Clin Infect Dis. 1996 Eriksson 1091 8

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1091

Erysipelas: Clinical and Bacteriologic Spectrum and Serological AspectsB. Eriksson, C. Jorup-Riinstriim, K. Karkkon en,rom the Department of Inf ectious Diseases, Karolinska Institute,A. C. Sjiiblom, and S. E. H olmuddinge Hospital, Huddinge; and the Department of ClinicalBacteriology, Umed University, Umed, Sw eden

The bacteriologic, serological, and clinical characteristics of 229 patients with erysipelas diagnosedduring a 2-year period at a un iversity hospital for infectious diseases in Sw eden are presented.fl-Hem olytic streptococci w ere detected in 34% of these patients. Group A was the dom inantserogroup, but group G streptococci were found in about half as many cases. Bacteremia was presentin 5%. A serological response with antistreptolysin 0 (ASO ) and antideoxyribonuclease B (AD NaseB) was seen primarily in patients harboring group A streptococci but also in those from whom nopathogen was isolated. ASO w as also found in high titers in some patients with group G streptococcalinfection. Th e clinical course was usually benign, w ith few complications, but recurrences werecommon (occurring in 21% of the patients). No c ases of streptococcal toxic shoc k w ere seen. Cultureof skin biopsy specimens had low sensitivity; /3-hemolytic streptococci w ere isolated from only twoof 15 patients.

Erysipelas is a superficial skin infection characterized by theacute onset of sharply demarcated erythema with associatedpain and swelling, most often accompanied by generalizedsymptoms such as fever and rigors and som etimes by nauseaand vo miting. It is usually a relatively mild disease with fewcomplications [1], but some patients present with pronouncedsept ic symptom s and m ay have local complicat ions such asskin necrosis or n ecrotizing fasciitis requiring surgical interven-tion [2]. The etiology is usually group A streptococci (GAS),but other groups of ,C3-hemolytic streptococci (BH S)no tably,group G streptococci (GGS)and Staphylococcus aureus havebeen implicated [1, 3, 4]. Other etiologic agents such as pneu-mococci and gram-negative bacteria may rarely cause a similarclinical picture in immunosuppressed patients [5-7], and inthe 19 30s Su lzberger et al . [8] reported an erysipelas-l ike dis-ease due to hypersensit ivity to derm al fungal infections.Less comm only, the differential diagnosis may involve non-infectious entities like deep venous thrombosis [9], Sweet'ssyndrome [10], and eosinophilic cellulit is [11]. Erysipelas canbe regard ed as a spe cific kind of superficial cellulitis. Cellulitisinvolves subcutaneous tissue as well as the superficial skin,and it is distinguished clinically from erysipelas by a morediffusely demarcated erythema without raised edges. In com-parison with erysipelas, besides GAS and o ther fi-hemolyticstreptococci, S. aureus and gram -negative bacteria are believedto be m ore comm only involved in cel lul it is.Erysipelas and cellulit is are com mon skin infections oftenrequiring hospitalization of the patient. The possibility that

Received 9 February 199 6; revised 5 July 1996.Financial support: Karolinska Institute and the Swedish M edical ResearchCoun cil (grant no. 10844).Reprints or correspondence: Dr. Bjorn Eriksson, Department of InfectiousDiseases, Karolinska Institute, Huddinge Hospital, 141 86 Huddinge, Sweden.Clinical Infectious Diseases 1996; 23:1091-81996 by The University of Chicago. All r ights reserved.1058-4838/96/2305 -0023$02 .00

S. aureus may cause a clinical picture resembling erysipelas hasimportant therapeutic implications and may necessitate primaryuse of broa d antibiotic regimens. In addition, the severity ofthis syndrome may be changing. Reports of an increased inci-dence in Sweden of sepsis due to GA S, often with a skin focus,appeared in 1988 [12]; such an increase has been noted in theWestern world s ince the middle of the 1980s . We thereforeundertook the following study of p atients with erysipelas toreview the clinical characteristics, bacteriology, and sero logicalaspects of this disease.Patients and Meth ods

Inclusion of patients. Patients admitted consecutively tothe Department of Infectious Diseases at Roslagstull Hospital(Stockholm) between 1 November 19 88 and 31 October 199 0for whom the diagnosis was erysipelas were studied prospec-tively. At that time the hospital served a population of900,000 residents in the southern and western parts of Stock-holm. Patients younger than 1 8 years of age or infected withHIV were excluded. The study was approved by the ethicscommittee of the Karolinska Institute (Huddinge, Sweden).Definition. Erysipelas was defined as a febrile conditionwith acute onset associated with a temperature of at least 38Cand a well-demarcated, warm, often painful area of erythema.

