Bacterial Skin and Soft Tissue Infections: A Review for the Dermatologist
The skin is the largest organ in the human body, and when
combined with the underlying soft tissues, it comprises
the bulk of the body’s solid mass. It is colonized with
resident microflora, including various species of staphylococci,
corynebacteria, and propionibacteria, that competitively inhibit
pathogenic microbes.1 It is important to differentiate between
normal colonization, which is not a disease process, and infection
with pathogenic strains, which may necessitate treatment.1
In the first century ad, Celsus described the classical symptoms
of an inflammatory infection as calor, rubor, tumor, and dolor (ie,
heat, redness, swelling, and pain).2,3 In modern medicine, skin and
soft tissue infections (SSTIs) are defined as invasion of pathogens
into the epidermis, dermis, and subcutaneous tissues, causing
subsequent inflammation. One might also augment Celsus’s
description with a fifth characteristic: functio laesa, or loss of function.
These infections often require treatment, and although it is
not within the scope of this review, the selection of suitable antibiotics
and their appropriate use is a key issue that physicians face.
SSTIs have developed into a much more complicated clinical
problem since Celsus first described them. They are becoming
increasingly common in both the outpatient and inpatient settings,
and microbial resistance is rising as more virulent strains
evolve. Bacterial SSTIs are among the most common diseases
seen by dermatologists, who are often the first point of care for
these patients.4 As the public health and economic burdens of
SSTIs rise, dermatologists continue to play a key role in identifying
and managing these diseases.
Epidemiology
Because bacterial SSTIs can manifest as various clinical entities, accurate assessment of incidence and prevalence has been difficult. 5 Furthermore, because many SSTIs resolve within 7 to 10 days, measurement of prevalence is variable.5 The estimated prevalence among all hospitalized patients is 7% to 10%,6 and from 2000 to 2004, hospital admissions for SSTIs increased by 29%.7 Approximately 70% to 75% of all SSTI cases are managed in an outpatient setting.8,9 A large portion of outpatient cases involve the lower extremity.9,10 In addition, the prevalence of SSTIs is higher in men, accounting for 60% to 70% of all cases, as well as in patients aged 45 to 64 years.5
Though the microbial makeup of SSTIs has been shifting over
the past 20 years, recent epidemiological studies yield conflicting
results.11 One study found that from 1997 to 2005, the annual
incidence of SSTIs rose from 32 to 48 clinical visits per 1,000 persons.
12 Greater than 95% of this increase in incidence was due to
the growing number of cases of cellulitis and abscesses.12 However,
other studies established that though the overall incidence
of SSTIs did not change during this time period, the frequency
of cellulitis and abscesses has indeed grown in number.13,14 Although
these studies differ in their outcomes with regard to
incidence, there is a consensus opinion that cellulitis in particular
is increasing in frequency, and that SSTIs are an increasingly
common occurrence.11 In addition, a recent study found that the
relative proportion of methicillin-resistant Staphylococcus aureus
(MRSA) isolates identified in an outpatient dermatology clinic
rose by 17.0% during the past 3 years.15 MRSA-related infections
have unquestionably increased in number and are likely responsible
for the rise in diagnoses.12,13,15
Microbiology
Most bacterial SSTIs are the result of aerobic Gram-positive cocci, particularly S aureus and Streptococcus species.1,8,11 Streptococcal infections can be further divided into several types, with groups A and B predominantly causing SSTIs.8 In recent years, S aureus has become an even more significant pathogen. The emergence of community-acquired MRSA strains has complicated treatment of bacterial SSTIs.11,16 Though S aureus infections are on the rise and are commonly identified on cultures, good clinical response to β-lactam antibiotics implies that Streptococcus species in Lancefield groups A, C, and G are still predominant microbes in skin infections.11,17,18 In particular, group A β-hemolytic streptococci is often identified.11
In addition, the microbiology of SSTIs varies in communityacquired
and hospital-acquired infections. The top 10 bacteria
overall in SSTIs are as follows: S aureus (45%), Pseudomonas
aeruginosa (11%), Enterococcus species (9.3%), Escherichia coli
(7.2%), Enterobacter species (4.8%), Klebsiella species (4.2%),
ß-hemolytic Streptococcus(4.1%), Proteus mirabilis (2.8%),
coagulase-negative Staphylococcus (2.8%), and Serratia species
(2.1%).19,20 However, hospital-acquired SSTIs demonstrate
a greater percentage of resistant species such as MRSA (up
to 40% of cases), P aeruginosa, and Enterococcus species.19 In
contrast, the majority of community-acquired SSTIs are caused
by β-hemolytic streptococci.5 According to the SENTRY Antimicrobial
Surveillance program, this pathogen appears as only
the seventh most common cause of SSTIs in North America20;
however, it is likely underrepresented, since mild or superficial
infections may not necessitate hospital admission and positive
cultures are difficult to obtain in streptococcal infections.19 It is
important to note that given the variable presentation of SSTIs
and the disparity in severity, assessing incidence and prevalence
is difficult; the statistics often vary between studies.5 It is
