Staphylococcal Diseases

Staphylococcal diseases are a broad group of conditions caused by Staphylococcus species, principally Staphylococcus aureus. They range from localised skin and soft tissue infection through invasive disease including bacteraemia, endocarditis and osteomyelitis, to toxin mediated syndromes including toxic shock syndrome and scalded skin syndrome.

Increasing prevalence of methicillin resistant strains in both healthcare and community settings is a major and ongoing consideration in empirical antibiotic selection across this entire disease spectrum.

Pathophysiology and classification

• Staphylococcus aureus colonises the anterior nares and skin of a substantial proportion of the general population asymptomatically.
• Invasive disease typically arises following a breach of normal skin or mucosal barriers.
• In specific toxin mediated syndromes, the systemic effect of exotoxins produced by colonising or infecting strains is responsible, rather than invasive bacterial spread itself.
• Methicillin resistant Staphylococcus aureus is resistant to beta lactam antibiotics through acquisition of the mecA gene encoding an altered penicillin binding protein. It has become increasingly prevalent as a healthcare associated pathogen and, of growing importance, as a cause of community acquired infection.
• Specific community strains are frequently associated with enhanced virulence through production of Panton Valentine leukocidin. This toxin is associated with severe necrotising skin and soft tissue infection and necrotising pneumonia.

• Localised skin and soft tissue infection (impetigo, furunculosis, carbuncle, abscess, cellulitis), addressed in detail under that specific condition, represents the commonest clinical manifestation of staphylococcal infection encountered in practice.
• Bacteraemia presents with fever and systemic upset. Staphylococcus aureus bacteraemia specifically carries substantial risk of metastatic seeding to distant sites (bone, joint, cardiac valves, other organs).
• Every episode requires careful evaluation for a potential source and for evidence of complicated, deep seated infection.
• Infective endocarditis is frequently caused by Staphylococcus aureus, particularly in the context of intravenous drug use or prosthetic cardiac material. It typically follows a more acute, aggressive course than streptococcal endocarditis.
• Osteomyelitis and septic arthritis are commonly caused by Staphylococcus aureus, whether through haematogenous seeding or direct inoculation.
• Toxin mediated syndromes include toxic shock syndrome and staphylococcal scalded skin syndrome. They reflect the systemic effects of specific circulating bacterial exotoxins.
• Staphylococcal scalded skin syndrome presents predominantly in young children with fever, skin tenderness, and widespread superficial epidermal desquamation. This reflects the action of exfoliative toxin on desmoglein 1 within the epidermis, distinguishing it from the deeper, full thickness involvement of toxic epidermal necrolysis.
• Staphylococcal food poisoning, addressed under food poisoning, reflects ingestion of preformed enterotoxin in contaminated food, producing rapid onset vomiting.

• Culture of blood, wound material, joint fluid or other relevant clinical specimen confirms the diagnosis and provides essential susceptibility testing. Distinguishing methicillin sensitive from methicillin resistant strains fundamentally guides subsequent antibiotic selection.
• Every episode of Staphylococcus aureus bacteraemia warrants a thorough search for a source and for evidence of metastatic complications.
• This includes repeat blood cultures to confirm clearance, and echocardiography to assess for endocarditis. Keep a low threshold for transoesophageal imaging, given the frequently more subtle presentation compared with typical endocarditis risk populations.
• Add further targeted imaging guided by specific symptoms or signs suggesting deep seated infection at another site.
• Nasal and skin swabs for methicillin resistant Staphylococcus aureus screening are performed in specific healthcare contexts (pre operative screening, contact tracing following identification of a case) rather than as part of routine diagnostic evaluation of active infection.
• Diagnosis of toxin mediated syndromes (toxic shock syndrome, scalded skin syndrome) is predominantly clinical, based on the characteristic pattern of presentation.
• Culture of a potential source site supports identification of the causative strain where feasible. Blood is typically negative in toxin mediated disease, given the localised nature of toxin producing infection.

• Methicillin sensitive Staphylococcus aureus infection is treated with flucloxacillin, given its narrow spectrum and reliable bactericidal activity against sensitive strains.
• Dose according to the severity and site of infection: typically 1 to 2 g intravenously four times daily for significant invasive infection, or 500 mg to 1 g orally four times daily for less severe presentations.
• Methicillin resistant Staphylococcus aureus infection requires alternative agents. Vancomycin (loaded then dosed to a target trough of 15 to 20 mg per litre for serious invasive infection) is a standard first line choice.
• Daptomycin 6 to 10 mg per kg intravenously once daily is an alternative. It is specifically avoided for pulmonary infection given inactivation by pulmonary surfactant.
• Linezolid 600 mg twice daily (oral or intravenous) is another alternative. It offers excellent bioavailability and tissue penetration including bone and soft tissue, though prolonged use needs caution given risk of myelosuppression and peripheral or optic neuropathy.
• These alternatives are particularly useful for vancomycin intolerant patients or specific clinical scenarios where they offer advantages.
• Bacteraemia, regardless of methicillin susceptibility, requires a minimum of two weeks of appropriate intravenous therapy for uncomplicated infection with a clear, removable source and prompt clearance on repeat cultures.
• Extend treatment to four to six weeks for complicated bacteraemia (persistent bacteraemia beyond forty eight to seventy two hours, endocarditis, or evidence of metastatic seeding).
• Specialist infectious disease input is strongly recommended, given evidence of improved outcomes with such involvement.
• Source control is essential alongside antibiotic therapy and should not be delayed. It includes drainage of any abscess or collection and removal of any infected intravascular device or other foreign material.
• Antibiotics alone frequently fail to clear infection in the presence of an undrained collection or retained infected foreign material.
• Toxic shock syndrome and scalded skin syndrome are addressed in detail under toxic shock syndrome. Management combines source control, appropriate antibiotic therapy (including an agent with antitoxin production suppressing activity such as clindamycin) and, for toxic shock syndrome specifically, aggressive haemodynamic support.
• Decolonisation protocols (nasal mupirocin, chlorhexidine body wash) are used in specific contexts. These include recurrent staphylococcal skin infection and pre operative preparation of identified carriers before high risk surgical procedures.
• The aim is to reduce the burden of colonising organisms and associated infection risk.