BEWARE OF BURULI ULCER

BEWARE OF BURULI ULCER

Throughout the years Buruli ulcer (BU) was known as a silent killer because of its unknown symptoms until five years now its symptoms and signs have been clearly shown and its cured has been improved massively with antimicrobial drugs and more overwhelming method of diagnosis. However its mode of transmission is still yet to be studied. The Buruli ulcer (BU) disease is still the national anthem of countries such Ghana, Togo and Gabon. The increasing impediment of Buruli ulcer and its related catastrophes has been associated with environmental factors such as dam constructions in remotes areas and many others

Mycobacterium ulcerans infection (Buruli ulcer) is a progressive necrotizing infection of the skin and subcutaneous tissue. The disease has been reported from at least 30 countries worldwide, mostly in tropical areas, where it mainly affects poor people living in rural areas. It can involve all age groups, although children aged less than 15 years are predominantly affected. Prevalence rates can be as high as 22%, as has been recorded in an endemic community in Ghana. The mode of transmission of Buruli ulcer is not entirely clear, but once M. ulcerans is introduced into the dermis or subcutaneous tissue, it proliferates and produces a toxin, designated mycolactone. This polyketide toxin has cytopathic activity and causes necrosis of the dermis, panniculus and fascia, usually leading to a single, painless, subcutaneous nodule, oedema or plaque. Fat cells enlarge and lose their nuclei and the skin that covers these lesions eventually sloughs off, together with the underlying tissues, forming an ulcer with undermined edges. Inflammatory cells are scarce in active lesions but, after an unspecified time period, a granulomatous response in the dermis and panniculus may be observed, followed by healing and scarring. In many cases calcification occurs. M. ulcerans may spread, presumably by lymphatic and haematogenous pathways, to distant foci. Occasionally metastatic bone lesions arise. The currently accepted definitive treatment is the surgical removal of the infected tissue, including healthy tissue at the peripheral and deep margins. Due to the non-specific clinical manifestations of the disease and its indolent course, those affected tend to postpone their presentation to the health facilities by researchers

Mode Of Transmission

Two main transmission hypotheses have been expounded; direct inoculation into broken skin through contact with contaminated environmental sources and vector-mediated transmission. Based on the detection of M. ulcerans DNA in the environment, many agents have been speculated as possible reservoirs and this has given support to the proposition that contact with environmental reservoirs is the source of transmission. However analysis of the M. Ulcerans genome and pathogenic mechanisms has revealed genome reduction and intracellular niche specialization in the environment thus indicating that biological reservoirs such as amoebae may also be likely candidates.

Laboratory Studies Of Buruli Ulcer

It has been demonstrated in laboratory studies that biting aquatic bugs (Naucoridae) fed on M. ulcerans-infested grub, could transmit M. ulcerans through bites and cause BU lesions in mice. In Australia, mosquitoes have also been implicated as possible insect vectors because M. ulcerans DNA has been detected in lysates of pooled mosquitoes. Also the M. ulcerans DNA positivity rate of sampled mosquitoes correlated with BU endemicity in local communities.

Additionally, a laboratory-based study showed that M. ulcerans DNA was found to transmit leprosy, and the intracellular-niche-requiring character of M. leprae led to the demonstration that Acanthamoeba spp could successfully maintain viable M. leprae intracellularly. This implicates Acanthamoeba spp as an important reservoir in the transmission of leprosy in nature. Similarly, we had earlier posited that Acanthamoeba spp may play an important role in BU transmission but did not support it with data. However a study by Gryseels et al. undermined the potential role of Acanthamoeba in BU transmission in the environment. The current study provides evidence, albeit in a laboratory model, in support of the hypothesis that Acanthamoeba spp may play a role in BU transmission. Furthermore, it was investigated whether Acanthamoeba polyphaga would enhance the virulence of M. ulcerans as reported for M. leprae and M. avium. Studies have demonstrated that injection of M. ulcerans into the footpad of mice, skin of grasscutters and guinea pigs results in BU, but topical application of M. Ulcerans on the abraded skin of the same guinea pigs did not lead to BU, suggesting that deeper dermal inoculation is required for transmission. It was show in an ICR mouse model that passive inoculation of naked M. ulcerans via contact with punctured skin could result in BU. We also show here for the first time that the mouse model could present undermined ulcer, which is the hallmark of BU by researchers.

Finally, this study demonstrates for the first time that A. polyphaga cocultured with M. ulcerans causes BU. Our study also demonstrates that coculturing A. polyphaga with M. ulcerans enhances BU pathogenesis. Persist in three successive instars of mosquito. A recent experimental mouse-tail infection model has shown that Anopheles notoscriptus, could transmit M. ulcerans to mice through bites and cause BU. Free living amoebae (FLA) have been reported severally in literature as possible reservoirs of pathogenic mycobacteria. The difficulty in implicating an arthropod vector for the

Signs and symptoms of Buruli Ulcer

Buruli ulcer often starts as a painless swelling (nodule). It can also initially present as a large painless area of induration (plaque) or a diffuse painless swelling of the legs, arms or face (oedema). Local immunosuppressive properties of the mycolactone toxin enable the disease to progress with no pain and fever. Without treatment or sometimes during antibiotics treatment, the nodule, plaque or oedema will ulcerate within 4 weeks with the classical, undermined borders. Occasionally, bone is affected causing gross deformities.

How To Control or Prevent Buruli Ulcer

The main control strategy, based on early detection and early treatment, is hampered in many places by the lack of awareness of the disease and limited access to health services. So far, no primary prevention strategy has been proposed for the population of rural regions where the disease is endemic. Studies aimed at identifying BU risk factors have repeatedly shown an association between the disease and activities such as wading or washing clothes in marshy areas of stagnant or slow-flowing waters. Farming in short clothes was also found to increase the risk of disease. The following measures would help prevent Buruli Ulcer.

Using a protected water source
Proper care of wounds, such as using alcohol to cleanse wounds
Hygienic practices, such as using soap for bathing
Wear protective cloths and boots especially those leaving in endemic areas.
Washing your skin or wounds that are exposed to the soil is required
In 2006, a case-control study performed in Akonolinga, in the endemic region of the Nyong valley in central Cameroon, showed for the first time that the use of a bed net was associated with protection against BU. This association was strong and independent of the socio-economic level of individuals, as it was found when comparing cases to both village and family controls by experts.