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Skin and soft tissue infections
SKIN AND SOFT TISSUE INFECTIONS
Skin and soft tissue infections
Impetigo Impetigo is an infection of the epidermis usually caused by Staph. aureus or group A streptococci. It is most common in hot, humid conditions and is often associated with overcrowding and poor hygiene. It may occur in outbreaks in households and institutions. Children are most commonly affected, and lesions typically occur on the face and hands. Impetigo is characterized by intra-epidermal vesicles, which rupture and crust to form a golden-yellow scab. Management – impetigo is treated by removal of the crusts and application of topical antibiotics such as mupirocin. Widespread infection responds better to oral antibiotics (e.g. flucloxacillin).
Estée Török Christopher P Conlon
The skin acts as a barrier between the host and the environment. It comprises several layers. The most superficial is the epidermis, a thin avascular layer overlying the dermis, which is a thicker layer containing hair follicles, sebaceous glands and sweat glands. Subcutaneous fat lies beneath the dermis and is separated from muscle by a tough layer of fascia. Infections may affect one or more of these layers. The skin is colonized by various micro-organisms that may invade and cause infection. Skin commensals include coagulasenegative staphylococci, of which Staphylococcus epidermidis is the most common. Staph. aureus and group A streptococci are the most important pathogens in skin and soft tissue infections. Other organisms (e.g. Gram-negative bacteria, anaerobes, viruses, fungi, parasites) may also cause infection. Infections of the skin and soft tissues are common and affect all age groups. They may occur as single or recurrent episodes, and may be mild and self-limiting or severe and progressive, leading to systemic complications such as bacteraemia and metastatic infection.
Ecthyma Ecthyma is a form of impetigo that penetrates deeper into the dermis and may scar. It starts as a vesicle and progresses to form a punched-out ulcer surrounded by a violaceous border. Ecthyma often occurs on the legs and is associated with insect bites, eczema, pediculosis and minor trauma. Most cases are caused by group A streptococci. Similar lesions, termed ‘ecthyma gangrenosum’, sometimes occur with Pseudomonas aeruginosa bacteraemia in neutropenic patients. Management is as for impetigo, unless the ecthyma is associated with P. aeruginosa bacteraemia, in which case appropriate intravenous antibiotics are required (e.g. ceftazidime, tazocin).
Folliculitis Folliculitis is an infection localized within the hair follicles and is characterized by clusters of small, erythematous papules or pustules. It is caused by a combination of occlusion of the hair follicle and infection, usually with Staph. aureus. It may also be caused by P. aeruginosa acquired from a swimming pool or jacuzzi (‘hot-tub folliculitis’). Fungi such as Candida and Pityrosporum orbiculare (Malassezia furfur) can sometimes cause folliculitis in patients who have diabetes or are receiving prolonged antibiotics or corticosteroid therapy. Management – staphylococcal folliculitis is treated with oral flucloxacillin. Hot-tub folliculitis is usually self-limiting. Fungal infection may require topical 1% clotrimazole for about 1 week. Folliculits often affects the beard area in men. When it is severe, topical 1% hydrocortisone may be needed in addition to antibiotics. Patients should use an electric razor until the condition settles.
Diagnosis A detailed history is essential to establish a specific diagnosis. It should include: • onset and duration of symptoms • appearance and anatomical distribution of the lesion • history of trauma • contact with insects and other animals • recent foreign travel • pre-existing medical conditions (e.g. diabetes mellitus, immunosuppression). When the diagnosis cannot be determined from the clinical features alone, investigations such as needle aspiration, biopsy or surgical debridement may be necessary to obtain appropriate specimens for microbiological examination and culture.
Furuncles and carbuncles Folliculitis may progress to involve the dermis, resulting in the development of a subcutaneous boil or abscess (furuncle). The usual cause is Staph. aureus. When a number of furuncles coalesce, the resulting inflammatory lesion is termed a ‘carbuncle’. Carbuncles are characterized by inflamed skin with pus draining from several hair follicles (Figure 1). Carbuncles are commonly found on areas of thickened skin such as the nape of the neck, the back and the thighs. Fever and malaise are common. Rarely, recurrent furuncles become a problem. Diabetes mellitus, and rare causes of immunodeficiency such as hyper-IgE syndrome (Job’s syndrome) and chronic granulomatous disease, should be considered.
Estée Török is Clinical Research Fellow in the Oxford University Clinical Research Unit, Viet Nam. Conflict of interests: none declared. Christopher P Conlon is a Consultant in Infectious Diseases and General Medicine in Oxford, UK. Conflict of interests: none declared.
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2 Erysipelas caused by Streptococcus pyogenes. (© 2005 C P Conlon) 1 Carbuncle on the dorsum of the foot. (© 2005 C P Conlon)
tions). Patients with diabetes, leg ulcers, lymphoedema, varicose veins or peripheral vascular disease are at increased risk. Cellulitis usually affects the legs and presents as a red, hot, swollen, tender area that is not as well demarcated or elevated as in erysipelas. Thrombophlebitis, lymphangitis, regional lymphadenopathy and fever are common. Local abscesses may develop and the overlying skin may necrose. Diagnosis of cellulitis is almost entirely clinical, because skin swabs are unhelpful and blood cultures, skin biopsies and tissue aspirates are seldom positive. Aspiration of blisters or collections may be helpful. Management – when staphylococcal infection is suspected or the cause is unknown, treatment is with intravenous flucloxacillin. When the patient is diabetic or has leg ulcers, intravenous cefuroxime and oral metronidazole may be used instead. Intravenous vancomycin should be used for cellulitis in patients who have been previously colonized with methicillin-resistant Staph. aureus. Vancomycin is toxic at high doses, so the dose may have
Management – small furuncles may burst and heal spontaneously; larger ones may require incision and drainage. Carbuncles usually require incision and drainage and systemic antistaphylococcal therapy (e.g. oral or intravenous flucloxacillin). Patients with recurrent furuncles who do not have underlying immunodeficiency should be considered for staphylococcal decolonization using 2% mupirocin ointment and oral antibiotics such as rifampicin and tetracycline.
