Skin and soft tissue infections

Skin and soft tissue infections

 

Bacterial skin and soft tissue infections

Bites and clenched fist injuries

 

Bites and clenched fist injuries often become infected. The organisms involved in human bites and clenched fist injuries are Staphylococcus aureus, Eikenella corrodens, Streptococcus species and beta-lactamase-producing anaerobic bacteria. The organisms involved in animal bites are Pasteurella species, Staphylococcus aureus, Capnocytophaga canimorsus, Streptococcus species and anaerobes. Cat bites have a higher incidence of infection than dog bites. In all cases a patient's tetanus immunisation status must be assessed. Postexposure rabies or Lyssavirus prophylaxis may need to be considered, eg bat bite.

 

The recommended management for human and animal bites and clenched fist injuries is thorough cleaning, debridement, irrigation, elevation and immobilisation.

 

Low risk

Antibiotics may not be necessary for mild wounds not involving tendons or joints that can be adequately debrided and irrigated and that are seen within 8 hours.

 

High risk

Wounds having a high risk of infection include:

·            wounds with delayed presentation (>=8 hours)

·            puncture wounds unable to be debrided adequately

·            wounds on hands, feet or face

·            wounds with underlying structures involved, eg bones, joints, tendons

·            wounds in the immunocompromised patient.

Presumptive therapy is necessary, use

amoxycillin+clavulanate (child: 22.5+3.2 mg/kg up to) 875+125 mg orally, 12-hourly for 5 days.

 

If the commencement of the above is likely to be delayed, give

procaine penicillin (child: 50 mg/kg up to) 1.5 g IM, as 1 dose, followed by amoxycillin+clavulanate as above.

 

For patients hypersensitive to penicillin, see Established infection below.

 

If obviously infected, a wound swab should be taken. Delaying primary wound closure should also be considered.

For severe and penetrating injuries, especially those involving joints and/or tendons, use initially

	metronidazole (child: 10 mg/kg up to) 400 mg orally, 12-hourly for 5 to 10 days
	PLUS EITHER
1	cefotaxime (child: 50 mg/kg up to) 1 g IV, 8-hourly for 5 to 10 days
	OR
1	ceftriaxone (child: 50 mg/kg up to) 1 g IV, daily for 5 to 10 days.

 

Alternatively, use

1	piperacillin+tazobactam (child: 100+12.5 mg/kg up to) 4+0.5 g IV, 8-hourly for 5 to 10 days
	OR
1	ticarcillin+clavulanate (child: 50+1.7 mg/kg up to) 3+0.1 g IV, 6-hourly for 5 to 10 days.

 

For patients with immediate penicillin hypersensitivity, use

	metronidazole (child: 10 mg/kg up to) 400 mg orally, 12-hourly for 5 to 10 days
	PLUS EITHER
1	doxycycline (child >8 years: 2 mg/kg up to) 100 mg orally, daily for 5 to 10 days
	OR
2	trimethoprim+sulfamethoxazole (child: 4+20 mg/kg up to) 160+800 mg orally, 12-hourly for 5 to 10 days
	OR
3	ciprofloxacin (child: 10 mg/kg up to) 500 mg orally, 12-hourly for 5 to 10 days.

 

Treatment should be modified according to Gram stain and culture.

If osteomyelitis is suspected, treatment duration should be extended.

Boils, carbuncles and folliculitis

 

In this topic:

Boils and carbuncles

Recurrent staphylococcal skin infection including boils

Folliculitis

Boils and carbuncles

 

The causative organism is generally Staphylococcus aureus, occasionally in association with Streptococcus pyogenes. If the lesions are small or few in number they may be managed by hot compresses with drainage if appropriate. If lesions are extensive or cause systemic symptoms, use

di/flucloxacillin (child: 25 mg/kg up to) 500 mg orally, 6-hourly for 5 to 7 days.

 

For patients hypersensitive to penicillin (excluding immediate hypersensitivity), use

cephalexin (child: 25 mg/kg up to) 500 mg orally, 6-hourly for 5 to 7 days.

 

For patients with immediate penicillin hypersensitivity, use

clindamycin (child: 10 mg/kg up to) 450 mg orally, 8-hourly for 5 to 7 days.

 

In areas where non–multiresistant MRSA strains are prevalent, a swab should be taken before initiating therapy. If this organism is isolated or strongly suspected, treatment should be guided by susceptibility testing. These strains are generally susceptible to clindamycin or trimethoprim+sulfamethoxazole as well as the drugs normally chosen for the multiresistant strains (vancomycin, rifampicin, sodium fusidate, quinupristin/dalfopristin and linezolid).

 

Recurrent staphylococcal skin infection including boils

 

Treat the acute lesions as described in boils and carbuncles. Once all lesions are healed, chronic carriage of pathogenic Staphylococcus aureus may be documented with nasal and or perineal swabs. Use

	mupirocin 2% nasal ointment intranasally, twice daily for 7 days
	PLUS
	wash daily with an antiseptic wash containing triclosan 1%, paying particular attention to hair-bearing areas, and wash clothes, towels and sheets in hot water. These measures should be continued for 4 weeks.

 

The whole family and close contacts may need similar treatment if these measures fail.

If lesions continue to recur despite good compliance, repeat the above regimen together with

	rifampicin (child: 7.5 mg/kg up to) 300 mg orally, 12-hourly for 7 days
	PLUS
	di/flucloxacillin (child: 12.5 mg/kg up to) 250 mg orally, 6-hourly for 7 days.

 

For MRSA use

fusidate sodium (child: 12 mg/kg up to) 500 mg orally, 12-hourly instead of di/flucloxacillin.

 

Successful eradication is unlikely if the strains are resistant to mupirocin or any of the antibiotics prescribed. Seek expert advice.

Folliculitis

 

This common condition presents with mildly itchy pustules on an erythematous base. It may affect any part of the hair-bearing skin in adults and children. It is often a problem in hot weather, and often occurs in macerated areas, including under wet dressings. The patient is often a chronic carrier of Staphylococcus aureus. Folliculitis is most often due to Staphylococcus aureus infection, but this should be confirmed by culture as Pseudomonas aeruginosa, Pityrosporum species, dermatophytes and herpes simplex virus may also cause folliculitis. Folliculitis may also be ‘sterile’, although in this situation Staphylococcus epidermidis is usually cultured. A variant known as eosinophilic folliculitis occurs in human immunodeficiency virus (HIV) disease but is not infective.

Determine the causative organism, if any, by culture of a swab. Viral cultures may be indicated if the lesions suggest herpes simplex infection.

For staphylococcal infection, treat as for impetigo with a staphylococcal carrier state, since this is usually the case. For pseudomonal folliculitis, which is due to contact with contaminated water, identify the source (eg hot water tank, spa) and cease contact with it until the water supply has been treated. Sterile folliculitis is usually due to maceration, particularly in obesity, heavy sweating, contact with occlusive substances such as oils, shaving and waxing. Attention to underlying problems is appropriate in these cases, but antiseptic washes, eg triclosan 1%, chlorhexidine 2%, are also required to diminish the overgrowth of skin flora in these cases.

Cellulitis and erysipelas

 

In this topic:

Introduction

Mild early cellulitis and erysipelas

Severe cellulitis

 

Cellulitis presents with spreading, tender erythema, associated with fever and systemic toxicity. It may be associated with lymphangitis and lymphadenopathy. As the rash progresses, blistering may occur. The causative organism is almost always Streptococcus pyogenes, but Staphylococcus aureus is important with wound-associated cellulitis. Now that Hib vaccination is widespread, Haemophilus influenzae is a rare cause of cellulitis. In immunosuppressed patients, a wide variety of organisms including Gram-negative bacteria, fungi and mycobacteria may also be responsible.

Cellulitis in children is often periorbital. Cellulitis in adults most often affects the lower legs. It is often unilateral, at least initially and there is usually an underlying abnormality, such as tinea pedis, fissured dermatitis, lymphoedema, lymphatic malformation, previous deep vein thrombosis, vascular surgery or radiotherapy. A search for a portal of entry should be made to prevent possible recurrences. Recurrent cellulitis may result in lymphoedema, which in itself worsens the situation. Cellulitis may also complicate wounds, eg cuts, abrasions, insect bites or scabies.

Erysipelas is a localised form of cellulitis involving the face, presenting with sudden onset of butterfly erythema associated with fever, and constitutional upset. There may be an underlying facial sinus or dental infection. It is almost always caused by Streptococcus pyogenes. Dental examination and imaging of sinuses is recommended.

 

If Streptococcus pyogenes is suspected, use

1	procaine penicillin (child: 50 mg/kg up to) 1.5 g IM, daily
	OR
2	phenoxymethylpenicillin (child: 10 mg/kg up to) 500 mg orally, 6-hourly.

 

If Staphylococcus aureus is suspected, (and also covering Streptococcus pyogenes) use

di/flucloxacillin (child: 25 mg/kg up to) 500 mg orally, 6-hourly.

 

For patients hypersensitive to penicillin, use

clindamycin (child: 10 mg/kg up to) 450 mg orally, 8-hourly.

 

To treat infection with either streptococci or staphylococci, use

di/flucloxacillin (child: 50 mg/kg up to) 2 g IV, 6-hourly.

