1. Disease Information
1.1 Disease definition and overview
Leishmaniasis is a neglected tropical disease caused by protozoan parasites of the genus Leishmania transmitted to humans (and other mammals) by infected female phlebotomine sandflies. Clinical expression spans cutaneous, mucocutaneous, and visceral disease forms, with post-kala-azar dermal leishmaniasis (PKDL) recognized as part of the visceral spectrum. (cosma2024leishmaniasisinhumans pages 2-4, mota2024classicalandinnovative pages 1-3)
Direct abstract support (definition quote): - “Leishmaniasis is classified as a neglected tropical disease (NTD), caused by protozoan parasites of the genus Leishmania, which are transmitted to humans and other animals through the bite of infected female phlebotomine sandflies.” (Cosma et al., 2024-10-??, DOI: 10.3390/tropicalmed9110258) (cosma2024leishmaniasisinhumans pages 2-4)
1.2 Key identifiers (ontology and clinical coding)
- MONDO ID: not available in retrieved evidence.
- MeSH: not available in retrieved evidence.
- ICD-10 / ICD-11: not available in retrieved evidence.
- Orphanet: not available in retrieved evidence.
1.3 Common synonyms / alternative names
- Visceral leishmaniasis: “kala-azar”. (sousa2024visceralleishmaniasistherapeutic pages 4-6, cosma2024leishmaniasisinhumans pages 2-4)
- Tegumentary leishmaniasis: used as an umbrella term for cutaneous and mucosal involvement in some clinical contexts. (chivinski2023intravenousliposomalamphotericin pages 6-7)
1.4 Evidence sources and aggregation level
The evidence used here includes: peer-reviewed reviews and systematic reviews/meta-analyses, observational clinical cohorts, and controlled human infection model (CHIM) data. These are aggregated disease-level resources with embedded patient-level study data; some sections also draw on retrospective chart review and case series evidence. (cosma2024leishmaniasisinhumans pages 2-4, lindner2024americancutaneousleishmaniasis pages 2-4, parkash2024safetyandreactogenicity pages 2-3, chivinski2023intravenousliposomalamphotericin pages 6-7)
2. Etiology
2.1 Disease causal factors
- Infectious agent: intracellular protozoa (Leishmania spp.). (cosma2024leishmaniasisinhumans pages 2-4, balahbib2023cutaneousleishmaniasisphysiopathology pages 1-4)
- Transmission: via bites of infected female sandflies. (cosma2024leishmaniasisinhumans pages 2-4, sousa2024visceralleishmaniasistherapeutic pages 4-6)
- Clinical heterogeneity: depends strongly on parasite species and host immunity. (cosma2024leishmaniasisinhumans pages 2-4, dey2024il32producingcd8+ pages 1-7)
2.2 Risk factors
Host factors - Immunocompromise (e.g., HIV, inborn errors of immunity) is associated with more severe disease and relapse risk in visceral infection. (lodi2024immuneresponseto pages 10-11)
Behavioral/environmental factors (mucosal disease) - Risk factors for mucocutaneous leishmaniasis include smoking, alcohol abuse, and large or multiple untreated skin lesions, especially on head/neck. (fischer2024treatmentofmucocutaneous pages 2-2)
Macro-environmental determinants (One Health) Climate change, deforestation, urbanization, globalization/migration can shift sandfly and reservoir distributions, increasing human exposure and expanding leishmaniasis into new latitudes/altitudes. (cosma2024leishmaniasisinhumans pages 2-4)
2.3 Protective factors
Not directly identified in the retrieved evidence corpus (no specific host genetic protective alleles or environmental protective exposures were evidenced).
2.4 Gene–environment interactions
Explicit gene–environment interaction evidence was not present in the retrieved corpus. The best-supported interaction framework here is “parasite species × host immune state × environment/vector ecology” determining clinical form and outcomes. (cosma2024leishmaniasisinhumans pages 2-4, fischer2024treatmentofmucocutaneous pages 2-2)
3. Phenotypes
3.1 Core clinical phenotypes by form (with suggested HPO terms)
Cutaneous leishmaniasis (CL) - Skin ulcer(s) / papules/plaques; lesions may persist months–years; atrophic scarring common. (balahbib2023cutaneousleishmaniasisphysiopathology pages 4-6, balahbib2023cutaneousleishmaniasisphysiopathology pages 1-4) - Suggested HPO: Skin ulcer (HP:0031432); Scar (HP:0100716); Skin papule (HP:0200037). - Typical incubation reported as 1–4 months and spontaneous healing over 2–10 months in some cases. (balahbib2023cutaneousleishmaniasisphysiopathology pages 1-4)
Mucocutaneous leishmaniasis (MCL/ML) - Destructive granulomatous lesions of oral/nasal/pharyngeal mucosa; complications include impaired swallowing/speech, aspiration pneumonia, bacterial superinfection/sepsis, and need for reconstructive surgery. (fischer2024treatmentofmucocutaneous pages 2-2) - Suggested HPO: Nasal septum perforation (HP:0011833); Dysphagia (HP:0002015); Dysarthria (HP:0001260).
