You are on page 1of 6

Pediatric mrmatology Vol. 4 No.

3 185—188

Impetigo: A Reassessment of
Etiology and Therapy
Leslie L. Barton, M.D. and Allan D. Friedman, M.D.
Department of PediatricslAdolescent Medicine, St. Louis I/niversit y School of Medicine, St. Louis,
Missouri

Abstract: Traditional concepts regarding the bacteriology and therapy of non-


bullous impetigo have been reexamined. Although in the United States the
disease is considered primarily of streptococcal origin and amenable to
peni- cillin therapy, we found that Staphylococcus aureus was the most common
isolate in 71 palients studied. Only two patients yielded pure cultures of
group A Q-hemolytic streptococci. All bul two isolates of S. aureus were
resistant to penicillin; one of these two isolates was also resistant to
erythromycin. Eryth- romycin appeared to be more efficacious than penicillin for
the treatment of impetigo.

Impetigo contagiosa is one of the most common


ined in the outpatient department between June and
skin infections in children. Since its classic descrip-
August 1986 with primarily nonbullous impetigo
tion by Fox in 1864 (1), numerous investigations ap-
were asked to participate in the study if they were
parently elucidated its etiology, pathogenesis, and
not receiving antibiotics at the time of being seen at
treatment (2—8). The majority of cases of impetigo
CGH, had not taken antibiotics during the preced-
were attributed to group A Q-hemolytic strepto-
ing week, had no history of allergy to either peni-
cocci. Older lesions were thought to be contami-
cillin or erythromycin, and had no known primary
nated or secondarily infected with Staphylococcus
or secondary immunodeficiency.
aureus. Only bullous impetigo was considered to be
Historical data obtained on each patient included
primarily staphylococcal in origin (9, 10).
the duration of impetiginous lesions, any preexist-
Recent data suggest that a shift in the major eti-
ing skin disorder, and siblings or other household
ologic agents of impetigo may have occurred (11,
members with similar lesions. Lesion morphology
12). We performed a study to delineate the current
was carefully and consistently noted on physical
causative agents and thus the appropriate antibiotic
examination.
management of this frequently encountered pediat-
After informed consent was obtained, a
ric dermatosis.
bacterial culture was obtained from a
representative lesion. The lesion was cleaned with
alcohol, allowed to dry, and the crust or vesicle
h4E7MODS was unroofed before the culture was obtained.
Antibiotic sensitivities were performed on all S.
The subjects were all outpatients at Cardinal Glen-
aureus isolates. The pa- tient was assigned to
non Children’s Hospital (CGH). All patients exam-
receive either erythromycin or penicillin in a
random, double-blind fashion by a
Address correspondence to Leslie L. Barton, M.D., Car-
dinal Glennon Children’s Hospital, 1465 South Grand
Boule- Vard, St. Louis, MO 63104. Telephone (314) 577-
5643.
185
186 Pediatric Dermatology Vol. 4 No. 3 November 1987

hospital pharmacist. Follow-up was done by one of


the two principal investigators seven days after the
initial visit. Patients who failed to keep their ap-
pointments were contacted by telephone or mail
either to reschedule the follow-up visit, or if this
was not possible, to report by telephone or inail
whether or not the patient’s lesions healed with 8T+O(2%)
therapy.
Patients were treated with either penicillin (pen-
icillin-VK), 50 mg per kg per day divided into four
doses, or erythromycin (erythromycin ethyl succi-
nate), 40 mg per kg per day divided into four doses.
Although follow-up was done seven days after ini-
tiating therapy, patients were asked to take the an-
tibiotic for 10 days.
Patients were asked to bring back their medicine
th -- S. aureus
bottles so that compliance could be judged. They ST - Group A bsl a hefT1OIytIC
were also asked about side effects of the medicine Streptococci
they had taken. Those who did not demonstrate im- 0 = Other
provement at the follow-up visit had their antibiot-
Figure 1. Distribution of Organisms
ics changed based on sensitivities obtained from
their original cultures.

