Import risk analysis:  
Pig s emen  
 
FINAL  
 
 
 
ISBN only for the final RA  
ISBN only for the final RA  
 
December  2012   This page is intentionally blank   
  
 
Ministry for Primary Industries  
Pastoral House  
25 The Terrace  
PO Box 2526  
Wellington 6011  
New Zealand  
 
Tel: 64 4 894 0100  
Fax: 64 4 894 0731  
 
 
 
Science and Risk Assessment  
Ministry for Primary Industries  
  
 
 
 
 
 
 
Import risk analysis : 
Pig s emen  
 
FINAL  
 
 
 
ISBN only for the final RA  
ISBN only for the final RA  
December  2012 
 
 
 
 
 
Approved for general release  
 
 
 
Lisa Oakley  
Manager, Risk Analysis  (Animals and Aquatic)  
Ministry for Primary Industries  
  This page is intentionally blank   
- i - CONTENTS  
1. Executive Summary  1 
2. Introduction 2 
3. Scope  2 
4. Commodity definition  2 
5. Risk analysis methodology  2 
6. Porcine adenovirus  15 
7. African swine fever virus  16 
8. Aujeszky’s disease virus  19 
9. Blue eye disease virus 24 
10. Classical swine fever virus and other pestiviruses 28 
11. Eastern equine encephalomyelitis virus  34 
12. Porcine haemagglutinating encephalomyelitis vir us 36 
13. Foot and mouth disease virus  38 
14. Japanese encephalitis virus 44 
15. Kunjin virus  48 
16. Menangle virus  50 
17. Murray Valley encephalitis virus 52 
18. Nipah virus  54 
19. Porcine reproductive and respiratory syndrome virus 57 
20. Porcine epidemi c diarrhoea virus  63 
21. Porcine myocarditis virus  65 
22. Porcine respiratory coronavirus 68 
23. Rabies virus 70 
24. Ross River virus 72 
25. Teschovirus serotype 1  74  
- ii - 26. Torque teno virus  76 
27. Transmissible gastroenteritis virus 78 
28. Rotavirus  80 
29. Porcine reovirus  82 
30. Swine influenza virus  83 
31. Swine pox v irus 85 
32. Swine vesicular disease virus 87 
33. Venezuelan encephalitis virus 91 
34. Vesicular exanthema virus 93 
35. Vesicular stomatitis virus  95 
36. West Nile virus 96 
37. Western equine encephalitis virus 98 
38. Bacillus anthracis 100 
39. Brucella sui s 102 
40. Burkholderia pseudomallei  106 
41. Clostridium botulinum  108 
42. Other Clostridium  spp. 109 
43. Leptospira spp.  111 
44. Mycoplasma  spp.  115 
45. Pasteurella multocida  117 
46. Salmonella spp.  119  
- iii - Contributors to this risk analysis  
 
 1. Author  
 
Bob Worthington  Contractor, Risk An alysis, M inistry for Primary Industries, 
Wellington  
 
Stephen Cobb  
 Principal Adviser, Risk Analysis, Ministry for Primary Industries,  
Wellington  
 
 
 
2. Internal Peer Review  
 
Stuart MacDiarmid  Principal International Adviser Risk Analysis, Ministry for 
Primary Industries, Wellington  
 
 
Lincoln Broad  Senior Adviser, Risk Analysis, Ministry for Primary Industries, 
Wellington  
 
Cathy Dyer  Senior Adviser, Animal Imports, Ministry for Primary Industries,  
Wellington  
 
Richard Soons  Senior Adviser, Animal Imports , Ministry for Primary Industries,  
Wellington  
 
José Derraik  Senior Adviser (Human Health), Ministry for Primary Industries,  
Wellington  
 
Sandy Toy  Senior Adviser (Indigenous Fauna), Ministry for Primary 
Industries, Wellington  
 
Howard Pharo  Manager, Impor t and Export (Animals), Ministry for Primary 
Industries, Wellington  
 
 
 
3. External Scientific Review  
 
Colin Wilks  Professor, School of Veterinary Science, Parkville, Melbourne, 
Australia  
 
Maurice Pensaert  Professor, Laboratory of Virology, Faculty of Ve terinary 
Medicine, University of Gent  
 
  
- iv - This page is intentionally blank   
Ministry for Primary Industries  Import risk analysis: Pig semen • 1 1. Executive Summary 
In March 2012, the Ministry for Primary Industries ( MPI) released a draft import health standard  
(IHS)  for the importation of pig semen into New Zealand  from all countries1
Following stakeholder  consultation on the draft IHS for the importation of porcine  semen into 
New Zealand , this final IRA  has been amended to assess the risks associated with  porcine  semen 
imported from all countries .  .  This was 
developed from the  2011 draft  import risk analysis  (IRA) for pig semen from Australia, the 
USA, Canada, the European Union, and Norway .  The 2011 draft IRA identified six organisms 
of potential concern  in porcine semen  (blue eye dise ase virus, foot and mouth disease virus, 
Nipah virus, Teschovirus serotype 1, Venezuelan encephalitis virus, and vesicular exanthema 
virus) but did not assess the risk due to these since Australia, the USA, Canada, the European 
Union and Norway claim freed om from these diseases.  
Twelve diseas e agents have been assessed to be  risks in the commodity. Options for risk 
management are presented for each of thes e:  
• Aujeszky’s disease virus  
• Blue eye  disease virus  
• Classical swine fever virus  
• Bovine viral diarrhoea virus  
• Foot and mouth disease virus   
• Japanese encephalitis virus  
• Porcine reproductive and respiratory syndrome virus  
• Porcine myocarditis virus  
• Swine vesicular disease virus  
• Brucella suis  
• Leptospira spp.  
• Salmonella spp.  
 
                                                
1 http://www.biosecurity.govt.nz/biosec/consult/draft-ihs -pigsemic.gen   
Ministry for Primary Industries  Import risk analysis: Pig semen • 2 2. Introduction  
This risk analysis has been undertaken at the request of t he Animal Imports team, MPI  in order 
to address matters of consistency between existing IHSs  and to consider new scientific 
information published since the existing IHSs were issued.  
An initial draft Import risk analysis: Pig semen from Australia, the USA,  Canada, the European 
Union, and Norway  was released in August 2009 for public consultation.  Two stakeholder 
submissions were received in response to this draft publication, from NZPork and PIC.  
Following clarification that stakeholder consultation sough t to elicit views on the risk 
management options presented in an import risk analysis, a further submission from NZPork was received in February 2010.   MPI considered these submissions  and made significant amendments 
to the August 2009 document to address stakeholder concerns in  the 2011 draft Import risk 
analysis: Pig semen from Australia, the USA, Canada, the European Union, and Norway . 
In March 2012, MPI released a draft IHS  for the importation of pig semen into New Zealand  
from all countries
2
3. Scope  .  Although  the conclusions of the 2011 draft import risk analysis  were valid 
for semen imported from Australia, the USA, Canada, the European  Union , and Norway , this 
final import risk analysis has been updated to assess  the risks as sociated with porcine  semen 
import ed from all  countries . 
This risk analysis is limited to the risks posed by infectious agents in imported porcine semen.  Genetic diseases and other risks that may be of commercial importance to importers are not 
assessed.   
This document does not consider speculative events that could occur in the future, such as the 
possible establishment of disease vectors due to climate change. MPI  has the flexibility to 
modify any IHS based on this risk analysis if future events make this appropriate.  
4. Commodity de finition  
The commodity is defined as fresh porcine semen from Australia or  frozen porcine semen from 
approved countries  collected and processed in accordance with international guidelines set out in 
the Terrestrial Animal Health Code  (OIE 2008a).  
It is ge nerally accepted that i f any testing of animals or semen is necessary to support 
certification of the health status of donors, it is carried out at a laboratory approved by the 
veterinary administration of the exporting country.  
5. Risk analysis methodology  
The methodology used in this risk analysis is described in MPI ’s Risk Analysis Procedures 
Version 1 (MAF 2006)  and is consistent with the g uidelines  in section 2 of the Code  (OIE 
2008a) .  
 
The risk analysis process is summarised in Figure 1.  
                                                
2 http://www.biosecurity.govt.nz/biosec/consult/draft-ihs -pigsemic.gen   
Ministry for Primary Industries  Import risk analysis: Pig semen • 3  
Figure 1.  The risk analysis process.  
 
 
Ministry for Primary Industries  Import risk analysis: Pig semen • 4 5.1. PRELIMINARY HAZARD L IST 
The hazard identification process begins with the collation of a list of organisms likely to be 
associated with the commodity.  The basis for the preliminary hazard list is all the 
diseases/disease agents of pigs that were listed by the OIE in 2008 as well as other diseases 
mentioned in the following sources:  
• MPI’s IHSs  and Overseas Market Access Requirements (OMARS) for pigs and pig 
products . 
• Diseases of Swine  (2006).  Edited by BE Straw, JJ Zimmerman, S D'Allaire, DJ Taylor, 
9th edition.  Blackwell Pub lishing, Ames, Iowa. ISBN -13: 978- 0-8138- 1703- 3. 
• Virus Infections of Porcines  (1989).  Edited by MB Pensaert, Elsevier Science Publishers , 
Amsterdam . ISBN 0 -444-42909- 3. 
• Infectious Diseases of Livestock  (2004). Edited by JAW Coetzer and RC Tustin, 2nd edition. 
Oxford University Press, Cape Town. ISBN 0 -19-578202 X.  
Organisms listed in the above sources that were not considered to be of concern were:  
Porcine retroviruses. The only retroviruses known in pigs are endogenous retroviruses which are integrated as part of the genome.  They are present in the DNA of all pigs and do not cause 
disease.  Therefore they are not regarded as pathogens and are of no relevance.  
Porcine lymphotrophic herpesviruses  occur widely in all countries and in all types of pigs.  They  
have not been associated with naturally occurring diseases.  They were unknown prior to 1999 
and since pigs were widely traded before this date they could be presumed to be universally 
distributed.  They are presently of some concern in relation to transp lantation experiments since 
they may be associated with post -transplant lymphoproliferative disease.  Since they are not 
associated with naturally occurring diseases and are universally distributed, they have been 
excluded from consideration in this risk a nalysis.  
Additional diseases or disease agents were included as a result of suggestions by experts reviewing the draft risk analysis or by interested parties that were consulted on the subject.  
Organisms/diseases identified in the above sources that were c onsidered to be organisms of 
potenti al concern are listed in Table 1.  The table indicates whether the organisms are zoonotic, 
and whether they are present in New Zealand and in the relevant exporting countries  that were 
the focus of the first two drafts o f this risk analysis .  References are given to substantiate the 
entries in the table.  
For agents that are known to be present in New Zealand, information about occurrence in other 
countries is generally irrelevant and references relating to the exporting countries have not 
always been given.   
Ministry for Primary Industries  Import risk analysis: Pig semen • 5 Table 1. Organisms of potential concern  
Disease agent  
 OIE List  Zoonotic  Present in 
NZ 
 Present in 
Australia  Present in 
USA and 
Canada  Present in 
EU or  
Norway  Prelim 
Hazard  
Viruses/diseases         
Adenovirus  No (OIE 
2008a)  No ? ? Yes 
(Kleiboeker 
2006) Yes 
(Kleiboeker 
2006)  Yes 
African swine fever virus  Yes (OIE 
2008a)  No No (OIE 
2008b; OIE 
2008c) No (OIE 
2008b; OIE 
2008c)  No (OIE 
2008b; OIE 
2008c)  Yes (OIE 
2008c)  Yes 
Aujeszky’s disease virus  Yes (OIE 
2008a) No No (OIE 
2008b; OIE 
2008c)  No (OIE 
2008b; OIE 
2008c)  Yes (OIE 
2008b; OIE 
2008c)  Yes (OIE 
2008b; OIE 
2008c)  Yes 
Blue eye disease virus  No (OIE 
2008a)  No No (Kirkland 
and Stephano 
2006) No (Kirkland 
and Stephano 
2006) No (Kirkland 
and Stephano 
2006) No (Kirkland 
and Stephano 
2006) No 
Bovine viral diarrhoea 1 
virus  Yes (OIE 
2008a)  No Yes (Vilcek 
et al 1998; 
Horner 2000)  Yes (Mahony 
et al 2005)  Yes 
(Potgieter 
2004) Yes 
(Barkema et 
al 2001; Drew 
et al 2002; 
Vilcek et al 
2003) No 
Bovine viral diarrhoea 2 
virus  Yes (OIE 
2008a)  No No (Vilcek et 
al 1998; 
Horner 2000) No (Mahony 
et al 2005) Yes 
(Potgieter 
2004) Yes 
(Barkema et 
al 2001; Drew 
et al 2002; 
Vilcek et al 
2003) Yes 
Classical swine fever 
virus  Yes (OIE 
2008a)  No No (OIE 
2008b; OIE 
2008c)  No (OIE 
2008b; OIE  
2008c)  No (OIE 
2008b; OIE 
2008c)  Yes (OIE 
2008b; OIE 
2008c)  Yes 
Congenital tremors virus  No (OIE 
2008a)  No Yes (Fairley 
1997) Yes Yes Yes No 
Cytomegalovirus  No (OIE 
2008a)  No Yes (Fairley 
1997) Yes Yes Yes No 
Eastern equine 
encephalitis virus  Yes (OIE 
2008a)  Yes No (OIE 
2008b; OIE 
2008c)  No (OIE 
2008b; OIE 
2008c)  Yes (OIE 
2008b; OIE 
2008c)  No (OIE 
2008b; OIE 
2008c)  Yes 
Encephalomyocarditis  
virus  No (OIE 
2008a)  No Yes 
(Sutherland et 
al 1977) Yes (Acland 
and Littlejohns 
1975; Seaman 
et al 1986)  Yes (Koenen 
2006) Yes (Koenen 
2006) No 
Foot and mouth disease 
virus  Yes (OIE 
2008a)  No No (OIE 
2008b; OIE 
2008c)  No (OIE 
2008b; OIE 
2008c)  No (OIE 
2008b; OIE 
2008c)  No (OIE 
2008b; OIE 
2008c)  No 
Hepatitis E virus  No (OIE 
2008a)  Yes Yes 
(Garkavenko 
et al 2001)  Yes Yes Yes No 
Japanese encephalitis 
virus  Yes (OIE 
2008a)  Yes No (CDC 
2006) Yes (Hanna 
et al 1999)  No (CDC 
2006) No (CDC 
2006) Yes 
Kunjin virus  No (OIE 
2008a)  Yes No Yes (Broom 
et al 2003)  No No Yes 
Menangle virus  
 No (OIE 
2008a)  Yes 
(Kirkland 
and 
Stephano 
2006) No Yes (Kirkland 
and Stephano 
2006) No (Kirkland 
and Stephano 
2006) No (Kirkland 
and Stephano 
2006) Yes 
Murray Valley 
encephalitis virus  No (OIE 
2008a)  Yes No Yes 
(Mackenzie et 
al 1994)  No No Yes 
Nipah virus  Yes (OIE 
2008a)  Yes No (Kirkland 
and S tephano 
2006) No (Kirkland 
and Stephano 
2006) No (Kirkland 
and Stephano 
2006) No (Kirkland 
and Stephano 
2006) No 
Porcine circovirus and 
PMWS  No (OIE 
2008a)  No Yes 
(Rawdon et al Yes (Raye et 
al 2005; Yes (Segales 
et al 2006)  Yes 
(Segales et al No  
Ministry for Primary Industries  Import risk analysis: Pig semen • 6 Disease agent  
 OIE List  Zoonotic  Present in 
NZ 
 Present in 
Australia  Present in 
USA and 
Canada  Present in 
EU or  
Norway  Prelim 
Hazard  
2004) Muhling et al 
2006)**  2006) 
Porcine epidemic 
diarrhoea virus  No (OIE 
2008a)  No No (MAF 
2007) No# No (Pensaert 
and Yeo 2006)  Yes 
(Pensaert and 
Yeo 2006)  Yes 
Porcine 
haemagglutinating 
encephalomyelitis virus  No (OIE 
2008a)  No 
(Pensaert 
2006) No# Yes (Forman 
et al 1979)  Yes 
(Pensaert 
2006) Yes 
(Pensaert 
2006) Yes 
Porcine myocarditis virus  No (OIE 
2008a)  unknown  No Yes (Biddle 
2007) No No Yes 
Porcine parvovirus  No (OIE 
2008a)  No Yes (Fairley 
1997) Yes Yes Yes No 
Porcine reproductive and 
respiratory syndrome virus Yes (OIE 
2008a)  No No (MAF 
2007) No (Animal 
Health 
Australia 
2007) Yes (Drew 
and Paton 
2004) Yes (Drew 
and Paton 
2004)  Yes 
Porcine respiratory 
coronavirus  No (OIE 
2008a)  No No (MAF 
2007) No# Yes (Saif and 
Sestak 2006)  Yes (Van 
Reeth and 
Pensaert 
2004) Yes 
Rabies virus  Yes (OIE 
2008a)  Yes No (OIE 
2008b)  No (OIE 
2008b)  Yes (OIE 
2008b)  Yes (OIE 
2008b)  Yes 
Ross River virus  No (OIE 
2008a)  Yes No 
(McFadden et 
al 2009)  Yes (Hu et al 
2007) No No Yes 
Rotavirus and Reovirus  No (OIE 
2008a)  No (Yuan 
et al 2006)& Yes ( Fu and 
Hampson 
1987; Fu et al 
1989) Yes 
(Nagesha and 
Holmes 1988; 
Nagesha et al 
1988; 
Nagesha et al 
1992) Yes (Yuan et 
al 2006)  Yes (Yuan et 
al 2006)  Yes***  
Rinderpest virus  Yes (OIE 
2008a)  No No (OIE 
2008b; OIE 
2008c)  No (OIE 
2008b; OIE 
2008c)  No (OIE 
2008b; OIE 
2008c)  No (OIE 
2008b; OIE 
2008c)  No 
Swine influenza virus  No (OIE 
2008a)  No 
(Thompson 
and 
Easterday 
2004)& Yes 
(Stanislawek 
2001) Yes 
(Thompson 
and Easterday 
2004) Yes 
(Thompson 
and Easterday 
2004) Yes 
(Thompson 
and 
Easterday 
2004) Yes** * 
Swine pox virus  No (OIE 
2008a)  No 
(Delhon et 
al 2006)  No (MAF 
2007) Yes (Delhon 
et al 2006)  Yes (Delhon 
et al 2006)  Yes (Delhon 
et al 2006)  Yes 
Swine vesicular disease 
virus  Yes (OIE 
2008a)  No No (OIE 
2008b; OIE 
2008c)  No (OIE 
2008b; OIE 
2008c)  No (OIE 
2008b; OIE 
2008c)  Some (OIE 
2008b; OIE 
2008c)  Yes 
Teschovirus serotype 1  No (OIE 
2008a)  No No (OIE 
2008b; OIE 
2008c)  No (OIE 
2008b; OIE 
2008c)  No (OIE 
2008b; OIE 
2008c)  No (OIE 
2008b; OIE 
2008c)  No 
Torovirus  No (OIE 
2008a)  No 
(Jamieson 
et al 1998; 
Wilhe lm et 
al 2003; 
Lodha et al 
2005) Yes (Horner 
1994) Yes Yes Yes No 
Torque teno virus  No (OIE 
2008a)  No ? ? Yes (Sibila et 
al 2009)  Yes (Sibila 
et al 2009)  Yes 
Transmissible 
gastroenteritis virus  Yes (OIE 
2008a)  No No (OIE 
2008b; OIE 
2008c)  No (OIE 
2008b; OIE 
2008c)  Yes (OIE 
2008b; OIE 
2008c)  Yes (OIE 
2008b; OIE 
2008c)  Yes 
Venezuelan encephalitis 
virus  Yes (OIE 
2008a)  Yes No (OIE 
2008c)  No (OIE 
2008c)  No (OIE 
2008c)  No (OIE 
2008c)  No  
Ministry for Primary Industries  Import risk analysis: Pig semen • 7 Disease agent  
 OIE List  Zoonotic  Present in 
NZ 
 Present in 
Australia  Present in 
USA and 
Canada  Present in 
EU or  
Norway  Prelim 
Hazard  
Vesicular stomatitis virus  Yes (OIE 
2008a)  Yes (Mare 
and Mead 
2004) No (OIE 
2008b)  No (OIE 
2008b; OIE 
2008c)  Yes (OIE 
2008b; OIE 
2008c)  No (OIE 
2008b)  Yes 
Vesicular exanthema 
virus   No (OIE 
2008a)  No (House 
and House 
1999) No (House 
and House 
1999) No (House 
and House 
1999) No (House 
and House 
1999) No (House 
and House 
1999) No 
West Nile virus  Yes (OIE 
2008a)  Yes No (OIE 
2008c)  No (OIE 
2008c)  Yes (OIE 
2008c)  Yes (OIE 
2008c)  Yes 
Western equine 
encephalitis virus  Yes (OIE 
2008a)  Yes No (OIE 
2008c)  No (OIE 
2008c)  Yes (OIE 
2008c)  No (OIE 
2008c)  Yes 
Bacterial agents/ 
diseases         
Actinobacillus 
pleuropneumoniae  No (OIE 
2008a)  No Yes (Hilbink 
et al 1992)   Yes 
(Gottschalk 
and Taylor 
2006) Yes 
(Gottschalk 
and Taylor 
2006) Yes 
(Gottschalk 
and Taylor 
2006) No 
Actinobacillus suis  No (OIE 
2008a)  No Yes (Carman 
and Hodges 
1982) Yes (Wilson 
and McOrist 
2000) Yes (Taylor 
2006b)  Yes (Taylor 
2006b; Taylor 
2006c)  No 
Actinobaculum suis 
(Eubacterium suis ) No (OIE 
2008a)  No Yes (Fairley 
1997) Yes (Taylor 
2006c)  Yes (Taylor 
2006c)  Yes (Taylor 
2006c)  No 
Arcanobacterium 
(Actinomyces or 
Corynebacterium)  
pyogenes  No (OIE 
2008a)  No Yes (Quinn 
et al 2002)  Yes Yes Yes No 
Bacillus anthracis  Yes (OIE 
2008a)  Yes 
(Taylor 
2006a)  No (Gill 
1992) Yes (OIE 
2008b; OIE 
2008c)  Yes (OIE 
2008b; OIE 
2008c)  Yes (OIE 
2008b; OIE 
2008c)  Yes 
Brucella suis  Yes (OIE 
2008a)  Yes 
(Macmillan 
et al 2006)  No (MAF 
2007) Yes (OIE 
2008b; OIE 
2008c)  Yes (OIE 
2008b; OIE 
2008c)  Yes (OIE 
2008b; OIE 
2008c)  Yes 
Burkholderia 
pseudomallei  No (OIE 
2008a)  Yes 
(Thomas 
1981; Inglis 
2004) No (MAF 
2007) Yes (Thomas 
1981; Inglis 
2004) No (Van der 
Lugt 2004)  No (Van der 
Lugt 2004)  Yes 
Chlamydia trachomatis  
Chlamydophila pecorum  
Chlamydophila psittaci  No (OIE 
2008a)  Yes (some 
species)  Yes  Yes Yes Yes No 
Clostridium tetani  No (OIE 
2008a)  Yes 
(Odendaal 
and Kriek 
2004) Yes (Ellison 
1992) Yes Yes Yes No 
Clostridium botulinum  No (OIE 
2008a)  Yes (Kriek 
and 
Odendaal 
2004) Some 
strains  Yes Yes Yes Yes***  
Other clostridial species  No (OIE 
2008a)  Some 
species/ 
strains  Some 
species/ 
strains  Yes Yes Yes Yes***  
Erysipelothrix 
rhusiopathiae  No (OIE 
2008a)  Yes 
(Wood and 
Henderson 
2006) Yes (Fairley 
1997) Yes Yes Yes No 
Escherichia coli  No (OIE 
2008a)                                 Yes Yes Yes Yes Yes No 
Lawsonia intracellularis  No (OIE 
2008a)  No 
(McOrist 
and 
Gebhart 
2006) Yes (Fairley 
1997) Yes Yes Yes No 
Leptospira serovars  Yes (OIE 
2008a)  Yes (Ellis 
2006) Yes 
(Midwinter 
1999) Yes Yes Yes Yes***   
Ministry for Primary Industries  Import risk analysis: Pig semen • 8 Disease agent  
 OIE List  Zoonotic  Present in 
NZ 
 Present in 
Australia  Present in 
USA and 
Canada  Present in 
EU or  
Norway  Prelim 
Hazard  
Mycobacterium spp. Yes (OIE 
2008a)  Yes 
(Cousins et 
al 2004)  Yes (OIE 
2008b; OIE 
2008c)  Yes (OIE 
2008b; OIE 
2008c)  Yes (OIE 
2008b; OIE 
2008c)  Yes (OIE 
2008b; OIE 
2008c)  No 
Mycoplasma 
hyopneumoniae  No (OIE 
2008a)  No Yes (Fairley 
1997) Yes Yes Yes No 
Mycoplasma hyorhinis  No (OIE 
2008a)  No Yes 
(MacPherson 
and Hodges 
1985) Yes Yes Yes No 
Mycoplasma 
hyosynoviae No (OIE 
2008a)  No No# Yes (Thacker 
2006) Yes (Thack er 
2006) Yes 
(Thacker 
2006) Yes 
Other Mycoplasma  spp.  No (OIE 
2008a)                                                        No  No# ? ? ? Yes 
Pasteurella multocida    Yes (OIE 
2008a)  No (De 
Jong 2006)   No (OIE 
2008b)  Yes (OIE 
2008b; OIE 
2008c)  Yes (OIE 
2008b; OIE 
2008c)  Yes (OIE 
2008b; OIE 
2008c)  Yes 
Pasteurella  spp. No (OIE 
2008a)  No Yes## Yes Yes Yes No 
Rhodococcus equi  No (OIE 
2008a)  No Yes (Carman 
and Hodges 
1987) Yes (Taylor 
2006d)  Yes  Yes No 
Exotic  Salmonella spp. No (OIE 
2008a)  Yes No Yes  Yes Yes Yes 
Serpulina pilosicoli  No (OIE 
2008a)  No Yes (Fairley 
1997) Yes Yes Yes No 
Brachyspira (Serpulina) 
hyodysenteriae  No (OIE 
2008a)  No Yes (Fairley 
1997) Yes Yes Yes No 
 
Table footnotes:  
     
**    Porcine circovirus 2 is present in Australia but PMWS has not been reported.  
***  Serotype/strain variation occurs.  
& Possibly zoonotic following reassortment with human viruses   
#      An extensive search of the literature revealed no evidence for the presence of the disease in the countries 
concerned.  
##    Commonly isolated and included in quarterly reports in the MAF publication Surveillance . 
 
The final version of this risk analysis also contains chapters assessing the risks associated with 
blue eye disease virus, foot and mouth disease virus, Nipah vir us, Teschovirus serotype 1, 
Venezuelan encephalitis virus , and vesicular exanthema virus  in porcine semen imported from 
countries other than Australia, the USA , Canada, the European Union or  Norway .  These agents 
were not assessed to be risks with s emen from those countries .  However, the development of an 
IHS for porcine semen from all countries requires an assessment of the risk posed by these 
additional pathogens.  
 Rinderpest virus is not subject to risk assessment as this disease was formally declared t o be 
globally eradicated in June 2011
3
5.2. HAZARD IDENTIFICATIO N . 
For each organism , the epidemiology is discussed, including a consideration of the following 
questions:  
                                                
3 See: http://www.fao.org/ag/againfo/programmes/documents/grep/A_RESO_18_FMD_Eradication.pdf   
Ministry for Primary Industries  Import risk analysis: Pig semen • 9 1. Could the imported commodity  act as a vehicle for the introduction of the 
organism?  
2. If the  organism requires  a vector, could competent vectors  be present in New 
Zealand?  
3. Is the organism exotic to New Zealand? 
4. If it is present in New Zealand,  
i. is it "under official control", which could be by government departments, 
by national or regional pest m anagement strategies or by a small -scale 
programme, or  
ii. are more virulent strains  known to exist in other countries?  
For any organism, if the answer to question one is “yes” (and the answer to question two is “yes” 
in the cases of organisms requiring a vect or), and the answers to either questions three or four are 
“yes”, it is classified as a potential hazard requiring risk assessment.  
 
Under this framework, organisms that are present in New Zealand cannot be considered as 
potential hazards unless there is evidence that strains with higher pathogenicity are likely to be 
present in the commodity to be imported. Therefore, although there may be potential for 
organisms to be present in the imported commodity, the risks to human or animal health are no 
different from risks resulting from the presence of the organism in this country already.  
If importation of the commodity is considered likely to result in an increased exposure of people to a potentially zoonotic organism already present in New Zealand, then that organism is also 
considered to be a potential hazard.  
5.3. RISK ASSESSMENT  
In line with the MPI  and the OIE risk analysis methodologies, the following analysis  is carried 
out for each potential hazard requiring risk assessment:  
 Risk Assessment  
  
 a) Entry ass essment -  the likelihood of the organism being imported in the 
commodity.  
 
 b) Exposure assessment - the likelihood of animals or humans in New 
Zealand being exposed to the potential hazard.  
 
 c) Consequence assessment - the consequences of entry, estab lishment or spread 
of the organism.  
 
 d) Risk estimation - a conclusion on the risk posed by the organism 
based on the release, exposure and consequence 
assessments. If the risk estimate is non -negligible, 
then the organism is classified as a hazard.  
It is important to note that all of the above steps may not be necessary in all risk assessments. 
The MPI and the OIE risk analysis methodologies make it clear that if the likelihood of release is 
negligible for a potential hazard, then the risk estimate is automatically negligible and the remaining steps of the risk assessment need not be carried out. The same situation arises where  
Ministry for Primary Industries  Import risk analysis: Pig semen • 10 the likelihood of release is non -negligible but the likelihood of exposure to susceptible species is 
negligible, or where both r elease and exposure are non -negligible but the consequences of 
introduction are concluded to be negligible.  
5.4. RISK MANAGEMENT  
For each organism classified as a hazard in the commodity , the risk management section 
identifies the options available for managin g the risk. Where the Code  lists recommendations for 
the management of a hazard, these are described alongside options of similar, lesser, or greater 
stringency where available.  In addition to the options presented, unrestricted entry or prohibition 
may a lso be considered for all hazards.  Recommendations for the appropriate sanitary measures 
to achieve the effective management of risks are not made in this document.  These will be determined when an import health standard (IHS) is drafted. As obliged unde r Article 3.1 of the 
WTO Agreement on Sanitary and Phytosanitary Measures (the SPS Agreement) , the measures 
adopted in IHSs will be based on international standards, guidelines and recommendations where 
they exist, except as otherwise provided for under Ar ticle 3.3  (where measures providing a 
higher level of protection than international standards can be applied if there is scientific justification, or if there is a level of protection that the member country considers is more 
appropriate following a risk a ssessment).  
5.5. RISK COMMUNICATION  
After an import risk  analysis has been written, MPI  analyses  the options available and proposes 
draft measures for the effective management of identified risks.  These are then presented in a 
draft IHS which is released togeth er with a risk management proposal that summarises the 
options analysis, and the rationale for the proposed measures.   This  package of documents is 
released for a six -week period of stakeholde r consultation . Stakeholder submissions in relation to 
these documents are reviewed before a final IHS is issued.  
 
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Ministry for Primary Industries  Import risk analysis: Pig semen • 15 6. Porcine adenovirus  
6.1. HAZARD IDENTIFICATIO N  
6.1.1. Aetiological agent  
Family: Adenoviridae , Genus; Mastadenovirus , Species: Porcine ade novirus (Benko et al 2005) . 
There are at least six serotypes of the virus (Kleiboeker 2006) . 
6.1.2. OIE list  
Not listed.  
6.1.3. New Zealand status  
Porcine adenovirus is widely distributed in the world and could be considered likely to be 
present in New Zealand. However, since there is no evidence to confirm its presence here, for the 
purposes of this risk ana lysis porcine adenovirus is assumed to be exotic.  
6.1.4. Epidemiology  
Swine are the only species known to be susceptible to porcine adenoviruses (Kleiboeker 2006) . 
While the role of the virus in causing diarrhoea is uncertain (Derbyshire et al 1966) , infections of 
caesarean -derived, colostrum -deprived pigl ets have resulted in gastroenteric disease.  The 
incubation period following faecal -oral transmission is 3 -4 days , and virus is found in 
enterocytes for up to 45 days post infection (Kleiboeker 2006) .  Infection by the respiratory route 
may also be possible.   
While antibodies are very commonly found in sows, th ey rarely excrete virus and there is a 
negative correlation between antibody levels and excretion of virus.  Most virus is shed during the post -weaning period (Derbyshire et al 1966) .  
 There is no indication that porcine adenovirus is excrete d in semen and the available information 
suggests that it is an enteric infection with virus found in enterocytes.  Most of the literature on the epidemiology of the virus is 20 -30 years old,  suggesting that this virus is no longer 
considered to be important.  
6.1.5. Hazard identification conclusion  
In view of the above, porcine adenovirus is not identified as a hazard in the commodity.  
 References  
 
Benko M, Harrach B, Both GW, Russell WC, Adair BM, Adam E, de Jong JC, Hess M, Johnson M, Kajon A, 
Kidd AH, Lemkuhl HD, Li QG, Mautner V, Pring -Akerblom P, Wadell C (2005).  Genus  Mastadenovirus . In: 
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Derbyshire JB, Clarke MC, Jessett DM (1966).  Observations on the faecal excretion of adenoviruses and 
enteroviruses in conventional and minimal disease pigs. Veterinary Record , 79, 595- 99. 
 
Kleiboeker SB (2006).  Porcine adenov irus. In: Straw BE, Zimmerman JJ, D'Allaire S, Taylor DJ (eds), Diseases of 
Swine . 9th edition. Pp. 287-90. Blackwell Publishing, Ames, Iowa.    
Ministry for Primary Industries  Import risk analysis: Pig semen • 16 7.  African swine fever virus  
7.1. HAZARD IDENTIFICATIO N 
7.1.1. Aetiological agent  
Family: Asfviridae , Genus; Asfvirus , Specie s: African swine fever virus  (ASFV)  (Sánchez -
Vizcaíno 2006) . 
7.1.2. OIE list  
Listed (OIE 2009a).  
7.1.3. New Zealand status  
Exotic notifiable organism (MAF 2009).  
7.1.4. Epidemiology  
The United States, Canada, Australia,  and Norway are free from African swine fever (ASF).  
With  the exception of Sardinia (Italy), all EU member states are free of ASF (OIE 2009b).  The 
European Commission decision 2005/362/EC has approved an eradication plan for ASF in 
Sardinia .  This  complies with the Directive 2002/60/EC which (amongst other meas ures) 
prohibits the movement of porcine semen from any holding within 10km of a premise infected with ASF.  T he Agreement between the European Community and New Zealand on sanitary 
measures applicable to trade in live animals and animal products  (97/132 /EC) prevents t he 
importation of any animal products to New Zealand that are unable to move freely in the EU.  
ASF is not recognised in any of the official EU candidate countries (Croatia, the Former Yugoslav Republic of Macedonia, and Turkey) or in any of the  recognised potential candidate 
countries (Albania, Bosnia and Herzegovina, Montenegro, Serbia,  and Iceland) (OIE 2009b).  
However, ASF is now spreading through Russia, the Ukraine, and neighbouring countries in the 
Caucasus (Callaway 2012) and is recognis ed as a potential source of possible incursions into the 
EU (Anonymous 2009).   ASF is considered to be endemic in most countries in sub -Saharan 
Africa (FAO 2012).  
When initially described, ASF infection of domestic pigs was associated with morbidity rates up 
to 100% and mortality rates often over 90%.  However, where the disease has become enzootic, 
a decrease in virulence may be seen resulting in fatality rates as low as 2 -3% (Mebus 1988).  
In African countries, ASF is maintained in a subclinically infected  wild pig population and 
transmitted to domestic pigs via the argasid tick Ornithodoros moubata , although other tick 
vectors ( O. savignyi  and O. porcinus porcinus ) have also been described (Kleiboeker et al 1998; 
Mebus 1988; Kleiboeker et al 1999; Burrage et al 2004).  In Europe, the soft tick O. erraticus  is 
recognised as the vector of ASFV (Wilkinson 1984) and it is thought that most Ornithodoros  
spp. of ticks that will feed on pigs are capable of acting as vectors for ASFV (Radostits et al 
2007).  
Once in fection is established in domestic pigs, it can spread rapidly between pigs by direct or 
indirect contact.  ASFV is present in a high titre in nasopharyngeal secretions  at the onset of 
clinical signs , and can be recovered from all organs of acutely sick pi gs (Radostits et al 2007).  
Viraemia develops within 48- 72 hours of infection,  and infectivity then persists for at least 7 
days.  The effect of the virus on haemostasis and on the vascular endothelium usually results in  
Ministry for Primary Industries  Import risk analysis: Pig semen • 17 death due to oedema and haemorrhage (Rodríguez et al 1996; Takamatsu et al 1999; Vallée et al 
2001).  
Some authors have suggested that ASF V can be found in boar semen and even transmitted to 
recipient sows (Thacker et al 1984; Wittmann 1989 ; Guérin and Pozzi 2005), although the only 
evidence for this provided in any of these sources appears to be a personal communication by 
DH Schlafer in 1984.  More recently, Maes et al 2008 stated that there is no published evidence 
to support this hypothesis.  
7.1.5. Hazard identification conclusion  
Of the countri es initially considered in this risk analysis, ASF is only found in Sardinia and 
legislative controls described above prohibit the movement of semen from any premises within 10Km of a property infected with this disease.  ASF is endemic in sub -Saharan Afri ca and is an 
emerging disease throughout Russia, the Ukraine, and neighbouring countries in the Caucasus.  
However , as there  is no published evidence to show that ASF V can be found in the semen of 
infected boars, ASF V is not  identified as a hazard in the co mmodity.  
 
