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Title: Prions in Milk from Ewes Incubating Natural Scrapie}
Article:
Abstract:
Since prion infectivity had never been reported in milk, dairy products originating from transmissible spongiform encephalopathy( TSE)-affected ruminant flocks currently enter unrestricted into the animal and human food chain. However, a recently published study brought the first evidence of the presence of prions in mammary secretions from scrapie-affected ewes. Here we report the detection of consistent levels of infectivity in colostrum and milk from sheep incubating natural scrapie, several months prior to clinical onset. Additionally, abnormal PrP was detected, by immunohistochemistry and PET blot, in lacteal ducts and mammary acini. This PrPSc accumulation was detected only in ewes harbouring mammary ectopic lymphoid follicles that developed consequent to Maedi lentivirus infection. However, bioassay revealed that prion infectivity was present in milk and colostrum, not only from ewes with such lympho-proliferative chronic mastitis, but also from those displaying lesion-free mammary glands. In milk and colostrum, infectivity could be recovered in the cellular, cream, and casein-whey fractions. In our samples, using a Tg 338 mouse model, the highest per ml infectious titre measured was found to be equivalent to that contained in 6 µg of a posterior brain stem from a terminally scrapie-affected ewe. These findings indicate that both colostrum and milk from small ruminants incubating TSE could contribute to the animal TSE transmission process, either directly or through the presence of milk-derived material in animal feedstuffs. It also raises some concern with regard to the risk to humans of TSE exposure associated with milk products from ovine and other TSE-susceptible dairy species.
Introduction:
Transmissible spongiform encephalopathies( TSE), or prion disease, are fatal neurodegenerative disorders occurring in sheep( scrapie), cattle( bovine spongiform encephalopathy- BSE), or humans( Creutzfeldt-Jakob disease- CJD). The key event in TSE is the conversion of a normal cellular protein( PrPc) into an abnormal isoform( PrPSc) which accumulates in tissues in infected individuals. According to the prion concept, abnormal PrP is the causative agent of TSEs[1] and PrPSc is currently considered to be the only TSE biochemical marker. Whereas its detection generally correlates with the presence of infectivity[2],[3], infectivity has been reported in the absence of detectable PrPSc[4]. A decade ago, a new variant form of CJD was identified. The emergence of this TSE form in humans was the consequence of the zoonotic transmission of BSE through dietary exposure to contaminated animal products[5],[6]. Since then, the control of human exposure to TSE agents has become a priority, and a sanitary policy has been implemented based on both the eradication of TSE in food producing animals and the exclusion of known infectious materials from the food chain. Because investigations carried out as early as the 1960's failed to reveal evidence of TSE agents in milk from affected ruminants, this product has continuously been considered as safe[7],[8]. However, more recently, disease associated prion protein( PrPSc) accumulation was reported in mammary glands from three scrapie-affected ewes. Deposits were associated with those mammary ectopic lymphoid follicles that develop in response to retroviral infection( Maedi)[9],[10]. Nevertheless, in the absence of definitive evidence of the presence of prion in milk, dairy products originating from TSE affected ruminant flocks continue to enter the animal and human food chain. In the past few months, however, evidence for the transmission of scrapie to lambs, via colostrum/milk, has been reported[11]. These data raise new concerns about the potential infectious character of milk from TSE affected small ruminants flocks.
