Parasite infections of domestic animals in the - CABI

MEETING ABSTRACTS Open Access

Parasite infections of domestic animals in theNordic countries – emerging threats andchallenges. Proceedings of the 22nd Symposiumof the Nordic Committee for Veterinary ScientificCooperation (NKVet)Helsinki, Finland. 7-9 September 2008

Published: 13 October 2010

These abstracts are available online at http://www.actavetscand.com/supplements/52/S1

S1Climate change, parasites and shifting boundariesLydden Polley1*, Eric Hoberg2, Susan Kutz31Department of Veterinary Microbiology, Western College of VeterinaryMedicine, University of Saskatchewan, Saskatoon, Saskatchewan S7N 5B4,Canada; 2National Parasite Collection, Agricultural Research Service, UnitedStates Department of Agriculture, Beltsville, Maryland 20705, USA;3Department of Ecosystem and Public Health, Faculty of Veterinary Medicine,University of Calgary, Calgary, Alberta T2N 4N1, CanadaE-mail: [email protected] Veterinaria Scandinavica 2010, 52(Suppl 1):S1

Background: Around the world the three major components of climatechange already evident and escalating in magnitude and significance are;1) warming; 2) altered patterns of precipitation; and 3) an increasedincidence of extreme climatic events [1]. For the structure and function ofecosystems, impacts of climate change vary with place and with time,and among the key outcomes are shifting boundaries for manycomponents and processes within the systems. Among thesecomponents are pathogens and infectious diseases, including thosecaused by helminth, arthropod and protozoan parasites in people,domestic animals, and wildlife [2].For host-parasite assemblages, boundaries potentially vulnerable toclimate change include those for spatial and temporal distributions ofhosts and parasites, for parasite survival and development in hosts and inthe environment, for risks of transmission to hosts at critical points inparasite webs, and for health effects on hosts, including the emergenceor resurgence of disease. The often complex and obscure linkages andinter-relationships among components of an ecosystem, coupled with theuncertain and variable trajectories for climate change, make it difficult toidentify all these vulnerabilities, particularly in the medium to long term.Also, faced with non-overwhelming “stress” most ecosystems display adegree of resilience that may mitigate some of the consequences ofclimate change [3,4], and in some circumstances the significance ofparasites remains essentially unchanged. Finally, some recent shifts indisease occurrence that intuition might suggest are associated with

climate change have proved likely to be wholly or partly the result ofother factors [5,6].The primary aim of this paper is to provide a framework for thinkingabout the critical potential connections between climate change,parasites, people, and wildlife in the circumpolar North, and betweenthese host groups, climate change, parasites and domestic animals inother areas of the world.Approaches: Much of the information currently available on climatechange and infectious disease relates to people and is based onretrospective analyses of associations between components of climateinvolved in climate change and the occurrence of disease in humanpopulations [7,8]. In other instances, features of parasite ecology have beenlinked to model-based scenarios for future climate change to generatemedium to long-term projections for parasite and disease distribution andoccurrence [9,10]. Underlying these approaches are observational andexperimental studies in a range of systems exploring, on a more intimatescale, the relationships between climate and parasite, and sometimes host,ecology [11-13]. All these lines of enquiry are increasing understanding ofthe mechanisms generating boundary shifts for parasites and diseasesresulting from climate change, and are assisting proper targeting ofmeasures to minimize their impacts on human and animal health.Encouragingly, effective climate-based forecasting, developed decades agofor ruminant fascioliasis [14], is now a reality for some epidemic humanmalaria in Africa [15] and is being evaluated for other human parasiticdiseases, for example human fascioliasis [16] and leishmaniasis [17] in SouthAmerica. Exploration of the effects of climate change on infectious diseaseecology presents many opportunities for valuable comparisons acrosspathogen and host groups, and across ecosystems.Central to understanding these climate change-host-parasite linkages isthe ability to detect and measure shifts in key features of parasites andhosts and to assemble data unequivocally establishing or refuting links toclimate change. Given relevant meteorological data, although monitoringand surveillance of parasitic infections and diseases may be possible tosome extent in people and domestic animals, even in remote areas withlimited infrastructure, it is usually more difficult in wildlife [18]. Aparticular issue for this host group, especially in Arctic and the North andother relatively isolated areas, is the currently limited understanding of

Acta Veterinaria Scandinavica 2010, Volume 52 Suppl 1http://www.actavetscand.com/supplements/52/S1

mailto:[email protected]

the parasite fauna, including species diversity and distribution, and itshealth significance, especially in the absence of obvious disease ormortality [19,20]. A recently initiated and very promising approach innorthern Canada and elsewhere is to recruit, train and fund northerners,particularly harvesters who have frequent contact with wildlife, as healthmonitors. This program is greatly enhanced in the longer term wherewildlife and wildlife health are introduced into curricula for schools innorthern communities (see http://www.ccwhc.ca/Sahtu/index.php).The fragile North: The North is among areas of the world where climatechange is already having significant and obvious effects and is impactingnortherners and the animal and plant resources vital to their health andwell-being [21,22]. For example, at risk on land are keystone wildlifespecies, including caribou, reindeer, moose, thinhorn sheep and muskoxen,waterfowl, and fish, together with berries and other foods of plant origin.In the surrounding oceans, polar bears, seals, walrus, seabirds and fish areall vulnerable. Among the elements of climate change threatening thehealth and sustainability of people and wildlife in the North, perhaps themost significant is warming, which is shifting boundaries for animals andplants [23], and for sea ice, permafrost, snow cover, and hydrology, as wellas local and regional infrastructure [22]. Warming is also a cause of risingsea levels and the consequent erosion and flooding of coastal areas anddisruption of coastal ecosystems and settlements [22].People and animals that inhabit the North are beset by an array of helminth,arthropod and protozoan parasites. Most of these are restricted to one ofthe two host groups, but several – the zoonoses – are transmissiblefrom animals to people, often through foods integral to traditional localcultures [18]. These zoonoses include (in North America) Trichinella,Anisakis, Diphyllobothrium, Echinococcus, and Toxoplasma, and perhapsCryptosporidium and Giardia. All of these can cause obvious clinical diseasein people, but not in everyone who is infected.Host and parasite vulnerabilities: Many aspects of host and parasiteecology in the North and elsewhere have been identified as potentiallyvulnerable to climate change. Among possible consequences are boundaryshifts that can alter the structure and function of host-parasiteassemblages [24,25]. The speed and extent of these shifts vary with placeand with time. For example, those linked to extreme climatic events maybe rapid and localized, whereas those resulting from warming may bemore gradual and widespread. For definitive and intermediate hosts,including arthropod vectors, these shifts include: 1) geographicdistributions – expansion into new areas and/or loss from old areas and, insome cases, local to regional extinctions, together with shifts in migrationroutes; 2) faunal structure – qualitative changes in the composition ofmulti-species host communities, including shifts in opportunities forcontacts between wildlife and domestic animals; 3) trophic linkages -including predator-prey relationships important for parasite transmission,especially for several zoonoses [26]; 4) phenology - especially the timing ofbreeding seasons and migrations, and the synchronization of the need forand availability of food; 5) level of nutrition – determined by thecomposition, availability, accessibility and quality of food and water; 6)health and wellbeing – including patterns of disease occurrence, andpossible detrimental synergies between parasites, other infectious agentsand other diseases; 7) host abundance – possibly affecting host densityand thus parasite transmission dynamics; 8) behavioural patterns –influencing exposure to parasite and in some cases subsequentenvironmental contamination with parasites; and 9) parasite evolution [27]- likely to be detected first among protozoans. For people dependent tosome extent on wildlife, as many northerners are, parasites may be one ofthe means by which climate change results in shifts in the availability andquality, or perceived quality, of their food and other key products (e.g.hides and pelts) of wildlife origin, and in the role of wildlife in their culturaland economic wellbeing and in the sustainability of northern communities.For parasites, some potential boundary shifts are similar to those for hosts.For example, as distributions and faunal structures for hosts shift, so too willthose for parasites. In some ecosystems, as a result of host switching, bothimmigrant (or invasive) and endemic hosts may experience new parasites,and these may be especially pathogenic for naïve hosts and may result inemergent or resurgent diseases. Shifts in parasite faunal structure may alsoresult from altered trophic linkages, and the levels of nutrition, health andwellbeing of hosts will influence their susceptibility to parasites and otherdiseases and may lead to shifts in the role of parasites in ecosystemdynamics. Outside their mammalian and avian hosts, many parasites havelife cycle stages in the environment or in ectothermic intermediate hosts

and vectors that are exposed directly to climate. Key potential boundaryshifts here are in parasite survival and development rates [12] and, for somespecies, in amplification rates for parasites developing in ectothermic hosts[11]. If warming from climate change enhances these rates, lengthens thesummers vital for the transmission of many northern parasites, and shortensand softens the winters then, simplistically, more infective stages ofparasites could be available sooner and the transmission period could beextended. In some instances, these shifts have the potential to generategreater parasite abundance in the definitive hosts and to increase theirhealth impacts.Some case studies: Despite our currently relatively limited under-standing of the ecology of host-parasite assemblages in the Arctic andthe North, it is possible to speculate how some might be influenced byclimate change. Although evidence transforming this speculation tocertainty remains sparse, it is important to consider these issues andespecially to identify potential high-risk scenarios for the emergence ofsignificant parasitic disease in people and in wildlife.Trichostrongyles of Ungulates: Trichostrongyles (e.g. Ostertagiagruehneri and Teladorsagia boreoarcticus) are non-zoonotic nematodesthat as adults parasitise the abomasum or intestines. They have direct lifecycles involving the development of eggs deposited in the feces to free-living, infective larvae in the environment. Infection of ungulate hosts isby ingestion of these larvae. Climate change, as well as its positive ornegative effects on the hosts, may shift patterns of development for theparasites’ free-living stages. For example, assuming adequate moisture,longer, warmer summers may increase survival and development ratesfor the free-living stages leading perhaps to shorter generation times andto greater abundance and increased longevity for infective larvae in theenvironment. This in turn may increase the infection pressure andparasite loads for hosts and lead to greater adverse impacts on hosthealth (e.g. weight loss and reduced conception rates) [28,29] and, forspecies important as food for northerners, on human health. In addition,altered summer transmission dynamics and fall climate may shift patternsof larval inhibition in the gastro-intestinal mucosa, an importantmechanism for overwinter survival by some trichostrongyles in otherareas of the world. A useful preliminary glimpse of the links betweenclimate change and altered ecology for trichostrongyles can be derivedfrom basic information about pre-patent periods and the relationshipsbetween environmental temperatures and larval survival anddevelopment rates as determined in the laboratory and in the field. Dataare plentiful on these aspects of trichostrongyles of domestic animals inseveral areas of the world [12], but caution is required when attemptingto extrapolate these data to the species of parasites infecting free-ranging hosts, particularly in the Arctic and the North.Protostrongylids of Ungulates: Protostrongylid nematodes (e.g.Umingmakstrongylus pallikuukensis, Parelaphostrongylus odocoiei andP. andersoni) are non-zoonotic and live as adults in the airways, lungparenchyma or skeletal musculature. Their life cycles are indirect, involvingdevelopment of first-stage larvae deposited in feces to infective larvae ingastropod intermediate hosts. Infection of ungulates is by ingestion of infectedgastropods or of infective larvae spontaneously emerged from the gastropods.The life cycle stages of these parasites outside the hosts havevulnerabilities to climate change generally similar to those of thetrichostrongyles but it is possible that gastropod mobility and avoidanceof extreme habitat conditions may protect the larvae from some of theeffects of a changed climate [30].For U. pallikuukensis, an empirical model derived from laboratory and fieldstudies demonstrated that warming in the North probably has alreadyshortened larval development times in gastropods and shiftedtransmission dynamics from a two-year to a one-year adult-to-adult cycle[31]. A similar model for P. odocoilei indicated that temperatureconstraints affecting larval development rates in gastropods may definethe northern limits of the parasite’s distribution, and that warming mayremove these and lead to an expanded parasite distribution [10]. Also, forU. pallikuukensis, attempted experimental infections indicated thatthinhorn sheep, potentially newly sympatric with muskoxen as a result ofshifts in host geographic distributions perhaps associated with climatechange, are not susceptible to the parasite [32].Trichinella nativa Trichinella is a genus of zoonotic nematode containingspecies that infect a range of vertebrates, including people, in many partsof the world. Trichinella nativa is the primary northern species. AdultTrichinella live in the small intestine, and the larvae produced by the


Page 2 of 31

http://www.ccwhc.ca/Sahtu/index.php

female parasites migrate to skeletal muscle and sometimes other tissues.These larvae are the parasite’s infective stage and transmission is bycarnivorism, including feeding on carrion. In the North many host speciesare infected, and of special concern are those consumed by people,especially polar and black bear, walrus, and seal. Other than in carrion,life cycle stages of Trichinella are not exposed to the environment andany effects of climate change are likely to result primarily from shifts inhost faunal structure and trophic linkages [26]. Outside the North, theecology of Trichinella may be modified by climate-induced shifts incontacts between wildlife and domestic animals, and perhaps throughbehavioural shifts in the utilization of infected hosts as food for people.Cryptosporidium and Giardia: Among the several species and genotypescurrently established for each of these two genera of protozoans some arezoonotic and infect a range of hosts but most seem restricted to a singlehost species [33]. Although some species/genotypes are shared betweenpeople and domestic animals, the significance of wildlife as sources ofhuman infections, and of people as a source of the parasites for wildlife,remain uncertain and unexplored. Both parasites live primarily in the smallintestine and the life cycles are direct. Infection is by ingestion of infectiveoocysts (Cryptosporidium) or cysts (Giardia) from the environment or fromcontaminated food or water. Climate change has the potential to altersurvival rates for the cysts and oocysts (which are infective when voided bythe hosts) and, because both parasites are found in surface water, shifts inlocal and regional hydrology may alter parasite distributions and the risks ofhuman and animal exposure. In human settlements altered patterns ofprecipitation and extreme climatic events may disrupt the integrity of theinfrastructure, particularly water supplies and sewage disposal, increasingthe risk of human infection. In addition, these elements of the climatechange may result in increased run-off and contamination of water withanimal feces, and increased risk of zoonotic transmission.Priorities for action: For people, domestic animals and especiallywildlife, in many situations around the world it is difficult to identify allthe causes of detectable shifts in disease occurrence and, correctly,efforts are directed principally at mitigation of the disease and ateffective control. Additionally, for all host groups, it may be difficult totease parasites from among other potential contributors to disease, andto determine the role of climate in shifts in disease ecology and hosthealth [34]. For wildlife, the detection of these shifts may also behampered by a lack of baseline data for the occurrence and significanceof pathogens and diseases. In exploring climate change as a cause ofnew patterns of disease, however, much can be learned from the manydata-derived relationships between key climatic factors and host, parasiteand disease ecology, and the integration of these with projections forclimate change trajectories. This capability, coupled with an integrative,multidisciplinary and ecological approach, makes possible theidentification of parasitic infections and diseases likely to be particularlysusceptible to climate change and, with adjustments for regionalvariations, the exploration of some of the possible consequences ofaccelerating climate change for the occurrence of these diseases and foranimal and human health. This is a very urgent need, and without suchan attempt to anticipate the possible, society is likely to be a more orless impotent spectator to the certainty of continual ecological calamities.References1. IPCC: Summary for Policymakers. In Climate Change 2007: The Physical Science

Basis. Contribution of Working Group I to the Fourth Assessment Report of theIntergovernmental Panel on Climate Change. Edited by: Solomon S, Qin D,Manning M, Chen Z, Marquis M, Averyt KB, Tignor M, Miller HL. CambridgeUniversity Press, Cambridge, United Kingdom and New York, NY, USA; 2007.

2. Patz JA, Graczyk TK, Geller N, Vittor AY: Effects of environmental changeon emerging parasitic diseases. Int. J. Parasitol 2000, 30:1395-1405.

3. Folke C, Carpenter S, Walker B, Scheffer M, Elmqvist , Gunderson L,Holling CS: Regime shifts, resilience, and biodiversity in ecosystemmanagement. Ann. Rev. Ecol. Evol. Syst 2004, 35:557-581.

4. Moore SE, Huntington HP: Arctic marine mammals and climate change:impacts and resilience. Ecol. Applic 2008, 18(Supplement):S157-S165.

5. Sumilo D, Asokliene L, Bormane A, Vasilenko V, Golovljova I, Randolph SE:Climate change cannot explain the upsurge of tick-borne encephalitis inthe Baltics. PLoS ONE 2007, 2:e500.

6. Sumilo D, Bormane A, Asokliene L, Vasilenko V, Golovljova I, Avsic-Zupanc T,Hubalek Z, Randolph SE: Socio-economic factors in the differentialupsurge of tick-borne encephalitis in Central and Eastern Europe. Rev.Med. Virol 2008, 18:81-95.

7. Cardenas R, Sandoval CM, Rodriguez-Morales AJ, Franco-Paredes C: Impactof climate variability in the occurrence of leishmaniasis in northeasternColombia. Am. J. Trop. Med. Hyg 2006, 75:273-277.

8. Curriero FC, Patz JA, Rose JB, Lele S: The association between extremeprecipitation and waterborne disease outbreaks in the United States.Am. J. Publ. Hlth 2001, 91:1194-1199.

9. Ogden NH, Maarouf A, Barker IK, Bigras-Poulin M, Lindsay LR,Morshed MG, O’Callaghan CJ, Ramay F, Waltner-Toews D, Charron DF:Climate change and the potential for range expansion of the Lymedisease vector Ixodes scapularis in Canada. Int. J. Parasitol 2006,36:63-70.

10. Jenkins EJ, Veitch AM, Kutz SJ, Hoberg EP, Polley L: Climate change andthe epidemiology of protostrongylid nematodes in northern ecosystems:Parelaphostrongylus odocoilei and Protostrongylus stilesi in Dall’s sheep(Ovis d. dalli). Parasitology 2006, 132:387-401.

11. Poulin R: Global warming and temperature-mediated increases incercarial emergence in trematode parasites. Parasitology 2006,132:143-151.

12. O’Connor LJ, Walkden-Brown SW, Kahn LP: Ecology of the free-livingstages of major trichostrongylid parasites of sheep. Vet. Parasitol 2006,142:1-15.

13. Van Dijk J, Morgan ER: The influence of temperature on thedevelopment, hatching and survival of Nematodirus battus larvae.Parasitology 2008, 135:269.

14. Ollerenshaw CB, Smith LP: Meteorological factors and forecasts ofhelminthic disease. Adv. Parasitol 1969, 7:283-323.

15. Cox J, Abeku TA: Early warning systems for malaria in Africa: fromblueprint to practice. Trends Parasitol 2007, 23:243-246.

16. Fuentes MV, Sainz-Elipe S, Nieto P, Malone JB, Mas-Coma S: GeographicalInformation Systems risk assessment models for zoonotic fasciolosis inthe South American Andes region. Parassitologia (Roma) 2005, 47:51-156.

17. Chaves LF, Pascaul M: Climate cycles and forecasts of cutaneousleishmaniasis, a non-stationary vector-borne disease. PLoS Medicine 2006,3:1320-1327.

18. Polley L: Navigating parasite webs and parasite flows: emerging andre-emerging parasitic zoonoses of wildlife origin. Int. J. Parasitol 2005,35:1279-1294.

19. Hoberg EP, Polley L, Jenkins EJ, Kutz SJ, Veitch AM, Elkin BT: Integratedapproaches and empirical models for the investigation of parasiticdiseases in northern wildlife. Emerg. Inf. Dis 2008, 14:10-17.

20. Kutz SJ, Asmundsson I, Hoberg EP, Appleyard GD, Jenkins EJ, Beckman K,Branigan M, Butler L, Chilton NB, Cooley D, Elkin B, Huby-Chilton F,Johnson D, Kuchboev A, Nagy J, Oakley M, Popko R, Scheer A, Simard M,Veitch A: Serendipitous discovery of a novel protostrongylid (Nematoda:Metastrongyloidea) in caribou, muskoxen, and moose from highlatitudes of North America based on DNA sequence comparisons. Can. J.Zool. 2007, 85:1143-1156.

21. Furgal C, Seguin J: Climate change, health, and vulnerability in Canadiannorthern aboriginal communities. Envir. Health Perspect 2006,114:1964-1970.

22. Anisimov OA, Vaughan DG, Callaghan TV, Furgal C, Marchant H, Prowse TD,Vilhjálmsson H, Walsh JE: Polar regions (Arctic and Antarctic). ClimateChange 2007: Impacts, Adaptation and Vulnerability. In Contribution ofWorking Group II to the Fourth Assessment Report of the Intergovernmental Panelon Climate Change. Edited by: Parry ML, Canziani OF, Palutikof JP, van derLinden PJ, Hanson CE. Cambridge University Press, Cambridge; 2007:653-685.

23. Root TL, Price JT, Hall KR, Schneider SH, Rosenzweig C, Pounds JA:Fingerprints of global warming on wild animals and plants. Nature 2004,421:57-60.

24. Brooks DR, Hoberg EP: How will global climate change affect parasite-host assemblages? Trends Parasitol 2007, 23:571-574.

25. Hoberg EP, Polley L, Jenkins EJ, Kutz SJ: Pathogens of domestic and free-ranging ungulates: global climate change in temperate to boreallatitudes in North America. Rev Sci Tech 2008, 27:511-528.

26. Rausch RL, George JC, Brower HK: Effect of climate warming on thePacific walrus, and potential modification of its helminth fauna. J.Parasitol 2007, 93:1247-1251.

27. Lebarbenchon C, Brown SP, Poulin R, Gauthier-Clerc M, Thomas F:Evolution of pathogens in a man-made world. Mol. Ecol 2008, 17:475-484.

28. Albon SD, Stien A, Irvine RJ, Langvatn R, Ropstad E, Halvorsen O: The roleof parasites in the dynamics of a reindeer population. Proc. R. Soc. Lond.B 2002, 269:1625-1632.


Page 3 of 31

http://www.ncbi.nlm.nih.gov/pubmed/11113264?dopt=Abstract



































29. Stien A, Irvine RJ, Ropstad E, Halvorsen O, Langvatn R, Albon SD: Theimpact of gastrointestinal nematodes on wild reindeer: experimentaland cross-sectional studies. J. Anim. Ecol 2002, 71:937-945.

30. Kutz SJ, Hoberg EP, Nishi J, Polley L: Development of the muskoxlungworm, Umingmakstrongylus pallikuukensis (Protostrongylidae) ingastropods in the Arctic. Can. J. Zool 2002, 80:1977-1985.

31. Kutz SJ, Hoberg EP, Polley L, Jenkins EJ: Global warming is changing thedynamics of arctic host-parasite systems. Proc. R. Soc. Lond. B 2005,272:2571-2576.

32. Kutz S, Garde E, Veitch A, Nagy J, Ghandi F, Polley L: Muskox lungworm(Umingmakstrongylus pallikuukensis) does not establish inexperimentally exposed thinhorn sheep (Ovis dalli). J. Wildl. Dis 2004,40:197-204.

33. Hunter PR, Thompson RCA: The zoonotic transmission of Giardia andCryptosporidium. Int. J. Parasitol 2005, 35:1181-1190.

34. Cattadori IM, Haydon DT, Hudson PJ: Parasites and climate synchronizered grouse populations. Nature 2005, 433:737-741.

S2GIS in vector borne diseasesGuy HendrickxAvia-GIS, Risschotlei 33, B-2980 Zoersel, BelgiumE-mail: [email protected] Veterinaria Scandinavica 2010, 52(Suppl 1):S2

Introduction: Since its origin in the late 1980’s, the development ofgeographical information science and of geographical informationsystems (GIS), the toolset enabling to conduct this type of research, hasnow reached the necessary maturity to be considered a main streamapplication: GIS evolved from the status of ‘a promising tool’ to the statusof ‘a tool achieving its promises’. To maintain this status the entire chainof events from data collection to data analysis must be adapted to thespecific needs and requirements of spatial analysis.From spatial data sampling to spatial information systems: Avia-GISis a consulting company specialized in the development of agro-veterinary and public health information systems. In Figure 1 below thedeveloped approach enabling the integration of the different stepsrequired for the development of data driven spatial information systemsis depicted. In this paper a selection of obtained results are shown whenapplying this approach to the field of vector borne diseases.First the principal of statistical spatial distribution models is highlightedusing the example of Rhipicephalus appendiculatus in Kenya, a ticktransmitting East Coast fever in cattle. The need for representative grounddata obtained using a robust spatial sampling strategy is highlighted andthe example of how this was achieved in MODIRISK, a project aiming atmapping mosquito species and biodiversity patterns in Belgium, is given.

Spatial model outputs using observed presence and absence data forAedes albopictus, an invasive species in (Southern) Europe, obtainedthrough an international network of scientific collaborators, are thencompared to potential distribution maps computed using a multicriteriadecision analysis approach (MCDA) based on expert knowledge. Thelimits and complementary value of both approaches are discussed.The impact of wind on the dispersal of airborne vectors of disease isillustrated using as an example the current invasion of Europe bybluetongue (BTV8) through endemic midges. Understanding thesedispersal patterns is an important step toward adding a dynamiccomponent to such models and increase there predictive potential aspart of planning tools for control measures: e.g. protection of cattletrough focussed vaccination. Ongoing work on the development of anairborne trapping device will further improve our knowledge of the 3Ddistribution patterns/ behaviour of the airborne midges and therefore thequality of the developed models.Finally the example of Vet-geoTools is used to show how an integratedspatial veterinary information system can contribute to the improvedmanagement of veterinary outbreaks.Conclusion: It is concluded that the development of such an integratedapproach using state of the art tools is essential to extract maximal valueof geographical information science outputs. This can only be achievedthrough combining state of the art research with state of the art tooldevelopment: a perfect meeting place, and play ground, for academicgroups and innovative SME’s.Further reading: Information on all projects and outputs mentionedabove can be downloaded directly from the Avia-GIS website at: http://www.avia-gis.com

S3Vector-borne nematodes, emerging parasites in Finnish cervidsSauli Laaksonen*, Antti OksanenFinnish Food Safety Authority Evira, Fish and Wildlife Health Research Unit,P.O.Box 517, FI-90101 Oulu, FinlandActa Veterinaria Scandinavica 2010, 52(Suppl 1):S3

Summary: There is a growing body of literature documenting theexpansion of emerging parasites to sub-arctic areas. The potential impactof global warming on shifts in the spatio-temporal distribution andtransmission dynamics of vector-borne diseases in domesticated and wildungulates may be remarkable [1]. Recent Finnish studies have revealedan array of Filarioid nematodes and associated diseases that appear to beemerging in northern ungulates [2-4].Members of the genus Setaria (Filarioidea: Onchocercidae) are found inthe abdominal cavities of artiodactyls (especially Bovidae), equids andhyracoids. All produce microfilariae which are present in host blood [5],and known vectors are haematophagous mosquitoes (Culicidae spp) andhorn flies (Haematobia spp.) [6].The Filarioid nematode Setaria tundra was first described in semi-domesticated reindeer (Rangifer tarandus tarandus) in Arkhangelsk area,Russia [7]. Setaria infections appear to have emerged in Scandinavian reindeernot later than in the 1960’s. In 1973, S. tundra was observed for the first timein northern Norway where there was an outbreak of peritonitis in reindeer, asthere was in Sweden, too. Also in 1973, tens of thousands of reindeer died inthe northern part of the Finnish reindeer husbandry area. Severe peritonitisand large numbers of Setaria worms were commonly found. Following this,the incidence of Setaria in reindeer in Scandinavia diminished.According to meat inspection data and clinical reports from practisingveterinarians, the latest outbreak of peritonitis in reindeer started in 2003in the southern and middle part of the Finnish reindeer herding area. Inthe province of Oulu, the proportion of reindeer viscerae condemned inmeat inspection due to parasitic lesions increased from 4.9 % in 2001 to47 % in 2004 and in Lapland from 1.4 % in 2001 to 43 % in 2006. Thefocus of the outbreak moved approximately 100 km northwards yearly sothat in 2005 only the reindeer in the northernmost small part of Finland(Upper Lapland) were free of changes. In the same time the outbreakseems to have settled in the southern area. [2].The causative agent was recognized both morphologically and molecularbiologically as S. tundra. DNA sequence of S. tundra parasitising reindeerin North Finland was deposited in GenBank under accession numberDQ097309. [2,3].