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 OIE (2009a)  Terrestrial Animal Health Code . 
http://www.oie.int/eng/normes/MCode/en_sommaire.htm , 
downl oaded 27/1/2009.  
 OIE (2009b)  World Animal Health Information Database (WAHID) Interface. 
http://www.oie.int/wahid -
prod/public.php?page=home , downloaded 11/12/2009.  
 
Radostits OM, Gay CC,  Hinchcliff KW, Constable PD (2007) African swine fever (African pig disease, wart hog 
disease). In: Veterinary Medicine  10th Edition, Saunders Elsevier, 1167-73.   
Ministry for Primary Industries  Import risk analysis: Pig semen • 18  
Rodríguez F, Fernández A, Pérez J, Marín de las Mulas J, Sierra MA, Jover A (1996)  African s wine fever: 
morphopathology of a viral haemorrhagic disease. Veterinary Record  139, 249-54.  
 Sánchez -Vizcaíno JM (2006)  African swine fever. In: Straw BE, Zimmerman JJ, D'Allaire S, Taylor DJ (eds), 
Diseases of Swine . 9th edition. Pp. 291 -307. Blackwell Publishing, Ames, Iowa  
 
Takamatsu H, Denyer MS, Oura C, Childerstone A, Andersen JK, Pullen L, Parkhouse RME (1999)  African 
swine fever virus: a B cell -mitogenic virus in vivo  and in vitro . Journal of General Virology  80, 1453-61.  
 Thacker B, Larsen R, Joo H S, Leman A (1984)  Swine diseases transmissible with artificial insemination. Journal 
of the American Veterinary Medical Association 185, 511 -6. 
 Vallée I, Tait SWG, Powell PP (2001)  African swine fever virus infection of porcine aortic endothelial cells le ads 
to inhibition of inflammatory responses, activation of the thrombotic state, and apoptosis. Journal of Virology  75, 
10372-82.  
 Wilkinson PJ (1984) The persistence of African swine fever in Africa and the Mediterranean. Preventive 
Veterinary Medicine  2, 71-82.  
 Wittmann G  (1989)   Die bedeutung viraler erkrankungen beim schwein für die besamung und den embryotransfer 
(Significance of viral diseases in pigs during artificial insemination and embryo transfer).  Tierärztliche Umschau  
44, 580-6.   
 
 
 
 
 
 
 
  
Ministry for Primary Industries  Import risk analysis: Pig semen • 19 8. Aujeszky’s disease virus 
8.1. HAZARD IDENTIFICATIO N 
8.1.1. Aetiological agent  
Family: Herpesviridae , Subfamily: Alphaherpesvirinae , Genus: Varicellovirus , Species: Suid 
herpesvirus  1, Aujeszky’s disease virus (Mocsari et al 1989;  Davison et al 2005) . 
8.1.2. OIE list  
Listed (OIE 2008a) . 
8.1.3. New Zealand status  
Exotic, notifiable organism (MAF 2009) .  
8.1.4. Epidemiology  
Aujeszky’s disease (AD) virus can infect most mammals e xcept primates, and is fatal in all 
animals except pigs. Therefore the pig is the only reservoir host, and all other animals are 
considered to be dead -end hosts (Pejsak and Truszczynski 2006) . 
Canada , Norway,  and Australia are free from AD. In the EU onl y Italy, Poland, Spain, Northern 
Ireland, and Portugal are reported to be infected or possibly infected. The virus is present in the 
USA (OIE 2008b) .  Elsewhere, Aujeszky’s disease is found in parts of Southeast Asia, and 
Central and South America including Mexico. The virus has also been reported from Cuba, Samoa , and Rwanda  (Center for Food Security and Public Health 2006).  
The disease has an incubation period ranging from 1 -11 days (Pejsak and Truszczynski 2006) . 
Respiratory and nervous signs may occur , but many pigs are subclinically infected. Mortality 
may be high in young pigs. The virus is found in nasal secretions and is transmit ted by direct 
nose-to-nose contact or over distances of a few meters by aerosols (Van Oi rschot 2004) . It is also 
found in vaginal secretions and semen, and therefore may be transmitted by natural breeding and by artificial insemination (Pejsak and Truszczynski 2006; Van Oirschot 2004; Wittmann 1986) .  
Pigs become long -term latent carriers after recovery from infection, and reactivation and 
excretion of the virus can occur due to stress or as a result of treatment with corticosteroids. 
However, reactivation is rare and it is considered insignificant in the epidemiology of the disease 
(Van Oirschot 2004) . The virus can be eradicated from infected herds by conventional test and 
slaughter pr ocedures. In the case of the New Zealand eradication programme, vaccination with 
deletion marker vaccines was used as an additional aid (Motha et al 1997) .  
Infection can be diagnosed by isolation of the virus, identification of viral DNA by PCR , or by 
serological methods, particularly t he ELISA (Pejsak and  Truszczynski 2006; Toma et al 2008; 
Van Oirschot 2004) . Since tissue culture is not an option for diagnosis of the virus in semen due 
to toxic effects of semen on cell lines, PCR is preferred (van Rijn et al 2004).  
8.1.5. Hazard identification conclusion 
Aujes zky’s disease virus (ADV) is an exotic , notifiable organism that is readily transmitted in 
pig semen. Therefore it is identified as a potential hazard in the commodity.   
Ministry for Primary Industries  Import risk analysis: Pig semen • 20 8.2. RISK ASSESSMENT  
8.2.1. Entry assessment  
Pigs may be sub -clinically infected, long -term latent  carriers of AD V. Therefore the likelihood 
of entry of the organism in the commodity is non -negligible for semen imported from any 
country where the virus is present.  
8.2.2. Exposure assessment  
Imported semen will be used to inseminate sows and the disease can be transmitted by infected 
semen. Therefore the likelihood of exposure of naïve New Zealand sows to virus in imported 
semen is non- negligible.  
8.2.3. Consequence assessment  
When previously introduced into New Zealand the virus spread through much of the North 
Island. Therefore, if reintroduced and left uncontrolled, it would likely become endemic over 
large areas. Production losses would be likely, particularly through mortality of young pigs. Introduction of the virus might interfere with New Zealand’s limited pig  exports. The 
consequences for domestic pigs are assessed  to be non- negligible.  
AD is not zoonotic and if introduced there would be no consequences for human health. ADV 
can infect a wide range of non -primate animals, and since infections of animals other than pigs 
are almost always fatal, they can be considered dead -end hosts. Moreover, infection of animals 
other than pigs is rare, occurring only where there is close contact with infected pigs (Pejsak and 
Truszczynski 2006) . Spread from inseminated pigs to other animals is therefore unlikely, but 
could occur under certain circumstances. Spread to other farmed pigs would be possible if inseminated pigs were moved between herds. Spread to wild pigs is theoretically possible if there 
is contact with farmed p igs, and virus might circulate in wild pig populations if they are of 
sufficient density. However, feral pigs seldom have contact with domestic pigs and when AD was endemic in the North Island, feral pigs remained free from infection. In the unlikely event  
that animals other than pigs did become infected, there would be no further spread as they are considered to be dead -end hosts. The consequences for the environment are therefore assessed  to 
be negligible.  
8.2.4. Risk estimation  
Entry, exposure and consequence are all assessed  to be non- negligible. As a result the risk 
estimate for ADV is non -negligible and it is assessed to be a risk in the commodity. Therefore 
risk management measures can be justified.  
8.3. RISK MANAGEMENT  
8.3.1. Options  
The Code  chapter on AD (OIE 2008a)  defines AD free countries, zones and establishments and 
provisionally free countries or zones.  
The Code  chapter on AD contains the following recommendations relating to importation of pig 
semen:  
Article 8.2.12.   Recommendations for importation from AD free countries or zones   
Ministry for Primary Industries  Import risk analysis: Pig semen • 21 Veterinary Authorities  should require the presentation of an international veterinary 
certificate attesting that:  
1. the donor animals:  
a. showed no clinical sign of AD on the day of col lection of the semen;  
b. were kept in an establishment  or artificial insemination centre  located in an 
AD free country or zone at the time of semen collection;  
2. the semen was collected, processed and stored in conformity with the provisions of 
Chapter s 4.5 and  4.6. 
Article 8.2.13.   Recommendations for importation from AD provisionally free countries or 
zones  
Veterinary Authorities  should require the presentation of an international veterinary 
certificate attesting that:  
1. the donor animals:  
a. have been kept for at least 4  months prior to semen collection in an artificial 
insemination centre  which has the status of AD free  establishment , and where 
all boars are subjected to a serological test to the whole AD  virus, with negative 
results, every 4  months;  
b. showed no cli nical sign of AD on the day of collection;  
2. the semen was collected, processed and stored in conformity with the provisions of Chapter s 4.5 and  4.6. 
Article 8.2.14.   Recommendations for importation from AD infected countries or zones  
Veterinary Authorities  should require the presentation of an international veterinary 
certificate attesting that:  
1. the donor animals:  
a. were kept in an AD free establishment  for at least 6  months prior to entering 
the artificial insemination centre ; 
b. have been kept for at least 4  months prior to semen collection in the artificial 
insemination centre  which has the status of AD free  establishment , and where 
all boars are subjected to a serological test to the whole AD virus, with negative results, every 4  months;  
c. were subjected to a serological test to the whole AD virus, with negative results, within 10  days prior to or 21  days after semen collection;  
d. showed no clinical sign of AD on the day of collection;  
2. the semen was collected, processed and stored in conformity with the provisions of 
Chapter s 4.5 and  4.6. 
Chapters 4.5 and 4.6 of the Code  (OIE 2009a)  contain requirements for AD for boars standing at 
semen collection centres.  Under these requirements, boars from a country or zone that is not free 
of AD must be clinically healthy, physiologically normal, not vaccinated against AD, kept 
exclusively in an AD -free establishment since birth, and subject to serological testing for whole 
AD virus with negative results within 30 days prior to entry into isolation at the quarantine 
station of the semen collection facility.  Boars must remain in this quarantine station for at least 
28 days and, at least 21 days after entering the quarantine station , must be tested negative for AD  
Ministry for Primary Industries  Import risk analysis: Pig semen • 22 as per Articles 8.2.12, 8.2.13, or 8.2.14 of the Code .  In countries, zones or compartments which 
are not free of AD, any boars resident in the semen collection facility must also be tested at least 
annually as per Arti cles 8.2.12, 8.2.13 or 8.2.14 of the  Code . 
The following options could be considered in order to effectively manage the risk of AD in 
semen:  
Option 1  
Aliquots of each batch of semen to be imported could be tested by PCR for the presence of virus 
(van Rijn et al 2004). Importation of semen giving positive results could be prohibited.  
Option 2  
Semen originating from collection centres certified as compliant with OIE Code Chapters 4.5 and 4.6 could be considered suitable for importation.  
Option 3  
Semen for exp ort to New Zealand could come from donor boars that were kept in an 
establishment or artificial insemination centre located in an AD -free country or zone at the time 
of semen collection.  
 
References  
 
Center for Food Security and Public Health (2006).  Aujes zkey’s Disease.  Available at: 
http://www.cfsph.iastate.edu/Factsheets/pdfs/aujeszkys_disease.pdf  
 
Davison AJ, Eberle R, Hayward GS, McGeogh DJ, Minson AC, Pellett PE, Roizman B, Studdert MJ, Thirly 
E (2005).  Genus  Variocellovirus . In: Fauquet CM, Mayo MA, Maniloff J, Desselberger U, Ball LA (eds), Eighth 
Report of the International Committee on Taxonomy of Viruses . Pp. 200-1, Elsevier Academic Press, Amst erdam.  
 
MAF (2009). The Unwanted Organisms Register. http://mafuwsp6.maf.govt.nz/uor/searchframe.htm.downloaded  
27/1/2009.  
 
Mocsari E, Szolnoki J, Glavits R, Zsak L (1989) . Horizo ntal transmission of Aujeszky's disease virus from sheep 
to pigs. Veterinary Microbiology , 19, 245 -52. 
 Motha J, MacDiarmid SC, Pannett GR (1997) . Evolution of Aujeszky's disease eradication in New Zealand. 
Surveillance , 24(2), 11- 3. 
 OIE (2008a) . Terrestrial Animal Health Code . 
http://www.oie.int/eng/normes/MCode/en_sommaire.htm , 
downloaded 27/1/2009.  
 
OIE (2008b) . World Animal Health Information Database (WAHID) Interface. http://www.oie.int/wahid -
prod/public.php?page=home , downloaded 27/1/2009.  
 
Pejsak ZK, Truszczynski MJ (2006).  Aujeszky's disease (pseudorabies). In: Straw BE, Zimmerman JJ, D'Allaire 
S, Taylor DJ (eds ), Diseases of Swine . 9th edition, Pp. 419-33, Blackwell Publishing, Ames, Iowa.  
 Toma B, Haddad N, Vannier P (2008).  Aujeszky's disease. In: OIE (eds), OIE Manual of Diagnostic Tests and 
Vaccines for Terrestrial Animals . Vol. 1, Pp. 145 -57, OIE, Paris.  
 
Van Oirschot JT (2004).  Pseudorabies. In: Coetzer JAW, Tustin RC (eds), Infectious Diseases of Livestock . Vol. 2, 
Pp. 909-22, Oxford University Press, CapeTown.  
  
Ministry for Primary Industries  Import risk analysis: Pig semen • 23 van Rijn PA, Wellenberg GJ, der Honing RH, Jacobs L, Moonen PLJM, Feitsma H (2004) Detection of  
economically important viruses in boar semen by quantitative RealTime PCR technology. Journal of Virological 
Methods 120, 151- 60. 
 
Wittmann G (1986). Aujeszky's disease. Revue Scientifique et Technique. OIE, 5, 959 -77. 
 
  
Ministry for Primary Industries  Import risk analysis: Pig semen • 24 9. Blue eye disease virus  
9.1. HAZARD IDENTIFICATION  
9.1.1. Aetiological agent  
Family : Paramyxoviridae , Genus : Rubulavirus .  Porcine rubulavirus (PoRV), also known as La -
Piedad -Michoacan -Mexico virus (LPMV) (King et al 2012).  
9.1.2. OIE list  
Not listed.  
9.1.3. New Zealand status  
There are no reports of porcine rubul avirus or related paramyxoviruses of pigs in New Zealand.  
9.1.4. Epidemiology  
Blue eye pig disease was described in 1980 in a commercial herd in La Piedad, Central Mexico 
(Stephao et al 1981; 1982, cited by Stephan et al 1988).  Although this disease has only bee n 
reported in Mexico (Center for Food Security and Public Health 2006) , closely related 
paramyxoviruses of pigs have been found in Australia  (Menangle virus, see Chapter 16 ), Canada  
(Salles et al 2011) , Japan (Sasahara et al 1954) ,  Israel  (Lipkind et al 1986), and the United States 
(Janke et al 2001).  
Infection of young pigs results in blue eye disease which is characterised by encephalitis, pneumonia, and corneal opacity.  The disease presents clinically with sudden onset pyrexia 
followed by progressive n eurologic signs such as weakness, ataxia, rigidity , or hyperexcitability 
(Center for Food Security and Public Health 2006).   Morbidity in affected litters is usually 
between 20 and 50% and mortality around 90%.  Pigs older than 30 days show moderate and 
transient clinical signs with fewer than 2% of this age group affected with low mortality. 
Reproductive failure is described in pregnant sows (Kirkland and Stephano 2006).  
Pigs are the only species clinically affected by PoRV with virus most commonly transmi tted by 
nose-to-nose contact between infected and susceptible pigs (Kirkland and Stephano 2006).   
Experimental infection (intranasal and intramuscular inoculation) of boars results in swelling of the epididymis, reduced spermatozoan motility and concentrat ion with viral antigen detectable in 
the head of the epididymis.  Viral antigen remains detectable in the epididymis for up to 10 weeks and detection of viral antigen in the lumina of the epididymal ductuli suggests the 
possibility of venereal transmission (Ramirez -Mendoza et al 1997).  A subsequent study 
demonstrated that PoRV could be detected in the semen of infected pigs between 2 and 49 days after infection, leading the authors to propose that semen from PoRV -infected boars could be an 
important route of virus transmission among and within farms (Solís et al 2007).   
Ministry for Primary Industries  Import risk analysis: Pig semen • 25 9.1.5. Hazard identification conclusion 
Although transmission in semen has not been proven experimentally, PoRV can be recovered 
from the semen of infected boars.  Two recent reviews of diseases in swine likely to be 
transmitted by artificial insemination have both included PoRV (Guérin and Pozzi 2005; Maes et al 2008).  PoRV is identified as a potential hazard in porcine semen.  
9.2. RISK ASSESSMENT  
9.2.1. Entry assessment  
Unilateral or bilateral swelling in the  testicular and epididymal regions of infected boars is 
described from 15 days after infection which may subside within the following 10 days although 
subsequent testicular atrophy has been recorded (Ramirez- Mendoza et al 1997).  However, overt 
clinical signs are not seen in all infected individuals so physical examination cannot be relied upon to detect boars infected with PoRV and virus can be recovered from the semen of infected 
boars up to 49 days post infection (Solís et al 2007) .  The likelihood of en try is assessed to be 
high.  
9.2.2. Exposure assessment  
Mumps virus is another member of the Rubulavirus genus and, although epididymo- orchitis is 
associated with human infections with the mumps virus and virus has been recovered from the semen of infected individ uals (Jalal et al 2004), no reports of venereal transmission of mumps 
virus could be found.  
Hernández -Jáuregui et al (2004) intranasally inoculated pregnant gilts at six weeks gestation 
with PoRV and were able to recover virus from the ovary, placenta, and  uterus between two and 
four weeks later.  Although transmission via infected semen has not been demonstrated, this 
study demonstrates that PoRV has a tropism for the tissues of the reproductive tract so the 
likelihood of exposure is assessed to be non -negligible.  
9.2.3. Consequence assessment  
Pigs are the only species clinically affected by PoRV.  Infection may cause progressive neurological disease in younger pigs with high mortality although less marked signs are 
described in older animals.  The consequences of  infection are assessed to be non -negligible.  
9.2.4. Risk estimation  
Since the entry, exposure,  and consequenc e assessments are all non-negligible, the risk is 
estimated to be non -negligible and PoRV is assessed to be a risk in porcine semen.  Risk 
management measures are  justified.  
9.3. RISK MANAGEMENT  
9.3.1. Options  
PoRV has only been described in Mexico so sanitary measures are not required for imports of porcine semen originating from pigs in any country other than Mexico.   
Ministry for Primary Industries  Import risk analysis: Pig semen • 26 A number of serological tests have been described  to detect exposure to PoRV including 
haemagglutination inhibition (Escobar -López et al 2012), virus neutralisation (Sánchez -
Betancourt et al 2012), indirect immunofluorescence, and enzyme- linked immunosorbent assays 
(Nordengrahn et al 1999).  All of these  serological tests detect seroconversion by the 8th day after 
infection ( Center for Food Security and Public Health 2006) . 
The following options could be considered in order to effectively manage the risk:  
 
Option 1  
Semen for export to New Zealand could co me from donor boars that were kept in an 
establishment or artificial insemination centre located in a PoRV -free country or zone at the time 
of semen collection.  
 
Option 2  
Donor boars could be subject to serological testing with negative results.  
 
References  
Center for Food Security and Public Health (2006).  Porcine Rubulavirus Infection. Available at: 
http://www.cfsph.iastate.edu/Factsheets/pdfs/blue_eye_disease.pdf  
Escobar -Lópe z AC, Rivera -Benitez JF, Castillo -Juárez H, Ramírez -Mendoza H, Trujillo -Ortega ME, 
Sánchez -Betancourt JI (2012).  Identification of antigenic variants of the porcine rubulavirus in sera of field swine 
and their seroprevalence. Transboundary and Emerging Dis eases  59, 416-420.  
Guérin B, Pozzi N (2005).  Viruses in boar semen: detection and clinical as well as epidemiological consequences 
regarding disease transmission by artificial insemination. Theriogenology  63, 556 -572.  
Hernández -Jáuregui P, Mendoza HR, Garc ía CM, Moreno -López J, Kennedy S (2004).  Experimental porcine 
rubulavirus (La Piedad-Michoacan virus) infection in pregnant gilts. Journal of Comparative Pathology  130, 1-6.  
Jalal H, Bahadur G, Knowles W, Jin L, Brink N (2004).  Mumps epididymo -orchitis wit h prolonged detection of 
virus in semen and the development of anti -sperm antibodies. Journal of Medical Virology  73, 147- 150. 
Janke BH, Paul PS, Landgraf JG, Halbur PG, Huinker CD (2001).  Paramyxovirus infection in pigs with 
interstitial pneumonia and enc ephalitis in the United States. Journal of Veterinary Diagnostic Investigation  13, 428-
433. 
King AMQ, Adams MJ, Carstens EB, Lefkowitz (2012).  Virus Taxonomy. Ninth report of the International 
Committee on Taxonomy of Viruses . Elsevier Academic Press, Lond on. 676-677.  
Kirkland PC, Stephano A (2006).  Chapter 27: Paramyxoviruses: Rubulavirus, Menangle, and Nipah virus 
infections. In Diseases of Swine , 9th Edition. Eds Straw BE, Zimmerman JJ, D’Allaire S, Taylor DJ. Blackwell 
Publishing, Oxford.  455-467.  
Lipkind M, Shoham D, Shihmanter E (1986).  Isolation of a paramyxovirus from pigs in Israel and its antigenic 
relationship with avian paramyxoviruses. Journal of General Virology  67, 427 -439.  
Maes D, Nauwynck H, Rijsselaere T, Mateusen B, Vyt P, de Kruif A, Van  Soom A (2008).  Diseases in swine 
transmitted by artificial insemination: An overview. Theriogenology  70, 1337-1345.   
Ministry for Primary Industries  Import risk analysis: Pig semen • 27 Nordengrahn A, Svenda M, Moreno -Lopez J, Bergvall A, Hernandez P, McNeilly F, Allan G, Merza M 
(1999).  Development of a blocking ELISA for screening antibodies to porcine rubulavirus, La Piedad Michoacan 
Virus. Journal of Veterinary Diagnostic Investigation  11, 319- 323. 
Ramírez -Mendoza H, Harnandez -Jauregui P, Reyes -Leyva J, Zenteno E, Moreno-Lopez J, Kennedy S (1997).  
Lesions in the reproduc tive tract of boars experimentally infected with porcine rubulavirus. Journal of Comparative 
Pathology  117, 237-252.  
Salles MWS, Scholes SFE, Dauber M, Strebelow G, Wojnarowicz C, Hassard L, Acton AC, Bollinger TK 
(2011).  Porcine techovirus polioencephalom yelitis in western Canada. Journal of Veterinary Diagnostic 
Investigation  23, 367-373.  
Sánchez -Betancourt JI, Trujillo ME, Mendoza SE, Reyes -Leyva J, Alonso RA (2012). Genetic and antigenic 
changes in porcine rubulavirus.  Canadian Journal of Veterinary Re search  76, 33 -37.  
Sasahara J, Hayashi S, Kumagai (1954). On a swine virus disease newly discovered in Japan. 1. Isolation of the 
virus. 2. Some properties of the virus. Virus 4, 131 -139.  
Solís M, Ramírez -Mendoza H, Mercado C, Espinosa S, Vallejo V, Reyes-Leyva J, Hernández J (2007).  Semen 
alterations in porcine rubulavirus -infected boars are related to viral excretion and have implications for artificial 
insemination. Research in Veterinary Science  83, 403-409.  
Stephan HA, Gay GM, Ramírez TC (1988).  Enceph alomyelitis, reproductive failure and corneal opacity (blue 
eye) in pigs, associated with a paramyxovirus infection. Veterinary Record 122, 6-10.  
Stephano HA, Gay GM, Ramírez TC, Maqueda AJJ (1981). Memorias XVII. Convención de la Asociación Mexicana de Veterinrios Especialistas en Cerdos, Ixtapa, México, 43.  
Stephano HA, Gay GM, Ramírez TC, Maqueda AJJ (1982). Proceedings of the 7
th International Pig Veterinary 
Society Congress, Mexico, 153.   
Ministry for Primary Industries  Import risk analysis: Pig semen • 28 10. Classical swine fever virus and other pestiviruses  
10.1. HAZARD IDENTI FICATION  
10.1.1.  Aetiological agent  
Family: Flaviviridae , Genus: Pestivirus , Species: Classical swine fever virus (CSFV) , Bovine 
viral diarrhoea virus  1 and 2 (BVDV -1 and 2), and Border disease virus  (BDV) (Barkema et al 
2001; Choi and Chae 2003; Thiel et al 2005) . See also Chapter 21  (porcine myocarditis virus).  
10.1.2.  OIE list  
Classical swine fever and bovine viral diarrhoea are listed diseases (OIE 2008a) . 
10.1.3.  New Zealand status  
BDV and BVDV- 1 are endemic in New Zealand, while BVDV -2 and CSFV are both exotic   
(Horner 2000; Vilcek et al 1998; OIE 2008b) . 
10.1.4.  Epidemiology  
CSFV is the causative agent of classical swine fever (CSF), a highly contagious disease of pigs. 
CSFV is ex otic to Australia, Norway, the USA, and Canada. Since 2007, outbreaks of CSF have 
been reported in the EU in Bulgaria, France, Germany, Hungary, Romania, and Slovakia (OIE 2008b) , possibly as a result of infected wild boars transmitting the virus to farmed pigs.   CSFV is 
found in much of Asia, some Caribbean islands, the African countries of Madagascar and Mauritius, and much of South and  Central America (Center for Food Security and Public Health 
2009).  
BVDV causes bovine viral diarrhoea in cattle, and BDV causes border disease in sheep. Both 
BVDV- 1 and BDV are endemic in New Zealand and , with the exception of Norway (OIE 
2008b),  in all t he countries considered in this risk analysis. Some strains of BVDV -2 cause a 
more severe disease in cattle than BVDV -1. BVDV- 2 is present in the EU (Barkema et al 2001; 
Cranwell et al 2005; Drew et al 2002; Nettleton and Gunn 2002; Vilcek et al 2002)  and North 
America (Nettleton and Willoughby 2008; Potgieter 2004) , but not in Norway or Australia 
(Horner 2000; Vilcek et al 1998) .  
Infection of pregnant sows with CSFV strains of low virulence can result in the birth of 
immunotolerant, per sistently infected pigs, particularly when infection occurs in late gestation 
(Van Oirschot 2004) . In pigs infected after birth the incubation period is 7 -10 days .  They are 
usually infect ive between days 5 and 14 post -infection, but can remain infective up to 3 months 
in cases of chronic  infections (OIE 2008a) . Pigs that recover from mild infections can carry the 
virus for long periods of time (Van Oirschot 2004) . Some pigs persistently infected with CSFV 
develop late- onset disease with typical signs of acute or  sub-acute infection after 4 -6 months 
(Van Oirschot 2004) . Infected pigs shed the vir us in saliva, nasal and ocular secretions, faeces 
and urine. Boars may shed the virus in semen (Choi and Chae 2003; De Smit et al 1999; Floegel et al 2000)  and sows can be infected by artificial insemination (Floegel et al 2000) .  
CSFV ca n be detected in semen by virus isolation in tissue culture, but reverse transcription PCR 
is a more sensitive method of detection which allows the detection of viral RNA for months after 
infection. For diagnosis of the disease a number of virus detection and serological tests are 
available. Serological testing is not suitable for detecting immunotolerant animals and cross 
reactions may occur with antibodies generated in response to BVDV infections. The virus can  
Ministry for Primary Industries  Import risk analysis: Pig semen • 29 also be demonstrated in tissues by immunolog ical staining methods (Drew 2008b) . Gross and 
histological lesions may be typical in cases of acute swine fever and are valuable diagnostic aids. 
Sensitive PCR methods are available that use group specific probes to detect all pestiviruses 
(BVDV- 1, BVDV- 2, BDV and CSFV) (Vilcek et al 1994)  and PCR methods are available for 
genotyping pestiviruses (Sandvik et al 1997) . 
BVDV and BDV can infect pigs (Nettleton 2004) , but the infection is usually subclinical. 
However, when these viruses infect naïve pregnant sows, infection of foetuses occurs and results in foetal mortality or birth of persistently -infected immunotolerant piglets. Piglets that have been 
infected in utero excrete large quantities of virus, but when they are infected at birth they excrete 
little or no virus (Le Potier et al 2006) . It is assumed that persistently -infected pigs can excrete 
BVDV in their semen since this occurs with CSFV in pigs and in cattle that are persistently infected with BVDV (Kirkland et al 1991; Potgieter 2004) . 
Concerns have been raised by domestic  stakeholders regarding the emergence of porcine 
neurologic and reproductive syndrome virus (novel Pesti -like virus in the US) and the occurrence 
of untypable or cross -reactive Pestivirus infections of swine in North America and elsewhere in 
the world (Cle ment 2009).  However, at a subsequent meeting with domestic stakeholders to 
discuss these  concerns (8th December 2009) , no further information regarding this specific 
matter was provided.  A literature search has identified one publication regarding the is olation of 
a novel viral agent (termed “Virus X” by the authors) associated with porcine reproductive and neurological syndrome and reproduction of the disease (Pogranichniy et al 2008).  This 
publication concluded that the possibility that Virus X is a pe stivirus cannot be completely ruled 
out.  However, there has been no further published confirmation of the identity of this agent or any studies which indicate that it is likely to be transmitted in semen.  
10.1.5.  Hazard identification conclusion 
Therefore CSFV is  identified as a  potential hazard. BVDV -1 and BDV are endemic in New 
Zealand and therefore are not potential hazards. BVDV -2 could infect pigs and be excreted in 
their semen and it is therefore also identified as  a potential hazard . 
 
There is insufficient evidence to conclude that other (novel) pestiviruses should be identified as a 
hazard in porcine semen.  
10.2. RISK ASSESSMENT  
10.2.1.  Entry assessment  
Blood, secretions and excretions (including oronasal and lacrimal secretions, urine, f aeces, and 
semen) and tissues f rom infected pigs contain CSFV.  Virus shedding can begin before the onset 
of clinical signs, and occurs throughout the course of acute or subclinical disease.  Chronically or 
persistently infected pigs can shed virus continuously or intermittently for months (Center for 
Food Security and Public Health 2009).  The likelihood of CSFV entry in the sem en of pigs from 
infected countri es is assessed to be high.  
 
In Germany and France the occurrence of CSF is associated with infection of wild boars that 
transmit the virus to farmed pigs. In most areas of Germany and France the likelihood of 
infection of pig semen is low. However, if donor pigs originate from areas where contact with infected wild pigs is possible, the likelihood of infection is assessed to be non -negligible.  
  
Ministry for Primary Industries  Import risk analysis: Pig semen • 30 Pigs originating from countries  where BVDV -2 is found  could be subclinically infected with 
BVDV- 2 and could excrete the virus in their semen. The likelihood for entry of BVDV -2 virus in 
pig semen from these countries is therefore non- negligib le.  
10.2.2.  Exposure assessment  
Imported semen will be inseminated into New Zealand pigs. As it has been demonstrated that 
sows can be infected with CSFV by artificial insemination with infected semen (Floegel et al 
2000) , it is assumed that this is also likely for pigs that are infected with BVD V-2, the likelihoo d 
of exposure of New Zealand pigs is assessed  to be non- negligible.  
10.2.3.   Consequence assessment  
Insemination of pigs would result in the transmission of the pestiviruses concerned to the 
recipients of the semen. Contact between infected pigs and other New Zealand pigs or ruminants 
could result in spread of imported pestiviruses. CSFV could cause disease that could spread 
widely in pigs due to movement of animals and contact transmission.  BVDV could be 
transmitted from pigs to cattle and establishment of viru lent strains of BVDV -2 could result in 
outbreaks of a disease that would have production -limiting and economic implications for the 
New Zealand cattle industries.  
 
CSF is an OIE listed disease. Introduction of virulent strains of CSFV could cause catastro phic 
mortality in a naïve pig population and bans on trade in New Zealand pig meat. Low virulence strains would cause less dramatic economic losses but would lead to difficulties in diagnosis and 
ongoing economic losses to pig farmers. Introduction of CSF would result in the need for an 
expensive eradication campaign involving stamping out of the disease or vaccination of the pig 
population.  
 BVDV and CSFV are not zoonotic and there would be no consequence for human health. BVD 
is not described as a disease of any significance in wild ruminants and therefore would be of no 
consequence to feral ruminants. CSF  could infect wild pigs that could then act as a reservoir of 
infection for domestic pigs. However, under New Zealand conditions the likelihood of contact 
between wild pigs and domestic pigs in commercial units that might be users of imported semen 
is assessed  to be low, but non- negligible.  
 Since BVDV -2 could be transmitted from infected pigs to cattle with subsequent spread of the 
virus between cattle t he consequences are assessed to be non -negligible. Introduction of CSFV  
could lead to high mortalities in pigs and limited trade bans.  
10.2.4.  Risk estimation  
Entry, exposure and consequence have all been assessed as non -negligible. As a result the risk 
estimate for CSFV and BVDV- 2 is non -negligible and they are classified as  a risk  in the 
commodity. Therefore risk management measures can be justified.  
10.3. RISK MANAGEMENT  
10.3.1.  Options  
Within the EU , CSF occurs only in Germany and France.   EU directive 2008/855/EC prohibit s 
movement of semen from areas infected with CSF and the Agreement between the European 
Community and New Zealand on sanitary measures applicable to trade in live animals and  
Ministry for Primary Industries  Import risk analysis: Pig semen • 31 animal products  (97/132/EC) prevents t he importation of any animal products to Ne w Zealand 
that are unable to move freely  in the EU.  
 