Erysipelas Erysipelas is a superficial infection of the dermis accompanied by lymphatic involvement. It is almost always caused by group A streptococci and is characterized by abrupt onset of a painful, erythematous, spreading rash with well-demarcated edges. There are often systemic features, and bacteraemia occurs in 5% of patients. Erysipelas previously occurred most commonly on the face (Figure 2), but now more commonly affects the legs. Predisposing factors include venous stasis, paraparesis, diabetes and alcohol abuse. Common portals of entry are trauma, ulcers, and eczematous, psoriatic or fungal skin lesions. Erysipelas tends to occur in areas of lymphatic obstruction and, because it also causes lymphatic obstruction, tends to recur. Management – treatment is with benzylpenicillin or clindamycin. If staphylococcal infection is likely, flucloxacillin should be used instead.
Cellulitis Cellulitis is rapidly spreading inflammation of the deep dermis and subcutaneous fat (Figure 3). The most common pathogens are group A streptococci and Staph. aureus. Other β-haemolytic streptococci (groups C, G and B) also sometimes cause cellulitis. Rare causes include Streptococcus pneumoniae, Enterobacteriaceae, Legionella pneumophila, Aeromonas hydrophila and Vibrio vulnificus. Cellulitis generally occurs after injury to the skin or as a result of breaches of the skin (e.g. ulcers, eczema, psoriasis, tinea infecMEDICINE 33:4
3 Typical severe inflammation of the skin and soft tissues in cellulitis of the lower leg.
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Management – the wound should be assessed carefully for evidence of damage to joints, muscles, tendons, nerves and blood vessels. A specialist hand surgeon should be consulted when the wound is to the hand. Prophylactic co-amoxiclav has been shown to be effective. Treatment comprises copious wound irrigation, debridement, elevation of the affected part and, if appropriate, tetanus and rabies immunization. Primary wound closure is usually undertaken only for facial wounds. MRI should be undertaken when there is clinical suspicion of osteomyelitis. Human bites should be managed with prophylactic antibiotics, but the risk of blood-borne viral infections should be considered. Recipients of monkey bites should be given prophylactic aciclovir because of the risk of simian herpesvirus B.
to be adjusted in response to trough plasma levels. Teicoplanin or linezolid are suitable alternatives. Analgesia, elevation of the limb and subcutaneous heparin are useful adjunctive measures.
Bursitis Staphylococcal infection of the deeper tissues may cause superficial redness, warmth and swelling of the skin, even though the skin itself is not infected. Examples include olecranon bursitis and prepatellar bursitis. There is often a history of recent trauma to the site. Diagnosis is clinical. Management – treatment is with intravenous flucloxacillin, elevation of the limb and, if necessary, aspiration of pus from the affected bursa.
Infections in intravenous drug-users Wound infections
Intravenous drug-users often introduce bacteria into normally sterile sites. Although septicaemia and endocarditis are the greatest dangers, skin and soft tissue infections are more common. The most common organism is Staph. aureus, but oral flora (e.g. α-haemolytic streptococci, Eikenella corrodens) may be found in those who lick their needles. Other causes include Strep. pneumoniae, Gram-negative bacteria, Clostridia spp. and fungi. Cellulitis or abscesses (Figure 4) may occur at the site of injection and can cause considerable soft tissue damage. Injections may also cause intramuscular abscesses (pyomyositis) or necrotizing fasciitis. Complications include bacteraemia, septic arthritis, osteomyelitis and infectious endocarditis. Management – intravenous antibiotics and, usually, surgical drainage or debridement are required.
The prevalence of surgical wound infections has decreased greatly since the advent of antibiotic prophylaxis. Several factors are known to contribute to the risk of wound infection: • host (immunity, nutritional status, diabetes) • surgical (type of procedure, surgical technique, use of foreign material) • microbial (microbial concentration and virulence, resistance to perioperative antibiotics). Surgical wound infections can be divided into superficial (involving skin or soft tissues) and deep (involving fascia or muscle). The most common pathogens are Staph. aureus, coagulasenegative staphylococci, enterococci, Escherichia coli, P. aeruginosa, Enterobacter spp., other enterobacteria, other streptococci, Candida spp. and anaerobes. Most superficial surgical wound infections present within days after the operation, with fever and local pain, swelling, erythema, tenderness, a purulent discharge or wound dehiscence. Ultrasonography or CT may be required to identify deep surgical wound infection in patients with clinical evidence of systemic infection but no local signs. Management of surgical wound infection primarily involves incision and drainage, debridement of any necrotic tissue, removal of any foreign bodies and local wound care. A deep pus or tissue sample should be sent for microbiological assessment. Surface swabs are not useful because they merely reflect colonizing organisms. Most superficial wound infections do not require any further therapy. The need for antimicrobial therapy should be guided by clinical findings (e.g. spreading cellulitis, systemic symptoms). The initial choice of antimicrobial agent should be directed towards the most likely organisms, according to the type of operation performed. Treatment can then be tailored in light of microbiological findings. Most incisional surgical wound infections are left open and allowed to heal by secondary intention.
