Rodents as shared indicators for zoonotic parasites of carnivores in urban environments

Rodents are shared intermediate or paratenic hosts for Echinococcus multilocularis, Toxocara spp. and Toxoplasma gondii, and may serve as valuable indicators for assessing the occurrence and the level of environmental contamination and infection pressure with free-living stages of these zoonotic parasites. We investigated 658 non-commensal rodents for parasite infections in the canton of Geneva, Switzerland. The prevalence of infection with E. multilocularis was highest in Arvicola terrestris captured in the north-western area (16·5%, CI: 10·1%-24·8%), possibly reflecting a higher red fox density due to the low incidence of sarcoptic mange in this part of the canton. The exposure rate to Toxocara spp. was highest in the urban area (13·2%, CI: 7·9%-20·3%), and may account for higher densities of domestic carnivore and red fox definitive hosts within the city. Exposure to T. gondii was widespread (5·0%, CI: 3·2-7·4%), indicating a ubiquitous distribution of infected cat definitive hosts. Interestingly, a widespread distribution of Taenia taeniaeformis, a parasite mainly transmitted by cats, was similarly evidenced in A. terrestris. Distinct spatial patterns for the different zoonotic parasites likely reflected differences in distribution, abundance, and habitat use of the respective definitive hosts. These results highlight the potential value of rodents as shared indicators for these pathogen

Challenging the growing rabbit with a moderately pathogenic E. coli under ad libitum or limited feed intake conditions: impact on digestive physiology, bacterial communities, and on post-weaning growth

