Aguiar, Julia

Debacker, Martine

Gryseels, Bruno

Guedenon, Augustin

Johnson, Roch C.

Kestens, Luc

Portaels, François

Scott, Janet T.

Emerging Infectious Diseases

English

PubMed

Scott, J.T.

Johnson, R.C.

Aguiar, J.

Debacker, M.

Guedenon, A.

Gryseels, B.

Portaels, Fran\ue7oise

Institutional Repository Universiteit Antwerpen

Schistosoma haematobium infection and Buruli ulcer

Janet T. Scott

Roch C. Johnson

Julia Aguiar

Martine Debacker

Luc Kestens

Augustin Guedenon

Bruno Gryseels

François Portaels

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Schistosoma haematobium Infection and Buruli Ulcer

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<i>Schistosoma haematobium</i>Infection and Buruli Ulcer

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LETTERSAddress for correspondence:  David H. Walker,Department of Pathology, University of TexasMedical Branch, 301 University Blvd., KeillerBldg., Galveston, TX 77555-0609, USA; fax:409-772-1850: email: dwalker@utmb.eduSchistosomahaematobiumInfection and Buruli Ulcer To the Editor: Buruli ulcer causedby Mycobacterium ulcerans was rec-ognized in 1997 as an emerging publichealth problem by the World HealthOrganization (WHO) (1). The diseaseis found in tropical Africa, theAmericas, Australia, and Asia (2). InBenin, severe disease with seriouscomplications is reported with increas-ing frequency. Buruli ulcer causesserious deformities and disability, par-ticularly since amputating limbs issometimes required in cases of severedisease such as osteomyelitis (3).Given the effect on the quality of lifeof those afflicted and the lack of ade-quate treatment, identifying host riskfactors for Buruli ulcer is an importantresearch imperative (2). We investigat-ed one potential risk factor, concurrentinfection with Schistosoma haemato-bium. Preliminary data indicate thatalthough S. haematobium is not a riskfactor for Buruli ulcer, it may be asso-ciated with osteomyelitis.Although Buruli ulcer and schisto-somiasis each exist in the absence ofthe other, close parallels exist betweentheir epidemiology, suggesting thatschistosomiasis could be one possiblerisk factor for Buruli ulcer. Both dis-eases are associated with the tropicalwetlands of west and central Africa.Cases of both schistosomiasis andBuruli ulcer have increased rapidly inthese areas since the 1980s, particu-larly after irrigation and dam con-struction. Buruli ulcer is most fre-quent in children <15 years of age;this group typically also has the high-est prevalence and intensity of schis-tosome infections. Schistosomiasis istransmitted through contact withinfected water when the cercarial lar-vae penetrate skin, and increasing evi-dence exists that M. ulcerans prolifer-ates in the bottom mud of stagnantwaters and may be harbored by aquat-ic insects (4). An immunologic rationale forlinking the two diseases has been pro-posed (5). Briefly, protective immuneresponses to other mycobacterial dis-eases are known to depend on a type 1cellular response, typified by interfer-on-gamma (IFN-γ). Helminth infec-tions, on the other hand, are classical-ly associated with type 2 responses,typified by interleukin (IL)-4 and IL-5 production. Therefore, a concurrentinfection with a bloodborne helminthsuch as S. haematobium may skew theimmune response away from a poten-tially protective type 1 response (5). A total of 113 patients wererecruited from Buruli ulcer treatmentcenters in Lalo (Couffo Department)and Zagnanado (Zou Department) inBenin. A team of experienced sur-geons clinically confirmed all cases ofBuruli ulcer. Controls (n = 429) wererecruited at random from residents ofeight current Buruli ulcer foci in theCouffo Department. Past or currentBuruli ulcer patients were excludedfrom the lottery for controls.Clinical records reported no caseof intestinal schistosomiasis in thisarea. This finding was confirmed by apreliminary survey of 60 Buruli ulcerpatients, which detected no concur-rent S. mansoni by using the KatoKatz method (6). Diagnosis of S.haematobium (urinary schistosomia-sis) was performed by filtering threeurine samples given on different days.Neither cases nor controls were askedto exercise (as is usual) before givingurine