The Code  defines CSF -free countries, zones and compartments and also countries free from CSF 
in domestic pigs but with a wild pig population.  The Code  chapter on CSF contains the 
following recommendatio ns relating to importation of pig semen:  
Article 15.3.8.   Recommendations for importation from countries, zones or 
compartments free of CSF  
Veterinary Authorities  should require the presentation of an international veterinary 
certificate attesting that:  
1. the donor animals:  
a. were kept in a country, zone  or compartment  free of CSF since birth or for 
at least 3  months prior to collection;  
b. showed no clinical sign of CSF on the day of collection of the semen;  
2. the semen was collected, processed and stored in confo rmity with the provisions of 
Chapter  4.5. and Chapter  4.6. 
Article 15.3.9.   Recommendations for importation from CSF infected countries or zones  
Veterinary Authorities  should require the presentation of an international veterinary 
certificate attesting tha t: 
1. the donor animals:  
a. were kept in a compartment  free of CSF since birth or for at least 
3 months prior to collection;  
b. showed no clinical sign of CSF on the day of collection of the semen and 
for the following 40 days;  
c. met one of the following conditions:  
i. have not been vaccinated against CSF and were subjected to a serological 
test performed at least 21 days after collection, with negative results; or  
ii. have been vaccinated against CSF and were subjected to a serological test 
in accordance with the Terrestri al Manual  performed at least 21 days after 
collection and it has been conclusively demonstrated that any antibody is 
due to the vaccine; or  
iii. have been vaccinated against CSF and were subjected to a virological test 
performed in accordance with the Terrestri al Manual  on a sample taken on 
the day of collection and it has been conclusively demonstrated that the boar is negative for virus genome;  
2. the semen was collected, processed and stored in conformity with the provisions of Chapter  4.5. and Chapter  4.6. 
Chap ters 4.5 and 4.6 of the Code  (OIE 2009a)  contain requirements for CSF for boars standing 
at semen collection centres.  Under these requirements, boars  must be clinically healthy, 
physiologically normal, kept in a CSF -free zone or compartment since birth or for the past three 
months  prior to entry into isolation at the quarantine station of  the semen collection facility , and 
neither be vaccinated against CS F nor the progeny of vaccinated sows  (unless there are OIE 
validated means of distinguishing vaccinated and infected pigs) .  Boars must remain in this  
Ministry for Primary Industries  Import risk analysis: Pig semen • 32 quarantine station for at least 28 days and, at least 21 days after entering the quarantine statio n 
must be tested negative for CSF  as per Articles 15.3.8 of 15.3.9 of the Code .  In countries, zones 
or compa rtments which are not free of CSF , any boars resident in the semen collection facility 
must also be tested at least annually as per Articles 15.3.8 or 15. 3.9 of the  Code . 
 
Available options, for exclusion of both CSFV and BVDV -2 are:  
Option 1  
Semen originating from collection centres certified as compliant with OIE Code Chapters 4.5 
and 4.6 could be considered suitable for importation.  
Option 2  
Every batch  of semen to be imported could be tested by a group- specific reverse transcriptase 
PCR test that detects all relevant pestiviruses (Drew 2008a; Nettleton and Willoughby 2008 ; 
Vilcek et al 1994) . A positive test on any batch of semen could result in disqualification of that 
semen.  
Option 3  
Donor boars could have lived their entire lives in countries that are free from  both CSFV and 
BVDV- 2.  
 
 
References  
References marked * were sighted as summaries in electronic media sources.  
Barkema HW, Bartels CJ, van Wuijckhuise L, Hesselink JW, Holzhauer M, Weber MF, Franken P, Kock 
PA, Bruschke CJ, Zimmer GM (2001). Outbreak of bovine virus diarrhea on Dutch dairy far ms induced by a 
bovine herpesvirus 1 marker vaccine contaminated with bovine virus diarrhea virus type 2. Tijdschrif voor 
Diergeneeskunde , 126(6), 158-65.* 
 Center for Food Security and Public Health (2009). Classical swine fever. Available at: http://www. cfsph.iastate.edu/Factsheets/pdfs/classical_swine_fever.pdf  
 
Choi C, Chae C (2003).  Detection of classical swine fever virus in boar semen by reverse transcription -polymerase 
chain reaction. Journal of Veterinary Diagnostic Investigation, 15(1), 35-41.  
 
Clement F (2009)  Re: Import risk analysis: Pig semen from Australia, the USA, Canada, the European Union and 
Norway – Draft for public consultation.  Personal communication. Letter to Reed CE, 4 November 2009.  
 
Cranwell MP, Jones JR, Wakeley PR (2005).  BVD v irus type 2 in British cattle. Veterinary Record, 156(8), 257 -
8. 
 
De Smit AJ, Bouma A, Terpstra C, Van Oirschot JT (1999).  Transmission of classical swine fever virus by 
artificial insemination. Veterinary Microbiology , 67(4), 239- 49. 
 Drew T (2008a). Bovi ne viral diarrhoea. In: OIE (eds), Manual of Diagnostic Tests and Vaccines for Terrestrial 
Animals . Vol. 2, Pp. 698 -711, OIE, Paris.  
 
Drew T (2008b). Classical swine fever (hog cholera). In: OIE (eds), Manual of Diagnostic Tests and Vaccines  for 
Terrestria l Animals . Vol. 2, Pp. 1092 -106, OIE, Paris.  
 
Drew T, Sandvik T, Wakeley PR, Jones T, Howard P (2002).  BVD virus genotype 2 detected in British cattle. 
Veterinary Record , 151(20), 551.  
  
Ministry for Primary Industries  Import risk analysis: Pig semen • 33 Floegel G, Wehrend A, Depner KR, Fritzemeier J, Waberski D, Moennig V (2000).  Detection of classical swine 
fever virus in semen of infected boars. Veterinary Microbiology , 77(1-2), 109-16.  
 
Horner GW (2000).  Typing of New Zealand strains of pestivirus. Surveillance , 27(3), 16.  
 Kirkland RD, Richards SG, Rothwell JT, Stanley DF (1991). Replication of bovine viral diarrhoea virus in the 
reproductive tract and excretion of virus in semen during acute and chronic infections. Veterinary Record , 128, 587-
90. 
 
Le Potier M -F, Mesplede A, Vannier P (2006).  Classical swine fever and ot her pestiviruses. In: Straw BE, 
Zimmerman JJ, D'Allaire S, Taylor DJ (eds), Diseases of Swine . 9th edition, Pp. 309- 22, Blackwell Publishing, 
Ames, Iowa.  
 
Nettleton PF (2004).  Border disease. In: Coetzer JAW, Tustin RC (eds), Infectious Diseases of Livestock . Vol. 2, 
Pp. 970-4, Oxford University Press, Cape Town.  
 Nettleton PF, Gunn G (2002).  BVD virus genotype 2 in British cattle. Veterinary Record , 151(20), 616.  
 
Nettleton PF, Willoughby K (2008). Border disease. In: OIE (eds), Manual of Diagnostic Tests and Vaccines for 
Terrestrial Animals. Vol. 2, Pp. 1041 -50, OIE, Paris.  
 
OIE (2008a).  Terrestrial Animal Health Code . 
http://www.oie.int/eng/normes/MCode/en_sommaire.htm , 
downloaded 27/1/2 009.  
 
OIE (2008b). World Animal Health Information Database (WAHID) Interface. http://www.oie.int/wahid -
prod/public.php?page=home , downloaded 27/1/2009.  
 
Pogranichniy RM, Schwartz KJ, Yo on K -J (2008) . Isolation of a novel viral agent associated with porcine 
reproductive and neurological syndrome and reproduction of the disease. Veterinary Microbiology  131, 35 -46. 
 
Potgieter LND (2004).  Bovine viral diarrhoea and mucosal disease. In: Coetz er JAW, Tustin RC (eds), Infectious 
Diseases of Livestock . Vol. 2, Pp. 946 -69, Oxford University Press, Cape Town.  
 Sandvik T, Paton DJ, Lowings PJ (1997).  Detection and identification or ruminant and porcine pestiviruses by 
nested amplification of the 5' untranslated cDNA regions. Virological Methods , 1, 43 -56.* 
 Thiel HJ, Collett MS, Gould EA, Heinz EX, Houghton M, Meyers G, Purcell RH, Rice CM (2005).  Genus  
Pestivirus . In: Fauquet CM, Mayo MA, Maniloff J, Desselberger U, Ball LA (eds), Eighth Report of the 
International Committee on Taxonomy of Viruses . Pp. 988 -92, Elsevier Academic Press, Amsterdam.  
 
Van Oirschot JT (2004). Hog cholera. In: Coetzer JAW, Tustin RC (eds), Infectious Diseases of Livestock . Vol. 2, 
Pp. 975-86, Oxford University Press, Cape Town.  
 
Vilcek S, Bjorklund HV, Horner GW, Meers J, Belak S (1998). Genetic typing of pestiviruses from New 
Zealand. New Zealand Veterinary Journal , 46, 35 -7. 
 
Vilcek S, Durkovic B, Bobakova M, Sharp G, Paton DJ (2002). Identification of bovine viral diarrh oea virus 2 in 
cattle in Slovakia. Veterinary Record , 151(5), 150-2.  
 Vilcek S, Herring AJ, Herring JA, Nettleton PF, Lowings JP, Paton DJ (1994).  Pestiviruses isolated from pigs, 
cattle and sheep can be allocated into at least three genogroups using polym erase chain reaction and restriction 
endonuclease analysis. Archives of Virology , 136(3- 4), 309 -23. 
 
  
Ministry for Primary Industries  Import risk analysis: Pig semen • 34 11. Eastern equine encephalomyelitis virus 
11.1. HAZARD IDENTIFICATIO N 
11.1.1.  Aetiological agent  
Family: Togaviridae , Genus: Alphavirus , Species: Eastern equine encephal omyelitis virus  
(EEEV) (Weaver et al 2005) . 
11.1.2.  OIE list  
Listed (OIE 2008) . 
11.1.3.  New Zealand status  
Notifiable disease (MAF 2008) . 
11.1.4.  Epidemiology  
EEEV is endemic in the eastern USA .  It is transmitted between birds by the mosquito Culiseta 
(Climacura) melanura, which frequents wetlands in the southern and southeastern USA, 
particularly those with peat -muck soil dominated with hardwood trees. These wet and murky 
habitats and hardwood r oot systems favour oviposition by C. (C.) melanura,  as its larvae require 
water with a high content of organic matter and protection from sunlight for development. 
Female C. (C.) melanura feed almost exclusively on birds, especially passerines, which maint ain 
the cycle of infection by the development of high viraemias. Because C. (C.) melanura is highly 
ornithophilic, other vectors are probably responsible for affecting the escape of the virus from 
the bird/mosquito cycle.  Coquillettidia perturbans  is susp ected of fulfilling this role, as it feeds 
on mammals and birds equally. Cases of encephalitis caused by EEEV tend to occur within 8 km of swampy habitats, which is within the flight range of C.  perturbans  (Gibbs 2004).  
Although EEEV has been isolated fro m over 20 different mosquito species in six genera, its 
establishment has been shown to require specific ecological conditions such as those found in 
hardwood wetlands of southeastern USA, particularly the presence of the highly ornithophilic mosquito C. (C.) melanura, and the specific passerine birds on which it feeds. This mosquito 
vector is not present in New Zealand (Belkin 1968) and neither are the specific passerines nor the forest ecosystems that it inhabits.  
EEEV  is mainly responsible for disease ou tbreaks in humans and horses, but has also been 
involved in outbreaks of disease in pigs (Elvinger et al 1994; Elvinger et al 1996a; Elvinger et al 
1996b) . In general, mammals are considered dead -end hosts because the very low virus titres that 
develop are insufficient to infect vectors. However, nursing pigs that were infected experim entally developed a high -titre viraemia that lasted up to 168 hours after infection, and 
virus could be isolated from oropharyngeal and rectal swabs up to 96 hours after infection (Elvinger and Baldwin 2006).  Experimental infection has been achieved by in tracranial, 
intradermal, intravenous, and oral routes of virus administration (Elvinger and Baldwin 2006).  However, there are no reports suggesting virus can be transmitted in porcine semen.  
11.1.5.  Hazard identification conclusion 
There is no evidence to suggest  that t ransmission of EEV by semen should be considered likely , 
so the virus is not identified as  a hazard in pig semen .  
  
Ministry for Primary Industries  Import risk analysis: Pig semen • 35 References  
 
Belkin JN (1968).   Mosquito Studies VII. The culicidae of New Zealand.  Contributions of the American 
Entomological Insti tute Vol 3, No. 1, 1968.  
 
Elvinger F, Baldwin CA, Liggett AD, Tang KN, Dove CR (1996a). Protection of pigs by vaccination of pregnant sows against eastern equine encephalomyelitis virus. Veterinary Microbiology , 51(3-4), 229-39.  
 
Elving er F, Baldwin CA, Liggett AD, Tang KN, Stallknecht DE (1996b) . Prevalence of exposure to eastern 
equine encephalomyelitis virus in domestic and feral swine in Georgia. Journal of Veterinary Diagnostic 
Investigation , 8(4), 481-4.  
 
Elvinger F, Liggett AD, Tang KN, Harrison LR, Cole JR, Jr., Baldwin CA, Nessmith WB (1994) . Eastern 
equine encephalomyelitis virus infection in swine. Journal of the American Veterinary Medical Association , 205(7), 
1014-6.  
 Elvinger F, Baldwin CA (2006).  Eastern Equine Encephalomye litis Virus. In: Straw BE, Zimmerman JJ, D'Allaire 
S, Taylor DJ (eds),  Diseases of Swine . 9th edition, Pp. 554-7, Blackwell Publishing, Ames, Iowa.  
 Gibbs EPJ (2004).  Equine encephalitides caused by alphaviruses . In: Coetzer JAW, Tustin RC (eds), Infectious 
Diseases of Livestock . Vol. 2, Pp. 1014- 22, Oxford University Press, Cape Town.  
 MAF (2008). The Unwanted Organisms Register. 
http://mafuwsp6.maf.govt.nz/uor/searchframe.htm , downloaded 
27/1/2009.  
 OIE (2008) . Terrestrial Animal Health Code. 
http://www.oie.int/eng/normes/MCode/en_sommaire.htm , 
downloaded 27/1/2009.  
 Weaver SC, Frey TK, Huang HV, Kinney RM, Rice CM, Roehrig  JT, Shope RE, Strauss EG (2005).  Genus  
Alphavirus . In: Fauquet CM, Mayo MA, Maniloff J, Desselberger U, Ball LA (eds), Eighth Report of the 
International Committee on Taxonomy of Viruses . Pp. 1003 -5, Elsevier Academic Press, Amsterdam.  
  
Ministry for Primary Industries  Import risk analysis: Pig semen • 36 12. Porcine haemagg lutinating encephalomyelitis virus  
12.1. HAZARD IDENTIFICATIO N 
12.1.1.  Aetiological agent  
Family: Coronaviridae , Genus: Coronavirus , Species: Porcine haemagglutinating 
encephalomyelitis virus (Spaan et al 2005) . 
12.1.2.  OIE list  
Not listed.  
12.1.3.  New Zealand status  
It is classified as an “other exotic virus” (MAF 2008) . 
12.1.4.  Epidemiology  
The virus occurs commonly in pigs and is probably distributed world- wide. It has not been 
described in New Zealand, but this may reflect a lack of investigation rather than true absence of 
the virus.  
The disease syndrome caused by this virus has been well described in several reviews (Andries 
1989; P ensaert 2004; Pensaert 2006) . Outbreaks of disease are rare and are usually confined to 
neonatal pigs which are susceptible to the virus unless protected by colostral antibody. Older pigs are resistant and infections are subclinical, but they develop anti body to the virus. If the 
virus is introduced into an immunologically naïve pig herd, young pigs develop signs which may include vomiting and wasting followed by severe encephalomyelitis and high mortality. Such 
outbreaks are generally self -limiting, lasti ng only a few weeks until sows have developed 
immunity. The incubation period under experimental conditions was 4 days. In natural outbreaks piglets as young as 2 days old may develop signs of infection, but the incubation period is 
usually considered to b e 4-7 days. Pigs older than 4 -5 weeks develop an age -related resistance to 
the disease and 43 -98 per cent of pigs are serologically positive in infected regions. Pigs excrete 
the virus in oronasal secretions for 8 -10 days and transmission is from exposure to nasal 
secretions. Long -term carriers are not described. Spread to the central nervous system is along 
nerve tracts and viraemia is believed to be of little importance in the pathogenesis of the disease. 
There is no evidence that the virus is excreted in  semen.  
12.1.5.  Hazard identification conclusion 
The disease is predominantly one of young pigs; animals older than 4 -5 weeks are resistant to the 
disease. Adult semen donors are therefore unlikely to be infected with the virus and there is no 
evidence that the vi rus is transmitted in semen. Therefore the virus is not identified as  a hazard in 
the commodity.  
 
References  
 
Andries K (1989).  Haemagglutinating encephalomyelitis virus. In: Pensaert MB (ed), Virus Infections of Porcines . 
Pp. 177-85, Elsevier, Amsterdam.  
 
MAF (2008). The Unwanted Organisms Register. http://mafuwsp6.maf.govt.nz/uor/searchframe.htm , downloaded 
27/1/2009.   
Ministry for Primary Industries  Import risk analysis: Pig semen • 37  
Pensaert MB (2004).  Haemagglutinating encephalomyel itis virus infection. In: Coetzer JAW, Tustin RC (eds), 
Infectious Diseases of Livestock . Vol. 2, Pp. 791 -4, Oxford University Press, Cape Town.  
 Pensaert MB (2006).  Hemagglutinating encephalomyelitis virus. In: Straw BE, Zimmerman JJ, D'Allaire S, Taylor 
DJ (eds), Diseases of Swine . 9th edition, Pp. 353-8, Blackwell Publishing, Ames, Iowa.  
 
Spaan WJM, Brian D, Cavanagh D, de Groot R, J, Enjuanes L, Gorbalenya AE, Holmes KV, Masters P, 
Rottier P, Taguchi F, Talbot P (2005).  Genus  Coronavirus . In: Fauquet CM , Mayo MA, Maniloff J, Desselberger 
U, Ball LA (eds), Eighth Report of the International Committee on Taxonomy of Viruses . Pp. 947-55., Elsevier 
Academic Press, Amsterdam.  
  
Ministry for Primary Industries  Import risk analysis: Pig semen • 38 13. Foot and mouth disease virus  
13.1. HAZARD IDENTIFICATIO N 
13.1.1.  Aetiological agent  
Family: Pic ornaviridae; Genus: Apthovirus, foot and mouth disease virus (FMDV). There are 
seven serotypes of the virus: O, A, C, SAT 1, SAT 2, SAT 3 and Asia 1 (OIE 2009).  
13.1.2.  OIE list  
Foot and mouth disease (FMD) is listed within the category of multiple species disease s. 
13.1.3.  New Zealand status  
FMD is an exotic notifiable disease that has never occurred here.  
13.1.4.  Epidemiology  
The disease has been eradicated from or has not occurred in North America, Australia and many 
European countries.  FMD is a highly contagious viral disease that causes high fever, vesicular 
lesions and ulcerations. FMD is considered the most contagious and economically devastating animal disease. The outbreaks of the disease in Britain in 2001 (Thompson et al 2002)  and in 
Taiwan in 1997 (Yang et al 1999)  cost those countries billions of dollars.  
 
The disease is widespread occurring endemically in areas o f South America, Africa and Asia. 
Currently, there are many unresolved disease events, including outbreaks in Europe (Bulgaria), China, North and South Korea, and South Africa (WAHID 2011).  
 Host species include cattle, zebus, domestic buffaloes, yaks, sheep, goats, swine, all wild 
rumin ants, wild Suidae  and members of the Camelidae  family. Although all cloven hoofed 
animals  are susceptible, expression of disease is variable from severe clinical signs to  inapparent 
infections (OIE 2009). Sheep may show no c linical signs whilst infectious , and pigs are an 
important amplifying host.  
 
The incubation period ranges from 2 -14 days. However, for the purposes of the Code  the 
incubation period is considered to be 14 days. Morbidity in domestic species is near 100% b ut is 
variable in wildlife. About 15 -50% of cattle become carriers following infection. The virus may 
persist in the pharyngeal region for up to 3.5 years. The virus type influences the duration of the carrier state. However, carriers are not epidemiologically important since evidence suggests that 
they do not act as a source of infection (USAHA 2008) . In pigs, a carrier state does not occur 
(Farez and Morley 1997).  
 
The levels of virus present in animals peak at around the time of onset of clinical signs, but 
significant levels of virus may be p resent before this time. FMDV  infected animals may excrete 
virus 4 days prior to clinical signs appearing (Geering et al 1995).   
 
Seven immunologically distinct types of FMDV have been identified. For each virus type, 
immunologically related subtypes also exist, creating 60 known type -subtype combinations. 
During an infection, virus recombinations, mutations , and host selection result in the constant 
generation of new FMD variants, creating challenges in vaccine strain selection (USAHA 2008) .   
Ministry for Primary Industries  Import risk analysis: Pig semen • 39  
Vaccination reduces virus shedding and prevents clin ical signs but does not necessarily prevent 
infection. Potent and highly purified vaccines protect animals from disease within 4- 6 days post 
vaccination. Vaccinated or u n-vaccinated animals that are infected with FMDV produce 
antibod ies to both non- structu ral and structural proteins. Vaccinated animals that are not infected 
with FMDV only produce antibodies to the structural proteins  (OIE 2009) . This feature permits 
serological tests to differentiate non -infected vaccinated animals from infected vaccinated 
animals.  
 Transmission occurs by direct contact with infected animals that excrete the virus in saliva, 
faeces, urine, milk, semen, ocular , and nasal discharges.  Infected animal products , contaminated 
objects , and transmission by aerosol for distances up to 60 km overland and 300 km by sea have 
been reported  (Gloster et al 1982) .  
13.1.5.  Hazard identification conclusion  
FMDV is identified as a potential hazard in porcine semen.  
13.2. RISK ASSESSMENT  
13.2.1.  Entry assessment  
Following infection, FMDV spreads from the original site of infection to the testes and accessory glands via the lymphatics and blood stream, and the virus may also multiply in the skin around 
the preputial orifice (Guérin and Pozzi 2005).  
FMDV has been isolated from porcine semen (Thacker et al 1984).   Mor e recently, quantitative 
real-time polymerase cha in reaction tests have shown that FMDV can be detected in the semen 
of an infected boar as soon as 1 day after infection (van Rijn et al 2004).  
The likelihood of entry is assessed to be high.  
13.2.2.  Exposure assessment  
Although artificial insemination using contaminated semen did not transmit infection to 
inseminated sows (McVicar et al 1977), these transmission studies have not been repeated.  
However, p igs are recognised to be important amplifying hosts for FMDV and are much more 
susceptible to infection by the oral route than are ruminants (AQIS 2000).  
The likeliho od exp osure is assessed to be low.  
13.2.3.  Consequence assessment  
Animals that become infected could become the focal point for an outbreak of foot and mouth 
disease. Where large numbers of pigs are infected, airborne spread over considerable distances 
has been described.  For example, the virus was transmitted by favourable winds from Brittany in France to the Isle of Wight in England (Gloster et al 1982) . Infected individuals may  infect 
fomites and t he movement of infected pigs could result in widespread exposure of other 
susceptible cloven -hoofed animals.  
 An outbreak  of FMDV  would cause serious disruption to the livestock industries, economic 
losses to individual farmers, very large expenses for an  eradication campaign, and significant 
disruption to export markets for both animals and animal products. The overall effects could be 
catastrophic as dramatically demonstrated by the losses that resulted from an outbreak of the  
Ministry for Primary Industries  Import risk analysis: Pig semen • 40 disease in Britain where th e costs to government were estimated at 3.1 billion pounds 
(Thompson et al 2002) . 
 
Foot and mouth disease infection of humans is extr emely rare and of no importance (Sanson 
1994) . Therefore, there would be negligible consequences for human health.  
 
The virus infects cloven -hoofed animals and could infect feral pigs, goats and deer thereby 
establishing the disease in feral populations, which could constitute an ongoing source of infection for domestic stock.  
 The cons equences are assessed to be high.  
13.2.4.  Risk estimation  
Entry, exposure and consequence have all been assessed as non -negligible. As a result the risk 
estimate for FMDV is non -negligible and it is assessed to be a risk in the commodity. Therefore 
risk management  measures can be justified.  
13.3. RISK MANAGEMENT  
13.3.1.  Options  
Article 8.5.15.  of the OIE Code  recommends that, for fresh porcine semen imported from FMD 
free countries or zones where vaccination is not practised or FMD free compartments , Veterinary 
Authorities  should require the presentation of an international veterinary certificate attesting that:  
1. the donor animals : 
a. showed no clinical sign of FMD on the day of collection of the semen;  
b. were kept for at least three months prior to collection in a FMD free country o r 
zone  where vaccination  is not practised or a FMD free compartment ; 
2. the semen was collected, processed and stored in conformity with the provisions of 
Chapters  4.5. and 4.6.  
Article 8.5.16.  of the OIE Code  recommends that , for f rozen p orcine semen import ed from FMD 
free countries or zones where vaccination is not practised or FMD free compartments , Veterinary 
Authorities  should require the presentation of an international veterinary certificate attesting that:  
1. the donor animals : 
a. showed no clinical sign of  FMD on the day of collection of the semen and for the 
following 30  days;  
b. were kept for at least three months prior to collection in an FMD free country or 
zone  where vaccination  is not practised or a FMD free compartment ; 
2. the semen was collected, processed and stored in conformity with the provisions of 
Chapters  4.5. and 4.6.  
Article 8.5.17.  of the OIE Code recommends that , for p orcine semen imported from FMD free 
countries or zones where vaccination is practised , Veterinary Authorities  should require the  
presentation of an international veterinary certificate attesting that:  
1. the donor animals :  
Ministry for Primary Industries  Import risk analysis: Pig semen • 41 a. showed no clinical sign of FMD on the day of collection of the semen and for the 
following 30  days;  
b. were kept for at least three months prior to collection in a FMD  free country or 
zone ; 
c. if destined to an FMD free country or zone  where vaccination  is not practised:  
i. have not been vaccinated and were subjected, not less than 21  days after 
collection of the semen, to tests for antibodies against FMD virus, with negative  results; or  
ii. had been vaccinated at least twice, with the last vaccination not more 
than 12  and not less than one  month prior to collection;  
2. no other animal  present in the artificial insemination centre  has been vaccinated within 
the month prior to collec tion; 
3. the semen:  
a. was collected, processed and stored in conformity with the provisions of Chapters  4.5. and 4.6.;  
b. was stored in the country of origin for a period of at least one month following collection, and during this period no animal on the establish ment  where the donor 
animals  were kept showed any sign of FMD.  
Article 8.5.18.  of the OIE Code recommends that, for porcine semen imported from FMD infected 
countries or zones , Veterinary Authorities  should require the presentation of an international 
veterinary certificate  attesting that:  
1. the donor animals : 
a. showed no clinical sign of FMD on the day of collection of the semen;  
b. were kept in an establishment  where no animal  had been added in the 30 days 
before collection, and that FMD has not occurred within 10 kilometres for the 
30 days before and after collection;  
c. have not been vaccinated and were subjected, not less than 21  days after 
collection of the semen, to tests for antibodies against FMD virus, with negative 
results; or  
d. had been vaccinated at least t wice, with the last vaccination not more than 12  and 
not less than one month prior to collection;  
2. no other animal  present in the artificial insemination centre  has been vaccinated within 
the month prior to collection;  
3. the semen:  
a. was collected, processed an d stored in conformity with the provisions of 
Chapters  4.5. and 4.6.;  
b. was subjected, with negative results, to a test for FMDV infection  if the donor 
animal has been vaccinated within the 12  months prior to collection;  
c. was stored in the country of origin f or a period of at least one month following 
collection, and that during this period no animal  on the establishment  where the 
donor animals  were kept showed any sign of FMD.  
Because of the extreme seriousness of the disease and the catastrophic consequences  that would 
result from its introduction, it may be concluded that importation of porcine semen should be limited to countries or zones that are free of FMDV in accordance with the OIE Code , or 
countries or zones in which compliance with measures in accord ance with the recommendations  
Ministry for Primary Industries  Import risk analysis: Pig semen • 42 of the OIE Code  for import of germplasm from FMD infected countries or zones has b een 
reviewed and accepted by MPI . 
The following options could be considered to effectively manage the risk:  
Option 1  
The international standards  described in articles 8.5.15 to 8.5.18. of the OIE Code  could be 
adopted to effectively manage the risk associated with FMDV in porcine semen.  
Option 2  
In addition to the measures described in Option 1, MPI may also require approval of  each semen 
collecti on and processing and storage facility/ies in the exporting country intended to be used 
during the preparation of an export  consignment to New Zealand. This approval may  be 
dependent  on the facility, its location and operating standards and that t he verifi cation systems of 
the Veterinary A uthority achieve a very high level of risk managem ent for FMD. The process for 
MPI approval may include site inspection. MPI  may also reserve  the right to supervise 
collection, require the use of New Zealand approved semen  collection personnel, or require any 
other measures deemed necessary to ensure compliance with facility and operating standards 
upon which the approval is based.  
Option 3  
Imports of porci ne semen could be limited to countries recognised to be free of FMDV  without 
vaccination . 
 
References  
 
AQIS (2000). Porcine semen import risk analysis: Risk assessment and risk management options. Australian 
Quarantine and Inspection Service, Canberra, Australia.  
 Farez S, Morley RS (1997).  Potential animal health hazards of pork and pork products. Review Scientifique et 
Technique , OIE , 16, 65-78. 
 
Geering WA, Forman AJ, Nunn MJ (1995). Exotic Disease of Animals: A field guide for Australian 
veterinarians, Australian Government Publishing Service, Canberra.  
 
Gloster J, Sel lers RF, Donaldson AI (1982).  Long distance spread of foot and mouth disease virus over the sea. 
Veterinary Record , 110, 47- 52. 
Guérin B, Pozzi N (2005).  Viruses in boar semen: detection and clinical as well as epidemiological consequences 
regarding diseas e transmission by artificial insemination. Theriogenology  63, 556 -572.  
McVicar JW, Eisner RJ, Johnson LA (1977). Foot and mouth disease and swine vesicular disease viruses in boar semen. Proce edings of the Annual Meeting of the United States Animal Heal th Association , 81, 231-243.  
 
OIE (2009).  Foot and Mouth Disease. In Terrestrial Manual . Available at: 
http://www.oie.int/fileadmin/Home/eng/Health_standards/tahm/2.01.05_FMD.pdf.  
 
Sanson RL (1994).  The epidemiology of foot -and-mouth disease: Implications for  New Zealand. New Zealand 
Veterinary Journal , 42, 41 -53. 
 Thacker BJ, Larse RE, Joo HS, Leman AD (1984). Swine diseases transmissible with artificial insemination. 
Journal of the American Veterinary Medical Association, 185, 511-516.  
  
Ministry for Primary Industries  Import risk analysis: Pig semen • 43 Thompson D, Muriel P,  Russell D, Osborne P, Bromley A, Rowland M, Creigh -Tyte S, Brown C (2002).  
Economic costs of the foot and mouth disease outbreak in the United Kingdom in 2001. Revue Scientifique et 
Technique, OIE, 21(3), 675-87.  
 
USAHA (2008).  United States Animal Health  Association. Foot and mouth disease. In Foreign Animal Diseases , 
Boca publications group, Boca Raton, pp. 261 -276.  
 
van Rijn PA, Wellenberg GJ, der Honing RH, Jacobs L, Moonen PLJM, Feitsma H (2004) Detection of 
economically important viruses in boar seme n by quantitative RealTime PCR technology. Journal of Virological 
Methods 120, 151- 60. 
 
WAHID (2011).  Home page for World Animal Health Information Database. Available at:  
http://web.oie.int/wahis/public.php?page=home&admin=0&newlang=1.  
 Yang PC, Chu RM, Chung WB, Sung HT (1999).  Epidemiological characteristics and economic costs of the foot 
and mouth disease epidemic in Taiwan. Veterinary Record , 145(25), 731-4.  
  
Ministry for Primary Industries  Import risk analysis: Pig semen • 44 14. Japanese encephalitis virus  
14.1. HAZARD IDENTIFICATIO N 
14.1.1.  Aetiological agent  
Family: Flaviviridae , Genus: Flavivirus , Species: Japanese encephalitis virus  (JEV) (Thiel et al 
2005) . 
14.1.2.  OIE list  
Listed (OIE 2008) .  
14.1.3.  New Zealand status  
Exotic notifiable organism (MAF 2008) . 
14.1.4.  Epidemiology  
Japanese encephalitis is a zoonosis that results in 30 -50,000 human disease cases per year in the 
parts of Asia where it is endemic (CDC 2006) . The causative virus is maintained in a bird 
(particularly egrets an d herons) to mosquito cycle. Pigs are the primary amplifying host (Geering 
et al 1995) . Infection of humans and horses may cause a severe and often fatal encephalitis. 
Although clinical signs are not common in pigs in endemic areas, there can be significant rates of 
abortion in immunologically naive sows (Hoke and Gingrich 1994; Platt and Joo 2006). 
Inapparent infections also occur in goats, sheep, cattle, and dogs, and have been reported in cats, rodents, bats, snakes, and frogs (Geering et al 19 95). 
Flaviviruses exhibit a high degree of specificity in their ability to infect and be transmitted by individual insect species, or even strains of individual species. Vector competence is under 
genetic control, with the susceptibility of the midgut epit helium being the primary determinant. 
In a susceptible insect, a sufficient concentration of the virus must be ingested to exceed the midgut infection threshold (Monath and Heinz 1996).   
Although 28 mosquito species have exhibited vector competence for JE V in field and laboratory 
studies, only a few species found in endemic areas develop sufficient abundance, have long 
enough flight ranges, exhibit sufficient longevity, and have the breadth of host feeding 
preferences to become natural vectors (Hoke and Gr ingrich 1994). In mainland Japan and 
Okinawa, the Philippines, the Korean peninsula, China, Taiwan, the Indochina peninsula (except Malaysia), Indonesia, Sri Lanka, India, and Nepal, the primary vectors belong to the Culex 
vishnui  group, mainly Cx. tritaen iorhynchus .  However, other mosquitoes are important vectors 
locally. These include Cx. vishnui in India, Thailand, and Taiwan, Cx. fuscocephala in Malaysia, 
Thailand and Taiwan, Cx. gelidus  in Indonesia, Thailand, and Vietnam, and Cx. annulus in 
Taiwan.  The type of available larval habitat determines which species will predominate.  Both 
Cx. tritaeniorhynchus  and Cx. vishnui  breed predominantly in rice paddies and are therefore the 
most important rural vectors (Hoke and Gingrich 1994).  
None of the above mosquito species are present in New Zealand (Belkin 1968). Nevertheless, t he 
introduced mosquito Cx. quinquefasciatus has been shown to be a competent vector of the virus under laboratory conditions, and the virus has also been isolated from naturally infe cted 
mosquitoes of this species (Van den Hurk et al 2003) .  
Ministry for Primary Industries  Import risk analysis: Pig semen • 45 JEV occurs throughout the temperate and tropical regions of Asia and has also spread to 
Indonesia, northern Australia, Papua New Guinea and possibly Pakistan (Center for Food 
Security and Public Health 2007). Despite rare appearances in northern Australia, the virus 
remains largely confined to the endemic areas of Asia and it is highly dou btful whether it could 
establish in New Zealand if introduced. The occurrence of JEV in Australia is sporadic and  
confined to the far northern regions and the Torres Strait islands (Johansen et al 2003; Liu et al 
2005; Mackenzie et al 1994; Ritchie and Rochester 2001) . 
JEV has been isolated from the testicles of boars with orchitis and from the semen  of infected 
boars for up to 5 weeks following infection ( Ogasa et al 1977; Guérin  1995).  
14.1.5.  Hazard identification conclusion  
Transmission by semen has been described . Therefore, JEV is identified as  a potential hazard in 
pig semen from infected areas.  
14.2. RISK  ASSESSMENT  
14.2.1.  Entry assessment  
Mosquitoes blown from Papua New Guinea seem to have been responsible for outbreaks of JE in 
the Torres Strait islands since 1995 and in Northern Australia in 1998, but there i s no evidence 
that the virus may  become established on the Australian mainland (Russell 1998). The last report 
of the virus on Australian territory involved a seropositive pig on a northern island in the Torres Strait, and it remains exotic to the Australian mainland (Anonymous 2007).  
Therefore the likeliho od of entry in pig semen from  countries where JEV is endemic or from  
northern Australia is assessed  to be non- negligible . 
14.2.2.  Exposure assessment  
Exposure in the first instance would be limited to inseminated animals. In view of the highly 
complex natural hist ory of this disease, which involves species of birds and high densities of pigs 
and insects in climates and ecosystems which are not found in New Zealand, even if the virus 
were introduced into New Zealand in this way it is extremely unlikely that any tran smission 
would occur. Climatographs, plotted on a monthly basis (Gerlach 1974), show that the hottest part of New Zealand is the far North in the month of February.  The mean daily temperature in 
that month is 20ºC (the mean daily minimum and the mean dail y maximum during that month is 
17ºC and 29ºC respectively).  However, summer is also the driest time of the year in New Zealand; the mean February rainfall in Northland is less than 100 mm.  Thus, even if a suitable 
vector did exist in New Zealand, the tim e of the year with the most suitable temperature for the 
development of the virus in vectors would be least suitable for the build -up of high vector 
densities.  In addition, amplification of the virus requires a high density of seronegative pigs, 
which wou ld probably only be found in areas where intensive pig production is practised, and 
this is limited in most parts of New Zealand, especially in the far north.  
Considering that the virus has never established outside the endemic areas of Asia, the absence 
of major mosquito vectors, the unsuitable climate and the absence of high densities of pigs, it is 
considered highly unlikely that JEV could establish in New Zealand. However, in view of the presence of a potential mosquito vector in this country, the likel ihood of exposure is assessed  to 
be non- negligible.   
Ministry for Primary Industries  Import risk analysis: Pig semen • 46 14.2.3.  Consequence assessment  
In the unlikely event that any consequences were to result from the insemination of sows with 
imported semen that might harbour JEV, the se would in the first instance be restricted  to the 
animals that were inseminated. The primary disease manifestation of infection in sows and gilts is abortion and abnormal farrowings. Sexually mature swine do not show any significant clinical 
signs of infection, but transient anorexia and a mild fe brile response have been observed (Platt 
and Joo 2006). As there are no reports of disease in non -pregnant sows, it is concluded that the 
immediate consequences of insemination with infected semen would be negligible.   
For any secondary consequences to ar ise beyond the inseminated sows, there would need to be 
viraemia in the inseminated animal and transmission by a competent vector mosquito. While the 
likelihood of this occurring in New Zealand is very low, for the purposes of this risk analysis it is 
assessed to be non- negligible.  
Infection of humans and horses may result in a severe and often fatal encephalitis. Further, if the virus were transmissible via mosquitoes in this country, there could be some level of abortions in 
immunologically naïve sows (H oke and Gingrich 1994).  
Therefore the consequences for infected humans, pigs and horses would be non -negligible .  As 
infections in other species are asymptomatic, the environmental consequences would be 
negligible.  
14.2.4.  Risk estimation  
Entry, exposure and cons equence assessments are non -negligible. Therefore, JEV is assessed to 
be a risk in semen from countries where the virus is endemic or n orthern Australia.  
14.3. RISK MANAGEMENT  
14.3.1.  Options  
The OIE Code  does not include recommendations for managing the risk of JEV in  semen of any 
species.  
The options available for managing the risk of the virus in the commodity are:  
Option 1  
Semen donors could be tested for presence of antibody at the time of collection and again 30 
days after collection of semen. Importation of seme n from donors that were positive at the time 
of collection could be permitted on the basis that seropositive animals are not viraemic. Semen from boars that were negative at the time of collection and negative 30 days later could be 
permitted while semen f rom donors that were negative at collection and positive 30 days later  
could be prohibited on the basis that they may have been viraemic at the time of semen collection.  
Option 2  
Importation could be restricted to semen collected from donors resident in regions that are free from JEV.  
References  
References marked * were sighted as summaries in electronic media sources  
Anonymous (2007). Animal Health Surveillance ; Quarterly Report Jan -Mar 2007, Vol 12 Issue 1, p 23.   
  
