Home About us Editorial board Search Ahead of print Current issue Archives Submit article Instructions Subscribe Contacts Login 
Home Print this page Email this page
Users Online:: 312

 Table of Contents  
Year : 2020  |  Volume : 23  |  Issue : 3  |  Page : 195-197

Blistering erysipelas in a black patient

1 Cardiology Unit, Department of Internal Medicine, Usmanu Danfodiyo University/Usmanu Danfodiyo University Teaching Hospital, Sokoto, Nigeria
2 Neurology Unit, Department of Internal Medicine, Usmanu Danfodiyo University Teaching Hospital, Sokoto, Nigeria
3 Dermatology Unit, Department of Internal Medicine, Usmanu Danfodiyo University Teaching Hospital, Sokoto, Nigeria
4 Dermatology Unit, Department of Internal Medicine, Usmanu Danfodiyo University/Usmanu Danfodiyo University Teaching Hospital, Sokoto, Nigeria
5 Gastroenterology Unit, Department of Internal Medicine, Usmanu Danfodiyo University/Usmanu Danfodiyo University Teaching Hospital, Sokoto, Nigeria

Date of Submission10-Jan-2019
Date of Decision25-Feb-2019
Date of Acceptance23-Apr-2019
Date of Web Publication7-Oct-2020

Correspondence Address:
Dr. Hayatu Umar
Department of Internal Medicine, Usmanu Danfodiyo University Teaching Hospital, Sokoto
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/smj.smj_63_19

Rights and Permissions

Blistering erysipelas bullosa constitutes a rare and severe variant of erysipelas, which is rarely reported in the medical literature. It is an acute inflammation of the epidermis and superficial lymphatics. The diagnosis is usually clinical. We report the case of blistering erysipelas of the lower limb complicated by sepsis in a young immunocompetent obese female. To the best of our knowledge, this is the first case being reported from sub-Saharan Africa. We recommend a high index of suspicion of this rare disease in a patient with suspected skin lesions and predisposing factors.

Keywords: Black patient, blistering erysipelas, insect bite, lower-limb erysipelas, obesity

How to cite this article:
Umar H, Akintomide FA, Abdullahi A, Muhammed J, Maiyaki AS. Blistering erysipelas in a black patient. Sahel Med J 2020;23:195-7

How to cite this URL:
Umar H, Akintomide FA, Abdullahi A, Muhammed J, Maiyaki AS. Blistering erysipelas in a black patient. Sahel Med J [serial online] 2020 [cited 2022 Oct 1];23:195-7. Available from: https://www.smjonline.org/text.asp?2020/23/3/195/297460

  Introduction Top

Erysipelas, which was formerly known by the name “ignis sacer,” “holy fire,” and “St. Anthony's fire,[1] is an acute bacterial-induced inflammation of the skin, with marked involvement of cutaneous and lymphatic vessels. Erysipelas and its' blistering form are most commonly caused by B-hemolytic Streptococcus of Group A, less so by Group B, C, or G Streptococci, and occasionally by Staphylococus aureus.[2],[3] However, there is still on-going debate whether erysipelas is also caused by S. aureus or Gram-negative bacteria.[4],[5],[6] The bullous form of erysipelas is a recognizable clinical entity which is rarely reported in the medical literature; it is more severe, predicts more aggressive course, besides, it often indicates a synergistic superinfection with staphylococcus.[7],[8] Complications of the disease include lymphangitis, lymphadenitis, thrombophlebitis, phlegmon, elephantiasis, septic vasculitis, sepsis, septic shock, necrotizing fasciitis, chronic recurrent erysipelas, and blistering erysipelas. Blistering erysipelas must be differentiated from cellulitis, Herpes zoster, impetigo contagiosa, contact dermatitis, diffuse inflammatory carcinoma of the breast, and angioedema.

  Case Report Top

A 22-year-old female was admitted to the Accident and Emergency Unit of Usmanu Danfodio University Teaching Hospital, Sokoto, Nigeria, with 3 days complaints of fever, headache, malaise, and generalized body weakness. A day after the onset of fever, she developed a rapidly expanding red-indurated painful skin rash with associated edema of the right leg. As the changes spread, blisters subsequently evolved. She has no history of diabetes mellitus, HIV and AIDS infection, insect bite, alcoholism, and tobacco use.

