Introduction
Background
Impetigo is a skin condition that is part of several different infectious skin diseases. This is a superficial, predominantly nonfollicular, infection. The name is believed to be derived from the Latin impetere (to assail).
It exists in 2 forms: bullous and nonbullous.
- Impetigo contagiosa (nonbullous) is a superficial, intra-epidermal, unilocular, vesiculopustular infection. It is the most common skin infection in children. Common impetigo is the term applied when the infection occurs in preexisting wounds. Impetigo can also present as folliculitis, which is considered to be impetigo of the hair follicles caused by Staphylococcus aureus.
Nonbullous impetigo with vesicles, pustules, and sharply demarcated regions of honey-colored crusts.
- Bullous impetigo is a toxin-mediated erythroderma in which the epidermal layer of the skin sloughs, resulting in large areas of skin loss.
- Ecthyma is a deeper, ulcerated infection, often occurring with lymphadenitis and may be a complication of impetigo.
Pathophysiology
Impetigo is an infection caused most commonly by coagulase-positive Staphylococcus aureus, and less often by group A beta-hemolytic streptococci (GABHS). The organisms are thought to enter through damaged skin and are transmitted through direct contact. After infection, new lesions may be seen on the patient with no apparent break in the skin. Frequently, however, upon close examination, these lesions will demonstrate some underlying physical damage.
Nonbullous (crusted) impetigo resulting from a chigger bite infected by group A beta-hemolytic streptococci. Courtesy of Professor David Taplin, Department of Dermatology and Cutaneous Surgery, University of Miami School of Medicine, Miami, Fla.
Besides skin trauma, common predisposing factors include warm and humid temperature and atopic disease.
The presentation of impetigo may take on more than one form. Some authors suggest that differences are due to the staphylococcal strain involved and the relative activity of the exotoxin.
In bullous impetigo, the separation of the epidermis is at the subgranular layer and due to an exotoxin (exfoliatoxins A-D) produced by staphylococci, which is the pathologic organism present in cases of bullous impetigo. The target molecule is desmoglien 1.
In impetigo, isolation of methicillin-resistant S aureus can be very high.
On histologic examination, the lesions in all presentations reveal a subcorneal neutrophilic infiltrate. Granular layer separation is noted in the bullous disease.
Frequency
United States
Approximately 9-10% of all children presenting to clinics with skin complaints have impetigo.
International
About 2.6 episodes per 100 person-weeks have been reported.
Multiple reports have noted a seasonal variance, with peak prevalence in August and September.
Sex
Impetigo occurs equally in males and females.
Age
- Impetigo occurs more commonly in children.
- The majority (90%) of bullous impetigo cases occur in children younger than 2 years.
Clinical
History
In impetigo contagiosa, the lesions begin with a single 2- to 4-mm erythematous macule that rapidly evolves into a vesicle or a pustule. This vesicle is very fragile and ruptures early, leaving a crusted exudate of a honey or yellow color over the superficial erosion. The infection spreads to contiguous and distal areas through inoculation of other wounds from scratching.
Bullous impetigo presents with small or large, superficial, fragile bullae. Often, these quickly appear and drain so that only the remnants of ruptured bullae are seen at the time of presentation. The separation of the epidermis is due to an exotoxin produced by staphylococci, which is the pathologic organism present in cases of bullous impetigo and is directed against epidermal desmoglein 1. In lesions of this type, isolation of methicillin-resistant S aureus has been as high as 20%. Some authors assert a continuum of disease including nonbullous impetigo, bullous impetigo, and abscess formation caused by S aureus with differing exotoxin characteristics.
