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From: TSS (216-119-144-34.ipset24.wt.net)
In Reply to: Re: 1 in 2 CHANCE OF GETTING BSE AKA MAD COW BY THE ORAL ROUTE (PRIMATE STUDY) posted by TSS on January 27, 2005 at 12:38 pm:
1: Dev Biol Stand. 1993;80:9-13. Transmission of human spongiform encephalopathies to experimental animals: comparison of the chimpanzee and squirrel monkey. Asher DM, Gibbs CJ Jr, Sulima MP, Bacote A, Amyx H, Gajdusek DC. Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD 20992. The agents of kuru and Creutzfeldt-Jakob disease have been consistently transmitted from patients with those diseases to chimpanzees and squirrel monkeys, as well as to other new-world primates, with average incubation periods of two or three years. No other animals have been found so consistently susceptible to the agents in human tissues. More rapid and convenient assays for the infectious agents would greatly facilitate research on the spongiform encephalopathies of humans. PMID: 8270119 [PubMed - indexed for MEDLINE] 1: J Med Primatol. 1976;5(4):205-9. Masters CL, Alpers MP, Gajdusek DC, Gibbs CJ Jr, Kakulas BA. The experimental host range for the slow virus infections causing subacute spongiform virus encephalopathies is enlarged in primates to include the gibbon for kuru, the pigtailed macaque for Creutzfeldt-Jakob disease, and the sooty mangabey for both diseases. The report is based on neuropathological evidence of the diseases in animals with preclinical lesions. A table lists all the species to which the subacute spongiform virus encephalopathies have been transmitted. PMID: 826636 [PubMed - indexed for MEDLINE] http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=826636 1: Brain. 1975 Dec;98(4):595-612. Experimental kuru in the spider monkey. Histopathological and ultrastructural studies of the brain during early stages of incubation. Beck E, Bak IJ, Christ JF, Gajdusek DC, Gibbs CJ Jr, Hassler R. The brains of 10 spider monkeys inoculated intracerebrally with brain suspension from kuru patients have been studied histologically and ultrastructurally. The animals were killed by perfusion of fixative from four to forty-one weeks after inoculation, when healthy and free of neurological signs. Definite histopathological changes had occurred as early as four weeks after inoculation, when moderate numbers of bi-nucleated neurons were found within the limbic cortex, striatum, the hypothalamus and amongst the Purkinje cells of the cerebellum. At later stages of incubation a moderate loss of neurons in the cerebral and cerebellar cortex and a mild to moderate proliferation of fibrous astrocytes here and also in the hypothalamus were the most striking features. None of our cases showed either status spongiosus or the generalized astrocytic proliferation and hypertrophy, characteristic of fully developed experimental kuru, in any region of the brain. The principal ultrastructural abnormalities consisted of the formation of membrane-bound intracytoplasmic vacuoles, predominantly within dendrites, and of concentric laminar arrays derived from the endoplasmic reticulum. The former were seen in all regions of the brain examined and at all stages of incubation. Concentric laminar arrays were confined to the cerebellar nodulus, where they were most numerous in dendrites and neuronal perikarya four weeks after inoculation. Both changes are interpreted as an indication that the kuru agent acts upon the plasma membrane from an early stage onwards and, by stimulating its growth, leads to the formation of complex, membrane-bounded vacuoles and to hyperplasia of the endoplasmic reticulum. The formation of vacuoles is further regarded as the first sign of status spongiosus on an ultrastructural level. Attention is drawn to the great similarities between the changes observed in the present material and those described in the brains of patients dying from kuru and of primates with fully developed experimental kuru. The significance of the relatively rapid spread of the kuru agent throughout the brain is discussed in relation to the concept of "slow virus" diseases. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=814967 1: Adv Neurol. 1975;10:291-317. Familial and sporadic chronic neurological degenerative disorders transmitted from man to primates. Gajdusek DC, Gibbs CJ Jr. PMID: 125030 [PubMed - indexed for MEDLINE] http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=125030 1: Intervirology. 1974;2(1):14-9. Transmission of kuru and Creutzfeldt-Jakob disease to marmoset monkeys. Peterson DA, Wolfe LG, Deinhardt F, Gajdusek DC, Gibbs CJ Jr. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=4207302 Gajdusek DC, Gibbs CJ Jr. Gajdusek DC, Rogers NG, Basnight M, Gibbs CJ Jr, Alpers M. 1: Ann N Y Acad Sci. 1969 Jul 3;162(1):529-50. Transmission experiments with kuru in chimpanzees and the isolation of latent viruses from the explanted tissues of affected animals. Gajdusek DC, Rogers NG, Basnight M, Gibbs CJ Jr, Alpers M. PMID: 5257421 [PubMed - indexed for MEDLINE] 53: Beck E, Daniel PM, Alpers M, Gajdusek DC, Gibbs CJ Jr. 1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8 Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery. Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC. Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them. PMID: 8006664 [PubMed - indexed for MEDLINE] TSS
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