Authors: Syed Rahil / Editor: Lynn Stevenson / Codes: DC1, DC3, DC6, DP1, IP1, SLO5 / Published: 02/05/2023

Group A Streptococcus is responsible for many skin and soft tissue infections. Knowledge of human skin anatomy helps to develop an understanding of the various clinical manifestations of this pathogen1. Based on the appearance of the associated skin rashes it is possible to differentiate between the variety of conditions caused by group A streptococcus.

Image 1: Anatomy of skin. Image via

Human skin is broadly divided into three layers: dermis, epidermis and subcutaneous tissue.

Epidermis is further divided into 4 layers (not discussed here)2.

Group A Streptococcus bacteria can affect any skin layer leading to different clinical sequelae.

  • Impetigo: superficial layers of epidermis
  • Ecthyma: epidermis and dermis
  • Erysipelas: upper dermis
  • Cellulitis: subcutaneous tissue and lower dermis
  • Necrotising fasciitis: subcutaneous tissue and fascial layers

The skin manifestations of each of these conditions will be discussed.



Impetigo is a common bacterial skin infection affecting the superficial layers of epidermis. It is more prevalent in children between the ages of two and five3. Pustules and honey-coloured crusted skin lesions are characteristic of Impetigo.

Impetigo can be caused by group A Streptococcus as well as Staphylococcus aureus and is classified into bullous and non-bullous types4.

Non-bullous impetigo can be caused by both pathogens. Face and extremities are the most commonly affected areas. It starts as erythematous lesions which transform into blisters (vesicles or pustules). They eventually rupture leading to typical honey coloured crust formation4.

It can spread rapidly due to autoinoculation.

Image 2: Impetigo via

Bullous impetigo is caused by Staphylococcus aureus (not discussed here).


Impetigo is treated by topical antiseptic creams like hydrogen peroxide 1% or povidone-iodine  ointment. Topical antibiotics (Fusidic acid/ Mupirocin) are used if topical antiseptics are ineffective.

When impetigo involves large bullae or when topical therapy is impractical, oral antibiotic therapy (like flucloxacillin) is the treatment of choice3.



Ecthyma is a more severe presentation of impetigo with deeper erosions of the skin into the dermis. Initially, it develops as a vesicle or a pustule on an inflamed area of skin. Soon it forms a hard crust over the blister. Removal of crust reveals an indurated ulcer oozing with pus. It resolves slowly and leaves a scar5,6,7.

Image 3: ecthyma via


Image 4: Erysipelas via

Erysipelas is a superficial form of cellulitis which affects the upper dermis. It extends into the superficial cutaneous lymphatics. Onset of symptoms and signs is usually abrupt8. The affected skin is bright red, firm and swollen with sharp, raised borders and it is associated with fever.

It commonly affects lower limbs but can also involve the face with a characteristic butterfly distribution of rash. It may become blistered and in severe cases it may also become necrotic.


Oral or intravenous penicillin is recommended as the antibiotic of choice. Treatment is usually for 10–14 days. The skin changes may take several weeks to resolve completely, however, no scarring tends to occur9.


It is not always possible to differentiate between cellulitis and erysipelas on clinical examination.

Cellulitis is a common bacterial skin infection affecting the lower dermis as well as subcutaneous tissue. Group A streptococcus is responsible for the two third cases of cellulitis10,11.

Cellulitis results in a localised area of red, painful, swollen skin and is associated with systemic symptoms11.

Spread of infection into lymph vessels and lymph nodes leads to lymphangitis and lymphadenitis.

Image 5: Cellulitia via


Management of cellulitis depends on the severity. Mild cellulitis may be treated with oral antibiotics and does not require hospital admission whereas patients with severe cellulitis with systemic symptoms should be hospitalised for intravenous antibiotics.

Penicillin-based antibiotics are the first choice (e.g. penicillin V or flucloxacillin). Clindamycin, clarithromycin, doxycycline and vancomycin can be used in patients with penicillin allergy.

Necrotising fasciitis

Necrotising fasciitis is a life-threatening infection of the soft tissue and fascia12. It is divided into three types. Type II, also known as the “flesh eating disease” is triggered by group A Streptococcus.

Necrotising fasciitis is a clinical diagnosis which can be easily missed. Late diagnosis and treatment of necrotizing fasciitis are linked to adverse outcomes, including multiple organ failure. Prompt identification is essential. This type of infection continues to be a significant cause of patient morbidity. Necrotising fasciitis should be suspected in any patient who presents with a skin rash associated with systemic features like hypotension and tachycardia.

The most common site of infection is the lower leg13. The other areas affected are upper limbs, trunk, perineum, buttocks, head and neck.

Infection starts in the superficial fascia and then spreads vertically into the deeper structures due to tissue necrosis caused by enzymes and toxins released by the bacteria.

