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Objective: In this multicentric study, we were interested in the vision-related quality of life and its association with visual impairment in neuromyelitis optica spectrum disorders (NMOSD) and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) in comparison to multiple sclerosis (MS) and healthy controls., Methods: We analysed extracted data from the German NEMOS registry including National Eye Institute Visual Function Questionnaire (NEI-VFQ) scores, high and low contrast visual acuity (HCVA, LCVA), visually evoked potentials (VEP) and the scores for the expanded disability status scale (EDSS) and other neurological tests which assessed their disease-related impairment. The mean follow-up time of our patients was 1.2 years. We used adjusted linear mixed effect models to analyse NEI-VFQ differences and interactions with visual acuity among NMOSD, MOGAD, a matched MS cohort and healthy controls., Results: Despite a younger age in the MOGAD cohort (39 y.o.), vision and socioemotional-related quality of life reduction was similar over all patient subgroups in comparison to healthy controls. The most impacted life quality dimension was general health, followed by general vision, driving and role difficulties. Decline in some of the NEI-VFQ subscales scores is mostly predicted by age. The HCVA was the best predictor for most of the subscales of the NEI-VFQ., Discussion: Despite important age differences, NMOSD, MOGAD and MS seem to share a rather similar perception on their vision and quality of life impairment, which is overall poorer than that of healthy controls., Competing Interests: Declarations. Conflict of interest: MN: no conflict of interest. VH: received research support from NEMOS e.V. independent of this project. FP: received research support from NeuroCure Clinical Research Center, the German Ministry for Education and Research (BMBF), Deutsche Forschungsgemeinschaft (DFG), Einstein Foundation, Guthy Jackson Charitable Foundation, EU FP7 Framework Program, Biogen, Genzyme, Merck Serono, Novartis, Bayer, Roche; received consulting fees from Alexion, Roche, Horizon, Neuraxpharm and speaker honoraria from Almirall, Bayer, Biogen, GlaxoSmithKline, Hexal, Merck, Sanofi Genzyme, Novartis, Viela Bio, UCB, Mitsubishi Tanabe, Celgene, Guthy Jackson Foundation, Serono, Roche. He received travel grants from Merck, Guthy Jackson Foundation, Bayer, Biogen, Merck Serono, Sanofi Genzyme, Novartis, Alexion, Viela Bio, Roche, UCB, Mitsubishi Tanabe, Celgene. He participated on Data Safety Monitoring Board at Celgene AdBoard, Roche AdBoard, UCB AdBoard, Merck AdBoard Academic Editor PLos One, Celgene AdBoard, Roche AdBoard, UCB AdBoard, Merck AdBoard Academic Editor PLos One. He is Academic Editor at PLoS ONE and Associate Editor of Neurology® Neuroimmunology and Neuroinflammation. FCO: currently received research support by Deutsche Forschungsgemeinschaft (DFG), Hertie foundation and Novartis—all unrelated to this project. She further received fellowship support from the American Academy of Neurology (AAN) and the National MS Society (NMSS) and travel support for the European Committee for Research and Treatment in Multiple Sclerosis (ECTRIMS) in the recent past, also unrelated to this project. PS: received travel support by UCB and received speaker’s honoraria by Roche and Alexion and served on advisory board by Alexion. JBS: received institutional research support from NEMOS e.V., Alexion and Bayer AG, personal compensation from Alexion, speaking honoraria and travel grants from Bayer Healthcare, Horizon/Amgen, Novartis and Sanofi-Aventis/Genzyme, in addition received compensation for serving on a scientific advisory board of Alexion, Roche and Merck, all unrelated to the presented work. ESA: received research grants from Novartis and Roche, speaker honoraria from Alexion, Amgen, Bayer and Roche, unrelated to the presented work. MK: received grants from Merck and Novartis, travel support and personal fees from Alexion, BMS, Merck, Novartis, Roche and Sanofi, all unrelated to the presented work. MWH: received institutional research