Skip to main content
Open Access Publications from the University of California

Dermatology Online Journal

Dermatology Online Journal bannerUC Davis

Bacterial colonization and antibiotic resistance in children with atopic dermatitis

Main Content

Bacterial colonization and antibiotic resistance in children with atopic dermatitis
Saeideh Farajzadeh, Zahra Rahnama, Zahra Kamyabi, Batool Ghavidel
Dermatology Online Journal 14 (7): 21

Dermatology Department, Afzalipour Hospital, Kerman University of Medical Sciences, Kerman, Iran.

Atopic dermatitis (AD) is a multifactor inflammatory dermatosis of unknown pathogenesis [1]. Many environmental factors including Staphylococcus aureus are able to exacerbate the disease [2, 3].

S. aureus and many other bacteria commonly colonize eczematous and uninvolved skin of AD patients. The rate of bacterial colonization is higher during exacerbations than during remission and are correlated with the severity of skin lesions [1, 4]. The extent and type of bacterial colonization and their antibiotic sensitivity according to age and disease severity are not fully determined [5]. Knowing the nature of antibiotic resistance in AD has great value in choosing the most appropriate empiric antibiotic for the treatment of infected AD.

Fifty consecutive children with AD aged 2 months to 15 years (18 girls and 32 boys) able to fulfill the Hanifin and Rajka criteria for AD [6] were included into the study. Children with infected AD and those on systemic or topical antibiotics for 1 week prior to the study were excluded from the study. Informed parental consent was obtained. A clinical evaluation of AD was performed using the SCORing Atopic Dermatitis (SCORAD) index [7, 8] as follows: mild (AD<25), moderate (25<AD<50), and severe (AD>50).

Skin swabs were taken from 2 active clinically non-infected eczematous lesions using sterile cotton tipped swab sticks rolled over the skin surface twice for identification of the bacterial pathogen. Microbiological cultures (by using EBM and Agar media) were performed.

Antimicrobial susceptibility was assessed by Muller Hinton media (Merck, Germany). The following antibiotic discs were used: cloxacillin, erythromycin, penicillin, cephalexin, and cefexime.

Data were analyzed using SPSS, version 10. Severity of AD was assessed by SCORAD, range 0-83, by a trained observer. The median SCORAD was calculated and comparisons between groups were undertaken using independent T-test and Pearson correlation coefficient. P-value<0.05 was considered to be statistically significant.

Eighteen girls and 32 boys were recruited, with a median age of 4.43 ± 3.5 years (range, 20 months to 14 years). A positive bacterial culture was detected in 74 percent of the patients. There was no statistically significant difference between the rates of positive culture in the boys (77.9%) and the girls (66.7%). The most common bacterium was Staphylococcus aureus (66%) in both sexes. Other detected bacteria were group A and B beta hemolytic streptococcus, entrobacter and Streptococcus viridans (Table 1).

There was no age related difference in the type and prevalence of bacterial colonization. Skin colonization rate was related to the severity of AD so that the more severe the dermatitis the higher the rate of the colonization (p<0.05). The bacterial resistance to antibiotics was assessed. Resistence to at least 1 antibiotic was found in 94 percent of the patients. Resistance to penicillin (90%), erythromycin (66.7%), cloxacillin (72.4%) and cephalexin (13.8%) was detected in smaller percentages.

Our study confirms previous findings of a high prevalence of S. aureus skin colonization in children with AD [3, 9, 10, 11]. Our study showed the association between the severity of AD and the skin bacterial colonization rate that is in line with the other reports [1] (Table 2). No difference has been noted in the skin colonization rate between the different sex and age groups.

The key finding in our study was the high rate of bacterial resistance to the antibiotics except cephalexin. Resistance to cloxacillin and erythromycin, commonly used in the treatment of infected AD [3, 5, 9], was remarkable.

Hoeger in 2004 found a high rate of erythromycin resistance (18%) among colonizing S. aureus strains in patients with AD. None of our study patients had resistance to cephalexin [9]. In our study resistance to erythromycin was noted in 66.7 percent of the patients. Only 18.3 percent of our patients showed resistance to cephalexin. These results are nearly in concordance with the Hoeger study. However, our study demonstrated a remarkable growing rate of resistance to these antibiotics.

