마잉주 정부의 미국산 쇠고기 광우병 위생검역 완화 협상으로 인해 한바탕 홍역을 치룬 대만에서 미국산 쇠고기 혀부위 수입을 둘러싸고 다시 논란이 발생했다는 소식입니다.

미국산 쇠고기 혀부위 453kg의 대만 수입이 최초로 허용됨에 따라 대만 정부는 전수검사를 통해 안전성을 보장하겠다고 발표했지만, 야당인 민진당(DPP) 의원들은 소의 혀부위도 내장으로 간주해서 수입을 중단시켜야 한다고 주장하고 있습니다.

대만정부와 미국정부는 혀(tongues), 음경(penises), 고환(testicles), 꼬리(tails), 힘줄(tendons), 횡격막( skirt=diaphragm) 등 6개 부위는 내장에 포함되지 않는다는 입장입니다.

대만의 검역당국은 미국산 소 혀 부위 중에서 혀 안쪽 뿌리 부근의 유곽돌기(circumvallate papillae)를 의무적으로 제거하기 때문에 안전성에 문제가 없다고 밝히고 있습니다. 참고로 소의 혀는 광우병 특정위험물질(SRM) 중에서 편도조직이 일부 분포하기 때문에 안전성 논란이 지속적으로 제기되고 있는 부위입니다.

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First local import permit issued for U.S. beef offal

출처 : Chinapost.com.tw Updated Tuesday, April 20, 2010 9:18 am TWN, The China Post news staff
http://www.chinapost.com.tw/taiwan/national/national-news/2010/04/20/253168/First-local.htm

TAIPEI, Taiwan — The Ministry of Economic Affairs has issued the first import permit for 453 kilograms of beef offal, and health authorities will conduct strict batch-by-batch inspections on U.S. beef tongues over which the public has doubts, MOEA officials said yesterday.

 To help ease any lingering public doubt about U.S. beef products, the Department of Health (DOH), the MOEA and the Council of Agriculture (COA) held a joint press conference earlier Monday to explain the existing standards.

Six types of beef offal such as beef tongues, penises, testicles, tails, tendons and skirt (diaphragm) are not classified as internal organs, so imports of those non high-risk beef products will be accepted, they said.

Lawmakers of the opposition Democratic Progressive Party (DPP) argued that the beef tongues and penises should be classified as internal organs, which would make them illegal to import.

The DOH said it decided last May that beef tongues are not classified as internal organs — unlike thoracic, abdominal, and pelvic organs, which are not allowed into Taiwan under a protocol signed with Washington last October.

Hsu Tien-lai, director general of the Bureau of Animal and Plant Health Inspection and Quarantine under the COA, said that high-risk circumvallate papillae, toward the base of the tongue, are required to be removed from beef tongues before entering Taiwan.

The U.S. announced on April 16 that exports of beef products to Taiwan will include bones with meat, hanging tenders, tongues, penises, testicles, tails, tendons and diaphragms from cattle younger than 30 months and slaughtered on or after April 1, seen as having a lower risk of carrying mad cow disease.

Strict Measures to Secure Safe Beef Products

Economics Minister Shih Yen-shiang said at the economic committee session of the Legislative Yuan that the government will enforce strict measures, including “three controls and five certifications,” in accordance with the existing law, to assure imports of U.S. beef products such as tongues and testicles are safe for consumers.

The measures set controls on beef imports at the source, at borders and in markets, while the five certifications refer to verifying certification documents, checking that shipments are marked with detailed product information, opening a high percentage of cartons of imported beef to check the product, conducting food safety tests and being able to get information on suspected problem products immediately.

Asked about the U.S. government’s announcement that beef exports to Taiwan will include tongues, testicles and tails, Shih cited Department of Health data as explaining that these products are not categorized as “internal organs” — which are not allowed to be exported to Taiwan according to a Taiwan-U.S. protocol signed last year.

The Bureau of Foreign Trade will decide whether or not to allow the import of such U.S. beef products based on the existing standard, Shih said.

