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REVIEW ARTICLE

Bacterial skin and soft tissue infections: review of the

epidemiology, microbiology, aetiopathogenesis and

treatment A collaboration between dermatologists and infectivologists

L. Tognetti,†,* C. Martinelli,‡ S. Berti,§ J. Hercogova,– T. Lotti,** F. Leoncini,‡ S. Moretti†

†Division of Clinical, Preventive and Oncologic Dermatology, Department of Critical Care Medicine and Surgery, Florence

University, Florence, Italy‡Infectious Diseases Unit, Azienda Ospedaliero Universitaria Careggi, Florence, Italy§Department of Sciences for Woman and Child’s Health, University of Florence, Florence, Italy–Dermatology department, 2nd Medical School, Charles University, Prague, Czech Republic

**Chair of Dermatology and Venereology, Guglielmo Marconi University, Rome, Italy

*Correspondence: L. Tognetti. E-mail: [email protected]

AbstractBacterial skin and soft tissues infections (SSTI) often determine acute disease and frequent emergency recovering,

and they are one of the most common causes of infection among groups of different ages. Given the variable

presentation of SSTI, a thorough assessment of their incidence and prevalence is difficult. The presence of patient-

related (local or systemic) or environmental risk factors, along with the emergence of multi-drug resistant pathogens,

can promote SSTI. These infections may present with a wide spectrum of clinical features and different severity, and

can be classified according to various criteria. Many bacterial species can cause SSTI, but Gram-positive bacteria

are the most frequently isolated, with a predominance of Staphylococcus aureus and Streptococcus pyogenes. The

diagnosis of SSTI requires an extended clinical history, a thorough physical examination and a high index of

suspicion. Early diagnosis is particularly important in complicated infections, which often require laboratory studies,

diagnostic imaging and surgical exploration. SSTI management should conform to the epidemiology, the aetiology,

the severity and the depth of the infection. Topical, oral or systemic antimicrobial therapy and drainage or

debridement could be necessary, along with treatment of a significant underlying disease. This review discusses theepidemiology, the pathogenesis and the classification of bacterial SSTI, describes their associated risk factors and

their clinical presentations. The authors provide a rational diagnostic and therapeutic approach to SSTI in respect of

antibiotic resistance and currently available antimicrobial agents.

Received: 6 April 2011; Accepted: 24 November 2011

Conflict of interest

None.

Funding source

None.

Epidemiology

Skin and soft tissue infections (SSTI) collectively refer to several

microbial invasions of the skin layers and of the underlying soft

tissues, inducing a host-response. SSTI can often determine acute

disease and they are one of the most common causes of infection

among groups of different ages.1–4 In particular, SSTI represent

the most common infection presentation in patients visiting emer-

gency room clinics in both hospitals and based practices, account-

ing for a substantial portion of emergency department visits and

hospital admissions.5–8 Despite that, it is difficult to make an

assessment of the exact incidence and prevalence of SSTI, probably

because of their variable presentation and their short duration.

Indeed, the majority of SSTI tend to resolve within 7–10 days.2

The estimated prevalence of SSTI among hospitalized patients was

7–10% in 2005, with 14.2 million ambulatory care visits, and the

incidence rate of SSTIs assessed in 2006 was 24.6 per 1000

ª 2012 The Authors JEADV 2 01 2 Jo ur nal o f t he E ur op ea n Ac ad em y o f D er ma to lo gy a nd V en er eo lo gy ª 2012 European Academy of Dermatology and Venereology

DOI: 10.1111/j.1468-3083.2011.04416.x JEADV


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person ⁄ year.9–11 The increased number of patients with immuno-

suppressed status (due to immunosuppressive drugs, cancer,

transplant surgery and HIV ⁄ AIDS), of invasive medical techniques

and of surgical wound infections, may have contributed to the

increasing incidence of severe SSTI over the last decades.3–5

Aetiopathogenesis and risk factors

Infections of the skin and underlying soft tissues can ensue from the

imbalance between the pathogenic power of a microorganism and

the immunological defenses of the host.12,13 Various physical and

chemical alterations of the skin can induce disruption of the cutane-

ous barrier, then predisposing to bacteria penetration, growth and

multiplication.12–15 Once the bacteria has penetrated the skin layers

and their virulence factors have overcame local host’s defenses, tis-

sue invasion occurs. Subsequent dissemination of microorganisms

in viable tissue triggers a series of systemic host responses.3,4,8,9 A

loss of integrity of the skin layers may be caused by lacerations, bite

or surgical wounds, scratches, burns or ulcers, along with inflamma-tory dermatoses and viral or fungal infections (e.g., tinea pedis can

predispose to leg cellulitits).16 Also variations of skin pH and tem-

perature,dryness and maceration should be considered.12–16

Risk factors for SSTI development can be classified as patient-

related, local or systemic, or environmental12–21: this classification

is reported in Table 1. Patient-related risk factors have been shown

to influence the course of the diseases and response to treatment,

but not to correlate with infection severity.2,3

Necrotizing soft tissue infections (NSTI) occurrence are

favoured by comorbidities, such as immunosuppression, cardio-

vascular or lung diseases and diabetes mellitus. Nevertheless, a nec-

rotizing infection can develop in immunocompetent people,

elicited by repetitive trauma (i.e. NSTI of the head and the neck) 22

or infections of urinary tract or perianal ⁄ retroperitoneal areas

(i.e. Fournier gangrene).1 In particular, about 20% of patients with

Fournier gangrene have no identifiable cause.1 The devitalised

tissue prevents cellular and humoral defence mechanisms from

reacting, by providing a growth medium for bacteria.1 Because of

its acidic pH, the necrotized tissue inactivates the antimicrobial

agents or prevents their delivering.7 NSTI may involve the fascia,

resulting in thrombosis of subcutaneous blood vessels and necrosis

of the underlying tissue.

