MAJOR ARTICLE
A High-Morbidity Outbreak of Methicillin-Resistant
Staphylococcus aureus among Players on a College
Football Team, Facilitated by Cosmetic Body Shaving
and Turf Burns
Elizabeth M. Begier,1,4 Kasia Frenette,1 Nancy L. Barrett,1,2 Pat Mshar,1 Susan Petit,1,2 Dave J. Boxrud,5
Kellie Watkins-Colwell,3 Sheila Wheeler,3 Elizabeth A. Cebelinski,5 Anita Glennen,5 Dao Nguyen,4,6 James L. Hadler,1
and the Connecticut Bioterrorism Field Epidemiology Response Teama
1
Infectious Diseases Division and 2Connecticut Active Bacterial Core Surveillance Project, Connecticut Department of Public Health, Hartford,
and 3Student Health Services of Sacred Heart University, Fairfield, Connecticut; 4Epidemic Intelligence Service Program, Centers for Disease
Control and Prevention, Atlanta, Georgia; 5Division of Public Health Laboratories, Minnesota Department of Public Health, Minneapolis, Minnesota;
and 6Los Angeles County Department of Health Services, Los Angeles, California
Background. Athletics-associated methicillin-resistant Staphylococcus aureus (MRSA) infections have become
a high-profile national problem with substantial morbidity.
Methods. To investigate an MRSA outbreak involving a college football team, we conducted a retrospective
cohort study of all 100 players. A case was defined as MRSA cellulitis or skin abscess diagnosed during the period
of 6 August (the start of football camp) through 1 October 2003.
Results. We identified 10 case patients (2 of whom were hospitalized). The 6 available wound isolates had
indistinguishable pulsed-field gel electrophoresis patterns (MRSA strain USA300) and carried the Panton-Valentine
leukocidin toxin gene, as determined by polymerase chain reaction. On univariate analysis, infection was associated
(P ! .05) with player position (relative risk [RR], 17.5 and 11.7 for cornerbacks and wide receivers, respectively),
abrasions from artificial grass (i.e., “turf burns”; RR, 7.2), and body shaving (RR, 6.1). Cornerbacks and wide
receivers were a subpopulation with frequent direct person-to-person contact with each other during scrimmage
play and drills. Three of 4 players with infection at a covered site (hip or thigh) had shaved the affected area, and
these infections were also associated with sharing the whirlpool ⭓2 times per week (RR, 12.2; 95% confidence
interval, 1.4–109.2). Whirlpool water was disinfected with dilute povidone-iodine only and remained unchanged
between uses.
Conclusions. MRSA was likely spread predominantly during practice play, with skin breaks facilitating infection. Measures to minimize skin breaks among athletes should be considered, including prevention of turf burns
and education regarding the risks of cosmetic body shaving. MRSA-contaminated pool water may have contributed
to infections at covered sites, but small numbers limit the strength of this conclusion. Nevertheless, appropriate
whirlpool disinfection methods should be promoted among athletic trainers.
Staphylococcal skin infections due to methicillin-susceptible Staphylococcus aureus (MSSA) are a well-documented complication of participation on athletic teams
Received 12 April 2004; accepted 29 June 2004; electronically published 26
October 2004.
a
Members of the study group are listed at the end of the text.
Reprints or correspondence: Dr. Elizabeth M. Begier, Connecticut Dept. of Public
Health, Infectious Diseases Div., 410 Capitol Ave., MS#11, Hartford, CT 06134
([email protected]).
Clinical Infectious Diseases 2004; 39:1446–53
2004 by the Infectious Diseases Society of America. All rights reserved.
1058-4838/2004/3910-0008$15.00
1446 • CID 2004:39 (15 November) • Begier et al.
[1–4]. Recently, community-acquired methicillin-resistant S. aureus (MRSA) infections have been increasingly
reported among athletes and, in some cases, have required hospitalization and surgery [5–7]. Transmission
via person-to-person contact during practice or competitive play has been implicated in outbreaks involving
wrestling and rugby football teams [5–7]. The sharing
of equipment (i.e., sensor wires) has been linked to
transmission of MRSA among fencers [5].
