The increasing incidence of atopic dermatitis and other allergic diseases in the last 30 years, especially in industrialized countries, has led to some serious thinking about the likely causes. Atopic dermatitis patients exhibit increased susceptibility to bacterial, viral and fungal microorganisms because of weakened immune systems. These microorganisms play an important part in the initiation and/or aggravation of AD.

To explain the increasing incidence, environmental factors like air pollution, poorly ventilated homes and diet have been cited. However, consistent evidence in support of this view is lacking.

Hygiene hypothesis

A new ‘hygiene hypothesis’ was put forward recently. According to this hypothesis, increasing susceptibility of people to atopic dermatitis is the result of decreased exposure to microorganisms, and thereby to infections, early in life.

The theory is based on certain irrefutable facts. The changed modern life style with its use of antibiotics and much increased hygienic and living standards have created a highly sanitized world in which the children are being brought up. As a result, children are being deprived of the much-needed exposure to microorganisms which play such a vital role in increasing their natural resistance and immunity to infections in later life. Also, desire for higher living standards has led to smaller families where frequency of atopic dermatitis is higher due to the fact that children in small families are less exposed to microorganisms. In larger families, children in the company of other children are more exposed to microbes and therefore they develop a higher tolerance to the development of eczema.

But the theory could not explain why some parasitic worm infections, which induce high levels of immunoglobulin E in the blood, do not cause allergy. Moreover, no such microorganisms have been discovered. As many as 64 studies published between 1966 and 2004 failed to cite any conclusive evidence that tuberculosis bacteria reduced the risk of eczema. On the contrary, some childhood bacterial and viral infections were found to increase the chances of developing eczema. However, microorganisms in a farming environment were found to reduce the risk of eczema development. This led to the view that the development of atopic dermatitis depended partly on the nature and the degree of exposure rather than infection per se.

Microbial colonization

There are mainly two types of skin colonizing microorganisms, which have a major role in the development of eczema. These are staphylococcus bacteria and malassezia furfur.

Staphylococcus bacteria: In eczema, bacterial colonization with staphylococcus bacteria is most common, found in almost 90% patients. The severity of atopic dermatitis increases with the bacterial count and a decrease in the count results in improvement in the condition. The factors involved in changed skin colonization of staphylococcus bacteria are, changed skin barrier, increased bacterial adhesion, defective bacterial clearance and reduced immune response. Further, the dry and cracked skin may facilitate colonization.

The immune system of the skin is the first line of defense against microorganisms. When the skin is damaged various kinds of antimicrobial peptides are produced which are quite effective against gram-negative microorganisms. However, these peptides are not as effective against the gram-positive staphylococcus bacteria. The immune system in atopic dermatitis is further weakened as the production of certain beneficial peptides in the sweat glands is reduced. These peptides, in healthy people, are quite effective against some pathogenic microorganisms but not so in atopic dermatitis affected patients. In atopic dermatitis affected people, even sweat production is reduced.

Malassezia furfur: The yeast, malassezia microorganism, is commonly part of the flora found on human skins and is plentiful in sites which produce sebum, such as the scalp, chest, and back. It is believed to contribute to atopic dermatitis initiation. These yeasts have been implicated in the pathogenesis of atopic dermatitis by inducing the production of IgE antibodies. Healthy people have developed IgG antibodies to these microorganisms, but in 30% to 80% of atopic dermatitis patients there is IgE and/or T-cell reactivity to the organism. Patients with atopic dermatitis on the head and the neck regions are more likely to produce malassezia specific IgE antibodies and a higher level of skin colonization, than patients with atopic dermatitis located elsewhere on the body. The malassezia microorganism is rarely produced when the skin is unaffected. This, combined with the fact of high prevalence of Type I sensitivity indicates that they have an important role in atopic dermatitis development. Various tests have shown malassezia present in 70% patients.

Malassezia is also active in promoting a variety of inflammatory responses, such as, by stimulating keratinocytes. However, antifungal studies have not been able to find the clinical significance of malassezia induced allergy in eczema.

In future, manipulation of the natural immune response to microorganisms may open the door to novel treatment methods. For example, a preliminary study on administration of probiotic bacteria to atopic dermatitis patients showed a beneficial effect on them.