SEARCH VEGSOURCE:

 

 

Follow Ups | Post Followup | Back to Discussion Board | VegSource
See spam or
inappropriate posts?
Please let us know.
  




From: TSS ()
Subject: Current status of transmissible spongiform encephalopathies in ruminants 2004
Date: August 26, 2005 at 10:21 am PST

B A

S E Biotechnol. Agron. Soc. Environ. 2004 8 (4), 221–228

Current status of transmissible spongiform

encephalopathies in ruminants

Etienne Thiry ( 1 ), Claude Saegerman ( 2 ), Laurence Xambeu ( 1 ), Julie Penders ( 1 )

(1) Virology-Epidemiology. Department of Infectious and Parasitic Diseases. Faculty of Veterinary Medicine. University of

Liège. Bd de Colonster 20 B43b. B–4000 Liège (Belgium). E-mail : etienne.thiry@ulg.ac.be

(2) Secretariat of the Scientific Committee. Administration of Control Policy. Federal Agency for the Safety of the Food

Chain. World Trade Center III. Avenue Simon Bolivar 30. B–1000 Brussels (Belgium).

Transmissible spongiform encephalopathies (TSE) encompass subacute neurological degenerative diseases for which the

prototypes are scrapie in sheep and some forms of Creutzfeldt-Jakob disease in man. The emergence of a new form of TSE

in cattle in United Kingdom (UK) since 1986, namely bovine spongiform encephalopathy (BSE), sharply increased the

interest for these diseases, especially because of the epidemic nature of BSE in UK, its subsequent spread in continental

Europe and the later discovery of its zoonotic character. The number of measures of veterinary public health taken to control

the disease and to prevent its spread to animals and human beings increased in time and culminated by the total feed ban.

Indeed, since the beginning of 2001, feed containing proteins of animal origin is prohibited for the feeding of production

animals, including ruminants and monogastric species. The effect of this total ban of mammalian meat and bone meal needs

to be evaluated. The incidence of BSE has a trend to decrease in UK and in most of the other European member states.

However, as BSE is a rare event distributed in a large bovine population, it is difficult to state unambiguously whether this

trend is significant. Furthermore, the evaluation of this measure will be only effective at least five years after its introduction,

since this period is the mean incubation time of BSE. The main concern is currently the eradication of BSE in the infected

countries. Additionally, the control of scrapie is also carried out due to the possible contamination of sheep with the BSE

agent. These actions must take into account several new facts: the recent discovery of BSE cases in countries with a low

geographical BSE risk level as Japan, Canada and the United States of America (USA); the growing incidence of chronic

wasting disease, a spongiform encephalopathy observed in deer in USA; the characterization of a new pattern of bovine

amyloidotic spongiform encephalopathy in Italy, atypical scrapie cases in sheep and atypical BSE cases in cattle in Europe

and the efficacy of sheep selection based on scrapie resistant genotypes.

1. INTRODUCTION

Transmissible spongiform encephalopathies (TSE) are

a group of invariably fatal transmissible

neurodegenerative disorders, due to the accumulation

of an abnormal isoform of the host-encoded prion

protein (PrP) causing spongiform vacuolation and

neuronal loss in the central nervous system

accompanied by proliferation of astrocytes and in

some cases deposition of amyloid plaques. They have

long incubation times and are transmissible within and

between species (Lasmézas, 2003; Trevitt, Singh,

2003). However the clinical picture is not pathognomonic

of BSE and a careful differential diagnosis

is always needed (Saegerman et al., 2003; 2004).

They differ from sporadic spongiform

encephalopathies by their transmissibility (Lasmézas,

2003). Nevertheless, the diagnostic methods cannot

d i fferentiate between the two categories. T h e s e

methods rely on the identification of the prion protein,

or more precisely to its resistant form PrPres, which is

associated with infectivity. The abnormal protein is

indeed resistant to protease activity and heat

treatment. These properties are used for the diagnosis

because of the degradation of the physiological form

of the prion protein, a glycoprotein present on the

membranes of neurons and other cell types, in the

samples submitted to the diagnosis. New diagnostic

methods rely on the use of antibodies specific of the

conformation of the abnormal protein.