Ministry for Primary Industries  Import risk analysis: Pig semen • 47 Belkin JN (1968).   Mosquito Studies VI I. The culicidae of New Zealand.  Contributions of the American 
Entomological Institute Vol 3, No. 1.  
 
CDC (2006) . Japanese encephalitis. http://0-www.cdc.gov.mill1.sjlibrary.org/ncidod/dvbid/jencephalitis/index.htm  , 
downloaded 27/1/2009.  
 
Center for Food Security and Public Health (2007). Japanese encephalitis. Available at: 
http://www.cfsph.iastate.edu/Factsheets/pdfs/japanese_encephalitis.p df   
 
Geering WA, Forman AJ, Nunn MJ (1995).  Japanese encephalitis. In: Exotic Diseases of Animals . Pp. 140-4, 
Australian Government Publishing Service, Canberra.  
 
Gerlach JC (1974).   Climatographs of New Zealand.  Ruakura Agricultural Research Centre Rese arch Bulletin 
74-1.  
 Guérin B (1995).  Viral excretion in boar semen and potential for contamination. Reproduction in Domestic 
Animals , 31 (1), 217-23.  
 Hoke CH, Gingrich JB (1994).   Japanese encephalitis.  In : Beran GW (ed).  Handbook of Zoonoses .  Second  
Edition.  Section B: Viral.  Pp 59 -69.  CRC Press, Boca Raton  
 
Johansen CA, Nisbet DJ, Zborowski P, van den Hurk AF, Ritchie SA, Mackenzie JS (2003) . Flavivirus 
isolations from mosquitoes collected from western Cape York Peninsula, Australia, 1999-2000. Journal of the 
American Mosquito Control Association , 19(4), 392-6.  
 
Liu C, Broom AK, Kurucz N, Whelan PI (2005). Communicable Diseases Network Australia: National Arbovirus 
and Malaria Advisory Committee annual report 2004-05. Communicable Disease Intellig ence, 29(4), 341-57.  
 
Mackenzie JS, Lindsay MD, Coelen RJ, Broom AK, Hall RA, Smith DW (1994) . Arboviruses causing human 
disease in the Australasian zoogeographic region. Archives of Virology , 136(3-4), 447- 67.* 
 
MAF (2008). The Unwanted Organisms Register . 
http://mafuwsp6.maf.govt.nz/uor/searchframe.htm , downloaded 
27/1/2009.  
 
Monath TP, Heinz FX (1996).   Flaviviruses.  In : Fields BN, Knipe DM, Howley PM (eds).  Fields Virology .  
Third Edit ion.  Pp 961- 1034.  Lippincott -Raven, Philadelphia.  
 Ogasa A, Yokoki Y, Fujisaki Y, Habu A (1977) Reproductive disorders in boars infected experimentally with 
Japanese encephalitis virus. Japanese Journal of Animal Reproduction  23(4), 171-5.  
 OIE (2008) . Terrestrial Animal Health Code.  
http://www.oie.int/eng/normes/MCode/en_sommaire.htm , 
downloaded 27/1/2009.  
 
Platt KB, Joo HS (2006).  Japanese Encephalomyelitis and West Nile Viruses. In: Straw BE, Zimmerman JJ, 
D'Allaire S, Taylor DJ (eds),  Diseases of Swine . 9th edition, Pp. 359-65, Blackwell Publishing, Ames, Iowa.  
 
Ritchie SA, Rochester W (2001) . Wind -blown mosquitoes and introduction of Japanese encephalitis virus into 
Australia. Emerg ing Infectious Diseases, 7(5). http://www.cdc.gov/ncidod/eid/vol7no5/ritchie.htm , downloaded 
27/1/2009.  
 
Russell RC (1998).   Vectors vs humans in Australia -  who is on top down under?  An u pdate on vector -borne 
disease and research on vectors in Australia. Journal of Vector Ecology  23(1), 1-46..  
 Thiel HJ, Collett MS, Gould EA, Heinz EX, Houghton M, Meyers G, Purcell RH, Rice CM (2005).  Genus   
Flavivirus . In: Fauquet CM, Mayo MA, Maniloff J,  Desselberger U, Ball LA, (eds), Eighth Report of the 
International Committee on Taxonomy of Viruses . Pp. 982 -8, Elsevier Academic Press, Amsterdam.  
 Van den Hurk AF, Nisbet DJ, Hall RA, Kay BH (2003) . Vector competence of Australian mosquitoes (Diptera: 
Culicidae) for Japanese encephalitis virus. Journal of Medical Entomology , 40(1), 82-90.*  
Ministry for Primary Industries  Import risk analysis: Pig semen • 48 15. Kunjin virus  
15.1. HAZARD IDENTIFICATIO N 
15.1.1.  Aetiological agent  
Family: Flaviviridae , Genus: Flavivirus , Species: Kunjin virus  (KUN) (Thiel et al 2005) . 
15.1.2.  OIE list  
Not listed . 
15.1.3.  New Zealand status  
Exotic . 
15.1.4.  Epidemiology  
KUN  is considered to be almost identical to West Nile virus (Spurr and Sandlant 2004) .  It 
occurs widely in Australia where it is considered endemic in the tropical regions of northern 
Western Australia, the Northern Territory, and northern Queensland (Hall e t al 2001; Mackenzie 
et al 2003).   
Human infections give rise to mild fever, headache, photophobia, rash, arthraligia, myalgia and 
lymphadenopathy , although severe encephalitis has also been described (Hall et al 2001).  
The principal mosquito vector of KU N is considered to be Culex annulirostris , although virus 
has also been recovered from Cx. australicus , Cx. squamous , Cx. Quinquefasciatus , and Aedes 
tremulus  (Mackenzie et al 1984).  Birds are the major vertebrate hosts of KUN, particularly 
ardeid waterbi rds of the order Ciconiiformes (Marshall et al 1982).  
Spradbrow (1972) described low -titre serological evidence of exposure of pigs to KUN in 
northern Queensland.  Similarly, serological evidence of infection of feral pigs in New South 
Wales was described by Gard et al (1976).  Experimental inoculation of pigs is followed by low 
levels of detectable antibody (Williams et al 2001).  There is no evidence to suggest that transmission of KUN in porcine semen should be considered likely.  
15.1.5.  Hazard identification co nclusion 
Although there is serological evidence of exposure of pigs in Australia to KUN, they are not 
considered to be a major vertebrate host of this virus and there is no evidence of virus being 
found in the semen of infected pigs.  KUN is not identified  as a hazard in porcine semen.  
 
References  
 
Gard GP, Giles JR, Dwyer -Gray RJ, Woodroofe GM (1976) Serological evidence of inter -epidemic infection of 
feral pigs in New South Wales with Murray Valley Encephalitis virus. Australian Journal of Experimental Bi ology 
and Medical Sciences  54 (3), 297 -302.  
 Hall RA, Scherrer JH, Mackenzie JS (2001) Kunjin virus: An Australian variant of West Nile? Annals of the New 
York Academy of Sciences  951 (1), 153- 60. 
 
Mackenzie JS, Lindsay MD, Coelen RJ, Broom AK, Hall RA, Sm ith DW (1994) Arboviruses causing human 
disease in the Australasian zoogeographic region. Archives of Virology  136, 447-67.  
  
Ministry for Primary Industries  Import risk analysis: Pig semen • 49 Mackenzie JS, Smith DW, Hall RA (2003) West Nile virus: is there a message for Australia? Medical Journal of 
Australia  178 (1), 5- 6. 
 
Marshall ID, Brown BK, Keith K, Gard GP, Thibos E (1982)  Variation in arbovirus infection rates in species of 
birds sampled in a serological survey during an encephalitic epidemic in the Murray Valley of south -eastern 
Australia, February 1974. Australia n Journal of Experimental Biology and Medical Science  60, 471 -8. 
 
Spradbrow PB (1972)  A survey for arbovirus antibodies in pigs and sheep in Queensland. Australian Veterinary 
Journal  48, 402-7.   
 
Spurr EB and Sandlant GR (2004) Preliminary risk assessment for the establishment of West Nile virus in New 
Zealand . Manaaki Whenua Press, Landcare Research, Lincoln, New Zealand.  
 Thiel HJ, Collett MS, Gould EA, Heinz EX, Houghton M, Meyers G, Purcell RH, Rice CM (2005).  Genus   
Flavivirus . In: Fauquet CM, Mayo MA , Maniloff J, Desselberger U, Ball LA, (eds), Eighth Report of the 
International Committee on Taxonomy of Viruses . Pp. 982 -8, Elsevier Academic Press, Amsterdam.  
 Williams DT, Daniels PW, Lunt RA, Wang L-F, Newberry KW, Mackenzie JS (2001)  Experimental inf ections 
of pigs with Japanese encephalitis virus and closely related Australian flaviviruses. American Journal of Tropical 
Medicine and Hygiene 65(4), 379-87.   
Ministry for Primary Industries  Import risk analysis: Pig semen • 50 16. Menangle virus  
16.1. HAZARD IDENTIFICATIO N 
16.1.1.  Aetiological agent  
The International Committee for the Tax onomy of Viruses has identified Menangle virus 
(porcine paramyxovirus) as a tentative species in the genus Rubulavirus of the family 
Paramyxoviridae (Lamb et al 2005) . 
16.1.2.  OIE list  
Not listed.  
16.1.3.  New Zealand status  
The virus is classified as “other exotic vi rus” (MAF 2008) . 
16.1.4.  Epidemiology  
The virus has only been f ound in Australia, where it caused a single outbreak of disease in 1997 
(Chant et al 1998; Kirkland and Stephano 2006; Philbey et al 1998) . All information in this  
section comes from these sources.  
Infection has been associated with reproductive disease including abortions, mummified foetuses 
and congenital defects. During the initial outbreak, returns to mating occurred and 
pseudopregnancy was common. The incubati on period has not been accurately determined and 
the period for which sows remain infected is not known.  A  carrier state does not occur.  
Therefore, it can be assumed that serologically -positive animals are not carriers of the virus. 
Sows become immune an d pass antibody to newborn piglets in their colostrum.  Once the 
population had become immune, only young pigs were infected after their maternal immunity 
had declined.  
The disease did not spread to other pig herds except to two associated growing farms t hat did not 
have any breeding sows and received pigs from the parent farm. A colony of fruit bats roosted 
within 200 meters of the parent farm. Virus neutralising antibody was found in approximately 
one-third of fruit bats in the colony on the affected far m and from fruit bats in a variety of 
locations in Australia. Therefore fruit bats were identified as the probable natural reservoir host of the virus. Pigs were infectious and the virus spread slowly through the entire pig population. 
Six months after the  estimated time of entry , 90% of pigs were positive to a virus neutralization 
test and antibody titres remained high for at least 2 years.  
Two workers on the affected farm became seropositive and developed a severe febrile illness 
with a rash and had high convalescent -phase antibody titres to the virus. There was no 
serological evidence of an alternative cause. It was concluded that there was strong evidence that the two men were infected with Menangle virus.  
The virus does not survive long in the environment and there have been no other recorded 
outbreaks of the disease. There is no evidence to suggest that transmission in the semen of 
infected pigs should be considered likely.   
Ministry for Primary Industries  Import risk analysis: Pig semen • 51 16.1.5.  Hazard identification conclusion 
Menangle virus occurs only in Australia .  Only one outbreak of the disease has occurred in 
Australia in the last 10 years , and the virus cannot be regarded as endemic in the pig population.  
There is no evidence that transmission occurs via semen.  Menangle virus is not  identified as a  
hazard in the  commodity.  
 
References  
 
Chant K, Chan R, Smith M, Dwyer DE, Kirkland PD (1998) . Probable human infection with a new virus 
described in the Family Paramyxoviridae . The NSW Expert Group. Journal of Emerging Diseases , 4(2), 273-5.  
 
Kirkla nd PD, Stephano A (2006).  Paramyxoviruses: Rubulavirus, Menangle and Nipah virus infections. Menangle 
virus.  In: Straw BE, Zimmerman JJ, D'Allaire S, Taylor DJ (eds), Diseases of Swine . 9th edition, Pp. 459 -62, 
Blackwell Publishing, Ames, Iowa.  
 
Lamb RA, Collins PL, Kolakofsky D, Melero JA, Nagai Y, Oldstone MBA, Pringle CR, Rima BK (2005).  
Genus  Rubulavirus . In: Fauquet CM, Mayo MA, Maniloff J, Desselberger U, Ball LA (eds), Eighth Report of the 
International Committee on Taxonomy of Viruses . Pp. 659 -60, E lsevier Academic Press, Amsterdam.  
 
MAF (2008). The Unwanted Organisms Register. http://mafuwsp6.maf.govt.nz/uor/searchframe.htm , downloaded 
27/1/2009.  
 
Philbey AW, Kirkland PD, Ross AD, Dav is RJ, Gleeson AB, Love RJ, Daniels PW, Gould AR, Hyatt AD 
(1998) . An apparently new virus (family Paramyxoviridae ) infectious for pigs humans and fruit bats. Emerging 
Infectious Diseases 4 , 4(2), 269 -71.  
Ministry for Primary Industries  Import risk analysis: Pig semen • 52 17. Murray Valley encephalitis virus 
17.1. HAZARD IDENTIFICATION  
17.1.1.  Aetiological agent  
Family: Flaviviridae , Genus: Flavivirus , Species: Murray Valley encephalitis virus (MVEV) 
(Thiel et al 2005) . 
17.1.2.  OIE list  
Not listed  
17.1.3.  New Zealand status  
Exotic unwanted organism (MAF 2008).  
17.1.4.  Epidemiology  
MVEV is found in Australia, Papua New Guinea, and probably islands in the  eastern part of the 
Indonesian archipelago (Mackenzie et al 1994).  Waterbirds are thought to be the major 
vertebrate host of the virus, especially members of the order Ciconiiformes, with the highest 
serological titres recognised in the rufous night hero n (Boyle et al 1983).  
Culex annulirostris  is recognised as the major vector of MVEV  in Australia.  The virus has also 
been recovered from other mosquito species including Aedes normanensis , Ae. 
pseudonormanensis , Ae. eidsvoldensis , Anopheles annulipes , Anopheles bancroftii , Cx. 
quinquefasciatus , Cx. australicus , Cx. palpalis , and Monsonia uniformis  (Mackenzie et al 1994) .  
Of these, only Cx. quinquefasciatus  (an introduced mosquito species known to be present in New 
Zealand [Holder 1999] ) has been shown exp erimentally to transmit MVE.   
Serological evidence of exposure to MVE has been described in domestic pigs in northern Queensland (Doherty et al 1964) and in feral pigs in New South Wales (Gard et al 1976).  
Experimental inoculation studies have shown that  pigs which develop low -grade viraemia 
following infection with MVEV should be considered low -grade amplifiers of this virus (Kay et 
al 1985).  There is no evidence to suggest that transmission of MVEV in porcine semen should 
be considered likely.  
17.1.5.  Hazard i dentification conclusion 
Although there is serological evidence of exposure of pigs in Australia to MVEV, pigs have been 
shown to develop only low -grade viraemia following infection and there is no evidence of virus 
being found in the semen of infected pig s.  MVEV is not identified as a  hazard in porcine semen.  
 
References  
 
Boyle DB, Marshall ID, Dickerman RW (1983) Primary antibody responses of herons to experimental infection 
with Murray Valley encephalitis and Kunjin viruses. Australian Journal of Experi mental Biology and Medical 
Science  61, 665 -74. 
 
Doherty RL, Carley JG, Gorman BM (1964) Studies of arthropod -borne virus infections in Queensland. IV. 
Further serological investigations of antibodies to group B arboviruses in man and animals. Australian Journal of 
Experimental Biology and Medical Science  42, 149 -64.  
Ministry for Primary Industries  Import risk analysis: Pig semen • 53  
Gard GP, Giles JR, Dwyer -Gray RJ, Woodroofe GM (1976) Serological evidence of inter -epidemic infection of 
feral pigs in New South Wales with Murray Valley encephalitis virus. Australian Journal  of Experimental Biology 
and Medical Science  54, 297-302.  
 Holder P (1999) The mosquitoes of New Zealand and their animal disease significance. Surveillance  24(4), 12-5  
 
Kay BH, Young PL, Hall RA, Fanning ID (1985) Experimental infection with Murray Valley  encephalitis virus. 
Pigs, cattle, sheep, dogs, rabbits, macropods and chickens.  Australian Journal of Experimental Biology and Medical 
Science  63, 109 -126.  
 MAF (2008). The Unwanted Organisms Register. 
http://mafuwsp6.maf.govt.nz/uor/searchframe.htm , downloaded 
27/1/2009.  
 Mackenzie JS, Lindsay MD, Coelen RJ, Broom AK, Hall RA, Smith DW (1994)  Arboviruses causing human 
disease in the Australasian zoogeographic region. Archives of Virology  136, 447-67.  
 Thiel HJ, Collett MS, Gould EA, Heinz EX, Houghton M, Meyers G, Purcell RH, Rice CM (2005).  Genus   
Flavivirus . In: Fauquet CM, Mayo MA, Maniloff J, Desselberger U, Ball LA, (eds), Eighth Report of the 
International Committee on Taxonomy of Vir uses. Pp. 982 -8, Elsevier Academic Press, Amsterdam.   
Ministry for Primary Industries  Import risk analysis: Pig semen • 54 18. Nipah virus  
18.1. HAZARD IDENTIFICATIO N 
18.1.1.  Aetiological agent  
Nipah virus (NiV) is a paramyxovirus in the subfamily Paramyxovirinae, and is classified in the 
new genus Henipavirus (Eaton et al 2006; Wang et al 2012).  
18.1.2.  OIE list  
Nipah virus encephalitis is an OIE -listed disease.  
18.1.3.  New Zealand status  
Nipah virus is exotic to New Zealand and listed as a Notifiable Organism (Tana et al 2011).  
18.1.4.  Epidemiology  
Nipah virus is a tropical disease that was first reported in Malay sia in 1998 and subsequently in 
Singapore, Bangladesh, and India ( Tan and Wong 2003; Katu 2004; Epstein et al  2006).  The 
disease is rare, appearing sporadically in tropical climates where the natural reservoir host 
Pteropid fruit bat species are found.  
Respiratory disease in pigs caused by NiV is often subclinical (OIE 2010).   Pigs excrete the virus 
in urine and respiratory droplets.  Chronic infections do not appear to be a feature of the disease. 
Experimental infections showed that virus was not excreted by pigs once neutralising antibodies 
appeared 14 -18 days post -infection (Middleton et al 2002).  Direct, close contact with pigs was 
the primary source of a major public health crisis, with the death of 105 people, when NiV first appeared (Katu 2004).  N ipah virus attacks the central nervous system and respiratory systems. 
Encephalitis is the main cause of death in humans.  The movement of infected pigs from Malaysia to an abattoir in Singapore resulted in the development of symptoms of encephalitis in 
35 abattoir workers with confirmed infection by NiV demonstrated in 11 of these individuals.  
One of these infected individuals died whilst four were reported to have persistent neurological deficits (Paton et al 1999; Chua et al 2000).  
In Bangladesh from 20 01 to 2005, five outbreaks were attributed to NiV infection. These 
involved much smaller numbers of affected humans and no animal disease was evident, differing from the Malaysian epidemic.  These outbreaks appear to have been due to spillover of virus 
directly from bats to humans ( Epstein et al 2006).  One outbreak was reported in 2001 in India, 
close to the Bangladesh border ( Chadha et al 2006).  Since 2001, almost annual human outbreaks 
of fatal encephalitis  caused by NiV  in Bangladesh and sporad ic outbr eaks in India have been 
reported . Although human- to-human transmission was not seen in the Malaysia and Singapore 
outbreak, the recent  outbreaks  in Bangladesh have led to the suspicion of  human- to-human and 
foodborne transmission of NiV (Lo et al 2012).   The threat to human health is significant since 
NiV infection has a high mortality rate of 33 -75% recorded in different outbreaks (Center for 
Food Security and Public Health 2007).   
Ministry for Primary Industries  Import risk analysis: Pig semen • 55 Virus isolation of NiV from unfixed samples followed by identification proce dures such as 
immunostaining, serum neutralisation , or molecular characterisation are described.  Real -time 
polymerase chain reaction is also available as a diagnostic test.  Immunohistochemistry of fixed 
tissue can also be used to detect NiV antigens.  Vi rus neutralisation tests and enzyme- linked 
immunosorbent assays are also available for serological diagnosis of NiV infection (OIE 2010).  
Virus spread between farms is usually associated with pig movements although transmission in semen has been suggested ( Center for Food Security and Public Health 2007).   NiV was not 
found in the urine of experimentally infected pigs although virus was detected in the kidneys of clinically infected individuals suggesting that urinary excretion of the virus may be possible 
(Middleton et al 2002).   NiV has been recovered from the urine of infected bats 
(Wacharapluesadee and Hemachudha 2007), cats (Mungall et al 2007), and humans (Chua et al 2001).  Natural infection of pigs with NiV leads to lesions in both the brain and lung s of an 
individual with tracheitis, pneumonia, and meningoencephalitis described.  The lungs and meninges are recognised as the most important target organs following experimental infection 
with vascular degeneration also described in the gastric submucosa and muscle, ureteral 
submucosal, spleen, and hepatic arterioles.  The spread of NiV from infected pigs is principally through coughed- up sputum and expired air, with excretion also possible via the placenta 
(Hooper et al 2001).   There is no evidence that  suggests NiV is shed in the semen of infected 
pigs.  
18.1.5.  Hazard identification conclusion 
There is no evidence to support the suggestion that NiV may be spread in the semen of infected 
boars. NiV is not identified as a hazard in porcine semen.  
 
 References  
 
Center for Food Security and Public Health (2007). Nipah virus infection. [Online] Available from:  
http://www.cfsph.iastate.edu/Factsheets/pdfs/nipah.pdf  [Accessed 29th March 2012].  
 
Chadha MS, Comer JA , Lowe L , Rota PA , Rollin PE , Bellini WJ , Ksiazek TG , Mishra A (2006). Nipah virus -
associated encephali tis outbreak Siliguri India.  Emerging Infectious Diseases  12, 235-240.  
 Chua KB, Bellini WJ, Rota PA, Harcourt BH, Tamin A, Lam SK, Ksiazek TG, Rollin PE, Zaki SR, Shieh W -
J, Goldsmith CS, Gubler DJ, Roehrig JT, Eaton B, Gould AR, Olson J, Field H, Danials  P, Ling AE, Peters 
CJ, Anderson LJ, Mahy BWJ (2000).  Nipah virus: A recently emergent deadly paramyxovirus. Science, 288, 
1432–1435.  
 
Chua KB, Lam SK, Goh KJ, Hooi PS, Ksiazek TG, Kamarulzaman A, Olson J, Tan CT (2001).  The presence 
of Nipah virus in respiratory secretions and urine of patients during an outbreak of Nipah virus encephalitis in Malaysia. Journal of Infection 42, 40-43.  
 
Eaton BT, Broder CC, Middleton D, Wang LF (2006). Hendra and Nipah viruses: different and dangerous.  
Nature Reviews  Microb iology  4, 23-35.  
 
Epstein JH, Field HE, Luby S, Pulliam JR, Daszak P (2006). Nipah virus: impact origins and causes of 
emergence.  Current Infectious Disease Reports  8, 59-65.  
 
Hooper P, Zaki S, Daniels P, Middleton D (2001). Comparative pathology of the di seases caused by Hendra and 
Nipah viruses. Microbes and Infection  3, 315 -322.  
 Katu Y (2004).  Nipah virus infection.  Uirusu. Journal of Virology  54, 237-242.   
Ministry for Primary Industries  Import risk analysis: Pig semen • 56  
Lo MK, Lowe L, Hummel KB, Sazzad HMS, Gurley ES, Hossain MJ, et al. (2012).  Characterization of N ipah 
virus from outbreaks in Bangladesh, 2008–2010. Emerging Infectious Diseases . Available from: 
http://dx.doi.org/10.3201/eid1802.111492
 [Accessed 21st March 2012).  
 
Middleton DJ , Westbury HA, Morrissy CJ , van der Heide BM , Russell GM , Braun MA , Hyatt AD  (2002). 
Experimental Nipah virus infection in pi gs and cats.  Journal of Comparative Pathology  126, 124-136.  
 
Mungall BA, Middleton D, Crameri G, Halpin K, Bingham J, Eaton BT, Broder CC (2007). Vertical 
transmission and fetal replication of Nipah virus in an experimentally infected cat. Journal of Infec tious Diseases  
196, 812-816.  
 OIE (2010) Hendra and Nipah virus diseases. Manual of Diagnostic Tests and Vaccines for Terrestrial Animals.  
Chapter 2.9.6.  Available at: 
http://www.oie.int/fileadmin/Home/eng/Health_standards/tahm/2.09.06_HENDRA_&_NIPAH_FINAL.pdf  
 
Paton NI, Leo YS, Zaki SR, Auchus AP, Lee KE, Ling AE, Chew SK, Ang B, Rollin PE, Umapathi T, Sng I, 
Chuan C, Lim E, Ksiazek TG (1999).  Outbr eak of Nipah -virus infection among abattoir workers in Singapore. 
Lancet, 354, 1253–1256.  
 
Tan CT, Wong KT (2003).  Nipah encephalitis outbreak in Malaysia.  Annals of the Academy of Medicine 32, 112-
117. 
 
Tana T, Murray-Cullen J, Johnston C, Lee E (2011).   Notifiable organisms. Surveillance  38(2), 20-24.  
 
Wacharapluesadee S, Hemachudha T (2007). Duplex nested RT -PCR for detection of Nipah virus RNA from 
urine specimens of bats. Journal of Virological Methods  141, 97-101.  
 
Wang LF, Collins PL, Fouchier RAM, K urath G et al (2012). Family Paramyxoviridae. In: King AM, Adams 
MJ, Carstens EB, Lefkowitz EJ (eds.) Virus Taxonomy . Elsevier, London, pp. 672-685.  
  
Ministry for Primary Industries  Import risk analysis: Pig semen • 57 19. Porcine reproductive and respiratory syndrome virus  
19.1. HAZARD IDENTIFICATIO N 
19.1.1.  Aetiological agent  
Family: Arteriviridae , Genus : Arterivirus, Species: Porcine reproductive and respiratory 
syndrome virus (PRRSv) (Snijder et al 2005) . 
19.1.2.  OIE list  
PRRS is listed in the Code , but it does not contain a chapter on this disease (OIE 2008a) . 
19.1.3.  New Zealand status  
Exotic, notifiable disease (MAF 2008) . 
19.1.4.  Epidemiology  
The disease/virus occurs in the USA, Canada and many EU countries but not in Norway, 
Sweden, or Australia (OIE 2008b) . The virus is highly infectious and spread rapidly through 
Europe and North America in the early 1990s. In infected reg ions 60- 80% of herds are typically 
infected (Zimmerman et al 2006) .  
Infection with virulent strains results in virae mia within 12 to 24 hours. Viral titres reach 
maximal levels by the seventh day after infection and are highest in the lung. Signs of infection 
are typically those of viraemia, followed by respiratory signs and reproductive problems such as 
abortion, foeta l deaths and reproductive failure (Zimmerman et al 2006) . 
Infected pigs shed the virus in saliva, nasal secretions, urine and semen (Zimmerman et al 2006) . 
Pigs may remain persistently  infected for periods of at least 150 days after infection (Allende et 
al 2000) , with virus multiplying in the  cells of subclinically infected pigs for several months 
(Zimmerman et al 2006) . The persistence of the virus in infected pigs is independent  of the route 
or time  of infecti on and occurs despite the concomitant  presence of antibody.  
Transmission commonly occurs through skin wounds . Oral and nasal transmission  is less 
efficient , and airborne transmission over short distances (1 -2.5 meters) has been demonstrated  
(Zimmerman et al 2006) . Airborne transmission  over longer distances is controversial but recent 
studies have shown that airborne spread from an infected herd is possible over distances of around 120 meters (Pitkin et al 2007) . Viral RNA has been demonstrated in semen 92 days after 
infection and the virus has been isolated from the bulbourethral gland 101 days after infection 
(Christopher -Henning et al 1995) . Artificial insemination has been a common method of 
transmission of the virus (Zimmerman et al 2006) . 
Diagno sis can be confirmed by isolation of the virus or by demonstration of viral RNA by PCR 
(Ludeman and Lager 2008; Zimmerman et al 2006) . Antibodies develop within 1- 2 weeks, ar e 
maximal 30 -50 days post infection, and decline to undetectable levels 3- 5 months after infection 
(Zimmerman et al 2006) . ELISA kits are commercially available with some using antigen 
prepared from both American and European strains of the virus (Ludeman and Lager 2008) . 
19.1.5.  Hazard identification conclusion 
Transmission of PRRSV in semen is well documented. The virus is identified as a potenti al 
hazard in porcine semen imported from countries where the virus is present.   
Ministry for Primary Industries  Import risk analysis: Pig semen • 58 19.2. RISK ASSESSMENT  
19.2.1.  Entry assessment  
PRRS is endemic in Canada, the USA, and most EU countries where the prevalence in many 
areas is high. The organism is commonly excreted in sem en. Therefore the likelihood of entry of 
the virus in imported semen is non- negligible.  
19.2.2.  Exposure assessment  
Since imported semen will used to inseminate sows, exposure of naïve New Zealand pigs to 
virus in imported semen would be inevitable.  
19.2.3.  Consequence a ssessment  
Insemination of New Zealand pigs with infected imported semen would almost certainly result in 
infection of the recipients. It can be expected that the virus would establish in herds that are 
infected by imported semen and spread rapidly as it d id in other countries. The disease would 
initially cause high losses to farmers and as the infection became endemic would lead to a continuous erosion of profits. It may be expensive and difficult to eradicate from New Zealand.  
The virus is not zoonotic an d there would be no consequences for human health. The only 
animals known to be infected by the virus are pigs and feral pigs would be the only susceptible 
species of wild or feral animals. However, transmission from domestic to feral pigs is unlikely. 
Furthermore it is likely that the disease would be self -limiting since under the conditions in 
which feral pigs live the virus may not re -cycle between litters of piglets.  Therefore the 
likelihood of deleterious effects on humans or the environment is assesse d to be negligible.  
19.2.4.  Risk estimation  
Entry, exposure and consequence have all been assessed as non -negligible. As a result the risk 
estimate for PRRS virus is non -negligible and it is classified as a risk  in the commodity. 
Therefore risk management measures  can be justified.  
19.3. RISK MANAGEMENT  
19.3.1.  Options  
The following relevant points were considered when drafting options for the effective management of PRRS virus in the commodity:  
• The virus is excreted in pig semen and transmission in semen is common.  
• Since pigs  may remain infected for at least 5 months, quarantine is not an option for 
preventing the introduction of the virus.  
• Serological tests and viral RNA detection tests (PCR) are available for diagnosis.  
• Introduction of the disease could have severe consequ ences for the pig industry.  
Of all the OIE -listed porcine diseases that are considered to be a hazard in porcine semen, it is 
noteworthy that PRRS is unique in that no Code  chapter has been written to outline standards for 
sanitary measures to manage the risk of international transmission of this disease.  
Chapters 4.5 and 4.6 of the Code  (OIE 2008a)  contain requirements for PRRSv for boars 
standing at sem en collection centres.  Under these requirements, boars from a country or zone 
that is not free of PRRS must be clinically healthy, physiologically normal, and subject to testing  
Ministry for Primary Industries  Import risk analysis: Pig semen • 59 complying with the standards in the Terrestrial Manual.  Boars must remain in  this quarantine 
station for at least 28 days and, at least 21 days after entering the quarantine station must be 
tested negative for PRRSv using a test compliant with the standards of the Terrestrial Manual.  
Any boars resident in the semen collection fac ility must also be tested at least annually using a 
test compliant with the standards in the Terrestrial Manual.  
These requirements from the Code  may provide some assurance that infected boars are not 
introduced into a stud, although ensuring a stud remains free of infection is recognised to be extremely challenging (Huinker 2002; Connor 2003; Polson and Reicks 2009) so annual testing 
alone (as described above) cannot be relied upon to ensure semen is free from PRRSv.  
Previously, PCR testing of semen has been used routinely in boar studs to monitor for PRRS 
(Connor 2003; Torremorell 2003).  However, following infection, virus can be detected sooner 
in blood than in semen (Christopher -Hennings et al 2001).  Serum PCR (using either a TaqMan 
PCR test or a nest ed PCR test) is more sensitive than semen PCR for PRRSv detection during the 
first six days following infection and boars are detected as PRRSv -positive by serum PCR before 
semen PCR (Reicks et al 2006a; Reicks et al 2006b) .  For testing boars, serum is cu rrently 
considered to be the preferred sample to use as PRRSv is in much higher levels in serum than in 
semen and is detectable at least 1 -2 days sooner (Reicks 2009).  PCR testing of pooled serum 
samples have been shown to be as effective for detection of  PRRSv in boar studs as testing 
individual samples (Rovira and Munoz -Zanzi 2006).  
The current state- of-the-art principles for early detection of PRRSv infection in boar studs 
include prohibition of vaccination together with avoidance of any seropositive animals, monthly 
serological testing of the stud population, antigen testing of donors at (weekly) collection, 
antigen testing of pooled semen samples (daily), and no use of semen until all individual animal 
tests have been completed.  However, despite these stringent measures, biosecurity breakdowns 
in boar studs are recognised (Clement 2010).  
In order to minimise the risk of distributing semen containing PRRSv, it has been recommended 
that boars should be sampled each day of collection. Additionally, a stat istical sampling of all 
boars on a stud should be collected each day, any boar showing clinical signs such as anorexia or pyrexia should be sampled immediately, and all semen should be withheld until negative results 
(using PCR testing of serum) are obtain ed.  Due to viral mutation, some strains of PRRSv may 
be undetected by PCR testing so additional weekly testing of boars by serum ELISA is also recommended (Reicks 2005; Reicks 2009).  
NZPork have stated that it would also be desirable to require semen to b e withheld for a period 
of three months after collection and only released if accompanied by certification that during the 
three months since the last collection date there has been no clinical or serological evidence of 
PRRS in the donor herds or the stud  itself (Clement 2010).  
Considering the above, the following options could be considered to effectively manage the risk of introducing PRRSv in imported porcine semen:  
Option 1  
Pig semen could be imported from countries that are recognised as free from PRR S without 
sanitary measures.  
Option 2  
 