 

For patients hypersensitive to penicillin (excluding immediate hypersensitivity), use

1	cephalothin (child: 50 mg/kg up to) 2 g IV, 6-hourly
	OR
1	cephazolin (child: 25 mg/kg up to) 1 g IV, 8-hourly.

 

For patients with immediate penicillin hypersensitivity, use

1	clindamycin (child: 10 mg/kg up to) 450 mg IV, 8-hourly THEN clindamycin (child: 10 mg/kg up to) 450 mg orally, 8-hourly
	OR
1	lincomycin (child: 15 mg/kg up to) 600 mg IV, 8-hourly THEN clindamycin (child: 10 mg/kg up to) 450 mg orally, 8-hourly
	OR
2	vancomycin (child: 20 mg/kg up to) 1 g IV, 12-hourly.

 

Intravenous home-based therapy may be used in suitable patients.

	cephazolin 2 g IV, 12-hourly for 4 to 7 days
	OR THE COMBINATION OF
	cephazolin 2 g IV, daily for 4 to 7 days
	PLUS
	probenecid 1 g orally, daily for 4 to 7 days.

 

For paediatric doses, consult an outpatient IV therapy service experienced with children.

Ceftriaxone has a broad spectrum of activity which is not required for routine cellulitis where streptococci and staphylococci are the likely pathogens.

 

Clostridial infection

 

This varies from mild cellulitis to overwhelming myonecrosis (gas gangrene). The basis of treatment is surgical debridement of necrotic tissue and antibiotic therapy. In severe infections, hyperbaric oxygen is an important adjunct if available. The diagnosis of gas gangrene is a clinical one. Neither the isolation of clostridia nor the presence of gas in tissue is diagnostic of the condition.

For cellulitis without myonecrosis, use

benzylpenicillin (child: 30 mg/kg up to) 1.2 g IV, 4-hourly.

 

For myositis/myonecrosis (gas gangrene), use

benzylpenicillin (child: 60 mg/kg up to) 2.4 g IV, 4-hourly.

 

For patients with immediate penicillin hypersensitivity, use

metronidazole (child: 12.5 mg/kg up to) 500 mg IV, 8-hourly.

 

Other measures, for example resuscitation, surgery and hyperbaric oxygen, are vitally important and require expert advice.

Compound fractures

 

Prophylaxis or early treatment directed particularly against Staphylococcus aureus should be given. The patient's immune status to tetanus should be assessed.

1	di/flucloxacillin (child: 50 mg/kg up to) 2 g IV, 6-hourly
	OR
2	cephalothin (child: 50 mg/kg up to) 2 g IV, 6-hourly
	OR
2	cephazolin (child: 25 mg/kg up to) 1 g IV, 8-hourly
	OR
3	clindamycin (child: 10 mg/kg up to) 450 mg IV, 8-hourly
	OR
3	lincomycin (child: 15 mg/kg up to) 600 mg IV, 8-hourly.

 

Duration of prophylaxis should be for 1 to 3 days.

If wound soiling or tissue damage is severe and/or devitalised tissue is present, add

1	gentamicin (child <10 years: 7.5 mg/kg; >=10 years: 6 mg/kg) 4 to 6 mg/kg IV, daily (adjust dose for renal function, see Monitoring of aminoglycosides)
	OR
2	ciprofloxacin (child: 5 mg/kg up to) 200 mg IV, 8-hourly THEN (child: 10 mg/kg up to)500 mg orally, 12-hourly.

 

If clindamycin or lincomycin are not used as the primary choice, then for clostridial species add either

	benzylpenicillin (child: 30 mg/kg up to) 1.2 g IV, 6-hourly
	OR
	metronidazole (child: 12.5 mg/kg up to) 500 mg IV, 12-hourly.

 

Alternatively, use

1	piperacillin+tazobactam (child: 100+12.5 mg/kg up to) 4+0.5 g IV, 8-hourly
	OR
1	ticarcillin+clavulanate (child: 50+1.7 mg/kg up to) 3+0.1 g IV, 6-hourly.

 

Duration of treatment should be for 5 to 7 days, or longer if bone infection is established, see Bone and joint infections.

Diabetic foot infections

 

Diabetic foot infections should always be regarded as serious, and treated vigorously. Culture may be unhelpful because of polymicrobial infections and superficial colonisation but may guide therapy particularly if Staphylococcus aureus or multiresistant pathogens are found. Anaerobic organisms are almost always involved, often with mixed Gram-positive and Gram-negative aerobic organisms. Surgical debridement is often necessary and antibiotic therapy should be effective against the mixed aerobic and anaerobic organisms frequently responsible. Underlying osteomyelitis should be considered. Vascular supply should be assessed.

For mild to moderate infection with no evidence of osteomyelitis, use

	metronidazole 400 mg orally, 12-hourly
	PLUS
	cephalexin 500 mg orally, 6-hourly.

 

Alternatively, use

amoxycillin+clavulanate 875+125 mg orally, 12-hourly.

 

For patients with penicillin hypersensitivity, use

	ciprofloxacin 500 mg orally, 12-hourly
	PLUS
	clindamycin 600 mg IV, 8-hourly.

 

For severe potentially limb-threatening infection, use

1	piperacillin+tazobactam 4+0.5 g IV, 8-hourly
	OR
1	ticarcillin+clavulanate 3+0.1 g IV, 6-hourly.

 

Alternatively, and for patients with penicillin hypersensitivity, use

	ciprofloxacin 750 mg orally, 12-hourly
	PLUS EITHER
1	clindamycin 900 mg IV, 8-hourly
	OR
1	lincomycin 900 mg IV, 8-hourly.

 

For patients with evidence of osteomyelitis, see Osteomyelitis.

For severe potentially life-threatening infections, see Severe sepsis

Depending on the organisms subsequently isolated from deep tissue specimens, other antibiotic combinations may be indicated. The duration of treatment will depend upon the response.

For further information on the management of diabetes see Diabetes: diagnosis and management plan, Diabetes: specific management, Diabetes: complications, or wound care see Diabetic foot ulcers.

Impetigo

This condition is caused by Staphylococcus aureus or Streptococcus pyogenes. Both organisms may be isolated in which case Strep. pyogenes is thought to be the primary pathogen. Strep. pyogenes is usually the primary pathogen in central and northern Australia.

Impetigo presents most often in children but may be seen at any age. Clinically it may be nonbullous, presenting with yellow crusts and erosions, or bullous, presenting with mildly irritating blisters that erode rapidly leaving a brown crust. The former tends to be a less acute condition. Diagnosis is confirmed by skin swab to define the infective organism and confirm antibiotic susceptibility. The condition is contagious. If due to Strep. pyogenes, glomerulonephritis may follow within 8 weeks.

Seek and treat underlying dermatosis such as dermatitis, scabies or head lice.

In situations where Streptococcus pyogenes is suspected or confirmed as the primary pathogen, use

	saline OR soap and water OR aluminium acetate solution OR potassium permanganate solution topically, 12-hourly to remove crusts (see Pompholyx - Specific treatments for dermatitis)
	PLUS
	phenoxymethylpenicillin (child: 10 mg/kg up to) 500 mg orally, 6-hourly for 10 days
	OR
	benzathine penicillin (child: 30 to 45 mg/kg up to) 900 mg IM, as 1 dose (see also dosing table for children).

 

For patients with penicillin hypersensitivity, use

roxithromycin 300 mg orally, daily (child: 4 mg/kg up to 150 mg orally, 12-hourly) for 10 days.

 

In situations where Staphylococcus aureus is suspected or confirmed as the primary pathogen, for mild or localised infections, use

	saline OR soap and water OR aluminium acetate solution OR potassium permanganate solution topically, 12-hourly to remove crusts (see Pompholyx - Specific treatments for dermatitis)
	PLUS
	mupirocin 2% topically, 8-hourly for 7 days.

 

For severe, widespread or longstanding infections where Staphylococcus aureus is suspected or confirmed, use

1	di/flucloxacillin (child: 12.5 mg/kg up to) 250 mg orally, 6-hourly for 10 days
	OR
2	cephalexin (child: 12.5 to 25 mg/kg up to) 250 mg orally, 6-hourly for 10 days
	OR
3	roxithromycin 300 mg orally, daily (child: 4 mg/kg up to 150 mg orally, 12-hourly) for 10 days.

 

Each of these drugs is active against both Staph. aureus and Strep. pyogenes.

Mastitis

 

Acute mastitis is usually associated with lactation and is frequently due to Staphylococcus aureus. Poor infant positioning and milk stasis are contributory factors to the infection. Suckling should be continued or milk from the infected breast expressed manually or by pump. In the absence of systemic symptoms in early mastitis, increased feeding on the affected side and gentle expression may prevent progression.

If systemic symptoms develop, early treatment with antibiotics is important to try to prevent abscess formation.

1	di/flucloxacillin 500 mg orally, 6-hourly
	OR
2	cephalexin 500 mg orally, 6-hourly.

 

If severe cellulitis has developed, antibiotics should be given IV.

1	di/flucloxacillin 2 g IV, 6-hourly
	OR
2	cephalothin 2 g IV, 6-hourly
	OR
2	cephazolin 1 g IV, 8-hourly.

 

For patients with immediate penicillin hypersensitivity, use

1	clindamycin 450 mg IV, 8-hourly THEN 450 mg orally, 8-hourly
	OR
1	lincomycin 600 mg IV, 8-hourly THEN clindamycin 450 mg orally, 8-hourly.
	OR
2	vancomycin 1 g IV, 12-hourly.