Lawmaker Ting Shou-chung of the ruling Kuomintang (KMT) suggested that the government take immediate action to prohibit the beef parts from entering Taiwan to prevent public outrage.

Taiwan’s agreement last year to lift its ban on U.S. bone-in beef and certain other beef products, including ground beef and offal, sparked a huge public outcry.

The ban was imposed in 2003 due to fears of bovine spongiform encephalopathy (BSE), or mad cow disease.

Under public pressure, the KMT-controlled legislature amended the Act Governing Good Sanitation Jan. 5 to deny the importing of beef products to Taiwan — including ground beef and other beef parts such as skulls, brains, eyes and spines — from countries with documented BSE cases over the past decades.

Progression of prion infectivity in asymptomatic cattle after oral bovine spongiform encephalopathy challenge

¹ Centro de Investigación en Sanidad (CISA-INIA), Valdeolmos, Madrid, Spain
² School of Biology and Environmental Science, University College Dublin, Belfield, Dublin 4, Ireland

Correspondence
Juan María Torres
jmtorres@inia.es

출처 : J Gen Virol 88 (2007), 1379-1383; DOI 10.1099/vir.0.82647-0
http://vir.sgmjournals.org/cgi/content/full/88/4/1379

The presence of BSE prion infectivity in asymptomatic cattle and its tissue distribution are important concerns for both human and veterinary health and food safety. In this work, a collection of tissues from asymptomatic cattle challenged orally with BSE and culled at 20, 24, 27, 30 and 33 months have been used to inoculate intracerebrally BoPrP-Tg110 mice expressing bovine PrP to assess their infectivity. Results demonstrate that BSE infectivity in asymptomatic cattle is essentially restricted to the nervous system, Peyer’s patches and tonsils, as reported previously for terminally BSE-diseased cattle. BSE infectivity was detectable in Peyer’s patches and tonsils at all time points analysed, but infectivity in nervous tissues (brainstem and sciatic nerve) was only detectable after 27 months from inoculation. Infectivity in brainstem increased markedly at 33 months after inoculation. All other investigated tissues or fluids (spleen, skeletal muscle, blood and urine) revealed no detectable infectivity throughout the time course studied.

	MAIN TEXT

Transmissible spongiform encephalopathies (TSEs) or prion diseases are associated with the accumulation of abnormal PrP^Sc conformer in the brain and subsequent neurodegeneration (Prusiner, 2004). The mechanism of conversion of PrP^C to PrP^Sc is not well understood, but it may occur by direct interaction of PrP^Sc with PrP^C, promoting refolding of the latter to produce additional PrP^Sc. The PrP^Sc conformer can be recognized by its partial resistance to proteinase K treatment.

Most TSEs are transmitted naturally by peripheral routes, either orally or transcutaneously. The mechanism(s) of spread from the periphery to the central nervous system (CNS) is an important issue. It is not clear how prions pass through the intestinal mucosa after oral uptake. M cells, which are portals for antigens and pathogens (Hathaway & Kraehenbuhl, 2000), may be involved in the transepithelial transport of prions (Heppner et al., 2001). Thus, the infectious agent may penetrate the mucosa through M cells and reach the Peyer’s patches. Although prion diseases are neurological disorders, critical events in their pathogenesis take place in restricted sites outside the nervous system, especially in peripheral lymph organs (Aucouturier et al., 2000).

Bovine spongiform encephalopathy (BSE) was recognized as a cattle prion disease during the 1980s (Wilesmith et al., 1988) in the UK. Ingestion of foods contaminated with BSE is the likely cause of the new variant Creutzfeldt–Jakob disease in humans (Bruce et al., 1997; Hill et al., 1997).

