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Infectious Disease Reports
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Editor’s Choice Articles

Editor’s Choice articles are based on recommendations by the scientific editors of MDPI journals from around the world. Editors select a small number of articles recently published in the journal that they believe will be particularly interesting to readers, or important in the respective research area. The aim is to provide a snapshot of some of the most exciting work published in the various research areas of the journal.

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9 pages, 350 KiB  
Article
Clostridioides difficile Infection in the United States of America—A Comparative Event Risk Analysis of Patients Treated with Fidaxomicin vs. Vancomycin Across 67 Large Healthcare Providers
by Sebastian M. Wingen-Heimann, Christoph Lübbert, Davide Fiore Bavaro and Sina M. Hopff
Infect. Dis. Rep. 2025, 17(4), 87; https://doi.org/10.3390/idr17040087 - 23 Jul 2025
Viewed by 270
Abstract
Background/Objectives: Clostridioides difficile infection (CDI) is a major cause of infectious diarrhea in the inpatient and community setting. Real-world data outside the strict environment of randomized controlled trials (RCTs) are needed to improve the quality of evidence. The aim of this study was [...] Read more.
Background/Objectives: Clostridioides difficile infection (CDI) is a major cause of infectious diarrhea in the inpatient and community setting. Real-world data outside the strict environment of randomized controlled trials (RCTs) are needed to improve the quality of evidence. The aim of this study was to compare different clinical outcomes of CDI patients treated with fidaxomicin with those treated with vancomycin using a representative patient population in the United States of America (USA). Methods: Comprehensive real-world data were analyzed for this retrospective observational study, provided by the TriNetX database, an international research network with electronic health records from multiple USA healthcare providers. This includes in- and outpatients treated with fidaxomicin (FDX) or vancomycin (VAN) for CDI between 01/2013 and 12/2023. The following cohorts were compared: (i) patients treated with fidaxomicin within 10 days following CDI diagnosis (FDX group) vs. (ii) patients treated with vancomycin within 10 days following CDI diagnosis (VAN group). Outcomes analysis between the two cohorts was performed after propensity score matching and included event risk and Kaplan–Meier survival analyses for the following concomitant diseases/events occurring during an observational period of 12 months following CDI diagnosis: death, sepsis, candidiasis, infections caused by vancomycin-resistant enterococci, inflammatory bowel disease, cardiovascular disease, psychological disease, central line-associated blood stream infection, surgical site infection, and ventilator-associated pneumonia. Results: Following propensity score matching, 2170 patients were included in the FDX group and VAN groups, respectively. The event risk analysis demonstrated improved outcomes of patients treated with FDX compared to VAN in 6 out of the 10 events that were analyzed. The highest risk ratio (RR) and odds ratio (OR) were found for sepsis (RR: 3.409; OR: 3.635), candidiasis (RR: 2.347; OR: 2.431), and death (RR: 1.710; OR: 1.811). The Kaplan–Meier survival analysis showed an overall survival rate until the end of the 12-month observational period of 87.06% in the FDX group and 78.49% in the VAN group (log-rank p < 0.001). Conclusions: Our comparative event risk analysis demonstrated improved outcomes for patients treated with FDX compared to VAN in most of the observed events and underlines the results of previously conducted RCTs, highlighting the beneficial role of FDX compared to VAN. Further big data analyses from other industrialized countries are needed for comparison with our observations. Full article
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12 pages, 939 KiB  
Brief Report
Pulmonary Hypertension Secondary to Fungal Infections: Underexplored Pathological Links
by Andrea Jazel Rodríguez-Herrera, Sabrina Setembre Batah, Maria Júlia Faci do Marco, Carlos Mario González-Zambrano, Luciane Alarcão Dias-Melicio and Alexandre Todorovic Fabro
Infect. Dis. Rep. 2025, 17(4), 84; https://doi.org/10.3390/idr17040084 - 12 Jul 2025
Viewed by 338
Abstract
Background/Objective: Pulmonary fungal infections are a significant diagnostic challenge, primarily affecting immunocompromised individuals, such as those with HIV, cancer, or organ transplants, and they often lead to substantial morbidity and mortality if untreated. These infections trigger acute inflammatory and immune responses, which may [...] Read more.