Microbiology

The different bacterial pathogens which can colonize the skin and

determine SSTI can be divided into two categories: resident flora

and transient flora.12,13 Skin resident flora, also called ‘microflora’,

includes many bacterial species (Gram-positive and Gram-nega-tive) that colonize epidermis and follicular pores. Microflora is

mainly distributed on anatomical sites presenting high moisture

level (i.e. axillae, groin and intertriginous areas) and depends on

age and gender.12–14,23 Gram-positive aerobic bacteria, coagulase-

negative staphylococci, streptococci and micrococci typically

affects exposed skin areas, whereas Gram-positive anaerobic bacte-

ria are generally present on cutaneous pleats. Skin transient flora,

also called ‘contaminant flora’, includes Staphylococcus aureus,

which is mostly localized in the nose and other orificial areas,

and some Gram-negative bacteria of the Enterobacteriaceae and

Table 1 Risk factors for most common SSTIsPatient related-risk factors Environmental risk factors

Local risk factors Systemic risk factors

Anatomical alterations Alcoholism Animal bites wounds caused by rats, dogs, cats,

spiders and reptiles

Chickenpox Chronic renal failure Close contact with an SSTI infected person: family,

school or work exposure

Fungal infections

(i.e. tinea pedis and onychomycosis)

Cardiovascular diseases Exposure to hot tub, seawater or infected freshwater

Infected wounds

(surgical, traumatic, bite-related)

Cirrhosis Human bites wounds

Inflammatory dermatoses

(i.e. contact dermatitis, atopiceczema, psoriasis)

Diabetes melli tus Invasi ve medi cal techniques: l iposuction,

endoscopic procedures and cathethers insertion

Lymphatic obstruction Elderly age i.v. Or subcutaneous drug abuse

Poor skin hygiene HIV-infection Piercing apposition

Pressure sores Iatrogenic immunosuppression

Pre-existing SSTI (e.g. cellulitis) Malnutrition

Repetitive trauma Neuropathy

Urinary tract infection Nicotine addiction

Perianal or retroperitoneal infection Obesity and sedentary lifestyle

Vascular ulcers Peripheral vascular insufficiency

Solid and haematologic tumours

SSTI, Skin and soft tissue infection.

ª 2012 The Authors JEADV 2 01 2 J ou rna l o f t he E ur op ean A ca dem y o f De rm at ol og y a nd V ene re ol og y ª 2012 European Academy of Dermatology and Venereology

2 Tognetti et al.


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Pseudomonaceae groups.12,14,23 Skin microflora composition is

reported in Table 2.

As some bacteria can be pathogenic under specific circum-stances, it is often difficult to give a thorough assessment of SSTI’s

microbiology.2–4 Infections of traumatic or surgical wounds are

usually caused by a mixture of aerobic and anaerobic micro-

organisms. Moreover, Gram-negative bacteria are frequently pres-

ent in wound infections caused by animal bites, trauma or surgery

or exposed to infected water.1,2,12–15 Hence, post-traumatic SSTI

often result in polymicrobial infections. A scheme of the most

common causative bacteria identified in SSTI is provided in

Table 3, where they are listed along with their associated risk fac-

tors and the type of infection they induce.

The predominant pathogens of SSTI are Gram-positive bacteria,

firstly S. aureus and Streptococcus pyogenes, followed by Enterococ-

cus faecalis and Corynebacterium species.2–4 S. aureus is the mostcommon identified causative agent, accounting for more than

40% of all SSTI cases in 2003, and represents a common cause of

cellulitis, abscesses and wound infections.1,4,17–20 During the last

decades, S. aureus has increasingly become resistant to methicillin

(methicillin-resistant S. aureus, MRSA) and has spread worldwide

both in healthcare and community settings.1,7,24–26 An increasing

prevalence of community-acquired MRSA (CA-MRSA) has been

assessed in many intensive care units and emergency departments

both in the United States and Europe,27–30 and numerous studies

have identifiedCA-MRSA as the most important cause of SSTI.31–36

Moreover, some MRSA isolates, phenotypically similar to

CA-MRSA strains, are likely to determine healthcare-associated

MRSA (HA-MRSA) infections.37 A few cases can be attributed to

methicillin-sensitiveS. aureus (MSSA).3,38

Regarding streptococci, those mostly associated with SSTIs fall

into groups A and B. Group A streptococci (S. pyogenes) often

cause necrotizing fasciitis or ‘flesh-eating’ infections, whereas

group B streptococci (S. agalactiae) are frequently identified in

diabetic patients.1,2,4,39 Pseudomonas aeruginosa is often isolated

from lower extremity infections, particularly in cases with periph-

eral vascular disease or puncture wounds and in cases involving

hydrotherapy.

