Keene WE, Markum AC, Samadpour M. Outbreak of Pseudomonas aeruginosa Infections Caused by Commercial Piercing of Upper Ear Cartilage. JAMA. 2004;291(8):981-985. doi:10.1001/jama.291.8.981
Author Affiliations: Acute & Communicable Disease Program, Oregon Department of Human Services, Portland (Dr Keene); Klamath County Department of Public Health, Klamath Falls, Ore (Ms Markum); and Department of Environmental Health, University of Washington School of Public Health, Seattle (Dr Samadpour). Dr Samadpour is now with the Institute for Environmental Health, Seattle.
Context Sporadic infections following ear piercing are well documented, but
common-source outbreaks are rarely recognized.
Objective To investigate reports of auricular chondritis subsequent to commercial
Design, Setting, and Subjects Outbreak investigation by Oregon public health agencies, including cohort
study of persons pierced at a jewelry kiosk in August-September 2000, environmental
sampling, and molecular subtyping of isolates. Confirmed cases had Pseudomonas aeruginosa cultured from ear wounds. Suspected cases had
signs and symptoms of external ear infection, including drainage of pus or
blood for at least 14 days.
Main Outcome Measures Risk factors for infection and comparison of bacterial isolates by molecular
Results From 186 piercings in 118 individuals, we identified 7 confirmed P aeruginosa infections and 18 suspected infections. Confirmed
cases were 10 to 19 years old. Most were initially treated with antibiotics
ineffective against Pseudomonas. Four were hospitalized,
4 underwent incision and drainage surgeries (1 as an outpatient), and several
were cosmetically deformed. Upper ear cartilage piercing was more likely to
result in either confirmed or suspected infection than was lobe piercing (confirmed:
RR undefined, P<.001; suspected: RR, 3.6; 95%
confidence interval, 1.5-8.5). All persons with confirmed infections had their
ear cartilage pierced with an open, spring-loaded piercing gun. Patient isolates
were indistinguishable by molecular subtyping, and matching isolates were
recovered from a disinfectant bottle and nearby sink. At least 1 worker admitted
sometimes spraying the disinfectant on the ear studs before piercing.
Conclusions Ear cartilage piercing is inherently more risky than lobe piercing.
Clinicians should respond aggressively to potential auricular chondritis and
consider Pseudomonas a possible cause pending culture
Although population-based data are scant, ear and body piercing appears
to be increasingly popular.1,2 Ear
piercing in particular is often performed in an unregulated or loosely regulated
environment1 by people with uncertain infection
control skills. Although the results are usually benign, ear piercing can
lead to serious infections.3- 9
In September 2000, an otolaryngologist in Klamath Falls, Oregon, was
consulted about a teenager with a suppurating ear infection. The patient was
admitted for surgery. The day before onset, the girl's ear had been pierced
at a jewelry kiosk. The previous day, the same physician had seen an outpatient
with a similar infection and a similar history of piercing at the same kiosk.
Both patients were pierced in upper ear cartilage; both wound cultures yielded Pseudomonas aeruginosa.
The physician alerted the local health department, noting that in 20
years of practice he had never seen this kind of infection. His report prompted
our investigation, which identified an ongoing common-source outbreak of disfiguring
upper ear infections.
Body and ear piercing businesses are regulated in Oregon, and state
licensing agency representatives provided information about the industry and
implicated kiosk. The kiosk was staffed by the owner or 1 of 3 employees.
We reviewed previous inspection reports and, with a state inspector, conducted
an initial visit on September 15, 2000. The owner agreed to suspend ear piercing
pending our investigation.
We conducted active surveillance at local medical facilities. Using
the kiosk's records, we reconstructed an arbitrary cohort of customers whose
ears were pierced from August 1 through September 15, 2000, and interviewed
them using a standardized questionnaire. Persons with active infections were
seen and referred for medical care as indicated. Pus or wound swabs were cultured
for Pseudomonas. We issued a press release to encourage
medical evaluation of active infections and to enhance case finding.
We defined confirmed infections among cohort members as any infection
at the piercing site that developed within 2 weeks of piercing from which P aeruginosa was cultured. Suspected infections were marked
by induration or erythema at the piercing site; local pain or tenderness;
and drainage of blood or pus lasting at least 14 days. We excluded persons
reporting minor problems not meeting either definition (eg, <14 days of
drainage) or whose piercing location could not be definitely classified as
lobe or cartilage.
We reviewed procedures and work schedules with the kiosk staff. We collected
environmental samples in and around the kiosk. Solid surfaces, including countertops,
plumbing fixtures, and ear-piercing guns, were wiped with saline-moistened
swabs. Disinfectant solutions were collected into sterile containers. Tap
water and sink aerators were collected into 1% sodium thiosulfate solutions
to neutralize chlorine. Kiosk workers were screened for Pseudomonas by stool and hand cultures. For the latter, workers donned
sterile gloves into which we poured approximately 50 mL of warmed sterile
saline solution. After 5 minutes of finger agitation, the gloves were removed
and the solution was decanted into sterile containers. Samples were enriched
in brain-heart infusion broth, plated onto membrane-filtration P aeruginosa agar and cetrimide agar, and cultured for Pseudomonas by standard methods. For comparison purposes, the local
hospital laboratory saved all P aeruginosa isolates
obtained from non−outbreak-associated patients during the next 3 months.