Necrotizing fasciitis Necrotizing fasciitis is an uncommon, severe infection of the subcutaneous tissue that results in progressive destruction of fascia and fat (Figure 5). Predisposing factors include diabetes, alcoholism and intravenous drug use. There are two clinical types – I and II. • Type I necrotizing fasciitis is a mixed infection caused by anaerobic bacteria (e.g. Bacteroides spp., Peptostreptococcus) and facultatively anaerobic bacteria (streptococci, enterobacteria). It
Bite wounds Domestic pets are the usual cause of bites. It is estimated that 3–18% of dog wounds and 28–80% of cat wounds become infected. Although most attention has focused on Pasteurella multocida, a wide spectrum of organisms have been isolated from bite wounds, including Capnocytophaga canimorsis, streptococci, enterococci, staphylococci, Haemophilus spp., Neisseria spp. and anaerobes.
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4 Injection abscess in an intravenous drug-user. (© 2005 C P Conlon)
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Management – treatment is with prompt surgical debridement and intravenous broad-spectrum antibiotics.
Gas gangrene Gas gangrene is a rare anaerobic infection most commonly caused by Clostridium perfringens. It is usually associated with a deep, penetrating injury that creates anaerobic conditions ideal for clostridia. Clinical features include sudden onset of pain 6–8 hours after injury. This is followed by increasing pain and tenderness, darkening of the skin to a purplish-red colour, formation of bullae, crepitus, fever, shock, and liver and renal failure. Gas in the soft tissues may be confirmed by plain radiography, CT or MRI. The diagnosis is confirmed by microbiological demonstration of Grampositive rods in the affected tissue. Management – aggressive surgical debridement combined with intravenous penicillin and clindamycin or tetracycline is required. Use of hyperbaric oxygen is controversial. Gas gangrene antitoxin may be useful if administered early.
5 Necrotizing fasciitis affecting the buttock. Note the tissue breakdown and the blue discoloration of subcutaneous tissue.
occurs in middle-aged and elderly individuals, most commonly after surgical procedures, and in those with diabetes or peripheral vascular disease. Infection usually starts in the feet and progresses rapidly along the fascia into the leg. Clinical presentation is with cellulitis and systemic signs of severe infection. Type I necrotizing fasciitis may also develop in the head and neck following a breach of the mucous membranes by surgery or instrumentation. • Type II necrotizing fasciitis is caused by group A streptococci and was previously termed ‘streptococcal gangrene’. It may occur in any age group. The cardinal symptom is excruciating pain with minimal cutaneous findings. Initially, there may also be fever, malaise, myalgia and diarrhoea. After 24–48 hours, erythema may develop, the skin may darken to a reddish-purple colour and bullae may develop. Patients are systemically unwell and may develop streptococcal toxic shock syndrome. Laboratory tests reveal neutrophil leucocytosis, thrombocytopenia and raised serum aspartate transaminase, creatine phosphokinase and creatinine. Radiological imaging (CT or MRI) may show subcutaneous and fascial oedema in addition to gas in the tissues, but should not delay prompt surgical exploration in patients in whom the diagnosis is clearly suspected. Management – prompt surgical exploration and debridement are essential. Intravenous broad-spectrum antibiotics (e.g. cefuroxime and metronidazole, clindamycin and gentamicin) are given until bacteriological data are available. Clindamycin has a theoretical advantage in that it may interrupt toxin production and reduce systemic toxic effects. Patients often require intensive care. Imaging studies may be helpful for monitoring progress and assessing the need for further surgery.
Uncommon infections Anthrax is caused by Bacillus anthracis and most commonly affects the skin, resulting in a ‘malignant pustule’. Infections occur in abattoir workers and result from inoculation of bacterial spores into skin abrasions caused by handling the hides of infected animals. After a few days, a papule forms at the site of infection; this develops into a vesicle and ulcerates to form a necrotic centre or eschar (Figure 6). Local oedema, painful regional lymphadenopathy and systemic features are often present. The diagnosis is confirmed by demonstrating Gram-positive bacilli in the ulcer fluid or tissues and by culturing the organism. Penicillin therapy is adequate, though quinolones and tetracyclines are also effective. An anthrax vaccine is available for military use. Cat-scratch disease – Bartonella henselae is the most common cause. Clinical features include regional lymphadenopathy, fever and a red papule at the inoculation site. Atypical presentations include Parinaud’s ocular glandular syndrome, maculopapular rash, erythema multiforme, erythema nodosum and leucocyto-
Fournier’s gangrene Fournier’s gangrene is a form of necrotizing fasciitis that affects the perineum. Although it may occur spontaneously, it most commonly affects debilitated, hospitalized men over the age of 50 years. Diabetes is a predisposing condition. Fournier’s gangrene is caused by penetration of the gastrointestinal or urethral mucosa by Gramnegative bacteria, enterococci or anaerobes such as Bacteroides spp. and peptostreptococci. Clinical features include severe pain and necrotizing fasciitis, which may involve the anterior abdominal wall, gluteal muscles, scrotum and penis.
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6 Cutaneous anthrax – small lesion with necrotic appearance. Gram-positive bacilli were visible on tissue biopsy, and Bacillus anthracis was found on culture.