Several studies indicate that, to date, the BSE agent has been found only in the brain, spinal cord and retinal (eye) tissue of BSE-diseased cattle. Infectivity assessment in several tissues from orally inoculated cattle, using bioassays based on RIII mice (Wells et al., 1994, 1998), revealed BSE infectivity in the CNS, all brain regions, the spinal cord, the optic nerve, the retina (neuronal cells) and the facial and sciatic nerves, as well as in distal ileum and bone marrow. The skeletal muscles, spleen and other lymphatic tissues were shown to be free of detectable infectivity. More recently, Wells et al. (2005) showed infectivity in tonsil tissue from cattle killed 10 months after oral BSE challenge by intracerebral inoculation in cattle. These finding are in contrast to the spreading of the scrapie agent in infected sheep, mice and hamsters in tissues such as spleen, other lymphatic tissues, muscles etc., even during the preclinical stage (Bosque et al., 2002; Heggebo et al., 2003; Thomzig et al., 2003, 2004). In addition, PrP^Sc can be found in the lymphoreticular system and is not restricted to the nervous system following oral inoculation of sheep and primates with the BSE agent (Bons et al., 1999; Jeffrey et al., 2001; Herzog et al., 2004; Andreoletti et al., 2006). Recently, experiments in transgenic mice overexpressing bovine PrP confirmed the essential restriction of infectivity to the nervous system in terminally BSE-diseased cattle (Buschmann & Groschup, 2005).

The distribution of BSE infectivity in asymptomatic cattle incubating the disease and its progression through the silent period from inoculation to the appearance of clinical signs is of particular interest in relation to food safety. In the present work, we have used a highly sensitive bioassay based on transgenic mice overexpressing bovine PrP (BoPrP-Tg110 mice) (Castilla et al., 2003) to assess the infectivity in a panel of tissues from asymptomatic cattle at different times (20–33 months) after oral challenge.

Tissues from asymptomatic cattle after oral BSE challenge were prepared and kindly provided by the Veterinary Laboratory Agency (VLA), New Haw, Addlestone, Surrey, UK, as part of the VLA Project SE1736. Cattle (4–6 months of age) were inoculated orally with 100 g doses of BSE-infected brainstem material derived from a homogenate of about 150 clinically sick and pathologically confirmed cases of BSE. Control animals were maintained under the same conditions, but not infected. Clinical signs were assessed monthly by veterinarian experts from the VLA (New Haw, Addlestone, Surrey, UK). At different times post-inoculation, three infected and one control animal were culled and a panel of tissues and fluids were sampled aseptically. The tissue and fluids were stored at –70 °C. In this study, tissues from animals culled at 20, 24, 27, 30 and 33 months post-infection were investigated. Homogenates (10 % in PBS) of each tissue or fluid from asymptomatic cattle sampled at the indicated times were used for infectivity assessment in BoPrP-Tg110 mice. Samples from the three inoculated cows at each time point were used as pools.

All pools, containing each tissue sampled from three different cattle at the same time after challenge, were tested for the presence of PrP^Sc before inoculation of BoPrP-Tg110 mice. PrP^Sc was analysed by Western blotting in brain tissues collected and homogenized in PBS. One hundred microlitres of 10 % (w/v) brain homogenate was pre-cleared by centrifugation at 2000 g for 5 min in 5 % sarcosyl. Samples were treated with 20 µg proteinase K ml^–1 (Roche) at 37 °C for 60 min and insoluble fractions were obtained by centrifugation at 25 000 g for 30 min. SDS sample loading buffer was added to all samples, boiled for 10 min and loaded on an SDS/12 % polyacrylamide gel. For the immunoblotting experiments, mAbs 2A11 (Brun et al., 2004) and Sha31 (Feraudet et al., 2005) were used at a 1 : 1000 dilution from ascitic fluid. Immunocomplexes were detected by horseradish peroxidase-conjugated anti-mouse IgG (Amersham Biosciences). The immunoblots were developed under conditions of enhanced chemiluminescence (Amersham Biosciences).

