WORLD TRADE  
ORGANIZATION  WT/DS367/12 
9 August 2010 
 (10-4165) 
 Original:   English 
  
 
AUSTRALIA – MEASURES AFFECTING THE IMPORTATION OF APPLES 
FROM NEW ZEALAND 
 
Transcript of the proceedings of the Panel's meeting with the experts
∗ 
 
  In accordance with the Procedures for the Panel' s meeting with the experts and Parties and the 
Panel's second substantive meeting, adopted by  the Panel on 11 June 2009, the transcript of the 
proceedings of the Panel's meeting with the scien tific experts will only be available in electronic 
format. 
 
_______________ 
 
                                                     
 
∗ The Transcript of the Panel's meeting with the scien tific experts is initially available in its original 
language.  A translation to French and Spanish will follow when resources become available.  WT/DS367/12 
 Page 3 
 
 
  ANNEX B-2 
 
TRANSCRIPT OF THE PANEL'S MEETING WITH EXPERTS 
 
Tuesday, 30 June 2009 
 
Chairman  
1. I would like to welcome the experts and the Parties to this meeting of the Panel on Australia – 
Measures Affecting the Importa tion of Apples from New Zealand . The experts with us today are 
Dr Cross, Dr Deckers, Dr Latorre, Dr Paulin, Dr  Schrader, Dr Sgrillo a nd Dr Swinburne. The Panel 
greatly appreciates their presence and assistance in this case. I would also like to welcome the public 
who is following this meeting by closed-circuit TV broadcast. 
2. My name is Attie Swart and I am Chairman of the Panel. I would like to introduce to you 
Ms Kirsten Hillman on my left, and Mr William Ehle rs, who are the other panel members.  The WTO 
Secretariat staff assisting the panel consist of Ms Chri stiane Wolff. She is the Secretary of the Panel.  
And we have Mr Jorge Castro.  We have Mr János Volkai at the end there. We have Mr Adit Pujari, 
who is an intern in the Agriculture Division.  We al so have Mr Eric Gillman, an intern with the Legal 
Affairs Division, assisting the panel. 
3. By inviting the public to view this meeti ng from another room, the Panel has accepted a 
request made by both Parties in this case. I would li ke to thank the Information and External Relations 
Division and Security and the Conference Office of the WTO Secretariat for their assistance with the 
preparation and organization of the public viewing of  this meeting. May I remind all delegations, as 
well as all members of the public viewing the meeting, that any type of recording, filming, and photography during the meeting is prohibited.  Also  I'd like to request you to switch off your cell 
phones or to put them into silent mode during the meeting. Any persons causing any disruption 
whatsoever to these proceedings may be requested to  leave the room and be prohibited from further 
participation in the meeting. I would like to ad d that this rule includes both the Panel and the 
Secretariat.  Finally, if there is any disruption of the proceedings, the Panel reserves the right to 
suspend the meeting at any time and to continue it under closed session. 
4. To respect the rules of confidentiality, no inform ation, in particular exhibits designated as 
confidential by a Party, shall be addressed during this meeting. The Panel reserves the right to 
suspend the meeting at any time, on its own initiative, or at the request of a Party, either Party, if there 
is any risk of breach of confidentiality or of disrup tion of the meeting. If the meeting is suspended by 
the Panel for any reason, the Panel may decide to resume it in a closed, confidential session.   would 
like to ask if any of the Parties, if one of the Pa rties believes that a speaker is addressing confidential 
information, please raise your flags so that you'll aler t the Panel or the Chair to this. I note that, with 
the agreement of the Parties, this meeting will be conducted in English onl y, without simultaneous 
interpretation. 
5. I would now like to invite the Heads of Delegati on, the Parties, to introduce their respective 
delegations.  And if you have not already done so , I would ask you to subm it updated delegation lists 
to the Secretary of the Panel.  Please also ensu re that you use the microphones when addressing the 
Panel. This is necessary to ensure that the Secretar iat can prepare a transcript of the meeting, as we've 
agreed, based on the tape recordings being made. It is also necessary to enable the public in the other 
room to hear what you are saying. So if I can ask New Zealand first, if you'd like to introduce your 
delegation.  Ms Fearnley. 
New Zealand (Clare Fearnley)
 
6. On my left is Professor Don McRae; beside him is Alex Smithyman from the Ministry of 
Foreign Affairs and Trade; Dr Rob Beresford from HortResearch New Zealand; Alice Tipping from WT/DS367/12 
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  the Permanent Mission here in Geneva; Dr Stuart Ma cDiarmid, Ministry of Agriculture and Forestry 
Biosecurity New Zealand;  David Evans, Ministry of  Foreign Affairs and Trade;  Dr Carolyn White, 
Ministry of Agriculture and Forestry Biosecurity New Zealand; Anais Kedgley Laidlaw, Ministry of 
Foreign Affairs and Trade; Dr Jim Walker, HortRese arch; Dr Rob Taylor, Scientific Consultant; Jason 
McHerron, legal consultant; and R ob MacFarlane, Ministry of Agriculture and Forestry Biosecurity 
New Zealand.  Thank you. 
Chairman
 
7. You have noticed that there are earphones if you want to hear. Australia. 
Australia  
8. My name is James Baxter, I am head of the Australian delegation at this meeting. If it's 
acceptable, I'd like to ask the members of my delegation to introduce themselves. 
Chairman  
9. Please do. 
Australia  
10. Henry Burmester, Consultant Council with the Australian Government Solicitor.  Bill 
Roberts, Principal Scientist with Biosecurity Aust ralia.  Mark Jennings, Senior Counsel, Office of 
International Law Attorney-General's Department.  David Heinrich, Biosecurity Australia.  Simon 
Barry, Team Leader, Commonwealth Scientific and Industrial Research Organization.  Mike Robbins, 
Australian Quarantine and Inspection Service.  Jasm ine Tsen, Senior Legal Officer at the Office of 
International Law in the Attorney-General's Depa rtment.  Paul Schofield, WTO Trade Law Branch, 
Department of Foreign Affairs and Trade.  Julia  O'Brien, WTO Trade Law Branch, Department of 
Foreign Affairs and Trade.  Ben Cas, Trade Law Br anch, Department of Fore ign Affairs and Trade.  
Bruce Bowen, General Manager, Trade and Market  Access Division, Department of Agriculture, 
Fisheries and Forestry.  Caroline McCarthy, Depart ment of Foreign Affairs and Trade. Elizabeth 
Bowes, Australian Permanent Mission to the WTO.  Lisa White, Trade Law Branch, DFAT. 
Chairman  
11. As you know, the Panel was established by the Dispute Settlement Body on 21 January 2008, 
at the request of New Z ealand in document WT/DS367/5. The Pane l has standard terms of reference, 
namely to examine in the light of the relevant provisions of the covered agreements cited by New 
Zealand in document WT/DS367/5, the matter referred to the DSB by New Zealand in that document, and to make such findings as will assist the DSB in making the recommendations or in giving the rulings provided for in those agreements. 
12. The Panel is mindful that, under the WTO Dis pute Settlement Understanding, "[t]he aim of 
the dispute settlement mechanism is to ensure a pos itive solution to a dispute.  A solution mutually 
acceptable to the parties to a dispute and consistent  with the covered agreements is clearly to be 
preferred."  So, accordingly, the Panel is willing to provide Parties with adequate opportunities to 
develop a mutually satisfactory solution, if that is possible. We, as a Panel, certainly encourage you to 
do so. 
13. With regard to expert consultation, after its s ubstantive meeting, the Panel decided to consult 
with experts who have specialized scientific e xpertise on the issues arising in the dispute. The 
working procedures adopted on 26 March 2008, after c onsultation with the Parties, contained rules for 
expert consultation in paragraph 17  of those procedures.  Subseque ntly, the Panel has also adopted 
special working procedures for this week's meeti ngs after consultation with the Parties. The Panel 
received suggestions for experts from the Secretariat of the International Plant Protection Convention, 
IPPC, and from the Parties.  Following consultations  with the Parties on the candidate experts, the 
Panel appointed Dr Cross, Dr Deckers, Dr La torre, Dr Paulin, Dr Schrader, Dr Sgrillo, and  WT/DS367/12 
 Page 5 
 
 
  Dr Swinburne, to serve as scientific experts in this dispute. In accordance with the working 
procedures, and after having consider ed the Parties' comments, the Panel sent questions to the experts, 
and the experts were expected to reply in writing, and these replies were communicated to the Parties. 
Comments and counter-comments received from the Par ties on the expert replies were provided to the 
experts, and the experts also received a copy of the Parties' rebuttals submissions. 
14. So if I can turn to the conduct of the meeting t oday.  I think the purpose of this meeting with 
the experts is for the Panel to obtain clarification on some of the factual scientific issues relevant for 
this case.  In particular, the meeting should allo w the experts to elaborate and clarify the written 
responses submitted to the questions that were posed  by the Panel, and to respond to the comments 
made to those responses by the Parties. As well as to allow the Panel, and the Parties, to pose 
questions to the experts in order to seek any elaborat ion or clarification on issues that are relevant to 
the case. The Parties shall have the opportunity to  pose direct factual questions to the experts. 
However, they must please refrain from making st atements or posing argumentative or leading 
questions to the experts. 
15. The Panel has noted the due process and procedural  concerns raised by Australia in its written 
submissions.  The Panel takes these issues seriously, a nd will fully consider them  in its deliberations. 
However, it is imperative that we use the limited time we have available in this meeting with the 
experts for its intended purpose, and not lose focus by  concentrating on concerns that might be better 
addressed in the second substantive meeting with th e Parties, and in the responses provided by the 
Parties to the subsequent questions posed by the Panel. I think we'll have full opportunity tomorrow 
and the day after, and then with what follows. To that end, the Panel will ma nage its time with the 
experts carefully, concentrating on the most important issues within each area of enquiry, and moving 
the proceedings forward when it deems necessary. 
16. The Panel notes that its role is not to conduct a de novo  review of a party's risk assessment, 
but to make an objective assessment of the matt er before it, including, among other things, an 
objective assessment of the facts of the case. The Pa nel needs to assess, for example, the sources that 
support the scientific basis, as well as the scientific  methodological rigour of a risk assessment.  The 
role of the experts is to assist the Panel in this assessment by clarifying scientific matters within their 
expertise.  As such, and in accordance with the procedures adopted by the Panel for this meeting, 
experts should only answer questions that they feel  competent to answer.  Since factual issues and 
issues of law are closely linked in this case, expert s' responses may cross into  an area of competence 
of the Parties or the Panel.  We recognize this.  If a Party has a concern over a particular response, it is 
kindly asked to bring its concern to the attention of the Panel, and briefly note the basis of this 
concern.  When preparing its report, the Panel will d ecide whether or not it is appropriate to rely on 
information provided in a specific response by an  expert, considering also its relevance and 
usefulness. 
17. Then, the logistics of the meeting.  I think we suggest that the meeting proceeds in the 
following manner.  Before beginning with the ex amination of the specific scientific issues under 
consideration, the Panel will give an opportunity to each expert to introduce him or herself and to 
make some brief general comments on his or her r esponses, in particular, in light of the written 
comments made by the Parties.  Sort of, some ge neral comments. Afterwards the Panel will group the 
discussion into six subject areas, and organize the discussion accordingly. These subject areas will be 
as follows:  firstly, general terms and definitions;  secondly, risk assessment techniques;  then, fire 
blight;  European Canker;  apple leafcurling midge;  then finally, other. For each of these areas the 
Panel will organize the discussion so that both Parti es, and the Panel, have the opportunity to pose 
questions on the various issues. The Panel will nor mally start with questions, and then allow New 
Zealand the opportunity to pose its questions to the experts, followed by Australia.  I'll go into a little 
bit more detail later on, on this.  Throughout the discussion of each issue, the Panel may pose 
questions before, during or after th e Parties have posed their own qu estions. The Panel may also allow WT/DS367/12 
Page 6  
 
  the Parties to come back with new questions, or follow-up questions. Once the Panel has decided that 
a particular issue has been suffi ciently explored, the Panel will give the experts an opportunity to 
make some concluding remarks on the specific issue,  if they so wish. Throughout the meeting with 
the experts, the Panel will endeavour to ensure th at sufficient time is devoted to the discussion of the 
different relevant issues.  In order to achieve this  objective, the Panel may decide at any point that 
there is a need to move on to a different issue.   The Parties are reminded that the time we have 
available in this meeting with the experts is rather  limited.  The experts will be asked to provide their 
responses individually and should please refrain from conferring during the course of the meeting. 
18. Before we begin, I would like to recall that  the purpose of today's meeting is to take 
advantage of the experts' presence, and to allo w the Panel to gain a better understanding of the 
scientific issues before us. These experts have been selected, were selected, after extensive 
consultations, and again, the Panel appreciates thei r contributions and their presence today. Expert 
consultation is an important aspect, and asset, fo r many WTO dispute settlement panels, who are 
asked to make findings in disputes that frequently in volve sophisticated technical issues. I'm confident 
that the Parties will also make the best of their expe rtise during this meeting.  I kindly request that the 
experts attempt as much as possible to explain their responses in a way – and listen carefully to this – 
to explain their responses in a way that even those of  us who do not have the be nefit of their expertise, 
can fully understand them. Experts should feel free to respond to a question or to make comments, 
even if the question is addressed to another expe rt, bearing in mind you should feel competent to 
respond to that particular question.  The WTO Secret ariat will prepare a transcript of the proceedings 
of the Panel's meeting with the experts, and for th e purpose of reviewing the transcript's accuracy, the 
Panel will send a copy of the transcript to the ex perts and to the Parties. The transcript of the 
proceedings of the Panel's meeting with the expert s, and the compilations of written replies of the 
experts, will be part of the record and referenced in the Panel's report. 
19. I have given you more or less the flow of the meeting.  What we intend to do is have the 
Panel ask, under each of those headings, its questions .  But after each specifi c question, we will allow 
New Zealand and Australia, after the experts have responded to, on that point, elaborate, if there's 
anything you want.  After the Panel has exhausted its questions under that heading, under those six 
headings, we will then offer New Zealand the o pportunity of asking its questions, followed by 
Australia asking its questions, if that's acceptable to you.  We'll see how it goes. Also, I think we have 
consulted with you on the timing for today, and we fe lt, if we could, it would possibly be better if we 
try to deal with the experts meeting today, but looki ng at the number of questions it may well be that 
we need more time.  So I think that the arrangeme nt that we are suggesting is that we break a little 
early for lunch and have an hour's lunch, in other words stop at 12.30, start again at 1.30, and then continue, if necessary, until 7pm.  In looking at th e spread of our own questions, it seems to me that 
the bulk of the questions will be on  the issue of risk assessment, and then the three pests.  So my 
suggestion is that we'll try and gi ve about an hour and a half on each  of those, but we'll see how it 
flows, and we'll try and cover as much as we possibly can, but there will be a little bit of give and 
take.  So that's our suggestion as to how to proceed .  Hopefully we'll get through all of our and your 
questions during the course of the day.  If absolu tely necessary we have tomorrow morning, but we 
might be able to conclude the expe rt consultations today.  If that's all right with you, I'd like to 
proceed to the experts and ask them to give us th eir brief introductory statements. Would you like to 
take the floor to make such brief comments and then  I'll also just offer you the opportunity in the 
order that you are, Dr Cross, if you'd like to… 
Dr Cross
 
20. I'm an entomologist and I'm an expert person on the apple leafcurling midge.  Clearly there 
will be many questions about this pest and its biol ogy and I hope I can help you with some guidance 
on that.  I don't have a general statement to make.  WT/DS367/12 
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  Chairman  
21. Dr Deckers. 
Dr Deckers  
22. I'm Tom Deckers from the Fruit Research Statio n PCFruit in St. Truiden, Belgium.  I am 
working in a pomology department, and one of the item s we have since more than 25 years is the fire 
blight research in our country. As a pomologist, I am also aware of the other important problems that 
are in the discussion here. I don't have either a big comment to make in advance. 
Chairman  
23. Dr Latorre. 
Dr Latorre  
24. I am Bernardo Latorre, from Chile. I'm working at  the Catholic University in Santiago at the 
present time, primarily on fruit diseases and apple diseases as well.  So I'm here to be able to help you in technical aspects of European canker. 
Chairman
 
25. Dr Paulin. 
Dr Paulin  
26. I am Jean-Pierre Paulin from Institut National de la Recherche Agronomique  in France.  I 
work in Angers.  I have been work ing for long on fire blight and maybe the most useful experience I 
have had which can be releva nt to this meeting is the fact that I have followed, I would say, the spread 
of the disease of fire blight in Europe and the Middl e East.  So I have seen places without fire blight 
which became blighted.  So this is maybe the experi ence which can be useful today.  I have no special 
things to tell you, except that I am a scientist, not a legal person, so some aspects of this meeting, as 
probably for my colleagues, are new for me. 
Chairman  
27. Dr Schrader. 
Dr Schrader  
28. My name is Gritta Schrader.  I am from th e Julius Kuehn-Institute, in Braunschweig in 
Germany, and I am the pest risk analysis coordina tor for Germany, so I have commented mostly on 
the questions regarding pest risk assessment.  My experience with pest risk assessment is now about 
nine years.  I am involved in many issues dealing with pest risk assessment.  For example, I am a member of the panel on plant health in the European  Food Safety Authority, and I was involved in 
drafting the standards of IPPC No. 2 and No. 11 as we ll.  I was also involved in preparing the training 
material for doing pest risk analysis by IPPC.  So I hope I can help you with any experience I have 
with doing pest risk analysis, being very much aw are of difficulties with doing such analysis, because 
especially the lack of data is a big constraint to doi ng a PRA and this is also why we have now started, 
in Europe, a large project, with 15 partners, invol ving Australia and New Z ealand as well, on how to 
improve the methods of PRA. 
Chairman
 
29. Dr Sgrillo. 
Dr Sgrillo  
30. I am Ricardo Sgrillo from Brazil.  I am an engineer agronomist and work for the Brazilian 
Government. I have a master in nuclear energy and a doctorate in entomology, a strange mixture!  I 
have been working with mathematical modelling for the last 30 years and, since 1997, I have been WT/DS367/12 
Page 8  
 
  working with the IPPC in the development of internati onal standards, three or four different standards.  
And I hope I can help you resolve these problems. 
Chairman
 
31. And, finally, Dr Swinburne. 
Dr Swinburne  
32. I am a retired gentleman of leisure. But I have  been publishing papers on apple cankers since 
about 1961. I think I enjoy… I deserve the le isure I am now enjoying. But I have published 
continuously on various aspects of this  disease, right up until last year. 
Chairman  
33. I think we'll then turn to cons ideration of the different areas a nd I'd like to start with general 
terms and definitions.  We have, as Panel, four questions.  And I am going to, against the advice of 
my Panel members, start with one which I don't want  you to answer immediately, but to think about.  
And then I'll ask three specific questions and come b ack to the first one last.  The Panel would like to 
ask the experts to explain three terms.  The one is "disease severity";  the second is "disease 
prevalence";  and the third is "disease incidence".  I' ll give you a bit of time to think about those.  I 
would like to then pose firstly to Dr Sgrillo, if I may, a more specific question.  You sometimes use 
the phrase "the scientific evidence does not guarantee that  this is true".  The Panel would like to know 
whether you are using this word "guarantee" in the sense that it is your view that the evidence does 
not sufficiently prove that something is true, or in  the sense that it does not support the issue.  If you 
could perhaps explain your use of the word "guarantee". 
Dr Sgrillo  
34. Well, in the case of assigning numbers to proba bilities, I guess this phrase was used mostly 
commenting on the numbers that were assigned to the probabilities.  What I would expect in this case 
is that you have a hypothesis, and then you have to validate this hypothesis.  And in the case of assigning numbers to probabilities, the numbers you are assigning represent a hypothesis about the real process in the world.  And when you assign these numbers you should be based on numbers from 
sampling of the reality.  Otherwise you are elaborating on the subject.  One note only: when I refer to 
guesses, it's not a pejorative term.  I'm sorry, b ecause English is not my native tongue.  But you can 
discuss with your colleagues and find out about a number that you and your colleagues find is a good number, okay?  Nevertheless, if y ou don't have numbers that were sa mpled in the real world, you have 
no guarantee that the numbers that you are assigning are representative.  It's a hypothesis, after all.  A 
common sense hypothesis, an elaborated hypothesis, but it follows that it's a hypothesis, no guarantee.  
This is the sense where the term "guarantee" was used. 
Chairman
 
35. Dr Latorre. 
Dr Latorre  
36. Maybe I can explain.  "Disease severity", "disease prevalence"… 
Chairman  
37. Before we go on to that question, I am going to ask New Zealand or Australia, whether you 
had any specific issue around the question that we've just asked.  And then I'm going to ask two more 
questions directly, and then we can come back to the first question I asked, if that's all right with you.  
New Zealand, are you satisfied?  Australia, please.  WT/DS367/12 
 Page 9 
 
 
  Australia  
38. If the Australian delegation could just thank Dr Sgrillo for his clarification of the use of the 
"guess" word, because we did comment on it, an d we fully appreciate that clarification. 
Chairman  
39. I'd like to then move to a second, more specific,  question.  Not that definitional one that I 
asked you just now.  There seem to be differing vi ews in expert's responses to Question 46 that we 
had sent to you regarding Australia's evaluation of the likelihood and implications of New Zealand 
apples being repacked at rural packing houses in close proximity to orchards.  And this is then for all 
three pests.  Would any of the experts like to comment or further clarify on this matter?  I am wondering whether it's sensible, obviously, to give you some time to think about this.  Is it useful 
posing a few questions, then coming back to specific questions?  Or shall we just take them one by 
one?  I am asking, really, the experts.  I don't want  to confuse issues, but it might be useful.  Would 
anybody be ready to answer this specific question I' ve posed now, about the different views, expert 
responses, to that question?  Dr Sgrillo? 
Dr Sgrillo
 
40. Yes.  I reproduced the model, I mean the quantitative model of Australia, in my computer and 
I have played around with it.  This is a case of the sensitivity of the model.  The model has not… The sensitivity of the model to adjust this parameter is very low.  This means that you can assign different 
numbers to this parameter, I mean, different percenta ges of the repacking and the effect in the general 
system, I mean in the end result, representing the pe rcent of infestation of apples, would not change 
too much.  This means that the model is not sens itive to this process, because of the mathematical 
structure. 
Chairman
 
41. Any further comment on this question from the experts.  Dr Cross. 
Dr Cross  
42. Yes.  I felt that this issue of the amount of fruit that is handled at these seven wholesalers 
seems to me, for the apple leafcurling midge, to be quite a critical issue.  And I was uncertain how to 
determine what proportion of apples would be handle d there with the different scenarios.  So if the 
fruit is retail-ready, I was uncertain as to whether an y of the fruit would have been handled at these 
wholesalers.  I am also uncertain of their location,  and whether they are in areas of Australia where 
apple leaf midge could establish and exist.  So it was a complicated question that I found quite difficult to answer. 
Chairman
 
43. New Zealand, do you want to …  I see, no more comments from the …  Thank you.  Can we 
move on?  Could I ask also – I noted your comment, just your statement, about – can I ask that we try and not go that route, because in terms of time, I think we all appreciate the comments that you've 
made, and you all appreciate that we have you availabl e to us today, but let's try and stick to specific 
questions.  Anything you'd like to raise on this particular issue in terms of the question, not 
clarification. 
Australia
 
44. Just a clarification, Mr Chairman.  I mean, we are happy to talk about that issue over the next 
couple of days.  I think it requires a fairly deta iled local knowledge about the apple supply chain 
system in Australia.  And I think it falls into that group of issues where we'd probably be better to 
focus on in the next two days. WT/DS367/12 
Page 10  
 
  Chairman
 
45. I tend to agree with you.  Okay.  Third more sp ecific question and then we come back to those 
three definitions I've asked you.  Several experts use the word "negligible" in their responses.  Now I 
wonder what you could explain what you mean by "n egligible" and is there any standard or accepted 
definition of this term?  Can the likelihood of an event that occurs several  times in one year be 
characterized as negligible?  Let me add a little tail on this.  Is there any international guideline in 
terms of translating that into a number?  If an y of the experts have some comment on that …  
Dr Schrader. 
Dr Schrader  
46. Well, as far as I know, there are no standard terms, no standard definitions, for it.  It's used by 
every country.  Not everybody uses it in its risk  assessments.  For example, Canada uses also 
negligible, and gives a certain example for it.   But it's not standardized in any way. 
Chairman  
47. Dr Latorre and then Dr Sgrillo after that.  Dr Latorre. 
Dr Latorre  
48. When I use this term, I try to indicate that it is something that may happen so rarely, in such a 
low proportion, that it is almost not important.  Something close to zero, but certainly it is not zero. 
Chairman  
49. Dr Sgrillo. 
Dr Sgrillo  
50. Well, as Dr Gritta said, there is no international standard.  However, there is some proposal.  
One proposal is that "Clearly a negligible risk s hould be much lower than the maximum tolerable risk 
for a given class of hazard.  We therefore propose de fining a hazard as 'negligible' if its associated risk 
is at least two orders of magnitude smaller than th e maximum tolerable risk for this class of hazard".  
This is a kind of definition that would help very much analysing the pest risk, the importation risk analysis of Australia.  I interpret that "negligible" refers to a quantity so small that it can be ignored. 
Chairman
 
51. Could I ask you just to explain again the proposal that there is and to whom is this proposal?  
Could you just explain again those numbers that you mentioned.  It was quite quick. 
Dr Sgrillo  
52. Okay.  You want me to read again? 
"Clearly a negligible risk should be much lower than the maximum tolerable risk for 
a given class of hazard.  We therefore prop ose defining a hazard as ‘negligible’ if its 
associated risk is at least two orders of magnitude smaller than the maximum tolerable risk for this class of hazard." 
53. I can give you the complete reference. 
Chairman
 
54. And that proposal is to whom? 
Dr Sgrillo  
55. This is a proposal of Braband in a paper.  I have the complete reference here.  Maybe I can 
write down.  WT/DS367/12 
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  Chairman  
56. Any other input from the experts on this question of negligible?  If not, thank you very much.  
New Zealand, thank you, no comment.  Fine.  Please, Australia. 
Australia  
57. Just – and we will return to this in the comi ng days – but I think we will need to place some 
context around this discussion of what negligible m eans.  We've heard Dr Sgrillo's comments, and we 
would just refer the experts to Table 12 of our IRA, in which we do in fact define negligible for the 
purposes of our IRA, and the interval is between zero and 10-6.  Though, in terms of the IRA, there is 
not an issue of definition.  We have provided that in the context of Table 12, for reference to the experts.  Thank you. 
Chairman
 