Classification

Several classification schemes have been proposed for SSTI, a lot

of them being complex and varied, and there is not an universally

accepted one yet.5,17,39

Every scheme organizes SSTI on the basisof a specific variable, such as aetiological agent, anatomical locali-

zation, skin extension (localized or spread infection), rate of pro-

gression (acute or chronic disease), clinical presentation (primary

and secondary infection) and severity (presence of comorbidi-

ties).1,4,18

According to the depth of the infection (Fig. 1), SSTI can be

classified into superficial infections, involving epidermis and ⁄ or

dermis, and deep infections, extending from deep dermis to sub-

cutaneous adipose tissue, muscular fascia and muscle.2,3,9,14

Skin and soft tissue infections can be further classified according

to the presence of complicating factors.6–8,17,18 This classification

scheme is the most used in clinical practice and generally coincideswith the previous one based on the depth of the infection, as

shown in Table 4. Indeed, uncomplicated infections (uSSTI) are

typically superficial, whereas complicated infections (cSSTI) usu-

ally have a deep involvement. As the description implies, cSSTI are

usually more severe, progress rapidly, involve deeper tissues such

as subcutaneous fat, deep fascia and muscle and possess a greater

risk of limb loss than uSSTI.39

Of particular concern is that, in most cases, an SSTI is uncom-

plicated at the time of initial presentation.6,7,18 Complicating fac-

tors such as diabetes mellitus and HIV-infection can easily

transform a mild infection into a life threatening condition, as

immunosuppression enables unusual or normally non-pathogenic

bacteria to cause infections or increase the likelihood of developingfulminant infections.4,7,40,41 Moreover, lesions located on the groin

area, on fingers, toes and head are more likely to be complicated.

Finally, otherwise uncomplicated SSTI occurring in specific ana-

tomical sites (e.g. rectal abscesses) and involving anaerobic or

Gram-negative organisms are considered complicated.7,40

Diagnosis

Although specific bacteria may cause a particular type of infection,

a considerable overlap in clinical presentations remains.2–4 SSTI

Table 2 Composition of skin resident and transient flora

Skin resident flora (microflora)

• Staphylococcus spp.

S. epidermidis: exposed skin areas, nose, cutaneous pleats,mouth, urethral orifice

S. saccharolyticus: upper trunk, forehead, forearms

S. saprophyticus: perineum

S. anginosus: cutaneous pleats

• Streptococcus spp.

S. mitis, S. salivarius, S. mutans: mouth

• Propionibacterium spp.

P. granulosum: sebaceous areas, follicular pores

P. acnes: sebaceous gland

• Corynebacterium spp.: high moisture level areas as cutaneouspleats, nose, mouth, urethral orifice and genital area

C. minutissimum: axillae, groin and intertriginous areas

C. xerosis: conjunctiva

Skin transient flora (contaminant flora)

Gram-positive species Gram-negative species

Staphylococcus spp: face,

scalp, nose and other

orificial areas ( S. aureus ),

exposed areas ( S. warneri )

Enterobacteriaceae: mouth ( E. coli )

Proteus spp: nose, conjunctiva,

exposed skin areas ( P. mirabilis )

Streptococcus pyogenes:

exposed skin areas, mouth

Corynebacteria: cutaneous

pleats ( C. minutissimum )

Pseudomonadaceae:

exposed skin areas ( P. aeruginosa )


Bacterial skin and soft tissue infections 3


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can present different features and severity according to their aetiol-ogy, severity and depth of the infection. An overview of most

common clinical presentation of SSTI is provided in Table 5.

Clinical history

To get an exact and early diagnosis, it is important to obtain an

extended clinical history including information about patient’s

travel, hobbies, trauma, animal bites and exposure to fresh or

saltwater. Medical history should always investigate the occurrence

of previous SSTI (i.e. recurrent cellulitis)11,16 and the immune

status of the patient.1,18 As many SSTI can be easily confused withother clinical syndromes, a careful history is essential to develop

an exact differential diagnosis.2

Physical examination

Diagnosis of most bacterial SSTI is based on clinical impression,

hence, a thorough physical examination is of basic importance in

making a correct clinical assessment and estimating the severity of

the infection.1 The minimum diagnostic criteria are a skin lesion

with the typical tetrad, that is erythema, oedema, warmth and pain

Table 3 Resident or transient bacteria species with their associated risk factors and SSTI

Causative bacteria Associated risk factors Type of infection

GRAM (+)

Clostridium spp. Cellulitis, gas gangrene, necrotizing fasciitis

Corynebacterium spp.C. minutissimum

C. xerosis

Human bites Erythrasma

Conjunctivitis

Enterococcus faecalis Immunosuppression Cellulitis, fasciitis, myositis, abscesses,

wound infections

Propionibacterium spp.

P. granulosum Severe acne

P. acnes Acne vulgaris

Staphylococcus spp.

S. aureus Neutropaenia, drug use, diabetic infections,

wounds, human bites

Bullous impetigo, furuncles, myositis, folliculitis,

purulent cellulitis

S. epidermidisS. aureus producing

exfoliative toxin

MRSA

human bites, diabetic foot infectionsImmunosuppression, diabetes,

neutropaenia, i.v. drug use

Wound infectionsSSSS

Abscesses, myositis, purulent cellulitis

S. saccharolyticus Cellulitis

S. saprophyticus Perianal abscesses

S. anginosus Hidradenitis suppurativa

Streptococcus spp.

