Abstract
Staphylococcus aureus has been thought to play the major role in eczema, but other staphylococci, including Staphylococcus epidermidis, all of which are normal flora on everyone’s skin, also play major roles. S. epidermidis and other staphylococci become pathogenic when they make biofilms. These biofilms, produced when the organisms are exposed to salt and water in sweat, protect the bacterial colonies. They also make these once-sensitive organisms multidrug resistant. The two parameters, biofilm production and multidrug resistance, are very closely aligned, making these staphylococci exceedingly difficult to kill when they assume a pathogenic role. We have found biofilm production and multidrug resistance in all the species we have recovered. The pathogenic role of the staphylococcal species producing biofilms is to form an occlusion in the eccrine sweat duct. This initiates a series of events that creates itching, and the prototypical rash then ensues.
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References
O’Brien JP. The etiology of poral closure. II. The role of staphylococcal infection in miliaria rubra and bullous impetigo. J Invest Dermatol. 1950;15(2):102–33. O’Brien noted similarities between miliaria and bullous impetigo, a disease largely believed to be caused by S. aureus, and hypothesized that miliaria, too, might be caused by infection with S. aureus. He examined 2,000 biopsy specimens from patients affected by acute miliaria and found a considerable degree of staphylococcal growth in the earliest obstructive lesions of the disease. O’Brien then inoculated skin with S. aureus and observed the development of lesions that appeared identical to those of miliaria. He concluded that S. aureus is the most probable organism responsible for the earliest lesions of miliaria.
Leyden JJ, Marples RR, Kligman AM. Staphylococcus aureus in the lesions of atopic dermatitis. Br J Dermatol. 1974;90(5):525–30. Leyden et al. quantified S. aureus in the chronic plaques and acute exudative lesions of atopic dermatitis. Ninety percent of cultures taken from chronic plaques were positive for S. aureus and the density exceeded 1 × 106/cm2 in 45 % of the samples. S. aureus was cultured from 100 % of acute exudative lesions with a mean density of 14 × 106/cm2.
Nickel JC, Ruseska I, Wright JB, Costerton JW. Tobramycin resistance of Pseudomonas aeruginosa cells growing as a biofilm on urinary catheter material. Antimicrob Agents Chemother. 1985;27(4):619–24. Nickel and colleagues developed biofilms by exposing disks of urinary catheter material to urine infected with Pseudomonas aeruginosa. They then treated these disks with tobramycin in a urine medium and found that a significant amount was still viable after exposure. Conversely, floating cells from the disks exposed to tobramycin were completely killed. The authors concluded that biofilms confer a degree of tobramycin resistance to the otherwise sensitive P. aeruginosa.
Sulzberger MB, Hermann F, Zak FG. Studies of sweating. I. Preliminary report with particular emphasis on a sweat retention syndrome. J Invest Dermatol. 1947;9(5):221–42. Dr. Sulzberger and his colleagues sought to prove that plugging of the sweat gland orifices played an important role in the pathogenesis of atopic dermatitis, ichthyosis, atypical seborrheic dermatitis and patchy prickly heat. They present cases where they exposed patients presumably with these diseases to transient heat and found that the patients had typical clinical and histologic findings. Clinically, they found immediately developed symptoms of pruritus and malaise and had decreased sweating as evidenced by starch iodine tests and increased pH on the skin surface. Subjects also developed new or more pronounced papulovesicles which had the low pH of sweat. On pathology, numerous sweat glands showed plugging. Biopsies after heat exposure showed increased vesicle formation and exocytosis.
Hölzle E, Kligman AM. The pathogenesis of miliaria rubra. Role of the resident microflora. Br J Dermatol. 1978;99(2):117–37. Hölzle and Kligman postulated that bacteria cause miliaria by creating a substance that blocks the lumens of sweat ducts. They caused anhidrosis in patients by covering the skin with a plastic film that was impermeable. They noted that as the density of resident aerobic bacteria on the skin increased, so did the degree of sweat suppression and miliaria. They also looked histologically at these specimens and noted that a PAS-positive, diastase-resistant amorphous mass clogged the acrosyringium after 2 days of occlusion.