Football teams, in particular, have emerged as a common population in which MRSA outbreaks occur, with
several high-profile outbreaks publicized during 2003
[8]. High school, college, and professional players have been
affected [8–10]. A recent report described 2 outbreaks among
college football players; possible risk factors were abrasions due
to artificial grass (i.e., “turf burns”), skin shaving, and sharing
unwashed bath towels, balms, and lubricants [5]. We describe
an MRSA outbreak among members of a college football team
to inform clinicians and public health practitioners and to guide
related policy.
METHODS
The Connecticut Department of Public Health was notified on
3 September 2003 about a cluster of skin infections due to
MRSA among members of a college football team and, at that
time, initiated enhanced surveillance for MRSA skin infections
among players and the community. All athletes with skin lesions
were evaluated at the student health center. Health center staff
obtained swab specimens from the anterior nares of players,
trainers, and coaching staff to identify individuals with nasal
carriage. Swab samples from the groin, axillae, and nares of
patients with recurrent infections were obtained for culture.
We contacted nearby hospital laboratories to identify cultures
of wound specimens obtained from persons 15–25 years during
the period of July through September 2003 that yielded MRSA.
We called student health facilities of the 3 opposing teams that
were played during the outbreak to identify individuals with
skin infections.
We visited the athletic center and interviewed athletic trainers, coaching staff, and infected players regarding player routines and hygienic practices at the athletic center. We performed
a retrospective cohort study of members of the 2003 football
team by use of a face-to-face questionnaire to assess skin injuries, hygienic practices (e.g., sharing of towels and equipment), and other exposures during the interval between the
arrival at football camp and the announcement of the outbreak
(i.e., from 6 August through 6 September 2003). We also asked
about known risk factors for MRSA (e.g., health care contacts
[such as physician visits, surgery, or hospitalization] and skin
conditions). We reviewed training room charts to obtain moredetailed information regarding whirlpool use.
We defined a case as culture-confirmed MRSA cellulitis or
skin abscess diagnosed in a player during the period from 6
August through 1 October 2003. Univariate relative risks were
calculated with use of Stata 7 software (Stata) [11]. We investigated confounding by use of stratified analysis and bivariate
logistic regression. MRSA isolates were subtyped at the Minnesota Department of Health’s Public Health Laboratory (Minneapolis) by PFGE. Methicillin resistance was confirmed at the
Minnesota Department of Health’s Public Health Laboratory
by detection of the mecA gene with PCR. The genetic element
carrying the mecA gene—staphylococcus cassette chromosome
mec (SCCmec)—was typed by PCR [12, 13]. Antibiotic susceptibility results from clinical laboratories were obtained. A subset
of isolates underwent quantitative susceptibility testing by broth
microdilution and testing for inducible clindamycin resistance
by the “D test” at the Minnesota Department of Health’s Public
Health Laboratory. All PFGE-indistinguishable wound and colonization isolates were tested at the Centers for Disease Control
and Prevention (Atlanta, GA) for enterotoxins A–E and H by
ELISA, for toxic shock syndrome toxin 1 by reverse passive
latex agglutination, and for the presence of Panton-Valentine
leukocidin toxin gene by PCR.
RESULTS
We identified 10 of 100 players who had skin infections due to
MRSA (attack rate, 10%). Skin infections due to MRSA were
not identified among trainers and coaching staff, non–football
players (i.e., other students and local residents), or members of
opposing teams. Primary MRSA infections occurred during a 3week period (between 16 August and 17 September) (figure 1).
Laboratory findings. Wound isolates were available from
6 of 10 case patients, and 3 colonization isolates were available
from the 2 hospitalized patients described below. PFGE showed
that all isolates had indistinguishable PFGE patterns indicative
of community-associated USA300 strain [14] and carried mecA
and SCCmec type IVa methicillin resistance gene alleles and
Panton-Valentine leukocidin toxin gene. Production of enterotoxins A–E and H and toxic shock syndrome toxin 1 were
not identified. Clinical laboratory testing revealed that all wound
isolates had identical susceptibility patterns revealing resistance
to cephalothin, erythromycin, oxacillin, and penicillin and susceptibility to ciprofloxacin, clindamycin, gatifloxacin, gentamicin, levofloxacin, linezolid, rifampin, tetracycline, trimethoprim-
Figure 1.
Date of onset of initial skin infections due to methicillinresistant Staphylococcus aureus (MRSA) among players on a college
football team during the period of August through September 2003.