Figure 1 (abstract S2) From spatial data to spatial information systems


Page 4 of 31








http://www.avia-gis.com

http://www.avia-gis.com

The habitus of reindeer calves heavily infected with S. tundra expresseddecreased welfare; low body condition and undeveloped winter fur coat.The meat inspection findings of peritonitic reindeer carcasses includedascites fluid, green fibrin deposits, adhesions and live and dead S. tundranematodes. Histopathologically, changes indicated granulomatousperitonitis with lymphoplasmacytic and eosinophilic infiltration. Nospecific bacterial growth was found. No significant impact on meat pHvalues nor on organoleptic evaluation of meat was found. There was asignificant positive correlation between worm count and the degree ofperitonitis and a negative correlation between the degree of peritonitisand back fat layer [2]. Earlier, Setaria yehi has been associated with lowgrade chronic peritonitis in Alaskan reindeer [8] and S. tundra with mildto severe peritonitis together with Corynebacterium sp. in Swedishreindeer [9]. Our studies revealed that S. tundra can act as a significantpathogen for reindeer, which was evident at both ante and post-morteminspection and in histological examination.In order to monitor the S. tundra parasite dynamics in nature, parasitesamples from wild cervids has also been collected [2]. In moose (Alcesalces), the most abundant wild cervid in the reindeer herding area, onlyfew cases of pre adult encapsulated S. tundra nematodes on the surfaceof the liver, but no peritonitis, were seen.The moose was evidently not asuitable host reservoir for the present S. tundra haplotype. The moosepopulation in northern Finland peaked in the years 2004 and 2005. Thereis a previous report of a peritonitis outbreak in moose in Finnish Laplandin 1989 associated with Setaria sp. nematodes [10]. The parasite wasgenetically identified as another haplotype of S. tundra. Although thisearlier outbreak took place within the reindeer husbandry area, noreports on associated increased morbidity in reindeer exist.According to our studies it is possible that the high percentage of theKainuu population of wild forest reindeer (Rangifer tarandus fennicus) withsigns of peritonitis caused by S. tundra (62 % of 34 animals examined) [2]is associated with the decrease of the population [11] from 1700individuals in 2001 to 1000 in 2005.Two roe deer (Capreolus capreolus) examined fresh in the field hadS. tundra nematodes in abdomen but no signs of peritonitis. According toour studies, the roe deer seems a capable host and asymptomatic carrierfor S. tundra. This conclusion is supported by the first S. tundraappearance in Scandinavia in the early 1970’s [2] simultaneously with theinvasion of the roe deer to North Scandinavia [12]. Further, there wereminor nucleotide differences between the reindeer S. tundra sequence(648 bp) and that from roe deer parasites in Italy (GenBank AJ544874)[13]. In the consideration of reservoir host capacity of roe deer it is worthnoting that especially young male roe deer can migrate hundreds ofkilometres from their birthplace [14].Our studies have revealed that S. tundra can have a significantpathogenic influence on the health of reindeer, and cause outbreaks alsoin moose population [10] and may further have consequences to cervidpopulation dynamics.The S. tundra outbreak in Sweden in 1973 was associated with unusuallywarm weather and appearance of larger than usual numbers ofmosquitoes and gnats [9]. The summers 1972 and 1973 were also verywarm in Finland, as were 2002 and 2003 (Finnish Meteorological Institutedata, personal communication S. Nikander 2004). Mosquitoes areconsidered vectors for S. tundra, but the life cycle in vectors is poorlyunderstoodClimate change is predicted to increase insect activity and thus promotevector-borne Filarioid nematodes’ emerge to North and becoming athreat to the wellbeing of arctic ungulates. Especially mosquito-bornediseases are among those diseases most sensitive to climate becauseclimate change would directly affect disease transmission by shifting thevector’s geographic range and increasing reproductive and biting ratesand by shortening the pathogen incubation period [15].Our research group has studied the invasion and reservoirs of S. tundra inFinnish cervid populations, which studies we shortly review in this paper.We highlight the possibility that vector borne parasites may, by theimpact of global climate change, further have consequences to wild anddomestic ungulates. The study revealed the absence of baselineknowledge concerning temporal parasitic biodiversity in cervids at highlatitudes. Therefore it is important to gain knowledge about theseparasites’ ecology, dynamics, and the impact on man and animal health.Acknowledgements: These studies were partly funded by Ministry ofAgriculture and Forestry (MAKERA).

References1. Hoberg EP, Polley L, Jenkins EJ, Kutz SJ, Veitch AM, Elkin BT: Integrated

approaches and empirical models for investigation of parasitic diseasesin northern wildlife. Emerg Inf Dis 2008, 14:10-17.

2. Laaksonen S, Kuusela J, Nikander S, Nylund M, Oksanen A: Parasiticperitonitis outbreak in reindeer (Rangifer tarandus tarandus) in Finland.Vet Rec 2007, 160:835-841.

3. Nikander S, Laaksonen S, Saari S, Oksanen A: The morphology of thefilarioid nematode Setaria tundra, the cause of peritonitis in reindeerRangifer tarandus. J Helminth 2007, 81:49-55.

4. Solismaa M, Laaksonen S, Nylund M, Pitkänen E, Airakorpi R, Oksanen A:Filarioid nematodes in cattle, sheep and horses in Finland. Acta Vet.Scand. 2008, 50:20.

5. Anderson RC: The Superfamily Filarioidea. In Nematode parasites ofvertebrates; their development and transmission. 2nd edition. CABI Publishing,New York; 2000:467-529.

6. Shol VA, Drobischenko NI: Development of Setaria cervi (Rudolphi, 1819)in Cervus elaphus maral. Helminthologia (Bratislava) 1973, 14:214-246,(Russian with English abstract).

7. Rajevsky SA: Zwei bisher unbekannten Nematoden (Setarien) vonRangifer tarandus und von Cervus canadensis asiaticus. Two hithertounknown nematodes Setaria species from Rangifer tarandus and from Cervuscanadensis asiaticus Z Infekt Krank. Hyg Haustiere 1928, 35:40-52, (InGerman).

8. Dieterich RA, Luick JR: The occurrence of Setaria in reindeer. J Wild Dis1971, 7:242-245.

9. Rehbinder C, Christensson D, Glatthard V: Parasitic granulomas in reindeer.A histopathological, parasitological and bacteriological study. Nordiskveterinaermedicin 1975, 27:499-507.

10. Nygren T: Riistantutkimusosaston tiedote. Bulletin of Finnish Game andFisheries Institute 1990, 104, (in Finnish).

11. Kojola I: Petojen vaikutus metsäpeurakannoissa. Suomen Riista 2007,53:42-48, (in Finnish).

12. Haugerud RE: Rådyret vandrer mot nord. Ottar 1989, 5:31-36, (inNorwegian).

13. Casiraghi M, Bain O, Guerro R, Martin C, Pocacqua V, Gardner SL,Franceshi A, Bandi C: Mapping the presence of Wolbachia pipientis onthe phylogeny of filarial nematodes: evidence for symbiont loss duringevolution. International J Parasit 2004, 34:191-203.

14. Cederlund G, Liber O: in Rådjuret, viltet, ekologin och jakten. Almqvist andWiksell Tryckeri, Uppsala 1995, 113-117, (in Swedish).

15. Patz JA, Epstein PR, Burke TA, Balbus JM: Global climate change andemerging infectious diseases. JAMA 1996, 275:217-23.

S4Human medical view on zoonotic parasitesAntti LavikainenDepartment of Bacteriology and Immunology, Haartman Institute, Universityof Helsinki, FinlandActa Veterinaria Scandinavica 2010, 52(Suppl 1):S4

Summary: From medical point of view, a zoonosis is any infectiousdisease that is naturally transmissible from vertebrate animals to humans[1]. A stricter definition is a disease that normally exists in othervertebrate animals, but can be accidentally transmitted to humans [2]. InNordic countries, parasites are rare (and zoonotic parasites even moreunusual) causative agents of human infections probably due to goodhygiene and climatic conditions. In most cases, parasitic infections are offoreign origin, except for some relatively common indigenous infestationssuch as enterobiasis (caused by the human pinworm, Enterobiusvermicularis) and pediculosis (caused by the human head louse, Pediculushumanus).Worldwide, the most significant genus of human parasites is Plasmodium.It is the causative agent of malaria, a severe tropical protozoan disease,which kills globally more than one million people every year [3]. InFinland, about twenty cases of malaria are diagnosed annually [4]. In2007, P. knowlesii infection was diagnosed in Finland in a tourist who hadtraveled in Malay Peninsula [4]. P. knowlesii is a Plasmodium of monkeys.This was second reported case of P. knowlesii malaria in a tourist. Duringthe 19th century, malaria was an indoors transmitted disease in Finland,as Anopheles mosquitoes hibernated in peoples’ households [5].


Page 5 of 31











Intestinal parasitoses are the most common parasitic infections. AmongFinnish asymptomatic population, pathogenic intestinal parasites (mostlyGiardia lamblia) can be found from 1.5 % of people [6]. However, only300 cases of clinical giardiasis are diagnosed in Finland annually [7], andreported numbers of diagnosed amebiasis cases (caused by Entamoebahistolytica) range from 30 to more than 100 [7,8]. These protozoans arehuman parasites, and infections caused by them can occur throughcontaminated food, water or by faecal-oral route. According to thestatistics of the Parasitological unit of HUSLAB (Laboratory of HospitalDistrict of Helsinki and Uusimaa county, Finland) from 2005 to 2007, themost important intestinal helminthes were pinworms, the humanwhipworm (Trichuris trichiura) and intestinal roundworms (Ascaris spp.).The swine roundworm (Ascaris suum), is a zoonotic parasite, but it wasnot routinely differentiated from human roundworm (A. lumbricoides).Formerly, the broad fish tapeworm (Diphyllobothrium latum) was a majorhealth problem in Finland, and it has been called “the national parasite ofFinland” [9,10]. Although it has been diminished drastically, it has notbeen totally eradicated. Around twenty human cases are still diagnosedannually in Finland, and the situation is similar in Sweden [11]. In contrastto diphyllobothriasis, which is mostly an indigenous disease, humanintestinal taeniases are imported cases. About a handful of taeniasis casesare diagnosted in HUSLAB yearly, and the beef tapeworm (Taeniasaginata) is more common finding than the pork tapeworm (T. solium). Inthe strict sense (see the definition above), diphyllobothriasis andtaeniases should not be called zoonoses, since humans are importantdefinitive hosts of D. latum and essential for T. saginata and T. solium,although vertebrate animals (fishes, cattle and swine, respectively) act assources of human infections.Echinococcus spp. are the most important zoonotic cestodes worldwide.Their larvae are causative agents of serious diseases calledechinococcoses. Until 1960’s, human cystic echinococcosis was asignificant public health problem among reindeer herding Sámipopulation in Swedish and Norwegian Lapland [12]. Human cases werefound also in Finnish Lapland, but only few reports have been published.Later, the parasite was eradicated from the reindeer-dog cycle, andendemic human cases have not been diagnosed for several decades. Inthe Parasitological unit of HUSLAB, eight echinococcosis cases werediagnosed between 2002 and 2008. These cases cover most of thediagnoses in Finland during that time period. All of them were caused byso-called sheep strain of E. granulosus. One of the patients was a Finn,but an endemic infection was excluded by the strain determination.Another endemic zoonotic parasitosis, which seems to be disappearedfrom Nordic countries as a human infection, is trichinellosis. This diseasecaused by larvae of nematodes of the genus Trichinella has not beendiagnosed for a long time. This contrasts the fact that Trichinella spp. arecommon in wild and domestic animals [13].Several exotic parasites, which occur as sporadic companions of travelers,can cause tissue lesions and even systemic disease. For example,leishmaniasis is the term given to diseases caused by protozoans of thegenus Leishmania[14]. These parasites are transmitted by sand flies, andsmall rodents and dogs are the reservoir of infection. There are two maintypes of clinical disease, cutaneous and systemic leishmaniases.Larvae of gastrointestinal nematodes of dogs and cats (Toxocara canisand T. cati, respectively), can cause disease called visceral larva migrans inhumans, chiefly in children [15,16]. Larvae migrate through inner organsand cause mechanical damage and eosinophilic lesions. Toxocara spp. aregeographically widely distributed. Larva migrans is obviously aunderdiagnosed zoonosis, and its prevalence in Nordic countries has notbeen studied recently. In HUSLAB material in 2007, seven patients hadpositive toxocariasis serology. One of these was most probably anunspecific seroreactivity because the same sample responded also againstseveral other helminth antigens. Six patients were children (age of 2-16years) and one was an elder person (75 years).Toxoplasmosis is a disease caused by the protozoan parasite, Toxoplasmagondii which infects up to one-third of the world human population [17].The definitive host of T. gondii is the cat; humans become infected byingesting oocysts (e.g., by eating vegetables contaminated with catfaeces or soil) or tissue cysts in meat. Toxoplasmosis in neonates andimmunocompromised patients can lead to severe disease and death. Ithas been estimated that 50-60 infants suffer from congenitaltoxoplasmosis annually (prevalence 1/1000) in Finland [18]. However,reported prevalences in Sweden, Norway and Denmark are much lower

(0.73-3.1/10,000) [19-21]. Anyway, due to the relatively high prevalence,indigenous occurrence and severe clinical manifestations toxoplasmosiscan be considered to be one of the most important true zoonoticparasitoses in the Nordic countries.In order to understand the transmission dynamics of zoonotic parasiticinfections to humans, it is essential to have knowledge on the life cycleand prevalence of infection in other animals, both domestic and wild.References1. World Health Organization: Zoonoses. [http://www.who.int/topics/zoonoses/

en/].2. Bannister BA, Begg NT, Gillespie SH: Infectious Disease. Oxford: Blackwell

Science 1996, 392.3. World Health Organization: Malaria. [http://www.who.int/mediacentre/

factsheets/fs094/en/index.html].4. Siikamäki H: Malariatapausten määrä pysyi ennallaan. Suomen Lääkärilehti

2008, 63:1847.5. Huldén L, Huldén L, Heliövaara K: Endemic malaria: an ‘indoor’ disease in

northern Europe. Historical data analysed. Malaria Journal 2005, 4:19.6. Siikamäki H, Kyrönseppä H, Jokiranta S: Suoliston parasiitti-infektiot.

Duodecim 2002, 118:1235-1247.7. National Public Health Institute: the Statistical Database of the Infectious

Diseases Register. [http://www3.ktl.fi/].8. Nohynek H, Siikamäki H, Peltonen R: Matkailijoiden infektiot. Mikrobiologia

ja infektiosairaudet II Helsinki: Kustannus Oy Duodecim: P Huovinen, S Meri,H Peltola, M Vaara, A Vaheri, V Valtonen , 1 2003, 653-668.

9. B von Bonsdorff: The fish tapeworm, Diphyllobothrium latum; a majorhealth problem in Finland. World Med J 1964, 11:170-172.

10. Konttinen Y, Hasenson S, Valovirta I, Malmström M, Ikonen E, Virtanen jaI:Unohdettu kansallisloinen–tapausselostus ja lyhyt kirjallisuuskatsaus.Duodecim 1997, 113:1549.

11. Dupouy-Camet J, Peduzzi R: Current situation of human diphyllobothriasisin Europe. Eurosurveill 2004, 9:31-35.

12. Lavikainen A: Ihmisen ekinokokkitauti Suomen, Ruotsin ja Norjan Lapissa.Suomen Eläinlääkärilehti 2005, 110:7-13.

13. L Oivanen L, Kapel CM, Pozio E, La Rosa G, Mikkonen T, Sukura A:Associations between Trichinella species and host species in Finland.J Parasitol. 2002, 88:84-8.

14. Király C: Kasvojen iholeishmanioosi etelänmatkan tuliaisena. Duodecim,1995, 111:1104.

15. Raether W: Gastrointestinal nematodes in dogs and cats. Parasitology infocus Berlin: Springer-Verlag: H Mehlhorn 1988, 841.

16. Vuento Risto: Koti- ja lemmikkieläimet tartuntatautien lähteenä. Duodecim1994, 110:555.

17. Birgisdóttir A, Asbjörnsdottir H, Cook E, Gislason D, Jansson C, Olafsson I,Gislason T, Jogi R, Thjodleifsson B: Seroprevalence of Toxoplasma gondiiin Sweden, Estonia and Iceland. Scand J Infect Dis 2006, 38:625-631.

18. Lappalainen M: Raskaudenaikaista toksoplasmainfektiota kannattaaseuloa? Suomen Lääkärilehti 1996, 51:1316.

19. Evengård B, Petersson K, Engman ML, Wiklund S, Ivarsson SA, Teär-Fahnehjelm K, Forsgren M, Gilbert R, Malm G: Low incidence oftoxoplasma infection during pregnancy and in newborns in Sweden.Epidemiol Infect 2001, 127:121-127.

20. Schmidt DR, Hogh B, Andersen O, Fuchs J, Fledelius H, Petersen E: Thenational neonatal screening programme for congenital toxoplasmosis inDenmark: results from the initial four years, 1999-2002. Arch Dis Child2006, 91:661-665.

21. Jenum PA, Stray-Pedersen B, Melby KK, Kapperud G, Whitelaw A, Eskild A,Eng J: Incidence of Toxoplasma gondii infection in 35,940 pregnantwomen in Norway and pregnancy outcome for infected women. J ClinMicrobiol 1998, 36:2900-2906.

S5Echinococcus spp. and echinococcosisBruno GottsteinFaculty of Medicine, Institute of Parasitology, University of Bern, Bern,SwitzerlandE-mail: [email protected] Veterinaria Scandinavica 2010, 52(Suppl 1):S5

Summary: Echinococcus spp. are cestode parasites commonly known assmall tapeworms of carnivorous animals. Their medical importance lies in


Page 6 of 31

http://www.who.int/topics/zoonoses/en/

http://www.who.int/topics/zoonoses/en/

http://www.who.int/mediacentre/factsheets/fs094/en/index.html

http://www.who.int/mediacentre/factsheets/fs094/en/index.html




http://www3.ktl.fi/















the infection of humans by the larval stage of the parasites,predominantly including Echinococcus granulosus, which is the causativeagent of cystic echinococcosis (CE) and Echinococcus multilocularis, whichcauses alveolar echinococcosis (AE).A few other species or genotypes are only very rarely or not at all foundin humans. Due to the emerging situation in many parts of Europe, thepresent article will predominantly focus on E. multilocularis .The natural life cycle of E. multilocularis involves predominantly red andarctic foxes as definitive hosts, but domestic dogs can also becomeinfected and represent an important infection source for humans inhighly endemic areas. In the definitive host, egg production starts asearly as 28 days after infection. After egg ingestion by a rodent or ahuman, larval maturation will occur practically exclusively within the livertissue. The geographic distribution of E. multilocularis is restricted to thenorthern hemisphere. In Europe, relatively frequent reports of AE inhumans occur in central and eastern France, Switzerland, Austria andGermany. Within the past ten years, the endemic area of Europe nowincludes many more countries such as Belgium, The Netherlands, Italy,and most former Eastern countries as far as up to Estonia. The Asianareas where E. multilocularis occurs include the whole zone from theWhite Sea eastward to the Bering Strait, covering large parts of Siberia,western and central parts of China and northern Japan. Worldwide thereare scant data on the overall prevalence of human AE. Some well-documented studies demonstrate a generally low prevalence amongaffected human populations. The annual mean incidence of new cases indifferent areas including Switzerland, France, Germany and Japan hastherefore been reported to vary between 0.1 and 1.2/100,000 inhabitants.The incidence of human cases correlates with the prevalence in foxesand the fox population density. Recently, a study documented that afour-fold increase of the fox population in Switzerland resulted in astatistically significant increase of the annual incidence of AE cases [1](Schweiger et al., 2007). This dramatic increase in red fox populations hasalso been reported throughout Europe, especially in urban areas. Theso-called city-fox phenomenon and, thereafter, the increased proximity offoxes with humans and an urban domestic dog – rodent cycle may,therefore, have significant public health implications [1-3].In infected humans the E. multilocularis metacestode (larva) developsprimarily in the liver. Occasionally, secondary lesions form metastases inthe lungs, brain and other organs. The typical lesion appearsmacroscopically as a dispersed mass of fibrous tissue with aconglomerate of scattered vesiculated cavities with diameters rangingfrom a few millimeters to centimeters in size. In advanced chronic cases,a central necrotic cavity containing a viscous fluid may form, and rarelythere is a bacterial superinfection. The lesion often contains focal zonesof calcification, typically within the metacestode tissue. Histologically, thehepatic lesion is characterized by a conglomerate of small vesicles andcysts demarcated by a thin PAS-positive laminated layer with or withoutan inner germinative layer [4]. Parasite proliferation is usuallyaccompanied by a granulomatous host reaction, including vigoroussynthesis of fibrous and germinative tissue in the periphery of themetacestode, but also necrotic changes centrally. In contrast to lesions insusceptible rodent hosts, lesions from infected human patients rarelyshow protoscolex formation within vesicles and cysts. Genetic andimmunologic host factors are responsible for the resistance shown bysome patients in whom there is an early ‘dying out’ or ‘abortion’ of themetacestode [5,6]. Therefore, not every individual infected withE. multilocularis is susceptible to unlimited metacestode proliferation anddevelops symptoms in the average within 5–15 years after infection. Thehost mechanisms modulating the course of infection are most likely of animmunologic nature, including primarily suppressor T cell interactions.Thus, the periparasitic granuloma, mainly composed of macrophages,myofibroblasts and T cells, contains a large number of CD4+ T cellsin patients with abortive or died-out lesions, whereas in patients withactive metacestodes the number of CD8+ T cells is increased. Animmunosuppressive process is assumed to downregulate the lymphoidmacrophage system. Conversely, the status of cured AE is generallyreflected by a high in-vitro lymphoproliferative response. The cytokinemRNA levels following E. multilocularis antigen stimulation of lymphocytesshow an enhanced production of Th2-cell cytokine transcripts IL-3, IL-4and IL-10 in patients, including a significant IL-5 mRNA expression inpatients and not in healthy control donors. A lack or deficiency of Th cellactivity such as in advanced AIDS is associated with a rapid and

unlimited growth and dissemination of the parasite in AE, recovery of theT cell status in AIDS is prognostically favorable.More detailed information about the host-parasite interplay that decidesabout the outcome of infection has been achieved with the murinemodel of AE. The involvement of cellular immunity in controlling theinfection is strongly suggested by the intense granulomatous infiltrationobserved in the periparasitic area of lesions. Immunodeficient athymicnude and SCID mice exhibited high susceptibility to infection anddisease, thus suggesting that the host cell mediated immune responseplays an important role in suppressing the larval growth. E. multilocularisappears to induce skewed Th2-responses. Based on in vitro and in vivostudies, Th2 dominated immunity was more associated with increasedsusceptibility to disease, while Th1 cell activation through IL-12, IFN .g,TNF.a and IFN.a was suggested to correlate with a more protectiveimmunity in AE. Nevertheless, effective suppression of larval growth bymeans of an immunological attack is hampered by the fact, that theparasite synthesizes a carbohydrate-rich laminated layer in order to beprotected from host effector mechanisms, as outlined above.Basically, the larval infection with Echinococcus multilocularis begins withthe intrahepatic postoncospheral development of a metacestode that – atits mature stage - consists of an inner germinal and the outer laminatedlayer as discussed above [4]. Several lines of evidence obtained in vivoand in vitro indicate the important bio-protective role of the laminatedlayer, e.g. as to protect the germinal layer from nitric oxide produced byperiparasitic macrophages and dendritic cells, and also to preventimmune recognition by surrounding T cells. On the other hand, the highperiparasitic NO production by peritoneal exudate cells contributes toperiparasitic immunosuppression [7], explaining why iNOS deficient miceexhibit a significantly lower susceptibility towards experimental infection[8]. The intense periparasitic granulomatous infiltration indicates anintense host-parasite interaction, and the involvement of cellularimmunity in control of the metacestode growth kinetics is stronglysuggested by experiments carried out in T cell deficient mouse strains [9].Carbohydrate components of the laminated layer, as the Em2(G11) andEm492 components discussed above, yield immunomodulatory effectsthat allow the parasite to survive in the host. I.e., the IgG response to theEm2(G11)-antigen takes place independently of alpha-beta+CD4+ T cells,and in the absence of interactions between CD40 and CD40 ligand [10].Such parasite molecules also interfere with antigen presentation and cellactivation, leading to a mixed Th1/Th2-type response at the later stage ofinfection. Furthermore, Em492 [11] and other (not yet published) purifiedparasite metabolites suppress ConA and antigen-stimulated splenocyteproliferation. Infected mouse macrophages (AE-MØ) as APCs exhibited areduced ability to present a conventional antigen (chicken ovalbumin,C-Ova) to specific responder lymph node T cells when compared tonormal MØ [12].Echinococcus granulosus parasitizes as a small tapeworm the smallintestine of dogs and occasionally other carnivores. The shedding ofgravid proglottids or eggs in the feces occurs within 4–6 weeks afterinfection of the definitive host. Ingestion of eggs by intermediate hostanimals or humans results in the development of a fully maturemetacestode (i.e. hydatid cyst) over a period of several months to years.Infections with E. granulosus occur worldwide, however predominantly incountries of South and Central America, the European and African part ofthe Mediterranean area, the Middle East and some sub-Saharan countries,Russia and China. Most cases observed in Central Europe and the USAare associated with immigrants from highly endemic areas. Various strainsof E. granulosus have been described, and differ especially in theirinfectivity for intermediate hosts such as humans. The most importantstrains for human infection include sheep (G1) and cattle (G5) asintermediate hosts.Cystic echinococcosis (CE) is clinically related to the presence of one ormore well-delineated spherical primary cysts, most frequently formed inthe liver, but other organs such as the lungs, kidney, spleen, brain,heart and bone may be affected too. Tissue damage and organdysfunction result mainly from this gradual process of space-occupyingdisplacement of vital host tissue, vessels or parts of organs.Consequently, clinical manifestations are primarily determined by thesite, size and number of the cysts, and are therefore highly variable.Accidental rupture of the cysts can be followed by a massive release ofcyst fluid and hematogenous or other dissemination of protoscolices.This can result in anaphylactic reactions and multiple secondary cystic


Page 7 of 31

echinococcosis (as protoscolices can develop into secondary cystswithin the same intermediate host). The parasite evokes an immuneresponse, which is involved in the formation of a host-derivedadventitious capsule. This often calcifies uniquely in the periphery ofthe cyst, one of the typical features found in imaging procedures. Inthe liver there may be cholestasis. Commonly, there is pressure atrophyof the surrounding parenchyma. Immunologically, the coexistence ofelevated quantities of interferon IFN-g, IL-4, IL-5, IL-6 and IL-10 observedin most of hydatid patients supports Th1, Th17 and Th2 cell activationin CE. In particular, Th1 cell activation seemed to be more related toprotective immunity, whereas Th2 cell activation was related tosusceptibility to disease.Prevention of both CE and AE focuses primarily on veterinaryinterventions to control the extent and intensity of infection in definitivehost populations, which may indirectly be approached by controlling theprevalence in animal intermediate hosts also. The first includes regularpharmacologic treatment and taking sanitary precautions for handlingdomestic dogs and to prevent infection and egg excretion, respectively.Regular praziquantel treatment of wild-life definitive host may contributeto lower the prevalence in affected areas.For diagnosis, imaging procedures together with serology will yieldappropriate results [13,14]. Sonography is the primary diagnosticprocedure of choice for hepatic cases [15], although false positives occurin up to 10% of cases due to the presence of nonechinococcal serouscysts, abscesses or tumors. Computerized tomography is the bestinvestigation for detecting extrahepatic disease and volumetric follow-upassessment; magnetic resonance imaging (MRI) assists in the diagnosis byidentifying changes in the intra- and extrahepatic venous systems.Ultrasonography is also helpful in following up treated patients assuccessfully treated cysts become hyperechogenic. Calcification ofvariable degree occurs in about 10% of the cysts. Aspiration cytologyappears to be particularly helpful in the detection of pulmonary, renaland other nonhepatic lesions for which imaging techniques and serologydo not provide appropriate diagnostic support. The viability of aspiratedprotoscolices can be determined by microscopic demonstration of flamecell activity and trypan blue dye exclusion. Immunodiagnostic tests todetect serum antibodies are used to support the clinical diagnosis ofboth AE and CE.Assessing the parasite viability in vitro following therapeutic interventionsmay be of tremendous advantage when compared with the invasiveanalysis of resected or biopsied samples. Such alternatives may beoffered by magnetic resonance spectrometry or positron emissiontomography (PET). The latter technique has recently been used forassessing the efficacy of chemotherapy in AE. PET positivity actuallydemonstrates periparasitic inflammatory processes due to a remaingactivity of the metacestode tissue. Serologic tests are more reliable in thediagnosis of AE than CE. The use of purified E. multilocularis antigenssuch as the Em2 antigen and recombinant antigens from the family ofEMR-proteins (EmII/3-10, EM10, EM4 and Em18, all four of themharbouring an identical immunodominant oligopeptide sequence)exhibits diagnostic sensitivities ranging between 91% and 100%, withoverall specificities of 98–100%. These antigens allow discriminationbetween the alveolar and the cystic forms of disease with a reliability of95%. Seroepidemiologic studies reveal asymptomatic preclinical cases ofhuman AE as well as cases in which the metacestode has died at anapparently early stage of infection (see above). Serologic tests are ofvalue for assessing the efficacy of treatment and chemotherapy onlywhen linked to appropriate imaging investigations. Prognostically,disappearance of anti-II/3–10 or anti-Em18 antibody levels coupled to PETnegativity indicates innactivation of AE. The management of CE and AEfollows the strategy recommended in the manual on echinococcosispublished in 2001 by the Office International des Epizooties and theWorld Health Organisation.References1. Schweiger A, Ammann R, Candinas D, Clavien PA, Eckert J, Gottstein B,

Halkic N, Muellhaupt B, Prinz BM, Reichen J, Tarr PE, Torgerson PR,Deplazes P: Human alveolar echinococcosis after fox population increase,Switzerland. Emerg Inf Dis 2007, 13:878-82.

2. Gottstein B, Saucy F, Deplazes P, et al: Is a high prevalence ofEchinococcus multilocularis in wild and domestic animals associated

with increased disease incidence in humans? Emerg Infect Dis 2001,7:408-12.

3. Reperant LA, Hegglin D, Fischer C, Kohler L, Weber JM, Deplazes P:Influence of urbanization on the epidemiology of intestinal helminths ofthe red fox (Vulpes vulpes) in Geneva, Switzerland. Parasitology Research2007, 101:605-611.

4. Gottstein B, Deplazes P, Aubert M: Echinococcus multilocularis:Immunological study on the “Em2-positive” laminated layer during invitro and in vivo post-oncospheral and larval development. ParasitologyResearch 1992, 78:291-297.

5. Sailer M, Soelder B, Allerberger F, Zaknun D, Feichtinger H, Gottstein B:Alveolar echinococcosis in a six-year-old girl with AIDS. J Pediatr 1997,130:320-3.

