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1. General Introduction
Skin and soft tissue infections are among the most common infections of man. Infections can range in severity from cosmetic to life-threatening depending upon the level of tissue penetration and, most importantly, the organism involved.
When attempting to ascertain the etiology of a skin or soft tissue infection, there are several important considerations:
- the appearance of the lesion
- epidemiologic factors that would put the patient in contact with particular etiologic agents
- the competency of host immune defenses
1.1. Appearance of the lesion
Specific types of skin infections, and sometimes even specific organisms, often have a typical characteristic appearance. The location, color, size and characteristics of lesion such as whether the lesion is singular or grouped, contiguous or separated over large distances, blanching or non-blanching can be important clues in determining the cause of an infection. An evaluation of the lesion for clues as to the depth of invasion (e.g.: presence of superficial bullous lesions, or crepitance—an indication of subcutaneous gas) may also be critical.
1.2. Epidemiologic factors
Infectious diseases of the skin are, like most infections, diseases of opportunity. Skin infection occur when organisms are contacted in their “natural environments” and begin to grow in the tissue of a patient.The most common agents of skin infections are typically coloizers of humans (e.g. Staphyloccous aureus in human nares) resulting in many opportunites for contact. It is important to elicit information from patients that may have put them at risk for infections with organisms that they would not ordinarily have contact with. For example, a skin infection developing around the site of a cat bite could be caused not only by bacteria present on the skin surface but also by bacteria present in the mouth of a cat.
While an understanding of epidemiological risk factors is important, one must not be overly reliant on epidemiology. Common infections remain common despite a patient’s history of exposure to an uncommon agent. Conversely, one may discount a particular disease etiology due to an incomplete understanding of the risk of infection with a particular agent (e.g.: the low risk of cutaneous anthrax in American postal workers was presumed prior to the discovery of its use in bioterrorism).
1.3. Host immune defenses
The competence of the host immune system plays a major role in determining which organisms may establish skin and soft tissue infections. The skin is the single largest organ in the body. Intact skin is the most important component in host defense against invasion from organisms in the external environment. Among the causes of breakdowns in this component of host defense are trauma, systemic illnesses affecting the skin (e.g. pedal edema and venous stasis causing “microbreaks” in skin), insertion of organisms beneath the skin by arthropod vectors and iatrogenesis (e.g.: surgery, intravenous catheter placement). Breakdowns in the skin barrier, or lack thereof, are important considerations in assessing risk for specific infections.
Once organisms have penetrated beyond the superficial epidermis, they encounter components of the innate and adaptive immune response including dendritic cells, macrophages, neutrophils and T and B lymphocytes. Specific deficiencies in any one or more of these components of the immune response can increase the risk for particular types of skin and soft tissue infection. For example, patients with chronic granulomatous disease (who have a defect in production of superoxide by phagocytic cells) are at risk for recurrent skin infections with Staphylococcus aureus. There are many examples of increased risk for specific infections with immunodeficiencies whether they are inherited, acquired (e.g. AIDS) or iatrogenic (e.g.: secondary to immunosuppressive agents used in transplantation).
2. Categorization of Skin and Soft Tissue Infections.
Skin and soft tissue infections may be categorized along several different axes. These include route of entry, class of organism and depth of infection.
2.1. Route of entry
There are only three pathways by which organisms can establish infections in the skin: they can either penetrate (or be inoculated) through the epidermis, they can extend directly from a deeper source of infection (e.g. a visceral abscess) or they can reach the skin from a distant site through hematogenous seeding. While some organisms may utilize more than one of these mechanisms, other organisms are capable of only one route of infection (see charts). Again, epidemiology and host factors (e.g.: risk factors for either a breakdown in the skin barrier or underlying septicemia) play a large factor in evaluating the likely cause of the skin infection.
2.2. Class of organism
Many bacteria, fungi, viruses and parasites can cause skin and soft tissue infections. Infections caused by these different classes of organisms typically have very different appearances and clinical courses. This is thought to be due to a complex mixture of factors including replication capacity of the organism, production of adhesion factors and proteases as well as immunogenicity and aspects specific to the host response. It is beyond the scope of this lecture to provide a comprehensive list of the manifestations of each of the organisms that may cause skin infections. Charts listing some of the more common bacterial and fungal causes of skin infections are found at the end of the text. Viral and parasitic causes of skin and soft tissue infections will be discussed with the individual organisms.