On examination, she was a young woman, restless, and confused with the Glasgow Coma Scale of 13, in obvious respiratory distress, icteric (yellowish tinge), acyanosed, not pale, and febrile (39.5°C). She was obese with body mass index of 37 kg/m2 and waist circumference of 98 cm. Her pulse rate was 118/min, blood pressure 90/50 mmHg, and respiratory rate of 28 counts/min. The quick sequential organ failure assessment (qSOFA) score was 3. Systemic examination was unremarkable. Examination of the right leg revealed extensive erythematous indurated plaque with raised and well-demarcated borders [Figure 1]. It was warm to touch, with bullae formation, edema, and tender inguinal lymphadenopathy.
Figure 1: Blistering erysipelas of the lower limbs

Click here to view

The most remarkable laboratory findings were leukocytosis of 16 × 103/μl, with neutrophilia and toxic granulation, serum urea of 9.7 mmol/L, and creatinine of 1.4 mg/dl. HIV screening was negative; erythrocyte sedimentation rate, hemoglobin, platelets, fasting blood sugar, fasting-lipid profile, and liver function tests were normal. Blood culture was negative. Gram stain revealed Gram-positive cocci in chains. Cultured bullous aspirate yielded streptococcal pyogenes, sensitive to penicillin (amoxicillin), ciprofloxacin, and erythromycin. The patient was empirically started on parenteral amoxicillin 500 mg 8 hourly for 5 days; this was subsequently changed to oral therapy for 9 days (total of 14 days antibiotic therapy). In addition, local treatment of the blister was done by the plastic surgical team. The patient achieved remarkable improvement, and she was discharged home. Follow-up in our medical outpatient clinic visit showed that she was enjoying good health.

  Discussion Top

Blistering erysipelas is a rare and more severe variant of erysipelas that is rarely reported in the medical literature. It is an acute and severe streptococcal skin infection, which usually predicts a more aggressive course of the disease.[7] The diagnosis is based on the detailed history, meticulous general, systemic and dermatological examination, and rarely microbial culture results. Early diagnosis and prompt treatment result in the excellent prognosis. In this immunocompetent, obese young female presenting with blistering erysipelas, there was neutrophilia; blister aspirate culture yielded the growth of streptococcus pyogenes. Blood culture was negative. However, other relevant investigations such as antistreptolysin O titer and C-reactive protein could not be carried out due to the lack of facilities.

A study from Sweden documented a good prognosis when there is a culture-positive skin lesion, as in our index case. Only 5% yielded positive blood culture among immunocompetent, hence the negative blood culture in our case, although she had sepsis by qSOFA criteria but not septic shock.[9] Respiratory tract specimen culture was seldom culture positive in some study, and their relevance to lower-limb erysipelas is doubtful except for the facial erysipelas; therefore, we did not do throat/nasal swab culture, which could be additional cost to the patient that could hardly pay for laboratory investigations and treatment in resource-poor settings such as our environment.

The etiopathogenesis of erysipelas begins with the disruption of local skin barrier, allowing the infective organism to penetrate the skin. Skin disruption occurs commonly with abrasion, trauma, interdigital tinea pedis, herpes simplex virus skin infections, but may result also from ulcers, puncture wounds, insect bite, exposure of a neonates umbilical stump, or postvaccination.[8] The source of infection in our index case followed an insect bite.

In erysipelas, cutaneous barrier disruption plays a major role as a risk factor. Furthermore, varied predisposing factors have been documented with erysipelas; this include obesity, diabetes mellitus, venous insufficiency, malignancy, cardiovascular disease, and alcoholism, of which only obesity has been shown to be a definitive risk factor for erysipelas.[9],[10],[11] Our patient had two of the major predisposing factors; obesity and disruption of cutaneous barrier. From studies, the most commonly affected site of infection as in our patient is the lower limbs.[12],[13]

In erysipelas, the distribution and speed of local inflammatory lesion formation are determined by the anatomical structure of the surrounding tissue.[14] The main morphologic determinants are erythema and edema, which rise above the surrounding normal skin, as seen in our index patient. Erythema, as rule, is the most striking finding. The margins though can have different shape arches like our index, and it can be saw tooth, and can spread with the varying level of intensity over the normal skin.[15] The periphery can be raised above the remaining parts of the erythema. The edema spreads beyond the erythema borders. Its severity depends on the localization of the inflammatory process. Its expression is the strongest in the areas with loose connective tissue (the eye lids, lips, and genitals).[14],[15] Blistering erysipelas can have varied clinical presentation and anatomic localization. The erythemobullous form of erysipelas has bullous lesions over an erythema which contains serous exudate.[15]

Penicillin is the empirical antibiotic treatment of choice. However, in patients allergic to penicillin, macrolides are usually recommended.[8] In our patient, the high index of suspicion and timely microbial diagnosis led to accurate diagnosis and prompt treatment with excellent prognosis. Blistering erysipelas being a localized skin infection rarely leads to sepsis (which was not the scenario in our index patient from the qSOFA criteria) and bacteremia, though our patient had a negative blood culture.

