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Effect of cobalt supplementation on serumvitamin B12 levels, weight gain and survival rate inlambs grazing cobalt‐deficient pastures

P. Vellema , L. Moll , H.W. Barkema & Y.H. Schukken

To cite this article: P. Vellema , L. Moll , H.W. Barkema & Y.H. Schukken (1997) Effectof cobalt supplementation on serum vitamin B12 levels, weight gain and survivalrate in lambs grazing cobalt‐deficient pastures, Veterinary Quarterly, 19:1, 1-5, DOI:10.1080/01652176.1997.9694727

To link to this article: http://dx.doi.org/10.1080/01652176.1997.9694727

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EFFECT OF COBALT SUPPLEMENTATION ON SERUM VITAMINB12 LEVELS, WEIGHT GAIN AND SURVIVAL RATE IN LAMBSGRAZING COBALT-DEFICIENT PASTURES

P. Vellema1,2, L. Moll1, H.W. Barkema1 and Y.H. Schukken3 Vet Quart 1997; 19: 1-5

Original Papers

SUMMARYThe effect of cobalt supplementation on serum vitaminB129 growth rate and survival rate was measured in con-trolled field experiments with Texel twin lambs of thesame sex, grazing cobalt-deficient pastures.The non-supplemented lambs had lower serum vitaminB12 concentrations than their supplemented brothers orsisters. During the experiments more lambs died in thenon-supplemented than in the supplemented group. Atthe end of the experiments supplemented lambs weighed(mean live weight) 7.2, 9.5, and 11.0 kg more than non-supplemented lambs in 1991, 1992, and 1993, respec-tively.Sex-related differences in weight gain and survival ratewere observed.

INTRODUCTIONIll-thrift diseases of sheep have been described in severalparts of the world (3). Diseased animals fail to thrive despitegrazing lush pasture, lose weight, and show listlessness, in-appetence, and serous ocular discharge. The role of cobalt inpreventing and curing this disease was demonstrated in 1935by Marston (10), who also suggested that many differentlynamed diseases of growing lambs probably had the sameaetiology.In 1972 a hitherto unrecognized disease of weaned lambs oc-curred almost simultaneously on three farms in the Nether-lands (28). The lambs showed, in addition to the above-mentioned symptoms, signs of acute photosensitization.Some lambs died, and on post-mortem examination theirlivers were swollen and sometimes pale. Because of the his-tological changes in the liver, Wensvoort and Herweijer (28)called this condition chronic hepatitis, the cause of whichthey believed to be infectious rather than toxic.A few years later a condition in lambs, which was probablyidentical to chronic hepatitis, was described in New Zealandand Norway and called white liver disease (5, 19, 24). Thedisease was thought to be caused by either a metabolic con-sequence of vitamin B12 deficiency or a toxic hepatopathy,probably as a result of exposure to a pasture mycotoxin,against which adequate dietary cobalt and/or adequate tissue

1 Animal Health Service in the Northern Netherlands, P.O. Box 361, 9200 AJ Drachten,the Netherlands.

2 Corresponding author. Mailing address: Animal Health Service in the NorthernNetherlands, P.O. Box 361, 9200 AJ Drachten, the Netherlands. Phone: (0)512570700. Fax: (0)512 520013.

3 Department of Herd Health and Reproduction. Faculty of Veterinary Medicine,Utrecht University, P.0 Box 80151, 3508 TD Utrecht, the Netherlands.

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vitamin B12 levels are protective. A similar disease was alsodescribed in Australia (15) and Northern Ireland (11). In1990 Ulvund described ovine white liver disease as a mani-festation of cobalt/vitamin B12 deficiency, which in lambs isaggravated by as yet unknown cofactors in grass (23).The aim of this study was to confirm the presence of co-balt/vitamin B12 deficiency in lambs in the Netherlands andto measure the effect of cobalt supplementation on serum vi-tamin B12, growth rate, and survival rate in lambs grazingcobalt-deficient pasture.