Background/Objective: Pulmonary fungal infections are a significant diagnostic challenge, primarily affecting immunocompromised individuals, such as those with HIV, cancer, or organ transplants, and they often lead to substantial morbidity and mortality if untreated. These infections trigger acute inflammatory and immune responses, which may progress to chronic inflammation. This process involves myofibroblast recruitment, the deposition of extracellular matrix, and vascular remodeling, ultimately contributing to pulmonary hypertension. Despite its clinical relevance, pulmonary hypertension secondary to fungal infections remains under-recognized in practice and poorly studied in research. Results/Conclusion: This narrative mini-review explores three key mechanisms underlying vascular remodeling in this context: (1) endothelial injury caused by fungal emboli or autoimmune reactions, (2) direct vascular remodeling during chronic infection driven by inflammation and fibrosis, and (3) distant vascular remodeling post-infection, as seen in granulomatous diseases like paracoccidioidomycosis. Further research and clinical screening for pulmonary hypertension in fungal infections are crucial to improving patient outcomes. Full article
(This article belongs to the Special Issue Pulmonary Vascular Manifestations of Infectious Diseases)
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23 pages, 1088 KiB  
Review
The Role of Type I Interferons in Tuberculosis and in Tuberculosis-Risk-Associated Comorbidities
by Florence Mutua, Ruey-Chyi Su, Terry Blake Ball and Sandra Kiazyk
Infect. Dis. Rep. 2025, 17(4), 81; https://doi.org/10.3390/idr17040081 - 8 Jul 2025
Viewed by 452
Abstract
The identification of a type I interferon-induced transcriptomic signature in active tuberculosis suggests a potential role for these interferons in the pathogenesis of tuberculosis. Comorbidities such as human immunodeficiency virus, diabetes, systemic lupus erythematosus, end-stage renal disease, and coronavirus disease are epidemiologically linked [...] Read more.
The identification of a type I interferon-induced transcriptomic signature in active tuberculosis suggests a potential role for these interferons in the pathogenesis of tuberculosis. Comorbidities such as human immunodeficiency virus, diabetes, systemic lupus erythematosus, end-stage renal disease, and coronavirus disease are epidemiologically linked to an increased risk for reactivation of latent tuberculosis infection. Notably, type I interferons are also implicated in the pathogenesis of these conditions, with a recognizable type I interferon transcriptomic signature. The mechanisms by which type I interferons in tuberculosis-risk-associated comorbidities may drive the progression of tuberculosis or maintenance of latent infection however remain largely unknown. This review summarizes the existing literature on the increased association between type I interferons, focusing on interferon-α and -β, and the heightened risk of tuberculosis reactivation. It also underscores the similarities in the immunopathogenesis of these comorbidities. A better understanding of these mechanisms is essential to guide the development of host-directed interferon therapies and improving diagnostic biomarkers in M. tuberculosis infection. Full article
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8 pages, 206 KiB  
Commentary
Clinical and Occupational Predictors of Mortality in Ebola Virus Disease: A Commentary from the Democratic Republic of Congo (2018–2020)
by Jean Paul Muambangu Milambo and Charles Bitamazire Businge
Infect. Dis. Rep. 2025, 17(3), 71; https://doi.org/10.3390/idr17030071 - 18 Jun 2025
Viewed by 379
Abstract
Background: This commentary analyzes demographic, clinical, and occupational characteristics associated with Ebola virus disease (EVD) outcomes during the 2018–2020 outbreak in the Democratic Republic of Congo (DRC). Methods: A total of 3477 EVD cases were included. Descriptive statistics and univariate and multivariate Cox [...] Read more.
Background: This commentary analyzes demographic, clinical, and occupational characteristics associated with Ebola virus disease (EVD) outcomes during the 2018–2020 outbreak in the Democratic Republic of Congo (DRC). Methods: A total of 3477 EVD cases were included. Descriptive statistics and univariate and multivariate Cox regression analyses were performed to evaluate associations between clinical outcomes and patient characteristics. Comorbidity estimates and healthcare worker (HCW) occupational exposure data were incorporated based on the literature. Results: The median age was 26.5 years (SD = 16.1), with the majority (59.7%) aged 20–59. Males represented 51.3% of the cohort. Most patients (81.8%) worked in occupations that were not disease-exposing. Overall, 450 patients (12.9%) died. Although comorbidities initially appeared predictive of mortality (unadjusted HR: 3.05; 95% CI: 2.41–3.87), their effect was not statistically significant after adjustment (adjusted HR: 1.17; 95% CI: 0.87–1.59; p = 0.301). The strongest predictor of death was clinical status at admission: patients classified as “very sick” had an alarmingly high adjusted hazard ratio (HR) of 236.26 (95% CI: 33.18–1682.21; p < 0.001). Non-disease-exposing occupations were also associated with increased mortality (adjusted HR: 1.75; 95% CI: 1.33–2.31; p < 0.001). Conclusions: Despite improvements in outbreak response, mortality remains disproportionately high among patients presenting in critical condition and those outside the health sector. These findings underscore the importance of early detection strategies and enhanced protection for all occupational groups during EVD outbreaks. Full article
(This article belongs to the Topic Vector-Borne Disease Spatial Epidemiology, Disease Ecology, and Zoonoses)
16 pages, 1995 KiB  
Review
Gut Microbiome in Pulmonary Arterial Hypertension—An Emerging Frontier
by Sasha Z. Prisco, Suellen D. Oliveira, E. Kenneth Weir, Thenappan Thenappan and Imad Al Ghouleh
Infect. Dis. Rep. 2025, 17(3), 66; https://doi.org/10.3390/idr17030066 - 9 Jun 2025
Cited by 1 | Viewed by 728
Abstract
Pulmonary arterial hypertension (PAH) is an irreversible disease characterized by vascular and systemic inflammation, ultimately leading to right ventricular failure. There is a great need for adjunctive therapies to extend survival for PAH patients. The gut microbiome influences the host immune system and [...] Read more.
