eMedicine Specialties > Dermatology > Bacterial Infections

Ecthyma

Loretta Davis, MD, Professor, Department of Internal Medicine, Division of Dermatology, Medical College of Georgia

Updated: Nov 6, 2009

Introduction

Background

Ecthyma is an ulcerative pyoderma of the skin caused by group A beta-hemolytic streptococci. Because ecthyma extends into the dermis, it is often referred to as a deeper form of impetigo.

Typical ecthyma lesions of the lower extremities.

The stages of ecthyma. The lesion begins as a pustule that later erodes and ultimately forms an ulcer.

Pathophysiology

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.

Frequency

International

The exact incidence of ecthyma worldwide remains unknown.

Mortality/Morbidity

Ecthyma rarely leads to systemic symptoms or bacteremia. Lesions are painful and can have associated lymphadenopathy. Secondary lymphangitis and cellulitis can occur. Ecthyma does heal with scarring. The rate of poststreptococcal glomerulonephritis is approximately 1%.

Race

No racial predisposition is recognized for ecthyma.

Sex

No sexual predisposition is recognized for ecthyma.

Age

Ecthyma has a predilection for children and elderly individuals. Outbreaks have also been reported in young military trainees.¹

Clinical

History

• 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

• 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.

Causes

• Ecthyma can be seen in areas of previously sustained tissue injury (eg, excoriations, insect bites, dermatitis).
• Ecthyma can be seen in patients who are immunocompromised (eg, diabetes, neutropenia, HIV infection).²
• Important factors contribute to the development of streptococcal pyodermas or ecthyma.
  • High temperature and humidity^3,4
  • 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.¹

Differential Diagnoses

Other Problems to Be Considered

Cutaneous diphtheria
Other bacterial, viral, and deep fungal infections of the skin
Excoriated insect bites
Ulcers of venous and arterial insufficiency

Workup

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.

Treatment

Medical Care

Medical treatment for ecthyma depends on the progression of the lesions. Hygiene is important. Maintain cleanliness by using bactericidal soap and frequently changing bed linens, towels, and clothing. Remove ecthyma crusts by soaking or using wet compresses and apply an antibiotic ointment daily.

• Consider topical therapy with mupirocin ointment for localized ecthyma.⁵
• More extensive ecthyma lesions require oral antibiotics; the duration of treatment varies because ecthyma may require several weeks of therapy to completely resolve.
• Penicillin should be adequate to treat ecthyma.
• Oral antistaphylococcal agents (eg, dicloxacillin, cephalexin, erythromycin, clindamycin) have been used to cover possible secondary Staphylococcus aureus infections. A study by Kelly et al has demonstrated that benzathine penicillin G eradicates streptococci; lesions heal clinically despite the concomitant presence of staphylococci.⁶
• Consider parenteral antibiotics for widespread ecthyma.

Surgical Care

Gently debride ecthyma crusts.

Medication

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

Antibiotics

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

Penicillin G benzathine (Bicillin LA)

DOC when a pyoderma is known to be caused by group A streptococci. Interferes with synthesis of cell wall mucopeptides during active multiplication, which results in bactericidal activity.

Dosing

Adult

600,000-1.2 million U IM

Pediatric

<60 lb: 600,000 U IM
>60 lb: 1.2 million U IM

Interactions

Probenecid can increase effectiveness by decreasing clearance; coadministration with tetracyclines can decrease effectiveness

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in impaired renal function; avoid intravascular injection

Penicillin VK (Veetids, Beepen-VK)

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

Dosing

Adult

0.25-0.5 g PO qid

Pediatric

25-50 mg/kg/d divided q6-8h

Interactions

Probenecid can increase effects by decreasing clearance; coadministration of tetracyclines can decrease effects

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in impaired renal function

Erythromycin (E.E.S., E-Mycin, Ery-Tab)

Suitable alternative for patients who are allergic to penicillin. Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest. For treatment of staphylococcal and streptococcal infections.
In children, age, weight, and severity of infection determine proper dosage. When bid dosing is desired, half-total daily dose may be taken q12h. For more severe infections, double the dose.