MRSA Outbreak in a College Football Team • CID 2004:39 (15 November) • 1447
Table 1. Predictors of infections due to methicillin-resistant Staphylococcus aureus (MRSA) among 90 football
players, Connecticut, 2003.
Type of exposure
since start of football camp
Player position
Neither cornerback nor wide receiver
No. of
case
patients
Total no.
of players
MRSA
attack rate,
% of players
Relative risk (95% CI)
P
a
2
70
2.9
Wide receiver
Cornerback
Traumatic skin breaks and protective pads
4
4
12
8
33.3
50.0
11.7 (2.4–56.8)
17.5 (3.8–81.0)
.004
.001
Any abrasion, cut, or turf burn vs. none
Turf burns vs. no turf burns
Elbow pads
Body shavingb
9
9
1
72
50
10
12.5
18.0
10.0
2.3 (0.3–16.6)
7.2 (1.0–54.5)
3.2 (0.6–17.9)
.680
.038
.301
7
25
28.0
6.1 (1.7–22)
.004
Never
Once
At least twice
Anatomical location
No area shaved
Chest or abdomen
Arms or legs
Groin or genitals
Other (ankle, foot, axilla)
Training room whirlpool
History of use
Never
⭐1 Time/week
3
3
4
65
10
13
4.6
30.0
30.8
1.0 (Reference)
6.5 (1.5–27.9)
6.7 (1.7–26.3)
.004
3
3
2
3
0
65
13
8
7
3
4.6
23.1
25.0
42.9
0.0
1.0
5.0
5.4
9.3
0.0
4
1
49
14
8.2
7.1
⭓2 Times/week
Shared use
Never
⭐1 Time/week
⭓2 Times/week
Hygienic practices
Ever wear practice or game uniform
without laundering
Ever shower ⭓2 h after practice
5
27
18.5
2.3 (0.7–7.7)
.220
5
1
4
61
10
15
8.2
10.0
26.7
1.0 (Reference)
1.2 (0.2–9.4)
3.3 (1.0–10.7)
.080
6
1
46
15
13.0
6.7
1.4 (0.4–4.7)
0.6 (0.1–4.1)
.740
1.000
2
4
28
29
7.1
13.8
0.5 (0.1–2.5)
1.4 (0.4–4.6)
.713
.721
3
1
0
9
8
8
33.3
12.5
0.0
0.8 (0.2–3.0)
0.6 (0.1–4.4)
0.0 (Not calculable)
Any vs. none
Frequency
Wash hands ⭐2 times/day
Ever sleep or nap in locker room
Other (all self reported)
Antibiotic use in previous year
Surgery or hospitalization in previous year
History of skin infection in previous 2 years
1.0 (Reference)
(Reference)
(1.1–22.1)
(1.1–27.7)
(2.3–37.6)
(Not calculable)
.055
.090
.010
1.000
1.0 (Reference)
0.9 (0.1–7.2)
1.000
1.000
.590
a
By Fisher’s exact test, except for frequency data, in which P values were from Cuzick’s nonparametric test for trend across ordered
groups (i.e., test for trend associated with increasing frequency of behavior).
b
Shaving a body area other than the face (excluding “shaving” the head with hair clippers to produce a crew cut).
sulfamethoxazole, and vancomycin. This pattern was confirmed
by quantitative broth microdilution testing. Isolates were negative
for inducible clindamycin resistance by D test.
Patient characteristics. All case patients were males and
aged 17–22 years. Ten case patients had 13 infections (9 cases of
abscess and 4 cases of cellulitis) at the following sites: elbow, 4
1448 • CID 2004:39 (15 November) • Begier et al.
cases; thigh, 2; hip, 2; chin, 1; forearm, 1; wrist, 1; knee, 1; and
tibial plateau, 1. Eight players were treated as outpatients only;
all but 1 required ⭓7 days of frequent visits (median, 10 days;
range, 1–21 days) for wound care (i.e., irrigation and packing).
Hospitalized patients. One player was hospitalized initially
in early September because of cellulitis and possible septic ar-
patients (table 1). Remaining case patients were a linebacker
and a tight end.