samples because many Buruliulcer cases were immobile. Allpatients positive for S. haematobiumwere offered praziquantel treatment. In the entire participating popula-tion, 11.5% (95% confidence interval[CI] 6% to 19%) of Buruli ulcer caseswere positive for S. haematobium;11.1% (95% CI 5% to 20%) of casesfrom Lalo and 12.2% (95% CI 4% to26%) from Zagnanado were positive.The difference between the two cen-ters was not statistically significant. Ofthe 429 non-Buruli ulcer controls,9.5% (95% CI 7% to 13%) were posi-tive for S. haematobium. No statistical-ly significant difference between casesand controls was detected. The oddsratio for S. haematobium infection in alogistic regression model (which alsoincluded age and sex) was 1.3 (95% CI0.63 to 2.4). Prevalence of S. haemato-bium infection did not significantlydiffer between controls’ residence(data not shown). Power analysis indi-cates that about 4,000 cases and con-trols would be required to find a statis-tically significant difference at thisprevalence of schistosomiasis.Both schistosomiasis and Buruliulcer are very local in nature; one vil-lage can have substantial numbers ofcases whereas the next village couldhave none. S. haematobium foci withinfection prevalence >50% do exist inBenin but in different settlementsfrom the Buruli ulcer foci. Should aBuruli ulcer focus coincide with aschistosomiasis focus with a higherprevalence of infection, some associa-tion between the two diseases couldappear.Detailed clinical information wasavailable for 36 patients tested for S.haematobium. In all cases, at least twoof four laboratory tests were positivefor M. ulcerans. These tests were: 1)acid-fast bacilli in a smear stained bythe Ziehl-Neelsen technique, 2) posi-tive culture of M. ulcerans, 3)histopathologic examination of a tis-sue specimen, and 4) positive poly-merase chain reaction (PCR) for M.ulcerans DNA. Five patients had con-firmed infection in bone samples, sothey were classified as osteomyelitisEmerging Infectious Diseases • www.cdc.gov/eid • Vol. 10, No. 3, March 2004 551LETTERSpatients. Two of these five had con-current S. haematobium, compared tono cases in nonosteomyelitis patients;a Fisher exact test showed this differ-ence to be significant (p < 0.02).These limited and preliminary dataare consistent with the relationshipbetween leprosy (caused by amycobacterium related to the onecausing Buruli ulcer, M. leprae) andconcurrent helminth infections. Theseverity of leprosy has recently beenlinked to intestinal helminth infection,whereas the presence or absence ofleprosy has not (7). The cytokine envi-ronment created by helminth infectionmay facilitate disease progression to amore severe form, or severe mycobac-terial disease and helminth infectionmay have a common risk factor.We were unable to furnish evi-dence of a link between the presenceor absence of S. haematobium infec-tion and Buruli ulcer, but concurrentinfections could influence Buruliulcer clinical manifestation and dis-ease severity.AcknowledgmentsWe thank the residents of Yamatouand Houada and the patients, families, andstaff of the Buruli ulcer treatment centersin Zagnanado and Lalo. We also acknowl-edge the contribution of Pr. Ayiou of LaCroix treatment center and thank K.Fissette for technical assistance. This work was financially co-sup-ported by the Belgian Directorate-Generalfor International Co-operation (DGCI).Janet T. Scott,* Roch C. Johnson,†Julia Aguiar,‡ Martine Debacker,*Luc Kestens,* Augustin Guedenon,§ Bruno Gryseels,* and Françoise Portaels**Institute of Tropical Medicine, Antwerp,Belgium; †Centre de Dépistage et deTraitement des Ulcères de Buruli de Lalo,Bénin; ‡Centre Sanitaire et NutritionnelGbemonten, Zagnanado, Bénin; and§Ministère de la Santé Publique, Cotonou,BéninReferences1. Asiedu K, Portaels F. Chapter 1: introduc-tion. In: Asiedu K, Scherpbrei R,Raviglione M, editors. Buruli ulcer:Mycobacterium ulcerans infection [mono-graph on the Internet]. Geneva: WorldHealth Organization; 2000. Available from:http://www.who.int/gtb-buruli/publica-tions/PDF/Buruli_ulcer_monograph.PDF2. van der Werf TS, van der Graaf WTA,Tappero JW, Asiedu K. Mycobacteriumulcerans infection. Lancet 1999;354:1013–8.3. Lagarrigue