Buruli Ulcer Disease Transmission

Human Activites

Outbreaks of Buruli ulcer have been associated with activities near water bodies.

(Barker & Carswell 1973; Radford 1975; Thangaraj et al. 1999). It has been shown that an increased incidence of disease in many areas has resulted from:

  • unprecedented flooding of lakes and rivers during heavy rainfall;
  • the damming of streams and rivers to create artificial lakes and wetlands;
  • resorts that modify wetlands;
  • deforestation practices leading to increased flooding;
  • construction of agricultural irrigation systems; and
  • population expansion, resettlement and migration closer to water bodies, thus putting more people at risk

Increased human activities (eg. mining) and urban development remove riparian forests and also change water quality through both point and non-point source pollution; these factors may in turn be tied to ecological changes and Buruli ulcer incidence. Duker et al. (2004) found significant spatial relationships among villages in Buruli ulcer affected areas and arsenic-enriched surface waters and adjacent farmlands. The authors suggested that increased Buruli ulcer risk was related to immunosuppression resulting from the consumption of arsenic-enriched drinking water and food crops. This hypothesis has not been clinically tested. Additionally, many water bodies associated with increased sedimentation and eutrophication have characteristically low dissolved oxygen concentrations that are documented to enhance the growth of M. ulcerans

Possible vectors investigated to date include the following:

Cases of Buruli ulcer reported in wild and domesticated animals in Australia (i.e., koalas, possums, and an alpaca) confirmed that it can infect some animals (Mitchell et al. 1984), but natural infections in non-human animals have not been reported from other endemic regions. The discovery of human cases in some endemic regions and the suspicion that the source of the bacteria in the environment (Hayman 1991b) have led other investigators to propose certain animals as possible reservoir hosts for M. ulcerans

Mammals, frogs, reptiles and bats have been tested without positive findings (Radford 1974).

Several arthropods (i.e., bedbugs, black flies, mosquitoes) associated with vectoring disease agents tested negative (Portaels et al. 2001; Revill & Barker 1972).

DNA of M. ulcerans has been identified from water and detritus (i.e., decaying plant and other organic matter) in Australia (Roberts & Hirst 1997; Ross et al. 1997; Stinear et al. 2000)

In several studies, Buruli ulcer was correlated with a plant species (Echinocloa pyramidalis) associated with rivers and swamps (Barker 1972; Barker et al. 1972), and Meyers et al. (1974) speculated that direct inoculation from contact with vegetation might occur. Marston et al. (1995) found that wearing long pants was protective against ulcers on the lower extremities.

Portaels and colleagues (1999) suspected that aquatic bugs (Hemiptera) could be reservoirs of M. ulcerans. A study of 123 aquatic insects (Hemiptera, water bugs; Odonata, dragonfly larvae; Coleoptera, beetle larvae) collected in Buruli ulcer positive swamps confirmed their previous findings, and showed that small fish also could be potential reservoirs of M. ulcerans (Portaels et al. 2001,Kotlowski et al. 2004). Marsollier et al. (2002, 2003) demonstrated experimentally that M. ulcerans could survive and multiply exclusively within the salivary glands of aquatic bugs (Naucoridae: Naucoris cimicoides), and the insects were able to transmit M. ulcerans to mice. Several Hemiptera are known to bite humans using a piercing stylet that normally functions for feeding on other invertebrates (Merritt and Cummins 1996a).

The role of other non-insect aquatic invertebrates (e.g., snails) as intermediate reservoir hosts for M. ulcerans has been suggested by several authors (Kotlowski et al. 2004; Marsollier et al. 2003; Marsollier et al. 2002; Portaels et al. 1999), and was recently investigated by Marsollier et al. (2004a). They experimentally confirmed that aquatic snails could be contaminated by M. ulcerans after feeding on aquatic plants with M. ulcerans biofilms. In the field, Kotlowski et al. (2004) recorded M. ulcerans DNA in aquatic snails from endemic regions of Ghana and Benin. Based on these studies, it is evident that M. ulcerans is associated with aquatic plants, as biofilm on the plant surface, and as part of decaying organic matter, all of which serve as food for certain aquatic invertebrates and fish, providing evidence for movement throughout the aquatic food web.

Taken together, these studies imply a direct transmission of M. ulcerans via skin contact, which may arguably be through trauma (Kotlowski et al. 2004; Marsollier et al. 2002; Marsollier et al. 2004a; Portaels et al. 1999). We suggest a possible scenario (Figure below) expanded and modified from an original hypothesis proposed by Portaels et al. (1999), for the movement of M. ulcerans among aquatic reservoirs. Our research seeks to better understand the role of M. ulcerans in the environment and its transmission.