In our study a few patients were afebrile after admission butwere included if they had had a h igh temperature within 2-3days before a dmission. Patients with localized erythema sur-rounding a wound infection or who had no recorded fever werenot included.Clinical characteristics. All patients were seen by a teammember sh ortly after admission for review of clinical features,underlying diseases, and any history of erysipelas. The C-reac-tive protein concentration and peripheral leukocyte count werenot parameters of the study bu t were determined routinely fornearly all patients admitted to the department and are thereforereported herein.


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1092riksson et al.ID 199 6;23 (November)Bacterial cultures. Bacterial cultures of specimens fromthe throat, nasopharynx, blood, wou nds, ulcers, or other skinlesions were performed as soo n as the patient was admitted tothe hospital. Conventional bacteriologic methods were usedfor isolation an d identification [13]. In cultures of throat an dnasopharyngeal specimens, only B H S were rout inely lookedfor. In 15 patients with erysipelas of the leg, a punch biopsy(area, 3 X 3 x 3 mm ) was performed at the advancing marginof the erythema. Biopsies were not performed on patients takinganticoagulant drugs o r with peripheral arterial vascular insuffi-ciency.Prior to biopsy, the skin was washed with isotonic salineand an esthet ized by cool ing with ethylchloride. The biopsyspecimen was crushed m echanical ly , and the contents werecultured on blood agar plates incubated aerob ically and anaero-bically and on hematin agar plates incubated in 5% carbondioxide. Any additional biopsy material was placed in thiogly-collate broth and incubated for 48 hours.Serology. Blood samples for streptococcal serology weredrawn on admission and at follow-up. Sera were frozen at 20C after centrifugation. Antistreptolysin 0 (ASO) and anti-deoxyribonuclease B (ADNase B) titers were determined witha neph elometer according to the m anufacturer's instructions(Behring, Marburg, Germ any). The prescribed method yieldscontinuous titer values, with lower detection limits of 57 and 7 8units for ASO and ADNase B, respectively. The manufacturerconsiders the normal upper l imit of each antibody to be 20 0U/ mL for adu lts, a limit internationally accepted for ASO. Allsera were analyzed at the same time at the Department ofClinical Bacteriology at U mea. University (Umea, Sweden).

Follow-up. A follow-up visit was scheduled for all pa-tients, who were to be seen 1 mo nth after admission for aclinical evaluation and a second serum sampling, as well asbacterial cultures of specimens from the throat, nasopharynx,and any wounds or ulcers. If no skin breach was present, amoistened swab was rubb ed over the intact skin at the formerarea of erysipelas and cultured to detect any streptococcal skincolonization.Recurrences. To identify the rate and m icrobiological fea-tures of recurrences, patients were asked to contact the depart-ment and were admitted again if symptoms recurred. Labora-tory tests and bacteriologic cultures were performed as during

the primary attack. Recurrences were recorded until 29 Febru-ary 1992.Results

Epidemiologic and clinical features. A total of 229 patientswere included in the study. There was a tendency toward theoccurrence of more cases in the winter (Novemb er Apri l :6-17 cases per month) than in the summer (May October :3-13 cases per month) (P = .05; Student's t-test).Erysipelas was the obvious diagnosis on admission for 199patients (87%). The average time from the onset of symptom s