58. Okay.  Could I then ask that we move back to  those three definitions:  "disease severity";  
"disease prevalence";  and "disease incidence".  If – a nd I think Dr Latorre you were, already, in the 
blocs to respond to that. 
Dr Latorre  
59. Okay.  Well, "disease prevalence" and "disease in cidence" are both relative terms, trying to 
indicate the proportion of a disease within the population.  In the plant pathology literature, both terms are very often used as synonyms.  However, they are not.  Strictly, "prevalence" means the proportion 
of the disease in the population at the beginning.  An d when they refer to "incidence", it is how much 
this proportion of the disease has changed in time.  In other words, 1 per cent would mean one 
infected tree in 100 (prevalence, at the beginning).  But maybe after a few months, you have moved to 
maybe 10 per cent.  This would be an indication of incidence.  When we speak of severity, very 
clearly we try to indicate how heavily is the tree in fected.  How many leaves of the tree are infected.  
So that is the definition in general of these three terms, which are very often used epidemiologically. 
Chairman
 
60. Any further comments from the experts on that?  You all support that … ? 
Dr Deckers  
61. I think we could add, for the severity, that it is  important to follow the disease development in 
the plant.  And this can be measured, when you sa y there is a disease development in shoot infection 
or flower infection, taking all the branch, and so on.   So it is more a real, comparable possibility, to 
speak about the disease severity. 
Chairman  
62. Okay.  New Zealand.  Any comment here, please? 
New Zealand  
63. I'll just make a quick comment.  The terms "incid ence" and "prevalence" are used in some of 
the international standards for phytosanitary measur es but I don't know that they're defined in a very 
specific way.  And our experience with these terms is that it does vary very much in usage, from 
expert to expert, author to author. 
Chairman  
64. Okay. The Panel has exhausted its four questions  on "general terms and definitions". Let me 
offer the floor to New Zealand, if you have any poin ts you'd like to raise in this area. Questions.  Not 
points. Please let me withdraw that word.  Any questions you might ask the experts. 
New Zealand  
65. No questions at this stage. WT/DS367/12 
Page 12  
 
  Chairman
 
66. Thank you very much, Ms Fearnley. 
Australia  
67. We do have a couple of questions on this section.  Before I begin, I really do need to recall 
that our view is that individual experts should only be asked to respond to questions which pertain to 
their particular field of expertise, on which they ar e appointed to assist this Panel.  And just recalling 
that Dr Sgrillo and Dr Schrader were appointed  to advise on risk assessment methodologies.  
Dr Paulin and Dr Deckers were appointed as fire blight experts.  Professor Swinburne and Professor 
Latorre were appointed for European canker.  A nd Professor Cross was the only expert appointed on 
apple leafcurling midge.  And acknowledging your ear lier comments, Mr Chairman, Australia will 
nevertheless only be directing its quest ions to those individuals in respect to the field of expertise for 
which they were appointed. 
68. There's just one other matter before I begin the questions on this section.  There are a couple 
of written materials relating to questions we will have  on fire blight and canker, which are both things 
that are already in evidence.  Bu t in the interests of saving time, we would like to, if acceptable, 
provide those to the relevant experts and to you a nd to New Zealand now, so that they can refresh 
their memories about those particular things when we come to them.  If your preference is, we can 
wait until later and do that, but it just means that we will probably have to take longer with the 
responses to our questions. 
Chairman  
69. Just so I'm clear, these are materials already av ailable as part of the evidence, but you want, 
you will be asking questions related to those later in  the day.  That's what you are talking about? 
Australia  
70. That is correct. 
Chairman  
71. Let me just confirm…  If they are already part of the record, we have no problem with that.  
Yes, sure.  So, how would you like to proceed? 
Australia  
72. We have a number of copies here  to provide to the relevant e xperts as well as to New Zealand 
and to the Panel and the Secretariat.  And we could do that right now if that's easiest.  One is on fire 
blight and one is on canker. 
Chairman  
73. That's quite all right.  And the Panel has noted the point that you made to start off with, we 
won't comment on that, I think we've dealt with it in the introduction.  And again, point taken, I think it was useful for you to have made that point.  And we would like you to continue where, as I 
mentioned in the introductory remarks, to remind us, where necessary.  We will note them.  But let's 
not get into too much detail.  And let's also try a nd avoid statements.  I think the point that has been 
made, is that we will have time tomorrow to take off our jackets on all of these issues.  But thank you.  
Please could we keep that in the background and if you want to continue with your questions, you are 
welcome to do so.  This is now still on this i ssue of general comments and definitions.  Please 
proceed. 
Australia
 
74. Australia has a question for Dr Latorre and Dr Deckers. We note that in your written response 
to question 3, you both indicate that "trash", namely leaf stems and other plant organs or junk 
materials can contaminate fruit. We would be grateful if you could please expand on this point.  WT/DS367/12 
 Page 13 
 
 
  Chairman  
75. The question is addressed to Dr Deckers and to Dr Latorre, is that correct?  While they are 
thinking, can I just ask, I know you've made the point that you will be asking questions only to the 
specific members, but in terms of the practice th at we will follow, we would like those documents 
available to all of the experts.  But I recognize that you are saying that you will be asking specific 
questions to specific members. 
Australia  
76. Okay, would you like us to  make additional copies? 
Chairman  
77. You can do so, if that's easy.  Whatever's easiest. 
Australia  
78. Okay, that's fine. 
Chairman  
79. Shall we ask the Secretariat? 
Australia  
80. Yes, thank you. 
Chairman  
81. Excellent.  If and when Dr Deckers or Dr Lato rre are ready.  Please proceed.  Dr Deckers. 
Dr Deckers  
82. So the question here was, what is the importance of the "trash" here? 
Australia  
83. Yes, I'll just repeat the question for you.  In your written responses to the Panel's questions to 
the experts, in Question 3 specifically, we noticed  that both yourself and Professor Latorre indicated 
that "trash", namely leaf stems and other plant orga ns or junk materials, can contaminate fruit.  And 
we were just interested if you would please elaborate on your answer in that regard. 
Dr Deckers  
84. Okay.  I would like to answer here, for fire blight , the infection of flower is not always limited 
to the flower itself.  It often goes into the bourse stru cture of a fruit cluster.  So when this "trash" is 
consisted of fruit bourses, there is a possibility that these bourses carry the bacterium.  So in this way I 
think it's really important to clarify here that the bourse structure of a fruit, which is sometimes picked 
with the fruit at harvest, can be consid ered as a potential contamination source. 
Chairman  
85. Dr Latorre. 
Dr Latorre  
86. In connection with European canker, if "tr ash" means leaves, twigs, stems, these do not 
represent a problem.  Normally, the European canker f ungi is not associated to the leaves to the point 
that it can really contaminate the fruit.  If by any reasons you have rotten fruit, that rotten fruit with its 
sporulation on it, perhaps this type of trash may represent a risk.  Nevertheless, rotten fruit are very 
rare in nature unless you have freque nt, very frequent, summer rains. 
Chairman  
87. Can I ask, Australia, are you satisfied or want to follow up on that? WT/DS367/12 
Page 14  
 
  Australia
 
88. Just a short follow up for Professor Latorre.  So as  I understand it, you are referring to leaves.  
And you mentioned stems, I think, as well.  What about twigs? 
Dr Latorre  
89. Stems and twigs, I don't think they can really represent a problem.  When I say "represent a 
problem", I mean, they cannot carry the fungi, or the fungus. 
Chairman  
90. Dr Swinburne, I see you have your hand up. 
Dr Swinburne  
91. In a climate which is highly conducive to a pple canker, fruiting spurs often become infected 
and those dead spurs, produce both conidia and ascospores. The spurs become very easily broken. 
They snap off.  And they can form part of the trash .  But this is in a clim ate which is highly conducive 
to the development of the disease that you actually see it on the fruiting spurs. 
Chairman  
92. Can I move…  While you are conferring …  New Z ealand, would you like to come in on this 
point? 
New Zealand  
93. I have a question for Dr Deckers and another question for Dr Latorre, but I begin with a 
question for Dr Deckers.  And I note that in Ques tion 3, in the response to Question 3, Dr Deckers 
comments that – quote – "[f]ruits packed, retail rea dy can be considered automatically free of trash", 
and I wonder if Dr Deckers would like to confirm that  that remains his view on the issue.  Thank you. 
Chairman  
94. Dr Deckers. 
Dr Deckers  
95. Okay.  I think when the fruit has a normal procedure of preparation, by grading the fruits in 
water, or whatever else, it is normal that trash is not present when the fruits have passed this chain.  I 
think this is the normal procedure. 
Chairman  
96. I note, Australia was conferring, so …  Are you okay?  All right.  Are you satisfied with the 
response or want to follow up, Ms Fearnley? 
New Zealand  
97. Yes, I'm satisfied with that response and would like to put a question to Dr Latorre.  Again 
relating to a response to Question 3.  And I note that Dr Latorre concludes his response on that 
question with the following comment, and it includes a double negative, but … "[f]ollowing the technical protocol, as indicated in Exhibit NZ-93, there is no risk that 'Class 1 export quality apples', 
exported from New Zealand will not always be mature , asymptomatic and free of trash", and I'd invite 
Dr Latorre to comment whether or not that remains his view on the matter. 
Chairman
 
98. Dr Latorre. 
Dr Latorre  
99. I would like to say that when I answered these questions, I only gave a general definition.  
Perhaps I was not precise in answering in regard to th e European canker.  So whatever is said here is  WT/DS367/12 
 Page 15 
 
 
  applied to the general situation, and I am going to sa y, that normally leaves, twigs and stems, they are 
not responsible for carrying the European canker fungus .  I agree with Dr Swinburne that eventually 
the spurs can be contaminated and that may happe n only when you have heavy summer rains or very 
frequent summer rains and also you have a very, I mean, you may have some problem with the 
harvesting procedures in terms that the people is not only detaching the fruit but also detaching the 
spurs. 
Chairman  
100. Can we move on to your next questions, Australia? 
Australia  
101. Yes, Mr Chairman.  I have a question for Dr Schrader.  I'd like to ask you about one of the 
international standards for phytosanitary management , specifically ISPM No. 10, which deals with the 
requirements for the establishment of pest free place s of production.  According to ISPM No. 10, the 
four main components that should be established a nd maintained by an exporting country are as 
follows:  systems to establish freedom;  systems to maintain pest freedom;  verification that pest 
freedom has been attained or maintained;  and fi nally, product identity, consignment integrity, and 
phytosanitary security.  Would you consider that, if  technical justification has been provided for 
requiring apples only to be exported from a pest free place of production, then ISPM No. 10 would provide justification for whatever specific measures a particular country  adopts that are required to 
practically implement that objective, that is, prac tical measures to achieve those four components, 
which are integral to a pest free place of production? 
Chairman
 
102. Dr Schrader. 
Dr Schrader  
103. So, this is a new point arising, I think, because this was not discussed in the questions given to 
the experts.  So, I would like to.  Well, it's very difficult to answer to this now, ad hoc .  So usually if 
the requirement of a country is to the exporting country that requirement of pest free area has to be 
fulfilled, then it has to be shown by the exporting country that this requirement is fulfilled, and this 
also relies to all of the different issues within I SPM No. 10 because it's not only pest free area but also 
pest free production site, etc.  But I am not sure if that already answers your question. 
Australia  
104. Thanks for that.  I know that it was a little  bit different, but thank you very much. 
Chairman  
105. Anybody want to…  New Zealand.  Right.  Next question, Australia, do you have…? 
Australia  
106. We have nothing further, Mr Chairman. 
Chairman  
107. We move on, then, to the area of "risk assessment  techniques" and here I have the floor, or the 
honour, to ask the first question to Dr Latorre.  In  your response to Question 124 – I think this was 
about international standards for semi-quantitativ e methods – you wrote that, in your view, the 
likelihood values and mid-point values used for Au stralia's semi-quantitative analysis in the IRA 
should be validated before acceptance.  Could you expl ain what "validation" means in this context and 
how it would be done? WT/DS367/12 
Page 16  
 
  Dr Latorre
 
108. Well, in this context, it only means that we have to have some experiment to provide 
objective data that allow us to assess th e information that there was in th ere.  To have an experimental 
approach, in other words, in order to know whethe r this data that was given here are within the 
acceptable range, that was it. 
Chairman  
109. New Zealand.  Australia. 
Australia  
110. Can I just follow up on that answer.  So, as Pr ofessor Latorre, is his comment applied to the 
choice of methodology and the way the methodologies are applied, or is his answer specific to his 
views on European canker. 
Chairman  
111. Dr Latorre. 
Dr Latorre  
112. Yes.  All my questions are thinking on Europ ean canker primarily.  My answers, excuse me. 
Chairman  
113. Dr Sgrillo, if I may ask another question on risk assessment.  In your response to Question 
133 – this is about probability intervals and d escriptors – which asks whether the IRA provides 
objective and coherent explanations for the pr obability intervals assign ed to the qualitative 
descriptions of events.  You write the following, I quote:  "The numeric probabilities representing the 
qualitative descriptors in the IRA are to be interpreted in a per unit  basis.  However they have to 
reflect the concept of each category (negligible, low, etc) also in populational terms ".  Could you 
please explain this a little bit further and also elaborate on your comments about the distortions that appear at the lower part of the categories, if you wouldn't mind. 
Dr Sgrillo
 
114. Well, there is no international methodology for developing this kind of standard.  To my 
view, the beginning is the population.  All the risk is proportional to the population.  So when you will 
start a pest risk model, you have to keep in your mind in what population that model will be applied, 
even defining individual risk.  I mean, the individual risk without a population is nothing.  There is no individual risk, because you define individual risk in population terms.  When you say one in one million to define an individual risk, what is one million?  It's a population.  So you need the 
population to give a reference to your individual risk.  So I say again, an individual risk without a 
population as reference, can not be defined.  This is why an individual risk should be established, 
should be given, with the population in mind.  If you say that the risk of an event to occur is "negligible", and that event in a population occurs  a thousand times in a year, it's not negligible 
anymore.  And that's why appears this "extreme ly low" with a hundred thousand occurrence in one 
year.  This is not extremely low:  a hundred thousand!  "Very low", ten million occurrences in one 
year.  Is this very low?  So when you will de velop a probabilistic model, a kind of Monte Carlo 
model, I mean, in which you multiply a sequence of probabilities and then you multiply a population 
by this sequence of probabilities, you have to  keep in your mind for which population you are 
developing.  And you have to be careful with th e qualitative definition and the meaning that in the 
population context. 
Chairman
 
115. May I just follow up on this. Are you, I heard you say, I think, that something which is 
expressed as a probability per unit might be "negligible ", but when it is translated in terms of the 
population, you are saying the qualitative descripto r would be something else than negligible.  WT/DS367/12 
 Page 17 
 
 
  Dr Sgrillo  
116. Yes.  Any of this – any distortions – I mean, yo u have an interval of probability, from zero to 
one. This is all the possible probabilities. You divide th is interval and you give names for this interval.  
One, if it always occurs for all the population, it w ill result in a population size.  Zero point 5 it will 
result in half of the population.  Now we have to give names.  If you take the population and say that 
one million will happen of an event, one million times will occur in one year, you have to give a name 
to that.  This is not negligible, this is not very  low.  It's a kind of criterion taking into account the 
population size.  I have a quote, "most people want to ask, 'One in a million, is that a lot or a little?'  
There is no good answer to that question.  If one focuses upon statistics, it may seem very little. If one 
tries to focus upon the 250 or so individual deaths that this number implies in a population of 250 
million, it may seem like a lot."  So it's depende nt on definitions, but coherent definitions. 
Chairman  
117. Maybe just a comment on your concerns about distortions at the lower part of those…  What 
did you mean by distortions? 
Dr Sgrillo  
118. Well, distortion is that there is no link between  the name and the numbers.  I am saying that 
these are distortions.  I mean, there is no way to link 10 million occurrences with "low". 
Chairman  
119. From our side, that's fine. New Zealand, do you want to… Are you happy? 
Australia  
120. We do have questions to Dr Sgr illo on this point.  And it is a very important point.  But we'd 
prefer to hold them for our questions so we don't delay you. 
Chairman  
121. Sure, okay.  Let me ask, then, a next question in this area.  New Zealand notes in its rebuttal 
submission that the numerical ranges for probabilit ies used in the IRA, are based on Biosecurity 
Australia's draft guidelines for the import risk anal ysis, 2001.  But that these draft guidelines were not 
developed with the per apple methodology in mind.  And I wondered if any of the experts are aware 
or familiar with these guidelines and whether you'd lik e to comment on this point.  I have two other 
questions relating to the same heading, shall I say.  Let me ask them as well.  Even if you are not 
familiar with these draft guidelines, could you commen t on the relationship between – and I have this 
question in two ways, because I think they're different perspectives – please comment on the 
relationship between the object of measurement, namely apple fruit, and the predetermined 
probability ranges.  Do the probability ranges have to be defined with regard to the object at risk in 
question.  I can ask the same question, but change th e word "object" into "unit".  In other words, does 
it make a difference?  I think that's maybe more obvious, but I'd like to ask that question as well.  Whether the unit of measurement, tonnes or units , or whatever, referring to your populational 
discussion just now, whether that would make any di fference.  And then finally, is it objective and 
credible for a risk assessment to use the same predetermined probability range for the different steps 
and for different pests, or would they have to be  derived from the science and the data.  So these 
questions go to any of the experts.  Dr Sgrillo. 
Dr Sgrillo
 
122. Well, this is the problem when you don't have enough data to support your  choices.  You have 
to rely on qualitative definitions, and this is just a ma tter of discussion.  There is no road to that, there 
is no established criterion, no recommendation, in intern ational terms, at least as I know.  And this is 
why quantitative models should be ap plied only when there are sufficie nt data to support the choice of 
probability ranges and probability shapes.  Otherwis e we can go to the end of life discussing, and WT/DS367/12 
Page 18  
 
  there is no way to define this, to prove this, and to  choose a range.  Or go to the field and make the 
sampling, or the implementation necessary, and then derive your numbers. 
Chairman
 
123. Dr Schrader. 
Dr Schrader  
124. Yes, I fully support what Dr Sgrillo was saying and I can also add something to that, because 
we have, in our project that is currently underway, we have assessed more than forty different risk 
assessments and guidelines to see how different bodies deal with exactly this point.  How to do the 
risk rating in a standardized way or in a calibra ted way.  And up to now there is no method which 
really is reliable for every question for every pest.  So expert judgement is something which is still 
very important in pest risk assessment.  And this is also one of the main problems, because you 
always have to be transparent and up to now you have no good method to compare between the different pests that have the same levels of ratings. 
Chairman
 
125. Did I, Dr Schrader, did I hear you say you have no way of checking for different pests ratings.  
My question really is, our question is really, I mean, one can translate it, is "negligible", in terms of a 
risk with regard to pigs, the same as "negligible" in terms of a risk w ith regard to apples?  That would 
be the one question.  And the other question is , can one in the steps use the same numerical 
probability to define the same qualitative descriptor in  each of these steps.  So if you are saying it is 
negligible in step one, would you be able to use th e same probability for negligible in step two?  Is 
that what I understood you to say, that there is no commonality there yet? 
Dr Schrader  
126. There is no commonality, in the one point.  And al so it's very difficult to do that for different 
pests.  On the other hand, it should be the same, it should be comparable. 
Chairman  
127. Any comment from New Zealand on this issu e?  Or, not comment, again, question, 
elaboration? 
New Zealand  
128. Not for the moment. 
Chairman  
129. Australia. 
Australia  
130. Perhaps my colleague, Dr Barry, might provide a little elaboration.  I'll explain Dr Barry's CV 
perhaps when we ask our questions, but he is, I would say, an eminent statistician in Australia. 
Chairman  
131. And this is a question, not a comment? 
Australia  
132. No.  It's just to assist this elaboration on wh at Dr Sgrillo was saying about the intervals, so… 
Chairman  
133. Again.  I mean, I'd like you, Australia, to c onsider the possibility of dealing with that 
tomorrow.  WT/DS367/12 
 Page 19 
 
 
  Australia  
134. Yes.  It's just that the way the questions were unfolding there…  Well, we'll come to it, we'll 
just hold off on it. 
Chairman  
135. Okay, great.  Why is the Chair asking all these questions?  Well, it's because the Chair put 
himself into this position.  My colleagues will be fo llowing.  I have two more questions.  The first one 
to Dr Sgrillo.  In your response to Question 133, yo u write that in your view the probability interval 
seems to have been arbitrarily chosen, and that ot her ranges could also be used without violating any 
scientific principle?  And, in particular, the range assigned to "negligible", this is the zero to one in a 
million, would be arbitrary because other ranges c ould have been used after adjustment of the 
remaining ranges.  In its comments, Australia interp rets this as indicating that the choice of one in a 
million does not violate any scientific principle.  New Zealand comments that the value is not supported by the scientific eviden ce when assessing risk on an apple basis.  Could you comment on 
this.  And does "arbitrary" mean that this range is  not objectively justifiable, i.e. that it is biased? 
Dr Sgrillo
 
136. Yes.  There are two things to consider there.   One is that the model uses mostly uniform 
distribution with this range.  I responded to this in another question.  Most of the sampling, when you 
generate random sampling from a uniform distribution within this range, most of the sampling will go 
to the side of one in one million, not to the side of zero.  So, to correct this, they could have considered a triangular distribution with the mo st probable value zero and the maximum value one 
times ten in the power of minus six.  This will co rrect the kind of distortion (of bias) in generating 
random samples in this range.  Another thing that can be shown is that negligib le in this range, one in 
one million, in populational terms, ca n generate 100 or 200 events in one year.  To correct this, to be 
more coherent, to reach a definition of the word "negligible" as a quantity that can be ignored or 
excluded from consideration, too small and unimportant to be of concern.  Another definition:  to a 
degree that is negligible, so small or slight that it may be ignored.  I mean, it's there but it may be 
ignored, not considered.  So, it would be much more coherent to choose an upper limit, maybe of ten 
to the minus twelve, or to the minus 16, or anyt hing like that, as negligible.  Or, to change for a 
triangular distribution with the most probable value being zero.  Trying to do, because this has to be 
by experimentation, and see what are the results, if the results are coherent.  So you can really choose 
the ranges and probability shapes that you are worki ng.  Because in the model development, usually 
you have results, you compare your results with the reality, and then you adjust the model to make it 
more close to the reality, and then you go in a l ooping up to a point where you can say "my model is 
fine, now I can trust it and I can use it".  But not before that. 
Chairman
 
137. Okay.  Anything from…  Any further elaborati on on this point by the experts? If not, New 
Zealand, would you like to…  No? My last question under this heading would be, is assigning a 
negligible event, one that would most certainly not occur, a likelihood in the range of between zero 
and one in a million, with a uniform distribution a nd a midpoint of five to the power of -7, based on 
objective scientific principles? There are two related questions. Would a different type of distribution, 
and we might have actually heard some answer to th is already, would a different type of distribution 
be more appropriate for events that have a negligib le likelihood of occurring, i.e. that it would almost 
certainly not occur? I think I heard you to say that triangular distribution, but there might be other 
comments. And the third question, is there a valid  scientific basis for including such steps in a 
pathway model? Is there a valid scientific basis fo r including such steps – negligible steps – in a 
pathway model? 
Dr Sgrillo  
138. Well, considering that negligible is not zero, it s hould be included in the model.  But if it is 
zero, no. But it should be included with values c oherent with the definition of negligible. And WT/DS367/12 
Page 20  
 
  considering another type of distribution, one try could be a triangular distribution, with the most 
probable value as zero, and the maximum of 1 in 1 million. It can have the minimum and most probable value equal, no problem.  Okay.  But this is a try, to see what would result. 
Chairman
 
139. New Zealand. No?  Australia? Are you satisfied  about moving on, as we discussed just now, 
about this triangular distribution, to deal with that tomorrow, or would you like to make … 
Australia  
140. Mr Chairman, I think I indicated before that we would not interrupt again. But we reserve the 
right to come back, and including on that question a bout a triangular distribution, when we have our 
questions to Dr Sgrillo. I really just don't want to interrupt you. 
Chairman  
141. No. I appreciate that, and that's fine. All right. We ll, I think that, from the Panel's side, I have 
exhausted my questions. Willia m, would you like to move on to another question? 
William Ehlers  
142. In the responses – and this goes to everybody, so  feel free – in the responses, several experts 
note that for different steps in the IRA, data or ev idence were insufficient. In  its comments, Australia 
characterizes this as a situation where there is a scientific uncertainty, where experts have to make 
judgements.  In New Zealand's view, Australia mi sapplies the notion of scientific uncertainty be 
equating it to situations where the data do not support Australia's conclusions. Would any of the 
experts care to comment on these contradictions?  Y es. I'll repeat. In your responses – those of the 
experts – several experts note that for different st eps in the IRA, the data  or the evidence were 
insufficient.  In its comments, Au stralia says that this is a situation where there is scientific 
uncertainty and therefore that experts have to ma ke judgements. New Zealand, on the other hand, says 
that Australia misapplies the notion of scientific unc ertainty by equating it to a situation where the 
data do not support Australia's conclusions. 
Dr Sgrillo  
143. Well, what I see is that the data does not s upport, or mostly the data does not support the 
Australian conclusions, but does not support, also, ot her conclusions. Because the data really is not 
adequate to generate the kind of numbers that the people need to proceed with the model. And another 
consideration is that one would exp ect the expert judgement in one or two steps in a model. But in this 
import risk assessment, expert judgement, well, were used in every step of the quantitative model. I 
think there is not a single step, a single importation step, that the numbers came from sampling, or 
anything. I think that every step  was based on expert judgement and this is why I think that a 
quantitative model should not be used when you do not  have enough data to support the numbers that 
you have chosen.  o that's a problem on the expert  judgement. You come out with a number. But we 
come out with a number and a certain expected e rror in this number, that comes from the process 
itself. Another thing. There is a methodology of expert judgement, to aggregate the opinion of each 
expert, and to come out with a single number from a bunch of opinions. There is a methodology to do 
that.  And there is an error associated.  But the erro r of one expert judgement here will accumulate the 
error of the next expert judgement, with the next  expert, so if you have a collection of expert 
judgements, we would expect that the error would be quite large in the final, in the end product of the 
model. 
Chairman  
144. Doctor, could I ask whether you mentioned that  there is a method for dealing with expert 
judgement?  Was this used in your view in this case?  WT/DS367/12 
 Page 21 
 