Visceral leishmaniasis (VL; kala-azar) - Systemic syndrome including fever, weight loss, hepatosplenomegaly, and cytopenias (pancytopenia/anemia). (balahbib2023cutaneousleishmaniasisphysiopathology pages 4-6, cosma2024leishmaniasisinhumans pages 2-4) - Suggested HPO: Fever (HP:0001945); Weight loss (HP:0001824); Splenomegaly (HP:0001744); Hepatomegaly (HP:0002240); Anemia (HP:0001903); Pancytopenia (HP:0001876).
Post-kala-azar dermal leishmaniasis (PKDL) - Recognized as post-VL dermal manifestation; detailed phenotype frequencies not evidenced in the retrieved set. (cosma2024leishmaniasisinhumans pages 2-4)
3.2 Quality of life impact
CL and MCL can cause scarring/disfigurement with substantial psychosocial morbidity. (cosma2024leishmaniasisinhumans pages 2-4, balahbib2023cutaneousleishmaniasisphysiopathology pages 4-6)
4. Genetic / Molecular Information
4.1 Human causal genes / Mendelian causes
Leishmaniasis is not a monogenic inherited disease; causal pathogen is Leishmania spp. Host genetics can modulate susceptibility and course, but specific loci were not evidenced in the retrieved corpus.
4.2 Molecular mechanisms (host–pathogen) and ontology suggestions
4.2.1 Cellular tropism and immune evasion (VL and CL)
- Parasite survival involves immune evasion mechanisms that favor anti-inflammatory environments, including immune checkpoint activity and cytokine skewing. (lodi2024immuneresponseto pages 10-11, dey2024il32producingcd8+ pages 1-7)
Phagosome manipulation (VL) - L. donovani lipophosphoglycan (LPG) can exclude vesicular proton-ATPase (V-ATPase) from phagosomes by impairing Synaptotagmin V recruitment, limiting acidification. (lodi2024immuneresponseto pages 10-11)
TLR pathway suppression - Parasites can exploit host deubiquitinating enzyme A20, a negative regulator of TLR signaling, to subvert innate responses. (lodi2024immuneresponseto pages 10-11)
Suggested ontologies: - GO biological process: response to protozoan (GO:0009617); phagosome maturation (GO:0090382); regulation of Toll-like receptor signaling pathway (GO:0034121). - CL cell types: macrophage (CL:0000235); neutrophil (CL:0000775); dendritic cell (CL:0000451); CD8-positive, alpha-beta T cell (CL:0000625); regulatory T cell (CL:0000815).
4.2.2 Immune checkpoints and localized immunosuppressive niches (human CL; 2024)
Spatial and single-cell profiling of human CL lesions identified myeloid-centered niches co-expressing PD-L1 (CD274) and IDO1, with neighboring IL-32–producing CD8+ memory T cells and Tregs. Mechanistically, IDO1-mediated tryptophan catabolism can suppress T-cell proliferation and promote regulatory phenotypes, and PD-L1 can suppress T-cell activation via PD-1 engagement. (dey2024il32producingcd8+ pages 7-11, dey2024il32producingcd8+ pages 11-15)
Quantitative prognostic finding (treatment response): Higher IL-32+ CD8+ T cell abundance was associated with slower cure; IL-32-low patients cured earlier with hazard ratios reported in the preprint. (dey2024il32producingcd8+ pages 11-15)
Suggested ontologies: - GO: tryptophan catabolic process (GO:0006569); negative regulation of T cell activation (GO:0050868).
4.2.3 Hypoxia–neutrophil–CD8 cytotoxic pathology in CL (2024)
A 2024 mechanistic study supports a causal chain in CL lesions: neutrophil recruitment increases oxygen consumption and reactive oxygen species (ROS) generation, amplifying local hypoxia; hypoxia drives Blimp-1/PRDM1 and induces cytolytic differentiation and granzyme B expression in lesion CD8+ T cells. Downstream, cytolysis activates NLRP3 inflammasome/IL-1β and perpetuates neutrophilic inflammation and tissue damage. Human CL lesions exhibit hypoxia transcriptional signatures correlated with neutrophils. (fowler2024neutrophilmediatedhypoxiadrives pages 1-2)
Suggested ontologies: - GO: response to hypoxia (GO:0001666); neutrophil degranulation (GO:0043312); T cell mediated cytotoxicity (GO:0001913); NLRP3 inflammasome complex assembly (GO:0072557).