 

Failure of symptoms to improve after 2 to 3 days suggests other pathogens or an abscess, requiring review, surgical drainage and bacteriological examination of the pus.

Necrotising fasciitis or synergistic gangrene

The basis of treatment is surgical removal of devitalised tissue, which reduces mortality and assists in diagnosis. Causative organisms are usually mixed aerobes and anaerobes, eg Escherichia coli, Bacteroides fragilis, streptococci and staphylococci. Use initially

	benzylpenicillin (child: 60 mg/kg up to) 2.4 g IV, 4-hourly
	PLUS
	gentamicin (child <10 years: 7.5 mg/kg; >=10 years: 6 mg/kg) 4 to 6 mg/kg IV, daily (adjust dose for renal function, see Monitoring of aminoglycosides)
	PLUS
	metronidazole (child: 12.5 mg/kg up to) 500 mg IV, 8-hourly.

 

Depending on the severity of the infection, and/or the organisms subsequently isolated, other antibiotics in combination may be indicated, eg the addition of di/flucloxacillin if Staphylococcus aureus is present.

For proven Streptococcus pyogenes necrotising fasciitis, use

	benzylpenicillin (child: 45 mg/kg up to) 1.8 g IV, 4-hourly
	PLUS EITHER
1	clindamycin (child: 15 mg/kg up to) 600 mg IV, 8-hourly
	OR
1	lincomycin (child: 15 mg/kg up to) 600 mg IV, 8-hourly.

 

For patients hypersensitive to penicillin (excluding immediate hypersensitivity), substitute for benzylpenicillin

1	cephalothin (child: 50 mg/kg up to) 2 g IV, 6-hourly
	OR
1	cephazolin (child: 25 mg/kg up to) 1 g IV, 8-hourly.

Paronychia

 

Chronic paronychia is painless and is a traumatic nail dystrophy. Pushing back the cuticles, or removal of the cuticles through keratolytics (as used by manicurists) damages the waterproof seal between the proximal nail fold and the nail plate that protects the nail matrix. Once damaged, water and debris can enter the nail matrix and produce inflammation of the undersurface of the proximal nail fold.

Loss of the cuticle is an essential feature of the diagnosis; if the cuticle is intact, consider other causes of swelling of the proximal nail fold. Nail biting is commonly associated. Treatment is dependent on correct care of the cuticle.

Secondary infection with Candida is common. Although Candida may aggravate the problem, it does not cause it; paronychia is essentially a problem caused by nail manicure that damages the integrity of the cuticle. Chronic paronychia may be aggravated by episodes of acute paronychia caused by secondary infection with staphylococci (see below).

Advise patients to:

·            not push back their cuticles or manicure their nails

·            avoid playing with or picking at their cuticles

·            never insert anything beneath the cuticle to clean out debris

·            keep their hands out of water, and wear cotton-lined rubber gloves when doing the dishes or other wet work

·            wear cotton gloves in the garden and leather gloves in cold weather

·            use a mild soap and shampoo to minimise irritation in the shower

·            continue with meticulous hand care until the cuticle regenerates (approximately 6 weeks).

 

Topical corticosteroids are helpful. Use

a potent or very potent topical corticosteroid topically, once daily for 14 to 21 days.

 

If there is secondary Candida infection, add

miconazole 2% tincture topically, twice daily for 5 to 7 days.

 

When there is persistent exudate, use an antiseptic tincture to dry out the area:

thymol 4% in alcohol 70%, applied with a dropper to the base of the nail.[Note 1]

 

When the area is dry and without exudate, to waterproof and protect the area, use

white soft paraffin topically, 5 to 10 times daily.

 

Refer unresponsive cases to a dermatologist.

 

Acute paronychia is due to bacterial (usually staphylococcal) or, rarely, viral (herpes simplex virus) infection. It may aggravate chronic paronychia. The proximal nail fold becomes painful and pus should be drained.

For staphylococcal infection not responding to drainage, use

di/flucloxacillin (child: 25 mg/kg up to) 500 mg orally, 6-hourly for 7 days.

 

For patients hypersensitive to penicillin (excluding immediate hypersensitivity), use

cephalexin (child: 12.5 mg/kg up to) 500 mg orally, 6-hourly for 7 days.

 

For patients with immediate penicillin hypersensitivity, use

clindamycin (child: 10 mg/kg up to) 450 mg orally, 8-hourly for 7 days.

 

For infection caused by herpes simplex virus (herpetic whitlow), use

1	valaciclovir 500 mg orally, 12-hourly for 7 to 10 days
	OR
2	famciclovir 250 mg orally, 12-hourly for 7 to 10 days
	OR
3	aciclovir (child: 5 mg/kg up to) 200 mg orally, 5 times daily for 7 to 10 days.

 

Aciclovir is the preferred treatment in children with acute paronychia caused by herpes simplex virus.

Superficial thrombophlebitis

Superficial thrombophlebitis may occur spontaneously and antibiotics are not indicated. However, thrombophlebitis related to an IV catheter is usually due to Staphylococcus aureus infection and antibiotic therapy should be given as for suspected bacteraemia in the presence of intravascular cannulae, see Severe sepsis, intravascular device source. The infected catheter should be removed and the tip, together with blood cultures from another site, sent for culture. Surgical drainage of purulent material and/or removal of the infected clot may sometimes be required.

 

Varicose or decubitus ulcers

 

Local measures similar to those for postoperative wound infections are most important. If there is surrounding cellulitis, treat with systemic antibiotics as for diabetic foot infections, as the organisms involved are similar.

Water-related skin and soft tissue infections

 

In a patient presenting with a wound infection, cellulitis or sepsis which may be related to contact with water, eg in fishermen, swimmers or aquarium owners, the following organisms may be encountered: Aeromonas species (source: fresh or brackish water); Mycobacterium marinum (source: fish tanks); Shewanella putrefaciens, Vibrio vulnificus, Vibrio alginolyticus and other noncholera vibrios (source: salt or brackish water).

Treatment of most of these infections is difficult and advice should be sought from a clinical microbiologist or an infectious diseases physician. In mild infection, treatment may be given as for mild early cellulitis.

 

Infections by Aeromonas species are associated with exposure to fresh or brackish water or mud (water activities, caving) through cuts and abrasions. The resulting illness may be a superficial skin infection, myositis or sepsis with metastatic complications. In about 25% of cases the patient has an underlying systemic illness.

ciprofloxacin (child: 5 mg/kg up to) 300 mg IV or (child: 10 mg/kg up to) 500 mg orally, 12-hourly.

 

Meropenem or imipenem are possible alternatives for polymicrobial infection.

 

Coral cuts are often infected with Streptococcus pyogenes, but infection may also occur with marine pathogens. For mild infection, treat as for impetigo, and if unresponsive or severe, treat as for severe cellulitis. Treatment may need to be modified depending on response and culture results.

 

For the treatment of Mycobacterium marinum infections, see Nontuberculous mycobacteria.

 

Vibrio species should be suspected in skin infections in patients who have been exposed to salt water. Local management of skin lesions may include incision, drainage and debridement. There is considerable variability in antimicrobial susceptibility. Initial treatment should include

doxycycline (child >8 years: 2 mg/kg up to) 100 mg orally, 12-hourly.

 

Alternative antibiotics which could be considered are cefotaxime, ceftriaxone, ciprofloxacin or minocycline.

Wound infections

 

Postoperative wound infections

 

Local measures such as surgical drainage and irrigation with sodium chloride 0.9% will usually suffice. Topical antibiotics may cause skin hypersensitivity and the emergence of resistant organisms, and are not recommended. In all cases a patient's tetanus immunisation status must be assessed.

For mild to moderate infection with surrounding cellulitis, use

1	di/flucloxacillin (child: 25 mg/kg up to) 500 mg orally, 6-hourly
	OR
2	cephalexin (child: 25 mg/kg up to) 500 mg orally, 6-hourly.

 

Alternatively, if Gram-negative organisms are suspected or known to be involved, use

amoxycillin+clavulanate (child: 22.5+3.2 mg/kg up to) 875+125 mg orally, 12-hourly.

 

For more severe infections particularly where systemic symptoms are present, use

1	di/flucloxacillin (child: 50 mg/kg up to) 2 g IV, 6-hourly
	OR
2	cephalothin (child: 50 mg/kg up to) 2 g IV, 6-hourly
	OR
2	cephazolin (child: 25 mg/kg up to) 1 g IV, 8-hourly.

 

If Gram-negative organisms are suspected or known to be involved, add

gentamicin (child <10 years: 7.5 mg/kg; >=10 years: 6 mg/kg) 4 to 6 mg/kg IV, daily (adjust dose for renal function, see Monitoring of aminoglycosides).

 

If there is a high incidence of MRSA in the surgical unit, use

vancomycin (child: 20 mg/

Post-traumatic wound infections

Generally, antibiotics are used in the early treatment of contaminated wounds following significant injury such as muscular, skeletal and soft tissue trauma, crush injuries and stab wounds. Antibiotics are not routinely required in all wounds. Careful cleaning and debridement of wounds is important in preventing infection, and immobilisation and elevation are also helpful. Likely pathogens include Staphylococcus aureus, Streptococcus pyogenes, Clostridium perfringens and aerobic Gram-negative bacilli. In all cases a patient's tetanus immunisation status must be assessed.

