Skin infections are usually obvious, with a combination of redness, swelling, heat and pain. Superficial infections may have exudates or puss. With more deep-seated infection, temperature and systemic upset with flu like symptoms may occur. Treatment will depend on the severity (depth) of infection, the presumed organism and the patient’s immune competency.

Skin infections usually result from an imbalance between the pathogenic power of micro-organisms and the immunological defences of a patient. Various physical and clinical alterations to the skin can disrupt the skin barrier function, predisposing to bacterial penetration. Once the bacteria has penetrated the skin’s defensive layer and their virulence factors have overcome local host defences, tissue invasion and infection occurs. Loss of the skin barrier may be caused by lacerations, bites, surgical wounds, scratching, burns, ulcers, inflammatory dermatoses (eczema/dermatitis), viral or fungal infections. Skin infections located on the groin, fingers, toes and the head are more likely to become complicated.

Most bacteria that cause skin infections are ones that colonise the skin or mucous membranes. Gram positive bacteria are the most frequently isolated, with a prominence of staphylococcus aureus and streptococcus pyogenes (see Table 1). The particular type of skin infection that these organisms cause will largely be determined by how they invaded the skin barrier and the depth of invasion. 

Group B streptococcus (strep agalactiae) are frequently identified in patients with diabetes. Pseudomonas aeruginosa is often isolated from lower extremity infections, particularly in cases of peripheral vascular disease or puncture wounds and in cases involving hydrotherapy (eg. jacuzzis).

Bites

Gram negative organisms are more likely in animal or human bites, surgical infections and IV drug users, and usually require a beta-lactimase antibiotic such as a amoxicillin/clavulanic acid or clarithromycin if allergic to penicillin. Good surgical toilet under local anaesthetic is most important for bites. With animal bites, consider tetanus risk and for human bites consider HIV, and hepatitis B and C risk.

Although specific bacteria may cause a particular type of skin infection, considerable overlap in clinical presentations remain. Most patients are treated empirically at presentation, pending culture results if taken. The empiric choice of antibiotic treatment must cover the most likely organism. Thus it is important to consider where and how the infection was acquired and the correct clinical diagnosis. Uncomplicated localised superficial skin infection in an immunocompetent host will often respond to topical antibiotics such as fusidic acid. Deeper and more extensive infections, particularly in patients who are immunocompromised, will need systemic treatment either orally for moderate infections or intravenously for severe infections. Once the causative agent and its susceptibility has been identified, treatment should be switched to a narrow spectrum antibiotic. Swabs for culture and sensitivity are not always necessary for skin infections but should be considered in more severe infections, recurrent infections or where resistant organisms are suspected (eg. nursing home patients and patients with chronic wounds in the community).

Impetigo

Staphylococcus aureus is most commonly known for causing the honey-coloured, crusty lesions seen in impetigo (‘aureus’ is Latin for gold) (see Picture 1). This is most common in preschool children and newborns; it can be quite infectious, spreading to siblings and classmates. It most commonly involves the face and exposed sites. The children are usually otherwise healthy. It usually starts with some small vesicles that rupture and develop a golden crust. This can spread locally after a few days. Satellite lesions occur around the original site and sometimes on distant sites. It can sometimes be confused with a herpes simplex and ringworm, as lesions are sometimes vesicular, discoid or annular. Sometimes a blister develops (bullous impetigo) most commonly in the skin folds; when this occurs it is more likely as a result of toxin producing staphylococcus aureus and is a localised form of staphylococcal scalded skin syndrome. 

Treatment of milder cases may respond to topical fusidic acid. However, resistance is becoming increasingly more common. Fortunately, resistance is not stable and will usually fade if the drug is stopped. Therefore, fusidic acid should be used for short courses of not more than two weeks, and courses should not be repeated for at least six to 12 weeks if possible. For more severe or widespread infection, oral flucloxacillin (or clarithromycin if allergic to penicillin) for at least seven to 14 days should be added to topical fusidic acid. Patients and carers should be instructed about careful handwashing and should be advised to use their own towels and facecloths to prevent cross infection. 

Folliculitis

Folliculitis is usually caused by staphylococci when the bacteria penetrate down through the hair shaft to cause a deep-seated infection in the hair follicles. This obviously occurs only in the hairy parts of the body, such as the beard area, scalp or on the trunk in men or in the legs or groin in women. Close inspection with good light and a magnifying lens will show multiple small areas of erythema around the hair shafts, which sometimes progress onto small papules and pustules. Like impetigo, minor cases might respond to topical fusidic acid but more deep-seated or wide-spread infection will require a long course of oral flucloxacillin for two to six weeks. For resistant cases, nasal swabs should be taken to rule out nasal carriage as a focus for reinfection. This can be treated with topical nasal antibiotics such as Naseptin or Bactroban. 

