughput SA nasal carriage genotyping effort that has been used to examine the SA transmission in athletes. Previous reports have shown that nasal carriage may play a key role in the epidemiology and pathogenesis of SA infections [6, 7]. The third part presents information on our current understanding on how SA can thrive on the skin and be easily transmitted from person to person via sweat. Thus, when a sport involves physical contact, this route is likely to be the major mode of transmission between the athletes. In the final section, we discuss the high-throughput genotyping effort

that has been undertaken in order to investigate SA transmission in athletes.

**Figure 1.** A hypothetical example of a *Staphylococcus aureus* infection resulting in an outbreak within an athletic setting. *Staphylococcus aureus* outbreaks are classified into three categories, which include "direct contact," "nosocomial infection," and "skin wound." These hypothetical schemes will need to be further examined in future experiments.

understood.

32 Frontiers in Frontiers in Staphylococcus Aureus *Staphylococcus aureus*

Since this initial report, various infectious disease outbreaks have been reported [9]. Sosin et al. [10] additionally reported an outbreak of furuncles in athletes in the state of Kentucky in the USA. The outbreak involved members of the high school football and basketball teams, with a total of 62 lesions reported in these affected athletes. In this school, the basketball season overlapped with the end of the football season, with the two teams sharing a locker room. In addition, six of the players participated on both of the teams. Based on these findings, the authors hypothesized that close physical contact was a risk factor for SA transmission in athletes. The majority of affected players were treated with oral antibiotics, with three players developing infections that did not respond to oral therapy, thereby requiring hospitalization for intravenous antibiotic therapy. One of these hospitalized players subsequently developed a disseminated SA infection and a lung abscess. A total of 81% of the observed lesions were found on the extremities. Moreover, players who sustained a skin injury were three times more likely to develop an infection compared to those who did not report any skin injury. The use of the school showers and locker room and the sharing of clothing and towels were not found to be risk factors for SA infections. Although SA was isolated from 14 of 52 (27%) nasal cultures collected from the athletes, this was not higher than the proportion of SA-positive nasal cultures found in a group of student controls.

These studies provided valuable information and have helped encourage the development of subsequent investigations into additional components affecting SA skin infections. Furthermore, the majority of all of the studies performed because the initial publication has focused on investigations of the effects of physical contact on SA skin infection.

As Suzuki and Tagami [11] discussed in detail, physical contact contributes to SA transmission. Their study identified several factors including an outbreak of SA skin infection in a collegiate men's rugby team. The athletes examined had all started the rugby season with a training camp that was in close proximity to where they lived and which was conducted between August 4 and 25 in 2011 (**Figure 2A**). SA infections were found in 14 (20%) of the 69 healthy rugby players between September 10 and October 21 of 2011 (**Table 1**). One team member required hospitalization during October 2011 in order to treat an abscess that was secondary to the SA infection. As other members of the team also developed skin infections,

**Figure 2.** Epidemic curve of the initial skin infections due to *Staphylococcus aureus* among collegiate rugby players (A). Field position diagram of players who developed *Staphylococcus aureus* infection (B). See **Table 1** for position-specific attack rates. 1 and 3, prop; 2, hooker; 4 and 5, lock; 6 and 7, flanker; 8, number 8; 9, scrum half; 10, fly half; 11 and 14, wings; 12 and 13, center back; and 15, fullback. Players infected with *Staphylococcus aureus* (×). Anatomical locations of infection sites (C). Front and back side of body. Filled circles, skin lesions (unpublished data).

screening was begun on October 6. The dispersion of the outbreak was trimodal, with 28, 50, and 21% occurring between September 10 and 20, between October 2 and 10, and between October 20 and 21 (**Figure 2A**). The infections developed in 11 forwards and three back-positioned players (**Figure 2B**). The infection rate was higher among the forwards versus the back positions (28 vs. 7%) (**Table 1**), with the flanker position exhibiting a greater likelihood of becoming infected compared to the other players. The forehead, back, elbow, and thumb comprised the primary sites of SA infection (**Figure 2B**). Infections tended to occur most frequently on the areas that were not covered by athletic apparel, such as the elbows, forearms, knees, and lower legs [1, 8]. These trends suggest that competitive practices lead to repeated direct contact. Nine crural abscesses were located on the front and back of the legs near or on


The overall attack rate = 10%.

screening was begun on October 6. The dispersion of the outbreak was trimodal, with 28, 50, and 21% occurring between September 10 and 20, between October 2 and 10, and between October 20 and 21 (**Figure 2A**). The infections developed in 11 forwards and three back-positioned players (**Figure 2B**). The infection rate was higher among the forwards versus the back positions (28 vs. 7%) (**Table 1**), with the flanker position exhibiting a greater likelihood of becoming infected compared to the other players. The forehead, back, elbow, and thumb comprised the primary sites of SA infection (**Figure 2B**). Infections tended to occur most frequently on the areas that were not covered by athletic apparel, such as the elbows, forearms, knees, and lower legs [1, 8]. These trends suggest that competitive practices lead to repeated direct contact. Nine crural abscesses were located on the front and back of the legs near or on

infection sites (C). Front and back side of body. Filled circles, skin lesions (unpublished data).

34 Frontiers in Frontiers in Staphylococcus Aureus *Staphylococcus aureus*

**Figure 2.** Epidemic curve of the initial skin infections due to *Staphylococcus aureus* among collegiate rugby players (A). Field position diagram of players who developed *Staphylococcus aureus* infection (B). See **Table 1** for position-specific attack rates. 1 and 3, prop; 2, hooker; 4 and 5, lock; 6 and 7, flanker; 8, number 8; 9, scrum half; 10, fly half; 11 and 14, wings; 12 and 13, center back; and 15, fullback. Players infected with *Staphylococcus aureus* (×). Anatomical locations of **Table 1.** Position-specific attack rates of clinical and *Staphylococcus aureus* and soft tissue infections among members of a rugby team (unpublished data).

the knee. In addition, most of the lesions were located on the extremities in areas that are not usually covered by the rugby uniform. However, SA isolates that resulted from the sharing of items, such as the contact bag, tackle bag, and bibs, were limited. Starting on November 3, oral fosfomycin calcium (1 g, two tablets) was administered three times daily for 5 days. After 22 days, there was a decrease in the number of SA nasal carriers. This intervention prevented further dissemination of the SA infection among the team members.

This report shows that the epidemic curves can provide considerable information about the outbreaks such as the pattern of the spread, magnitude, time trend, and exposure and disease incubation periods. The epidemic curve in the present study was trimodal, with continuous, intermittent exposure and gradual increases in the numbers of infections. This type of epidemic curve is typical of person-to-person spread [12]. Classic epidemic curves from propagating outbreaks comprise successively taller peaks, distanced one incubation period apart. The two most common sources of SA spread were contaminated hands and physical contact with athletes [13, 14]. Multimodal peaks are representative of SA outbreaks and comprise a risk factor for such outbreaks during physical contact sports [8]. These previous studies support a person-to-person contact method for the transmittal of the disease, with skin injuries serving as an entrance point for the infectious organisms.