Surgical removal of devitalised tissue and other measures are vitally important and require expert advice.

 

Antibiotics are seldom necessary, however, if management is delayed or debridement difficult, use

	di/flucloxacillin (child: 25 mg/kg up to) 500 mg orally, 6-hourly for 5 to 7 days
	PLUS
	metronidazole (child: 10 mg/kg up to) 400 mg orally, 12-hourly for 5 to 7 days.

 

Alternatively, use

amoxycillin+clavulanate (child: 22.5+3.2 mg/kg up to) 875+125 mg orally, 12-hourly for 5 to 7 days.

 

 

	di/flucloxacillin (child: 50 mg/kg up to) 2 g IV, 6-hourly
	PLUS
	gentamicin (child <10 years: 7.5 mg/kg; >=10 years: 6 mg/kg) 4 to 6 mg/kg IV, daily (adjust dose for renal function, see Monitoring of aminoglycosides)
	PLUS
	metronidazole (child: 12.5 mg/kg up to) 500 mg IV, 12-hourly.

 

Alternatively, use

	metronidazole (child: 12.5 mg/kg up to) 500 mg IV, 12-hourly
	PLUS EITHER
1	cephalothin (child: 50 mg/kg up to) 2 g IV, 6-hourly
	OR
1	cephazolin (child: 50 mg/kg up to) 2 g IV, 8-hourly.

 

Duration of treatment should be at least 5 days.

If antibiotic prophylaxis against gas gangrene is required, to the initial regimen add

benzylpenicillin (child: 60 mg/kg up to) 2.4 g IV, repeat in 4 hours if necessary.

Tetanus prophylaxis 

Time since vaccination	Type of wound	Tetanus toxoid	Tetanus immunoglobulin
History of 3 or more doses of tetanus toxoid
<5 years	all wounds	no	no
5 to 10 years	clean minor wounds	no	no
	all other wounds	yes	no
>=10 years	all wounds	yes	no
Uncertain vaccination history or <3 doses of tetanus toxoid
	clean minor wounds	yes	no
	all other wounds	yes	yes

Viral skin and soft tissue infections

 

Eczema herpeticum

 

This is defined as dermatitis with secondary herpes simplex virus infection and should be considered as a possible cause of any acute flare of dermatitis. The signs are grouped vesicles and erosions on a weeping dermatitis, with associated fever and malaise. Skin tenderness is more common than itching. A viral swab is needed for diagnosis. Hospital admission may sometimes be required. Staphylococcus aureus commonly colonises but diffuse redness and crusting suggest bacterial infection (see Impetigo). This condition is more often seen in children than adults. Treatment is with antiviral drugs

1	valaciclovir 500 mg orally, 12-hourly until healed
	OR
2	famciclovir 250 mg orally, 12-hourly until healed
	OR
3	aciclovir (child: 5 mg/kg up to) 200 mg orally, 5 times daily until healed.

 

For more severe disease, use

aciclovir (for all ages) 5 mg/kg IV, 8-hourly initially, THEN an oral regimen as above.

 

Initial topical therapy should include wet dressings or compresses with potassium permanganate or aluminium acetate solution. Topical corticosteroids should be avoided until the infection is under control. See Specific treatments for dermatitis.

Herpes simplex infections of the skin and and soft tissue

Herpes simplex labialis (cold sores)

 

 

Herpes simplex virus infections are very common in children and adults; on serology over 90% of the population have been exposed to the virus by adult life. The primary attack often occurs in childhood with fever, toxicity and oral ulceration associated with lymphadenopathy. Healing occurs in 2 weeks, but during this time it may be difficult for the child to eat and drink and hospitalisation may be required.

Recurrent attacks usually occur on the lips, but if the primary attack has been on the skin recurrences can occur on that area of skin. Recurrences are usually mild and infrequent, but are occasionally very frequent and disabling. Sun protection is important in preventing recurrences of facial herpes simplex.

In children with atopic dermatitis and in immunosuppressed patients, herpes simplex virus may disseminate, causing a generalised eruption requiring hospitalisation for IV antiviral therapy. In patients with HIV infection, herpes simplex may become chronic with recalcitrant crusted lesions and ulceration. Herpes simplex may be complicated by erythema multiforme, which is often more disabling than the infection itself.

 

For symptomatic treatment, use

povidone iodine 10% paint applied 3 times daily.

 

For antiviral therapy, use

aciclovir 5% cream applied every 4 hours while awake for 4 days, at the first sign of recurrence.

 

1	famciclovir 125 mg orally, 12-hourly for 5 days
	OR
1	valaciclovir 500 mg orally, 12-hourly for 5 days
	OR
2	aciclovir (child: 5 mg/kg up to) 200 mg orally, 5 times daily for 5 days.

 

Aciclovir may be used in children, both orally and parenterally.

 

1	valaciclovir 500 mg orally, daily
	OR
2	famciclovir 250 mg orally, 12-hourly
	OR
3	aciclovir (child: 5 mg/kg up to) 200 mg orally, 8-hourly OR (child: 10 mg/kg up to) 400 mg orally, 12-hourly.

 

Treatment should be interrupted every 6 months to determine the natural history of the disease in any given patient but may be restarted in the event of recurrence.

Herpetic whitlow

 

Herpetic whitlow may masquerade as an acute pyogenic infection; see also paronychia.

1	valaciclovir 500 mg orally, 12-hourly for 7 to 10 days
	OR
2	famciclovir 250 mg orally, 12-hourly for 7 to 10 days
	OR
3	aciclovir (child: 5 mg/kg up to) 200 mg orally, 5 times daily for 7 to 10 days.

 

Mucocutaneous herpes simplex

 

Aciclovir is recommended for the treatment of acute symptomatic episodes in immunocompromised patients.

aciclovir 5 mg/kg IV, 8-hourly for 7 to 10 days.

 

For an alternative to parenteral therapy, use

1	valaciclovir 1 g orally, 12-hourly for 7 to 10 days
	OR
2	famciclovir 500 mg orally, 12-hourly for 7 to 10 days
	OR
3	aciclovir (child: 5 to 10 mg/kg up to) 200 to 400 mg orally, 5 times daily for 7 to 10 days.

Herpes zoster (shingles)

Acute herpes zoster

 

Approximately 20% of people will experience herpes zoster (shingles), mostly when they are elderly. Pain due to herpes zoster may occur before, with or following the rash. Postherpetic neuralgia is pain persisting for longer than four weeks after crusting of the vesicles. About 10% of patients with herpes zoster will subsequently have postherpetic neuralgia. Older patients are more likely to experience severe pain and complications. Postherpetic neuralgia occurs in up to 75% of those over 70 years of age affected with herpes zoster.

The aims of treatment are to:

        relieve the acute pain

        prevent postherpetic neuralgia

        decrease the chance of neurological or ophthalmic complications.

Motor effects are not uncommon and usually unimportant, but may on rare occasions be severe. Secondary infection must always be considered and treated if present.

For further information regarding ophthalmic herpes zoster, see Ophthalmic herpes zoster.

If the rash has been present for less than 72 hours, treatment with famciclovir, valaciclovir or aciclovir has been shown to significantly reduce acute pain, the duration of the rash, viral shedding and ophthalmic complications.

Whether antiviral therapy reduces the duration of postherpetic neuralgia remains contentious, although data are suggestive of some benefit. A study has shown that famciclovir reduces the duration of postherpetic neuralgia, especially in patients over 50 years of age. The same may possibly be true for valaciclovir and aciclovir, although the evidence is less clear.

Acute herpes zoster is a greater risk in immunocompromised patients in whom there is an increased risk of dissemination involving skin, adjacent dermatomes and deep tissues and rarely, visceral involvement.

The treatment is effective in anyone; however, it is most useful in those patients:

        treated within 72 hours of the onset of vesicles

        who are immunocompromised

        who are more than 50 years of age

        with severe acute pain

        with involvement of critical areas, eg eye, perineum, limbs, neck.

There is no proven value of antiviral therapy in the immunocompetent patient if it is commenced more than 72 hours after onset of rash.

If there are clear indications for antiviral therapy, then start as early as possible with

famciclovir 250mg orally, every 8 hours for 7 days

OR

valaciclovir 1g orally, every 8 hours for 7 days

OR

aciclovir (child: 20mg/kg up to) 800mg orally, 5 times daily for 7 days.

 

Herpetic lesions are usually painful. Occasionally pain precedes the rash. The pain is usually mild, but can be intense, especially on the face. In most cases its severity diminishes gradually and resolves completely over a few weeks. Ice packs and protective dressings may provide relief. The elderly are more likely to have severe and/or persistent pain.

aspirin 300 to 600mg orally, every 4 hours as necessary (avoid in children)

OR

paracetamol 0.5 to 1g orally, every 4 to 6 hours as necessary, up to 4g daily

 

If pain is severe, add

an opioid orally, see Getting to know your analgesics and adjuvants - Opioids.