to admission was 4 days (range, 1-22 days). Diarrhea or vom-i t ing occurred in 8% of the cases. Six patients (3% ) had onlyfever and constitutional symptoms on admission and were be-l ieved to have sepsis or pnem onia until the typical erythemaappeared, usu ally a day later. Differential diagnoses consideredinitially included herp es zoster, acute gout, and septic arthritis.Fifteen patients (7%) who w ere initial ly suspected of havingdeep venous thrombosis of the leg underwent ascending phleb-ography before be ing referred to the department. No patientwas in circulatory shock upon admission to the hosp ital, andstreptococcal toxic shock syndrome developed in none.An overview of clinical features in relation to the site of theerysipelas is given in table 1 . Most p atients were elderly (me-dian age, 67 years; range, 19-95 years). Forty-five percent ofthe men vs. 23% of the women were younger than age 60 years(P < .01; x 2 test). There were more men (131; 57%) thanwomen (98; 43%) in the study group as a whole and in allsubgroups, except that of patients with erysipelas of the arm.In that group there were four women with lymphedema of thearm that occurred following a mastectomy for breast cancer.In 153 patients (67%) a portal of entry was noted, mo st oftena leg ulcer or skin fissure (31%), followed by skin trauma(17% ), eczema or other skin disease (9% ), an interdigital ulcerof the toes with suspected mycosis (6%), and a pustule orparonychia (2%).Fifty-three patients (23%) had no underlying disease,whereas one or more underlying diseases were noted in 77% .Most frequen t was cardiovascular disease (33%), followed byperipheral arterial or venous (or combined) disease (24% ), dia-betes (9%), skin disease (9%), alcoholism (8%), malignancy(4%), and lymphedem a (2%). Mo st pat ients with per ipheralvascular disease had venous insufficiency with chronic or re-lapsing leg ulcers. Four patients had erysipelas of the leg aftersaphenous venectomy in coronary artery surgery. Twelve pa-tients were being treated with steroid drugs, in most casesbecause of a rheumatic disorder. One patient was treated withimmunosuppressive drugs after kidney transplantation.A history of a single previous episode of erysipelas wasrecorded for 27 patients (12% ). Thirty-six patients (16%) hadhad two or more previous episodes.

Treatment and complications. Antibiotic therapy had beeninstituted before admission for 94 patients (41%). After admis-sion, 70% were treated with penicillin,(;*/0 with an isoxazo lyl-penicillin, and 11 % with a com bination of penicillin and isoxa-zolylpenicillin. Some other combination of two /3-lactamantibiotics or a cephalosporin was given in 6% of the cases.Non-/3-lactam antibiotics, usually clindamycin or erythromy-cin, were administered to 8%, in most cases because of anallergy to penicillin. Thirty-five percent o f the patients rec eivedonly oral antibiotic treatment.Co mplications, mainly local skin necrosis or abscess forma-t ion, were n oted in 14% (31 pat ients). Severe complicat ionswere unusual . Two pat ients had sept ic ar thr it is of the knee.Three patients had extensive tissue necrosis requiring skin


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CID 19 96;23 (November)haracteristics of Erysipelas09 3Table 1. Clinical characteristics in relation to site of erysipelas in 229 patients.Clinical characteristic

Data per indicated site of erysipelasFace*

(n = 29 ) Arm or hand(n = 12 ) Leg or foot(n = 177) Others(n = 11) Al l(n = 229)Years of age, median (range)Men 61 44 62 66 62 (19-92)Women 62 73 73 30 73 (19-95)Male/female ratio 1.9 0.71 1.3 1.7 1.3No. (%) of patients with:Underlying disease 15 (52) 9 (75) 145 (82) 7 (64) 176 (77)History of erysipelas 3 (10 ) 2 (17) 54 (31) 4 (36) 63 (28)Portal of entry noted 14 (48) 7 (58) 130 (73) 2 (18) 153 (67)Bullous or he morrhagic erysipelas 1 (3) 2 (17) 19 (11) 1 (9) 23 (10)Complication 1 (3) 2 (17) 27 (15) 1 (9) 31 (14)Recurrence 4 (14) 0 39 (22) 5 (45) 48 (21 )Temperature (C)* 38.5 38.2 38.3 38.7 38.4 (36.0-41.1)CRP (mg/L), mean (range) 10 7 157 17 0 220 163 (


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1094riksson et al.ID 1996;23 (November)Table 2. Bacteriologic findings for patients with erysipelas.No. of patients for whom culture of indicated specimen yielded isolate(s)/no. ofpatients being treated with antibiotics at t ime of culture