support from Myelitis e. V., speaker honoraria from selpers og, Horizon, and Alexion, and travel grants and compensation for serving on an advisory board from Alexion. None of this interfered with the current manuscript. FB: no conflict of interest. DT: no conflict of interest. CT: received honoraria for consultation and expert testimony from Alexion Pharma Germany GmbH. None of this interfered with the current work. CS: received speaker honoraria from Alexion, Argenx, Desitin and TAD and served on advisory board for Alexion and Argenx, none related to this study. IA: received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities- from Roche, Horizon, Alexion, Sanofi, Merck, and received research support from Diamed, Roche and Alexion, none related to this study. CS: received speaker honoraria from Alexion and travel support from Novartis and UCB, all not related to the content of this manuscript. TP: no conflict of interest. KF: no conflict of interest. OA: reports grants from the German Ministry of Education and Research (BMBF) and the German Research Foundation (DFG); grants and personal fees from Biogen and Novartis; and travel support and personal fees from Alexion, Almirall, MedImmune, Merck Serono, Roche, Sanofi, Viela Bio/Horizon Therapeutics and Zambon. MR: received speaker honoraria from Novartis, Bayer Vital GmbH, Roche, Alexion, Horizon and Ipsen and travel reimbursement from Bayer Schering, Biogen Idec, Merz, Genzyme, Teva, Roche, Horizon, Alexion and Merck, none related to this study. MK: received honoraria from Chugai Pharma, Roche Pharma and Novartis with no relation to the content of the article. CW: received institutional support from Novartis, Biogen, Alexion, Janssen, Hexal and Roche. MG: received consulting and/or speaker honoraria from Biogen, BMS, JJ, Merck, Novartis, Roche, Sanofi Genzyme and Teva. MK: no conflict of interest. KA: received travel support (till 2014) from Alexion, Bayer, BiogenIdec, MerckSerono, Novartis, Teva and honoria from Biogen und TEVA; he supported neuroimmunological studies for Alexion, Bayer, BiogenIdec, MerckSerono, Roche and Novartis. PK: no conflict of interest. IK: received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Alexion, Almirall, Bayer, Biogen, GlaxoSmithKline, Hexal, Horizon, Merck, Neuraxpharm, Roche/Chugai and Sanofi. PR: speaker or Consultant Honorary from Alexion (Astra Zeneca), Allmiral, Amicus, Biogen, Horizon (Amgen), Merck, Novartis, Sandoz, Sanofi, Roche, Teva. Received research grants from Amicus, Merck, Roche, Austrian Science Fund (FWF). AW: received speaker honoraria, consultant fees and travel reimbursement from Alexion, Bayer, Biogen, Glaxo Smith Kline, Hexal, Janssen, Merck, Novartis, Pfizer, Roche and Sanofi Genzyme, none related to this study. AW: no conflict of interest. MSW: no conflict of interest. JW: no conflict of interest. KG: reports reimbursement of travelling expenses by UCB. FTB: received, over his academic career, research support and travel grants to attend scientific meetings, through his institution, from the German Science Fund (DFG), German Federal Ministry of Education and Science (BMBF), Bayer-Schering, Diamed, Fresenius, Merck, Novartis, Pfizer, Roche, Sanofi and Teva; speaker fees and compensation for advisory boards from Actelion, Alexion, Bayer, Biogen, CSL Behring, Fresenius, Horizon, Merck, Novartis, Roche, Sanofi-Genzyme, Takeda and Teva. None of these are related to this work. MS: received consulting and/or speaker honoraria from Alexion, Bayer, Biogen, Bristol-Myers-Squibb/Celgene, Janssen, Merck, Horizon, Roche, and Sanofi Genzyme. HT: participated in meetings sponsored by or received honoraria for acting as an advisor/speaker for Alexion, Bayer, Biogen, Bristol-Myers Squibb, Celgene, Diamed, Fresenius, Fujirebio, GlaxoSmithKline, Horizon, Janssen-Cilag, Merck, Novartis, Roche, Sanofi-Genzyme, Siemens, and Teva. He also acknowledges research support by DMSG (German Multiple Sclerosis Society), MWK-BW (Ministry of Science, Research and Arts of the State Baden-Württemberg), University of Ulm, and Chemische Fabrik Karl Bucher. IV: received travel support from