Analysis of Buruli Ulcer Prevalence in Amansie West District: A Geostatistical Approach

Research Article

Austin Biom and Biostat. 2015;2(1): 1011.

Analysis of Buruli Ulcer Prevalence in Amansie West District: A Geostatistical Approach

Frank B Osei1* and Alfred A Duker2

1Department of Mathematics and Statistics, University of Energy and Natural Resources, Ghana

2Department of Geomatic Engineering, Kwame Nkrumah University of Science and Technology, Ghana

*Corresponding author: Osei FB, Department of Mathematics and Statistics, University of Energy and Natural Resources, Sunyani, Ghana.

Received: October 27, 2014; Accepted: January 05, 2015; Published: January 06, 2015


Buruli Ulcer (BU) is a disease caused by Mycobacterium Ulcerans (MU). The exact mode of transmission is yet unknown. However, the occurrences of BU cases in some specific discrete foci suggest a space-confined distribution pattern; this motivates this study. We incorporate a geostatistical technique to investigate the spatial patterns of BU prevalence in part of the Amansie West district of Ghana. A semivariogram model was computed to summarize the spatial variation and to determine the strength and spatial scale of the pattern. Ordinary kriging was used to produce a spatially continuous risk map of BU. The semivariogram model indicated a wider range of spatial dependence. Such nature of spatial dependence could be attributed to poor nature of public health interventions and the nature of BU risk factors. Spatial distribution of BU was observed to be high at the southern parts of the study area. Empirical classification of the study area into low, moderate and high risk zones showed that20% of the communities are within the high risk zone; 7% within the moderate risk zone; and 73% within the low risk zone.

Keywords: Mycobacterium ulcerans; Buruli ulcer; WHO; Topographic maps


Buruli Ulcer (BU) is a disease caused by Mycobacterium Ulcerans (MU) that manifests as disfiguring skin ulceration which is difficult to treat. In its advanced stage the disease does not respond to drugs and requires surgery, sometimes even limb amputation. It often starts as a painless, mobile swelling under the skin called a nodule. The disease can present as a large area of indurations- plaque- or a diffuse swelling of the legs and arms - edema. Because of the local immunosuppressive properties of mycolactone, or perhaps as a result of other unknown mechanisms, the disease progresses with no pain and fever, which may partly explain why those affected often, do not seek prompt treatment [1]. If untreated BU may lead to extensive soft tissue destruction, with inflammation extending to deep fascia. The parts of the body most affected are the extremities. Subsequent complications may include contracture and deformities. The main form of treatment was excision surgery and skin grafting while, occasionally amputation of limb is unavoidable. Today, however, according to WHO the overwhelming evidence is that, 8 weeks of streptomycin-rifampicin or 4 weeks of rifampicin-streptomycin followed by 4 weeks of rifampicin-clarithromycin or 8 weeks of other oral regimens all achieve recurrence-free healing with an acceptable level of side-effects. This is true for ulcers of all sizes, even without additional surgery to remove necrosis or skin grafting to accelerate healing [2].

In recent years, there has been increased incidence of BU in West Africa (including Benin, Burkina Faso, Cote d'Ivoire, Ghana, Guinea, Liberia and Togo), Mexico, French Guyana, Papua New Guinea and Australia. The disease seems to affect mostly impoverished inhabitants in remote and rural areas; children are the most vulnerable, accounting for approximately 70% of the cases [3]. The World Health Organization (WHO) has recognized BU as the third most prevalent mycobacterium disease after tuberculosis and leprosy and has called for urgent action to control [3,4].

The disease was first described by Cook in Uganda in1897 [5] and the etiologic agent was characterized by [6] and others in Australia. Since [7] reported the first case of Buruli ulcer identified in Ghana in 1971 awareness of the public health importance of the disease has been increasing [8]. Due to the ugly appearance of the deformities it leaves, Buruli ulcer is greatly feared and stigmatized in the endemic areas, and is often attributed to witchcraft and curses [9].

