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7: Soft Tissue, Bone and Joint Infections MJA PracticeMJ AEssentials Practice Essentials InfectiousInfectious Diseases Diseases 7: Soft tissue, bone and joint infections Thomas Gottlieb, Bridget L Atkins and David R Shaw Although many of these infections are trivial, some may threaten life or limb SOFT TISSUE, BONE AND JOINT INFECTIONS cause consid- Abstract erable morbidity in hospitals and the community. Their severityThe variesMedical from Journal trivial of Australia to lethal. ISSN: These 0025-729X infections 17 Junecom- 2002 ■ Soft tissue infections are common and usually respond monly176 arise 12 609-615 from skin breaches or bacteraemia, but occa- rapidly to oral antibiotics; if empirical therapy fails then sionally©The they Medical are Journala manifestation of Australia 2002of awww.mja.com.au more generalised exposure to unusual organisms should be considered. MJA Practice Essentials — Infectious Diseases infection, such as endocarditis. Rarely, a localised soft tissue ■ Septic arthritis requires early recognition, identification of infection can produce a profound systemic illness with the infecting pathogen and urgent joint washout to prevent severe pain, tissue necrosis, hypotension and rapid progres- irreversible cartilage and bone destruction. sion to multisystem failure and death. Early recognition is essential, as, without treatment, mortality is high. ■ Prosthetic joint infection is uncommon but has high morbidity; the best outcomes are achieved with removal of the prosthesis and replacement after at least six weeks of Soft tissue infections antibiotic therapy. Soft tissue infections can be subdivided according to the skin ■ Osteomyelitis often complicates diabetic foot infection compartment involved (Box 1). Diagnosis is based on the with ulceration and is rarely cured by antibiotics alone; appearance of lesions, degree of pain and systemic toxicity. early surgical intervention achieves the best outcome. Knowledge of the organisms involved does not always help define the tissue depth of disease, but aids choice of antimi- MJA 2002; 176: 609-615 crobial therapy. Investigation and management of common soft tissue infections are summarised in Box 1. Skin abscesses and furuncles S. aureus is the leading pathogen that causes furuncles and Impetigo abscesses in the community. Certain phage types are associ- ated with recurrent episodes of furunculosis and may spread Impetigo is most common in children and usually involves among family members. Staphylococcal bacteraemia may the skin of the face, often around the mouth and nose. It has result from a minor skin lesion or furuncle, with potentially two forms: severe complications, including osteomyelitis, septic arthri- ■ Non-bullous, which is most commonly caused by Strepto- tis and endocarditis.6 coccus pyogenes (group A streptococci) and is typified by Recently, infections caused by community-acquired, “honey-crust” lesions (Box 2); and methicillin-resistant S. aureus have been described in both ■ 4 Bullous, which is caused by Staphylococcus aureus; rup- adults and children in Australia.7 These bacteria are resist- ture of the bullae leaves a thin “varnish-like” crust. ant to ␤-lactam antibiotics, but retain susceptibility to agents such as clindamycin, in contrast to multiresistant S. Folliculitis aureus, which is usually hospital-acquired. This ␤-lactam Infection of the hair follicles may occur after exfoliation, use resistance may delay effective therapy (case history, Box 3). of a loofah sponge and shaving, or may be spontaneous. A In patients with recurrent S. aureus soft tissue infection, specific form is “whirlpool” (“hot tub” or “spa”) folliculitis, attempts can be made to eradicate the causative strain from caused by Pseudomonas aeruginosa.5 long-term carriage in the nasal passages and on skin with nasal mupirocin and skin antiseptic solutions.8 Penicillins and cephalosporins are ineffective in eradicating nasal carriage. Series Editors: M Lindsay Grayson, Steven L Wesselingh Department of Microbiology and Infectious Diseases, Cellulitis Concord Hospital, Sydney, NSW. Thomas Gottlieb, FRACP, FRCPA, Senior Specialist. Cellulitis is an acute, spreading inflammation involving the Oxford Radcliffe Hospitals, Nuffield Orthopaedic Centre, epidermis, dermis and subcutaneous fat. The most common Oxford, UK. causes are S. aureus and ß-haemolytic streptococci (most Bridget L Atkins, MRCP, Consultant, Department of Microbiology, commonly group A [S. pyogenes], but also groups C and G). Infectious Disease Unit and Bone Infection Unit. Host factors may predispose to cellulitis and should be Infectious Diseases Unit, Royal Adelaide Hospital, Adelaide, SA. corrected if possible. These are infective (eg, varicella, tinea David R Shaw, FRACP, Director. Reprints will not be