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clastic vasculitis. The diagnosis is confirmed serologically and by polymerase chain reaction analysis. Treatment is with azithromycin or doxycycline. Cutaneous larva migrans occurs in returning travellers, particularly those who have visited tropical beaches. It is caused by infection with animal hookworm larvae such as Ancylostoma brasiliense, A. caninum and Uncinaria stenocephala, and presents as an itchy cluster of lesions or a sinuous track on exposed areas. Treatment is with albendazole. Erysipeloid is a rare condition is caused by Erysipelothrix rhusiopathiae. It is usually acquired from infected animals, and affects veterinary surgeons, farmers and butchers. The organism is inoculated into the skin and causes characteristic dark, purplish lesions with swelling of the digits (Figure 7). Rarely, septicaemia occurs and may be complicated by endocarditis. The condition is treated with penicillin. Erythema chronicum migrans is the cutaneous manifestation of Lyme disease, which is caused by Borrelia burgdorferi. It is acquired by inoculation from a tick bite. A red, circular lesion develops and spreads from the site of the bite. Other features include fever, malaise and arthralgia. Diagnosis is serological. Treatment is with doxycycline. Leishmaniasis – cutaneous leishmaniasis is acquired from a sandfly bite. ‘Old world’ leishmaniasis, caused by Leishmania major, L. tropica and L. aethiopica, is endemic in Africa, Asia, India, the Middle East and the Mediterranean. ‘New world’ leishmaniasis, caused by L. brasiliensis, L. mexicana and L. panamensis, is endemic in Latin America. Clinical presentation is with a crusted sore on the face, hand or leg 6–8 weeks after returning from an endemic area. Diagnosis is clinical and confirmed histologically. Lesions often resolve spontaneously, but some may require cryotherapy or treatment with pentavalent antimony, amphotericin B or pentamidine. Patients with L. brasiliensis should be treated to avoid the possibility of espundia (mucocutaneous disease). Leprosy – infection with Mycobacterium leprae causes a spectrum of clinical disease ranging from tuberculoid to lepromatous leprosy. In tuberculoid leprosy, anaesthetic macules or plaques, pigmentary change and thickened peripheral nerves develop. In
lepromatous leprosy, macules, papules, nodules and ulceration occur, resulting in collapse of the nasal bones and coarsening of facial tissues, producing the characteristic ‘leonine’ facies. The diagnosis is confirmed by biopsy and split-skin smears. Treatment is with dapsone, clofazimine and rifampicin. Lupus vulgaris is a cutaneous infection caused by M. tuberculosis. It most commonly affects the face and neck, and appears as firm, translucent, yellow-brown ‘apple jelly’ nodules. Untreated lesions spread, leading to disfiguring scarring and contractures. Diagnosis is confirmed by biopsy, which shows tuberculoid granulomata in the mid-dermis. Treatment is with antituberculous chemotherapy. Molluscum contagiosum is a benign condition caused by a pox virus. It usually affects children or the immunocompromised (e.g. HIV-infected patients). The lesions are most commonly seen on the face and trunk, and are papular with a central punctum. Orf is an infectious cutaneous lesion caused by a pox virus acquired from sheep. It commonly affects farmers (particularly those who bottle-feed lambs) and veterinary surgeons. A red papule develops, commonly on the sides of the fingers, and grows rapidly, often becoming vesicular, before developing a central necrotic area. Lymphangitis, regional lymphadenopathy and fever are common. Recovery is spontaneous. Scabies is a pruritic skin lesion caused by infestation with Sarcoptes scabei. It is associated with poor socioeconomic conditions and overcrowding. The female mite lays her eggs in a burrow in the stratum corneum, generating a local hypersensitivity reaction; when the eggs hatch, the cycle is repeated. Diagnosis is confirmed by extraction of the mite from a burrow. Treatment comprises topical acaricides (e.g. permethrin) and washing of all clothing and linen. All members of the household should be treated at the same time. Tick typhus – African tick typhus, caused by Rickettsia conorii and R. africae is commonly seen in patients returning from safari in southern Africa. Endemic typhus is caused by R. typhi and transmitted by the rat flea. Epidemic typhus is caused by R. prowazekii and transmitted by the human louse. Clinical features include fever, headache, malaise, myalgia, lymphadenopathy and splenomegaly. There may be an eschar at the site of inoculation and a maculopapular rash, though some spotted fevers produce few if any spots. Diagnosis is confirmed serologically. Treatment is with doxycycline.
FURTHER READING Bisno A L, Stevens D L. Streptococcal infections of the skin and soft tissues. N Engl J Med 1996; 334: 240. Brook I. Microbiology and management of human and animal bite wound infections. Prim care 2003; 30: 25–31. Ebright J R, Pieper B. Skin and soft tissue infections in injection drug users. Infect Dis Clin North Am 2002; 16: 697–12. Guay D R. Treatment of bacterial skin and skin structure infections. Expert Opin Pharmacother 2003; 4: 1259–75. Seal D V. Necrotizing fasciitis. Curr Opin Infect Dis 2001; 14: 127–32. Shwarz M N. Clinical practice. Cellulitis. N Engl J Med 2004; 350: 904–12. Shwarz M. Cellulitis and subcutaneous tissue infections. In: Mandell G L, Owen R, Bennett J E et al., eds. Principles and practice of infectious diseases. 5th ed. New York: Churchill Livingstone, 2000: 1037–57.
