ABSTRACT.    Leishmania parasites cause complex of diseases called leishmaniases. Symptoms of leishmaniases range from subclinical to extensive systemic disease. It was established that many genes control the disease, but the basis of variation of symptoms is still unknown. The dissection of genetic and functional aspects of susceptibility to infection of L. major was performed using two inbred strains: susceptible BALB/cHeA, resistant STS/A and a set of 20 CcS/Dem recombinant congenic (RC) strains. Each of the 20 CcS/Dem strains carries different random subset of 12.5% genes of the strain STS/A in a BALB/cHeA background. We analyzed the response of the intermediately resistant RC strain CcS-9. In the (CcS-9_BALB/cHeA)F₂ hybrids we mapped five loci that influence cutaneous or visceral pathology. We confirmed the position and found new functions of Lmr15 (chromosome 11) and Lmr18 (chromosome 16) and mapped three novel loci: Lmr24 (chromosome 2) controls parasite load in draining lymph nodes, Lmr25 (chromosome 4) controls splenomegaly, skin lesions and level of IFNγ in serum and Lmr26 (chromosome 17) determines skin lesions. The definition of genes controlling response to L. major infection will permit a better understanding of pathways and genetic diversity underlying the course of disease.