Typical descriptors used in impetigo are as follows:
- Tender, red rash
- Honey-colored crusts
- Pruritus
- Poorly healing wound
The following symptoms usually are absent in impetigo contagiosa but may be present in bullous impetigo:
- Fever
- Diarrhea
- Generalized weakness
Physical
- Type and location of impetigo lesions
- Most frequently on the face (around the mouth and the nose) or at a site of trauma
- Red macule or papule as early lesion
- Lesions with ruptured bullae and crusted edges
- Lesions with honey-colored crusts
- Thin-roofed vesicle or bullae (usually nontender)
- Pustules
- Weeping, shallow, erythematous ulcer
- Satellite lesions (often at multiple sites)
- Bullae on the buttocks, trunk, and face
Nonbullous impetigo from an abrasion infected by group A beta-hemolytic streptococci. Courtesy of Professor David Taplin, Department of Dermatology and Cutaneous Surgery, University of Miami School of Medicine, Miami, Fla.
Nonbullous impetigo secondary to group A beta-hemolytic streptococci. Courtesy of Professor David Taplin, Department of Dermatology and Cutaneous Surgery, University of Miami School of Medicine, Miami, Fla.
Streptococcal impetigo from an infected insect bite. Courtesy of Professor David Taplin, Department of Dermatology and Cutaneous Surgery, University of Miami School of Medicine, Miami, Fla.
- Regional lymphadenopathy
- Common in impetigo contagiosa
- Rare in bullous impetigo
Causes
The causative agents are discussed in Pathophysiology. The incidence of community-acquired methicillin-resistant S aureus (CA-MRSA) has increased in some locales to as high as 50% of the isolates.
More on Impetigo |
 Overview: Impetigo |
| Differential Diagnoses & Workup: Impetigo |
| Treatment & Medication: Impetigo |
| Follow-up: Impetigo |
| Multimedia: Impetigo |
| References |
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References
Sarabi K, Khachemoune A. Tinea capitis: a review. Dermatol Nurs. Dec 2007;19(6):525-9; quiz 530. [Medline].
Popovich D, McAlhany A. Accurately diagnosing commonly misdiagnosed circular rashes. Dermatol Nurs. Aug 2008;20(4):294-300. [Medline].
Allen CH, Patel B, Endom EE. Primary bacterial infections of the skin and soft tissues, changes in epidemiology and management. Clin Ped Emerg Med. 2004;5:246-255.
Dagan R. Impetigo in childhood: changing epidemiology and new treatments. Pediatr Ann. Apr 1993;22(4):235-40. [Medline].
Elsayed S, Laupland KB. Emerging gram-positive bacterial infections. Clin Lab Med. Sep 2004;24(3):587-603, v. [Medline].
Epps RE. Impetigo in pediatrics. Cutis. May 2004;73(5 Suppl):25-6. [Medline].
Leyden JJ. Review of mupirocin ointment in the treatment of impetigo. Clin Pediatr (Phila). Sep 1992;31(9):549-53. [Medline].
Loffeld A, Davies P, Lewis A, Moss C. Seasonal occurrence of impetigo: a retrospective 8-year review (1996-2003). Clin Exp Dermatol. Sep 2005;30(5):512-4. [Medline].
Luby S, Agboatwalla M, Schnell BM, Hoekstra RM, Rahbar MH, Keswick BH. The effect of antibacterial soap on impetigo incidence, Karachi, Pakistan. Am J Trop Med Hyg. Oct 2002;67(4):430-5. [Medline].
Nishijim S, Ohshima S, Higashida T, Nakaya H, Kurokawa I. Antimicrobial resistance of Staphylococcus aureus isolated from impetigo patients between 1994 and 2000. Int J Dermatol. Jan 2003;42(1):23-5. [Medline].
Oranje AP, Chosidow O, Sacchidanand S, et al. Topical retapamulin ointment, 1%, versus sodium fusidate ointment, 2%, for impetigo: a randomized, observer-blinded, noninferiority study. Dermatology. 2007;215(4):331-40. [Medline].
Zetola N, Francis JS, Nuermberger EL, Bishai WR. Community-acquired meticillin-resistant Staphylococcus aureus: an emerging threat. Lancet Infect Dis. May 2005;5(5):275-86. [Medline].
Further Reading
Keywords
impetigo, impetigo contagiosa, group A beta-hemolytic streptococci, GABHS, Staphylococcus aureus, bullous impetigo, impetigo bullosa, common impetigo, folliculitis, follicular impetigo, ecthyma, vesiculopustular infection
