Pediatr Clin N Am 49 (2002) 743 – 751

Infections associated with pediatric

sport participation
E. Stephen Buescher, MD
Center for Pediatric Research, Eastern Virginia Medical School,
Children’s Hospital of The King’s Daughters, 855 West Brambleton Avenue, Norfolk, VA 23510, USA

The pathophysiology of infections in athletes appears to be little different from

that of infections in nonathletes, but the immunology of athletes compared to that
of nonathletes can be altered according to training level. Some authors suggest that
a J-curve relationship may exist between the levels of physical training in athletes
and their predisposition toward upper respiratory infections (URI), such that if the
rate of URI in nonathletes is considered the baseline, then moderate training is
associated with fewer URIs, while extensive or overtraining is associated with an
excess of upper respiratory infections over the baseline rate [1]. If this relationship
applies to other types of infections, it may be an important consideration when
trying to minimize the risk of an infectious illness developing during crucial
competitions. It may also be an important consideration when an athlete wishes to
persist with strenuous training during an infectious illness, which often results in
degradation of athletic performance accompanied by worsening of the infectious
illness [2]. It is therefore important to have an understanding of the infectious
syndromes that occur in athletes, their mechanisms of acquisition and spread, the
risks they pose to other athletes, and the approaches to their management. This
information may help to minimize the risk of acquiring infections and the
morbidity associated with infections in athletes.

Routes of exposure
There are many factors that potentially impact the development of infections in
athletes. Skin abrasion caused by person-to-person contact or by contact with
athletic equipment (eg, ‘‘mat burn’’ in wrestlers) is common in athletics. Excessive
sweating without prompt evaporation can result in skin maceration or otherwise
alter the skin’s normal defense mechanisms. Heavy exertion, shouting, or cough-

E-mail address: sbuesche@chkd.com (E.S. Buescher).

0031-3955/02/$ – see front matter D 2002, Elsevier Science (USA). All rights reserved.
PII: S 0 0 3 1 - 3 9 5 5 ( 0 2 ) 0 0 0 1 6 - 0
744 E.S. Buescher / Pediatr Clin N Am 49 (2002) 743–751

ing can result in aerosolization of respiratory secretions. Other aspects of the sports
world that are associated with acquisition or spread of infection in athletes: sharing
or having common-source contact with less-than-clean practice clothing or
support equipment (eg, water buckets, water bottles, towels, contaminated
equipment, swimming pools, showers); close person-to-person contact that may
be repetitive or physically injurious (eg, skin-to-skin contact in wrestlers, physical
contact in football players); massed audiences in closed environments; and
pressure from coaches or teammates to ‘‘play hurt or ill.’’

Skin contact/skin exposure

In sports that involve skin contact, particularly those where skin injury can
result from the contact, transmission of Herpes simplex virus, the agent that
causes Molluscum contagiosum superficial fungal infections, or the staphylo-
coccal/ streptococcal causes of impetigo are well described in athletes.
Herpes simplex virus (HSV) infection in wrestlers (Herpes gladiatorum) and
rugby players (scrumpox) is widely recognized and probably the most common
infection transmitted person-to-person in sports. The pathophysiology of infection
is thought to be direct inoculation of HSV from a vesicle on the skin of an athlete
into the normal or abraded skin of a competitor or teammate. Pre-existing
abrasions or underlying skin conditions may predispose one to the development
of this infection. Local replication of the virus occurs, producing single or clus-
tered vesicular lesions with erythematous bases at the site of inoculation. When a
recurring problem, prodromal signs (burning, itching, stinging) often occur at the
site where lesions will appear. In primary infection, constitutional symptoms such
as malaise, fever, and regional adenopathy may accompany the appearance of the
vesicles after an incubation period of 2 to 14 days. In all cases, the vesicle fluid is
rich in infectious Herpes simplex virus, explaining why a risk of transmission is
present whenever vesicles are present and/or ruptured. Competitors should be
disqualified from practice and competition involving skin-to-skin contact that
might allow virus transmission until their vesicles are dry and scabbed. As with
other forms of Herpes simplex virus infection, local recurrences of vesicles are
common and can be precipitated by stress. Diagnosis can be made by either culture
of the vesicle fluid for HSV, or by preparation of a Tzank smear from a vesicle
floor, which confirms the presence of virus from the Herpes family but does not
specify HSV as the causative agent. Effective treatment of cutaneous Herpes
simplex infection can be achieved with acyclovir (pediatric: 40 to 80 mg/kg/d in
three to four doses for 7 to 10 days; adult: 200 mg by mouth three times per day
for 10 days), valacyclovir (not approved in children < 18 years old; adult: 1 g/d in
two divided doses for 5 days), or famciclovir (not approved in children < 18 years
old; adult 250 mg/d in two doses for 5 days), which will decrease the duration of
viral shedding from lesions and the time to scabbing of vesicles. Effective
prophylaxis against Herpes gladiatorum in wrestlers with more than a two-year
history of the condition using valacyclovir has been recently reported [3], using
500 mg given orally daily.
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Varicella zoster virus (VZV) is the cause of chickenpox and shingles.