7 Erysipeloid affecting the hand. (© 2005 C P Conlon)
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Skin and soft tissue infections
Impetigo Impetigo is an infection of the epidermis usually caused by Staph. aureus or group A streptococci. It is most common in hot, humid conditions and is often associated with overcrowding and poor hygiene. It may occur in outbreaks in households and institutions. Children are most commonly affected, and lesions typically occur on the face and hands. Impetigo is characterized by intra-epidermal vesicles, which rupture and crust to form a golden-yellow scab. Management – impetigo is treated by removal of the crusts and application of topical antibiotics such as mupirocin. Widespread infection responds better to oral antibiotics (e.g. flucloxacillin).
Estée Török Christopher P Conlon
The skin acts as a barrier between the host and the environment. It comprises several layers. The most superficial is the epidermis, a thin avascular layer overlying the dermis, which is a thicker layer containing hair follicles, sebaceous glands and sweat glands. Subcutaneous fat lies beneath the dermis and is separated from muscle by a tough layer of fascia. Infections may affect one or more of these layers. The skin is colonized by various micro-organisms that may invade and cause infection. Skin commensals include coagulasenegative staphylococci, of which Staphylococcus epidermidis is the most common. Staph. aureus and group A streptococci are the most important pathogens in skin and soft tissue infections. Other organisms (e.g. Gram-negative bacteria, anaerobes, viruses, fungi, parasites) may also cause infection. Infections of the skin and soft tissues are common and affect all age groups. They may occur as single or recurrent episodes, and may be mild and self-limiting or severe and progressive, leading to systemic complications such as bacteraemia and metastatic infection.
Ecthyma Ecthyma is a form of impetigo that penetrates deeper into the dermis and may scar. It starts as a vesicle and progresses to form a punched-out ulcer surrounded by a violaceous border. Ecthyma often occurs on the legs and is associated with insect bites, eczema, pediculosis and minor trauma. Most cases are caused by group A streptococci. Similar lesions, termed ‘ecthyma gangrenosum’, sometimes occur with Pseudomonas aeruginosa bacteraemia in neutropenic patients. Management is as for impetigo, unless the ecthyma is associated with P. aeruginosa bacteraemia, in which case appropriate intravenous antibiotics are required (e.g. ceftazidime, tazocin).
Folliculitis Folliculitis is an infection localized within the hair follicles and is characterized by clusters of small, erythematous papules or pustules. It is caused by a combination of occlusion of the hair follicle and infection, usually with Staph. aureus. It may also be caused by P. aeruginosa acquired from a swimming pool or jacuzzi (‘hot-tub folliculitis’). Fungi such as Candida and Pityrosporum orbiculare (Malassezia furfur) can sometimes cause folliculitis in patients who have diabetes or are receiving prolonged antibiotics or corticosteroid therapy. Management – staphylococcal folliculitis is treated with oral flucloxacillin. Hot-tub folliculitis is usually self-limiting. Fungal infection may require topical 1% clotrimazole for about 1 week. Folliculits often affects the beard area in men. When it is severe, topical 1% hydrocortisone may be needed in addition to antibiotics. Patients should use an electric razor until the condition settles.
Diagnosis A detailed history is essential to establish a specific diagnosis. It should include: • onset and duration of symptoms • appearance and anatomical distribution of the lesion • history of trauma • contact with insects and other animals • recent foreign travel • pre-existing medical conditions (e.g. diabetes mellitus, immunosuppression). When the diagnosis cannot be determined from the clinical features alone, investigations such as needle aspiration, biopsy or surgical debridement may be necessary to obtain appropriate specimens for microbiological examination and culture.
Furuncles and carbuncles Folliculitis may progress to involve the dermis, resulting in the development of a subcutaneous boil or abscess (furuncle). The usual cause is Staph. aureus. When a number of furuncles coalesce, the resulting inflammatory lesion is termed a ‘carbuncle’. Carbuncles are characterized by inflamed skin with pus draining from several hair follicles (Figure 1). Carbuncles are commonly found on areas of thickened skin such as the nape of the neck, the back and the thighs. Fever and malaise are common. Rarely, recurrent furuncles become a problem. Diabetes mellitus, and rare causes of immunodeficiency such as hyper-IgE syndrome (Job’s syndrome) and chronic granulomatous disease, should be considered.
Estée Török is Clinical Research Fellow in the Oxford University Clinical Research Unit, Viet Nam. Conflict of interests: none declared. Christopher P Conlon is a Consultant in Infectious Diseases and General Medicine in Oxford, UK. Conflict of interests: none declared.
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2 Erysipelas caused by Streptococcus pyogenes. (© 2005 C P Conlon) 1 Carbuncle on the dorsum of the foot. (© 2005 C P Conlon)
tions). Patients with diabetes, leg ulcers, lymphoedema, varicose veins or peripheral vascular disease are at increased risk. Cellulitis usually affects the legs and presents as a red, hot, swollen, tender area that is not as well demarcated or elevated as in erysipelas. Thrombophlebitis, lymphangitis, regional lymphadenopathy and fever are common. Local abscesses may develop and the overlying skin may necrose. Diagnosis of cellulitis is almost entirely clinical, because skin swabs are unhelpful and blood cultures, skin biopsies and tissue aspirates are seldom positive. Aspiration of blisters or collections may be helpful. Management – when staphylococcal infection is suspected or the cause is unknown, treatment is with intravenous flucloxacillin. When the patient is diabetic or has leg ulcers, intravenous cefuroxime and oral metronidazole may be used instead. Intravenous vancomycin should be used for cellulitis in patients who have been previously colonized with methicillin-resistant Staph. aureus. Vancomycin is toxic at high doses, so the dose may have
Management – small furuncles may burst and heal spontaneously; larger ones may require incision and drainage. Carbuncles usually require incision and drainage and systemic antistaphylococcal therapy (e.g. oral or intravenous flucloxacillin). Patients with recurrent furuncles who do not have underlying immunodeficiency should be considered for staphylococcal decolonization using 2% mupirocin ointment and oral antibiotics such as rifampicin and tetracycline.
