In terms of medicine statistics, Buruli ulcer is a disease like any other. It has found mention in International Encoding. The virus is the mycobacterium ulcerans from the family of mycobacteria. But does this mean that all scientific secrets have been revealed?
Buruli ulcer confronts science with important, but unanswered questions. The biggest riddles are still the path of transmission and the habitat of the bacteria in environment, plant, animal or humans. Another question is why Buruli ulcer is on the increase in the sub-tropical and tropical countries of West and Central Africa.
Why is this the case? The disease is particularly frequent in circumscribed zones ("cluster"), and it spreads particularly well in swamplands and grasslands in the vicinity of rivers. Possibly, ecological changes have contributed to the spread, like for example the decline of the natural cover of mangroves or of the tree stock in the bank zones of rivers. What is important for the causative elimination of the disease is the localisation of a vector, which transmits the disease to humans.
Another characteristic of Buruli ulcer is the only moderate effectiveness of antibiotics during the cure of the disease. Only in the early forms with small dimensions (as a rule under 10 cm), a marked improvement in most cases can be achieved through streptomycin and rifampicin in the course of a treatment lasting up to 12 weeks. But even here, the removal of the pod through operation is mostly still required. If Buruli ulcer has reached the stage of ulcus or if it has already extensively invaded the sub-skin tissue, the only option left is extensive surgical removal. Antibiotics have either no effect or only very little effect on the healing process in these cases.
Another problem in the case of Buruli ulcer is the high remission rate. Depending upon the stage of the disease and quality of the treatment, up to 30% of the diseased must reckon with a relapse.
Buruli ulcus begins with a painless, often itchy lump or nodule of the skin. If left untreated, it develops into massive skin ulcerations with subsequent scar and contracture formation. Through the inflammations, organs can be damaged or destroyed, especially eyes, breasts and sexual organs. If the disease attacks the bones or if there are super-infections of the ulcerative regions, it can result in serious inflammations with sepsis and death. Destroyed or inflamed bones and joints lead to loss of limbs through amputation. If left untreated, the infection burns out in the course of months up to years and leaves behind grave contractures and deformities.
Mycobacterium ulcerans produces a toxin (mycolacton), which blocks the cellular immune defence system of the affected tissue and simultaneously destroys the tissue. Even the extensive painlessness of the spread of the inflammation can be ascribed to this toxin.
The breakout of Buruli ulcer as endemic disease was often the result of ecological changes or floods. Mostly, the multiplication of the number of diseased cases was preceded by the formation and expansion of swamplands. Even artificial irrigation systems appear to promote the spread of Buruli ulcer, as examples from West Africa have shown. Natural and artificial augmentation of swampy, stagnant water and of moist zones is conducive to the spread of the disease.
Buruli ulcer afflictions are reported in the following countries:
- Africa: Angola, Benin, Burkina Faso, Congo, Democratic Republic of Congo, Ivory Coast, Gabon, Ghana, Guinea, Cameroon, Liberia, Nigeria, Sierra Leone, Sudan, Togo, Uganda and Central African Republic
- West Pacific: Australia, China, India, Indonesia, Japan, Malaysia, Papua New Guinea
- America: Bolivia, French Guyana, Mexico, Peru, Surinam
Further information on our local Buruli work can be found here:
Like in the case of tuberculosis and leprosy, the mycobacterium ulcerans can be recognised through a simple microscopic analysis of the wound secretion of an ulcer caused by Buruli.
Microscopy is cheap and, therefore, the first choice means in the poor endemic countries of Buruli ulcer.
The differential diagnosis for other ulcer-causing tropical skin diseases can be found therewith (tropical ulcer, actinomycosis, skin diphtheria, noma, atypical skin mycobacteria like "mycobacterium abscessus", scrofuloderma, leishmaniasis of the skin, yaws).
Mycobacterium ulcerans grows well in conventional culture medium (Löwenstein-Jensen).The growth is slow, so that a reliable result is available after two weeks at the earliest, as a rule even as late as after six to eight weeks. The culture diagnosis of mycobacterium ulcerans is the "gold standard" of UB diagnostics.
The culture diagnosis is unfortunately expensive and laborious. The necessary standards during sampling and transport often cannot be observed under field conditions.
Mycobacterium ulcerans grows best at 32 degree Celsius and is killed quickly at higher temperatures. This distinctiveness, additionally, makes the transport of the samples under tropical conditions difficult.
Polymerase Chain Reaction (PCR) proves the genetic material of the virus. Wound secretion is needed for this as well as for microscopy and culture. PCR is 96% sensitive and 100% specific as compared to the "gold standard" bacteria culture. The results of the findings are available as early as after about 24 hours.