None of the samples was scored positive by Western blotting using mAb 2A11 (Table 1 and data not shown). In addition, samples were analysed by using the highly sensitive Bio-Rad ELISA TeSeE test (Grassi et al., 2001) according to the manufacturer’s recommendations. Only brainstem sampled at 33 months post-inoculation was scored positive with this test (Table 1). The presence of infectivity in the different samples was analysed by intracerebral inoculation of BoPrP-Tg110 transgenic mice. These mice overexpress bovine PrP (around eightfold) under the control of the murine Prnp gene promoter from the MoPrP.Xho vector (Borchelt et al., 1996) and are highly susceptible to BSE infection (Castilla et al., 2003, 2004). Groups of six mice (6–7 weeks old, weighing around 20 g) were inoculated with 20 µl of the appropriate tissue pool in the right parietal lobe by using a 25-gauge disposable hypodermic needle. After inoculation, the mice were observed daily and their neurological status was assessed twice weekly. Mice showing at least three of ten signs of neurological dysfunction (Scott et al., 1989, 1993) over several consecutive days were sacrificed and samples were collected for diagnostic evaluation. Survival times were calculated as the time between inoculation and death. All mice in an experiment were tested for PrP^Sc accumulation in their brains, and only those positive for PrP^Sc were included in the calculation of survival times.

The PrP^Sc electrophoretic profiles found in the brain of BoPrP-Tg110 mice inoculated with the different tissues showed no apparent differences when positive tissues were compared with each other or with PrP^Sc from the brain of a natural BSE case (Fig. 1).

View larger version (53K): [in this window] [in a new window]   Fig. 1. Western blot of brain homogenates from selected BoPrP-Tg110 mice inoculated with a pool of tissues from BSE-infected asymptomatic cattle (33 months after oral challenge). Bovine tissues used for the inoculation of BoPrP-Tg110 mice are indicated above each line, with the exception of BSE2, which is a BoPrP-Tg110 mouse inoculated with BSE2 derived from a natural case of BSE in cattle (Castilla et al., 2003). mAb 2A11 was used as indicated in the text. Molecular mass is given on the right in kDa.

In brainstem, the detection of infectivity was only achieved 27 months after oral challenge. The infectivity found in brainstem at 27 or 30 months after challenge was low, as only one-third of the BoPrP-Tg110 mice inoculated were scored positive and with long incubation times. Previous work using the RIII mouse bioassay failed to detect infectivity in the CNS before 32 months after inoculation (Wells et al., 1998). In contrast, the pool of brainstem material from cattle sampled 33 months after oral challenge contained a high titre of infectivity, as shown by the maximum percentage of infected BoPrP-Tg110 mice found. This indicates a marked accumulation of the infectious agent in at least one of the three pooled animals during the last few months (from 30 up to 33 months) after challenge. This increased infectivity is confirmed by the detection of PrP^Sc by the Bio-Rad ELISA TeSeE test in this brainstem pool. As only one of the three animals used for each pool needs to be positive to transmit the disease to the BoPrP-Tg110 mice, we cannot be sure that the differences detected in the infectivity levels were not due to differences between individual cattle. A low level of infectivity was also detected in the sciatic nerve from animals sampled at 30 and 33 months after challenge. All other tissues or fluids investigated, including skeletal muscle, blood and urine, revealed no detectable infectivity throughout the time course studied (Table 1). Tissues with no detectable infectivity in the highly sensitive bioassay based on transgenic mice (without a transmission barrier for BSE prions) may be considered as being of very low risk for oral infection in humans, where a strong transmission barrier is present (Lasmezas et al., 2005).

In conclusion, our results confirm that BSE infectivity in asymptomatic cattle is essentially restricted to the nervous system, as reported previously for terminally BSE-diseased cattle (Buschmann & Groschup, 2005), and is consistent with the idea that BSE infectivity, after oral uptake, propagates only poorly in some intestinal lymphatic tissues (mainly Peyer’s patches) and from there spreads centripetally to the CNS, probably by intraneural spread via the peripheral nervous system.