TABLE 1. Distribution o/ Streptoco‹ cal and


RESULTS Sr uph yloc’occ'aI Impeiiyinous Lesions
Seventy-one patients were enrolled in the study; 65 Body Site
were culture positive and 44 were evaluable for ef-
fectiveness of therapy. All of the 38 patients who Organism Face Trunk Extremities
were examined in follow-up were compliant as S. aureus 10 11 14
measured by the amount of antibiotic remaining in Group A streptococci 1 0 I
their medicine bottles. The compliance of six pa- S. aureus and group A 6 2 11
streptococci
tients, whose therapeutic outcome was assessed by
telephone or postcard, could not be ascertained.
Figure I illustrates the distribution of organisms
cultured from the lesions. Staphylococcus aureus
was cultured alone or in combination with other or-
ganisms from 60 (92%) of the 65 patients with iden-
tified organisms. The organism was found in impe-
tigo regardless of body site (Table 1) and was o•-
cultured from children of all ages (Fig. 2).
Lesions in which pure cultures of S. aureus grew 7

were described as vesicular (26PoJ, crusted f60Po),


or bullous (14%); yellow-brown (29%) or honey-col-
ored (71No); and deep (l2Wo), superficial (78%), or
a combination of deep and superficial (10%).
While 35 patients (53%) grew only S. aureus,
only 2 (3%) grew group A Q-hemolytic
streptococci alone. Both of these cases of
streptococcal impetigo occurred in older children 0-6 7-12 1618 1&24 ZS-@ 3J-d6 >3•5 >5
(age 3 years or older). One of these patients had a
culture taken from the face, the other from an
extremity. Group A Q-hemolytic streptococcal Figure 2. Age Distribution
impetigo was described
Barton and Friedman: Impetigo 187

as yellow-brown or honey-colored, superficial,


dominantly adult Boston practice was caused by
and crusted.
Of the 71 patients enrolled, 39 (55Wo) were male S. aureus (l 1). A concurrent study in Florida re-
and 32 (45%) were female. Eighty-three percent vealed that of 101 children with impetigo, 77%
were black, which approximates the racial dis- yielded a pure growth of S. aureus, 9Wc S. aureus
tribution in our entire hospital population. Both and group A Q-hemolytic streptococci, and ldc
S. aureus and S. aureus with group A B-hemolytic group A Q-hemolytic streptococci alone; 13% had
streptococci were isolated as often from early le- no growth from their lesions (12). In the children
sions as from later lesions. Of the 35 patients who from whom 5. aureus was the only isolate, none
grew S. aureus only, follow-up was available on 29. failed treatment with cloxacillin, in contrast to 47%
Fourteen (48Wo) received erythromycin and all were failure with penicillin V. These data thus conflicted
cured. Fifteen (52Wo) received penicillin; of these, 11 with earlier studies, presented a therapeutic di-
(73Vo) improved or were cured, in contrast to 4 lemma, and were the impetus for the current study.
The results of our investigation demonstrate that
(27%) who were treatment failures (P 0.1). All 11
in our Midwestern patient population, S. aureus has
who were treated and cured with penicillin had pen-
become the most common etiologic agent of impe-
icillin-resistant S. aureus as determined by sensitiv-
tigo. That organism was the only bacterial isolate in
ity testing. Although one patient had a penicillin-
53Pc of the patients. occurred in association with
sensitive S. aureus, he was randomized to the
group A }3-hemolytic streptococci in an additional
erythromycin group. One patient randomized to the
30Fr, and with other bacteria in an additional 9Po of
penicillin group had an organism resistant to both
the study patients. Only 3Pr of the patients had im-
penicillin and erythromycin.
petiginous lesions that yielded a pure growth of
group A |3-hemo1ytic streptococci. Also, S. aureus
was isolated from children of all ages, and was as
DISCUSSION common in new as in older lesions. In contrast to
Lookingbill (16), we found that neither lesion mor-
Studies performed in the United States in the 1960s
phology nor site differentiated lesions caused by
and early 1970s demonstrated the superiority of
staphylococci from those caused by streptococci.
systemic antibiotics to topical antibiotics for
There were no treatment failures with erythromy-
the treatment of impetigo (2—6, 13). Burnett com-
cin, while 27Yc of infections that yielded S. aureus
pared oral erythromycin to placebo, wet dressings,
failed to respond to penicillin. Eleven patients in
and topical neomycin-bacitracin ointment (14, 15).
this study responded to penicillin despite the pres-
Erythromycin had superior therapeutic efficacy in
ence of penicillin-resistant staphylococci. The ex-
all instances. In a comparison of erythromycin
planation for this previously observed phenomenon
and topical neomycin-bacitracin-polymyxin (Neo-
remains speculative (3).
sporin), erythromycin markedly hastened healing
Thus it appears that data from different geo-
and decreased the recurrence rate (2). Parenteral
graphic locales support the increased frequency of
penicillin was more effective than either topical
S. aureus in impetigo. Rational therapy is predi-
Neosporin or gentamicin for the therapy of strep-
cated upon knowledge of the major prevailing etio-
tococcal pyoderma (3). It is interesting that in all of
logic agents and their antibiotic sensitivities. The
the early studies, erythromycin and penicillin were
ideal therapeutic agent is inexpensive, easily admin-
associated with virtually identical cure rates, even
istered, well tolerated, and highly efficacious. We
when penicillin-resistant staphylococci were iso-
do not recommend the use of cefaclor or amoxicil-
lated from skin lesions (3, 13). This observation
lin-clavulanic acid, as recently suggested (17), as
appeared to confirm the primary role of group A
their expense and side effects outweigh potential
|3-hemo1ytic streptococci in the pathogenesis of im-
benefits. In another study, clindamycin and eryth-
petigo. Prospective studies in an area endemic for
romycin achieved 90% cure (13); however, gastroin-
impetigo also demonstrated the sequence of spread
testinal side effects were far more common with
of group A Q-hemolytic streptococci from normal to
clindamyctn. In our hospital, 95P• of S. aureus iso-
damaged skin to respiratory tract, in contrast to the
lates are resistant to penicillin, whereas 90To are
spread of staphylococci from the respiratory tract
sensitive to erythromycin and 88% to cloxacillin. A
to normal skin (7, 8).
comparative study of the last two antibiotics for the
More recently, it was noted that the vast major-
treatment of impetigo contagiosa has yet to be
ity of pyoderma, including impetigo, in a pre-
published.
188 Pediatric Dermatology Vol. 4 No. 3 November 1987

