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Leishmania spp. (Kinetoplastida) are unicellular parasites causing leishmaniases, neglected tropical diseases of medical and veterinary importance. In the vertebrate host, Leishmania parasites multiply intracellularly in professional phagocytes, such as monocytes and macrophages. However, their close relative with intracellular development—Trypanosoma cruzi—can unlock even non-professional phagocytes. Since Leishmania and T. cruzi have similar organelle equipment, is it possible that Leishmania can invade and even proliferate in cells other than the professional phagocytes? Additionally, could these cells play a role in the long-term persistence of Leishmania in the host, even in cured individuals? In this review, we provide (i) an overview of non-canonical Leishmania host cells and (ii) an insight into the strategies that Leishmania may use to enter them. Many studies point to fibroblasts as already established host cells that are important in latent leishmaniasis and disease epidemiology, as they support Leishmania transformation into amastigotes and even their multiplication. To invade them, Leishmania causes damage to their plasma membrane and exploits the subsequent repair mechanism via lysosome-triggered endocytosis. Unrevealing the interactions between Leishmania and its non-canonical host cells may shed light on the persistence of these parasites in vertebrate hosts, a way to control latent leishmaniasis. Full article

The reactivation of latent Leishmania infection in chronic diseases and immunocompromised hosts is a broad and heterogeneous field in medicine and infectious diseases. We reported one of the first cases of Visceral Leishmaniasis occurring in a Caucasian middle-aged man living in an endemic country (Italy) for Leishmania infantum infection following secukinumab treatment for psoriatic arthritis. The patient was cured with a Liposomal Amphotericin B (L-AmB, 3 mg/Kg on days 1–5, followed by a dose on days 10, 17, 24, 31 and 38) regimen, after which his anti-interleukin 17 treatment was restarted—without recurrence in the follow-up. Full article

Reactivation of latent tuberculosis infection (LTBI) or latent parasitic infection (LPI) during drug-induced immunosuppression can have serious consequences. The Division of tropical and humanitarian medicine of the Geneva University Hospitals runs a specific consultation for parasitic screening of immunosuppressed or pre-immunosuppressed patients. We sought to determine the seroprevalence of LTBI and LPI in such patients and explore its relationship with country of origin or previous travel in a retrospective, single-centre observational study from 2016 to 2019. Demographic data, travel history, ongoing treatments and results of the parasitological (Strongyloides stercoralis, Trypanosoma cruzi, Echinococcus multilocularis, Entamoeba histolytica and Leishmania spp.) and TB screening were collected to calculate LPI or LTBI prevalence. Risk factors for LTBI and strongyloidiasis were analysed using Poisson regression with robust variance. Among 406 eligible patients, 24/353 (6.8%) had LTBI, 8/368 (2.2%) were positive for Strongyloides stercoralis infection, 1/32 (3.1%) was positive for Entamoeba histolytica and 1/299 (0.3%) was positive for Leishmaniasis. No cases of Trypanosoma cruzi (0/274) or Echinococcus multilocularis (0/56) infection were detected. Previous travel to or originating from high-prevalence countries was a risk factor for LTBI (PR = 3.4, CI 95%: 1.4–8.2 and 4.0, CI 95%: 1.8–8.9, respectively). The prevalence of serological Strongyloidiasis in immunosuppressed patients is lower in comparison to those without immunosuppression (PR = 0.1, CI 95%: 0.01–0.8). In conclusion, screening before immunosuppression needs to be individualized, and LTBI and LPI need to be ruled out in patients who originate from or have travelled to high-prevalence countries. The sensitivity of strongyloidiasis serology is reduced following immunosuppression, so an algorithm combining different tests or presumptive treatment should be considered. Full article