Variable Nasopharynx Throat BloodtWound

or ulcer3 Joint fluidTotal no. of patients 196 (77) 192 (76) 161 (51) 119 (41) 2 (2)Isolate(s):None or no rmal flora 187 (77) 181 (74) 153 (49) 24 (10) 0 (0)Group A streptococci 7 (0) 6 (0) 5 (0) 42 (9) 2 (2)Group B streptococci 0 (0) 0 (0) 1 (1) 0 (0) 0 (0)Group C streptococci 0 (0) 0 (0) 0 (0) 2 (0) 0 (0)Group G streptococci 2 (0) 5 (2) 2 (1) 19 (4) 0 (0)Enterococci ND ND 0 (0) 12 (7) 0 (0)

Staphylococcus aureus ND ND 0 (0) 61 (16) 0 (0)Gram-negative bacteria ND ND 0 (0) 21 (12) 0 (0)NOTE. ND not routinely detected.t Usually two sets of aerobic and anaerobic blood cultures were performed per patient.t Patients frequently had more than one type of species isolated from wo unds/ulcers.Twenty-seven isolates were recovered from 21 patients: Escherichia coli (3), Enterobacter cloacae (6), Enterobac-

ter agglomerans (1), Klebsiella oxytoca (2), Proteus mirabilis (3), coliforms (not further specif ied; 1), Pseudomonasspecies (10), and Acinetobacter species (1).

the mean age (61-7 0 years) did not differ significantly betweenthe subgroups.The serological findings are summarized in figure 1. ASOtiters of >200 were noted in 30% of acute sera, whereastiters above this normal limit were noted in 61% of the conva-lescent sera. A significant increase in ASO titers betweenserum specimens one and two was noted in the no-pathogengroup (P = .0006), the GAS group (P = .001), and the GGSgroup (P = .0006) (Wilcoxon's signed rank test). No suchincrease was noted in the enterococci group (P = .34) or theS. aureus group (P = .07) (Wilcoxon's signed rank test).An AD Nase B titer of >200 was noted in 30% of the acutesera and in 51% of the convalescent sera. Very high levels ofADNase B were found in two patients in the no-pathogengroup. A significant difference in ADNase B titers betweenserum specimens one and two was recorded in the no-patho gengroup (P= .0001), the GAS group (P= .02), and the S. aureusgroup (P = .02) but not in the GG S group (P = .1) or theenterococci group (P = .22) (Wilcoxon's signed rank test).

Follow-up. Fol low-up was done for 109 pat ients. Sevenpatients were colonized with GAS, three with GGS, five withenterococci, and 16 with S. aureus, usually in skin lesions.Four patients who were culture-negative on admission harboredBH S at follow-up. In no case were BH S found in cultures ofswab specimens from the surface of intact skin overlying theformer site of erysipelas.

Recurrences. One or more recurrences of erys ipelas oc-curred in 48 patients (21%) during the observation period.Twenty-four patients had 1 recurrence, 16 patients had 2 and 8had 3. Twenty-three percent of patients with any underlyingdisease had a recurrence, vs. 13% of those without such disease,but this difference wa s not statistically significant (P > .10;

x2 test). One of the four patients who underwent a saphenousvenectomy in corona ry artery surgery relapsed. The time fromthe first admission until the second attack varied between 3and 157 weeks (median, 14 weeks). Cultures were performedon 34 of the occasions of relapse, and GAS w ere isolated on8, GGS on 6, enterococci on 2, and S. aureus (as a singlepathogen) on 2.

DiscussionErysipelas is generally a sporadic disease of which therehave been few reported o utbreaks [14 ]. In classic reports fromthe beginning of the century, it was descr ibed as a comm ondisease affecting mainly children an d elderly patients. It wascommonly located in the face, but erysipelas of the trunk, leg,or umbilicus was associated with a higher case-fatality rate.

Most cases were seen in the winter and spring months, inparallel with scarlet fever and streptococcal throat carriage[15-19].

In a survey of scarlet fever and erysipelas in Norway, Mad -sen [20] reported an incidence of erysipelas of 10 cases per10,000 people per year between 1880 and 19 70. A few reportsfrom Europe and Israel have shown a recent increase in hospitaladmissions due to this diagnosis [21-23]. Except for the Nor-wegian report, however, there seem to be few reliable popula-t ion-based data; most reports have co me from hospitals. In aprevious study in Sweden [24], a l i ttle over 100 cases per yearwere noted in an infectious disease department serving about700,000 people. This corresponds w el l to our o wn study, inwhich there were 229 recorded admissions during a 2-yearobservation period among a population of 900 ,000 people.