MATERIALS AND METHODSFarmThe study was carried out in the Northern Netherlands, in theprovince of Fryslan on a dairy farm near the sea. The soiltype on this farm is sea clay. Besides dairy cows, approxima-tely 1.5 ewes of the Texel breed are kept per hectare. Thefarmer fertilized the pasture yearly, with 200 kg of nitrogenper hectare (740 kg of a commercial nitrogen fertilizer (27%nitrogen)) and with composted manure. At the start of the ex-periments perennial ryegrass (80%) and white clover (15%)were the most important crops.The sheep lambed in March and were only kept indoorsaround the lambing time. When a few days old the lambs wentoutside during the daytime, and as soon as the weather permit-ted they stayed outside day and night. Indoors they were fed onhay. Ewes were given concentrates, at a maximum of 1 kg perewe per day, from 1 week before until 2 weeks after parturi-tion. Lambs were never given concentrates.Lambs on this farm had a history of illthrift during the sum-mer months. Cobalt/vitamin B12 deficiency was diagnosedin 1988, and after cobalt supplementation lambs grew well.Dairy calves on the farm were not affected.

AnimalsThe experiments were performed with 18, 20, and 25 regis-tered Texel twins in 1991, 1992, and 1993, respectively. Thetwin lambs were the same sex. Of the 63 twins, 37 were fe-male and 26 male. In 1991 and 1992 all twins of the same sexborn on the farm before 1 April were used. In 1993 the lambswere bought from five different farms. The twin lambs of1993 were born before 1 April and were brought with theirdams to the experimental farm a few weeks later. They werefoot-trimmed and foot-bathed, vaccinated against pasteurel-losis and clostridial diseases (Heptavac-P®, Hoechst AnimalHealth, Bucks, UK), drenched with oxfendazole (Synan-thic® 2.265%, Janssen Pharmaceutica B.V., Tilburg, theNetherlands) and closantel (Flukiver®, Janssen Pharma-ceutica B.V.), and preventively treated against lice and kedswith a deltamethrine pour-on formulation (Sputop/S®,Pitman-Moore, Houten, the Netherlands) on arrival. Duringthe grazing season all the lambs were treated with oxfenda-zole and closantel at least two times.

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Allocation of treatmentAt the start of each experimental year one lamb of a twin wasrandomly allocated to either the supplemented or the non-supplemented group. The second lamb was allocated to theother group (13). The lambs in the supplemented group re-ceived a cobalt pellet (each 10-g pellet contains 3 g cobaltoxide; Permaco® cobalt pellet, Coopers Animal Health,North Ryde, Australia). In 1991 the lambs in the supplemen-ted group received a cobalt pellet once at the start of the ex-periment (22/4/1991). In 1992 the lambs received a pellettwice (14/5/1992 and 17/7/1992), and in 1993 they receiveda pellet at the end of April, the end of June, and in earlySeptember. Since in the two preceding years some supple-mented lambs had lost a cobalt pellet by regurgitation, in1993 seven lambs received an extra cobalt pellet on the nextsampling date after their serum vitamin B12 had dropped be-low 200 pmo1/1.

Grass samplesGrass samples were collected by picking, imitating the waysheep graze, and avoiding soil contamination. The grasssamples were dried and cobalt analyses were performed byusing flameless atomic absorption spectrophotometry (AAS,graphite oven).

Weighing and samplingDuring the experiments the lambs were managed as a singleflock and fed on grass only. They were weighed and bloodsamples were taken at least every three weeks. At the end ofthe experiment of 1991 only ten of the surviving lambs wereslaughtered, while in 1992 and 1993 all surviving lambswere slaughtered.

Analytical proceduresBlood samples were collected at the same time the animalswere weighed. Immediately after arrival in the laboratory theserum samples were stored at 4 °C and vitamin B12 was mea-sured in a chemiluminescence assay (Magic® Lite VitaminB12 Assay, Ciba Corning Magnetic Immunochemistries)within 24 hours after blood collection.

Clinical observationsThe lambs were observed at least two times a week.Necropsy was performed on all lambs that died, were killedfor health reasons, or were slaughtered.

Carcase weightThe carcase weight of a lamb is the weight after slaughter.Total carcase weight at the end ofthe experimental period isthe sum of the carcase weights of all lambs that did not dieduring the exj)eriments.

Statistical analysisPrior to statistical analysis, observations were checked forunlikely values; no data were excluded for this reason.Missing values routinely caused a record to be dropped if theanalysis included that variable (1).Differences in serum vitamin B12 andbody weight betweensupplemented and non-supplemented lambs were analysedusing a paired t-test (18). This means that as soon as onelamb of a twin died the data for the other lamb were left out.The difference in survival between supplemented and non-supplemented lambs was analysed using a life table analysis(14). The relative risk of not surviving was calculated using

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the Logrank test (14). Sex differences in mean live weightswere compared using Student t-tests (18). Sex differences insurvival between supplemented and non-supplementedlambs were analysed using Pearson's Chi-square test on con-tingency tables (4). The statistical significance level waschosen at P = .05.