available from the authors. Correspondence: Dr D R pedis and scabies) and non-infective (eg, eczema, trauma, Shaw, Infectious Diseases Unit, Royal Adelaide Hospital, North Terrace, local ischaemia, venous, arterial or vasculitic ulceration, Adelaide, SA 5000. [email protected] lymphatic impairment, surgery and radiotherapy). Rarer MJA Vol 176 17 June 2002 609 Infectious Diseases MJA Practice Essentials 1: Investigation and management of soft tissue infections* Syndrome Common pathogens Investigations Management Impetigo Streptococcus ■ None ■ If uncomplicated and localised: wash crusts off, apply topical (epidermis) pyogenes mupirocin or sodium fusidate.2 Staphylococcus ■ If multiple lesions present or not responding to topical aureus treatment: oral dicloxacillin. ■ If severe or extensive, systemically unwell or not responding to oral treatment: intravenous flucloxacillin.3 Folliculitis S. aureus ■ None ■ Usually self-limiting, no specific treatment required. (hair follicle) Pseudomonas ■ Avoid precipitating factor (eg, exfoliation). aeruginosa (“spa” or ■ In “spa” folliculitis, spa should be drained, cleaned and “whirlpool” folliculitis) chlorinated on refilling. Skin S. aureus ■ Gram stain and culture of pus ■ Incision and drainage. abscesses, ■ Antistaphylococcal antibiotics (initially intravenous if severe). furuncles (hair follicles) Cellulitis ß-Haemolytic ■ Blood cultures ■ Elevate limb. (epidermis, streptococci ■ Gram stain and culture of aspirate ■ Intravenous antibiotics directed at staphylococci and dermis, S. aureus from blister or pustule, if present, or streptococci (eg, flucloxacillin, cephalothin or, for home- subcutaneous fat) Rarely: Haemophilus (in immunosuppressed patient) based therapy, cephazolin); or broader spectrum (eg, influenzae, others from leading edge of cellulitis ceftriaxone and fluoroquinolones) if need to cover waterborne ■ Consider unusual causes if rele- pathogens, such as Aeromonas or Vibrio spp., or patient is vant exposure (Box 4); may require immunocompromised. tissue biopsy for histopathological ■ Consider hospital admission (Box 5). examination, microscopy (Gram and acid-fast stain) and culture (including fungal and mycobacte- rial culture), or directed nucleic acid amplification tests. Necrotising fasciitis S. pyogenes ■ Gram stain and culture of surgical ■ Urgent surgical debridement (multiple debridements may be (fascia) Mixed bowel flora samples needed). ■ Blood cultures ■ Intravenous antibiotics: initially broad spectrum to cover ␤-haemolytic streptococci, enteric gram-negative rods, and anaerobes; and modified on culture and susceptibility results. Clindamycin should be added if S. pyogenes is identified. Clostridial Clostridium ■ Gram stain and culture of surgical ■ Urgent surgical debridement plus intravenous antibiotics myonecrosis (gas perfringens samples (penicillin plus clindamycin). gangrene) (muscle) ■ Blood cultures ■ Hyperbaric oxygen may have a role. *Summarised from Therapeutic guidelines: antibiotic.1 causes of cellulitis are associated with specific exposures (Box 4). Infection with S. pyogenes may also be confined to 2: Non-bullous form of impetigo the dermis, termed erysipelas. Clinical features: Streptococcal infections often have an abrupt “wildfire” onset with localised pain in the affected limb. Rigors may precede visible signs of skin involvement or lymphangitis by 24 hours. Tender regional lymphadeni- tis often develops. Often fever abates, and leukocyte count and C-reactive protein level decrease before any improve- ment at the site of cellulitis. Indeed, the area involved, blistering and local necrosis may continue to increase for days after a systemic clinical response. Desquamation occurs on recovery. Diagnosis and management: In practice, the specific causative organism is usually not isolated: blood cultures are usually negative,10 and skin swabs are rarely diagnostic. However, culture of an aspirate from an intact blister may be helpful, “Honey-crust” lesion typical of Streptococcus pyogenes impetigo. and, in the immunosuppressed patient or after unusual 610 MJA Vol 176 17 June 2002 MJA Practice Essentials Infectious Diseases 3: Case history — community-acquired methicillin-resistant Staphylococcus aureus Presentation: A 14-year-old girl presented with a four-week history of progressive swelling in the left submandibular region. Despite treatment with oral flucloxacillin for 10 days she experienced increasing pain, fever and torticollis. Management: The girl was admitted to hospital and given intravenous flucloxacillin and penicillin for three days without improvement. Further history revealed that both the girl and her younger brother had experienced recurrent boils since a family visit to Samoa a year previously. Swabs of pus from a boil, as well as
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