6. Zingg W, Renner-Schneiter EC, Pauli-Magnus C, Renner EL, van Overbeck J,Schläpfer E, Weber M, Weber R, Opravil M, Gottstein B, Speck RF: Swiss HIVCohort Study. Alveolar echinococcosis of the liver in an adult withhuman immunodeficiency virus type-1 infection. Infection 2004,32:299-302.

7. Dai WJ, Gottstein B: Nitric oxide-mediated immunosuppression followingmurine Echinococcus multilocularis - infection. Immunology 1999,97:107-116.

8. Dai WJ, Waldvogel A, Jungi T, Stettler M, Gottstein B: Inducible nitric oxidesynthase-deficiency in mice increases resistance to chronic infectionwith Echinococcus multilocularis. Immunology 2003, 10:238-44.

9. Dai WJ, Waldvogel A, Siles-Lucas M, Gottstein B: Echinococcusmultilocularis proliferation in mice and respective parasite 14-3-3 geneexpression is mainly controlled by an alphabeta CD4 T-cell-mediatedimmune response. Immunology 2004, 112:481-488.

10. Dai WJ, Hemphill A, Waldvogel A, Ingold K, Deplazes P, Mossmann H, et al:Major carbohydrate antigen of Echinococcus multilocularis induces animmunoglobulin G response independent of alpha beta(+) CD4(+) Tcells. Inf Immun 2001, 69:6074-6083.

11. Walker M, Baz A, Dematteis S, Stettler M, Gottstein B, Schaller J, et al:Isolation and characterization of a secretory fraction of Echinococcusmultilocularis metacestode potentially involved in modulating the host-parasite interface. Infect Immun 2004, 72:527-36.

12. Mejri N, Gottstein B: Intraperitoneal Echinococcus multilocularis infectionin C57BL/6 mice inhibits the up-regulation of B7-1 and B7-2 co-stimulator expression on peritoneal macrophages and causes failure toenhance peritoneal T cell activation. Parasite Immunol 2006, 28:373-385.

13. Ammann RW, Renner EC, Gottstein B, Grimm F, Eckert J, Renner EL, SwissEchinococcosis Study Group: Immunosurveillance of alveolarechinococcosis by specific humoral and cellular immune tests:prospective long-term analysis of the Swiss chemotherapy trial (1976-2001). J Hepatol 2004, 41:551-59.

14. Pawlowski ZS, Eckert J, Vuitton DA, et al: Echinococcosis in humans:clinical aspects, diagnosis and treatment. WHO/OIE Manual onechinococcosis in humans and animals. Paris: WHO/OIE Eckert J et al. 2001,20-71.

15. WHO: International classification of ultrasound images in cysticechinococcosis for application in clinical and field epidemiologicalsettings. Acta Trop 2003, 85:253-61.

S6Dogs and echinococcosis in IcelandSigurdur SigurdarsonThe Icelandic Food- and Vetarinary Authority Austurvegur 64, 800 Selfoss,IcelandActa Veterinaria Scandinavica 2010, 52(Suppl 1):S6

History: Hydatid disease was first described in Icelandic literature aboutthe year 1200. According to the first qualified physician in Iceland, BjarniPálsson (1719-1779) was echinococcosis about 1760 one of the mostfrequent diseases among the human population, and was also commonlyobserved in sheep and cattle. Autopsies and questionaries indicate that20-25% of the inhabitants might have been infested by hydatidosis about1850. The nature of the disease was still unknown at that time. The dogpopulation was estimated to be 15.000-20.000, or about one dog forevery three or four people. At the same time there were in Copenhagen


Page 8 of 31

































1 dog for every 30-32 persons. Obviously there were too many dogs inIceland. The sheep, cattle, dogs and humans lived in close contact. Thedogs often shared a room and even bed with the family, and were thebest playmate for the children. The people lived mostly in primitivehouses at that time and under primitive hygienic conditions. It istherefore not wonder that the hydatid disease flourished as long as thenature of the disease was still obscure.In 1849 the Danish physician P.A.Schleisner (1819-1900) concluded thatone out of every six Icelanders suffered from hydatid disease. In 1862doctor Harald Krabbe (1831-1917) from the Royal Veterinary andAgricultural University in Copenhagen studied the hydatid problem inIceland. He found that 28 out of 100 dogs and most of the old sheep andcows that were slaughtered were infested with echinococcus cysts.Experiments he carried out in cooperation with an Icelandic physician JónC Finsen (1826-1885) proved the relationship between taenias in dogs andthe hydatid cysts in humans. Doctor H. Krabbe realized that mostimportant was to inform the people of the nature of the disease in orderto prevent the infestations of humans and animals with eggs ofthe intestinal parasites of the dog. H. Krabbe was a chief adviser to theIcelandic government on hydatid disease and prophylactic measures in theperiod 1860-1890. His recommendations were followed strictly for morethan 100 years and partially they still are. New infestations by E. granulosuspractially dissappeared in Iceland the decade 1890-1900. That is based on7333 autopsies of people performed in the period 1932-1966. And basedon 15.888 autopsies 1932-1982 only few human infestations occurred after1900.The most recent human cases are a person born in 1937 who wasautopsied in 1960, another person born in 1905 operated 1984 and thethird person born in 1920 operated in 1988. In 1863 an autopsy survey of100 dogs were carried out. E. granulosus was found in 28 of them, 75 dogscarried T. marginata. In the period one hundred years later 200 dogs wereautopsied (1950-1960). T. marginata was found in 11 dogs but none ofthem carried E. granulosus. Reports of meat inspectors from Icelandicabattoirs did not record hydatid cysts in cattle, pigs and horses after 1961.However in the period 1953-1979, cysts of echinococcus were recorded ina total of 21 old ewes, all of which came from few farms on 2 small areasin East-Iceland. There was an indication that the parasite had beenintroduced to the country by an imported dog. After 1979 no hydatid cystshave been found in any animal in Iceland.Why so successful control of hydatid disease in Iceland: Echino-coccosis is a great public health and economic problem in manycountries. It has been extremely difficult to eliminate it in many endemicareas. Apparently it was done in Iceland rather easily. How?The campaign against hydatid disease in Iceland was for more than onecentury and partially still is based on Harald Krabbe´s recommendations:1) Succesful information to the people. Most people in Iceland had losteither relatives or friends as a victim to hydatid disease and the memoryof this disease was and still is dreaded. When people knew what to do,strong parcipitation of both young and old was easy to activate.2) Reduction of the dog population by taxes on all dogs, higher tax onunnessesary dogs and a ban on keeping a dog without permission.Outbrakes of distemper in 1870, 1888 and 1890 reduced the number ofdogs considerably, 3)Preventing the dog gaining access to raw offaland burning cysts in organs 4) Caution in dealing with dogs, esp.Children, 5) Yearly anthelmintic treatment of all dogs after theslaughtering sesion. Some factors that assisted in the campaign: -Ceasingof milking sheep on the farms, - improvement of the houses and hygiene,-strictly practiced caution on the contact between dogs and animals/people. Building of slaughterhouses all over the country in the period1900-1920, then slaughtering on the farms almost ceased. The hydatiddisese was never found in horses, rodents or in wild animals in Iceland.References1. Pálsson PA: Echinococcosis and its elimination in Iceland. In a book in regi

of Ivan Katić Köbenhavn Harald Krabbe Dagbog fra Island 2000, 93-100,Ferðasaga(1863, 1870, 1871).

2. Þórarinsdóttir KH: Echinokokkosen i Island og dr. Harald Krabbes indsatsfor dens bekæmpelse. Köbenhavn OSVAL II – opgave, KöbenhavnsUniversity, medicinske fakultet 1999.

3. Dungal N: New Zealand medical journal. 1957, 56:212-222.4. Einarson M: Búnaðarrit. 1901, 15:125-164.5. Einarson M: Dýralækningabók. Reykjavík 1931, 91-93, 232-235.

6. Finsen J: Iagtagelser angaaende Sygdomsforholdene I Island. Köbenhavn1874, 177.

7. Hlíðar Sig E: Lækning húsdýra Akureyri. 1915, 66-68, 102-104.8. Jónassen J: Ekinokoksygdommen belyst ved islandske Lægers Erfaring.

Köbenhavn 1882, 268.9. Jónsson V: Skírnir. 1954, 128:134-175.10. Jónsson S: Tidsskrift for Veterinærer. 1879, 137-178, 2. Rk., 9 Bd,.11. Krabbe H: Athugasemdir handa Íslendingum um sullaveikina og varnir

móti henni. Köbenhavn 1864, 18.12. Krabbe H: Helmintologiske Undersögelser I Danmark og paa Island med

særlig hensyn til Blæreormlidelserne ............ paa Island. Köbenhavn 1865,64.

13. Magnússon G: Yfirlit um sögu sullaveiki á Íslandi. Reykjavík 1913, 83.14. Pálsson PA, Vigfússon H, Henriksen K: Læknablaðið. 1971, 57:39-51.15. Sigurðsson J: Nordisk Medicinhistorisk Årsbog. 1970, 182-198.16. Thoroddsen Þ: Landbúnaður á Íslandi. 1922, 2:73-84.17. Bang B: Biografier af lærere ved De Danske Veterinærskole. Medlemsblad

for Den Danske Dyrlægeforening, 6. Aargang, Köbenhavn 1923, 93-99.18. Schultz Forlag JH: Dansk Biografisk Leksikon. Bnd. 13 Köbenhavn 1938.19. Dungal N: Er sullaveikin að hverfa á Íslandi? Læknablaðið 1942, 28:121-128.20. Dungal N: Eradication of Hydatid Disease in Iceland. New Zealand Medical

Journal 1957, 56:212-222.21. Eschricht D: Afhandling om de Hydatider, der fremkaldte den I Island

endemiske leversyge. I: Oversigt over Videnskabernes Selskabs Forhandlinger1857, 211-239.

22. Faust EC: Echinococcus Disease. Nelson Loose-Leaf Medicine II New York, 11920, 433.

23. Fenger E: Plan til en Forelæsnings-Cyclus. Kbh 1843.24. Fridriksson G: Saga Reykjavíkur 1870-1940. Reykjavík: Iðunn 1994.25. Garcia LS, Bruckner DA: Diagnostic medical parasitology. 1997.26. Jónasson J: Íslenskir Þjóðhættir. 3 utg Reykjavík: Ísafoldarprentsmiðja 1961.27. Jónsson V: Sullaveikirannsóknir Jóns Finsen og Haralds Krabbe. Skírnir

1954, 128:134-175.28. Krabbe H: Om Echinokokkerne, I. del I: Ugeskrift for Læger. Række 2 1862,

37(15):225-235.29. Krabb H: Om Echinokokkerne, II. del. I: Ugeskrift for Læger. 2 Række 1862,

37(16):241-259.30. Krabbe H: Echinokokksygdommen på Island. Ugeskrift for læger 1864,

41(1):1-19, 2. Række.31. Krabbe H: Blæreormlidelserne på Island og de imod dem trufne

Foranstaltninger. Tidsskrift for Veterinærer 1865, 20:205-222, 2. Række.32. Krabbe H: Helmintologiske Undersögelser I Danmark og paa Island med

særlig hensyn til Blæreormlidelserne paa Island. 1: Det Kongelige DanskeVidenskabernes Selskabs Skrifter 5. Række, naturvidenskabelig og mathematiskAfdeling 1865, 7:347-408, Köbenhavn, 64 pp.

33. Leared A: Athugasemdir um sullaveikina á Íslandi. Íslendingur 1862,3:105-106.

34. Leared A: Athugasemdir um sullaveikina á Íslandi. Þjóðólfur 1862, 15:33-34.35. Magnússon G: Yfirlit yfir sögu sullaveikinnar á Íslandi. Fylgirit Árbókar

Háskóla Íslands fyrir háskólaárið 1912-1913. Reykjavík 1913.36. Einarsson Matthías: Hvernig fær fólk sullaveiki? Læknablaðið 1925,

11:98-100.37. Nielsen JB: Parasitologi – et kompendium. Köbenhavn: FADL´s Forlag, 2

1994.38. Olafsens og Povelsens Reise gennem Island. Soröe 1772.39. Pálsson PA, Vigfússon H, Henriksen K: Læknablaðið. 1971, 57:39-51.40. Pálsson PA: Echinococcosis and its elimination in Iceland. Hist Med Vet

1976, 1:4-10.41. Pálsson PA: Echinococcosis in Iceland – historical review. XVII.

Interrnational Congress of Hydatology, Limassol, Cyprus, nov. 6-10 1996.42. Pétursson J: Lækningabók fyrir Almúga. Köbenhavn: Udg. Af Thorsteinn

Jónsson 1834.43. Roberts L, Janovy J: Foundations of Parasitology. Boston: Wm.C. Brown

Publishers, 5 1996.44. Schleisner PA: Island undersögt fra et lægavidenskabeligt Synspunkt.

Köbenhavn: Boghandler C.G.Iversen 1849.45. Sun T, Rackson M, Farber B: Current status of Hydatid Disease. Digestive

Diseases 1988, 6:170-184.46. Thorsteinsson B, Jónsson B: Íslandssaga til okkar daga. Reykjavík: Sögufélag

1991.


Page 9 of 31







S7Toxoplasma gondii in the Subarctic and ArcticKristin W Prestrud1*, Kjetil Åsbakk1, Antti Oksanen2, Anu Näreaho3,Pikka Jokelainen31Norwegian School of Veterinary Science, Department of Food Safety andInfection Biology, Section of Arctic Veterinary Medicine, Tromsø, Norway;2Finnish Food safety Authority Evira, Fish and Wildlife Health Research Unit(FINPAR), Oulu, Finland; 3Department of Basic Veterinary Sciences, Faculty ofVeterinary Medicine, University of Helsinki (FINPAR), Helsinki, FinlandActa Veterinaria Scandinavica 2010, 52(Suppl 1):S7

Summary: The coccidian protozoan Toxoplasma gondii has a world-widedistribution. It causes toxoplasmosis, a potentially very serious disease tohumans and other warm-blooded animals. Infection has in many studiesbeen shown to be rather common in the Nordic countries also, where itsprevalence both in domestic animals and wildlife can be explained bycontacts with cats and their faeces, cats and wild felids being the onlydefinitive hosts of the parasite known.Before the discovery of the complete life cycle of the parasite, otherinfection routes to animals were studied e.g. in Russia, where lateraltransmission of infection in a reindeer herd was reported. The vehicle ofinfection was apparently body fluids, such as e.g. saliva and lacrimal fluidcontaining parasite tachyzoites, which might invade another reindeer viamucosal membranes. According to the finding, toxoplasmosis might beapprehended to be also a sexually transmitted disease. Following thediscovery of the pivotal role of the cat in the epidemiology of T. gondii,possible alternative pathways of infection have generally been ignored. InFennoscandian semi-domesticated reindeer, a clear association of theseroprevalence of antibodies to T. gondii was seen with the degree ofdomestication, and, thus, with cat contacts [1].In the high Arctic of Svalbard, there is a considerably high seroprevalenceof infection both in polar bears and Arctic foxes [2-4]. The source ofinfection is unlikely to be found in the seals constituting the major partof the polar bear’s diet, as in one study, antibodies were not found inNorth Atlantic marine mammals. However, in other, less arctic andremote, cetacean and pinniped populations studied, T. gondii infectionhas been found.Because Svalbard reindeer and sibling voles studied have been free fromT. gondii infection, it can be assumed that sexual stages of infection (indefinitive hosts) leading to oocyst production is not a major part of theSvalbard T. gondii life cycle [2]. Then, carnivores probably get theinfection with food, anyhow. Cannibalism is considered common in polarbears and Arctic foxes, and probably can explain a lot. One parasiteisolate from an Arctic fox proved to belong to the Type II strain, thepredominant T. gondii lineage in the world [3]. This somewhat objects tothe suggested idea of a specific Arctic life cycle of the parasite, butincorporates the Arctic to the global T. gondii infection network. Furthersupport to the hypothesis is gained from the finding that Svalbardbarnacle geese (Branta leucopsis) are rather commonly infected. They mayget the infection when wintering in Scotland. So, perhaps migratory birdsare important in T. gondii globalisation.Cats are crucial to T. gondii epidemiology. However, the Arctic exampleproves that the successful parasite can thrive even in the absence of cats.References1. Oksanen A, Åsbakk K, Nieminen M, Norberg H, Näreaho A: Antibodies

against Toxoplasma gondii in Fennoscandian reindeer — Associationwith the degree of domestication. Parasitology International 1997,46:255-261.

2. Prestrud KW, Åsbakk K, Fuglei E, Mørk T, Stien A, Ropstad E, Tryland M,Gabrielsen GW, Lydersen C, Kovacs KM, Loonen MJ, Sagerup K, Oksanen A:Serosurvey for Toxoplasma gondii in arctic foxes and possible sources ofinfection in the high Arctic of Svalbard. Vet Parasitol 2007, 150:6-12.

3. Prestrud KW, Dubey JP, Åsbakk K, Fuglei E, Su C: First isolate ofToxoplasma gondii from arctic fox (Vulpes lagopus) from Svalbard. VetParasitol 2008, 151:110-114.

4. Oksanen A, Åsbakk K, Prestrud KW, Aars J, Derocher A, Tryland M, Wiig Ø,Dubey JP, Sonne C, Dietz R, Andersen M, Born EW: Prevalence of antibodiesagainst Toxoplasma gondii in polar bears (Ursus maritimus) from Svalbardand East Greenland. J Parasitol 2008, 1, [Epub ahead of print].

S8Trichinella in the NorthNiina Airas1, Seppo Saari1, Taina Mikkonen1, Anna-Maija Virtala1, Jani Pellikka1,Antti Oksanen2, Marja Isomursu2, Antti Sukura1*1Department of Basic Veterinary Sciences, Faculty of Veterinary Medicine,University of Helsinki, Helsinki, Finland; 2Finnish Food Safety Authority Evira,Oulu, FinlandActa Veterinaria Scandinavica 2010, 52(Suppl 1):S8

Background: Endemic human trichinellosis has been rare in Norway,Sweden and Finland. In Norway the last outbreak involving five personsis from 1953 and before that there were reported six epidemics with 711patients since 1881 (reference in [1]). In Sweden 10 outbreaks involving504 patients were documented 1917-1969 (reference in [2]). In Finlandonly eight human cases have been reported since 1890, the latest beingthree hunters at 1977 who got the infection from bear meat (referencein [1]).Sporadic cases of trichinellosis in production animals have beendetected in pig meat inspection in these countries. In Norway therewas a peak of positive pigs in the 1950’s and 1960’s but since 1981 nopositive finding in pigs has been reported. In Sweden, 127 positive pigswere reported 1970-1999 and no cases since 2000. The first infectedFinnish pig was found 1954, and the total number of positive pigs infifty years was up to 714 (1954-2003). There was a peak of cases in the1980’s and 90’s when a total of 671 pigs were found positive. During1981-2000, the positive animals originated from 0-19 farms yearly. Since

Figure 1 (abstract S8) Prevalence gradient is seen in all sampledanimal species with sample size over 100 individuals.


Page 10 of 31





2004 no trichinella has been found in pigs. The decrease in Trichinellaprevalence and incidence in domestic swine has been speculated to bedue the change in Finnish swine industry since Finland joined the EU in1995 [3]. During recent years, the industry has moved towards large-scale enterprises with corporative ownership with new facilities. Theseare better protected against the Trichinella infection commonly presentin surrounding wildlife in Finland [3]. High sylvatic trichinellosisprevalence has been reflected to farmed wild boars in whichcondemnation due trichinelllosis has been relatively more commonthan in pig. To clarify the spatial variation of sylvatic trichinellaprevalence suggested in earlier studies, a new Finnish sample set wasanalyzed.Material and methods : Muscle samples of 2487 carnivorous wildanimals from eight host species during 1999-2005 were collected byvolunteer hunters. Molecular identification was performed on larvalisolates with multiplex PCR.Results : Out of 2487 animals analyzed, Trichinella spp were revealedfrom 618 animals. Different host species showed variable sampleprevalence (range: 0- 46 %). Almost half of the lynx harbouredTrichinella spp (46%); in species rank, lynx were followed by wolves(39%), raccoon dogs (28%), and red foxes (19%). Lower than tenpercent prevalences were detected in sampled pine martens, badgers,bears, and otters. No larvae were detected from mink. The overallTrichinella prevalence from all sampled host species was notgeographically equally distributed varying from 2.6% (Lapland) up to67% on different game districts (P< 0.001), showing obviousdiminishing gradient form south to north (figure 1).Molecular analysis was performed with 328 larval isolates. Trichinellaspecies were successfully identified from 303 animals, from 25 animalsamplification did not give specific reaction (7.6%). Four species werediscovered: T. spiralis, T. nativa, T. britovi, and T. pseudospiralis. SingleTrichinella species were revealed from 281 (93%) of the infected hostanimals and 22 (7%) showed mixed infections. T. nativa was the mostcommon single species (80.1%) followed by T. spiralis (12.8%) T. britovi(6.0%) and T. pseudospiralis (1.1%), which was found in single infectionin only three animals but in mixed infection in four more individuals.From mixed infections, never more than two different species werefound, but all possible two-species combinations of four species werediscovered. Species geographic distribution showed that all fourspecies were discovered only from the southern part of the country; inthe middle and northern part, only T. nativa and T. spiralis wererevealed.The parasite burden was not normally distributed. Different hosts showedvariations in the infection density and also different Trichinella speciesmade different parasite burdens. There was a significant interactionbetween animal species and Trichinella species showing for example thatT. spiralis gave a higher larval burden in raccoon dog than in otheranimals. However, in raccoon dogs, the host specie with the highestburden, infection densities did not differ between infecting Trichinellaspecies.Conclusion: In Finland sylvatic trichinellosis is very common with biggeographical differences showing clear diminishing along south to northgradient. T. nativa was the most prevalent species in the country but,remarkably, the domestic species T. spiralis was isolated from 15% ofsylvatic isolations. T. spiralis was recovered all around in Finland.Intriguingly, T. spiralis was revealed form the very north in a fox in anarea where never any domestic outbreak of trichinellosis has beenreported, and seldom any swine has been seen, indicating that T. spiralismay exist in sylvatic cycle without external sources from synanthropicanimals.When population sizes are considered, the major reservoir animals inFinland are the raccoon dog and the red fox.References1. Oivanen L: Endemic trichinellosis – experimental and epidemiological

studies. Dissertation 2005, Yliopistopaino, Helsinki.2. Pozio E, Christensson D, Steen M, Marucci G, La Rosa G, Bröjer C, Mörner T,

Uhlhorn H, Ågren E, Hall M: Trichinella pseudospiralis foci in Sweden. VetParasitology 2004, 125:335-342.

3. Oivanen L, Oksanen A: Synanthropic Trichinella infection in Finland. VetParasitol 2009, 159:281-284.

S9Detection of infection with Angiostrongylus vasorum (Nematoda,Strongylida) by PCRMohammad Al-Sabi1*, Pia Webster2, Jacob Willesen3, Peter Deplazes4,Alexander Mathis4, Christian Kapel11Department of Agriculture and Ecology, University of Copenhagen, DK-1871Frederiksberg C, Denmark; 2Department of Disease Biology, University ofCopenhagen, DK-1871 Frederiksberg C, Denmark; 3Small animal hospital,University of Copenhagen, DK-1871 Frederiksberg C, Denmark; 4Institute ofParasitology, University of Zurich, CH-8057 Winterthurerstrasse 266A, Zurich,SwitzerlandActa Veterinaria Scandinavica 2010, 52(Suppl 1):S9

Background: The French heart worm Angiostrongylus vasorum is aparasitic nematode of the pulmonary arteries and heart of canines oftenwith severe and in some cases fatal outcome. The diagnosis is based ondetection and species identification of larvae in faeces which can beproblematic in Veterinary praxis especially in cases with low excretinganimals. A reliable technique is thus needed for correct diagnosis andestimation of the true prevalence of infection in a population as well asfor monitoring and control campaigns.Materials and methods: A PCR was developed from the ITS2 region ofthe rDNA of A. vasorum. The sensitivity of the primers was tested withDNA from adult A. vasorum from a naturally infected fox and first stagelarvae (L1) from an experimentally infected foxes. The specificity of theprimers was tested against DNA from the most common helminthparasites of canines in Denmark and neighbouring countries. Furthermorethe PCR system was applied as a confirmative test in a screening study ofDanish hunting dogs and an epidemiological study of helminth parasitesof wildlife in Denmark.Results: The designed primers were very sensitive and could detect asingle A. vasorum L1. The primers were also very specific and did notreact with DNA from any of the common canine helminths. When usedas a confirmative test, the PCR system proved to be robust and easy towork with detecting a single larva, and for use in post mortemexamination of wildlife. There are practical problems that can face thePCR system such as isolating dead larvae from frozen samples and theknown problem of intermittent larval excretion in dogs. These twoproblems can be solved by isolation of larvae by sieving instead of byBaermann sedimentation if samples were frozen, and examiningconsecutive fresh faecal samples.Conclusions: We were able to design a new PCR to detect DNA ofA. vasorum in canines. The test proved to be very sensitive and specificwhen tested in clinical and epidemiological studies. The test will befurther applied in many epidemiological and clinical studies to come.

S10Wild life surveillance on Echinococcus multilocularis in SwedenBirgitta Andersson*, Bodil Christensson, Susanne Johansson,Eva Osterman Lind, Göran ZakrissonNational Veterinary Institute, Department of Virology, Immunobiology andParasitology, Section for Parasitological Diagnostics; SE-751 89 Uppsala,SwedenActa Veterinaria Scandinavica 2010, 52(Suppl 1):S10

Background: Echinococcus multilocularis is a tapeworm whose adultstages parasitize the intestine of canids such as foxes and wolves. Alsodomestic dogs and cats can act as definitive hosts. The sylvatic lifecycle includes small rodents as intermediate hosts but humans maybecome accidentally infected by ingestion of eggs. Sweden, Finland,UK, Ireland, and Malta are considered to be free of this parasite andtherefore have maintained their national rules as regards deworming ofpets at movement into the countries. According to the EC regulation,these national rules can be applied during a transitional period to2010.In order to confirm the absence of E. multilocularis in Sweden, monitoringof foxes is being carried out continuously. These investigations arefinanced by the Swedish government.


Page 11 of 31


Materials and methods: In 2007, 245 red foxes were shot and sent toSVA by local hunters in different parts of Sweden. To kill potentialtapeworm eggs, the carcasses were placed in –80° C for at least oneweek before sampling. Faecal samples were then collected from therectum and sent to Switzerland for testing by coproantigen ELISA(Deplazes et al., 1999). Forty-eight foxes that were positive in the ELISAand additional 28 randomly selected individuals were also examined by asedimentation technique according to the OIE guidelines.Results and discussion: Forty-eight foxes out of 245 were positive forEchinococcus sp. by the coproantigen ELISA. With the sedimentationtechnique however, Echinococcus sp was not detected in any of theexamined animals, including those who had been positive in the ELISA.One possible explanation for obtaining false positive ELISA results wasthat some kind of cross-reaction had taken place. The majority of thefoxes were infected with other parasites, for example Taenia sp,Mesocestoides sp, Alaria alata, Toxocara canis, Toxascaris leonina.Conclusions: There is a need for good screening methods with highsensitivities and specificities. The results obtained by the sedimentationtechnique indicate that Sweden was still free from the fox tapeworm in2007.Reference1. Deplazes P, Alther P, Tanner I, Thompson RCA, Eckert J: Echinococcus

multilocularis coproantigen detection by enzyme-linked immunosorbentassay in fox, dog and cat populations. J. Parasitol 1999, 85:115-121.

