Buruli ulcer

What is buruli? ulcer?

Buruli ulcer is a necrotizing 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. Most cases occur in central and western Africa. Cases have also been reported from Australia, Southeast Asia, and Central and South America. In the last 2 decades, the incidence of Buruli ulcer has increased, despite the significant underreporting of cases. In 1999 there were 6,000 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 wetlands. Although the exact mode of transmission is unknown, M. ulcerans most probable 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 mycobacterial infection may follow an infected mosquito bite.

People of any age can be affected, but most cases are in children under 15 years of age.

What are the clinical features of Buruli ulcer?

the incubation period varies from a few weeks to months. Buruli ulcer begins as a firm, painless ache. nodule (swelling) on the skin, which is about 1 to 2 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 (like fever, discomfortor expanded lymph nodes)

Over the next several weeks, the nodule ruptures to form a sore necrotic ulcer with undercut edges (destruction of tissue underlying intact skin). the necrosis may extend several centimeters beyond the edges of the ulcer, causing the injury appears smaller than its actual size. The ulcer can spread into deeper tissues destroying nerves, blood vessels, muscles, and sometimes bone. The extremities, particularly the lower extremities, are the most commonly involved.

What are the complications of Buruli ulcer?

Tissue destruction can be extensive (involving up to 15% from the patient's skin surface) and secondary infection can occur. Other complications include osteomyelitis (bone infection) and metastatic injuries (the spread of wounds to distant sites). Extensive lesions heal with scars, which can cause irreversible deformities, secondary lymphedema (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.

Antibiotic treatment can sometimes cause a paradoxical effect. inflammatory reaction and enlargement ulceration.

How is Buruli ulcer diagnosed?

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 clusters of acidic bacilli (mycobacteria) under a microscope.
• Polymerase chain reaction (PCR) you can quickly confirm M. ulcerans on swabs from an ulcer or tissue biopsy.

• Biopsy of the lesion may reveal features microscopic changes and agglomerations of acid fast bacilli.

• M. ulcerans It can also be grown from swabs taken from an ulcer or from a biopsy of fresh tissue, but it takes 6 to 8 weeks or longer for the result to be reported.

What is the treatment for Buruli ulcer?

Current WHO recommendations for treatment are as follows:

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

The BCG vaccine appears to offer some short-term protection (less than a year) against the disease.