Players who sustained turf burns had a risk of infection that
was 7 times higher than that for players without turf burns
(relative risk [RR], 7.2; 95% CI, 1.0–54.5). An additive interaction was seen between player position and turf burns, suggesting that players in high-risk positions were particularly at
risk if they sustained such abrasions (table 2). Times to wound
cleaning, wound coverage, and receipt of wound care by team
trainers were not predictive of infection risk. Only 10 players
used protective elbow pads. Use of such pads was associated
with a trend toward a higher risk of infection (RR, 3.2; 95%
CI, 0.6–17.9).
Overall, 25 players (28%) reported body shaving (i.e., shaving
an area of the body other than the face). Players reported
shaving the following sites: chest, 12 players; groin, 7; arms, 6;
legs, 2; abdomen, 2; ankle/foot, 2; and axillae, 1. Seven of these
25 players shaved 2 sites. Players who reported body shaving
were 6.1 times more likely to develop MRSA infections. Shaving
genitals or the groin was associated with a higher infection risk
(43%) than shaving other body sites (RR, 9.3; 95% CI, 2.3–
37.6). Three of 4 players with infections of covered sites (areas
normally covered by the football uniform, including hips and
thighs) had recently shaved these areas. The fourth player reported shaving the affected area before the start of camp. No
case patients reported sharing razors. As with turf burns, additive interaction was seen between player position and body
shaving, suggesting that players in high-risk positions increased
their risk by body shaving (table 2).
Training room charts recorded only therapeutic whirlpool
use. Chart reviews documented that only 5 players were directed
thritis. Gram stains of synovial fluid specimens obtained from
this patient showed rare WBCs and no organisms (fluid cell
count was not performed). Culture of the synovial fluid yielded
negative results, but arthrocentesis was performed several hours
after receipt of the first dose of ciprofloxacin. The patient received intravenous vancomycin for 3 weeks to treat presumed
septic arthritis due to MRSA. Three weeks after completing
antibiotic treatment, he developed a chin abscess due to MRSA
strain USA300. After diagnosis of the second infection, samples
obtained from the groin and axillae were obtained for culture,
which also yielded MRSA USA300. Results of nasal culture,
which were initially negative during the team-wide survey, again
did not yield S. aureus.
Another case patient who originally presented with a thigh
abscess subsequently developed cellulitis of the elbow. After
receipt of oral ciprofloxacin for a total of 5 weeks and resolution
of the second infection, he was hospitalized because of an abscess on his forearm due to MRSA (which again was susceptible
to ciprofloxacin) and received intravenous vancomycin for 14
days. Swab samples were obtained from the axillae, groin, and
nares for culture, but only nares culture yielded MRSA USA300;
the patient’s initial nares culture had yielded MSSA.
Colonization results. A total of 97 of 100 players had nares
swab specimens obtained for culture. Forty-three cultures
yielded MSSA. No MRSA was found. All 29 members of the
athletic training and coaching staff had nares swabs obtained
for culture: 6 cultures yielded MSSA, and 0 yielded MRSA.
Disease risk factors. Ninety players (90%) (including all
10 case patients) completed face-to-face interviews. Cornerback
defensive backs and wide receivers had the highest infection
risk (50% and 33%, respectively), accounting for 8 of 10 case
Table 2. Additive interaction of player position with turf burns and body shaving, 2
markers of interruption of skin integrity.
High-risk
a
position
No. of
case
patients
Total no.
of players
MRSA
attack rate,
% of players
Attributable risk
of MRSA infection,
% of players
No
No
Yes
0
2
3
53
17
12
0.0
11.8
25.0
Reference
11.8
Reference
Yes
5
8
62.5
37.5
No
Yes
No
No
No
Yes
0
2
1
32
38
8
0.0
5.3
12.5
Reference
5.3
Reference
Yes
Yes
7
12
58.3
45.8
Risk factor
Body shavingb
No
Yes
No
Yes
Turf burnc
NOTE. We were unable to assess multiplicative interaction because the attack rate in the reference
group is 0. MRSA, methicillin-resistant Staphylococcus aureus.
a
Cornerback or wide receiver.
Shaving body areas other than the face (excluding shaving the head with hair clippers to produce
a crew cut).
c
Abrasions due to artificial grass.
b
MRSA Outbreak in a College Football Team • CID 2004:39 (15 November) • 1449
Table 3. Attacks rate of methicillin-resistant Staphylococcus aureus (MRSA), by frequency
of shared use of the training room whirlpool, for infections at covered sites only.