4.2.4 Epigenetic regulation and IL-10/IL-12 reciprocity (macrophage; 2024)
Single-cell ATAC-seq analysis in a macrophage infection model identified a transient “sleepy macrophage” state and a reciprocal IL-10/IL-12 axis; the work emphasizes transcription-factor-driven chromatin remodeling and epigenetic control of inflammatory cytokine programs in infected macrophages. (khandibharad2024singlecellatacsequencing pages 1-2)
Suggested ontologies: - GO: chromatin remodeling (GO:0006338); regulation of interleukin-10 production (GO:0032666); regulation of interleukin-12 production (GO:0032655).
4.2.5 Single-cell atlas of parasite development in the vector (2024)
Single-cell analysis of Leishmania development in sandflies identified heterogeneity in transmitted parasite forms beyond classical nondividing metacyclic promastigotes, including “replicating early metacyclics” and haptomonad stages, with in vivo mouse infection indicating pathology is not restricted to a single transmitted stage. (parkash2024safetyandreactogenicity pages 2-3)
5. Environmental Information
5.1 Environmental and ecological drivers (One Health)
Environmental disruptions (climate change, deforestation, urbanization) and human/animal movement can expand sandfly range and human-vector contact, contributing to emergence in previously non-endemic areas. (cosma2024leishmaniasisinhumans pages 2-4)
5.2 Reservoirs and zoonotic ecology
Domestic dogs are highlighted as primary reservoirs for zoonotic visceral leishmaniasis in some settings, with additional roles for wild reservoirs. (sousa2024visceralleishmaniasistherapeutic pages 4-6)
6. Anatomical Structures Affected
6.1 Primary organs/tissues
- Skin (cutaneous lesions; scarring). (balahbib2023cutaneousleishmaniasisphysiopathology pages 4-6)
- Suggested UBERON: skin of body (UBERON:0002097)
- Mucosa of upper aerodigestive tract (nasal/oral/pharyngeal). (fischer2024treatmentofmucocutaneous pages 2-2)
- Suggested UBERON: nasal mucosa (UBERON:0001707); oral mucosa (UBERON:0000344)
- Spleen, liver, bone marrow (visceral leishmaniasis systemic involvement and diagnostic sampling sites). (cosma2024leishmaniasisinhumans pages 2-4, gritti2024epidemiologicalclinicaland pages 30-35)
- Suggested UBERON: spleen (UBERON:0002106); liver (UBERON:0002107); bone marrow (UBERON:0002371)
6.2 Subcellular compartments
Not explicitly evidenced in the retrieved corpus; infection is intracellular (amastigotes in host cells). (mota2024classicalandinnovative pages 1-3)
7. Temporal Development
- CL incubation: reported 1–4 months in a 2023 review; typical spontaneous healing 2–10 months (variable). (balahbib2023cutaneousleishmaniasisphysiopathology pages 1-4)
- MCL evolution: may occur after untreated/inadequately treated CL, potentially years later. (balahbib2023cutaneousleishmaniasisphysiopathology pages 4-6, fischer2024treatmentofmucocutaneous pages 2-2)
- VL progression: can be fatal if untreated; Sousa 2024 reports untreated mortality exceeding 95%. (sousa2024visceralleishmaniasistherapeutic pages 4-6)
8. Inheritance and Population
8.1 Epidemiology (recent statistics)
- Global annual incidence often cited as 700,000–1,000,000 new cases/year. (cosma2024leishmaniasisinhumans pages 2-4)
- For CL, WHO reported 253,435 new cases in 2018; a review cites 500,000–1,000,000 new cases annually. (balahbib2023cutaneousleishmaniasisphysiopathology pages 4-6)
- For VL, a 2024 review estimates 50,000–90,000 new cases/year, with only 25–45% officially reported, and untreated mortality >95%. (sousa2024visceralleishmaniasistherapeutic pages 4-6)
- VL is concentrated in India, Sudan, Brazil, and Kenya (reported as 68% of cases). (sousa2024visceralleishmaniasistherapeutic pages 4-6)
8.2 Geographic distribution and expansion
Leishmaniasis is endemic across Africa, Asia, Southern Europe, the Middle East, and Central/South America, with recent reports of autochthonous transmission in previously non-endemic Western Europe and North America attributed to climate and migration drivers. (cosma2024leishmaniasisinhumans pages 2-4)
9. Diagnostics
9.1 Parasitological diagnosis (microscopy, histology, culture)
- VL: microscopy sensitivity differs by sampling site: splenic aspirate/biopsy microscopy reported >90% sensitivity, bone marrow aspirate 50–80%, with a quoted 0.1% fatality risk for splenic sampling. (gritti2024epidemiologicalclinicaland pages 30-35)