 

Although a variety of topical therapies have been used, there is little good supportive evidence. Lignocaine ointment or lignocaine+prilocaine cream may be tried for a few days on nonulcerated skin and even if only partially effective, may supplement other measures. They should not be used on ulcerated skin because of possible systemic toxicity. Occlusive dressings may enhance the efficacy of topical local anaesthetics.

lignocaine 5% ointment or lignocaine+prilocaine cream topically, with an occlusive dressing if possible, to the painful areas. Beware of skin reactions.

 

There is no proof that systemic corticosteroids alone prevent postherpetic neuralgia or other neurological complications of herpes zoster, but one large study did show that pain and abnormal sleep patterns in the acute phase resolved faster when prednisolone was given in a tapering regimen from 40mg daily over 21 days in combination with aciclovir.

Use of amitriptyline, nerve blocks and opioids, if necessary, soon after the development of acute herpetic pain may also help prevent the sensitisation of the central nervous system that may lead to persistence of the pain, see Dorsal horn of the spinal cord: the gate control theory and central sensitisation. However, the value of the latter measures has yet to be proven.

Postherpetic neuralgia

 

The pain of postherpetic neuralgia is usually severe. It may present as burning, aching and monotonous pain, or it may present as paroxysmal shock-like stabbing or lancinating pain. The patient almost always has an atypical response (allodynia) of severe pain to a light stimulus, such as gentle brushing of the skin. The skin of the affected area may be depigmented and scarred but the degree of scarring bears no relationship to the severity or quality of pain.

Postherpetic neuralgia is difficult to treat. It is largely a disease of the elderly, in whom consideration must always be given to problems associated with other diseases, particularly those affecting cognition and to the maintenance of physical function and continued socialisation.

Treatment should begin with the simplest and safest approaches, such as aspirin, paracetamol or any NSAID, ice massage, transcutaneous electrical nerve stimulation (TENS), topical capsaicin or lignocaine. If these produce inadequate relief, try either a tricyclic antidepressant (TCA) such as amitriptyline or nortriptyline or an antiepileptic drug such as carbamazepine or gabapentin. It may then be reasonable to try oral opioids.

For pain relief commence with

aspirin 300 to 600mg orally, every 4 hours as necessary (avoid in children)

OR

paracetamol 0.5 to 1g orally, every 4 to 6 hours as necessary, up to 4g daily

OR

any NSAID orally, in the recommended regimens outlined. The elderly are particularly at risk of gastrointestinal toxicity from NSAIDs. Specific COX-2 inhibitors, are safer in this regard and this favours their use in patients aged over 65 years, although they have all the other NSAID adverse effects.

 

This may be sufficient for some patients without the need for other interventions and is worth trying for a few days.

Ice massage may be helpful.

If the above produce inadequate relief, an early treatment step should be to use TENS. This should be combined with a TCA or an antiepileptic.

transcutaneous electrical nerve stimulation, applied as often as necessary (up to 16 hours a day) for at least 2 weeks.

 

TCAs are the most effective drug therapy for postherpetic neuralgia, delivering a response rate of around 40% to 65%. Most controlled studies have used amitriptyline. It appears that the ability to block the reuptake of noradrenaline into neurones is important and thus selective serotonin reuptake inhibitors probably have little value in this condition.

Some antiepileptic drugs have proven efficacy in the treatment of postherpetic neuralgia. Either gabapentin or carbamazepine may be used. These may be better tolerated than TCAs in the elderly.

A decision on which drug to use is largely dependent on consideration of efficacy, adverse effects and cost. Other indications, eg need for sedation, or contraindications, eg prostatism, may influence the choice of agent.

Success is more likely if therapy is commenced early. The patient needs to be told that it may take weeks before they experience maximal effect. TCAs should be taken for three to six months after pain is reduced or abolished.

amitriptyline 10 to 25mg orally, at night, increasing every 7 days to a usual maximum dose of 75 to 100mg at night. Use with care in the elderly and those with ischaemic heart disease; if sedation is a problem, an alternative such as nortriptyline or doxepin can be used

OR

carbamazepine 50mg (elderly patient) or 100mg (younger, larger patient) orally, twice daily initially, increasing as tolerated and according to response every 3 days to a maximum of 400mg twice daily. A controlled-release preparation may reduce peak-related toxicity

OR

gabapentin 300mg orally, daily initially, increasing as tolerated and according to response every 4 days from once daily to 3 times daily, to a usual maximum daily dose of 2400mg. Gabapentin is renally excreted and much lower doses should be used in the elderly and those with renal impairment.

 

Topical therapy with capsaicin, which depletes substance P, or lignocaine ointment, gel or transdermal patch has also been advocated.

capsaicin 0.075% cream topically, 4 times daily. Regular application is necessary for effect; this may present practical difficulties. Response may not occur for a week or more. Severe burning on application can be intolerable for up to one-third of patients. Ice massage or topical local anaesthetic applied 20 minutes prior to capsaicin may help

OR

lignocaine 5% ointment or 10% gel (requires extemporaneous preparation) topically, with an occlusive dressing if possible, to the painful areas

OR

lignocaine 5% patch transdermally, to the painful areas (available in Australia under the Special Access Scheme (SAS) at the time of writing).

 

An opioid analgesic may be needed for the pain, see Getting to know your analgesics and adjuvants - Opioids. Where possible, this should be under the supervision of a pain clinic, or specialists experienced in their use for this condition. However, patients should not be denied effective analgesia while waiting for an appointment at a pain clinic.

In one trial, intrathecal methylprednisolone given with lignocaine was shown to be effective, in particular in the reduction of allodynia. However, uncertainty remains about possible long-term effects, eg arachnoiditis. Intrathecal corticosteroids are best reserved for patients who do not have a response to any other measures.

Psychological approaches should not be forgotten, see Nonpharmacological pain management techniques.

Many other treatments have been advocated and used. These include other antiepileptic drugs, including phenytoin and sodium valproate, local and systemic corticosteroids and anaesthetic injections, and antipsychotics. None are particularly effective.

Surgical and nerve destruction techniques are not recommended.

Herpetic lesions are usually painful. Occasionally pain precedes the rash. The pain is usually mild, but can be intense, especially on the face. In most cases its severity diminishes gradually and resolves completely over a few weeks. Ice packs and protective dressings may provide relief. The elderly are more likely to have severe and/or persistent pain.

aspirin 300 to 600mg orally, every 4 hours as necessary (avoid in children)

OR

paracetamol 0.5 to 1g orally, every 4 to 6 hours as necessary, up to 4g daily

 

If pain is severe, add

an opioid orally, see Getting to know your analgesics and adjuvants - Opioids.

 

Although a variety of topical therapies have been used, there is little good supportive evidence. Lignocaine ointment or lignocaine+prilocaine cream may be tried for a few days on nonulcerated skin and even if only partially effective, may supplement other measures. They should not be used on ulcerated skin because of possible systemic toxicity. Occlusive dressings may enhance the efficacy of topical local anaesthetics.

lignocaine 5% ointment or lignocaine+prilocaine cream topically, with an occlusive dressing if possible, to the painful areas. Beware of skin reactions.

 

There is no proof that systemic corticosteroids alone prevent postherpetic neuralgia or other neurological complications of herpes zoster, but one large study did show that pain and abnormal sleep patterns in the acute phase resolved faster when prednisolone was given in a tapering regimen from 40mg daily over 21 days in combination with aciclovir.

Use of amitriptyline, nerve blocks and opioids, if necessary, soon after the development of acute herpetic pain may also help prevent the sensitisation of the central nervous system that may lead to persistence of the pain, see Dorsal horn of the spinal cord: the gate control theory and central sensitisation. However, the value of the latter measures has yet to be proven.

Ophthalmic herpes zoster

 

Aciclovir and related agents decrease pain, corneal damage and anterior uveitis. Early treatment is recommended as soon as the diagnosis is suspected. An ophthalmologist should be consulted. For children, hospital admission is recommended.

1	famciclovir 250 mg orally, 8-hourly for 7 days
	OR
2	valaciclovir 1 g orally, 8-hourly for 7 days
	OR
3	aciclovir (child: 20 mg/kg up to) 800 mg orally, 5 times daily for 7 days.

 

If sight is threatened, use

aciclovir 10 mg/kg IV, 8-hourly for 7 days.

 

The above treatment may be supplemented with aciclovir 3% eye ointment, 5 times daily.

 

Human papilloma virus (warts)

 

These benign tumours are seen in all ages but are most common in children. Common warts occur mostly on hands, feet and extensor surfaces. Warts on the face often take the form of multiple tiny plane lesions. Warts adjacent to mucosal surfaces are frequently filiform. There is no specific or reliably effective treatment. In children, warts frequently resolve spontaneously, making aggressive therapy inappropriate.

topical keratolytics (over-the-counter preparations of salicylic acid, Upton’s paste) with and without occlusion and serial paring. Normal skin should be covered with adhesive elastic plaster, with a hole left for the wart and the substance applied to the wart. More tape is applied over the top to increase occlusion. The tape is removed the following day and the wart is pared with a scalpel or filed with a pumice stone. When using Upton’s paste on plantar warts, the tape should be left in place for a week.

OR

cryotherapy to each wart every 2 to 4 weeks until resolved

OR

ablative therapy, using cautery and less commonly CO₂ laser, to each wart, but only in situations where scarring is unlikely or unimportant.

