건강과 대안 » SPECIES BARRIER

[구제역] Foot and mouth disease: the human consequences

건강과대안 — Mon, 27 Dec 2010 16:59:21 +0000

BMJ. 2001 March 10; 322(7286): 565–566.

PMCID: PMC1119772

Foot and mouth disease: the human consequences

The health consequences are slight, the economic ones huge

Henry Prempeh, specialist registrar public health medicine

Robert Smith, clinical scientist (zoonoses)

(Email: robert.smith@cdsc.wales.nhs.uk

)

Berit Müller, epidemiologist

PHLS Communicable Disease Surveillance Centre, London NW9 5EQ

This article has been cited by other articles in PMC.

The current major outbreak of foot and mouth disease (FMD) is the latest in a series of disasters that are putting British agriculture under stress.¹ The disease affects all cloven-hoofed animals and is the most contagious of animal diseases. It is caused by a virus of the family Picornaviridae, genus Aphthovirus, of which there are seven serotypes (O, A, C, SAT1, SAT2, SAT3, and Asia1). The current outbreak in the United Kingdom is due to the highly virulent pan-Asiatic serotype O.¹ In animals the disease presents with acute fever, followed by the development of blisters chiefly in the mouth and on the feet. Infected animals secrete numerous virus particles before clinical signs appear.²

Foot and mouth disease is a zoonosis, a disease transmissible to humans, but it crosses the species barrier with difficulty and with little effect. Given the high incidence of the disease in animals, both in the past and in more recent outbreaks worldwide, its occurrence in man is rare³ so experience of the human infection is limited. The last human case reported in Britain occurred in 1966, during the last epidemic of foot and mouth disease.⁴ The circumstances in which it does occur in humans are not well defined, though all reported cases have had close contact with infected animals. There is one report from 1834 of three veterinarians acquiring the disease from deliberately drinking raw milk from infected cows.⁵ There is no report of infection from pasteurised milk, and the Food Standards Agency considers that foot and mouth disease has no implications for the human food chain.

The type of virus most often isolated in humans is type O followed by type C and rarely A. The incubation period in humans is 2-6 days. Symptoms have mostly been mild and self limiting, mainly uncomfortable tingling blisters on the hands but also fever, sore throat, and blisters on the feet and in the mouth, including the tongue.³ Patients have usually recovered a week after the last blister formation. In the unlikely event of human cases in the current outbreak in Britain they should be reported to the Communicable Disease Surveillance Centre (0208 200 6868) duty doctor, who can direct professional inquiries towards expert advice on management and diagnosis.² Suspected and confirmed human cases must have no contact with susceptible livestock to avoid transmitting the disease. Person to person spread has not been reported.

Foot and mouth disease should not be confused with the human disease hand, foot, and mouth disease. This is an unrelated and usually mild viral infection, principally of children, caused by different viruses, principally coxsackie A virus.⁶

Foot and mouth disease is endemic in many countries, including much of Africa, Asia, and South America, where its importance relates to the reduced productivity of livestock, the cost of vaccination, and the restrictions placed on international trade in live animals and animal products.⁷ To be listed among the “FMD free countries where vaccination is not practised” the Office International des Epizooties, the international regulatory body concerned with animal infections,⁸ requires a country to have a record of regular and prompt animal disease reporting and to supply documented evidence of an effective system of surveillance. Such a country should also not import animals vaccinated against foot and mouth disease⁹ since serological testing cannot differentiate between infected and vaccinated animals. A “foot and mouth free zone” may be established in a country in which parts are infected, separated from the rest by a buffer zone.

As international trade barriers become increasingly subject to scrutiny, foot and mouth disease remains one of the few remaining constraints to international trade in live animals and animal products. The occurrence of even a single case of foot and mouth disease in a previously disease free country results in an immediate ban on an economically valuable export trade. The European Commission in 1990-1, after undertaking a cost benefit analysis, implemented a policy of non-vaccination to increase export opportunities and to ensure high animal health standards.¹⁰ This outbreak containment policy requires an export ban on all livestock and animal products from any affected country, along with movement restrictions and the slaughter and burning of all cloven-hoofed animals that are either infected, on infected premises, or in contact with infected animals. Until now the European Union has remained free of foot and mouth disease since an outbreak in Greece in 1996.

The highest risk to European Union countries is through legal and illegal imports of infected live animals and contaminated meat or dairy products from infected countries then being eaten by animals. International travellers bringing back food from endemic countries could spread the disease. The foot and mouth disease virus can survive for long periods in a range of fresh, partially cooked, cured, and smoked meats and in inadequately pasteurised dairy products. Currently animals and animal products need to be checked only when they enter the European Union. Once inside, and with correct documentation, they can be moved around without restriction. For these reasons other countries have banned the import of animal products from the UK.