Group A ( S. pyogenes ) Human bite, wounds, poor hygiene,

diabetes mellitus

Impetigo, ecthyma, necrotizing fasciitis

Groups B ( S. agalactiae ) Diabetes mellitus Erysipelas

Group C, D and G Stasis dermatitis, lymphoedema Wound infections, impetigo

GRAM (–)

Acinetobacter (dry areas) Burn wounds

Aeromonas hydrophila Wounds occurred i n i nfected water Severe cell ul iti s

Capnocytophaga canimorsus Dog bite wounds Cellulitis

Enterobacteriaceae spp. Hidradenitis suppurativa, cellulitis necrotizing fasciitis

Haemophilus influentiae Orbital cellulitesNocardia spp. Immunosuppression Abscesses

Pseudomonas aeruginosa Neutropenia, i.v. drug abuse, hydrotherapy

exposure (hot tub) surgical wounds

Cellulites, sepsis, hidradenitis suppurativa,

hot water folliculitis

Pasteurella multocida Cat bite wounds Cellulitis

Proteus spp. Folliculitis, proteus syndrome

Mycobacteria spp.

M. marinum(exposed skin areas)

Exposure to infected water Cellulitis, granulomas

M. mucogenicum

(wounds, urethral orifice)

Exposur e to peri toneal dialysi s Post-traumatic SSTI

Mycobacterium ulcerans Wounds Chronic cutaneous ulcers

SSTI, Skin and soft tissue infection; SSSS, Staphylococcal scalded skin syndrome.


4 Tognetti et al.


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or tenderness.2 Local signs that would suggest a severe SSTI

include erythema, oedema, bullae, haemorrhagic lesions, crepitus;then, when a NSTI has developed, we will observe dysfunction of

the affected area and skin discoloration (due to tissue ischaemia

from locally thrombosed vessels).1–4 Systemic symptoms such as

hypotension, tachycardia, hypothermia or fever and altered mental

status are suggestive of a more serious infection and the presence

of two or more of these signs is usually associated with worse

prognosis.1,8,40 A necrotizing infection should be suspected on

clinical grounds only and an early diagnosis is essential to protect

limbs and to save lives.7,12,18 Indeed, NSTI are generally fulminant

(they typically progress within 24–48 h) and often life-threatening,and they can have devastating consequences such as the destruc-

tion, with a widespread loss of tissue, of the underlying fat, the

fascia and the muscle.6,9,17,18 Clinical appearance of impetigo and

erysipelas infection is showed in Figs 2, 3 and 4.

Laboratory studies

Laboratory investigations including blood cultures, needle aspira-

tion and tissue swab with culture, can help confirm diagnostic

suspicion.1–4,12 Although the yield is very low in cSSTI, patients

Figure 1 Distribution of most common SSTIs by the depth of

the infection. (Modified from: Maleville J, Traibe A, Massicot P.

Infections bacté riennes communes. In: Dermatologie et Vènè-

reologie. Saurat JH, Grooshans E, Laugier P, Lachapelle JM,

eds; 2nd edn. Fribourg: Masson, 1990: 117–120.)

Figure 2 Bullous impetigo in a six-month-old baby. (Courtesy of

dra. S Berti)

Figure 3 Non-bullous impetigo in a five-month-old baby with

atopic dermatits. (Courtesy of dra. S Berti)

Figure 4 Erysipelas of the upper trunk spreading to the right

arm in a 62-year-old man. (Courtesy of dra. S Berti)




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who present with severe infection or sepsis syndrome should have

blood cultures obtained.18 Other blood tests may be helpful for

diagnosis, including abnormal findings, such as elevated white

blood cell count, anaemia and thrombocytopenia.39 Tissue speci-

mens obtained by biopsy or curettage are preferred to swabs of

superficial skin lesions or drainage, which may be contaminated

with normal skin flora. If there is no open wound, needle aspira-tion of fluid at the leading edge of infection may be helpful.

Cultures of the skin rarely yield a definitive pathogen in most

uSSTI. Otherwise, gram staining and culture specimens obtained

from complicated wounds usually help guide therapy, especially

when MRSA is a suspected pathogen.1,40

In patients with erysipelas, laboratory investigations reveal

elevation of erythrocyte sedimentation rate (ESR) and reactive

C protein (RCP) and leukocytosis with neutrophilia. Because of

the superficial nature of the infection, bacteriemia is often not

found, making blood culture unnecessary, whereas more useful

are the cultures from bullae fluid, which give positive responses in

5–40% cases.41,42

Diagnostic imaging

To obtain more information, SSTI sometimes require diagnostic

imaging. X-ray radiography (x-ray) and ultrasonography (US) are

used to explore subdermal involvement: x-ray can reveal air fluid

levels or air presence in the soft tissues, suggesting the need for

urgent debridment, whereas US detects abscess or fascial inflamma-

tion. X-ray is indicated in patients with diabetic foot infection to

adscertain the presenceof osteomyelitis.43 Computered tomography

(CT) and magnetic resonance imaging (MRI) give a more detailed

exploration of deeper soft-tissues, hence, they are particularly

beneficial in patients with rapidly progressive infections. CT is

helpful in identifying gas and fluid collections or foreign objects.