Chickenpox is the clinical manifestation of primary VZV infection, and localized
recurrences of VZV infection, called zoster or shingles, are caused by the
reactivation of VZV, not by the acquisition of new infection. Chickenpox can
be spread to susceptibles in sports environments [4], probably through airborne or
droplet spread. Zoster can also mediate spread of VZV because the vesicles of
both chickenpox and zoster contain fluid that is full of infectious VZV particles;
therefore, skin-to-skin contact with an athlete showing shingles can potentially
transmit VZV to a nonimmune host. As with HSV, athletes who have shingles
and whose sports involve skin-to-skin contact should probably be restricted from
competition or practice until all vesicular lesions have dried and scabbed.
Molluscum contagiosum is a cutaneous infection caused by a recently iden-
tified poxvirus, the only member of the Molluscipox virus family. The lesion is
a translucent to flesh-colored, rounded papule, some of which have central um-
bilication. Transmission is thought to occur from person-to-person via direct
contact and via fomites, including towels. Molluscum congiatosum is an asymp-
tomatic nuisance condition that usually affects small areas of the skin in normal
hosts, but in compromised hosts it can become disseminated and affect the entire
skin surface.
Treatment of molluscum contagiosum is still based on physical removal of the
keratinized plug (the molluscum body) at the center of each lesion. Topical
cantharidin (0.7% in collodion), topical salicylic acid plasters, electrocautery, or
treatment with liquid nitrogen can be successful alternatives for removal of lesions.
Warts (human papillomavirus infection) result from person-to-person or skin-
to-skin contact. Common warts are usually a mere cosmetic nuisance unless they
involve areas of skin that are required for specific athletic activities (eg, between
the fingers or on the hands of gymnasts). Warts involving callused areas (eg,
plantar warts on the soles of the feet) can be painful and, therefore, are of more
concern to the athlete. In some instances, these warts appear to be calluses, but
upon superficial scraping of the painful area of callus, punctate bleeding occurs as
a result of the vascularization of the papilloma (wart); when this is done to callus,
only deeper layers of callus are revealed. Dark clotted blood vessels in plantar
warts give rise to their common name of ‘‘seed’’ warts. Treatment of both
common and plantar warts with daily topical salicylate plasters that can be
purchased over the counter is effective but requires dedication and time.
Physician-administered liquid nitrogen treatments can be used if salicylate
plasters fail or if more rapid removal is necessary.
Tinea corporis (ring worm), tinea pedis (athletes foot), tinea cruris (jock itch),
and Tinea unguium are all superficial skin or fingernail/toenail infections
involving dermatophyte fungi. Tinea corporis is frequently caused by organisms
of the genus Trichophyton and produces roughly round-to-oval areas of affected
skin that have slightly raised and reddened edges with central clearing (ie, looks
like a ring), and are often pruritic and scaly. Tinea pedis is caused by Trichophyton
rubrum, Trichophyton mentagrophytes, or Epidermophyton floccusum, and takes
the form of moist, scaly/peeling areas between the toes that crack and may be
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painless or produce burning sensations. Tinea cruris is usually caused by the same