For microrestriction fingerprinting (MRF), DNA was extracted from Pseudomonas isolates grown overnight on tryptic soy agar
as previously described.10 Ten to twenty microliters
(approximately 1.5 µg/µL) of the DNA preparations was digested
with NcrI (American Allied Biochemical, Aurora, Colorado).
DNA fragments were electrophoretically separated on 15 × 20-cm agarose
gels in Tris-borate EDTA (17 hours at 70 V). Antibiograms for patient isolates
were abstracted from laboratory records.
To gauge the frequency of auricular chondritis subsequent to ear piercing,
in 2002 we mailed all otolaryngologists licensed in Oregon (outside Klamath
County) a brief questionnaire, including case photographs, asking how many
patients with piercing-related chondritis they had seen during the past year
and cumulatively during earlier years in practice. Follow-up telephone calls
were made to nonrespondents. No effort was made to identify specific patients
or to exclude potentially duplicative patient reports.
Relative risks (RRs), 95% confidence intervals (CIs), and 2 ×
2 table P values (by Fisher exact test) were calculated
for selected exposure variables using EpiInfo software (version 6.04b; Centers
for Disease Control and Prevention, Atlanta, Ga). Each piercing was treated
as an independent event.
We identified receipts for 124 individuals during the 45-day period
and interviewed 118; 6 could not be located. These 118 individuals underwent
186 ear piercings (defined as new holes) during this period, of which 7 (4%)
resulted in confirmed P aeruginosa infection and
18 (10%) led to suspected infections. Staphylococcus aureus was cultured from one person with a suspected earlobe infection; no
other pathogens were identified. Twenty-six piercings (14%) resulted in minor
symptoms not meeting either case definition; no problems were reported after
130 piercings (70%), and the outcome of 5 piercings (3%) could not be determined. Figure 1 shows the occurrence of ear piercings
during this period and their outcomes.
At least 63 of 186 piercings (34%) were done in upper ear cartilage,
including all 7 with confirmed P aeruginosa infection;
112 (60%) were lobe piercings and the locations of 11 (6%) were ambiguous.
Relative to lobe piercing, cartilage piercing was associated with an increased
risk of both confirmed (RR, undefined; P<.001)
and suspected (RR, 3.6; 95% CI, 1.5-8.5) infections.
Worker A performed the plurality of piercings (82 [44%]), including
6 of 7 that resulted in confirmed infections and 4 of 18 that resulted in
suspected infections (Figure 1).
Restricting analysis to piercings by worker A, cartilage piercing remained
associated with an increased risk of confirmed infection (RR, undefined; P<.001). The risk of developing confirmed or suspected
infections was higher for cartilage piercing by other workers as well (RR,
3.2; 95% CI, 1.2-8.5).
At least 14 persons sought medical attention. The 7 patients with confirmed P aeruginosa infection were aged 10 to 19 years. Their
symptoms began within a few hours to 3 days after piercing (median, 1 day);
they presented for medical attention 2 to 8 days (median, 5) after symptom
onset. All had abscess formation with associated swelling, pain, bleeding,
and drainage. Two reported retroauricular lymphadenopathy. Reported systemic
signs and symptoms were minor and nonspecific. On initial presentation, most
patients were treated with cephalosporins or other drugs ineffective against P aeruginosa (Table 1).
Six patients with confirmed infection were referred to otolaryngologists—3
only after the health department intervened. Four patients were hospitalized:
3 for incision and drainage surgery and 1 to receive intravenous therapy.
Another refused admission and underwent incision and drainage as an outpatient.
Four were treated with fluoroquinolones. The active infections resolved within
1 to 3 months and several resulted in significant disfigurement of the pinna
(Figure 2). By 2002, all but 2 patients
had been lost to follow-up.
The jewelry kiosk had been routinely inspected in January 2000, 8 months
before the outbreak was recognized. At that time, the operator was cited for
improper record keeping, hand washing, and equipment disinfection practices,
as well as use of improper equipment (open, spring-loaded guns) to pierce
cartilage. Although approved for lobes, these devices were not legal for cartilage
piercing in Oregon.
Citations notwithstanding, kiosk workers had continued to use the guns
on both lobes and cartilage. Each worker gave a somewhat different account
of "standard" procedures, none of which could be verified. All stated that
a customer's ear was first wiped with alcohol. A sterile ear stud was loaded
into a gun, ideally without touching either the stud or the part of the gun
that touched the ear. The piercing gun was then positioned and triggered,
driving the stud through the ear.
Worker A stated that before using the piercing gun, she would mist the
assemblage with disinfectant from an atomizer bottle—a practice other
operators denied. Although originally containing another product and not intended
to be reused, the disinfectant atomizer had been used for months and refilled
many times. The contents could not be verified but were reported to be a blend
in uncertain proportions of a "double" quaternary ammonium disinfectant, a
phenolic disinfectant, and tap water from a nearby utility sink.
