The infectivity in tissues from cattle exposed orally to the agent of BSE was assayed by the intracerebral inoculation of cattle. In addition to the infectivity in the central nervous system and distal ileum at stages of pathogenesis previously indicated by mouse bioassay, traces of infectivity were found in the palatine tonsil of cattle killed 10 months after exposure. Because the infectivity may therefore be present throughout the tonsils in cattle infected with BSE, observations were made of the anatomical and histological distribution of lingual tonsil in the root of the tongue of cattle. Examinations of tongues derived from abattoirs in Britain and intended for human consumption showed that macroscopically identifiable tonsillar tissue was present in more than 75 per cent of them, and even in the tongues in which no visible tonsillar tissue remained, histological examination revealed lymphoid tissue in more than 90 per cent. Variations in the distribution of the lingual tonsil suggested that even after the most rigorous trimming of the root of the tongue, traces of tonsillar tissue may remain.
Scrapie belongs to a group of diseases known as the transmissible spongiform encephalopathies or prion diseases. Two different categories of naturally occurring scrapie have been identified: classical scrapie, which was first recorded around 1750, and atypical scrapie or 'Nor-98', which was first identified in Norway in 1998. The molecular characteristics of atypical scrapie have been well defined, but detailed descriptions of the neuropathological phenotype are rare since the majority of cases have been detected through active surveillance programmes where only brainstem and cerebellum are collected for statutory diagnosis. In order to characterise the neuropathology of naturally occurring atypical scrapie in sheep, we examined multiple brain levels from 15 whole brains from field cases of atypical scrapie, both clinical suspects and fallen stock, collected in Great Britain between 2004 and 2006. We found that the distribution of disease-associated prion protein (PrP(Sc)) and vacuolation in atypical scrapie cases are very different to both classical scrapie and experimental bovine spongiform encephalopathy in sheep. Immunolabelling for PrP(Sc) is mild and restricted at the obex and more intense and widespread rostrally, particularly in the cerebellum, substantia nigra, thalamus and basal nuclei. Intracellular immunolabelling types are not seen, but distinctive white matter immunolabelling is widespread. Vacuolation associated with PrP(Sc) deposits was not observed in the brainstem neuroanatomical areas commonly affected in classical scrapie and bovine spongiform encephalopathy, but was instead most prominent in the cerebellar cortex and neocortex. This is the largest comprehensive descriptive study of atypical scrapie pathology to date, and provides baseline data against which other natural or experimental cases can be compared. It also reinforces the current recommendation to collect cerebellum in addition to brainstem to enable confident confirmation of this distinct disease phenotype within surveillance programmes.
This study examines tissues from sequential-kill, time-course pathogenesis studies to refine estimates of the age at which disease-specific PrP (PrP Sc ) can first be detected in the central nervous system (CNS) and related peripheral nervous system ganglia of cattle incubating bovine spongiform encephalopathy (BSE). Such estimates are important for risk assessments of the age at which these tissues should be removed from cattle at slaughter to prevent human and animal exposure to BSE infection. Tissues were examined from cattle dosed orally with 100 or 1 g BSE-infected brain. Incubation period data for the doses were obtained from attack rate and the sequential-kill studies. A statistical model, fitted by maximum likelihood, accounted for the differences in the lognormal incubation period and the logistic probability of infection between different dose groups. Initial detection of PrP Sc during incubation was invariably in the brainstem and the earliest was at 30 and 44 months post-exposure for the 100 g-and 1 g-dosed sequential-kill study groups, respectively. The point at which PrP Sc in 50 % of the animals would be detected by immunohistochemistry applied to medulla-obex was estimated at 9.6 and 1.7 months before clinical onset for the 100 g-and 1 g-dosed cattle, respectively, with a low probability of detection in any of the tissues examined at more than 12 months before clinical onset. PrP Sc was detected inconsistently in dorsal root ganglia, concurrent with or after detection in CNS, and not at all in certain sympathetic nervous system ganglia.
Background: Active surveillance for transmissible spongiform encephalopathies in small ruminants has been an EU regulatory requirement since 2002. A number of European countries have subsequently reported cases of atypical scrapie, similar to previously published cases from Norway, which have pathological and molecular features distinct from classical scrapie. Most cases have occurred singly in flocks, associated with genotypes considered to be more resistant to classical disease. Experimental transmissibility of such isolates has been reported in certain ovinised transgenic mice, but has not previously been reported in the natural host. Information on the transmissibility of this agent is vital to ensuring that disease control measures are effective and proportionate.
Very low levels of somatic mitochondrial (mt)DNA deletions have been identified in the semen of infertile men. It has been suggested that these mutations cause infertility through an effect on sperm motility, but there has been no direct evidence to show that mutant mtDNA can affect sperm function. We have carried out semen analysis on a male harbouring the A3243G mtDNA mutation and show that high levels of mutant mtDNA strongly correlate with low sperm motility.
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