Folliculitis can sometimes be due to traumas, such as from shaving or waxing. In addition, applications of tar, oils, or greasy ointments can also lead to folliculitis. When prescribing greasy moisturisers, such as emulsifying ointment, doctors should always instruct the patient or carer to rub the ointments downwards, as rubbing ointments upwards can irritate hair follicles and lead to folliculitis. 

Folliculitis can sometimes be caused by gram negative organisms such as pseudomonas or E coli, especially in acne patients taking oral tetracyclines. They usually respond to stopping the tetracyclines and giving ampicillin/clavulanic or trimethoprim or isotretinoin.

Swimming pool or jacuzzi folliculitis is also due to gram negative organisms such as pseudomonas and may resolve spontaneously by staying out of the water or to ciprofloxacin. Yeasts such as pityrosporum ovale can cause a low grade folliculitis on the trunk in young adults and it responds to topical or oral anti-yeast medications such as ketaconazole. Ingrown hairs in the neck in men can cause a folliculitis-like reaction (pseudofolliculitis barbae), which can be managed by physically removing the ingrowing hairs or by growing a beard. 

Boils (carbuncles and furuncles)

These can be considered a localised severe folliculitis, which again is most commonly due to staphylococcus aureus. The point of entry again is usually through the hair follicle, but the infection spreads locally to cause a painful, tender boil, which can sometimes progress on to a skin abscess. All patients with boils or abscesses should be checked for diabetes. Since this is a deep-seated infection, topical treatments are usually ineffective and treatment involves giving high dose oral or systemic flucloxacillin (oral clarithromycin if the patient is penicillin allergic) for at least seven to 14 days. If an abscess is fluctuant and pointing, it should be incised and drained, either under local or general anaesthetic. Swabs should be taken to identify the responsible organism, and its sensitivity to antibiotics. 

Secondary infection of eczema

The most common cause of an acute exacerbation of atopic eczema, particularly in children, is secondary infection, usually by staphylococcus aureus. Most cases need systemic antibiotics, usually with flucloxacillin (or clarithromycin if penicillin allergic) for at least seven to 14 days in the maximum dose allowed for the particular age group. 

MRSA 

Methicillin resistant staphylococcus aureus (MRSA) was considered a hospital infection until a few years ago. However, it is now commonly found in the community. Many patients in nursing homes and patients in the community with chronic wounds, such as leg ulcers, can be infected by MRSA. MRSA is not more virulent than ordinary staph aureus but when it causes an infection it is harder to treat because of its resistance to multiple drugs. Many patients in nursing homes and those discharged from hospitals may be carriers of the MRSA strain without having a clinical infection. With such patients, simple hygienic precautions, such as wearing gloves and hand washing, may be all that is required.

Leg ulcers

Patients with chronic leg ulcers should have their wounds swabbed to identify if they are carrying MRSA. In some cases the MRSA may be colonising the wound and may not be responsible for any obvious underlying clinical infection. Therefore, even in the presence of MRSA, good wound care with topical antiseptics, elevation and compression when indicated, should help to heal the wound. If there is obvious clinical infection, such as pain, erythema, heat and swelling, the patient may respond to high dose oral or systemic flucloxacillin, even though the wound is colonised with MRSA. However, it is important to identify MRSA in the wound to protect healthcare workers, other residents in a nursing home and family members from getting contaminated and spreading the MRSA to other people. 

Streptococci infections

Erysipelas

Erysipelas is a deeper infection than impetigo, usually affecting the superficial dermis (see Picture 2). It usually develops suddenly with redness, heat, swelling and tenderness in the affected area. It spreads out rapidly from the original site, which is often a small area of broken skin as a result of a patch of localised eczema. The patient often feels feverish and has flu-like symptoms and perhaps a low-grade temperature. The rash usually has a well demarked, erythematous, palpable border, and the face and lower legs are the most common sites infected. Vesicles and bullae may appear after a few days. Lymphangitis and regional lymph node enlargement are sometimes associated. It is most commonly caused by beta haemolytic streptococcus and responds to high dose oral or systemic penicillin (benzylpenicillin IM or IV or oral penicillin V in high doses). Erysipelas-like cellulitis can sometimes be caused by staphylococcus aureus and so in severe infections it may be necessary to combine penicillin V and flucloxacillin orally in high doses, or admit the patient for systemic antibiotics. Rest and elevation are important, particularly if the lower limb is involved. 

Cellulitis

This causes a similar but deeper and more diffuse infection of the lower dermis than erysipelas. Again the patient usually presents with a painful, red, hot and swollen rash, which can spread rapidly. The patient may have a low-grade fever and flu-like symptoms. It often involves the lower leg; a leg ulcer or a break in the skin from a fungal infection of the feet can be the portal of entry for the streptococcus. Treatment is the same as erysipelas with high dose penicillin V, adding flucloxacillin for more severe infections (clarithromycin can be used if penicillin allergic).