No. of
case
patients
Total no.
of players
MRSA
attack rate,
% of players
Relative risk (95% CI)
Never
⭐1 Occasion per week
1
0
61
10
1.6
0.0
1.0 (Reference)
0.0 (Not calculable)
⭓2 Occasions per week
3
15
20.0
Frequency of
whirlpool sharing
12.2 (1.4–109.2)
P
a
.020
a
By Cuzick’s nonparametric test for trend across ordered groups (i.e., test for trend associated with increasing
frequency of behavior).
by athletic trainers to use the whirlpool, whereas 38 players
reported whirlpool use on the questionnaire. Players who reported sharing the cold whirlpool in the training room with
another athlete were 2 times as likely to have an MRSA infection
(RR, 2.4; 95% CI, 0.8–7.7), although this difference was not
statistically significant. However, for infections of covered sites,
risk increased significantly with more-frequent whirlpool sharing. Those who shared the whirlpool ⭓2 times a week were 12
times more likely to have infections due to MRSA on covered
sites than were those who never shared the whirlpool (RR, 12.2;
95% CI, 1.4–109.2) (table 3). Infections of covered sites occurred throughout the outbreak, and whirlpool maintenance
practices were not altered from those described below until the
end of September.
Health care–associated risk factors for MRSA, such as antibiotic use and surgery or hospitalization during the previous
year, and hygienic practices were not significantly associated
with infection risk. Additional risk factors not found to be
associated with disease were having a football player as a roommate, dormitory of residence, and locker location. Sharing of
personal items was relatively infrequent (towels, 4% of players;
creams and ointments, 6% of players; nonspray deodorant, 6%
of players; and bar soap, 20% of players) and not associated
with infection.
Skin infections due to MSSA. In addition to skin infections
due to MRSA, 6 minor skin infections due to MSSA were
identified during active surveillance. Nasal carriage of MSSA
and other assessed exposures were not statistically associated
with MSSA infection (P 1 .05).
Facility inspection and staff interviews.
No soap was
available in showers used by the athletes. Water used to wash
towels was 44.4C rather than 71C [15], and chlorine bleach
was not used. Wound care and coverage was optional and left
to the discretion of the players. Several case patients reported
having played football with open wounds.
Two 416-L (100-gallon) whirlpools in the athletic trainers’
room were filled in the morning, and povidone-iodine was
added as a disinfectant (30 mL per 75.7 L [1 fluid ounce per
20 gallons] of water). Usually, 2 players used a pool at once.
Pool water was unchanged throughout the day. Players were
1450 • CID 2004:39 (15 November) • Begier et al.
instructed to shower before use, and players with open wounds
were reportedly not allowed in the whirlpool, although case
patients with turf burns described having used the whirlpool.
Whirlpools were drained and cleaned with heptagon at the end
of each day. Whirlpools were kept at temperatures of 7C–
15.5C (cold pool) and 35C–40.5C (hot pool; used only at
the end of the outbreak).
DISCUSSION
We hypothesize that MRSA was spread between players largely
by frequent direct contact between cornerbacks and wide receivers during practice scrimmage and drills. Whirlpools may
have provided an additional mechanism for the spread of
MRSA, because of unproven and limited water disinfection
practices. Infection appears to have been facilitated by interruptions of skin integrity, including turf burns and microabrasions likely sustained while body shaving. Nasal colonization with MRSA does not appear to have played a role in
this outbreak.
Despite prompt recognition of methicillin resistance by the
treating clinician, these previously healthy players experienced
significant morbidity from their infections, with nearly all requiring daily wound care for 11 week and 2 requiring hospitalization. Outbreak wound isolates carried mecA and SCCmec
type IVa gene alleles for methicillin resistance, as well as the
Panton-Valentine leukocidin toxin gene. This gene allele combination has been frequently identified in community-associated MRSA isolates, particularly those from patients with primary skin infections and necrotizing pneumonia [16–18].
Whether Panton-Valentine leukocidin toxin or other associated
exotoxins are responsible for increased clinical virulence requires study [16].