Spread of the virus is facilitated by the development of long distance animal trading. Dense livestock populations may also enhance local spread in the vicinity of an outbreak. Awareness of the disease among livestock owners is crucial, as are the UK’s excellent diagnostic facilities. Spread can take place on the wind and mechanically by the movement of animals, people, and vehicles that have been contaminated with the virus. Thus the whole British population has a role in combating the disease. Restriction of non-essential movement both into and out of affected farms and more widely in the countryside is important. This is requiring close collaboration between veterinary, health, and local authorities. If these measures are not successful, however, the major review of safeguards announced by the agriculture minister may lead to major changes in animal husbandry in the UK.¹¹

References

1. Ministry of Agriculture, Fisheries, and Food. Foot and mouth disease – FAQ [online]. London: MAFF; 2001. www.maff.gov.uk/animalh/diseases/fmd/qa1.htm . (Accessed 05 March 2001). This site is being regularly updated during this outbreak.

2. Foot and mouth disease outbreak- no threat to public health. Commun Dis Rep CDR Wkly. 2001;11:1–2.

3. Bauer K. Foot-and-mouth disease as zoonosis. Arch Virol. 1997;13 (suppl):95–97.

4. Armstrong R, Davie J, Hedger RS. Foot-and-mouth disease in man. BMJ. 1967;4:529–530. [PMC free article] [PubMed]

5. Hertwig CA. ?bertragung tierischer Ansteckungsstoffe auf den Menschen. Med Vet Z 1834;48.

6. Chin J, editor. Control of communicable diseases manual. 17th ed. Washington, DC: American Public Health Association; 2000. Coxsackievirus diseases; pp. 129–131.

7. Donaldson AI, Doel TR. Foot-and-mouth disease: the risk for Great Britain after 1992. Vet Record 1992; 8 Aug;131:114-20.

8. Kitching RP. Foot and mouth disease: current world situation. Vaccine. 1999;17:1772–1774. [PubMed]

9. Recommendations applicable to specific diseases: Foot and mouth disease International Animal Health Code – 2000. Paris: Office International des Epizooties; 2000.

10. Report from the Commission to the Council on a study carried out by the Commission on policies currently applied by Member States in the control of foot-and-mouth disease. Brussels: CEC; 1989.

11. Minister of Agriculture, Fisheries, and Food. Foot and mouth disease: thorough review of measures to reduce disease risk [online]. 2001. p. 3.http://www.maff.gov.uk/inf/newsrel/2001/010303a.htm Mar. http://www.maff.gov.uk/inf/newsrel/2001/010303a.htm.

[광우병] 종간장벽에 대한 미 농무부의 자료

건강과대안 — Sun, 09 Aug 2009 12:22:23 +0000

광우병 인자의 소-인간 종간장벽에 대한 미 농무부 동식물검역청의 자료

일반적으로 종간 장벽은 1(감소가 전혀 나타나지 않음)에서 1000 사이의 범위에 있는 인자(因子)에 따라 전염의 효능성을 감소시키는 것으로 추정된다. 종간장벽이 1(즉, 효과적인 종간장벽이 전혀 없다는 말이다) 이라는 가정은 최악의 사례가 되는 시나리오로 간주된다. 소에게서 인간에게로 광우병 전염에 대한 종간장벽에 대한 의견 중에는 EU 과학전문가위원회가 1에서 10만 사이의 전염 효능 범위에 대한 종간 장벽의 영향을 가능성 있는 변수로 평가한 것이 있다. 이 범위는 훗날 10에서 10만 사이로 업데이트 되었다. 그러나 EU 과학전문가위원회는 현재까지 알려진 과학지식의 범위 내에서 소와 인간사이의 광우병 종간장벽의 참값을 측정하는 것은 불가능하다는 결론을 내렸다.

(이 내용은 EU과학전문가위원회의 업데이트된 종간장벽 내용을 약간 왜곡했다고 판단됩니다. 왜냐하면 EU과학전문가위원회는 훗날(2000년을 가리킵니다) 종간장벽에 관한 내용을 업데이트하면서 과학적 데이터가 서로 상충되고 불확실성이 존재할 경우 종간장벽을 1로 간주하는 가정을 반드시 포함시켜야 한다고 결론에서 명시적으로 밝혔기 때문입니다.)

제목 : Evaluation of the Potential for Bovine Spongiform Encephalopathy in the United States
(Harvard Center for Risk Analysis Harvard School of Public Health, November 26, 2001)
(전문은 첨부파일 참조)

출처 : 미 농무부 동식물검역청 자료
http://www.aphis.usda.gov/newsroom/hot_issues/bse/background/documents/mainreporttext.pdf

2.1.2 The Species Barrier (7쪽~8쪽)

Interspecies transmission of TSEs is mitigated by a so called “species barrier”. This
barrier represents the decreased efficiency with which TSEs are passed from one animal to a
second animal of a different species, compared with the efficiency with which the TSE is passed among animals of the same species. That is, a much greater amount of infective material is necessary to infect an animal from a different species than is needed to pass the disease to an animal of the same species. The species barrier is also associated with an increase in the disease’s incubation period (i.e., the delay between exposure to the agent resulting in infection and the manifestation of disease). In some instances the species barrier seems to confer complete resistance to transmission. It is at least conceptually possible that an animal failing to develop the disease following cross species challenge would become infected if administered a sufficiently large dose of infectivity, or would manifest clinical signs of disease if it somehow lived longer than the incubation period associated with the species barrier (Hill et al., 2000).

