Infection à rotavirus

Rotavirus infection is a viral illness caused by group A rotavirus (RVA), a non-enveloped RNA virus classified by VP7 (G) and VP4 (P) genotypes, with G3P and G14P predominating in equine populations and analogous strain diversity described in humans ^[1][2]. In children, rotavirus is recognised as the infectious agent most strongly linked to severe acute gastroenteritis and dehydration ^[3][4].

In children, rotavirus gastroenteritis commonly presents with diarrhoea, vomiting, and dehydration, with severity assessed through established scoring systems; dehydration reflects overall severity and is a key determinant of hospitalisation ^[3][4]. In foals, the principal manifestations are diarrhoea, fever, lethargy, and anorexia with reduced suckling ^[1]. Beyond the gastrointestinal tract, rotavirus infection has been associated with extraintestinal and autoimmune sequelae, indicating a systemic component that broadens its clinical picture ^[2].

Equine group A rotavirus (RVA) is one of the most important pathogens causing diarrhoea in foals, and according to G and P classification (defined in accordance with the VP7 and VP4 genes), the predominant equine RVAs circulating in horse populations globally are G3P and G14P equine RVAs, although currently available vaccines contain only the G3P equine RVA strain ^[1].

The principal transmission route for rotavirus is faecal–oral, reflecting the non-enveloped nature of the virus and its environmental stability ^[1]. Diagnosis in equine practice is frequently supported by human immunochromatographic rapid antigen detection kits because of their speed and ease of use ^[1].

Maternal vaccination strategies, such as intramuscular inoculation of pregnant mares to provide colostral antibodies, have been used against equine RVA, although current vaccines contain only the G3P strain despite the broader circulation of G14P ^[1]. In children, the introduction of rotavirus vaccines has reduced but not eliminated severe gastroenteritis, and ongoing public-health planning must account for host genetic and microbiome factors that modulate vaccine effectiveness ^[4][2]. Disinfection practices are constrained by the virus's non-enveloped structure, with amphoteric soaps and quaternary ammonium compounds generally ineffective against RVA, whereas alcohol-based products, aldehydes, and chlorine- or iodine-based compounds retain activity ^[1]. Selected probiotic strains have shown consistent efficacy in preventing hospital-acquired diarrhoea, though evidence for prevention in day-care and community settings remains lacking ^[5].

1. 1 Nemoto M et al. Equine rotavirus infection. J Equine Sci. 2021 Mar. PMID: 33776534. doi: 10.1294/jes.32.1. PubMed: https://pubmed.ncbi.nlm.nih.gov/33776534/
2. 2 Gómez-Rial J et al. Rotavirus infection beyond the gut. Infect Drug Resist. 2019. PMID: 30636886. doi: 10.2147/IDR.S186404. PubMed: https://pubmed.ncbi.nlm.nih.gov/30636886/
3. 3 Guarino A et al. European Society for Pediatric Gastroenterology, Hepatology, and Nutrition/European Society for Pediatric Infectious Diseases evidence-based guidelines for the management of acute gastroenteritis in children in Europe: update 2014. J Pediatr Gastroenterol Nutr. 2014 Jul. PMID: 24739189. doi: 10.1097/MPG.0000000000000375. PubMed: https://pubmed.ncbi.nlm.nih.gov/24739189/
4. 4 Posovszky C et al. Acute Infectious Gastroenteritis in Infancy and Childhood. Dtsch Arztebl Int. 2020 Sep 11. PMID: 33263539. doi: 10.3238/arztebl.2020.0615. PubMed: https://pubmed.ncbi.nlm.nih.gov/33263539/
5. 5 Poeta M et al. Acute Infectious Diarrhea. Adv Exp Med Biol. 2024. PMID: 39060736. doi: 10.1007/978-3-031-58572-2_9. PubMed: https://pubmed.ncbi.nlm.nih.gov/39060736/