S11Emerging alveolar echinococcosis (AE) in humans and high prevalenceof Echinococcus multilocularis in foxes and raccoon dogs in LithuaniaMindaugas Šarkūnas1*, Rasa Bružinskaitė1,4, Audronė Marcinkutė2,Kęstutis Strupas3, Vitalijus Sokolovas3, Alexander Mathis4, Peter Deplazes41Department of Infectious Diseases, Lithuanian Veterinary Academy, Tilžės str.18, LT–47181, Kaunas, Lithuania; 2Clinic of Infectious Diseases, Microbiologyand Dermatovenereology, Vilnius University, Lithuania; 3Santariškių Clinic,Vilnius University, Lithuania; 4Institute of Parasitology, WHO CollaboratingCentre for Parasitic Zoonoses, University of Zürich, SwitzerlandE-mail: [email protected] Veterinaria Scandinavica 2010, 52(Suppl 1):S11

Summary: The presence of the most important definitive andintermediate hosts suggests that conditions for the live cycle ofE. multilocularis are favorable in Lithuania. While the main rodent hostshave not been investigated systematically in Lithuania, E. multilocularishas already been identified in one of 5 muskrats (Ondatra zibethicus)captured in the Šilutė district. The high prevalence of E. multilocularis inred foxes and raccoon dogs as well as a notable increase of AEin humans document that E. multilocularis is of emerging concern inLithuania. The human AE cases were recorded from many parts of thecountry suggesting that the whole territory of Lithuania should beconsidered as an endemic area for E. multilocularis. Considering the longprepatent period of AE in humans we suggest that this zoonosis ispresent in the area investigated for at least a few decades.Introduction: Echinococcus multilocularis is a small tapeworm exploitingmainly wild animals with the red fox (Vulpes vulpes) being the crucialdefinitive host in Europe [1]. Dogs and raccoon dogs are also highlysusceptible definitive hosts of E. multilocularis, while reproduction of thisparasite is significantly lower in cats as shown by experimental infections[2]. Humans may get infected by uptake of eggs, and the tumor-likegrowth of the metacestode stage mainly in the liver may lead to aserious disease – alveolar echinococcosis (AE).Although a rare disease, the numbers of AE cases have increased inendemic areas in Central Europe [3]. AE is of considerable public healthimportance because of its high lethality if untreated and high treatmentcosts [4].The known central–European endemic area of E. multilocularis hasexpanded during the 1990s especially to the North and East [5], and theparasite was recently reported in the Baltic and neighboring regions i.e.Poland [6], Belarus [7] and Estonia [8]. The presence of the mostimportant definitive and intermediate hosts [9] suggests that conditionsfor the live cycle of E. multilocularis are therefore favorable in Lithuania.While these main rodent hosts have not been investigated systematically

in Lithuania, E. multilocularis has already been identified in one of 5muskrats (Ondatra zibethicus) captured in the Šilutė district [10]. The highprevalence of E. multilocularis in red foxes and raccoon dogs as well as anotable increase of AE in humans was also recently documented [11,12].Human infection: In the early eighties, sporadic cases of cysticechinococcosis caused by the larval stage of E. granulosus werediagnosed in humans in Lithuania. However, during the last decades, thediagnostic techniques have improved and the incidence of human AE hasrisen to considerable levels, with an increasing concern among thehuman population and the health authorities.From 1997 to July 2008, 96 AE cases have been diagnosed at the StateHospital for Tuberculosis and Infectious Diseases in cooperation with theSantariškių Clinic (Vilnius University). Eighty-one percent of AE patientswere farmers or persons involved in agricultural activities. Most of thepatients (59%) owned dogs. The AE cases were recorded from many partsof the country suggesting that the whole territory of Lithuania should beconsidered as an endemic area [11,12].Animal infection: The helminth fauna of carnivores from Lithuania wasinvestigated in earlier studies, but no record was made onE. multilocularis [13,14]. The methods used in these studies are not welldocumented but the reported findings of E. granulosus as well as othersmall helminths in dogs and wolves indicate that E. multilocularis wouldmost probably have been detected in the 122 foxes investigated, at leastif highly prevalent at that time.In neighboring Poland, E. multilocularis in red foxes was recorded for thefirst time in the Gdansk region in 1995 [6] which is close to theLithuanian border. Interestingly, the parasite’s prevalence in red foxes(35%) in the southern part of Lithuania [11] is comparable to the one(34.5%) reported from Poland [15]. However, based on these limited data,it remains unclear whether the East Baltic region is a newly establishedendemic area of an extending distribution to the eastern part of Europe,or just a hitherto unnoticed one.In Lithuania, E. multilocularis was detected in 158 (58.7%, 95%CI 50.2%–64.1%) of 269 red foxes examined. It was present in foxes frommost tested localities with the highest prevalence of 62.3% (CI 49.0–74.4%)being observed in the Kaunas district. Mean worm burden was 1309(1-20,924) worms per fox in this district [11]. It was found that 17% of theinfected adult red foxes were harboring heavy infections (>1000 wormsper animal) while none of the juvenile foxes were heavily infected. Thisfinding differs from other studies suggesting that juvenile foxes play amore important role in the life cycle of E. multilocularis [16,17]. However,our result may be biased by the low number of juvenile foxes investigated.The high prevalence (58.7%) of E. multilocularis in red foxes in theexamined areas suggests that these animals may play the most importantrole in the zoonotic transmission of this tapeworm in Lithuania.The raccoon dog is a highly susceptible definitive host for E. multilocularis[2] and there are reports on infected animals from Germany [18], Poland[19] and Lithuania [11]. However, the prevalence of E. multilocularis inraccoon dogs is relatively low in these countries when compared to thoseof the red foxes (2.7%, 8% and 10%, respectively). Further, thesignificance of the raccoon dogs regarding the transmission ofE. multilocularis to the intermediate host population is poorly understood.In addition to the morphological detection of E. multilocularis in one of 5muskrats (Ondatra zibethicus) captured in the Šilutė district of Lithuania[10], infertile and calcified metacestodes of E. multilocularis wereidentified by PCR in 0.4% (3/685) of pigs, and 2 of 240 examined dogs(0.8%) from the same area excreted E. multilocularis eggs [20] ascharacterised by multiplex PCR using primers specific for E. granulosus,E. multilocularis and Taenia spp. according to Trachsel et. al. [21].Conclusions: The identification of AE in pigs and of E. multilocularisin dogs demonstrates that transmission of E. multilocularis is occurring inthe rural environment in close vicinity to the human population. Redfoxes may be considered as the most important species for transmissionof E. multilocularis to humans while the respective epidemiologicalimportance of rural dogs and raccoon dogs is still unknown and deservesfurther studies.The high number of human AE cases and the high prevalence ofE. multilocularis in definitive wild hosts as well as its presence in pigs anddogs document that E. multilocularis is of emerging concern in Lithuania.Considering the long prepatent period of AE in humans we suggest thatthis zoonosis is present in the area investigated for at least a few decades.


Page 12 of 31




Acknowledgments: The study was financially supported by the Foodand Agriculture Organization of the United Nations (FAO, project TCP/LIT/ 3001 (T)), the SwissBaltNet (supporter: GEBERT RÜF STIFTUNG),Lithuanian Veterinary Academy, Hospital of Tuberculosis and InfectiousDiseases and Santariškių Clinic of Vilnius University. The authors wishto thank Regina Virbalienė and Jolanta Ž i l iukienė , ParasitologyLaboratory, National Public Health Centre, Aušrinė Barakauskienė, MD,PhD, National Centre for Pathology and Jonas Valantinas MD, PhD,Santariškių Clinic for their valuable assistance in diagnosing humanechinococcosis.References1. Eckert J, Deplazes P: Biological, epidemiological, and clinical aspects of

echinococcosis, a zoonosis of increasing concern. Clin Microbiol Rev 2004,17:107-35.

2. Kapel CM, Torgerson PR, Thompson RC, Deplazes P: Reproductive potentialof Echinococcus multilocularis in experimentally infected foxes, dogs,raccoon dogs and cats. Int J Parasitol 2006, 36:79-86.

3. Schweiger A, Ammann RW, Candinas D, Clavien PA, Eckert J, Gottstein B,Halkic N, Muellhaupt B, Prinz BM, Reichen J, Tarr PE, Torgerson PR,Deplazes P: Human alveolar ecihnococcosis after fox population increase,Switzerland. Emerg Infect Dis 2007, 13(6):878-882.

4. Torgerson PR, Schweiger A, Deplazes P, Pohar M, Reichen J, Ammann RW,Tarr PE, Halkik N, Müllhaupt B: Alveolar echinococcosis: from a deadlydisease to a well-controlled infection. Relative survival and economicanalysis in Switzerland over the last 35 years. J Hepatol 2008, 49(1):72-77.

5. Romig T, Dinkel A, Mackenstedt U: The present situation ofechinococcosis in Europe. Parasitol Int 2006, 55:S187-191.

6. Malczewski A, Rocki B, Ramisz A, Eckert J: Echinococcus multilocularis(Cestoda), the causative agent of alveolar echinococcosis in humans firstrecord in Poland. J Parasitol 1995, 81:318-321.

7. Shimalov VV, Shimalov VT: Helminth fauna of red fox (Vulpes vulpesLinnaeus, 1758) in southern Belarus. Parasitol Res 2003, 89:77-78.

8. Moks E, Saarma U, Valdmann H: Echinococcus multilocularis in Estonia.Emerg Infect Dis 2005, 11(12):1973-1974.

9. Prūsaitė J, Mažeikytė R, Pauža D, Paužienė N, Baleišis R, Juškaitis R, et al:Fauna of Lithuania. Mokslas, Vilnius 1988, (In Lithuanian).

10. Mažeika V, Paulauskas A, Balčiauskas L: New data on the helminth fauna ofrodents of Lithuania. Acta Zoologica Lituanica 2003, 13:41-47.

11. Bružinskaitė R: Epidemiology of Echinococcus species with reference tohelminths of red foxes (Vulpes vulpes) and raccoon dogs (Nyctereutesprocyonoides) in Lithuania. PhD Thesis Lithuanian Veterinary Academy,Department of Infectious Diseases 2007.

12. Bružinskaitė R, Marcinkutė A, Strupas K, Sokolovas V, Deplazes P, Mathis A,Eddi C, Šarkūnas M: Alveolar echinococcosis, Lithuania. Emerg Infect Dis2007, 13(10):1618-1619.

13. Danilevičius E: Echinococcosis in Lithuanian SSR and immunodiagnosis ofechinococcosis in pigs. PhD Thesis Lithuanian Veterinary Institute 1964, (inRussian).

14. Kazlauskas J, Prūsaitė J: Helminths of carnivores in Lithuania. ActaParasitologica Lituanica 1976, 12:33-40, (in Russian).

15. Gawor J, Malczewski A, Stefaniak J, Nahorski W, Paul M, Kacprzak E, et al:Risk of alveococcosis for humans in Poland. Przegl Epidemiol 2004,58:459-465, (in Polish).

16. Tackamnn K, Loschner U, Mix H, Staubach C, Thulke HH, Conraths FJ:Spatial distribution patterns of Echinococcus multilocularis (Leucart1863) (Cestoda: Cyclophyllidea: Taeniidae) among red foxes in anendemic focus in Branderburg, Germany. Epidemiol Infect 1998,120:101-109.

17. Hofer S, Gloor S, Muller U, Mathis A, Hegglin D, Deplazes P: Highprevalence of Echinococcus multilocularis in urban red foxes (Vulpesvulpes) and voles (Arvicola terrestris) in the city of Zurich, Switzerland.Parasitol 2000, 120:135-142.

18. Thiess A, Schuster R, Nockler K, Mix H: Helminth findings in indigenousraccoon dogs Nyctereutes procyonoides (Gray, 1834). Berliner undMunchener Tieraztlichr Wochenschrift 2001, 114:273-276, (in German).

19. Machnicka B, Dziemian E, Rocki B, Kolodziej-Sobocinska M: Detection ofEchinococcus multilocularis antigens in faeces by ELISA. Parasitol Res2003, 91:491-496.

20. Bružinskaitė R, Šarkūnas M, Torgerson PR, Mathis A, Deplazes P:Echinococcosis in pigs and intestinal infection with Echinococcus spp. indogs in Southwestern Lithuania. Vet Parasitol in press.

21. Trachsel D, Deplazes P, Mathis A: Identification of eggs of canine Taeniidsby multiplex PCR. Parasitology 2007, 134:911-920.

S12A survey for Toxoplasma gondii in red fox (Vulpes vulpes) fromFinnmark County, NorwayRenate Sjølie AndresenNorwegian School of Veterinary Science, Department of Food Safety andInfection Biology, Section of Arctic Veterinary Medicine, Stakkevollveien 23,NO-9010 Tromsø, NorwayActa Veterinaria Scandinavica 2010, 52(Suppl 1):S12

Summary: Samples (blood or tissue fluid) from 405 red foxes (Vulpesvulpes) from Finnmark, Northern Norway, were assayed for antibodiesagainst T. gondii using the direct agglutination test (DAT). The proportionof seropositive animals was 42.5 %, with no significant relationshipbetween sex and infection. The proportion of seropositives seemed toincrease with age, in agreement with findings in previous studies in otherspecies. Genotyping of brain tissue by PCR was not successful whatconcerned T. gondii genomic DNA. This first report of Toxoplasma gondiiinfection in Norwegian red foxes from Finnmark County indicates thatT. gondii is fairly common in red foxes from this area, and the highseroprevalence might be explained by widespread of the parasite in thediet of the foxes. This implies that the red fox is a host of significance inthe maintaining of T. gondii in this northern region.

S13Toxoplasma gondii in Australian smallgoodsTatjana MomcilovicNorwegian School of Veterinary Science, P.O.Box 8146, 0030 Dep Oslo,NorwayActa Veterinaria Scandinavica 2010, 52(Suppl 1):S13

Summary: Toxoplasma gondii is one of the most common parasiticinfections of humans and other warm-blooded animals. In most adults itdoes not cause serious illness, but severe disease may result frominfection of fetuses and immuno-compromised people. Consumption ofraw or undercooked meats has been consistently identified as animportant source of exposure to T. gondii. Several studies indicate thepotential failure to inactivate T. gondii in the processes of cured meatproducts, referred to as smallgoods in Australia.This publication presents a qualitative risk-based assessment of theprocessing of ready-to-eat smallgoods. The raw meat ingredients arerated with respect to their likelihood of containing T. gondii cysts and anadjustment is made based on whether all the meat from a particularsource is frozen. Next the effectiveness of common processing steps toinactivate T. gondii cysts are assessed, including addition of spices,nitrates, nitrites and salt, use of fermentation, smoking and heattreatment, and the time and temperature during maturation. It isconcluded that processing steps which may be effective in theinactivation of T. gondii cysts include freezing, heat treatment andcooking, and the interaction between salt concentration, maturation timeand temperature. The assessment is the illustrated using a Microsoft Excelbased software tool which was developed to facilitate the easyassessment of four hypothetical smallgoods products.

S14Echinococcus granulosus (‘pig strain’, G6/7) in Southwestern LithuaniaMindaugas Šarkūnas1*, Rasa Bružinskaitė1,3, Audronė Marcinkutė2,Alexander Mathis3, Peter Deplazes31Department of Infectious Diseases, Lithuanian Veterinary Academy, Kaunas,Lithuania; 2Clinic of Infectious Diseases, Microbiology andDermatovenereology, Vilnius University, Vilnius, Lithuania; 3Institute ofParasitology, University of Zürich, SwitzerlandActa Veterinaria Scandinavica 2010, 52(Suppl 1):S14

Background: Cystic echinococcosis (CE) of pigs is widespread and knownsince many years in Lithuania [1]. Recently, the number of diagnosed


Page 13 of 31




























cases of human CE began to increase [2] but only limited information isavailable on the main epidemiological aspects of this zoonosis.Material and methods: During 2005-2006, post slaughter examinationand morphological identification of cysts from pigs from small familyfarms (n=612) and industrial farms (n=73) was performed. Dog fecalsamples (n=240) were collected in 12 villages and microscopicallyexamined by egg flotation/sieving (F/Si) [3] and modified McMastermethods [4]). For the genetic identification of E. granulosus to species/strain level, PCR was performed with DNA from typical hydatid cysts frompigs (n=2), morphologically unidentifiable lesions from pigs (n=3),nonfertile cysts from cattle (n=3) and taeniid eggs from dog faecalsamples (n=34) [5]. Risk factors for cystic echinococcosis were evaluatedby a questionnaire.Results: CE was prevalent in 13.2% (81/612) of the pigs reared in smallfamily farms and 4.1% of those reared in industrial farms. Molecularanalysis of isolated taeniid eggs revealed in 10.8% of the dogsinvestigated Taenia spp., in 3.8% E. granulosus (G 6/7) and in 0.8%E. multilocularis. In addition, three samples from livers of human and froma cow were confirmed as E. granulosus larval stage by PCR. Sequenceanalysis confirmed the ‘pig strain’ (G 6/7) in all pig, dog, cattle andhuman isolates investigated. No significant risk factor for infections withE. granulosus or Taenia spp. could be identified.Conclusion: The ‘pig strain’ of E. granulosus is highly prevalent in thesouthwestern part of Lithuania, and transmission is more likely in smallfamily farms indicating a high exposure to cestode eggs in rural areas.Therefore control programs should be initiated with special reference tosmall family farms.References1. Danilevičius E: Cystic echinococcosis and immunodiagnosis in pigs in

Lithuania. PhD thesis. Kaunas 1964, (in Lithuanian).2. Marcinkutė A, Bareišienė MV, Bružinskaitė R, Šarkūnas M, Tamakauskienė R,

Vėlyvytė D: Cystic echinococcosis in Lithuania. Lithuanian GeneralPractitioner 2006, 10:8-11.

3. Mathis A, Deplazes P, Eckert J: An improved test system for PCR-basedspecific detection of Echinococcus multilocularis eggs. J Helminthol 1996,70:219-222.

4. Roepstorff A, Nansen P: The epidemiology, diagnosis and control ofhelminth parasites of swine. FAO Animal Health Manual 3, Food andAgriculture Organization of the United Nations 1998, Rome, Italy.

5. Trachsel D, Deplazes P, Mathis A: Identification of taeniid eggs in thefaeces from carnivores based on multiplex PCR using targets inmitochondrial DNA. Parasitology 2007, 134:911-920.

S15Sylvatic Trichinella reservoir not found among voles in FinlandHanna Välimaa1*, Jukka Niemimaa2, Antti Oksanen1, Heikki Henttonen21Finnish Food safety Authority Evira, Fish and Wildlife Health Research Unit(FINPAR), Oulu, Finland; 2Finnish Forest Research Institute, Vantaa ResearchUnit, FinlandActa Veterinaria Scandinavica 2010, 52(Suppl 1):S15

Background: Sylvatic Trichinella infection has been found to be verycommon in Finnish wild carnivores [1], especially locally in Southern andpartly Central Finland. Cannibalism and carrion feeding have beenregarded as the major source of infection to red foxes and raccoon dogs.Voles have been found the major food items of red foxes [2]. They areregarded as herbivorous, but many herbivores consume animal tissuesoccasionally. Therefore, voles might be assumed potentially to take part inTrichinella life cycle in the wild. Microtus spp and Myodes spp have beenfound to be infected with Trichinella, e.g. [3]. In Finland, refuse tip rats havebeen found to be rather commonly infected with Trichinella spiralis [4].Material: A total of 1761 bank voles Myodes glareolus, and 138 field volesMicrotus agrestis, trapped on 30 transect sampling locations in Finland. Inaddition, also 60 shrews, Sorex spp. accidentally found succumbed in thetraps, were also included in the study. After killing, during dissection, theright hind leg of each animal was removed and frozen until thawed atlaboratory. Left hind legs were spared for confirmation analyses. Followingthawing, the legs were treated as meat inspection samples according toCommission Regulation (EC) No 2075/2005 utilizing pepsin-HCl digestion.Results and discussion: No Trichinella spp larva was found in any of thesamples. Therefore, microtid rodents in Finland cannot be confirmed to

take part of the Trichinella spp life cycle. The opposite cannot beconfirmed, either, as absence of evidence is not equal to evidence ofabsence. The predilection sites of Trichinella muscle larvae in microtidrodents are not well-known. Perhaps the right hind leg is not a goodmatrix for Trichinella larvae. In addition, even though the materialconsisting of 1899 small mammals may appear large at topical inspection,the potential impact of microtid rodents on Trichinella transmissionbiology is based on the high numbers of animals. The Finnish volepopulation fluctuates all the time, but during the peaks there areestimated to be about 200 000 000 voles in the country.References1. Oivanen L: Endemic trichinellosis – experimental and epidemiological

studies. Dissertation 2005, Yliopistopaino, Helsinki.2. Dell’Arte GL, Laaksonen T, Norrdahl K, Korpimäki E: Variation in the diet

composition of a generalist predator, the red fox, in relation to seasonand density of main prey. Acta Oecologica 2007, 31:276-281.

3. Holliman RB, Meade BJ: Native trichinosis in wild rodents in HenricoCounty, Virginia. J. Wildl. Dis 1980, 16:205-207.

4. Mikkonen T, Valkama J, Wihlman H, Sukura A: Spatial variation ofTrichinella prevalence in rats in Finnish waste disposal sites. J. Parasitol2005, 91:210-213.

S16Aggregation in cattle dung-colonizing insect communitiesRichard Wall*, Colin LeeVeterinary Parasitology & Ecology Group, School of Biological Sciences,University of Bristol, Woodland Road, Bristol, BS8 1UG, UKActa Veterinaria Scandinavica 2010, 52(Suppl 1):S16

Background: Ruminant dung is a highly ephemeral, patchily distributedresource, which is utilized by a diverse community of invertebrate species. Thisecologically important community may be affected adversely by insecticideand endectocide residues in the faeces of treated cattle. The aim of thepresent work was to quantify the aggregation of the insects colonising cow-dung in cattle pastures and test the hypothesis that the dung-pat communityassemblage observed is the result of stochastic colonization events.Methods: Fresh dung from dairy cattle was used to construct arrays ofstandardised, 1.5kg, artificial cow pats in cattle pastures. Batches of tenpats were placed out each week for 24 weeks, between May and Octoberin 2001. Pats were left exposed in the field for seven days, to allowcolonisation. Pats were then brought back to the laboratory and insectcolonizers were collected and identified.Results: Individual pats contained on average, only half the number ofinsect taxa present in an entire batch put out at any one time. Among sixrepresentative taxa of Diptera and four of Coleoptera, significant levels ofintraspecific aggregation were observed in all but one (Mesembinameridiana), with the abundance of most taxa within pats approximating anegative binomial distribution. A simulation analysis was used to showthat the observed relative frequency of taxa within pats does not differfrom that expected by chance if colonisation is a random binomial eventin which each species colonises a pat independently of all other species.Conclusion: The highly aggregated distributions observed in this studyhighlight the need for relatively large sample sizes when attempting toassess the abundance and distribution of individual taxa in cow dung. Inaddition, the results suggest that the aggregated populations of evenhighly abundant insects will be more susceptible to the deleteriouseffects of insecticidal residues in dung than if they were evenlydistributed, if by chance they colonize a pat containing insecticidalresidues from a recently treated animal.

S17Important ectoparasites of Alpaca (Vicugna pacos)Set BornsteinDep. of Virology, Immunobiology and Parasitology, National VeterinaryInstitute, Uppsala, SwedenActa Veterinaria Scandinavica 2010, 52(Suppl 1):S17

Summary: Background: Alpacas (Vicugna pacos), earlier named Lamapacos, belong to the family Camelidae of which there are 7 livingspecies. Four are native to South America and of those four two are


Page 14 of 31










domestic species, the alpaca (Vicugna pacos) and the llama (Lamaglama) and two are wild, the vicuña (Vicugna vicugna) and the guanaco(Lama guanicoe). These species are often referred to as the New Worldcamels (NWCs) or the South American Camels (SACs) [1]. To the threeOld World camels (OWCs) belong the bactrians or the two-humpedcamel (Camelus bactrianus). Lately it has been established that there aretwo different species of bactrians, one domesticated and one wildendangered species [2]. The latter lives on the border betweenMongolia and China. The other domesticated OWC species is the morewell known, the one-humped or the dromedary camel (Camelusdromedarius).The Camelidae evolved and developed parallel to the Ruminantiae over35 million years ago in North America [1] and have developed specialanatomical and physiological features which are of great significance totheir biology, well adapted to the extreme climatic environments of therough countries of deserts and semi-deserts of Asia, the Middle East andNorthern Africa (OWC) and the high altitude country of the Andes inSouth America (SAC/NWC), respectively. The Camelidae (long neck andsmall head) are members of the order of Artiodactyla (even number ofdigits), suborder Tylopoda (modified ruminants with pad or callus oneach foot).All camelids have 37 pairs of chromosomes and the karyotypes are quitesimilar. The SACs can interbreed and produce fertile offspring.

Important livestock: The alpacas as well as the llamas were and still arevery important livestock in large areas of South America, particularly inPeru, Bolivia, Ecuador, Chile and Argentina ([3,4,1]. Since the llamas andalpacas were domesticated about 4-5000 BC [1], they have been the mostimportant resource of human culture and survival in the high altitudeenvironments of the Andes. The SACs are better adapted than any otherdomesticated species to the very cold, hard and fragile areas with verylow oxygen pressure (altitudes between 4-5000m).Alpaca provide meat, hides, fuel, manure and particularly very fine fibres(wool), which are highly priced. Today more than 500,000 peasantfamilies are raising SACs in the Andes and these livestock are the mainsource of income for the campesinos. Increasing numbers of alpaca arebeing imported to various countries outside of South America includingEurope for wool production, breeding and as companion animals. This isa fairly recent phenomenon that started with larger exports from Chile in1983-84, first to North America [1].Ectoparasites: The alpacas as other livestock are exposed to and affectedby a range of ectoparasites (see Table 1). Of particular importance are themange mites, the burrowing Sarcoptes scabiei and the non-burrowingChorioptes sp and Psoroptes sp and lice, both biting and suckingPhthiraptera. The mange mites have been reported to be commoninfestations on alpacas also in countries outside of South America.Problems with mange are reported frequently from several countries in

Table 1 (abstract S17) Ectoparasites of alpaca belonging to the Phylum, Arthropoda

Order Family Species Disease

Astigmata Sarcoptidae Sarcoptes scabiei sarcoptic mange

Psoroptidae Chorioptes sp chorioptic mange

Psoroptes sp psoroptic mange (ear canker)

Prostigmata Demodicidae Demodex sp demodectic mange

Metastigmata Argasida (Soft ticks)

Otobius mengnini otitis

Ixodidae (Hard ticks)1

Ixodes holocyclus Tick paralysis

Dermacentor spp Tick toxicosis

Phthiraptera Sucking lice2 Microthoracius spp

Biting lice3 Bovicola (Damalinia) brevis

Siphonaptera Flees Vermipsylla sp

Diptera (flies)

Culicidae (mosquitos)

Simulidae (black flies)

Tabanidae Tabanus spp (horse flies, deer fly)

Muscidae Musca domestica (house fly)

M autumnalis (face fly)

Stomoxys calcitrans (biting stable fly)

Hydrotea spp

Haematobia spp

Sarcophagidae

Calliphoridae

(blowflies) Calliphora sp

Cochliomyia hominivorax (primary screw worm)

Phaenicia spp (green blow fly)

Phormia spp (black blow fly)

Oestridae (Bot flies)

Oestrus sp

Cephenomyia sp1 Alpacas are at risk to be infested by native ticks e.g. in Scandinavia by various Ixodes and Haemophysalis spp, many that are known vectors of pathogens2 Suborder; Anoplura3 Suborder; Mallophaga


Page 15 of 31

Europe [5-10]. In the UK e.g. 23 % of alpaca owners were concerned [8]and in Switzerland alpaca owners regarded mange as one of the fourmost frequent health problems [11]. Sarcoptes scabiei var aucheniae isvery prevalent in alpacas as well as in other SACs [3]. It is said to beresponsible for 95 % of all losses due to ectoparasites in alpacas [12,13].Infestations with Chorioptes sp are also very common. Some regardChorioptes mites as the most common ectoparasite infesting SACs [14].The mite is assumed to be C bovis [15,16]. Psoroptes (aucheniae) ovis mayalso be found to infest particularly the earlaps (pinna) and the outer earcanals, but can also be found elsewhere on the body of alpacas. Mixedinfections occur with two and even three of the mite species [9,17,16].Mange: Sarcoptic mange: The early acute manifestation of sarcopticmange include mild to severe pruritus with erythema, papules andpustules, developing soon to crusting, alopecia and lichenification andthickening of the skin (hyperkeratosis), the chronic stage. Lesions may beseen on the limbs (often between the toes), medial thighs, ventralabdomen, chest, axilla, perineum, prepuce, the head including the lipsand ears. Fibre-free areas are said to be more often affected. Damage tothe fibre and loss of condition occur. In very severe infections the diseasemay result in death [3,17]. There are historical accounts of largeepidemics of S scabiei var aucheniae affecting SACs in South America(1544, 1545, 1548, 1826, 1836 and 1839) causing havoc in SACs withmortalities of over two thirds of the populations [3].Prevalence of the infection among the alpaca of peasant communities inthe Andes is between 20-40 % [12]. The earlier high prevalence of theinfection also seen in the alpacas imported and bred in USA has beensubstantially reduced, most probably due to the frequent use ofivermectin [18]. In Europe there are several case reports [11,17,10], but noproper study addressing the prevalence of sarcoptic mange infections.A concern is that S scabiei has a zoonotic potential and that somevariants are not host-specific.Chorioptic mange: Previously Chorioptes sp infestations were consideredrelatively rare in SACs [18,15], although Cremers [19] was of the oppositeopinion. Today chorioptic mange is a very common condition in manyherds worldwide [14,20].Clinical signs of chorioptic mange may mimic sarcoptic mange, butanimals affected usually exhibit a milder pruritus and sometimes none atall (subclinical). Individuals with a heavy infestation may be free of anysymptoms of mange although others in the same herd with lowerinfestations may show severe extensive skin lesions [20]. Often alopeciaand scaling are seen on the feet – often as in sarcoptic mange betweenthe toes and the base of the tail. Lesions may spread to the ventralabdomen, medial limbs and often the ears.Psoroptic mange: Psoroptic mange is often seen at predilection sites;pinna and outer ear canals, as erythema, crusting, papules serumexudates and alopecia. Pruritus is evident emanating from these lesions.Typical lesions seen in the outer ear canals are big flakes. Pusoccasionally appears which is most likely due to secondary infections.Ears and parotid regions may become grossly swollen in severe lesions[3]. However, lesions may be generalised as well as pruritus with orwithout involvement of the outer ear canal. Other sites with lesionsreported include; nares, axillae, groin, neck and legs, abdomen, perineum,shoulders, back and its sides and the base of the tail [16]. Intermittentbilateral ear twitching and short-duration head shaking may indicateotitis due to Psoroptes sp infestations [6].The Psoroptes sp of alpacas and llamas have previously been referred to asP auchenia or P communis auchinae [6], but adequate identifications of thedifferent isolates of the mites have not yet been done. There is a concernthat the Psoroptes sp isolated from SACs, referred to as P communis, thecosmopolitan ear mite of many herbivores [21], might be able to infestsheep and cattle i.e act as reservoirs for the very serious sheep scab.Psoroptic mange was reported recently in two alpacas in the UK [13]. Oneof the animals came from Chile and the other was born in the UK.Cross-transmission: The possibility of cross-transmission of any of theother mange mites and other ectoparasites of alpacas to domestic sheepand other livestock and vice versa is a concern and, to my knowledge,has not yet been sufficiently investigated. Sarcoptes scabiei var aucheniaewas reported to be able to infect sheep and horses [22]. AnotherSarcoptes scabiei variant (var. cameli), a common pathogen indromedaries, was shown experimentally to be able to infect sheep andgoats [23], and S scabiei derived from goats and sheep readily infecteddromedaries experimentally [24].

