Atopic dermatitis (AD), also known as atopic eczema, is a chronic inflammatory disorder that causes significant morbidity and has a wide range of allergic and non-allergic comorbid disorders.
Comorbidity is a concurrence of multiple diseases or disorders in association with a given disease. The patient with AD has an increased risk of developing one or more of a number of other diseases/conditions that share many immunological features with AD.
| Cutaneous (skin) infections including:-
1, 2, 3, 4, 5, 6, 7
Patients with AD are highly susceptible to certain bacterial, fungal and viral infections.
They have also been noted to have an increased incidence of warts caused by the human papillomavirus (HPV), and fungal infections caused by Trichophyton rubrum and also have a higher incidence of the fungal infections:- tinea pedis, tinea unguium, tinea manuum, tinea cruris, and tinea corporis, as well tinea barbae.7
AD Patients are also susceptible to severe infections caused by herpes simplex type 1 virus (eczema herpeticum or Kaposi’s varicelliform), vaccinia virus (eczema vaccinatum) coxsackie A virus and molluscum contagiosum virus. These viral infections can cause serious complications in AD patient and if not treated promptly have the potential to be life threatening.7
Signs of Secondary Infection include:
- Sudden flaring (worsening) of eczema all over the body.
- Weeping crusted areas – crusts are often a golden colour
- Clusters of pustules (yellow/white pimples).
- Fever, Shivering and extremely painful skin.
- Chicken pox-like blisters and sores – this can be caused by the cold sore virus and may require urgent medical attention (Kaposi’s varicelliform)
BACTERIA and ATOPIC DERMATITIS (AD)
The skin is colonized by various different species of bacteria, fungi, and viruses that together are known as the skin microbiome, mainly Corynebacterium spp., Propionibacterium acnes and Staphylococcus epidermidis.
Each person will carry a different combination of these depending upon health and environment. The colonization of bacteria on specific regions on the body depends upon the local skin environment including moisture levels, pH, and keratinocyte cell surface adhesion proteins (Skin Barrier). For instance, Staphylococcus and Corynebacterium species thrive in specific environments on the skin such as the sole of the foot and the back of the knee. Dry environments such as the inside forearm and palm of hand are more prone to harbour a mixed population of bacteria including Propionibacterium acnes. 7
Babies are born microbe free until exposure to the external environment allows for immediate colonization of their skin, this first colonization usually starts as they pass through the vagina. As the child grows and they are exposed to different environments and in physical contact with different people their microbiome will change.7
Environmental factors such as diet, age, and gender also play a role in the makeup of the skin microbial flora.7
Staphylococcus aureus (S. aureus) and Staphylococcus epidermidis (S. epidermidis) are the two most common clinical isolates of the microbiota that is normally found in the nasal passages and on the skin of healthy people. They are Gram-positive cocci found in clusters. S. epidermidis comprises greater than 90% of the aerobic resident flora found on the skin and is considered a normal inhabitant of the skin surface. Some strains of S. epidermidis produce bacteriocins that are toxic to other bacterial species such as Staphylococcus aureus. S. epidermidis can also target S. aureus can prevent S. aureus biofilm formation and growth thus promoting a stronger skin barrier and immune response.7
In AD patients, when the patient suffers skin barrier breakdown and lowered immunity both S. aureus readily colonizes the affected skin lesions. Studies have shown that between 80% and 100% of patients with AD present nasal and skin colonization by with S. Aureus, as opposed to the prevalence of only between 5 to 30% in individuals without AD. To further break down the colonization statistics S. aureus has been isolated from 55–75% of unaffected AD skin, 85–91% of chronic lichenified (thickened/ scratched) lesions and 80–100% of acute exudative (weepy) skin lesions.7, 8
Impetigo contagiosum (contagiosa)
Impetigo is a skin infection caused by Staphylococcus aureus and Streptococcus pyogenes. In Europe and colder climate regions, Staphylococcus aureus is the most common cause. Impetigo can affect any one but is more common in children aged 2yrs. – 6 yrs. of age. It is highly contagious and is spread by direct contact. Children and those affected need to be kept home from day care, kindergarten, school and work.9
Impetigo is commonly found in people who have skin conditions that cause impaired skin barrier e.g. eczema, scabies, fungal infections or via skin trauma e.g. insect bites. It is also common in crowded environments e.g. schools, day care centres etc. It can be spread through contact sports e.g. wrestling. Impetigo caused by Streptococcus pyogenes is common in hot humid regions.