Dosing

Adult

250-500 mg PO qid

Pediatric

30-50 mg/kg/d PO divided q8-12h

Interactions

Coadministration may increase toxicity of theophylline, digoxin, carbamazepine, and cyclosporine; may potentiate anticoagulant effects of warfarin; coadministration with lovastatin and simvastatin increases risk of rhabdomyolysis; coadministration of strong CYP3A inhibitors (eg, diltiazem, verapamil, nitroimidazole antifungal agents) increases risk of sudden death from ventricular arrhythmias

Contraindications

Documented hypersensitivity; hepatic impairment

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in liver disease; estolate formulation may cause cholestatic jaundice; adverse GI effects are common (give doses pc); discontinue use if nausea, vomiting, malaise, abdominal colic, or fever occur

Cephalexin (Keflex, Biocef)

First-generation cephalosporin arrests bacterial growth by inhibiting bacterial cell wall synthesis. Bactericidal activity against rapidly growing organisms. Primary activity against skin flora; used for skin infections or prophylaxis in minor procedures. Active against Streptococcus pyogenes and S aureus.

Dosing

Adult

250-500 mg PO qid

Pediatric

25-50 mg/kg/d PO divided qid

Interactions

Coadministration with aminoglycosides increases nephrotoxic potential

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Patients with a history of IgE-mediated allergic reactions to penicillin may have similar reactions to cephalosporins; adjust dose in renal impairment

Clindamycin (Cleocin)

Lincosamide for treatment of serious skin and soft tissue staphylococcal infections. Also effective against aerobic and anaerobic streptococci (except enterococci). Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

Dosing

Adult

150-300 mg PO qid

Pediatric

10-20 mg/kg/d PO divided tid/qid

Interactions

Increases duration of neuromuscular blockade induced by tubocurarine and pancuronium; erythromycin may antagonize effects; antidiarrheals may delay absorption

Contraindications

Documented hypersensitivity; regional enteritis, ulcerative colitis, hepatic impairment, antibiotic-associated colitis

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in severe hepatic dysfunction; no adjustment necessary in renal insufficiency; associated with severe and possibly fatal colitis

Dicloxacillin (Dycill, Dynapen)

Treatment of infections caused by penicillinase-producing staphylococci. May use to initiate therapy when staphylococcal infection is suggested.

Dosing

Adult

125-500 mg PO qid

Pediatric

12.5-50 mg/kg/d PO divided into 4-6 doses

Interactions

Probenecid may increase effect of penicillins; tetracyclines may decrease effect of penicillins with concurrent use

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in impaired renal function

Mupirocin (Bactroban)

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

Dosing

Adult

Apply thin film to affected area bid

Pediatric

Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Prolonged use may result in growth of nonsusceptible organisms; local reactions have been reported (ie, burning, pain, pruritus, erythema, dry skin, tenderness, cellulitis)

Follow-up

Deterrence/Prevention

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

Complications

• Ecthyma rarely produces systemic symptoms.
• Invasive complications of streptococcal skin infections include cellulitis, erysipelas, gangrene, lymphangitis, suppurative lymphadenitis,⁷ bursitis,¹ lobar pneumonia,¹ 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.¹
• Possible sequelae of secondary untreated Staphylococcus 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.

Prognosis

• Ecthyma lesions are slow to heal but do respond to appropriate antibiotics over several weeks; prognosis is favorable.

Patient Education

• For excellent patient education resources, see eMedicine's Skin, Hair, and Nails Center. Also, see eMedicine's patient education article Impetigo.

Multimedia

Media file 1: Typical ecthyma lesions of the lower extremities.

Media file 2: The stages of ecthyma. The lesion begins as a pustule that later erodes and ultimately forms an ulcer.

References

1. [Best Evidence] Wasserzug O, Valinsky L, Klement E, et al. A cluster of ecthyma outbreaks caused by a single clone of invasive and highly infective Streptococcus pyogenes. Clin Infect Dis. May 1 2009;48(9):1213-9. [Medline].