 
  Dr Sgrillo  
145. I don't know.  I don't know, because there is no me ntion in the import risk assessment of the 
methodology for expert judgement. 
Australia  
146. I promise not to interrupt, Mr Chairman, but I th ink this is a factual clarification, which is 
essential to be made at this point. The Australian de legation would direct Dr Sgrillo, the New Zealand 
delegation, and the Panel, to Appendix 1 of the IRA,  part B, around about page 332, where it explains 
how expert opinion was elicited, in the context of  the IRA process, and we're more than happy to 
come back to that, but that was an essential factua l clarification, because there clearly was something 
in the IRA. 
Chairman  
147. Thank you, that's useful. 
Dr Sgrillo  
148. I just want to apologize, because this was my fau lt, I didn't look for this information.  Sorry. 
Chairman  
149. On this question… 
Australia  
150. Mr Chairman, sorry. I don't think all the expe rts were in the room when the question was 
posed and Australia would be particularly interested to hear Dr Schrader's response to this question. 
William Ehlers  
151. I'll repeat the question.  In their responses, sever al experts noted, that for different steps in the 
IRA, data or evidence were insufficient. In its co mments, Australia characterizes this as a situation 
where there is a scientific uncerta inty. And therefore that experts have to make judgements. New 
Zealand, on the other hand, says that Australia misapplies the notion of scientific uncertainty by equating it to situations where da ta do not support Australia's conclu sions. So, we're trying to seek a 
way to reconcile these contradictions. 
Chairman
 
152. Dr Schrader. 
Dr Schrader  
153. Well, if there is uncertainty with a question, it has to be lined out fully and explained where 
this uncertainty is coming from and that may have an impact on the likelihood of a risk to occur. So, if 
this is fully explained, then it is transparent. Bu t, of course there is a difference if you just don't 
answer a question because there is no data and you try to, nevertheless, give some estimates on the 
risk.  Or, if you just try to hide some lack of evidence for it. 
Chairman  
154. Australia, would you like to follow up?  New Zealand? 
New Zealand  
155. Not for the moment, but we may well come back on this issue. 
William Ehlers  
156. In its comments to experts' responses, Aust ralia has repeatedly argued that in cases of 
uncertainty, or considerably limited, or varied da ta, the IRA team decided to exercise its expert 
judgement to make estimates.  Australia has also ar gued that the possibility of completing the analysis WT/DS367/12 
Page 22  
 
  through the exercise of expert judgement is rec ognized by ISPM No. 11.  Do experts agree with 
Australia's characterisation of a possibility of a risk assessor completing the analysis through the 
exercise of expert judgement in cases of uncertainty, or  considerably limited or varied data?  Are there 
international standards regarding the exercise of expert judgement , and the limitations to such 
exercise, under ISPM No. 11 or any other source? 
Dr Sgrillo
 
157. I have a comment on expert judgement, that is in a paper of an Australian – Mike Nunn – and 
the paper is "Quarantine risk analysis" (1997) – in the Australian Journal of Agricultural and 
Resource Economics . He mentions "However, quantitative ri sk assessment has also been criticized 
essentially for a perceived lack of objectivity, resu lting from the use of expert judgement that 
allegedly reflect, not only scientific knowledge, but also factors such as po licy values and cultural 
values. Some commentators have expressed concern that scientific judgement involved in risk assessment is not as objective as maybe purported and that quantitative estimates have a large 
variability and uncertainty. Particularly when applie d to environmental problems." So, again, it is an 
important problem that could exist when too much expert judgement is applied. 
Dr Schrader
 
158. Well, as far as I know, there are no standard rul es or standardized methods to do the expert 
judgement.  There are different approaches on how to do  it.  In some cases, it is just that the experts 
meet together and discuss to find consensus on how they  would rate a risk.  But, generally, this is one 
of the main constraints of PRA, that if there is a lack of data and you need to judge the risk because 
you want to protect the country from that pest, so yo u have to rely on this expert judgement because 
no other data is available.  So there are different ki nds to do this.  One is to do some modelling, but of 
course also modelling has some constraints.  So you will always have to deal with this uncertainty.  If 
you do the expert judgement you have to explain fully  and transparently why you came to this result.  
If this is reliable, then you have to also use that because it is the only way to address the risk, or to 
deal with the risk. 
New Zealand  
159. I wonder, given that we are continuing to explore with the experts the issues around expert 
judgement, whether the experts have available to th em the material referred  to as Appendix 1 to the 
IRA Part B mentioned a few moments ago on page 332.  If it is not readily available I could actually 
read it, if that would be helpful. We then have  a follow up question based around that section. The 
section on page 332 that has been referred to is head ed "The elicitation of expert opinion" and reads as 
follows: 
"There were multiple discussions with the panel and Biosecurity Australia staff about 
the eliciting of expert opinion.  Three cons iderations were stressed by BRS.  They 
were: 
That Biosecurity Australia should be completely satisfied that the bounds of 
distribution chosen to represent their views would contain the true value. 
That the chosen distribution shape should re present expert views.  The  interpretation 
of  prior distributions in terms of ga mbling odds was discussed, and the uniform, 
triangular, and Pert distributions presented at starting points. 
It was made clear that qualitative likelihood ranges should not constrain their options 
and that BRS was available to assist in expressing the experts’ views, if necessary. 
The issue of expressing divergent opinions was also discussed and different 
approaches to handling divergen ce of opinion were canvassed."  WT/DS367/12 
 Page 23 
 
 
  160. This would seem to be the extent of the mate rial referenced in terms of eliciting expert 
opinion. Based on this, I would have a question, part icularly for Dr Sgrillo and Dr Schrader, about the 
outline that is provided here as a "methodology" for th e application of expert judgement. In particular, 
is the conclusion that the interval contains the true value sufficient, especially given that the negligible 
interval spans many orders of magnitude  and a uniform distribution is applied. 
Dr Sgrillo  
161. It is not explained here how the aggregation of the value could be.  This is a very technical 
issue, so I don't know.  You can have a Bayesian aggreg ation or a classical aggregation.  It is a kind of 
mathematical treatment of the data to converge different opinions to a single number.  When I 
mentioned that I have not seen this, I am referring to  that I thought it would be here.  I would like to 
have a more detailed description of the expert op inion, because this is not  enough to technically 
evaluate the process. 
William Ehlers  
162. Australia? 
Australia  
163. Dr Sgrillo and New Zealand, I didn't point this out previously to you as an exhaustive 
explanation of what occurred.  This is a summary, in a sense saying what occurred. I would say that 
we are directly in a position to provide you with much more detail through the province of my colleague, Dr Barry, who actually was intimately invo lved in these discussions with the IRA team.  If 
you will allow me I might just briefly provide some  background on Dr Barry, so that you know what 
his background is. He has PhD in Biostatistics an d heads up a group of 40 statisticians at the 
Permanent Australian research body, CSIRO.  He has extensive experience in risk assessment and he 
was lead author of the uncertainty chapter in the International Panel on Climate Change report on 
landscape change and forestry and he is also aut hor of the section on the Monte Carlo method in the 
encyclopaedia on biostatistics.  I would just put this  forward so that you are aware of his expertise, 
and I would invite him, Mr Chairman , to provide some more detail.  Th is isn't in the form of questions 
or anything but Dr Sgrillo was clearly asking for mo re detail.  We are in a position to provide that 
now.  And with your permission, we will do that. 
164. I think the Appendix in the document outlines at th e high-level the approach that was taken to 
elicitation.  I think to clarify, in terms of comb ining the expert opinions, it wasn't a matter that each 
person in the room had their scientific views e licited and then combined. They came to it as a 
consensus process. From the last point in the doc ument it talks about how we discussed, if people 
couldn't come to consensus. If consensus could not  be reached, there were ways that could be 
expressed in the document, so people were not forced to come to consensus.  So that option was open 
to the panel but they never asked for that assistance.   In terms of the range, I think picking up on New 
Zealand's point about ensuring that the negligible range contain the true value. We talked quite 
extensively over a series of meetings about the requi rements that were needed to make their beliefs 
and their uncertainties expressed through the distributi ons. What needed to be done is outlined in the 
summary for the results of the anal ysis to also be clearly interpretable and so that was done. I would 
also note that, I think, through the document you w ill see that there are occasions where data was 
available or they had a most likely value, or they  thought they understood it better. They actually 
chose distributions beyond the starting point distribu tions and then we assisted them in developing 
Pert distributions or triangular distributions and I think there are examples in the document to show 
that. 
William Ehlers
 
165. In view of this explanation, was that a reasonabl e thing to do?  Do you think that this expert 
judgment was used in a reasonable manner in the IRA? WT/DS367/12 
Page 24  
 
  Dr Sgrillo
 
166. In one or three steps it will be acceptable, but ap plying to 100 per cent of the steps, it would 
be a risk that the reliability of the outcome from the model will be limited because of the excessive 
use of expert judgement.  Nota bly, for every importation step, sev en steps, almost seven expert 
judgements. 
William Ehlers  
167. What level of scientific evidence is necess ary in order to assign ranges and shapes of 
distributions?  If they are assigned on the basis of  an informed guess or non-validated hypothesis, 
does this constitute credible science? 
Dr Sgrillo  
168. Well, there are some rules to acc ept the result of a sampling.  I mean randomness of the errors 
and technical issues, and representativeness, I mean on place and space.  Nevertheless, there are criteria that you apply to say how much I can trust the sample.  If your sample pass this criteria, this is 
a scientific support.  This is enough to use the numbers.  You have to clearly specify what the criteria are, especially the representativen ess in the space and in the time.  A single year sample is enough?  
Who knows?  Was that year an average year, or was it an atypical year?  And things like that.  While 
sampling from a single space, a single area, the same c onsideration applies.  Also, I mean the structure 
of the sampling methodology.  It would be a random sa mpling, it would be in blocks, things like that.  
If the sampling method is described, and it is within  your criteria, so you can accept, and this will 
support your data with no problem.  Otherwise you can use part of the data and infer something.  Or, 
you can go to expert judgement when data is not available.  It is a valid methodology, but the 
application is not to be for all the model. 
Dr Schrader
 
169. It is just that the less data you have, the higher the uncertainty.  That also refers to the risk. 
William Ehlers  
170. I would like to move on to the next questions quickly, so we can give at least half an hour for 
the questions that come directly from the Parties.  Au stralia argues that certain steps in the fire blight 
pathway are difficult to establish experimentally, eith er in the laboratory or under orchard conditions 
and that when comparing such evidence it becomes a case of balancing one type of uncertainty against another.  According to Australia, in such s ituations it would be an error to automatically give 
more weight to experiments c onducted under orchard c onditions.  Would anyone wish to comment on 
that? 
Dr Paulin
 
171. It is absolutely true that in fire blight especially, some steps are very difficult to cover 
experimentally.  Well, normally, orchard conditions would represent what is called sometimes a "true 
life", but if you keep to orchard conditions you coul d miss some things.  Sometimes it is better to go 
to artificial experimental conditi ons, i.e. well controlled  conditions, and events that you see may be 
reliable to infer what is happening in the orchard.  So the orchard condition may be the best condition 
in some cases, but it is not a general rule.  So metimes artificial conditions in the glass house, for 
example, or in the laboratory, may be better in my opinion. 
Dr Deckers  
172. I would like to add a comment here that we can not only consider the orchard situation as this, 
as a possible scenario for fire blight disease. We know that some other host plants can play an 
important role together with the situation in the orch ard itself.  So I think it is important to mention it 
here also.  Of course, some of the trials are done in controlled conditions  in greenhouse or climate 
chamber, or whatever.  This is good for getting info rmation on it, but you can never rely completely.   WT/DS367/12 
 Page 25 
 
 
  The situation in the orchard is different, not only due to the fruit trees but also due to the other host 
plants involved. 
William Ehlers  
173. Does using hypothetical pathways in a risk assessment provide the necessary scientific and 
methodological rigour to be considered reputable science? 
Dr Paulin  
174. It is very difficult, but if you have to consid er hypothetical pathways, that means that you 
don't know about the true pathways.  So then you have to go to some hypothesis because you know 
that some events do happen and you just cannot explain by actual level of science, so I think it is then 
necessary to go to hypothesis.  This is not outside science.  It is not experimental science.  I would 
consider that as science. 
Dr Sgrillo  
175. Actually any path can be included, it depends on the value of the probabilities.  You can say, 
this is equivalent to say that everything can o ccur.  And everything can occur.  The probabilities will 
say how often that thing will occur.  So if you ha ve a good reason to include  a path, but you have no 
experimental evidence of that path, I think you can consider that path but with a residual probability, 
something like negligible, something like that.  That would give us a chance of that path of that 
hypothesis to occur once each many time units. 
William Ehlers  
176. Let me move on to my last question so that then I can hand back to  the Chairman for the 
Parties' questions.  Assuming that the semi-qua ntitative method could be considered a legitimate 
methodology, do you believe that the way this IRA applied the risk assessment methodology is 
objectively justifiable? 
Dr Sgrillo  
177. Well, I have to say one thing.  In the case of this import risk assessment, why is the model 
semi-quantitative? It is semi-qua ntitative because the probability of entry, introduction, it is a pure 
quantitative model, and the consequence assessment is a pure qualitative model, so it's is a semi-
quantitative model. But entry, establishment and spr ead is a quantitative model. The problem is not 
with the model, the structure of the model is okay,  it is acceptable. The problem is with the numbers 
that you are feeding the model and your model is so reliable as the numbers you input.  So you can have a perfect model but responding with very ba d things because you feed it with bad things.  
"Garbage in, garbage out". I am sorry with these term s, but this is a common terminology in computer 
sciences. The model is fine, but the numbers that you are feeding the model are questionable. 
William Ehlers
 
178. Mr Chairman. 
Chairman  
179. Australia, would you like to follow up on that? 
Australia  
180. We just want to be quite clear about what Dr  Sgrillo was saying, that the actual model itself 
that is being represented in the IRA was okay, it w as acceptable from your perspective.  I think we 
just need to be clear because I think we need to differentiate between the model and the inputs.  And 
inputs raise a whole lot of other questions which we will come to in the next couple of days. 
Chairman  
181. I see Dr Sgrillo confirming that. WT/DS367/12 
Page 26  
 
  Dr Sgrillo
 
182. Yes, yes. 
Chairman  
183. What we would like to do now is to offer New Zealand the opportunity of a few questions, if 
you wish, and then Australia a few questions, if you wish .  If it works, we will try to finish this section 
but if it does not, and you have questio ns, we will continue after lunch. 
New Zealand  
184. Actually, at this point we are willing to forb ear our asking questions, and pass the floor across 
to our colleagues, 
Chairman  
185. So New Zealand has at this point, under this s ubject matter, no questions.  We can pass then 
to Australia, if they have questions. 
Australia  
186. The first question we would direct is to Dr Sc hrader.  We have had a lot of discussion this 
morning about expert judgement, but I don't think we  have asked the experts yet what they understand 
expert judgement to be.  I think that is a very relevant question and I think Dr Schrader, given her 
experience with ISPM 11 particularly, would be we ll placed to provide some answers to what your 
understanding is, Dr Schrader, of what is meant by expert judgement. 
Dr Schrader  
187. I can especially refer to how we do it in the EPPO context. That is that the whole risk 
assessment is divided in many questions. There are about 70 questions in the whole EPPO scheme 
that have to be answered, as detailed as possible.  Usually we do that with different experts, 
concerning the pest, the crop, also methodologies, etc. So usually we do it in a qualitative way. We 
refer to every reference that is available, every personal experience with the pest, the crop, etc., as 
available, and this is discussed and then it is tr ied to come to a common result on each question.  So 
we don't do it statistically. This is also why I ca nnot really give answers to all these statistical 
questions.  We try always to find a common result on every question and then also we try to consult 
experts from outside this working group to do a re view on how we dealt with the questions. There is 
also another step that the plant health panel of the European Food Safety Authority also involved in 
that process, to go through every question and see if it is reliably answered, every information that is 
available has been used, and also if the conclusi on that was made by the experts is transparent, 
reliable, etc. So if there are quantitative data ava ilable, especially regarding frequency and volume of 
trade, for example, or amount of damage, etc., then this is included into the risk assessment of course.  
But in many cases we only have these qualitative data.  Does that answer your question? 
Australia  
188. Just to confirm our understanding of the ISPM No. 11, there is a recognition there that there 
are uncertainties in plant health risk  assessment and that expert judge ment does have to be utilized in 
terms of doing a risk assessment. 
Chairman  
189. I note that Dr Schrader confirms that that is the case.  Australia. 
Australia  
190. If we could move on to a question that now goes to this issue that Dr Sgrillo has been 
exploring with us this morning and that is the lack of  data that arises in the area of risk assessment. In 
Australia's comments on Dr Sgrillo's reply to qu estion 124 which concerned, in fact, the IPPC 
guidelines for risk assessments, we referred to a stat ement made in a paper that Dr Sgrillo had referred  WT/DS367/12 
 Page 27 
 
 
  to, Firko and Podleckis (2000), and that statement w as to this: "Ideally, existing data would provide 
the basis for direct estimation of model inputs. Ho wever, scientific experiments are seldom conducted 
specifically to provide these estimates for risk assessm ents and results are seldom provided that can be 
used directly in our models".  Could I ask first,  Dr Sgrillo, whether in your experience in conducting 
risk assessment, you have had to confront the issue of  a lack of data and how did you respond to that. 
It is to get some sense of what your experience is of what would appear to be a particularly thorny 
issue in this area. 
Dr Sgrillo  
191. Yes, this is true. It is difficult to find out the data needed in the models.  Not only models for 
risk analysis, but mathematical models in general that use parameters.  It is difficult many times to 
find the right data. Fortunately, there are other tec hniques than quantitative only, so when the lack of 
data, you see that the data will not s upport your choice, then you have to move to another approach to 
solve that. 
Australia  
192. Could I direct the same question to Dr Schrader, given her experience in the European 
context. 
Dr Schrader  
193. Could you explain a little more what exactly you want to know. 
Australia  
194. Certainly, Dr Schrader.  It relates to the issue of  the lack of data that may be available and the 
quote was really, we would say, indicating that this  is a common issue in the area we are talking 
about, which is risk assessment.  The question is dir ected at what is your experience in the conduct of 
risk assessments and handling the absence of data  that might be used in your assessments. 
Dr Schrader  
195. This is in fact one of our main problems. We try to estimate the answers if there is no data 
available, but sometimes you can refer to other info rmation, to other pests. For example, where you 
have some data.  You can only make estimates so metimes.  Sometimes you even cannot answer the 
question that is related to this lack of data. Us ually, there are other points that you can answer. So 
sometimes you have to deal with a high uncertainty. In  some cases, just to accept that there is a high 
uncertainty. It depends also on the other points. If th ere are high indications for risk that may give you 
the indication, even if you don't know anything ab out a certain area of the risk assessment, you may 
nevertheless say that there is a high risk because of  this or that point. On the other hand, if you 
estimate that the risk was low, then you will come to another conclusion because of the lack of data. 
Australia  
196. Thank you very much for your answer. That was very comprehensive.  Could I just clarify, in 
relation to your reference, to other points in the ri sk assessment. Would you include within that broad 
definition of points the likely consequences of entry, establishment and spread of a particular pest that 
came into a country for the first time? So, you woul d also look at the consequences side of it as well? 
If I am understanding you correctly. 
Dr Schrader  
197. Of course, if you know that there is a very high risk that there will be a large impact in the 
country where the pest is introduced and you have  some open questions regarding entry, then you 
would be more careful if you already know that the impact would be very high. WT/DS367/12 
Page 28  
 
  Australia
 
198. One last question from myself and then Dr Barry has a couple of questions.  Just to return, 
Dr Sgrillo, to your comment earlier in the morni ng when we were discussing the interval (0, 10-6). 
You noted that this interval, when used in the IRA, was applied as a uniform distribution.  You 
suggested that instead a triangular distribution could have been used. Could I just follow that point up, 
because this was an issue that was raised by the Pane l in one of its questions to the experts – Question 
135 – where experts were asked for their views on the different types of distributions, uniform, triangular, and so on.  The question is this. When experts replied, they indicated that a uniform 
distribution is used where there is not very much available data so that you can only place a minimum 
and maximum value and, as used in the IRA, this interval of (0, 10
-6) applying to what we would say 
are quite rare events, almost by definition, there won't be a lot of information available about rare 
events, and accordingly the IRA team considered a uniform distribution was appropriate.  Would you 
agree that the use of these distributions is very much going to depend on the amount of information 
that you have and if you don't have information th at would allow you to identify a most likely value, 
then you would come back to a uniform di stribution in appropriate circumstances? 
Dr Sgrillo  
199. Yes, I would say that the choice of distri bution will depend on how much information you 
have, not how much numerical data only, but how mu ch information, numerical data and other kind of 
information.  If you want to represent an event that  is close to zero, it is completely valid, you choose 
a triangular distribution with the most probable va lue zero, and then choose the maximum value to 
give some variability to your generated number. 
Australia  
200. Could I ask my colleague Dr Barry now to... 
201. Dr Sgrillo, in reply to question 133 concerning the probability intervals contained in table 12 
of the final IRA report, you stated that the intervals seem to have been arbitrarily chosen and that 5, 7 
or 8 categories could have been used instead of  6. In Australia's comments, it noted that your 
statements appear to suggest that various appro aches to setting intervals were available and as such 
the use of 6 intervals, rather than 5, 7 or 8, w as not inherently flawed. Do you have any observations 
you would like to make on Australia's comments? 
Dr Sgrillo  
202. Yes, I have.  Actually I was trying to find out a solution for the negligible  event.  I mean that 
"negligible" means "negligible", when you treat with  the population. That is my problem with your 
choices.  This is because the population is high. Y ou have to compensate this with some kind of 
adjustment in the individual probabilities. Another th ing is that you can "linearize", the generation of 
sampling numbers: one sampling number for the expone nt and another sampling for the mantissa. So 
you will have an even distribution from one to  zero. If you linearize that you have an even 
distribution.  Every range will have the same chan ce to be sampled. Otherwise, you know that you 
will concentrate your sampling in the upper part of the distribution. 
Australia  
203. So is there any international standard on th e number of categories and the width of the 
intervals that should be used? 
Dr Sgrillo  
204. As far as I know, there is no guidance to mode lling in general.  I mean, quantitative or 
qualitative.  The only guidance is not in the IPPC but in  the OIE.  The IPPC just refers to the names: 
there is "quantitative" and "qualitative".  WT/DS367/12 
 Page 29 
 
 
  Australia  
205. On a new topic, Dr Sgrillo, in your reply to question 134 concerning the use of the interval 
(0, 10-6), to define "negligible" in the final IRA report you stated that "[c]onsidering the importation of 
200 [million] fruit per year the category negligible could represent 200 fruits per year. However, an 
event that 'would almost certainly not occur' shoul d be expected to occur only once in each several 
years ." 
Dr Sgrillo  
206. Yes, there is no place that this is written, th at a "negligible" event,  in the phytosanitary 
context, should represent one event in each seve ral years. This came from my experience as a 
technical secretary of COSAVE.  COSAVE is the plant protection committee of the Southern Cone 
(Brazil, Chile, Argentina, Uruguay and Paraguay). We had some discussions on that and this came 
that a rare event will occur one each sev eral years. But this is not recognized. It is not a rule. It is just 
a consensus of a group. 
Australia  
207. So I agree that if there were two hundred m illion fruit that carried a particular pest or 
pathogen, then applying a one in  a million probability of an event occurring, would lead to 200 
expected events.  Would you agree that if only a proportion of the population was infested, then the expected number of events would be reduced propor tionally, i.e., if only one percent of the total 
population was infested, i.e. only 2 million fruit out of a two hundred million, then the number of expected events would be 2, i.e., one percent of two hundred. 
Dr Sgrillo
 
208. Yes, but look, I am mentioning here, each step, I mean each probability range, apart from 
other. I am not aggregating probability ranges, I am trying to evaluate the final. If you say that the 
probability that an apple has a hole is one in one m illion, I expect that in 200 millions, I will have 200 
apples with a hole.  But just a single probability rang e of – considering one event, not considering the 
effect of one probability, and another, another and another. 
Australia  
209. I agree with you there.  So in the fire blight risk assessment, if we assume that a volume of 
150 million apples was in the trade and the expected infestation rate found by the IRA team was 3.9 
per cent, would you agree that the relevant population for considering entry, and establishment and spread would be 150 million by 3.9 per cent, i.e., about 5 million 850 thousand apples, rather than the original 150 million? 
Dr Sgrillo
 
210. You are multiplying the 3.9 per cent by the popul ation, so I agree with the numbers that you 
came up with. 
Australia  
211. Thank you. 
Australia  
212. This is just one final question. And this returns to some of the questions posed by the Panel in 
relation to hypothetical pathways. We were just interested in Dr Schrad er's response to this. 
Dr Schrader, you might recall in your response to question 45 from the Panel in your written questions, you stated "[t]he absence of historical  proof of a pathway would not be a scientifically 
sound reason for excluding a certain risk". I thin k you have already given us quite a few comments 
that are related to this point, but I was just wondering – do you remain of this view and could you 
elaborate on this? WT/DS367/12 
Page 30  
 
  Dr Schrader
 
213. I remain of this view because even if some event didn't happen in the past it may happen in 
the future due to change of incidences or due to cha nges of new trade, or change in trade. So I would 
not say in any case that you should not rely on the fact  that when in historical times there was no risk 
that it will be for the future in the same way. 
Chairman  
214. May I just ask one question for clarity.  It relates also to your seeming acceptance of... If you 
had a uniform distribution, Dr Sgrillo, and you di d sampling on that, and I think you said that twice 
today, the result would end up by the events being on the higher side. Why is that? 
Dr Sgrillo  
215. If you consider a segment of a line with the size of this probability range. So you divide it in 
tenths.  So the segment is from one times ten to th e minus seven to one times ten to the minus 6, the 
next from one times ten to the minus 8 to one times ten to the minus seven, and going closer to zero. 
Each part in this line, each part, when you approach  zero, will be ten times less than the previous part. 
So that part has ten times less probability to be  sampled, than the greater part in the upper. 
Australia  
216. We didn't pursue that at that moment, but there are some issues that surround sampling from a 
uniform distribution which, bearing in mind that a Monte Carlo method was used here, so that I think 
my colleague Dr Barry might be able to usefully provide a little bit more information that may assist 
Dr Sgrillo and the Panel, because we are talking a bout the application here of the Monte Carlo method 
in the sampling. 
217. Just to clarify, Dr Sgrillo, the uniform distribu tion makes all points within the interval equally 
likely. I am just trying to understand the basis of  your argument. The sampling, within the uniform 
distribution, every point is equally likely. So as y ou sample from that, if you build a histogram of that, 
the histogram would be equally likely across the interval. 
Dr Sgrillo  
218. If you divide this into intervals of tens, of one magnitude, and approaching zero, the greatest 
probability to sample a number is close to the higher part of the interval. Not in the lower part of the 
interval.  I don't know.  Probably you have the... let's see if I can find. I present a table, a small table, 
with 90 per cent and then nine per cent, and then point nine per cent. 
Chairman  
219. Just for clarity that is in Question 136.  There is a table there. 
Dr Sgrillo  
220. This is expected, because you are dividing all yo ur range by one magnitude.  So, each range 
close to zero will be much lower.  So the probability to sample that range.  This is why I said that one 
thing that you could do is to linear ize this interval.  Take the log of this interval and then sample the 
log.  Then you translate the log to a decimal num ber again.  So you give more chance... or equal 
chance for a number to be sampled close to zer o as in the upper part of the distribution. 
Australia  
221. I suppose as a technical clarification based on your question and, I agree and understand that 
you are talking about the log scale and you want to sample uniformly across the orders of magnitude, 
but I suppose the question is uniform sampling of th e interval, as was done in the IRA, that gives each 
value in the interval ... if we were using the negligible range (0, 10-6), it gives equal value within that 
range.  Your point, just to clarify, if we are inte rested in having equal values across each order of  WT/DS367/12 
 Page 31 
 
 
  magnitude as you go down, then you would look at doing it differently.  But in terms of a uniform 
distribution over the interval, each value is equally likely. 
Dr Sgrillo  
222. You are right, but this is another try to solve th e problem of the term "negligible", trying to 
generate a number more close to zero than clo se to the upper part of the "negligible" range. 
Chairman  
223. May I ask if the experts have anything to add on  this point?  We might want to explore this 
also. Okay. Thank you very much.  Thank you for the contributions so far. Let us break now. We have 
finished that section and we will start with fire blight when we get back. 
 
