Updated: Mar 08, 2019
Author: Loretta S Davis, MD; Chief Editor: William D James, MD 



Ecthyma is an ulcerative pyoderma of the skin well known to be caused by group A beta-hemolytic streptococci. Concomitant Staphylococcus aureus is often isolated from lesional skin.[1] On occasion, S aureus alone has been isolated.[2] Because ecthyma extends into the dermis, it is often referred to as a deeper form of impetigo.

Typical ecthyma lesions of the lower extremities. Typical ecthyma lesions of the lower extremities.
The stages of ecthyma: the lesion begins as a pust The stages of ecthyma: the lesion begins as a pustule that later erodes and ultimately forms an ulcer with adherent crust.


Ecthyma begins similarly to superficial impetigo. Group A beta-hemolytic streptococci may initiate the lesion or may secondarily infect preexisting wounds. Preexisting tissue damage (eg, excoriations, insect bites, dermatitis) and immunocompromised states (eg, diabetes, neutropenia) predispose patients to the development of ecthyma. Spread of skin streptococci is augmented by crowding and poor hygiene.


Ecthyma can be seen in areas of previously sustained tissue injury (eg, excoriations, insect bites, dermatitis). Insect bites in the setting of recent travel have been associated with ecthyma.[2]

Ecthyma can be seen in patients who are immunocompromised (eg, diabetes, neutropenia, HIV infection).[3]

Important factors that contribute to the development of streptococcal pyodermas or ecthyma include the following:

  • High temperature and humidity [4, 5]
  • Crowded living conditions
  • Poor hygiene

Untreated impetigo that progresses to ecthyma most frequently occurs in patients with poor hygiene.

Some strains of Streptococcus pyogenes have a high affinity for both pharyngeal mucosa and skin. Pharyngeal colonization of S pyogenes has been documented in patients with ecthyma.[6] Ecthyma has also been reported in the setting of perianal streptococcal disease.[7]



The exact incidence of ecthyma worldwide remains unknown.


No racial predisposition is recognized for ecthyma.


No sexual predisposition is recognized for ecthyma.


Ecthyma has a predilection for children and elderly individuals. Outbreaks have also been reported in young military trainees.[6]


Ecthyma lesions are slow to heal but do respond to appropriate antibiotics and local wound care; prognosis is favorable.

Ecthyma rarely leads to systemic symptoms or bacteremia. Lesions are painful and can have associated lymphadenopathy. Secondary lymphangitis and cellulitis, as well as poststreptococcal glomerulonephritis, can occur. Ecthyma does heal with scarring.

Patient Education

For patient education resources, see the Skin Conditions and Beauty Center. Also, see the patient education article Impetigo.




Ecthyma usually arises on the lower extremities of children, persons with diabetes, and neglected elderly patients. During wartime in tropical climates, ecthymatous ulcers are commonly found on the ankles and dorsi of the feet.

Physical Examination

Ecthyma begins as a vesicle or pustule overlying an inflamed area of skin that deepens into a dermal ulceration with overlying crust. The crust of ecthyma lesions is gray-yellow and is thicker and harder than the crust of impetigo. A shallow, punched-out ulceration is apparent when adherent crust is removed. The deep dermal ulcer has a raised and indurated surrounding margin.

Ecthyma lesions can remain fixed in size (sometimes resolving without treatment) or can progressively enlarge to 0.5-3 cm in diameter.

Ecthyma heals slowly and commonly produces a scar.

Regional lymphadenopathy is common, even with solitary lesions.


Ecthyma rarely produces systemic symptoms.

Invasive complications of streptococcal skin infections include cellulitis, erysipelas, gangrene, lymphangitis, suppurative lymphadenitis,[8] bursitis,[6] lobar pneumonia,[6] and bacteremia.

Nonsuppurative complications of streptococcal skin infections include scarlet fever and acute glomerulonephritis. Prompt antibiotic therapy does not appear to reduce the rate of poststreptococcal glomerulonephritis. Streptococcal toxic shock syndrome has been reported.[6]

Possible sequelae of secondary untreated S aureus pyodermas include cellulitis, lymphangitis, bacteremia, osteomyelitis, and acute infective endocarditis. Some S aureus strains produce exotoxins that can lead to staphylococcal scalded skin syndrome and toxic shock syndrome.





Laboratory Studies

Gram stain and culture of ecthyma lesions reveal gram-positive cocci that represent group A streptococci, with or without Staphylococcus aureus. Prior group A streptococci infection can be detected by anti-DNase beta testing.