Although transmission of a TSE from one species to another may be less efficient than
the transmission within the same species, once it occurs, the TSE may become “adapted” to the new host. Because it has adapted to the new species, it can be transmitted more efficiently among members of that species, and the incubation period becomes shorter and less variable. For example, when scrapie is transmitted experimentally from one species to another, the incubation period is usually longer in the first passage than that seen in subsequent passages within the new species (Dickinson et al., 1976).

The species barrier probably reflects some combination of factors including differences
between the donor’s and recipient PrP. Scrapie studies conducted in mice, rats, and hamsters demonstrate the presence of a species barrier. These findings include pathogenesis differences between the first and subsequent passages in the new species, and how rapidly the transmitted strain replicates in the new host (Kimberlin et al., 1987, Kimberlin and Walker, 1989), and others.

The response of some TSEs exhibits heterogeneity within a species, a characteristic that
appears to be due to the existence of different strains of the agent. Strains are distinguished by highly replicable differences in the incubation period, neuropathology, and host range (Fraser and Dickinson, 1968, Bruce et al., 1989). CJD, scrapie, TME, and CWD show strain diversity, while BSE appears to be a single, stable strain (Bruce et al., 1994, Bruce et al., 1997). vCJD (i.e., the new form of CJD related to exposure to the BSE agent) does not demonstrate morphologic strains (Will et al., 1996, Hill et al., 1997, Bruce et al., 1997, Scott et al., 1999).

Recipient characteristics also affect the efficiency with which TSEs are transmitted
across species. Some species, such as rabbits or chickens, do not develop disease when
challenged with specific TSEs, while other species do. It has been postulated that the similarities between the PrP structure between the donor and the recipient explain the differences in transmission efficiency (Priola et al., 1994, Raymond et al., 2000).

Because the presence of a TSE agent is often assessed by inoculating a test species (e.g.,
mice) with the suspect material, the species barrier compromises the sensitivity of these
bioassays. Cattle-to-cattle transmission of BSE by the intracerebral route is known to be 1,000 times more efficient than cattle-to-mouse transmission by the same route (MAFF, 2000b). It is often assumed that the species barrier decreases transmission efficiency by a factor of between 1(no decrease) and 1,000 (Det Norske Veritas, 1997). The assumption that the species barrier is 1(i.e., that there is effectively no species barrier) is considered to be a worst-case scenario. In an opinion on the species barrier for transmission of BSE from cattle to humans, the EU Scientific Steering Committee suggested that plausible values for the impact of the species barrier on transmission efficiency range from between 1 and 100,000 (SSC, 1999a). This range was later updated to between 10 and 100,000 (SSC, 2000b). However, the committee concluded that it is impossible to estimate the true value for BSE species barrier between cattle and humans within an order of magnitude given current knowledge (SSC, 2000b).

[광우병] 광우병 원인물질의 인간에 대한 경구 노출 : 감염량 및 종간장벽

건강과대안 — Sun, 09 Aug 2009 12:15:50 +0000

유럽과학전문가위원회에서 2000년에 발표한 의견서인 [광우병 원인물질의 인간에 대한
경구 노출 : 감염량 및 종간장벽]의 결론 35쪽에 “제시된 서로 상충되는 과학적 데이터와
이번 문서 속에 소개된 소-인간의 종간장벽의 불확실성을 고려할 때, 비록 입수할 수
있는 증거가 현실적으로 종간장벽 수치가 1보다 훨씬 높을 것 같다고 하더라도,
종간장벽을 1로 간주 하는 최악의 사례 시나리오에 대한 가정을 반드시 포함시켜야 한다.”고
명시적으로 밝히고 있습니다.

다시 말해 과학적 데이터가 상충되고 불확실성이 있는 상황에서는 종간장벽을 1로 간주하는
최악의 시나리오를 반드시 포함시켜 예방대책을 세워야 한다는 것을 유럽과학전문가
위원회에서 명시적으로 밝힌 중요한 문서라고 할 수 있습니다.

ORAL EXPOSURE OF HUMANS TO THE BSE AGENT:
INFECTIVE DOSE AND SPECIES BARRIER (전문은 첨부파일 참조)

출처 : EU Scientific Steering Committee(6 AND 27 MARCH 2000)

p35

Given the conflicting scientific data and thus the uncertainties about the bovineto-
human species barrier as outlined in this document, the assumption of a worst
case scenario considering no (=1) barrier should be included, although available
evidence indicates that values greater than 1 are likely to be more realistic.