Some variants of S scabiei are known to cross-infect humans resulting inpseudo-scabies. Successful experimental infections of humans withSarcoptes scabiei from alpacas have been reported [16,25]. Some authorsdo recognize that S scabiei var aucheniae should be regarded as zoonotic[16].Diagnosis: The above highlights the importance of correct diagnosis. Forall three mite species apply the same traditional skin scrapingprocedures, particularly deep skin scrapings for the burrowing Sarcoptesmites with microscopic identification of the species. In relatively acuteinfections the mites may be difficult to find. Multiple skin scrapings,employing a blunted scalpel blade often coated with liquid paraffin, arenecessary to make on the same individual and on several animals inthe affected herd, preferably on all animals. The thickly crusted partsof chronic lesions often yield high numbers of sarcoptic mites.Recommended procedures of taking skin scrapings and the followinganalytical procedures vary [14]. Often the recommendations are to placethe skin scrapings on a glass slide and mix it either with a drop or two ofthe solution of potassium hydroxide (NaOH) followed by applying heatfor a few minutes or mix the skin scraping material with liquid paraffin,followed by applying a glass cover slip. This is then examined for thepresence of ectoparasites under low power.Another laboratory procedure is to place the scrapings (scabs and debris)preferably in centrifuge tubes allowing the material to be soaked in a10 % solution of potassium hydroxide and place the mix in a water bath(370C) for a few hours after which the material is centrifuged at about3000 r.p.m. Then the supernatant is discarded and the sedimentexamined in a microscope under low power after having added 1-2drops of glycerine to the sediment.One can often short-cut above procedure by first examining the collectedskin scrapings in a small petri-dish which is left in room temperature or< 350C for an hour or two followed by examining the scrapings under lowmagnification (stereo-microscope). The raised temperature (> +180C) willstimulate any live ectoparasite present to move enhancing the possibilityof detecting parasites which then may be isolated and identified. If noectoparasite is found the previous described procedures follow.In regards to Chorioptes sp animals may harbour a relatively low level ofinfestation showing no clinical disease, while other individuals mayexperience a hypersensitivity reaction with moderate to severe skinlesions including pruritis, similar to a clinical reaction to acute S scabieiinfections. A recommended site for performing skin scrapings in search ofChorioptes sp is the dorsal interdigital (between the toes) and axillaeareas [14].Low power microscopical examination of material from superficial skinscrapings and swabs rubbed into the outer ear canal may identifyPsoroptes sp. For proper identification isolates should be sent to expertsin the field.When diagnosis is not conclusive skin biopsies are recommended in skindisease. Mites are seldom seen in acute cases in histological sections ofthe skin. However, in cases of chronic sarcoptic mange, S scabiei mayoften be seen in the epidermis.Differential diagnosis: Any pruritic dermatitis may mimic infections/infestations by mange mites There are several other causes of skin lesionswhich should be mentioned as differential diagnostic possibilities apartfrom dermatitis of bacterial, viral and fungal etiology; e.g. immunemediated skin disease, hypersensitivity reactions, pemphigus likeconditions, nutritional/metabolic disease, idiopathic hyperkeratosis,mineral deficiencies i.e. zinc responsive dermatosis. Unfortunately thelatter diagnosis (zinc responsive dermatosis) has become a very populardiagnosis that is seldom proven correct.Phthiriosis (lice): Bovicola (Lepikentron) breviceps Rudow, 1866 (the bitingor more appropriate the chewing louse), varying in size from 0.5x1.2 mmto 1.5x4 mm, is more common in llamas than in alpacas. The colour ofthe body of the louse is white or light tan and it has a blunt broad headthat is distinctly different from the elongated mouthparts of the suckinglice. Infestations are mostly seen on the dorsal midline, base of the tail,on the side of the neck and along the sides of the body.Clinical signs of infestations are often a lack of lustre and a raggedlooking coat. Infested animals exhibit pruritus. Heavy infestations result inmatting and loss of fibres [15], but do not seem to have negative effectson the quality of the fibres or pose any health risk to alpacas [26].Alpacas are more often infested with the sucking lice, Michrothoraciusmazzai Werneck 1932 characterized by its elongated spindle-shaped


Page 16 of 31

head, which is almost as long as its abdomen. Earlier in the literature theformer species has been misnamed M prealongiceps [27]. Preferred sitesof attachment are around the flanks, head, neck and withers. Althoughthese lice are large enough to be seen with the naked eye, about twothirds the size of the biting lice, they are often partly imbedded in theskin taking a blood meal and thus may be difficult to see.Clinical signs are pruritus, restlessness, hair loss and poor growth. Severeinfestations can cause anaemia. The biting lice may be found by partingthe fibres down to the skin using a bright light in search of tiny movingspecks. Nits (eggs) may be seen attached to the fibres. The smallersucking lice can be seen clinging to the fibres close to the skin orimbedded in it.Treatment: A variety of insecticides and acaricides have been used onSACs with varying levels of success. In the past there have been severalsubstances and dosage regimes employed to treat mange mites. ThePeruvian Indian peasants believed that the fat of condors was a goodcure. This practice was later replaced by used motor oil [3]. Relatively fewof the commonly used acaricidal substances and insecticides have beenscientifically tested on SACs. The modern macrocyclic lactones e.g. havebeen tried but not undergone proper testing for efficacy or safety onthese animals that have such a unique physiology and metabolismcompared to other domestic species. Pharmacokinetic studies ofmacrocyclic lactones as well as other well known therapeutic productsare limited in SACs [28,29]. As yet there are few if any therapeuticproducts available licenced for these particular animals. This forces theclinicians to use off-label products licenced for other production animals,mostly ruminants. However, several well known therapeutic substancesnot licensed for use on camelids have been and are used on SACs, somewith good results.A number of authors have used ivermectin at 200 µg/kg by subcutaneousinjection with variable but often good results against mange miteinfestations and sucking lice in SACs [15,16]. Some have employed higherdoses e.g. 400 µg/kg and with more frequent applications (even weekly)than the recommended standard dosages used for other livestock. Alsotopical use of products containing eprinomectin, doramectin andmoxidectin have proved efficacious in some treatments, but not in others[16,10]. Applying injectibles (systemic therapy) in combination withtopical treatments is often required to get better results [30]. Particularlypatients with chronic lesions with thickened crusty hyperkeratotic skinneed to be treated aggressively. In addition, perhaps an earlierrecommendation to employ hand-dressing (with a brush) of the thickhyperkeratotic areas of the skin with tepid water with soap andkeratolytic agents (e.g. salicylic acid solutions) would shorten the recoverytime and reduce the amount of acaricides used [31,32].Chorioptes sp infestations have often showed to be difficult to control anderadicate [9]. Also Sarcoptes scabiei infections have been very difficult tosuccessfully treat [17]. Whether ``fomites`` play any significant role inregards to re-infection/infestation is debatable. Sarcoptes scabiei outsidetheir host will not survive more than about three weeks. However,Chorioptes spp may survive for a little more than 60 days.The fibres of alpacas do not contain lanolin which is necessary for theeffective spreading of topically applied products, i.e. pour-ons,formulations designed for other livestock than camelids e.g. cattle andsmall stock. This may partly explain therapeutic failures on alpacas [6].When using pour-ons it is essential to apply the products direct on theskin.There are numerous insecticides including pyrethrins, chlorinatedhydrocarbons, carbamates and organic phosphates which may eradicatelice, but the problem is the administration of the products. The clue tosuccessful treatment is to establish contact with the parasites. Liceinfestations are easier to treat than the above mentioned mange mites.Ivermectin at a dose rate of 200µg/kg body weight administeredsubcutaneously is effective against sucking lice [15], but not against thebiting or chewing lice. Cypermethrin at a dose rate of 10 mg/kg has beenused with good effect [33,34]. A single treatment is thought to beenough but two treatments 14 days apart is recommended as back-up[33]. Eradication of infestations require repeated treatments and isolationuntil the animals are found to be completely free of the parasites [33].The results of several case reports indicate the need to treat morefrequently and with higher dosages of some of the acaricidal substancesused, compared to the formula for ruminants [16]. It is vital to closelymonitor the results of treatment i.e. the clinical resolution following the

therapies employed before deciding on whether to stop treatment orchange the regimen. Successful treatment should be followed byeffective biosecurity measures to prevent the risk of re-infection/infestations. In addition it is recommended to treat all the animals in theherd at the same time.Acknowledgement: The author is grateful to Mrs Anita Lilburn forvaluable linguistic revision of the manuscript and to Dr Aiden P Foster forletting me use valuable images of his case material.References1. Hoffman E: The complete alpaca book. Bonny Doon Press, Santa Cruz,

California; 2003.2. Cui P, Ding F, Gao H, Meng H, Yu J, Hu , Zhang HA: Complete

mitochondrial genome sequence of the wild two-humped camel(Camelus bactrianus ferus): an evolutionary history of camelidae. BMCGenomics 2007, 18:241.

3. Alvarado J, Astrom G, GBS Heath: An investigation into remedies of Sarna(sarcoptic mange) of alpacas in Peru. Expl Agric 1966, 2:245-254.

4. Aba MA: Hormonal interrelationships in reproduction of female Llamasand Alpacas. PhD Thesis Swedish University of Agricultural Sciences,Uppsala 1998.

5. Petrikowski M: Chorioptic mange in an alpaca herd. In Advances inVeterinary Dermatology. Edited by: Kwocka, K.W., Willemse, T., von Tscharner,C. 1998, 3:450-450.

6. Bates P, Duff P, Windsor R, Devoy J, Otter A, Sharp M: Mange mites speciesaffecting camelids in the UK. Vet Rec 2001, 463-464.

7. Frame NW, Frame RKA: Psoroptes species in alpacas. Vet Rec 2001, 128.8. Tait SA, Kirwan JA, Fair CJ, Coles GC, Stafford KA: Parasites and their

control in South American camelids in the United Kingdom. Vet Rec2002, 150:638-639.

9. Geurden T, Deprez P, Vercruysse J: Treatment of sarcoptic, psoroptic andchorioptic mange in a Belgian alpaca herd. Vet Rec 2003, 153:332-333.

10. Lau P, Hill PB, Rybnicek J, Steel L: Sarcoptic mange in three alpacastreated successfully with amitraz. Vet Dermatol 2007, 18:272-277.

11. Burri HI, Martig I, Sager H, Liesegang A, Meylan M: South Americancamelids in Switzerland. I. Population, management and healthproblems. Schweiz Arch Tierhheilk 2005, 147:325-334.

12. Leguia G: The epidemiogy and economic impact of llama parasites.Parasitology Today 1991, 7:54-55.

13. DÁlteiro GL, Batty A, Laxon K, Duffus P: Psoroptes species in alpacas. VetRec 2001, 96.

14. DÁlteiro GL, Callaghan C, Just C, Manner-Smith A, Foster AP, Knowles TG:Prevalence of Chorioptes sp. mite infestation in alpaca (Lama pacos) inthe south-west of England: implications for skin health. J Sm Rumin Res2005, 57:221-228.

15. Fowler ME: Medicine and Surgery of South American Camelids Llama,Alpaca, Vicuña, Guanaco. Sec ed; Iowa State Press; 1998.

16. Foster A, Jackson A, DÁlteiro GL: Skin diseases of South Americancamelids. In Practice 2007, 29:216-223.

17. Borgsteede FHM, Timmerman A, Harmsen MM: Een geval ernstigeSarcoptes-schurft bij alpaca´s (Lama pacos). Tijdschr Voor Diergeneeskunde(Voor de praktijk) 2006, 131:282-283.

18. Rosychuk RAW: Llama Dermatology. Veterinary Clinics of North America:Food Animal Practice 1989, 51:228-239.

19. Cremers HJWM: Chorioptes bovis (Acarina: Psoroptidae) in somecamelids from Dutch zoos. Vet Quart 1985, 7:198-199.

20. Plant JD, Kutzler MA, Cebra CK: Efficacy of topical eprinomectin in thetreatment of Chorioptes sp. infestation in alpacas and llamas. VetDermatol 2007, 18:59-62.

21. Bates P: Inter- and intra-specific variation within the genus Psoroptes(Acari: Psoroptidae). Vet Parasitol 1999, 83:201-217.

22. Neveu-Lemaire J: Traite dÉntomologie Medicale et Veterinaire. VigotFreres , 1 1938, Paris.

23. Nayel NM, Abu-Samra MT: Experimental infection of the one humpedcamel (Camelus dromedarius) and goats with Sarcoptes scabiei var.cameli and S. scabiei var. ovis. Ann Trop Med Parasitol 1986, 80:553-561.

24. Nayel NM, Abu-Samra MT: Experimental infection of the one humpedcamel (Camelus dromedarius) and goats with Sarcoptes scabiei var.cameli and S. scabiei var. caprae. Brit Vet J 1986, 142:264-269.

25. Mellanby K: Sarcoptic mange in the alpaca, Lama huanaco var. paca.J Soc Trop Med Hyg 1946 1947, 40:359.

26. Vaughan JL, Carmichael I: Control of the camelid biting louse, Bovicolabreviceps in Australia. Alpacas Australia 1999, 27:24-28.


Page 17 of 31


















27. Cicchino AC, Muñoz Cobeñas ME, Bulman GM, Diaz JC, Laos A:Identification of Microthoracius mazzai (Phthiraptera: Anoplura) as aneconomical important parasite of alpacas. J Med Entomol 1998,35:922-930.

28. Hunter RP, Isaza R, Koch DE, Dodd CC, Goately MA: Moxidectin plasmaconcentrations following topical administration to llamas (Lama glama)and alpacas (Lama pacos). J Small Rumin Res 2004, 52:273-277.

29. Hunter RP, Isaza R, Koch DE, Dodd CC, Goately MA: The pharmacokineticsof topical doramectin in llamas (Lama glama) and alpacas (Lama pacos).J Vet Pharmacol Therap 2004, 27:187-189.

30. Curtis CF, Chappell SJ, Last R: Concurrent sarcoptic and choriopticacariosis in a British llama (Lama glama). Vet Rec 2001, 149:208-209.

31. Nayel NM, Abu-Samra MT: Sarcoptic mange in the one-humped camel(Camelus dromedarius). A clinico-pathological and epizootiological studyof the disease and its treatment. J Arid Environm 1986, 10:199-211.

32. Bornstein S, Wernery U, Kaaden O-R: Infectious Diseases in Camelids. 2ndedition. Blackwell Science Berlin Vienna; 2002:267-387.

33. Palma RL, McKenna PB, Aitken P: Confirmation of the occurrence of thechewing louse Bovicola (Lepikentron) breviceps (Insecta: Phthiraptera:Trichodectidae) on alpacas (Lama pacos) in New Zealand. New Zealand J2006, 54:253-254.

34. Vaughan JL: Eradication of the camelid biting louse. Austral Vet J 2004,82:218-219.

S18Coccidiosis in farmed silver foxes (Vulpes vulpes) and blue foxes (Alopexlagopus) in Finland: a case report:Tapio Juokslahti1*, Teija Korhonen2, Antti Oksanen31Helsinki University, Faculty of Veterinary Medicine (Docent), Helsinki, Finland;2Finnish Food safety Authority Evira, Production Animal Health ResearchUnit, Seinäjoki, Finland; 3Finnish Food safety Authority Evira, Fish and WildlifeHealth Research Unit (FINPAR), Oulu, FinlandActa Veterinaria Scandinavica 2010, 52(Suppl 1):S18

Summary: Fur animal farming was initiated during the 1890s on PrinceEdward Island in Canada. Farmed silver foxes descend from animals caughtfrom the wild on the island. Finnish fur farming increased during the post warperiod and in mid-1980s, there were about 6000 fur animal farms, mostlylocated in Southern Ostrobothnia (Fig.), producing about 8 million fur animalsyearly. Currently, there are approximately 1300 fur farms and the yearlyproduction in 2007 was about 2 million fox and 2 million mink furs. The globalproduction at the same time was about 7 million fox and 58 million mink furs.An outbreak of clinical enteric coccidiosis was encountered at a fox farmwith silver foxes (Vulpes vulpes) and blue foxes (Alopex lagopus) inintensive farming district of Osthrobothnia in Finland during summer2008. The breeding animal stock of the farm consists of 1500 silver foxfemales and 4000 blue fox females. The whelping period of the silverfoxes was from April 20 to May 25, and the whelping period of the bluefoxes was from ay 5 to June 10.The first clinical signs were seen on silver fox whelps at the age of threeweeks. The whelps were unthrifty, their stools were watery, and theylittered the floors of the wooden whelping boxes. Their fur was moist andclamped. The females also had moist fur coat, which clamped in thecervical and abdominal areas. There was not increased mortality. Themorbidity was about 50 %, with all the whelps in affected culls showingthe symptoms. At this time the females are still nursing their whelps, andthe whelps keep themselves mostly inside the whelping boxes. After thesefirst symptoms, all whelps were studied clinically. They showed markedunthriftyness and poor growth. The body size of the animals wassignificantly smaller than the normal at this age. Affected whelps weresubmitted to post-mortem examination to Finnish Food Safety AuthorityEvira laboratory in Seinäjoki. In parasitological flotation test from intestinalcontents, coccidian oocysts were detected. Faecal samples were submittedfor quantitative parasitological analysis and species identification.Of the six silver fox whelp faecal samples, coccidian oocysts were foundin 4; max 5600 oocysts per gram (opg), and of the four blue fox whelpfaeces, oocysts were found in two, max 120 opg. Two species of Isosporawere found. Oocysts of the first one were 30-37x24-28 µm (mean [n=20]35.3 (SD 0.9) x 26.2 (SD 0.4) µm, and sporocysts measured 15-16x14-15µm (mean [n=20] 15.5 (SD 0.2) x 14.8 (SD 0.5). Sporozoites measuredwithin sporocysts within oocysts were about 13x5 µm (cannot be

measured very accurately). The oocyst surface is colourless, smooth andclear. There is neither Stieda body nor micropyle in the oocyst orsporocyst. No oocyst granule, but sporocyst residuum sometimes present.This species was identified as Isospora canivelocis (Weidman, 1915)Wenyon, 1923. Duszynski et al. [1] consider it possible that this species isidentical with Isospora buriatica Yakimoff and Matschoulsky, 1940 inMatschoulsky, 1941 from the Corsac fox and Indian fox, and, moreinterestingly, with Isospora canis Nemeseri, 1959 from the domestic dog.The other species oocysts measured 21-26x16-21 µm (mean [n=10] 23.4(SD=1.2) x 18.4 (SD=1.0) µm, and sporocysts measured 11-13x10-13 µm(mean [n=10] 12.2 (SD=1.0) x 11.4 (SD=1.0). The oocyst of this species isslightly smaller but essentially indistinguishable from Isospora ohioensisDubey, 1975, which was described to be 24x21 (21-27x19-23) µm in size.Variation in oocyst size can be caused by e.g crowding in heavyinfections. Also the infection phase can affect oocyst size.The animals were treated with oral sulfadiatzine-trimethoprim (ratio 5:1)medication at a dose of 120 g per ton of semimoist feed for five days, theeffect was variable, but the whelps later gained their normal condition andstarted to gain weight. The treatment was judged to be satisfactory.A second outbreak was observed on the same farm in blue fox whelps,when they reached the age of three weeks. The symptoms were similarto that of the silver foxes earlier, but more severe. The mortality was lowalso at this outbreak, but morbidity was higher, and the weightdevelopment was more affected. Whelps were submitted to post-mortemexamination, and coccidiosis was confirmed. The affected whelps weretreated with one individual oral dosing of toltrazuril by syringe at 10 mgper whelp and with oral sulfadiatzine-trimethoprim medication for fivedays, similar to the silver fox whelps. The recovery in the blue foxoutbreak was pronounced, and better than that of the silver fox outbreak.Discussion: The whelps most probably received the infection from theirdams, which are known to shed parasites at puerperal period. Alsohorizontal infection within litters in the whelping boxes is to beconsidered. The hygienic conditions on the farm deserve attention, andon this farm they may have contributed to the outbreak.The farm is located in the intensive fur farming district with proximity toother fur animal farms. The spread of the parasites within the farm andpossibly also between other farms may have been facilitated by black-headed gulls (Larus ridibundus), which frequently feed under the cagenettings and the feeding boards of the foxes. They may be vectors forthe parasite spread with their feet.Clinical coccidiosis is reported on fur animals [2], clinical case of thisseverity is the first one encountered in Finland. From the Internet, itappears that in Chinese veterinary medical literature, silver fox coccidiosisis described as a well-known disease and an important problem [3].This reported outbreak calls for closer examination of the occurrence ofclinical coccidiosis amongst Finnish fox farms, the coccidian speciescapable of infecting both blue foxes and silver foxes, and the controlmeasures of the clinical coccidiosis including potential infection routes,vehicles, and the therapy.References1. Duszynski DW, Couch L, Upton SJ: Coccidia (Eimeriidae) of Canidae and

Felidae. Supported by NSF-PEET DEB 9521687 2000 [http://biology.unm.edu/biology/coccidia/carniv1.html].

2. Wenzel UD, Berestov VA: Pelztierkrankheiten. VEB Deutscher, Berlin;1986:98-99.

3. Ping JiXing, Hongyong Wang, Zhou Zhenghong, Zhenchun to: Silver Foxcoccidiosis treatment. Cure of the silver fox Coccidiosis. Poujian throughpathology and laboratory checks to early diagnosis of the Silver Foxcoccidiosis, and to Treatment. Coccidia powder words of the diseasehave a better effect, in addition, sanitation is also extremely important.Hubei Animal Husbandry and Veterinary 2003, 01.

S19Haemonchosis in a sheep flock in North FinlandSaana-Maaria Manninen*, Antti OksanenFinnish Food Safety Authority (FINPAR), Evira Fish and Wildlife Research Unit,Oulu, FinlandActa Veterinaria Scandinavica 2010, 52(Suppl 1):S19

Background: In May 2008 two sheep from a farm in Ylikiiminki (65°N26°E) were autopsied at Finnish Food Safety Authority Evira in Oulu and


Page 18 of 31






http://biology.unm.edu/biology/coccidia/carniv1.html

http://biology.unm.edu/biology/coccidia/carniv1.html

diagnosed with a Haemonchus contortus infection. Haemonchus contortushas a few years ago been reported on the island of Hailuoto just outsideOulu, where it led to a lethal infection. Although this to sheep highlypathogenic nematode has been detected in Finland already in 1933 byAgnes Sjöberg [1], it has apparently never been reported so far up northin Finland. In Sweden H. contortus has almost reached the Arctic Circle[2]. It does not survive the Nordic winter on pasture, but with almost 100% arrested development in the early fourth larval stage it is capable ofsurviving the Nordic winter within its host [3].The farm the infected sheep originated from is a small sheep farm withalso a few goats and other domestic animals such as horses, turkeys andrabbits. They had bought their first sheep in November 2006, part of theewes being pregnant at time of purchase and lambed in January. Thesheep are of Finnish race, Texel-Oxford, Kainuu grey and cross-breeds. Inthe winter the sheep are housed in an approximately 150 m2 barn withthick straw bedding and access to a corral sized about 500 m2. Grazinggrounds from May until snowfall (in October) consists of approximately4 ha of pasture and 1 ha of mixed forest. According to the owner thetotally about 35 sheep and 4 goats mainly used the pasture grass as theirnutrition, but were also given hay in round bales, when the feeding areabecame very contaminated with faeces. The drinking water wasaccessible in the nearby river Kiiminkijoki. The animals were treated withfenbendazole in the autumn of 2007.In the spring of 2008 many of the sheep (age 1+) became weak anddeveloped an oedema under the jaw. Two of these animals (one died andone shot) were autopsied and the rest of the ones with symptoms were killedand buried. The autopsy findings included oedema under the jaw, palenessdue to anemia and abomasitis caused by a severe parasite infection.Materials, methods and results: Contents of the abomasum were rinsedinto 2L of water and a 200 mL sample was collected, the adult wormscollected, counted and identified. In one of the sheep 300 abomasalnematodes were found, where of 90 % were identified as Haemonchuscontortus, the rest being Teladorsagia circumcincta. In the faecal flotationusing a modified McMaster method an egg count (epg) of 5880 wascounted and eggs identified as Trichostrongylidae spp. The other animalhad a more severe infection, and approximately 1600 adult worms werefound in the abomasum, also with 90 % H. contortus and 10 %T. circumcincta. The results of the faecal egg count for this individualwere following: Trichostrongylidae spp. 36 000 EPG, Strongyloides sp. 400epg and Eimeria sp. 2040 oocysts per gram faeces.Discussion: The results indicate that Haemonchus contortus is becominga potential threat to sheep in North Finland and the distribution of thenematode should be monitored. The parasite is hereby proven to causevery severe disease in the North Ostrobothnian sheep production.Considering the effects of the climate change, that can be veryaffirmative for H. contortus life cycle, and the increasing amount of sheepin North Finland [4], the occurrence of this parasite in these latitudesshould not be left without attention. Moreover, it may be transmitted toother species such as reindeer [5]. In case of an infection with H.contortus, the flock could be recommended treatment with a macrocycliclactone antoparasitics, as eradication of the parasite on an individual farmpossible with correct administration of anthelmintics in the winterperiodwhen the animals are housed [6].References1. Sjöberg-Klaavu A: Om nematoder i matsältningsorganen hos får i

Finland. [About nematodes in the gastrointestinal tract in sheep inFinland]. In 4. Nordiska veterinärmötet, section IX Helsingfors, Tilgmannstryckeri, (In Swedish).

2. Lindqvist Å, Ljungström B-L, Nilsson O, Waller PJ: The dynamics,prevalence and impact of nematode infections in organically raisedsheep in Sweden. Acta vet. scand 2001, 42:377-389.

3. Waller PJ, Rudby-Martin L, Ljungström BL, Rydzik A: The epidemiology ofabomasal nematodes of sheep in Sweden, with particular reference toover-winter survival strategies. Veterinary Parasitology 2004, 122:207-220.

4. TE-keskus: Statistics. 2008, Available online: http://www.te-keskus.fi/Public/download. [Accessed 20. July 2008].

5. Hrabok JT, Oksanen A, Nieminen M, Rydzik A, Uggla A, Waller PJ: Reindeeras hosts for nematode parasites in sheep and cattle. VeterinaryParasitology 2006, 136:297-306.

6. Waller PJ, Rydzik A, Ljungström BL, Törnquist M: Towards the eradicationof Haemonchus contortus from sheep flocks in Sweden. VeterinaryParasitology 2006, 136:367-372.