a. Boars should be sourced from donor herds that do not vaccinate against PRRSv, and be shown to be negative for PRRSv before entering the stud as described in Chapters 4.5 
and 4.6 of the Code .  
Ministry for Primary Industries  Import risk analysis: Pig semen • 60 b. Individual donor boa rs should be tested by serum PCR each day of collection with 
negative results.  
c. During each day of the collection period, all boars on the stud should be tested for 
PRRSv by serum PCR, with the number of boars sampled sufficient to give a 95% 
confidence of detecting a 5% prevalence rate.  
d. 30 to 50 days after the final sample collection, boars on the stud should be tested by a multi- valent serum ELISA for PRRSv  that uses both European and American strain 
antigens , with the number of boars sampled suffic ient to give a 95% confidence of 
detecting a 5% prevalence rate.  
Option 3  
 a. Boars should be sourced from donor herds that do not vaccinate against PRRSv, and be 
shown to be negative for PRRSv before entering the stud as described in Chapters 4.5 
and 4.6 of the Code . 
b. Individual donor boars should be tested by serum PCR each day of collection with negative results.  
c. During each day of the collection period, all boars on the stud should be tested for 
PRRSv by serum PCR, with the number of boars sample d sufficient to give a 95% 
confidence of detecting a 5% prevalence rate.  
d. 30 to 50 days after the final sample collection, boars on the stud should be tested by a multi- valent serum ELISA for PRRSv  that uses both European and American strain 
antigens , with the number of boars sampled sufficient to give a 95% confidence of 
detecting a 5% prevalence rate.  
e.   Semen should be accompanied by certification that during the three months since the last 
collection date there has been no clinical or serological e vidence of PRRS in the donor 
herds or the stud itself.  
Option 4 (the current measures in place based on an earlier risk analysis)  
a. The semen collection centre could be required to have a documented absence from 
PRRS. All pigs entering the semen collectio n centre must originate from herds which  
have never recorded a clinical case of PRRS.  
b. The semen collection centre could be required to have never used a modifi ed live PRRS 
virus vaccine nor introduced pigs from herds that have used a modified live PRRS  virus 
vaccine.  
c. All pigs in the semen collection centre could be required to have completed a 5 week 
period of isolation .  While undergoing this  5 week isolation period the pigs must be 
exposed throughout the isolation period to direct contact with at least an equal number of sentinel grower pigs and the total number of pigs in the semen collection centre 
undergoing isolation could be required to be at least ten  at all times.   
Ministry for Primary Industries  Import risk analysis: Pig semen • 61 d. The sentinel grower pigs used could be required to be between 12 and 24 we eks of age 
and derived from 3 or more herds which have been shown by an approved multi -valent 
ELISA to be free of PRRS within two months prior to the commen cement of the isolation 
period.  
e. During the isolation period, al l pigs undergoing isolation could  be tested for PRRS using 
an approved multi -valent ELISA test, on two occasions at the start and finish of the 
isolation period, with a negative result in each case.  
f. Semen collected from donor boars during the 5 week period of isolation (either during 
approval of the semen collection centre or prior to entry of a donor boar onto an approv ed 
semen collection centre) could  become eligible for export to New Zealand upon 
successful completion of isolation (i.e. no positive test for PRRS in any donor boar or 
sentinel simultaneously undergoing isolation).  
Option 5  
Reflecting that breakdowns in boar studs still occur despite intensive monitoring, the importation of pig semen from countries with PRRSv could be prohibited.  
 
 
References  
References marked * were si ghted as summaries in electronic media sources.  
Allende R, Laegried WW, Kutish JF, Galeota JA, Wills RW, Osorio FA (2000). Porcine reproductive and 
respiratory disease virus. Description of persistence in individual pigs upon experiment al infection. Journal of 
Virology , 74, 10834-7.* 
 
Christopher -Hennings J, Nelson EA, Hines RJ, Nelson JK, Swenson SL, Zimmerman JJ, Chase CCL, Yaeger 
MJ, Benfield DA (1995). Persistence of porcine reproductive and respiratory syndrome virus in serum and se men of 
adult boars. Journal of Veterinary Diagnostic Investigation , 7, 456-64.  
 
Christopher -Hennings J, Holler LD, Benfield DA, Nelson EA (2001) Detection and duration of porcine 
reproductive and respiratory syndrome virus in semen, serum, peripheral blood  mononuclear cells, and tissues from 
Yorkshire, Hampshire, and Landrace boars. Journal of Veterinary Diagnostic Investigation,  13, 133 -42. 
 Clement F (2010)  Personal communication.  Porcine semen draft IRA - response to proposed risk management 
measures.  E-mail to Pharo HP, 18 Feb 2010.  
 Connor JF (2003) Farms and boar studs: how can we prevent PRRSV contamination.  Annual Meeting of the 
American Association of Swine Veterinarians , 523 -524 
 Huinker CD (2002)  How boar studs are adapting to the recent PRRS bre aks. Allen D Leman Swine Conference , 65-
67. 
 Ludeman LR, Lager KM (2008).  Porcine reproductive and respiratory syndrome. In: OIE (eds), Manual of 
Diagnostic Tests and Vaccines for Terrestrial Animals. Vol. 2, Pp. 1116-27, OIE, Paris. 
 
MAF (2008). The Unwan ted Organisms Register. 
http://mafuwsp6.maf.govt.nz/uor/searchframe.htm , downloaded 
27/1/2009.  
 
OIE (2008a) . Terrestrial Animal Health Code . http://www.oie.int/eng/normes/MCode/en_sommaire.htm , 
downloaded 27/1/2009  
 
OIE (2008b) . World Animal Health Information Database (WAHID) Interface. http://www.oie.int/wahid -
prod/public.php?page=home, downloaded 4/8/2009.   
Ministry for Primary Industries  Import risk analysis: Pig semen • 62  
Pitkin A, Deen J, Dee SA (2007) . Aerosol transmission of PRRSV: Application to the field, Allen D. Leman Swine 
Conference. Volume 34. Veterinary Continuing Education, University of Minnesota, University of Minnesota, pp. 
85. 
 
Polson D and Reicks D (2009)  The naïve boar s tud PRRS dilemma -  prevention, detection, or both? Annual 
Meeting of the American Association of Swine Veterinarians , 23-32. 
 
Reicks DL (2005) Boar stud PRRS monitoring – science and economics. ISU Swine Disease Conference for Swine 
Practitioners , 141 -145.  
 
Reicks DL, Munoz -Zanzi C, Mengeling W, Christopher -Hennings J, Lager K, Polson D, Dee S, Rossow K 
(2006a)  Detection of porcine reproductive and respiratory syndrome virus in semen and serum of boars during the 
first six days after inoculation. Journal of  Swine Health and Production 14, 35-41.  
 
Reicks DL, Munoz -Zanzi C, Rossow K (2006b) Sampling of adult boars during early infection with porcine 
reproductive and respiratory syndrome virus for testing by polymerase chain reaction using a new blood collectio n 
technique (blood -swab method). Journal of Swine Health and Production  14, 258-264.  
 
Reicks DL (2009)  Monitoring boar studs for early detection of PRRS virus to avoid complete depop -repop of studs 
and infection of downstream breeding herds. Proceedings of  the American Association of Swine Veterinarians 2009, 
19-22.  
 
Rovira A and Munoz -Zanzi C (2006)  Evaluation of the potential use of pooling in PRRSV monitoring protocols 
for boar studs. Proceedings of the 19th IPVS Congress , Copenhagen, Denmark Volume 2, 19.  
 
Snijder EJ, Brinton MA, Faaberg KS, Godeny EK, E. GA, MacLachlan NJ, Mengeling WL, Plageman PGW 
(2005).  Genus  Arterivirus . In: Fauquet CM, Mayo MA, Maniloff J, Desselberger U, Ball LA (eds), Eighth Report of 
the International Committee on Taxonomy of V iruses. Pp. 965 -74, Elsevier Academic Press, Amsterdam.  
 
Torremorell M (2003)  Monitoring boar studs. Annual Meeting of the American Association of Swine Veterinarians , 
259-260.  
 
Zimmerman J, Benfield DA, Murtagh MP, Osorio F, Stevenson GW, Torremorell M (2 006).  Porcine 
reproductive and respiratory syndrome virus  (Porcine Arterivirus) . In: Straw BE, Zimmerman JJ, D'Allaire S, 
Taylor DJ (eds), Diseases of Swine . 9th edition, Pp. 387-417, Blackwell Publishing, Ames, Iowa.  
  
 
 
   
Ministry for Primary Industries  Import risk analysis: Pig semen • 63 20. Porcine epidemic diarrhoea vir us 
20.1. HAZARD IDENTIFICATIO N 
20.1.1.  Aetiological agent  
Family: Coronaviridae , Genus: Coronavirus,  Species: Porcine epidemic diarrhea virus (Spaan 
et al 2005) . 
20.1.2.  OIE list  
Not list ed. 
20.1.3.  New Zealand status  
Listed as an “other exotic virus” (MAF 2008) .  
20.1.4.  Epidemiology  
Information given below is derived from a comprehensive review of the subject (Pensaert and 
Yeo 2006) .  
Porcine epidemic diarrhoea occurs in the EU but neither in North America nor Australia. The disease was probably first recognized in England in 1 971, but the cause was not established until 
1978. The disease spread from England to Europe. Outbreaks of diarrhoea occur in pigs of all ages.  Older pigs generally recover within a week, while mortality in piglets under 7 days old is 
around 50% and may a pproach 100%. The morbidity may be close to 100% in naïve herds. The 
prevalence of the disease in Europe has declined and it is now rare. The disease may become 
endemic on a farm where the number of pigs is high and the virus is maintained by circulation i n 
litters of piglets.  
Experimentally -infected, colostrum -deprived piglets develop the disease in 22 -36 hours, and on 
farms with susceptible populations of pigs the disease appears 4 -5 days after introducing new 
pigs. The virus multiplies only in the cells  of the digestive tract and is transmitted by the faecal -
oral route. There is no evidence to indicate that the virus is excreted in semen or that semen is a vehicle for the transmission of virus.   
20.1.5.  Hazard identification conclusion 
Porcine epidemic diarrhoea is predominantly a disease of very young piglets. The causative virus 
multiplies only in the cells of the digestive tract and there is no evidence that it is excreted in 
semen. Therefore, this virus is not identified as a  hazard in the commodity.  
 
References  
 
MAF (2008).  The Unwanted Organisms Register. http://mafuwsp6.maf.govt.nz/uor/searchframe.htm , downloaded 
27/1/2009.  
 
Pensaert MB, Yeo S -G (2006). Porcine epidemic d iarrhoea. In: Straw BE, Zimmerman JJ, D'Allaire S, Taylor DJ 
(eds). Diseases of Swine . 9th edition , Pp. 367 -72. Blackwell Publishing, Ames, Iowa.  
 
Spaan WJM, Brian D, Cavanagh D, de Groot R, J., Enjuanes L, Gorbalenya AE, Holmes KV, Masters P, 
Rottier P, Taguchi F, Talbot P (2005).  Genus Coronavirus . In: Fauquet CM, Mayo MA, Maniloff J, Desselberger  
Ministry for Primary Industries  Import risk analysis: Pig semen • 64 U, Ball LA (eds). Eighth Report of the International Committee on Taxonomy of Viruses . Pp. 947-55. Elsevier 
Academic Press, Amsterdam.  
  
Ministry for Primary Industries  Import risk analysis: Pig semen • 65 21. Porcine myocarditis vi rus 
21.1. HAZARD IDENTIFICATIO N  
21.1.1.  Aetiological agent  
The aetiological agent of this new disease has been identified as a pestivirus and given the name 
Bungowannah virus (Kirkland et al 2007) . 
21.1.2.  OIE list  
Not listed.  
21.1.3.  New Zealand status   
Exotic.  
21.1.4.  Epidemiology  
A new disease occurred in pigs in Australia in 2003 (McOrist et al 2004) . The disease was 
shown to be caused by an infectious agent and characterized by neonatal death s and stillbirths. 
The pathological changes consisted of multifocal non -suppurative myocarditis and sometimes 
myonecrosis with crystalline arrays of virus particles identified in heart tissue (Kirkland et al 
2007; McOrist et al 2004) .  
The condition was confined to two farms. There was some movement of breeding sows between the two properties (McOrist et al 2004) . Since no further cases have been described it has 
apparently not sp read.  
The virus has characteristics of a pestivirus but shows significant divergence from other known 
pestiviruses (Kirkland et al 2007) . It has been isolated in culture and identified by 
immunoperoxidase staining using polyclonal antibody from a pig infected with  the virus. Sera 
from infected pigs react weakly with other pestiviruses in an agar gel immunodiffusion test but 
do not exhibit neutralizing activity against other pestiviruses.  
The epidemic features of the disease outbreak suggest that the epidemic spread by contact 
through naïve breeding sows and ceased when naïve sows were no longer available. There was 
no evidence indicating that long term carriers of the disease occurred. Despite the severity of the 
outbreaks the herds made relatively rapid recoveries .  
The disease has not been described in any other country.   A recent report has c onfirmed 
Bungowannah -like Pestivirus is unlikely to be present in swine in the upper Midwestern USA 
(Abrahante et al 2012).   
21.1.5.  Hazard identification conclusion 
As Bungowannah v irus is a pestivirus, it is considered likely that it is present in semen from 
infected boars. Since the virus occurs only in Australia, it is identified as  a potential hazard in the 
commodity from that country.   
Ministry for Primary Industries  Import risk analysis: Pig semen • 66 21.2. RISK ASSESSMENT  
21.2.1.  Entry assessment  
Although the disease occurs extremely rarely and there is no evidence suggesting that long -term 
carriers of virus occur, given that the Bungowannah virus has been identified as a Pestivirus, it is 
assumed that there is a non -negligible likelihood of transmission in  semen (see Chapter 8).  
21.2.2.  Exposure assessment  
Imported semen will be inseminated into New Zealand pigs. As it has been demonstrated that sows can be infected with CSFV by artificial insemination with infected semen (Floegel et al 
2000) , it is assumed that this is also likely for pigs that are infected with Bun gowannah virus, the 
likelihood of exposure of New Zealand pigs is assessed  to be non- negligible.  
21.2.3.  Consequence assessment  
As described above, infection of pigs is characterized by neonatal deaths and stillbirths, with pathological changes described as multi focal non -suppurative myocarditis and sometimes 
myonecrosis with crystalline arrays of virus particles identified in heart tissue.  The consequences of infection are therefore assessed  to be non- negligible.  
21.2.4.  Risk estimation  
Entry, exposure and consequence have all been assessed as non -negligible. As a result the risk 
estimate for Bungowannah virus is non -negligible and it is classified as a risk  in the commodity. 
Therefore risk management measures can be justified.  
21.3. RISK MANAGEMENT  
21.3.1.  Options  
Porcine myocardit is is confined to a single enterprise composed of a number of small properties 
in New South Wales and there have been no other reports of the disease outside this enterprise.  
This enterprise includes an AI facility which used boars from the positive site after testing with a 
protocol to e nsure they are antibody positive and serum negati ve for Bungowannah virus (Biddle 
2010).  Since this enterprise has was placed under quarantine in 2003, approximately 275,000 semen doses each year have been used to insemin ate 50,000 sows in both the positive site and in 
negative farms with no further spread of this disease.  Considering there has been no further spread of the virus, it is reasonable to conclude that these current measures are effectively 
managing the risk o f spread in porcine semen.  
A peroxidise -linked assay to detect antibodies to Bungowannah virus and an RT -PCR test to 
detect Bungowannah virus RNA have been described (Finlaison et al 2009).  
 
Option 1  
Porcine semen could be imported from countries other tha n Australia without sanitary measures.  
Option 2  
Semen originating from Australian studs which can be certified as not including individuals from 
properties where porcine myocarditis has been identified could imported without any further 
sanitary measures.   
Ministry for Primary Industries  Import risk analysis: Pig semen • 67 Option 3  
Donor boars originating from properties where porcine myocarditis has been recognised should 
be isolated and tested to demonstrate they are seropositive and negative for Bungowannah virus 
RNA before entering the collection centre.  
 
 References  
Abrahante JE, Zhang JW, Rossow K, Zimmerman JJ, Murtaugh MP (2012).  Surveillance of Bungowannah 
Pestivirus in the upper Midwestern USA. Transboundary and Emerging Diseases . Article first published online: 27 
Nov 2012. DOI:  10.1111/tbed.12035 . 
Biddle R R (2007).  Personal communication. Letter from Dr R R Biddle, Australian Chief Veterinary Officer to Dr 
Barry O’Neil, 16 May 2007.  
 
Biddle R R (2010) Personal communication. Letter fro m Dr R R Biddle, General Manager Animal Health 
Programs, Department of Agricultu re Fisheries and Forestry, to Dr Howard Pharo, 4 March 2010.  
 
Finlaison DS, King KR, Frost MJ, Kirkland PD (2009)  Field and laboratory evidence that Bungowannah virus, a 
recently recognised Pestivirus, is the causative agent of the porcine myocarditis synd rome (PMC). Veterinary 
Microbiology , 136 (3-4), 259-265.  
 
Floegel G, Wehrend A, Depner KR, Fritzemeier J, Waberski D, Moennig V (2000) . Detection of classical swine 
fever virus in semen of infected boars. Veterinary Microbiology , 77(1-2), 109-16.  
 
Kirkland PD, Frost MJ, Finlaison DS, King KR, Ridpath JF, Gu X (2007).  Identification of a novel virus in 
pigs--Bungowannah virus: a possible new species of pestivirus. Virus Research , 129(1), 26-34.  
 
McOrist S, Thornton E, Peake A, Walker R, R obson S, Finlaison D, Kirkland P, Reece R, Ross A, Walker K, 
Hyatt A, Morrissy C (2004).  An infectious myocarditis syndrome affecting late -term and neonatal piglets. 
Australian Veterinary Journal , 82(8), 509-11.  
   
Ministry for Primary Industries  Import risk analysis: Pig semen • 68 22. Porcine respiratory coronavirus  
22.1. HAZARD I DENTIFICATION  
22.1.1.  Aetiological agent  
Family: Coronaviridae , Genus: Coronavirus . The International Committee on Taxonomy of 
Viruses considers Transmissible gastroenteritis virus  and Porcine respiratory coronavirus  to be 
a single species (Spaan et al 2005) . 
22.1.2.  OIE list  
Not listed.  
22.1.3.  New Zealand status  
Listed as an “other exotic organism” (MAF 2008).  
22.1.4.  Epidemiology  
Porcine respiratory coronavirus (PRCV) is probably a deletion mutan t of the transmissible 
gastroenteritis virus (TGEV) (Rasschaert et al 1990) . PRCV was first isolated in 1984 following 
the discovery of unexplained antibody titres to TGEV in pigs (Pensaert et al 1986) . The virus 
spread widely through Europe and late r through North America (Saif and Sestak 2006) . Natural 
infections with the virus are generally subclinical, but experimental infections with high 
challenges of virus may result in mild respiratory signs. Concomitant infections with other 
viruses, particularly porcine respiratory and reproductive syndrome virus , result in more severe 
signs (Saif and Sestak 2006) . The emergence of the virus in Europe coincided with the decline in 
the occurrence of TGE and has lead to speculation that infection with PRCV provides protection 
against TGEV (Saif and Sestak 2006) . Experimental studies have shown that infection with 
PRCV provides partial protection against TGEV (Cox et al 1993; Wesley and Woods 1993; Wesley and Woods 1996) .  
PRCV multiplies in the res piratory tract and tonsils and may be isolated from these sites. Limited 
multiplication may occur at enteric sites where only a few scattered cells containing virus may be 
demonstrated, even following direct inoculation of virus into the intestinal lumen (Saif and 
Sestak 2006) . No reports could be found that suggest that PRCV is excreted in semen.  
Infection with PRCV is of little economic importance as it usually causes only subclinical infections. It may even be beneficial in providing at lea st a partial immunity against TGEV. 
However, the presence of PRCV in a pig population complicates the diagnosis of TGE due to cross reactions.  
22.1.5.  Hazard identification conclusion 
PRCV causes a mild, usually subclinical, infection in pigs. There is no evidenc e that the virus is 
excreted in semen. Therefore it is not identified as a  hazard in the commodity.  
 
References  
References marked * were sighted as summaries in electronic media sources.  
Cox E, Pensaert MB, Callebaut P (1993) . Intestina l protection against challenge with transmissible gastroenteritis 
virus of pigs immune after infection with porcine respiratory coronavirus. Vaccine , 11, 267-72.*  
Ministry for Primary Industries  Import risk analysis: Pig semen • 69  
MAF (2008).  The Unwanted Organisms Register. http://mafuwsp6.maf.govt.nz/uor/searchframe.htm , downloaded 
27/1/2009.  
 Pensaert M, Callebaut P, Vergote J (1986) . Isolation of a porcine respiratory, non-enteric coronavirus related to 
transmissible gastroenteritis virus. Veterinary Quar terly, 8, 257-61.*  
 Rasschaert D, Duarte M, Lause H (1990). Porcine respiratory coronavirus differs from transmissible 
gastroenteritis virus by a few genomic deletions. Journal of General Virology , 71, 2599-607.  
 
Saif LJ, Sestak K (2006).  Transmissible gas troenteritis and porcine respiratory coronavirus . In: Straw BE, 
Zimmerman JJ, D'Allaire S, Taylor DJ (eds), Diseases of Swine . 9th edition, Pp. 489- 516, Blackwell Publishing, 
Ames, Iowa.  
 
Spaan WJM, Brian D, Cavanagh D, de Groot R, J., Enjuanes L, Gorbalenya AE, Holmes KV, Masters P, 
Rottier P, Taguchi F, Talbot P (2005).  Genus   Coronavirus . In: Fauquet CM, Mayo MA, Maniloff J, Desselberger 
U, Ball LA, (eds), Eighth Report of the International Committee on Taxonomy of Viruses , Pp. 947-55., Elsevier 
Academic Press, Amsterdam.  
 
Wesley RD, Woods RD (1993). Immunization of pregnant gilts with PCRV produces lactogenic immunity for 
protection of nursing piglets from challenge with TGEV. Veterinary Microbiology , 38, 31-40.  
 
Wesley RD, Woods RD (1996). Induction of protective immunity against transmissible gastroenteritis virus after 
exposure or neonatal pigs to porcine respiratory coronavirus. American Journal of Veterinary Research, 57, 157-62.  
 
   
Ministry for Primary Industries  Import risk analysis: Pig semen • 70 23.  Rabies virus  
23.1. HAZARD IDENTIFICATIO N 
23.1.1.  Aetiological agent  
Family: Rhabdoviridae , Genus : Lyssavirus , rabies virus. In addition to the true rabies virus there 
are a number of closely related lyssaviruses such as the European bat Lyssavirus which cause 
similar diseases.  
23.1.2.  OIE list  
Listed (OIE 2 008a) . 
23.1.3.  New Zealand status  
Exotic, notifiable organism (MAF 2008) . 
23.1.4.  Epidemiology  
Rabies is a disease of all mammals including man. It is characterized by severe nervous signs 
and is invariably fatal.  
 With some exceptions (particularly islands), rabies is found wo rldwide.  The United Kingdom , 
Ireland, Sweden , Norway, Finland, Iceland, Japan, Australia, New Zealand, Singapore, most of 
Malaysia, Papua New Guinea, the Pacific Islands, the Indonesian island chains east of Java, and 
Iranian Jaya have been free of classical rabies virus for many years (Center for F ood Security 
and Public Health 2005;  OIE 2008b ). 
 In all endemically -infected countries the virus is maintained in a population  of domestic or wild 
carnivores, and in some European countries and Australia related lyssaviruses occur in bats 
(Fooks et al 2003; Swanepoel 2004; Thompson 1999) . 
 The virus is carried mainly by carnivores and, in the final stages of the disease, they excrete the 
virus in their saliva and transmit the disease to other animals when they bite them. Other forms of transmission such as aerosol transmission in bat colonies (Swanepoel 2004)  and per os 
infection of kudu (Hubschle 1988)  are rare exceptions. Following deposition of virus in a bite 
wound the virus enters peripheral nerves and is transported through the nerves to the central 
nervo us system. After entering the peripheral nerves the virus is not found in any other body 
tissues or in the blood. Amputation of limbs of mice experimentally infected in the footpads has been shown to prevent the virus from progressing to the brain (Swanepoel 2004) . The passage of 
virus through the nervous system is a slow process and depending on the site  of infection, the 
dose of virus and the animal concerned , the incubation period before the appearance of clinical 
signs may vary from weeks to years. In pigs the incubation period has been reported to vary from a few days to several weeks (Elvinger 2006) .The occurrence of viraemia is an exceptional event , 
except in exper imental infections of young mice with large doses of virus (Swanepoel 2004) . 
The virus spreads to the  salivary glands at about the stage that there is generalized dissemination 
of infection in the brain. It then multiplies in the salivary glands and is excreted in the saliva. In the terminal stages of the disease animals become incoordinated and may be ag gressive.  
  
Ministry for Primary Industries  Import risk analysis: Pig semen • 71 The disease in pigs lasts from a few days to a few weeks and invariably ends fatally , although i t 
has been suggested that pigs m ay recover from the disease (Elvinger 2006) . Typically animals 
become uncoordinated, may be aggressive and salivate excessively or develop a paralytic form 
of the disease (Swanepoel 2004) . Pigs are generally dead -end hosts since they are unlik ely to bite 
other animals or humans .  
The virus is confined to the nervous tissues until the final stages of the disease when the clinical 
signs  are dramatic and obvious. The likelihood of contamination of semen with virus collected 
from healthy animals which have remained healt hy for 60 days aft er collection  is negligible.   
23.1.5.  Hazard identification conclusion 
Rabies virus is not identified as a hazard in s emen collected from healthy boars housed at 
collection centres that have been approved by the veterinary authority of the exporting country.  
 
References  
 
Center for Food Security and Public Health (2005).  Rabies. Available at: 
http://www.ivis.org/advances/Disease_Factsheets/rabies.pdf  
 Elvinger F (2006).  Rabies. In: Straw BE, Zimmerman JJ, D'Allaire S, Taylor DJ (eds),  Diseases of Swine . 9th 
edition, Pp. 557-60, Blackwell Publishing, Ames, Iowa.  
 
Fooks AR, Brookes SM, Johnson N, McElhinney LM, Hutson AM (2003) . European bat lyssaviruses: an 
emerging zoonosis. Epidemiology and Infection, 131(3), 1029-39.  
 
Hubschle OJ (1988) . Rabie s in kudu antelope. Reviews of Infectious Diseases , 19(Supplement 4), S629-33.  
 
MAF (2008). The Unwanted Organisms Register. 
http://mafuwsp6.maf.govt.nz/uor/searchframe.htm , downloaded 
27/1/2009.  
 
OIE (2008a) . Chapter 8.11, Rabies. Terrestrial Animal Health Code ,  
http://www.oie.int/eng/normes/MCode/en_chapitre_1.8.11.htm , downloaded 27/1/2009.  
 OIE (2008b) . World Animal Health Information Database (WAHID) Interface. 
http://www.oie.int/wahid -
prod/public.php?page=home , downloaded 27/1/2009.  
 
Swanepoel R (2004).  Rabies. In: Coetzer JAW, Tustin RC (eds), Infectious Diseases of livestock . Terrestrial Animal 
Health Code, Vol. 2, Pp. 1123-82, Oxford University Press, Oxford.  
 
Thompson GK (1999) . Veterinary surgeon's guide to Australian bat lyssavirus. Australian Veterinary Journal , 
77(11), 710-2.  
  
Ministry for Primary Industries  Import risk analysis: Pig semen • 72 24. Ross Ri ver virus 
24.1. HAZARD IDENTIFICATIO N 
24.1.1.  Aetiological agent  
Family: Togaviridae , Genus: Alphavirus , Species: Ross River virus  (RRV) (Weaver et al 2005) . 
24.1.2.  OIE list  
Not listed . 
24.1.3.  New Zealand status  
Exotic . 
24.1.4.  Epidemiology  
RRV is a mosquito -borne alphavirus that occurs in Australia. It has not been reported in Nor th 
America or Europe (Harley et  al 2001; Russell 2002; Russell and Doggett 2006) . RRV is a 
zoonotic virus but is not known to cause clinical disease in domestic animals.  
 
Approximately 5,000 human cases of Ross River fever (characterised by fever, polyarthritis, and 
rash) are notified  annually in Australia (Harley et al 2001; Russell 2002; Russell and Doggett 
2006) .  RRV has been isolated from at least 30 species of mosquitoes and transmission has been 
demonstrated from at least 13 species (Harley et al 2001) . The major mosquito vectors are Culex 
annulirostris  in freshw ater habitats, and Aedes vigilax  and Aedes camptorynchus  in northern and 
southern coastal regions. Other species involved in transmission include Aedes normanensis, 
Coquillettidia linealis,  and Aedes notoscriptus . Based mainly on serological evidence, the 
reservoir hosts for the virus are believed to be large marsupials such as kangaroos and wallabies (Russell 2002; Russell and Doggett 2006; Vale et al 1991) . However, antibodies to the virus 
have been found in a wide variety of placental and marsupial mammals, and viral is olations from 
naturally infected vertebrates have only been recorded in eight cases including two cases from 
macropods and two from horses (Harley et al 2001) . Humans may also act as reservoirs of 
infection and a mosquito -human cycle probably occurs during outb reaks of the disease.  
 
RRV is normally confined to Australia, Papua New Guinea, and the Solomon Islands. In the 
latter two countries the virus may be introduced periodically from Australia (Russell 2002) . An 
outbreak that occurred in the Pacific region in 1979 -80 involved Fiji, American Samoa, the Cook 
Islands, and New Caledonia, and probably also Tonga, Kiribati, and Western Samoa. The 
outbreak seems to have been started by a single traveller from Australia infecting mosquitoes in Fiji (Harley et al 2001; Russell 2002) . Since the virus is known to be transmitted by Aedes 
aegypti  and Aedes albopictus  the potential exists for outbreaks of disease to occur in countries 
where these species of mosquitoes are present.  
 RRV has not occurred in New Zealand. Aedes notoscriptus , a pr obable vector of Ross River 
virus (Russell and Doggett 2006)  and Aedes camptorhynchus,  a known vector of the virus, have 
become established in New Zealand (Derraik and Calisher 2004) . However, Aedes  
camptorhynchus  has subsequently been the subject of a successful eradication campaign
4
                                                
4 See: http://www.biosecurity.govt.nz/pests/southern -saltmarsh -mosquito  .  
Ministry for Primary Industries  Import risk analysis: Pig semen • 73  
No records of natural infection of pigs with RRV have been found , although pigs in Taiwa n have 
serological evidence of repeated exposure to a closely related alphavirus (Sagiyama virus).  Experimental infection of pigs with Sagiyama virus is non -pathogenic and leads to a short -lived 
period of viraemia (Chang et al 2006).  There is no evidence  to suggest that Sagiyama virus is 
likely to be transmitted in porcine semen.  
 
24.1.5.  Hazard identification conclusion 
Since there is no evidence  that pigs can act as reservoirs of RRV  and no evidence to suggest that 
transmission of alphaviruses in porcine semen should be considered likely,  RRV  is not identified 
as a hazard in the commodity.  
 
 References  
 
References marked * have been sighted as summaries  in electronic media . 
Chang C-Y, Huang C-C, Huang T -S, Deng M -C, Jong M -H, Wang F -I (2006). Isolation and chara cterization of 
Sagiyama virus fro m domestic pigs. Journal of Veterinary Diagnostic Investigation , 18, 156-61.  
 
Derraik JG, Calisher CH (2004).  Is New Zealand prepared to deal with arbvoviral diseases? Australian and New 
Zealand Journal Public Health , 28(1) , 27-31. 
 
Harley D, Sleigh A, Ritchie S (2001).  Ross river virus transmission, infection and disease: a cross -disciplinary 
review. Clinical Microbiology reviews , 14(4), 909- 32. 
 
Russell RC (2002).  Ross River virus: Ecology and distribution. Annual Review of Entomology , 47, 1 -31. 
 
Russell RC, Doggett SL (2006).  Ross river and Barmah forest. 
medent.usyd.edu.au/fact/ross%20river%20&%20barmah%20forest.htm . 
 