Although some forms of TSE are known for a long

time, as scrapie in sheep and Creutzfeldt-Jakob

disease (CJD) in man, bovine spongiform

encephalopathy (BSE) is a newly emerged disease. Its

origin is still in debate: either the adaptation of a strain

of scrapie or the passage from a sporadic bovine case

into a TSE by recycling the agent via meat and bone

meal.

Keywords. Transmissible spongiform encephalopathy, prion, scrapie, bovine, sheep.

BSE is the most likely cause of variant CJD in man

(Bruce et al., 1997; Hill et al., 1997; Hill, Collinge,

2003). The identification of BSE as a potential

zoonosis in the nineties led to the development of a

large set of measures in order to further prevent the

spread of the agent in cattle and to enhance human

food safety. Fortunately, the incidence of the variant

CJD did not increase too much since the identification

of the first cases in 1996. However, due to the long

duration of the incubation period of this disease, new

human cases are still expected.

This paper intends to review the current

epidemiological situation of BSE in Europe and in the

world with emphasis to the evolution of its profile

over the last years. It also reviews the last

developments in the recognition of unusual disease

patterns, known as atypical BSE and scrapie forms,

and the growing importance of chronic wasting

disease in deer in North America.

2. PATHOGENESIS OF BSE

In experimental conditions, oral transmission of BSE

agent is 105 less efficient than the intracerebral route

(European Commission, 2000). Only a few

inoculation experiments have been performed.

Therefore the knowledge of the pathogenesis is still

very scarce. The currently available data can be

summarized as follows. In this paper, PrPsc refers to

the abnormal, pathologic prion protein; PrPres refers to

the fraction of PrPsc which is resistant to heat or

protease treatment and which therefore remains in the

sample after this treatment.

Oral inoculation of calves aged 4–6 months was

performed with 100 g of pooled cerebral tissues from

75 clinically affected bovines. PrPres protein can be

detected:

– from 6 to 18 months post infection (PI): in the distal

part of the ileum, especially in Peyer’s patches;

– from 10 months PI in the tonsils;

– from 32 months PI in trigeminal ganglia;

– from 36 months PI in the enteric nervous system;

– at 36–40 months of age: in the central nervous

system of clinically affected animals.

These studies suffer from a severe bias: indeed,

from 18 to 32 months of age, the stage of

neuroinvasion is unknown (Wells et al., 1998; Terry

et al., 2003).

The hypothetic pathogenesis of BSE is as follows.

The primary site of multiplication and the route of

dissemination are unknown. The distal ileum seems to

be the portal of entry. BSE agents then replicate in

cells of the reticulo-lymphocytic system at an early

stage. The infection of these cells is proven in sheep

affected by scrapie and deer affected by chronic

wasting disease. The peripheral autonomous nervous

system is susceptible to be the route of BSE towards

the central nervous system (Prince et al., 2003; Wells,

2003), as also evidenced in mouse scrapie (Kimberlin,

Walcker, 1980). Although myocytes have been found

to accumulate prion protein in scrapie-infected sheep

several months before the onset of clinical disease,

muscle infection has not been observed in BSE

infected cattle (Andreoletti et al., 2004).

3. EPIDEMIOLOGICAL SITUATION IN

EUROPE

The epidemiological situation must be envisaged

taking into account three pivotal years: the first

notification of BSE in United Kingdom (UK) in 1986,

the first diagnosis of BSE in continental Europe in

1990 in Switzerland, and the introduction of

compulsory testing of bovine carcasses in 2001 in

European member states belonging to level III of

geographical BSE risk (GBR) (Table 1).

UK experienced the emergence of BSE in 1986.

The peak incidences were recorded in 1992 and 1993.

Indeed the role of meat and bone meal was early

suspected in the transmission of BSE and the first

measures of prevention were enforced as early as

1988. The effects of these measures were visible in

1994 by a first decrease of the incidence.