	ACKNOWLEDGEMENTS

 
We thank the VLA (New Haw, Addlestone, Surrey, UK) for kindly providing tissues of experimentally infected cows at different time points. The authors wish to thank Dr J. Grassi from CEA (Commissariat à l’Energie Atomique), France, for providing the Sha31 antibody. Thanks are also due to Bio-Rad for supplying the ELISA TeSeE kits. This work was supported by grants INIA-CAL01-018, UE-FAIR-CT97-3306 and INIA-RTA-2006-0091.

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Received 16 October 2006; accepted 22 December 2006.

10월 22일자로 대만과 미국이 새롭게 미국산 쇠고기 수입위생조건을 체결했다는 소식입니다.

국회를 통하여 입수한 자료(첨부파일)에 따르면… 2009년 한국의 수입위생조건과 거의 유사합니다. 30개월 이상의 연령제한 및 부위제한을 OIE 기준에 따라 완전히 철폐했습니다.

수입위생조건 영문 내용을 보시면 아시겠지만… 대만은 중국정부의 “하나의 중국” 정책으로 인해 주권국가로 인정받지 못하고… 그냥 “주미 대만대표부”로 취급당하고 있는 형편이라 미국에 강력하게 저항하기 힘든 정치외교적 상황을 고려한다면… 주권국가인 R.O.K의 이명박 정부보다 2년 가까이 미국의 압력에 더 버텨냈다는 사실을 인정해야 한다고 생각합니다.

한국의 이명박 정부의 졸속협상이 대만의 협상력을 떨어뜨린 결과라고 볼 수 있습니다. 한미FTA 협정도 분명히 그러한 측면이 강하게 존재합니다. 편향되고 잘못된 외교정책의 결과가 주변 국가에 얼마나 민폐를 끼칠 수 있는지를 보여주는 사례 중의 하나로 기록될 것으로 생각합니다.

미-대만 간 체결된 미국산 쇠고기 수입위생조건의 핵심 내용은 다음과 같습니다.

* 수입부위 : SRM(광우병 위험물질) 제외, MSM/MRM(기계적 분리육/기계적 회수육) 제외, 30개월 이상의 두개골과 척주에서 분리한 AMR(선진회수육) 제외한 쇠고기. 선진회수육에는 광우병 위험물질이나 중추신경계조직(CNS)이 들어있지 않아야 하며, 갈은 쇠고기(ground beef)에는 선진회수육은 허용되나 광우병 위험물질 또는 기계적 분리육/기계적 회수육이 포함되지 않아야 함

==> 30개월 이상의 쇠고기까지 전면 개방. 2008년 한국의 2단계 개방안 보다 더 수입조건 완화. 30개월 미만의 쇠고기만 수입하는 현행 한국의 수입위생조건보다 더 개방했음. 쇠고기 및 쇠고기 제품의 정의를 ‘미국연방육류검사법’으로 기술한 한국과 차이가 있음.

* SRM 규정 : 모든 연령에서 회장원위부와 편도 / 30개월령 이상에서 뇌, 두개골, 안구, 삼차신경절, 척수, 척주(등뼈 ; 미추 제외, 흉추 및 요추의 횡돌기 제외, 천추의 날개(익) 제외), 등배신경절

==> SRM의 범위를 OIE 기준으로 대폭 완화함. 2008년 한국의 기준과 동일.

* 광우병 발생 시 미국은 즉시 역학조사를 실시하고 그 결과를 대만에 통보해줌. 추가 광우병 사례가 미국이 OIE로부터 부여받은 등급에 부정적 변화를 가져올 경우 수입중단

==> 2008년 한국의 수입조건과 동일.

* 육류작업장에 대한 요건 : 수출작업장 승인권은 미국 정부에 있음. 작업장은 사전에 대만에 통보해야 함. 미국 정부의 수출작업장에 대한 정기적인 모니터링과 점검 프로그램 유지.
 
==> 2008년 한국의 수입조건과 동일.

