Leishmaniases: From Clinical Presentation, to Pathogenesis and Basic Science

A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Parasitic Pathogens".

Deadline for manuscript submissions: closed (15 December 2025) | Viewed by 2282

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Guest Editor
Centro de Investigações em Agravos Tropicais Emergentes e Negligenciados, Instituto de Doenças Tropicais Natan Portella, Universidade Federal do Piauí, Rua Artur de Vasconcelos 151-Sul, Teresina 64002-510, PI, Brazil
Interests: leishmania infantum; visceral leishmaniasis; pathogenesis; immunology

Special Issue Information

Dear Colleagues,

Most patients with viscerotropic Leishmania species do not develop visceral leishmaniasis or kala-azar disease. However, the disease is lethal if not treated quickly and adequately. Transmission occurs from bites from a species of sandfly. Host immunity status, including whether they are suffering from AIDS and using drug immunosuppression, their sex and genetic background, and sandfly-related factors, seem to modulate susceptibility to infection. Disease severity and mortality are mediated by Leishmania virulence factors that must be precisely identified. Patients develop a protracted course of disease with fever, anemia, wasting, hepatosplenomegaly, generalized edema, jaundice, diarrhea, and other signs and symptoms. Laboratory changes include neutropenia, lymphocytopenia, a low platelet count, low albumin, high gammaglobulins, elevated C-reactive proteins, and a higher erythrocyte sedimentation rate. HIV is a common risk factor, but the interaction of both pathogens is not well known. Hemorrhages are likely due to disseminated intravascular coagulation, and bacterial infections seem to result from a process known as immunoparalysis. Understanding these factors may help uncover the pathogenic basis of many infectious diseases and may help find new treatment opportunities for these diseases to avoid fatalities.

Prof. Dr. Carlos Henrique Nery Costa
Guest Editor

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Keywords

  • leishmania infantum
  • leishmania donovani
  • visceral leishmaniasis
  • kala-azar
  • hemorrhages
  • HIV

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Published Papers (2 papers)

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Research

17 pages, 1972 KB  
Article
Leishmaniavirus Type 1 Enhances In Vitro Infectivity and Modulates the Immune Response to Leishmania (Viannia) Isolates
by Armando A. Bonilla Fong, Vanessa J. Pineda, José E. Calzada, Marcia Dalastra Laurenti, Luiz Felipe Domingues Passero, Davis Beltran, Luis Fernando Chaves, Azael Saldaña and Kadir González
Pathogens 2025, 14(12), 1263; https://doi.org/10.3390/pathogens14121263 - 10 Dec 2025
Viewed by 194
Abstract
Leishmania RNA virus 1 (LRV-1) is a double-stranded RNA virus identified in several Leishmania spp. LRV-1 has been associated with increased disease severity and therapeutic failure in cutaneous leishmaniasis (CL). Although LRV-1 has been reported in the Americas, its influence on [...] Read more.
Leishmania RNA virus 1 (LRV-1) is a double-stranded RNA virus identified in several Leishmania spp. LRV-1 has been associated with increased disease severity and therapeutic failure in cutaneous leishmaniasis (CL). Although LRV-1 has been reported in the Americas, its influence on parasite infectivity and host immune responses remains poorly characterized in Panamanian isolates. In this study, we investigate the in vitro infectivity and immunomodulatory effects of LRV-1-positive (LRV-1+) versus LRV-1-negative (LRV-1) isolates of Leishmania (Viannia), including clinical strains of L. (V.) panamensis and L. (V.) guyanensis. A total of 21 isolates (nine LRV-1+, nine LRV-1, and three reference strains) were used to infect human U937 macrophages. The infectivity index (II) was measured at 24, 48, and 72 h post-infection. Cytokine levels of TNF-α, IFN-γ, IL-4, IL-6, IL-10, and IL-17 were quantified by flow cytometry, and IL-1β by ELISA at 24 and 48 h. LRV-1+ isolates exhibited significantly higher infectivity at 48 h (mean II = 1386.2) and 72 h (mean II = 1316.8) compared to LRV-1 isolates (mean II = 714.4 and 571.0, respectively; p < 0.001). Two L. (V.) panamensis LRV-1+ isolates associated with complicated CL cases displayed the highest II values. Cytokine analysis revealed that LRV-1+ isolates induced elevated TNF-α (p < 0.01) and IL-1β (p < 0.001), along with reduced IFN-γ (p < 0.01), while no significant differences were observed for IL-4, IL-6, IL-10, or IL-17. These findings indicate that LRV-1 enhances parasite infectivity and promotes a pro-inflammatory cytokine profile, which may contribute to disease persistence and treatment failure. Full article
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11 pages, 490 KB  
Article
Low Plasma Lipids Are Associated with Relapsing and Lethal Visceral Leishmaniasis in HIV-Infected Patients
by Renata V. S. Silva, Silvia R. B. Uliana, Jenicer K. U. Y. Yasunaka, Cláudio S. Veloso, Emille Sousa, Maria M. L. Ferreira, Vivianne S. Carvalho, Gabriel R. Ferreira, Dorcas L. Costa and Carlos H. N. Costa
Pathogens 2024, 13(6), 450; https://doi.org/10.3390/pathogens13060450 - 25 May 2024
Cited by 1 | Viewed by 1368
Abstract
Visceral leishmaniasis (VL) results from protozoa Leishmania infantum and L. donovani infection. This study investigated whether host factors would explain the relapses. First, susceptibility to amphotericin B of L. infantum isolates was evaluated in vitro. Then, clinical data and the lipid profile of [...] Read more.
Visceral leishmaniasis (VL) results from protozoa Leishmania infantum and L. donovani infection. This study investigated whether host factors would explain the relapses. First, susceptibility to amphotericin B of L. infantum isolates was evaluated in vitro. Then, clinical data and the lipid profile of patients with relapsing and non-relapsing VL were assessed. Susceptibility to amphotericin B was similar between the isolates. CD4+ lymphocytes were reduced in both groups of patients in the first episode and with relapsing VL. Still, the strongest blood cell indicator associated with relapses was low total lymphocyte counts. Total plasma cholesterol, high-density lipoprotein, low-density lipoprotein, and, uniquely, triglycerides of the six individuals in the first episode and twenty-three with relapsing VL were lower in relapsing patients than those in the first episode. Deceased patients had extremely low low-density lipoprotein. After CD4+ decreases, lymphocyte CD8+ reduction is the final stage of immunological failure. The lower lipid concentrations appear to be secondary to the depletion of fat stores by inflammation-induced cachexia and fat exhaustion provoked by the co-occurrence of both diseases, which can finally lead to death. Full article
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