Prevalence and characterization of the seven major serotypes of Shiga toxin-producing Escherichia coli (STEC) in veal calves slaughtered in France.

Shiga toxin (Stx)-producing Escherichia coli (STEC) belonging to the "top 7″ serotypes (i.e. O157:H7, O26:H11, O45:H2, O103:H2, O111:H8, O121:H19 and O145:H28) are considered as the main pathogenic enterohemorrhagic E. coli (EHEC). As ruminants, including calves, are a reservoir of pathogenic STEC, we investigated the prevalence, major virulence genes and genetic relatedness of top7 STEC in veal calves slaughtered in France, through the analysis of 500 fecal samples collected over one year. Thirty top7 STEC isolates were recovered from 28 calves. The two serotypes O103:H2 and O26:H11 accounted for 73% of STEC strains, followed by O145:H28 and O157:H7. STEC super-shedding levels were identified for two calves carrying STEC O103:H2 and O157:H7, respectively. Thirty-nine atypical enteropathogenic E. coli (aEPEC) were also recovered from calves. Overall, a prevalence of 5.6% top7 STEC-positive calves was found, thus higher than that previously determined for the French slaughtered adult cattle (1.8%), confirming the impact of animals age on STEC carriage. Most top7 STEC strains carried the stx1a subtype suggesting a low pathogenicity for humans. Seasonal variation in STEC carriage was also observed, with two peaks of higher prevalence during spring and fall. Genetic similarity of top7 STEC isolates was found for calves originating from the same fattening facilities, reflecting STEC circulation between animals kept in groups. This study indicates that veal calves grown for meat production are at higher risk of shedding top7 STEC compared to adult cattle. They thus represent ideal targets for the implementation of farm interventions aimed at reducing STEC burden in cattle and the food chain.

Sleep disorders in obese children are not limited to obstructive sleep apnoea syndrome.

AIM: This study was to characterise respiratory and nonrespiratory sleep disorders in obese children and evaluate the diagnostic and therapeutic impact of a specific sleep consultation. METHODS: A descriptive study was conducted in obese French children who received multidisciplinary care management from the hospital centre for paediatric obesity in Bordeaux. This followed a specific sleep consultation between 2007 and 2015, because their paediatrician had identified symptoms suggestive of sleep disorders. RESULTS: The sleep specialist confirmed the presence of a sleep disorder in 98.4% of the 128 obese children, with a mean age of 12.1 ± 3.2 years. These included respiratory sleep disorders, hypersomnolence, insomnia and circadian rhythm sleep-wake disorders. Polysomnography revealed that 46.1% had respiratory sleep disorders and 24.2% had obstructive sleep apnoea syndrome (OSAS). Just under half (47.6%) were referred to an otorhinolaryngologist for sleep care management, 30.5% were referred to an orthodontist, 17.9% had melatonin treatment and 13.3% received continuous positive airway pressure ventilation. CONCLUSION: Sleep disorders in obese children were not limited to respiratory sleep disorders including OSAS. A systematic specific consultation with a sleep specialist is essential for the diagnosis and care of such children and would be beneficial when treating paediatric obesity.

The secreted form of dengue virus nonstructural protein NS1 is endocytosed by hepatocytes and accumulates in late endosomes: implications for viral infectivity.

The flavivirus nonstructural protein NS1 is expressed as three discrete species in infected mammalian cells: an intracellular, membrane-associated form essential for viral replication, a cell surface-associated form that may be involved in signal transduction, and a secreted form (sNS1), the biological properties of which remain elusive. To determine the distribution of the dengue virus (DEN) sNS1 protein in vivo, we have analyzed by immunohistological means the tissue tropism of purified DEN sNS1 injected intravenously into adult mice. The sNS1 protein was found predominantly associated with the liver, where hepatocytes appeared to represent a major target cell. We further showed that sNS1 could be efficiently endocytosed by human Huh7 and HepG2 hepatocytes in vitro. After its internalization, the protein was detected intracellularly for at least 48 h without being substantially degraded. Colocalization studies of sNS1 with markers of the endolysosomal compartments revealed that the protein was specifically targeted to lysobisphosphatidic acid-rich structures reminiscent of late endosomes, as confirmed by electron microscopy. Intracellular accumulation of sNS1 in Huh7 cells enhanced the fluid phase uptake of rhodamine-labeled dextran. Furthermore, preincubation of Huh7 cells with sNS1 increased dengue virus production after infection with the homologous strain of DEN-1 virus. Our results demonstrate that the accumulation of DEN sNS1 in the late endosomal compartment of hepatocytes potentializes subsequent dengue virus infection in vitro, raising the possibility that sNS1 may contribute to viral propagation in vivo.

Introduction of West Nile virus in the Middle East by migrating white storks.

West Nile virus (WNV) was isolated in a flock of 1,200 migrating white storks that landed in Eilat, a town in southern Israel, on August 26, 1998. Strong, hot westerly winds had forced the storks to fly under considerable physical stress before reaching the agricultural land surrounding the town. Most of the flock were fledglings, <1 year old, which had hatched in Europe. Thirteen dead or dying storks were collected 2 days after arrival and submitted to the laboratory for examination. Four WNV isolates were obtained from their brains. Out of 11 storks tested six days after arrival, three had WNV-neutralizing antibodies. Comparative analysis of full-length genomic sequences of a stork isolate and a 1999 flamingo isolate from the USA showed 28 nucleotide (nt) (0.25%) and 10 amino acid (0.3%) changes. Sequence analysis of the envelope gene of the stork isolate showed almost complete identity with isolates from Israeli domestic geese in 1998 and 1999 and from a nonmigrating, white-eyed gull in 1999. Since these storks were migrating southwards for the first time and had not flown over Israel, we assume that they had become infected with WNV at some point along their route of migration in Europe.