 

Bleomycin has been used by dermatologists. Immunotherapy with topical sensitisers, dinitrochlorobenzene (DNCB) and diphencyprone is effective but can be hazardous because of the risk of severe allergic contact dermatitis and the possible mutagenicity of DNCB. Specialist referral is recommended.

tretinoin 0.05% cream applied daily, particularly for plane warts on the face

OR

cryotherapy to each wart every 2 to 4 weeks until resolved

OR

keratolytics, see above, used with caution on the face: a small area should be tested first and the preparation applied sparingly and accurately.

 

However, plane warts on the face are very difficult to treat and are often best left untreated.

The treatment of genital warts is discussed in Genital skin diseases.

Topical keratolytics or cryotherapy, see above, may be used.

In general, cautery is useful only in situations where scarring is unlikely or unimportant.

In children with multiple warts, use cimetidine 40mg/kg/day, orally in 2 divided doses for up to 12 weeks. This does not appear to be useful in adults. Cimetidine is thought to act as an immunostimulator. This treatment remains controversial as some trials have shown it to be no more useful than placebo.

 

Molluscum contagiosum

This common poxvirus infection is seen often in young children where lesions occur anywhere on the body and in adults where it is seen most often as a sexually acquired infection of the genital area. In human immunodeficiency virus (HIV) infection, lesions may be widespread and atypical. In children, infection is usually acquired from family members or others with whom they swim or bathe. The typical lesion is a pearly papule with a central umbilication and a core that may be extracted with the tip of a needle.

The infection may be complicated by dermatitis, particularly in atopic patients, and by bacterial superinfection. Spontaneous resolution is the rule in immunocompetent patients but may take up to 2 years.

Chemical therapies are ineffective in treating these lesions. In children, conservative management is usually best, unless lesions are widespread and interfering with lifestyle and function. If treatment is required, the most effective treatment is extracting the core with a large needle or curetting the lesions if small. In children with numerous lesions, this may require a general anaesthetic. In adults, cryotherapy is effective.

Treat secondary dermatitis with topical therapy, see General treatment of dermatitis and Control of xerosis.

To avoid secondary infection following extraction, use

mupirocin 2% ointment or cream OR povidone iodine 10% alcoholic solution.

 

Avoiding heated swimming pools and showering rather than bathing reduces the spread of these lesions. It is not practicable or necessary to isolate children with molluscum contagiosum.

In patients with HIV infection, treatment may be very difficult, although where the lesions are few in number cryotherapy may be effective.

Varicella (chicken pox)

In the nonhospitalised patient with a normal immune system and uncomplicated varicella, antivirals are not recommended because the benefits are only marginal.

In immunocompromised patients with severe disease and in normal patients with complications of varicella, eg pneumonitis or encephalitis, use

aciclovir 10 mg/kg IV, 8-hourly for 7 to 10 days.

 

For less severe disease, use oral therapy as for herpes zoster.

Superinfection of varicella skin lesions with Streptococcus pyogenes and Staphylococcus aureus may occur and should be treated as for impetigo or cellulitis as appropriate.

Fungal skin and soft tissue infections

 

Pityriasis versicolor

 

This chronic, superficial yeast infection of the skin can present with areas of hyperpigmentation or hypopigmentation.

It is caused by the budding yeast Malassezia furfur, which is the mycelial phase of the yeast Pityrosporum orbiculare, which is part of the normal skin flora.

The hypopigmentation is due to tyrosinase inhibition by dicarboxylic acids produced by the pityrosporum, with consequent suppression of melanin production. Abnormal melanosomes may also be produced by a disruption in this pathway, accounting for the hyperpigmentation seen in other patients with this disorder.

Pityriasis versicolor is seen in young patients, with a peak incidence between 20 and 30 years of age. It is common in tropical climates. The sex incidence is equal and there may be a genetic predisposition to develop this reaction to normal skin flora.

Patients present with well demarcated pale or tan-coloured macules, some of which may coalesce, with fine scale, usually on the upper trunk alone. However, the condition may involve the whole trunk, the upper arms and the neck. There may be a slight itch.

Skin scrapings reveal spherical budding yeasts and coarse mycelia on microscopy.

Topical therapy is with

ketoconazole 2% shampoo applied daily for 10 minutes and washed off, for 10 days

OR

selenium sulfide 2.5% shampoo applied daily for 10 minutes for 7 days

OR

sodium thiosulfate 20% solution applied twice daily for 2 weeks.

 

If the disease is localised to a small area it is reasonable to use

imidazole cream or lotion, topically, twice daily for 10 days.

 

In unresponsive cases, use systemic therapy with

ketoconazole 200mg orally, daily for 10 days OR itraconazole 200mg orally, daily for 5 days.

 

Note:

Griseofulvin is ineffective against this yeast.

 

The hypopigmentation may persist for some months until adequate sun exposure repigments the areas of pallor. It can be recurrent in some individuals and repeated courses of treatment may be necessary. Alternatively, intermittent doses of systemic medication (pulse therapy) can be used to suppress the growth of the yeast. Use

ketoconazole 400mg OR itraconazole 200mg orally, once every 30 to 90 days.

Tinea

Tinea: introduction

 

The causative agents in this condition are dermatophyte species, which may be acquired from animals, other humans or soil. Any part of the skin, hair and nails may be affected. Typically, tinea on the body presents with itchy, scaly erythematous lesions, with an annular or geographic shape and a tendency to clear centrally. Lesions may sometimes be pustular. The lesions expand slowly in most cases but an acute onset of multiple annular lesions can occur.

If the diagnosis has been missed and the infection treated with a topical corticosteroid, the typical morphology is lost, but it can usually be appreciated that the lesions have a definite edge.

Tinea of the hands and feet presents with interdigital maceration, and a nonspecific scaly erythema with fissuring and pustules that is often asymmetrical, distinguishing it from dermatoses such as psoriasis and dermatitis, which are usually bilaterally symmetrical. The infection commonly spreads to involve the nails with white or yellow discolouration, nail plate dystrophy and subungual debris. Foot tinea is often associated with tinea of the groin.

Tinea of hair-bearing areas presents with patchy alopecia, scaling and broken hairs. Hair may break at the scalp surface, producing a ‘black dot’ appearance. Inflammation is variable and ranges from nonexistent to the pustular, boggy mass seen with a kerion.

Diagnosis of tinea in hair-bearing areas is supported by fluorescence under Wood’s light examination, but many species do not fluoresce and a negative test does not rule it out. Diagnosis is confirmed by microscopy and culture of skin scrapings, subungual debris, clipped nail or plucked hair. Culture results are available in 3 to 4 weeks.

As fungal culture is a simple and inexpensive test, confirmation of diagnosis is always recommended prior to treatment with antifungals, particularly systemic agents, as tinea is often confused with eczema and other annular or patchy conditions such as pityriasis rosea and granuloma annulare. If microscopy is positive or there is a high index of suspicion of fungal infection, it is reasonable to begin treatment prior to the results of microscopy and culture. If antifungals have recently been used, these should be ceased for 1 week prior to attempting culture. When taking a fungal culture, scaly material should be scraped with a scalpel blade from the edge of the lesion. This may be deposited in a sterile container or inoculated straight onto a fungal culture plate. Material should be sent for direct microscopy. False negative results may be encountered with fungal culture, particularly with nail clippings, where the rate may be up to 40%. Negative culture may occur after positive microscopy. Reasons for negative culture include sampling error and overgrowth of nonpathogenic species in the laboratory. If there is still a strong diagnostic suspicion, a trial of therapy may be the ultimate diagnostic tool.

Tinea corporis, pedis and cruris

 

1	bifonazole 1% topically, once daily, continued for 14 days after symptoms resolve.
	OR
1	terbinafine 1% topically, once or twice daily, continued for 14 days after symptoms resolve.
	OR
2	clotrimazole 1% topically, 2 or 3 times daily, continued for 14 days after symptoms resolve.
	OR
2	econazole 1% topically, 2 or 3 times daily, continued for 14 days after symptoms resolve.
	OR
2	ketoconazole 2% topically, twice daily, continued for 14 days after symptoms resolve.
	OR
2	miconazole 2% topically, twice daily, continued for 14 days after symptoms resolve.

 

If unresponsive, use

1	terbinafine (child <20 kg: 62.5 mg; 20 to 40 kg: 125 mg) 250 mg orally, daily for at least 2 weeks, depending on the response
	OR
2	griseofulvin fine particle (child: 10 mg/kg up to) 500 mg or ultrafine particle (child >2 years: 5.5 mg/kg up to) 330 mg orally, daily for at least 4 weeks.

Tinea of the nails (onychomycosis, tinea unguium)

 

Onychomycosis is the term used for fungal infection of the nail. The condition is unsightly and may cause discomfort. Toenails are affected more commonly than fingernails. It is most commonly produced by dermatophyte moulds such as Trichophyton rubrum and Trichophyton mentagrophytes var interdigitale. T. rubrum infections usually also involve the sole of the foot, particularly the areas of thick skin, and frequently produce moccasin tinea pedis. T. rubrum is an anthropophilic fungus—humans are the natural reservoir of infection. Infections are frequently chronic and resistant to therapy. T. mentagrophytes var interdigitale is also an anthropophilic fungus and frequently infects the toe web spaces or the soft parts of the sole of the foot.