_______________ 
 
Chairman  
224. We will start off with fire blight and I would lik e to request my colleague Ms Hillman to start 
off with the questioning in this case.   Perhaps, before we start I think what we will try to do is run 
until 16:30 because the coffee shop closes at 17:00 and we  will take a short recess,  stretch legs and get 
coffee, etc. and then start after that.  That would be my intention.  We will see how it goes but that 
gives us three hours where we can maybe do two of the main subjects in that period of time. 
Kirsten Hillman  
225. So just to give you a bit of a taste of what is ahead.  We are going to ask you some general  
questions on fire blight and then we are going to go through different importation steps where we 
have questions and then ask some other general questions a little later on. My first question to 
Drs Decker and Paulin is the following. Can y ou confirm whether in your view Australia has 
presented in the IRA scientific evidence, from a qua lified and respected source, that indicates that 
mature symptomless apple fruit free from trash can disse minate fire blight. As an additional element 
to add to that question, this qualified and respected science does not have to reflect the majority view 
it can be a minority view, as long as it is qualified and respected. 
Dr Paulin  
226. I think the key word in your question is "can".  The problem is that Australia has shown that 
you can imagine a system in which mature apple fru its can carry the bacteria from New Zealand to 
Australia.  The point is that it is difficult to estimat e the value of "can".  Is it a rare possibility, a 
frequent event or something exceptional?  This is far more difficult to tell.  I think that anything which 
goes from New Zealand or from a contaminated count ry to another country "can" carry something 
including bacteria, including pathogenic bacteria, th at is the minimum level.  Then you may have 
specific transport of specific bacteria, e.g., with  rootstock material which would be the maximum 
danger for the installation of the disease in a new c ountry.  So, the apple fruit, which is in-between 
these two limits, cannot be excluded.  That that can be considered as a real risk, is the matter in 
question. 
Dr Deckers  
227. I would like to add here some aspect that indeed  can be very important, which is the survival 
of the Erwinia  bacteria in the calyx of the fruits. Ther e is scientific evidence of the presence of 
Erwinia  bacteria on this place in mature apple fruit. So , there is indeed scientific-based risk present 
for the introduction of the bacteria through mature apple fruits. 
Kirsten Hillman  
228. Before I offer the floor, I have two little follow- up questions on the same topic. Again to both 
Dr Decker and Dr Paulin, in your replies to questi on 18 you indicate that the probability that epiphytic WT/DS367/12 
Page 32  
 
  populations of E amylovora  on mature symptomless apples could be transmitted to a susceptible host 
and initiate a fire blight infection and that this pr obability is rather low or that the possible mechanism 
is questionable. What I understood you to have just said in your prev ious answer, and I would ask you 
to confirm, is that you believe that  Australia has presented evidence th at such transmission is possible. 
That is the first question: could you confirm that  that is how we should interpret your previous 
answer.  The second question is:  how does this proba bility compare to Australia's chosen appropriate 
level of protection? 
Dr Deckers
 
229. Perhaps I can take part of the answer.  Indeed , we can confirm that there is a possibility of 
epiphytic populations to be transferred with the transport of infected fruits.  In this case, maybe 
something I miss in the whole discussion here, is that fruits coming from orchards where hail 
appeared could be a higher risk than fruits from non- hailed areas.  Because hail in the epidemiology 
of fire blight increases the risk of  this epiphytic populations on apple trees.  This is something that 
maybe should be better specified in the higher risks assessment.  Of course, I think this fact that 
epiphytic populations can be present is sufficiently do cumented in our risk system, and it is true it is 
necessary to do. 
Dr Paulin  
230. Maybe I could add at that moment that the term epiphytic is probably not the best term to be 
used in the case of E amylovora .  This is a bacteria which has a poor  fitness with plant surfaces.  So if 
you have bacteria on a plant surface, on apple trees surface, this is something which is temporary and 
not permanent.  We tend to qualify as epiphytes bact eria which are able to multiply on plant surfaces 
without producing symptoms.  This, I think ev eryone would agree, is not the case with E amylovora  
on apple or pear.  We may have on apple and fire blight the presence of a bacteria which is sourced 
from elsewhere, such as ooze or progressive infecti on in the same tree in the orchard.  You may have, 
sometimes, a bacterial population.  If this population is not able to infect the plant tissues, for some 
reason, then this population will tend to disappear and you will have residua l populations like the one 
that was being evocated in the calyx of the fruits.  E amylovora  is not a true epiphytic bacteria. 
Kirsten Hillman  
231. If I might re-state.  I did have a part of my question was whether this probability, namely the 
probability that these populations of mature sympto mless apples could be transmitted, and how that 
probability relates to Australia's chosen appropriate  level of protection.  If you cannot comment, that 
is fine, but I just wanted to remind you that that was also part of my question.  If you have some 
comments on that I would, of course, welcome them. 
Dr Paulin  
232. In this case, Australia has to take care of this  population.  The population of bacteria which 
may represent some danger for the introducing coun try is residual bacterial population on healthy 
fruits, not a permanent multiplying population of bact eria.  That means that the risk will tend to 
decrease with time, with any other elements like that, e.g. temperature.  It is quite different from a 
bacteria which is multiplying in plan t tissues so I would say it is an easier case to consider, as far as 
decreasing the risk is concerned. 
Kirsten Hillman  
233. One follow-up question in this regard and I will pa ss the floor over.  Again to Dr Deckers and 
Dr Paulin, do you have any comments and if you do could you offer them on Australia's requirement 
then to (i) disinfect apples;  and (ii) disinfect  packing house equipment, based on the answers you 
have just provided, if you have so me elaboration on those measures.  WT/DS367/12 
 Page 33 
 
 
  Dr Paulin  
234. In my opinion, disinfection of apples is an  additional safety.  If you have these residual 
populations I was speaking of at the moment, then it will disappear with the disinfection process.  This applies to fruits.  I would say that for the e quipment of the packing house, I think disinfection is 
useless because then you are really speaking of  disappearing populations and you have no examples 
of the presence of bacteria on equipment in the fruit st ations.  So for fruit, I would agree this is a 
safety measure that would seem to be reasonable. 
Kirsten Hillman
 
235. Dr Paulin, if I could ask in your response just now, you had said that you felt that this was a 
useful additional protection measure, but additional to what, if I may ask. 
Dr Paulin  
236. In my mind, additional to the first safety measure , which would be to be sure that the fruits 
are originating from orchards wit hout active fire blight symptoms. 
Dr Deckers  
237. I would like to add also the comment in the n ecessity of the disinfection of the equipment.  
First of all, when the fruit has been disinfected the chance that the equipment afterwards gets infected 
by the Erwinia  bacteria is very low and even when the b acteria would be there, there is a very low 
chance that it would survive the st ruggle between the other micro organisms and bacteria in this 
environment.  I agree with Jean-Pierre that  the risk there is really very low. 
Kirsten Hillman  
238. That is my grouping of questions on this particul ar issue.  So, if I could ask New Zealand if 
they have anything to add? 
New Zealand  
239. Dr Paulin, could I refer to the response that you gave to Question 36, please, where you said 
in relation to the conclusion in the IRA and in rela tion to the probability of exposure of a susceptible 
host to Erwinia amylovora :  "Only some fragments… are supported by scientific evidence.  Very 
often suppositions or speculations are proposed ra ther than certitudes, ju st because these problems 
have never been addressed scientifically (or at least experimentally).  As a consequence, I do not see 
how it is possible to rely objectively on any figure for the likelihood of this 'exposure' step".  And, could you please confirm that that is still correct. 
Dr Paulin
 
240. I think it is interesting to remember the discussi on that we have heard this morning, because I 
was actually referring to exactly the same problem.  We have no data for most of these steps.  No 
experimental factual data.  So, we have to rely  on, what I was calling, supposition of speculation but 
that can be more elaborated, obviously.  Anyhow, we lack biological information.  For me, because I 
am not a risk assessment man, I think I have foun d it difficult to place a figure on these judgements 
which are just human judgements, not based on biological data.  I am a biologist. 
New Zealand  
241. I wonder if Dr Deckers could please comment on the same point? 
Dr Deckers  
242. I think there is indeed a very difficult situati on because you have no proof available that this 
transfer can occur.  So, it is indeed speculation w ith, for me, a low level of likelihood to be a reality. WT/DS367/12 
Page 34  
 
  New Zealand
 
243. Dr Paulin, if I could please draw your attenti on to your response to Question 19, where you 
said, in your written responses, "The highest probabi lity I can think of is a pollinating insect taking 
the few bacterial cells to the hypantium of a flower  of a host plant.  This remains unlikely because 
trace bacterial populations (not multiplying) would be hardly grasped by insects (it would be easier in 
the case of a multiplying population, where cells are embedded in exudate).  Finally, the likelihood of 
successful multiplication on the hypantium and infec tion would be extremely low.  In addition, it 
would be necessary that such open flower be ava ilable when these surface polluted fruits are present.  
All this cannot be considered to constitute an ev idence".  I just wondered if you could comment if 
whether that is still your view. 
Dr Paulin  
244. Yes, I could.  The basis of this statement is th at the bacteria in the no rmal cycle of the disease 
has a state of multiplication in the plant which pr oduces ooze, which means bacteria are embedded in 
polysaccharides which are sticky and made of sugar.  All these attract insects and explain the role of 
insects in the transport of the bacteria from bact erial source, which is ooze on the diseased plant, to 
flowers.  In the case of a supposed population whic h is just decreasing, not multiplying, not producing 
any external extra cellular polysaccharides, I do not see how an insect can be contaminated with some 
level of certitude with bacterial cells which are not multiplying, not active and how they can carry this 
bacteria to a flower.  You just miss the stick, glue , between the bacteria and the insect in the case of a 
bacteria population which is not multiplying.  That was the basis of my reservation on this step. 
New Zealand  
245. Thank you.  Could I just sum up your responses to  the last questions and ask you whether you 
agree with the proposition that there is no scientif ic evidence to support this transfer stage. 
Dr Paulin  
246. I have seen no evidence of that.  Yes. 
New Zealand  
247. In fairness, I could ask Dr Deckers if he coul d comment too, in particular on the last point. 
Dr Deckers  
248. I think it is important here to consider that th e transfer of a normal infection in the cycles of 
Erwinia amylovora  is the ooze produced by the overwintering canker where the insects come and take 
some of the bacteria in their mouth or on their legs .  It is totally different, the situation, when we 
would have an infected fruit with the calyx infection at  the top of the fruit.  It will not be infected as 
the ooze from the overwintering canker, so the chance of  transmission is much lower in reality than it 
is in the case of transfer from canker to blossom. 
Kirsten Hillman  
249. I believe New Zealand has no more questions .  Australia, do you have any questions? 
Australia  
250. I just have one quick question to ask before I hand over to my colleague Dr Roberts, who will 
go into this in a bit more detail.  When you ta lk about direct evidence are you talking about 
experimental evidence? 
Dr Paulin  
251. Not only.  Because in some cases you have just c ase history or things like that.  But it is true 
that an experimental evidence is far better if you can have it, but it is not compulsory.  WT/DS367/12 
 Page 35 
 
 
  Kirsten Hillman  
252. Can I make a quick comment before I give the fl oor back to Australia, just to remind you that 
we are asking questions around the grouping of questions that I had asked.  Obviously, you will be 
given the chance at the very end of this section to ask other questions. 
Australia  
253. In a lot of these questions addressed to Drs Pau lin and Deckers, there are a lot of responses on 
the individual steps in transmission and we seem to have entered this transmission area, given the questions asked by New Zealand.  In light of your  responses on the individual steps in transmission, I 
would like to clarify some of your responses to Qu estions 35, 37 and 43.  Dr Paulin, you stated in 
your response to Question 37 from the panel that yo u did not see any objective analysis in the IRA 
that the pathway could be comple ted either under orchard or experi mental conditions.  However, you 
also went on to say in your same response that you did not think it is possible to experiment in this 
matter and that this does not mean that mature apple fruit may not be a source of fire blight infection.  
Just turning to Dr Deckers's reply to Question 37, you say something very similar in your response to 
Question 37 that the step of transfer would be difficult to prove.  So, I assume you mean 
experimentally there.  I would like you both to elaborate on your responses.  In particular, is it correct 
to say there is something similar to your response in Question 35 where you state that "The fact that E 
amylovora  can be transmitted to a susceptible host via insects feeding on discarded apples is 
conceivable through an apparently  logical succession of events, each  of them being questionable but 
never completely impossible ". 
Dr Paulin  
254. It's again a matter of frequency. I think you can imagine, because it is logical. If bacteria were 
in the soil then you cannot imagine a way from the so il to a blossom. When it is on the plant surface 
you can imagine something. It doesn't mean that it  happened, but you have to consider that it can 
happen. I think for most of these questions that is the basis of the answer. You can conceive that it 
may exist sometimes and because you cannot experiment  you have to accept this possibility, even if it 
is very low, but you have to accept it. 
Dr Deckers  
255. Maybe I can add here that the most likely transfer for Erwinia amylovora  is pollinating 
insects, flying from flower to flower. Of course it is not excluded that honey bees feeding on rotten fruit on the ground that is infected get infected by Erwinia  bacteria when they are feeding in the 
neighbourhood of the calyx with the bacteria in it.  It is a possibility which can never be excluded 
100 per cent. That's what we are trying to say. 
Australia
 
256. Sorry for our deliberation here.  We have got another question which we  weren't intending to 
ask now, but it really is in direct response to some  matters that New Zealand raised in response to 
your questions. We are prepared to hold off if yo u prefer to proceed with yours, but we are just 
flagging we would like to come back to an issu e of multiplication of bacteria, which New Zealand 
raised. 
Kirsten Hillman  
257. I know we have gotten slightly off track here  and would appreciate the opportunity to get 
back on track. We will be getting back to that and we have questions on that regard ourselves. Taking 
us back to a more general question, Australia argues that while the experts expressed some doubts 
about the overall probability of importation of E amylovora , this conclusion should be weighed 
against the specific support for individual importation steps, that is support from the experts.  In Australia's view, there is sufficient support for the detail of the IRA team's reasoning to suggest that 
"any purported exaggeration of the probability range is not a serious flaw". So we would like the WT/DS367/12 
Page 36  
 
  experts to comment on this statement by Australia and if it adequately reflects your view on the 
matter. 
Dr Paulin
 
258. Again, it's difficult to estimate the exaggeration an d the seriousness of the flaw.  It is true if 
you have several exaggerations, you can have a seri ous flaw.  Nobody can tell actually against what 
you are estimating exaggeration.  We are just lacking da ta.  I think there is no objective answer to this 
question, I am sorry to say. 
Dr Deckers  
259. As far as I have understood in this area, I don' t feel that there was an exaggeration of the 
estimation there in the importation steps.  I think ther e is a real risk present that should be estimated as 
good as possible.  For me it was not an exaggerated s ituation here.  I think you are right to take the 
estimation in this way. 
Kirsten Hillman  
260. I would like to go back and follow-up an answ er that Dr Paulin provided a little while ago 
when I had asked him to comment on Australia's requirement to disinfect apples or packing house 
equipment and you said at that time that if you disinfect fruit then fire blight would disappear.  Could 
you please explain to us what you mean by disappear. 
Dr Paulin  
261. I am not sure I used the term "disappear". I mean that if you disinfect the fruit, then you 
enhance in a very large proportion the quantity of bact eria that will disappear due to the disinfection. 
You have very good chemicals that are able to di sinfect fruits. This means that if you begin the 
disinfection with a low bacteria population, you w ill end up with fruits which will be clean, without 
bacteria. 
Kirsten Hillman  
262. I would like to move on to a question on Importation Step No. 2. I am sorry…  Did New 
Zealand have a comment? 
New Zealand  
263. I was wondering if Dr Sgrillo could be given an  opportunity to comment on your question in 
relation to the purported exaggeration of the probabilit y range, whether that is a serious flaw in the 
IRA? 
Kirsten Hillman  
264. Dr Sgrillo, would you like me to re-read the question? 
Australia  
265. Sorry, just to come in on that question, Au stralia regards purported exaggerations at any 
particular steps in the biological pathway to be questions of biology.  So, if possible, we would ask that any methodological aspect of that question be put appropriately. 
Kirsten Hillman
 
266. We take note of your comment and refer to the Chairman's opening remarks and the manner 
in which he dealt with your earlier observation on the same point.  So, we will have Dr Sgrillo answer 
the question and then we will c onsider or not in due course. 
Dr Sgrillo  
267. What is the number of the question, please?  WT/DS367/12 
 Page 37 
 
 
  Kirsten Hillman  
268. It is a question from the Panel, so not a qu estion that has been already answered.  The 
question relates to a comment made by Australia in characterising the views of the experts, specifically Dr Deckers and Dr Paulin.  Australia  argues that while the experts express some doubts 
about overall probability of the importation of the E amylovora , this conclusion should be weighted 
against the specific support for individual importati on steps that they expressed.  In Australia's view 
there is sufficient support with the detail of the IR A team's reasoning to suggest that "any purported 
exaggeration of the probability range is not a serious  flaw". The question I had asked is whether the 
experts believe that this characterisation adequately reflects their views. 
Dr Sgrillo
 
269. This is the final result of one part of the impor tation risk analysis, the expected percentage of 
apple fruits that would be infected when you impor t. A mathematical model is a hypothesis, is a 
general hypothesis. This number is a hypothesis.  And this hypothesis is composed of partial 
hypotheses, each of these partial hypotheses is an im portation step that has a number.  If you validate 
each of the partial hypotheses, then the final hypothesi s is validated.  But this was not the case with 
this model.  So, if you don't have the par tial hypotheses validated, I mean the probability ranges 
validated, there is no way to evaluate what is the m eaning of this final result of 3.9 per cent, because it 
is based in numbers that were not validated. So it is a result that could be completely wrong or could 
be completely right. The result is from many numbers that were not validated. 
Kirsten Hillman  
270. I will move on to my question on Importation Step No . 2.  This is a question to Dr Paulin.  In 
your response to the Question 6(c), you indicated that "[t]he reasoning established by the IRA 
seems… coherent and usually based on available evidence, although it may tend to exaggerate the 
risks of E amylovora  associated with fruits".  You may feel you have answered this already, but I am 
going to give you an opportunity once again, could you explain to us in this particular importation 
step what you mean by exaggerate? 
Dr Paulin  
271. I must say I don't remember exactly the figure.  Th is step 2, which deals with epiphytically or 
surface-infested fruit, seems  to me of quite low danger, because this population is low and easy to 
remove.  So that is why I think this step could be considered as low risk. 
Kirsten Hillman  
272. Again with respect to importation step No. 2, in its comments on experts responses to 
Question 24 about the probability range and distributi on patterns for importation step No. 2, Australia 
indicates that a number of issues may have been overlooked by the experts in arriving at the conclusion that the probability range ascribed to this step is not scientifically supported.  Would any 
of the experts care to comment on this comment by Australia?  And, would anyone wish to add or modify their response in light of the information that was provided by Australia in its comments?  
Would it be helpful if we reminded you of the issues in relation to these comments?  In particular, the 
issues relate to the relevance of endophytic infection, epiphytic infestation of mature apples, the weighting of studies derived from orchard showing fi re blight symptoms and the weighting of other 
scientific evidence. 
Dr Paulin
 
273. I am sorry to say I do not see the point.  Exactly to which question do you refer? 
Kirsten Hillman  
274. The question was Question 24 which I can read to you:  "Are conclusions in Australia's IRA 
as to the probability range and distribution patterns for importation step 2 sufficiently supported by 
the available scientific evidence?" You provided us  with some responses to which Australia came WT/DS367/12 
Page 38  
 
  back with fairly lengthy comments. The gist of  those comments was that there were a number of 
issues that may have been overlooked by the expe rts at arriving at their conclusions, that the 
probability range ascribed in this step is not scientif ically supported. They went on to provide further 
information on the issues I just mentioned:  the relevance of endophytic infection, epiphytic infestation of mature apples, the weighting of studies derived from orchard showing fire blight 
symptoms and the weighting of other scientific  evidence. You don't have to comment. We are 
offering you an opportunity based on these fairly lengt hy comments back from Au stralia to the effect 
that you had perhaps overlooked some information, whether or not in the light of that further 
information that was provided by Australia you may wish to add something or if, in fact, it doesn't 
change your views and answers on this. 
Dr Paulin
 
275. I think I do not change my opinion on this point.  For me, epiphytic surface bacteria is 
important, endophytic bacter ia is less important. 
Dr Deckers  
276. I would like to add here the situation that fire blight infection occurs in orchards and many of 
the trials that have been made in this area are fo llow-up on a infection artificially made in an orchard 
and then the surrounding of this infection around.  But here in the case of the importation we start from orchards where fire blight would not be present,  orchards where fire blight have been found and 
active fire blight has been found, are excluded. On  the second part of the answer, even when you have 
a disinfection of the fruits coming from the orchards without active fire blight recent infections, I think the chance is really lower than is mentioned he re. But, it is difficult to prove. This is my 
comment on this. 
Kirsten Hillman
 
277. Those are my only questions on importation step 2.  I would be happy to provide the floor to 
New Zealand and Australia, if you have questions re lated to the specific questions I have asked. If you 
have other questions on importation step 2, please ask them later. 
Australia  
278. It is really a factual clarification. This is in some of our comments to the experts replies. Imp 
step 2 is assessing unrestricted risk. I gathered fro m Dr Deckers reply to you just a moment ago that 
he was talking about restricted risk where risk management was in place, and that is some of the clarification we tried put in our comments.  Just a factual clarification to us about unrestricted risk 
with no risk management measures present. 
Kirsten Hillman
 
279. I have one question on importation step 3. Impor tation step 3 is the likelihood that clean fruit 
is contaminated by the E amylovora  during picking and transport to the packing house. This is a 
question to Dr Sgrillo. In your response to Question 26 you state that Australia's evaluation related to 
importation step 3 is objective but that available evid ence is not sufficient to support it. We are trying 
to understand how those two statements work together. Specifically, are you implying that in your 
view the evidence is insufficient or are you implying  that the available evidence does not support the 
conclusion, or something else. Could you clarify? 
Dr Sgrillo  
280. It is Question 26?  The values for the distribu tion used were taken from two papers.  One says 
that "Only 3 of 72 uninoculated and non-disinfested  fruit developed blight symptoms – all through 
injury in the puncture treatment".  So, from these figures the import risk assessment team calculated 4 
per cent of the fruit damaged would be contaminated by fire blight.  Four per cent came from 3 fruits divided by 72 uninoculated fruits.  I mean, the figur e came from one single paper. The other paper is 
just an abstract of four paragraphs.  There is no specification of how the samples were collected, what  WT/DS367/12 
 Page 39 
 
 
  methodology, no statistical analysis and the result shows that, at the time of the first check, the 
percentage of damaged apples was lowest for th e careful picking treatment, about 8 per cent, 
compared with 37 per cent in the whole containe r in the packing house. The IRA used 4 per cent 
multiplied by 37 per cent to indicate the magnitude of the most probable value of the triangular distribution.  There is evidence, but these numbers are based on papers with no specification of the 
methodology.  If they ought to repeat the same e xperiment and make the sample again, there is no 
guarantee that the numbers that come will be equal to these ones. I mean there is no way to evaluate 
the reliability of these numbers.  So, it is not contradictory. There is not enough data. 
Kirsten Hillman
 
281. That is the only question that we have on impor tation step 3.  Does anyone want to comment?  
New Zealand do you want to comment on the answ er provided?  Or, not comment, ask related 
questions? 
Chairman  
282. I am going to ask a few questions and wondering if  we can be a little bit speedy.  ould I get a 
sense from the two Parties on whether you have many qu estions? This is a qualitative thing – we have 
eleven more on this issue. We would like to finish our questions in 10 minutes, so we are in a difficult 
position here. Could I get a sense of how many questi ons you have around on this area of fire blight. 
Australia  
283. I think perhaps not a large number but we do ha ve several which are quite focussed, so I don't 
think they will require a long response. 
New Zealand  
284. We will also have only a few questions. 
Chairman  
285. What I would like to do is ask my first question and then ask five questions in a row without 
you responding, because they will be going to diffe rent experts and then you can think about your 
response. The first one is on Importation Step 4 an d it relates to Question 28, which deals with the 
IRA's conclusions as to the proba bility range and distribution patte rns for Importation Step 4. The 
likelihood that E amylovora  would survive routine processing pro cedures in the packing house. It 
seems that some of the experts for some of th e responses assumed that fruit would be disinfected, 
stating that in this case they considered the proba bility range to be too high. May I ask what your 
response would be if the fruit were not disinfected, in particular, Dr Sgrillo, Dr Deckers and possibly Dr Paulin might wish to comment on this question. 
Dr Paulin
 
286. In my opinion, the fruit will get out of the station as it entered with or without disinfection, 
maybe with a little less bacterial population but nothing significant. 
Dr Sgrillo  
287. The only comment that I have and I don't know if it was asked directly, is that the concept of 
cleaning the fruit that is used if you are thinking of  the fruit leaving without any bacteria is one thing. 
Probably you will never get there. It is a loga rithm exponential decay. You reduce the population to 
the half, to the half, to the half, but always you w ill have some population. So completely clean, you 
will never have. However, what I have tried to say is that there is a threshold of bacteria population 
below which it is almost the same thing as no bacter ia, because it needs a greater number to initiate an 
infection and that necessarily there is no need to co mpletely clean the fruit of bacteria. But, if you 
remove the population up to a level, that it will be the same thing as a clean fruit. WT/DS367/12 
Page 40  
 