The strong association with certain player positions provides
evidence for person-to-person spread, because cornerbacks and
wide receivers were a subpopulation with frequent direct person-to-person contact with each other during scrimmage play
and drills. Two other investigations of MRSA outbreaks among
athletes implicated person-to-person spread during prolonged
close contact [6, 7]. One occurred among wrestlers, in which
teammates passed MRSA to each other during practice but not
to opponents exposed only for a brief 3-min match [7]. An
outbreak among rugby players was attributed to person-toperson contact during play because of a high attack rate among
those playing the position of forward [6]. An increased rate of
infection among rugby forwards has also been seen in outbreaks
of cutaneous herpes simplex [6].
We did not find evidence that playing with uncovered wounds
increased the risk of infection. However, several case patients
reported having played football with uncovered wounds that were
subsequently diagnosed as MRSA infections, which likely provided the opportunity for such patients to pass MRSA to others
before diagnosis. Before the outbreak, athletic staff left wound
care largely to the discretion of the players, allowing the players
to seek care and wound coverage if they wished. As a control
measure, we required the exclusion of case patients from all play
until the wounds healed, and all players were required to cover
open wounds during play. These interventions have been routinely used in similar outbreaks [1, 2, 5]. We recommend that
players routinely and consistently comply with covering wounds
as a participation requirement to limit the potential for and extent
of future outbreaks of infection.
MRSA infection appears to have been facilitated by interruptions of skin integrity, including those caused by body shaving. Although some athletes (e.g., swimmers) practice body
shaving to enhance performance, body shaving is largely a cosmetic practice among football players and other young men
[20]. Body shaving is likely to produce microabrasions. Surgical
literature has documented increased risk of postoperative infection associated with shaving surgical sites [21, 22]. Body
shaving has not previously been conclusively linked to infections among athletes, although it was a possible risk factor in
an MRSA outbreak among college football teammates in 2000
[5]. This emerging cosmetic behavior among young men may
contribute to the risk of infection in populations of athletes,
especially in areas covered by clothing (e.g., the groin and
thighs). Education regarding the risks of body shaving for participants in contact sports should be considered.
Open wounds [3, 4] and possibly turf burns [5] have been
associated with staphylococcal infections, including MRSA,
during past outbreaks among football players. We found increased risk associated with turf burns, although these abrasions
were not always directly adjacent to infection. We did not find
an association with the type and timing of care of turf burns,
suggesting that avoiding such abrasions entirely would be the
best way to prevent infection. Although the negative impact of
artificial turf on the rates and severity of more debilitating
injuries such as concussions [23, 24] and musculoskeletal injuries [25, 26] has been described, the specific effects of the
characteristics of artificial turf on the risk of abrasion warrants
study. Additionally, the impact of wearing uniforms that cover
more skin merits testing [3], particularly given recent advances
in textiles that likely improve the tolerability of such clothing.
We found a trend toward increasing risk of infection associated with the use of elbow pads. Investigation of 2 previous
MSSA outbreaks found that use of elbow pads significantly
increased the risk of infection [3, 4]. Although pads should
prevent abrasions, it is possible that they promote moisture
buildup and bacterial growth or skin breaks due to chafing.
Study is needed to better define the positive and negative effects
of elbow pads.
In our initial survey, we found no MRSA nasal colonization
among players or staff. We did identify a high rate of colonization with MSSA, suggesting that nasal swabs were a sensitive
means of detecting staphylococcal colonization. Two other investigations of outbreaks of MRSA among athletic teams found
similarly low rates of nasal carriage of the outbreak strain [6,
7]. We identified axilla and groin (but not nasal) colonization
with the outbreak strain in 1 player with a well-documented
MRSA skin infection following a possible MRSA joint infection,
suggesting that alternative carriage sites may have played a role
in infection, including recurrent infection. Additionally, at the
time of this player’s second infection, after the outbreak period,
his roommate (a running back on the same football team)
became infected with the outbreak strain. We also found a
higher risk associated with groin shaving, compared with shaving of other body sites, again suggesting that groin carriage of
MRSA by athletes should be investigated further.
Given the full-body nature of the players’ routine contact,
particularly in hot weather promoting perspiration, sites of
carriage among participants in contact sports might reasonably
differ from those among health care workers, who predominantly have hand contact with patients. In an MRSA outbreak
in a child care center, culture of throat and anal swab specimens
were found to have a higher sensitivity for identifying MRSA
carriage than was culture of nares specimens [27]. Because no
new cases occurred after initial control measures were implemented, groin and axilla swab samples for culture were not
obtained from the entire team. Such a survey involving a 20member rugby team was conducted during an MRSA outbreak.