V, Portaels F, Meyers WM,Aguiar J. L’ulcère de Buruli: attention auxatteintes osseuses! A propos de 33 casobservés au Benin. Med Trop (Mars)2000;60:262–6.4. Portaels F, Elsen P, Guimaraes-Peres A,Fonteyne PA, Meyers WM. Insects in thetransmission of Mycobacterium ulceransinfection [letter]. Lancet 1999;353:986.5. Stienstra Y, van der Graaf WTA, MeermanGJT, The TH, de Leij LF, van der Werf TS.Susceptibility to development ofMycobacterium ulcerans disease: review ofpossible risk factors. Trop Med Int Health2001;6:554–62.6. Katz N, Chaves A, Pellegrino J. A simpledevice for quantitative stool thick smeartechnique in Schistosomiasis mansoni. RevInst Med Trop Sao Paulo 1972;14:397–400.7. Diniz LM, Zandonade E, Dietze R, PereiraFE, Ribeiro R. Short report: do intestinalnematodes increase the risk for multibacil-lary leprosy? Am J Trop Med Hyg2001;65:852–4.Address for correspondence: Janet Scott,Institute of Tropical Medicine, Nationalestraat,155, 2000, Antwerpen, Belgium; fax: 00-32-3-2476-231; email: jscott@itg.be1998 DengueHemorrhagic FeverEpidemic in Taiwan To the Editor: The rapid spread-ing of dengue viruses has led toincreasing incidence rates of denguefever (DF), dengue hemorrhagic fever(DHF), and dengue shock syndrome(DSS) worldwide in the past 20 years.The global pandemic of DF and DHFin 1998 was associated with thelargest DF epidemics many tropical orsubtropical countries had ever experi-enced (1,2). Here we report the uniqueepidemiologic characteristics of DFand DHF caused by dengue virus type3 (DEN-3) in Taiwan, where dengueis not endemic. The recent epidemics of dengue inTaiwan started when dengue virustype 2 (DEN-2) was first introducedinto the southern off-islet of Hsiao-Liu-Chiu in 1981 after an absence of38 years since World War II. TainanCity in southern Taiwan had not had adengue epidemic since l942–1943until three dengue outbreaks occurredthere in the last decade. The first out-break of DEN-1 in 1994 and the sec-ond of DEN-2 in 1997 involved fewconfirmed cases. The third epidemicof dengue, which was attributed toDEN-3, began in October 1998 andcontinued into January 1999. From August 1, 1998, to January31, 1999, physicians in all the hospi-tals and clinics in Tainan City wererequired to report any suspecteddengue cases who met the criteria offever (>38oC) and two or more of thefollowing symptoms and signs:headache, retroorbital pain, myalgia,arthralgia, rash, and hemorrhagicmanifestations. Patients who met thecriteria were invited to participate inthe study; informed consent wasgiven by the patients, and plasma orserum samples were collected for lab-oratory confirmation. When a physi-cian reported a suspected denguecase, a minimum of 100 blood sam-ples would be collected from thepatient’s neighbors by the Tainan CityHealth Bureau staff. The blood speci-mens were transported to the labora-tory at the National Institute ofPreventive Medicine for confirma-tion. A confirmed dengue case wasrequired to be positive by eitherreverse transcription–polymerasereaction (3), or demonstrate serocon-version by dengue-specificimmunoglobulin (Ig) M and seroneg-ativity for Japanese encephalitis virus(JEV)-specific IgM by IgM-enzyme-552 Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 10, No. 3, March 2004

A simple device for quantitative stool thick smear technique in Schistosomiasis mansoni. Rev Inst Med Trop Sao Paulo

Address for correspondence: Janet Scott, Institute of Tropical Medicine, Nationalestraat, 155, 2000, Antwerpen, Belgium; fax: 00-32-3-2476-231; email: jscott@itg.be

Chapter 1: introduction. In: Asiedu

Insects in the transmission of Mycobacterium ulcerans infection [letter]. Lancet

L’ulcère de Buruli: attention aux atteintes osseuses! A propos de 33 cas observés au Benin. Med Trop (Mars)

Short report: do intestinal nematodes increase the risk for multibacillary leprosy?

The global pandemic of DF and DHF in

The TH, de Leij LF, van der Werf TS. Susceptibility to development of Mycobacterium ulcerans disease: review of possible risk factors. Trop Med Int Health

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Schistosoma haematobium infection and Buruli ulcer

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