Retrospectively, the analysis of the epidemic curve

allowed to estimate at five years the mean incubation

period of BSE in cattle. Therefore the shape of the

epidemic curve in UK was not the reflect of a natural

evolution of the disease but was the result of the

stringent control measures. The Over Thirty Months

Rule (OTMS), which means that all animals over 30

months of age slaughtered are proscribed for human

consumption, was introduced in UK in 1996 (Arnold,

Wilesmith, 2003). In 2003, 612 new cases of BSE

were still diagnosed. Several hypotheses are raised

about the origin of these cases: insufficient respect of

the control measures, other routes of transmission than

feeding, maternal transmission or sporadic cases, e.g.

(Figure 1).

In most of the other European member states BSE

was firstly diagnosed in the nineties. The first cases

recognized in Ireland in 1989 are explained by the

close vicinity with UK. Furthermore, the cases

diagnosed the same year in the Falkland Islands and

the Oman Sultanate are imported cases. Several

European countries declared positive cases only from

2001 (Figure 2). It is surprising that most of these

countries, although belonging to the same GBR level

as France or Belgium, for example, did not identify

cases earlier. One can speculate about the quality of

the epidemiosurveillance network which was greatly

222 Biotechnol. Agron. Soc. Environ. 2004 8 (4), 221–228 Thiry E. et al.

Current status of TSE of ruminants 223

improved in late 2000 and mostly in 2001 by the start

of the compulsory testing of carcasses at

slaughterhouses by the use of rapid tests (Pastoret et

al., 2001) (Table 2).

In non European countries, where imported cases

are excluded, the disease was identified from 2001 in

Japan and in 2003 in Canada. One case imported from

Canada was found in USA in 2004 (Table 2).

In Europe, the evolution of the annual incidence is

difficult to interpret because the cases have been

recruited from different epidemiosurveillance

networks. The Belgian situation can be taken as an

example for the other European countries. The first

case was reported in 1997. This does not preclude that

BSE affected cows could have been present in

Belgium before but not diagnosed. Until 2001, all the

cases were obtained by the clinical epidemiosurveillance

network. The two complementary

programs, testing at slaughterhouse and at rendering

plants, added cases to the incidence (Deslys et al.,

2001). It is therefore impossible to simply compare the

incidences before and after 2001 (Figure 3). The

introduction of these two programs was simultaneous

to a sharp decrease of the identification of cases by

clinical investigation on living animals.

A decrease in incidence was observed in Belgium

in 2002 and 2003. The same evolution was observed

in France and several other countries. It can be the

result of the measures taken to ban the meat and bone

meals in ruminants and other food-producing animals.

However, as BSE is a rare event distributed in a large

bovine population, it is difficult to state

unambiguously whether this trend is significant. It

must be confirmed by a steady decrease of the

incidence until 2006, i.e. five years after the start of

the total ban of mammalian meat and bone meal,

because this period is the mean incubation time of

BSE in cattle. Moreover for healthy slaughtered

animals the lower limit of age is not the same for all

countries: 24 months in France, Germany, Spain and

Italy, and 30 months in the other European countries.

This situation induces a bias in epidemiological

indicators because BSE is rarely confirmed in animals

younger than 30 months (Saegerman et al., 2003).

A d i fficult epidemiological situation is

encountered in countries which recently showed an

increase in incidence: Ireland, Spain and Portugal

(Figure 2). This feature suggests that BSE appeared

Table 1. Countries are classified in four groups following the evaluation of their geographical risk of exposure to BSE (GBR)

(European Commission, 2004b).

GBR level GBR definition European member states belonging Non European countries belonging

to the level to the level

I Highly unlikely Argentina, Australia, Botswana, Brazil,

Chile, El Salvador, Iceland, Namibia, New

Caledonia, New Zealand, Nicaragua,

Norway, Panama, Paraguay, Singapore,

Swaziland, Uruguay, Vanuatu

II Unlikely but not Sweden (in revision) Canada (in revision), Colombia, Costa Rica,

excluded India, Kenya, Mauritius, Nigeria, Pakistan,

USA (in revision)

III Likely but not Austria, Belgium, Cyprus, Czech Albania, Belarus, Former Yugoslavia,

confirmed or Republic, Denmark, Estonia, Finland Principality of Andorra, Bulgaria, Croatia,

confirmed, at a France, Germany, Greece, Hungary, Israel, Japan, Macedonia, Romania,

lower level Ireland, Italy, Latvia, Lithuania, San Marino, Switzerland, Turkey

Luxembourg, Malta, Netherlands,

Poland, Slovakia, Slovenia, Spain

IV Confirmed at a Portugal, United Kingdom

higher level

40000

35000

30000

25000

20000

15000

10000

5000

0

Year

F i g u re 1 . Annual incidence of BSE cases in United

Kingdom since the emergence in 1986 (Office international

des Epizooties, 2004).