The mode of MU infection is still unknown; yet several hypotheses have been described. The first hypothesis is trauma to the skin by a contaminated environment (e.g., soil, water, vegetation, insect vector) [10]. The second hypothesis is that, as MU has been shown to be aerosolized from suspensions of tap water [11] it could be inhaled or ingested [11-13] and then reactivated in low temperature areas of the body at the sites of trauma. The second hypothesis is demonstrated in an extensive outbreak among residents of Philip Island [14,15]. One could argue, however, that there are either three hypotheses, or basically only one hypothesis: i.e., whatever mechanism or vector transmission, the basic idea is that there is some unknown environmental reservoir (in water-or mud plant bio films; snails; amoebae; fish; faecal pellets of certain rodents; etc.). These suggest some space-confined environmental reservoir, which justifies the definition of the risk of infection to space or place-defined risk; and therefore the analysis based on a geostatistical approach. Since environmental processes that play a role in mediating BU disease are spatially continuous in nature [16] BU rates are expected to display some spatial pattern, i.e. BU rates measured in communities that are geographically closer should be more similar than the rates recorded over larger separation distances.

Past studies of spatial patterns have relied mostly on methods based on the examination of the mean and variance or on the frequency distribution of observed disease incidence [17]. Deterministic approaches to interpolation (trend surface, inverse distance weighting, triangulation, and splinting) are based upon a priori mathematical models of spatial variation. It is assumed that the sampled data has no errors, which is often an incorrect assumption. In practice, error cannot be eliminated but only minimized. Therefore, in most cases one cannot produce the best representative map of estimated values in un-sampled locations with these techniques. However, these methods do not incorporate information on the location of the samples and in particular they fail to consider the degree of dependency between neighbouring observations (i.e., spatial dependence). Recently, methods that recognize such dependency have been proposed [18]. Geostatistics, as introduced by geologists, quantifies the spatial dependence and has been applied successfully in agro forestry, agronomy, and entomology [19]. In this study, we incorporate a geostatistical technique to investigate the spatial patterns of BU prevalence.

Materials and Methods

Study area

In Ghana, the first case of BU was reported in 1971 and, between 1991 and 1997, more than 2000 cases have been reported [4]. Approximately 6000 cases were recorded in a national survey in 1999. BU is the third most widespread mycobacterium infection in the country with an overall prevalence of 22.7 per 100,000. Cases have been identified in all ten regions of the country and in 90 out of 110 districts [20]. The Ashanti Region (which accounts for 10.2% of the land area and 19.1% of the population of Ghana) is the worst affected, accounting for 60% of all reported cases (Figure 2), with the Amansie West District (of the Ashanti Region) having the highest prevalence of 150.8 per 100,000 [20]. Figure 1 shows the prevalence of suspected active cases of Buruli Ulcer by region. In the Amansie West District high incidence of BU occurs in communities in close proximity to the off in River. Reports also show that 44% of BU patients are farmers [21]. This district is therefore placed in a suitable setting for studying the relation between BU and environmental factors that may potentially contribute to infection. The Amansie West District lies between latitudes 6°00'N and 6°45'N and longitudes 1°30'W and 2°15'W and covers an area of approximately 1,136 km2. The District is underlain by Lower Proterozoic volcanic greenstones with intervening sedimentary rocks and granitoid intrusions [22]. The District is drained by the off in and Oda rivers and the landscape varies from gentle to broken. Vegetation thrives on ferric fluvisols (the major soil types), which have been developed through yearly rainfall ranging from 125 to 200 cm and temperatures of 22 to 30° C. Vegetation is secondary forests, thicket, swamp and for b re growth (i.e., soft-stemmed leafy herbs, mostly the weeds, which appear on farms and have to be cut regularly). Of the 310 settlements in the Amansie West District, 19 have a population of 1000 or more, and their total population in 2000 was 108,726. There are approximately equal percentages of males and females. In terms of occupation, 70% are farmers and 22% are engaged in legal and 'Galamsey' (or illegal) gold mining. Since the national BU case search in 1999, the Amansie West District Health Administration and the mission hospital (St. Martin's Hospital) at Agroyesum have consistently collected data on BU.