Tufts OpenCourseware
Author: Susan Hadley, M.D.
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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:

  1. the appearance of the lesion
  2. epidemiologic factors that would put the patient in contact with particular etiologic agents
  3. 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.

3. Therapy

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)
Erysipelothrix rusiopathae (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
(Lyme disease)
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
Cutaneous inoculation
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
Disseminated infections
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
Trichosporon beigelii
Fusarium spp.
Pseudallescheria boydii

5. Ancillary Material

5.1. Readings

5.1.1. Suggested

  • Schaechter, Chapter 61: pp 573-8