High prevalence of scrapie in a dairy goat herd: tissue distribution of disease-associated PrP and effect ofPRNPgenotype and age

Abstract

-Following a severe outbreak of clinical scrapie in 2006-2007, a large dairy goat herd was culled and 200 animals were selected for post-mortem examinations in order to ascertain the prevalence of infection, the effect of age, breed and PRNP genotype on the susceptibility to scrapie, the tissue distribution of diseaseassociated PrP (PrP d ), and the comparative efficiency of different diagnostic methods. As determined by immunohistochemical (IHC) examinations with Bar224 PrP antibody, the prevalence of preclinical infection was very high (72/200; 36.0%), with most infected animals being positive for PrP d in lymphoreticular system (LRS) tissues (68/72; 94.4%) compared to those that were positive in brain samples (38/72; 52.8%). The retropharyngeal lymph node and the palatine tonsil showed the highest frequency of PrP d accumulation (87.3% and 84.5%, respectively), while the recto-anal mucosa-associated lymphoid tissue (RAMALT) was positive in only 30 (41.7%) of the infected goats. However, the efficiency of rectal and palatine tonsil biopsies taken shortly before necropsy was similar. The probability of brain and RAMALT being positive directly correlated with the spread of PrP d within the LRS. The prevalence of infection was influenced by PRNP genetics at codon 142 and by the age of the goats: methionine carriers older than 60 months showed a much lower prevalence of infection (12/78; 15.4%) than those younger than 60 months (20/42; 47.6%); these last showed prevalence values similar to isoleucine homozygotes of any age (40/80; 50.0%). Two of seven goats with definite signs of scrapie were negative for PrP d in brain but positive in LRS tissues, and one goat showed biochemical and IHC features of PrP d different from all other infected goats. The results of this study have implications for surveillance and control policies for scrapie in goats.scrapie / goat / prion disease / transmissible spongiform encephalopathy

Scrapie e seu diagnóstico diferencial em ovinos no Mato Grosso do Sul

“…A doença pode apresentar-se na forma clássica em ovinos e caprinos geneticamente susceptíveis (AVMA 2002, Goldmann & Baylis 2004, González et al 2009, OIE 2009) e na forma atípica, diagnosticada na Noruega, por Benestad et al (2003), denominada "Nor98", posteriormente observada em outras partes do mundo (Arsac et al 2007,Cosseddu 2007, Jeffrey & González 2007, Seuberlich et al 2007, Colussi et al 2008, Fediaevsky et al 2008, Loiacono et al 2009, Martinez 2010 (Fernandes et al 1978), mas a primeira notiϐicação oϐicial à Organização Mundial de Saúde Animal (OIE) foi de um surto, também no RS, ocorrido em 1985, (Pereira 1996). Posteriormente, entre 1995 e 2010, foram registrados surtos, no RS, Paraná (PR), Mato Grosso do Sul (MS), Mato Grosso (MT), Minas Gerais (MG) e São Paulo (SP) (OIE 2011a).…”

Scientific Opinion on BSE/TSE infectivity in small ruminant tissues

“…The prevalence of clinically and sub-clinically affected animals in Classical scrapie-affected flocks has been investigated by different research groups in different European countries and it varied between 3% (Jeffrey et al, 2002) and 41% (Ligios et al, 2006). Evidence for similar prevalence differences were obtained from affected goat herds (Gonzalez et al, 2009). …”

“…Central nervous system invasion occurs at both the obex and thoracic spinal cord level through the autonomic nerve roots (EFSA Panel on Biological Hazards (BIOHAZ), 2009). Similar investigations were carried out in the UK (Gonzalez et al, 2009) Additionally, goat kids (n=54) were orally challenged with Classical scrapie around birth (1.5g brain homogenate from naturally affected goats administered through natural suckling) (Project UMR INRA1225 -AFSSA Niort).…”

“…This diversity in interaction with the goat PrP genotype may impact on the kinetics of the dissemination and on the distribution of the TSE agent in the organs. For instance development of clinical Classical scrapie was recently reported, in the absence of PrP Sc accumulation in lymphoid tissues in some naturally affected goats (Gonzalez et al, 2009;Konold et al, 2007a). EFSA Journal 2010;8(12):1875…”

The influence of the commensal and pathogenic gut microbiota on prion disease pathogenesis

“…Although prions do not accumulate within the large intestinal GALT during the early stages of infection (Donaldson et al, 2015b;Gonzalez et al, 2009;Thomsen et al, 2012;van Keulen et al, 2000), pathogen-induced pathology in the large intestine might influence disease susceptibility by enhancing the uptake of prions into GALT within it. Infection with the helminth T. muris is entirely restricted to the caecum and proximal colon (Fig.…”