Histologic Findings

Ecthyma lesions show dermal necrosis and inflammation. A deep and superficial granulomatous perivascular infiltrate occurs along with endothelial edema. A heavy crust covers the surface of the ecthyma ulcer.



Medical Care

Oral antibiotics are used to treat ecthyma. Hygiene is also important. Maintain cleanliness by using bactericidal soap and frequently changing bed linens, towels, and clothing. Remove ecthyma crusts by soaking or using wet compresses. Lesions should then be covered with petroleum jelly or mupirocin ointment.[9]

Oral penicillin is the standard of care for documented streptococcal ecthyma. Typically, a 7-day course is adequate.[10] If concomitant or primary S aureus infection is suspected, oral dicloxacillin and cephalexin are recommended as isolates are typically methicillin-susceptible.[10] Of interest, a 1971 study by Kelly et al demonstrated benzathine penicillin G eradication of streptococci and clinical healing of ecthyma lesions despite the concomitant presence of staphylococci.[1] If methicillin-resistant S aureus is isolated or suspected, doxycycline, clindamycin, and sulfamethoxazole-trimethoprim are therapeutic options.[10] Consider parenteral antibiotics for widespread ecthyma and in the setting of community outbreaks of poststreptococcal glomerulonephritis.[10]

Additional FDA-approved antibiotics for the treatment of acute bacterial skin and skin structure infections include oritavancin (Orbactiv), dalbavancin (Dalvance), and tedizolid (Sivextro). These agents are active against Staphylococcus aureus (including methicillin-susceptible and methicillin-resistant S aureus [MSSA, MRSA] isolates), Streptococcus pyogenes, Streptococcus agalactiae, and Streptococcus anginosus group (includes Streptococcus anginosus, Streptococcus intermedius, and Streptococcus constellatus), among others. For complete drug information, including dosing, see the following monographs:

  • Oritavancin

  • Dalbavancin

  • Tedizolid


Surgical Care

Gently debride ecthyma crusts.


Maintaining cleanliness is critical for preventing ecthyma. Using insect repellants to prevent bites also may decrease the prevalence of ecthyma.



Guidelines Summary

The Infectious Diseases Society of America recently updated their guidelines for the diagnosis and management of skin and soft tissue infections. For the full guidelines, see Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America.[10, 11]



Medication Summary

The goals of pharmacotherapy for ecthyma are to reduce morbidity and to prevent complications.


Class Summary

Topical antibiotics should be considered adjunctive therapy in addition to systemic antibiotics for the treatment of ecthyma.

Penicillin G benzathine (Bicillin LA)

Penicillin G benzathine is the drug of choice when a pyoderma is known to be caused by group A streptococci. It interferes with the synthesis of cell wall mucopeptides during active multiplication, which results in bactericidal activity.

Penicillin VK (Veetids, Beepen-VK)

Penicillin VK inhibits biosynthesis of cell wall mucopeptide and is effective during the stage of active multiplication. Inadequate concentrations may produce only bacteriostatic effects.

Cephalexin (Keflex, Biocef)

Cephalexin is a first-generation cephalosporin that arrests bacterial growth by inhibiting bacterial cell wall synthesis. It has bactericidal activity against rapidly growing organisms. Its primary activity is against skin flora; it is used for skin infections or prophylaxis in minor procedures. It is active against Streptococcus pyogenes and S aureus.

Dicloxacillin (Dycill, Dynapen)

Dicloxacillin is used for treatment of infections caused by penicillinase-producing staphylococci. It can be used to initiate therapy when staphylococcal infection is suggested.

Clindamycin (Cleocin)

Clindamycin is a lincosamide for the treatment of serious skin and soft-tissue staphylococcal infections. It is also effective against aerobic and anaerobic streptococci (except enterococci). It inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

Trimethoprim/sulfamethoxazole (Bactrim, Bactrim DS, Cotrim)

This combination agent inhibits the biosynthesis of proteins and nucleic acids needed for bacterial growth. It typically is effective for methicillin-resistant S aureus.

Doxycycline (Doxycin, Acticlate, Adoxa)

Doxycycline inhibits bacterial growth by inhibiting protein synthesis. It often is effective for methicillin-resistant S aureus. It is not recommended for children younger than 8 years.

Mupirocin (Bactroban)

Mupirocin selectively binds to bacterial isoleucyl transfer-RNA synthetase, inhibiting protein synthesis.