Infectious Diseases in Critical Care Medicine

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Severe Skin and Soft Tissue Infections

in Critical Care

Mamta Sharma and Louis D. Saravolatz
Division of Infectious Disease, Department of Internal Medicine, St. John Hospital and Medical Center, and
Wayne State University School of Medicine, Detroit, Michigan, U.S.A.

INTRODUCTION
Skin and soft tissue infections are common and vary widely in severity from minor pyodermas
to severe necrotizing infections. Most of these infections are superficial and treated with
regimens of local care and antimicrobial therapy. However, others like necrotizing infections
are life-threatening and require a combined medical and surgical intervention. Prompt
recognization and treatment is paramount in limiting the morbidity and mortality associated
with these infections, and thus a thorough understanding of the various etiologies and
presentation is essential in the critical care setting. It is also important to discriminate between
infectious and noninfectious causes of skin and soft tissue inflammation. A detailed history
and examination are necessary to narrow the possible etiologies of infection. In many
instances, surface cultures are unreliable and misleading because surface-colonizing organisms
can be mistaken for pathogens. In instances in which the diagnosis is in doubt, aspiration,
biopsy, or surgical exploration of the skin can be considered. Typically, soft tissue infections
result from disruption of the skin by exogenous factor, extension from subjacent infection, or
hematogenous spread from a distant site of infection.


MICROBIAL FLORA
Normal skin functions as a protective barrier that prevents microorganisms from causing soft
tissue infection.
Physiological factors that control the bacterial skin flora include humidity, water content,
skin lipids, temperature, and rate of desquamation. The pH of the skin is usually around 5.6.
Besides containing secretory immunoglobulin (IgA), sweat also possesses sufficient salt to
create a high osmotic pressure, which may be responsible for inhibiting many microbial
species. In spite of these barriers to colonization, the skin provides an excellent venue of
various microenvironments. Differences in cutaneous microflora may relate to variability in skin
surface temperature and moisture content as well as the presence of different concentrations of
skin surface lipids that may be inhibitory to various microorganisms. Colonization with
organisms sensitive to desiccation, such as gram-negative bacilli, is not favored. The
predominant bacterial flora of the skin is the various species of coagulase-negative staphylococci
(Staphylococcus epidermidis,S. capitis, S. warneri, S. hominis, S. haemolyticus, S. lugdunensis, and
S. auricularis),Corynebacteriumspp. (diphtheroids), andPropionibacteriumspp. Humans are a
natural reservoir forS. aureus, and asymptomatic colonization is far more common than
infection. Colonization of the anterior nares, perineum, or skin, particularly if the cutaneous
barrier has been disrupted or damaged, may occur shortly after birth and may recur anytime
thereafter (1–4). The anterior nares are reservoirs forS. aureus. Approximately 20% of
individuals always carry one type of strain and are called persistent carriers. A large proportion
of the population approximately 60% harborsS. aureusintermittently, and the strains change
with varying frequency. Such persons are called intermittent carriers. Finally, approximately
20% almost never carryS. aureusand are called noncarriers (5–7). Carriage rates are higher than
in the general population for injection drug users, persons with insulin-dependent diabetes,
patients with dermatological conditions, patients with long-term indwelling intravascular
catheters, and those with human immunodeficiency virus infection. High nasal carriage rates
are found in patients withS. aureusskin infections as demonstrated from nasal cultures taken at
the time theS. aureusinfection was present (5).Micrococcusspp.,Peptostreptococcus,Streptococcus

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