There are two types of impetigo. The most common is called crusted or non-bullous impetigo. It starts as small blisters, which quickly burst and crust over. The other type, called bullous impetigo, causes large blisters that break easily. It is less common, and mainly affects babies.
Non Bullous Impetigo normally presents as:
- Small vesicles that rupture, dries and forms golden- coloured, brown or even brownish black crusts/scabs.
- Lesions can be up to 2cm in diameter.
- Usually found on the face – around the mouth and nose, but they can also be found on the limbs.
- In mild cases there is normally no systemic symptoms, but if it is an extensive eruption, it may be accompanied by fever and swelling.
Bullous Impetigo presents as:
- Large fluid filled blisters > 2cm, which rupture easily.
- May be golden in colour, brown or even brownish black.
- The limbs and torso are more likely to be affected.
- It is normally accompanied by fever and swelling.
Bullous impetigo is only caused by S aureus.
Impetigo has been commonly called “school sores”. It is important, due to the contagious nature of the condition, that hands are washed regularly and especially after having touched or scratched the impetigo lesions. Anything that has been in contact with the sores e.g. clothing or anything that has been on the sores can spread the infection to other family members, friends and colleagues. In order to prevent the spread of the condition it is very important that clothes, towels, pillows and bed linen, nail scissors, razors or toothbrushes etc. are not shared. Clothing, towels and bedding etc. should be washed separately using hot water, washing powder and a disinfectant or eucalyptus/tea tree oil added to the wash.
- Simpson EL.; Comorbidity in Atopic Dermatitis; Curr Dermatol Rep. 2012 March 1; 1(1): 29–38. doi:10.1007/s13671-011-0003-5
- Augustin M. et al.; Epidemiology and Comorbidity in Children with Psoriasis and Atopic Eczema; Dermatology 2015;231:35–40 DOI: 10.1159/000381913
- Deckert S. et al.; Nonallergic comorbidities of atopic eczema: an overview of systematic reviews; Allergy 69 (2014) 37–45 © 2013
- Ellis CN. et al.; Validation of Expert Opinion in Identifying Comorbidities Associated with Atopic Dermatitis/Eczema; Pharmacoeconomics 2003; 21 (12)
- Silverberg J.I. and Silverberg N.B.; Atopic Dermatitis: Update on Pathogenesis and Comorbidities
- Cogen A.L. et al.; Skin microbiota: a source of disease or defence?; Br J Dermatol. 2008 March ; 158(3): 442–455. doi:10.1111/j.1365-2133.2008.08437.x
- Williams M. R. et al.; The Role of the Skin Microbiome in Atopic Dermatitis; Curr Allergy Asthma Rep (2015) 15: 65 DOI 10.1007/s11882-015-0567-4
- Baviera G. et al.; Staphylococcus Aureus And Atopic Dermatitis: Which Came First, The Chicken Or The Egg?; EMJ Dermatol. 2015;3:92-97.
- Petry V. et al.; Bacterial skin colonization and infections in patients with atopic dermatitis; An Bras Dermatol. 2012;87(5):729-34.
- Leung DYM.; The role of Staphylococcus aureus in atopic eczema; Acta Derm Venereol 2008; Suppl 216: 21–27
- Baker S.; The role of microorganisms in atopic dermatitis; 2006 British Society for Immunology, Clinical and Experimental Immunology, 144: 1–9