dermatophyte fungi that cause tinea pedis, and appears as scaly or pruritic, slightly
reddened skin in the groin and inguinal areas. Its development may be associated
with pre-existing tinea pedis that was possibly caused by spores carried to the
groin and inguinal areas by underwear pulled over infected feet. Tinea unguium is
a chronic, usually painless infection of the nails of the hands or feet. Frequently
associated with tinea pedis, it is caused by the same dermatophyte fungi found in
tinea pedis and usually starts at the lateral edges of the nail. Over time, increasing
amounts of the middle and distal underside of the nail become involved, ultimately
producing soft, brownish nails with pits and grooves that ultimately separate from
the underlying base. Transmission of dermatophyte infections from person-to-
person appears to occur via fungal spores acquired from the environment (eg,
common showers) or from direct skin-to-skin contact in some sports (eg,
wrestling). These infections are often overlooked and/or ignored because they
are unlikely to have any related short- or long-term morbidity. Their development
in athletes appears to be associated with common conditions found in sports:
sweat-soaked clothing/underwear, infrequently washed/sanitized practice cloth-
ing, occlusive clothing, and local skin trauma associated with form-fitting
equipment that create environments conducive to the growth and spread of the
causative fungi, making them almost ubiquitous to athletic activities.
Treatment of these conditions (except tinea unguium) usually involves
prolonged applications of topical antifungal medications (clotrimizole, micona-
zole, ketoconazole, terbinafine, tolnaftate) plus changing the environmental
conditions that facilitate their spread/transfer to the skin (frequent and regular
washing of practice equipment and clothing, wearing shower sandals, putting on
clean socks before putting on underwear). Continuing treatment for 2 weeks after
the disappearance of physical signs is recommended. Topical corticosteroid
preparations can have dramatic effects on decreasing symptoms associated with
these infections, but they are for symptomatic treatment only; their discontinua-
tion is usually promptly followed by exacerbation of symptoms.
In some instances of widespread tinea corporis and in all instances of tinea
unguium, oral antifungal treatment is necessary. Oral treatment with ketoconazole
(children: 3 to 6 mg/kg/d, once per day; adults 100 to 200 mg/d) or itraconazole
(children 10 to 15 mg/kg/d, once per day; adults 100 to 200 mg once per day) has
been reported to give good results for tinea corporis, but it is expensive and long-
term treatment can be associated with liver toxicity. For tinea unguium, oral
griseofulvin ultramicrosize form 5 to 10 mg/kg/d (maximum dose 750 mg) once
per day; microsize form 10 to 20 mg/kg/d divided two times per day (maximum
dose 1000 mg), itraconazole (same doses as above), and terbinafine (adults:
250 mg/d) [5] have been used with success, but treatments must be continued until
the entire affected nail has been completely replaced by new nail, usually 6 to
12 months, and recurrences are common.
Bacterial skin infections of athletes include those with recognized transmissi-
bility but minimal morbidity (eg, impetigo), those with minimal transmissibility
and morbidities (folliculitis, dermatitis), and those with potential to develop into
 E.S. Buescher / Pediatr Clin N Am 49 (2002) 743–751 747

