SAN DIEGO Patients with atopic dermatitis are highly colonized with Staphylococcus aureus but do not appear to be preferentially infected with community-acquired methicillin-resistant S. aureus.
Up to 79% of patients with atopic dermatitis have S. aureus in their anterior nares, 64%75% have it on their normal skin, and more than 90% have it on their lesional skin.
In contrast, up to 30% of atopic-free adults have S. aureus in their nasal carriage and 10% have it on their skin, Dr. Sheila Fallon Friedlander said at a conference sponsored by Rady Children's Hospital, San Diego.
A reason why patients with atopic dermatitis may have trouble with S. aureus is that they appear to lack an adequate number of cathelicidins, said Dr. Friedlander, director of pediatric dermatology at the University of California, San Francisco.
"The end result clinically is that they don't have as much antimicrobial peptide helping to ward off infection. Atopics also have an impaired skin barrier, sometimes as a result of abnormal or decreased filaggrin. With increasing dryness and lack of appropriate adhesion, there is also increased skin surface area for the S. aureus to adhere to," she said.
In addition, she said S. aureus can elaborate superantigens, "which have the ability to stimulate the production of alternative glucocorticoid receptors. These receptors are more resistant to the effects of steroids. So often when S. aureus is present in the skin, there is elaboration of a receptor [that] makes it more difficult for the patient to respond to topical corticosteroid treatment."
A recent study estimated that 40%66% of patients with atopic dermatitis develop S. aureus skin infections (Pediatr. Derm. 2000;17:1114). Another concluded that the condition is a risk factor for invasive S. aureus infection in this patient population, including bacteremia, osteomyelitis, and endocarditis (Am. J. Med. 2005;118:104851).
However, Dr. Friedlander described the link between atopic dermatitis and invasive disease as "a controversial issue" with data that remain unclear.
"In some papers, it appears that there are lower levels of invasive disease in patients with atopic dermatitis," she said. "Invasive disease does occur, but atopics don't seem to be at higher risk for invasive disease. Further studies are required to clarify this issue."
The good news is that patients with atopic dermatitis do not seem to be preferentially affected with community-acquired methicillin-resistant S. aureus (CA-MRSA). An estimated 6%19% of children with atopic dermatitis were found to have the condition (Arch. Dermatol. 2002;138:93941).
Another group of researchers concluded that the "observed incidence of cutaneous CA-MRSA lesions in patients with atopic dermatitis or other non-intact skin barrier is less than reported in other at-risk groups" (J. Clin. Dermatol. 2007;8:25970).
Dr. Friedlander explained that, compared with the hospital-acquired form of MRSA, the community-acquired form is clonal, has many drug options, and has a predilection for skin disease. "It preferentially infects the skin; skin and soft tissue infections are what we see," she said. "But you must remember that you can have invasive disease from this organism."
Clinically, CA-MRSA presents as furuncles or folliculitis 65%95% of the time. "Parents will say, 'my child keeps getting a spider bite,'" Dr. Friedlander said. Most patients look well, but 40%50% will have fever.
Most often, CA-MRSA organisms possess Panton-Valentine leukocidin, a virulence factor that is a bicomponent cytotoxin. This virulent toxin "destroys our leukocytes by punching holes in the membrane," she said. "This leads to capillary dilation and significant necrosis."
CA-MRSA also may possess an aberrant fibronectin-binding protein gene, which enables the S. aureus "to adhere better to our tissue and therefore enhances invasion."
Incision and drainage alone appears to suffice in CA-MRSA skin and soft tissue lesions smaller than 5 cm. "If a lesion is bigger than that, you need to be aggressive," she said. "Please culture these lesions. In the old days, people used to drain these and throw the exudate away. Do not throw it away because the antibiotic susceptibility patterns differ from the hospital-acquired form, and you may need this information to determine the best therapy for your patient."
Dr. Friedlander often starts patients on clindamycin. However, some organisms may be resistant, and therefore you need to check for inducible resistance in these patients. "Sometimes you need to use trimethoprim/sulfamethoxazole," she said.
"In older children, you can use minocycline or doxycycline, but remember, these drugs can damage the teeth of young children, and I will not use tetracyclines in children less than 8 years of age."
Attempts to eradicate MRSA with various combinations of antibiotics have had mixed results, but recent studies have found the use of bleach baths in combination with nasal mupirocin to be useful.