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lnrern;iri(Mial lournal of Dcriiiarology, Vol. ^5. No. I I, November 1 996
REVIEW
ERYSIPELAS: AN UPDATE
CHRISTIAN CHARTIER, M.D., AND E D O U A R D G R O S S H A N S , M.D.
Erysipelas consists of a superficial skin infection with
lymphatic involvement. In general review articles of
streptococcal infections published in the early 1970s,
erysipelas is either barely mentioned or alluded to as
an infection on tbe way to extinction; however, in
some countries, a dramatic increase in tbe incidence of
tbis infection bas been observed and, above all, it is the
site of erysipelas tbat bas cbanged. Facial sites bave be-
come rare and now erysipelas of tbe legs is commonly
observed witb a bigb rate of atypical and recurrent
forms.' Recent papers bave added new clinical, diag-
nostic, microbiologic, and tberapeutic information.
EPIDEMIOLOGY
From 1940 to 1970, tbe decline in streptococcal infec-
tions bas been related to antimicrobial therapy, improved
living conditions, and decreased virulence of the infecting
organisms. In the past few years, tbe incidence of
erysipelas bas been increasing. In our clinic, tbis increas-
ing incidence became striking from 1973 on. (Fig. l).'--^
Tbe upsurge in erysipelas is confirmed by most au-
tbors in industrialized countries.'"' At particular risk for
infection are the young, tbe elderly, and immunocompro-
mised patients.* But there are no satisfying explanations
for tbe comeback of tbis disease. Epidemic forms and
nosocomial infections are rare; erysipelas affects only iso-
lated individuals. Streptococcal resistance to antimicro-
bials and subsequent failure of tberapy cannot be consid-
ered as a possible explanation. Tbere is, perhaps, a
bacteriologic explanation with tbe increase of some M-
serotypes. A potential explanation may be tbe loss of col-
lective immunity against virulent streptococcal strains.''
BACTERIOLOGIC FEATURES
Streptococci were determined to be the causative agent
in 79% of tbe cases of erysipelas in the retrospective
analysis of Bernard et al."* In this report, group A strep-
From the Dermatology Clinic, Faculty of Medicine, Louis
Pasteur University, Strasbourg, France.
Address for correspondence: F-douard Grosshans, M.D.,
Dermatology Clinic, Faculty of Medicine, 1 Place de l'Hopital,
F-67091 Strasbourg, France.
tococci predominated in 67% of tbe cases (group G:
23%; group C: 7%, and group B: 3%). Norby et al.«
sbowed a dominance of serotype Tl M1, but serotyp-
ing data of streptococci isolated from erysipelas are
seldom available in tbe otbers reports.
One sbould be aware of tbe possibility of otber
causative agents, given tbe particular tberapeutic con-
siderations: Staphylococcus aureus, Piieumococcus,
Klebsiclla pneumoniae, Yersinia enterocolitica and
Haemophilus influenzae. Cox et al.' described a patient
witb an acute ulcerated preseptal erysipelas with subse-
quent spread across tbe face, in wbom conjunctival
swabs demonstrated tbe presence of Moraxella species.
CLINICAL DATA
Erysipelas classically involves the face, but currently
tbe predominant location is tbe lower extremities tbat
are favored by local trophic disorders.'-'" In the series
reported by Mainetti et al.," six of 583 cases of ery-
sipelas seen between 1981 and 1991 were localized to
the buttock and bip. Five patients had had a dynamic
hip screw implanted for coxartbritis on tbe side, wbere
tbe skin infection developed. Tbe possible surgical
compromise of the venous-lymphatic circulation of tbe
buttocks appears to be tbe causative factor rather than
superinfection of the surgical wound. Clinically atypi-
cal forms are frequent and some clinical features, such
as bullae and purpura, are not rare.
DIAGNOSIS—BACTERIOLOGIC TESTS
A positive diagnosis of erysipelas is, above all, based
on tbe clinical findings. Bacteriologic tests are useful.
Blood cultures are not always positive even if tbey are
performed in tbe early septic pbase, wben tbe patient
bas a bigb fever. Tbese cultures are positive in 5% of
tbe cases. Swabs can easily be obtained from tbe local
portal of entry or from the fluid of intact pustules or
bullae developing on tbe surface of tbe inflammatory
plaque. The injection-reaspiration metbod, altbougb
easy to perform, is also disappointing. In the report of
Bernard et a I.,** detection of streptococci in skin speci-
mens was better witb direct immunofluorescence (64%),
tban with latex agglutination (47%) or classic culture
tecbniques (28%).
779
International Journal of Dermatology
Vol. 35, No. t 1, November 1996
Figure 1. A frequency curve of erysipelas in the Dermatol-
ogy Clinic of Strasbourg, France, from 1959 to 1995.