Physical examination findings include local and systemic features:


  • Severe pain out of proportion to physical findings
  • Oedema
  • Redness
  • Skin blisters/ necrosis
  • Skin tenderness
  • Crepitus


  • Fever
  • Tachycardia
  • Hypotension
  • Shock
Image 6: Necrotising fasciitis via


Emergency surgical debridement

Prompt and effective surgical intervention is essential for successful treatment of infected subcutaneous tissue. The devitalized tissue must be completely removed and any infected fluids must be drained. Surgical debridement should be conducted as soon as possible, ideally within the first 12 hours of admission to the hospital14.

Empirical antibiotic therapy

Choice of empirical antibiotics depends on the local hospital policy. Suitable antibiotics include Piperacillin/ Tazobactam, Meropenem, Ceftriaxone or Ciprofloxacin and Clindamycin14.

For example:

  • Piperacillin/ Tazobactam (Tazocin) + Clindamycin (if no Penicillin allergy)
  • Meropenem/ Clindamycin (if Penicillin allergy)

Please refer to your local trust protocol or microbiologist.


Image 7: Scarlet fever rash via

Scarlet fever

Image 8: Pastia lines via

Scarlet fever  is an infectious disease caused by group A streptococcus and can be recognised based on the appearance of skin rash.

The typical rash in Scarlet fever is described as “sandpaper like” due to diffuse erythema interspersed with numerous small papules, giving it a sandpaper like appearance.

Rash develops 12-48 hours after onset of fever. It generally starts on the upper body (below ears/ chest/ armpits) before spreading downwards15.

Examination of the face can reveal a strawberry tongue and circumoral pallor. Palms and soles are usually spared.

“Pastia lines” are another characteristic feature of Scarlet fever. These are petechial lesions distributed in linear fashion over flexural areas like axillae, antecubital fossa etc.17.

The rash starts to fade and peel by about the sixth day of infection.


Penicillin antibiotics (like penicillin V) is first choice, prescribed for a duration of 10 days18.



  1. Stevens DL, Bryant AE. Impetigo, Erysipelas and Cellulitis. 2016 Feb 10. In: Ferretti JJ, Stevens DL, Fischetti VA, editors. Streptococcus pyogenes: Basic Biology to Clinical Manifestations [Internet]. Oklahoma City (OK): University of Oklahoma Health Sciences Center; 2016-.
  2. Kolarsick, Paul A. J. BS; Kolarsick, Maria Ann MSN, ARHP-C; Goodwin, Carolyn APRN-BC, FNP. Anatomyand Physiology of the Skin. Journal of the Dermatology Nurses’ Association 3(4):p 203-213, July 2011.
  3. Hartman-Adams H, Banvard C, Juckett G. Impetigo: diagnosis and treatment. Am Fam Physician. 2014 Aug 15;90(4):229-35.
  4. Brown J, Shriner DL, Schwartz RA, Janniger CK. Impetigo: an update. Int J Dermatol. 2003 Apr;42(4):251-5.
  5. Sonthalia S, Singal A, Khurana R. Ecthyma. Indian Pediatr. 2014 Jun;51(6):510-1. PMID: 24986304.
  6. Ecthyma. Health jade team (
  7. Ngan V. Ecthyma. DermNet ( 2003. Reviewed in 2016.
  8. Bonnetblanc JM, Bédane C. Erysipelas: recognition and management. Am J Clin Dermatol. 2003;4(3):157-63.
  9. Stanway A. Erysipelas. DermNet ( 2001. Reviewed in 2016.
  10. Raff AB, Kroshinsky D. Cellulitis: A Review. JAMA. 2016 Jul 19;316(3):325-37.
  11. Stanway A. Cellulitis. DermNet ( 2001. Reviewed in 2016.
  12. Leiblein M, Marzi I, Sander AL, Barker JH, Ebert F, Frank J. Necrotizing fasciitis: treatment concepts and clinical results. Eur J Trauma Emerg Surg. 2018 Apr;44(2):279-290.
  13. Tso DK, Singh AK. Necrotizing fasciitis of the lower extremity: imaging pearls and pitfalls. Br J Radiol. 2018 Jul;91(1088):20180093.
  14. Sartelli, M., Guirao, X., Hardcastle, T.C. et al. 2018 WSES/SIS-E consensus conference: recommendations for the management of skin and soft-tissue infections. World J Emerg Surg 13, 58 (2018).
  15. Herdman MT, Cordery R, Karo B, Purba AK, et al. Clinical management and impact of scarlet fever in the modern era: findings from a cross-sectional study of cases in London, 2018-2019. BMJ Open. 2021 Dec 24;11(12):e057772.
  16. Kang JH. Febrile Illness with Skin Rashes. Infect Chemother. 2015 Sep;47(3):155-66.
  17. Drago F, Ciccarese G, Merlo G, Trave I, Javor S, Rebora A, Parodi A. Oral and cutaneous manifestations of viral and bacterial infections: Not only COVID-19 disease. Clin Dermatol. 2021 May-Jun;39(3):384-404.
  18. National Institute for Health and Care Excellence. Phenoxymethylpenicillin | Prescribing information | Scarlet fever | CKS | NICE. Last revised: February 2023.