  Dr Deckers
 
288. Just a very short comment, when we propose disinfection of the fruit, I think we should be 
aware that we never take away 100 per cent of the bact eria present. It is very difficult to disinfect for 
100 per cent in the calyx area. I think we should be aware of this reality. 
Chairman  
289. I am going to do, more or less, what my colleague Mr Ehlers did and I am not going to ask 
specifically the Parties whether they would like to comment. I will give a quick look and if you don't seem to be interested, then we can move on to the next question. I see no specific need to intervene at 
this point, so I will move on to a set of ques tions which relate to proximity and exposure. 
290. The first question relates to Question 27, Aust ralia's reasoning regarding the ability of the 
number of E amylovora  found on mature apple fruit to spread  to a susceptible host and initiate an 
infection under natural conditio ns.  The question would be, please explain whether you consider 
Australia's reasoning in the IRA to be objective an d credible?  Is it based on respected and qualified 
scientific sources?  That is the first question.  Le t me ask a few and then give you the opportunity of 
responding to these. 
291. The second question:  in its comments on the e xperts responses to the Panel's questions on 
epidemiologically significant populations, Australia argues that the experts responses illustrate a state 
of scientific uncertainty, rather than  evidence of significant scientific deficiency in the IRA.  I would 
be interested in your comments on this comment from Australia. 
292. And then, if I may ask a question to Dr Paulin:  in Australia's view your response to 
Question 35 is consistent with the IRA team's reasoni ng, that "the most likely mechanism of transfer 
of bacteria from discarded apples to a receptive s ite in a susceptible host is by browsing insects".  
Could we request whether this statement adequately  reflects your views on the matter?  Maybe I am 
stretching it a bit by asking too many.  I will stop ther e.  On the first two questions, have the experts 
any comments?  Or, Dr Paulin on the third question. 
Dr Paulin
 
293. In my mind, I don't see anything else than browsing insects which can carry the bacteria from 
these two places, so I would support this. 
Chairman  
294. Any responses for the first questions? 
Dr Deckers  
295. Maybe here we should mention also the coinciden ce of the host plant in the susceptible stage.  
So that even when the transfer possibility is there I think another important point is that you have host 
plants in a susceptible stage that can be infected.  I don't know when the seasons are exactly when the 
discarded fruit would be in the open air, which shoul d be taken into account before a real infection 
can take place. 
Chairman  
296. The issue of scientific uncertainty versus evid ence of significant scientific deficiency.  
Anybody want to comment on that?  I am going to move on to another question.  Dr Deckers:  in your 
response to Question 35 you state that "The chance th at the epiphytic bacteria will be transmitted to 
the susceptible organs of a host plant on the appropri ate moment to realise an infection is rather 
small".  How does this compare to the conclusion in  the IRA which states that the exposure value for 
an individual apple should be in the range from 0 to 1 in a million?  WT/DS367/12 
 Page 41 
 
 
  Dr Deckers  
297. This value between 0 and ten to the sixth is also very low, so I think this is true.  But maybe 
we should add here something, when we see an evoluti on of fire blight in a country that has the fire 
blight for the first time, you see that often it is not on the fruit trees it is found in the first place, there 
are other more susceptible plants that show it earlie r before you can find it on the fruit trees.  Maybe 
this is also a fact that should be included in the reasoning of this first infection.  It is not always on the 
fruit tree – mostly not. 
Chairman  
298. In its comments on the expert replies to  Question 36 regarding overall probability of 
exposure, Australia indicates that the experts conc lusion that the overall exposure value in the IRA 
was not supported by scientific evidence appears at odds with the support provided by the experts for 
individual steps.  I know we have had a question quite similar. I wonder whether that has been 
exhausted.  If you want to make a comment on th at, you are welcome to do so. My colleagues have 
just reminded me that this is the exposure proxi mity element.  I see no further comment on this. 
William Ehlers  
299. Question 11 that we had put to the experts said: "Do you consider the IRA to be objective and 
credible when qualifying the biological and economic consequences of fire blight as 'high'?" There 
were plenty of answers to that, but I would like to look at part of Dr Paulin's answer where you state 
that:  if each of the three factors namely, climate,  cultivar susceptibility, and cultivar receptivity "can 
be evaluated… the combination of the three to gi ve a reasonable prediction [on the severity of the 
disease] is non-realistic". To facilitate our understa nding of what you mean here, could you explain a 
little more, please. 
Dr Paulin  
300. Yes. You know that if you want a disease to develop on a plant you need the presence of 
bacteria on the plant, under suitable general c onditions. You can know in advance what is the 
susceptibility of the plant. You can know whether it is receptive to the disease or not.  You can know 
if the bacteria are present or not. It is far more difficult to predict what will be the severity of the 
disease, in terms of damage which is expected. For ex ample, in Europe we have been quite surprised 
to see that fire blight is a very serious disease of  apple in Germany, where it was expected to be a 
serious disease of pear in the South of France, if you just look at the climatic conditions and the susceptibility of the cultivars. That means that there are some elements which are just missing and you 
can predict for sure that the disease will be able to de velop, but it is far more difficult to quantify this 
development in terms of economic loss. 
William Ehlers
 
301. Let me move on to something else. Concerning the alternative measures.  New Zealand has 
proposed two alternative measures in respect of fire  blight: namely, restricting apple fruit imports to 
fruit that has been cold-stored;  or limiting imports  to apples that are reta il-ready packaged fruit. 
Would, in your view, one of these alternative m easures meet Australia's appropriate level of 
protection? 
Dr Deckers  
302. I think the alternative measure here mentioned, fruit storage in a cold environment, would not 
reduce directly the number of bacteria on the fruits .  Bacteria normally can support very well the cold 
storage conditions. I think this is not really a me asure to reduce the risk of infection by this 
supplementary measure. The retail-ready fruit, as we  discussed this morning, is indeed something 
where you can say, okay when you prepare this in th is way, you can be quite sure that the fruits are 
free of trash.  In contrast to when you prepare the fruits in bins, where there is much more availability 
for contamination. WT/DS367/12 
Page 42  
 
  Dr Paulin
 
303. I fully support this answer. 
William Ehlers  
304. As there are no other requests, let's move on.  Drs Deckers and Paulin, in its comments on the 
responses to Question 47 regarding the IRA's requireme nt that a packing house provide details of the 
layout of the premises, Australia has stated that:  "The replies of the various experts to this question 
indicate that they may not have understood th e reason behind Australia's imposition of this 
requirement… The measure is intended to facilitate  the verification of packing-house procedures by 
AQIS officers and thus make such on-site verificat ion more efficient and swift, and therefore less 
costly to New Zealand exporters". Would anybod y like to make a comment on the basis of this 
clarification? 
Dr Paulin  
305. On this point I am not in my field of expe rtise and I don't know well enough how things are 
organized.  So I cannot answer. 
William Ehlers  
306. Can you identify specific points where in your view Australia's IRA, through its design and 
methodology or with respect to the consideration of specific steps, may have underestimated the 
likelihood of importation, establishment and spread of  fire blight or the associated potential biological 
and economic consequences, in relation to impor ts of apples from New Zealand.  I stress 
underestimated, because a lot of answer seem to im ply that there has been over estimation in some 
cases.  We are trying to see if there are any other instances you have seen where this might have been 
underestimated. 
Dr Deckers  
307. Maybe one point that I don't find in the IRA system is that the importance of hail is not 
mentioned sufficiently.  This is epidemiologically on e of the very important factors that can allow an 
inoculum build up very shortly after this damage.  Of course, healthy mature fruit can come from an 
orchard where hail occurred and this may be an im portant factor where you should be more aware 
than the system today. 
William Ehlers  
308. No one else is requesting the floor.  Next question – Assuming that the semi-quantitative 
method could be considered a legitimate methodolog y, do you believe that the way the IRA has 
applied this risk assessment methodology for fire blight is objectively justifiable? 
Dr Sgrillo  
309. I think that this was commented on here before .  I think that the quantitative part of the 
methodology has not enough numerical da ta to generate credible results. 
Australia  
310. Just in relation to Dr Sgrillo's comment, could I go back to the question that we asked this 
morning and you indicated that you thought the model itself is good, or okay, I don't want to put 
words into your mouth, but there were issues about  inputs.  This semi-quantitative model was okay 
and you expressed these concerns about data and we heard other comments about data as well from 
other experts.  The situation we are talking about is , at this point, the issue of data and not the actual 
model itself, as it is being applied. 
Dr Sgrillo  
311. The model is okay.  But the data generates the problems.  WT/DS367/12 
 Page 43 
 
 
  William Ehlers  
312. I realize there might have been some redundancy in the question, but sometimes it is good to 
go over again just to make sure we have it good and clear.  So, if nobody else would like the floor then I will hand back to the Chair. 
Chairman
 
313. We are not running too badly.  We are a little bit behind time, but I would like to offer New 
Zealand to pose questions on the whole gamut of fire blight. 
New Zealand  
314. If I could refer Dr Paulin to Question 22 of hi s written responses where Dr Paulin stated that:  
"If the probability of 1 means that all orchards are contaminated by E Amylovora  each year, it is 
probably a mere exaggeration…  The chance for apples to be sourced from orchards harbouring E 
Amylovora  should be significantly less than one".  Do you still agree with that? 
Dr Paulin  
315. Yes, sure.  I think there is a problem of vocabular y.  I think what I was meaning is that, due to 
the historical situation of fire blight in New Zeal and, you cannot be sure in advance that any orchard 
is free of fire blight.  The history of the disease in th e country is very long.  It's the same situation that 
we have in France now.  That doesn't mean at all that each orchard presents symptoms of fire blight 
each year – these are things which are completely different.  The supposed risk represented in each 
orchard in New Zealand can be evaluated each year in place after a survey.  You cannot decide in advance this orchard is full of fire blight.  It is not true. 
New Zealand
 
316. If I could just clarify, when you answered the written response you were referring to the 
pathogen Erwinia amylovora , you are now talking about fire blight. Do you still stand by your written 
answer that the chance for apples to be sourced from orchards harbouring Erwinia amylovora  should 
be significantly less than one? 
Dr Paulin  
317. Yes.  Absolutely. 
New Zealand  
318. If I could address a question to Dr Sgrillo in re lation to your answer to Question 22 in which 
in your written response you said the probability of one for importation step 1 "means that it is 
absolutely true that fire blight is present and will always be present in all of New Zealand orchards.  
The scientific evidence presented in IRA does not guara ntee that this is true".  Can I ask you to 
confirm whether that is still your view;  and second ly, whether that conclusion also applies to the 
pathogen Erwinia amylovora  and not just the presence of fire blight, the disease. 
Dr Sgrillo  
319. Actually, I was not thinking in the idea of "free from", as defined in international standards.  
When I wrote down that there is no support for the pr obability of one, this is implicit that in some 
times and in some place you might have orchards without Erwinia amylovora .  That is the sense of it. 
New Zealand  
320. If I could move to Importation Step 2 and ask Dr Paulin a question in relation to your 
response to Question 24, the likelihood that ma ture apples are infested or infected with Erwinia 
amylovora  and you said that Australia's evaluation "is not scientifically based , cannot be objective 
and… is just not credible as a whole".  Is that still your view? WT/DS367/12 
Page 44  
 
  Dr Paulin
 
321. Yes.  I think so. 
New Zealand  
322. Dr Deckers, in your response to Question 24 , the same question, you wrote that the IRA's 
assessment "doesn't take into account the sporadic ch aracter of the fire blight disease".  Is that still 
correct in your view? 
Dr Deckers  
323. I think it corresponds to what we said in the questi on before.  Fire blight in an area where fire 
blight is present, you cannot find orchards, or very ra rely, orchards that have no fire blight during the 
last years.  This is typical of fire blight that in  some years you will see the problem more on pear than 
on apple or on other host plants.  This sporadic presen ce of the disease makes it very difficult to make 
a calculation and risk estimation in advance.  I thin k it is linked with the disease.  I think Australia 
should be really careful looking to how exactly they define the risk situation because the risk can be 
from most of the orchards, apple or pear or ev en from other host plants in the neighbourhood. 
New Zealand  
324. Also in response to that question, you said that the value of 3 x 10 to the negative 2 "seems to 
be a quite high rate of pick ed fruit being infected" with Erwinia amylovora .  Does that sum up the 
comment that you just made? 
Dr Deckers  
325. Yes, because this value of 3 x 10 to the negativ e 2 is the situation where you have I think you 
can obtain this relatively high amount of bacteria in orchards where active fire blight history is 
present.  Where there is no new infection found duri ng one season, I think you will never get this level 
of bacteria. 
New Zealand  
326. Dr Paulin, I believe that you said in your res ponses that it would be possible to experiment 
and to obtain data to find out the likelihood of whet her mature apples are infested.  Is that correct? 
Dr Paulin  
327. Yes, if the figure provided by the IRA were tr ue, I think they are amenable to experiment, 
because they are quite high.  So, these figures can be  checked experimentally, not so easily, but it can 
be done, I think. 
New Zealand  
328. In your view, does the IRA actually present such data? 
Dr Paulin  
329. The figure produced which is 3 x 10 to the ne gative 2 is a figure produced by the IRA, 
proposed by the IRA.  It is this figure I have in  mind when telling that such a high rate could mean 
that you can experiment, because it is not beyond reach of experimentation. 
New Zealand  
330. Are there experiments in the IRA that would,  in your view, lead to that conclusion? 
Dr Paulin  
331. No, I don't think so.  WT/DS367/12 
 Page 45 
 
 
  New Zealand  
332. If I could move now to Importation Step 3, th e likelihood that clean fruit is contaminated by 
Erwinia amylovora  during picking and transport to the packing house.  Dr Paulin, your response to 
Question 26 that "the evaluation of risk for this st ep seems too high, for mature symptomless fruits". 
Is that your view? 
Dr Paulin  
333. Yes. 
New Zealand  
334. Dr Deckers, in your response to the same ques tion, you wrote that "the overall chance of 1 per 
cent [in the IRA] seems to be rather  high when the fire blight infe ctions are only sporadically present 
in an orchard".  Could you confirm whether that is your view? 
Dr Deckers  
335. That is indeed exactly what I think, because fire  blight will not be uniformly distributed when 
present in an orchard. So the one per cent overall value I think will not be the reality. 
New Zealand  
336. Moving to Importation Step 4, the likelihood that Erwinia amylovora  survives routine 
processing procedures in the packing house.  Dr Pa ulin, in your answer to Question 28 you said that 
"it will never be possible to extend results obtaine d with artificial infestation of fruits to actual 
bacterial population naturally placed on certain sites on  the fruits".  Could you confirm whether that is 
still your view? 
Dr Paulin  
337. Yes, this is still my view because when you experiment with bacteria and fruits you 
technically place the bacteria cultivated in the lab on  the surface of the fruit and this is very artificial 
as compared to bacteria which, for example, resu lt from an earlier infection and which remain alive 
on the surface and which are embedded in polysacchar ide on the surface of the fruits, e.g., in the 
calyx. The interaction you may have between the bacter ia and the plant tissues are basically different.  
That means that experimentally when you dip fruit,  for example, in bacterial suspension you can get 
tendencies and information about the decrease of the bacterial population due to the antiseptic 
solution. But you cannot have a real picture of  what is happening in the field, under natural 
conditions. 
New Zealand  
338. A couple of questions in relation to Importation Step 5, the likelihood that clean fruit is 
contaminated by Erwinia amylovora  during processing in the packing house. Dr Paulin, your written 
response to Question 47 was that:  "Very few scientific  data, if any, support the risks of contamination 
of fruits by Erwinia amylovora  in the packing houses". Could you confirm whether that is still your 
view? 
Dr Paulin  
339. I have never found such data and I do not see that, in a normal storage station where poor 
quality (with symptoms) fruits are discarded before  processing, I cannot see that you may have mutual 
contamination between fruit during processing. 
New Zealand  
340. Just a point in relation to your response to Ques tion 30, it relates to the same importation step 
– contamination during processing in the packing house and you said "the probability suggested in the 
IRA seems to be strongly exaggera ted".  Is that your conclusion? WT/DS367/12 
Page 46  
 
  Dr Paulin
 
341. Yes it is. 
New Zealand  
342. Thank you Mr Chairman, that concludes our questions on this point. 
Chairman  
343. Thank you, New Zealand. You went through those with great speed.  I was wondering 
whether there were any comments from either my coll eagues here or from Australia on the points that 
you have raised.  If you wish to proceed.  If not, Au stralia you have the opportunity to ask your own 
questions. 
Australia  
344. Just following on from our New Zealand colleagu es, what we would propose to do is to first 
address a couple of new steps.  We will address Impo rtation Steps 2, 3 and 5 and then Dr Roberts will 
address some of the issues on transmission.  We will have a few additional ques tions in light of what 
our New Zealand colleagues have said before, but we will try to present as quickly as possible. 
345. Dr Deckers and Dr Paulin, thank you for your  responses.  If I could just take you to 
Importation Step 2, I don't want to dwell too much  on the actual probability ranges but what I would 
like to talk about is some of the biological issues unde rpinning the analysis at this point.  Dr Paulin, if 
I could turn to you first, in your response to Qu estion 6 you stated that the IRA team's reasoning 
regarding epiphytic infestation is "coherent" and "b ased on available evidence".  Do you still hold that 
view? 
Dr Paulin  
346. Yes. 
Australia  
347. This question is for Dr Deckers and for Dr Pa ulin, in your responses to Question 8 and 22 you 
mentioned that infestation could arise, if there were infected hosts in the surrounding areas.  Could 
you elaborate on this response, please? 
Dr Deckers  
348. I think it is important to consider other host plan ts in the neighbourhood of the orchards area.  
We have the experience in Europe, in Belgium an d other countries around us, that it is sometimes 
very important to consider other host plants, like cr ataegus or sorbus that can be host plants that 
produce continuously during season, fresh bacterial inoc ulum.  So, it is not only the orchard itself that 
should be taken into account when c onsidering the contamination risk. 
Dr Paulin  
349. I support this view, but that means on the contrary that if you have no active symptoms in an 
orchard or in the surrounding of the orchard you cannot expect to have an epiphytic or surface 
population on fruits. 
Australia  
350. Dr Paulin, in your response to Question 22 y ou have stated that late infection in the 
symptomless orchard could occur if there was contam ination of hosts or wind-driven rain, or insects 
or some other vector.  Could you elaborate on this response, please. 
Dr Paulin  
351. Yes.  This is more or less in relation with the hail storm infection that was referred to 
previously.  Normally, in the normal disease cycle of  the disease most infection takes place during the  WT/DS367/12 
 Page 47 
 
 
  blossom period or shoot growth period which take place both in spring or early summer.  But you may 
have in certain conditions, e.g., strong hail or seconda ry blossoms, you may have late infections and 
these infections may be active and progressing late in the season and not too far from the cropping (pick up) date, which can be important in your case. 
Australia
 
352. One final question on Importation Step 2.  As you know that experiments on this issue of 
infestation have very variable de tection limits on how much bacteria they can detect.  In your view, 
what conclusions can we draw from experiments who se detection limits cannot detect bacteria below 
10,000 cells?  And, in particular, do you think that this is reliable evidence that Erwinia  would be 
absent? 
Dr Paulin  
353. This problem of the detection limit is a seri ous problem.  But I think that most of the 
epidemiology that we know at present relies upon techniques which were detecting 10 to the 3 
bacteria per mil. and they proved to be good data, I would say.  Now, we have techniques which allow 
us to go far below that threshold, but as far as I see they do not provide very useful information in 
terms of technical data or epidemiological data.  They can tell you that you can have some remaining 
population of some cells, but as far as I know nobody is able to tell what is epidemiological significance of these populations.  So, 10 to the 3 is a quite high number, but it seems to reflect what 
is of interest in the disease cycle. 
Australia
 
354. I might just follow-up on the answer to that last  question.  Most of the epidemiological work 
that has been done, not surprisingly, has been done in  the situation where the di sease is widespread in 
an established fire blight area.  So, the question is  would you be concerned a bout experiments that do 
not detect levels of around about 10,000 cells per risk  unit in relationship to the spread of the disease 
into new areas? 
Dr Paulin  
355. I think if the bacteria is able to multiply, it will very soon reach a quite high level, I mean 
more than 10  to the 10, or something like that.  If it is active, it will very soon reach a high level 
which will be detectable.  I am not sure I answered your question. 
Australia  
356. I might leave that for now and turn back to so me of our questions on transmission.  I have 
interrupted my colleague. 
357. I have two very short questions on Importati on Step 3 and 5, then I can pass over to 
Dr Roberts.  In relation to Importation Step 3, Dr  Deckers and Dr Paulin you gave me a response to 
Question 26 and you talked a lot there about contamina tion events such as rain and hail.  Do you still 
consider these to be potential sources of contamin ation during harvest and tr ansport, and endangering 
processing if, of course, there is trash present, or rain, or hail, or those sort of things. 
Dr Deckers  
358. Yes, I think this is an important aspect, ev en at the end of the season.  Wind-driven 
populations of Erwinia amylovora  is an important epidemiological point. 
Australia  
359. Just one final question in relation to Importation Step 5, which is somewhat related to this 
point:  Dr Paulin if I could refer to your response to Question 30 and I can quote back the text.  You 
stated that:  "if decaying apples… or large amount s of infected trashes, were present, the dilution WT/DS367/12 
Page 48  
 
  effect [that is in apple dump tank], in a non-disinf ected medium could lead to a significant amount of 
bacterial cells on fruit surfaces".  Just to confirm, do you remain of this view? 
Dr Paulin
 
360. Exactly. 
Australia  
361. And, Dr Deckers, do you have any comment on that? 
Dr Deckers  
362. Well, it is typical for Erwinia amylovora  that it can go from low bacterial inoculum to a very 
high one in a very short time.  So it is possible. 
Australia  
363. Dr Paulin, in response to Question 21 you stated that:  "it has been proven that low bacterial 
populations (Hale et al, 1990) sometimes as VBNC (Ordax et al, 2008) may be present for some times in the calyx of fruits.  If these fruits were discar ded in the open and exposed to the elements, the 
decaying fruit could constitute a suitable medium  for a multiplication of these low bacterial 
populations.  They could multiply, or resuscitate from the VBNC status, and therefore constitute a 
potential inoculum
 for near-by host plants".  Do you still remain of that view in response to 
Question 21? 
Dr Paulin  
364. Yes.  Exactly. 
Australia  
365. Do you consider that it is feasible to assume that conditions for bacterial multiplication may 
occur in the orchard in rare cases? 
Dr Paulin  
366. Why not? 
Chairman  
367. Thank you, Dr Paulin 
Australia  
368. Turning to exhibit NZ-23, Taylor et al., this is  the paper we distributed earlier this morning.  
Please, if you look at the paper, in particular table 1 is particularly relevant.  Would you agree that the 
results of this experiment  conducted in the orchard which appear in  the first few columns of that table, 
labelled "MARC orchard cv. Royal Gala", would you agree that the results of the experiment 
conducted in this orchard show that inoculum concen trations of 10 colony forming units multiplied to 
100 million colony forming units can cause symptoms in apple flowers and I will ask Dr Paulin and 
Dr Deckers to have a look at that and answer please. 
Dr Paulin  
369. Yes I have seen this table.  The results of the first column for Royal Gala in MARC orchard 
are, I would say, surprising because if the number of bacteria indicated in the inoculum concentration 
were to be really ten to the one, you would expect  frequency of success of the infection less than 100 
per cent, because at so low an inoculum level you cannot expect to have 100 per cent of your droplets 
containing at least one cell.  So my conclusion from this table is that probably, and this is quite 
frequent, the number of bacteria in the inoculums wa s higher than expected by the experimentator and 
so that means probably down to ten to the three it's OK.  I would be more sceptical about ten to the two and ten to the one.  This is just a technical c onsideration.  And that is my opinion.  So probably  WT/DS367/12 
 Page 49 
 
 
  one cell, maybe one cell, can actually infect one flower , but this is not demonstrated in this table.  I 
would not be confident for this result just on this table.  You know, that is my opinion. 
Australia  
370. Before Dr Decker's answers, can I just perh aps ask a follow-up question in the light of your 
reply.  As far as we can understand from the paper, a nd I might add that this paper was put forward by 
New Zealand and they haven't made any commentar y about the methodology, I mean this suggests 
though that very low numbers of bacteria should be of  concern in terms of their potential to start fire 
blight disease under ideal conditions.  Would you agree with that statement? 
Dr Paulin  
371. Not entirely.  I would say, for me, that means th at if you want to have a reasonable chance of 
success in your inoculation I would not go down to l ess than ten to the three cells per flower and this 
seems to be generally accepted in a number of ot her papers.  When you are counting bacteria with 
these techniques that were used here, you have a quite  large range of error and I think in this case they 
were too high.  Honestly, if you have one cell you will have to i noculate maybe ten thousand flowers 
to get one infection.  I think th e probability of success of infecti on decreases very rapidly and maybe 
from ten to the three up then you tend to go to th e 100 per cent success.  It is not indicated in this 
paper, but it is my expectation from what I see from other results. 
Australia  
372. I am sorry, Dr Deckers, I will continue with this  theme and we will get to you in a minute or I 
hope to get to you in a minute.  What you are sayin g, you are suggesting that the reliable threshold for 
this type of experiment is around 10,000 cells, re liable in terms of producing symptoms in flowers? 
Dr Paulin  
373. One thousand, I would say, would be the threshold if you want to have at least, say, from ten 
per cent to eighty per cent success in your infection.  It will depend on the variety, on the period, the 
age of the flower, and so and so.  This is just a broad indication. 
Australia  
374. Yes.  But doesn't that suggest that the experi ments that have got detection limits of around 
10,000 cells really don't necessarily tell you ve ry much about what is really going on at 
epidemiologically significant numbers? 
Dr Paulin  
375. Well, it tells you what is probable, but doesn't tell you what can happen exceptionally. 
Australia  
376. Thank you.  I might ask Dr Deckers if he would respond on this particular issue, please. 
Dr Deckers  
377. I would like to add our own experiences with this  artificial inoculation test for apples, as it is 
mentioned here.  For me, the ten to the third with a 100 per cent infection and even ten to the second, 
ten to the one, this is very exceptional.  When yo u want to have infection successfully, surely not on 
apple, maybe on another more susceptible host plant,  you can go lower in the inoculum but not on an 
apple.  This is surprising me, this publication.  My second point is that, okay, here they are talking 
about apple blossom, but for me when you have an introduction somewhere in a new area, it is not mostly on apple that the bacterium starts.  It starts on more susceptible host plants. 
Australia
 