No axilla or groin carriage was identified [6], but small numbers
limit firm conclusions based on those findings.
We found that an increasing infection risk was associated
with an increased frequency of sharing the cold whirlpool in
the trainer’s room and with unproven water disinfection practices that did not meet Connecticut regulations. All public
pools, even therapeutic whirlpools, must be disinfected with
an automatic disinfection feeder [19]. In this study, povidoneiodine was added only in the morning, and whirlpool water
remained unchanged all day. Research concerning hydrotherapy
whirlpools has documented that staphylococci can persist in
whirlpools even when water is changed between users [28] and
MRSA Outbreak in a College Football Team • CID 2004:39 (15 November) • 1451
when chlorine disinfection is performed to enable use by multiple people [29]. Furthermore, transmission of MRSA has been
linked to contaminated hydrotherapy equipment [30] and
bathtubs [31] in nosocomial outbreaks. Athletic trainers were
instructed to empty, disinfect, and refill whirlpools after each
use, because pools lacked recirculation and filtration equipment, including automatic disinfection feeders. Because informal conversations with athletic trainers suggested that use of
dilute povidone-iodine for disinfection of whirlpools was a
common practice, we sent a communication to similar Connecticut facilities to clarify whirlpool maintenance practices that
comply with Connecticut’s public health code.
We found several practices that did not accord with basic
principles of good hygiene and infection prevention (e.g., soap
not available in showers), as has been the case in other outbreaks [3, 5]. We recommended installing soap dispensers with
antibacterial soap in team showers and washing towels with
water consistently ⭓71C. Players were urged to shower immediately after practice and to clean and dress cuts and turf
burns as soon as possible. Although all of these measures were
implemented in the days after the outbreak report, the end of
the outbreak was most closely temporarily associated with the
installation of soap dispensers, and recurrent cases coincided
with times at which the dispensers were temporarily empty and
awaiting refill.
Given repeated findings of inadequate routine hygienic practices and increased risk of infection associated with skin breaks,
disseminating guidelines for schools and universities via the
American College Health Association or other national health
organizations would be appropriate to publicize the best effective practices to prevent outbreaks of MRSA. Such measures
would enable trainers and athletic department staff to use
straightforward approaches to prevent or limit the extent of
MRSA outbreaks.
There are several study limitations. The outbreak’s small
size—only 10 case patients—made full multivariate analysis
impossible; however, bivariate analysis did not suggest that confounding explains our results. We also could not ascertain the
actual number of days of whirlpool use by case patients. With
such information, we could have more conclusively determined
the risk of infection associated with whirlpools. Additionally,
whirlpool water and surfaces were not sampled for culture, so
we cannot say if MRSA was actually present in these whirlpools.
In summary, in this high-morbidity outbreak of MRSA infection among young healthy athletes, we identified both modifiable risk factors for infection and breaks in adherence to
standard hygiene recommendations. Because of increasing reports of virulent community-acquired MRSA nationwide, athletic and coaching staff should note the special risk associated
with athletes, and common-sense prevention guidelines should
be implemented.
1452 • CID 2004:39 (15 November) • Begier et al.
STUDY GROUP MEMBERS
The Connecticut Bioterrorism Field Epidemiology Response
Team members involved in the investigation include Brenda Esponda, Diana Mlynarski, Ava Nepaul, and Terry Rabatsky-Ehr.
Acknowledgments
We thank Arthur Leffert, Sands Cleary, MariJo Panettieri, Matt Cartter,
Richard Dicker, Bill Sawacki, Bob Howard, Arjun Srinivasan, Joanne Bartkus, Ruth Lynfield, Nolan Lee, Tim Naimi, Andre Weltman, Virginia Dato,
Eddy Bresnitz, Corey Robertson, Dan Jernigan, and members of the university administration and athletic department staff. We also thank George
Killgore and Gregory Fosheim (Centers for Disease Control and Prevention;
Atlanta, GA) for performing toxin testing on the outbreak-associated MRSA
isolates and Jeff Hageman for facilitating this analysis.
Potential conflicts of interest. All authors: No conflict.
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