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LETTERS TO THE ED I TOR

Leishmania braziliensis in blood 30 yearsafter cure

SIR,-Leishmaniasis caused by Leishmania braziliensis ischaracterised by chronicity, latency, and metastatic behaviour.Recurrent lesions with mucosal involvement can be found in

patients who are clinically cured, which makes the treatment verydifficult and more expensive. Two mechanisms may explainrecurrent lesions:1 reactivation of persistent infections, andreinfection. The former implies either a failure in treatment or thatin this type of leishmaniasis, clinical cure, but seldom radicalelimination of the parasite, is achieved.2To get direct evidence of the presence of L braziliensis in patients’

blood, we tested a drop of blood obtained by finger prick with aspecific polymerase chain reaction (PCR) assay.3 The drop wasretrieved with a non-heparinised capillary tube and was

centrifuged. The buffy coat and serum were collected from thecapillary, treated with proteinase K, and boiled before PCR. Bloodwas taken from a 41-year-old woman infected in a high endemicarea of Merida State, Venezuela. She had presented with threelesions on her lower right leg that had healed spontaneously within 3months. 30 years later, the only evidence of leishmaniasis was threescars each of about 15 mm diameter. Her intradermal reaction was

positive (16 x 14 mm) after 72 h, whereas indirectimmunofluorescence with L braziliensis antigen was positive at adilution of 1/256. Blood cultures were negative. As a control, bloodwas also taken from a 23-year-old female volunteer who had neverlived in an endemic area.As shown in the figure, DNA of L braziliensis was found in the

blood of the woman who had had leishmaniasis (lanes 2 and 3). Thisis evidence of persistent infection, because it is difficult to accountfor the presence of this DNA in the absence of parasite. Thepresence of latent L braziliensis infection demands a revision ofseveral aspects of the epidemiology and management of humantegumentary leishmaniasis including: the role of the human host as areservoir, and the intradomiciliary transmission of the disease; thepossible transmission in non-endemic areas where the insect vectoris present; the contamination in urban areas by blood transfusions;the reactivation of leishmaniasis in immunosuppressed patients;4,5and treatment with immunosuppressive drugs. Furthermore, the

Southern blot hybridisation of PCR samples.Lane 1 =buffy coat of control lanes 2 and 3= patient’s buffy coat

and serum, lane 4=pedal biopsy of L braziliensis infected hamster.Arrow points to the PCR products indicating their size in base pairs(bp).

fact that a well-nourished infected person can harbour the parasitewithout any apparent handicap supports the view that Americantegumentary leishmaniasis, like American visceral leishmaniasis, isa disease that affects mainly the poor and under-nourished indeveloping countries.6

This work was supported by grants CONICIT Sl-2323, CDCH-UCVC.03.10.2890, and RLA 0083 009 UNDP to J. L. R., and CONICITSl-2121 and CDCHT-ULA. C.48390 to N. A. We thank Dr Ana Lugo forthe IFI test and Miss Carolina Gonzalez for technical help.

Grupo de Genética Molecular,Centro de Biología Celular,Universidad Central de Venezuela,Caracas 1041-A, Venezuela

PALMIRA GUEVARAJOSÉ LUIS RAMÍREZ

Núcleo Universitario Rafael,Trujillo, Venezuela

ELINA ROJASJOSÉ VICENTE SCORZA

Facultad de Ciencias,Mérida, Venezuela

NÉSTOR GONZÁLEZNESTOR AÑEZ

1. Saravia NG, Weigle K, Segura I, et al. Recurrent lesions in human Leishmaniabraziliensis infection: reactivation or reinfection? Lancet 1990; 336: 398-402.

2. Arargot de Rossell R, de Duran R, Rossell O, Rodriguez AM. Is leishmaniasis evercured? Trans R Soc Trop Med Hyg 1992; 86: 251-53.

3. Guevara P, Alonso A, Da Silveira JF, et al. Identification of new world Leishmaniausing ribosomal gene spacer probes. Mol Biochem Parastiol 1992; 56: 15-26.

4. Clauvel JP, Couderc LJ, Belmin J, Daniel MT, Rabian T, Seligmann M. Visceralleishmaniasis complicating acquired immunodeficiency syndrome (AIDS). TransR Soc Trop Med Hyg 1986; 80: 1010-11.

5. Machado E, Braga M, Da-Cruz AM, et al. Disseminated American muco-cutaneousleishmaniasis caused by Leishmania braziliensis braziliensis in a patient with AID S: acase report. Mem Inst Oswaldo Cruz 1992; 87: 487-92.

6. Badaró R, Jones TC, Lorenco R, et al. A prospective study of visceral leishmaniasis inan endemic area of Brazil. J Infect Dis 1986; 154: 639-49.

Topical melarsoprol for trypanosomiasisSIR,-Reactive arsenical encephalopathy is usually considered to

be the major side-effect associated with melarsoprol therapy oflate-stage human trypanosomiasis. Another importantcomplication is the damage caused to the vascular system by theinjection, which is supplied as a 36% solution in propylene glycol.This formulation is irritating and care has to be taken that theinjections are strictly intravenous with no leakage.! In youngpatients, at the end of a melarsoprol treatment regimen, it can beimpossible to find veins for further intravenous injections.2,3 Theseeffects can be long-lasting, with reports that the veins of patients hadnot fully recovered 2 years after melarsoprol therapy/* This effect isalmost certainly due to the propylene glycol and the vasculardamage could be avoided by changing the solvent or by finding analternative formulation that avoids intravenous injections.However, melarsoprol is insoluble in most solvents and unstable as asolid. Even if a suitable solvent were found, a new formulationwould still have to undergo the complicated registration procedurefor use in man.