Discussion:
Failure to transmit TSE using milk from scrapie affected or incubating ewes in conventional rodents models, has been previously reported[7]. In our study, the use of a transgenic mouse model expressing the ovine PRP gene reduced or abolished the species barrier phenomenon[25] and could explain, at least partially, the positive results we obtained. However the low infectivity level we measured( 100. 1 to 101. 6 ID50/ml) indicates that, even in this transgenic animal model, direct inoculation with 20 µl per mouse of whole milk or colostrum would be unlikely to transmit disease. It also means that, despite no PK resistant PrP being detected in milk and colostrum fractions, the approach we used( i. e immunoprecipitation of all detectable PrP on beads) was sufficiently efficient to concentrate infectivity. Measurements of the concentrative efficacy of this method are currently under investigation and will be reported elsewhere. A recently published study reported the successful transmission of scrapie to lambs through consumption of colostrum/milk collected from ewes at the late incubation or clinical stage of the disease[11]. This study was the first to identify Prion presence in mammary secretions from Scrapie affected ewes. However, because of its design, this study did not elicit information as to which fraction, colostrum or milk, induced disease transmission. Moreover, since lateral contamination occurred between lambs and in some cases several ewes were used to feed a lamb, it was not possible in this experiment to clearly determine which of the donor ewes were shedding infectivity in colostrum/milk. The data we provided here brings definitive and unambiguous evidence of the presence infectivity in both milk and colostrum from naturally incubating scrapie ewes. In our model, infectivity was detected up to 20 months before clinical disease onset and a majority of ewes( 10 out of 13 at the moment of writing) were demonstrated to have shed prion infectivity in their milk. Taken together, the results reported by Konold et al.[11] and those obtained in our study, raise the issue of the use of sheep milk or milk by-products for animal feeding. Currently ruminants' milk represents a major source of protein in milk-replacer and feedstuffs used in a variety of farm animal species. The use of TSE incubating ewe milk in such products could give rise to dietary exposure of animals both intra and interspecies. Given the low level of infectivity apparent in milk and the species barrier phenomenon, the interspecies transmission risk associated with ewe milk certainly remains limited. However, in the current stage of knowledge, the possibility of such transmission cannot be ruled out. As all scrapie samples in our study were collected from a single flock, it is likely that investigated ewes were exposed to only a limited range of TSE agents and possibly to a single one. Consequently, caution should be taken before inferring those observations to other situations. Interactions between host genotype and TSE agent are known to impact on the kinetics of prion dissemination in ewes. Such interactions could also influence, not only how early the shedding of infectivity via colostrum and milk takes place but also the levels of infectivity. Prion infectivity was detected here in sheep with healthy mammary glands as well as those with chronic lymphoproliferative mastitis. However, our preliminary results suggest that the presence of ectopic lymphoid follicles in ewes with lymphoproliferative mastitis could increase prion shedding in milk. Acute and subacute bacterial mastitis are extremely common in dairy animals and can impact on milk composition[26]. The effect of these conditions on milk prion shedding was not addressed in this study and remains to be evaluated. Our study was carried out in a flock affected by Maedi-Visna Lentivirus. This non oncogenic retrovirus is largely spread in sheep population even if its exact prevalence remains difficult to evaluate. In several countries or sheep production areas, up to 70% of flocks were reported to be infected[27]. While Maedi-Visna Lentivirus generally induces a persistent infectious with no associated pathology, it can cause, in a fraction of infected individuals, lymphoproliferative changes including a diffuse interstitial infiltration and/or peri-ductal follicle-like aggregations in the mammary gland. In such affected ewes disease has a subclinical course with secretion of apparently normal milk[28],[29]. A potential enhancement of the prion infectivity shedding in milk from persistently Maedi Virus infected ewes( with no pathological manifestations) cannot be ruled out[30]. However, because of the relative high prevalence of such infection in dairy ewes production areas, such hypothetical effect would not impact, in our opinion, on the significance of our observations. There are major differences in terms of peripheral pathogenesis between BSE in cattle and TSE in other ruminants. In cattle BSE, peripheral tissues PrPSc accumulation and infectivity is marginal and this is particularly true of lymphoid tissues[31]. Such differences prevent the observations reported here in sheep being directly extrapolated to BSE in cattle. Nevertheless, these results clearly call for the re-examination of milk from BSE affected cattle for the presence of prions. Finally, the consequences for humans of the presence of prions in sheep milk should certainly be given consideration. However, it is our opinion that its relative impact on global TSE dietary exposure is of lower magnitude than other prion sources, such as lymphoid tissues from small ruminants incubating TSE[32],[33].
A decade ago , a new variant form of Creutzfeldt-Jakob disease was identified . The emergence of this prion disease in humans was the consequence of the zoonotic transmission of bovine spongiform encephalopathy through dietary exposure . Since then , the control of human exposure to prions has become a priority , and a policy based on the exclusion of known infectious materials from the food chain has been implemented . Because all investigations carried out failed to reveal evidence of infectivity in milk from affected ruminants , this product has continuously been considered as safe . In this study , we demonstrate the presence of prions in colostrum and milk from sheep incubating natural scrapie and displaying apparently healthy mammary glands . This finding indicates that milk from small ruminants could contribute to the transmission of prion disease between animals . It also raises some concern with regard to the risk to humans associated with milk products from ovine and other dairy species .