Vale TG, Spratt DM, Cloonan MJ (1991).  Serological evidence of arbovirus infection in native an domestic 
mammals on the south coast of New South Wales. Australian Journal of Zoology , 39, 1 -7.* 
 Weaver SC, Frey TK, Huang HV, Kinney RM, Rice CM, Roehrig JT, Shope RE, Strauss EG (2005).  Genus   
Alphavirus . In: Fauquet CM, Mayo MA, Maniloff J, Desselberger U, Ball  LA, (eds), Eighth Report of the 
International Committee on Taxonomy of Viruses . Pp. 1003 -5, Elsevier Academic Press, Amsterdam.   
Ministry for Primary Industries  Import risk analysis: Pig semen • 74 25. Teschovirus serotype 1 
25.1. HAZARD IDENTIFICATIO N 
25.1.1.  Aetiological agent  
Family: Picornaviridae , Genus: Teschovirus . Eleven serotypes o f porcine Teschovirus (PTV) are 
recognised, PTV -1 to PTV -11.  Virulent strains of PTV -1 are associated with Teschovirus 
encephalitis (Teschen disease) whereas less virulent strains of PTV -1 are associated with milder 
disease (Talfan disease, benign enzooti c paresis, or poliomyelitis suum) (Zell et al 2001; Center 
for Food Security and Public Health 2009).  
25.1.2.  OIE list  
Not listed.  
25.1.3.  New Zealand status  
Enterovirus encephalomyelitis virus is exotic to New Zealand and listed as a Notifiable 
Organism (Tana et al 2011) . 
25.1.4.  Epidemiology  
Most of the eleven serotypes of PTV are widely distributed in pigs and cause few clinical problems.  However, virulent strains of PTV -1 cause Teschovirus encephalomyelitis.  Teschen 
disease (a fatal, nonsuppurative encephalomyelitis of pigs)  was first described in the Czech 
republic in 1929 and later spread throughout Europe (OIE 2008).  A milder form of disease 
(Talfan disease or poliomyelitis suum) was later recognised in Wales and Denmark (Yamada et 
al 2009).  Clinical signs of infection w ith virulent strains of  PTV -1 include fever, anorexia, 
depression and incoordination followed by hypersensitivity, paralysis and death.  Less virulent 
strains of PTV -1 (and strains of PTV -2, -3, -4, -5, -6, -9, and -10) are associated with 
neurological di sease in younger animals characterised by ataxia and paresis which may progress 
to paralysis (OIE 2008;  Center for Food Security and Public Health 2009).  
Teschovirus encephalomyelitis has not been reported in Western Europe since 1980.  Since 
1996, the dis ease has been reported in Belarus, Japan, Latvia, Madagascar, Moldavia, Romania, 
Russia, Uganda, and Ukraine  (OIE 2008).  
PTV enters the body via the oral route and multiplies in the gastrointestinal tract and associated lymphoid tissues before being shed i n faeces and oral secretions  (Center for Food Security and 
Public Health 2009).  
Following experimental intravenous infection with PTV -1, viral antigen was detected in spinal 
ganglia, degenerate nerve fibres, brainstem grey matter, and ventral horn of the s pinal cord as 
well as in bronchiolar epithelial cells, hepatocytes, tonsillar epithelium and myenteric nerve 
plexus of the small and large intestine.  Viral antigen was only seen in the enterocytes of the 
duodenum and jejunum and in the tonsils following o ral infection with PTV -1 (Yamada et al 
2009).  Histological studies on field outbreaks of disease suggest pathological lesions are limited to the brain and spinal cord (Pogranichniy et al 2003).   
Ministry for Primary Industries  Import risk analysis: Pig semen • 75 PTV infections only occur in swine.  Other animal species are not known to be susceptible (OIE 
2008).  
25.1.5.  Hazard identification conclusion 
There is no evidence to support the suggestion that PTV -1 may be spread in the semen of 
infected boars. PTV -1 is not identified as a hazard in porcine semen.  
 
References  
Center for F ood Security and Public Health  (2009). Teschovirus encephalomyelitis and porcine Teschovirus 
infection. [Online] Available from: http://www.cfsph.iastate.edu/Factsh eets/pdfs/enterovirus_encephalomyelitis.pdf  
[Accessed 15th November  2012].  
OIE (2008). Teschovirus encephalomyelitis (previously enterovirus encephalomyelitis or Teschen/Talfan disease). 
Chapter 2.8.10 in: Manual of Diagnostic Tests and Vaccines for Terre strial Animals . OIE, Paris.  
Pogranichniy RM, Janke BH, Gillespie TG, Yoon K -J (2003).  A prolonged outbreak of polioencephalomyelitis 
due to infection with a group I porcine enterovirus. Journal of Veterinary Diagnostic Investigation 15, 191- 194. 
Tana T, Mu rray -Cullen J, Johnston C, Lee E (2011).   Notifiable organisms. Surveillance  38(2), 20-24.  
Yamada M,  Kozakura R, Nakamura K, Yamamoto Y, Yoshii M, Kaku Y, Miyazaki A, Tsunemitsu H, Narita 
M (2009).  Pathological changes in pigs experimentally infected with porcine Teschovirus. Journal of Comparative 
Pathology  141, 223-228.  
Zell R, Dauber M, Krumbholz A, Henke A, Birch -Hirschfeld E, Stelzner A, Prager D, Wurm R (2001).  
Porcine Teschoviruses comprise at least eleven distinct serotypes: Molecular and evolutiona ry aspects. Journal of 
Virology  75, 1620-1631.   
Ministry for Primary Industries  Import risk analysis: Pig semen • 76 26. Torque teno virus  
26.1. HAZARD IDENTIFICATIO N 
26.1.1.  Aetiological agent  
Genus: Anellovirus , Species: Torque teno virus (TTV) (Biagini  et al 2005) .  Two species -specific 
genogroups have been described in pigs (TTV1 and TTV2) (Niel et al 2005).  
26.1.2.  OIE list  
Not listed . 
26.1.3.  New Zealand status  
Testing of a small number of samples from New Zealand pigs has not found positive animals, 
but no surveillance related to this virus has occurred in New Zealand (Clement 2009).  
26.1.4.  Epidemiology  
TTV infection of pigs was first reported in t he United States (Leary et al 1999) and later 
characterised in Japan (Okamoto et al 2002).  Infection has subsequently been recognised in pigs 
in Canada, Spain, China, Korea, Thailand (McKeown et al 2004), and Brazil (Niel et al 2005).  A 
study of TTV in s ix different countries demonstrated that approximately 66% of pigs were 
positive for TTV DNA, suggesting that TTV should be considered ubiquitous in swine populations (McKeown et al 2004).  
Porcine TTV is not known to be associated with any swine disease ( McKeown et al 2004) 
although experimental infection of gnotobiotic piglets resulted in mild histologic changes in the 
lung, liver and kidney which were not accompanied by overt clinical signs (Krakowka and Ellis 
2008).  There is some speculation that TTV m ay contribute to the expression of postweaning 
multisystemic wasting syndrome in porcine circovirus 2 -infected pigs (Kekarainen et al 2006; 
Ellis et al 2008)
 
Vertical transmission of TTV has been described in pigs (Pozzuto et al 2009) and TTV can be found in porcine semen.  69% of TTV -seropositive boars were shown to have detectable TTV 
DNA in their semen using a nested PCR assay (Kekarainen et al 2007).  
26.1.5.  Hazard identification conclusion 
TTV is ubiquitous and where surveillance for exposure to this virus has  been undertaken a high 
seroprevalence is demonstrated.  There is a high likelihood that TTV would be present in porcine 
semen and, in the absence of sanitary measures for TTV, it is inevitable that this virus has been 
introduced into New Zealand in this c ommodity.  Given the absence of clinical disease 
associated with TTV infection, any claim that New Zealand should be considered free of this virus would have little credibility.  TTV is not identified as a  hazard in the commodity.  
 
References  
 
Biagini P, Todd D, Bendinelli M, Hino S, Mankertz A, Mishiro S, Neil C, Okamoto H, Raidal S, Ritchie BW, 
Teo GC (2005).  Genus   Anellovirus . In: Fauquet CM, Mayo MA, Maniloff J, Desselberger U, Ball LA, (eds), 
Eighth Report of the International Committee on Taxonomy of  Viruses . Pp. 335-41, Elsevier Academic Press, 
Amsterdam.  
  
Ministry for Primary Industries  Import risk analysis: Pig semen • 77 Clement F (2009) . Re: Import risk analysis: Pig semen from Australia, the USA, Canada, the European Union and 
Norway – Draft for public consultation.  Personal communication. Letter to Reed CE, 4 N ovember 2009.  
 
Ellis JA, Allan G, Krakowka S (2008).  Effect of coinfection with genogroup 1 porcine torque teno virus on 
porcine circovirus type 2 -associated postweaning multisystemic wasting syndrome in gnotobiotic pigs.  American 
Journal of Veterinary Re search  69, 1608- 14. 
 
Kekarainen T, Sibila M, Segalés J (2006).  Prevalence of swine Torque teno virus  in post -weaning multisystemic 
wasting syndrome (PMWS) -affected and non -PMWS-affected pigs in Spain. Journal of General Virology  87, 833 -7. 
 
Kekarainen T, L ópez -Soria S, Segalés J (2007).  Detection of swine Torque teno virus genogroups 1 and 2 in boar 
sera and semen. Theriogenology  68, 966 -71. 
 Krakowka S, Ellis JA (2008).  Evaluation of the effects of porcine genogroup 1 torque teno virus in gnotobiotic 
swine . American Journal of Veterinary Research 69, 1623 -9. 
 Leary TP, Erker JC, Chalmers ML, Desai SM, Mushahwar I (1999).  Improved detection systems for TT virus 
reveal high prevalence in humans, non- human primates and farm animal. Journal of General Virology  80, 2115-20.  
 McKeown NE, Fenaux M, Halbur PG, Meng XJ (2004). Molecular characterization of porcine TT virus, an 
orphan virus, in pigs from six different countries. Veterinary Microbiology  104, 113-7.  
 
Niel C, Diniz -Mendes L, Devalle S (2005). Rolling -circle amplification of Torque teno virus  (TTV) complete 
genomes from human and swine sera and identification of a novel swine TTV genogroup. Journal of General 
Virology  86, 1343-7.  
 
Okamoto H, Takahashi M, Nishizawa T, Tawara A, Fukai K, Muramatsu U, Naito Y , Yoshikawa A (2002).  
Genomic characterization of TT viruses (TTVs) in pigs, cats and dogs and their relatedness with species -specific 
TTVs in primates and tupaias. Journal of General Virology  83, 1291-7.  
 
Pozzuto T, Mueller B, Me ehan B, Ringler SS, McInto sh KA, Ellis JA, Mankertz A, Krakowka S (2009).  In 
utero  transmission of porcine torque teno viruses. Veterinary Microbiology  137, 375-9.  
  
 
 
 
  
Ministry for Primary Industries  Import risk analysis: Pig semen • 78 27. Transmissible gastroenteritis virus 
27.1. HAZARD IDENTIFICATIO N 
27.1.1.  Aetiological agent  
Family: Coronaviridae , Genus: Coro navirus , Species: Transmissible gastroenteritis virus  
(TGEV) (Spaan et al 2005) . 
27.1.2.  OIE list  
Listed (OIE 2008a) . 
27.1.3.  New Zealand status  
Notifiable disease (MAF 2008) . 
27.1.4.  Epidemiology  
Transmissible gastroenteritis causes high mortality in neonatal pigs. It occurs in North America 
and in many European countries but not in Norway or Australia (OIE 2008b) . The close 
relationship to PRCV has been discussed in Section 18. There is an overall nucleotide seque nce 
homology of 96% between TGEV and PRCV , but the latter has a deletion of 621 -681 
nucleotides in the S gene (Saif and Sestak 2006) .  
When introduced into a naïve herd TGEV infects all age groups , and pigs under 7 days 
invariably die. Sucklin g pigs older than 7 days usually survive but remain stunted. Older pigs 
generally show inappetance and diarrhoea for a few days before recovering (Saif and Sestak 
2006) . Lactating sows may become very sick with signs of inappetance, vomiting, diarrhoea, and 
agalactia (Saif and Sestak 2006) . Cats and dogs can be subclinically infected (Pensaert and Van 
Reeth 2004) .  
Pigs commonly carry the virus for about 2 weeks after infection (Pensaert and Van Reeth 2004) , 
but chronic and/or persistent shedding of the virus for periods up to 18 months has been reported (Derbyshire et al 1969) . After an outbreak of the disease some herds eliminate the virus, but in 
larger herds with frequent  farrowings the virus may become endemic (Saif and Sestak 2006) . 
Transmission is usually by t he faecal -oral route when susceptible pigs come in contact with 
infected pigs or when faeces are carried on fomites (Saif and Sestak 2006) . There are no 
descriptions of transmission by semen or of insemination being significant in the epidemio logy 
of the disease.  
27.1.5.  Hazard identification conclusion 
The virus is not transmitted in semen, and therefore it is not identified as a  hazard in the 
commodity.  
 
References  
References marked * were seen as abstracts in electronic databases.  
Derbyshire JB, Jessett DM, Newman G (1969) . An experimental epidemiological study of porcine transmissible 
gastroenteritis. Journal of Comparative Pathology , 79(4), 445 -52.*  
 
MAF (2008). The Unwanted Organisms Register. http://mafuwsp6.maf.govt.nz/uor/searchframe.htm , downloaded 
27/1/2009.   
Ministry for Primary Industries  Import risk analysis: Pig semen • 79  
OIE (2008a) . Terrestrial Animal Health Code . http://www.oie.int/eng/normes/MCode/en_ sommaire.htm , 
downloaded 27/1/2009.  
 OIE (2008b) . World Animal Health Information Database (WAHID) Interface. 
http://www.oie.int/wahid -
prod/public.php?page=home , downloaded 27/1/2009.  
 Pensaert MB, Van Reeth K (2004).  Transmissible gastroenteritis. In: Coetzer JAW, Tustin RC (eds), Infectious 
Diseases of Livestock . Vol. 2, Pp. 780 -3, Oxford University Press, Cape Town.  
 Saif LJ, Sestak K (2006).  Transmissible gastroenteritis and porcine respiratory coronavirus. In: Straw BE, 
Zimmerman JJ, D'Allaire S, Taylor DJ (eds), Diseases of Swine . 9th edition, Pp. 489- 516, Blackwell Publishing, 
Ames, Iowa.  
 
Spaan WJM, Brian D, Cavanagh D, de Groot R, J., Enjuanes L, Gorbalenya AE, Holmes KV, Masters  P, 
Rottier P, Taguchi F, Talbot P (2005).  Genus  Coronavirus . In: Fauquet CM, Mayo MA, Maniloff J, Desselberger 
U, Ball LA (eds), Eighth Report of the International Committee on Taxonomy of Viruses , Pp. 947-55., Elsevier 
Academic Press, Amsterdam.  
    
Ministry for Primary Industries  Import risk analysis: Pig semen • 80 28. Rotavirus  
28.1. HAZARD IDENTIFICATIO N 
28.1.1.  Aetiological agent  
Family: Reoviridae , Genus: Rotavirus , Species: Rotavirus E  (Ramig et al 2005) .   
28.1.2.  OIE list  
Not listed.  
28.1.3.  New Zealand status  
Group A rotavirus has been described in New Zealand pigs (Fu and Hampson 1987; Fu and 
Hampson 1989; Fu et al 1989; Fu et al 1990) . However, due to the limited numb er of 
investigations reported and the confused state of the taxonomy of rotaviruses , it is uncertain if all 
types of rotaviruses that occur in pigs are present in New Zealand.  
28.1.4.  Epidemiology  
Rotaviruses are generally described as occurring universally (Steele et al 2004; Yuan et al 2006)  
and there is consi derable confusion about the naming and classification of the different species. 
The International Committee on the Taxonomy of Viruses recognises Rotavirus A -E with 
tentative species F and G. Group A, B, and C rotaviruses have been detected in pigs  as well as in 
other animals and humans. Type E has been found only in pigs and groups D, F and G have been 
detected only in birds. The basis for recognition of a species is considered to be “the ability to 
exchange (reassort) genome segments during coinfection, t hereby exchanging genetic 
information and generating novel progeny virus strains” (Ramig et al 2005) . Rotaviruses  are 
double -stranded RNA viruses in which reassortments occur. The basis for classifying species is 
more theoretical than practically useful and the taxonomy of the group is likely to be unstable. Serological characteristics are of more practical importance for classifying species. Rotavirus  
group A strains have been described in pigs in New Zealand (Fu and Hampson 1987; Fu and 
Hampson 1989; Fu et al 1989; Fu et al 1990) .  Most importantly, all the rotaviruses are enteri c 
viruses transmitted by the faecal -oral route and have not been reported as being excreted in 
semen. Semen, natural breeding and artificial insemination have not been reported as being 
relevant to the epidemiology of the disease.  
28.1.5.  Hazard identification co nclusion 
The virus is not excreted in semen and therefore the likelihood of importing rotavirus virus in 
semen is negligible and it is not identified as a  hazard in the commodity.  
 References  
 
Fu ZF, Hampson DJ (1987). Group A rotavirus  excretion patterns in naturally infected pigs. Research in 
Veterinary Science , 43(3), 297-300.  
 
Fu ZF, Hampson DJ (1989). Natural transmission of group A rotavirus within a pig population. Research in 
Veterinary Science , 46(3), 312-7.  
 
Fu ZF, Hampson DJ, Blackmore DK (1989). Detection and survival of group A rotavirus in a piggery. Veterinary 
Record , 125, 576-8.   
Ministry for Primary Industries  Import risk analysis: Pig semen • 81  
Fu ZF, Hampson DJ, Wilks CR (1990) . Transfer of maternal antibody against group A rotavirus from sows to 
piglets and serological responses follow ing natural infection. Research in Veterinary Science , 48(3), 365-73.  
 Ramig RF, Ciarlet M, Mertens PPC, Dermody TS (2005).  Genus  Rotavirus . In: Fauquet CM, Mayo MA, 
Maniloff J, Desselberger U, Ball LA (eds), Eighth Report of the International Committee on Taxonomy of Viruses , 
Pp. 484-96, Elsevier Academic Press, Amsterdam.  
 Steele AD, Geyer A, Gerdes GH (2004).  Rotavirus infections. In: Coetzer JAW, Tustin RC (eds), Infectious 
Diseases of Livestock . Vol. 2, Pp. 1256- 64, Oxford University Press, Cape Town.  
 
Yuan L, Stevenson GW, Saif LJ (2006).  Rotavirus and Reovirus. In: Straw BE, Zimmerman JJ, D'Allaire S, 
Taylor DJ (eds), Diseases of Swine .  9th edition, Pp. 435-54, Blackwell Publishing, Ames, Iowa.  
   
Ministry for Primary Industries  Import risk analysis: Pig semen • 82 29. Porcine reovirus  
29.1. HAZARD IDENTIFICATIO N 
29.1.1.  Aetiological agent  
Family: Reoviridae , Genus: Orthoreovirus , Species: Mammalian orthoreovirus  1-4 (Chappell et 
al 2005) . 
29.1.2.  OIE list  
Not listed.  
29.1.3.  New Zealand status  
Reoviruses have been isolated from poultry (Green et al 1976; Saifuddin et al 1980)  and 
antibodies are frequently detected in poultry. Reovirus also occurs in cats. However, a 
retrospective electronic search of Surveillance  and the New Zealand Veterinary J ournal  revealed 
no evidence that the virus has ever been found in pigs in this country.  
29.1.4.  Epidemiology  
Reoviruses are regarded as orphan viruses occurring in the respiratory system and gut. They have been isolated from diseased and healthy pigs but experimental inoculations have not consistently 
caused disease (Yuan et al 2006) .    
29.1.5.  Hazard identification conclusion 
Reoviruses are not considered to be pathogenic in pigs and are not identified as a hazard  in the 
commodity.  
 References  
 
Chappe ll JD, Duncan R, Mertens PPC, Dermody TS (2005).  Genus Orthoreovirus . In: Fauquet CM, Mayo MA, 
Maniloff J, Desselberger U, Ball LA (eds), Eighth Report of the International Committee on Taxonomy of Viruses , 
Pp. 455-65, Elsevier Academic Press, Amsterdam.  
 
Green AF, Clarke TK, Lohr JE (1976) . Avian reoviruses in New Zealand. New Zealand Veterinary Journal , 
24(8), 181 -3. 
 Saifuddin M, Wilks CR, Christensen NH, Fu ZF, Rice M (1980) . Isolation of a reovirus from a broiler chicken 
flock with high early mortality . New Zealand Veterinary Journal , 37, 12 -4. 
 Yuan L, Stevenson GW, Saif LJ (2006).  Rotavirus and Reovirus. In: Straw BE, Zimmerman JJ, D'Allaire S, 
Taylor DJ (eds),  Diseases of Swine . 9th edition, Pp. 435-54, Blackwell Publishing, Ames, Iowa.  
   
Ministry for Primary Industries  Import risk analysis: Pig semen • 83 30. Swine inf luenza virus  
30.1. HAZARD IDENTIFICATIO N 
30.1.1.  Aetiological agent  
Family: Orthomyxoviridae , Genus: Influenzavirus  A, Species: Influenza A virus  (Kawaoka et al 
2005) . 
30.1.2.  OIE list  
Avian influenza is listed in the Code , but swine influenza is not listed as a pig disease (OIE 
2008) . 
30.1.3.  New Zealand status  
Antibody to H3N2 influenza A virus was found 88.6% of pig sera in a survey of 429 pigs. No 
antibodies were found to H1N1, the other strain of influenza A virus commonly found in pigs 
overseas (Stanislawek 2001) . 
30.1.4.  Epidemiology  
Influenza A, B, and C viruses are recognized as separate genera (Kawaoka et al 2005) . Only 
influenza A viruses are important in pigs (Olsen et al 2006; Thompson and Easterday 2004) . All 
influenza viruses are classified serologically according to the combination of the haemagglutinin 
(H) and neuraminidase (N) an tigens they express. There are 16 different forms of H and 9 of N 
and all combinations of these are possible (Olsen et al 2006) . Influenza viruses are segmented 
negative sense RNA viruses and therefore genetically unstable. Major reassortmen ts of RNA 
segments are possible due to recombination events and smaller mutations cause antigenic drift. However, the situation in pigs has remained relatively stable and only H1N1, H3N2, and more 
rarely H1N2 are of known significance (Olsen et al 2006) .  
Because pigs are susceptible to both avian and human influenza viruses they are thought to be important hosts for the generation of recombinants that could potentially cause a pandemic in 
humans (Olsen et al 2006) . The factors  necessary for creating a new virulent strain are still only 
partially understood (Neumann and Kawaoka 2006) . 
Swine influenza is a mild disease of pigs characterised by a sudden onset of respiratory signs and 
an abrupt recovery about 5- 7 days lat er (Olsen et al 2006) . More severe signs can occur when 
infection with influenza virus is complicated by the simultaneous occurrence of other infections such as porcine respiratory  and reproductive syndrome  or various bacterial infections (Olsen et al 
2006) . However, the infection is often subclinical as evidenced by the fact that the disease has 
not been described in New Zealand but antibodies occur commonly in pigs.  
Influenza in swine is primarily an infection of the respirat ory tissues. In lung tissue the virus 
multiplies to a high titre (Olsen et al 2006 ; Thompson and Easterday 2004)  but viraemia is not 
considered to be a feature of the disease (Zou 2006) . Howeve r, it has been shown to occur 
irregularly in experimentally infected mice and in humans with subsequent transient infections of 
other organs including muscles, liver and brain (Davis et al 2000; Mori et al 1995; Tsuruoka et al 
1997) . No evidence could be found that the virus is transmitted in semen.   
Ministry for Primary Industries  Import risk analysis: Pig semen • 84 30.1.5.  Hazard identification conclusion 
Swine influenza is a comparatively mild infection of little economic importan ce. The disease has 
a short course or is subclinical and long -term carriers are not known. Consequently, the 
likelihood that semen donors resident in collection centres, where all pigs are healthy and 
quarantined on entry, would be infected with swine infl uenza virus at the time of semen donation 
is negligible. In addition the virus is not transmitted in semen. Therefore the virus is not identified as a  hazard in the commodity.  
 References  
References marked * were sighted as summaries in electronic media so urces.  
Davis LE, Kornfeld M, Daniels RS, Skehel JJ (2000) . Experimental influenza causes a non -permissive viral 
infection of brain, liver and muscle. Journal of Neurovirology , 6(6), 529-36.* 
 
Kawaoka Y, Cox NJ, Haller O, Hongo S, Kaveri n N, Klenk H -D, Lamb RA, McCauley J, Palese P, Rimsted 
E, Webster RG (2005).  Genus:  Influenzavirus A . In: Fauquet CM, Mayo MA, Maniloff J, Desselberger U, Ball LA 
(eds), Eighth Report of the International Committee on Taxonomy of Viruses , Pp. 685 -7, Elsevi er Academic Press, 
Amsterdam.  
 
Mori I, Komatsu T, Takeuchi K, Nakakuki K, Sudo M, Kimura Y (1995) . Viremia induced by influenza virus. 
Microbial Pathogenesis , 19(4), 237 -44. 
 Neumann G, Kawaoka Y (2006). Host range restriction and pathogenicity in the cont ext of influenza pandemic. 
Emerging Infectious Diseases , 12(6). http://www.cdc.gov/ncidod/eid/vol12no06/05-1336.htm, downloaded 
27/1/2009.  
 
OIE (2008) . Terrestrial Animal Health Code. 
http://www.oie.int/eng/normes/MCode/en_sommaire.htm , 
downloaded 27/1/2009.  
 Olsen CW, Brown IH, Easterday BC, Van Reeth K (2006).  Swine influenza. In: Straw BE, Zimmerman JJ, 
D'Allaire S, Taylor DJ (eds), Diseases of Swine . Pp. 469-82, Blackwell Publishing,  Ames, Iowa.  
 
Stanislawek W (2001) . Serological survey for influenza A in New Zealand pigs. Surveillance , 28(22), 7-8.  
 
Thompson GR, Easterday BC (2004).  Swine influenza. In: Coetzer JAW, Tustin RC (eds), Infectious Diseases of 
Livestock . Vol. 2, Pp. 775 -8, Oxford University Press, Cape Town.  
 
Tsuruoka H, Xu H, Kuroda K, Hosaka Y (1997) . Viremia in influenza: detection by polymerase chain reaction. 
Nippon Rinsho , 55(10), 2714-8.* 
 Zou S (2006) . Potential impact of pandemic influenza on blood safety and avai lability. Transfusion Medicine 
Reviews , 20(3), 181-9.* 
   
Ministry for Primary Industries  Import risk analysis: Pig semen • 85 31. Swine pox virus  
31.1. HAZARD IDENTIFICATIO N 
31.1.1.  Aetiological agent  
Family: Poxviridae , Genus: Suipoxvirus , Species: Swinepox virus  (Buller et al 2005) .  
31.1.2.  OIE list  
Not listed.  
31.1.3.  New Zealand status  
Classified as an “other exotic organism” (MAF 200 8). 
31.1.4.  Epidemiology  
Information in this section is taken from two authoritative reviews (Delho n and Tulman 2006; 
Munz and Dumbell 2004) .  
Swine pox virus is widely distributed in the world and causes a mild disease of little economic 
significance. The disease is transmitted by contact between acutely infected pigs or by lice or 
biting flies which act as mechanical vectors. Lice remain infected for weeks or months. The 
incubation period of the disease is from 4 -14 days and the virus may persist in dried scabs for 
months. Toward the end of the incubation period virus is also shed from saliva and lachrymal fluid. A viraemic state is postulated but has not been demonstrated. Pox lesions develop 
especially on the abdomen and thin skin regions. The lesions scab over and then heal in about 
three weeks. Diagnosis is usually made from the typical signs and l esions , and virus can be 
confirmed by isolation or electron microscopy. Antibody development is often poor or absent and serological tests are unreliable.  
There is no evidence that pigs are long -term carriers of virus and there is no evidence that the 
virus can be transmitted in semen.  
31.1.5.  Hazard identification conclusion 
The signs of infection are obvious and long -term carriers do not occur. Consequently, the 
likelihood that boars that have been quarantined before introduction to a semen collection centre will be infected at the time of collection is negligible. In addition the virus is not transmitted in 
semen. Therefore, the virus is not identified as a  hazard in the commodity.  
 
References  
 
Buller RM, Arif BM, Black DN, Dumbell KR, Esposit o JJ, Lefkowitz EJ, McFadden G, Moss B, Mercer AA, 
Moye r RW, Skinner MA, Tripathy DN (2005). Genus Suipox . In: Fauquet CM, Mayo MA, Maniloff J, 
Desselberger U, Ball LA (eds), Eighth Report of the International Committee on Taxonomy of Viruses , Pp. 127, 
Elsevier Academic Press, Amsterdam.  
 
Delhon G, Tulman ER (2006).  Swine pox. In: Straw BE, Zimmerman JJ, D'Allaire S, Taylor DJ (eds), Diseases of 
Swine , Pp. 483- 7, Blackwell Publishing, Ames, Iowa.  
 MAF (2008).  The Unwanted Organisms Register. 
http://mafuwsp6.maf.govt.nz/uor/searchframe.htm , downloaded 
27/1/2009.   
Ministry for Primary Industries  Import risk analysis: Pig semen • 86  
Munz E, Dumbell K (2004).  Swine pox. In: Coetzer JAW, Tustin RC (eds), Infectious Diseases of Livestock . Vol. 
2, Pp. 1293-5, Oxford U niversity Press, Oxford.  
  
Ministry for Primary Industries  Import risk analysis: Pig semen • 87 32. Swine vesicular disease virus 
32.1.  HAZARD IDENTFICATION  
32.1.1.  Aetiological agent  
Family: Picornaviridae , Genus: Enterovirus, Species: Swine vesicular disease vir us (SVDV). 
SVDV is considered to be a porcine variant of Human coxsackievirus  B5 (Stanway et al 2005) . 
32.1.2.   OIE list  
Listed (OIE 2008a) . 
32.1.3.  New Zealand status  
Exotic notifiable disease (OIE 2008b) . 
32.1.4.  Epidemiology  
Swine vesicular disease (SVD)  first e merged in Italy in 1966 (Nardelli et al 1968) and was 
subsequently diagnosed throughout Europe and Asia (Lubroth et al 2006).  
SVDV is exceptionally stable outside the host and indirect contacts such as transport vehicles or 
waste feeding play an important role in the spread of disease (Hedger and Mann 1989).  
Experimental inoculation or exposure to a contaminated environment is followed by the rapid 
development of viraemia (Dekker et al 1995).  
Viral titres are greatest in the myocardium and brain of infected individuals, suggesting these are the most likely sites of viral replication (Chu et al 1979; Lai et al 1979) .  Experimental 
inoculation studies have demonstrated high viral titres in lymph nodes (Dekker et al 1995).  SVDV has been recovered from the sem en of infected boars up to 4 days post infection , although 
artificial insemination using infected semen failed to transmit disease to sows (Maes et al 2008).  
32.1.5.   Hazard identification conclusion 
SVDV can be recovered from the semen of infected boars.  SVDV is  therefore identified as  a 
potential hazard in semen imported from infected countries.  
32.2. RISK ASSESSMENT  
32.2.1.  Entry assessment  
SVDV has been reported in a number of European countries  and is currently recognised in Italy 
(OIE 2008b; Sabirovic et al 2009; Sabiro vic et al 2010a; Sabirovic et al 2010b).  As SVDV can 
be found in the semen of infected pigs (Maes et al 2008), the likelihood of entry is assessed  to be 
non-negligible.  
32.2.2.  Exposure assessment  
Imported semen will be inseminated into New Zealand pigs. Maes et  al (2008) noted that 
artificial insemination using SVDV -infected semen failed to transmit disease to sows.  Similarly, 
van Rijn et al (2004) were unable to isolate virus directly from the semen of boars artificially 
infected with SVDV intravenously althou gh virus isolation carried out following the blind 
passage of semen samples in cell culture did detect SVDV.  PCR testing of semen from  
Ministry for Primary Industries  Import risk analysis: Pig semen • 88 artificially infected boars gave weak positive results, suggesting low numbers of SVDV RNA 
(van Rijn et al 2004).  
The li kelihood of exposure is very low . 
32.2.3.  Consequence assessment  
Reflecting the results of van Rijn et al (2004) described above, there is a very low likelihood that insemination of pigs would result in the transmission of SVDV to the recipients of the semen.   
 Infection of pigs with SVDV results in vesicular lesions whose severity may be heavily 
influenced by environmental factors (Hedger and Mann 1989).  These lesions may be 
accompanied by fever, inappetance and general malaise.  SVDV infection may be clinicall y 
indistinguishable from foot and mouth disease so an initial presentation of clinical SVD (before laboratory confirmation of the viral aetiology) would be likely to trigger the massive initial 
response usually reserved for foot and mouth disease.  
 The con sequences of exposure are assessed  to be non -negligible.  
32.2.4.  Risk estimation  
Entry, exposure and consequence have all been assessed as non -negligible. As a result the risk 
estimate for SVDV is non -negligible and it is classified as a risk  in the commodity. Therefore 
risk management measures can be justified.  
32.3. RISK MANAGEMENT  
32.3.1.  Options  
 The Code  defines SVD -free countries, and SVD -infected zones.  The Code  chapter on SVD 
contains the following recommendations relating to importation of pig semen:  
Article 15.4.9.   Recommendations for importation from SVD free countries  
Veterinary Authorities  should require the presentation of an international veterinary 
certificate attesting that:  
1. the donor animals:  
a. showed no clinical sign of SVD on the day of collection of the  semen;  
b. were kept in an SVD free country for not less than 6 weeks prior to 
collection;  
2. the semen was collected, processed and stored in conformity with the provisions of Chapter  4.5. and Chapter  4.6. 
Article 15.4.10.   Recommendations for importation fr om countries considered infected 
with SVD  
Veterinary Authorities  should require the presentation of an international veterinary 
certificate attesting that:   
Ministry for Primary Industries  Import risk analysis: Pig semen • 89 1.  the donor animals:  
a. showed no clinical sign of SVD on the day of collection of the semen and w ere 
subjected to the virus neutralisation test for SVD with negative results;  
b. were kept in the exporting country for the 28 days prior to collection, in an 
establishment or artificial insemination centre where no case of SVD was 
officially reported duri ng that period, and that the establishment or artificial 
insemination centre was not situated in an SVD infected zone.  
2.   the semen was collected, processed and stored in conformity with the provisions of 
Chapter  4.5. and Chapter  4.6. 
Chapters 4.5 and 4. 6 of the Code  (OIE 2009a)  contain requirements for SVD for boars standing 
at semen collection centres.  Under these requirements, prior to entry into iso lation at the 
quarantine station of the semen collection facility, boars must be clinically healthy, 
physiologically normal, and either kept in a SVD -free country since birth or for the past six 
weeks, or kept since birth or for the past six weeks in an es tablishment outside an SVD infected 
zone where no case of SVD was officially reported during that period and been subject to a virus 
neutralisation test for SVD with negative results.  Boars must remain in this quarantine station 
for at least 28 days and, at least 21 days after entering the quarantine station must be tested 
negative for SVD as per Articles 15.4.9 or 15.4.10 of the Code .  In countries, zones or 
compartments which are not free of SVD, any boars resident in the semen collection facility 
must a lso be tested at least annually as per Articles 15.4.9 or 15.4.10 of the Code . 
 
Available options for exclusion of SVD are:  
 
Option 1  
Semen originating from donor boars that have lived their entire lives in countries free from SVD 
could be imported withou t further sanitary measures.  
Option 2  
Semen originating from donor boars from countries considered infected with SVD could be 
required to comply with the recommendations contained in 15.4.10 of the OIE Code , including 
compliance with Chapters 4.5 and 4.6 o f the Code . 
Option 3  
Every batch of semen to be imported could be tested by PCR as described by van Rijn et al 
(2004). A positive test on any batch of semen could result in disqualification of that semen.   
 
 
 
References  
 
Chu RM, Moore DM, Conroy JD (1979).  Experimental swine vesicular disease, pathology and 
immunofluorescence studies. Canadian Journal of Comparative Medicine  43, 29 -38.  
Ministry for Primary Industries  Import risk analysis: Pig semen • 90  
Dekker A, Moonen P, de Boer -Luijtze EA, Terpstra C (1995).  Pathogenesis of swine vesicular disease after 
exposure of pigs to an infected environment. Veterinary Microbiology  45, 234 -50. 
 Hedger RS, Mann JA (1989).  Swine vesicular disease virus. In Pensaert MB (ed) Virus Infections of Vertebrates, 
Volume 2. Virus Infections of Porcines .  Pp 241- 50, Elsevier Science Publishers.   
 
Lai SS, McKercher PD, Moore DM, Gillespie JH (1979). Pathogenesis of swine vesicular disease in pigs. 
American Journal of Veterinary Research  40. 463 -8. 
 Lubroth J, Rodríguez L, Dekker A (2006). Vesicular diseases. In: Straw BE, Zimmerman JJ, D’Allaire S, Taylor 
DJ (eds)  Diseases of Swine  9th Edition, pp 517 -35, Blackwell Publishing.  
 