significant medical illnesses (cellulitis, furuncules, and carbuncles). Impetigo is a

clinical syndrome characterized by development honey-colored crusting over
areas of involved skin. The skin around the crusts is often erythematous, and
manual removal of crusts frequently results in bleeding from the affected, weeping
skin. Usually associated with staphylococcal and streptococcal pathogens, impe-
tigo responds to local cleaning of the affected skin plus oral antibiotics appropriate
for staphylococci and streptococci (eg, dicloxacillin, cephalexin). Impetigo can be
spread by skin-to-skin contact, so athletes with large or multiple affected areas of
skin that are crusted, moist, or draining should be disqualified from practice or
competition until the areas are dry. Once they are dry, participation with the
affected areas covered can be allowed until these areas return to normal.
Development of folliculitis (punctate inflammation/infection of hair follicles)
or dermatitis (inflammation of the skin), typically caused by minor superficial
bacterial infection of these structures, is not usually a cause for disqualification
from competition and will usually respond to measures aimed at local care and
prevention of contact with the offending process. Prolonged contact with
ineffectively chlorinated warm/hot water (eg, hot tubs, whirlpool baths, swim-
ming pools) can alter skin integrity to allow local invasion by organisms in the
water, often Staphylococcus aureus or Pseudomonas aeruginosa, into hair
follicles and sweat glands of hairy areas or the buttock to produce these
conditions. Folliculitis lesions are usually papular and often are more pruritic
than painful. Rather than producing papules, dermatitis involves areas of skin,
with signs varying from mild discomfort to intense pruritus or pain. When they
occur, avoidance of these facilities will usually allow natural resolution of the
conditions. Decontamination of the facilities by emptying and cleaning with
antiseptic solutions and then refilling with adequately chlorinated water usually
resolves the problem for future users. Obviously, use of hot tub or whirlpool by
an individual with either folliculitis or dermatitis may result in contamination of
the equipment and spread to other users, so athletes should be restricted from
these facilities until their conditions resolve.
In some instances, the superficial infection of skin or hair follicles can spread
to involve deeper layers and cause cellulitis or furuncle/carbuncle formation.
Cellulitis is a condition of diffuse inflammation of the soft tissue; a furuncle is
essentially a single-chambered abscess in the soft tissue, and a carbuncle is a
multiloculated abscess that is a coalescence of multiple furuncles. Spread of
furunculosis among high school athletes has been reported [6] to result from
contact with others who have furuncles and/or skin abrasions. When any of these
conditions occur, they are commonly caused by S. aureus and require some form
of specific treatment, including antibiotics with/without incision and drainage for
their effective resolution.
Spread of infections caused by Streptococcus pyogenes have also been
described in athletes. Streptococcal infection of the ‘‘turf-burn’’ injuries that
result from falls on nonskid surfaces during indoor football is reported [7], as is
an epidemic pyoderma caused by a nephritigenic strain of S. pyogenes in rugby
players, ‘‘scrum kidney’’ [8].
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Human ectoparasites (eg, scabies, lice) can also be acquired by athletes,

usually via fomite contact (ie, sharing of used/unsanitized clothing, equipment, or
towels). Scabies is caused by Sarcoptes scabei, the scabies mite, which
superficially burrows into human skin to lay its eggs. Allergic reactions to mites
and/or their feces excreted into the skin during egg-laying can result in intense
pruritus, which is usually the presenting complaint of the condition. Preferring
dark, warm, and moist areas of the skin, scabies commonly occurs around the
belt line, the perineum and axillae, and between the fingers. Diagnosis is made by
identification of either the mite itself or mite eggs in skin scrapings taken from
the affected area, and topical treatment with permethrin cream or lindane cream is
usually effective for eliminating the infestation. Lice infestations in humans
usually involve hairy areas and are caused by Pediculus humanus capitis (head
louse), Pediculus humanus corporis (body louse), or Phthiris pubis (pubic or
crab louse). All three lice types feed on human blood and attach their eggs (nits)
firmly to individual hair shafts. Topical applications of permethrin (1%) will kill
adult lice and eggs. Retreatment after 7 to 10 days is recommended. Very fine –
toothed combs (‘‘nit combs’’) are passed through hairy areas to physically
remove the nits.