The findings of Goh et al. in 1997 indicated that 87 percent of S. aureus isolated from AD was penicillin resistant, which is in concordance with the results of our study. All S. aureus isolated in the Goh study was sensitive to cloxacillin and cephalexin, but in our study a high resistance to cloxacillin was detected. Staphylococcal resistance to methecillin and closely related penicillins has been noted since the introduction of penicillinase stable B-lactams (methicillin, cloxacillin, flucloxacillin) [10]. This concern necessitates finding an appropriate antibiotic for the treatment of infected AD. First generation cephalosporins such as cephalexin and cefadroxil are particularly suitable for the treatment of infected AD in our patient population. Their antimicrobial spectrum is restricted to Gram-positive bacteria and a limited number of Gram-negative strains. They have a good gastrointestinal absorption and have a low rate of gastrointestinal side effects [9]. Unfortunately, recent isolates of methicillin resistant Staphylococcus aureus (MRSA) have also been shown to transfer antibiotic resistance, including cephalexin, on to the other previously sensitive staphylococcus [11, 12, 13].

This study is subject to a number of important limitations: the lack of assessment of staphylococcal resistance to methicillin, the small sample size, and the fact that it is a single center study.

Increasing rates of resistance to cloxacillin and erythromycin that are the mainstay of therapy for infected AD have been detected. Low rates of resistance to cephalexin in this study may make it an ideal candidate for treating infected AD in our population.

Acknowledgment: We would like to thank Kerman Medical University research center for its financial support.


1. Breuer K, Kapp A, Werfel T. Bacterial infections and atopic dermatitis. Allergy 2001; 56: 1034-41. PubMed

2. Morishita Y, Tada J, Sato A, et al. Possible influences of staphylococcus areus on atopic dermatitis-the colonizing features and the effects of staphylococcal enterotoxins. Clinical and Experimental Allergy 1999; 1110-17. PubMed

3. Goh CL, Wong JS, Giam YC. Skin colonization of staphylococcus aureus in atopic dermatitis patients seen at the National Skin Care, Singapore. International Journal of Dermatology 1997; 36: 653-657. PubMed

4. Guzik TJ, Bzowska M, Kasprowicz A, et al. Persistent skin colonization with staphylococcus aureus in atopic dermatitis: relationship to clinical and immunological parameters. Clinical Exp Allergy 2005; 35: 448-455. PubMed

5. Arkwright PD, Daniel To, Sanyal D, David TJ, Patel L. Age-Related prevalence and antibiotic resistance of pathogenic staphylococci and streptococci in children with infected atopic dermatitis at a single-speciality center. Arch Dermatol 2002; 138: 939-941. PubMed

6. Hanifin JM, Rajka G. Diagnostic features for atopic dermatitis. Acta Dermatol venerol 1980; 92: 744-747.

7. Gelmetti C, Colonna C. The value of SCORAD and beyond. Towards a standardized evaluation of severity? Allergy 2004; 59 (supple. 78): 61-65. PubMed

8. Pucci N, November E, Cammarata M, et al. Scoring atopic dermatitis in infants and young children: distinctive features of the SCORAD index. Allergy 2005; 60: 113-116. PubMed

9. Hoeger PH. Antimicrobial susceptibility of skin-colonizing S. aureus strains in children with atopic dermatitis. Pediatr Allergy Immunol 2004; 15: 474-477. PubMed

10. Perera G, Hay R. A guide to antibiotic resistance in bacterial skin infections. JEADV 2005; 19: 531-545. PubMed

11. Abeck D, Mempel M. Staphylococcus aureus colonization in atopic dermatitis and its therapeutic implications. British Journal of Dermatology 1998; 139 (S3): 13-16. PubMed

12. Adachi Y, Akamatsu H, Horio T. The effect of antibiotics of the production of superantigen from staphylococcus aureus isolated from atopic dermatitis. J Dermatol Sci 2002; 28: 76-83. PubMed

13. Trividic M, Gauthier ML, Sparsa A, et al. Methicillin resistant staphylococcus aureus in dermatological practice: origin, risk factors and out come. Ann Dermatol Venereal 2002; 129: 27-29. PubMed

© 2008 Dermatology Online Journal