2.3. Depth of infection
The skin consists of multiple different compartments. An avascular superficial layer, the epidermis performs the barrier functions of the skin and consists of a tough layer of protein and lipids (stratum corneum). The dermis underlies the epidermis. The dermis contains blood vessels, lymphatics and fibroblasts which produce the collagen and elastic tissue of the skin. The dermis also contains the skin appendages which include the eccrine and sebaceous glands and hair follicles. These may provide routes of entry for pathogens as they provide breaks in the protective epidermis. Below the dermis is a layer of subcutaneous fat which sits on top of a fascial layer which separates the skin from deeper muscle layers.
See image: Cutaneous anatomy, sites of infection, and infecting organisms. Infectious diseases, / [edited by] Sherwood L. Gorbach, John G. Bartlett, Neil R. Blacklow. Philadelphia : Saunders, c1992, p. 1065.
Therapy for skin and soft tissue infections depends upon the depth of invasion and the invading organism. Superficial infections such as impetigo can often be treated with topical antibiotics. Deeper infections such as cellulitis require systemic antimicrobials and the deepest infections (e.g.: necrotizing fasciitis) require a combination of systemic antimicrobials and extensive surgical debridement. Because culture data is often unavailable for patients with skin and soft tissue infections, antimicrobial therapy is often initiated empirically based on what are thought to be the most likely organisms causing a particular type of infection.
4. Skin and Soft Tissue Infections Tables
4.1. Skin and Soft Tissue Infections Table I
|Most Common Organisms||Layer involved||Route of entry||Appearance/localization||Risk factors/Comments|
|Impetigo||Staphylococcus aureusStreptococcus pyogenes||stratum corneum||cutaneous||vesicles, pustules, “honey crusts”||contagious, poor hygiene|
|Folliculitis||Staphylococcus aureus||stratum corneum dermis||cutaneous||papules and pustules around hair follicles|
|Many other bacteria, fungi|
|Pseudomonas aeruginosa||as above||as above||papules and pustules||“hot tub” folliculitis|
|Erysipelas||Streptococcus pyogenes Group C, G streptococci||superficial dermis||cutaneous with lymphatic spread||bright red, well circumscribed lesions occ. bullous; typically face and legs||infants, elderly, saphenous vein harvest|
|Ecthyma||Staphylococcus aureus Streptococcus pyogenes||dermis||cutaneous||ulcerations with adherent scabs||poor hygiene|
|(gangrenosum)||Pseudomonas aeruginosa||dermis||hematogenous||deep ulcerations with black eschars||bacteremia, neutropenia|
|(“ecthyma-like”)||Bacillus anthracis||dermis||cutaneous||as above||wool and mail sorting|
|Abscess||Staphylococcus aureus||dermis||cutaneous||tender, fluctuant mass with overlying erythema;||defects in phagocytosis Hidradenitis suppurativa (recurrent infections in intertriginous areas|
|non-tuberculous mycobacteria||dermis||cutaneous||as above, occ. ulcerating or with lymphangitic spread of nodules||trauma; for M. marinum- water exposure.|
|Cellulitis||Staphylococcus aureus||deep dermis||cutaneous||spreading erythema, occ, lymphangiitis vesicles, abscess formation||condutions causing bacterial colonization of skin (psoriasis eczema, chronic ulceration)|
|Pasturella multocida||as above||cutaneous||as above||cat bite, (typically rapid onset)|
|Bacteroides fragilis Prevotella spp, Fusobacterium||as above||cutaneous||as above||human bites|
|Aeromonas hydrophila||as above||cutaneous||as above||water exposure|
|Vibrio vulnificus||rarely hematogenous||cirrhosis (Vibrio)|
|Clostridium spp||as above||cutaneous||as above, +/- crepitance||abdominal surgery|
|Pseudomonas aeruginosa||as above||cutaneous||as above,||lower extremities puncture wounds through old shoes|
