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place approximately 60 km east of Kathmandu, the capi-tal of Nepal, and she had not previously been to India.Only her son, who brought her to us because the faciallesion was persistent and not responding to any localtherapy, visited her periodically. Furthermore, the statesmentioned in the letter are to the west of India, andNepal is contiguous with the eastern areas of India, notablyBihar and eastern Uttar Pradesh. The distance betweenKathmandu, Nepal, and Rajasthan, the area of investiga-tion in the study by Peters et al. (1981), is more than1500 km.

The study quoted for the identification of Leishmaniaisolates in India (Peters et al., 1981) was carried out 27years ago, using technology that is now obsolete. Peters etal. identified Leishmania major in Rajasthan canal regionusing isoenzyme and serotyping procedures. In the serotyp-ing method, cross-reactivity is commonly found. In theisoenzyme analysis the results were not very clear cut asthey found differences in the enzyme glucose phosphateisomerase (GPI); therefore, they mention that the strainresembles L. major. In the 27 years since this study therehas been no further report of L. major in the Rajasthan area.Recent studies based on molecular methods have identifiedL. tropica and L. donovani in Himachal Pradesh in North India(Sharma et al., 2005) and L. tropica in Rajasthan (Kumar etal., 2007).

In our study, we used the latest molecular methods,including PCR and PCR-RFLP, for characterisation of the par-asite in a clinical sample from a patient from Nepal (Kumaret al., 2008). Results were authenticated by sequencing thePCR product and comparing with the sequence of WHO ref-erence strains of L. major, L. donovani and L. tropica. Thesequence was 100% identical to the sequence of the WHOreference strain of L. major.

Moreover, we did not perform an HIV test in our patientas there was no such indication. Furthermore, in a relatedcondition, post-kala-azar dermal leishmaniasis, on which wehave been working for the past two decades, we have notcome across a single patient who was co-infected with HIV.

Funding: None.

Conflicts of interest: None declared.

Ethical approval: Not required.

References

Kumar, R., Bumb, R.A., Anasari, N.A., Mehta, R.D., Salotra, P.,2007. Cutaneous leishmaniasis caused by Leishmania tropica inBikaner, India: parasite identification and characterization usingmolecular and immunological tools. Am. J. Trop. Med. Hyg. 76,896—901.

Kumar, R., Ansari, N.A., Avninder, S., Ramesh, V., Salotra, P., 2008.Cutaneous leishmaniasis in Nepal: Leishmania major as a cause.Trans. R. Soc. Trop. Med. Hyg. 102, 202—203.

Peters, W., Chance, M.L., Chowdhury, A.B., Dastivar, B.G., Nandy,

A., Kalra, N.L., Sanyal, R.K., Sharma, M.I.D., Srivastav, L.,Schnur, L.F., 1981. The identity of some stocks of Leishmaniaisolated in India. Ann. Trop. Med. Parasitol. 75, 247— 249.

Sharma, N.L., Mahajan, V.K., Kanga, A., Sood, A., Katoch, V.M.,Mauricio, I., Singh, C.D., Parwan, U.C., Sharma, V.K., Sharma,

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R.C., 2005. Localized cutaneous leishmaniasis due to Leishma-nia donovani and Leishmania tropica: preliminary findings of thestudy of 161 new cases from a new endemic focus in HimachalPradesh, India. Am. J. Trop. Med. Hyg. 72, 819— 824.

Rajesh Kumara

Nasim Akhtar Ansari a

Singh Avnindera

V. Rameshb

Poonam Salotraa,∗a Institute of Pathology (ICMR),

Safdarjung Hospital Campus, New Delhi 110029, Indiab Department of Dermatology & Regional

STD Centre, Safdarjung Hospital andV.M. Medical College, New Delhi 110029, India

∗ Corresponding author.E-mail address: salotra@vsnl.com (P. Salotra)

19 February 2008oi: 10.1016/j.trstmh.2008.03.005

ater hyacinth and the transmission of schis-osomiasis

n the 1960s, detailed studies in Uganda on the Entebbeeninsula at the north end of Lake Victoria revealed lowransmission of Schistosoma mansoni (Prentice et al., 1970).he bottom-dwelling snail, Biomphalaria choanomphala,as implicated as the intermediate host. Biomphalaria

udanica tanganyicencis was very difficult to infect in theaboratory, and mammalian-type cercariae were rarelyound in field-collected samples. However, at the southernnd of the lake, B. s. tanganyicencis was an importantntermediate host (Webbe, 1962). More recent studies haveeported relatively high levels of infection, particularlyn mothers and children on the shores of Lake VictoriaOdugwu et al., 2006). The major change in the area haseen the invasion of the water hyacinth, Eichhornia sp.,nd the presence of B. sudanica that is susceptible tonfection with S. mansoni, although B. choanomphala cantill contribute to transmission. Similarly, in the same periodlate 1960s) a search for snails on the shore of Lake Albertas unrewarding (G.C. Coles, personnel observation), butigh levels of transmission are now present in some partsf the shoreline (Pinot de Moira et al., 2007). We suggesthat the invasion of water hyacinth has played a majorole in the increased transmission of schistosomiasis onhe shoreline of the great lakes of eastern Africa by eitherntroducing susceptible snails and/or providing a suitablenvironment for their multiplication.

unding: None.

onflicts of interest: None declared.

thical approval: Not required.

eferences

dugwu, S.E., Ramamurthy, N.K., Kabatereine, N.B., Kazibwe, F.,Tukahebwa, E., Webster, J.P., Fenwick, A., Stothard, J.R., 2006.

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Schistosoma mansoni in infants (aged <3 years) along the Ugan-dan shoreline of Lake Victoria. Ann. Trop. Med. Parasitol. 100,315—326.

inot de Moira, A., Fulford, A.J., Kabatereine, N.B., Kazibwe, F.,Ouma, J.H., Dunne, D.W., Booth, M., 2007. Microgeographicaland tribal variations in water contact and Schistosoma mansoniexposure within a Ugandan fishing community. Trop. Med. Int.Health 12, 724—735.

rentice, M.A., Panesar, T.S., Coles, G.C., 1970. Transmission ofSchistosoma mansoni in a large body of water. Ann. Trop. Med.Parasitol. 64, 339—348.

ebbe, G., 1962. Population studies of intermediate hosts inrelation to transmission of bilharziasis in East Africa, in:Wolstenholme, G.E.W., O’Connor, M. (Eds), Bilharziasis. CibaFoundation Symposium. J&A Churchill Ltd., London, pp. 7—22. d

Correspondence

G.C. Coles ∗

School of Clinical Veterinary Science,University of Bristol, Langford House,

Bristol BS40 5DU, UK

N.B. KabatereineVector Control Division, Ministry of Health,

P.O. Box 1661, Kampala, Uganda

∗ Corresponding author.E-mail address: gerald.c.coles@bristol.ac.uk

(G.C. Coles)

3 January 2008

oi: 10.1016/j.trstmh.2008.01.009