- CL: microscopy of skin biopsy for amastigotes is used; one cited study reports direct exam sensitivity ~89.3%, decreasing with older lesions. (balahbib2023cutaneousleishmaniasisphysiopathology pages 9-12, balahbib2023cutaneousleishmaniasisphysiopathology pages 12-15)
- Culture: reported as uncommon in some settings due to long growth time; sensitivity cited as 60–85%. (gritti2024epidemiologicalclinicaland pages 35-39)
9.2 Serology
- rK39 antigen is cited as useful for VL; performance may vary by geography (high performance in Indian subcontinent, lower sensitivity in Eastern Africa and southern Europe). (balahbib2023cutaneousleishmaniasisphysiopathology pages 12-15, gritti2024epidemiologicalclinicaland pages 35-39)
9.3 Molecular diagnostics and species typing
- PCR can detect as few as 10 parasites/mL, with sensitivity 86–95% in acute lesions but lower in chronic disease (~45.5% in one report). (balahbib2023cutaneousleishmaniasisphysiopathology pages 12-15)
- For imported ACL cases in Germany, diagnosis was clinical + PCR confirmation, with typing via ITS1/SSU rRNA PCR-RFLP and later HSP70 PCR-RFLP. (lindner2024americancutaneousleishmaniasis pages 2-4)
- Molecular typing: MLEE is described as historical gold standard but laborious and requires culture; high-copy targets used for molecular typing include kDNA minicircles, miniexon, and hsp70 (widely validated for species typing). (gritti2024epidemiologicalclinicaland pages 39-44, gritti2024epidemiologicalclinicaland pages 35-39)
9.4 Diagnostics used in recent spatial-omics CL studies
Studies of human CL lesions used slit-skin smears (Giemsa), PCR/qPCR confirmation, and RNA-FISH probes (e.g., amastin) for parasite detection in tissue sections. (dey2024il32producingcd8+ pages 19-22)
10. Outcome / Prognosis
- VL is described as potentially fatal if untreated; one 2024 review states untreated mortality exceeds 95%. (sousa2024visceralleishmaniasistherapeutic pages 4-6)
- In Brazil, a 2024 narrative review reports 50,478 cases and 3,945 deaths through Aug 2024 with mortality 7.02% (as reported in that secondary source). (sousa2024visceralleishmaniasistherapeutic pages 4-6)
- CL and MCL often lead to chronic morbidity via scarring/disfigurement and mucosal destruction. (fischer2024treatmentofmucocutaneous pages 2-2, cosma2024leishmaniasisinhumans pages 2-4)
11. Treatment
11.1 Standard pharmacotherapy and real-world use
Common antileishmanial agents across syndromes include pentavalent antimonials, amphotericin B (including liposomal), miltefosine, paromomycin, and pentamidine; choice often depends on setting/availability and host factors. (sousa2024visceralleishmaniasistherapeutic pages 4-6, fischer2024treatmentofmucocutaneous pages 2-2)
11.2 Quantitative treatment outcomes from recent evidence
Liposomal amphotericin B for cutaneous/mucosal disease (systematic review/meta-analysis; 2023)
- Pooled cure rate (case series): 87.0% (95% CI 79–92%) across 38 case series. (Chivinski et al., 2023-07, DOI: 10.1093/ofid/ofad348) (chivinski2023intravenousliposomalamphotericin pages 1-2)
- Case reports cure: 65/92 (82.3%). (chivinski2023intravenousliposomalamphotericin pages 1-2)
- Adverse reactions: in pooled data, adverse reactions reported in 40.7% of cases; most commonly renal toxicity and infusion reactions. (chivinski2023intravenousliposomalamphotericin pages 7-9)
Mucocutaneous leishmaniasis therapies (systematic review; 2024)
- Species-stratified outcomes show high reported success for L-AmB in multiple small series (e.g., L. braziliensis 57/64 (89%)). (fischer2024treatmentofmucocutaneous pages 4-4)
- Combination therapy NMA + pentoxifylline had 9/10 cured in one report and an overall cure rate reported as 95% for the combination. (fischer2024treatmentofmucocutaneous pages 6-7)
Post-kala-azar dermal leishmaniasis (PKDL) randomized trial (2021)
- Per-protocol final cure: 74.5% (liposomal amphotericin B) vs 86.9% (miltefosine). (pandey2021arandomizedopenlabel pages 3-4)
- Adverse events: 82% vs 56% (mostly grade I–II). (pandey2021arandomizedopenlabel pages 3-4)
11.3 Treatment guidelines (evidence limitation)
Formal WHO/IDSA guideline text was not retrieved in this corpus; treatment regimen details referenced in the meta-analysis include mention of guideline cumulative dosing (e.g., IDSA cumulative 18–21 mg/kg for L-AmB) but without full guideline retrieval. (chivinski2023intravenousliposomalamphotericin pages 7-9)
11.4 MAXO term suggestions (treatments)
- Liposomal amphotericin B therapy: MAXO:0000743 (antifungal/antiparasitic drug therapy) (placeholder—MAXO IDs not evidenced in corpus).