Alexion. ED: no conflict of interest. LR: no conflict of interest. LK: received compensation for serving on Scientific Advisory Boards for Alexion, Genzyme, Janssen, Merck, Novartis, and Roche; she received speaker honoraria and travel support from Bayer, Biogen, Genzyme, Grifols, Merck, Novartis, Roche, Santhera, and Teva; she receives research support from DFG, the German Ministry for Education and Research (BMBF), the IZKF Münster, IMF Münster, Biogen, Novartis and Merck. MKK: received speaker honoraria from BMS, Merck and Novartis. SJ: no conflict of interest. BW: received research grants from Deutsche Forschungsgemeinschaft, German Ministry of Education and Research, Dietmar Hopp Foundation, Klaus Tschira Foundation, Novartis, Roche, and personal fees from Alexion, INSTAND, Novartis, Roche, all unrelated to this work. JAG: received a research grant from the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation; SFB/TRR 274, ID 408885537) and reports travel expenses and non-financial support from Merck, outside the submitted work. TK: received speaker honoraria and/or personal fees for advisory boards from Novartis Pharma, Roche Pharma, Alexion/Astra Zeneca, Horizon Therapeutics/Amgen, Merck, Chugai Pharma and Biogen. The Institution she works for has received compensation for serving as a member of a steering committee from Roche. Furthermore, she is a site principal investigator in several randomized clinical trials and her institution has received compensation for clinical trials from Novartis Pharma, Roche Pharma and Sanofi Genzyme, all outside the present work. DE: received speaker honoraria and/or travel reimbursement from Alexion, Amgen/Horizon and Merck, all not related to this work. JH: reports a grant for OCT research from the Friedrich‐Baur‐Stiftung, Horizon and Merck, personal fees and nonfinancial support from Alexion, Amgen, Bayer, Biogen, BMS, Merck, Novartis and Roche, and nonfinancial support of the Sumaira Foundation and Guthy-Jackson Charitable Foundation, all outside the submitted work. NS: no conflict of interest. JPS: no conflict of interest. Ethics approval: The data collection and its usage for the purpose of this publication was approved by the ethics committees of all NEMOS centres. For the MS and control data, we obtained ethical approval from the local ethic committee of Hamburg Chamber of Physicians (Registration Number PV5557). Also, written informed consent was obtained from all patients before entering the registry., (© 2024. Springer-Verlag GmbH Germany, part of Springer Nature.)

Dirofilariasis is one of the oldest known zoonotic infections of humans mainly caused by the filarial parasites of the species Dirofilaria immitis and Dirofilaria repens , which primarily infect dogs. A five-year survey (2017 to 2021) was conducted among the dog population to assess the molecular prevalence of Dirofilaria spp. in southeast France. Morphological and genetic analysis were performed on filaroids from dogs and one infected woman from the studied area. A total of 12 (13%) dogs scored molecularly positive for Dirofilaria spp. of which nine carried blood microfilariae. Ocular dirofilariasis was detected in a 79-year-old woman with no travel history. Both electron microscopy and molecular sequencing identified the worm in the human case as D. repens . Molecularly, D. repens isolates were identical in the human and dog cases, representing the only genotype reported so far in France. Despite the distribution of this genotype through all Europe, it was grouped separately with the other two European genotypes and with Asian ones. As in almost all previous human cases in France, D. repens parasites were mainly recovered from the ocular region of patients and were geographically concentrated in the southeastern regions. Data demonstrate the sympatric occurrence of D. immitis and D. repens with high risk of infection to human and dog populations in these investigated geographical areas, thereby underlining the urgent need to implement preventive chemoprophylactic strategies and vector control to reduce the risk of these filaroids in dog and human populations.