The first stage of onychomycosis is hyperkeratosis of the undersurface of the distal nail plate and the distal nail bed (hyponychium). This is known as distal subungual onychomycosis (DSO). The fungus seems to travel underneath the nail plate in the longitudinal folds of the nail bed to produce spears of subungual hyperkeratosis. These spears are one of the most useful clues to the diagnosis of onychomycosis. Progressive nail involvement produces total dystrophic onychomycosis (TDO).

T. mentagrophytes var interdigitale may also produce an unusual form known as white superficial onychomycosis (WSO). The diagnosis is confirmed by taking scrapings from the nail surface. WSO is responsive to topical imidazoles, whereas DSO and TDO are unresponsive.

Because many other disorders can mimic tinea of the nail, it is important to establish a diagnosis of tinea microbiologically before commencing treatment. This is done by first taking clippings of the affected distal nail plate and then scraping any subungual hyperkeratosis.

Microscopy and then culture will be positive in approximately 80% of cases of onychomycosis. Nail plate histology can be used if the culture is negative. For histology, a clipping of the distal nail plate is sent to the pathologist in formalin and stained with PAS (periodic acid Schiff reaction) to demonstrate the fungal hyphae. This increases the diagnostic yield in difficult cases.

Treatment options must be carefully considered, particularly if treatment is for cosmetic reasons only, as effective drugs are expensive and can have serious adverse drug reactions. However, the toenails can be a reservoir of infection which can precipitate recurrent cellulitis in association with tinea pedis.

First-line treatment for all types of nail tinea consists of

1	terbinafine (child <20 kg: 62.5 mg; 20 to 40 kg: 125 mg) 250 mg orally, daily for 6 weeks for fingernails and 12 weeks for toenails
	OR (if terbinafine is not tolerated)
2	itraconazole 400 mg orally daily for 7 days every month for 3 to 4 months
	OR
3	fluconazole 150 mg to 450 mg orally, once weekly for 12 to 52 weeks.

 

Terbinafine has a cure rate of 70% to 80%. Itraconazole and fluconazole have been used extensively overseas and a 3-month course has a cure rate of 60% to 70%. There is limited published data for use of itraconazole or fluconazole for tinea of the nails in children; terbinafine is currently the drug of choice.

Prior to the release of terbinafine, ketoconazole and griseofulvin were the main treatments, both of which needed to be taken continuously for 12 to 18 months. Ketoconazole use was limited by the potential complication of severe hepatic toxicity. Griseofulvin is safe but relatively ineffective; it has a cure rate of around 30% after 12 or more months of continuous therapy.

Topical nail lacquers are also available over-the-counter in pharmacies for the treatment of onychomycosis. These agents have no effect on TDO, but may have limited efficacy on DSO in patients intolerant of oral antifungals or not wanting to take oral medication for this problem.

For superficial or distal nail involvement, use

amorolfine 5% nail lacquer topically, weekly (may require up to 12 months therapy).

 

One difficulty in treating onychomycosis is determining when treatment has failed and a second course is required. At the end of the 3-month treatment period most nails still look abnormal, as a totally dystrophic nail takes up to 9 months to grow out. If normal nail is emerging proximal to the dystrophic nail, a scratch with a scalpel blade should be made at the base of the dystrophy. This scratch can then be followed by the patient until it grows out. If the dystrophic nail is growing out it remains distal to the scratch and no further treatment is required. If the dystrophy moves proximal to the scratch, this indicates ongoing fungal invasion of the nail which requires further treatment.

 Tinea in children

 

 

In children, tinea (dermatophyte infection) most commonly involves the scalp, face and body. Tinea pedis is less common in children than in adults, but is seen often in children with Down syndrome. The incidence rises with increasing age, reaching adult levels by late adolescence. In children, tinea is commonly acquired from dogs, cats and guinea pigs but human pathogens may also be responsible, especially in the case of tinea pedis. The animal dermatophytes tend to produce a more inflammatory and acute form of tinea. A kerion is a very acute form of tinea capitis, usually caused by an animal dermatophyte, in which a large boggy, pustular mass appears on the scalp.

 

These dermatophyte infections like tinea capitis are caused by fungi of the genera Trichophyton, Microsporum and Epidermophyton. Confirm the diagnosis by fungal culture of scrapings and plucked hairs prior to commencing therapy. This is important to confirm the diagnosis and for future monitoring. Topical therapy is ineffective in treating tinea capitis.

1	terbinafine (child <20 kg: 62.5 mg; 20 to 40 kg: 125 mg) 250 mg orally, daily for 4 weeks
	OR
2	griseofulvin fine particle (child: 10 mg/kg up to) 500 mg or ultrafine particle (child >2 years: 5.5 mg/kg up to) 330 mg orally, daily for 4 to 8 weeks.

 

Hair may not have completely regrown at the end of therapy, but this improves with time. Scarring alopecia is unusual as a sequel of tinea capitis.

Ketoconazole and selenium sulfide shampoos are a useful adjunct to therapy, in that they reduce shedding of spores; however, used alone they are ineffective as treatment.

The use of antibiotics, oral corticosteroids and surgical debridement does not add to the management of kerion and is contraindicated.

 

Prior to commencing treatment, perform a fungal scraping for culture. Many rashes that are common in children, such as dermatitis and psoriasis, may mimic tinea.

For mild or localised cases, use

imidazole cream applied 3 times daily for a minimum of 3 weeks

OR

terbinafine 1% cream applied twice daily for minimum of 2 weeks.

 

For extensive cases or tinea that has received prolonged treatment with topical corticosteroid, use

griseofulvin fine particle (child: 10 mg/kg up to) 500 mg or ultrafine particle (child >2 years: 5.5 mg/kg up to) 330 mg orally, daily for minimum of 3 weeks.

 

Clinical improvement usually occurs promptly, but premature cessation of treatment will result in relapse. .

 

Antifungal agents used in dermatology 

 

Drug	Dose form and strength	Indication
Note: Dose requirements for antifungal agents are given in individual sections
imidazoles, topical
- bifonazole	cream (1%)	tinea corporis, candidiasis, pityriasis versicolor
- clotrimazole	cream, solution (1%)	tinea corporis, candidiasis, pityriasis versicolor
- econazole	cream, lotion, dusting powder, foaming solution (1%)	tinea corporis, candidiasis, pityriasis versicolor
- ketoconazole	cream (2%) shampoo (1%, 2%)	tinea corporis, candidiasis, pityriasis versicolor, adjunct to treatment of tinea capitis
- miconazole	cream, lotion, ointment, oral gel, powder, shampoo, solution, spray, tincture (2%)	tinea corporis, candidiasis, pityriasis versicolor
nystatin	cream (100 000U/g)	candidiasis
selenium sulfide	shampoo (2.5%)	pityriasis versicolor
terbinafine	cream, gel (1%)	tinea corporis, candidiasis
amorolfine	nail lacquer (5%)	tinea of nails
fluconazole	oral (50mg, 100mg, 150mg, 200mg, 50mg/5mL)	candidiasis, pityriasis versicolor, tinea
griseofulvin	oral (125mg, 330mg, 500mg)	tinea capitis, tinea resistant to topical therapy
itraconazole	oral (100mg, 10mg/mL)	candidiasis, pityriasis versicolor, tinea
ketoconazole	oral (200mg)	candidiasis, pityriasis versicolor, tinea
terbinafine	oral (250mg)	tinea onychomycosis, tinea resistant to griseofulvin or patients unable to take griseofulvin

Candidiasis

 

Candida infection occurs on skin and mucosal surfaces, and is usually seen in subjects with predisposing factors, including therapy with broad-spectrum antibiotic, diabetes, iron deficiency, obesity and immobility, particularly where the skin is macerated and overheated. Candida infection may supervene on other dermatoses, particularly in the genital area and the flexures. General debility and immune incompetence also predispose to this infection. Otherwise healthy infants may suffer from oral candidiasis.

The clinical presentation is patches of moist, confluent erythema with a soggy, scaly edge, sometimes with vesicles and satellite pustules. The location is usually the flexures, submammary area and other skin folds. On mucosal surfaces, curd-like white material is seen on a red base. Diagnosis is readily confirmed by culture of a swab; however, a scraping for microscopy and fungal culture may also be done.

As the underlying factors predisposing to Candida albicans infection may not be readily modified, suppressive treatment is often required. Investigate for diabetes mellitus and iron deficiency. Treat underlying dermatoses if present. Cease oral antibiotics unless essential. In immunocompetent patients, use

imidazole cream OR nystatin 100 000U/g cream applied 2 to 3 times daily. Continue treatment for 2 weeks after symptoms resolve.

 

Note:

Griseofulvin is not active against Candida albicans.

 

If necessary for inflammation, use

hydrocortisone 1% cream topically, 2 to 3 times daily.

 

If there is a poor response to therapy, or it is impracticable to apply topical treatment, use a course of an oral antifungal agent

ketoconazole 200mg orally, daily for 10 days OR itraconazole 100mg orally, twice daily for 7 days OR fluconazole 150mg orally, as a single dose.

 

In immunodeficient patients, use

ketoconazole 200mg OR itraconazole 100mg OR fluconazole 50mg orally, daily.

 

Treatment is continued until all clinical signs of candidiasis have subsided; however culture may remain positive. Long-term intermittent dosing is usually required to maintain remission of symptoms. Ketoconazole should be monitored by monthly liver function tests (LFTs) and fluconazole and itraconazole should be monitored by LFTs at 6-monthly intervals once the patient is on maintenance therapy.