- Cryotherapy for localized CL lesions (used in CHIM recurrences): MAXO:0000549 (cryotherapy) (placeholder—MAXO IDs not evidenced in corpus). (parkash2024safetyandreactogenicity pages 1-2)
12. Prevention
12.1 Vector/reservoir control and One Health prevention
Integrated surveillance and prevention strategies targeting vectors, animal reservoirs (notably dogs), and human exposure are emphasized in the One Health literature; drivers such as climate change and land-use change motivate adaptive surveillance. (cosma2024leishmaniasisinhumans pages 2-4, sousa2024visceralleishmaniasistherapeutic pages 4-6)
12.2 Vaccines and CHIM as a vaccine-enabling technology (2024)
A major 2024 development is the establishment of a controlled human infection model (CHIM) for sand fly–transmitted L. major CL to accelerate vaccine development. (parkash2024safetyandreactogenicity pages 2-3, parkash2024safetyandreactogenicity pages 1-2)
Direct abstract support (CHIM quote): - “The leishmaniases are globally important parasitic diseases for which no human vaccines are currently available.” (Parkash et al., Nature Medicine, 2024-08, DOI: 10.1038/s41591-024-03146-9) (parkash2024safetyandreactogenicity pages 1-2)
13. Other Species / Natural Disease (One Health)
- Dogs are highlighted as primary domestic reservoirs for visceral leishmaniasis in the Americas, with implications for zoonotic transmission and control. (sousa2024visceralleishmaniasistherapeutic pages 4-6)
- Leishmaniasis is framed as a human–animal–environment system, influenced by pet trade, breeding, and migration affecting reservoir movement. (cosma2024leishmaniasisinhumans pages 2-4)
14. Model Organisms and Experimental Systems
14.1 Human CHIM (real-world implementation for translational research)
- Model: sand fly–transmitted CL CHIM (L. major via Phlebotomus duboscqi). (parkash2024safetyandreactogenicity pages 2-3)
- Take rate: 64% overall (9/14), 82% among confirmed bites (9/11). (parkash2024safetyandreactogenicity pages 2-3)
- Trial registration: NCT04512742. (parkash2024safetyandreactogenicity pages 1-2)
- Safety: no severe/serious adverse events; recurrences treated successfully with cryotherapy; scarring observed. (parkash2024safetyandreactogenicity pages 1-2)
14.2 Mouse models
Mechanistic work in mice supports roles for neutrophils/hypoxia and CD8 cytotoxicity in CL pathology. (fowler2024neutrophilmediatedhypoxiadrives pages 1-2)
14.3 Macaque model (visceral persistence; single-cell)
A rhesus macaque VL model with post-treatment tissue reservoirs and single-cell transcriptomic profiling is described (preprint), highlighting parasite persistence in spleen, bone marrow, and lymph nodes after miltefosine. (parkash2024safetyandreactogenicity pages 2-3)
15. Clinical Trials and Development Pipeline (selected)
ClinicalTrials.gov trials retrieved include: - NCT04512742: sand fly-transmitted CL CHIM (vaccine-enabling model). (parkash2024safetyandreactogenicity pages 1-2) - VL combination therapy trials (completed): NCT01122771, NCT00696969, NCT00523965, NCT00371995. (clinical-trials tool output; not chunk-cited in current evidence set) - Cutaneous/mucosal treatment trials: NCT01377974 (miltefosine for mucosal leishmaniasis), NCT03829917 (oral miltefosine + topical paromomycin in ACL). (clinical-trials tool output; not chunk-cited in current evidence set)
Expert interpretation and analysis (2023–2024 emphasis)
- Diagnostics are moving toward molecular confirmation and species typing, driven by heterogeneous treatment response across Leishmania species and the need to guide therapy; PCR-RFLP and HSP70 typing are used in real-world clinical practice for imported cases. (lindner2024americancutaneousleishmaniasis pages 2-4, gritti2024epidemiologicalclinicaland pages 39-44)
- Pathophysiology is increasingly understood as spatially compartmentalized immunopathology, where distinct immune niches and checkpoints exist within lesions; spatial transcriptomics and single-cell methods identify actionable pathways (PD-L1/IDO1; hypoxia-driven cytotoxicity). (dey2024il32producingcd8+ pages 7-11, fowler2024neutrophilmediatedhypoxiadrives pages 1-2)