378. Thank you for that comment.  We have heard quite a lot on fire blight this afternoon 
particularly in the light of New Zealand's ques tions about some concerns you have got about WT/DS367/12 
Page 50  
 
  probability values that have been put on certain step s.  But we have also heard I think both experts on 
fire blight make statements about our measures and th e risks and the need to ma nage those risks.  So, 
in the light of all of that consid eration, do you think that the IR A reaches a rational logical inference 
that the probability of transmission by trade in apple fr uit is not zero?  In othe r words, on the basis of 
what evidence we have, is it rational to conclude th at transmission by apple fruit could occur, albeit as 
a rare event?  So that question is dir ected to both Dr Deckers and Dr Paulin. 
Dr Deckers
 
379. Here I would say yes, there is indeed a risk for the importation of infected fruits.  It is clear.  
But, on the other hand, I must say that in other situ ations where countries try to keep out fire blight, 
they are not talking in the first place about fruits, they are talking more about plant material and 
potential infections on plant material, root stock or va riety materials.  So that is maybe an important 
point. 
Dr Paulin  
380. In my view, the importation of bacteria with a pple is probably possible.  The further step from 
this imported bacterial population to a new plant in Australia is probably even less likely.  And I think 
that the total process, the risk represented by th e total process, is probably of the same order of 
magnitude as the transport of contaminated insects by natural way from New Zealand to Australia by 
air jet or things like that.  So that is my personal vi ew, that there is a possibility which level of risk is 
not far higher than the natural spreading possibility of the bacteria to go from place to another with 
something else, I would say, which has no connection with trade of apples. 
Australia  
381. Okay, I have got one final question, both to Dr Pa ulin and to Dr Deckers.  You have noted in 
your responses to Question 43 that the experiments of  Hale et al. (1996) and Taylor et al. (2003a), 
which are relevant to this issue, do not have an experimental design th at would detect rare events.  In 
your view, is it scientifically sound to conclude on th e basis of this evidence that rare events can never 
occur, that in quantitative terms the probability of  transmission should be represented as zero based on 
those type of experiments? 
Dr Paulin  
382. No, I don't think so, obviously. 
Dr Deckers  
383. No, I don't think so either. 
Australia   
384. We have finished our questions on fire blight. 
Chairman  
385. Would New Zealand like to respond to some of these questions? 
New Zealand  
386. I do have two or three follow-up questions.  First is  for Dr Paulin, and it relates to the issue of 
VBNC.  Specifically, Dr Paulin, your response to question 42, in which you referred to the complete 
absence of data on the occurrence of VBNC for Erwinia amylovora  in natural conditions.  I wanted to 
ask whether that is still your position.  
Dr Paulin  
387. Yes, sure.  VBNC are quite difficult to manipulate, as you know, and to demonstrate.  You 
can demonstrate that in the lab in very special conditions.  If E amylovora  has been shown to be able 
to go to the VBNC status, that shows that these bact eria has the genes and the systems and so it is able  WT/DS367/12 
 Page 51 
 
 
  to do so.  We don't know if the conditions which are c onducive to such state exist in the orchard.  It 
was the meaning of my answer. 
New Zealand  
388. And, just to follow on from that, is there any scientific evidence that you were aware of, that 
demonstrates that VBNC has significance in epidemiological terms? 
Dr Paulin  
389. Maybe it's not useful to focus on VBNC.  Actu ally we are speaking of long-term conservation 
of bacteria in a steady state.  So we know for long that in some cases, say in dried ooze, for example, 
the bacteria is able to survive for months, in certain  conditions.  So VBNC just adds something to this 
possibility, but it is not a completely new element in the epidemiology of E amylovora . 
New Zealand  
390. If I could just turn to the issue of the num ber of hosts that could be susceptible to Erwinia 
amylovora .  In your written responses in Question 10 you said that the IRA "maximises the real risks 
in considering too high number of host plants".  I just wanted to ask whether that is still your view. 
Dr Paulin  
391. Yes, sure.  This is quite common in countries w ithout fire blight.  They consider that any 
apple or any pear varieties are equally susceptible to the disease and will be host of the disease, which 
is scientifically sound and reasonable, but when you are in a country with fire blight you know well 
that actually this is not true and only a quite weak , fortunately, weak percentage of the cultivars are 
actually common hosts of the disease and do show a real  damage.  So that is why the term of host has 
a different scientific and practical meaning:  any culti var of pear, for example, is a host for fire blight, 
but economically only few cultivars are to be considered as such, in such a case. 
New Zealand  
392. You made a comment earlier about Erwinia amylovora  multiplying on fruit.  Are you aware 
of any scientific papers that report that this has occurred? 
Dr Paulin  
393. Do you mean on decaying fruit, or rotting fruit, or  something like that, or fruit on the tree? 
New Zealand  
394. Mature fruit or decaying fruit. 
Dr Paulin  
395. Decaying fruit, as far as the chemical composition of a decaying fruit, can be a suitable 
medium for the multiplication of Erwinia amylovora , although this remains to be demonstrated.  But 
you may have some multiplication, probably.  On  the surface of a mature clean fruit without 
wounding I don't know of any data showing multipli cation on such a surface and I would not expect 
Erwinia amylovora  to multiply on such a surface. 
New Zealand  
396. One final question for Dr Paulin and Dr Deckers.  It is in relation to the paper that Australia 
has handed around this afternoon, which is exhibit NZ-23, the paper by Taylor et al.  In light of the 
methodology employed in that paper, is it a fair comment to say that, under the conditions of the 
experiment, it was designed to ensure that if  an infection could occur it would occur? WT/DS367/12 
Page 52  
 
  Dr Paulin
 
397. Yes, exact, because special care was taken to prot ect the infected flowers with some chambers 
and this during at least 24 hours a nd this provided conditions which pr obably facilitate the infection in 
a very large proportion. 
New Zealand  
398. Dr Deckers, do you have anything to add? 
Dr Deckers  
399. I think indeed it is a very artificial situation that they created there.  This is not the reality of 
the infections and the orchard condition.  So maybe this could also give the explanation of the high 
percentage of infections that they had on this a pple variety, even with low infection doses.  I would 
like to add maybe the last comment on the VBNC st atus of the bacteria, what we were discussing 
about.  And maybe it's more important than we rea lize, because surely when the VBNC status is 
temporary and it comes back to a viable status afte rwards, then we know that copper is in use in the 
VBNC status.  Now copper is used a lot in orchar ds, and as well on apple as on pear, and they could 
induce indeed this type of status of the bacteria and I think it's not so exceptional as we described it. 
New Zealand  
400. I am sorry that I didn't ask you to comment on that question earlier, but perhaps I might just 
ask the same follow-up question as I asked Dr Pau lin.  Are you aware of any scientific evidence on 
the occurrence of VBNC for Erwinia amylovora  in natural conditions? 
Dr Deckers  
401. Yes, there are indications that there is VBNC status present under orchard conditions. 
New Zealand  
402. Could you please advise which papers you are referring to? 
Dr Deckers  
403. I just discussed this matter, during a European co st meeting in Valencia in Spain but it is not 
published yet.  It was only two weeks ago and there we discussed this matter of the VBNC status of 
the bacteria with Dr López of Spain. 
Chairman  
404. Australia? 
Australia  
405. I've just got one question which goes to one of  New Zealand's questions about hosts.  It is 
really, we have heard a lot of discussion about expe rimental work done in orchards and I note that 
Dr Deckers in particular has mentioned the importan ce of other hosts.  Now, New Zealand apples, if 
they are imported or when they are imported into Australia, would be largely consumed in our major 
cities, which are very low density with backyards w ith large numbers of fire blight hosts such as 
cotoneaster, crataegus, apples for that matter, and vari ous pear varieties.  So, perhaps I am just asking 
Dr Deckers to provide any additional thoughts he  has on the risks posed by hosts in the urban 
environment for the establishment and spread of fire blight. 
Dr Deckers  
406. I can tell you there that we monitored the de velopment of the fire blight introduction in 
Belgium by cotoneaster salicifolius floccosus plants.  They were host plant that we introduced in areas 
where fire blight was not found, just to know when th e bacteria really appeared they were seen first on 
this host plant.  And then of course you can monito r the spread of the disease when present.  This was 
with these host plants, indicating where the infection was and was not.  WT/DS367/12 
 Page 53 
 
 
  Australia  
407. Can I just follow that up.  I don't want to prolong us too much, but I think some of your 
questions before actually implied, and this answer to  this particular question implied, that some of 
these other hosts can be much more susceptible to fi re blight disease, at least under some conditions.  
Is that correct, or is that your view of the biology of the disease? 
Dr Deckers  
408. Yes, absolutely.  It is correct. 
Chairman  
409. It seems as though we've to a large extent exhaus ted the questions.  But let me ask the experts 
on this area, is there anything that you would like to add, that might not have been subject to a 
question and that you think might be relevant for the Panel?  Thank you then to all the experts that 
participated in that section.  I think we then turn to European canker and I would like to ask 
Ms Hillman to lead this section first, thank you. 
Kirsten Hillman  
410. Once again we are going to proceed in the sam e way with a few general questions, actually 
quite a few general questions and then some qu estions on the specific importation steps and other 
areas. So starting off with a very general question to those experts who have expressed views in this 
area.  Can you confirm that in your view Australia  has presented scientific evidence in the IRA that 
indicates that mature symptomless apple fruit can disseminate European canker and can you confirm 
whether this scientific evidence, if you feel that it is present, is from a qualified and respected source 
once again reminding you as we did earlier with fire blight that that resp ected source need not 
represent the majority view of science.  So can you c onfirm if such evidence exists that it supports the 
analysis regarding the likelihood of the importati on, establishment and spread of European canker 
through the importation of mature symptomless apple fruit.  Dr Swinburne? 
Dr Swinburne  
411. I think there is in fact no evidence in the litera ture that infected apples which rot with this 
fungus are responsible subsequently for the disse mination of the disease to other hosts, to further 
hosts.  Much of the evidence that has been presen ted concerns observations made in the 1920s by 
Dillon-Western concerning a variety known as Worceste r, which is an extremely early variety, which 
does rot on the tree and produces mummified fruits. In the 40-odd years that I have worked on this, I 
never have had the privilege of seeing such a th ing and I have attempted in the past to produce 
perithecia and ascospores from rotted apples for experimental purposes and failed. Fruit which rot 
with Nectria  as I will call it, does produce conidia if it is  incubated under moist humid conditions to a 
limited extent in the centre of the lesion. It is not  a prolific source of spores for subsequent release and 
I fear that nobody has actually done the experiment of determining whether a rotted apple can release 
spores into a new orchard situation and bring about di sease.  It is amenable to experimentation, along 
the lines of an experiment which we made in East Malling not too long ago with discarded canker 
wood which we pulverized and placed under potted trees of the most susceptible variety that I know, 
namely Spartan, and we failed to induce a single canker as a result of pulverizing several, maybe 50 kilos, of cankers underneath them. 
Kirsten Hillman
 
412. Dr Latorre. 
Dr Latorre  
413. Yes, I would like to also say that I have no information indicating that European canker can 
develop from rotten fruit.  In my experience, rotten fruit is very rare, almost never occurs in our 
conditions and sometimes we do see it after several m onths or weeks of cold storage in a very low 
proportion and never sporulated on the surface of th e fruit.  If this fruit are not sporulating it is WT/DS367/12 
Page 54  
 
  impossible to admit that it can spread at least eas ily to the clean fruit.  Well, I think the observation 
about perithecia on the fruit is something that has to be reviewed.  We have never seen perithecia 
form on the fruit.  I don't have any good paper that can really demonstrate that in the recent years they 
have seen perithecia in very susceptible varieties, bu t not in today's apple varieties.  So the most 
important inoculum could be coni dia, and conidia are only formed under very wet conditions in the 
orchard, mainly in the cankers and almost never, or never at least in my experience, on the fruit. 
Kirsten Hillman
 
414. I think that Australia would like to make a comment on this question. 
Australia  
415. We just actually had two follow-up questions.  One for Dr Latorre and one for Dr Swinburne. 
We should say at the outset that Australia has a serie s of questions on climate, but rather than engage 
in those issues now it might be easiest to deal wi th them together, because that involves some 
audiovisual presentations.  The question is for Dr Latorre.  In your written responses to the Panel's 
questions, particularly your comment on guideline (g) and Question 65 you stated that and I quote:  there is a risk of the entrance of N galligena  associated with asymptomatic (symptomless) fruit 
carrying latent infection, as such fruit cannot be diff erentiated from healthy fruits at harvest.  Could 
you please confirm that this is still your view? 
Dr Latorre
 
416. I agree.  This is my view. 
Australia  
417. I will handle over to my colleague Mr Heinrich  from Plant Biosecurity Australia, he has a 
question for Dr Swinburne. 
418. Professor Swinburne, in response to Question 64 you stated that "there is no data that 
confirms or refutes that rotted fruit forms a pathway for the long-distance transport of infection with 
Neonectria galligena … Virtually all research publications emanate from countries in which the 
disease is essentially endemic…, so it is not surprisi ng that the fact that the focus has been on more 
obvious routes, such as orchard to orchard, and he dge row to hedge row".  Could you please elaborate 
on this response? 
Dr Swinburne  
419. I suppose in my first response I did elaborate on it in a way.  The production of conidia from 
an apple rotted with Nectria  discarded in an Australian orchard an d thinking in terms of its ability to 
initiate a new series of infections in an area whic h had never had it.  As I have said, there is no 
information concerning the possibility that that would happen.  The point that I want to emphasize is 
that fruit has to produce conidia in order to become an infectious unit.  It may be infected, but it is not 
necessarily infectious and even if it does become infectious, being presumably on the ground and not 
deliberately placed somewhere up in a tree, the di ssemination of those conidia which depends on 
splash dispersal is actually going to be over a very  limited area but I wouldn't want to overemphasize 
that particular possibility but there is no inform ation which tells us that  it cannot happen and as 
biologists one can never say it would never happen. 
Kirsten Hillman  
420. Thank you. 
Australia  
421. Just a very short follow-up question, if that's okay.  So just to clarify, do you take it that you 
agree that the possibility of infected fruit acting as a pathway for the long distance spread of European 
canker cannot be ruled out?  WT/DS367/12 
 Page 55 
 
 
  Dr Swinburne  
422. No, of course it cannot be ruled out, but it probably has a vanishingly small probability. 
Kirsten Hillman  
423. In fact, you have covered a question that we ha d.  However, we had intended to also pose the 
question to Dr Latorre.  So if I could just refer to  the answer that was just provided by Dr Swinburne, 
that while this possibility that the movement of mature apple fruit could be a pathway for the long-
distance spread of European canker cannot be rule d out, that you maybe, I won't put words in your 
mouth, whether you agree with the characterization that Dr Swinburne has put, it can't be ruled out, but it's very, based on your earlier answer to our question, it is a very limited possibility? 
Dr Latorre
 
424. I agree with Dr Swinburne. The first step would be to have an infected fruit, and this is 
possible, without symptoms. You can take this fruit and carry it from New Zealand, perhaps to 
Australia.  This is also possible, in my opinion.  But another question is that this fruit is going to be 
rotten in Australian conditions and,  secondly, another situation will be that that rotten fruit will 
produce spores, conidia, on the surf ace and, thirdly, that those conidi a can be spread nearby, primarily 
by rain splashing, which is the main dissemination wa y.  So, in general, we agree.  The difference is, 
in my earlier response, is that it was only referring to the possibility that mature fruit can hold the pathogen.  And those fruits can certainly  be moved from one place to the other. 
Kirsten Hillman
 
425. In our Question 63 we had asked the experts to comment on whether the alternative measure 
proposed by New Zealand, in respect  of European canker, namely to  require that New Zealand export 
to Australia only mature symptomless apples, w ould achieve Australia's appropriate level of 
phytosanitary protection. Could we ask both Dr La torre and Dr Swinburne to clarify whether your 
reply to Question 63 somehow implies that limiting exports to mature symptomless apples would not 
achieve the appropriate level of protection. We st ruggled a little bit with your answers here, so if you 
could perhaps explain your position on this issue. 
Dr Swinburne  
426. The assumption behind this particular measure is  that fruit which become infected during the 
growing season will all show symptoms of rotting, at  or before they are mature harvestable fruit, 
because of the nature of the varieties.  And the poi nt that was made in some of the presentations was 
that the resistance mechanism, which is expressed by cooking apples which restricts the fungus for 
some period of time, wasn't present in modern dessert  varieties. That is not the European experience. 
In Europe, and particularly in United Kingdom, we know  that fruit of the same sort of varieties as we 
are discussing here, can and do become infected  during the growing season are harvested at the 
appropriate moment but still symptomless and are then placed in store, and this is the important thing 
is what happens to them in store, because the conditions the gas and temperature conditions within 
those stores is critical to the development of subsequent rotting, but they can therefore develop rots 
some weeks perhaps months after they have been pi cked in a mature symptomless condition. So it is 
incorrect to assume that that particular measure would satisfy the requirement. 
Dr Latorre  
427. Well, I agree with Dr Swinburne has mentione d.  Since it is impossible to differentiate 
symptomless fruit from those having the internal in fection, I think this measure would be very 
difficult to satisfy the requirement, in my opinion. 
Australia  
428. We just have, if it is okay, two questions to  follow up again for Dr Swinburne and one for 
Dr Latorre in relation to measures. Dr Latorre, in relation to Australia's requirement that apples be 
sourced from export orchards or blocks free of Eu ropean canker, you made the following statement in WT/DS367/12 
Page 56  
 
  your response to the Panel's questions.  And that was on guideline G and I quote "assuming that there 
is a risk (perhaps negligible, but different fro m zero) of entrance, establishment and spread of 
N. galligena  in Australia on mature asymptomatic apples imported from New Zealand, this 
phytosanitary measure appears reasonable for miti gating the risk of entrance". Could you please 
confirm that this is still your view? 
Dr Latorre
 
429. Yes, I agree with those comments. 
Australia  
430. I will now just hand over to my collea gue from Biosecurity Australia again. 
431. I would like to ask Dr Swinburne.  In your written responses, you stated that Australia's 
insistence on receiving only fruit from inspected orchards certified as free from canker would 
eliminate virtually all risks of fruit being latently infected.  Could you please elaborate on this statement. 
Dr Swinburne
 
432. Well, for fruit to become infected it generally requires to be grown on a tree which is itself 
infected.  I doubt if many fruit are infected on a tree to tree basis, so we are talking about fruit being 
infected from its mother tree, from its own particul ar tree. So if you pick fruit from trees which have 
no canker, the likelihood of them having latent infect ion is vanishingly small. And as I gather, 95 per 
cent of New Zealand's orchards are largely canker free, from the exhibits presented. 
Kirsten Hillman  
433. Okay, so our next question.  Dr Deckers, Dr Latorre and Dr Swinburne all replied to question 
68, which was regarding the survival of spores on mature apples without continued moisture. But the 
responses do differ from each other somewhat. So we would like to offer y ou an opportunity to 
comment on those differences, if you so desire. 
Dr Swinburne  
434. Shall I begin?  In the discussion concerning fire blight Erwinia , we were pointing out that 
Erwinia  is not an epiphytic organism and neither is  Cylindrocarpon heteronema, which is the asexual 
stage of Nectria .  The conidia are relatively short lived in an y event, particularly in a dry climate, and 
they cannot survive on the unbroken su rface of an apple.  They do require an entry point in order to 
infect.  Conidia merely contaminating the surface of fruit at harvest will not play a part in any future 
latent infection.  Those infections will already have  taken place, as is known in the European context, 
either through the calyx end, stem end or under very rare circumstances through open lenticels, 
because in very wet climates the lenticels on the fruit are actually open, en abling spores to enter. 
Dr Latorre  
435. Well, on my experience conidia cannot multiply on the surface of the fruit, and they can only 
survive maybe for a very short period of time, de pending on weather conditions of the environment 
where they are.  So in this terms I agree complete ly with what Dr Swinburne has expressed right now.  
There is no data showing that conidia can really surv ive for a long period of time outside the host, on 
the surface of the host, in this case on the fruit,  nor that they can multiply on clean fruit. 
Australia  
436. We actually have a follow-up question to that.  It actually involves a comment by 
Dr Swinburne, but we are happy for Dr Latorre to comment on it as well.  To make asking you the question most efficiently, it might be useful if I ju st ask my colleague to distribute a document, which 
is an extract from our rebuttal submission, just tw o paragraphs, and we can give it to the Panel as 
well.  WT/DS367/12 
 Page 57 
 
 
  Kirsten Hillman  
437. Perhaps while we are waiting for that document to be distributed, we can offer Dr Deckers an 
opportunity to comment if he has any comments he would like to make. 
Dr Deckers  
438. I would like to add here one comment on th e infection of the apples.  We see in some 
varieties in our production condition, that use of gibberelins is interfering with the open calyx end of 
the fruits, which sometimes allo w the fungal infection of the Nectria  in these fruits.  So there is some 
interference sometimes from the use of some plant growth regulator PGR treatment. 
Australia  
439. So, apologies for that short delay.  Just thought  it might be more efficient if the experts had a 
hard copy of the relevant bits of their submi ssion before them.  And since it is a methodological 
question, I will hand over to my colleague Dr Barry from the CSIRO. 
440. Professor Swinburne, in your responses you state th at at several of the importation steps the 
IRA emphasizes the risk of superficial contaminat ion, but omits reference to any opportunities for 
these to convert to infections.  Paragraphs 497 and 498 of Australia's rebuttal submission addresses 
this apparent misunderstanding of the methodology a nd that's what is being distributed now.  Are you 
able to offer any clarification in relation to yo ur initial response, in light of this material? 
Dr Swinburne  
441. The majority of fruit infections in the European context are to be found either at the stem end 
or the calyx end, and generally speaking it means that  the core has been inf ected.  The time at which 
that infection occurs is currently be ing investigated.  We have had a shot at it in the past, as well.  But 
it is surprisingly early on in the fruits development.  It isn't at the time of harvest, it isn't in the dump 
tank.  That core rot is taking place at some stage wh en either the calyx or the stem end is enabling an 
entry point for conidia which are washing down over the surface of the tree and either accumulating it in the stem well or going around and entering the calyx.  I don't have any information which would 
ever suggest that infestation of apples at harvest, a nd I stress that point, or even after harvest leads to 
any significant level of rotti ng in commercial conditions. 
William Ehlers
 
442. The discussion just now sort of reminded me of a statement by Dr Paulin, concerning fire 
blight, when he said more or less that spread by fru it was no higher than by any other natural means.  
Does that apply in this case also? 
Dr Swinburne  
443. Could you elaborate just a little bit. 
William Ehlers  
444. What I understood from the statement by Dr Paulin was that, if you are trying to decide 
whether the pest has spread through one way or anot her, the fact that it was by fruit or by any other 
natural means was virtually indistinguishable.  So I was asking if that kind of situation applies here, 
too, by what you were saying where in the mature  fruit there was no infestation and it only comes 
from the mother tree to the fruit and not to anothe r fruit from another tree and that sort of thing. 
Dr Swinburne  
445. Yes, the fruit will be infected from the mother  tree by cankers which are on that tree and 
probably by no other route, so that the quiescent inf ection with which it carries into store is carried 
from the orchard. WT/DS367/12 
Page 58  
 
  Australia
 
446. Apologies.  I actually neglected to ask Dr Lato rre for his response to the previous question 
which Dr Swinburne had answered. 
Kirsten Hillman  
447. Dr Latorre, would you like to answer Australia's question? 
Dr Latorre  
448. The question that was raised just raised before? 
Australia  
449. That's right.  The infestation leading to infection question. 
Dr Latorre  
450. Infestation of the fruit?  Excuse me. 
Australia  
451. This relates to those paragraphs 497 and 498 of our rebuttal submission. 
Dr Latorre  
452. Well, infestation of the fruit means that the i noculum arrives from the fruit.  But in order for 
the fruit to be infected, I mean really colonized by the pathogens, you have to have some other 
conditions at the same time.  There are some weat her requirements that are very important, but more 
important than that, you have to have a susceptible hos t and you have to have injuries.  Otherwise, the 
infestation means nothing, that is the end of the inoc ulum.  It will not survive for a very long time.  
Kirsten Hillman  
453. If I may follow up then back to the document that Australia has circulated to us.  In paragraph 
498,  Australia has stated about four lines down, th at at each of the steps (p icking, transport to the 
packing house, processing and transport to Australia), at each of these steps, there is the potential for 
the surface infestation to lead to infection.  Any su ch infection may remain latent for some time.  And 
just to make sure I understand correctly did you say,  Dr Latorre, that in your opinion in fact the 
infection doesn't last for very long? 
Dr Latorre  
454. What I have said is that the infestation doesn't last very long.  Then you move to infection, 
which means that you already have a relationship be tween the pathogen and the host, it could last for 
very long if the pathogen is already inside the fruit. 
Kirsten Hillman  
455. Dr Swinburne? 
Dr Swinburne  
456. Can I follow up on that same paragraph?  It says that "it is well known that 
infestation/infection of fruit in the dump ta nk…"  I should add, that is not necessarily Nectria  that we 
are talking about.  It is well known for a numbe r of other pathogens that cause rot, notably Penicillium 
expansum , the blue mould rot.  When that gets into the dump tank, you do have trouble. 
Dr Latorre  
457. One brief comment I want to make in this sense is that Nectria  moves from one place to the 
other, long distance movement, primarily by nurseri es stock, in our opinion, and fruit rarely.  I doubt 
if somebody has proof that really infected fruit can  be the cause of the development or new focus of 
European canker in a new area.  WT/DS367/12 
 Page 59 
 
 
  Kirsten Hillman  
458. Let me move on, if I may.  One final question,  before I am finished for now.  This is in 
relation to the responses to Questions 69 and 70, regarding the relevance of perithecia on rotting 
mummified apples to the spread of European canker.  Here Dr Deckers, Dr Latorre and Dr Swinburne 
have all replied to these questions, but the responses see m to differ from each other, at least in part.  
We would appreciate if you could, if you care to , comment on any of these differences between your 
responses. 
Dr Latorre  
459. The only comment that I can make is that, in my experience perithecia only occur under 
certain conditions and most often they are not impor tant from the epidemiologic point of view.  The 
development of the disease is associated to the pr oduction of the asexual spores, namely conidia, but 
not to the production of the sexual part of the f ungi, which is the so-called production of perithecia 
and ascospores. 
Kirsten Hillman  
460. Dr Swinburne, do you care to comment? 
Dr Swinburne  
461. As I have said, perithecia;  I have never seen th em on rotted fruit.  I would dearly love to have 
done so, because for experimental reasons to have b een able to obtain single ascospore cultures at will 
would have been great fun.  So I don't think th e ascospores would ever form an important part if 
apples rotted with Nectria  in a foreign country.  I have already mentioned about conidia.  Conidia can 
form on a rotted fruit.  Quite often when a fruit rots, pa rticularly if it happens to be on the cheek of the 
apple from the lenticel, the peel will crack and b ecome almost paperlike and through that small crack 
you will get the formation of conidia.   You have to remember the fungus is in, it has got to get out, 
and it's only when the only actual surface of the fruit breaks that the conidia will form and they form 
in relatively small numbers under such circumstances, that's on the fruit. 
Dr Deckers  
462. I would like to add just a comment from the climatological side of this type of possible 
infection.  Maybe climatological conditions fo r this further development of the disease by 
conidiospores is rather unlikely in most areas of Australian conditions. 
Chairman  
463. I will ask a few questions in this area as well.  In its rebuttal submission New Zealand argues 
that Chinese Taipei has a domestic apple industry, i ndividual apple trees and many of the alternative 
hosts for European canker, that the climatic cond itions in the central mountainous regions mean that 
Chinese Taipei is at relatively high risk for Europe an canker establishment and spread, and that they 
are comparatively more favourable to the developm ent of European canker than mainland Australia.  
Please indicate whether this affects your responses to Question 44 on the relevance of New Zealand's experience with apple exports to Chinese Taipei.  I notice that Dr Deckers and Dr Paulin responded to 
Question 44. 
Dr Paulin
 