ACKNOWLEDGMENTS
7. Ferrieri P, Dajani A. Wannamaker L, Chapman S.
This study was funded by a grant from the Fleur de Natural history of impetigo. I. Site sequence of ac-
Lts Foundation. We thank the pediatric housestaff, quisition and familial patterns of spread of cutaneous
streptococci. J Clin Invest 1972;5 l:285l—2862.
ambulatory faculty, and personnel for their partici- 8. Dajani A, Ferrieri P, Wannamaker L. Natural history
pation in the study. Mrs. Nelka Lindsey aided in of impetigo. II. Etiologic agents and bacterial inter-
the preparation of the manuscript. actions. J Clin In vest 1972;5 I:2863—2871.
9. Tunnessen W. Cutaneous infections. Pediatr Clin
North Am 1983;3:515—532.
10. Tunnessen W. Practical aspects of bacterial skin in-
REFERENCES fections in children. Pediatr Dermatol 1985;2:255—
1. Fox W. On impetigo contagiosa or porrigo. Br Med J 265.
1864;1:467—4fi9. 11. Finnerty E, Folan D. Changing antibiotic sensitivities
2. Hughes W. Wan R. Impetigo contagiosa: etiology, of bacterial skin disease. Cutis l979;23:227—230.
complications, and comparison of therapeutic effec- 12. Schachner L, Taplin D, Scott G. Morrison M. A ther-
tiveness of erythromycin and antibiotic ointment. Am apeutic update of superficial skin infections. Pediatr
I Dis Child 1967;113:44W53. Clin North Am 1983;30: 397—404.
3. Esterly N, Markowitz M. The treatment of pyoderma 13. Dillon H. Topical and systemic therapy for pyoder-
in children. JAMA 1970;212: l6fi7—1670. mas. Inf I Dermatol 1980:19:443—451.
4. Derrick C, Dillon H. Further studies on the treatment 14. Burnett J. Management of pyogenic cuianeous infec-
of streptococcal skin infection. J Pediatr 1970;77:69b tions. N Engl J Med l9fi2;266: 164—169.
— 700. 15. Burnett J. The route of antibiotic administration in
5. Dillon H. The treatment of streptococcal skin infec- superficial impetigo. N Engl Med 1963;268:72—75.
tions. 3 Pediatr 1970;76:676—684. 16. Lookingbill D. Impetigo. Pediatr Rev 1985 ;7:177—
6. Dajani A, Hill P, Wannamaker L. Experimental in- 181.
fection of the skin in the hamster simulating human 17. Jaffe A , O’ Brien C. Reed M, Blumer J. Randomized
impetigo. II. Assessment of various therapeutic reg- comparative evaluation of A ugmentin and cefaclor in
imens. Pediatrics 1971;48:83—90. pediatric skin and soft-tissue infections. Curr Ther
Res 1985 ;38: 160—I69.
This document is a scanned copy of a printed document. No warranty is given
about the accuracy of the copy. Users should refer to the original published
version of the material.

You might also like