[EN] The impact of a challenge with moderately pathogenic Escherichia coli O128:C6 on the digestive physiology and gut bacterial community of growing rabbits under two feeding programmes was analysed. Upon weaning (28 d old), 180 rabbits were allocated to four groups (9 cages of 5 rabbits per group) for two weeks: group C100 was non-inoculated and fed ad libitum; C70 was non-inoculated and feed intake was limited to 70% of C100; I100 and I70 were inoculated and fed ad libitum or restricted to 70%, respectively. At the age of 31 d (D0), rabbits were orally inoculated with E. coli (2.2×108 colony forming units/rabbit). The effects of inoculation spiked on D4, with a 28% lower growth rate for I100 than for C100. Limited feed intake reinforced the inoculation’s effects on growth: I70 had a 66% lower growth rate than C70. The morbidity rate peaked at 42% between D4 and D7 for inoculated groups, without significant effect of the feed intake level. E. coli concentration peaked on D5/D6 in the caecum of the I100 and I70 groups. Inoculation reduced by 30% (P<0.05) the villus height/crypt depth and villus/crypt area ratios in the ileum, with no significant effect of the intake level. Inoculation was associated with a tenfold increase in serum haptoglobin (P<0.001) for both ad libitum and restricted rabbits. On D5, the inoculation modified the structure of the ileal bacterial community (P<0.05), but not that of the caecum. The feed intake level did not affect either the structure or diversity of the bacterial community, both in the ileum and caecum.The authors would like to thank Alain Milon and Stéphane Bertagnoli (ENV Toulouse) who provided the E. coli O128:C6 strain we used. We are also grateful to ANSES staff in the “Service d’Elevage et d’Expérimentation en Pathologie Aviaire” (M. Amelot, L. Le Moal, T. Le Coq, D. Courtois and M. Morvan) and for the technical help of F. Lalande (HQPAP, ANSES) and L. Gordon.Martignon, M.; Burel, C.; Licois, D.; Reperant, E.; Postollec, G.; Valat, C.; Gidenne, TN. (2021). Challenging the growing rabbit with a moderately pathogenic E. coli under ad libitum or limited feed intake conditions: impact on digestive physiology, bacterial communities, and on post-weaning growth. World Rabbit Science. 29(1):1-10. https://doi.org/10.4995/wrs.2021.14089OJS110291Agnoletti F. 2012. Update on rabbit enteric diseases: despite improved diagnostic capacity, where does disease control and prevention stand? In: Proc. 10th World Rabbit Congress, World Rabbit Science Association (WRSA) publ., Sharm El Sheik, Egypt, 1113-1127.Allison S.D., Martiny J.B.H. 2008. Resistance, resilience, and redundancy in microbial communities. Proc. Nat. Academy Sci., 105: 11512-11519. https://doi.org/10.1073/pnas.0801925105Antonopoulos D.A., Huse S.M., Morrison H.G., Schmidt T.M., Sogin M.L., Young V.B. 2009. Reproducible community dynamics of the gastrointestinal microbiota following antibiotic perturbation. Infect. Immunity 77: 2367-2375. https://doi.org/10.1128/IAI.01520-08Bennegadi N., Gidenne T., Licois D. 2001. Impact of fibre deficiency and sanitary status on non-specific enteropathy of the growing rabbit. Anim. Res., 50: 401-413. https://doi.org/10.1051/animres:2001135Boisot P., Licois D., Gidenne T. 2003. Une restriction alimentaire réduit l'impact sanitaire d'une reproduction expérimentale de l'entéropathie épizootique (EEL) chez le lapin en croissance. In: Proc. "10èmes Journées de la Recherche Cunicole", Paris, France, 267-370.Camguilhem R., Milon A., 1989. Biotypes and O serogroups of Escherichia coli involved in intestinal infections of weaned rabbits: clues to diagnosis of pathogenic strains. J. Clin. Microb., 27: 743-747. https://doi.org/10.1128/JCM.27.4.743-747.1989Cantey J.R., Inman L.R. 1981. Diarrhea due to Escherichia coli strain RDEC-1 in the rabbit. The Peyer's patch as the initial site of attachement and colonization. J. Infect. Diseases, 143: 440-446. https://doi.org/10.1093/infdis/143.3.440Combes S., Nice F., Licois D., Fortun-Lamothe L., Gidenne T. 2009. Response of digestive bacterial community of rabbits after experimental infection of epizootic enteropathy syndrome (ERE). In: Proc. 13èmes Journées de la Recherche Cunicole (Bolet G., Ed.), ITAVI publ., Paris., France, 227-230.Combes S., Massip K., Martin O., Furbeyre H., Cauquil L., Pascal G., Bouchez O., Le Floc'h N., Zemb O., Oswald I.P., Gidenne T., 2017. Impact of feed restriction and housing hygiene conditions on specific and inflammatory immune response, the cecal bacterial community and the survival of young rabbits. Animal, 11: 854-863. https://doi.org/10.1017/S1751731116002007Coussement W., Ducatelle R., Charlier G., Okerman L., Hoorens J. 1984. Pathology of experimental colibacillosis in rabbits. J. Vet. Med., 31: 64-72. https://doi.org/10.1111/j.1439-0450.1984.tb01282.xEuropean Union 2003. Protection of Animals used for Experimental Purposes. Directive 86/609/EEC of 24th novembre 1986, amended 16th septembre 2003. In: Official Journal of European Union.Fortun-Lamothe L., Boullier S. 2007. A review on the interactions between gut microflora and digestive mucosal immunity. Possible ways to improve the health of rabbits. Livest. Sci., 107: 1-18. https://doi.org/10.1016/j.livsci.2006.09.005Foubert C., Duperray J., Boisot P., Guyonvarch A. 2008. Effect of feed restriction with or without free access to drinking water on performance of growing rabbits in healthy or epizootic rabbit enteropathy conditions. In: Proc. 9th World Rabbit Congress (Xiccato G., Trocino A., Lukefahr S.D., Eds.). Fond. Ini. Zooprofilattiche E Zoot. Publ., Brescia Italy, 667-671.Georgieva T., Penchev Georgiev I., Tanev S., Vachkov A., Petrov V., Eckersall P. D., Sotirov L., Lazarov L., Christov T.S., Nikolov J. 2009. Variations of acute phase protein (haptoglobin, fibrinogen and ceruloplasmin) concentrations in weaning rabbits after experimental infection with E. coli. Rev. Médecine