Chapter 27 Bacterial infections
3. Is Staphylococcus aureus the only bacterium that causes impetigo?
Older textbooks state that the most common cause of impetigo (impetigo contagiosum) is group A β-hemolytic Streptococcus. In recent years, most infections in the United States have been due to S. aureus, but the prevalence varies geographically. Although impetigo may be due to either organism, in many cases, both can be cultured. In these cases, it is thought that the streptococci are the primary infection and the staphylococci are secondary invaders after the infection has damaged the skin.
4. What does staphylococcal impetigo look like?
Early lesions of staphylococcal impetigo appear as thin, flaccid blisters that may demonstrate cloudy contents or layering of pus (Fig. 27-1). The base of the blister may demonstrate variable erythema. Histologically, the blisters are very superficial; the split occurs beneath the stratum corneum. For this reason, the blisters quickly collapse and may demonstrate a shiny lacquered appearance. Older lesions demonstrate a yellowish crust.
5. Why is staphylococcal impetigo frequently bullous?
Bullous impetigo is caused by staphylococci that produce toxins (exfoliative toxins A and B) capable of causing the split in the epidermis by targeting the epidermal adhesion molecule, desmoglein 1 (Dsg-1). Group II staphylococci are most commonly implicated.
6. How is bullous impetigo diagnosed?
The clinical appearance is usually suggestive but not diagnostic, and other superficial blistering or pustular disorders need to be considered, such as pemphigus, some bullous drug eruptions, and subcorneal pustular dermatosis. A Gram stain of the blister contents should demonstrate abundant Gram-positive cocci, but the definitive test is a culture that not only establishes the cause but also provides sensitivities to different antibiotics. The diagnosis can also be established by doing a biopsy, which demonstrates a subcorneal blister with neutrophils and cocci in the blister cavity.
7. How is bullous impetigo treated?
Oral dicloxacillin or cephalexin is the antibiotic of choice for severe infections. Oral erythromycin is frequently used in penicillin-allergic patients, although up to 20% or more of all staphylococci are resistant. Topical mupirocin is also effective and can be used if the patient cannot take oral antibiotics or if the infection is localized to a small area.
9. How do furuncles present?
Furuncles may be solitary or multiple and present as painful, erythematous, deep-seated follicular abscesses (Fig. 27-2). Patients may demonstrate mild constitutional symptoms in severe cases, or lesions may progress into carbuncles or staphylococcal cellulitis.
10. What is the best way to treat furuncles?
Nonsuppurative solitary lesions are best treated with local heat until they become fluctuant. Fluctuant furuncles should be opened and drained. Smaller lesions may be punctured with a no. 11 blade and the contents drained, while large abscesses may require a larger incision, drainage, and a wick. Patients with many lesions, evidence of surrounding cellulitis or with systemic symptoms should be considered for oral antibiotics.
As always, the diagnosis should be confirmed with a culture and antibiotic sensitivities performed at the initial visit, since not all follicular-based abscesses are due to staphylococci. The initial antibiotic choice before the culture and antibiogram results is usually oral dicloxacillin, oral cephalexin, or oral amoxicillin/clavulanate. Oral erythromycin, azithromycin, or clarithromycin can be used if the patient is allergic to penicillin. However, if MRSA infection is clinically suspected then the initial antibiotic choice is different (see question 16).
11. Why do some patients develop recurrent staphylococcal impetigo or recurrent furunculosis?
Recurrent infections occur when Staphylococcus aureus establishes itself as a part of the resident microbial flora. This occurs in up to 20% of individuals. The most common sites of carriage are the anterior nasal vestibule, axilla, groin, and feet. Patients who have virulent strains are prone to the development of recurrent impetigo or furunculosis, depending on the strain. A variety of host factors, such as abnormal neutrophil chemotaxis (e.g., hypergammaglobulinemia IgE syndrome), deficient intracellular killing (e.g., chronic granulomatous disease), and immunodeficiency states (e.g., AIDS), are important in a minority of patients. Diabetes mellitus is listed in many references as being associated with recurrent furunculosis, but this is controversial.
El-Gilany AH, Fathy H: Risk factors of recurrrent furunculosis, Dermatol Online J 15:16, 2009.
12. How is staphylococcal carriage eliminated?
Standard treatment regimens, such as oral dicloxacillin, oral cephalexin, oral erythromycin, or even intravenous vancomycin, eliminate active infection but not staphylococcal carriage. The most commonly used regimen to eliminate staphylococcal carriage is rifampin in combination with dicloxacillin. Less common regimens utilize oral clindamycin, topical mupirocin ointment, or replacement of the microflora with a less pathogenic strain of S. aureus (strain 502A). The success of these regimens varies from 50% to 70%; however, recolonization is common.
13. What is staphylococcal scalded-skin syndrome?
Staphylococcal scalded-skin syndrome typically occurs in neonates, infants, or immunocompromised adults. Like bullous impetigo, it is due to group II staphylococci that produce an exfoliatoxin; however, it differs in that the infection occurs at a distant site, such as a conjunctivitis or abscess. In neonates and infants, the kidneys are not able to excrete the exfoliatoxin adequately. The high level of exfoliatoxin produces diffuse, tender erythema associated with fever that rapidly progress to flaccid bullae; the bullae wrinkle and exfoliate, leaving an oozing erythematous base (Fig. 27-3). Mortality in neonates is usually not due to the infection but is secondary to impaired temperature regulation or fluid balance.
Figure 27-3. Early staphylococcal scalded-skin syndrome demonstrating diffuse erythema and early desquamation.
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