Buruli Ulcer (Mycobacterium ulcerans) in Victoria: Recognition & Treatment

Victorian Epidemiology & Vector Transmission

Mycobacterium ulcerans infection (historically known as the Bairnsdale ulcer in Victoria) is an environmentally acquired necrotising skin and soft tissue infection. While historically confined to coastal regions (Bellarine and Mornington Peninsulas, Frankston, and East Gippsland), cases have increasingly emerged across regional Victoria and inland river corridors.

Landmark Australian medical research has established the unique transmission pathway:

• Native Animal Reservoir: Native possums (particularly common ringtail and brushtail possums) act as major environmental mammalian reservoirs, shedding vast quantities of M. ulcerans in their faecal pellets.
• Mosquito Vector: Mosquitoes (predominantly Aedes notoscriptus) feed on infected possum faeces or skin lesions, subsequently transmitting the mycobacteria to humans via subsequent bites. The incubation period is remarkably long, averaging 4 to 5 months (ranging from 1 to 9 months), meaning an infection diagnosed in winter was frequently inoculated during the preceding summer.

Clinical Stages of Infection

The disease progresses through characteristic clinical phases, predominantly affecting exposed areas of the limbs (ankles, calves, forearms, elbows):

1. Papule / Nodule Stage: A small, firm, non-tender, painless erythematous bump or subcutaneous nodule mimicking an ordinary insect bite.
2. Oedematous / Plaque Stage: Firm, non-pitting, painless swelling spreading across the subcutaneous tissues.
3. Ulcerative Stage: The overlying skin breaks down, revealing a deep, crater-like ulcer with characteristic undermined edges (the subcutaneous necrosis extends far beneath the visible skin margin) and a white/yellow necrotic slough base. Systemic symptoms (fever, chills) are characteristically absent.

Definitive Laboratory Diagnosis: IS2404 PCR

Standard bacterial swabs and routine cultures are useless for diagnosis, as M. ulcerans takes over 8 to 12 weeks to grow on specialised Lowenstein-Jensen media. The gold-standard diagnostic test is Polymerase Chain Reaction (PCR) targeting the insertion sequence IS2404:

• For Ulcerated Lesions: A dry sterile synthetic swab rubbed firmly along the undermined edge of the ulcer (where viable mycobacteria reside).
• For Non-Ulcerated Nodules: A fine-needle aspirate or 3 mm punch biopsy submitted for mycobacterial PCR.
• Victorian Statutory Notification: Buruli ulcer is a Group B notifiable condition in Victoria; laboratories and diagnosing medical practitioners must notify the Victorian Department of Health within 5 days.

Evidence-Based Dual Oral Antibiotic Therapy

Modern clinical management has eliminated the historical need for mutilating wide surgical excision. Curative medical therapy achieves cure rates exceeding 95%:

• First-Line Regimen: Oral Rifampicin (10 mg/kg up to 600 mg daily) PLUS Oral Clarithromycin (7.5 mg/kg up to 500 mg twice daily) for a total of 8 weeks. (For patients intolerant to clarithromycin, moxifloxacin or ciprofloxacin is substituted under specialist infectious diseases guidance).
• Paradoxical Reactions: In up to one-third of patients, the ulcer may temporarily look larger, more inflamed, or discharge more exudate 4 to 8 weeks into treatment. This represents a robust host immunological response to dead bacterial antigens, not treatment failure, and is managed with supportive wound dressings and short-course oral corticosteroids if severe.
• Wound Care & Physiotherapy: Dedicated non-adherent foam dressings, compression therapy (if limb oedema is present), and gentle joint range-of-motion exercises to prevent functional contractures.