Maes D, Nauwynck H, Rijsselaere T, Mateusen B, Vyt P, de Kruif A, Van Soom A (2008)  Diseases in swine 
transmitted by artificial insemination: An overview. Theriogenology  70, 1337-45.  
 Nardelli L, Lodetti E, Gualandi GL, Burrows R, Goodridge D, Brown F, Cartwright B (1968).  A foot and 
mouth disease syndrome in pigs caused by an enterovirus. Nature  219, 1275-6.   
 OIE (2008a) . Terrestrial Animal Health Code . 
http://www.oie.int/eng/normes/MCode/en_sommaire.htm , 
downloaded 27/1/2009.  
 
OIE (2008b) . World Animal Health Information Database. http:/ /www.oie.int/wahid -prod/public.php?page=home , 
downloaded 27/1/2009.  
 
Sabirovic M, Roberts H, Papadopoulou C, Lopez M, Hancock R, Calistri P (2009).  International disease 
monitoring, July to September 2009. Veterinary Record  165, 552-5.  
 Sabirovic M, Robe rts H, Lopez M, Hancock R (2010a).  International disease monitoring, October to December 
2009. Veterinary Record  166, 160-2.  
 
Sabirovic M, Roberts H, Lopez M, Hancock R (2010b).  International disease monitoring, January to March. 
Veterinary Record  166, 483-6.  
 
Stanway G, Brown F, Christian P, Hovi T, Hyypia T, King AMQ, Knowles NJ, Lemon SM, Minor PD, 
Pallansch MA, Palmenberg AC, T. S (2005).  Genus  Enterovirus . In: Fauquet CM, Mayo MA, Maniloff J, 
Desselberger U, Ball LA (eds), Eighth Report of the Internat ional Committee on Taxonomy of Viruses , Pp. 760-3, 
Elsevier Academic Press, Amsterdam  
 
van Rijn PA, Wellenberg GJ, der Honing RH, Jacobs L, Moonen PLJM, Feitsma H (2004) Detection of 
economically important viruses in boar semen by quantitative RealTime PCR  technology. Journal of Virological 
Methods 120, 151- 60. 
 
 
  
Ministry for Primary Industries  Import risk analysis: Pig semen • 91 33. Venezuelan encephalitis virus  
33.1. HAZARD IDENTIFICATIO N 
33.1.1.  Aetiological agent  
Family: Togaviridae , Genus: Alphavirus  (King et al 2012).  Six subtypes of Venezuelan equine 
encephalomyelitis (VEE) virus a re recognised (OIE 2008).  
33.1.2.  OIE list  
Venezuelan equine encephalomyelitis is an OIE -listed disease.  
33.1.3.  New Zealand status  
Equine encephalitis viruses (including VEE  virus) are exotic to New Zealand and listed as 
Notifiable Organisms (Tana et al 2011).  
33.1.4.  Epidemiology  
Venezuelan equine encephalomyelitis is an arthropod -borne inflammatory viral infection of 
equines and humans that results in mild to severe febrile and, occasionally fatal, encephalitic 
disease.  Horses serve as an amplifying host for epizootic strains of VEE while enzootic VEE 
viruses cycle primarily between sylvatic rodents and mosquitoes (OIE 2008).  
 Bowen (1976) summarised experimental studies using VEE virus and concluded that pigs could 
be eliminated as important epizootic hosts because of their lo w susceptibility to infection or low 
viraemias.  There are a few reports of serological evidence of VEE in pigs but isolation of virus has not been reported in this species. It appears that pigs are not significant in the epidemiology 
of the disease becaus e they do not produce a significant viraemia (AQIS 2000).  
 The pig is generally regarded as a dead -end host, and there is no evidence suggesting that pigs 
might transmit the virus to mosquitoes. Overall, the likelihood of the VEE virus being present in the semen of a donor boar and being transmitted to a recipient sow was assessed by AQIS (2000) 
to be negligible.  
33.1.5.  Hazard identification conclusion 
Consistent with the findings of AQIS (2000), VEE virus is not identified as a hazard in porcine semen.  
 
References  
AQIS (2000).  Porcine Semen Import Risk Analysis:  Risk assessment and risk management options. 
http://www.daff.gov.au/__data/assets/pdf_file/0018/15345/00-020a.pdf  
 
Bowen G S (1976) . Experimental infection of North American mammals with epidemic Venezuelan encephalitis 
virus.  The American Journal of Tropical Medicine and Hygiene 25, 891 -899.  
King AMQ, Adams MJ, Carstens EB, Lefkowitz (2012).  Virus Taxonomy. Ninth report of th e International 
Committee on Taxonomy of Viruses . Else vier Academic Press, London. 1103- 1110 .  
Ministry for Primary Industries  Import risk analysis: Pig semen • 92 OIE (2008).  Venezuelan equine encephalomyelitis. Chapter 2.5.14 in: Manual of Diagnostic Tests and Vaccines for 
Terrestrial Animals. OIE, Paris.  
Tana T, Murray-Cu llen J, Johnston C, Lee E (2011).   Notifiable organisms. Surveillance  38(2), 20-24.   
Ministry for Primary Industries  Import risk analysis: Pig semen • 93 34. Vesicular exanthema virus  
34.1. HAZARD IDENTIFICATIO N 
34.1.1.  Aetiological agent  
Family: Caliciviridae , Genus: Vesivirus . Vesicular exanthema of swine virus (VESV) and 
vesiviruses isola ted from marine species are phylogenetically grouped together as “marine 
vesiviruses” (King et al 2012).  
34.1.2.  OIE list  
Not listed.  
34.1.3.  New Zealand status  
Vesicular exanthema has never been decribed in New Zealand.  
34.1.4.  Epidemiology  
The primary reservoir hosts of marine vesiviruses are thought to be certain fish species which 
can pass on infections to secondary hosts such as seals or pigs.  Vesicular exanthema was first 
described in pigs in the United States in 1932 and outbreaks continued until it was eradicated in 
1956.   Only one outbreak has been described outside of the United States (in Iceland, associated 
with pigs fed raw garbage from a United States military post) (Anon 1988).  
 
Vesicular exanthema is clinically indistinguishable from either foot and mouth disease o r 
vesicular stomatitis.  Infected pigs present with vesicles on the snout, lips, tongue, and mucosae of the oral cavity and on the sole, Interdigital spaces, and coronary band of the foot.  Lesions 
directly attributable to VESV, other than vesicle formatio n, have not been described (Madin and 
Traum 1955).  
 
VESV is principally transmitted between pigs by direct contact when ruptured vesicles release 
large amounts of infective virus into the environment. Transmission of virus associated with 
feeding waste (ga rbage) food to pigs is also recognised (Madin and Traum 1955).  No references 
could be found that described the presence of VSEV in boar semen and VSEV is not listed in recent reviews of pathogens likely to be found in boar semen (Guérin and Pozzi 2005; Maes et al 
2008).  
34.1.5.  Hazard identification conclusion 
Vesicular exanthema has  not been reported since 1956 and there is no evidence to support the 
suggestion that VSEV may be spread in the semen of infected boars. VSEV is not identified as a 
hazard in porcine s emen.  
 
References  
Anon (1988). Vesicular exanthema of swine. Surveillance  15(4), 13-14.   
Ministry for Primary Industries  Import risk analysis: Pig semen • 94 Guérin B, Pozzi N (2005).  Viruses in boar semen: detection and clinical as well as epidemiological consequences 
regarding disease transmission by artificial inseminatio n. Theriogenology  63, 556 -572.  
King AMQ, Adams MJ, Carstens EB, Lefkowitz (2012).  Virus Taxonomy. Ninth report of the International 
Committee on Taxonomy of Viruses . Else vier Academic Press, London. 977-986 . 
Madin SH, Traum J (1955).  Vesicular exanthema of  swine. Bacteriological Reviews  19, 6-19.  
Maes D, Nauwynck H, Rijsselaere T, Mateusen B, Vyt P, de Kruif A, Van Soom A (2008).  Diseases in swine 
transmitted by artificial insemination: An overview. Theriogenology  70, 1337-1345.   
Ministry for Primary Industries  Import risk analysis: Pig semen • 95 35. Vesicular stomatitis virus  
35.1. HAZARD IDENTFICATION  
35.1.1.  Aetiological agent  
Family: Rhabdoviridae , Genus: Vesiculovirus , Species: Vesicular stomatitis Alagoas virus , 
Vesicular stomatitis Indiana virus , Vesicular stomatitis New Jersey virus (Tordo et al  2005) . 
Many authors regard the three species of virus as serotypes of the same species.  
35.1.2.   OIE list  
Listed (OIE 2008) . 
35.1.3.  New Zealand status  
Exotic notifiable disease ( MAF 2008) .  
35.1.4.  Epidemiology  
Vesicular stomatitis is primarily an insect -borne virus but it can also be transmitted by contact 
(Lubroth et al 2006) . Outbreaks of disease occur sporadically in the USA and are always 
associated with insect transmission (Lubroth et al 2006; Rodriguez 2002; Rodriguez et al 1996) . 
The virus is found in epithelial tissues o f the mouth, nose, coronary region of the hooves , teats 
and lymph nodes (Lubroth et al 2006) . It is not found in blood (Lubroth et al 2006) . There are no 
references to it being excreted in semen.  
35.1.5.  Hazard identification conclusion 
Since the virus is an a rbovirus and is not excreted in semen it is not identified as a  hazard in the 
commodity.  
 
References  
References marked * were sighted as abstracts in electronic databases.  
Lubroth J, Rodriguez L, Dekker A (2006).  Vesicular stomatitis . In: Straw BE, Zimmerman JJ, D'Allaire S, Taylor 
DJ (eds), Diseases of Swine . 9th edition, Pp. 525-35, Blackwell Publishing, Ames, Iowa.  
 
MAF (2008). The Unwanted Organisms Register. http://maf uwsp6.maf.govt.nz/uor/searchframe.htm , downloaded 
27/1/2009.  
 
OIE (2008) . Terrestrial Animal Health Code (mammals, birds and bees). 
http://www.oie.int/eng/normes/MCode/en_sommaire.htm , downloaded 27/1/2009.  
 
Rodriguez LL (2002) . Emergence and re-emergence of vesicular stomatitis in the United States. Virus Research , 
85(2), 211 -9.* 
 
Rodriguez LL, Fitch WM, Nichol ST (1996). Ecological factors rather than temporal factors dominate the 
evolution of vesicular stomatitis virus. Proceedings of the National Academy of Sciences USA , 93(23), 13030 5.*  
 Tordo N, Benmansour A, Calisher C, Dietzgen RG, Fang R-X, Jackson AO, Kurath G, Nadin-Davis S, Tesh 
RB, Walker PJ (2005).  Genus  Vesiculovirus . In: Fauquet CM, Mayo MA, Maniloff J, Desselberger U, Ball LA 
(eds), Eighth Report of the International Committee on Taxonomy of Viruses , Pp. Elsevier Academic Press, 
Amsterdam.   
Ministry for Primary Industries  Import risk analysis: Pig semen • 96 36. West Nile virus  
36.1. HAZARD IDENTIFICATIO N 
36.1.1.  Aetiological agent  
Family: Flaviviridae ; Genus: Flavivirus , Species: West Nile virus  (WNV) (Thiel  et al 2005) . 
36.1.2.  OIE list  
Listed . 
36.1.3.  New Zealand status  
Exotic organism, not listed as unwanted or notifiable by MAF.  
36.1.4.  Epidemiology  
West Nile virus was originally isolated in Uganda in 1937. It is found all ov er Africa and has 
also been found in France (1962), Romania (1996), and Russia (1999) (Bunning et al 2004) . The 
virus spread to the United States in 1999 and since then has spread throughout the USA (CDC 
2003a)  and adjoining countries. Disease is seen mainly in humans and horses , but the virus also 
causes deaths in wild birds. Most cases in humans are asymptomatic, but there have been over 15,000 cases of disease and over 600 deaths in the epidemic in the USA (Higgs et al 2005) . 
 The virus is transmitted by mosquitoes and maintained in a bird- mosquito cycle (CDC 2003b) . 
At least 43 species of mosquitoes have been suspected as vectors of the disease (Gingrich and Williams 2005) . The virus can be transmitted fro m infected mosquitoes to non -infected 
mosquitoes when they feed together on non -infected hosts (Higgs et al 2005) .  
 
Experimental inoculation studies of pigs using mosquitoes infected with WNV have sho wn that 
adult pigs are very unlikely to show clinical disease when infected with this virus and rarely develop a very low level transient viraemia.  Weanling pigs are more likely to develop viraemia 
following infection but this is also of short duration and insufficient to infect mosquitoes.  Pigs 
are therefore considered unlikely to serve as amplifying hosts of WNV (Teehee et al 2005).   
36.1.5.  Hazard identification conclusion 
Since pigs are dead -end hosts for WNV, the likelihood that virus would be present in im ported 
semen is assessed  to be negligible. Therefore, the organism is not identified as a  hazard in the 
commodity.  
 
 References  
 
Bunning MI, Wilson TM, Bowen RA (2004).  West Nile virus infection. In: Coetzer JAW, Tustin RC (eds). 
Infect ious Diseases of livestock . Pp. 1004- 11. Oxford University Press, Oxford.  
 
CDC (2003a).  West Nile Virus: Statistics, Surveillance, and Control. 
www.cdc.gov/ncidod/dvbid/westnile/surv&control05Maps.htm . 
 CDC (2003b).  West Nile Virus: What you need to know.  www.cdc.gov/ncidod/dvbid/westnile/birds&mammals.htm . 
  
Ministry for Primary Industries  Import risk analysis: Pig semen • 97 Gingrich JB, Williams GM (2005).  Host-feeding patterns of suspected West Nile virus mosquito vectors in 
Delaware, 2001- 2002. Journal of the American Mosquito Control Association , 21(2), 194-200.  
 
Higgs  S, Schneider BS, Vanlandingham DL, Klingler KA, Gould EA (2005).  Nonviraemic transmission of West 
Nile virus. Proceedings of the National Academy of Science USA , 102(25), 8871-4.  
 
Teehee ML, Bunning ML, Stevens S, Bowen RA (2005). Experimental infection o f pigs with West Nile virus. 
Archives of Virology  150, 1249-56.  
 Thiel HJ, Collett MS, Gould EA, Heinz EX, Houghton M, Meyers G, Purcell RH, Rice CM (2005).  Genus   
Flavivirus . In: Fauquet CM, Mayo MA, Maniloff J, Desselberger U, Ball LA, (eds), Eighth Repo rt of the 
International Committee on Taxonomy of Viruses . Pp. 982 -88, Elsevier Academic Press, Amsterdam.  
  
Ministry for Primary Industries  Import risk analysis: Pig semen • 98 37. Western equine encephalitis virus 
 
37.1. HAZARD IDENTIFICATIO N 
37.1.1.  Aetiological agent  
Family: Togaviridae ; Genus: Alphavirus , Species: Western equine encepha litis virus (WEEV). 
(Weaver  et al 2005) . 
37.1.2.  OIE list  
Listed.  
37.1.3.  New Zealand status  
Exotic notifiable disease (MAF 2008) .  
37.1.4.  Epidemiology  
WEEV is found predominantly in the western United States and Canada (Radostits et al 2007) 
and is normally maintained in a host -vector relationship by cycling between mo squitoes ( Culex 
tarsalis  in the western United States and Culiseta melanura in the eastern and southern United 
States) and the definitive host (wild birds, especially passerines) (Hayes and Wallis 1977; 
Iversen 1994).  Pigs are an accidental host of the vi rus (Radostits et al 2007).  
Although surveys have described evidence of exposure to WEEV in pigs (Scherer et al 1966), there is no evidence that would suggest this species should be considered anything other than a 
dead -end host.  An extensive literature s earch has found no evidence of clinical disease in pigs 
associated with WEEV, nor any suggestion that this virus is likely to be found in the semen of infected pigs.  
37.1.5.  Hazard identification conclusion 
Since pigs are dead -end hosts for WEEV, the likelihood that virus would be present in imported 
semen is considered to be negligible. Therefore, the organism is not identified as a  hazard in the 
commodity.  
 
References  
 
Hayes CG, Wallis RC (1977). Ecology of Western Equine Encephalomyelitis in the Eastern United S tates. 
Advances in Virus Research  21. 37-83.  
 Iversen JO (1994) . Western equine encephalomyelitis. In: Beran GW, (ed), Handbook of zoonoses, Second edition. 
Section B: viral.  Pp. 25- 31, CRC Press, Boca Raton.  
 MAF (2008). The Unwanted Organisms Register. 
http://mafuwsp6.maf.govt.nz/uor/searchframe.htm , downloaded 
27/1/2009.  
 Radostits OM, Gay CC, Hinchcliff KW, Constable PD (2007)  Viral diseases characterized by nervous signs. 
Eastern and west ern viral encephalomyelitis of horses. In: Veterinary Medicine  10
th Edition, Saunders Elsevier, 
1368-72.  
  
Ministry for Primary Industries  Import risk analysis: Pig semen • 99 Scherer WF, Campillo Sainz C, De Mucha Macias J, Rubio -Brito R, Miura T, Dickerman RW, Warner DW, 
Dyer M (1966).  Serologic survey for neutralizing ant ibodies to eastern equine and western equine encephalitis 
viruses in man, wild birds and swine in southern Mexico during 1961. American Journal of Tropical Medicine and 
Hygiene  15, 211 -8. 
 
Weaver SC, Frey TK, Huang HV, Kinney RM, Rice CM, Roehrig JT, Shope  RE, Strauss EG (2005).  Genus   
Alphavirus . In: Fauquet CM, Mayo MA, Maniloff J, Desselberger U, Ball LA, (eds), Eighth Report of the 
International Committee on Taxonomy of Viruses . Pp. 1003 -5, Elsevier Academic Press, Amsterdam.  
  
Ministry for Primary Industries  Import risk analysis: Pig semen • 100 38. Bacillus anthracis  
38.1. HAZARD IDENTFICATION  
38.1.1.  Aetiological agent  
Bacillus anthracis . 
38.1.2.   OIE list  
Listed (OIE 2008) . 
38.1.3.  New Zealand stat us 
Exotic notifiable disease (MAF 2008) .  
38.1.4.  Epidemiology  
Anthrax is generally an acute bacterial infection of many species including pigs. Pigs are more 
resistant to infection than ruminants (Taylor 2006) . Animals are infected by the oral route with 
spores which occur in the soil , but infected animals are not contagious (Taylor 2006) . Bacilli 
sporulate when bl ood from infected animal carcasses is exposed to air , and spores can remain 
viable in soil for many years (De Vos and Turnbull 2004; Turner et al 1999a; Turner et al 
1999b) . Anthrax may present as the pharyngeal, intestinal, or septicaemic form in pigs. The first 
two syndromes may be mild and animals may recover spontaneo usly. The septicaemic form is 
usually an acute or peracute infection and death may occur without any signs being observed 
(Taylor 2006) .  
Diagnosis is made by identification of the organism in blood smears taken from dead animals, or if the carcass has been opened from lymph nodes, spleen or kidney. The organism can be 
cultured from blood or tissues.  
There are no reports indicating that the organism is excreted in semen of healthy animals, and the Code  gives no recommendations for trade in semen, thereby indicating that no trade restrictions 
are required.  
38.1.5.  Hazard identification conclusion 
The likelihood that a healthy boar housed at a semen collection centre would be excreting Bacillus anthracis  spores in its semen is negligible. Therefore Bacillus anthracis  is not identified 
as a hazard in the commodity.  
 
References  
 
De Vos V, Turnbull PCB (2004).  Anthrax. In: Coetzer JAW, Tustin RC (eds),  Infectious Diseases of Livestock , 
Vol. 3. Pp. 1788 -818, Oxford University Press, Cape Town.  
 
MAF (2008). The Unwanted Organisms Reg ister. http://mafuwsp6.maf.govt.nz/uor/searchframe.htm , downloaded 
27/1/2009.  
 OIE (2008) . Terrestrial Animal Health Code. 
http://www.oie.int/eng/normes/MCode/en_sommaire.htm , 
downloaded 27/1/2009.  
 Taylor DJ (2006).  Miscellaneous bacterial infections . Anthrax. In: Straw BE, Zimmerman JJ, D'Allaire S, Taylor 
DJ (eds), Diseases of Swine . 9th edition, Pp. 817-22, Blackwell Publ ishing, Ames, Iowa.   
Ministry for Primary Industries  Import risk analysis: Pig semen • 101  
Turner AJ, Galvin JW, Rubira RJ, Condron RJ, Bradley T (1999a) . Experiences with vaccination and 
epidemiological investigations on an anthrax outbreak in Australia. Journal of Applied Microbiology , 87(2), 294 -7. 
 Turner AJ, Galvin JW, Rubira RJ, Miller GT (1999b) . Anthrax explodes in an Australian summer. Journal of 
Applied Microbiology , 87(2), 196-9.  
 
  
Ministry for Primary Industries  Import risk analysis: Pig semen • 102 39.  Brucella suis  
39.1. HAZARD IDENTFICATION  
39.1.1.  Aetiological agent  
Brucella suis . 
39.1.2.  OIE list  
Listed (OIE 2008a) .  
39.1.3.  New Zealand status  
Exotic, notifiable organism (MAF 2008) . 
39.1.4.  Epidemiology  
Brucellosis is a venereal disease in pigs, with sows readily infected when mated with infected 
boars or inseminated with semen containing B. suis  (MacMillan et al 2006).   Infected boars may 
shed 104 to 105 CFU of B. suis  per ml of semen (Lord et al 1998) .   Infection of semen cannot be 
eliminated by using antibiotics , as the amount of antimicrobial required may be incompatible 
with semen survival ( Algers et al 2009)  
Apart from domestic pigs, reservoirs of B. suis infection are recognised in European hares 
(Bendtsen et al 1954) and feral pigs (Drew et al 1992).  Transmission of infection from wild boars to domestic pigs is though t to be through the venereal route .  Waste feeding of hare offal 
has also been implicated as a method of introduction (Algers et al 2009).  
Bacteraemia follows 1 to 7 weeks after exposure to B. suis  and persists for an average of about 5 
weeks , although intermittent bacteraemia lasting as long as 34 months has been decribed.  
Bacteraemia may precede the development of a detectable serological response by as much as 6 
to 8 weeks (MacMillan et al 2006).  
Infection with B. suis is associated with reproductive failure characterised b y abortion, stillbirth, 
infertility, and testicular lesions.  B. suis localises to the placenta of pregnant sows, leading to 
placentitis with subsequent malnut rition and hypoxia , and abortion in mid -to-late pregnancy 
(Algers et al 2009).  However, the clin ical evidence of infection varies considerably between 
herds and clinical signs may be only transient or absent.  Death is rare (MacMillan et al 2006).  
Porcine brucellosis is a significant public health concern, with occupational B. suis infections 
describ ed in farmers, veterinarians, abattoir workers, and individuals who have direct contact 
with feral swine (MacMillan et al 2006).  
39.1.5.  Hazard identification conclusion 
Following infection, B. suis  is commonly found in porcine semen and is therefore identified as  a 
potential hazard.   
Ministry for Primary Industries  Import risk analysis: Pig semen • 103 39.2. RISK ASSESSMENT  
39.2.1.  Entry assessment  
B. suis has never been recognised in Norway.  The disease may be present in the other countries 
although it appears to be restricted to wildlife in the United States, Canada, Australia, and some 
EU me mber states (OIE 2008b; 2008c).  Pigs originating from those countries where B. suis is 
present could be subclinically infected with B. suis  and could excrete the organism in their 
semen. The likelihood for entry of B. suis in pig semen from these countrie s is therefore non-
negligible.  
39.2.2.  Exposure assessment  
Imported semen will be inseminated into New Zealand pigs.  Sows are readily infected when 
mated with infected boars or inseminated with semen containing B. suis (MacMillan et al 2006).  
The likelihood of  exposure of New Zealand pigs is assessed  to be non- negligible.  
39.2.3.   Consequence assessment  
Insemination of pigs would result in the transmission of B. suis to the recipients of the semen  and 
the establishment of infection .  Although affected herds may have no clinical signs of 
brucellosis, reproductive losses, infertility, paralysis and lameness may be seen as a result of infection.  Once introduced into the environment, B. suis can persist in organic matter at near -
freezing temperatures for over 2 years (MacMillan et al 2006) , and subsequent spread to other 
domestic herds would be likely.  Infection may also become established in New Zealand’s feral 
pig population.  
 Occupational exposure may result in infection of farm staff, abattoir workers, and veterinari ans. 
 The consequences of introduction are assessed to be non -negligible.  
39.2.4.  Risk estimation  
Entry, exposure and consequence have all been assessed as non -negligible. As a result the risk 
estimate for B. suis is non -negligible and it is assessed to be a risk in the commodity. Therefore 
risk management measures can be justified.  
39.3. RISK MANAGEMENT  
39.3.1.  Options  
The Code  chapter on porcine brucellosis contains the following recommendations relating to 
importation of pig semen:  
Article 15.3.5.   Recommendations for the importation of semen of pigs  
Veterinary Authorities  of importing countries  should require the presentation of an 
international veterinary certificate attesting that:  
1. the donor animals showed no clinical sign of porcine brucellosis on the day of 
collection of the semen;  
2. the donor animals were kept in a herd  free from porcine brucellosis;   
Ministry for Primary Industries  Import risk analysis: Pig semen • 104 3. the donor animals were subjected to a diagnostic test for porcine brucellosis with 
negative results during the 30  days prior to collection;  
4. the semen does not contain Brucel la agglutinins;  
5. the donor animals were kept in the exporting country , for the 60  days prior to 
collection, in an establishment  or artificial insemination centre  where the herd is free 
from porcine brucellosis;  
6. the semen was collected, processed and stored in conformity with the provisions of 
chapters  4.5. and 4.6. 
Chapters 4.5 and 4.6 of the Code  (OIE 2009a)  contain requirements for B. suis  for boars stand ing 
at semen collection centres.  Under these requirements, prior to entry into isolation at the 
quarantine station of the semen collection facility, boars must be clinically healthy, 
physiologically normal, kept in a herd free of porcine brucellosis and s ubject to a diagnostic test 
for porcine brucellosis with negative results .  Boars must remain in this quarantine station for at 
least 28 days and, at least 21 days after entering the quarantine station , must be tested negative 
for B. suis  as per Articles 1 5.3.5 of the Code .  In countries, zones or compartments which are not 
free of porcine brucellosis, any boars resident in the semen collection facility must also be tested 
at least annually as per Articles 15.3.5 of the Code . 
The OIE Manual (Olsen 2009) des cribes the indirect and competitive ELISAs, as well as the 
Rose Bengal test, complement fixation test, and fluorescence polarisation assay as suitable serological tests for international trade.  N one of the serological tests described are considered 
reliab le for diagnosis in individual pigs , although all of these tests are sensitive enough to be 
used as screening tests to detect an infected herd (Algers et al 2009).  For international trade, the 
disease status of the herd and of the area in which the herd i s situated are of more importance 
than tests on individual animals (Olsen 2009).  
Available options for exclusion of B. suis are:  
Option 1  
The requirements of Article 15.3.5.  (including compliance with Chapters 4.5 and 4.6) would 
ensure that imported seme n was free from B. suis.  
Option 2  
Semen from donor boars that have lived their entire lives in countries that are free from B. suis 
could be imported without restrictions.   
 
 References  
 
Algers B, Blokhuis HJ, Bøtner A, Broom DM, Costa P, Domingo M, Greine r M, Hartung J, Koenen F, 
Müller -Graf C, Mohan R, Morton DB, Osterhaus A, Pfeiffer DU, Roberts RU, Sanaa M, Salman M, Sharp 
JM, Vannier P, Wierup M (2009). Scientific Opinion of the Panel on Animal Health and Welfare (AHAW) on a 
request from the Commission  on porcine brucellosis ( Brucella suis ). The EFSA Journal  1144, 1-112.  
 
Bendtsen H, Christiansen M, Thomsen A (1954).  Brucella enzootics is swine herds in Denmark – Presumably 
with hare as a source of infection. Nordisk veterinaermedicin  6, 11- 21. 
 Drew ML , Jessup DA, Burr AA, Franti CE (1992).  Serological survey for brucellosis in feral swine, wild 
ruminants, and black bear of California. Journal of Wildlife Diseases  28, 355 -63.  
 Lord VR, Cherwonogrodzky JW, Schurig GG, Lord RD, Marcano MJ, Meléndez GE (1 998). Venezuelan field 
trials of vaccines against brucellosis in swine. American Journal of Veterinary Research  59, 546-51.   
Ministry for Primary Industries  Import risk analysis: Pig semen • 105  
MacMillan AP, Schleicher H, Korslund J, Stoffregen (2006). Brucellosis. In: Straw BE, Zimmerman JJ, 
D'Allaire S, Taylor DJ (eds), D iseases of Swine . 9th edition, Pp. 603-11, Blackwell Publishing, Ames, Iowa.  
 
MAF (2008).  The Unwanted Organisms Register. http://mafuwsp6.maf.govt.nz/uor/searchframe.htm , downloaded 
29/11/2007.  
 OIE (2008a). Terrestrial Animal Health Code . 
http://www.oie.int/eng/normes/MCode/en_sommaire.htm , 
downloaded 29/11/2007.  
 OIE (2008b).  Handistatus II. 
http://www.oie.int/hs2/report.asp , Downloaded 27/1/2009.  
 
OIE (2008c).  World Animal Health Information Database (WAHID) Interface. http://www.oie.int/wahid -
prod/public.php?page=home , downloaded 10/12/2009.  
 Olsen S (2009).  Chapter 2.8.5. Porcine brucellosis. In: OIE (eds), Manual of Diagnostic Tests and Vaccines for 
Terrestrial Animals., OIE, Paris.   
Ministry for Primary Industries  Import risk analysis: Pig semen • 106 40. Burkholderia pseudomallei  
40.1. HAZARD IDENTIFICATIO N 
40.1.1.  Aetiological agent  
Burkholderia pseudomallei . 
40.1.2.   OIE list  
Not listed . 
40.1.3.  New Zealand status  
Listed as an exotic unwanted organism (MAF 2008) . 
40.1.4.  Epidemiology  
Burkholderia pseudomallei  is the cause of melioidosis, a disease of humans and animals .  It 
occurs predominantly in the tropical and subtropical regions of Asia , northern Australia and in 
some foci in Africa (Groves and Harrington 1994; Inglis 2004; Inglis et al 2004) , and was 
recorded over 20 years ago in a piggery in southeastern Queensland (Ketterer et al 1986) . It 
occasionally spills over into temperate regions and an imported case has occurred in New 
Zealand (Corkill and Cornere 1987) . The aetiological agent occurs in the environment and is 
widely distributed in water and soil (Sprague and Neubauer 2004) . It has been trans mitted to 
animals via oral mucosa, nasal mucosa, ingestion, parental inoculation, and skin scarification 
(Groves and Harrington 1994) . Infection in natural cases is probably by contact with infected 
water and mud , especially through abrasions and wounds. Water was implicated as a possible 
source of infection in six locations in one study (Inglis et al 2004) . The disease has been 
described in pigs (Taylor 2006; Thomas 1981) . Many cases are subclinical , but fever and 
occasional deaths may occur. The infection is usually discovered at post -mortem when abscesses 
are found in the internal organs and lymph nodes.   
There is no evidence that the infection is transmitted in pigs by semen. Theoretically the 
organism could be excreted in se men during the bacteraemic phase of the disease. However, this 
has not been described and it is considered extremely unlikely to occur in a healthy pig used as a semen donor.  
40.1.5.  Hazard identification conclusion 
Burkholderia pseudomallei  is an organism found in the environment in tropical and subtropical 
areas, but has not established in temperate climates. It appears to be an opportunistic pathogen 
and there are no descriptions of it being transmitted by pig semen. For these reasons it is not 
identified as a  hazard in the commodity.  
 References  
References marked * were sighted as summaries in electronic media sources.  
Corkill MM, Cornere B (1987) . Melioidosis: a new disease in New Zealand. New Zealand Medical Journal , 100, 
106-7.  
  
Ministry for Primary Industries  Import risk analysis: Pig semen • 107 Groves MG , Harrington KS (1994).  Glanders and melioidosis. In: Beran GW (eds), Handbook of Zoonoses 
Section A: Bacterial, Rickettsial, Chlamydial and Mycotic. Pp. 149-65, CRC Press, Boca Raton, Ann Arbor, 
London, Tokyo.  
 
Inglis TJJ (2004) . Melioidosis in man and ot her animals: epidemiology, ecology and pathogenesis. Veterinary 
Bulletin , 74(10), 39N -48N.  
 Inglis TJJ, Foster NF, Gal D, Powell K, Mayo M, Norton R, Currie BJ (2004) . Preliminary report on the 
northern Australian melioidosis environmental surveillance pro ject. Epidemiology and Infection, 132(5), 813- 20. 
 
Ketterer PJ, Webster WR, Shield J, Arthur RJ, Blackall PJ, Thomas AD (1986) . Melioidosis in intensive 
piggeries in south eastern Queensland. Australian Veterinary Journal , 63(5), 146-9.  
 MAF (2008). The Un wanted Organisms Register. 
http://mafuwsp6.maf.govt.nz/uor/searchframe.htm , downloaded 
27/1/2009.  
 
Sprague LD, Neubauer H (2004). Melioidosis in animals: A review on epizootiology, diagnosis  and clinical 
presentation. Journal of Veterinary Medicine B, Infectious Diseases and Public Health , 51(7), 305-20.  
 Taylor DJ (2006).  Miscellaneous bacterial infections. Melioidosis  (Burkholderia pseudomallei infection) . In: Straw 
BE, Zimmerman JJ, D'Alla ire S, Taylor DJ (eds), Diseases of Swine . Pp. 822, Blackwell Publishing, Ames, Iowa.  
 Thomas AD (1981) . Prevalence of melioidosis in northern Queensland. Australian Veterinary Journal , 57(3), 146-
8. 
  
Ministry for Primary Industries  Import risk analysis: Pig semen • 108 41. Clostridium botulinum  
41.1. HAZARD IDENTFICATION  
41.1.1.  Aetiologic al agent  
Clostridium botulinum . Types A, B, C α, Cβ, D E, F, and G have been identified (Kriek and 
Odendaal 2004) .   
41.1.2.  OIE list  
Not listed.  
41.1.3.  New Zealand status  
Type C botulism has been identified in New Zealand (Fairley 1997; Gardner 1990; Gardner 
1992) . It is not clear whether other t ypes occur in New Zealand.  
41.1.4.  Epidemiology  
Animals are poisoned when they eat decaying meat, bones, vegetable matter or other food items 
that are contaminated with botulinum toxin (Cobb et al 2002; Kriek and Odendaal 2004; Songer 
and Taylor 2006) . Therefore botulism is a toxicosis , not an infectious disease, except in rare 
cases of toxicoinfectious botulism where the organism multiplies i n the gut or in wounds (Kriek 
and Odendaal 2004) . Affected animals are not infectious. There are no reports of C. botulinum  or 
its toxin being excreted in semen.  Pigs are highly resistant to botulism and the disease is rarely reported in them (Songer and Taylor 2006) . 
41.1.5.  Hazard identification conclusion 
C. botulinum  is an environmental contaminant and  not a disease agent transmitted by animals. 
Therefore, it is not identified as a  hazard in the commodity.  
 
References  
 
Cobb SP, Hogg RA, Challoner DJ, Brett MM, Livesey CT, Sharpe RT, Jones TO (2002).  Suspected botulism in 
dairy cows and its implications for the safety of human food. Veterinary Record  150, 5-8.  
 
Fairley R (1997). Infectious diseases of pigs in New Zealand. Surveillance , 24(2), 5 --7. 
 
Gardner DE (1990) . Clostridial diseases of animals in New Zealand. Surveillance , 17(4),  19-21. 
 Gardner DE (1992) . Botulism in New Zealand. Surveillance , 19(2), 26-7.  
 Kriek NPJ, Odendaal MW (2004).  Botulism. In: Coetzer JAW, Tustin RC (eds),  Infectious Diseases of Livestock  
Vol. 3, Pp. 1885 -902, Oxford University Press, Cape Town.  
 Songer J G, Taylor DJ (2006).  Clostridial infections. Botulism. In: Straw BE, Zimmerman JJ, D'Allaire S, Taylor 
DJ (eds), Diseases of Swine , Pp. 624-8, Blackwell Publishing, Ames, Iowa.  
  