MRI can exactly reveal even little changes associated with NSTI and

it is superior to CT in detecting the muscular fascia involvement.

Hence, MRI is helpful when myositis or necrotizing fasciitis is

suspected.44

Concerning cellulitis diagnosis: X-ray and CT are useful tools

in complicated cases (e.g., when underlying osteomyelitis is

suspected), while they are usually not necessary in uncomplicated

cellulitis.11,20 Moreover, US can help detecting a subcutaneous

abscess consequent to cellulitis, and guiding tissue aspiration.

Otherwise, when cellulitis complicates a chronic lymphoedema

and the affected extremity rapidly increases in volume, gallium-

67-scintigraphy should be performed. Because CT and US are not

sufficient to differentiate between cellulitis and necrotizing fasciitis,

MRI is the investigation of choice for this specific differential diag-

nosis.12

When using contrast enhanced MRI, the main diagnosticcriterion for necrotizing fasciitis (NF) is the involvement of deep

muscular fascia: as a fluid collection occurred, the fascia results

thickened after contrast agent absorption.

Surgical exploration

Surgical exploration has a diagnostic and therapeutic role therefore

it should be not delayed once the disease is suspected.17,18 Surgical

exploration can provide the definitive identification of necrotizing

soft tissue infection, by revealing loss of fascial integrity, lack of

bleeding and ‘dishwater fluid’ in the surgical incision wound.12 No

investigations or preparations should delay operative intervention,

and early specialist surgical consultation for radical, repeateddebridement takes precedence. The ‘finger test’ represents a very

specific surgical exploration technique for NF diagnosis, and it is

performed as follows: the apparently healthy skin surrounding the

lesion is incised vertically up to the muscular fascia level, then the

index finger is introduced until it reaches the subcutis-muscular

fascia junction. If this junction is altered, with subcutis and fascia

detached instead of normally tight fitting, the test is positive.

Other diagnostic signs that can be observed are moderate bleeding

and pus ooze from the surgical incision (generally 2 cm deep),

that is consequently used for necrotic debridement and ⁄ or

drainage.45

TreatmentThe management of SSTI should conform to the aetiology, the epi-

demiology and the distribution by the depth of the infection.1,12,17

The choice between oral and parenteral therapy is generally sug-

gested by the severity of the infection. Parenteral therapy is pre-

ferred when the infection is rapidly spreading and comorbidities

(i.e. diabetes mellitus, neutropenia, heart failure, hepatic cirrhosis

and renal failure) are present. Moreover, parenteral therapy is cho-

sen, at least initially, to ensure rapid serum and tissue antimicrobial

levels.1,17,18

Table 4 Classification schemes based on the depth of the

infections and on the presence of complicating factors

Uncomplicated

infections

Complicated infections

Superficial

infections

Impetigo Erysipelas

Ecthyma Lymphangitis

Folliculitis Diabetic foot infections

Furunculosis Venous stasis ulcers

Carbuncles Infected pressure sores

Abscess Staphylococcal scalded

skin syndrome (SSSS)

Hidradenitis

supppurativa

Deep

infections

Cellulitis

Myositis

Necrotizing soft-tissue infections

Necrotising cellulitis

Necrotizing fasciitis

MyonecrosisPyomiositis

Phlegmon

Post-operative wounds infections

SSSS, staphylococcal scalded skin syndrome


6 Tognetti et al.


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Table 5 Most common clinical presentation of SSTI

SSTI Aetiopathogenesis Clinical features

Impetigo Patients: children aged 2–5 years (peak of

incidence), newborns, adults in economically

disadvantaged areas. Atopic dermatitis is an

important risk factorTransmission: person-to-person or via fomites. The

infection takes 10 days after skin colonization to

become clinically apparentLocalization: exposed body areas, orificial areas,

face, scalp and the back of the hands

(non-boullous impetigo); skin folds

(bullous impetigo)

Non-bullous impetigo (contagious impetigo): papules surrounded

by an area of erythema that become superficial vesicles and then

pustules which gradually enlarge and break down over a period

of 4–6 days to form characteristic thick, honey-coloured crusts.Multiple spread lesions (auto-inoculation). Caused by

S. pyogenes or S. aureus or both

Bullous impetigo: caused by toxin-producing S. aureus, is alocalized form of staphylococcal scalded skin syndrome. Vesicles

that rapidly evolve into flaccid bullae filled with clear yellow fluid.

Then the fluid becomes darker, more turbid and, sometimes,

purulent. The bullae can easily break leaving a thin

yellow-brownish crust with oozing result

Pathognomonic finding: ‘collarette’ of scale surrounding the blister

roof at the periphery of ruptured lesions

Ecthyma Patients: healthy people living in tropical areas

(or in tourists came back from these) and

immunosuppressed peoplePathogenesis: b-haemolytic Streptococci penetrates

the skin barrier through even minimal trauma

leading to an inflammation of the epidermic anddermal layers

A vesicle or pustule overlying an inflamed area of skin that

deepens into a dermal ulceration with overlying grey-yellow crust.

