Cases of the ‘flesh-eating’ Buruli ulcer have increased significantly in Victoria over recent years. Until 2015 there were less than 100 cases annually; however, since 2017, there have now been between 200 and 340 cases every year (Health.vic 2022a).
But what exactly is this illness, why is it described as ‘flesh-eating’ and is it a cause for concern?
What is Buruli Ulcer?
Buruli ulcer is a chronic bacterial infection causing necrosis of the skin and underlying tissue (Healthdirect 2021; Hartley et al. 2014). It’s sometimes referred to as Bairnsdale ulcer, as its first discovery in Australia was in the regional town of Bairnsdale during the late 1930s (Johnson 2019).
Buruli ulcer is caused by the bacteria Mycobacterium ulcerans, which belongs to the same family as the bacteria responsible for leprosy and tuberculosis (Healthdirect 2021).
Mycobacterium ulcerans bacteria produce a toxin known as mycolactone that weakens the body’s immune response and is toxic to the cells, resulting in extensive tissue damage, ulceration and skin loss. If left untreated, this ulceration can extend to the nerves, blood vessels, muscles and even bone (Hartley et al. 2014; Better Health Channel 2018; Health.vic 2022a).
It’s for this reason that the condition is often described as a ‘flesh-eating ulcer’ (Hendrie 2018).
Buruli ulcer has been detected in 33 countries, predominantly in central and west Africa. Most cases in Australia occur in Victoria, particularly in the East Gippsland, Mornington Peninsula and Bellarine Peninsula areas (Healthdirect 2021).
People have also contracted the infection in Queensland and the Northern Territory (Better Health Channel 2018).
What Causes Buruli Ulcer?
Mycobacterium ulcerans bacteria are found naturally in the environment and have been detected in mosquitoes, possum faeces, vegetation and areas of swampy and stagnant water (Better Health Channel 2018; Healthdirect).
It’s currently not known how humans become infected with Mycobacterium ulcerans, however, most cases occur in areas where mosquitoes and possums have been found to be carrying the bacteria (Better Health Channel 2018; Health.vic 2022b).
It’s been speculated that mosquitoes transmit the bacteria through bites, or that the bacteria enters the body through the inoculation or contamination of a wound (Hartley et al. 2014).
The bacteria can’t be transmitted from person-to-person (Healthdirect 2021).
Symptoms of Buruli Ulcer
Symptoms typically develop between a few weeks to months after infection (Hartley et al. 2014).
The first sign of the infection is a firm, painless nodule on the skin. The nodule will most commonly appear on an arm or leg, over a joint. It may be itchy and will typically be between 1 and 2 cm in diameter, resembling a mosquito or spider bite (Healthdirect 2021; Hartley et al. 2014; Better Health Channel 2018).
Over the next days or weeks, the nodule will gradually grow larger and may form a crusty, non-healing scab that eventually ulcerates (Better Health Channel 2018).
The resulting ulcer is usually painless with undermined edges, signifying tissue damage under the skin. If left untreated, the ulcer will continue to extend and may destroy other tissue, muscle and bone (Healthdirect 2021; Hartley et al. 2014).
Occasionally, the infection will present without localisation. The patient may experience localised pain and swelling accompanied by a fever, raised lumps, or thickened or raised areas of flat skin (Better Health Channel 2018).
Complications of Buruli Ulcer
Significant tissue destruction (up to 15% of the skin surface)
Secondary infection
Osteomyelitis (bone infection)
Metastatic lesions (spread of wounds to different parts of the body)
Scarring
Secondary lymphoedema due to fluid retention
Impaired joint movement.
(Hartley et al. 2014)
While mortality is rare, lifelong disability, disfigurement and socioeconomic burden are common consequences of the infection, particularly if recognition is slow and access to treatment is limited (Hartley et al. 2014).
Diagnosis of Buruli Ulcer
The fastest, easiest and most accurate way to diagnose Buruli ulcer is via polymerase chain reaction (PCR) test to detect the presence Mycobacterium ulcerans, using a swab or tissue biopsy of the affected area (O'Brien et al. 2019; Healthdirect 2021).
The characteristic ulcer might resemble lesions or wounds caused by diabetes, or arterial or venous insufficiency. It’s important to rule out these differential diagnoses during assessment (WHO 2022).
Early diagnosis is crucial in ensuring prompt treatment and preventing the progression of the illness (Healthdirect 2021).
Treatment of Buruli Ulcer
Treatment comprises both antibiotics and complementary management (WHO 2022).
Currently, the recommended course of antibiotics is a combination of rifampicin and clarithromycin (WHO 2022).
An alternative combination of rifampicin and moxifloxacin is commonly used in Australia, but there is limited evidence proving its efficacy (WHO 2022).
Complementary treatments may involve:
Wound and lymphoedema management
Surgical intervention (debridement and skin grafting) to speed up the healing process
In severe cases, physiotherapy to prevent disability
Long-term rehabilitation (in cases of disability).
(WHO 2022)
Preventing Buruli Ulcer
Due to the mode of transmission being unknown, it’s not understood how exactly Buruli ulcer can be prevented. Despite this, protecting against potential sources of infection such as soil and mosquito bites may help to reduce the risk (Better Health Channel 2018). Precautions may include:
Wearing gloves, long-sleeved shirts and long pants when working outdoors
Using insect repellents
Using plasters to protect cuts and abrasions
Washing and covering any wounds sustained while working outdoors
Seeking medical advice in the case of a slow-healing skin lesion.
(Better Health Channel 2018)
Overall, however, the risk of Buruli infection in Australia is low (Better Health Channel 2018).
Johnson, P D R 2019, ‘Buruli Ulcer in Australia’, in G Pluschke & K Röltgen (eds.) Buruli Ulcer: Mycobacterium Ulcerans Disease, viewed 23 June 2022, https://www.ncbi.nlm.nih.gov/books/NBK553830/