Ministry for Primary Industries  Import risk analysis: Pig semen • 109 42. Other Clostridium  spp. 
42.1. HAZARD IDENTIFICATIO N 
42.1.1.  Aetiological agents  
The followi ng clostridial species are associated with syndromes occurring in swine  
(Songer and Taylor 2006) : 
 
 Clostridium perfringens type A  
C. perfringens type C  
C. difficile  
C. tetani  
C. novyi  
C. septicum  
C. chauvoei  
42.1.2.  OIE list  
Not listed.  
42.1.3.  New Zealand status  
The following have been identified  as occurring in New Zealand (Gardner 1990) : 
 
C. tetani  
C. botulinum  
C. difficile  
C. chauvoei  
C. septicum  
C. oedematiens ( novyi ) 
C. perfringens  (types A and D)  
 
C. haemolyticum (a synonym for  C. novyi type D) (A nonymous 1979)  and more recently C. 
sordellii (Simpson 1999)  have also been isolated.   
42.1.4.  Epidemiology  
Clostridia are generally regarded as being universally distributed , occurring as vegetative 
organisms or as spores in soil and the environment. Of the organisms identified as being 
important in pigs, all are already present in New Zealand , except  possibly C. perfringens  type C. 
The disease syndrome in young pigs caused by C. perfringens  type C , has also not been 
described in New Zealand (Fairley 1997) . Therefore only C. perfringens  type C is considered in 
this section.  
The peracute and acute forms of the disease in young pigs are characterised by haemorrhagic 
diarrhoea and death within 12 -48 hours .  At post mortem there is necrohaemorrhagic enteritis 
(Songer and Taylor 2006) . The organism is probably carried in the gut of infected sows where it 
occurs in low numbers and is difficult to identify , as it is massively outnumbered by the total 
population of C. perfringens  of other types (Songer and Taylor 2006) . The le thal necrotising beta  
Ministry for Primary Industries  Import risk analysis: Pig semen • 110 toxin of C. perfringens  type C is the primary factor involved in the pathogenesis of the disease, 
but other factors may also be involved (Songer and Taylor 2006). The organism is transmitted by 
the oral route and there is nothing in t he literature to suggest that it is transmitted by semen. 
Indeed, if any animal were to be septicaemically infected by the organism it would be clearly sick and obviously unsuitable for semen donation.  
42.1.5.  Hazard identification conclusion 
Since the organism is  not transmitted in semen it is not identified as  a hazard in the commodity.  
 
 
References  
 
Anonymous (1979). Laboratory reports: Invermay Animal Health Laboratory. Surveillance , 6(4), 26-7.  
 
Fairley R (1997). Infectious diseases of pigs  in New Zealand. Surveillance , 24(2), 5 --7. 
 Gardner DE (1990) . Clostridial diseases of animals in New Zealand. Surveillance , 17(4), 19- 21. 
 Simpson B (1999) . Clostridium sordellii -  the ‘new clostridium’. New Zealand Vetscript , 12(9), 11.  
 Songer JG, Tayl or DJ (2006).  Clostridial infections.  Botulism. In: Straw BE, Zimmerman JJ, D'Allaire S, Taylor 
DJ (eds), Diseases of Swine . 9
th edition, Pp. 624- 8, Blackwell Publishing, Ames, Iowa.  
   
Ministry for Primary Industries  Import risk analysis: Pig semen • 111 43. Leptospira spp.  
43.1. HAZARD IDENTIFICATIO N 
43.1.1.  Aetiological agent  
The species Leptospira interrogans  contains over 200 Leptospira serovars classified into 23 
serogroups (Bolin 2004) . A newer and alternative taxonomic scheme based on genomic 
characteristics clas sifies the pathogenic organisms into eight species, and the species are 
subdivided into serovars. For the purposes of this risk analysis the older method of classifying 
leptospires as serovars of Leptospira interrogans  is used and serovars are written as i f they were 
single species , e.g., Leptospira hardjo, L. pomona , etc. 
43.1.2.  OIE list  
Although leptospirosis is listed by the OIE, from 2004 to 2009 the Code chapter did not contain 
recommendations for leptospirosis, only a statement that it was “under study”. At the OIE General Session in May 2009, the International Committee accepted the recommendation of the 
Terrestrial Animal Health Standards Commission that the empty Code chapter on leptospirosis 
should be deleted from the Code . 
43.1.3.  New Zealand status  
L. hardjo, L . pomona, L. balcanica, L. copenhageni , L. ballum  and L. tarrasovi  have been 
isolated from animals in New Zealand (Midwinter 1 999). A single isolation of L. australis  has 
been reported from a human (Thompson 1980) .  Serological diagnosis indicates that five of the 
species that have been found in farm animals can also infect humans, but L. balcanica  which is 
associated with possums has not been diagnosed in humans (ESR 2004) . Other Leptospira spp. 
are classified by MAF as “other exotic organisms” (MAF 2008) . 
L. pomona  and L. tarassovi have been identified in pigs in New Zealand (Fairley 1997) . 
43.1.4.  Epidemiology  
Leptospira spp. occur throughout the world , but it is not possible to accurately define which 
serovars occur in each country. Exotic Leptospira spp. that have been found in pigs include L. 
bratislava, L. canicola, L. icterohaemorrhagiae, L. sejroe and  L. grippotyphosa.  
Leptospirosis is not a single disease but a complex of diseases caused by many different 
leptospires. Most serovars are adapted to a particular host species in which they may exist for 
long periods without causing disease signs. Species othe r than the maintenance host may be 
more resistant to infection , but if infected are more susceptible to disease. L.  pomona , for 
example , causes subclinical infection in pig herds but may be responsible for causing sporadic 
cases of disease in other species  such as humans (accidental hosts). In maintenance hosts, 
Leptospira localise in the kidneys and continue to be excreted in urine for protracted periods.  
The organisms are shed in urine and infection can occur through mucous membranes, venereally, by mout h or through the skin, particularly through abrasions and wounds (Hunter 2004). 
Leptospira spp. are also excreted in semen and remain viable in semen prepared for artificial 
insemination (Hunter 2004; Masri et al 1997) . Clinically diseased animals shed more organisms 
and are more im portant sources of infection than chronic carriers (Horsch 1989) .  
Ministry for Primary Industries  Import risk analysis: Pig semen • 112 In accidental hosts the incubation period ranges  from 2 -16 days and is followed by a period of 
bacteraemia (Hunter 2004). Most cases of leptospirosis in pigs are subclinica l. A variety of signs 
may be shown by diseased animals including abortion, haemolytic anaemia, icterus and 
nephritis. Chronic leptospirosis is characterised by abortions, stillbirths and the birth of weak 
piglets. The disease can be diagnosed by the isolat ion of the organism, but because this is a 
difficult process it is usually diagnosed by serological methods. A rising titre suggests a recent infection while  a stable, often low -level titre indicates resolution or a chronic infection. The 
microscopic agglu tination test is still the most commonly used herd test .  A number of variations 
of ELISA are also available,  but generally lack serovar specificity (Bolin 2004) . Leptospirosis is 
seldom the cause of economically serious disease in animals. It is a zoonotic disease that 
occasionally causes serious disease in humans (Thornley et al 2002) .   
Leptospira spp. are sensitive to several antibiotics (Alt et al 2001; Gerritsen et al 1994; Gerritsen 
et al 1993; Hodges et al 1979; Minis try of Agriculture and Forestry 2007; Murray and 
Hospenthal 2004; Oie et al 1983) . Leptospiruria has been successfully treated using streptomycin 
(Alt et al 2001; Gerritsen et al 1994; Hodges et al 1979) . Streptomycin and penicillin have been 
used extensively for prophylaxis and treatment of live animals, semen and embryos in international trade. Streptomycin was found to be the drug of choice in pigs and tetracycline was 
also effective (Alt and Bolin 1996).  
43.1.5.  Hazard identification conclusion 
Since Leptospira spp. exotic to New Zealand occur in the countries included in this  risk analysis, 
they are identified as a potential hazard . 
43.2. RISK ASSESSMENT  
43.2.1.  Entry assessment  
Acutely infected animals  or chronic carriers of infection may excrete the organism in their semen 
(Hunter 2004; Masri et al 1997) . Therefore the likelihood of entry in imported semen is non-
negligible.  
43.2.2.  Exposure assessment  
Carriers and acutely infected animals shed the organism in their semen and inseminate d sows are 
likely to become infected. Therefore the likelihood of exposure of sows inseminated with imported semen is high.  
43.2.3.  Consequence assessment  
Introduction of new Leptospira serovars is unlikely to have a major impact on the New Zealand 
pig population or other farmed animals although cases of disease and reproductive failure may occur.  
The establishment of a new Leptospira serovar to which humans are susceptible could lead to the 
sporadic occurrence of leptospirosis in humans. The number and se verity  of the cases would 
depend on the serovars involved and contact with infected animals. Some serovars are not important as human pathogens .   For example, in New Zealand L. balcanica is common in its 
maintenance host the brush- tailed possum, but infections of  humans have not occurred despite 
close contact between possums and possum hunters (ESR 2004) .   
Ministry for Primary Industries  Import risk analysis: Pig semen • 113 There are not likely to be noticeable consequences for feral or wild animals , but some serovars 
such as L. grippotyphosa, L. canicola , L. sejroe  and L. sa xkoebing  could become established in 
mice and rats (Horsch 1989)  and subsequently infect humans.  
The likelihood of establishment of new Leptospira serovars is low but non- negligible. 
Establishment of new serovars could cause sporadic cases of disease in humans. Therefore the 
consequences of establishment are non -negligible. Cases of disease and reproductive failure may 
occur in pigs.  
43.2.4.  Risk estimation  
Entry, exposure and consequence have all been assessed as non -negligible. As a result the risk 
estimate for Leptospira spp. is non -negligible and they are classified as a risk  in the commodity. 
Therefore risk management measures can be justified.  
43.3. RISK MANAGEMENT  
43.3.1.  Options  
When drafting options for managing the risk posed by Leptospira spp. in semen , the following 
points were considered:  
• Because of the occurrence of long -term carriers of infection, quarantine is not a suitable 
option.  
• Diagnosis in donor boars by means of serology is complex to perform and the results are 
difficult to interpret b ecause of the many serovars and the difficulty in interpretation of 
cross reactions and low -titre reactions.  
• Testing of semen samples by culture or PCR is problematic because isolation of 
organisms is difficult and selection of primers for PCR that will r ecognise all serovars 
has not yet been achieved.  
• Leptospira are sensitive to a variety of antibiotics , and treatment of animals or inclusion 
of antibiotics in prepared semen has traditionally been used to prevent dissemination of Leptospira spp. by intern ational trade.  
• The OIE Terrestrial Animal Health Standards Commission considers that international trade does not increase the risks to human or animal health.  The Code  gives no 
recommendations for leptospirosis.  
Option 1  
The disease could be considered to  be of negligible risk to human or animal health , and trade 
without restrictions could be permitted.  
Option 2  
Donor boars could be tested serologically with a variety of antigens that occur in the exporting 
country and not in New Zealand, with negative res ults. 
Option 3  
Donor boars could be treated with effective antibiotics within one week of semen collection.  
Streptomycin is the antibiotic of choice although it may not be available in all countries.   
Ministry for Primary Industries  Import risk analysis: Pig semen • 114 Option 4 
Semen diluents containing antibiotics that are  effective against Leptospira spp. could be used in 
the preparation of the semen.  
 
References  
References marked * were sighted as abstracts in electronic databases.  
Alt DP, Zuerner RL, Bolin CA (2001) . Evaluation of antibiotics for trea tment of cattle infected with Leptospira 
borgpeterseni i serovar hardjo. Journal of the American veterinary Medical Association , 219(5), 636-9.  
 
Bolin CA (2004).  Leptospirosis. In: OIE (eds), Manual of Diagnostic Tests and Vaccines for Terrestrial Animals . 
Vol. 1, Pp. 316 -27, OIE, Paris.  
 ESR (2004).  Notifiable and other diseases in New Zealand. Annual Report 2003, pp. 26-7., Institute of Environment 
and Science Research, New Zealand. 
http://www.surv.esr.cri.nz/PDF_surveillance/AnnSurvRpt/2003AnnualSurvRpt.pdf , downloaded 27/1/2009.  
 
Fairley R (1997). Porcine leptospirosis in New Zealand. Surveillance , 24(4), 15.  
 
Gerritsen MJ, Koopmans MJ, Dekker TC, De Jong MC, Moe rman A, Olyhoek T (1994). Effective treatment 
with dihydrostreptomycin of naturally infected cows shedding Leptospira interrogans  serovar hardjo subtype 
hardjobovis. American Journal of Veterinary Research, 55(3), 339-43.  
 Gerritsen MJ, Koopmans MJ, Olyhoe k T (1993). Effect of streptomycin treatment on the shedding of and the 
serologic responses to Leptospira interrogans  serovar hardjo  subtype hardjobovis  in experimentally infected cows. 
Veterinary Microbiology , 38(1 -2), 129-35.  
 
Hodges RT, Thomson J, Townsend KG (1979). Leptospirosis in pigs: the effectiveness of streptomycin in leptospiruria. New Zealand Veterinary Journal , 27(6), 124-6.  
 
Horsch F (1989).  Leptospirosis. In: Blaha T (eds),  Applied Veterinary Epidemiology , Pp. 95 -102, Elsevier Science 
Publis hers, Amsterdam.  
 Hunter P (2004).  Leptospirosis. In: Coetzer JAW, Tustin RC (eds), Infectious Diseases of Livestock . Vol. 3, Pp. 
1445-6, Oxford University Press, Cape Town.  
 Masri SA, Nguyen PT, Gale SP, Howard CJ, Jung SC (1997). A polymerase chain react ion assay for the 
detection of Leptospira  spp. in bovine semen. Canadian Journal of Veterinary Research , 61(1), 15 -20. 
 
Midwinter A (1999) . Spirochaetes in New Zealand. Surveillance , 26(3), 10-2.  
 
MAF (2008). The Unwanted Organisms Register. 
http://mafuwsp6.maf.govt.nz/uor/searchframe.htm , downloaded 
27/1/2009.  
 Murray CK, Hospenthal DR (2004) . Determination of susceptibilities of 26 Leptospira  sp. serovars to 24 
antimicrobial agents by a bro th microdilution technique. Antimicrobial Agents and Chemotherapy , 48(10), 4002-5.  
 
Oie S, Hironaga K, Koshiro A, Konishi H, Yoshii Z (1983) . In vitro susceptibilities of five Leptospira  strains to 
16 antimicrobial agents. Antimicrobial Agents and Chemothe rapy, 24(6), 905- 8. 
 Thompson A (1980) . The first New Zealand isolation of Leptospira interrogans  serovar australis . New Zealand 
Medical Journal , 91(651), 28.  
 
Thornley CN, Baker MG, Weinstein P, Maas EW (2002) . Changing epidemiology of human leptospirosis  in New 
Zealand. Epidemiology and Infection , 128(1), 29-36.   
Ministry for Primary Industries  Import risk analysis: Pig semen • 115 44. Mycoplasma  spp.  
44.1. HAZARD IDENTIFICATIO N 
44.1.1.  Aetiological agent  
Mycoplasma hyopneumoniae , M. hyorhinis , and M. hyosynoviae are recognized pathogens of 
pigs. Other Mycoplasma spp. and related Mollicute s are regarded as non -pathogenic (Thacker 
2006) . 
44.1.2.  OIE list  
Not liste d. 
44.1.3.  New Zealand status  
M. hyorhinis and  M. hyopneumoniae have been isolated from pigs (MacPherson and Hodges 
1985) . 
44.1.4.  Epidemiology  
M. hyopneumoniae, M. hyorhinis, and  M. hyosynoviae are widely distributed in the world 
(Thacker 2006) .  Of these , only M. hyosynoviae  has not been described in New Zealand.  Since 
there have been no restrictions in the past to prevent the introduction of this organism, it seems 
unlikely that it is not already here. It commonly occurs along with M. hyorhinis , which is faster 
growing and easier to culture .  Unless a culture medium that contains inhibitors for M. hyorhinis  
is used, M. hyosynoviae  may be overlooked (Friis 1979; Friis et al 1991) . 
M. hyosynoviae  colonises the upper respiratory tract. In the acute phase of infection, which lasts 
1-2 weeks, it spreads systemically and infects joints and other tissues .  Infection can persist 
indefinitely in the tonsils (Friis et al 1991; Hagedorn -Olsen et al 1999a; Hagedorn -Olsen et al 
1999b; Thacker 2006) . 
Signs of infection with M. hyosynoviae  occur after an incubation period of 4 -9 days  and include 
lameness in 3 -5 month old pigs, with acute signs persisting for 3 -10 days. Many animals recover 
with no further lameness. In some animals stiffness or arthritis may persist and may be complicated by osteochondrosis (Thacker 2006) . The diagnosis can be confirmed by isolation of 
the organism from joint fluid during the acute phase, or a ntibody can be detected by complement 
fixation or ELISA . These  tests are not generally available in the USA (Thacker 2006) , and are 
unlikely to be available in New Zealand. In some herds no signs of disease are seen and infection is confined to the tonsils (Hagedorn -Olsen et al 1999b) .  
The available evidence suggests that the organism persists in tonsils and synovial surfaces. The organi sm spreads systemically during the early stages of infection, indicating bacteraemia.  
However, a search of the literature including three electronic databases produced no evidence that the organism is excreted in semen or that semen or artificial insemina tion is implicated in 
the transmission of the disease.  
44.1.5.  Hazard identification conclusion 
M. hyosynoviae  has not been described as occurring in New Zealand, but surveillance has not 
been conducted  in a systematic way. There is no evidence to suggest that th e organism is 
excreted in semen and therefore it is not identified as a  hazard in the commodity.   
Ministry for Primary Industries  Import risk analysis: Pig semen • 116 References  
References marked * were sighted as summaries in electronic media sources.  
Friis NF (1979) . Selective isolation of slowly growin g acidifying mycoplasmas from swine and cattle. Acta 
Veterinaria Scandinavica , 20, 607- 9. 
 
Friis NF, Ahrens P, Larsen H (1991) . Mycoplasma hyosynoviae  isolation from the uppe r respiratory tract and 
tonsils of pigs. Acta Veterinaria Scandinavica, 32(4), 425- 9.** 
 Hagedorn -Olsen T, Nielsen NC, Friis NF (1999a) . Induction of arthritis with Mycoplasma hyosynoviae  in pigs: 
clinical response and re-isolation of the organism from body fluids and organs. Zentralblatt für Veterinärmedizin. 
Reihe A, 46(6), 317-25.  
 
Hagedorn -Olsen T, Nielsen NC, Friis NF, Nielsen J (1999b) . Progression of Mycoplasma hyosynoviae  infection 
in three pig herds. Development of tonsillar carrier state, arthritis and antibodies in serum and synovial fluid in pigs 
from birth to slaughter. Zent ralblatt für Veterinärmedizin. Reihe A , 46(9), 555-64.* 
 MacPherson MR, Hodges RT (1985) . The occurrence of mycoplasmas in the lungs of pigs in New Zealand. New 
Zealand Veterinary Journal , 33(11), 194-7.  
 Thacker EL (2006).  Mycoplasmal diseases. In: Straw BE, Zimmerman JJ, D'Allaire S, Taylor DJ (eds), Diseases of 
Swine . 9
th edition, Pp. 701 -17, Blackwell Publishing, Ames, Iowa.  
  
Ministry for Primary Industries  Import risk analysis: Pig semen • 117 45. Pasteurella multocida  
45.1. HAZARD IDENTIFICATIO N 
45.1.1.  Aetiological agent  
Pasteurella multocida  strains that produce a dermonecrotic protein toxin (Penrith 2004) . 
45.1.2.  OIE list  
Listed (OIE 2008a) .  
45.1.3.  New Zealand status  
Notifiable organism (MAF 2008) .  
45.1.4.  Epidemiology  
Progressive atrophic rhinitis occurs in all countries that are considered in this risk analysis (OIE 
2008b) . The disease is caused by toxigenic strains of P. multocida and is most commonly seen in 
young pigs about 4 -12 weeks old, but older pigs can also be infected. The first signs are those of 
acute rhinitis with snu ffling and sneezing. As the disease progresses, snout deformities are seen 
and retardation of growth rate is common (De Jong 2006; Penrith 2004) . In some cases pigs may 
be subclinically infected. The organism may be found in the nasal passages and it usually 
colonises the tonsils (De Jong 2006; Penrith 2004) . Colonisation of the nasal mucosa causes the 
most severe lesions, but lesions can develop as a result of toxin produced in the tonsils without colonisation of the nasal passages (De Jong 2006; Penrith 2004) . The organism may be isolated 
from tonsils, nasal passages and lungs, but has also been isolated from the vagina (De Jong 2006) .  
An extensive review of the literature revealed no description of the isolation of the organism from the male genital tract or of excretion of the organism in semen. The Australian Quarantine 
and Inspection Service (AQIS) found no information on excretion of P. multocida in semen 
(AQIS 1999) . Further, in reply to a question about their draft import risk analysis, AQIS said  
“transmission of P. multocida via artificial insemination is considered a very unlikely event” 
(AQIS 2000) . Therefore, it is concluded that the organism is not excreted in semen. In addition, 
the organism is sensitive to a wide range of antibiotics including those that are used in semen 
diluents (Penrith 2004)  and would like ly be inactivated in semen prepared for artificial 
insemination.   
45.1.5.  Hazard identification conclusion 
P. multocida is not excreted in semen and is not identified as a hazard in the commodity.  
 
References  
 
AQIS (1999). Porcine semen Import  Risk Analysis: Technical Issues Paper. 
http://www.daff.gov.au/__data/assets/pdf_file/0018/15282/99-025a.pdf , downloaded 27/1/2009.  
 
AQIS (2000). Animal Quarantine Polic y Memorandum 2000/20. 
http://www.daff.gov.au/__data/assets/pdf_file/0016/15343/00-020.pdf , downloaded 27/1/2009.  
  
Ministry for Primary Industries  Import risk analysis: Pig semen • 118 De Jong MF (2006).  Progressive and nonprogressive atroph ic rhinitis. In: Straw BE, Zimmerman JJ, D'Allaire S, 
Taylor DJ (eds), Diseases of Swine . Pp. 577 -602, Blackwell Publishing, Ames, Iowa.  
 
MAF (2008). The Unwanted Organisms Register. http://ma fuwsp6.maf.govt.nz/uor/searchframe.htm , downloaded 
27/1/2009.  
 OIE (2008a) . Terrestrial Animal Health Code . 
http://www.oie.int/eng/normes/MCode/en_sommaire.htm , 
downloaded 27/1/2009.  
 
OIE (2008b) . World Animal Health Information Database. http://www.oie.int/wahid -prod/public.php?page=home , 
downloaded 27/1/2009.  
 
Penrith M -L (2004).  Progressive atrophic rhinitis. In: Coe tzer JAW, Tustin RC (eds), Infectious Diseases of  
Livestock . Vol. 2, Pp. 1707 -13, Oxford University Press, Cape Town.  
  
Ministry for Primary Industries  Import risk analysis: Pig semen • 119 46. Salmonella spp.  
46.1. HAZARD IDENTIFICATIO N 
46.1.1.  32.1.1 Aetiological agent  
There are approximately 2,500 known serovars in the Salmonella genus (Davies 2008) . All 
organisms considered in this section belong to the species enterica  and the subspecies enterica  
except for Salmonella arizonae , which belongs to the subspecies arizon ae. Using correct 
conventions, the names such as Dublin and Typhimurium, which do not have species status, 
should not be italicised. The correct name for the serovar Typhimurium is Salmonella enterica 
subsp. enterica  serovar Typhimurium. However, in this r isk analysis the simplified form such as 
Salmonella Typhimurium is used. Phage typing of Salmonella spp. is also commonly used to 
classify strains. The definitive phage type (Alley et al 2002)  number is giv en after the species 
name , e.g., Salmonella Typhimurium DT104. In this chapter the term species or its abbreviations 
sp. (singular) or spp. (plural) are used broadly to include species, subspecies, serotypes and 
phage types , e.g., Salmonella spp. 
46.1.2.  OIE list  
Not listed.  
46.1.3.  New Zealand status  
Salmonella Abortus ovis, S. arizonae , S. Dublin, S. Enteritidis DT4, S.  Gallinarum, S. Pullorum, 
S. Typhimurium DT44 and DT104 and Salmonella spp. (exotic affecting animals), are listed as 
unwanted organisms (MAF 2008) .  
46.1.4.  Epidemiology  
Salmonella spp. isolated in New Zealand are identified to serovar and phage type by the 
Environmental Science and Research (ESR)  laboratory and recorded on a database (ESR 2007) . 
Isolations from both medical and animal health laboratories are included.  
S. Typhimurium DT104 is of particular importance because it exhibits mu ltiple resistance to 
commonly used antibiotics and is a threat to human health (Hogue et al 1997;  Jones et al 2002; 
Plagemann 1989) . S. Typhimurium is endemic in New Zealand in both animals and humans , but 
in 2006 the definitive phage type DT104 occurred only three times and DT44 did not occur in 
1,404 isolates from humans. These page types were not identified in 1,417 isolates from animals. 
S. Enteritidis DT4 was isolated six times in humans and not at all from animals in the same 
period (ESR 2007) . The occurrence of these phage types in a few cases in humans may indicate 
that they have not become established in the New Zealand animal population and are rare in 
humans.  
S. Choleraesuis  is the main cause of salmonellosis in pigs in the USA and S. Typhimu rium is the 
principle pathogen in Europe (Griffith et al 2006; Penrith et al 2004) . S. Choleraesuis is a pig -
adapted strain and has rarely been isolated from other animals. It is no t present in New Zealand 
(ESR 2007) . Disease in pigs is usually characterised by septicaemia and pneumonia and 
sometimes meningoencephalitis. Enterocolitis  occurs infrequently (Griffith et al 2006; Penrith et 
al 2004) . S. Typhi murium commonly causes enterocolitis and may cause septicaemia and 
abortion (Griffith et al 2006; Penrith et al 2004) .  
Ministry for Primary Industries  Import risk analysis: Pig semen • 120 Outbreaks of disease in pigs caused by S.  Typhisuis have been reported from Asia, Europe and 
the USA (Penrith et al 2004) . Other Salmonella spp. are commonly isolated from healthy and 
diseased pigs and, although they are usually not a s ignificant cause of disease in pigs, pigs can 
act as a source of infection for humans (Penrith et al 2004) . 
Once a herd becomes infected with a Salmonella sp. the organism spreads through the herd and 
many pigs become carriers that excrete the organism intermittently. Identification  of carrier 
animals is difficult and requires repeated culturing of faeces.  
Since septicaemia occurs in infected animals, infection of semen could occur.    
46.1.5.  Hazard identification conclusion 
S. Choleraesuis  is an exotic, zoonotic organism and S. Typhimurium  type DT104 and DT44 and 
S. Enteritidis DT4 are unwanted and zoonotic organisms.  Other exotic zoonotic Salmonella spp. 
may occur in pigs. Therefore these organisms are identified as a potential hazard  in the 
commodity.  
46.2. RISK ASSESSMENT  
46.2.1.  Entry assessment  
Animals infected with Salmonella spp. may carry them for long periods and excrete them 
intermittently in faeces. Donor boars could be chronic carriers or be recently infected with 
Salmonella spp. Therefore the likelihood that donors could be infected with Salmonella 
organisms is non -negligible. In sheep S. Abortus ovis may be transmitted during mating (Vodas 
and Marinov 1986)  and S. Morbificans has been described as a secondary invader of the bovine 
reproductive tract (Boryczko and Furowicz 19 71). It is therefore possible that septicaemic pigs 
could excrete Salmonella spp. in semen. Although the likelihood that Salmonella spp. could be 
present in pig semen is low, it is assessed  to be non- negligible.  
46.2.2.  Exposure assessment  
Imported semen would b e inseminated into sows and therefore exposure of New Zealand farmed 
pigs is inevitable.  
46.2.3.  Consequence assessment  
Salmonella spp. could be transmitted by the faecal -oral route amongst pigs and infected pigs 
could develop disease or become subclinically -infected carriers. Newly introduced Salmonella 
spp. could spread widely due to stock movements and could result in the establishment of 
production -limiting salmonellosis in livestock. An example of how an emerging Salmonella sp. 
can effect New Zealand animal industries can be seen in the case of S.  Brandenburg,  which first 
emerged in 1997 and subsequently spread to many farms causing abortions in hundreds of sheep 
flocks within a few years (Kerslake and Perkins 2006) . Introdu ction of new Salmonella spp. 
could therefore have significant economic consequences for the animal industries.  Establishment of exotic zoonotic Salmonella spp. in animal populations , e.g., S. Typhimurium 
DT 104,  could cause human disease requiring expensi ve treatment and possibly death in rare 
cases (Davies 2001; Hogue et al 1997) . 
 There would be n o particular consequences for the environment other than possibly sporadic 
cases of salmonellosis in wild or feral animals such as deer, goats, and birds. S. Typhimurium 
(DT160) was reported to be associated with several hundred deaths in sparrows (Alley et al 
2002) . The outbreak was self -limiting and did not cause lasting damage to the sparrow  
Ministry for Primary Industries  Import risk analysis: Pig semen • 121 population. However, Salmonella infections can establish in wild bird populations and cause 
mortalities over many years (Pennycott 2001) . 
 
Introduction of infected semen could lead to the establishment of new Salmonella spp. that have 
the potential to cause disease in humans, production -limiting disease of dom estic animals and 
disease in wild and feral animals. Therefore the consequences are non -negligible.  
46.2.4.  Risk estimation  
Entry, exposure and consequence have all been assessed as non -negligible. As a result the risk 
estimate for exotic Salmonella spp. is non -negligible and they are assessed to be a risk in the 
commodity. Therefore risk management measures can be justified.  
46.3. RISK MANAGEMENT  
46.3.1.  Options  
When drafting options for managing the risk posed by Salmonella spp. in semen the following 
points were considered : 
• Donor boars should be healthy and show no signs of salmonellosis.  
• Culturing of faeces from donor animals is unreliable due to the intermittent excretion of the organism by carrier animals. Therefore isolation attempts could be repeated several 
times to increase the likelihood of detecting carriers.  
• Serological tests are not presently available that can reliably detect a wide variety of Salmonella serovars in individual carrier animals.  
• Processed semen will generally contain antibiotics but, since resist ance to antibiotics is 
widespread, they cannot be relied upon to inactivate Salmonella spp. (Jones et al 2002; 
Wray et al 199 1).  
• Culture of Salmonella spp. from a variety of animals and animal sources is well 
documented and comparatively simple to perform (Davies 2008) . 
There are no recommendations in the  Code  relating to Salmonella  in semen.  
The following options, given in ascending order of stringency , are available:  
Option 1  
Semen from healthy pigs not showing clinical signs of salmonellosis and housed on an artificial 
insemination centre could be impo rted without restriction.  
Option 2  
Faecal samples from donor boars could be cultured using suitable pre -enrichment and 
enrichment media (Davies 2008) , on at least 3 occasions, twice i n the 3 weeks prior to semen 
collection and once within 1 week of the completion date of collection of semen. All isolated Salmonella spp. could be identified to serotype and for S.  Typhimurium and S. Enteritidis to 
phage type. The results could be reported to the director of Biosecurity New Zealand. Semen from boars carrying exotic Salmonella spp. could be prohibited from importation. The decision 
whether to import semen from boars infected with endemic species could be made by the importer.   
Ministry for Primary Industries  Import risk analysis: Pig semen • 122 Option 3  
An al iquot of semen from each batch could be cultured using suitable pre -enrichment and 
enrichment media (Davies 2008) . When culturing processed semen it could be assumed that if 
Salmonell a spp. are not isolated they are not present or have been inactivated by the antibiotics 
used in preparation of the semen. Culturing from processed semen samples could therefore be 
recommended. Any isolated Salmonella spp. could be fully identified to serotype, and to phage 
type for S. Typhimurium and S. Enteritidis, and the results reported to the director of Biosecurity 
New Zealand. Semen infected with exotic Salmonella spp. could be prohibited from importation. 
The decision whether to import semen infect ed with an endemic Salmonella spp. could be made 
by the importer.  
 
 
References  
References marked * were sighted as summaries in electronic media sources.  
Alley MR, Connolly JH, Fenwick SG, Mackereth GF, Leyland MJ, Rogers LE, Haycock M,  Nicol C, Reed 
CEM (2002) . An epidemic of salmonellosis caused by Salmonella Typhimurium DT 160 in wild birds and humans 
in New Zealand. New Zealand Veterinary Journal , 50(5), 170-6.  
 
Boryczko Z, Furowicz A (1971) . Changes in the semen and blood of bulls a fter experimental orchitis and 
inflammation of the seminal vesicles. 1. Results of physical, biochemical and bacteriological examinations. 
Medycyna Weterynaryjina , 27(7), 423-8.  
 
Davies R (2001) . Salmonella Typhimurium DT 104 in Great Britain. Udgivet af D ansk Zoonoscenter , 
http://zoonyt.dzc.dk/0101/artikler/art5.htm , downloaded 27/1/2009.  
 
Davies R (2008).  Salmonellosis. In: OIE (eds), Manual of Diagnostic Tests and Vaccines for Terrestrial Animals . 
Vol. 2, Pp. 1267 -83, OIE, Paris.  
 
ESR (2007) . Database of the enteric reference 
laboratory. http://www.surv.esr.cri.nz/enteric_reference/enteric_reference.php , downloade d 27/1/2009.  
 Griffith RW, Schwartz KJ, Meyerhotz DK (2006).  Salmonella. In: Straw BE, Zimmerman JJ, D'Allaire S, Taylor 
DJ (eds), Diseases of Swine . Pp. 739-54, Blackwell Publishing, Ames, Iowa.  
 
Hogue A, Agula F, Johnson R, Petersen K, Saini P, Schlosser  W (1997).  Situation assessment: Salmonella 
Typhimurium DT 104, United States Department of Agriculture, Food Safety and Inspection Service, Washington 
DC 20250. 
http://www.fsis.usda.gov/OPHS/stdt10 4.htm , downloaded 27/1/2009.  
 
Jones YE, Chappell S, McLaren IM, Davies RH, Wray C (2002) . Antimicrobial resistance in Salmonella  isolated 
from animals and their environment in England and Wales from 1988 to 1999. Veterinary Record , 150, 649-54.  
 Kerslake JI, Perkins NR (2006) . Salmonella  Brandenburg: case -control survey in sheep in New Zealand. New 
Zealand Veterinary Journal , 54(3), 125 -31. 
 
MAF (2008). The Unwanted Organisms Register. 
http:// mafuwsp6.maf.govt.nz/uor/searchframe.htm , downloaded 
27/1/2009.  
 
Pennycott T (2001) . Death in finches and sparrows. http://www.bvpa.org.uk/papers/penn01wb.htm , downloaded 
27/1/2009.  
 Penrith M -L, Neser JA, Henton MM (2004).  Porcine salmonellosis. In: Coetzer JAW, Tustin RC (eds), Infectious 
Diseases of Livestock . Vol. 3, Pp. 1601- 7, Oxford University Press, Cape Town.  
 
Plagemann O (1989). Differential diagnosis of Salmonella Abortus ovis and Yersinia pseudotuberculosis from 
abortions in ewes. Journal of Veterinary Medicine. Series B , 36(7), 509 -14. 
  
Ministry for Primary Industries  Import risk analysis: Pig semen • 123 Vodas K, Marinov MF (1986) . Role of rams in the epizootiology of salmonella abortion in sheep. 
Veterinaromeditski Nauki, 23(9), 61-8.  
 
Wray C, Beedel l YE, McLaren IM (1991) . A survey of microbial resistance in salmonellas isolated from animals 
in England and Wales during 1984- 1987. British Veterinary Journal , 147(4), 356-69.  
   
Ministry for Primary Industries  Import risk analysis: Pig semen • 124