  Conclusion Top

Blistering erysipelas can be treated with good outcome if the diagnosis and treatment are prompt. We recommend a high index of suspicion in patients with suspected blistering lesions and major risk factors.

Consent for publication

Written informed consent was obtained from the patient for the publication of this case report. A copy of the written consent is available for review by the editor of this journal.

Declaration of patient consent

The authors certify that they had obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images, and other clinical information to be reported in the journal. The patient understands that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Jorup-Rönström C. Epidemiological, bacteriological and complicating features of erysipelas. Scand J Infect Dis 1986;18:519-24.  Back to cited text no. 1
Bisno AL, Stevens DL. Streptococcal infections of skin and soft tissues. N Engl J Med 1996;334:240-5.  Back to cited text no. 2
Bennett JE, Dolin RB. Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases, US Elsevier Health Bookshop. 8th ed. Philadelphia: Elsevier; 2015. p. 3577.  Back to cited text no. 3
Eriksson B, Jorup-Rönström C, Karkkonen K, Sjöblom AC, Holm SE. Erysipelas: Clinical and bacteriologic spectrum and serological aspects. Clin Infect Dis 1996;23:1091-8.  Back to cited text no. 4
Bernard P, Bedane C, Mounier M, Denis F, Catanzano G, Bonnetblanc JM. Streptococcal cause of erysipelas and cellulitis in adults. A microbiologic study using a direct immunofluorescence technique. Arch Dermatol 1989;125:779-82.  Back to cited text no. 5
Siljander T, Karppelin M, Vähäkuopus S, Syrjänen J, Toropainen M, Kere J, et al. Acute bacterial, nonnecrotizing cellulitis in Finland: Microbiological findings. Clin Infect Dis 2008;46:855-61.  Back to cited text no. 6
Krasagakis K, Samonis G, Maniatakis P, Georgala S, Tosca A. Bullous erysipelas: Clinical presentation, staphylococcal involvement and methicillin resistance. Dermatology 2006;212:31-5.  Back to cited text no. 7
Mossad S. Common infections in clinical practice: Dealing with the daily uncertainties. Cleve Clin J Med 2004;71:129-30, 133-8, 141-3.  Back to cited text no. 8
Dupuy A, Benchikhi H, Roujeau JC, Bernard P, Vaillant L, Chosidow O, et al. Risk factors for erysipelas of the leg (cellulitis): Case-control study. BMJ 1999;318:1591-4.  Back to cited text no. 9
Lazzarini L, Conti E, Tositti G, de Lalla F. Erysipelas and cellulitis: Clinical and microbiological spectrum in an Italian tertiary care hospital. J Infect 2005;51:383-9.  Back to cited text no. 10
Swartz MN. Clinical practice. Cellulitis. N Engl J Med 2004;350:904-12.  Back to cited text no. 11
Brishkoska-Boshkovski V, Dimitrovska I, Kondova-Topuzovska I. Clinical presentation and laboratory characteristics in acute and recurrent erysipelas. Open Access Maced J Med Sci 2019;7:771-4.  Back to cited text no. 12
Kosior E, Reich A. Evaluation of antibiotic treatment on the duration of hospitalization of patients with erysipelas and bacterial cellulitis. Dermatol Ther (Heidelb) 2019;9:159-66.  Back to cited text no. 13
Czarnecki L, Franke-Nawrocka I, Klobut Z. Diphtheria of the glans penis with coexistent erysipelas of the right inguinal fold in a 51-year-old man. Pol Tyg Lek 1967;22:518-20.  Back to cited text no. 14
Bakardzhiev I. Erysipelas penis. J IMAB Annu Proc Sci Pap 2011;17:146-8.  Back to cited text no. 15


  [Figure 1]


Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

  In this article
  Case Report
   Article Figures

 Article Access Statistics
    PDF Downloaded106    
    Comments [Add]    

Recommend this journal