RESULTSGrassThe mean cobalt content of the monthly grass samples of thepastures on which the lambs grazed during the experimentalperiods of 1991, 1992, and 1993 was .10 (range .04-.23), .06(range .02-.09), and .05 (range .02-.08) mg/kg dry matter(DM), respectively. The cobalt content of non-deficient pas-tures is at least .11 mg/kg DM (26).

Serum vitamin B12No difference in serum vitamin B12 concentrations of sup-plemented and non-supplemented lambs was found at thestart of the three experimental periods (Figure 1; 1991: P =.90, 1992: P = .24, 1993: P = .43). After the first samplingdate, the non-supplemented lambs always had lower serumvitamin B12 concentrations than their supplemented siblings(Figure 1; P < .01).The serum vitamin B12 concentrations of the supplementedlambs were different in 1991, 1992, and 1993, whereas theconcentrations of the non-supplemented lambs were com-parable. In 1991 the serum vitamin B12 concentrations of thesupplemented lambs fell below 400 pmo1/1 at the end ofJulyand stayed low, reaching about the same concentrations asthose of the non-supplemented lambs at the end of the exper-

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Figure 1. Mean serum vitamin B12 of supplemented and non-supplemen-ted lambs in 1991, 1992, and 1993. Arrows indicate moment of cobaltsupplementation.

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imental period (Figure 1). In 1992 the serum vitamin B12concentrations of the supplemented lambs dropped duringand towards the end of the experimental period to 238 and304 pmo1/1, reaching the deficiency threshold. In 1993 themean serum vitamin B12 concentrations were 300 pmo1/1 onthe second and 223 pmo1/1 on the third occasion of cobaltsupplementation, and 705 pmo1/1 at the end of the exper-imental period.

Weight gainNo differences in weight between supplemented and non-supplemented lambs were found at the start of the three ex-perimental periods (Figure 2; 1991: P = .75, 1992: P = .74,1993: P = .74). The differences in mean live weight at theend of the experiment were 7.2, 9.5, and 11.0 kg (P < .01) in1991, 1992, and 1993 respectively (Figure 2). The mean dif-ference in weight gain between the sexes during the three ex-perimental periods is shown in figure 3. From day 82 afterthe start of the experiments there was a difference in weightgain between ewe lambs and ram lambs (P < .05).

Clinical symptomsBesides a reduced weight gain and loss of weight, inappetence,listlessness, and serous ocular discharge were often seen in thenon-supplemented lambs. In 1992 one and in 1993 four of thenon-supplemented lambs showed signs of acute photosensiti-zation. Neurological signs were not seen at any time.

SurvivalIn 1991 none of the lambs died. In 1992 four of the non-sup-plemented lambs died and one was killed because of severephotosensitization. In 1993 a supplemented ewe lamb died

from enterotoxaemia and a supplemented ram lamb was re-moved because teeth problems prevented the animal fromgrazing. From the end ofJuly until the end of the experimen-tal period eight non-supplemented lambs died (P < .01).Thus non-supplemented lambs had a 6.7-fold higher risk ofdying than supplemented lambs had. The pathology of theselambs will be reported elsewhere. In the non-supplementedlambs that died there was a clear difference between sexes:only 1 of the 13 lambs was a ewe lamb (P < .01).

Carcase weightAt the end of the experimental periods of 1991, 1992, and1993, the difference in total live weight of the surviving sup-plemented and non-supplemented lambs was 129, 311, and399 kg respectively (Table 1; P < .01). The difference in totalcarcase weight of the supplemented and non-supplementedlambs was 206 kg in 1992 and 239 kg in 1993 (P < .01). Thusat the end of the experimental periods there was a considera-ble difference in the economic value of supplemented andnon-supplemented lambs (27).

DISCUSSIONThe mean cobalt content of the grass on which the lambs gra-zed was .07 (range .02-.23) mg/kg DM. Kennedy et al. (8)state that the pasture cobalt content needs to be below .07mg/kg DM for sheep to develop vitamin B12 deficiency. Ourfindings however support those of Ulvund and Pestalozzi(26), and Clark et al. (5), who found vitamin B12 deficiencyin lambs grazing pastures with cobalt contents up to .21

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Table 1. Differences between cobalt-supplemented and non-supplemented lambs at the end of the experimentalperiods in 1991, 1992, and 1993.