224 Biotechnol. Agron. Soc. Environ. 2004 8 (4), 221–228 Thiry E. et al.

later in these countries and makes therefore impossible

to speculate about an effective control of BSE in these

countries.

4. SUBCLINICAL CASES

Both experimental and field data support the existence

of subclinical forms of TSEs (Hill, Collinge, 2003).

These subclinical cases can have various origins:

crossing of the species barrier, resistant genotype,

prolonged incubation period, e.g. The epidemiosurveillance

in European countries reveals that most of

the BSE cases reported since 2001 have been

identified by the systematic sampling in

slaughterhouses. Other animals were identified in the

rendering plants, therefore suggesting a disease

causing death. Therefore all these animals were not

recruited by the clinical epidemiosurveillance

network. Those reported positive at abattoirs can be

considered as subclinically infected at the time of

slaughter or it may be that they had very faint clinical

signs. As shown in figure 3, most of the detected BSE

cases are therefore animals in good condition, without

clinical signs or only very few. It is indeed impossible

to predict if these animals would have developed

clinical BSE if they were kept alive. It cannot be

excluded that they could constitute later on a cohort of

Figure 2. Annual incidence rates of BSE per million bovines of over 24 months of age in all countries which reported cases

from 1999 to 2003 except United Kingdom. Some figures are so low that they are not or hardly visible in the diagram. It is

the case for Austria (0.96 in 2001), for Canada (0.16 in 2003), for Denmark (1.14 in 2000), for Germany (1.07 in 2000), for

Japan (1.44 in 2001, 0.97 in 2002), for the Netherlands (1.03 in 1999, 1.07 in 2000), for Poland (1.28 in 2002, 1.49 in 2003)

and for Spain (0.59 in 2000). On the other hand, Portugal experienced high BSE incidences reaching figures that fall outside

the scale of the graph: 199.50 in 1999, 186.95 in 2000, 137.88 in 2001, 107.80 in 2002 and 137.19 in 2003. The reported data

are raw rates. Indeed, depending on the country, the minimum age of tested carcasses at slaughterhouse may vary: Germany

performs a voluntary testing under 24 months of age and a compulsory testing over 24 months; France, Italy and Spain have

a compulsory testing over 24 months and the other European member states over 30 months. These variations must be taken

into account if the epidemiological situations are compared (European Commission, 2004a; Office International des

Epizooties, 2004).

100

90

80

70

60

50

40

30

20

10

0

Country

1999

2000

2001

2002

2003

Table 2. Year of first diagnosis of bovine spongiform

encephalopathy (Office International des Épizooties, 2004).

Year Country

1986 United Kingdom

1989 Ireland, Oman Sultanate (2 imported cases)

Falkland Islands (imported case)

1990 Switzerland

1991 France

1994 Portugal

1997 Belgium

1998 Netherlands

2000 Germany, Denmark, Spain

2001 Austria, Czech Republic, Finland, Greece, Italy

Japan, Slovakia, Slovenia

2002 Israel, Luxemburg, Poland

2003 Canada

2004 USA (imported case)

Current status of TSE of ruminants 225

animals which segregates from the typical BSE cases.

Furthermore some of the atypical cases reported in the

following sections could be also part of the subclinical

cases.

5. ATYPICAL BOVINE SPONGIFORM

ENCEPHALOPATHIES

The epidemiosurveillance network which was set up

in Europe and several other non European countries

identifies hundred of BSE and scrapie cases every

year. Strain variation was already demonstrated for

s c r a p i e agent, but not for BSE so far. The recent

identification of atypical cases could modify the

epidemiology of BSE if these cases are attributed to

new strains. Furthermore, these new data add to the

complexity of the system and reveal that other situations

can be encountered in natural conditions than those

observed during the first phases of the BSE epidemic.