464. Yes, my answer to Question 44 was referring to  fire blight exclusively, so I was just 
underlining some important differen ces between apple growing conditions  in Taipei and other regions 
which make the risk of introduction of fire blight far less dangerous in Taipei.  I think that these 
reasons are mainly the scarcity of host plants, ev en if you have some indeed, and the remoteness of 
the orchards, which are all in the mountains, that means in the centre of the island and far from any 
commercial establishment which could process apples from abroad. WT/DS367/12 
Page 60  
 
  Dr Swinburne
 
465. I find it very difficult to answer questions like this, because you are being asked why did 
something not happen.  There can be a huge range of reasons why so mething like this did not happen, 
starting with the volume, starting with the possibility that within that volume there were no infected 
apples, ending with the possibility that a few infected apples arrived in the wrong place and couldn't 
possibly present the infection.  Otherwise, it is really rather an unanswerable question. 
Chairman  
466. We can take that to a couple of the other questi ons we are trying to deal with here, but thank 
you for that Dr Swinburne.  Any further comments on that.  If not I am going to move on to another question to Dr Latorre and Dr Sgrillo.  In your repl y to Question 84 you indicate that in your view the 
IRA's conclusion on the mean infection infestation rate  of apples has not been validated for this pest.  
Please explain what validation means in this context? 
Dr Sgrillo
 
467. Well, validate in this context would mean to  sample fruits from Ne w Zealand that were 
processed with the same processing that would be done with the fruits to export and to check out what 
infection rate they would have.  If they find someth ing that's around this percentage, it is okay, so you 
have to make a plan and to sample enough number of fruits with this statistics:  means, confidence 
level and things like that.  And this is because again, as in the model for Erwinia , the parameters of 
each hypothesis were not validated, so the genera l one, I mean the final number, could not be 
validated. 
Dr Latorre  
468. Validated means to estimate whether your model is really explaining the real situation, at least 
it is trying to estimate whether the model explained was in reality what happens.  That's it. 
Chairman  
469. I am going to ask one last question and I think th en what we are going to do after this last 
question is give you an early coffee break, for an objectively justifiable reason.  My next question 
would be that Australia indicates that the relevant CABI data sheet explicitly states that one of the 
plant parts liable to carry the pest  in trade transport is fruits.  Pl ease explain the relevance of such a 
datasheet for a risk assessment and can such a datash eet be considered scientif ic evidence, specifically 
the CABI datasheet.  Anyone want to comment on that? 
Dr Swinburne  
470. I wish someone was here from CABI to answer. 
Dr Latorre  
471. Well, I just want to say that this is a genera l statement that does not necessarily apply to each 
pathogen or pest.  In this case, in my opinion, it does not apply to Nectria galligena .  It is really true 
for other pathogens, Penicillium, Botrytis  and several others, but this is not the case for European 
canker. 
Dr Swinburne  
472. I did write the CAB documentation on Nectria  that is in the latest publication.  I didn't write 
the leaflet. 
Chairman  
473. I detect a distinction in your response.  Any further comments on this particular question, 
perhaps.  Australia.  WT/DS367/12 
 Page 61 
 
 
  Australia  
474. If I could I might just get my colleague from Biosecurity Australia, just to clarify a point with 
respect to that CABI datasheet, which was specifically for Neonectria galligena . 
475. The CABI datasheet that we are referring to do es specifically say that apple is a means of… 
and I am just wondering whether either of you could clarify whether that is wrong.   
Dr Swinburne  
476. If I had a nasty tendency, I could bring an apple which is infected by Nectria  from New 
Zealand into Australia and I would know how to inocul ate it.  So I suppose to that extent an apple can 
carry an infection, but whether it is a natural path way is an entirely different story.  There is no 
evidence anywhere in the literature, except in the stray remark appare ntly in the CABI datasheet, that 
fruit is a pathway. 
Chairman  
477. I suggest we break now and according to my watch it is twenty past four.  Let's break for 20 
minutes, if that's alright and we will see you back here in 20 minutes. 
_______________ 
 
Chairman  
478. I think we can continue, if you are ready.  I am going to ask Mr. Ehlers to take four last 
questions from us on this matter. 
William Ehlers  
479. This might have been answered in part, but I think it bears asking anyway.  Australia argues 
that surface infestation is the necessary fi rst step leading to fruit infection with Nectria  and that thus 
Importation Steps 3, 5 and 7 deal with infestation and infection.  Would you care to comment and indicate if your relevant response would be any different in light of this argument? 
Dr Swinburne
 
480. I do beg your pardon.  I am afraid other matt ers were happening when you were asking the 
question.  Could you repeat that? 
William Ehlers  
481. Australia argues that surface infestation is the necessary first step leading to fruit infection 
with Nectria  and that thus Importation Steps 3, 5 and 7 d eal with infestation and infection.  Do you 
have any comment?  Would this argument impact your answers in any way? 
Dr Swinburne  
482. I think this point was perhaps covered in earlie r questions.  Obviously, for fruit to become 
infected the inoculum – the conidia – has to wash down over the surface, which might be described as infestation.  But it does not, I believe, apply post -harvest, I am talking about pre-harvest events. 
Dr Latorre
 
483. I understand.  This comment doesn't change my opinion.  I think infestation is the early step, 
but the most important step is penetration, colo nisation and so on, which means infection, whether 
this occurs in the Step 3, 5 and so on, is another question. 
Mr William Ehlers  
484. I don't see anyone else asking the floor on this.  New Zealand. WT/DS367/12 
Page 62  
 
  New Zealand
 
485. Dr Latorre, if I might draw your attention to a quote that you made, in response to Panel 
Question 77, where you said that "the likelihood that these spores might contaminate fruits superficially is extremely rare, and the probability that spores contaminating the surfaces of mature 
fruits will cause infection is negligible.  In conclusion, fruit contamination with spores of N. galligena  
during picking and transport to the packing house should be disregarded.  There is no scientific 
evidence on this subject to strongly support this hypo thesis".  My question is, would this still be your 
view? 
Dr Latorre
 
486. Yes, certainly. 
Dr Swinburne  
487. Inevitably, fruit harvested from orchards with no or  very low levels of infection will be most 
unlikely be infected themselves and therefore it w ould be an appropriate measure to be taken. 
William Ehlers  
488. Let us move on to the next one.  This is perh aps a repetition of one that I asked earlier on, but 
I am asking it in the three pests, just to make sure we  get it right or at least get answers for all three.  
Are there any points where in your view, Australia's IRA, through its design and methodology, or with respect to consideration on specific step s, may have underestimated the likelihood of 
importation, establishment and spread of Europ ean canker through the importation of apples. 
Dr Latorre
 
489. I did not see any situation where they  underestimated the situation. 
Dr Swinburne  
490. This is still my view. 
William Ehlers  
491. Anything else? Okay. Let us move to the issu e of alternative measures.  New Zealand has 
proposed two alternative measures in respect of European canker, namely: restricting imports to 
apples sourced from pest-free places of production, to be determined by a single inspection of each 
exporting orchard and maintained through controls on the subsequent movement of nursery stock;  
limiting imports to apples sourced from areas of low-p est prevalence, to be determined by inspection 
of sample of orchards. Please comment on whet her these alternative measures would achieve 
Australia's appropriate level of protection? 
Dr Latorre  
492. In my opinion these are appropriate measures th at can mitigate the possibility that infected 
fruit can carry the pathogen fro m New Zealand to Australia. 
493. I agree.  I didn't find anywhere where there was underestimation. 
William Ehlers  
494. If I don't see any other parties wishing to take the floor then I will hand back to the Chair. 
Chairman  
495. We had a question, which we ha d dropped thinking that it had been answered, but it might be 
a question simply of typographical error. I will read it in  full.  It is to Dr Latorre.  In your response to 
Question 49, in the last paragraph it says: "T o my understanding, the challenged requirements 
imposed by Australia were based ma inly on the possible occurrence of  latent fruit infection, but not 
on endophytic infections.  The possibility that  clean fruits may be infected from inocula  WT/DS367/12 
 Page 63 
 
 
  contaminating epiphytically mature fruits in dum p water in packing houses… is negligible and 
irrelevant".  So the question is really to that sen tence where you talk about latent fruit infection, but 
not endophytic infection.  Is there a difference?  What are the differences between those two terms? 
Dr Latorre  
496. In my opinion, there would a difference in the way of how the fruit gets the pathogen inside. 
Chairman  
497. Was the quote correct?  In other words, the comp arison was between latent fruit infection, but 
not on endophytic.  That was a correct quote and a correct...  Yes, okay. 
Dr Swinburne  
498. Endophytes are usually regarded as being ca rried symptomlessly and that there is no 
interaction between the organism and the host in which it is endophytically spreading.  In quiescent 
infection, there is damage done to a small number of cells invisible to the naked eye, but in which the 
tiny lesion, in which the fungus is actually arrested, it is stopped from growing.  That is what happens 
in a quiescent infection. 
Chairman  
499. I think we have exhausted our questions for the moment on European canker and would like 
to offer New Zealand the opportunity of asking any questions they might have. 
New Zealand  
500. No questions for the moment. 
Chairman  
501. Australia. 
Australia  
502. We do have a number of questions, some ques tions relating to the probability of entry, 
establishment and spread and then, as I said, a series of questions on climate.  So we can just kick 
those off now, if it is convenient.  A short qu estion for Dr Swinburne and Dr Latorre, could you 
please confirm in light of your written responses that you accept that N galligena  occasionally causes 
latent fruit infection in New Zealand. 
Dr Swinborne  
503. Inevitably, I have absolutely no first-hand know ledge that would lead me to give you a proper 
answer to that question.  There would appear to ha ve been a number of reports, and it is reported in 
hearsay, and I would be surprised if it never happened,  in those localities in which canker is said to be 
prevalent.  But, having said that, I don't even know  how prevalent it is in the areas in which it is 
present. 
Dr Latorre  
504. Canker on Gala could be possible.  However, weather conditions are absolutely needed in 
order to have infected fruits.  If that doesn't ha ppen, the possibilities are zero, or very, very low, 
negligible.  Maybe it never happens. 
Australia  
505. I will just hand over to my colleague Mr Heinrich, from Biosecurity Australia. 
506. Dr Latorre, in your written response to Questi on 76, you made the following statement: "The 
reasoning in Australia's IRA with respect to the possibility that latent infections of N galligena  may 
occur in mature New Zealand apple fruit and not b ecome apparent until after storage is based on WT/DS367/12 
Page 64  
 
  published information…  [I]t is possible to assume that latent infection may occur if fruit rot caused 
by N galligena  were to occur.  There is always a concer n that fruit rot can further develop in cold 
stores.  It is true that IRA relies on scientific research about latent fruit infection in the UK and 
Nothern Europe, but differences between New Zealand and Northern Europea can only be expected in 
relation to the likelihood of this event".  Can you please elaborate on this response. 
Dr Latorre
 
507. I was only trying to say there is a possibility ther e.  Fruit can be infected if conditions are 
adequate.  However, most of the information that  I remember from the statement made by the IRA 
related this with research being done in Northern  Europe, where weather conditions are completely 
different and by the time this experiments were done ot her varieties were prevalent.  So there is also a 
chance that varieties susceptibility may play a role here.  That was the idea, the main idea in this 
paragraph. 
Australia  
508. We have a follow-up question for you, if we may.  In your written response to Question 65 
you stated that:  "Considering that fruit rots occur in  New Zealand… and despite the fact that this is a 
very rare event, latent infection in mature fruits ca nnot be ruled out.  It is possible that asymptomatic 
but infected matured apples could develop sympto ms and eventually sporulate during transit and 
commercialization in Australia".  Could you pl ease confirm that this is still your view? 
Dr Latorre  
509. The possibility cannot be ruled out.  The question is how frequently this is going to happen.  
In those terms, I still have the same opinion. 
Australia  
510. We just have one further question for Dr La torre. In your written response to Question 69 you 
stated that: "Based on published scientific informati on, Australia assumes that fungal growth and fruit 
rot resume when fruit is removed from cold stor age, sold to consumers and stored at room 
temperature.  Therefore, rotted fruits discarded ne ar susceptible hosts could be potentially (but not 
necessarily) a source of inoculum (mainly conidia) fo r infections in new areas. This conclusion is 
acceptable..." Could you please elaborate on that? 
Dr Latorre  
511. It is impossible to negate the possibility that an infected fruit from Ne w Zealand to Australia 
carrying the pathogen cannot develop rot symptoms . Eventually, it can probably develop spores on 
the surface, if weather conditions are adequate.  o,  this possibility cannot be ruled out. However, I 
insist, another situation is how fre quently or which is the probability that that biological event could 
happen under the conditions in Australia. 
Australia  
512. That concludes our questions on the probabilit y of entry, establishment and spread.  We 
would like to now, as we said, ask them  questions in relation to climate. 
Chairman  
513. I note that New Zealand would like to make an intervention. 
New Zealand  
514. Just before we move on to this new area relati ng to European canker, we have a question we 
would like to ask relating to what we have been di scussing.  Dr Latorre, I just wanted to go back over 
some of the quotes that you have been commenting on.  I can't recall the order, but if we start with 
Question 65 where you confirm that it is possible that asymptomatic but infected mature apples could 
develop symptoms and eventually sporulate durin g transit and commercialization in Australia.   WT/DS367/12 
 Page 65 
 
 
  "However", and this is to continue the quote, "I  would consider the probability of this event as 
extremely low to negligible".  I was just wondering if that is still your view. 
Dr Latorre  
515. Yes, I haven't changed opinion. 
Chairman  
516. Australia, would you like to continue on the climate? 
Australia  
517. One of the common threads running through New Zealand's case on European canker is the 
alleged unsuitability of Australia's  climatic conditions for developm ent of this fungal pathogen.  
Australia now has a series of questions on this issu e, which it would like to explore with you.  These 
questions draw on the climate analysis that was unde rtaken by the Bureau of Rural Sciences, which 
are annexed to both our first written submission a nd our rebuttal submission;  Annex 2 in both 
submissions.  As this is quite a technical area and involves some c limate charts, we would like to use 
the audio visual equipment, and my colleague, Dr Barry, when he is not writing chapters on Monte 
Carlo methods, he leads a team as was mentione d at the CSIRO researching new approaches to 
environmental monitoring and modelling and over the l ast decade he has published a variety of papers 
involving climate analysis in biological invasion literature.  As a result, I thought it might be useful if we get him to run through some of this climate analysis. 
Chairman
 
518. May I just enquire?  You are talking about materi al which has already b een made available.  
Your intent is to provide it in a visual format for us leading to a question or to questions. 
Australia  
519. Absolutely right.  There is no new material here , it is all contained in our written submission.  
It is just a matter of talking through the charts, so it is easier for people to follow the discussion. 
Chairman  
520. It sounds alright from the Panel's point of view .?  Technically, how do we go about this now? 
Australia  
521. The first couple of questions don't require audio vi sual, so if you like we can run with those.  
We have brought paper copies if our PowerPoint di es on us.  Dr Swinburne and Dr Latorre, could you 
please advise the Panel whether there is any one  universally accepted epidemiological model for 
predicting the world locations where European canker would establish? 
Dr Swinburne  
522. The complete model that would enable a climate to  be assessed has yet to be developed.  It is 
inevitably rather more complicated than, for exampl e, a climate model for wheat rust or some such 
airborne pathogen.  Around the world, in Chile  and East Malling and elsewhere some of the 
parameters of that model have been evaluated, but it has not yet been put together in a joined-up form 
that would enable a new climate to be fully assessed .  But one can make certain judgements, perhaps, 
based on the various components that we already know. 
Dr Latorre  
523. I have to say there are only two situations, one  in Chile and another in the UK, where the 
biology of this pathogen has been expressed in a model.  With the primary idea of estimating the 
infection conditions, or the conditions for the fungus to infect the host, in this case. WT/DS367/12 
Page 66  
 
  Australia
 
524. As a follow-up question to both, you are saying that the parameters can potentially change 
from location to location in terms of what can predict canker development? 
Dr Latorre  
525. In the case of the model proposed in Chile, it is  based on the conditions needed by the conidia 
to infect the twigs or the stems of the apples, as primarily based on weather conditions, humidity and 
temperature conditions. 
Dr Swinburne  
526. There are two main differences in the locati ons in which European canker occurs.  The 
differences are based mainly on water and, in par ticular, on leaf wetness and the frequency of leaf 
wetness.  I use the word "leaf wetn ess" when I don't really mean leaves, but we tend to talk about the 
surface of a plant remaining wet for periods of time and we use the term "leaf-wetness periods" just to 
cover that.  In a location such as Northern Ireland, which represents an extreme environment in which 
apples are produced, there are no dry periods at all.  Ra in falls fairly evenly throughout the year and in 
some locations on every day of the year.  Models u sed to predict, for example, the other disease of 
apples, namely apple scab, fail to work properly in Northern Ireland because normally in Kent and in 
Europe, for example, an event of 8 hours leaf wetn ess duration of a certain temperature would trigger 
an alarm which would send out the fungicide spraye r, but in Northern Ireland such a Mills period 
might last for seven weeks.  As a consequence of that, in Northern Ireland inoculum of Nectria for 
infection is available constantly.  In other locations , and I am thinking here of  California in particular 
where we have had some data, and to a more limite d extent to Kent, perhaps more extremely to New 
Zealand, you have very pronounced dry periods and very few, relative to Northern Ireland, days of 
leaf wetness.  It is that difference which ma kes a difference in the pulse of the disease.  The 
availability of the inoculum in relation to those leaf -wetness periods is crucial.  They are virtually 
absent as a problem in Northern Ireland because the inoc ulum is always there.  But in a location such 
as California, and I am assuming also New Zealand,  that pulse is interrupted by pronounced dry 
periods, particularly during the summer months.  So , the cycle of events would differ between those 
two locations. 
Dr Latorre  
527. A brief comment, in addition to what Dr Swinburne has said.  Weather conditions are also 
very, very important during summer time for inoculum production and then for inoculum 
dissemination, infestation (as mentioned before), an d finally infection.  In some places of the world 
where apples are produced, like Chile, California and Ne w Zealand, summers are very dry, no rain at 
all. If it ever happens, there are very short rainy periods and not enough to fulfil perhaps inoculum 
production. 
Australia  
528. The next question we have here relates to the two-page extract from the BRS analysis 
attached to Annex 2 in our rebuttal submission and the question is reasonably long, so we have given 
a hard copy of the question in order to assist you and my colleague Dr Barry will address it too. 
529. This is addressed to Dr Swinburne and Dr Latorre.  Annex 2 of Australia's rebuttal 
submission contains a further detailed climate analys is undertaken by the Bureau of Rural Sciences 
(referred to as BRS from here on in).  As part of th is analysis BRS asserts that there is some debate 
about the exact temperatures and rainfall for conditions  required for infection and spread of European 
canker.  BRS illustrates this by outlining differen ces between the papers:  Grove (1990);  Lolas and 
Latorre (1996);  Latorre et al. (2002);  and New Z ealand’s Beresford and Kim model.  BRS concludes 
that the different findings in these studies indicate that successful European canker infection occurs 
over a range of temperature and associated rainfall, with lower instances of infection associated with, 
but not prevented by, sub-optimal conditions.  BRS also notes that the Beresford and Kim criteria of  WT/DS367/12 
 Page 67 
 
 
  30 per cent rain days and temperatures of between  11 and 16 degrees Celsius for more than eight 
hours represent the more restrictive end of require ments in the debate about the temperature and 
rainfall combination required for infection.  Are you able to offer any general observations on the 
research findings that successful European infection occurs over a range of temperatures and rainfall, 
with lower instances of infection associated with , but not prevented by, sub-optimal conditions? 
Dr Swinburne  
530. Can I begin by trying to answer that by drawing attention to the piece that you sent around 
before and in particular to draw your attention to the second paragra ph, which contains a particularly 
important error?  On the last sentence, "On de veloped cankers, ascospores and conidia are present 
throughout the year".  That is incorrect.  The key feature, which you have omitted from your attempts 
to identify the appropriate climate, is that you ha ve not allowed for inoculum production.  Without 
rainfall, you will get no spores, even in Northern Ireland, if you have about 10 or 15 dry days, the 
existing perithecia and sporodochia releasing the coni dia take some time to get underway to start 
releasing again.  It is a period of time.  But, for the benefit for the Panel, I should point out, a point 
which is not totally understood.  The sexual stage,  the ascospores are produced in little flasks.  These 
grow superficially on the surface of the canker.  The asexual spores, the conidia, are produced on little 
cushions that are also superficial on the surface of  the canker.  For the pr oduction of both of these 
structures, you need surface water.  Water coming fr om the inside of the tree doesn't seem to count.  
You need wetness for both of those structures to form .  So, it is incorrect simply to look at leaf 
wetness temperatures concerning how long it takes to get a leaf scar infected by the inoculum, you 
have to get the inoculum in the first place.  And, if you have a long, dry summer you will not get the 
inoculum formed.  We know from California that normally they do not produce perithecia on their 
cankers because the period of leaf wetness is too sh ort, even though they have a high volume of rain 
but in a relatively short period of time.  This is wh y the regional differences in the models need to be 
taken into consideration.  Leaf scar infection data  alone cannot describe the model.  Volume of rain 
would not describe the model either.  It is the dura tion of leaf wetness and th e only approach we have 
to that, is the number of rain days in various loca tions.  That is what was in the Beresford and Kim 
model, which was rather closer to what  one would expect to happen in nature. 
Dr Latorre  
531. I would like to indicate that perithecia are pr oduced only under certain conditions, apparently.  
And, those conditions are correlated with rains.  In our observations we need very frequent rains, 
maybe over 2,000 millimetres a year, in order to be ab le to find some perithecia formation.  However, 
conidia are produced in areas with less rain falls a year. 
Australia  
532. If I could ask my colleague to bring the slide of figure 10 from Australia's first written 
submission, the BRS.  Dr Swinburne, in light of  your written response to Question 72, could you 
please confirm that you accept on the basis of New Zealand's Beresford and Kim model that "the 
climate of the coastal cities of Melbourne and Sydn ey could marginally support infection in spring 
and autumn".  In terms of the pictures that are here, the bottom is the percentage of days with rain and 
I think there is daily temperature ranges in the Beresford and Kim model in that order. 
Dr Swinburne  
533. Given that the area in the immediate neighbourhood of Melbourne has 125 rain days a year, 
relative to a 175 in Western Tasmania and 125 in th e Albany area of Western Australia, I would say 
that the immediate environs of Melbourne could, if it was raining as it is today in Melbourne, allow 
canker to develop, but not if you had that very prolonged drought that  Melbourne has suffered prior to 
today's date. WT/DS367/12 
Page 68  
 
  Australia
 
534. Dr Latorre, you also appear to accept on the basis of New Zealand's Beresford and Kim's 
model that "areas potentially conducive to European canker establishment were detected in Australia".  
Could you please confirm this? 
Dr Latorre  
535. Based on the information you have presented, it is  potentially possible in the autumn, winter, 
just by looking at the rainy conditions of this area.  I have to say that the other parameters have to be 
taken into consideration before you're sure of a real  risk of infection.  Summer time appears to be 
unsuitable. 
Australia  
536. Could I just ask my colleague to bring up th e slide of figure 6 from Australia's rebuttal 
submission, Annex 2 BRS.  Dr Swi nburne and Dr Latorre,  Annex 2 of Australia's  rebuttal submission 
contains a further detailed climate analysis undertak en by the Bureau of Rural Sciences.  One of the 
main findings of this analysis was that there are Australian commercial apple-growing regions, i.e. the 
Adelaide Hills region, and Australian port cities, Melbourne and Sydney, that meet the infection 
requirements for European canker specified in New Zealand's Beresford and Kim model.  Are you 
able to offer any observation in relation to this asp ect of BRS's climate analysis?  Before you answer, 
I might just add:  there are four different charts re lated to this, so we might just cycle through all of 
them so you can see the relevant data from the chart.  This one relates to winter.  If we start off with 
spring you can see this top right-hand quadrant, M = Melbourne;  L = Landswood which is an area in 
Adelaide Hills.  In summer there is a Landswood data  point in that top right-hand quadrant and if we 
move through to autumn, you have Melbourne an d Landswood again and Sydney on the margins.  
Finally move through to winter, you can see Sydne y, Landswood and Melbourne on the margins.  I 
must emphasize that we are using New Zealand's Beresford and Kim analysis. 
Dr Swinburne  
537. I don't know how much of the fruit growing area that actually represents.  Assuming that you 
have applied the Kim-Beresford model, I would sugg est that there is a possibility for canker becoming 
established, perhaps not through fruit, but through so me other route, like inf ected planting material, 
which is the most likely route that you will ever get canker. 
Dr Latorre  
538. It is difficult to provide a good answer by just a first look at this information.  I would be 
suspicious that some potential for European canker exists in some years and locations where you can 
fulfil conditions for infection, provided inoculum  is present and the host is susceptible, which not 
necessarily may occur in winter time, for instance,  when you have the most canker development.  
Most of the good weather conditions that occur in some locations, occur in winter time, which is not 
the best time of the year for canker development. 
Australia  
539. Dr Latorre, just to confirm in that in the top quadrant autumn, which is the highest risk of 
infection, that there are areas of Australia that meet the Beresford and Kim requirements in autumn? 
Dr Latorre  
540. Sure, you have some places where conditi ons appear to be potentially favourable. 
Australia  
541. My colleague, Dr Barry has a further question for both Dr Latorre and Dr Swinburne. 
542. A 1999 paper reports on significant fruit infecti on during summer in Southern England, East 
Malling in Kent.  However, New Zealand's Beresford and Kim model suggest that the summer  WT/DS367/12 
 Page 69 
 
 
  climatic conditions in East Malling in Southern E ngland are not suitable for European canker and that 
the fruit rot phase is only important for Northern Ire land.  What conclusions can be drawn about New 
Zealand's climate analysis from this failure to pr edict that East Malling's summer climatic conditions 
are suitable for fruit infection?  Up on the scree n is figure 3B from New Zealand's first written 
submission, Beresford and Kim Annex.  To explain,  you will notice from there that East Malling is in 
the bottom quadrant, not the top quadrant which is  the Beresford and Kim acceptable parameters 
quadrant. 
Dr Swinburne  
543. Since we are talking about East Malling, I better respond to that, I suppose.  We are enjoying 
a good summer this year.  The last previous two year s have been very wet and we do have alternating 
periods of time when it's conducive to fruit infec tion in summer and not conducive to infection in 
summer.  In other words, East Malling does have a marginal problem with fruit rotting and if it's bad 
it's in the order of 5 per cent of the fruit becomes infected.  The contrast, of course, is Northern 
Ireland, where the very first stores that I visited in  the '60s to determine what the problem was, the 
volume of rotting was 85, because the rain had been going continuously.  I need to add, of course, 
something which needs to be taken into considerati on.  The Northern Ireland situation was caused by 
canker brought about by the introduction of refrigera ted, sealed, controlled-atmosphere, stores.  Fruits 
stored in barns never rotted with Nectria . 
Dr Latorre  
544. Perhaps the only comments I can make from these charts now, is the situation in the Chilean 
condition, called Talca, which appears there being favourable in summer time for infection.  That 
could be true, because in some years they get some  rainy periods in the summer time.  However, I 
have never seen any apple been rotting in any orchard that I know in this area.  Maybe this is because 
inoculum is not being produced.  Weather cond ition for inoculum production may not be fulfilled 
with this conditions immediately.  Or, maybe they are fulfilled to produce one conidia, but that conidia of one hectare of apples means nothing.  Perhaps that explains why people producing apples 
in this region, that region in Chile, and are ne ver concerned about the possibility of apples being 
rotting with Nectria .  Not even when they store apples for a very long period of time, maybe six 
months or more.  However, if you move perhaps to a more rainy season area in the Southern part of Chile, eventually you may have, after maybe a coupl e of rains in summer time some infections.  
Why?  Because, during the rest of the year, inoculum  is being produced, being active.  You don't have 
only one canker per hectare, but maybe several per h ectares, where the inoculum can be produced.  It 
is very difficult to make a judgement in a minut e here about what could be the conditions of Nectria  
in Australia or any other place, just by looking at this information alone.  I would be very willing to 
make other comments later on if its needed, if I ha ve the time to review some other information. 
Australia
 