A shallow, punched-out ulceration appears when adherent crustis removed (which rapidly form a hard brown-blackish crust

covering the underlying ulceration). Then, lesion become multiple,

mostly localized on the legsEcthyma gangrenosum: necrotic skin ulcer which can pass as a

primary or secondary infection; secondary infection set in

typically in course of sepsis caused by P. aeruginosa, among

transplanted, neutropenic or diabetic patients.

Erysipelas Patients: childhood and adults aged 56–67

(two peaks of incidence)

Localization: lower extremities (adults); face (adults

and children), especially the butterfly area, with

oedematous and closed eyelids

Course of infection: short, infrequent relapses

Elevate fever with heat and shiver can precede skin

manifestations, consisting in intense, warm and aching erythema

and oedema that rapidly extend to the surrounding skin areas

with a well-demarcated erythematous border (‘step sign’). Flaccid

vesicles and bullae filled with purulent fluid may appear on

2 ⁄ 3 days after infection. Lymphangitis and regional lymph nodes

inflammation are often associated

Cellulitis Localization: extremities, face

Course of infection: long, frequent relapses, local

complications; recurrent cellulitits is usually caused

by Staphylococcus and Streptococcus spp.

Erythema, oedema, warmth and tenderness of the affected area,

tender lymphadenopathy and fever. The involved area is poorly

demarcatedS. aureus and Bacterioides spp.: cellulitis in diabetic patients

Pseudomonas spp. and Enterobacteriaceae: in hospitalizedpatients

Clostridium spp: in exposed fractures and penetrating trauma

Streptococcus spp. plus Haemophilus influentiae: orbital cellulitis,

occurring as a primary infection in healthy children aged under

5 years, or as secondary infection after sinusitis

Necrotizing

fasciitis (NF)

Patients: adults aged 50–60

Localization: extremities, abdomen, perineum

Pathogenesis: streptococcal haemolytic toxins

(streptolysin O and S) damageRisk factors: immunosuppression, chickenpox

Disproportion between ache and skin manifestation

NF type 1: polymicrobial infection, destroys the subcutaneous fat

and the muscular fascia, sometimes sparing the skin of the lower

extremities, perineum and abdominal wallNF type 2 (‘streptococcal gangrene’): caused by S. pyogenes

alone or associated with S. aureus, presents with severe local

pain and rapidly spreading erythema followed by necrosis.Fascial necrosis and myonecrosis may occur, with no gas

production

Myonecrosis

(MN)

Patients: traumatologic or oncologic

MN is an acute life-threatening infection that cancomplicates with many conditions, most common

being gangrene

Gas gangrene: slowly expanding ulceration confined to the

superficial fascia, determines necrosis of muscle, gas in thetissues and systemic toxicity; is caused by Clostridium spp.

Traumatic gangrene: becomes clinically apparent after an

incubation period that can range from 6 h to 4 days, presents

with acute severe pain on the wound area, where the skin is

initially pale-pink, then becomes bronze and finally purple-reddish

with bullae, oedema and crepitus. The patient rapidly develops

signs of sepsis as tachycardia, rapid breathing, mental confusionand fever

SSTI, skin and soft tissue infection; NF, necrotizing fasciitis; MN, myonecrosis.




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Uncomplicated SSTI

Superficial uSSTI typically respond to topical treatment, as they

generally can be managed with a topical antibiotic agent, heat

packs or incision and drainage, and, when necessary, with one

cycle of oral antibiotics. They seldom require oral antimicrobial

treatment and patient’s hospitalization.2,5,6,39

Complicated SSTI

Otherwise, deep cSSTI including infected ulcers, burns, major

abscesses, infections in diabetics and deep-space wound infections,

often require debridement and systemic antibiotic therapy along

with hospitalization.1,7–9 Moreover, hyperbaric oxygen is also

believed to enhance wound healing.46 Surgical incision followed

by drainage is a mainstay in the treatment of abscesses, as it

removes a large portion of the microbes causing the infection

along with the purulent material.39,40,47 Antibiotic therapy for

abscesses and wound infections is then recommended when there

is no response to incision and drainage (e.g. when abscesses arelocalized in areas difficult to drain) and in the following condi-

tions: >5 cm erythema around the wound, rapid progression,

associated cellulitis or phlebitis, signs of systemic infection (tem-

perature >38 C, tachycardia, leukocytosis), comorbidities, immu-

nosuppression.7,38–40,48 Systemic treatment for major abscesses

and complicated wound infections may require one therapy cycle

with b-lactam antibiotics, associated or not with clindamycin.49

The management of NSTI include an immediate surgical inter-

vention along with parenteral antibiotic therapy.17,18,39

Several antibiotic classes have been shown to be effective, alone

or in combination, in treating cSSTI: a treatment scheme is

provided in Table 6.

