Experimental infection of mink with bovine spongiform encephalopathy

Robinson, Mark; Hadlow, W. J.; Huff, T. P.; Wells, G. A. H.; Dawson, M.; Marsh, Richard F.; Gorham, J. R.

doi:10.1099/0022-1317-75-9-2151

Cited by 60 publications

(37 citation statements)

References 8 publications

(24 reference statements)

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“…Histopathologic studies showed more severe spongiform changes, especially at rostral levels, in cattle infected with TME ( 7 ) than infected with typical BSE, and these changes were also observed in TgOvPrP4 mice infected with L-type BSE at second passage. Conversely, mink infected with typical BSE had a greater degree of spongiform change in the brainstem than mink infected with TME ( 10 ). Similar changes were also observed in TgOvPrP4 mice infected with typical BSE.…”

Section: Discussionmentioning

confidence: 99%

“…These TME outbreaks happened before bovine spongiform encephalopathy (BSE) was identified in Europe or before 3 cases of BSE had occurred in the United States after 2003. Despite a potential link of TME with a cattle TSE, clinical and histologic studies indicate that mink inoculated with BSE have features that distinguish this disease from natural and experimental TME ( 7 , 8 , 10 ). …”

mentioning

confidence: 99%

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Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and L-type Bovine Spongiform Encephalopathy in a Mouse Model

Baron

Bencsik

Biacabe

et al. 2007

Emerg. Infect. Dis.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and L-type Bovine Spongiform Encephalopathy in a Mouse Model

Baron

Bencsik

Biacabe

et al. 2007

Emerg. Infect. Dis.

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“…BSE has been transmitted experimentally by parenteral routes from cattle to mice (Fraser et al, 1988(Fraser et al, , 1992, cattle (Dawson et al, 1990a), sheep and goats (Foster et al, 1993;Fraser & Foster, 1994), mink (Mustela vison) (Robinson et al, 1994), marmoset (Callithrix jacchus) (Baker et al, 1993), cynomolgus macaque (Lasmézas et al, 1996) and guinea pig (M. Dawson, P. Griffiths & S. J. Ryder, unpublished data). The present study shows that BSE is transmissible from cattle to pigs that were exposed parenterally.…”

Section: Discussionmentioning

confidence: 99%

“…This observation is in marked contrast to the now-considerable body of evidence that BSE has been transmitted, by natural or accidental means, via foodstuffs to several other animal species and to man (Bruce et al, 1994;Kirkwood & Cunningham, 1994;Bruce et al, 1997;Hill et al, 1997). It has also been transmitted by feeding BSEaffected brain to mice (Barlow & Middleton, 1990) and mink (Robinson et al, 1994) and by the oral dosing of sheep and goats (Foster et al, 1993, Fraser & Foster, 1994 and cattle (Wells et al, , 1998. Transmission of BSE to lemurs (Microcebus murinus) after oral dosing with infected brain has been reported (Bons et al, 1999).…”

Section: Time After Exposure When Killed (Weeks)mentioning

confidence: 99%

Studies of the transmissibility of the agent of bovine spongiform encephalopathy to pigs

Wells

Hawkins

Austin³

et al. 2003

Journal of General Virology

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Studies to test the transmissibility of the bovine spongiform encephalopathy (BSE) agent to pigs began in 1989. Parenteral inoculation of the agent by three routes simultaneously (intracranially, intravenously and intraperitoneally) produced disease with an incubation period range of 69-150 weeks. Pre-clinical pathological changes were detected in two pigs killed electively at 105 and 106 weeks post-inoculation. Infectivity was detected by bioassay in inbred mice in the CNS of those pigs that developed spongiform encephalopathy. Infectivity was also found in the stomach, jejunum, distal ileum and pancreas of terminally affected pigs. These findings show that pigs are susceptible to BSE. In contrast, disease failed to occur in pigs retained for 7 years after exposure by feeding BSE-affected brain on three separate days, at 1-2 week intervals. The amounts fed each day were equivalent to the maximum daily intake of meat and bone meal in rations for pigs aged 8 weeks. No infectivity was found in tissues assayed from the pigs exposed orally. This included tissues of the alimentary tract. It is suggested that these pigs did not become infected. The relatively high oral exposure used in these experiments compared with feed-borne exposure in the field may explain the absence of an epidemic of spongiform encephalopathy in domestic pigs concurrent with the BSE epidemic in the UK.

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“…In nature, BSE is transmitted to cattle (Wells & Wilesmith, 1995), several zoo ruminants (Kirkwood & Cunningham, 1994) and wild and domestic cats (Wyatt et al, 1990(Wyatt et al, , 1991. Experimentally, BSE has been transmitted to mice (Fraser et al, 1992), sheep, goats , minks (Robinson et al, 1994), marmosets (Baker et al, 1998), macaques (Lasmézas et al, 1996) and lemurs (Bons et al, 1999). Furthermore, BSE has been transmitted to humans, in whom it causes variant Creutzfeldt-Jakob disease (vCJD) (Collinge et al, 1996;Hill et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

Alteration of the biological and biochemical characteristics of bovine spongiform encephalopathy prions during interspecies transmission in transgenic mice models

Yokoyama

Masujin

Iwamaru

et al. 2009

Journal of General Virology

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In the interspecies transmission of prions, the species barrier influences the susceptibility of the host. Bovine spongiform encephalopathy (BSE) prions affect a wide range of host species but do not affect hamsters. In order to study this species barrier, this study analysed the transmissibility of BSE prions to several lines of transgenic (Tg) mice, including those expressing mouse and hamster chimeric prion proteins (MH2M and MHM2 mice). BSE prions were transmitted to tga20, MHM2 and ICR mice, and the incubation period was approximately 400 days. Thus, these mice were classified as 'susceptible mice'. However, BSE prions were not transmitted to MH2M and TgHaNSE mice, and these mice were classified as 'resistant mice'. After the BSE prions were passaged once in wild-type mice, they could be transmitted to resistant mice. The characteristics of the accumulated abnormal isoform of PrP (PrP Sc ) in susceptible and resistant mice were determined using Western blotting. A BSE-like glycoform pattern of PrP Sc was detected in all of the susceptible mice using two different antibodies that recognized either the N-or the C-terminal end of the 27-30 kDa protease-resistant fragment of PrP (PrP 27-30 ) as the epitope. In contrast, proteinase digestion followed by deglycosylation analysis showed that, in addition to PrP 27-30 , truncated PrP Sc fragments existed in resistant mice. These mixed PrP Sc fragments may have resulted from the adaptation of resistant mice to BSE prions.

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Experimental infection of mink with bovine spongiform encephalopathy

Cited by 60 publications

References 8 publications

Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and L-type Bovine Spongiform Encephalopathy in a Mouse Model

Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and L-type Bovine Spongiform Encephalopathy in a Mouse Model

Studies of the transmissibility of the agent of bovine spongiform encephalopathy to pigs

Alteration of the biological and biochemical characteristics of bovine spongiform encephalopathy prions during interspecies transmission in transgenic mice models

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