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CID 19 96;23 (November)haracteristics of Erysipelas09 5Table 3. Bacteriologic findings in skin b iopsies (and cultures of other spe cimens) for 15 patients with erysipe las of the leg.Patientno .

Patient's age(y)/sex

Under ly ingconditions

Antibioticreceivedbeforebiopsy

Findings in culture of indicated specimenNasopharynx

or throat Skin lesion Blood Skin biopsy1 78/M CVD, alcoholism Penicillin N eg Enterobacter cloacae,

Acinetobacter species,Staphylococcusepidermidis

NG Streptococcus millerigroup

2 29/M Obesity, recurrenterysipelas

None GG S GGS, S. epidermidis NG GG S3 78/F Leg ulcers None N eg ND GA S GA S4 74/M CVD, recurrent

erysipelasNone N eg N eg NG E. cloacae

5 61/M Hypostatic eczema None N eg N eg NG S. epidermidis,Clostridiumspecies6 59/M Healthy None N eg ND NG S. epidermidis7 77/M Diabetes, artificial

heart valve, legulcer

None N eg GAS, S. aureus NG NG

8 71/M Artificial heartvalve, leg ulcer

None N eg ND NG NG9 66/M Recurrent erysipelas None N eg ND NG S. epidermidis

10 81/F Diabetes, recurrenterysipelas,sarcoidosis,chronic leg ulcer

None N eg ND NG Morganellamorganii,coliforms

11 68/F Healthy None N eg GAS, S. aureus NG NG12 57/M CV D None ND GAS, Enterobacter species,Klebsiella oxytoca

ND NG13 82/F Charnley prosthesis Penicillin N eg S. epidermidis NG NG14 51/M Alcoholism,psoriasis, chronichip infection withfistula, burn

None N eg GAS, S. aureus NG NG

15 48/F Healthy buttraumatic wound NoneN eg ND NG NG

NO TE. CV D = cardiovascu lar disease ; GAS = group A streptococc i ; GGS = group G streptococc i ; ND = not done; Neg = no growth or normal f lora ;NG = no growth.

All our cases were sporadic and had n o epidemiologic con-nection, but there was a tendency toward increased frequencyin the cold months. The age an d sex distribution in our ownand other recent reports is similar [21-24]. Erysipelas of thelegs is now m ore frequent than facial localization, and m ostpatients have one or more underlying diseases [21-24]. Aprevious attack in itself seems to be a pred isposition for recur-rences.General and local symptom s are usually helpful in the correctdiagnosis of erysipelas, but prodromal symptoms are commonand may b e misleading. In 13% of our patients the diagnosiswas unclear on admission, and in 3% the skin changes wereobserved later. Thus, patients with severe streptococcal diseaseand sept ic shock m ay be ini tia lly suspected of having gram-negative sepsis.The C -reactive protein level was usually strongly elevated,but leukocytosis was not a con sistent finding (54%). In a recent

study [25], a C-reactive protein concentration of >20 0 m g/Lwas taken as an indication of the development o f necrotizingfasciitis in patients with erysipelas. In our study, however,about one-third of the patients with uncomplicated erysipelashad concentrations of >200 mg/L.Penicil lin is the drug o f choice for the antibiotic treatmentof erysipelas. Sixty-five percent of our pa tients received intra-venous treatmen t at some time in the course of the disease.Jorup-ROnstrOm et al. [26] have shown that treatment with oralpenicillin is adequ ate for most patients. Skin concentrations ofpenicillin were studied in a subgroup of our patients receivingoral medication and were sho wn to be above M IC values forhemolytic streptococci for about 4 hours after adm inistrationof 1 gram of phenoxymethylpenicil l in to normal-weight pa-tients [27]. Howe ver, septic symptom s and vom iting may b epronounced , and in these cases cl inicians may choose to giveparenteral therapy initially.