Erysipelas Erysipelas is a superficial infection of the dermis accompanied by lymphatic involvement. It is almost always caused by group A streptococci and is characterized by abrupt onset of a painful, erythematous, spreading rash with well-demarcated edges. There are often systemic features, and bacteraemia occurs in 5% of patients. Erysipelas previously occurred most commonly on the face (Figure 2), but now more commonly affects the legs. Predisposing factors include venous stasis, paraparesis, diabetes and alcohol abuse. Common portals of entry are trauma, ulcers, and eczematous, psoriatic or fungal skin lesions. Erysipelas tends to occur in areas of lymphatic obstruction and, because it also causes lymphatic obstruction, tends to recur. Management – treatment is with benzylpenicillin or clindamycin. If staphylococcal infection is likely, flucloxacillin should be used instead.
Cellulitis Cellulitis is rapidly spreading inflammation of the deep dermis and subcutaneous fat (Figure 3). The most common pathogens are group A streptococci and Staph. aureus. Other β-haemolytic streptococci (groups C, G and B) also sometimes cause cellulitis. Rare causes include Streptococcus pneumoniae, Enterobacteriaceae, Legionella pneumophila, Aeromonas hydrophila and Vibrio vulnificus. Cellulitis generally occurs after injury to the skin or as a result of breaches of the skin (e.g. ulcers, eczema, psoriasis, tinea infecMEDICINE 33:4
3 Typical severe inflammation of the skin and soft tissues in cellulitis of the lower leg.
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Management – the wound should be assessed carefully for evidence of damage to joints, muscles, tendons, nerves and blood vessels. A specialist hand surgeon should be consulted when the wound is to the hand. Prophylactic co-amoxiclav has been shown to be effective. Treatment comprises copious wound irrigation, debridement, elevation of the affected part and, if appropriate, tetanus and rabies immunization. Primary wound closure is usually undertaken only for facial wounds. MRI should be undertaken when there is clinical suspicion of osteomyelitis. Human bites should be managed with prophylactic antibiotics, but the risk of blood-borne viral infections should be considered. Recipients of monkey bites should be given prophylactic aciclovir because of the risk of simian herpesvirus B.
to be adjusted in response to trough plasma levels. Teicoplanin or linezolid are suitable alternatives. Analgesia, elevation of the limb and subcutaneous heparin are useful adjunctive measures.
Bursitis Staphylococcal infection of the deeper tissues may cause superficial redness, warmth and swelling of the skin, even though the skin itself is not infected. Examples include olecranon bursitis and prepatellar bursitis. There is often a history of recent trauma to the site. Diagnosis is clinical. Management – treatment is with intravenous flucloxacillin, elevation of the limb and, if necessary, aspiration of pus from the affected bursa.
Infections in intravenous drug-users Wound infections
Intravenous drug-users often introduce bacteria into normally sterile sites. Although septicaemia and endocarditis are the greatest dangers, skin and soft tissue infections are more common. The most common organism is Staph. aureus, but oral flora (e.g. α-haemolytic streptococci, Eikenella corrodens) may be found in those who lick their needles. Other causes include Strep. pneumoniae, Gram-negative bacteria, Clostridia spp. and fungi. Cellulitis or abscesses (Figure 4) may occur at the site of injection and can cause considerable soft tissue damage. Injections may also cause intramuscular abscesses (pyomyositis) or necrotizing fasciitis. Complications include bacteraemia, septic arthritis, osteomyelitis and infectious endocarditis. Management – intravenous antibiotics and, usually, surgical drainage or debridement are required.
The prevalence of surgical wound infections has decreased greatly since the advent of antibiotic prophylaxis. Several factors are known to contribute to the risk of wound infection: • host (immunity, nutritional status, diabetes) • surgical (type of procedure, surgical technique, use of foreign material) • microbial (microbial concentration and virulence, resistance to perioperative antibiotics). Surgical wound infections can be divided into superficial (involving skin or soft tissues) and deep (involving fascia or muscle). The most common pathogens are Staph. aureus, coagulasenegative staphylococci, enterococci, Escherichia coli, P. aeruginosa, Enterobacter spp., other enterobacteria, other streptococci, Candida spp. and anaerobes. Most superficial surgical wound infections present within days after the operation, with fever and local pain, swelling, erythema, tenderness, a purulent discharge or wound dehiscence. Ultrasonography or CT may be required to identify deep surgical wound infection in patients with clinical evidence of systemic infection but no local signs. Management of surgical wound infection primarily involves incision and drainage, debridement of any necrotic tissue, removal of any foreign bodies and local wound care. A deep pus or tissue sample should be sent for microbiological assessment. Surface swabs are not useful because they merely reflect colonizing organisms. Most superficial wound infections do not require any further therapy. The need for antimicrobial therapy should be guided by clinical findings (e.g. spreading cellulitis, systemic symptoms). The initial choice of antimicrobial agent should be directed towards the most likely organisms, according to the type of operation performed. Treatment can then be tailored in light of microbiological findings. Most incisional surgical wound infections are left open and allowed to heal by secondary intention.