Water contact/exposure
Water contact occurs in essentially all sports, either intentionally (swimming,
water polo, or showering) or unintentionally (kayaking, canoeing, or steeple-chase
running). In swimmers, paddlers, and other athletes with ear exposures to water,
otitis externa (swimmers ear), usually caused P. aeruginosa, is a common
localized problem. In the ear canal, little tissue separates the skin surface from
the underlying cartilage, and development of inflammation in the soft tissue of the
ear canal readily results in pain in the region. Movement of the pinna exacerbates
the pain of otitis externa, and is a useful diagnostic maneuver to differentiate
infection/inflammation in the external ear canal from middle ear infection. In
addition to the pseudomonas, culture of the external ear canal often also yields
fungi, but their role in the process is unclear and, therefore, antifungal treatment is
not usually administered. Physical examination typically shows erythematous,
edematous (often weeping) skin in the ear canal that may obstruct the canal.
Removal of debris from the canal along with drying the area (using Burrows
solution for several days) may be necessary to allow penetration of antibiotic
drops. A topically applied preparation containing polymixin B, neomycin, and
corticosteroid is usually used two to three times per day, sometimes with a cotton
wick placed in the canal to assure passage of the drops throughout the external
canal. Oral antibiotic therapy is rarely needed. Prevention centers on minimizing
the duration of water contact with the external canal by either aggressively drying
the ears after water exposures or by wearing earplugs to prevent water contact.
Infections caused by inadvertent water exposures, usually involving ingestion
of unchlorinated (ie, contaminated) water sources include giardiasis, cryptospo-
ridiosis, salmonellosis, shigellosis, and leptospirosis. All except leptospirosis
 E.S. Buescher / Pediatr Clin N Am 49 (2002) 743–751 749

usually have prominent gastrointestinal symptomatology (vomiting or diarrhea,

gastrointestinal upset) that will usually send the athlete seeking medical aide.
Giardiasis develops 10 to 14 days after ingestion of contaminated water, usually
somewhere in the wild or in environments with inadequate sanitation. Presenta-
tions can vary: anorexia, bloating, distention, and flatulence or belching, with or
without vomiting or diarrhea. Without treatment, spontaneous resolution may
occur or complaints may persist for weeks or months as a chronic illness.
Diagnosis is best made by detection of giardia antigens in the stool because direct
visual examination of stool for cysts and trophozoites only detects about 70% of
cases. Treatment with metronidazole is preferred (adults: 250 mg by mouth three
times a day for 5 to 7 days) and is usually effective.
Cryptosporidiosis has risk factors similar to those of giardiasis, consumption
of contaminated water, but because the causative agent, Cryptosporidium
parvum, is relatively resistant to the effects of chlorination, outbreaks related
to swimming pool water contact have occurred. Watery diarrhea that varies in
frequency and volume is the usual manifestation, and in the immunocompetent
host, the disease is usually self-limited over 2 to 4 weeks. In the immunocom-
promised, infections can become chronic. Management of the illness is mostly
supportive because of the lack of effective therapies for this protozoan.
Aeromonas hydrophila, Salmonella, and Shigella species are bacterial enteric
pathogens that are usually acquired by contact/ingestion of contaminated water.
The latter two can also be acquired via fecal-oral contamination from improperly
prepared or stored foods. In addition to causing a significant gastroenteritis,
Aeromonas can also cause severe cellulitis after contaminated water contact with
a superficial wound. Salmonella and Shigella species usually cause dysenteric
illness (bloody, cramping diarrhea) that may or may not require antibiotic
treatment. In many cases, the illnesses caused by Salmonella or Shigella are
self-limited over 3 to 4 days, but usually they significantly incapacitate
the athlete.
Acquisition of leptospirosis has recently been associated with participation in
triathlons [9]. Clinical manifestations include fever, chills, headache, myalgia,
conjunctivitis, abdominal pain, vomiting, diarrhea, skin rashes, and meningeal
symptoms. The severity of illness can vary, as does the incubation period,
which can vary from several days to 4 weeks. Diagnosis is made by culture,
development of IgM antibody, a four-fold rise in IgG antibody, or immuno-
histochemical testing of infected tissues. Severe cases are treated with intra-
venous penicillin.
Viral agents can also be spread via contact with contaminated water or by fecal-
oral contact. Adenovirus pharyngoconjunctivitis has been reported after contact
with a swimming pool that was inadequately chlorinated [10]. Enterovirus and
Norwalk virus outbreaks have occurred in association with contact sports
(football) [4,11,12], with spread occurring both within a team – probably through
shared drinking containers – and from one team to the other, the latter suggesting
spread during athletic competition. Taken together, these episodes suggest that
athletes with active gastrointestinal illness, particularly those associated with
750 E.S. Buescher / Pediatr Clin N Am 49 (2002) 743–751