5.1. Atypical BSE cases in Japan

Since 2001, all cattle slaughtered at abattoirs in Japan

are screened for BSE using a rapid test. A 23 months

old steer was detected positive at the slaughterhouse.

It was apparently healthy before slaughter. T h e

histology showed no spongiform changes and

immunohistochemistry revealed no accumulation of

PrPres typical of BSE. The analysis of PrPres from the

obex region revealed an electrophoretic profile

different from the typical cases: the low content of the

diglycosylated form, a faster migration of the non

glycosylated form and less resistance against protease

digestion than typical cases (Yamakawa et al., 2003).

5.2. Atypical BSE cases in France

Three cases among those diagnosed at the

slaughterhouse (two cases) and rendering plants (one

case) in animals over 24 months old were confirmed

BSE positive by Western blot detection of PrPres

extracted from the brain stem. These three samples

showed relatively low levels of PrPrres. They showed a

atypical electrophoretic profile: it was mainly

characterized by a higher molecular mass of the

unglycosylated PrPres. The same profile was identified

previously in a cattle which had been experimentally

inoculated intracerebrally with scrapie; however no

genetic polymorphism was observed between atypical

and typical BSE cases. The three apparently healthy

cows were aged 8, 10 and 15 years, respectively.

The explanations of these atypical cases are still

hypothetical: cattle may have been infected by another

source of TSE agent like scrapie agent from sheep or

goat; another possibility could rely on sporadic cases

of BSE, as it has been already demonstrated in humans

with CJD (Biacabe et al., 2004).

5.3. Atypical BSE cases in Italy

Two healthy cows aged 11 and 15 years were positive

among other cattle by histopathology, Western blot

and immunohistochemistry. They exhibited however

distinct features as predominance of the low molecular

weight glycoform and a PrPres fragment of lower

molecular weight, as identified by Western blot.

A d d i t i o n a l l y, the pattern of PrPs c deposits was

different in the central nervous system: the two cases

showed large PrPs c aggregates and dense PrPs c

amyloid plaques, instead of the amyloid deposition in

typical BSE cases. Furthermore, the localization of the

lesions was different in the brain. Therefore these

cases are called bovine amyloidotic spongiform

encephalopathy (BASE). This phenotype was

unrecognized previously in BSE positive cattle. BASE

was observed in old cows and shows similarities with

a distinct subtype of sporadic CJD in humans

(Casalone et al., 2004).

5.4. Atypical BSE case in Belgium

A slaughtered 64 months old cow was positive in the

abattoir by the rapid test. Further testing was carried

30

25

20

15

10

5

0

1997 1998 1999 2000 2001 2002 2003

Year

Figure 3. Incidence of BSE cases in Belgium, from the first

case in 1997 till 2003, following the three networks of

epidemiosurveillance: clinical suspicions identified in the

field; carcasses over 30 months of age tested at slaughterhouse

and over 24 months of age tested at rendering plants,

which started in 2001. All cases were confirmed by the

histopathological examination, immunohistochemistry and

search for scrapie associated fibrils (Federal Agency for the

Safety of the Food Chain, 2004).

Clinical suspicion

Slaughterhouse

Rendering

226 Biotechnol. Agron. Soc. Environ. 2004 8 (4), 221–228 Thiry E. et al.

out on this case. No spongiform changes were

observed by histopathology, no PrPsc accumulation

was seen by immunohistochemistry and the search for

scrapie-associated fibrils was negative. Western blot

testing was however positive, but the electrophoretic

profile of PrPsc was different from typical BSE cases.

This atypical case is very similar to those already

identified in Japan (De Bosschere et al., 2004b).

6. RESISTANCE TO SCRAPIE AND ATYPICAL

CASES IN SHEEP

Scrapie is not transmitted from sheep to humans. The

human risk is associated with a possible exposure of

sheep to BSE-contaminated feed. Since 2002,

European Union has initiated a scrapie program:

among several measures, the genotyping of 1% of the

sheep population must be performed. Furthermore, it

is also possible to select in the sheep population

animals which exhibit a genotype resistant to scrapie.

