Volume 10, Number 3—March 2004
Schistosoma haematobium Infection and Buruli Ulcer
To the Editor: Buruli ulcer caused by Mycobacterium ulcerans was recognized in 199
Volume 10, Number 3—March 2004
Schistosoma haematobium Infection and Buruli Ulcer
To the Editor: Buruli ulcer caused by Mycobacterium ulcerans was recognized in 1997 as an emerging public health problem by the World Health Organization (WHO) (1). The disease is found in tropical Africa, the Americas, Australia, and Asia (2). In Benin, severe disease with serious complications is reported with increasing frequency. Buruli ulcer causes serious deformities and disability, particularly since amputating limbs is sometimes required in cases of severe disease such as osteomyelitis (3). Given the effect on the quality of life of those afflicted, and the lack of adequate treatment, identifying host risk factors for Buruli ulcer is an important research imperative (2). We investigated one potential risk factor, concurrent infection with Schistosoma haematobium. Preliminary data indicate that although S. haematobium is not a risk factor for Buruli ulcer, it may be associated with osteomyelitis.
Although Buruli ulcer and schistosomiasis each exist in the absence of the other, close parallels exist between their epidemiology, suggesting that schistosomiasis could be one possible risk factor for Buruli ulcer. Both diseases are associated with the tropical wetlands of west and central Africa. Cases of both schistosomiasis and Buruli ulcer have increased rapidly in these areas since the 1980s, particularly after irrigation and dam construction. Buruli ulcer is most frequent in children <15 years of age; this group typically also has the highest prevalence and intensity of schistosome infections. Schistosomiasis is transmitted through contact with infected water, when the cercarial larvae penetrate skin, and increasing evidence exists that M. ulcerans proliferates in the bottom mud of stagnant waters and may be harbored by aquatic insects (4).
An immunologic rationale for linking the two diseases has been proposed (5). Briefly, protective immune responses to other mycobacterial diseases are known to depend on a type 1 cellular response, typified by interferon-gamma (IFN-γ). Helminth infections, on the other hand, are classically associated with type 2 responses, typified by interleukin (IL)-4 and IL-5 production. Therefore, a concurrent infection with a bloodborne helminth such as S. haematobium may skew the immune response away from a potentially protective type 1 response (5).
A total of 113 patients were recruited from Buruli ulcer treatment centers in Lalo (Couffo Department) and Zagnanado (Zou Department) in Benin. A team of experienced surgeons clinically confirmed all cases of Buruli ulcer. Controls (n = 429) were recruited at random from residents of eight current Buruli ulcer foci in the Couffo Department. Past or current Buruli ulcer patients were excluded from the lottery for controls.
Clinical records reported no case of schistosomiasis in this area. This finding was confirmed by a preliminary survey of 60 Buruli ulcer patients, which detected no concurrent S. mansoni by using the Kato Katz method (6). Diagnosis of S. haematobium was performed by filtering three urine samples given on different days. Neither cases nor controls were asked to exercise (as is usual) before giving urine samples because many Buruli ulcer cases were immobile. All patients positive for S. haematobium were offered praziquantel treatment.
In the entire participating population, 11.5% (95% confidence interval [CI] 6% to 19%) of Buruli ulcer cases were positive for S. haematobium; 11.1% (95% CI 5% to 20%) of cases from Lalo and 12.2% (95% CI 4% to 26%) from Zagnanado were positive. The difference between the two centers was not statistically significant. Of the 429 non-Buruli ulcer controls, 9.5% (95% CI 7% to 13%) were positive for S. haematobium. No statistically significant difference between cases and controls w