The onset of impetigo may occur at any age and is transmitted by autoinoculation, direct contact, or contaminated objects. It produces non-scarring epidermal lesions, well delimited, usually in exposed areas. It may be bullous or non-bullous. In the non-bullous form, caused by S. pyogenes, S. aureus (alone or in co-infection) and, occasionally, by group C and G streptococci, the lesions evolve from macula to papules, vesicles and pustules, which finally form a thick meliceric crust. In the bullous form, caused by S. aureus exfoliative toxins, the lesions evolve to vesicles and then to blisters with yellow more or less turbid and even purulent fluid, and finally form a fine crust. The main complication is local dissemination (cellulitis, lymphadenitis) or even systemic complications (pneumonia, osteoarthritis, sepsis).

In non-complicated mild cases, topical disinfectants can be used, mupirocin or fusidic acid every 8h, or retapamulin every 12h, for 5–7 days. If the lesions are extensive or with systemic symptoms, oral antibiotic therapy with amoxicillin–clavulanic acid, a first- or second-generation cephalosporin, or cloxacilin is recommended.5

Perianal bacterial dermatitis consists of an erythema around the anus caused by S. pyogenes or less frequently by S. aureus, alone or associated with S. pyogenes.6 Incidence peaks at 3–5 years of age, predominantly in males (70%), although prevalence is the same in both sexes if vulvovaginitis is included,8 which together with balanoposthitis constitute what is known as perineal disease.

It manifests as a non-elevated erythema, measuring 2–3cm, around the anus, with well-delimited edges, sometimes accompanied by pruritus, painful bowel movement, constipation, overflow incontinence, haematochezia and fissures.9 Boys may present with balanoposthitis and girls with vulvovaginitis with secretion and dysuria.10 There are usually no general symptoms, unlike cellulitis. In the acute phase (<6 weeks progression) the lesion is red, bright, humid and painful, and may present a whitish pseudo-membrane. Without treatment, lesions become chronic, with painful fissures, mucous secretion or psoriasis-like plates with yellowish periphery crust. When the cause is staphylococcus, there may be pustules and the erythema extends towards the adjacent skin.6

Patients or members of the household may have presented acute pharyngoamigdalitis or a skin infection7 in the previous 3 months or simultaneously with perianal dermatitis, or be pharyngeal or perianal carriers of S. pyogenes.7,8 Recurrence after treatment with penicillin or amoxicillin is frequent (up to 37%),11 especially if there are non-diagnosed cases in relatives.

It is believed that transmission is by contact, whether through autoinoculation (infection or pharyngeal or skin carrier) or interfamilial contagion, especially if bath water is shared10 or if a relative has presented acute pharingoamigdalitis or perianal dermatitis.7

Diagnosis is based on clinical analysis and confirmation is bacteriological. Samples from the perianal area must be gathered from all patients (A-II) and pharyngeal samples if there are symptoms (B-III), for a rapid antigen detection test for S. pyogenes (100% positive predictive value)7 or a culture. If the result of the test is negative, it is recommended to prepare a culture due to the possibility of false negatives or S. aureus as a cause of the condition (A-II). Potential cases in persons cohabiting with the patient should be investigated and a rapid diagnostic test or a culture for symptomatic patients (B-III) carried out, since this is a frequent cause of recurrences within the family.

Although good results have been reported with topical antibiotic therapy in monotherapy (B-II), the use of systemic antibiotics is recommended in all cases (A-II). If no rapid diagnostic test available or if it is positive, oral treatment with penicillin or amoxicillin for 10 days is recommended (B-II), which may be prolonged to 14–21 days based on clinical progress (C-III).10 If there is no response after one cycle of amoxicillin, or if the diagnostic test was negative, and while waiting for the result of the culture, amoxicillin–clavulanic acid may be used (C-III).

When choosing the initial antibiotic therapy, a familial history of streptococci or staphylococcus infection must be taken into consideration (C-II).

For recurrent infection cefuroxime is recommended11 for 7–10 days (C-II). The association of oral and topic treatment seems to decrease recurrences (A-II).6

The aetiological agent of hair follicle infection is S. aureus, followed by gram-negative bacilli. Predisposing factors include obesity, diabetes, hyperhidrosis, immunosuppression and atopical dermatitis.