This genotype relies on amino acid substitutions in the

PrPsequence, in positions 136, 154 and 171. The most

resistant sheep belong to the genotype ARR/ARR1.

However, several studies revealed that their resistance

is not absolute. A few percentage of these resistant

animals can be effectively infected by the scrapie

agent (Ikeda e t a l ., 1995). Furthermore, one

ARR/ARR1 sheep died after intracerebral inoculation

of BSE agent (Houston et al., 2003).

A positive effect of this new surveillance program

is the increase of the number of analyses. Among the

positive results obtained, new scrapie cases were

identified from sheep possessing a highly resistant

genotype ARR/ARR1 (Agence française de sécurité

sanitaire des aliments, 2004). However there is no

indication of a link between these cases and BSE.

Several atypical cases of scrapie were identified in

Norway since 1998 (Benestad et al., 2003). Recently

a similar case was diagnosed in Belgium (De

Bosschere e t a l ., 2004a). These sheep possess

genotypes which are rarely associated with scrapie

(AHQ/AHQ1; AHQ/ARQ1). They also do not show

the typical histopathological brain lesions.

Furthermore, other possible atypical scrapie cases in

France and Germany can be missed by the usual rapid

tests (Buschmann et al., 2004) and their identification

requires therefore very sensitive methods.

7. CHRONIC WASTING DISEASE IN CERVIDS

A chronic wasting disease is described in the USA

since 1967 in three deer species: mule deer

(Odocoileus hemionus), white-tailed deer (Odocoileus

virginianus) and Rocky Moutain elk (Cervus elaphus

nelsoni). This disease is also a TSE (Miller, Williams,

2003). It remained for many years as a scientific

curiosity but recently the interest in this disease grew

due to the emergence of BSE and an increase of the

incidence and the geographic distribution of the

disease. The death of three hunters by CJD in 2003

was enough to produce a "mediatic" emergence in the

USA although no link was evidenced with chronic

wasting disease and a human TSE. The disease is not

observed outside North America.

8. CONCLUSIONS

After the initial BSE epidemic in Europe, the current

trend is a decrease in incidence in most European

countries. Fortunately, the number of variant CJD

cases is kept low although any human case is

dramatic. However, the relatively high number of BSE

positive animals in UK and the increase in incidence

in a few European member states require to maintain

a high level of epidemiosurveillance. The continuous

surveillance of BSE and scrapie reveals now the

existence of so called "atypical cases" which need a

careful attention.

TSEs are still emerging diseases. Although the

scientific knowledge is steadily increasing, many

aspects of the pathogenesis and the epidemiology of

these diseases remain to be elucidated. However,

efficient control measures were enforced in most of

the European member states. Every measure which

can improve the detection of infected animals and the

quality and the respect of the feed ban is a step

towards eradication of BSE in cattle.

Acknowledgements

This work is financially supported by a grant from the

"Service public fédéral, santé publique, sécurité de la

chaîne alimentaire et environnement. Fonds budgétaire

pour la santé et la qualité des animaux et des produits

animaux". The authors thank Dr S. Roels (CERVA-CODA,

Brussels) for providing them with in press papers. C. Espert

is acknowledged for her help in the preparation of the

manuscript.

Bibliography

Agence française de sécurité sanitaire des aliments.

Communiqué de presse de l’Agence française de

sécurité sanitaire des aliments relatif à la mise en

évidence de cas de tremblante chez des animaux de

génotype résistant ARR/ARR. 9 janvier 2004,

[28/05/04], Available 1 One letter IUPAC code for amino acids with A = a l a n i n e ,

H = histidine, R = arginine and Q = glutamine.

Current status of TSE of ruminants 227

actu/CommuniqueARR90104.pdf>

A n d r e o l e t t i O., Simon S., Lacroux C., Morel N . ,

Tabouret G., Chabert A., Lugan S., Corbiere F., Ferre P.,

F o u c r a s G., Laude H., Eychenne F., Grassi J . ,

Schelcher F. (2004). PrP(Sc) accumulation in myocytes

from sheep incubating natural scrapie. Nat. Med. 10,

p. 591–593.