- A major translational development is the CL CHIM that directly supports vaccine development by enabling controlled assessment of protective immunity and lesion biology in humans, including spatial immune mapping. (parkash2024safetyandreactogenicity pages 1-2, parkash2024safetyeffectivenessand pages 13-17)
- One Health framing is essential: climate change and land-use shifts are not only upstream risk drivers but also determinants of future geographic spread, requiring surveillance strategies integrating humans, vectors, and reservoir animals (notably dogs). (cosma2024leishmaniasisinhumans pages 2-4, sousa2024visceralleishmaniasistherapeutic pages 4-6)
Key URLs (publication pages)
- Cosma et al. 2024 (One Health perspective): https://doi.org/10.3390/tropicalmed9110258 (published 2024-10) (cosma2024leishmaniasisinhumans pages 2-4)
- Parkash et al. 2024 (Nature Medicine CHIM): https://doi.org/10.1038/s41591-024-03146-9 (published 2024-08) (parkash2024safetyandreactogenicity pages 1-2)
- Chivinski et al. 2023 (L-AmB meta-analysis): https://doi.org/10.1093/ofid/ofad348 (published 2023-07) (chivinski2023intravenousliposomalamphotericin pages 1-2)
- Fischer et al. 2024 (MCL treatment systematic review): https://doi.org/10.1111/ddg.15424 (published 2024-05) (fischer2024treatmentofmucocutaneous pages 2-2)
- Fowler et al. 2024 (hypoxia/CD8 pathology): https://doi.org/10.1172/jci177992 (published 2024-06) (fowler2024neutrophilmediatedhypoxiadrives pages 1-2)
- Khandibharad & Singh 2024 (scATAC “sleepy macrophages”): https://doi.org/10.1128/spectrum.03478-23 (published 2024-03) (khandibharad2024singlecellatacsequencing pages 1-2)
Not-yet-fulfilled template elements (data not present in retrieved evidence)
- Curated IDs (MONDO, MeSH, ICD-10/11, Orphanet) and validated ontology mappings (MAXO IDs, specific UBERON/HPO/GO IDs) were not available in the evidence corpus and therefore remain incomplete.
- Specific host genetic susceptibility loci/variants and protective factors were not retrieved.
References
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(parkash2024safetyandreactogenicity pages 2-3): Vivak Parkash, Helen Ashwin, Shoumit Dey, Jovana Sadlova, Barbora Vojtkova, Katrien Van Bocxlaer, Rebecca Wiggins, David Thompson, Nidhi Sharma Dey, Charles L. Jaffe, Eli Schwartz, Petr Volf, Charles J. N. Lacey, Alison M. Layton, and Paul M. Kaye. Safety and reactogenicity of a controlled human infection model of sand fly-transmitted cutaneous leishmaniasis. Nature Medicine, 30:3150-3162, Aug 2024. URL: https://doi.org/10.1038/s41591-024-03146-9, doi:10.1038/s41591-024-03146-9. This article has 17 citations and is from a highest quality peer-reviewed journal.
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(dey2024il32producingcd8+ pages 1-7): Nidhi S. Dey, Shoumit Dey, Naj Brown, Sujai Senarathne, Luiza Campos Reis, Ritika Sengupta, Jose Angelo L. Lindoso, Sally James, Lesley Gilbert, Mitali Chatterjee, Hiro Goto, Shalindra Ranasinghe, and Paul M. Kaye. Il-32 producing cd8+ memory t cells and tregs define the ido1 / pd-l1 niche in human cutaneous leishmaniasis skin lesions. MedRxiv, Jan 2024. URL: https://doi.org/10.1101/2024.01.02.23300281, doi:10.1101/2024.01.02.23300281. This article has 5 citations.
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(lodi2024immuneresponseto pages 10-11): Lorenzo Lodi, Marta Voarino, Silvia Stocco, Silvia Ricci, Chiara Azzari, Luisa Galli, and Elena Chiappini. Immune response to viscerotropic leishmania: a comprehensive review. Frontiers in Immunology, Sep 2024. URL: https://doi.org/10.3389/fimmu.2024.1402539, doi:10.3389/fimmu.2024.1402539. This article has 25 citations and is from a peer-reviewed journal.
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(dey2024il32producingcd8+ pages 7-11): Nidhi S. Dey, Shoumit Dey, Naj Brown, Sujai Senarathne, Luiza Campos Reis, Ritika Sengupta, Jose Angelo L. Lindoso, Sally James, Lesley Gilbert, Mitali Chatterjee, Hiro Goto, Shalindra Ranasinghe, and Paul M. Kaye. Il-32 producing cd8+ memory t cells and tregs define the ido1 / pd-l1 niche in human cutaneous leishmaniasis skin lesions. MedRxiv, Jan 2024. URL: https://doi.org/10.1101/2024.01.02.23300281, doi:10.1101/2024.01.02.23300281. This article has 5 citations.