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1erum: 110,000; 00 0 001 , 0 0 0 : 0 00100 NoneASGSnt.. aureusA00000 I I )1S. aureus01 , 0 0 0 o0 0 000NoneASGSnt.C 100 : Serum: 1 BI1096riksson et al.ID 1996;23 (November)IsoatedpathogenIsoatedpathogenFigure 1. Box plot of log titers of (A ) antistreptolysin 0 (ASO) and (B) antideoxyribonuclease B (ADNase B) in p atients with erysipelas,from whom various pathogens were isolated. Medians and 25th and 75th percentiles are indicated by central, lower, and upper horizontal linesof the box, respectively. The 10th and 90th percentiles are indicated b y horizontal lines below and ab ove the box, respectively. Circles representindividual values below or ab ove the 10th and 90th percentiles. Serum 1 and 2 are the acute and convalescent serum samples. Patients weregrouped according to isolated pathogen: none = no isolated pathogen (33 patients); GAS = group A streptococci (33); GGS = group Gstreptococci (18); Ent. = enterococci (6); and S. aureus = Staphylococcus aureus (6).

Complications were relatively few and usually nonsevere.Severe complications such as retropharyngeal abscess, medi-astinitis, pleural effusion, upper-airway obstruction, and ocularinvolvement have been reported [28-30] but were not observedin this study.No patient died as a direct result of the erysipelas. Madsen[20] reported decreasing mortality due to the disease in Norwayduring the first half of the century an d virtually no deaths afterthe advent of antibiotic treatment. The Western world is nowexperiencing a resurgence of serious GAS infections, includingsepsis and streptococcal toxic shock syndrome. About half ofthese severe or fulminant infections originate from a skin orsoft-tissue infection [31].Du ring the winter of 1988-198 9, there was an outbreak ofGAS bacteremia in Sweden, mainly caused by M1 strains andassociated with high mortality [12]. The GAS strains fromour study were serotyped, and the production of streptoccocalpyrogenic exotoxins was studied [32]. The M1 serotype alsowas predominant in the patients with erysipelas, and thosestrains had profi les of toxin produ ction and D NA restrict ionpatterns of the em m gene region similar to those of the bacter-emia-associated strains [33, 34]. The reasons for low mortalityand the absence of streptococcal toxic shock syndrome in ourpatients are unclear, but there may be h igher levels of toxin-neutralizing antibodies in p atients with erysipelas than in pa-tients with sepsis [32].The relapse rate was 21%, and equally high rates have beenrecorded previous ly , especial ly among pat ients with venousinsufficiency [24] or after saphenous venectom y in coronarysurgery [35]. Long-term antibiotic prophylaxis has b een triedin a subgroup of our patients [36], and it was found to beeffective for mo st of them. Such effectiveness has also beenshown in a few o ther studies [37, 38].

Bacteriologic proof of the suspected streptococcal et iologyof erysipelas is often difficult to obtain. From o nly about on e-third of our p at ients could BH S be isolated. Blood cultureswere positive for only 5% of the patients; therefore, such cul-tures seem to be of low value for patients who are not immu no-suppressed and have no signs of septic shock. Cellulitis orerysipelas caused by gram-negative bacil l i has been reportedto occur mainly in patients with cirrhosis or other severe under-lying diseases [39, 40]. In these cases, cultures of blood, skin-blister fluid, or material obtained during surgical procedu resusually have been diagnostic.Respiratory tract specimens were seldom culture-positive inour study, and their relevance to the skin infection may bedoubtful. Our data do not support the theory that the respiratorytract is the main reservoir of streptococcal infection in casesof erysipelas. However, in so me cases of facial erysipelas, thenasopharynx may be the reservoir.Most of the BHS recovered in our study were isolated fromskin lesions. Whether these streptococci were the true etiologicpathogens is difficult to assess. The use of fine-needle aspirationof the skin to determine the etiology of cellulitis was first advo-cated by Uman and Kunin in 1 975 [41], but the sensitivity of thismethod has been d isappointingly low [42]. One explanation maybe that the den sity of organisms in the inflamed tissue is low[43]. Some authors, using fine-needle aspiration techniques, havefound that patients with diabetes, malignancy, or other underlyingdiseases are more frequently culture-positive [44]. The low sensi-tivity of skin biopsy culture was verified in our study, and thistechnique was abando ned after its use for 15 patients. The findingsof cultures of skin-lesion specimens are probably as reward ingand representative as those of m ore invasive techniques [45].Detection o f streptococcal antigens in skin biopsy specimensby mea ns of latex agglutination [46] and direct immunofluo-


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CID 1996;23 (November)haracteristics of Erysipelas09 7rescence methods [47] has been shown to be more sensitiveand has dem onstrated a c lear predom inance of BHS in casesof erysipelas as well as cellulitis. Moreover, the location ofstreptococci in the dermis-hypodermis, as visualized by theimmunofluorescence technique, was similar in patients witherysipelas and those with cellulitis, indicating that these condi-t ions may b e two aspects of the same d isease process .

