Most common bacterial skin infections are caused by coagulase-positive Staphylococcus aureus or group A beta-hemolytic streptococci. Before the widespread availability of antibiotics, many common skin infections resulted in serious illness and even death. In the 1950s following the widespread use of antibiotics, most staphylococcal and streptococcal skin infections responded well to the use of the penicillins. However, scattered cases of methicillin-resistant Staphylococcus aureus (MRSA) were already being reported by the early 1960s. From late 1960s to the mid-1990s, MRSA infections became a major problem especially in large urban hospitals. In the past decade, hospital-acquired MRSA infections began to decrease as hospitals instituted more aggressive infection control measures, but during that same time community-acquired MRSA infections increased.
Syphilis has been called "the great masquerader" and "the great imitator" based on the many varied presentations of the cutaneous and other organ system findings. Patients with secondary syphilis usually present with rashes that mimic common papulosquamous skin diseases, but can present with skin findings that mimic almost any cutaneous disorder.
Impetigo is a common, highly contagious, superficial skin infection that presents with either a bullous or nonbullous appearance. Nonbullous impetigo accounts for the majority of cases. It occurs in children of all ages, as well as adults, whereas the bullous form is most common in newborns. Impetigo is limited to the epidermis.
Coagulase-positive Staphylococcus aureus is the most common cause of bullous and nonbullous impetigo. Group A beta-hemolytic streptococci including the nephritogenic strains may also cause impetigo.1,2
Nonbullous impetigo represents a host response to the infection, whereas staphylococcal toxin causes bullous impetigo and no host response is required to manifest clinical disease.3
History and Physical Examination
Nonbullous impetigo begins as a single lesion typically manifesting as a red macule or papule that quickly becomes a vesicle. The vesicle ruptures, forming an erosion and the contents dry to form the characteristic honey-colored crust commonly seen with impetigo (Figure 12-1). Nonbullous impetigo usually occurs on the face or extremities. Impetigo may occur concomitantly with herpes simplex and atopic dermatitis.
Bullous impetigo begins as a superficial vesicle that rapidly progresses to a flaccid bulla, with sharp margins and no surrounding erythema. When the bulla ruptures, a moist yellow crust forms. Impetigo is often spread to surrounding areas by autoinoculation. Bullous impetigo usually arises on grossly normal skin and favors moist intertriginous areas, such as the diaper area, axillae, and neck folds.
Ecthyma is an uncommon variant of impetigo that initially presents as a typical impetigo infection that spreads into the dermis. It usually presents on the lower legs with thick crusts overlying superficial ulcers. It is more common in young children, immunosuppressed patients, and in patients with poor hygiene.