Vét. 160: 133-139.Gidenne T., Licois D. 2005. Effect of a high fibre intake on the resistance of the growing rabbit to an experimental inoculation with an enteropathogenic strain of Escherichia coli. Anim. Sci., 80: 281-288. https://doi.org/10.1079/ASC41570281Gidenne T., Combes S., Fortun-Lamothe L. 2012. Feed intake limitation strategies for the growing rabbit: effect on feeding behaviour, welfare, performance, digestive physiology and health: a review. Animal 6: 1407-1419. https://doi.org/10.1017/S1751731112000389Gidenne T., Lebas F., Savietto D., Dorchies P., Duperray J., Davoust C., Fortun-Lamothe L. 2015. Nutrition et alimentation. In: Le lapin. De la biologie à l'élevage (Gidenne T., Ed.). Quae Éditions Publ., Paris, France, 152-196.Goodlad R.A., Levi S., Lee C.Y., Mandir N., Hodgson H., Wright N.A. 1991. Morphometry and cell proliferation in endoscopic biopsies: evaluation of a technique. Gastroenterology, 101: 1235-1241. https://doi.org/10.1016/0016-5085(91)90072-SKimsé M., Combes S., Fortun-Lamothe L., Cauquil L., Monteils V., Bayourthe C., Gidenne T. 2011. Physiopathologic and microbiologic characterisation of Rabbit Epizootic Enteropathy in the growing rabbit - first results. In: Proc. 13èmes Journées de la Recherche Cunicole (Bolet G., Ed.). ITAVI Publ. Paris, 155-158.Le Bouquin S., Jobert J.L., Larour G., Balaine L., Eono F., Boucher S., Huneau A., Michel V. 2009. Risk factors for an acute expression of Epizootic Rabbit Enteropathy syndrome in rabbits after weaning in French kindling-to-finish farms. Livest. Sci., 125: 283-290. https://doi.org/10.1016/j.livsci.2009.05.010Le Floc'h N., Knudsen C., Gidenne T., Montagne L., Merlot E., Zemb O. 2014. Impact of feed restriction on health, digestion and faecal microbiota of growing pigs housed in good or poor hygiene conditions. Animal, 8: 1632-1642. https://doi.org/10.1017/S1751731114001608Licois D. 2004. Domestic rabbit enteropathies. In: Proc. 8th World Rabbit Congress (Becerril C., Pro A., Eds.). Colegio de Postgraduados for WRSA publ., Puebla, Mexico, 385-403. Available at http://www.world-rabbit-science.com/WRSAProceedings/Congress-2004-Puebla/Papers/Pathology/P0-Licois.pdf Accessed July 2020.Licois D., Reynaud A., Federighi M., Gaillard-Martinie B., Guillot, J.F. 1991. Scanning and transmission electron microscopic study of adherence of Escherichia coli O103 enteropathogenic and/or enterohemorrhagic strain GV in enteric infection in rabbits. Infect. Immunity, 59: 3796-3800. https://doi.org/10.1128/IAI.59.10.3796-3800.1991Licois D., Guillot J.F., Mouline C., Reynaud A. 1992. Susceptibility of the Rabbit to an Enteropathogenic Strain of Escherichia coli 0103 - Effect of Animals Age. Ann. Rech. Vét., 23: 225-232.Maertens L. 2011. Strategies to Reduce Antibiotic Use in Rabbit Production. J. Agric. Sci. Technol., 1: 783-792.Marlier D., Dewree R., Delleur V., Licois D., Lassence C., Poulipoulis A., Vindevogel H. 2003. A review of the major causes of digestive disorders in the European rabbit. Ann. Rech. Vét., 147: 385-392.Martignon M.H., Combes S., Gidenne T. 2010. Digestive physiology and hindgut bacterial community of the young rabbit (Oryctolagus cuniculus): Effects of age and short-term intake limitation. Comp. Biochem. Phys. Part A, 156: 156-162. https://doi.org/10.1016/j.cbpa.2010.01.017Michelland R.J., Dejean S., Combes S., Fortun-Lamothe L., Cauquil L. 2009. StatFingerprints: A friendly graphical interface program for processing and analysis of microbial fingerprint profiles. Molec. Ecol. Ress., 9: 1359-1363. https://doi.org/10.1111/j.1755-0998.2009.02609.xMichelland R.J, Monteils V., Combes S., Cauquil L., Gidenne T., Fortun-Lamothe L. 2011. Changes over time in the bacterial communities associated with fluid and food particles and the ruminal parameters in the bovine rumen before and after a dietary change. Canadian J. Microb., 57: 629-637. https://doi.org/10.1139/w11-053Milon A., Esslinger J., Camguilhem R. 1990. Adhesion of Escherichia coli strains isolated from diarrheic weaned rabbits to intestinal villi and hela-cells. Infect. Immunity, 58: 2690-2695. https://doi.org/10.1128/IAI.58.8.2690-2695.1990Milon A., Esslinger J., Camguilhem R., 1992. Oral vaccination of weaned rabbits against enteropathgenic Escherichia coli-like E. coli O103 infection: use of heterologous strains harboring lipopolysaccharide or adhesin of pathogenic strains. Infect. Immunity, 60: 2702-2709. https://doi.org/10.1128/IAI.60.7.2702-2709.1992Peeters J.E., Pohi P., Okerman L., Devriese, L. 1984. Pathogenic properties of Escherichia coli strains isolated from diarrheic commercial rabbits. J. clin. Microb., 84: 34-39. https://doi.org/10.1128/JCM.20.1.34-39.1984Peeters J.E., Charlier G., Raeymaekers R. 1985. Scanning and transmission electron microscopy of attaching effacing Escherichia coli in weanling rabbits. Vet. Pathol., 22: 54-59. https://doi.org/10.1177/030098588502200109Peeters J.E., Geeroms R., Orskov F., 1988. Biotype, serotype, and pathogenicity of attaching and effacing enteropathogenic Escherichia coli strains isolated from diarrheic commercial rabbits. Infect. Immunity, 56: 1442-1448. https://doi.org/10.1128/IAI.56.6.1442-1448.1988Ramette A. 2007. Multivariate analyses in microbial ecology. FEMS Microb. Ecol. 62: 142-160. https://doi.org/10.1111/j.1574-6941.2007.00375.xRantzer D., Svendsen J., Westrom B. 1996. Effects of a strategic feed restriction on pig performance and health during the post-weaning period. Acta Agric. Scand. A, 46: 219-226. https://doi.org/10.1080/09064709609415874Rosenzweig M.L. 1995. Species Diversity in Space and Time. Cambridge, UK: Cambridge University Press. https://doi.org/10.1017/CBO9780511623387Skrivanová E., Molatová Z., Skrivanová V., Marounek M. 2009. Inhibitory activity of frabbit milk and medium-chain fatty acids against enteropathogenic Escherichia coli O128. Vet. Microb., 135: 358-362. https://doi.org/10.1016/j.vetmic.2008.09.08