Our own study supports the view that GAS are the usualet io logic agents in erys ipelas, but GG S were found in abo uthalf as many cases. Streptococci of groups B and C wererarely involved. Enterococci were recovered from patients withchronic leg ulcers, mostly in mixed flora with gram-negativeenteric bacteria or P s e u d o m o n a s species. Such culture findingsare frequently regard ed as non representative of the invadingorgan ism in pa tients with typical erysipelas. However, sinceserology showed no significan t increase in antibodies to strepto-cocci in this group of patients with chronic leg ulcers, theseculture findings may have been relevant. Such patients usuallyare elderly, have grave underlying vascular diseases, and re-quire longer hospitalization than the average patient with ery-sipelas (median, 17 days vs. 6 days). Whether they wouldbenefit from broad er antibiotic treatment than administration o fpenicillin alone has not been determ ined. Our p atients usuallyreceived conventional penicillin treatment on ly.

The signif icance of f inding S . a u r e u s in ulcers or skin lesionsof patients with classic erysipelas is difficult to assess. Fewstudies have shown d irect evidence of this pathogen in casesof erysipelas. A study in Austria with use of an invasive tech-nique of scarification identified S . a u r e u s as a cause of erysipe-las in a few cases [48]. In the previously cited studies usingskin-biopsy antigen-detection methods [46, 47], S . a u r e u s wa sindirectly im plicated in a few of the cases of cellulitis but innone o f those of c lassic erysipe las . Many of our own pat ientsharboring s taphylococc i as the sole presumptive pathogenswere receiving antibiotic treatment at the t ime of culture. Theserologic data for this group were inc onclusive. There was asignificant increase in titers of ADNase B but not in titers ofASO (P = .07). Som e of these patients may thus have had astreptococcal infection but negative cultures because of an tibi-otic treatment or a sam pling error.

The levels of antistreptococca l antibodies have been shownto be a ge-related [49], peaking in the age g roup of 10-20 yearsand declining well below the traditionally accepted normalupper limit of 200 U/mL in older age groups. Mean ages inthe subgroups of our pat ients were between 60 and 70 years,and al l values (down to the detect ion l imits of the m ethods)were therefore included in the analysis of antibody titers. Asigni f icant increase in t i ters of both ASO and ADNase B wasnoted in the groups from whom G AS or no pathogens wereisolated (the GAS and n o-pathogen group s), implying that GASwere the probable p athogens in these patients.

Deoxyribonuc lease B production is specific for GAS [50],and the significant increase in ADNase B titers in the staphylo-cocci group ma y implicate GAS in som e of these cases as well ,

as discussed above. A rise in ASO titers but not ADNase Btiters was noted in the GGS group , a finding co nsistent withthe fact that GGS strains produce streptolysin 0 but not deoxy-ribonuclease B [50]. The small group of patients harboringenterococci had no s igni f icant increase in ASO or ADNase Btiters. It therefore seems unlikely that an undetected infectiondue to GAS or GGS was common in this group of patientswith erysipelas. Another serologic study of erysipelas and cel-lulitis [51] found evidence of infection with GAS in 40% ofthe patients with erysipelas (7 of 15). In the same study, all20 patients with cellulitis had a high o r rising titer of antibodiesagainst group A, C, or G streptococcal antigens.

In summ ary, erysipelas is generally caused by BHS m ostlyGAS or GGS an d rarely other serogroup s. S . a u r e u s probablydoes not cause a cl inical picture of classic erysipelas but maycause cellulitis. For patients with mild disease, cultures of skinlesions and emp ir ical treatment d irected aga inst BHS seemadequa te. For severely il l patients and those who ha ve graveunderlying diseases or are receiving im munosuppressive treat-men t, more extensive diagnostic studies are necessary, such asculture of blood, needle aspirations o f skin or bullous fluid, orculture of tissue obtained during surgical debridement. Clinicalsigns of necrotizing fasciitis requiring promp t surgical interven-tion should be looked for.

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