Microbiology of Skin and Wounds

The skin has multiple layers of dead epithelial cells, which provides a barrier against pathogens
The skin surface is inhabited by a variety of normal microbiota, including bacteria, yeasts, and fungi
The skin generates antimicrobial peptides, and sweat has a low pH that inhibits the growth of most pathogens
Sebum, a skin secretion, has a low pH that makes the skin inhospitable to most microorganisms

The skin is colonized by an array of organisms, with relatively fewer organisms in dry areas and more in moist areas
Normal skin microbiota includes bacteria such as Staphylococcus epidermidis, Propionibacterium, Corynebacterium, Lactobacillus, Bacteroides, Prevotella, and Haemophilus
Yeasts such as Malassezia and Candida are also present on the skin

Skin and soft tissue infections are the second most common infections encountered in primary care settings
Skin microbial diseases can occur through three pathways: breach of intact skin, skin manifestations of systemic infections from blood-borne spread, and toxin-mediated skin damage from microbial toxins produced elsewhere in the body

Pathogen: Staphylococcus aureus, a facultative anaerobic, Gram-positive bacterium that forms grape-like clusters of spherical cells
Virulence factors: coagulase, hyaluronidase, staphylokinase, β-lactamase, protein A, cytolytic toxins, leukocidin, exfoliative toxins, and toxic shock syndrome toxin
Pathogenesis: bacteria on the surface of the skin grow into hair follicles and, in some cases, invade the surrounding tissues, leading to inflammation, fever, and symptom development
Signs and symptoms: folliculitis, furuncle or boil, and carbuncle
Diagnosis: based on characteristic clinical presentation, with laboratory tests unnecessary in most cases
Treatment: incision and drainage of abscesses, topical antibiotic therapy with mupirocin, and oral antibiotics such as clindamycin and trimethoprim-sulfamethoxazole
Prevention: good hygiene and cleanliness

Pathogens: Staphylococcus aureus and Streptococcus pyogenes (most cases caused by both bacteria)
Pathogenesis: bacteria colonize the skin and then invade through scratches, abrasions, or other wounds, leading to inflammation and symptom development
Signs and symptoms: characteristic red patches, oozing, pus-filled vesicles on a red base, and a thick, honey-colored, sticky crust
Diagnosis: visual inspection, with laboratory tests unnecessary in most cases
Treatment: topical mupirocin, with oral antibiotics such as dicloxacillin or cephalexin required in some cases
Prevention: good hygiene and cleanliness, with frequent handwashing and avoiding close contact with infected individuals

Pathogen: Streptococcus pyogenes, a Gram-positive coccus arranged in chains
Pathogenesis: bacteria enter the skin through a cut or break, leading to inflammation and symptom development
Signs and symptoms: reddening of the skin, swollen local lymph nodes, pain, fever, chills, and leukocytosis
Diagnosis: visual inspection, with laboratory tests unnecessary in most cases
Treatment: oral penicillin, with intravenous penicillin required in severe cases
Prevention: good hygiene and cleanliness, with prompt wound care and avoidance of close contact with infected individuals

Pathogen: Staphylococcus aureus, which secretes exfoliative toxins that cause SSSS
Pathogenesis: exfoliative toxins cause the dissolution of epidermal desmosomes, leading to skin sloughing
Signs and symptoms: reddening and wrinkling of the skin, followed by large blisters that contain clear fluid, and fever
Diagnosis: based on distinctive skin lesions and histological examination
Treatment: intravenous antimicrobial drugs such as cloxacillin, with vancomycin used to treat resistant strains
Prevention: little can be done to prevent SSSS, as S. aureus is normally present on moist skin

Pathogens: multiple bacteria, but most commonly Streptococcus pyogenes
Pathogenesis: bacteria enter the body through breaks in the skin, spread rapidly along muscle fascia, and secrete enzymes that allow the bacterium to invade body tissues
Signs and symptoms: hot, intensely painful, sunburn-like rash at the site of infection, followed by fever, tiredness, and muscle aches
Diagnosis: combination of clinical evaluation, imaging studies, laboratory tests, and sometimes surgical exploration
Treatment: immediate removal of dead tissue, repeated daily until bacterial destruction of tissue is halted, and intravenous broad-spectrum antimicrobial drugs
Prevention: prompt wound care, good hygiene, and cleanliness