Effects of infection-induced migration delays on the epidemiology of avian influenza in wild mallard populations

Wild waterfowl populations form a natural reservoir of Avian Influenza (AI) virus, and fears exist that these birds may contribute to an AI pandemic by spreading the virus along their migratory flyways. Observational studies suggest that individuals infected with AI virus may delay departure from migratory staging sites. Here, we explore the epidemiological dynamics of avian influenza virus in a migrating mallard (Anas platyrhynchos) population with a specific view to understanding the role of infection-induced migration delays on the spread of virus strains of differing transmissibility. We develop a host-pathogen model that combines the transmission dynamics of influenza with the migration, reproduction and mortality of the host bird species. Our modeling predicts that delayed migration of individuals influences both the timing and size of outbreaks of AI virus. We find that (1) delayed migration leads to a lower total number of cases of infection each year than in the absence of migration delay, (2) when the transmission rate of a strain is high, the outbreak starts at the staging sites at which birds arrive in the early part of the fall migration, (3) when the transmission rate is low, infection predominantly occurs later in the season, which is further delayed when there is a migration delay. As such, the rise of more virulent AI strains in waterfowl could lead to a higher prevalence of infection later in the year, which could change the exposure risk for farmed poultry. A sensitivity analysis shows the importance of generation time and loss of immunity for the effect of migration delays. Thus, we demonstrate, in contrast to many current transmission risk models solely using empirical information on bird movements to assess the potential for transmission, that a consideration of infection-induced delays is critical to understanding the dynamics of AI infection along the entire flyway.<br /