1991 1992 1993

non-suppl. suppl. non-suppl. suppl. non-suppl. suppl.Number alive 18 18 15 20 17 23Number dead 0 0 5 0 8 2Tota live weight (kg) 683 812 489 800 524 923Total carcase weight (kg) ndl) nd 215 421 228 467I) nd: not determined.

(range .08- .21) mg/kg DM.The non-supplemented lambs always had serum vitamin B12concentrations around or below 200 pmo1/1 at the start of theexperimental periods and these values dropped to below 100pmo1/1 during the experiments. Suttle (20) suggested that aserum vitamin B12 concentration of 188 pmo1/1 is probablythe threshold between marginal and functional deficiency,while others indicate the margin to be between 150 and 300pmo1/1 (2, 6, 7, 9, 16, 21,22). This indicates that the non-sup-plemented lambs were B12 deficient shortly after the start ofthe experiment.During the first months of 1991 the supplemented lambs hadhigher vitamin B12 concentrations than in 1992 and 1993. Thisprobably was caused by the higher cobalt content of the grassin 1991. From the end of July the serum vitamin B12 concen-trations dropped below 400 pmo1/1 and were 207 pmo1/1 at theend of the period. In between they even reached values as lowas 140 pmo1/1. This means that these supplemented lambswere B12 deficient during part of the experimentalperiod.Year-to-year differences in weight gain (Figure 2) and in thesevereness of clinical signs in cobalt/vitamin B12-deficientlambs have also been reported by others (9, 25). The clinicalsigns of the non-supplemented lambs were identical to thosedescribed elsewhere (5, 11, 15, 19, 23, 24, 28). The smallerdifference in mean live weight between supplemented andnon-supplemented lambs in 1991 may have been partly cau-sed by the higher cobalt content of the grass, resulting in bet-ter growth and less severe clinical signs in the non-supple-mented lambs compared to those of the non-supplementedlambs in 1992 and 1993. However, this difference may alsohave been partly caused by the low serum B12 concentrationsof the supplemented group during the second half of the ex-periment in 1991. Whether or not the differences in weightgain in the different years resulted from the different numbersof cobalt pellets the supplemented lambs received or reflectedthe normal differences in weight gain between different yearscannot be concluded from these trials. It is likely that in 1991both the low serum vitamin B12 concentrations of the supple-mented lambs at the end of the experimental period and thehigher cobalt content of the grass played a role.The difference in weight gain we found was smaller than thatfound by Ulvund and Pestalozzi (26) in Norway. This couldhave been caused by our method of cobalt supplementation.In Norway cobalt pellets increased the average daily weightgain less than other methods (cobalt sulphate by mouth, gra-zing of moderately or heavily cobalt fertilizedpastures, vita-min B12 injections, access to cobalt lickstone, grazing of die-ease free pastures) of supplementation (56 vs 60-115 g/day).Cobalt pellets can become coated with calcium phosphate orbe lost by regurgitation (25, 12), thus reducing the effective-ness of supplementation.

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The considerable difference we found between the value of thecarcases of supplemented and non-supplemented animals (27)is likely to be underestimated because some of the carcases ofthe non-supplemented lambs were unsaleable because of theirbad conformation. This was not included in the analysis.We found sex-related differences in weight gain and survi-val. In field observations of cobalt/vitamin B12 deficiencywe had often had the impression that ram lambs were moreseriously affected than ewe lambs. Differences betweensexes in survival and body weight response have also beensuggested by others (17 ,28).Further research is needed to determine which other factorsin grass besides the cobalt content influence the developmentof vitamin B12 deficiency. It is also not known which mecha-nisms underlie the complex of symptoms caused by vitaminB12 deficiency.

CONCLUSIONSOur results demonstrate that in the Netherlands cobalt/vita-min B12 deficiency can occur in lambs grazing cobalt-defi-cient pasture. Cobalt supplementation results in higher se-rum vitamin B12 concentrations, better live weight gains andprevents clinical symptoms and death.

ACKNOWLEDGEMENTSWe wish to thank mr. and mrs. Zwaagstra, the owners of the farm where thetrial was performed, for their cooperation and their care of us and the experi-mental lambs. We also thank Els Louwersefor her assistance in the field andDirk Vermeulen for his skilful technical assistance.