Dobson RL, Lobitz WC. Some histochemical observations on the human eccrine sweat glands: the pathogenesis of miliaria. AMA Arch Dermatol. 1957;75(5):653–66. Dobson and Lobitz sought to uncover the initial alteration of the eccrine sweat gland that produces miliaria. They produced clinical cases of miliaria in patients using iontophoresis and subsequent sweating. Biopsy specimens from the treated areas were then analyzed at various intervals. They found that treated sites first developed aggregates of Schiff-positive, diastase-resistant material that filled the distal portion of the epidermal sweat-duct unit, causing complete occlusion. They described this plugging of the distal sweat pore as the primary anatomic alteration leading to initial cases of miliaria. They showed that this plugging led to degeneration of the sweat-duct unit, or a parakeratotic keratin plug, which in turn perpetuates the process by plugging the newly regenerated sweat-duct unit.
Mowad CM, McGinley KJ, Foglia A, Leyden JJ. The role of extracellular polysaccharide substance produced by Staphylococcus epidermidis in miliaria. J Am Acad Dermatol. 1995;3:729–33. Mowad et al. looked at the ability of several species of coagulase-negative staphylococci to induce miliaria. The study group’s aim was to induce miliaria by inoculating the forearm of patients with differing strains of coagulase-negative staphylococci under an occlusive dressing that thermally stimulated the area. Only strains of S. epidermidis were able to induce miliaria in the subjects studied. S. epidermidis alone is capable of producing the PAS-positive extracellular polysaccharide substance (EPS). Therefore, the authors concluded that it is the EPS that obstructs delivery of sweat to the skin in miliaria and that it is this that plays a key role in the pathogenesis of miliaria.
Allen HB, Jones NP, Bowen SE. Lichenoid and other clinical presentations of atopic dermatitis in an inner city practice. J Am Acad Dermatol. 2008;58(3):503–4. Allen et al. report on the incidence and different presentations of atopic dermatitis seen in an inner city clinic over an 8-month interval and describe a new presentation of atopic dermatitis seen in African Americans, the lichen planus–like variant.
Gagnon RD. Outpatient visits to US physicians by diagnosis. In: Sober AJ, Fitzpatrick TB, editors. Yearbook of dermatology. Chicago: Yearbook Medical Publishers; 1992.
Laughter D, Istvan JA, Tofte SJ, Hanifin JM. The prevalence of atopic dermatitis in Oregon schoolchildren. J Am Acad Dermatol. 2000;43(4):649–55. Laughter and colleagues investigated the prevalence of atopic dermatitis in childhood. They studied 5- to 9-year-old children from rural and urban Oregon using the Schultz-Larsen questionnaire. They found a prevalence of 17.2 % in this population.
Kay J, Gawkrodger DJ, Mortimer MJ, Jaron AG. The prevalence of childhood atopic eczema in a general population. J Am Acad Dermatol. 1994;30(1):35–9. Kay and colleagues investigated the epidemiology of atopic eczema in the general population. They drew subjects from a general practice in Birmingham, England. They found a lifetime prevalence of 20 % in children aged 3–11 years.
Nnoruka EN. Current epidemiology of atopic dermatitis in south-eastern Nigeria. Int J Dermatol. 2004;43(10):739–44.
Kajiyama S, Tsurumoto T, Osaki M, Yanagihara K, Shindo H. Quantitative analysis of Staphylococcus epidermidis biofilm on the surface of biomaterial. J Orthop Sci. 2009;14(6):769–75. doi:10.1007/s00776-009-1405-0. Epub 2009 Dec 8.
Kong HH, Oh J, Deming C, et al. Temporal shifts in the skin microbiome associated with disease flares and treatment in children with atopic dermatitis. Genome Res. 2012;22(5):850–9. Kong and colleagues classified all the organisms found on normal skin controls and in children with atopic dermatitis at different stages of the disease presentation. Our findings, in comparison, demonstrate one of our crucial theories: we believe that what the organisms are doing on the skin is of considerably greater importance than which organisms are present there.
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Allen, H.B. (2015). Microbiology. In: The Etiology of Atopic Dermatitis. Springer, London. https://doi.org/10.1007/978-1-4471-6545-3_2
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DOI: https://doi.org/10.1007/978-1-4471-6545-3_2
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