diarrhea, should be removed from competition and practice until their illnesses
have resolved.
Respiratory viral infections can also be spread via athletic competition and
may involve spectators as well as athletes. Measles outbreaks epidemiologically
associated with attendance at indoor athletic games have occurred, as has spread
of VZV [4,13]. Influenza infections during the wintertime ‘‘flu’’ season can also
be athletic event associated [4] because the current epidemiology suggests that
each year, spread of illness through children and adolescents in school are
important factors that influence the extent, duration, and severity of the annual
season. Influenza infection significantly alters pulmonary function, and while the
constitutional symptoms may only last 7 to 10 days, staccato-type cough may
persist for weeks, significantly impacting the athlete’s endurance and function.
Prevention of influenza infection centers around annual immunization, which is
strongly recommended by those wishing to decrease their risk of influenza. The
duration and severity of influenza A infection can diminished by administration
of amantidine. Oseltamivir (oral dosing for adults: 75 mg two times a day for
5 days; children < 15 kg: 30 mg two times a day for 5 days; children 15 to 23 kg:
45 mg two times a day for 5 days; children 23 to 40 kg: 60 mg two times a day
for 5 days) or zanamavir (inhaled dosing for adults: 10 mg two times a day for
5 days; not approved in children < 12 years old) started within the first 36 hours
of symptoms can significantly alter the course and severity of infection with
either influenza A or B. Spread of Epstein-Barr Virus (EBV) linked to shared
water bottles/cups can occur, as can streptococcal pharyngitis. Infectious
mononucleosis caused by EBV can have a range of severities, from subclinical
illness to severe fatigue, hepatitis, hemolytic anemia, and splenomegaly. Time to
recovery from mononucleosis is variable, but when the athlete returns to training
too soon or with too much effort, relapses with increased fatigue are common.
Splenic rupture caused by trauma during mononucleosis has been discussed
extensively and is a consideration for the athlete. Sonographic evaluation of
spleen size may help with deciding when the athlete can return to his or her
sport. A common rule of thumb is to avoid strenuous exercise, weight lifting,
and physical contact for at least 3 weeks after the clinical illness, and that
intensity of training/participation may be increased if an initial week of about
50% effort is well tolerated [14].
Although much consideration has been given to the risk of blood-borne
pathogen (hepatitis B virus, hepatitis C virus, and human immunodeficiency
virus) infections in athletes, current consensus is that the risk of acquiring these
agents during athletic practice or competition is small. While acquisition and
spread of hepatitis B associated with sumo wrestling [4] and American football
have occurred [15], in most instances, acquisition of these infections usually
resulted from nonathletic ‘‘off-the-field’’ activities rather than activities directly
related to sports. Therefore, prevention of these infections focuses more on
education about risks in nonathletic rather than athletic environments [16]. The
American Academy of Pediatrics has recently published a statement about blood-
borne pathogen infections and the risks to athletes [17].
 E.S. Buescher / Pediatr Clin N Am 49 (2002) 743–751 751

Summary
Infections occur in childhood and adolescent athletes just as they do in all
children and adolescents. Because of the sports environment, and in some
instances the sport itself, athletes can be prone to infections that will alter their
athletic performance or present risks to other athletes. Recognition of the
infectious risks related to sports and the options for their treatment or, better
yet, prevention, can help young athletes perform to their utmost potential.

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