 

Parasitic skin and soft tissue infections

Cutaneous larva migrans

 

Animal hookworms usually cause this condition. Although self-limiting, treatment alleviates symptoms.

1	ivermectin (child >5 years) 200 micrograms/kg orally, as 1 dose
	OR
2	albendazole (child <=10 kg: 200 mg) 400 mg orally, daily for 3 days.

Ectoparasites

 

Scabies (Sarcoptes scabiei)

 

 

Scabies is a dermatosis caused by infestation with the mite Sarcoptes scabiei var hominis. This insect is a human pathogen and is spread by close physical contact between infected persons. Human scabies is not acquired from animals. Scabies is common in school-age children and in closed communities such as nursing homes. If untreated, it will usually spread to all members of a patient’s family.

The diagnosis of scabies is often difficult, especially if it is not suspected. This is because the clinical picture is variable and signs may be subtle. An allergic reaction to the presence of the mite is responsible for signs and symptoms. The degree of this reaction is variable and may sometimes be absent. Sometimes the only complaint is itch without an obvious rash. The itch exacerbates at night and after hot showers. Typically there is an itchy, excoriated but nonspecific rash on the trunk, associated with scaly burrows on the fingers and wrists. Papular lesions are often seen around the major flexures in children, on the penis in men, or on the nipples in women. In babies and young children, there are often vesicles and pustules on the palms and soles and sometimes on the scalp. Nodules may occur in axillae, groin and sometimes other parts of the skin. Secondary bacterial infection may occur.

Confirmation of the diagnosis is made by microscopy of scrapings from a burrow. The main pitfall in using this technique is the selection of a suitable burrow, as these are few in number and difficult to identify. This procedure therefore requires some skill. Response to antiscabetic medication may therefore be used as the most practical diagnostic test. In doubtful cases, or where the patient has difficulty accepting the diagnosis, a scraping is very useful. The burrow is a superficial lesion, which involves only the epidermis, and its contents may easily be scraped from the skin surface using a scalpel blade. The material is smeared onto a drop of oil or potassium hydroxide 10%. Microscopy of this material reveals the mite, eggs or faecal material.

 

If secondary bacterial infection is present, treat as for impetigo at the same time as scabicide treatment.

1	permethrin 5% cream (child >6 months) topically, to the whole body including face and hair (avoid eyes and mucous membranes), leave overnight
	OR
2	benzyl benzoate 25% emulsion (child <2 years: dilute with 3 parts of water; child 2 to 12 years and sensitive adult: dilute with equal parts of water) topically to the whole body, including face and hair (avoid eyes and mucous membranes), leave for 24 hours.

 

Treat family and close contacts even if free of symptoms, since these can take several weeks to develop and contacts may by then have become a source of re-infection. After the recommended treatment, wash clothing and bedclothes and hang in the sun. Clothing or bedding that cannot be washed should be placed in plastic bags for 7 days.

Children under 2 months of age can be treated with sulfur 5% cream daily for 2 to 3 days or crotamiton 10% cream daily for 3 to 5 days, according to the manufacturer's instructions. These agents are less efficacious and cure may not occur. If relapse occurs, consider treatment with permethrin.

For moderate and severe infections, repeat scabicide treatment in 14 days.

 

Contact tracing, notification and treatment are essential to prevent treatment failure. All members of the patient’s family and close contacts should be treated simultaneously. In closed communities such as nursing homes, all patients and staff require treatment. If a school-age child has had scabies, the school should be notified, but treatment of clinically uninvolved children is not required.

 

The itching of scabies does not resolve immediately after treatment and may take 3 weeks to subside. Part of this itching may be irritation from the antiscabetic agent itself. Patients must be warned and instructed not to apply further antiscabetic agents. During this time, relieve the itch and dermatitis that occurs secondarily.

Use

	a moderately potent topical corticosteroid applied 2 to 3 times daily
	AND
	an emollient.

 

Postscabetic nodules may last for months despite treatment with a topical corticosteroid.

 

In this variant of scabies, the mite population on the patient is very high due to a poor host response. This is seen in physically incapacitated and immunocompromised patients, including those with HIV infection. It presents with gross, fissured thickening of the skin, particularly on the back of the neck and around the hands and feet and under the nails. Often there is secondary dermatitis but, paradoxically, itch may be absent. Diagnosis is easily made by a scraping because of the vast number of lesions.

For crusted (Norwegian) scabies, consider ivermectin (child >5 years) 200 micrograms/kg orally initially as a single dose, in association with scabicides. Topical keratolytics containing, for example, lactic acid 5% and urea 10% can be applied daily after washing, on days when scabicides are not applied. It may be necessary to repeat scabicides twice-weekly for 2 to 6 weeks, together with repeated ivermectin doses. One regimen for severe crusted scabies is ivermectin (child >5 years) 200 micrograms/kg orally on days 1, 2, 15, 16 and 29.

 

The source of a scabies outbreak in this situation is frequently a new, infested patient. If possible, this patient should be identified, as they may have Norwegian scabies. The safety of ivermectin in elderly and debilitated patients has not yet been established.

The affected ward should be quarantined and all patients, medical and nursing staff and their families should be treated. Bedding, clothes and towels should be laundered and communal sitting areas sprayed with insecticide. If staff from the affected ward have worked elsewhere, that area should also be treated.

 

The recommended treatment is permethrin 5% cream, see Background and treatment. Permethrin is classified as category B2; however, this must be balanced against the significant morbidity of untreated scabies. Patients may elect to postpone treatment if scabies is acquired in the first trimester of pregnancy.

Alternative treatment with sulfur 5 to 10% in sorbolene cream may be used if the clinician judges the risks of treatment with permethrin to outweigh the benefit.

 

Scabies in HIV-infected individuals may be resistant to repeated attempts at topical therapy. In this situation, use

ivermectin 200 micrograms/kg orally, weekly.

 

Note:

Ivermectin is available in Australia but is not specifically approved for use in scabies. It is not recommended in geriatric patients.

 

If treatment fails after the use of permethrin, consider the possibility of a wrong diagnosis, an unidentified source of reinfestation, inadequate contact tracing or noncompliance with instructions. Recommended measures are to consider other diagnoses and treat accordingly, to supervise treatment (inpatient, community nurse) or specialist referral.

If topical treatment fails, and the diagnosis of scabies is not in doubt, use

ivermectin 200 microgram/kg orally, as a single dose.

Lice

 

 

Head lice are common and not indicative of poor hygiene. The only complication is secondary infection from scratching.

Approximately one-third of cases can be cured by wet combing (applying hair conditioner or olive oil to wet hair and using a fine nit comb) every 3 to 4 days for several weeks after detection.

Alternatively, topical insecticides can be used

1	maldison 0.5 to 1% topically, according to the manufacturer’s instructions. Not to be used in children <6 months
	OR
1	permethrin 1% topically, according to the manufacturer’s instructions
	OR
1	pyrethrins 0.165% + piperonyl butoxide 1.65% to 4% topically, according to the manufacturer’s instructions.

 

Apply to hair (avoiding contact with eyes and mucous membranes), leave for the time advised, then rinse thoroughly with warm water. Wash hands thoroughly after use. Two to 3 days after the treatment, comb hair with a fine comb. If pyrethrins or permethrin are used, treatment should be repeated at 7 to 10 days.

Family and other intimate contacts should be examined and treated.

After 1 or 2 treatments, persisting adult lice suggest resistance, so re-treatment with an alternative regimen may be necessary. Pyrethrins and permethrin are chemically similar, but maldison has a different mode of action. This may be important, as head lice may become resistant to each group of agents.

 

For head lice that are resistant to topical insecticides, the recommended treatment is

olive oil applied thickly to scalp and hair for 8 hours on treatment days 1, 2, 5, 9, 13, 17 and 21, to coincide with the lifecycle of the louse. Then comb out with a fine comb.

 

The basis for this treatment is that the oil suffocates the lice. If this fails, use

trimethoprim+sulfamethoxazole 80+400mg orally, twice daily for 3 days. Repeat after 10 days.

 

It is thought that the effectiveness of trimethoprim+sulfamethoxazole is due to the destruction of symbiotic bacteria in the gut of the lice.

 

Phthirus pubis colonises pubic, axillary, beard and body hair. It may also involve eyebrows and eyelashes. It is transmitted by close physical contact, often sexual. It is most often seen in adults. In children sexual abuse should be considered but is not invariable. The main symptom is itching with the louse and eggs visible on hairs. Treatment is the same as for head lice (above). Contact tracing is essential. The whole body surface should be examined, including eyelashes and eyebrows. Shaving pubic hair is also helpful. Underwear and bedclothes should be washed. Treatment failure may be due to re-infection, and family and sexual partner(s) should therefore be checked and treated as appropriate.

 

Treat as for head lice (above) applying the preparation to the whole body, but avoiding contact with eyes and mucous membranes. The parasites and eggs are found in clothing and bedclothes, which should be discarded, hot washed or sealed in plastic bags for 30 days.

 

White soft paraffin is applied thickly to the eyelashes twice a day for 8 days to suffocate the insects. The nits may then be physically removed with fine forceps. This may be difficult, requiring slit lamp control. In this situation, referral to an ophthalmologist is recommended.