Empirical treatment

In many cases, an aetiologic diagnosis is difficult at presentation

time, thus most patients are initially treated empirically, pending

culture results. The empiric choice of antibiotic therapy must

cover the most likely organisms, thus it is important to consider

where and how the infection was acquired. An empirical antibiotic

treatment is also recommended when mixed flora polymicrobical

infection is suspected: for example, infections of the surgical site

after intra-abdominal procedures need extended spectrum penicil-

lins or carbapenems.1–3,7 Agents that provide coverage for both

S. aureus and S. pyogenes (e.g. penicillins, cephalexin, oxacillin)

are commonly used as empiric therapy for both uSSTI andcSSTI.1–3,7,48 Clindamycin or metronidazole can be added to a

regimen to cover for anaerobes, depending on the clinical situation

and spectrum of other agents being used.2,7 Beta-lactams (i.e.

amoxicillin ⁄ clavulanic, cefazolin) are indicated when Gram-

negative are likely to be involved (e.g. animal or human bites,

surgical infections and intravenous drug users).1–3,7 However,

broad-spectrum antibiotics (e.g. fluoroquinolones, cephalosporins)

should be reserved for severe or polymicrobial infections, or if

organisms are resistant to the more narrow spectrum agents.1,7

Once the causative agent and its susceptibility has been identified,

clinicians must switch to narrow-spectrum antibiotics.

Antibiotic resistance

Antibiotic resistance is a concern, given that many SSTIs are

caused by MRSA and multidrug resistance is common with both

CA-MRSA and HA-MRSA infections.5 HA-MRSA is generally sus-

ceptible to vancomycin, linezolid and trimethoprim-sulphameth-

oxazole (that will also cover Streptococcus spp. and Gram-negative

organisms), whereas CA-MRSA is usually sensitive to these anti-

microbial agents as well as to clyndamicin, quinolones and tetracy-

clines.1–3,7,48 Pending culture data, an empirical therapy in

hospitalized patients with cSSTI should be based on vancomycin

or linezolid or daptomycin or telavancin or clindamycin. For

empirical coverage of CA-MRSA in outpatients with SSTI (i.e.

purulent cellulitis) or in patients that do not respond to b-lactams,

the current IDSA guidelines recommend one of the following:

trimetoprim-sulphamethoxazole, doxycicline or minocycline andlinezolid.48 Tigecycline (a semi-synthetic glycylcycline), also has

broad spectrum activity against MRSA.7

Macrolide resistance among group A and group B streptococci

has also risen, but organisms have remained susceptible to penicil-

lins and cephalosporins.1,2,6 Management of non-purulent cellulitis

should include empirical coverage for S. pyogenes.48 Once S. pyoge-

nes is isolated in necrotizing fasciitis or myonecrosis, patients

should be treated high dose G penicillin and clyndamicin.49

Treatment duration

There are no guideline indications for duration of SSTI therapy. In

general, short-course therapy for uSSTI is the standard of care.Treatment duration for cSSTI is variable, and depends on patient

response (influenced by immunological status, comorbidities, age,

etc.), severity of infection and causative agent. On average, treat-

ment for most lesions requires 7–14 days of antibiotics therapy.1–3,7

Immunoglobulin therapy

The use of intravenous immunoglobulin (IVIG) is based on the

theoretical mechanism that IG can promote clearance of S. pyoge-

nes by the immune system, neutralize streptococcal superantigens

and act as an immunomodulatory agent, through the binding with

streptococcal derived exotoxin.50–52 Some positive results have

been reported in myonecrosis and necrotizing fasciitis caused by

S. pyogenes.50,51,53 However, all of these patients would requireadditional surgical debridement. Suggested IVIG dosage varies,

but most authors recommend 2 g ⁄ kg with an option of a second

dose, if necessary after 24 h.52 Side effects are seldom reported, but

the major contraindications include selective IgA deficiency or a

history of anaphylaxis with immunoglobulins.50,51

Treatment recommendations

Some medication-related factors, including route of delivery,

patient allergies, side effect profile, drug interaction potential,


8 Tognetti et al.


9/11

pharmacodynamics and cost, have to be considered when select-

ing an antimicrobial agent.2,6,47,54 To prevent recurrent SSTI, it

is recommended to maintain good personal hygiene and keepdraining wounds covered with clean, dry bandages.48 Finally, it

is essential to manage a significant underlying disease (e.g. diabe-

tes mellitus, peripheral vascular disease, ischaemic ulceration and

chronic lymphoedema) that may complicate the therapy

response.1,8,17,18

Antibiotic drugs

The following provides an overview of the antimicrobial agents

used to treat SSTIs.

b-Lactam antibiotics Several b-lactam antibiotics, such as semi-

synthetic penicillins (e.g., nafcillin, dicloxacillin) or first-generation

cephalosporins (e.g., cephalexin, cefazolin) are still effective againstMSSA and streptococci1–3,55 Although staphylococci are now

almost universally resistant, streptococci remain sensitive to peni-

cillin. Regarding MRSA, therapy with a b-lactam drug is generally

no longer sufficient.7,18,19,48

Clindamycin Clindamycin can suppress bacterial toxin produc-

tion, including streptococcal pyrogenic exotoxin A, PVL, and

staphylococcal enterotoxin B.1,3 Thus, it represents an important

adjunct to therapy. After exposure to clindamycin, however,

Table 6 Antimicrobial agents commonly used in patients with SSTIs

Antibiotics Usual dose Notes

Impetigo

Amoxicillin–clavulanic acid 500 mg p.o. q8–12 h qid for 10 days The therapy prevents post-streptococcal

glomerulonefritis

Erythromycin 250–500 mg p.o. q6 h Efficacy reduced in erythromycin-resistantS. aureus strains