Clinically, patients present with lesions on hair-bearing sites on the face, neck, armpits or glutei, ranging from a papule-vesicle with a erythematosus base (folliculitis, which affects the superficial hair follicle), to tender erythematosus nodules (furuncle, extending to the deep dermis), to warm, tender, erythematous plaques (carbuncle, affecting the surrounding subcutaneous cellular tissue).

The diagnosis is clinical and a microbiological study is only recommended for lesions that are atypical or respond poorly to treatment.12

Treatment is initially topical with mupirocin or fusidic acid, and in recurrent or extensive forms not responding to topical treatment, a combination of amoxicillin–clavulanic acid, clindamycin, cefadroxil, cefalexin or cefuroxime. For furuncles and carbuncles, it is recommended to apply local heat and assess the possibility of making an incision and surgical drainage.

This is defined as the inflammation of the lymphatic vessels of the subcutaneous tissue. The organisms most frequently involved are S. pyogenes, S. aureus and Pasteurella multocida (P. multocida) (the latter after an animal bite). There is usually systemic involvement, even before the distal oedema and linear cord to regional nodes are evident.

Empirical treatment in mild to moderate forms is amoxicillin–clavulanic acid or a first- or second-generation cephalosporin.

This is a superficial infection affecting the superior dermis, the subcutaneous cellular tissue and sometimes the lymphatic system, in most cases caused by S. pyogenes or streptococci of groups B, C or G.1,13–18

The triggering factors include abrasions, ulcers, intertriginous fungal infections of the feet, venous or lymphatic obstruction and chronic oedema. In neonates, the infection may originate in the umbilical cord and extend to the abdominal wall.

Onset is acute, characterised by an erythematosus plate with well-defined and slightly elevated edges. It is more frequent in lower limbs and face, and may be associated with regional lymphadenitis. There are usually general symptoms (fever, chills, discomfort), sometimes before cutaneous signs. Systemic complications are also possible (sepsis, streptococcal toxic-shock syndrome, endocarditis, etc.), although they are rare in otherwise healthy patients. When the infection is resolved it produces scaling and hyperpigmentation.

The diagnosis is clinical (A-II); haemocultures and cultures of skin biopsies or aspirates have a low yield.

Treatment consists of administration of oral penicillin or amoxicillin (A-III).1 Patients with lesions of more than 5cm or generally poor condition, infants and immunodepressed patients may require hospitalisation and parenteral treatment (A-II). The care of wounds and their predisposing factors are also important aspects of the treatment (A-II).

This is an acute infection affecting the dermis and subcutaneous cellular tissue. Predisposing factors include trauma, wounds and pre-existing infections. It appears as a warm, tender, poorly defined erythematous plaque, which sometimes causes phlyctena, petechial or local necrosis and may be accompanied by lymphadenitis and systemic symptoms.17

The main cause is S. aureus and S. pyogenes. Other less frequent microorganisms are Streptococcus agalactiae and gram-negative bacilli in neonates and enterobacteria in immunosuppressed patients.

Its location may provide an aetiological orientation: in the periauricular region and the sole of the foot with puncture wounds P. aeruginosa is more frequent, while in bites, P. multocida is common.

The diagnosis is clinical, but a microbiological study is recommended in the cases discussed in the section on general treatment. An ultrasound scan may be useful to differentiate cellulitis from non-fluctuant abscesses.

A systemic antibiotic treatment with good coverage against S. aureus and S. pyogenes must always be recommended. In mild cases and under strict surveillance, oral treatment with amoxicillin–clavulanic acid, cloxacilin, cefadroxil, cefalexin, cefuroxime or clindamycin may be considered.

Tables 2 and 3 summarise of other infectious conditions of clinical relevance, and Table 4 details the recommended dosage of the most widely used anti-infective drugs.

Most superinfections of the wounds produce clinical manifestations in the first 12h, generally erythema, pain or some other type of secretion through the wound. In human bites, fever above 38°C, abscess and lymphagitis are established criteria of superinfection, as well as the presence of at least 4 of the following: erythema extending more than 3cm from the edge of the wound, pain on palpation, inflammation, purulent drainage or leukocyte count of over 12,000cells/ml.

In superinfections of puncture wounds in the foot, clinical symptoms usually begin during the first 5–7 days if the causative agent is Staphylococcus, and after 7 days if it is produced by Pseudomonas. It is important to note the infection of bones and deep tissues.23,24

In addition to local cleaning and debridement, prophylactic antibiotic treatment is recommended only in the cases listed in Table 5 (A-I) and according to the guidelines in Table 6.