REFERENCES1. Analytical software, 1992. Statistix, version 4.0 user's manual. Analy-

tical Software, St. Paul, MN, USA.2. Andrews ED, and Stephenson BJ. Vitamin B12 in the blood of grazing

cobalt-deficient sheep. N Z J Agric Res 1966; 9: 491-507.3. Aston BC. Bush-sickness investigation. Five years' work at the

Mamaku demonstration farm. N Z J Agric 1924; 28: 215-38.4. Bishop YMM, Fienberg SE, and Holland PW. Discrete multivariate

analysis. MIT Press, 1975, Cambridge, Massachusetts.5. Clark RG, Cornforth IS, Jones.,BAH, McKnight LJ, and Oliver J. A

condition resembling ovine white liver disease in lambs on irrigatedpasture in South Canterbury. N Z Vet J 1978; 26: 316.

6. Clark RG, Wright DF, Millar KR, and Rowland JD. Reference curvesto diagnose cobalt deficiency in sheep using liver and serum vitaminB12 levels. N Z Vet J 1989; 37: 7-11.

7. Fraser AJ. Production related reference ranges. Surveillance. Specialissue on trace elements 1982; 9: 4-7.

8. Kennedy DG, Blanchflower WI, Scott JM, Weir OG, Molloy AM,Kennedy S, and Young PB. Cobalt-vitamin B12 deficiency decreasesmethionine synthase activity and phospholipid methylation in sheep. JNutr 1992; 122: 1384-90.

9. MacPherson A, Moon FE, and Voss RC. Biochemical aspects of co-balt deficiency in sheep with special reference to vitamin status and apossible involvement in the aetiology of cerebrocortical necrosis. BrVet J 1976; 132: 294-308.

10. Marston HR. Problems associated with 'Coast Disease' in South

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Australia. J Counc Sci Ind Res (Aust) 1935; 8: 111-6. deficiencies in grazing livestock. Vet Rec 1986; 119: 148-52.11. McLoughlin MF, Rice DA, and Taylor SM. Liver lesions resembling

ovine white liver disease in cobalt deficient lambs. Vet Rec 1984; 115:21. Suttle NF, Linklater KA, and Jones DG. Disorders related to trace ele-

ment deficiencies. In: Martin WB, Aitken ID, eds. Diseases of sheep.325. Oxford: Blackwell Scientific Publications 1991; 238-50.

12. Millar KR, and Albyt AT. A comparison of vitamin B12 levels in the li-ver and serum of sheep receiving treatments used to correct cobalt de-ficiency. N Z Vet J 1984; 32: 105-8.

22. Ulvund MJ. Ovine white-liver disease (OWLD). Vitamin B12 andmethyl malonic acid (MMA) estimations in blood. Acta Vet Scand1990a; 31: 267-75.

13. Peto R, Pike MC, Armitage P, Breslow NE, Cox DR, Howard SV,Mantel N, McPherson K, Peto J, and Smith PG. Design and analysis ofrandomized clinical trials requiring prolonged observation of each pa-

23. Ulvund MJ. Ovine white-liver disease. Manifestations of cobalt/vita-min B12 deficiency in lambs. Oslo, Norway: The Norwegian Collegeof Veterinary Medicine, 1990b.

tient. I. Introduction and design. Br J Cancer 1976; 34: 585-612. 24. Ulvund MJ, and Overhs J. Chronic hepatitis in lambs in Norway, a14. Peto R, Pike MC, Armitage P, Breslow NE, Cox DR, Howard SV,

Mantel N, McPherson K, Peto J, and Smith PG. Design and analysis ofcondition resembling ovine white liver disease in New Zealand. N ZVet J 1980; 28: 19.

randomized clinical trials requiring prolonged observation of each pa-tient. II. Analysis and examples. Br J Cancer 1977; 35: 1-39.

25. Ulvund MJ, and Pestalozzi M. Ovine white-liver disease (OWLD) inNorway: clinical symptoms and preventive measures. Acta Vet Scand

15. Richards RB, and Harrison MR. White liver disease in lambs. Aust Vet 1990a; 31: 53-62.J 1981; 57: 565-8. 26. Ulvund MJ, and Pestalozzi M. Ovine white-liver disease (OWLD).

16. Russel AJF, Whitelaw A, Moberly P, and Fawcett AR. Investigationinto diagnosis and treatment of cobalt deficiency in lambs. Vet Rec

Botanical and chemical composition of pasture grass. Acta Vet Scand1990b; 31: 257-65.