S20Comparative evaluation of efficiency of traditional McMaster chamberand newly designed chamber for the enumeration of nematode eggsAsta Pereckiene1*, Saulius Petkevicius1,2, Antanas Vysniauskas11Veterinary Institute of Lithuanian Veterinary Academy, Instituto 2, LT-56115Kaisiadorys, Lithuania; 2Department of Infectious Diseases, LithuanianVeterinary Academy, Tilzes 18, LT-47181 Kaunas, LithuaniaE-mail: [email protected] Veterinaria Scandinavica 2010, 52(Suppl 1):S20

Summary: The objective of this study was to perform the comparativeevaluation of efficiency of traditional McMaster chamber and the newlydesigned chamber for the enumeration of nematode eggs in differentagriculture animals. Thirteen pig, two horse and two sheep farms wererandomly selected, and 815 of pig faecal samples, 264 of horse and 264of sheep faecal samples were examined. The positive samples wereidentified by Henriksen and Aagaard (1976) [1] modification of McMastermethod. Furthermore, experimental horse faeces were examined by [1]and Urquhart et al., 1996) [2] modifications, whereas pig and sheepfaeces were examined by [1] and Kassai, 1999 [3] modifications,respectively. All samples were evaluated in two replicates: usingtraditional McMaster 0.3 ml chamber – I and newly designed 1.5 mlchamber – II [4]. In pig farms, 11.5% and 18.2% (chambers I and II,P<0.05) of pigs were found infected with Ascaris suum. Furthermore,14.6% and 17.8% (chambers I and II, P<0.05) of pigs were found infectedwith Oesophagostomum dentatum and 3.7% and 8.2% (chambers I and II,P<0.05) with Trichuris suis, respectively. In horse farms, 65.5% and 83.7%horses infected with strongyles were identified (chambers I and II, P<0.05.In sheep farms, the number animals of positive to strongyle infection was81.4% and 96.2% (I and II chambers, P<0.05). The new modification ofchamber [4] demonstrated statistically higher sensitivity for enumerationof nematode eggs and for evaluation of farms with infected animalscompared to McMaster modifications described in [1-3].Introduction: Faecal examination is an important tool for monitoringworm infections in farm animals and an important adjunct to maintainingeffective worm control programmes. Described faecal examinationmethods are either qualitative or quantitative. Qualitative methodsprovide information on the species present, whereas quantitativemethods provide an indication of the levels of infections. Both have theirown importance in determining the health status of a herd anddetermining appropriate treatments and control measures. Quantitativeexaminations are performed by different modifications of the McMastermethod, which is the most widely used and standard quantitativetechnique with sensitivity from 10 to 100 eggs per 1 g of faeces [5-15].Furthermore, the following chambers are used for egg count: traditionalMcMaster chamber with two chambers (2 x 0.15 ml), Gordon-Whitlockchamber (3 x 0.15), Whitlock McMaster chamber (3 x 0.3 ml), Whitlockuniversal chamber (4 x 0.5 ml), FECPAK 1 ml chamber (2 x 0.5 ml), andmodified MAFF 1 ml chamber (2 x 0.5 ml) [5,7,16-19].We produced a new type of chamber and tested it by the highperformance modification of McMaster method using the highestpossible amount of faeces and reducing the sensitivity coefficient. Thenew chamber was compared with the traditional McMaster chamber inboth cases using the McMaster method modifications [1-3]. Thetraditional (I) and the new chambers (II) were used for comparativeanalysis to evaluate the performance and stability of faecal examinationresults.Materials and methods: Thirteen pig, two horse and two sheep farmswere randomly selected, and 815 of pig faecal samples, 264 of horse and264 of sheep faecal samples were examined. The positive samples wereidentified by [1] modification of McMaster method. Experimental horsefaeces were examined by [1] and [2] modifications, whereas pig andsheep faeces were examined by [1] and [3] modifications, respectively. Allsamples were evaluated in two replicates: using traditional McMaster0.3 ml chamber – I, and newly designed 1.5 ml chamber - II [4]. The newegg count chamber (II) has a bead, which prevents the faeces suspensionfrom seeping out and protects the optics of microscope from adverseeffect. Comparisons were made as to the number of samples found to bepositive by each of the chamber.Results: Ascaris suum infection was identified in all investigated pigfarms, but the number of infected pigs estimated with the two chambers


Page 19 of 31











was significantly different − 11.5% (94/815) of pigs positive (chamber I)and 18.2% (148/815) of pigs positive (chamber II). Whipworm infectionwas identified only in 8 farms (chamber I) and in 11 farms (chamber II) −3.7% (30/815) and 8.2% (67/815) of samples were positive to T. suisinfection. Nodular worm infection was identified in 5 and 7 farms(chambers I and II) − 14.6% (119/815) and 17.8% (145/815) of positivepigs, respectively. The number of positive samples (chamber II) to Ascarissuum was on 1.6, Oesophagostomum dentatum on 1.2, and Trichuris suison 2.2 times higher compared results with chamber I. In farms where upto 10% of samples were identified as infected with chamber I, thedifference coefficient was highest (1.8). However, in the farms where>50% of infected pigs were identified with chamber I, the differencecoefficient was lowest (1.02).In horse farms, 65.5% (173/264) and 83.7% (221/264) of horses wereidentified infected with strongyles (chambers I and II, P<0.05). The numberof samples positive to Strongylus spp. was on 1.2 times and to Parascarisequorum on 3.4 times higher with chamber II compared to chamber I. Insheep farms, the number of animals positive to strongyle infection was81.4% (215/264) and 96.2% (254/264) (I and II chambers, P<0.05). Thenumber of samples identified as infected with Trichostrongylus spp. was 1.3times higher for chamber II compared to chamber I, 3.1 times higher forToxocara vitulorum, 2.5 times higher for Nematodirus filicollis, and 1.9 timeshigher for Trichuris ovis, respectively.Conclusion: The experimental examination of pig, horse and sheep faecesusing the new 1.5 ml chamber (II) helped to identify a higher percentage ofinfected animals compared to the traditional McMaster 0.3 ml chamber (I).The new modification of chamber [4] demonstrated statistically highersensitivity for enumeration of nematode eggs and for evaluation of farmswith infected animals compared to McMaster modifications desribed in [1-3].References1. Henriksen SA, Aagaard KA: A simple flotation and McMaster method. Nord

Vet. Med 1976, 28:392-397.2. Urquhart GM, Armour J, Duncan JL, Dunn AM, Jennings FW: Veterinary

Parasitology. Blackwell Science Ltd., Oxford, UK; 1996:307.3. Kassai T: Veterinary Helminthology. Butterworth-Heinemann, Oxford;

1999:260.4. Vyšniauskas A, Pereckienė A, Kaziūnaitė V: Comparative analysis of

different modifications of McMaster method. Veterinarija ir Zootechnika2005, 29:61-66, (in Lithuanian).

5. Whitlock HV: Some modifications of the McMaster helminth egg-counting technique and apparatus. J. Counc. Sci. Ind. Res 1948, 21:177-180.

6. MAFF (Ministry of Agriculture, Fisheries and Food): Manual of VeterinaryParasitological Laboratory Techniques. HMSO, London, 3 1986, 24.

7. Anon : Manual of veterinary parasitological laboratory techniques.Ministry of Agriculture 3rd edition. 1986, 24-25.

8. Coles GC, Bauer C, Borgsteede FHM, Geerts S, Taylor MA, Waller P, Wold J:Assotiation for the Advancement of Veterinary Parasitology (W.A.A.V.P.)methods for the detection of anthelmintic resistance in nematodes ofveterinary importance. Vet. Parasitol 1992, 44:35-44.

9. Ihler CF, Bjørn H: Use of two in vitro methods for the detection ofbenzimidazole resistance in equine small strongyles (Cyatostoma spp.).Vet. Parasitol 1996, 65:117-125.

10. Ward MP, Lyndal-Murphy M, Baldock FC: Evaluation of a compositemethod for counting helminth eggs in cattle faeces. Vet Parasitol 1997,73:186-187.

11. Roepstorff A, Nansen P: A Simple McMaster technique. Epidemiology,diagnosis and control of helminth parasites of swine. FAO. Animal HealthManual. Rome, Italy; 1998:47-56.

12. Craven J, Bjørn H, Barnes A, Henriksen SA, Nansen P: A comparison of invitro tests and a faecal egg count reduction test in detectinganthelmintic resistance in horse strongyles. Vet. Parasitol 1999, 85:49-59.

13. Varady M, Konigova A, Čorba J: Benzimidazole resistance in equinecyatostomes in Slovakia. Vet. Parasitol 2000, 94:67-74.

14. Mercier P, Chick B, Alves-Branco F, White CR: Comparative efficacy,persistent effect, and treatment intervals of anthelmintic pastes. Vet.Parasitol 2001, 99:29-39.

15. Pook JF, Power ML, Sangster NC, Hodgson JL, Hodgson DR: Evaluation oftests for anthelmintic resistance in ciathostomes. Vet. Parasitol 2002,106:331-343.

16. Whitlock HV, Kelly JD, Porter CJ, Griffin DL, Martin ICA: In vitro fieldscreening for anthelmintic resistance in strongyles of sheep and horses.Vet. Parasitol 1980, 7:215-232.

17. Lyndal-Murphy M: Anthelmintic resistance in sheep in Australianstandard diagnostic techniques for animal diseases. Edt. Corner L. A.,Bagust T., J. 1993, 3-9.

18. Cringoli G, Rinaldi L, Veneziano V, Capelli G, Scala A: The influence offlotation solution, sample dilution and the choice of McMaster slide area(volume) on the reliability of the McMaster technique in estimating thefaecal egg counts of gastrointestinal strongyles and Dicrocoeliumdentriticum in sheep. Vet. Parasitol 2004, 123:121-131.

19. Presland SL, Morgan ER, Coles GC: Counting nematode eggs in equinefaecal samples. Vet. Rec 2005, 156:208-210.

S21Metastrongylus spp. infection in a farmed wild boar (Sus scrofa) inFinlandPaula Syrjälä1*, Antti Oksanen2, Outi Hälli3, Olli Peltoniemi3, Mari Heinonen31Veterinary Bacteriology Research Unit, Finnish Food Safety Authority Evira,Kuopio, Finland; 2Fish and Wildlife Health Research Unit, Finnish Food SafetyAuthority Evira, Oulu, Finland; 3Department of Production Animal Health,University of Helsinki, Pohjoinen pikatie 800, 04930 Saarentaus, FinlandActa Veterinaria Scandinavica 2010, 52(Suppl 1):S21

Summary: Metastrongylus spp. (Nematoda, Metastrongylidae) are lungworms of swine and occur worldwide. Species in the family includeM. apri, M. pudendotectus, M. asymmetricus, and M. salmi. Earth worms areintermediate hosts and pigs get infected when eating earth worms.In Finland wild boar farming began in the 1980s and now there are overhundred farms and over 2000 wild boars in different parts of the country.This case report is part of a study aiming to get more information aboutthe diseases that occur in the farmed wild boar population in Finland.Lungworms were detected in an eight month old farmed wild boar sentfor necropsy from a farm situated in eastern Finland. In the group of25 animals of about the same age, the farmer had noticed poor growthand gait abnormalities. He submitted two euthanized boars (A and B) fornecropsy. A routine necropsy was performed and tissue samples werecollected for histopathology, bacteriology and parasitology.The boar A was in a poor nutritional condition. The lungs were slightlymottled, but otherwise normally inflated. Large numbers of white threadlike nematodes were detected in the bronchi (Fig. 1.). Bones were soft. Inthe faecal sample, 7500 EPG Metastrongylus spp. eggs were detected withflotation (Fig. 2.). The boar B was in a moderate nutritional condition. Nolung worms were detected. The main pathological diagnosis of both wasosteomalacia due to deficiency of mineral feeding. However, the the poornutritional condition of the boar A infected with lung worms was possiblypartly due to the lung worm infection. Four additional faecal sampleswere sent from remaining boars from the farm and two of them werealso positive for Metastrongylus spp. eggs (100 and 200 EGP).In Finland Metastrongylus spp. has occurred sporadically in pigs decadesago in southeastern parts of the country [unpublished, Nikander, [1]. It

Figure 1 (abstract S21) Cross section of Metastrongylus spp. in the lung.


Page 20 of 31























was not detected in domestic pigs in a large study done in all Nordiccountries in 1980 ’s [1]. It was also not found in a study of Danishorganic swine herds [2]. In natural wild boar in many countries thisparasite is common [3-6]. In the modern pig industry this infectionseems to have been disappeared, because there is no contact with theintermediate host, the earth worms. However, in the farmed wild boar,and in situations where pigs are kept outdoors, Metastrongylus spp.should be considered as a possible cause of poor growth andrespiratory signs.References1. Roepstorff A, Nilsson O, Oksanen A, Gjerde B, Richter SH, Örtenberg E,

Christensson D, Martinsson KB, Bartlett PC, Nansen P, et al: Intestinalparasites in swine in the Nordic countries, prevalence and geographicaldistribution. Vet Parasitol 1998, 76:305-319.

2. Carstensen L, Vaarts M, Roepstorff A: Helminth infections in Danishorganic swine herds. Vet Parasitol 2002, 106:253-264.

3. Järvis T, Kapel Ch, Moks E, Talvik H, Mägi E: Helminths of wild boar in theisolated population close to the northern border of its habitat area. VetParasitol 2007, 150:366-369.

4. Morita T, Haruta K, Shibata-Haruta A, Kanda E, Imai S, Ike K: Lung worms ofwild boars in the western region of Tokyo, Japan. J Vet Med Sci 2007,69:417-420.

5. de-la-Muela N, Hernandez-de-Lujan S, Ferre I: Helminths of wild boar inSpain. J Wildl Dis 2001, 37:840-843.

6. Barutzki D, Schoierer R, Gothe R: Helminth infections in wild boars inenclosures in southern Germany: species spectrum and infectionfrequency. Tierarztl Prax 1990, 18:529-534.

S22Rare canine parasites survive in the wild fox populationMarja Isomursu*, Niina Salin, Antti OksanenFinnish Food safety Authority Evira, Fish and Wildlife Health Research Unit,Oulu, FinlandActa Veterinaria Scandinavica 2010, 52(Suppl 1):S22

Summary: Members of the canid family – e.g. domestic dog Canisfamiliaris, wolf Canis lupus, red fox Vulpes vulpes and raccoon dogNyctereutes procyonoides – share a wealth of parasite species. Nowadays,the diversity of the parasitic fauna of domestic dogs is reduced byantiparasitic medications and disposal of faeces, but a thriving populationof wild foxes can host even rare parasite species. Finnish Food SafetyAuthority Evira, Fish and Wildlife Health Research Unit, examines approx.250 fox carcasses for zoonoses every year. Some rarely seen canineendoparasites were observed in the winter 2007-2008.In January 2008, one of the first Finnish domestic cases of Spirocerca sp.infection was observed in a fox hunted from North Lapland fjeld area inUtsjoki (69° N 27°E). The previous one reported was imported fromTanzania [1]. A 30 x 15 mm granuloma containing two large, red, coiled

nematodes was formed on the curvatura major of the stomach. The foxwas a male individual in good condition.In a 1.5 year-old female fox from Pyhtää, Southeast Finland, a solitaryfemale individual of French heartworm Angiostrongylus vasorum waslodged in the right ventricle, in the opening of the pulmonary artery. Theexistence of this parasite in Finland is very inadequately known, but it isspreading in Europe, e.g. in Denmark [2].A massive liver fluke Metorchis albidus infection was observed in an aged(6.5 yrs) female fox from Virolahti, Southeast Finland. The flukes hadcaused a severe cholangitis. Although Metorchis is a very occasionallyseen parasite in Finland, it is regarded as common in Germany [3].In addition to these isolated cases, a small survey of the occurrence ofthe bladder hairworm Capillaria plica was conducted in February 2008.Scrapings of urinary bladder wall were taken from 44 foxes from NorthLapland and 7 of them (16%) were positive for eggs or worms. In aDanish study, about 80 % of foxes examined were found infected withthis parasite [2]. All four parasite species mentioned above have at leastone intermediate or paratenic host which may facilitate their persistencein the nature.It is interesting to notice that a similar amount of raccoon dogs are alsoexamined and comparable findings to the abovementioned have notbeen made. The raccoon dog often harbours higher Trichinella infectiondensities than the red fox does, and this has been speculated to becaused by some innate or acquired cause of immunoincompetence(unpublished). Therefore, raccoon dogs might be expected to harbouroccasional parasite infections even more commonly than foxes.References1. Nikander -S: Sukkulamadon (Spirocera lupi) aiheuttama osteosarkooma

koiran ruokatorvessa. [Oesophageal osteosarcoma associated withSpirocerca lupi in a dog.]. Suomen Elainlaakarilehti. 1994, 100(3):173-177.

2. Saeed I, Maddox-Hyttel C, Monrad J, Kapel CMO: Helminths of red foxes(Vulpes vulpes) in Denmark. Veterinary Parasitology. 2006, 139(1/3):168-179.

3. Schuster R, Bonin J, Staubach C, Heidrich R: Liver fluke (Opisthorchiidae)findings in red foxes (Vulpes vulpes) in the eastern part of the FederalState Brandenburg, Germany—a contribution to the epidemiology ofopisthorchiidosis, Parasitol. Res 1999, 85:142-146.

S23Control of livestock ectoparasites with entomopathogenic fungi: areviewStephen Abolins, Richard Wall*

Veterinary Parasitology & Ecology Group, School of Biological Sciences,University of Bristol, Woodland Road, Bristol, BS8 1UG, UKActa Veterinaria Scandinavica 2010, 52(Suppl 1):S23

The abundance of ectoparasites requires ongoing management and thisis most commonly achieved with insecticides or endectocides. However,the growth in resistance, the slow rate of development of new actives,coupled with environmental and health concerns associated with thecontinued use of some of the existing neurotoxic insecticides, suggestthat alternative approaches to their management need to be identified.Here one possible alternative approach, the use of entomopathogenicbiological control agents, is reviewed highlighting the remainingobstacles that should be overcome to enable their practical application.

S24Anthelmintic resistance. An overview of the situation in the NordiccountriesCarl Fredrik IhlerDepartment of Companion Animal Clinical Sciences, Norwegian School ofVeterinary Science, P:O 8146, 0030 Dep Oslo, NorwayE-mail: [email protected] Veterinaria Scandinavica 2010, 52(Suppl 1):S24

Introduction: Gastrointestinal nematodes in grazing animals cause majorproduction losses and represent an animal welfare problem worldwide.For decades use of anthelmintics has been central in the controlprograms of these parasites. This intensive use of anthelmintic drugs hasresulted in problems with resistance to the anthelmintic drugs availabletoday. Resistance to all classes of broad-spectrum anthelmintics available

Figure 2 (abstract S21) Metastrongylus spp. egg with a larva inside.


Page 21 of 31

















benzimidazoles (BZ), imidothiazoles-tetrahydropyrines and macrocycliclactones has been reported [1].The time from introducing a new class ofanthelmintic drugs until resistance has been detected seems to be lessthan 10 years [1]. As time has passed problems of multiresistance tomore than one class has occurred as well. Multiresistant Haemonchuscontortus has become a major threat to the whole small ruminantindustry in part of South Africa and in the South-East of USA [2,3].At present, resistant nematode populations are detected in allour naturally grazing species; sheep, goats, cattle and horses [1].In pigs, resistance to pyrantel, levamisole and benzimidazoles inOesophagostumum spp have been detected [4,5].Development of anthelmintic resistance: Anthelmintic resistance (AR)is defined by Køhler as genetically transmitted loss of sensitivity of a drugin worm populations that were previously sensitive to the same drug [6].In a worm population, alleles coding for resistance will be present as aresult of mutations, also in unexposed populations. Resistance willdevelop if there are survival advantages for parasites carrying thesealleles [7]. Treating worms with drugs corresponding to the “resistance”alleles will give these worms an advantage and the frequency of resistantworms in the population will increase. The frequency of alleles coding forresistance at the time of exposure to a drug will be important for therate of the development of a resistant population.The amount of anthelmintic drugs used and thereby the exposure willinfluence the development of AR. Therefore, it is important to establishde-worming strategies that take this into consideration. Parasite controlprograms must have a specific aim and the use of drugs must be kept toa minimum to achieve this aim. For horses a reasonable aim of a parasitecontrol program would be to eliminate the large strongyles and have thecyathostomes and Parascaris equorum infestations under control.The prepatent period of a parasite will be of importance. Species withshort prepatent periods will have more generations during a grazingseason. Frequent anthelmintic treatment will then expose moregenerations of these parasites than species with longer generationintervals. The trichostrongyles in ruminants (prepatent period approx.3 weeks) and cyathostomes in horses (prepatent period 6-8 weeks) areexamples of short generation interval species. Strongylus vulgaris has,however, a prepatent period of 6 months. This difference in generationinterval might be the reason why resistance is common in cyathostomesand has not been reported in S. vulgaris so far.Parasites in refugia represent the fraction of the worm population notexposed to the drug when animals are treated. The free living stages ofthe parasites are the most important part of the refugia. The higher theproportion of parasites in refugia the slower the development ofresistance as the selection pressure of the whole population is lower [8,9].The importance of refugia can be illustrated by looking at the differencein development of resistance in Australia compared to New Zealand. InNew Zealand, where the climate is wet, up to 75% of the H. contortuspopulation are larval stages on the pasture [10], which is considerablyhigher than in the more dry climate in Australia. In spite of the fact thatthe benzimidazoles and levamisole have been used over the same periodof time, the resistance to these drugs was detected much later in NewZealand [11].In the Nordic countries parasites which do not overwinter on the pasture,such as H. contortus, have only a small proportion in refugia and hencehave a greater selection pressure when animals are treated in this periodthan in species where larval stages overwinter on pasture.Selective treatment of animals will also have impact on the refugia. Inhorses selective treatment of animals expelling > 200 eggs per gramwhen treated in the grazing season has been suggested. This will reducethe exposed proportion of the population and thus dilute the resistantalleles in the population. Such strategy will, however, need an egg countof faeces from every single animal before treatment. This strategy iswidely used in Denmark [12].Detection of anthelmintic resistance: Different methods, both in vivoand in vitro methods, have been used to detect and monitor AR. Faecalegg count reduction test is the most used in vivo method and gives anestimation of the efficacy of the drug by comparing the egg counts preand post treatment. Guidelines for the method are described by Coles etal. [13]. The accuracy of the method depends on a correlation betweenegg counts and worm burdens which is not always present. Nematodeslike Trichostrongylus colubriformis and Ostertagia circumcincta show littlecorrelation whereas H. contortus show good correlation [14,15].

The controlled test is the most reliable method but is rarely used becauseof high costs. This test uses untreated control groups and the parasitizedanimals are euthanized about 10 days post treatment and a necropsy issubsequently preformed.Different in vitro methods are described. The egg hatch assay (EHA) wasfirst described by Le Jambre for the detection of BZ- resistance [16].Modification of the original method is developed by Taylor et al. [17] andthe method is mostly used for the detection of possible BZ resistance insheep and horses [18].The larval development assay (LDA) uses the abilityof the anthelmintic to arrest the normal development from eggs to L3larvae. By observing the proportion of L3 larvae developed in differentconcentrations of an anthelmintic, a LC50 value can be determined. Inthis assay anthelmintics with different modes of action can be tested atthe same time and it has been useful in surveys of sheep nematodes[19]. The test has shown to be difficult to use in equine strongyles due torepeatability problems [20].A biochemical test for detection of BZ resistance based on reducedaffinity to tubulin has also been introduced [21]. The method requires alarge number of larvae and is therefore unsuitable for field surveys [17].Molecular based tests are only in use for detection of BZ resistance as themolecular mechanisms for resistance to tetrahydropyrimidenes andmacrocyclic lactones are not fully understood [18]. The principle of thediagnosis of resistance relies on a multiple allele specific PCR. Themethod has been used for testing ovine trichostrongyles and equinesmall strongyles for BZ resistance. The most common mechanism for BZresistance in ovine trichostrongyles involves a phenylalanine to tyrosinemutation located at residue 200 of the isotype 1 beta-tubulin gene [22].The same polymorphism is described in equine small strongyles [23].Anthelmintic resistance in gastrointestinal nematodes in the Nordiccountries: AR most likely represents a problem of all Nordic countriesalthough few studies have been performed in Finland and Iceland(Oksanen and Sigurdsson, personal communication).The Danish veterinary parasitologists have been important expandingour knowledge of AR in the Nordic countries. In the early 90s theCentre for Experimental Parasitology in Copenhagen, lead by theenthusiastic Professor Peter Nansen, performed many studies andresearch programs in this field involving PhD students from manycountries. The Centre through Dr. Henrik Bjørn, also inspired researchon anthelmintic resistance in Sweden and Norway together with Dr.Peter Waller.In Denmark, several studies have been performed on AR in smallruminants, horses and swine. The first study on resistance in sheepnematodes in Denmark was published in the early 90s where resistanceto levamisole in Ostertagia circumcincta was described [24]. Later Maingiet al. [25] reported evidence of BZ, ivermectin and levamisole resistancein caprine trichostrongyles in a survey from 15 Danish goat herds. Mostother studies concerning AR in sheep nematodes in Denmark havefocused on comparison of different in vitro tests with the faecal eggcount reduction test and to my knowledge no surveys have beenperformed to evaluate changes in the resistance situation over the last10-15 years.In Sweden there are no published surveys on resistance in small ruminantnematodes while there is one single report on the situation in Norway[26]. In this report BZ-resistance was detected in four out of 26 herds.Resistance in O. circumcincta was found in all 4 herds while resistance inNematodirus battus and H. contortus were suspected in one of theseherds.In swine, Roepstorff et al. [4] confirmed resistance to pyrantel citrate inOesophagostomum spp. in Denmark. Later Bjørn et al. [27] confirmed side-resistance between levamisole and pyrantel in the same species. To myknowledge no studies on AR in swine parasites have been conducted inthe other Nordic countries. The prevalence of resistant Oesophagostomumspp. is reported from Germany is estimated to 2-3.5 % [5].No studies concerning resistance in cattle nematodes have so far beenpublished from the Nordic countries. Worldwide there are howeverstudies confirming resistance to all three major classes of anthelminticdrugs in cattle nematodes [1]. Looking at the experience of othercountries, anthelmintic resistance in cattle nematodes might be a threatto the cattle industry in our countries as well.Anthelmintic resistance in intestinal parasites of the horse is withoutdoubt the area where most studies concerning AR are conducted in theNordic countries. In Sweden Nilsson et al. [28] reported BZ-resistance in


Page 22 of 31

equine small strongyles. Later Bjørn et al. [29] and Ihler [30] publishedhigh prevalence of BZ-resistance in Denmark and Norway.Pyrantel resistance in small strongyles has also been reported from theNordic countries [30-32]. Resistance to macrocyclic lactones in the equinesmall strongyles has so far not reported, but there is a worldwideagreement that it is just a question of time before this will occur.However, reports on resistance to ivermectin in the equine roundwormP. equorum have been published. From Denmark Schougaard and Nielsen[33] have reported reduced efficacy of ivermectin as have Lindgren et al.from Sweden [34]. Resistance to ivermectin in the equine roundworm issuspected in Norway, but a proper study on this has not been conducted yet.Although most reports on AR in nematodes concern anthelmintics toruminant and horse parasites, there are also reports of resistance in thecanine hookworm Ancylostoma caninum to pyrantel [35,36]. No reports inthe Nordic countries on resistance to canine nematodes have beenpublished.Reducing the development of AR: AR is a major problem whencontrolling parasite infections in production animals and horsesworldwide. As documented, the reason for development of resistance toanthelmintics is a selection of resistant individuals in the wormpopulation as a result of anthelmintic exposure. Therefore, efforts toreduce this exposure will slow down further development of resistancebut will not reverse the existing resistance in a population. The mostobvious way to reduce the exposure is to reduce the use of anthelminticdrugs and look to other ways to control parasites beside anthelminticuse.As no new broad-spectrum anthelmintic drugs with new modes of actionhave been introduced since the macrocyclic lactones in the 80s, it isnecessary to take the warnings of AR as a major problem seriously.Improvement of the grazing management is important in reducing theuse of anthelmintics. Reduction of the stocking rate, reducing the grazingseason on the pastures and mixed grazing between animal species are allkey factors. Furthermore, the animals have to be treated at times whenthe effect of treatment is best and underdosing is to be avoided.Biological control of nematodes is an interesting way of reducing the useof anthelmintic drugs. The principle of biological control is the use of thenatural enemies of the nematodes to reduce the infection level onpastures [37]. These methods have no intention of eliminating the freeliving larval stages but aim to reduce them to a level where no clinical orsubclinical effects are present while stimulating an acquired immuneresponse. Nematode destroying fungi have been a potential candidate inbiological control and the fungus Duddingtonia flagrans has shown to beeffective through several studies [38-41]. Most studies on the effect offeeding D. flagrans have been based on daily intake of the fungi throughfeed supplementation. Mineral blocks containing fungal spores or slow-release devices might be practical ways of feeding the fungal material inthe future and make the method practical in commercial farming.Development of effective vaccines against intestinal parasites will allowthe opportunity to reduce the use of antiparasitic drugs. In spite of greatefforts making vaccines protecting grazing animals against helminthinfections, only a vaccine against the bovine lungworm Dictyocaulusviviparus is commercially available [42]How to deal with the challenge of AR in the Nordic countries:Keeping in mind that new classes of anthelmintic drugs with differentmode of action have not been introduced since the 80s and that the ARproblem seems to escalate worldwide, we have to take action.Monitoring the resistance situation by systematic surveys in differentworm populations is an important means to control AR. I think that theagricultural industry has to be financially responsible for this workthrough their organisations. We have good knowledge on thedevelopment of AR and we know how to deal with it, but we lackinformation on the development AR over time in our region.Prescription from veterinarians must be the only way for the farmers toobtain anthelmintics. This will subsequently demand a qualified advicefrom the veterinarians in order to give the best advice concerning typeof formulations and when to treat the animals to achieve the best effectof the treatment and at the same time take development of AR intoconsideration. This is a challenge in the education of both veterinarystudents and veterinary colleagues.References1. Kaplan RM: Drug resistance in nematodes of veterinary importance. A

status report. Trends Parasitol 2004, 20:477-481.

2. Van Wyk JA, Stenson MO, Van der Merwe JS, Vorster RJ, Viljoen PG:Anthelmintic resistance in South-Africa: surveys indicate indicate anextremely serious situation in sheep and goat farming. Onderspoort J VetRes 1999, 66:273-284.

3. Mortensen LL, Williamson LH, Terrill TH, Kircher RA, Larsen M, Kaplan RM:Evaluation of prevalence and clinical implications of anthelminticresistance in gastrointestinal nematodes of goats. J Am Vet Med Assoc2003, 223:495-500.

4. Roepstorff A, Bjørn H, Nansen P: Resistance of Oesophagostomum spp. inpigs to pyrantel citrate. Vet Parasitol 1987, 24:229-239.

5. Gerwert S, Failing K, Bauer C: Prevalence of levamisole and benzimidazoleresistance in oesophagostomum populations of pig breeding farms inNorth Rhine-Westphalia, Germany. Parasitol Res 2002, 88:63-68.

6. Køhler P: The biochemical basis of anthelmintic action and resistance. IntJ Parasitol 2001, 31:336-345.

7. Gilleard JS, Beech N: Population genetics of anthelmintic resistance inparasitic nematodes. Parasitology 2007, 134:1133-1147.

8. Martin PJ, Le Jambre LF, Claxton JH: The impact of refugia on thedevelopment of thiabendazole resistance in Haemonchus contortus. IntJ Parasitol 1981, 11:35-41.

9. van Wyk JA: Refugia- overlooked as perhaps the most potent factorconcerning the development of anthelmintic resistance. Onderspoort JVet Res 2001, 66:55-67.

10. Le Jambre LF: Anthelmintic resistance in gastro intestinal nematodes ofsheep. In The epidemiology and control of gastro intestinal parasites of sheep.Edited by: Donald AD, Southcott WH, Dineen JK. CSRIO, Division of AnimalHealth, Melbourne; 1979:109.

11. Kettle PR, Vlassoff A, Lukies JM, Ayling JM, McMurtry LW: A survey ofnematode control measures used by sheep farmers and of anthelminticresistance on their farms. Part I. North Island and the Nelson region of theSouth Island. NZ Vet J 1981, 29:81-83.

12. Nielsen MK, Monrad J, Olsen SN: Prescription-only anthelmintics- aquestionnaire survey of strategies for surveillance and control of equinestrongyles in Denmark. Vet Parasitol 2006, 135:47-55.

