Microbes of the skin belong to the microbial ecosystem of the body. The terms microbiota (micro-organisms) and microbiom (includes genetic material) are used interchangeably, despite some differences exist.
9.1.4 Cutaneous Microbiology
The cutaneous microbiome encompasses the microbes that live in and on the skin, including bacteria, fungi and viruses. It is dynamic, continously evolving and diversifying with age, environment (height, lattitude, temperature, clothes, skin moisture, pH, sebum), personal hygiene, stress, nutrition status, culture, exposure to skin irritating or protecting agents, UV-light, antibiotics and/or genetic and epigenetic factors (barrier function, innate and adaptive immune system).
In contrast to adults, there are no anatomical differences in the microbiom of the skin in the newborn. However the type of delivery has an impact on the composition of the microbiom:
- Natural delivery: mothers′ vaginal flora: predominantly Lactobacilla.
- Delivery by Caesarean section: mothers′ skin flora: Staphylococci, Streptococci, Corynebacteria, and Cutibacteria.
3rd week up to the 3rd month of life
- Anatomic site‐specific bacterial profiles, but still different from adults before adolescence. Colonization interfollicular, intrafollicular and acrosyringeal.
- Around the 6th week of life: Staphylococcus and Corynebacterium.
- Around 1 month: Malassezia colonization increased with age, becoming adult‐like by 1 month of life.
Microbiome and Microbiota
An average healthy human body possesses 10x 14 microorganisms, including bacteria, fungi, mites and viruses – 10-fold the number of human cells. A single square centimeter of the human skin can contain up to one billion microorganisms.
Depending on commensal or pathogenic microbes living on the skin the local and systemic immune response is different
- Commensal microbes: homeostatic balance with the host.
- Pathogenic microbes: disruption of the cutaneous „eco-„ system and induction of innate and adaptive defense mechanisms responding with pro- and anti inflammatory mediators and activation of cells depending on the nature of the antigen.
Stress can modulate the composition of the microbiome.
An infection by intracellular pathogens initiates the development of T helper 1 (TH1) cells, whereas extracellular pathogens induce the differentiation of TH2 and TH17 subsets (atopic dermatitis, acne).
At the beginning of life in the late in utero status and after delivery the vernix caseosa is a key player in the development of early cutaneous innate immunity.
Risk for Diseases
A dysbiosis (dysbacteriosis) occurs when the „healthy“ microbiome is altered, for example by overwashing, humidity, clothes, antimicrobials, and resulting in conditions like erythema toxicum neonatorum, superficial folliculitis, body or feet odor, atopic dermatitis, and acne.
Spectrum of primary and secondary skin diseases with change of microbiota (Examples); see respective chapters
In general, we differentiate primary infections of the skin, skin diseases which become secondary superinfected ( impetiginized) , and skin diseases in which changes of the microbiota aggravate the course of a disease.
Erythema toxicum neonatorum
Macular erythema, papules and pustules in neonates, mostly self-limited. Most probably related to coccal microbes entering the opening of the follicle.
Superficial and Deep Folliculitis
Overgrowth of staphyloccal species in the acro – and infrainfundibulum of the follicle, showing superficial pustules, infiltrated lesions with papules and finally abcesses leading to furuncle or carbuncle.
Mostly seen in the first decade of life . Staphyloccocal or streptococcal are highly contagious infections, Staph.aureus of the intrafollicular epidermis, streptococci interfollicular epidermis. For treatment topical desinfectants and antimicrobials are preferred instead of topical antibiotics.
This is a quite common world wide to diagnose superficial infection with a Malassezia furfur species showing multiple asymptomatic scaly hyperpigmented (winter) or hypopigmented (summer) macules. Seborrhoic dermatitis is triggered by M. furfur. Hot and humid environments, occlusive clothes, increased sweating , immunosuppression, malnutrition, pregnancy, are precipitating factors. Wood (UVA) light examination for diagnosis.
Atopic Dermatitis (AD)
Barrier dysfunction and microbes contribute to the pathogenesis of AD. 70% of patients with AD are colonized with Staphylococcus aureus at lesional sites. Early exposure to Staphylococcus may reduce the development of AD ( adaptive immune response). AD patients are more prone to suffer from herpes (eczema herpeticatum) or malassezia infections.
Acne vulgaris originates in the pilosebaceous unit of the skin starting in (pre)puberty. Increased and modified sebum production, disturbance of follicular keratinocyte differentiation and release of inflammatory mediators are the primary driving forces of acne. The second step in the pathogenic cascade is colonization of this unit by Cutibacterium acnes, a commensal bacterium followed by additional triggering of inflammation.
C. acnes produces numerous enzymes and proteinases incl. lipases that alltogether alter the sebaceous lipid composition and contribute to the production and release of antimicrobial and immunomodulatory molecules.
Psoriasis is characterized by hyper-proliferation of keratinocytes with increased desquamation and increased inflammation. The disturbed barrier function of psoriasis gives rise to an altered microbiome. Throat and nasal Streptococcal infection have been shown to trigger initiation and exacerbation of psoriasis. Skin microbiota in Psoriasis display a higher degree of diversity compared to healthy skin.
Laboratory & other workups
- Swaps, scarification (Lepra), extraction of follicular material.
- Cyanoacrylate stripes.
- Wood light (malassecia).
- Biopsy: mycobacteria, deep mycoses, parasites.
- Serology, culture, PCR for further specification.
For STIs refer to the respective chapters.
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