Skin and soft tissue infections occur in all races, all ethnic groups, and all geographic locations, although some have unique geographic niches. In modern times, the frequency and severity of some skin and soft tissue infections have increased for several reasons. First, microbes are rapidly disseminated throughout the world via efficient air travel, acquiring genes for virulence factors and antibiotic resistance. Second, natural disasters, such as earthquakes, tsunamis, tornadoes, and hurricanes, appear to be increasing in frequency, and the injuries sustained during these events commonly cause major skin and soft-tissue damage that predisposes to infection. Third, trauma and casualties resulting from combat and terrorist activities can markedly damage or destroy tissues and provide both endogenous and exogenous pathogens with ready access to deeper structures. Unfortunately, because the marvels of modern medicine may not be available during human-instigated and natural disasters, primary treatment may be delayed and the likelihood of severe infection and death increased.
ANATOMIC RELATIONSHIPS: CLUES TO THE DIAGNOSIS OF SOFT TISSUE INFECTIONS
Skin and soft tissue infections have been common human afflictions for centuries. However, between 2000 and 2004, hospital admissions for skin and soft tissue infections rose by 27%, a remarkable increase that was attributable largely to the emergence of the USA300 clone of methicillin-resistant Staphylococcus aureus (MRSA). This chapter provides an anatomic approach to understanding the types of soft tissue infections and the diverse microbes responsible.
Protection against infection of the epidermis depends on the mechanical barrier afforded by the stratum corneum, since the epidermis itself is devoid of blood vessels (Fig. 26-1). Disruption of this layer by burns or bites, abrasions, foreign bodies, primary dermatologic disorders (e.g., herpes simplex, varicella, ecthyma gangrenosum), surgery, or vascular or pressure ulcer allows penetration of bacteria to the deeper structures. Similarly, the hair follicle can serve as a portal either for components of the normal flora (e.g., Staphylococcus) or for extrinsic bacteria (e.g., Pseudomonas in hot-tub folliculitis). Intracellular infection of the squamous epithelium with vesicle formation may arise from cutaneous inoculation, as in infection with herpes simplex virus (HSV) type 1; from the dermal capillary plexus, as in varicella and infections due to other viruses associated with viremia; or from cutaneous nerve roots, as in herpes zoster. Bacteria infecting the epidermis, such as Streptococcus pyogenes, may be translocated laterally to deeper structures via lymphatics, an event that results in the rapid superficial spread of erysipelas. Later, engorgement or obstruction of lymphatics causes flaccid edema of the epidermis, another characteristic of erysipelas.
Structural components of the skin and soft tissue, superficial infections, and infections of the deeper structures. The rich capillary network beneath the dermal papillae plays a key role in the localization of infection and in the development of the acute inflammatory reaction.