COMl'LICATIONS
The necrotizing fasciitis is tnore a clinical form of
streptococcal dertnohypodertnal infections, rather than
a complication. A significant increase in the frequency
of necrotizing fasciitis caused by group A streptococci
has recently been noted.'^ Serotypes 1, 3, 12, and 28
are usually involved; the virulence of some serotypes
tnight be explained by the acquisition of a toxic gene.
But in the retrospective analysis of Bernard et al.,"* the
annual incidence of necrotizing fasciitis was much
lower and more constant.
The "toxic-strep" sytidrome consists of a Strepto-
coccus pyogenes group A infection, complicated by
tnulti-organ failure. This syndrome has been described
in close relation to erysipelas by Ligtenberg et al."
The iticidence of deep vein throtnbosis in patients
with erysipelas of the leg is unknown. In our report,'
we observed deep throtnbophlebitis in 0.9% and su-
perficial thrombophlebitis in 1.3% of patients in a se-
ries of .529 cases with erysipelas.
In a prospective study of 40 patients with erysipelas
of the leg, Mahe et al.''' looked for deep vein throtnbo-
sis, using systematically pulsed Doppler vein exploration
combined with ultrasonography and, when necessary, a
second Doppler exatnination and phlebography. Six
cases of deep vein throtnbosis were diagnosed (among
them, five patients at high risk for deep venous throm-
bosis; in these cases, it had never been suspected at the
clinical examination).
THERAPY
Erysipelas requires antimicrobial therapy. Treatment
regimens vary widely, in both the dermatologic and in-
fectious disease literature. Streptococcus pyogenes con-
tinues to be susceptible to S-lactam antimicrobials;
numerous studies have detnonstrated the clinical effica-
cy of penicillin; classically, a macrolide is used only,
when there is a documented allergy to penicillin. It is
not necessary to cover Staphylococcus aureus, but if
penicillin, given as first line treattnent, fails, the diagno-
sis of the streptococcal origin has to be recotisidered.
Two drugs—not available in the United States—are very
useful in the treatment of erysipelas: roxithrotnycin and
pristinamycin. Bernard et al." cotiducted a prospective,
randotnized, multicenter trial to evaluate the efficacy
and safety of roxithrotnycin (150 mg b.i.d. orally) and
penicillin (2.5 tnillion units (Mil) x 8, daily tv until
apyrexial, then 6 MtJ daily orally) in the treatment of
erysipelas. Both antitnicrobials were continued utitil
the patient had been apyrexial for at least 10 days. The
overall efficacy rates were 84 % (26/31) in the rox-
ithrotnycin group and 76 % (29/38) in the penicillin
group. Oral roxithromycin was also well tolerated
treatmetit (no side effects, whereas skin eruptions oc-
curred in two cases in the penicillin group). Treattnent
with pristinatnycin, continued until the patient had
been apyrexial for 10 days (3 g daily orally), give the
satne results; in a prospective trial, Bernard et al."' re-
ported the efficacy rate to be 86%. Quinolones and
cephalosporins are not itidicated in the treatment of
erysipelas. The adtninistration of clitidatnyciti in addi-
tion to penicillin seetns advisable in patients with strep-
tococcal toxic-shock syndrome.'^
Recurretices of erysipelas are especially prevaletit in
patients suffering frotn local impairtnetit of circulation.
The tnechanistns of recurrence are notwell utider-
stood; pharytigeal carrier state of streptococci group A
can be associated with or precede the relapse. In these
cases, antimicrobial prophylaxis tnay be introduced for
a longer titne, by daily adtninistration of penicilliti V
orally or intratnuscularly (i.e., benzathine penicillin 2.4
MtJ every 3 weeks for 1 or 2 years). Recurrences of
erysipelas appeared to be reduced, but the effect is not
dratnatic. Continuous antibiotic prophylaxis is indicat-
ed only in patients with a high recurrence rate."*
CONCLUSIONS
Erysipelas has chatiged. On an epidemiologic basis, iso-
lated cases are still the rule with epidemic forms being
rare; however, currently, a dratnatic increase in the inci-
dence of this infection has been observed, whereas the
annual incidence of necrotizing fasciitis is more constant.
On a diagnostic basis, laboratory investigations are
becoming iticreasitigly informative, given the advetit of
new diagnostic techniques such as detection of strepto-
cocci in skin specimens with direct itntnunofluorescence.
Therapeutically, penicillin is the antitnicrobial agreed
upon by all; however, the macrolides are also very use-
ful for this itidicatioti.
DRUG NAMES
benzathine penicillin G: Pertnapen
clindamycin: Cleocin
780
Hrysipeias
Ciiaiticr and Grosshans
penicillin V: Compocillin V, Ledercilliti VK,
Robicillin-VK, V-Cillin, and others
penicillin V Betizathine: Pen-Vee
pristinamycin BAN
roxithromyciti USAN
REFERENCES
1. Chartier C, Grosshatis E. Erysipelas. Int J Dertnarol
1990; 29:459-467.
