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Buruli ulcer

Author: Marie Hartley, Staff writer. Reviewed and updated by Dr Amanda Oakley Dermatologist, Hamilton, New Zealand; and Vanessa Ngan, Staff Writer; June 2014.


What is Buruli ulcer?

Buruli ulcer is a necrotising disease (causing tissue death) of the skin and underlying tissue.

Buruli ulcer is also called Bairnsdale ulcer, Searles ulcer, Daintree ulcer, and Sik-belonga-sepik.

What is the cause of Buruli ulcer?

Buruli ulcer is caused by bacteria called Mycobacterium ulcerans. These bacteria are atypical mycobacteria and come from the same family of organisms that cause leprosy and tuberculosis.

Who gets Buruli ulcer?

Buruli ulcer is found in more than 30 tropical, subtropical, and temperate countries. The majority of cases occur in central and western Africa. Cases have also been reported from Australia, South East Asia, and Central and South America. Over the last 2 decades, the incidence of Buruli ulcer has increased, despite significant underreporting of cases. In 1999 there were 6000 new cases in Ghana; in Australia, there were 25 cases in 2004, 47 in 2005 and 72 in 2006. In 2018, there were more than 340 cases in the state of Victoria alone.

Buruli ulcer predominantly affects poor rural communities living near swampy terrain. Although the exact mode of transmission is unknown, M. ulcerans most likely cause infection through inoculation or contamination of a traumatic wound. In Victoria, Australia, the infection has been found in wild animals such as ring-tailed possums, and in mosquitoes. It has been speculated that the mycobacterial infection may follow an infected mosquito bite. 

People of any age can be affected, but most cases are among children aged less than 15 years.

What are the clinical features of Buruli ulcer?

The incubation period ranges from a few weeks to months. Buruli ulcer begins as a firm, painless nodule (swelling) in the skin, which is around one to two cm in diameter. M. ulcerans produces a toxin, called mycolactone, which is directly toxic to cells and also dampens the immune system. The toxin causes extensive tissue destruction, without any systemic symptoms (such as fever, malaise, or enlarged lymph nodes).

Over the following weeks, the nodule breaks down to form a painless necrotic ulcer with undermined edges (tissue destruction underlying intact skin). The necrosis may extend several centimetres beyond the edges of the ulcer, making the lesion appear smaller than its actual size. The ulcer can extend down into deeper tissues destroying nerves, blood vessels, muscles, and occasionally bone. The limbs, particularly the lower limbs, are most commonly involved.

What are the complications of Buruli ulcer?

Tissue destruction can be extensive (involving up to 15% of the patient's skin surface) and secondary infection may occur. Other complications include osteomyelitis (infection of the bone) and metastatic lesions (the spread of the wounds to distant sites). Extensive lesions heal with scarring, which may cause irreversible deformity, secondary lymphoedema (swelling due to fluid retention), and restriction of joint movement. Few people die from Buruli ulcer, but it often causes long-term disability, disfigurement, and a significant socioeconomic burden.

Treatment with antibiotics can sometimes cause a paradoxical inflammatory reaction and enlarging ulceration.

How is the diagnosis of Buruli ulcer made?

In endemic areas, Buruli ulcer is often diagnosed and treated based on clinical findings.

  • A direct smear is taken from the necrotic base of the ulcer, stained with Ziehl-Neelsen stain to reveal clumps of acid-fast bacilli (mycobacteria) under a microscope.
  • Polymerase chain reaction (PCR) can rapidly confirm M. ulcerans in swabs of an ulcer or tissue biopsy.
  • Biopsy of the lesion can reveal characteristic microscopic changes and clumps of acid-fast bacilli.
  • M. ulcerans can also be cultured from swabs taken from an ulcer or fresh tissue biopsy, but the result takes 6 to 8 weeks or more to be reported.

What is the treatment of Buruli ulcer?

Current WHO recommendations for treatment are as follows:

  1. A combination of rifampicin and either streptomycin, amikacin, clarithromycin, moxifloxacin or ciprofloxacin for eight weeks as a first-line treatment for all forms of the active disease. Antibiotics can promote healing of smaller lesions and decrease disease recurrence. The best outcomes occur with early treatment (ulcers < 5 cm).
  2. A paradoxical flare-up may require oral prednisone to be added to the antibiotic regime.
  3. Surgery may be necessary to remove necrotic tissue, cover skin defects, and correct deformities.
  4. Interventions to minimise or prevent disabilities.

BCG vaccination appears to offer some short-term protection (less than one year) from the disease.



  • Lupi O, Madkan V, Tyring SK. Tropical dermatology: bacterial tropical diseases. J Am Acad Dermatol. 2006 Apr;54(4):559–78. PubMed

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