Buruli ulcer (BU) is a necrotizing cutaneous infection caused with Mycobacterium ulcerans bacteria, which is categorised as a non-tuberculous mycobacterium. BU is also a neglected, debilitating skin disease, It was first definitely described in 1948, M. ulcerans infections have been reported from 34 countries, mainly with tropical, subtropical and temperate climates. Although the exact mechanisms by which M. ulcerans spreads are yet unknown, wetlands are frequently found around infection centers. It is extremely probable that M. ulcerans, which developed from the fish pathogen M. marinum, may have been influenced by an environmental niche.
Depending upon the geographical areas where they are found they have different names while naming a few; Buruli ulcer, Bairnsdale ulcer, Daintree ulcer, Mossman ulcer, Kumasi ulcer or Searls ulcer. Although in the late 1800s Sir Albert Cook described cases of chronic disfiguring skin ulcers in Uganda, it was in 1948 by MacCallum and the group who linked those chronic skin ulcers to mycobacterium in six cases from rural Australia.The disease was named after Buruli County, where in the 1960s a large number of cases were reported.
M. ulcerans grow at temperatures between 29-33 °C whereas M. tuberculosis grows at 37°C. M. ulcerans needs a low (2.5%) oxygen concentration. The organism produces toxin-mycolactone-which causes tissue damage and inhibits the immune response. The exact mode of transmission of M.ulcerans is still unknown (WHO) but there is a possibility that the disease is passed to humans from some insects that are found in water. With no proven link between human and animal infection, some animals can get the disease. Laboratory tests from Victoria- Australia, confirmed the disease in several animals, including horses, dogs, alpacas, koalas, possums (CDC).
Signs and symptoms (CDC).
The symptoms of Buruli ulcer include:
- Swelling of the skin
- Destroyed skin and soft tissue
- One or more slow growing, generally painless ulcers.
They have to see the doctors as soon as they feel that they are sick or similar symptoms, as antibiotics can cure them easily. If antibiotics are not taken on time, this disease can lead to:
- Bone infection
- Functional disability (limited joint movement etc.)
- Secondary bacterial infection of skin ulcer lesions
YOU MAY ALSO BE INTERESTED IN Antimicrobial Resistance and How it’s Affecting Our Everyday Lives
Diagnosis and treatment
- Diagnosis should be confirmed via nucleic acid detection by polymerase chain reaction.
- For non-ulcerative lesions (oedematous, plaques or nodules), swab specimens may produce false-negative results, and a fine-needle aspirate or biopsy is required to obtain tissue fluid fresh tissue for diagnosis.
Use of antibiotics
- Recommended for most lesions unless contraindicated, not tolerated, or declined by the patient.
- The recommended antibiotic therapy is oral rifampicin combined with either clarithromycin or a fluoroquinolone (moxifloxacin or ciprofloxacin) as s second oral agent.
- Antibiotics should be administered for 8 weeks unless the lesion involves deeper structures (eg. bone or joint) or is associated with prednisolone therapy for severe paradoxical reaction, when it may be prolonged up to 12 weeks.
- Antibiotics should be administered for a minimum of 4 weeks before surgery aimed at definitive wound closure.
- Paradoxical reactions occur= in up to 20% of patients and do not represent a failure of antibiotic treatment
- Severe paradoxical reactions may cause significant tissue necrosis, which may be managed with oral corticosteroids (prednisolone 0.5-2.0mg/kg daily, tapered over 4-8 weeks)
Role of surgery
- As microbiological and clinical cure is achieved with antibiotic treatment, surgery is not required for cure in addition to antibiotics.
- Surgery alone is an acceptable and effective alternative if:
- Antibiotics are declined, contraindicated, or not tolerated; or
- Patient preference is for wide excision and direct closure of small lesions without antibiotics.
Note that there is a risk of relapse when surgery is performed without adjuvant antibiotics. The likelihood of relapse varies with patient characteristics, the lesion site and whether the margins of excision are clear.
- In lesions with significant skin or soft-tissue necrosis, conservative surgical debridement is indicated in combination with antibiotics to remove necrotic tissue and prepare the area for skin grafting or flap closure
- Surgery may be required to repair large defects or to hasten the closure of a wound
- Röltgen K, Pluschke G. Buruli Ulcer: History and Disease Burden. 2019 Apr 30. In: Pluschke G, Röltgen K, editors. Buruli Ulcer: Mycobacterium Ulcerans Disease [Internet]. Cham (CH): Springer; 2019
- Guarner J. Buruli Ulcer: Review of a Neglected Skin Mycobacterial Disease. J Clin Microbiol. 2018 Mar 26;56(4):e01507-17. doi: 10.1128/JCM.01507-17. PMID: 29343539; PMCID: PMC5869816.
- Zingue D, Bouam A, Tian R, Drancourt M. 2018. Buruli ulcer, a prototype for ecosystem-related infection, caused by Mycobacterium ulcerans. Clin Microbiol Rev 31:e00045-17.
- Zingue D, Bouam A, Tian RBD, Drancourt M. Buruli Ulcer, a Prototype for Ecosystem-Related Infection, Caused by Mycobacterium ulcerans. Clin Microbiol Rev. 2017 Dec 13;31(1):e00045-17.