A r n o l d M., Wi l e s m i t h J. (2003). Modelling studies on

bovine spongiform encephalopathy occurrence to assist

in the review of the over 30 months rule in Great

Britain. P roc. R. Soc. London B. Biol. Sci. 2 7 0,

p. 2141–2145.

B e n e s t a d SL., Sarradin P., T h u B., Schonheit J . ,

Tranulis MA., Bratberg B. (2003). Cases of scrapie with

unusual features in Norway and designation of type,

Nor98. Vet. Rec. 153, p. 202–208.

Biacabe AG., Laplanche JL., Ryder S., Baron T. (2004).

Distinct molecular phenotypes in bovine prion diseases.

EMBO Rep. 5 (1), p. 110–115.

B r u c e ME., Wi l l RG., Ironside J W., Mc C o n n e l l I . ,

D r u m m o n d D., Suttie A., Mc C a r d l e L., Chree A . ,

Hope J., Birkett C., Cousens S., Fraser H., Bostock CJ.

(1997). Transmissions to mice indicate that "new

variant" CJD is caused by the BSE agent. Nature 389,

p. 498–501.

B u s c h m a n n A., Biacabe AG., Ziegler U., Bencsik A . ,

M a d e c J Y., Erhardt G., Lühken G., Baron T. ,

G r o s c h u p MH. (2004) Atypical scrapie cases in

Germany and France are identified by discrepant

reaction patterns in BSE rapid tests. J. Virol. Methods

117, p. 27–36.

Casalone C., Zanusso G., Acutis P., Ferrari S., Capucci L.,

Ta g l i a v i n i F., Monaco S., Caramelli M. (2004).

Identification of a second bovine amyloidotic

spongiform encephalopathy: molecular similarities with

sporadic Creutzfeldt-Jakob disease. Proc. Natl. Acad.

Sci. U S A 101, p. 3065–3070.

D e B o s s c h e r e H., Roels S., Benestad S L . ,

Vanopdenbosch E. (2004a). A Nor98 case diagnosed in

Belgium via active surveillance. Vet. Rec. in press.

De Bosschere H., Roels S., Va n o p d e n b o s c h E. (2004b).

Atypical case of bovine spongiform encephalopathy in

an East-Flemish cow in Belgium. J. Appl. Res. Vet. Med.

2, in press.

Deslys JP., Comoy E., Hawkins S., Simon S., Schimmel H.,

We l l s G., Grassi J., Moynagh J. (2001). Screening

slaughtered cattle for BSE. Nature 409, p. 476–478.

European Commission (2000). Preliminary opinion on the

oral exposure of humans to the BSE agent: infective

dose and species barrier, adopted by the Scientific

Steering Committee at its meeting of 2–3 March 2000.

Brussels: European Commission, Scientific Steering

Committee, Health and Consumer Protection

Directorate General, 53 p.

European Commission (2004a). Report on the monitoring

and testing of ruminants for the presence of

transmissible spongiform encephalopathy (TSE) in the

EU in 2003, including the results of the survey of prion

protein genotypes in sheep breeds. Document 04-D-

42525, May 2004. Brussels: European Commission,

Health and Consumer Protection Directorate General,

84 p.

European Commission (2004b). [01/06/04] Av a i l a b l e

< h t t p : / / e u r o p a . e u . i n t / c o m m / f o o d / f s / s c / s s c / o u t c o m e _ e n .

html>

Federal Agency for the Safety of the Food Chain.

[15/05/04] Available

Hill AF., Debruslais M., Joiner S., Sidle KC., Gowland I.,

Collinge J., Doey LJ., Lantos P. (1997). The same prion

strain causes vCJD and BSE. Nature 389, p. 448–450.

Hill AF., Collinge J. (2003). Subclinical prion infection in

humans and animals. Br. Med. Bull. 66, p. 161–170.

H o u s t o n F., Goldmann W., Chong A., Jefff r e y M . ,

Gonzalez L., Foster J., Parnham D., Hunter N. (2003).

Prion diseases: BSE in sheep bred for resistance to

infection. Nature 423, p. 498.

