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For those not familiar with it, and maybe those too familiar with it, it causes itching as the main problem. It looks scabby, scratched and “bad” to mothers and especially grandmas.
A general sequence is for a child in infancy to erupt with a dry, scabby rash over the face, especially the cheeks, scalp and behind the ears. It can get weepy. Eczema means bubbling up, weeping or crusting. In childhood, it tends to find the flexures or bends, like in elbows and behind knees. It often, but not always, softens in adolescence. In adulthood (for those of you who made it) it frequently fires up hands, sometimes insufferably.
The person’s skin is congenitally drier, itches more (cannot wear wool as a prototype of a rough cloth!), stings more with alcoholic lotion components, etc. And it tends to become colonized on normal-appearing skin as well as the eczema by Staph aureus, which is a different concept than infected, although the words are incorrectly used interchangeably.
There are more than 300 different strains of S. aureus as cataloged by the Centers for Disease Control and Prevention in their DNA sequencing bank in Atlanta. Nothing’s simple anymore. The strains that grow on atopic dermatitis are not often the ones that cause the bad infections you hear about. How and why they get to that skin is still very much part of the mystery.
As genetic analysis is becoming more the norm to study diseases, those abnormalities of atopic dermatitis are emerging. It was always felt to have genetic roots somehow.
In the 1920s, the word atopy was coined, meaning nowhere. It attempted to connote family pedigrees of atopic dermatitis, clustering with allergies to the environment and asthma. For so long, and even yet, the idea that allergies were the sole cause was dominant. But more than 60 percent of kids develop it in their first year, and 50 percent have no evidence of allergy in the first two years. Some families have only the atopic dermatitis and no respiratory component.
In 1974, Albert Kligman, dermatology hero at the University of Pennsylvania, showed the Staph aureus cultures went way down with an antibiotic given to which they were sensitive, and the eczema cleared much better than without. A review article in the April 3 New England Journal of Medicine by Thomas Bieber, a German dermatologist, tried to offer a unifying theory of atopic dermatitis. Many, many theories have come and gone. He attempted to resolve, in an exceedingly complicated discussion, the interactions of innate immunity, skin barrier dysfunction (one of the main issues), Staph aureus colonization and its stimulation of the inflammation, and how the interaction of environment creating allergic sensitization through the broken skin barrier occurs. One of his key points is that bacterial overgrowth needs to be controlled since it can’t be totally eliminated.
When we humans try to understand something, we separate it into segments. But that is artificial, because the interplay among the skin barrier malfunction, bacteria on it, and both internal and external influences is a dynamic process, fluctuating from moment to moment. This is true for every living organism, from walruses to viruses. It is hard for our “static picture minds” to grasp or wrap themselves around it.
The practical point of this theoretical tangle is: If you or your kiddo is getting treated with whatever for atopic dermatitis, and it isn’t working, consider the Staph aureus source. It may take a culture of the eczema to test for antibiotic sensitivities in order to choose the appropriate drug.
I just heard the story again. Once the child had the intense, even agonizing, itch quelled, his personality and sleep improved vastly when given the antibiotic. And everyone else in the house slept better, too. Atopic dermatitis affects the whole fam damily. Happy baby, happy parents — and grandparents.