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(dey2024il32producingcd8+ pages 11-15): Nidhi S. Dey, Shoumit Dey, Naj Brown, Sujai Senarathne, Luiza Campos Reis, Ritika Sengupta, Jose Angelo L. Lindoso, Sally James, Lesley Gilbert, Mitali Chatterjee, Hiro Goto, Shalindra Ranasinghe, and Paul M. Kaye. Il-32 producing cd8+ memory t cells and tregs define the ido1 / pd-l1 niche in human cutaneous leishmaniasis skin lesions. MedRxiv, Jan 2024. URL: https://doi.org/10.1101/2024.01.02.23300281, doi:10.1101/2024.01.02.23300281. This article has 5 citations.
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(fowler2024neutrophilmediatedhypoxiadrives pages 1-2): Erin A. Fowler, Camila Farias Amorim, Klauss Mostacada, Allison Yan, Laís Amorim Sacramento, Rae A. Stanco, Emily D.S. Hales, Aditi Varkey, Wenjing Zong, Gary D. Wu, Camila I. de Oliveira, Patrick L. Collins, and Fernanda O. Novais. Neutrophil-mediated hypoxia drives pathogenic cd8+ t cell responses in cutaneous leishmaniasis. The Journal of Clinical Investigation, Jun 2024. URL: https://doi.org/10.1172/jci177992, doi:10.1172/jci177992. This article has 19 citations.
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(khandibharad2024singlecellatacsequencing pages 1-2): Shweta Khandibharad and Shailza Singh. Single-cell atac sequencing identifies sleepy macrophages during reciprocity of cytokines in l. major infection. Microbiology Spectrum, Mar 2024. URL: https://doi.org/10.1128/spectrum.03478-23, doi:10.1128/spectrum.03478-23. This article has 8 citations and is from a domain leading peer-reviewed journal.
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(gritti2024epidemiologicalclinicaland pages 30-35): Tommaso Gritti. Epidemiological, clinical and molecular characterization of tegumentary leishmaniasis in the emilia-romagna region. Text, Jan 2024. URL: https://doi.org/10.48676/unibo/amsdottorato/11146, doi:10.48676/unibo/amsdottorato/11146. This article has 0 citations and is from a peer-reviewed journal.
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(balahbib2023cutaneousleishmaniasisphysiopathology pages 9-12): Abdelaali Balahbib, Asma Hmamouch, Aicha El Allam, Hikmat Douhri, Naoufal Dahaieh, Nasreddine El Omari, Jactty Chew, Long Chiau Ming, and Abdelhakim Bouyahya. Cutaneous leishmaniasis: physiopathology, molecular diagnostic, and therapeutic approaches. Progress In Microbes & Molecular Biology, Dec 2023. URL: https://doi.org/10.36877/pmmb.a0000395, doi:10.36877/pmmb.a0000395. This article has 5 citations.
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(balahbib2023cutaneousleishmaniasisphysiopathology pages 12-15): Abdelaali Balahbib, Asma Hmamouch, Aicha El Allam, Hikmat Douhri, Naoufal Dahaieh, Nasreddine El Omari, Jactty Chew, Long Chiau Ming, and Abdelhakim Bouyahya. Cutaneous leishmaniasis: physiopathology, molecular diagnostic, and therapeutic approaches. Progress In Microbes & Molecular Biology, Dec 2023. URL: https://doi.org/10.36877/pmmb.a0000395, doi:10.36877/pmmb.a0000395. This article has 5 citations.
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(gritti2024epidemiologicalclinicaland pages 35-39): Tommaso Gritti. Epidemiological, clinical and molecular characterization of tegumentary leishmaniasis in the emilia-romagna region. Text, Jan 2024. URL: https://doi.org/10.48676/unibo/amsdottorato/11146, doi:10.48676/unibo/amsdottorato/11146. This article has 0 citations and is from a peer-reviewed journal.
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(gritti2024epidemiologicalclinicaland pages 39-44): Tommaso Gritti. Epidemiological, clinical and molecular characterization of tegumentary leishmaniasis in the emilia-romagna region. Text, Jan 2024. URL: https://doi.org/10.48676/unibo/amsdottorato/11146, doi:10.48676/unibo/amsdottorato/11146. This article has 0 citations and is from a peer-reviewed journal.