I k e d a T., Horiuchi M., Ishiguro N., Muramatsu Y., Kai-

U w e GD., Shinagawa M. (1995). Amino acid

polymorphisms of PrPwith reference to onset of scrapie

in Suffolk and Corriedale sheep in Japan. J. Gen. Virol.

76, p. 2577–2581.

K i m b e r l i n RH., Wa l c k e r CA. (1980). Pathogenesis of

mouse scrapie: evidence of neural spread of infection to

the CNS. J. Gen. Virol. 51, p. 183–187.

L a s m é z a s CI. (2003). The transmissible spongiform

encephalopathies. Rev. Sci. Techn. Off. Int. Epiz. 22 (1),

p. 23–36.

M i l l e r M W., Wi l l i a m s ES. (2003). Horizontal prion

transmission in mule deer. Nature 425, p. 35–36.

Office International des Epizooties. [15/05/04] Available

P a s t o r e t P P., Gouff a u x M., Saegerman C., Roels S . ,

Dechamps P., Thiry E., Vanopdenbosch E. (2001). Le

diagnostic immunologique rapide des encéphalopathies

spongiformes transmissibles. Ann. Méd. Vét. 1 4 5,

p. 164–173.

P r i n c e MJ., Bailey JA., Barrowman PR., Bishop K J . ,

Campbell GR., Wood JM. (2003). Bovine spongiform

encephalopathy. Rev. Sci. Techn. Off. Int. Epiz. 22 (1),

p. 37–60.

S a e g e r m a n C., Claes L., Dewaele A., Desmecht D . ,

Rollin F., Hamoir J., Gustin P., Czaplicki G., Bughin J.,

Wu l l e p i t J., Laureyns J., Roels S., Berkvens D . ,

Va n o p d e n b o s c h E., T h i r y E. (2003). Diff e r e n t i a l

diagnosis of neurologically expressed disorders in

Western European cattle. Rev. Sci. Techn. Off. Int. Epiz.

22 (1), p. 83–102.

S a e g e r m a n C., Speybroeck N., Roels S . ,

Va n o p d e n b o s c h E., T h i r y E., Berkvens D. (2004).

Decision support tools for clinical diagnosis of disease

in cows with suspected bovine spongiform

encephalopathy. J. Clin. Microbiol. 42, p. 172–178.

228 Biotechnol. Agron. Soc. Environ. 2004 8 (4), 221–228 Thiry E. et al.

Te r r y LA., Marsh S., Ry d e r SJ., Hawkins S A C . ,

Wells GAH., Spencer YI. (2003). Detection of diseasespecific

PrP in the distal ileum of cattle exposed orally

to the agent of bovine spongiform encephalopathy. Vet.

Rec. 152, p. 387–392.

Trevitt CR., Singh PN. (2003). Variant Creutzfeldt-Jakob

disease: pathology, epidemiology, and public health

implications. Am. J. Clin. Nutr. 78 ( s u p p l ) ,

p. 651S–656S.

Wells GA. (2003). Pathogenesis of BSE. Vet. Res. Commun.

27 (Suppl 1), p. 25–28.

We l l s GAH., Hawkins SAC., Green RB., A u s t i n A R . ,

D e x t e r I., Spencer YI., Chaplin MJ., Stack M J . ,

Dawson M. (1998). Preliminary observations on the

pathogenesis of experimental bovine spongiform

encephalopathy (BSE) : an update. Vet. Rec. 1 4 2,

p. 103–106.

Ya m a k a w a Y., Hagiwara K., Nohtomi K., Nakamura Y. ,

N i s h i j i m a M., Higuchi Y., Sato Y., Sata T., Expert

Committee for BSE Diagnosis, Ministry of Health,

Labour and Welfare of Japan (2003). A t y p i c a l

proteinase K-resistant prion protein (PrPres) observed in

an apparently healthy 23-month-old Holstein steer.

Japan. J. Infect. Dis. 56 (5-6), p. 221–222.

(32 ref.)

http://www.bib.fsagx.ac.be/library/base/text/v8n4/221.pdf

TSS




Follow Ups:



Post a Followup

Name:
E-mail: (optional)
Subject:

Comments:

Optional Link URL:
Link Title:
Optional Image URL: