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Response to Letter:

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We would like to take this opportunity to thank Rodriguez and colleagues for their interest in our study. We agree that only six New World Leishmania species were identified from 20 patients. A typographical error resulted in the sentence “more than 25 species identified capable of producing disease.” This should have read “more than 25 species identified with most capable of producing disease.” In addition, we agree that of the 25 species identified, less than 20 have been definitely associated with human disease.

Additional epidemiological history, such as an extensive travel history, site, location and number of lesions, treatment, and therapeutic responses, would have greatly added to our study. However, as described in the methods, our laboratory served as the referral center for speciation and definitive diagnosis of Leishmania. Thus, these details, including therapeutic decisions made by the treating physician, were unavailable for a number of cases.

The clinical spectrum of Leishmania braziliensis, when compared to other New World species, was discussed in the article along with the risks of disease progression to the mucocutaneous form, so we are at a loss to explain why this is repeated by Rodriguez and colleagues. The authors also comment that the incidence of Chagas’ disease should have been investigated in those patients who had traveled to South America. However, this is out of the scope of a paper whose specific message was on the emergence of imported Leishmania infections and clearly not possible given the limitations in the methods referred to above.

The reasons for the choice of amphotericin B to treat cutaneous disease in Australia include the relative difficulty in obtaining pentavalent antimonial compounds that require importation and specific permission from health authorities. This consequently limits clinical experience with these compounds. Liposomal amphotericin B has less toxicity than the pentavalent antimonial compounds and demonstrates excellent efficacy. All our patients treated with amphotericin B responded well to treatment.

Leishmania infections are not notifiable in Australia, and thus, rates of infection within the country are unknown. However, our laboratory has seen a steady increase in Leishmania speciation requests from no cases prior to 2004 to the current level of 22 from 2005 to 2008. While we were unable to provide denominator data, we think that this represents a true increase.

With respect to miltefosine treatment for cutaneous disease, Rodriguez and colleagues would be aware of the research suggesting that miltefosine therapy for L (Viannia) braziliensis from Guatemala is suboptimal.1 Reasons for clinical failure and/or “resistance” include reduced intrinsic sensitivity of L (Viannia) braziliensis species to miltefosine in vitro.2 Rodriguez and colleagues state that no miltefosine-resistant Leishmania species have been isolated to date from clinical cases. However, this is not correct as Yardley and colleagues (2005) tested 15 clinical Peruvian New World Leishmania isolates and found that most of the isolates typed to the L (Viannia) braziliensis complex were insensitive to miltefosine. Thus, as discussed in our report, we would argue that speciation of Leishmania is of critical importance to guide therapeutic decisions. However, further species-specific drug research would greatly assist in these management decisions.

Finally, we certainly agree that the recent discovery of a novel Leishmania species in kangaroos in Australia along with the report of possible suitable vectors warrants further study to ascertain the potential risk for local human transmission.

References

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