2. Grosshans E. The red face: erysipelas. Clin Dertnatol
1993; 11:307-313.
3. Solberg CO, Chelsom J. Infeksjoner med gruppe A-
streptokokker. Nord Med 1995; 110:50-52.
4. Bernard P, Bedane C, Mounier M, et al. Dertnohypo-
dermites bacterietities de l'adulte. Incidence et place de
l'etiologie streptococcique. Atin Dertnatol Venereol
1995; 122:495-500.
5. Bernard P. Dertno-hypodermal bacterial infections.
Current concepts. Fur J Med 1992; 1:97-104.
6. Bratton RL, Nesse RE. St Anthotiy's fire: diagnosis and
management of erysipelas. Am Fani Physician 1995;
51:401-404.
7. Eeingold DS, Weinberg AN. Group A streptococcal in-
fections. An old adversary reetnerging with new tricks .'
Arch Dertnatol 1996; 132:67-70.
8. Norrby A, Eriksson B, Norgren M, et al. Virulence
properties of erysipelas-associated group A streptococci.
EurJ Cliti Microhiol Infect Dis 1992; 11:1 136-1 143.
9. Cox NH, Knovvles MA, Porteus ID. Pre-septal celluliris
and facial erysipelas due to Moraxella species. Clin F"xp
Dertnatol 1994; 19:321-323.
10. Crickx B, Chevron F, Sigal-Nahum M, et al. Erysipele:
dontiees epidemiologiques, clitiiques et therapeutiques.
Ann Dertnatol Venereol 1991; 1 18:1 1-16.
1 1. Maitietti C, Bernard P, Saurat JH. Hip surgery skin ccl-
luhtis. Eur J Med 1992; 1:52-54.
12. Simonart T, Simonart JM, Schoutens C, et al. Epidemi-
ologie et etiopathogenie des fasciites necrosantes et du
sytidrotne de choc streptococcique. Ann Dermatol
Venereol 1993; 120:469-472.
13. Ligtenberg G, Blankestiin PJ, Koomans HA. Erysipelas:
not always innocent. Nerh J Med 1993; 43:179-182.
14. Mahe A, Destelle JM, Bruet A, et al. Thromboses
veineuses profondes au cours des erysipeles de jamhe.
Etude prospective de 40 observatiotis. Presse Med 1992;
21:1022-1024.
15. Bernard P, Plantin P, Roger H, et al. Roxithrotnycin ver-
sus penicillin in the treatment of erysipelas in adults: a
cotnparative study. BrJ Dertnatol 1992; 127:155-159.
16. Bernard P, Risse L, Bonnetblanc JM. Trairement des
dertnohypodertnites aigues bacteriennes de l'adulte par
la pristinainyciiie: etude ouverte de 42 malades. Ann
Dertnatol Vetiereol 1996; 123:16-20.
17. Bisno AL, Stevetis DL. Streptococcal infections of skin
atid soft tissues. N Etigl J Med 1996; 334:240-245.
18. Sjoblotn AĈ , Friksson B, Jorup-Ronstrom C, et al. An-
tihiotic prophylaxis in recurrent erysipelas. Infection
1993; 21:390-.S93.
Drug Eruptions
It is well known tbat tbe introduction of various drugs into tbe stomach is some-
times followed by the appearance of a cutaneous eruption, and that the connec-
tion between tbem is one of cause and effect. One of tbe tnost cotnmon of tbe
so-called medicinal eruptions, consisting of tbe acnefortn, pustular, and some-
times furuncular lesions due to the administration of tbe iodide or bromide of
potassium, has been attributed to direct irritation of tbe glands of tbe skin be-
cause of tbe attempted cutaneous elimination of the drug from tbe system, and
tbe detection of iodine and bromine in the pus obtained from the cutaneous le-
sions gives to this idea apparent support. Tbe histological character of sucb le-
sions, however, according to Duckworth, does not indicate that the cutaneous
glands are primarily involved, wbile more recent microscopic investigation shows
that, although lesions caused by the ititernal use of iodine and brotnine prepara-
tions may originate in dilatation and cellular infiltration of the capillary network
whicb surroutids the sebaceous glands, the same process also affects blood-vessels
wbicb bave nothing to do witb the glandular apparatus of tbe skin, and may de-
velop to sucb an extent that the consequent lesions represent a pustular dertnati-
tis. Tbe attribute of an eliminative patbogenesis, tberefore, cannot be given to tbis
variety of eruption until more evidence in its favor is forthcoming, altbough the
occasional inception of tbe process in tbe lieigbborhood of tbe cutaneous glands
is suggestive of the ancient maxim, ubi irritatio, ibi affluxus. From Tilden GH.
Dermatitis medicament (Eczema chapter). In: Piffard HG, Morrow PA, eds. J
Cutan Venereol Diseases. Vol 3. Netv York: W Wood, 1885:347.
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