Pseudomonas aeruginosa was not recovered from
any of the solid surfaces that were swabbed, from tap water at the 2 sinks
used by shop employees, or from faucet aerators, but it was cultured from
2 of 4 workers (1 from stool, 1 from hands), from the atomizer solution, and
from waste water in traps beneath both sinks.
All 7 patient isolates had indistinguishable antibiograms. Five isolates
were available for further subtyping; all were indistinguishable by MRF subtyping
and indistinguishable from the atomizer and the utility sink trap isolates.
They differed from the bathroom sink and worker isolates, which were heterogeneous.
The 13 community isolates collected by the hospital between October and December
2000 comprised 12 MRF patterns, none of which matched the outbreak strain.
Of 136 otolaryngologists licensed in Oregon, 13 (10%) were retired,
dead, or unlocatable. Of the remaining 123, we received responses from 94
(76%). They reported seeing 53 patients with ear piercing–related auricular
chondritis within the previous year, and 8 (15%) of these patients had P aeruginosa infection. In their cumulative 1406 practice-years
of experience, the otolaryngologists estimated having seen an additional 190
patients with piercing-related auricular chondritis, 27 (14%) of them with P aeruginosa infection. Twenty-seven (29%) of the responding
clinicians reported never having seen piercing-related auricular chondritis.
Pseudomonas aeruginosa is known to cause sporadic
cartilage infections following ear piercing or other trauma,9,11- 14 but
we found no descriptions of previous common-source outbreaks. This unfortunate
natural experiment confirms the assertion that ear cartilage is more prone
to serious infection than the lobe is.7,11,13- 15 It
also underscores the importance of infection control training wherever invasive
procedures are performed—even in nonmedical settings.
A constellation of events aligned to cause this outbreak. First, open
piercing guns were used to drive relatively blunt studs through cartilage,
rather than recommended16 (and, in Oregon,
legal) alternatives such as needle piercing. Second, a "single-use" disinfectant
bottle was refilled repeatedly, becoming contaminated with P aeruginosa, presumably at the sink where organisms were recovered.
Finally, at least 1 worker sometimes sprayed the sterile studs and piercing
gun with disinfectant, not appreciating that sterile implements would not
benefit from a spray with any disinfectant, much less a contaminated one.
The size of this outbreak is difficult to assess. The specificity of
our suspected case definition for Pseudomonas infections
could not be determined, but the asymmetrical timing of confirmed vs suspected
infections (Figure 1) suggests that
more cases would have been confirmed had more persons—particularly those
with cartilage infections—been cultured during their first weeks of
symptoms. The outbreak may have begun well before August; following news media
reports, we learned of several similar-sounding infections from individuals
pierced before the study period.
The incidence of serious sequelae following ear piercing is not well
known. Several surveys in selected populations have found high rates of minor
outbreak subsequent to lobe piercing (staphylococcal infections at a children's
party4) and a case-control study implicating
lobe piercing as a risk factor for hepatitis B transmission18 were
reported in the 1970s. Noninfectious problems, notably metal hypersensitivity,
may be more common than serious infection.2 Case
reports aside, there are essentially no data about the incidence of auricular
chondritis following piercing. The physician survey results suggest that specialist
visits are uncommon.
Cartilage wounds can be slow to heal and may demand aggressive therapy,
including surgical debridement and drainage.7,11,14,19 While
cultures are recommended, empirical therapy of auricular chondritis should
include coverage for Pseudomonas, which may be the
most common cause.12- 15 Given
limited options for outpatient therapy, ciprofloxacin has been recommended
as the drug of choice,13,14 notwithstanding
concerns about pediatric use.
Culturing Pseudomonas from a bottle of disinfectant
has ample precedent.20,21 Whatever
it was, the atomizer solution was clearly not pseudomonicidal.
In commercial settings, better worker training is a worthwhile goal,
but the most effective interventions may include both changes to ear-piercing
equipment that reduce the potential for worker error and increased regulatory
attention.9 This outbreak prompted revisions
to Oregon regulations, adopted in 2001, that included a ban on the use of
open, spring-loaded piercing guns as well as increased educational and training
requirements for workers. Of course, given the ubiquity of Pseudomonas in plumbing fixtures and other aqueous environments, some
risk of infection will remain until the wound heals.
Although P aeruginosa infections per se are
not reportable in any state, suspected common-source outbreaks of any kind
are reportable in every state.22 Reporting
obligations may be overlooked by clinicians, especially when the offending
organism is not specifically named on reporting lists. This outbreak smoldered
for weeks—perhaps months—until 2 patients happened to be referred
to the same otolaryngologist, who promptly notified the local health department.
Had the outbreak occurred in a larger community, with more specialists and
hospitals, or had the clinician not contacted the health department, it might
have continued indefinitely—unnoticed, uninvestigated, and uncontrolled.