Buruli ulcer pathophysiology

Jump to navigation Jump to search

Buruli ulcer Microchapters


Patient Information


Historical Perspective



Differentiating Buruli ulcer from other Diseases

Epidemiology and Demographics

Risk Factors

Natural History, Complications and Prognosis


History and Symptoms

Physical Examination

Laboratory Findings

Chest X Ray

Other Diagnostic Studies


Medical Therapy


Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Buruli ulcer pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides


American Roentgen Ray Society Images of Buruli ulcer pathophysiology

All Images
Echo & Ultrasound
CT Images

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Buruli ulcer pathophysiology

CDC on Buruli ulcer pathophysiology

Buruli ulcer pathophysiology in the news

Blogs on Buruli ulcer pathophysiology

Directions to Hospitals Treating Buruli ulcer

Risk calculators and risk factors for Buruli ulcer pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]


Buruli ulcer is an infectious disease caused by the tuberculous agent Mycobacterium ulcerans. The infection causes painless swelling, with lesions developing in the skin later on.


Being one of the less known diseases caused by mycobacteria, means of Buruli ulcer infection are not completely clear. However, the mycobacterium has been identified in stagnant or slowly moving water sources in endemic areas and in aquatic insects (Naucoridiae). Transmission to man may be by means of insects or by a contaminated aerosol generated from decaying vegetation in the water source. Infection in Australia has occurred in an alpaca, in koalas, possums and other marsupials.

The disease is primarily an infection of subcutaneous fat, resulting in a focus of necrotic (dead) fat containing myriads of the mycobacteria in characteristic spherules formed within the dead fat cells. Skin ulceration is a secondary event. The mycobacterium produces a toxin, named mycolactone, which causes this fat necrosis and inhibits an immune response. Healing may occur spontaneously but more often the disease is slowly progressive with further ulceration, granulation, scarring, and contractures. Secondary infection may occur with other nodules developing and infection may occur into bone. Although seldom fatal, the disease results in considerable morbidity and hideous deformity.

Th1-mediated immune responses are protective against M. ulcerans infection, whereas Th2-mediated responses are not.