1975; 96: 194-8. 27. Vellema P, Moll L, Barkema HW, Schukken YH, and Wentink GH.17. Shallow M, Ellis NJS, and Judson GJ. Sex-related responses to vita- Cobalt supplementation in Texel lambs: a randomized trial. In:

min B12 and trace element supplementation in prime lambs. Aust Vet J1989; 66: 250-1

Schukken YH, Lam TJGM, eds. Proceedings of the Annual Meeting ofthe Dutch Society for Veterinary Epidemiology and Economics, 14

18. Sokal RR, and Rohlf FJ. Biometry. WH Freeman and Company, 1981,New York.

December 1994, Utrecht. Dutch Society for Veterinary Epidemiologyand Economics, Utrecht, the Netherlands: 1994; Vol 7: 121-35.

19. Sutherland RJ, Cordes DO, and Carthew GC. Ovine white liver disea-se - an hepatic dysfunction associated with vitamin B12 deficiency. N

28. Wensvoort P, and Herweijer CH. Chronische hepatitis bij lammeren.Tijdschr Diergeneeskd 1975; 100: 221-8.

Z Vet J 1979; 27: 227-32.20. Suttle NF. Problems in the diagnosis and anticipation of trace element Accepted for publication: August 22, 1996.

ESTIMATING THE RATE OF PSEUDORABIES VIRUSINTRODUCTION INTO PIG-FINISHING HERDS ATREGIONAL LEVEL

A.Stegeman1,2, A. R.W. Elbers1, M.C.M. de Jong2, B. Oosterlaak3, andA.A. Dijkhuizen4

SUMMARYFrom February to June 1995, 5-12 blood samples werecollected in each Dutch pig herd and tested for antibodiesagainst pseudorabies virus (PRV). The percentage ofPRV-seropositive pig-finishing herds in three regionswith more than 1,000 pigs/km2 (regions 2, 4 and 7) was6% (region 2), 12% (region 7), and 25% (region 4). Thepercentage of PRV-seropositive pig-finishing herds infive regions with fewer than 1,000 pigs/km2 (regions 1, 3,5, 6, and 8) was 3% (region 1), 9% (region 3), 6% (region5), 0% (region 6), and 4% (region 8). The small samplesize allows only the detection of major outbreaks and thepercentages of PRV-seropositive herds therefore under-estimate the actual virus circulation in the regions. Thefraction of PRV introductions that will result in a majoroutbreak depends on the herd immunity and thus on thevaccination programme of the herds. By combining foreach herd the occurrence or absence of a major outbreakwith the herd immunity induced by the vaccination pro-

Animal Health Service, P.O.Box 4, 5280 AA Boxtel, the Netherlands.2 Department of Pathobiology and Epidemiology. Institute for Animal Science and

Health (ID-DLO), P.O. Box 65, 8200 AB Lelystad, the Netherlands. Also correspon-dence-address.

3 Animal Health Service, P.O. Box 9, 7400 AA Deventer, the Netherlands.4 Department of Farm Management, Wageningen Agricultural University, P.O. Box

338, 6700 AH Wageningen, the Netherlands.

Vet Quart 1997; 19: 5-9

gramme, we estimated the average rate at which PRVwas introduced into finishing herds in the eight regions.The average number of PRV introductions per finishingherd per finishing period (16 weeks) in the pig-dense re-gions was estimated at 0.20 in region 2, 0.83 in region 4,and 0.48 in region 7. In the less densely populated regionsthis rate was estimated at 0.08 in region 1, 0.34 in region3, 0.17 in region 5, 0.00 in region 6, and 0.09 in region 8.The eight regions could be classified into four areas witha statistically different (P < 0.05 in Mann Whithey U test)rate of PRV introduction: i) regions 1, 6, and 8; ii) regions2 and 5; iii) regions 3 and 7; and iv) region 4.

INTRODUCTIONTo enable free trade of pigs, several countries within theEuropean Union are under pressure to eradicate pseudora-bies virus (PRV, Aujeszky's disease virus). In some coun-tries this goal has been achieved by depopulation followedby repopulation and test-and-removal (1,18). However, inregions in which PRV is enzootic, it is economically unfeasi-ble to eradicate PRV by either of these two traditional me-thods. Fortunately, the results of field studies that have beencarried out on a limited scale indicate that PRV can be eradi-cated in such regions by area-wide vaccination (12). On thebasis of these results, several countries of the EuropeanUnion have started an area-wide vaccination campaign (9).

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