2. Ko WT, Adal KA, Tomecki KJ. Infectious diseases. Med Clin North Am. Sep 1998;82(5):1001-31, v. [Medline].

3. Singh G. Heat, humidity and pyodermas. Dermatologica. 1973;147(5):342-7. [Medline].

4. Allen AM, Taplin D, Twigg L. Cutaneous streptococcal infections in Vietnam. Arch Dermatol. Sep 1971;104(3):271-80. [Medline].

5. Dagan R, Bar-David Y. Double-blind study comparing erythromycin and mupirocin for treatment of impetigo in children: implications of a high prevalence of erythromycin-resistant Staphylococcus aureus strains. Antimicrob Agents Chemother. Feb 1992;36(2):287-90. [Medline].

6. Kelly C, Taplin D, Allen AM. Streptococcal ecthyma. Treatment with benzathine pencillin G. Arch Dermatol. Mar 1971;103(3):306-10. [Medline].

7. Duve S, Voack C, Rakoski J, Hoffmann H. Extensive inguinal lymphadenitis. Ecthyma with inguinal lymphadenitis. Arch Dermatol. Jul 1996;132(7):823, 826. [Medline].

8. Epstein ME, Amodio-Groton M, Sadick NS. Antimicrobial agents for the dermatologist. I. Beta-lactam antibiotics and related compounds. J Am Acad Dermatol. Aug 1997;37(2 Pt 1):149-65; quiz 166-8. [Medline].

9. Hewitt WD, Farrar WE. Bacteremia and ecthyma caused by Streptococcus pyogenes in a patient with acquired immunodeficiency syndrome. Am J Med Sci. Jan 1988;295(1):52-4. [Medline].

10. Leyden JJ, Kligman AM. Rationale for topical antibiotics. Cutis. Oct 1978;22(4):515-20, 522-8. [Medline].

11. Peter G, Smith AL. Group A streptococcal infections of the skin and pharynx (first of two parts). N Engl J Med. Aug 11 1977;297(6):311-7. [Medline].

12. Pichichero ME. Group A beta-hemolytic streptococcal infections. Pediatr Rev. Sep 1998;19(9):291-302. [Medline].

13. Ray WA, Murray KT, Meredith S, Narasimhulu SS, Hall K, Stein CM. Oral erythromycin and the risk of sudden death from cardiac causes. N Engl J Med. Sep 9 2004;351(11):1089-96. [Medline].

14. Sadick NS. Current aspects of bacterial infections of the skin. Dermatol Clin. Apr 1997;15(2):341-9. [Medline].

15. Witkowski JA, Parish LC. Bacterial skin infections: management of common streptococcal and stapylococcal lesions. Postgrad Med. Oct 1982;72(4):166-8, 171-3, 176-8 passim. [Medline].

Keywords

ecthyma, ulcerative pyoderma, cutaneous pyoderma, impetigo, deep impetigo, pyodermic lesion, skin streptococci, group A beta-hemolytic streptococci, group A beta-hemolytic GABHS, ecthymatous ulcer, ecthymatous ulceration, group A streptococci, GAS, group A

Contributor Information and Disclosures

Author

Loretta Davis, MD, Professor, Department of Internal Medicine, Division of Dermatology, Medical College of Georgia
Loretta Davis, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

Medical Editor

Donald Belsito, MD, Clinical Professor, Department of Internal Medicine, Division of Dermatology, University of Missouri at Kansas City; Private Practice, American Dermatology Associates, LLC
Donald Belsito, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Contact Dermatitis Society, Dermatology Foundation, Kansas Medical Society, Noah Worcester Dermatological Society, Phi Beta Kappa, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Pharmacy Editor

David F Butler, MD, Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic
David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Managing Editor

Lester F Libow, MD, Dermatopathologist, South Texas Dermatopathology Laboratory
Lester F Libow, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, and Texas Medical Association
Disclosure: Nothing to disclose.

CME Editor

Joel M Gelfand, MD, MSCE, Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania
Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology
Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds None; Genentech Consulting fee Consulting; Centocor Consulting fee Consulting; Centocor Grant/research funds None; Covance Consulting fee Consulting; Shire  Consulting

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

The authors and editors of eMedicine gratefully acknowledge the contributions of previous Chief Editor, William D. James, MD, and previous author, Carmen Mays, MD, to the development and writing of this article.

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