Schistosomiasis, a neglected tropical disease caused by parasitic worms of the genus Schistosoma and transmitted through freshwater snails, affects over 200 million people worldwide. Climate change, through rising temperatures, altered rainfall patterns, and extreme weather events, is influencing the distribution and transmission dynamics of schistosomiasis. This scoping review examines the impact of climate change on schistosomiasis transmission and its implications for disease control. This review aims to synthesize current knowledge on the influence of climate variables (temperature, rainfall, water bodies) on snail populations, transmission dynamics, and the shifting geographic range of schistosomiasis. It also explores the potential effects of climate adaptation policies on disease control. The review follows the Arksey and O’Malley framework and PRISMA-ScR guidelines, including studies published from 2000 to 2024. Eligible studies were selected based on empirical data on climate change, schistosomiasis transmission, and snail dynamics. A two-stage study selection process was followed: title/abstract screening and full-text review. Data were extracted on environmental factors, snail population dynamics, transmission patterns, and climate adaptation strategies. Climate change is expected to increase schistosomiasis transmission in endemic regions like Sub-Saharan Africa, Southeast Asia, and South America, while some areas, such as parts of West Africa, may see reduced risk. Emerging hotspots were identified in regions not currently endemic. Climate adaptation policies, such as improved water management and early warning systems, were found effective in reducing transmission. Integrating climate adaptation strategies into schistosomiasis control programs is critical to mitigating the disease’s spread, particularly in emerging hotspots and shifting endemic areas.

Background: Leishmaniasis is a neglected tropical disease with diverse clinical forms, heterogeneous geographical distribution, and persistent diagnostic and treatment challenges. Although substantial primary research exists, evidence remains fragmented, limiting integrated and context‐specific control strategies. This scoping review synthesizes global evidence on disease distribution, diagnostic performance, and treatment outcomes, and identifies critical evidence gaps. Methods: A scoping review was conducted in accordance with the Arksey and O′Malley framework and PRISMA‐ScR guidelines. Four electronic databases were searched for studies published between January 2000 and January 2026. Data were synthesized narratively. A total of 118 studies were included in the review, of which 75 were analyzed to assess the geographical distribution of Leishmaniasis, while the remaining 43 studies were used to evaluate diagnostic tools and treatment outcomes. Results: Seventy‐five studies from 53 countries were included. Cutaneous leishmaniasis was reported in 58 studies (77.3%) and was the most geographically widespread form, whereas visceral leishmaniasis was reported in 26 studies (34.7%) and showed marked focality, particularly in East Africa, South Asia, and Brazil. Molecular diagnostics demonstrated superior performance, with PCR and qPCR sensitivities ranging from 89% to 100% and specificities from 57% to 100%, depending on target gene and sample type. Loop‐mediated isothermal amplification showed sensitivities of 89.7%–95% and specificities of 63.6%–100%. In contrast, microscopy showed lower sensitivity (32.8%–80.8% for cutaneous and 44%–67% for visceral leishmaniasis) but high specificity (> 95%). Serological tests and rapid diagnostic tests performed well for visceral leishmaniasis, with rK39‐based assays showing sensitivities of 78–96.4% and specificities of 93%–97%, and direct agglutination tests achieving sensitivities of 97.3%–99.1% and specificities of 97.5%–98.8%. Fewer than one‐third of studies evaluated operational feasibility. Liposomal amphotericin B achieved the highest cure rates for visceral leishmaniasis, whereas antimonials remained the most frequently used treatment for cutaneous disease. Relapse was predominantly reported in visceral leishmaniasis. Conclusion: Leishmaniasis exhibits substantial global heterogeneity, with molecular diagnostics offering high analytical accuracy but limited real‐world deployment. Addressing operational constraints and integrating emerging technologies are critical priorities for strengthening global leishmaniasis control. Molecular and antigen‐based diagnostics offer improved accuracy but remain underutilized in resource‐limited settings. Effective treatment is complicated by toxicity, cost, and relapse. Expanding diagnostic capacity, optimizing treatment protocols, and strengthening surveillance systems are critical for effective global leishmaniasis control and elimination.

Background: Acinetobacter baumannii is a major cause of hospital‐associated infections (HAIs) globally, particularly in intensive care units (ICUs). Its remarkable environmental resilience and ability to acquire extensive antimicrobial resistance (AMR) have made it a critical threat to patient safety and a top priority pathogen according to the World Health Organization. This scoping review synthesizes global evidence on (1) the epidemiological distribution of A. baumannii –associated HAIs, (2) the genetic mechanisms underlying its multidrug‐resistant (MDR) and extensively drug‐resistant (XDR) phenotypes, and (3) the structural interconnectivity of resistance determinants. Methods: We systematically reviewed 34 epidemiological and 30 molecular studies published between 2007 and 2024 from four databases (PubMed, Scopus, Web of Science, and Google Scholar), following PRISMA‐ScR and Joanna Briggs Institute guidelines. Data on infection types, resistance phenotypes, and molecular mechanisms were extracted and analyzed. A structured resistance network was constructed using Cytoscape to visualize co‐occurring resistance genes. Results: A. baumannii was frequently implicated in ventilator‐associated pneumonia, bloodstream infections, urinary tract infections, and wound infections, with ICU settings being the most affected. Thirty studies analyzing A. baumannii isolates revealed widespread MDR and XDR profiles. The most frequent resistance genes included blaOXA‐23‐like, blaNDM, and blaOXA‐58‐like, alongside aminoglycoside‐modifying enzymes (e.g., aph(3 ^′ )‐Ia and aac(6 ^′ )‐Ib) and efflux pumps (AdeABC and adeR/S). Methyltransferases (armA and rmtB) and mobile elements such as ISAba1 were commonly codetected. Resistance extended across aminoglycosides, carbapenems, β ‐lactams, fluoroquinolones, and sulfonamides, reflecting a multifactorial resistance mechanism among clinical isolates. Conclusions: A. baumannii poses a severe and evolving threat to healthcare systems due to its multifaceted resistance mechanisms and nosocomial adaptability. Enhanced molecular surveillance, integrated diagnostic systems, and novel therapeutic strategies targeting resistance networks are urgently needed to combat this high‐priority pathogen.