Rodents as shared indicators for zoonotic parasites of carnivores in urban environments

Rodents are shared intermediate or paratenic hosts for Echinococcus multilocularis, Toxocara spp. and Toxoplasma gondii, and may serve as valuable indicators for assessing the occurrence and the level of environmental contamination and infection pressure with free-living stages of these zoonotic parasites. We investigated 658 non-commensal rodents for parasite infections in the canton of Geneva, Switzerland. The prevalence of infection with E. multilocularis was highest in Arvicola terrestris captured in the north-western area (16.5%, CI: 10.1%-24.8%), possibly reflecting a higher red fox density due to the low incidence of sarcoptic mange in this part of the canton. The exposure rate to Toxocara spp. was highest in the urban area (13.2%, CI: 7.9%-20.3%), and may account for higher densities of domestic carnivore and red fox definitive hosts within the city. Exposure to T. gondii was widespread (5.0%, CI: 3.2-7.4%), indicating a ubiquitous distribution of infected cat definitive hosts. Interestingly, a widespread distribution of Taenia taeniaeformis, a parasite mainly transmitted by cats, was similarly evidenced in A. terrestris. Distinct spatial patterns for the different zoonotic parasites likely reflected differences in distribution, abundance, and habitat use of the respective definitive hosts. These results highlight the potential value of rodents as shared indicators for these pathogens

Nicotinic receptors

Regulation of normal or abnormal behaviour is critically controlled by the central serotonergic systems. Recent evidence has suggested that serotonin (5-HT) neurotransmission dysfunction contributes to a variety of pathological conditions, including depression, anxiety, schizophrenia and Parkinson’s disorders. There is also a great amount of evidence indicating that 5-HT signalling may affect the reinforcing properties of drugs of abuse by the interaction and modulation of dopamine (DA) function. This chapter is focused on one of the more addictive drugs, nicotine. It is widely recognised that the effects of nicotine are strongly associated with the stimulatory action it exhibits on mesolimbic DAergic function. We outline the role of 5-HT and its plethora of receptors, focusing on 5-HT2 subtypes with relation to their involvement in the neurobiology of nicotine addiction. We also explore the novel pharmacological approaches using 5-HT agents for the treatment of nicotine dependence. Compelling evidence shows that 5-HT2C receptor agonists may be possible therapeutic targets for smoking cessation, although further investigation is required.peer-reviewe

Toxocariasis: a silent threat with a progressive public health impact

Background: Toxocariasis is a neglected parasitic zoonosis that afflicts millions of the pediatric and adolescent populations worldwide, especially in impoverished communities. This disease is caused by infection with the larvae of Toxocara canis and T. cati, the most ubiquitous intestinal nematode parasite in dogs and cats, respectively. In this article, recent advances in the epidemiology, clinical presentation, diagnosis and pharmacotherapies that have been used in the treatment of toxocariasis are reviewed. Main text: Over the past two decades, we have come far in our understanding of the biology and epidemiology of toxocariasis. However, lack of laboratory infrastructure in some countries, lack of uniform case definitions and limited surveillance infrastructure are some of the challenges that hindered the estimation of global disease burden. Toxocariasis encompasses four clinical forms: visceral, ocular, covert and neural. Incorrect or misdiagnosis of any of these disabling conditions can result in severe health consequences and considerable medical care spending. Fortunately, multiple diagnostic modalities are available, which if effectively used together with the administration of appropriate pharmacologic therapies, can minimize any unnecessary patient morbidity. Conclusions: Although progress has been made in the management of toxocariasis patients, there remains much work to be done. Implementation of new technologies and better understanding of the pathogenesis of toxocariasis can identify new diagnostic biomarkers, which may help in increasing diagnostic accuracy. Also, further clinical research breakthroughs are needed to develop better ways to effectively control and prevent this serious disease

