Pathogen fitness landscapes change when transmission cycles establish in non-native environments or spill over into new vectors and hosts. The introduction of Leishmania infantum in the Americas into the Neotropics during European colonization represents a unique case study to investigate mechanisms of ecological adaptation of this important parasite. Defining the evolutionary trajectories that drive L. infantum fitness in this new environment are of great public health importance as they will allow unique insight into pathways of host/pathogen co-evolution and their consequences for region-specific changes in disease manifestation. This review summarizes current knowledge on L. infantum genetic and phenotypic diversity in the Americas and its possible role in the unique epidemiology of VL in the New World. We highlight the importance of appreciating adaptive molecular mechanisms in L. infantum to understand the parasites’ successful establishment on the continent.

The description of the genus Leishmania as causative agents of leishmaniasis occurred during this modern age. But evolutionary studies suggest that the origin of Leishmania can be traced back to the Mesozoic era. Subsequently, during its evolutionary process, it sustained a worldwide dispersion predating the breakup of the Gondwana supercontinent. It is assumed that this parasite evolved from monoxenic Trypanosomatidae. Phylogenetic studies locate the dixenous Leishmania in a well-supported clade, recently named subfamily Leishmaniinae, which includes also monoxenous trypanosomatids. Virus-Like Particles were reported in many species of this family. So far, several Leishmania species have been reported as infected by Leishmania RNA Virus (LRV) and Leishbunyavirus (LBV). Since the first descriptions of LRV decades ago, differences in its genomic structure have been highlighted, leading to the designation of a LRV1 in L. (Viannia) species and a LRV2 in other L. (Leishmania) species. There are strong indications of virus infecting Leishmania spp. ability to enhance parasitic survival both in human and experimental infections, through highly complex and specialized mechanisms. Phylogenetic analyzes of these viruses have shown that their genomic differences correlate with the infected parasite species, suggesting a coevolutionary process. Herein, we will present unpublished results regarding the relationship Leishmania – endosymbiotic Leishmania viruses and will explore what has been described in the literature, and what is known about this association that could contribute to discussions about the worldwide dispersion of Leishmania.

Diagnosis of canine leishmaniosis (CanL) still represents a major challenge due to the variable clinical manifestations and the large number of asymptomatic dogs. Serological tests are most commonly used to detect infected animals, revealing anti-Leishmania antibodies, mainly of IgG isotype. Recently, a new diagnostic antigen, rKLi8.3, containing 8.3 kinesin tandem repeats (TR) from an Leishmania infantum strain from Sudan has been shown to provide excellent specificity and sensitivity to Leishmania infected humans and dogs. However, asymptomatic animals with very low antibody titers are often difficult to detect by serodiagnosis. Thus, we wondered whether addition of an anti-IgG-enhancing step in the protein A/G-based rKLi8.3-ELISA will improve the diagnostic performance without decreasing the specificity. For this, parasitologically confirmed CanL cases with low or high clinical score, uninfected healthy controls and dogs with other infections were tested by rKLi8.3-ELISA as well as two different immunochromatographic rapid tests, rKLi8.3-lateral flow test (LFT) and Dual Path Platform (DPP®) based on the rK28 antigen. Our results show that the diagnostic accuracy of the rKLi8.3-ELISA and LFT was similar to that of DPP, missing several asymptomatic animals. However, addition of a secondary, amplifying anti-dog IgG antibody in the protein A/G-based rKLi8.3-ELISA enabled the detection of nearly all asymptomatic dogs without affecting its specificity.