Nasal carriage of Staphylococcus aureus in patients undergoing Mohs micrographic surgery is an important risk factor for postoperative surgical site infection: a prospective randomised study.

BACKGROUND: Surgical site infection (SSI) can be a problematic complication of Mohs micrographic surgery (MMS). Previous reports have cited nasal Staphylococcus aureus (S. aureus) carriage as a risk factor for SSI, but none thus far in dermatologic surgery. OBJECTIVE: The aim was to determine the difference in infection rates between nasal carriers of S. aureus and non-carriers, and whether decolonisation with intranasal mupirocin ointment and chlorhexidine wash would reduce the infection rate in nasal carriers. METHODS: In all, 738 patients presenting for MMS at the Oxford Day Surgery and Dermatology underwent a nasal swab to determine their S. aureus carriage status. S. aureus carriers were randomised for decolonisation with intranasal mupirocin ointment and chlorhexidine body wash. Non-carriers were untreated. All patients were followed up for SSI. RESULTS: The rate of SSI was 11 per cent in untreated S. aureus carriers, 4 per cent in treated carriers, and 3 per cent in non-carriers. The difference in infection rate between carriers and non-carriers was significant (P < 0.001). The difference between treated and untreated carriers was also significant (P = 0.05). CONCLUSION: Nasal S. aureus carriage is an important risk factor for SSI in MMS, conferring an over threefold increase in SSI risk. A pre-operative nasal swab provides a simple and effective risk stratification tool. The use of a topical decolonisation regimen reduces the infection rate in carriers to a level approaching non-carriers without exposure to systemic antibiotics.

Retrospective analysis of adult patients with cutaneous leukocytoclastic vasculitis.

A retrospective analysis was conducted on 93 adult patients with cutaneous leukocytoclastic vasculitis from St. Vincent's Hospital Melbourne to determine the classification, aetiology, severity and prognosis of this population of patients. We developed a new classification system for the purposes of our study based on modifications to the Chapel Hill Consensus Conference definitions for vasculitic syndromes. The results of our study indicate that an obvious cause was not found in 44.1% of patients. Of the patients with secondary vasculitis, the commonest causes were drugs and infections, accounting for a total of 40.9% of patients. Extracutaneous involvement was found in 39.8% of patients. Patients with symptoms resolving in less than 3 months accounted for 59.1% of the population, whereas 24.8% of patients had either symptoms lasting three or more months or evidence of recurrent symptomatology. There were 6 deaths (6.91%) and the rest were lost to follow up. The majority of patients in this retrospective series were classified as having hypersensitivity vasculitis, which is a relatively benign disorder limited mostly to skin with a low incidence of extracutaneous involvement (15.8%). Nevertheless, evidence of systemic involvement or sepsis need to be excluded as this may have important implications for patient treatment and outcome.

Fixed drug eruption with interferon-beta-1b.

A 32-year-old woman with multiple sclerosis who developed non-injection-site-related fixed drug eruption with interferon-beta-1b. Erythematous plaques started appearing 1 month after the drug was introduced, and increased in number following each administration. The histopathology of a skin biopsy was consistent with fixed drug eruption. The drug was subsequently ceased, with resolution of the rash 6 weeks later.

Pyoderma gangrenosum complicated by herpes simplex virus infection.

High-dose immunosuppression used in the treatment of pyoderma gangrenosum predisposes patients to opportunistic infections. A 66-year-old man presented with recalcitrant pyoderma gangrenosum in which the ulcer itself became infected with herpes simplex virus type 1. This patient was immunosuppressed with multiple agents including topical and oral corticosteroids, cyclosporin, mycophenolate mofetil, intravenous immunoglobulin and infliximab. However, the patient's ulcer continued to extend despite this. It was not until the presence of this virus was detected using polymerase chain reaction on a viral swab of the lesion and oral aciclovir was commenced that the ulcer began to heal. In addition, a fungal granuloma developed on this patient's left forearm as a complication of the potent immunosuppression, which was resolved following treatment with oral voriconazole.