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Background    L. tropica  can cause both cutaneous and visceral leishmaniasis in humans. Although the  L. tropica -induced cutaneous disease has been long known, its potential to visceralize in humans was recognized only recently. As nothing is known about the genetics of host responses to this infection and their clinical impact, we developed an informative animal model. We described previously that the recombinant congenic strain CcS-16 carrying 12.5% genes from the resistant parental strain STS/A and 87.5% genes from the susceptible strain BALB/c is more susceptible to  L. tropica  than BALB/c. We used these strains to map and functionally characterize the gene-loci regulating the immune responses and pathology.    Methods  We analyzed genetics of response to  L. tropica  in infected F 2  hybrids between BALB/c×CcS-16. CcS-16 strain carries STS-derived segments on nine chromosomes. We genotyped these segments in the F 2  hybrid mice and tested their linkage with pathological changes and systemic immune responses.    Principal Findings  We mapped 8  Ltr  ( Leishmania tropica  response) loci. Four loci ( Ltr2 ,  Ltr3 ,  Ltr6  and  Ltr8 ) exhibit independent responses to  L. tropica , while  Ltr1 ,  Ltr4 ,  Ltr5  and  Ltr7  were detected only in gene-gene interactions with other  Ltr  loci.  Ltr3  exhibits the recently discovered phenomenon of transgenerational parental effect on parasite numbers in spleen. The most precise mapping (4.07 Mb) was achieved for  Ltr1  (chr.2), which controls parasite numbers in lymph nodes. Five  Ltr  loci co-localize with loci controlling susceptibility to  L. major , three are likely  L. tropica  specific. Individual  Ltr  loci affect different subsets of responses, exhibit organ specific effects and a separate control of parasite load and organ pathology.    Conclusion  We present the first identification of genetic loci controlling susceptibility to  L. tropica . The different combinations of alleles controlling various symptoms of the disease likely co-determine different manifestations of disease induced by the same pathogen in individual mice.

Mapping the Genes for Susceptibility and Response to Leishmania tropica in Mouse