13. Coles GC, Bauer C, Borgsteede FH, Geerts S, Klei TR, Taylor MA, Waller PJ:World Association of Advancement of Veterinary Parasitology (WAAVP)methods for detection of anthelmintic resistance in nematodes ofveterinary importance. Vet Parasitol 1992, 44:35-44.

14. Sangster NC, Whitlock HV, Russ IG, Gunawan M, Griffin DL, Kelly JD:Trichostrongylus colubriformis and Ostertagia circumcincta resistant tolevamisol, morantal tartrate and thiabendazole: occurrence of fieldstrains. Res Vet Sci 1979, 27:106-110.

15. Martin PJ, Anderson N, Jarrett RG: Resistance to benzimidazole resistancein field strains of Ostertagia and Nematodirus in sheep. Aust Vet J 1985,62:38-43.

16. Le Jambre LF: Egg hatch as an vitro assay of thiabendazole resistance innematodes. Vet Parasitol 1976, 2:385-391.

17. Taylor MA, Hunt KR, Goodyear KL: Anthelmintic resistance detectionmethods. Vet Parasitol 2002, 28:183-194.

18. Coles GC, Jackson F, Pomroy WE, Prichard RK, von Samson-Himmelstjerna G, Silvestre A, Taylor MA, Vercruysse J: The detection ofanthelmintic resistance in nematodes of veterinary importance. VetParasitol. 2006, 136:167-85.

19. Lacey E, Redwin JM, Gill JH, Demargherity VM, Waller PJ: A larvaldevelopment assay for the simultaneous detection of broad spectrumanthelmintic resistance. Resistance of parasites to antiparasitic drugs.MSDAGVET, Rahway, NJ.: Boray JC 1990, 177-184.

20. Tandon R, Kaplan RM: Evaluation of a larval development assay(DrenchRite®) for the detection of anthelmintic resistance incyathostomin nematodes of horses. Vet Parasitol 2004, 121:125-142.

21. Sangster NC, Prichard RK, Lacey E: Tubulin and benzimidazole resistancein Trichostrongylus colubriformis (nematoda). J Parasitol 1985, 71:645-651.

22. Elard L, Cabaret J, Humbert JF: PCR diagnosis of benzimidazole-susceptibility or-resistance in natural population of the small ruminantparasite, Teladorsagia circumcincta. Vet Parasitol 1999, 80:231-237.

23. Pape M, Posedi J, Failing K, Schnieder T, von Samson-Himmelstjerna G:Analysis of the beta-tubulin codon 200 genotype distribution inbenzimidazole-susceptibility and –resistance cyathostome population.Parasitology 2003, 127:53-59.

24. Bjørn H, Monrad J, Nansen P: Anthelmintic resistance in nematodeparasites of sheep in Denmark with special emphasis on levamisoleresistance in Ostertagia circumcincta. Acta vet Scand 1991, 32:145-154.


Page 23 of 31









































25. Maingi N, Bjørn H, Thamsborg SM, Bøgh HO, Nansen P: A survey ofanthelmintic resistance in nematode parasites of goats in Denmark. VetParasitol 1996, 66:53-56.

26. Reiersen A, Ihler CF: Ormemiddelresistens hjå saueparasittar i Norge.Proceedings Husdyrforsøksmøtet 1996, 401-405.

27. Bjørn H, Roepstorff A, Waller PJ, Nansen P: Resistance to levamisole andcross-resistance between pyrantel and levamisole in Oesaphagostomumqudrispinulatum and Oesophagostomum dentatum of pigs. Vet Parasitol1990, 37:21-30.

28. Nilsson O, Lindholm A, Christensson D: A field evaluation of anthelminticsin horses in Sweden. Vet Parasitol 1989, 32:163-171.

29. HBj rn, Sommer C, Schougrd H, Henriksen SA, Nansen P: Resistance tobenzimidazole anthelmintics in small strongyles (Cyathostominae) ofhorses in Denmark. Acta vet Scand 1991, 32:253-260.

30. Ihler CF: A field survey on anthelmintic resistance in equine smallstrongyles in Norway. Acta vet Scand 1995, 36:135-143.

31. Craven J, Bjørn H, Henriksen SA, Nansen P, Larsen M, Lendal S: Survey ofanthelmintic resistance on Danish horse farms, using 5 differentmethods of calculating faecal egg count reduction. Equine vet J 1998,30:289-293.

32. Lind EO, Kuzmina T, Uggla A, Waller PJ, Höglund J: A field study on theeffect of some anthelmintics on cyathostomins of horses in Sweden. VetRes Commun 2007, 31:53-65.

33. Schougaard H, Nielsen MK: Apparent ivermectin resistance of Parascarisequorum in foals in Denmark. Vet Rec 2007, 160:439-440.

34. Lindgren K, Ljungvall O, Nilsson O, Ljungström BL, Lindahl C, Höglund J:Parascaris equorum in foals and in their environment on a Swedish studfarm, with notes on treatment failure of ivermectin. Vet Parasitol 2008,151:337-343.

35. Jackson R, Lance D, Townsend K, Stewart K: Isolation of antehelminticresistant Ancylostoma caninum. N Z Vet J 1987, 35:215-216.

36. Kopp SR, Kotze AC, McCarthy JS, Coleman GT: High-level pyrantelresistance in the hookworm Ancylostoma caninum. Vet Parasitol 2007,143:299-304.

37. Larsen M: Biological control of nematodes in sheep. J Anim Sci 2006, 84:E133.

38. Faedo M, Barnes EH, Dobson RJ, Waller PJ: The potential ofnematophagous fungi to control the free-living stages of of nematodeparasites of sheep.: Pasture plot study of Duddingtonia flagrans. VetParasitol 1998, 76:129-135.

39. Larsen M, Faedo M, Waller PJ, Hennessy DR: The potential ofnematophagous fungi to control the free-living stages of of nematodeparasites of sheep: Studies with Duddingtonia flagrans. Vet Parasitol1998, 76:121-128.

40. Fontenot ME, Miller JE, Peña MT, Larsen M, Gillespie A: Efficiency offeeding Duddingtonia flagrans chlamydospores to grazing ewes onreducing availability of parasitic nematode larvae on pasture. VetParasitol 2003, 118:203-213.

41. Waller PJ, Schwan O, Ljungström BL, Rydzik A, Yeates GW: Evaluation ofbiological control of sheep parasites using Duddingtonia flagrans undercommercial farming conditions on the island of Gotland, Sweden. VetParasitol 2004, 126:299-315.

42. Smith WD, Zarlenga DS: Developments and hurdles in generatingvaccines for controlling helminth parasites of grazing ruminants. VetParasitol 2006, 139:347-459.

S25Parasite surveillance and novel use of anthelmintics in cattleJohan HöglundDepartment of Biomedical Sciences and Veterinary Public Health, Div. ofParasitology and Virology (SWEPAR), Swedish University of AgriculturalSciences (SLU), SE-751 80 Uppsala, SwedenActa Veterinaria Scandinavica 2010, 52(Suppl 1):S25

Background: Cattle are economically the most important livestock forfarmers in Sweden. However, both dairy and beef production has beensubjected to considerable structural change over recent decades.Currently, there are approximately 1.5 million cattle, including ≈370 000dairy cows producing milk worth 1 m€ [1]. The trend is that the numbersof dairy cows are decreasing slowly, while beef cows are somewhatincreasing. At the same time as the productivity has been intensified

since the 1950’s in the cattle sector, herd size has increased and thenumber of production units, especially the number of dairy farms, havebeen dramatically reduced. In contrast, the numbers of organic farms aresteadily increasing. The goal of the Swedish government is to increasethe Swedish organic production of agricultural commodities to 20%within a three-year period.According to the Swedish animal welfare regulations, both conventionaland organic cattle must have access to pasture for a period of 2–3months per year [2]. The grazing season normally occurs between earlyMay and October. As pasture-borne parasites are ubiquitous whereveranimals are grazing, they remain one of the most important productivityconstraints in Swedish cattle production. These parasites have in commonthat they often exhibit simple direct life cycles with infective stagestransmitted on pasture by the faecal–oral route. The most importantpasture-borne parasites of grazing cattle in Sweden are thegastrointestinal (GI) nematodes Ostertagia ostertagi and Cooperiaoncophora. To a lesser degree, the lungworm Dictyocaulus viviparus, andalso the coccidian Eimeria alabamensis, are important pathogens.Furthermore, in wet areas the liver fluke Fasciola hepatica, with a complexlife cycle, sometimes cause problems.The importance of GI-nematodes and lungworms on the productivity infirst-season grazing (FSG) cattle has been demonstrated in a range ofindependent grazing trials conducted at SWEPAR over the last decade[3-8]. According to the results, the weight-gain penalties in unprotectedset stocked FSG animals were on an average in the range of 20 to 65 kg,compared to simultaneously grazed calves but that were fully protectedfrom parasites by the use of effective anthelmintics. Combined, thesetrials demonstrate the importance of nematode parasites on animalproductivity under Swedish climatic and management conditions. Theyalso show that good levels of nematode control can be achieved throughthe correct use of anthelmintics. However, at the same time there areconcerns that over-dependence on ‘chemical’ control may lead to long-term difficulties. This occurs partly through development of anthelminticresistance, but also because these substances are not widely acceptedamong consumers. Routine prophylactic use of anthelmintics is notaccepted in organic livestock farming [9]. However, “blanket” treatment ofthe whole grazing group or herd is accepted, even on organic farms, inresponse to a worm problem after it has been diagnosed.Although the results from our grazing trials also have shown that goodlevels of parasite control can be achieved without anthelmintics, some ofthe alternative non-chemical parasite control approaches that we havetested are impractical. For example, when it comes to the use of naturalpasturelands there are situations where high grazing pressure must bemaintained in order to maintain a profile necessary for the generation ofsubsidies. Young and adult stock on Swedish dairy farms are also oftengrazed on dedicated pastures, which omits the opportunities for mixedgrazing between different age groups. There are many examples oforganic cattle farmers who have obtained exemptions from the organicguidelines because their animals have suffered from nematode parasites.In this contribution, the focus is on diagnostic methods that can be usedfor individual and/or herd parasite monitoring in parasite surveillanceprogrammes. I will also briefly discuss future ways to refine the use ofanthelmintics through targeted selective treatments (TSTs). The latter is asustainable deworming method that can be applied in both conventionaland organic cattle production. Finally, some results from an ongoing EUproject (PARASOL, http://www.parasol-project.org/) will be presented.Sustainable use of anthelmintics: For the foreseeable future it can beassumed that anthelmintics will constitute the cornerstone of mostparasite control programmes, irrespective of whether they are used aloneor in an integrated programme. However, to preserve the efficacy and toreach a wider level of acceptance, including organic producers, it isunavoidable to refine the ways in which anthelmintics are used. Onepossibility is to replace current treatment regimes with TSTs. Today inSweden, anthelmintics are either administered at strategic times to allfirst grazing season cattle at risk (e.g. against GI-nematodes), or given asmetaphylactic mass treatments following the appearance of clinical signsin some animals in a grazing group (e.g. against lungworm). In order tocreate low input and sustainable programs for nematode control, TSTstrategies must not only be further developed but also validated underpractical farming conditions. The long-term aim with TST is to minimisethe number of whole herd/flock anthelmintic treatments by directingtreatments towards only those animals/herds that are likely to suffer from


Page 24 of 31









































http://www.parasol-project.org/

disease and production loss. Overall, this will reduce the opportunities forany associated environmental and health risks, while maintainingagricultural productivity.The concept of TST is simple and easy to accept, especially in situationswhere animals with a high worm burden are easily identified, forexample by showing clinical signs such as coughing, diarrhoea,emaciation or reduced productivity. However, it is well recognised thatthe greatest losses associated with pasture-borne nematode parasites ingrazing livestock are sub-clinical. Economic assessments have also shownthat the financial costs associated with sub-clinical parasitism areenormous [10]. It can also be argued that it is suboptimal and often toolate to treat with an anthelmintic when clinical signs have already beenobserved, as animals showing signs of disease are most likely topropagate infection. Essential for the TST approach is that there beaccess to good and reliable indicators, and identification of treatmentthresholds.Potential TST indicators: There are many potential TST indicators, whichcan be grouped according to whether they are parasitological,pathophysiological or performance factors. Those indicators based ontraditional parasitological techniques, such as faecal egg counts (FEC),and in particular pasture larval counts and tracer tests, are generallyimpractical, as they are either extremely laborious and/or non-informativewhen required [11]. Accordingly, it can be expected that they will not befeasible as indicators for the purpose of monitoring cattle health. Oneexception might be the recently developed FECPAC technology (http://www.fecpak.com/), which might serve its purpose. However, thistechnology must first be carefully tested and evaluated in field before itcan be recommended as a routine measure.Among the serological tests there are several promising candidates.Recently it has been demonstrated that both serum pepsinogenconcentrations (SPC) and antibody levels at housing provide veryuseful information about previous exposure to nematode parasites.SPC is a pathophysiological indicator measuring the damage caused tothe abomasal mucosa, and it has been shown to correlate with theoccurrence of parasitic gastroenteritis, both in naturally infectedanimals [12] and in young cattle experimentally infected with differentlevels of O. ostertagi [13]. However, the use of SPC is restricted, as itcan only be used to predict exposure of FSG animals to this particularparasite.Another option is to detect specific IgG antibody serum levels withimmunological methods using ELISA. Currently there are several in-house ELISAs for the detection of Ostertagia and Cooperia spp. Ofparticular interest is the ELISA using crude proteins from whole wormextracts of O. ostertagi, as it has been demonstrated that this ELISA notonly reflects parasite exposure [13] but also reflects the damage causedin terms of reduced production traits and milk yield [14,15].Interestingly, this test was recently evaluated to measure antibody levelsagainst this abomasal parasite in bulk tank milk [16]. To what levelparasite exposure in cows is correlated with the situation found inheifers and calves on the same farm remains obscure. Although thisaspect is currently being investigated within PARASOL, it is certainly atopic that requires more attention in the future. Milk is commonlytested for a range of infectious diseases, and results from the Ostertagiatest could then easily be incorporated into existing herd healthsurveillance programmes.If not tested beforehand, the suitability of using milk ELISAs against otherimportant parasites should also be explored. It is important to realise thatthe costs of sampling and testing must be minimised before a herdhealth monitoring programme can reach more general acceptanceamong representatives in authorities, livestock organisations and, notleast, the farming community.Ongoing research: Since 2006 SWEPAR has been actively involved inthe PARASOL project. This is an ongoing STREP activity coordinated byProfessor Joseph Vercruysse, Ghent University, Belgium, and aimed athelminth control in grazing ruminants. The work in Sweden has mainlybeen focussed on cattle, with the the specific aims: (1) to compare thepepsinogen and antibody levels against O. ostertagi in FSG animals athousing, and (2) to predict the situation in the FSG stockby investigating the antibody levels in bulk tank milk from the sameherds.A total of 44 dairy farms in south-central Sweden were randomlyselected in 2005. From each farm bulk tank milk was sampled along

with serum from ~10 FSG at the time of housing. The same farmswere also approached to participate the following year, and in 200636 farms participated together with one additional farm. In both yearsthe farmers were asked to complete a form containing questionsabout the management of the cattle on the farm, including questionsconcerning deworming practices. In the second year the form wasmore detailed, and it then also contained questions about utilizationof the pastures and figures on the milk production. Pepsinogenconcentrations and O. ostertagi antibody levels were measured in serafollowing ring-testing and according to standard operating procedures(SOP). In each run a set of standard samples was included to validatethe test results. Also, the milk samples were analysed in a similarfashion using the O. ostertagi-ELISA from SVANOVA biotechnology,Uppsala, Sweden.It was found that the majority of the herds were stabled in Septemberto October. However, the housing dates varied a lot. Notably, somefarmers housed their animals in late December. In both years, mostfarmers treated their FSG with an anthelmintic. However, a largeproportion (38%) was left untreated. The preferred anthelmintic in2006 was the oxfenbendazole intermittent release device (SystamexRepidose®). This drug was used on 85% of the farms. No samples hada serum pepsinogen concentration that exceeded the proposed cut-offconcentration of 3.5 U tyrosin, indicative of subclinical ostertagiosis.The highest value measured was 2.9 U tyrosin. Still, both the meanpepsinogen concentrations and serum antibody levels againstO. ostertagi were on an average higher for calves from the untreatedherds. However, there was only a weak positive correlation betweenthe Ostertagia- antibody levels and pepsinogen concentrations whenthe results of the same serum samples was compared (R=0.34).Furthermore, there was no association between the Ostertagia-antibody levels in bulk tank milk and in sera from the FSG from thesame herd. On the other hand, there was a good agreement betweenOD values obtained in different years, and in particular for the milksamples.A retrospective study was also carried out to assess the possibility ofusing daily weight gain in first-season grazing cattle (FSG) as a marker fortreatment decisions to prevent parasite-induced losses caused bygastrointestinal (GI) nematodes. Data were combined from threeindependent grazing trials, each of which was repeated over 2–3 years, inorder to investigate the influences of parasites on the performance ofFSG cattle subjected to different levels of parasite control. ROC analysesshowed that anthelmintic treatment of animals with a daily weight gain(Dwgt) of <0.75 kg/day by mid-season had a sensitivity of ~70% and aspecificity of ~50%. It thus seems feasible to base a targeted selectivetreatment for FSG cattle on Dwgt recorded approximately 4–8 weeksafter turn-out, provided that it is accepted that some animals will bedewormed without need. However, these data were pooled from anumber of disparate trials, so that these sources of variation wereincluded in the experiment but their individual effects cannot bedetermined. The next stage is to validate the conclusions in a controlledfield trial.Acknowledegements: The financial support of PARASOL (ParasiteSolutions), EU thematic priority areas Food Quality and Safety (FP6,FOOD-2004-T5.4.6.6), and FORMAS (220-2007-1616) and the linguisticrevision by David Morrison is gratefully acknowledged.References1. Anon: Jordbruksstatistisk årsbok. 2008, (tab 10.2).2. DFS: Djurskyddsmyndighetens författningssamling. Saknr L 2007,

100D.3. Dimander SO, Höglund J, Uggla A, Spörndly E, Waller PJ: The impact of

internal parasites on the productivity of young cattle organically rearedon semi-natural pastures in Sweden. Veterinary Parasitology 2000,90:271-284.

4. Dimander SO, Höglund J, Spörndly E, Waller PJ: Evaluation of gastro-intestinal nematode parasite control strategies for first-season grazingcattle in Sweden. Veterinary Parasitology 2003, 111:193-209.

5. Höglund J, Svensson C, Hessle A: A field survey on the status of internalparasites in calves on organic dairy farms in southwestern Sweden.Veterinary Parasitology 2001, 99:1-17.

6. Höglund J, Viring S, Törnqvist M: Seroprevalence of Dictyocaulus viviparusin first grazing season calves in Sweden. Veterinary Parasitology 2004,125:343-352.


Page 25 of 31

http://www.fecpak.com/

http://www.fecpak.com/











7. Höglund J, Törnqvist M, Rydzik A, Ljungström B-L: Best use of doramectinin first season grazing cattle in Sweden. Svensk Veterinärtidning 2008,4:11-18, (In Swedish with an English summary).

8. Larsson A, Dimander SO, Rydzik A, Uggla A, Waller PJ, Höglund J: A 3-yearfield evaluation of pasture rotation and supplementary feeding tocontrol parasite infection in first-season grazing cattle-Effects on animalperformance. Veterinary Parasitology 2006, 142:197-206.

9. KRAV: Standards for organic certified production. Heatlh and medical care2007, 5.4:50-52.

10. Corwin RM: Economics of gastrointestinal parasitism of cattle. VetParasitol 2007, 72:451-457.

11. Eysker M, Ploeger HW: Value of present diagnostic methods forgastrointestinal nematode infections in ruminants. Parasitology 2000, 120:S109-119.

12. Dorny P, Shaw DJ, Vercruysse J: The determination at housing ofexposure to gastrointestinal nematode infections in first-grazing seasoncalves. Veterinary Parasitology 1999, 80:325-340.

13. Ploeger HW, Kloosterman A, Borgsteede FH: Effect of anthelmintictreatment of second-year cattle on growth performance during winterhousing and first lactation yield. Veterinary Parasitology 1990,36:311-323.

14. Ploeger HW, Kloosterman A, Bargeman G, von Wuijckhuise L, van denBrink R: Milk yield increase after anthelmintic treatment of dairy cattlerelated to some parameters estimating helminth infection. VeterinaryParasitology 1990, 35:103-116.

15. Ploeger HW, Kloosterman A, Rietveld FW, Berghen P, Hildersson H,Hollanders W: Quantitative estimation of the level of exposure togastrointestinal nematode infections in first-year calves. VeterinaryParasitology 1994, 55:287-315.

16. Sanchez J, Dohoo IR, Markham F, Leslie K, Conboy G: Evaluation of therepeatability of a crude adult indirect Ostertagia ostertagi ELISA andmethods of expressing test results. Veterinary Parasitology 2002,109:75-90.

S26Changes in production systems and effects on parasitic infectionsAllan Roepstorff*, Stig Milan Thamsborg, Helena MejerDanish Centre for Experimental Parasitology, Department of Disease Biology,Faculty of Life Sciences, University of Copenhagen, Dyrlægevej 100, DK-1870Frederiksberg C, DenmarkActa Veterinaria Scandinavica 2010, 52(Suppl 1):S26

Summary: A plentity of parasites of great diversity is the rule for allanimals in nature. A successful parasite has to be transmitted from onehost to the next and this transmission is often the weakest point in thelife cycle, as the parasites depend on the surrounding environment fordays to months to become infective either as free-living stages orwithin intermediate hosts. For domestic animals, housing and otherfactors characterizing the production system thus have a great impacton transmission, the ectoparasites being an exception due to theirtransmission by physical contact between host animals. In the presentpaper, the effects of production systems on parasitic infections arediscussed with focus on pigs. During the last century pigs have movedfrom traditional husbandry systems with poor hygiene and access tooutdoor areas towards highly intensive, exclusively indoor industries, aprocess which has gradually reduced the number of endoparasitespecies. Furthermore, ectoparasitic arthropods are easily eradicated bydrug treatment in modern pig enterprises. It is thus only a smallnumber of protozoan parasites that are common across farms. Atpresent, the trend of decreasing parasitism is for the first time reversed.Organic pigs or other free-range pigs make up the best and mostextreme example, and these pigs may harbour many more parasitesthan conventional pigs. Only a small minority of domestic pigs,however, live in organic/free-range herds. It may therefore be moreimportant in the future that conventional pig herds are also changingtheir housing system due to animal welfare issues; straw bedding isbeing reintroduced, the pregnant sows are untethered to become free-moving, and facilities may include water sprinkling devices which willincrease the humidity and thereby the survival of transmission stages.The future challenge of domestic pigs may therefore, for the first time,be to control an increasing parasite load.

S27Alternative approaches to control of parasites in livestock: Nordic andBaltic perspectivesStig Milan Thamsborg*, Allan Roepstorff, Peter Nejsum, Helena MejerDanish Centre for Experimental Parasitology, Department of VeterinaryDisease Biology, Faculty of Life Sciences, University of Copenhagen, DenmarkActa Veterinaria Scandinavica 2010, 52(Suppl 1):S27

Introduction: It is evident from several on-farm surveys that levels ofparasite infections vary markedly between livestock production systemsand from one farm to another [1]. The background for these differencesrelates to livestock breeds, different management factors and otherpractices that directly or indirectly affect parasite infections, and also tofarmers’ attitudes e.g. the chosen threshold for intervention. This paperdeals with practices or interventions that can be actively applied byfarmers aiming specifically at control of mainly helminth infections, eitherby reducing the parasite infrapopulations directly, e.g. by means ofantiparasitic crops, or by limiting the uptake of external stages, e.g. bypasture management. The term “alternative” approaches has beenapplied (despite several options not being very alternative or novel butrelatively old) to denote only limited focus on use of commercialanthelmintics. Focus will be on approaches relevant to primarily ruminantand pig production and which can be applied in the Nordic-Baltic contextafter some modification or which may serve as a guideline for relevantresearch in our region. For practical reasons the options will be dealt withone at a time although, as pointed out in several reviews [2,3], thecombination of two or more options, or the combination with limited useof anthelmintics, will in many cases be the optimal approach.Pasture management: The basic principle of pasture management islimiting the intake of infective stages of pasture-borne parasite infections.Pasture management encompasses practices related to grazing: time ofturn-out, length of grazing period, age composition of flocks, co-grazingwith other species and frequency of pasture changes, although otherfactors like type of herbage and productivity, stocking rates and parasitecontamination levels at turn-out also are very important. On mostruminant farms, pasture management is guided by nutritionalrequirements of animals in combination with customary practices, and ingeneral little attention is paid to parasites when the season’s grazing isplanned. Pasture management practices aiming at parasite control havebeen extensively researched (and reviewed by [2,4,5] and in most casesdemonstrated to be quite successful in controlling mainly gastrointestinalnematodes of ruminants. The strategies can be grouped as preventive i.e.starting off with low (or nil) infection levels in animals and on pastures,evasive i.e. moving animals away from pastures before harmfulcontamination levels are generated, or dilutive strategies i.e. lowering theratio between susceptible and resistant animals (or lowering the overallstocking rate). Despite obvious benefits, these strategies are not readilyadopted by cattle farmers, although still more by organic thanconventional farmers [6,7], and this may be related to the relative easeand low cost of using anthelmintics compared to labour-intensive fencingand moving. Furthermore, in sheep grazing management is difficult topractice totally without drugs.In dairy cattle, the most susceptible group of animals, i.e. first seasongrazing calves, is uninfected at turn-out and if placed on an uninfected(or lightly contaminated) pasture this will result in good control for thefirst half of the season. By repeated moves to clean pastures (e.g. 2-3times), excellent control is obtained for the entire season [8]. Eventhough the first paddock is contaminated, infections are reduced if theflock is moved by 15 July to a paddock ungrazed the same year [9]. Arecent Swedish study showed very convincingly that a practice of turningout first year grazing steers (castrated bulls) on paddocks grazed bysecond year grazers in the previous season combined with a mid-summermove to clean pasture, result in acceptable control of gastrointestinalnematodes [10]. Male animals are generally more susceptible to parasitesthan females and steers are believed to have intermediate susceptibility[11]. Recent Danish studies on nematode infections showed susceptibilityin steers to be very similar to that of heifers [9]. Several studies haveindicated an exacerbating effect of high stocking rates on gastrointestinalnematode infection levels in both cattle and sheep [12,13] whereas theeffect is less clear in outdoor pigs [14], which presumably is because pigstend to stay in the feeding area instead of utilising the paddocks evenly.