Necrotizing fasciitis Necrotizing fasciitis is an uncommon, severe infection of the subcutaneous tissue that results in progressive destruction of fascia and fat (Figure 5). Predisposing factors include diabetes, alcoholism and intravenous drug use. There are two clinical types – I and II. • Type I necrotizing fasciitis is a mixed infection caused by anaerobic bacteria (e.g. Bacteroides spp., Peptostreptococcus) and facultatively anaerobic bacteria (streptococci, enterobacteria). It
Bite wounds Domestic pets are the usual cause of bites. It is estimated that 3–18% of dog wounds and 28–80% of cat wounds become infected. Although most attention has focused on Pasteurella multocida, a wide spectrum of organisms have been isolated from bite wounds, including Capnocytophaga canimorsis, streptococci, enterococci, staphylococci, Haemophilus spp., Neisseria spp. and anaerobes.
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4 Injection abscess in an intravenous drug-user. (© 2005 C P Conlon)
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Management – treatment is with prompt surgical debridement and intravenous broad-spectrum antibiotics.
Gas gangrene Gas gangrene is a rare anaerobic infection most commonly caused by Clostridium perfringens. It is usually associated with a deep, penetrating injury that creates anaerobic conditions ideal for clostridia. Clinical features include sudden onset of pain 6–8 hours after injury. This is followed by increasing pain and tenderness, darkening of the skin to a purplish-red colour, formation of bullae, crepitus, fever, shock, and liver and renal failure. Gas in the soft tissues may be confirmed by plain radiography, CT or MRI. The diagnosis is confirmed by microbiological demonstration of Grampositive rods in the affected tissue. Management – aggressive surgical debridement combined with intravenous penicillin and clindamycin or tetracycline is required. Use of hyperbaric oxygen is controversial. Gas gangrene antitoxin may be useful if administered early.
5 Necrotizing fasciitis affecting the buttock. Note the tissue breakdown and the blue discoloration of subcutaneous tissue.
occurs in middle-aged and elderly individuals, most commonly after surgical procedures, and in those with diabetes or peripheral vascular disease. Infection usually starts in the feet and progresses rapidly along the fascia into the leg. Clinical presentation is with cellulitis and systemic signs of severe infection. Type I necrotizing fasciitis may also develop in the head and neck following a breach of the mucous membranes by surgery or instrumentation. • Type II necrotizing fasciitis is caused by group A streptococci and was previously termed ‘streptococcal gangrene’. It may occur in any age group. The cardinal symptom is excruciating pain with minimal cutaneous findings. Initially, there may also be fever, malaise, myalgia and diarrhoea. After 24–48 hours, erythema may develop, the skin may darken to a reddish-purple colour and bullae may develop. Patients are systemically unwell and may develop streptococcal toxic shock syndrome. Laboratory tests reveal neutrophil leucocytosis, thrombocytopenia and raised serum aspartate transaminase, creatine phosphokinase and creatinine. Radiological imaging (CT or MRI) may show subcutaneous and fascial oedema in addition to gas in the tissues, but should not delay prompt surgical exploration in patients in whom the diagnosis is clearly suspected. Management – prompt surgical exploration and debridement are essential. Intravenous broad-spectrum antibiotics (e.g. cefuroxime and metronidazole, clindamycin and gentamicin) are given until bacteriological data are available. Clindamycin has a theoretical advantage in that it may interrupt toxin production and reduce systemic toxic effects. Patients often require intensive care. Imaging studies may be helpful for monitoring progress and assessing the need for further surgery.
Uncommon infections Anthrax is caused by Bacillus anthracis and most commonly affects the skin, resulting in a ‘malignant pustule’. Infections occur in abattoir workers and result from inoculation of bacterial spores into skin abrasions caused by handling the hides of infected animals. After a few days, a papule forms at the site of infection; this develops into a vesicle and ulcerates to form a necrotic centre or eschar (Figure 6). Local oedema, painful regional lymphadenopathy and systemic features are often present. The diagnosis is confirmed by demonstrating Gram-positive bacilli in the ulcer fluid or tissues and by culturing the organism. Penicillin therapy is adequate, though quinolones and tetracyclines are also effective. An anthrax vaccine is available for military use. Cat-scratch disease – Bartonella henselae is the most common cause. Clinical features include regional lymphadenopathy, fever and a red papule at the inoculation site. Atypical presentations include Parinaud’s ocular glandular syndrome, maculopapular rash, erythema multiforme, erythema nodosum and leucocyto-
Fournier’s gangrene Fournier’s gangrene is a form of necrotizing fasciitis that affects the perineum. Although it may occur spontaneously, it most commonly affects debilitated, hospitalized men over the age of 50 years. Diabetes is a predisposing condition. Fournier’s gangrene is caused by penetration of the gastrointestinal or urethral mucosa by Gramnegative bacteria, enterococci or anaerobes such as Bacteroides spp. and peptostreptococci. Clinical features include severe pain and necrotizing fasciitis, which may involve the anterior abdominal wall, gluteal muscles, scrotum and penis.
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6 Cutaneous anthrax – small lesion with necrotic appearance. Gram-positive bacilli were visible on tissue biopsy, and Bacillus anthracis was found on culture.