Crossing the Interspecies Barrier: Opening the Door to Zoonotic Pathogens

The number of pathogens known to infect humans is ever increasing. Whether such increase reflects improved surveillance and detection or actual emergence of novel pathogens is unclear. Nonetheless, infectious diseases are the second leading cause of human mortality and disability-adjusted life years lost worldwide [1], [2]. On average, three to four new pathogen species are detected in the human population every year [3]. Most of these emerging pathogens originate from nonhuman animal species

Highly Pathogenic Avian Influenza Virus H5N1 Infection in a Long-Distance Migrant Shorebird under Migratory and Non-Migratory States

Corticosterone regulates physiological changes preparing wild birds for migration. It also modulates the immune system and may lead to increased susceptibility to infection, with implications for the spread of pathogens, including highly pathogenic avian influenza virus (HPAIV) H5N1. The red knot (Calidris canutus islandica) displays migratory changes in captivity and was used as a model to assess the effect of high plasma concentration of corticosterone on HPAIV H5N1 infection. We inoculated knots during pre-migration (N = 6), fueling (N = 5), migration (N = 9) and post-migration periods (N = 6). Knots from all groups shed similar viral titers for up to 5 days post-inoculation (dpi), peaking at 1 to 3 dpi. Lesions of acute encephalitis, associated with virus replication in neurons, were seen in 1 to 2 knots per group, leading to neurological disease and death at 5 to 11 dpi. Therefore, the risk of HPAIV H5N1 infection in wild birds and of potential transmission between wild birds and poultry may be similar at different times of the year, irrespective of wild birds' migratory status. However, in knots inoculated during the migration period, viral shedding levels positively correlated with pre-inoculation plasma concentration of corticosterone. Of these, knots that did not become productively infected had lower plasma concentration of corticosterone. Conversely, elevated plasma concentration of corticosterone did not result in an increased probability to develop clinical disease. These results suggest that birds with elevated plasma concentration of corticosterone at the time of migration (ready to migrate) may be more susceptible to acquisition of infection and shed higher viral titers—before the onset of clinical disease—than birds with low concentration of corticosterone (not ready for take-off). Yet, they may not be more prone to the development of clinical disease. Therefore, assuming no effect of sub-clinical infection on the likelihood of migratory take-off, this may favor the spread of HPAIV H5N1 by migratory birds over long distances

Spatial and Temporal Association of Outbreaks of H5N1 Influenza Virus Infection in Wild Birds with the 0°C Isotherm

Wild bird movements and aggregations following spells of cold weather may have resulted in the spread of highly pathogenic avian influenza virus (HPAIV) H5N1 in Europe during the winter of 2005–2006. Waterbirds are constrained in winter to areas where bodies of water remain unfrozen in order to feed. On the one hand, waterbirds may choose to winter as close as possible to their breeding grounds in order to conserve energy for subsequent reproduction, and may be displaced by cold fronts. On the other hand, waterbirds may choose to winter in regions where adverse weather conditions are rare, and may be slowed by cold fronts upon their journey back to the breeding grounds, which typically starts before the end of winter. Waterbirds will thus tend to aggregate along cold fronts close to the 0°C isotherm during winter, creating conditions that favour HPAIV H5N1 transmission and spread. We determined that the occurrence of outbreaks of HPAIV H5N1 infection in waterbirds in Europe during the winter of 2005–2006 was associated with temperatures close to 0°C. The analysis suggests a significant spatial and temporal association of outbreaks caused by HPAIV H5N1 in wild birds with maximum surface air temperatures of 0°C–2°C on the day of the outbreaks and the two preceding days. At locations where waterbird census data have been collected since 1990, maximum mallard counts occurred when average and maximum surface air temperatures were 0°C and 3°C, respectively. Overall, the abundance of mallards (Anas platyrhynchos) and common pochards (Aythya ferina) was highest when surface air temperatures were lower than the mean temperatures of the region investigated. The analysis implies that waterbird movements associated with cold weather, and congregation of waterbirds along the 0°C isotherm likely contributed to the spread and geographical distribution of outbreaks of HPAIV H5N1 infection in wild birds in Europe during the winter of 2005–2006