Page 26 of 31




















Coccidia in ruminants are often transmitted by overwintering pastureinfections from one year’s young stock to the next [15], and cleanpastures at turn-out (read ungrazed the previous year) are thus crucial incontrol [16]. This is a fact often overlooked by sheep or cattle farmers,e.g. if they have a permanent, after-lambing collecting paddock or ifcalves as a rule are grazed in close vicinity of the farm [17]. In the case ofsheep, similar management practices may also result in problems ofnematodirosis in early season (“lamb-to-lamb” disease) as observed inDenmark [18]. Increasing problems with liver flukes (Fasciola hepatica) arebecoming evident in many places in Northern Europe where grazing ofcattle is re-introduced on natural wetlands for aesthetical reasons and tomaintain biodiversity [19]. In many cases control is achieved by strategicapplication of flukicides but it would be relevant to employ evasivegrazing i.e. a move in mid-August as a means of control. However, fewstudies, if any, have addressed this approach.The majority of the pig production in Nordic countries is indoor butpasture management is relevant in conventional outdoor and organicfarming where the breeding stock, or all stock, have to be outside for apart of the year. The most common helminths (Ascaris suum and Trichurissuis) are characterized by hard-shelled eggs and thus sustained longevityon pasture – up to 10 years (reviewed by [1], despite initial high deathrates [20]. Ongoing Danish experiments using parasite-naïve pigs to tracethe levels of contamination on pastures after initial deposition of eggs,have yielded 2 interesting results: firstly, transmission levels are increasingthe first 2 years, indicating an unexpected slow development toinfectivity; secondly, infection levels were not markedly decreased after 4years (Mejer and Roepstorff, 2006, unpublished data). This demonstratesfully that at present we cannot provide evidence-based recommendationswith regard to paddock rotation in pigs – 2-3 years are obviously notenough! In contrast, it seems that Oeosphagostomum spp. have a poorsurvival over winter [14,21,22] and do not constitute a problem in strictlyoutdoor sow herds [23] while the coccidian parasite Isospora suis seemsto be controlled by routine moving of the farrowing huts betweenfarrowings [24].The principles of pasture management may be applied to indoor stablingof pigs in large pens with plenty of straw bedding, e.g. deep-littersystems. In these cases, the continuous use of a pen will inevitably leadto increasing levels of parasite infections [25] and all-out-all-in systemsneed to be applied. With the forthcoming implementation of EU-legislation stipulating loose housing in enriched environments (e.g.wallowing) for sows for part of the gestation, an increased risk ofhelminth transmission may be anticipated.Bioactive crops and nutrition: It is difficult to draw a clear distinctionbetween bioactive crops, plant (herbal) medicine and nutrition as such.Bioactive crops (nutraceuticals) are plants containing secondarymetabolites that are considered beneficial for their positive effect onanimal health (in casu helminth control) rather than their directnutritional value [26]. These crops can be used as fresh forages forgrazing or as conserved feed in the daily ration without any adverseeffect. They may be grown in the normal crop rotation and thereforedraw some attention from commercial seed companies. In plant medicinedosing is usually a very critical issue and extraction steps are oftenincluded.In small ruminants, extensive studies worldwide on bioactive crops havefocused on forages rich in condensed tannins (4-8% of dry matter) andtheir effect on gastrointestinal nematodes [26,27]. The relevanttemperate/subtropical forages include sainfoin (Onobrychis viciifolia), sulla(Hedysarum coronarium) and larger trefoil (Lotus pedunculatus), all withlimited distribution in Nordic-Baltic countries. Condensed tannins aresecondary metabolites related to plant defence against herbivory andconstitute a poorly defined group of polyphenolic compounds, based onflavan-3-ol monomers (prodelphinidins or procyanidins) and characterizedby a protein-binding capacity (tanning!) [28]. The variability is large withincondensed tannins and is related to plant species, growth conditions,stage of development, cuts etc. Due to this variability many findings areinconsistent or even contradictory. However, there is now ampleevidence from in vitro and in vivo studies that forages with condensedtannins may affect all stages of parasitic nematodes, leading to reducedestablishment of infective larvae, lowered fecundity of adult nematodesand in some cases, reduction in worm burdens. Effects have beenobserved against both abomasal and intestinal nematodes but this may,like in many other instances, depend on plant species or stage, e.g. the

ratio between prodelphinidins and procyanidins [29]. It has long beendebated whether the effects are direct by harming residing/incomingnematodes, or indirect by improving immunity through more rumen-by-pass protein [28]. Recent studies have clearly indicated direct effects ofcondensed tannins from conserved sainfoin including inhibitedexsheathment of infective larve, diminished pathological changes inlarvae following short term exposure and reduced penetration ofabomasal mucosa ([29,30]; Severine Brunet, pers. communication, 2008). Aleafy cultivar of chicory (Cichorium intybus) suitable for ruminant grazing,although not rich in condensed tannins, does exhibit similar effects onnematodes, and this forage may prove to be more appropriate in theNordic-Baltic context [31,26].It has been known for more than a decade that structure andcomposition of the feed may influence establishment and fecundity ofintestinal nematodes of monogastric animals [32]. A low fibre contentand high level of easily fermentable carbohydrates may lower parasitism.Roots of chicory (Cichorium intybus) and seeds of lupin are rich in suchfermentable carbohydrates, particularly fructans (inulin). In pigs, almostcomplete reduction of the egg output of Oesophagostomum spp. hasbeen acheived by adding purified inulin [33] or dried chicory roots to thediet [22]. High reductions in worm counts have been observed in somestudies [33,34] but not in all [22]. Incomplete elimination of worms mayexplain why depression of egg excretion has been partially reversible asegg counts were shown to increase when the carbohydrates werewithdrawn from the diet ([33]; Helena Mejer, unpublished data, 2008).The fermentable carbohydrates are only partially degraded in the smallintestine, and the mechanism of action is most likely related to theproduction of short chain fatty acids during their fermentation in thelarge intestine [35]. It is believed that the short chain fatty acids directlyor indirectly cause adverse conditions for residing nematodes just asthere is a shift in microbial composition [36]. Consequently, T. suis,another inhabitant of the large intestine, is moderately affected butresults are inconsistent [37-39]. Furthermore, early larval stages of A. suumpenetrate the large intestine before the migratory liver phase andestablishment of incoming infections may be affected [22] but notestablished adult infections (Helena Mejer, unpublished data, 2008). Asthe major targets of nematode control in pig outdoor production in theNordic context are indeed A. suum and T. suis, these findings needfurther investigation to be of practical relevance.Selective breeding for host resistance: In ruminants, faecal egg counts,nematode worm counts and related morbidity markers, like pepsinogenfor cattle and anaemia scores for sheep with haemonchosis, showmoderate heritabilities (0.3-0.4), and this forms the basis for a breedingapproach to control of gastrointestinal nematodes, as reviewed by e.g.[40] and [41]. In large wool producing countries (New Zealand andAustralia) selective breeding for host resistance is now implemented onmany commercial enterprises. Quantitative Trait Loci (QTLs) have beenidentified and a first DNA test for sheep is now commercially available(Catapult Genetics NZ) but breeding values are in most instances stillbased on faecal egg counts. Reduction rates in faecal egg counts areestimated to be approx. 2% annually [42] but the reduction inanthelmintic treatment frequency remains to been demonstrated.Selective breeding for resistance has been associated with disadvantages,e.g. low productivity when unexposed, or increased tendency to scouringassociated with larval exposure, due to higher immunologicalresponsiveness [43]. Combining low faecal egg counts with other traits, e.g. productivity, in a selection index is therefore presently consideredmost suitable [41].In pigs, Danish studies based on examination of 200 offspring of knownmatings revealed heritabilities of faecal egg counts of A. suum of 0.3-0.4and of T. suis of 0.4-0.7 [44]. For T. suis the heritabilities depended ontime in relation to start of infection: during the early expulsion phaseheritabilities were highest, probably indicating close genetic control ofthe onset of immunity. For Ascaris a number of other parameters likeactual worm burden, total egg output and antibody-levels were alsoheritable whereas this was not the case for the size and fecundity of theworms (Peter Nejsum, unpublished data, 2009). It is obvious thatbreeding for increased host resistance is also an option within the pigindustry and may be highly relevant in free-range systems.Conclusions: Other options, apart from those mentioned above, remain,including biological control with nematode-trapping fungi against free-living larvae, copperoxide needles against abomasal nematodes,


Page 27 of 31

vaccination against gastrointestinal nematodes of sheep, etc. For differentreasons these options are not expected to be available in the Nordic orBaltic context in the foreseeable future. In contrast, many forms ofgrazing management do work in ruminants and should always form thebackbone of any control program. Nutritional supplementation to grazingruminants is also immediately available but the costs and benefits needto be considered – if herbage amount and quality is sufficient very littleextra is gained by additional supplementation. Selective breeding is anobvious option in small ruminants and perhaps in pigs and beef/dualpurpose cattle. More basic research is needed on bioactive forages withregard to mode of action and possible active compounds in order toselect the most appropriate forage species/cultivars. None of theseapproaches should be considered ’stand alone’ control measures due totheir moderate efficacy and integration with anthelmintics will continueto be a necessity.Today it is widely recognized that with the limited arsenal ofanthelmintics and the constant spread of anthelmintic resistance, wecannot keep livestock free of nematodes during their entire productionlife by drug application alone. We need to provide support for thesusceptible young stock, e.g. optimal nutrition and limited parasitechallenge, during the phase of acquisition of immunity until they cancope with infections. Thus, our mission as veterinarians andparasitologists has changed accordingly and a new approach to achievesufficient levels of immunity with acceptable levels of production lossand uncompromised animal welfare by prudent (read minimal) use ofanthelmintics has emerged. This represents a shift in paradigm, becausepreviously the issue of most concern was achieving the highestproduction possible. Now we must consider how to transfer this newmessage ‘across the fence’ to farmers and extension staff. The futurechallenges are indeed numerous.Acknowledgements: The authors are grateful for valuable commentsfrom Dr. A. L. Willingham on an earlier version of this paper.References1. Roepstorff A: Ascaris suum in pigs: population biology and

epidemiology. Doctorate Thesis, The Royal Veterinary and AgriculturalUniversity, Copenhagen 2003, 227.

2. Waller PJ: Sustainable nematode parasite control strategies for ruiminantlivestock by grazing management and biological control. Animal FeedScience and Technology 2006, 126:277-289.

3. Waller PJ, Thamsborg SM: Nematode control in ‘green’ ruminantproduction systems. Trends in Parasitology 2004, 20(10):493-497.

4. Barger I: Grazing Management for the Control of Nematode Parasites. InSustainable Parasite Control in Small Ruminants. Editeb by: LF Le Jambre, MRKnox. ACIAR; 1996:146-150.

5. Thamsborg SM, Roepstorff A: Parasite problems in organic livestockproduction systems and options for control. Journal of Parasitology 2003,89:S277-S284.

6. Svensson C, Hessle A, Höglund J: Parasite control methods in organic andconventional dairy herds in Sweden. Livestock Production Science 2000,66:57-69.

7. Weinreich LL, Thamsborg SM, Jensen AM, Vaarst M, Rasmussen J: Parasitecontrol in Danish organic dairy herds and farmers’ attitudes toagricultural production. In Enhancing Animal Health Security and FoodSafety in Organic Livestock Production. Proceedings of the 3rd SAFO Workshop.16–18 September 2004, Falenty, Poland. Edited by: Hovi, M., Zastawny, J. andPadel, S. Sustaining Animal Health and Food Safety in Organic Farming,University of Reading, Reading; 2005:165.

8. Eysker M, van der Aar WM, Boersema JH, Githiori JB, Koyman FNJ: Theeffect of repeated moves to clean pasture on the build up ofgastrointestinal nematode infections in calves. Veterinary Parasitology1998, 76:81-94.

9. Kristensen T, Thamsborg SM, Andersen HR, Søegaard K, Nielsen AL: Effectsof grazing system on production and parasitism of dairy breed heifersand steers grazing wet marginal grasslands. Animal Science 2006,82:201-211.

10. Larsson A, Dimander SO, Rydzik A, Uggla A, Waller PJ, Höglund J: A 3-yearfield evaluation of pasture rotation and supplementary-feeding tocontrol parasite infection in first-season grazing cattle – Effects onanimal performance. Veterinary Parasitology 2006, 142:197-206.

11. Barger I: Influence of sex and reproductive status on susceptibility ofruminants to nematode parasitism. International Journal for Parasitology1993, 23:463-469.

12. Thamsborg SM, Jørgensen RJ, Nansen P: Internal parasitism of steersgrazing extensively at different stocking rates. Acta vet. scand 1998,39:311-323.

13. Thamsborg SM, Jørgensen RJ, Ranvig H, Bartlett P, Waller PJ, Nansen P: Theperformance of grazing sheep in relation to stocking rate and exposureto nematode infections. Livestock Production Science 1998, 53:265-277.

14. Thomsen LE, Mejer H, Wendt S, Roepstorff A, Hindsbo O: The influence ofstocking rate on transmission of helminth parasites in pigs onpermanent pasture during two consecutive summers. VeterinaryParasitology 2001, 99:129-146.

15. Svensson C: Survival of oocysts of Eimeria alabamensis on pasturesunder different climatic conditions in Sweden. Acta Vet. Scand 1995,36:9-20.

16. Lindqvist A: Animal Health and Welfare in Organic Sheep and GoatFarming - Experiences and reflections from a Swedish outlook. In:Veterinary challenges in Organic Farming. Proc. 14th Nordic Committee forVeterinary Scientific Cooperation Symposium, Acta vet. Scand. 2001,95:27-31.

17. Nielsen B, Thamsborg SM, Kristensen T: Feed supplements for young dairybreed calves after turn-out to pasture: Effect on weight gain andsubclinical coccidiosis in organic production systems. Acta AgriculturaScandinavica, Section A, Animal Science 2003, 53:1-10.

18. Thamsborg SM, Githigia SM, Larsen ML, Nansen P, Henriksen SAa: Infektionmed Nematodirus battus, en ny parasit hos får i Danmark (Nematodirusbattus, a new parasitic infection in sheep in Denmark). DanskVeterinærtidsskrift 1996, 79:231-232.

19. Pritchard GC, Forbes AB, Williams DJ, Salimi-Bejestani MR, Daniel RG:Emergence of fasciolosis in cattle in East Anglia. Vet.Rec 2005,157:578-582.

20. Larsen MN, Roepstorff A: Seasonal variation in development and survivalof Ascaris suum and Trichuris suis eggs on pastures. Parasitology 1999,119:209-220.

21. Roepstorff A, Murrell KD: Transmission dynamics of helminth parasites ofpigs on continuous pasture: Oesophagostomum dentatum andHyostrongylus rubidus. International Journal for Parasitology 1997,27:553-562.

22. Mejer H: Transmission, infection dynamics and alternative control ofhelminths in organic swine. Ph. D. Thesis, The Royal Veterinary andAgricultural University, Copenhagen 2006.

23. Carstensen L, Vaarst M, Roepstorff A: Helminth infections in Danishorganic swine herds. Veterinary Parasitology 2002, 106(3):253-264.

24. Roepstorff A, Jørgensen RJ, Nansen P, Henriksen SAa, Skovgaard J,Andreasen MPetersen: Parasitter hos økologiske svin (Parasites in certifiedorganic production of swine). Project report from Danish Abattoirs 1992, 36.

25. Holmgren N, Nilsson O: Inverkan av produktionsplanering ochskabbsanering på tarmnematoder hos bis-grisar (Influence of productionplanning and mange control on nematodes of pigs). Project report fromKöttböndernas Forskningsprogram project No. G37-97, SvenskaDjurhälsovården 1998.

26. Hoste H, Jackson F, Athanasiadou S, Thamsborg SM, Hoskin SO: The effectsof tannin-rich plants on parasitic nematodes in ruminants. Trends inParasitology 2006, 22(6):253-261.

27. Hoste H, Torres-Acosta JF, Alonso-Diaz MA, Brunet S, Sandoval-Castro C,Adote SH: Identification and validation of bioactive plants for the controlof gastrointestinal nematodes in small ruminants. Proc. of 5thInternational Workshop: Novel Approaches to the Control of HelminthParasites of Livestock. Tropical Biomedicine 2008, 25(1 Supplement):56-72.

28. Mueller-Harvey I: Unravelling the conundrum of tannins in animalnutrition and health. Journal of Science, Food and Agriculture 2006,86:2010-2037.

29. Brunet S, Jackson F, Hoste H: Effects of sainfoin (Onobrychis viciifolia)extract and monomers of condensed tannins on the association ofabomasal larvae with fundic explants. International Journal for Parasitology2008, 38:783-790.

30. Brunet S, Aufrere J, Babili F El, Fouraste I, Hoste H: The kinetics ofexsheathment of infective nematode larvae is disturbed in the presenceof a tannin-rich plant extract (sainfoin) both in vitro and in vivo.Parasitology 2007, 134:1253-1262.

31. Thamsborg SM, Mejer H, Bandier M, Larsen M: Influence of differentforages on gastrointestinal nematode infections in grazing lambs. Proc.of 19th International Conference of WAAVP, New Orleans 2003, 189.


Page 28 of 31



































32. Bjørn H, Roepstorff A, Nansen P: A possible influence of diet compositionon the establishment of nematodes in the pig. Veterinary Parasitology1996, 63:167-171.

33. Petkevičius S, BachKnudsen KE, Murrell KD, Wachmann H: The effect ofinulin and sugar beet fibre on Oesophagostomum dentatum infectionin pigs. Parasitology 2003, 127:61-68.

34. Petkevičius S, Bach Knudsen KE, Nansen P, Murrell KD: The effect of dietarycarbohydrates with different digestibility on the populations ofOesophagostomum dentatum in the intestinal tract of pigs. Parasitology2001, 123:315-324.

35. Petkevičius S, Murrell KD, Bach Knudsen KE, Jørgensen H, Roepstorff A,Laue A, Wachmann H: Effects of short-chain fatty acids and lactic acidson survival of Oesophagostomum dentatum in pigs. VeterinaryParasitology 2004, 122:293-301.

36. Mølbak L, Thomsen LE, Jensen TK, Knudsen KEB, Boye M: Increasedamount of Bifidobacterium thermacidophilum and Megasphaera elsdeniiin the colonic microbiota of pigs fed a swine dysentery preventive dietcontaining chicory roots and sweet lupine. Journal of Applied Microbiology2007, 103(5):1853-1867.

37. Thomsen LE, Petkevičius S, Bach Knudsen KE, Roepstorff A: The influence ofdietary carbohydrates on experimental infection with Trichuris suis inpigs. Parasitology 2005, 131:857-865.

38. Petkevičius S, Thomsen LE, Bach Knudsen KE, Murrell KD, Roepstorff A,Boes J: The effect of inulin on new and on patent infections of Trichurissuis in growing pigs. Parasitology 2007, 134:121-127.

39. Thomsen LE, Knudsen KEB, Jensen TK, Christensen AS, Møller K,Roepstorff A: The effect of fermentable carbohydrates on experimentalswine dysentery and whip worm infections in pigs. VeterinaryMicrobiology 2007, 119:152-163.

40. Sonstegard TS, Gasbarre LC: Genomic tools to improve parasiteresistance. Veterinary Parasitology 2001, 101:387-403.

41. Hunt PW, McEwan JC, Miller JE: Future perspectives for theimplementationm of genetic markers for parasite resistance in sheep. In:Proc. of 5th International Workshop: Novel Approaches to the Control ofHelminth Parasites of Livestock. Tropical Biomedicine 2008, 25(1Supplement):18-33.

42. Pomroy WE: Anthelmintic resistance in New Zealand: a perspective onrecent findings and options for the future. New Zealand Veterinary Journal2006, 54(6):265-270.

43. Karlsson LJE, Pollott GE, Eady SJ, Bell A, Greeff JC: Relationship betweenfaecal worm egg counts and scouring in Australian Merino sheep.Animal Production Australia 2004, 25:100-103.

44. Nejsum P, Roepstorff A, Jørgensen CB, Fredholm M, Göring HHH,Anderson TJC, Thamsborg SM: High heritability for Ascaris and Trichurisinfection levels in pigs. Heredity 2009, 102:357-364.

S28Gastrointestinal helminths and lungworms in suckler cow beef herds inSouthern Finland, a pilot studyU Eerola1*, H Härtel2, A Oksanen3, T Soveri41Private Practitioner, Hämeentie 22, 16900 Lammi, Finland; 2LSO Foods Oy,Animal Health Service, Forssa, Finland; 3Finnish Food Safety Authority Evira,Fish and Wildlife Health Research Unit, Oulu, Finland; 4Department ofProduction Animal Medicine, Faculty of Veterinary Medicine, University ofHelsinki, FinlandE-mail: [email protected] Veterinaria Scandinavica 2010, 52(Suppl 1):S28

Introduction: The number of suckler cow beef herds is increasing inFinland. Prevalence studies about gastrointestinal parasites andlungworms of grazing beef cattle in southern Finland are not available.Systematic anthelmintic treatment is not widely used and there is norecommended treatment protocol available. The aim of this study wasto obtain basic knowledge of the prevalence of gastrointestinalparasites and lungworms in grazing suckler cow beef herds in southernFinland.Materials and methods: The study was conducted in summer 2002. Itincluded 13 voluntary beef cattle herds (herd size 26 – 95 adultanimals) in southern Finland. None of the herds had clinical symptomsof parasitic infection. None of the herds was treated in the spring and11 of the herds had not used anthelmintic treatments within a year.The first set of faecal samples were taken from 4-10 calves on 10 farms,4-10 heifers on 7 farms and 8-12 cows on 13 farms. The first samplingwas done more than 3 weeks after the beginning of the grazing periodand the second sampling was done at the end of the grazing period inautumn. Faecal samples were investigated at Finnish Food SafetyAuthority Evira, Oulu. The methods used were modified McMaster forgastrointestinal helminth eggs and the Baermann technique fordetecting Dictyocaulus viviparus. Egg count less than 50 eggs/gramfaeces (epg) was considered low infection, 50-500 epg moderateinfection and more than 500 epg heavy infection consideringTrichostrongylidae spp. Dictyocaulus viviparus infections were evaluatedon herd level as negative or positive.Results: Trichostrongylidae spp were found in all herds in all groupsexamined. The egg counts in individual calves varied from 0 to 1540 epgat the first and from 0 to 780 epg at the second sampling. Egg counts inheifers varied between 0 - 120 epg and 0 - 140 epg, in older cowsbetween 0 - 360 epg and 0 - 200 epg, respectively. Only three individualsamples had egg count higher than 500 epg. Median values for calves,heifers and cows are presented in Table 1.

Table 1 (abstract S28) Median egg count values (epg) of Trichostrongylidae spp. in 13 beef cow herds

calves in summer calves in autumn heifers insummer heifers in autumn cows in summer cows in autumn

Farm 1 50 60 M M 0 0

Farm 2 0 70 M 10 0 0

Farm 3 0 0 M 60 60 0

Farm 4 20 30 20 0 0 0

Farm 5 60 120 20 20 0 0

Farm 6 10 50 0 0 0 0

Farm 7 20 40 0 M 10 0

Farm 81 50 M 0 0 30 M

Farm 9 40 20 M M 0 0

Farm 10 M 2 40 M 50 20 0

Farm 11 M 0 M M 0 0

Farm 121 M M 70 70 0 0

Farm 13 60 160 0 M 0 01 Dictyocaulus viviparus positive herd2 M = Information missing


Page 29 of 31




























Dictyocaulus viviparus was detected in two herds. Other thantrichostrongylid gastrointestinal parasites (Capillaria sp., Nematodirus sp.,Moniezia sp., Paramphistomum sp.) were detected in very few samples atlow levels.Discussion : Gastrointestinal parasites, mainly Trichostrongylidae spp.,were found widely in beef cattle, but the parasite egg counts were lowor moderate at all farms in all groups of animals. None of the herdshad clinical signs of infection and did not seem to need regularanthelmintic treatment. However, summer 2002 was exceptionally dryand warm in southern Finland which may be one reason for low eggcounts. Other gastrointestinal parasites (Capillaria sp., Nematodirus sp.,Moniezia sp ., Paramphistomum sp.) were rare and considered notimportant.The most important finding of this study was some farms having asubclinical Dictyocaulus viviparus infection. In light of the low incidence ofdisease in Finland, subclinical infections are a risk in cattle trade andshould be considered.

S29The prevalence of internal parasites in wild boar farms in FinlandOuti Hälli*, Eve Ala-Kurikka, Olli Peltoniemi, Mari HeinonenDepartment of Production Animal Medicine, University of Helsinki,Saarentaus, FinlandActa Veterinaria Scandinavica 2010, 52(Suppl 1):S29

Background: In Finland, the most important internal parasites indomestic pigs are nematode Ascaris suum and coccidia Isospora suis. Asthe environmental conditions and management practices in wild boar(Sus scrofa) outdoor farming are suitable for parasites during mostseasons, we wanted to explore the parasite burden of wild boars inFinland. This kind of research has not been carried out earlier in ourcountry. Economical losses caused by internal parasites, especiallyascarids, are mainly due to reduced daily weight gain and feedconversion ratio [1].Materials and methods: Based on a national record of wild boar farmers,a sampling frame of farms was compiled. Every farm on that list wascontacted first by mail and the non-responders received a phone call fromresearch group personnel. All volunteer farms that still had wild boarswere included. From all animals slaughtered in study farms during thestudy period (autumn 2007 – spring 2008), a faecal sample was obtaineddirectly from rectum after slaughter. Faecal egg or oocyst counts regardingAscaris suum, coccidia, Strongylus and Trichuris suis were counted by theconcentration McMaster technique. The number of positive farms (at leastone animal with parasite eggs in faecal sample) and summary statistics ofegg counts for every parasite type was calculated.Results: Altogether 113 samples were collected from 22 farms, a medianof 4 samples (1-15) per herd. The median age of sampled wild boars was18 months. Mean age was found to be 21,5 months (standard deviation14,5). The number of positive farms can be seen in Figure 1. andsummary statistics for egg or oocyst counts for different parasites studiedcan be found in Table 1.Conclusion: Almost all farms were positive regarding coccidia. The exactdiagnosis of the species of the oocysts was not reached, whether theywere Isospora or Eimeria. Although the established oocyst countsprobably are harmless for adult animals, the risk for piglets could besubstantial because of environmental contamination, especially in case of

Isospora. Smaller number of animals and farms were Strongylus or Ascarissuum positive. Adult animals are known to be able to develop immunitytowards ascarids, thus the low egg burden in sampled animals was quiteexpected.Reference1. Corwin RM, Stewart TB: Internal Parasites. In Diseases of Swine. Edited by:

Straw BE, D’Allaire S, Mengeling WL, Taylor DJ Ames, Iowa: Iowa StateUniversity Press; 1999:713-730.

S30Cross-infection of gastrointestinal nematodes between winter corralledsemi-domesticated reindeer (Rangifer tarandus tarandus) and sheep(Ovis aries)Saana-Maaria Manninen*, Antti Oksanen, Sauli LaaksonenFinnish Food Safety Authority Evira, Fish and Wildlife Health Research Unit,Oulu, FinlandActa Veterinaria Scandinavica 2010, 52(Suppl 1):S30

Summary: The increasing number of sheep (Ovis aries) in the reindeer(Rangifer tarandus tarandus) herding area in North Finland andsupplementary winter feeding of reindeer in corrals shared with sheepcauses potential for cross-infection of gastrointestinal nematodesbetween reindeer and sheep. The aim of this study was to elucidatethis potential. The study included 46 animals, of which 12 reindeerand 8 sheep had shared a corral. Twelve reindeer had no knowncontact with sheep. Both reindeer groups shared free ranging areaswith wild moose (Alces alces). Two moose were included in this study,as were 12 sheep which had no contact with other ruminants. Afterslaughter in September-November abomasa and proximal smallintestines were collected and examined for gastrointestinalnematodes. The parasites were collected, counted and identified.Following species were found in reindeer: Ostertagia gruehneri ,Ostertagia arctica, Spiculopteragia dagestanica, Nematodirus tarandi,Nematodirella longissimespiculata and Bunostomum trigonocephalum.Sheep were infected with Teladorsagia circumcincta , Teladorsagiatrifurcata, Ostertagia gruehneri, Ostertagia arctica, Nematodirus filicollisand Nematodirus spathiger. Spiculopteragia dagestanica and Ostertagiagruehneri were identified in moose. Ostertagia gruehneri, which isconsidered to be a reindeer parasite, was only found in the sheep thathad shared a corral with reindeer. These sheep were not found to beinfected with other abomasal nematodes. The reindeer that hadshared a corral with sheep were not infected with nematodes usuallyhaving sheep as their primary host.

Figure 1 (abstract S29) Number of farms with at least one pig positive for different parasites in fecal examination (22 farms included in the study).

Table 1 (abstract S29) Summary statistics for egg counts(epg) for coccidia, Strongylus, Ascaris suum and Trichuris suis.

Parasite Mean, epg SD, epg Min, epg Max, epg

Coccidia 6 118 1987 0 102 000

Strongylus 300 945 0 6 150

Ascaris suum 29 15 0 1 450

Trichuris suis 0 0 0 0


Page 30 of 31

S31Intestinal parasite infection exposes grouse to canine predatorsMarja Isomursu1*, Osmo Rätti2, Pekka Helle3, Tuula Hollmén41Finnish Food Safety Authority Evira, Research Department, Fish and WildlifeHealth Research Unit, P.O.Box 517, FI-90101 Oulu, Finland; 2Arctic Centre,University of Lapland, P.O.Box 122, FI-96101 Rovaniemi, Finland; 3FinnishGame and Fisheries Research Institute, Oulu Game and Fisheries Research,Tutkijantie 2 E, FI-90570 Oulu, Finland; 4Alaska Sealife Center, 301 RailwayAvenue, P.O. Box 1329, Seward, AK 99664, USAActa Veterinaria Scandinavica 2010, 52(Suppl 1):S31

Background: Sublethal parasite infections may cause mortality indirectlyby exposing the host to predation. The best known example of thisamong birds is red grouse in which caecal nematode infection causesincreased risk of predation and can even affect population dynamics [1].Intestinal helminth parasites are common in forest grouse, capercaillieTetrao urogallus, black grouse Tetrao tetrix and hazel grouse Bonasabonasia [2], and these grouse are valuable prey for several species ofpredators. We evaluated the hypothesis that parasite infection makes thehost more vulnerable to predation by comparing the intestinal parasiteinfection status of grouse hunted with a trained dog to that of grousehunted without a dog. Hunting with a dog can be regarded as closesimulation of natural predation because the dog presumably locates theprey by the same cues as wild canine predators.Material and methods: We collected whole grouse intestines fromhunters and received 623 samples of which the bird species, age classand sex were determined. All sample birds were shot with a shotgunduring legal hunting season in September and October. Intestines werecut open and parasites visible to naked eye or stereomicroscope wereextracted and identified. The associations between host sex, age, species,the month of sampling, the use of dog and the occurrence of intestinal

helminths were studied using hierarchical loglinear modelling withbackward elimination procedure (P = 0.05) (SPSS programme ver. 11.5).Two different models were studied, one for cestodes (all three speciespooled together) and one for nematodes.Results and conclusions: Grouse were infected by four helminth species:a nematode Ascaridia compar and cestodes Skrjabinia cesticillus, Paroniellaurogalli and Hymenolepis sp. Nematode infection was not connected todog-assisted hunting. However, there was a significant interactionbetween cestode infection and the use of dog (P < 0.01). Cestodes weremore common in grouse hunted with a dog (see Figure 1). Cestodeswere mostly parasites of juvenile grouse but even among juveniles only,cestodes were more prevalent in the dog-assisted hunting bag. Theresults suggest that mammalian predators prey more selectively onparasitized individuals and that intestinal parasites may contribute to thehigh mortality of juvenile grouse through increased predation.This abstract is based on a recent paper published in Annales ZoologiciFennici by the same authors [3].References1. Dobson A, Hudson P: The interaction between the parasites and

predators of red grouse Lagopus lagopus scoticus. Ibis 1995, 137:S87-S96.2. Isomursu M, Helle P, Rätti O: Intestinal helminths in Finnish grouse.

Suomen Riista 2004, 50:90-100, (In Finnish with English summary).3. Isomursu M, Rätti O, Helle P, Hollmén T: Parasitized grouse are more

vulnerable to predation as revealed by a dog-assisted hunting study.Ann Zool Fennici 2008 in press.

Cite abstracts in this supplement using the relevant abstract number,e.g.: Isomursu et al.: Intestinal parasite infection exposes grouse tocanine predators. Acta Veterinaria Scandinavica 2010, 52(Suppl 1):S31

Figure 1(abstract S31) Prevalence of cestodes in grouse hunted with adog or without a dog. Shaded bars = with dog, open bars = withoutdog.


Page 31 of 31



Documents

Parasite infections of domestic animals in the - CABI