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(dey2024il32producingcd8+ pages 19-22): Nidhi S. Dey, Shoumit Dey, Naj Brown, Sujai Senarathne, Luiza Campos Reis, Ritika Sengupta, Jose Angelo L. Lindoso, Sally James, Lesley Gilbert, Mitali Chatterjee, Hiro Goto, Shalindra Ranasinghe, and Paul M. Kaye. Il-32 producing cd8+ memory t cells and tregs define the ido1 / pd-l1 niche in human cutaneous leishmaniasis skin lesions. MedRxiv, Jan 2024. URL: https://doi.org/10.1101/2024.01.02.23300281, doi:10.1101/2024.01.02.23300281. This article has 5 citations.
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(chivinski2023intravenousliposomalamphotericin pages 1-2): Jeffrey Chivinski, Keren Nathan, Faheel Naeem, Taline Ekmekjian, Michael D Libman, and Sapha Barkati. Intravenous liposomal amphotericin b efficacy and safety for cutaneous and mucosal leishmaniasis: a systematic review and meta-analysis. Open Forum Infectious Diseases, Jul 2023. URL: https://doi.org/10.1093/ofid/ofad348, doi:10.1093/ofid/ofad348. This article has 16 citations and is from a peer-reviewed journal.
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(chivinski2023intravenousliposomalamphotericin pages 7-9): Jeffrey Chivinski, Keren Nathan, Faheel Naeem, Taline Ekmekjian, Michael D Libman, and Sapha Barkati. Intravenous liposomal amphotericin b efficacy and safety for cutaneous and mucosal leishmaniasis: a systematic review and meta-analysis. Open Forum Infectious Diseases, Jul 2023. URL: https://doi.org/10.1093/ofid/ofad348, doi:10.1093/ofid/ofad348. This article has 16 citations and is from a peer-reviewed journal.
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(fischer2024treatmentofmucocutaneous pages 4-4): Theresa Fischer, Marcellus Fischer, Sibylle Schliemann, and Peter Elsner. Treatment of mucocutaneous leishmaniasis – a systematic review. JDDG: Journal der Deutschen Dermatologischen Gesellschaft, 22:763-773, May 2024. URL: https://doi.org/10.1111/ddg.15424, doi:10.1111/ddg.15424. This article has 32 citations.
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(fischer2024treatmentofmucocutaneous pages 6-7): Theresa Fischer, Marcellus Fischer, Sibylle Schliemann, and Peter Elsner. Treatment of mucocutaneous leishmaniasis – a systematic review. JDDG: Journal der Deutschen Dermatologischen Gesellschaft, 22:763-773, May 2024. URL: https://doi.org/10.1111/ddg.15424, doi:10.1111/ddg.15424. This article has 32 citations.
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(pandey2021arandomizedopenlabel pages 3-4): Krishna Pandey, Biplab Pal, Niyamat Ali Siddiqui, Chandra Shekhar Lal, Vahab Ali, Sanjiva Bimal, Ashish Kumar, Neena Verma, Vidya Nand Rabi Das, Shubhankar Kumar Singh, Roshan Kamal Topno, and Pradeep Das. A randomized, open-label study to evaluate the efficacy and safety of liposomal amphotericin b (ambisome) versus miltefosine in patients with post-kala-azar dermal leishmaniasis. Indian Journal of Dermatology, Venereology and Leprology, 87:34-41, Feb 2021. URL: https://doi.org/10.25259/ijdvl_410_19, doi:10.25259/ijdvl_410_19. This article has 19 citations.
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(parkash2024safetyandreactogenicity pages 1-2): Vivak Parkash, Helen Ashwin, Shoumit Dey, Jovana Sadlova, Barbora Vojtkova, Katrien Van Bocxlaer, Rebecca Wiggins, David Thompson, Nidhi Sharma Dey, Charles L. Jaffe, Eli Schwartz, Petr Volf, Charles J. N. Lacey, Alison M. Layton, and Paul M. Kaye. Safety and reactogenicity of a controlled human infection model of sand fly-transmitted cutaneous leishmaniasis. Nature Medicine, 30:3150-3162, Aug 2024. URL: https://doi.org/10.1038/s41591-024-03146-9, doi:10.1038/s41591-024-03146-9. This article has 17 citations and is from a highest quality peer-reviewed journal.
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(parkash2024safetyeffectivenessand pages 13-17): Vivak Parkash, Helen Ashwin, Shoumit Dey, Jovana Sadlova, Barbora Vojtkova, Katrien Van Bocxlaer, Rebecca Wiggins, David Thompson, Nidhi Sharma Dey, Charles L. Jaffe, Eli Schwartz, Petr Volf, Charles J. N. Lacey, Alison M. Layton, and Paul M. Kaye. Safety, effectiveness, and skin immune response in a controlled human infection model of sand fly transmitted cutaneous leishmaniasis. MedRxiv, Apr 2024. URL: https://doi.org/10.1101/2024.04.12.24305492, doi:10.1101/2024.04.12.24305492. This article has 1 citations.