|Necrotizing fasciitis||Streptococcus pyogenes||deep underlying||cutaneous||similar to cellulits, pain||diabetes|
|Clostridium spp.||tissue||occ||hematogenous||out of proportion to appearance|
|(Fournier’s gangrene)||gram negative enteric bacteria||deep underlying tissue||cutaneous extension from UTI||scrotal pain, erythema, swelling||healthy men|
|Purpura fulminans||Neisseria meningitis||deep tissue||hematogenous||initially maculo-papular, followed by petichiae and ultimately deep purpuric, necrotic lesions||complement but also healthy hostsdeficiency|
|Cutaneous manifestations of vector-borne bacterial diseases|
|Erythema migrans||Borrelia burgdorferi||dermis||cutaneous with hematogenous||painless erythematous lesions occ. “target-like”||exposure to ticks in endemic areas|
|Rocky Mountain Spotted Fever||Rickettsia rickettsii||dermis, vasculature||cutaneous with hematogenous dissemination||petechiae macules progressing toand palpable purpura. Often involves hands and soles.||exposure to ticks in endemic areas|
|Ricketsialpox||Rickettsia akari||dermis||cutaneous||eschar at site of mite bite||exposure to mouse mite in urban settings|
|.Scrub typhus||Ricketssia prowazekii||epidermis||cutaneous with hematog. dissemin||maculopapular, blanching rash||crowded living, louse exposure|
|Murine typhus||Rickettsia typhi||epidermis||cutaneous with hematog. dissem||maculopapular, petichial||exposure to infected fleas (Central America)|
|Tularemia||Francisella tularensis||dermis||cutaneous with hematog dissem||papule at bite site followed by eschar Ulcerations over lymphadenopathy||exposure to infected animals, ticks (all 50 states)|
|Sexually transmitted bacterial infections|
|Syphilis||Treponema pallidum||dermis||cutaneous with hematog. dissem.||1o: painless ulceration (chancre)|
|2o: maculopapular, occ. pustular, plaque-like|
|3o: painless nodules, gummas|
|Chancroid||Haemophilus ducreyi||dermis||cutaneous||nodule that breaks down into painful ulcer|
|Donovanosis (granuloma inguinale)||Calymmatobacterium granulomatis||dermis||cutaneous||firm nodule that erodes into painless ulcer|
|Lymphogranuloma venereum||Chlamydia trachomatis||lymph nodes||cutaneous||inguinal lymphadenopathy (bubos)|
4.2. Skin and Soft Tissue Infections Table II
|Fungi||Other names||Layer involved||Appearance/localization||Risk factors|
|Microsporum, Trichophyton||Tinea capitus||stratum corneum||erythema, scaling, hair loss||person to person transmission|
|Microsporum, TrichophytonEpidermophyton||Tinea corporus||stratum corneum||red, raised, scaly, sometimes circular, often grouped lesions|
|Candida spp.||stratum corneum||vesicopustules progressing to erythema and maceration. Typically in intertriginous regions||obesity, diabetes|
|Sporothrix schenckii||“Rose gardener’s disease”||dermis||nodule progressing to pustule and ulceration Subcutaneous nodules extending along Lymphatic drainage channe||trauma from plant materials|
|Actinomyces||“Madura foot”||initially stratum corneum but can penetrate deeply||nodules progressing to ulcers with granulomata||trauma|
|“Mucor” (Rhizopus, Mucor)||dermis||dark, necrotic lesions||trauma, burns, diabetes|
|Malessezia spp||folliculitis Tinea versicolor||epidermis||papulopustular hypo and hyper pigmented macules|
|Candida spp||disseminated candidiasis||epidermis, dermis||pustules||intravenous catheterization, neutropenia|
|Coccidioides immitis||Valley fever||dermis, deeper tissue||papules, pustules, granulomata, abscesses||exposure in SW US, Mexico, S. America|
|Cryptococcus neoformans||dermis||nodular or ulcerative lesions||defects in T cell immunity (AIDS, steroids)|
|Aspergillus spp||dermis, deeper tissue||erythematous papules, pustules, necrotic ulcerations||severe and extended immunosuppression|