Standard prophylaxis should always be considered in the case of rabies, tetanus and other diseases transmitted through wounds.

In the United States, where up to 80% of staphylococci isolated in ambulatory patients are resistant to methicillin, Community-acquired methicillin- resistant S. aureus (CA-MRSA) represents a public health problem.25 In Spain, some studies in paediatric populations report a frequency of resistance to methicillin in S. aureus of 9–14.8%,26–29 but there are no studies at the national level. The frequency in neonates was investigated in the Community of Madrid30 from 2007 to 2009, and a prevalence of 3.3% was reported.

The role of methicillin resistance as an indicator of seriousness is starting to be questioned, and more relevance is being given to other virus factors, such as Panton–Valentine leukocidin (PVL),32 although most strains of PVL are also resistant to methicillin.31,33 Nosocomial MRSA is associated with certain multidrug-resistant genotypes, but this is not the case in CA-MRSA, which only rarely presents resistance to macrolides and lincosamides.27,31,33

Although they may cause pneumonia, sepsis and osteoarthritis, most CA-MRSA infections are limited to the skin and soft tissues.

There are no clinical criteria to differentiate skin infections produced by methicillin-sensitive S. aureus from those caused by MRSA,34 although in the latter, therapeutic failure and formation of abscesses and necrosis with black superficial crust similar to a spider bite are more frequent.3 Given the implications for treatment, any non-fluctuant lesions suggestive of abscesses detected during physical examination should be studied under ultrasound examination (C-III). If possible, it is recommended to take samples for culture, determination of LPV and genetic profiling.

The current low incidence of AC-MRSA in the paediatric population does not justify amending empirical antibiotic therapy guidelines. However, under certain circumstances changes must be considered, such as extensive cellulitis, abscesses or necrosis, the presence of recurrent abscesses in children or in other members of their household, poor response to conventional treatment, patients living in highly endemic areas (Asia, America or Eastern Europe) or living with known carriers (C-III).

In minor, non-suppurating infections (impetigo, mild superinfection of wounds, etc.), topical treatment with mupirocin is usually sufficient35 (A-III). In skin abscesses, incision and early surgical drainage are essential. This has been shown to be effective with otherwise healthy patients with non-complicated infections to achieve full healing with no adjuvant antibiotic therapy35–38 (A-II). Systemic antibiotic treatment is recommended in other localised infections, as adjuvant if drainage has been incomplete, if there is intense local infection (abscesses of more than 5cm) and in patients under 2 years of age or with other risk factors (immunosuppression, moderate-serious atopical dermatitis, etc.) (A-III).

The drug of first choice is oral clindamycin, which also inhibits the production of LPV35 (A-II). Trimethoprim–sulfamethoxazole is an effective alternative in areas where there is high resistance to clindamycin (A-II), in the event of intolerance, or when capsules are not suitable for the patient. Linezolid must be avoided in mild-moderate infections, because it is expensive, has potential adverse effects and leads to development of resistances. The presence of LPV does not require changes in the therapeutic approach although it is associated with a greater need for incision and surgical drainage.3,31

If empirical treatment is initiated with any of these drugs, changing to a betalactamic is recommended as soon as its sensitivity can be proved.

It is estimated that 19.3% of the Spanish population is colonised by S. aureus, of which only 1.3% are MRSA.39 The most frequent areas of colonisation are the nostrils, but axilla inguinal and intestinal carriers have also been described.40 Considering the low incidence of MRSA in paediatrics, the systematic study of persons living with the patient is not recommended, and should be limited to outbreaks in limited communities (families, institutions, etc.) and recurrent infections3 (C-III). In these cases, decolonisation in the child and carriers living in their household should consist of nasal mupirocin every 12h and washing the body and hair with 4% chlorhexidine soap for 5–10 days (C-III). In the event of therapeutic failure with mupirocin, topical fusidic acid every 12h along with oral trimethoprim–sulfamethoxazole for 7 days should be used3,35 (C-III).

The main transmission pathway seems to be intimate skin-to-skin contact.40 General prevention measures consist in minimising the risk of skin trauma (use of protection during sports activities, etc.) (C-III), keeping wounds clean and covered (A-III), frequent hand washing and body hygiene (A-III), avoiding sharing towels and clothes (A-III) and proper disposal of contaminated objects35,40 (C-III).