Pulmonary arterial hypertension (PAH) is an irreversible disease characterized by vascular and systemic inflammation, ultimately leading to right ventricular failure. There is a great need for adjunctive therapies to extend survival for PAH patients. The gut microbiome influences the host immune system and is a potential novel target for PAH treatment. We review the emerging preclinical and clinical evidence which strongly suggests that there is gut dysbiosis in PAH and that alterations in the gut microbiome may either initiate or facilitate the progression of PAH by modifying systemic immune responses. We also outline approaches to modify the intestinal microbiome and delineate some practical challenges that may impact efforts to translate preclinical microbiome findings to PAH patients. Finally, we briefly describe studies that demonstrate contributions of infections to PAH pathogenesis. We hope that this review will propel further investigations into the mechanisms by which gut dysbiosis impacts PAH and/or right ventricular function, approaches to modify the gut microbiome, and the impact of infections on PAH development or progression. Full article
(This article belongs to the Special Issue Pulmonary Vascular Manifestations of Infectious Diseases)
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19 pages, 7883 KiB  
Article
Differential Effects of Human Immunodeficiency Virus Nef Variants on Pulmonary Vascular Endothelial Cell Dysfunction
by Amanda K. Garcia, Noelia C. Lujea, Javaria Baig, Eli Heath, Minh T. Nguyen, Mario Rodriguez, Preston Campbell, Isabel Castro Piedras, Edu Suarez Martinez and Sharilyn Almodovar
Infect. Dis. Rep. 2025, 17(3), 65; https://doi.org/10.3390/idr17030065 - 6 Jun 2025
Viewed by 781
Abstract
Background: Human Immunodeficiency Virus (HIV) infections remain a source of cardiopulmonary complications among people receiving antiretroviral therapy. Still to this day, pulmonary hypertension (PH) severely affects the prognosis in this patient population. The persistent expression of HIV proteins, even during viral suppression, has [...] Read more.
Background: Human Immunodeficiency Virus (HIV) infections remain a source of cardiopulmonary complications among people receiving antiretroviral therapy. Still to this day, pulmonary hypertension (PH) severely affects the prognosis in this patient population. The persistent expression of HIV proteins, even during viral suppression, has been implicated in vascular dysfunction; however, little is known about the specific effects of these proteins on the pulmonary vasculature. This study investigates the impact of Nef variants derived from HIV-positive pulmonary hypertensive and normotensive donors on pulmonary vascular cells in vitro. Methods: We utilized well-characterized Nef molecular constructs to examine their effects on cell adhesion molecule gene expression (ICAM1, VCAM1, and SELE), pro-apoptotic gene expression (BAX, BAK), and vasoconstrictive endothelin-1 (EDN1) gene expression in endothelial nitric oxide synthase (eNOS) nitric oxide and the production and secretion of pro-inflammatory cytokines over 24, 48, and 72 h post-transfections with Nef variants. Results: HIV Nef variants SF2, NA7, and PH-associated Fr17 and 3236 induced a significant increase in adhesion molecule gene expression of ICAM1, VCAM1, and SELE. Pulmonary normotensive Nef 1138 decreased ICAM1 gene expression, but had increased VCAM1. PH Nef ItVR showed a consistent decrease in ICAM1 and no changes in SELE and VCAM1 expression. Further gene expression analyses of pro-apoptotic genes BAX and BAK demonstrated that Nef NA7, SF2, normotensive Nef 1138, and PH Nef Fr8, Fr9, Fr17, and 3236 variants significantly increased gene expression for apoptosis. Normotensive Nef 1138, as well as PH Nef Fr9 and ItVR, all displayed a statistically significant decrease in BAX expression. The expression of EDN1 had a statistically significant increase in samples treated with Nef NA7, SF2, normotensive Nef 2044 and PH Nef 3236, Fr17, and Fr8. Notably, PH-associated Nef variants sustained pro-inflammatory cytokine production, including IL-2, IL-4, and TNFα, while anti-inflammatory cytokine levels remained insufficient. Furthermore, eNOS was transiently upregulated by all Nef variants except for normotensive Nef 2044. Conclusions: The distinct effects of Nef variants on pulmonary vascular cell biology highlight the complex interplay between Nef, host factors, and vascular pathogenesis according to the variants. Full article
(This article belongs to the Special Issue Pulmonary Vascular Manifestations of Infectious Diseases)
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