* 위반제품을 야기한 절차가 계속 되었을 경우 FSIS는 적절한 개선 및 방지조치가 취해졌다고 결정될 때까지 즉시 해당절차 중단. FSIS가 개선조치가 적절하다고 결정하는 경우 생산재개
 
==> 2008년 한국의 수입조건과 동일.

* 대만 정부는 미국의 쇠고기 수출작업장에 대한 표본검사 실시 가능

 ==> 2008년 한국 수입위생조건과 동일
 
* 미국에서 100일 이상 사육해야 미국산으로 인정
 
 ==> 2008년 한국의 수입조건과 동일.

* 특정위험물질 발견된 경우 수입중단 불가하며 미국 정부는 원인을 규명하기 위한 조사.
 
==> 2008년 한국의 수입조건과 동일.

* 동일작업장에서 최소 2회 발견된 경우, 개선조치 취해질 때까지 중단.
 
==> 2008년 한국의 수입조건과 동일.

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Taiwan reopens to U.S. bone-in beef after 6-year ban

By Ralph Jennings Ralph Jennings – Fri Oct 23, 2:25 am ET

출처 : 로이터통신(Reuters)  Fri Oct 23, 2:25 am ET

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대만, 뼈있는 미국산 쇠고기 금수 해제

(서울=연합뉴스) 대만 정부가 뼈 있는 미국산 쇠고기에 대한 금수 조치를 해제했다.

대만 위생서는 23일 월령 30개월 미만 소에서 생산된 제품에 한해 뼈 있는 미국산 쇠고기에 대한 수입 금지 조치를 철회하기로 했다고 발표했다고 dpa 통신 등 외신들이 전했다.

   대만 정부가 금수 조치를 해제한 품목에는 소의 뇌, 등뼈 부위 등도 포함된다.

위생서는 이날 성명을 통해 “미국산 쇠고기에 대한 엄격한 평가 절차 및 위험 분석 과정을 거친 끝에, 현재 수입이 허용된 뼈 없는 쇠고기 이외의 제품에도 시장을 개방하기로 했다”고 밝혔다.

   위생서는 소비자의 불안을 감안, 뼈 있는 쇠고기의 경우 대만으로 수출되기 전 미 농무부의 검사 과정을 거치도록 할 예정이며, 미국에서 광우병 사태가 재발할 경우 금수 조치를 재개할 것이라고 강조했다.

   뼈 있는 쇠고기의 경우 통상 광우병으로 알려진 BSE(소해면양뇌증) 감염 부위가 포함될 가능성이 훨씬 높은 것으로 알려져 있다.

   앞서 대만 정부는 미국에서 광우병에 걸린 소가 발견된 직후인 지난 2003년 12월 미국산 쇠고기에 대한 금수 조치를 취한 바 있다.

   대만 정부는 이후 2006년 뼈 없는 미국산 쇠고기 대한 금수 조치를 해제했으나, 뼈 있는 쇠고기에 대해서는 수입 금지 방침을 유지해 왔다.

   대만 정부가 6년 만에 미국산 뼈 있는 쇠고기에 대한 금수 조치를 해제하자, 미국은 즉각 환영 입장을 밝혔다.

   대만 주재 미국대표부의 대변인은 대만 정부의 조치를 환영한다고 밝히면서, 대만 정부의 금수 철회는 국제 기준에 따른 과학적 판단에 의한 것이라고 평가했다.

   반면 대만소비자재단은 정부가 미국의 정치적 압력에 굴복해 국민의 동의도 구하지 않고 미국산 쇠고기에 대한 금수 조치를 철회했다며 정부의 결정을 비난했다.

   미국은 대만 당국의 금수 조치가 있기 전까지 대만의 최대 쇠고기 공급국이었으며, 지금도 현지 쇠고기 시장에서 32%의 점유율을 보이고 있다.

   대만 정부는 뼈있는 미국산 쇠고기 수입이 재개될 경우 교역 규모가 연간 6천만달러에 이를 것으로 예상하고 있다.

   rainmaker@yna.co.kr