Cefalexin 500 mg p.o. q12 h

Mupirocin (ointment) 1 application q12 h

Fusidic aci d (oi ntment) 1 appli cation q8 h

Erysipelas

Amoxicillin–clavulanic acid 1 g p.o. q8 h

Ampicillin–sulbactam 3 g i.v. q6 h

Cefalexin 500 mg p.o. q8 h

Cefazolin 1–1.5 g i.v. q8 h

Ceftriaxone 1–2 g i.v. 24 h

Erythromycin 250–500 mg p.o. qid for 10 days

Peni ci ll in G procai ne 0.6–1.2 mil li onU i .m. qid for 10 days

Cellulitis

Ampicillin–sulbactam 3 g i.v. q6 h

Ceftriaxone 1–2 g i.v. q24 h

Daptomycin 4–6 mg ⁄ kg i.v. q24 h

Ertapenem 1 g i.v. q24 h

Levofloxacin 750 mg i.v. or p.o. q24 h

Linezolid 600 mg p.o. or i.v. q12 h

Moxifloxacin 400 mg i.v. or p.o. q24 h

Oxacillin 2 g i.v. q4 h

Piperacillin–tazobactam 3.375 g i.v. q6 h First choice awaiting culture test results in

hospital-acquired SSTIs

Tygeciclin 100 mg i.v. · 1dose, then 50 mg i.v. q12 h

Vancomycin 15–20 mg ⁄ kg q12 h or 400 mg q24 h First choice awai ti ng culture test results i n

hospital-acquired SSTIsNecrotizing fasciitis and myonecrosis

Penicillin G 4 or 8–10 million U ⁄ day divided q4 h For community-acquired SSTIs

+ Clindamicyn 600 mg i.v. q6 h or 900 mg i.v. q8 h For community-acquired SSTIs

Oxacillin 2 g i.v. q4 h

+ Gentamycin 3 mg ⁄ kg ⁄ day i.v. divided q8 h If penicillin is controindicated

Metronidazole 15 mg ⁄ kg i.v. · 1dose, then 500 mg i.v. q6–8 h First choice awaiting culture test results

+ Imipenem ⁄ meropenem 500 mg i.v. q6 h or 1 g i.v. q12 h First choice awaiting culture test results

+ Vancomycin 1 g i.v. q12 h First choice awaiting culture test results

SSTIs, skin and soft tissue infections.




10/11

MRSA can become resistant via an inducible erm gene. Hence, it

is useful to perform a disc diffusion test, known as a D-test, to

determine if inducible resistance is present.56

Daptomycin Daptomycin is approved for the treatment of cSSTI

caused by susceptible strains of S. aureus (including MRSA),

S. pyogenes, S. agalactiae,Streptococcus dysgalactiae and vancomycin-

susceptible strains of E. faecalis, as 4–6 mg ⁄ kg intravenous

daily.39,57 The most common adverse events seen with dapto-

mycin include constipation, nausea, injection site reactions

and headache. An advantage of daptomycin is a once-daily

dosing, which is allowed by its long half-life and its prolonged

postantibiotic effect.

Ertapenem With a spectrum of activity similar to other carba-

penems, it is active against Gram-positive, Gram-negative and

anaerobic bacteria, such as S. aureus (MSSA), S. pyogenes, S. pneu-

moniae, E. coli, K. pneumoniae and Peptostreptococcus species;however, ertapenem lacks activity against P. aeruginosa.58 It is also

efficacious for the treatment of mixed anaerobic and aerobic cSS-

TIs.59 Ertapenem, 1 g intravenous daily, is approved for cSSTI due

to S. aureus (MSSA), S. pyogenes, E. coli and Peptostreptococcus

species. The most common adverse events include nausea, diar-

rhoea, infusion-related reactions and headache.

Linezolid It is active against many Gram-positive organisms

including S. aureus (MRSA and MSSA), coagulase-negative staph-

ylococci, vancomycin-susceptible and vancomycin-resistant E. fae-

cium and E. faecalis and streptococci (including penicillin-

resistant strains). Linezolid, 600 mg b.i.d. intravenous or oral, isapproved for the use of cSSTI without osteomyelitis caused by

S. pyogenes, S. agalactiae and MSSA or MRSA.60 Another advan-

tage of using linezolid is the ability to continue therapy as an out-

patient, thus decreasing the length of stay and overall cost.

Although it may be given as first-line therapy, linezolid is best

used for transitioning of care to outpatient status and as an alter-

native to standard therapy.

Tigecycline Many organisms that in the past had acquired resis-

tance to tetracycline are now susceptible to tigecycline. The spec-

trum of activity of tigecycline includes many clinically important

bacteria, such as Streptococcus species, MSSA and MRSA, Enterococ-

cus species, Enterobacteriaceae and anaerobic bacteria.61 It is gener-ally well tolerated, with mild to moderate nausea and vomiting

being the most commonly encountered adverse effects. Although

more studies are needed to test tigecycline against other commonly

used comparator regimens, tigecycline has shown promise as an

alternative for the initial empiric treatment of cSSTIs.

Conclusions

The emergence of antibiotic-resistance has been reported by

numerous studies in the field of bacterial SSTI. Nevertheless,

several recent antibiotics classes with narrow activity spectrum are

available at present time, but their side effect has to be considered.

Hence, a collaboration between dermatologists and infectivologists

can promote a rational approach to the aetiology and epidemiol-

ogy of SSTI and a more functional therapeutic approach, which

are necessary in clinical practice.

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