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clastic vasculitis. The diagnosis is confirmed serologically and by polymerase chain reaction analysis. Treatment is with azithromycin or doxycycline. Cutaneous larva migrans occurs in returning travellers, particularly those who have visited tropical beaches. It is caused by infection with animal hookworm larvae such as Ancylostoma brasiliense, A. caninum and Uncinaria stenocephala, and presents as an itchy cluster of lesions or a sinuous track on exposed areas. Treatment is with albendazole. Erysipeloid is a rare condition is caused by Erysipelothrix rhusiopathiae. It is usually acquired from infected animals, and affects veterinary surgeons, farmers and butchers. The organism is inoculated into the skin and causes characteristic dark, purplish lesions with swelling of the digits (Figure 7). Rarely, septicaemia occurs and may be complicated by endocarditis. The condition is treated with penicillin. Erythema chronicum migrans is the cutaneous manifestation of Lyme disease, which is caused by Borrelia burgdorferi. It is acquired by inoculation from a tick bite. A red, circular lesion develops and spreads from the site of the bite. Other features include fever, malaise and arthralgia. Diagnosis is serological. Treatment is with doxycycline. Leishmaniasis – cutaneous leishmaniasis is acquired from a sandfly bite. ‘Old world’ leishmaniasis, caused by Leishmania major, L. tropica and L. aethiopica, is endemic in Africa, Asia, India, the Middle East and the Mediterranean. ‘New world’ leishmaniasis, caused by L. brasiliensis, L. mexicana and L. panamensis, is endemic in Latin America. Clinical presentation is with a crusted sore on the face, hand or leg 6–8 weeks after returning from an endemic area. Diagnosis is clinical and confirmed histologically. Lesions often resolve spontaneously, but some may require cryotherapy or treatment with pentavalent antimony, amphotericin B or pentamidine. Patients with L. brasiliensis should be treated to avoid the possibility of espundia (mucocutaneous disease). Leprosy – infection with Mycobacterium leprae causes a spectrum of clinical disease ranging from tuberculoid to lepromatous leprosy. In tuberculoid leprosy, anaesthetic macules or plaques, pigmentary change and thickened peripheral nerves develop. In
lepromatous leprosy, macules, papules, nodules and ulceration occur, resulting in collapse of the nasal bones and coarsening of facial tissues, producing the characteristic ‘leonine’ facies. The diagnosis is confirmed by biopsy and split-skin smears. Treatment is with dapsone, clofazimine and rifampicin. Lupus vulgaris is a cutaneous infection caused by M. tuberculosis. It most commonly affects the face and neck, and appears as firm, translucent, yellow-brown ‘apple jelly’ nodules. Untreated lesions spread, leading to disfiguring scarring and contractures. Diagnosis is confirmed by biopsy, which shows tuberculoid granulomata in the mid-dermis. Treatment is with antituberculous chemotherapy. Molluscum contagiosum is a benign condition caused by a pox virus. It usually affects children or the immunocompromised (e.g. HIV-infected patients). The lesions are most commonly seen on the face and trunk, and are papular with a central punctum. Orf is an infectious cutaneous lesion caused by a pox virus acquired from sheep. It commonly affects farmers (particularly those who bottle-feed lambs) and veterinary surgeons. A red papule develops, commonly on the sides of the fingers, and grows rapidly, often becoming vesicular, before developing a central necrotic area. Lymphangitis, regional lymphadenopathy and fever are common. Recovery is spontaneous. Scabies is a pruritic skin lesion caused by infestation with Sarcoptes scabei. It is associated with poor socioeconomic conditions and overcrowding. The female mite lays her eggs in a burrow in the stratum corneum, generating a local hypersensitivity reaction; when the eggs hatch, the cycle is repeated. Diagnosis is confirmed by extraction of the mite from a burrow. Treatment comprises topical acaricides (e.g. permethrin) and washing of all clothing and linen. All members of the household should be treated at the same time. Tick typhus – African tick typhus, caused by Rickettsia conorii and R. africae is commonly seen in patients returning from safari in southern Africa. Endemic typhus is caused by R. typhi and transmitted by the rat flea. Epidemic typhus is caused by R. prowazekii and transmitted by the human louse. Clinical features include fever, headache, malaise, myalgia, lymphadenopathy and splenomegaly. There may be an eschar at the site of inoculation and a maculopapular rash, though some spotted fevers produce few if any spots. Diagnosis is confirmed serologically. Treatment is with doxycycline.
FURTHER READING Bisno A L, Stevens D L. Streptococcal infections of the skin and soft tissues. N Engl J Med 1996; 334: 240. Brook I. Microbiology and management of human and animal bite wound infections. Prim care 2003; 30: 25–31. Ebright J R, Pieper B. Skin and soft tissue infections in injection drug users. Infect Dis Clin North Am 2002; 16: 697–12. Guay D R. Treatment of bacterial skin and skin structure infections. Expert Opin Pharmacother 2003; 4: 1259–75. Seal D V. Necrotizing fasciitis. Curr Opin Infect Dis 2001; 14: 127–32. Shwarz M N. Clinical practice. Cellulitis. N Engl J Med 2004; 350: 904–12. Shwarz M. Cellulitis and subcutaneous tissue infections. In: Mandell G L, Owen R, Bennett J E et al., eds. Principles and practice of infectious diseases. 5th ed. New York: Churchill Livingstone, 2000: 1037–57.
7 Erysipeloid affecting the hand. (© 2005 C P Conlon)
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