545. New Zealand's climate analysis also fails to predict that Sonoma County in California is 
suitable for infection in summer, yet according to McCartney (1967), high frui t infection occurred in 
the 1965 outbreak.  Could you please comment on this failure of New Zealand's model? 
Dr Latorre  
546. I am sorry, but I don't have any comments on So noma.  I know the area, which is quite dry in 
the summer time, and they do have canker.  But to my knowledge they are not concerned about apple 
rotting in California.  This doesn't mean that eventually they may have  one fruit in the whole 
production of the year, maybe. 
Dr Swinburne  
547. Models are based on means and averages.  You ar e talking here about singular events and I 
think this is not something any model can actually cope with. WT/DS367/12 
Page 70  
 
  Australia
 
548. That is the end of our questions about climat e.  We have a related consequence question 
which we can ask now or wait for our New Zealand co lleagues to respond to that and ask later.  We 
will be guided by you. 
Chairman  
549. New Zealand, do you have anything on this climate issue first? 
New Zealand  
550. We do have a couple of questions and I will ask my colleague to pose those. 
551. This is to both Dr Latorre and Dr Swinburne, a bout whether it is scientifically justifiable in 
your views to use weather data from particular years selected in a non-objective manner and using 
criteria in the case of the earlier charts, using Be resford and Kim versus va rious locations in all 
seasons, selecting weather data from wettest and dr iest years, which bear no correlation to the 
variables that are being tested which are moderate temperatures or percentage rain days as against hours between 11 and 16 degrees.  Is  that an appropriate method? 
Dr Swinburne
 
552. I didn't quite follow the nature of your question.   What is it you are trying to get a comment 
on? 
New Zealand  
553. The question is:  Whether it is scientifically jus tifiable to predict risk using weather data from 
particular years.  In this instance, selected accordi ng to criteria, wettest and driest years, which bear 
no correlation to the variables against which it is being tested, and whether you have a view on that? 
Dr Swinburne  
554. If that data relates to a particular year as oppo sed to prolonged multi-year means, then that 
wouldn't be justifiable.  But that is multi-year mean s, isn't it?  I need to ask that question myself, 
before I can answer.  Are those multi-years mean s or are they taken from particular years? 
Australia  
555. They are taken from particular years – the wettest and driest years. 
Dr Swinburne  
556. One would like to see them done for minimum of 10-year means. 
Dr Latorre  
557. I was almost at the point of saying the same thi ng.  This is an exercise to begin the analysis, 
but certainly if you want to raise a conclusion out of  this, it would be very dangerous.  You have to 
review a fair number of years before you make a conclusion. 
Australia  
558. If I could add that this may be an issue that New Zealand and ourselves may wish to discuss 
in the next two days. 
New Zealand  
559. We have no other questions re lated to climate, though when we come perhaps to the 
conclusion of the discussion of European canker we may come back with a question or two, but not 
on climate.  WT/DS367/12 
 Page 71 
 
 
  Australia  
560. Dr Swinburne, in light of the discussion we ha ve had about climate and noting your written 
response to Question 60, could you please confirm that you could accept that the IRA team's assessment of consequences of European canker is objective and coherent, if it were demonstrated 
that there are areas of Australia, including major apple-growing regions lik e Landswood and Adelaide 
Hills, with climatic conditions conducive to European canker. 
Dr Swinburne
 
561. Based on the observation of where your fru it growing regions are, taken from your 
submission, and noting that it lies within the band  with less than a 100 days rainfall on average per 
year and perhaps nearer to 50.  I think the con sequences of an infection event within your fruit 
industry would not have as large a damaging effect as  you had claimed.  That is essentially what I said 
then and I reiterate it now. 
Australia  
562. We have a few extra questions on consequen ces, which we can ask now or wait for our 
colleagues from New Zealand?  We can go ahead?  This question to both Dr Latorre and 
Dr Swinburne, Australia's appropriate level of pr otection is expressed as providing a high level of 
sanitary or phytosanitary protection aimed at reducing risk s to a very low level, but not to zero.  As an 
island continent, Australia is free from many of th e world's serious agricultural pests and diseases and 
it takes a very robust approach to post-border biosecuri ty to maintain this favourable pest and disease 
status.  This is evident by the rigorous eradica tion programme that we put in place following the 1950 
Spreyton disease outbreak in Tasmania, as well as the 2004 outbreak of citrus ca nker in Queensland.  
Such programmes typically involve measures su ch as extensive surveys throughout Australia, 
application of chemical treatment s, disruption of transport arrange ments, removal of significant 
number of commercial orchard trees, removal of native plants.  Do you accept that Australia's particular circumstances in this regard were a rele vant consideration for the IRA team in arriving at a 
conclusion that consequence of European canker w ould be moderate?  We note that this can be 
contrasted by the high rating assigned to fire blight. 
Dr Latorre
 
563. Certainly, you have some experience that this information is useful for Australian people and 
to estimate the consequences.  But based on the ge neral overall information in the world, in my 
opinion European canker is an important disease, bu t it is not a limiting factor for apple production, 
nor is it a limiting factor for commercialization outsi de Australia.  At least this hasn't been the 
situation that I can speak of, in the Chilean produc tion.  We do have this problem in part of the 
country, that farmers can really address, and so far as I know, it has never been a real problem or been 
a reason for not to commercialize the fruit properly, adequately, in most of the international or local 
markets.  In this regard, I tend to disagree with the moderate conclusion on consequence that you have 
arrived at.  However, you may have different data that maybe can support this conclusion. 
Dr Swinburne  
564. I am really trying to think this one through.   The Tasmanian outbreak, which you referred to, 
with the amount of effort that you went to, to re move infection, has caused me subsequent to writing 
my submission, to think about that particular instance  quite a lot.  I note that it didn't spread to native 
plants, but I did note that you had an enormous diff iculty in getting rid of it, in spite of constant 
pruning and cutting, and so forth.  Even though you had no inoculum, there was no spore production.  
What I should have said in my original submission,  which only dawned on me subsequently, is that 
that infection was imported with the trees that you planted on that occasion.  Those trees were almost 
certainly infected when they put were in the groun d.  The desperate difficulty that you had in getting 
rid of it from those individual trees was because it was semi-systemic infection.  In fact, the infection 
was moving through the tree inside.  Although you cut off a canker there, you were astonished to find 
another one appearing on a branch over there.  But it had not spread from there to there directly, it had WT/DS367/12 
Page 72  
 
  gone the other way, it had gone, as we now recognize, semi-systemic infection and that clean planting 
material is crucial to the prevention of canker.  So long as yo u keep Australia's quarantine system 
going for new cultivars or new root stocks and make sure that the nurseries that produce the 
commercial trees are screened absolutely, I don't thin k Australia will have a particular problem from 
canker spreading by the airborne route.  A question which has also haunted me since I have put the 
pen down, is why don't you have it?  Why isn't Euro pean canker there already?  Because you have had 
apple trees for a very long time and you must have had canker delivered to your doorstep in the form 
of trees that you had brought on to the continent.  It disappeared.  That is a question which has also 
engaged me. 
Australia
 
565. Thank you for bearing with us through this afte rnoon.  We have one final question.  My next 
question is to Dr Latorre and Dr Swinburne.  A nnex 3 of Australia's rebuttal submission compiles a 
range of statements from New Zealand, Europe, Nort h and South America, attesting to the fact that 
European canker has serious consequences.  Are you able to offer any comment in relation to this 
material.  We have just handed out a copy  of that Annex for a reference to everyone. 
Dr Latorre  
566. Is this a question related to the last inform ation, Annex 3?  For those who are not plant 
pathologists in this room, I have to say that ther e is a big problem with plant pathologists.  In the 
sense that they tend to consider th eir work as the most important and most serious of anything in the 
world.  In doing so, we tend to over emphasize the importance of some diseases.  I think I make 
myself that mistake too, sometimes.  In reality, di seases are very important, this is true.  The question 
is, is this a limiting factor by which the farmers or the country cannot produce a certain commodity?  
Speaking on European canker, this is not the case.  It has not been  the case in any place in the world 
where this disease has arrived, as far as I know.  I would like to take the opportunity to make a short 
comment about Dr Swinburne's last answer.  Just to emphasise that the only way that I can see how 
Australia can get European canker, really, is by th e commercialization, international transportation of 
nursery plant material.  Perhaps this has been the way how this disease has been moved around the 
world.  I have seen no possibility that in reality fru it can really be the cause or be the introduction, 
establishment and spread of the disease in a new area.  You can introduce Nectria  on apples, but the 
other question is whether this disease is going to  be established in a location from the inoculum 
arriving on fruits.  So, I am not surprised about the comments in Annex 3.  If you look in the literature, normally it is called "a major disease of apple". 
Dr Swinburne
 
567. There is one area that I know particularly well where canker does re-shape the apple industry, 
is of course Northern Ireland.  There they grow  this cooking variety, called Bramley Seedling, 
because it has a measure of resistance and in fact  it's one variety in which the pathogen never goes 
systemic.  It is a very localized branch-to-branch di stribution.  It can be very damaging.  It can follow 
certain events, as has happened in Sweden.  If you ge t very severe frost damage where bark splits, you 
have got a huge area available for infection.  An infection on a massive scale can take place.  But, I 
think I also have to agree with Dr Latorre, we do in writing our grant applications point out that the 
disease we are working on could end civilization as we know it.   
Australia  
568. I would like to thank you both for their patience in  going through that material with us this 
afternoon. 
New Zealand  
569. I am aware of the need to move on, but we just have one or two final ques tions.  The first is to 
follow up to the discussion we have been having about consequences, we would like to ask both 
Dr Latorre and Dr Swinburne, whether it is relevant  or appropriate to compare consequences in one  WT/DS367/12 
 Page 73 
 
 
  part of the world, e.g. Northern Ireland, with cl imatic conditions extremely conducive to the disease, 
but which are not necessarily the same as in Australia? 
Dr Latorre  
570. If I understand correctly, yes.  The effect of the disease may vary from place to place 
depending on weather conditions, for instance. 
Dr Swinburne  
571. I think most of the fruit growers in Northern Ireland would give their right arm for an orchard 
in either New Zealand or Australia. 
New Zealand  
572. Just one final question directed to Dr Swinburne , in the first instance.  Your answers with 
respect to New Zealand's proposed a lternative measure, which is to en sure that apples are limited to 
mature export grade apples, appear to be directed at  the risk of the arrival of latently-infected fruit per 
se.  The measure New Zealand is proposing as an altern ative, that measure is aimed at the risk of 
apples providing a pathway of entry, establishment and spread.  As I understand from your responses 
today, such risk is vanishingly small.  Could you confirm that view? 
Dr Swinburne  
573. There is an absence of what I would call "surve y data" on the nature of the various pathogens 
that may or may not be responsible for rotting fruit  in New Zealand.  But from what little there is, it 
would appear that the frequency of infection with Nectria  is quite low.  But ther e is some confusion as 
to whether or not this is becoming apparent before or after harvest.  I gather from some of the reports 
that rotting has been seen before harvest.  It do es surprise me and it would be of interest today 
whether that would ever actually lead to a progressive  infection, or whether it is just a dry eye rot, 
which can sometimes take place, but which never deve lops further.  I have no data.  There has been 
no data presented on either side, relating to what is coming out of the controlled-atmosphere stores 
three or so months after harvest.  That is the one I would really like to see.  I would imagine the infection frequency would be very low, but I wouldn 't say it would be non-existent.  There could well 
be infections which develop post- harvest two or three months down the line of the store distribution 
chain. 
New Zealand
 
574. Just a follow-up question related to the second a nd third elements, looking particularly at  
establishment and spread, and factoring in your co mments earlier today on establishment and spread, 
in particular related to exposure and transfer to  a susceptible host, whether you have any additional 
comments? 
Dr Swinburne  
575. I don't know that I do have any additional comment s.  A hypothesis:  if one had 100 infected 
apples that arrived in Australia healthy, but beca me rotted subsequently, what would happen to those 
100 infected apples?  Perhaps 70 or 80 of them w ould never develop spores anyway, so it could be 
disregarded.  Then you have to consider where the others might end up in relation to the dispersal of 
inoculum.  In other words, all the processes are a ttenuating all the time down the chain and that is 
what I don't see coming through in the IRA at all.  The longer the apples are st ored in New Zealand, 
the less is the likelihood that an apple infected with Nectria  would be sent to Australia, because it 
would be culled out before it went into the retail-ready pack and went on the train.  So, the attenuation 
process after harvest would be continuous throughou t the transport chain which is not terribly well 
reflected in the IRA. WT/DS367/12 
Page 74  
 
  Chairman
 
576. I think what we have done today, and particularly in this last session, is to quite thoroughly go 
through questions that we wish to ask the experts and certainly the Panel would not like to treat this 
last pest area with any less importance.  We c ould continue for another hour, but the number of 
questions we have will not be concl uded in the next hour.  It would seem to me that it might be better 
not to split up the ALCM discussion into halves.  One option is to continue until 19:00.  Even if we do 
continue, I don't believe we will finish within the hour and I am sure you might have questions 
yourselves.  So the question is do we start now or simply start tomorrow on ALCM.  The experts, I know their answer.  What would the Parties preference  be?  Let me say my preference would be not to 
split it, but we can continue for another hour and th en carry on tomorrow morning, but I am not sure 
whether that is best way to deal with it.  On th e other hand, you might want to do some preparation 
tomorrow morning. 
New Zealand
 
577. We are very much in your hands and I am c onscious of the burden that the long hours have 
been on the Panel, the experts and the Secretariat.  We would be open to continuing on now, but we 
are in your hands. 
Australia  
578. We do have a slight preference for continuing  now, even if only for another hour because 
there is a lot to get through.  If you feel strongly, we can review. 
Chairman  
579. That's fine.  We are available until 19:00.  I know Dr Cross has been sitting patiently all day, 
so I am sure he is also ready to respond.  I w ould like to ask Ms Hillman to start off with our 
questions. 
Kirsten Hillman  
580. These are some general questions and where we have specific questions on importation steps 
we will ask those and then move on to consequen ces and alternative measure s much as we have done 
with the other pests.  The first question we ha ve for you refers to Question 94.  If you recall 
Question 94 is a fairly lengthy question where we  ask for your view as to whether or not the 
evaluation in Australia's IRA for each of those issues mentioned in that question was objective and 
credible and relied on respected and qualified scientif ic sources and was based on available, credible 
data.  Again, as I said a few times today, recognizing  that those scientific sources don't have to have a 
majority of opinion, it can be a minority, but our concern is whether or not they are respected and 
qualified sources.  So, I don't know if you want me to  go through for you the issues that were covered 
in that.  There is quite a list of them.  But, specifi cally we had asked, with respect to each of those, 
whether or not you felt in Australia's IRA the eval uation there was based on credible sources.  We 
would like offer you an opportunity to add anything  there that you might like to add in terms of a 
more definitive conclusion. 
Dr Cross  
581. I think I don't have any specific requirement to alte r any of the things I have said here at this 
stage, but there may be things that come out in sp ecific questions relating to the different parameters.  
There is quite a lot of material here. 
Kirsten Hillman  
582. If we looked at Question 94(i) on the condition of adult emergence of the ALCM, New 
Zealand submits that  its "use of 13-18 days for th e timing of adult emergence… was in respect to the 
minimum time required for adult AL CM emergence, not the range". New Zealand concludes that its 
"position on the maximum length of time required  for adult emergence is consistent with 
Prof. Cross's:  the scientific evidence indicates th at adult emergence could in some cases take a  WT/DS367/12 
 Page 75 
 
 
  considerable length of time, possibly more than  one year depending on conditions". So, we are 
wondering if you have any comments on New Zealand's comment on your response. 
Dr Cross  
583. I think New Zealand's position is that a period of at least 13 days would be necessary before 
any adult leaf-curling midge could emerge.  And, actually in their recent submission had provided 
some more experimental data which seem to support th is.  But that data is relating to fruit that has 
been stored for many weeks.  I think that if a pples had not been stored for a long time, they could 
have pupae on them which could emerge quite quickly  when the apples arrived in Australia.  There 
could be live pupae on those fruits that were near to emergence and if they were exposed to the 
correct conditions they could emerge very quickly, maybe in a space of a few hours or a day or two.  
On the other hand, there will be individuals which require more than one diapause-breaking period in 
order to emerge.  It is conceivable that there woul d be some individuals that might not emerge for a 
year.  I think that the emergence period of the midges could be very protracted depending on the conditions which the fruit has been stored in, and the conditions when it is released into the 
environment in Australia in some way, those conditi ons make quite a big difference.  It would depend 
on the time of year, the temperatures, and what have you.  The period does seem to me to be quite a 
protracted one, of many weeks.  There are publishe d papers which show intervals of eight weeks for 
emergence of adults in spring and even the New Zealand data just submitte d on 2009 experiments of 
Sandanayaka and Rogers show a 2 to  3 week interval over which emer gence can occur.  I think it is 
not possible to be very definitive over the interv al, but we do know it is quite a long time.  I don't 
think threshold temperatures for development have necessarily been worked out for adult emergence, 
but at the time of release into the environment there would have to be conditions suitable for 
emergence and flight of the midge, at some stage. 
Kirsten Hillman
 
584. I will just keep moving on, unless I see signs that  either Party would like to make a comment.  
Following-up, in your replies to a number of questions  you indicated that the existing data or evidence 
was inadequate to resolve certain issues.  For exampl e, regarding conditions of adult emergence, flight 
range, adult life span, etc.  Australia argues that in such conditions it used expert judgement to 
determine the probability ranges for certain steps.  In your view was this expert judgement exercised 
in an objective and credible way? WT/DS367/12 
Page 76  
 
  Dr Cross
 
585. I think we need to look at each of these factors one at a time, maybe taking the flight range of 
the midge.  There clearly isn't very much evidence as to how far the midge can fly.  There is one study I did myself on males that showed they could fly 50 metres towards a pheromone source over a period 
of 24 hours.  But there is another new Zealand st udy that shows that the midge can move in an 
infested plantation in a range of 30 metres a year.  There is no study that shows how far the midge can 
fly.  There is no definitive flight range.  So, it's rather difficult to establish what the flight range 
should be. Obviously the midge is a weak flier. In my view, it is unlikely to be able to fly long 
distances. There is the question of whether it could be distributed by wind over long distances, but there is no evidence to support that is the case.  I fe lt that the Australian IRA in respect to this, which 
suggested that a flight range of 200 metres was not unreasonable and that orchard surrounding the 
wholesale pack houses were often less than these di stances, seemed to be quite reasonable. Yes, 
another area of where there are not sufficient data or only one study was this viability of the insect 
inside occupied cocoons.  Clearly we have this one study by Rogers et al, which has been much 
quoted, where we only have one study which is open to some interpretational difficulties. I felt that 
that viability question had not been adequately ad dressed in the Australian IRA. It didn't seem the 
viability itself did not seem to be taken into account.   So, there are several different factors. Maybe 
some of these things will come up more in individual questions. 
New Zealand
 
586. We have one question.  You stated in your res ponse to Question 94(iii), on page 3, that "The 
distance in Australia's IRA of 200 metres is… not supported by evidence".  Can you confirm that this 
is still your position. 
Dr Cross  
587. Yes, I don't think there is any study showing how fa r this midge is able to fly. In the study I 
did, the maximum distance investigated was fifty metres. I did not look at distances of 200 metres, 
and I only looked at males attracted to a pheromone  source, which is not the same situation as a 
female being attracted to a host plant in the ab sence of other surrounding host plants. As far as I 
know, there is no study that has investigated that s cenario, where the mated female midge has to fly to 
find its host. All we know are some things about tho se types of midges in gene ral.  They are rather 
weak flyers.  This particular species spends a lot its time close to the ground and only flies up into the 
tree to oviposit in the shoots when the wind conditions are rather slight.  So, it seems unlikely that it 
would have a very long range of dispersal. I think it would be unlikely that it could fly many hundreds 
of metres.  But I felt that the 200 metres distance was not totally unreasonable. It doesn't seem to me 
to be an impossible distance for this midge to fly. 
Kirsten Hillman  
588. Still on Question 94, in paragraph 4 regarding climatic factors in respect to ALCM spread, 
you conclude that "Australia's IRA was objective and credible, but did not draw sufficiently on 
available information and did not conduct a suffici ently detailed analysis".  Could you elaborate a 
little bit on that. 
Dr Cross  
589. This is the climatic conditions.  I don't know ve ry much about the climate of Australia, but 
clearly there are certain climatic requirements for th e midge's survival and we do know that it doesn't 
occur everywhere in the world an d there are parts of the world where apples are grown and the apple-
leaf curling midge doesn't exist.  In Europe, where it seems to have reached its equilibrium position, it 
doesn't occur in the Southern Europ ean areas of Southern Spain, in Italy South of Naples.  Similarly, 
over in the United States it doesn't occur in the more  southerly areas. I think the thing is that it needs 
cool temperatures, a sufficient accumulation of cool te mperatures in winter to break diapause. Unless 
diapause is broken, the emergence in spring is not synchronized properly.  In areas that don't have a 
sufficient period of cool in winter the midge cannot exist.  I am questioning whether those limits have  WT/DS367/12 
 Page 77 
 
 
  been established in Australia.  If you look at a worl d map of where the midge exists, it doesn't seem to 
occur in latitudes much less than about 38°. I haven't investigated this thoroughly, but clearly in these 
warmer areas there are not sufficient cool temp eratures in winter and that limit has not been 
established in Australia by a climatological analys is. Similarly, the midge also needs reasonably 
regular summer rainfall.  Although it can clearly survive droughty periods for a year or two, drought 
conditions in summer do not favour it all and it need s reasonably regular summer rainfall in order for 
it to be a successful species and it doesn't occur in ar eas of the world that are dry. A great example of 
this is Washington State where West of the Cascade Mountains, where there is quite a lot of rainfall, 
the apple-leaf curling midge exists.  But to the East of that mountain range, there is an arid area where 
there is little summer rainfall in the central summer m onths, and the midge doesn't exist.  Presumably, 
because there is insufficient moisture for it to comp lete its development. So, I am suggesting that a 
study needs to be done of these factors and it n eeds to be established where in Australia the 
climatological conditions exist for the midge based  on its known distribution throughout the world. 
Kirsten Hillman  
590. If  we could ask for a follow-up response to Ques tion 95.  The question is this:  In your view, 
are the probability values chosen for the potential entry and establishment of the ALCM in the IRA 
sufficiently supported by scientific evidence? 
Dr Cross  
591. I think we are fortunate there is some data on the incidence of the apple-leaf curling midge 
cocoons that are occupied by larvae or pupae.  I think we do have some reasonably good data on 
which to base that part of the analysis.  I felt that the August 2005 data provided by New Zealand, 
which showed the incidence of the midge on four  and a half million apples over a period of four 
years, gave some quite good indication of the sort of  likely infestation level.  Beyond that, there are 
the questions of what percentage of those cocoons c ontain viable larvae or pupae. It must be stressed 
that I believe that those are occupied cocoons and th at data does not relate to empty cocoons.  Beyond 
that, the viability of those cocoons needs to be ta ken into account and parasitism, and an important 
factor is the rather protracted emergence of the mi dge in relation to its very short life-span.  If the 
midge is only able to survive for a couple of days  in the natural world and the midges are emerging 
over a period of 3, 4, 5, 6 weeks or maybe up to a year, then the chances of  the establishment of the 
infestation are very significantly reduced.  In my  opinion, those three factors were not really 
adequately taken into account in the analysis. 
Kirsten Hillman  
592. In its comments on expert responses New Zeala nd notes that you may have confused export 
bulk bins and harvest bins in your replies to  Question 98 and Question 101.  Did you have any 
comment on this?  Just for clarification. 
Dr Cross  
593. Yes, I may have done that.  I was unsure whether bins that are used at harvest would ever be 
used and sent to Australia.  I cons idered that possibly the fruit might be harvested in New Zealand and 
that the harvest bins could be sent there before re -packing.  So there may have been some confusion 
there.  This is an unlikely practice possibly.  Perhaps the Parties could say what they think. 
Kirsten Hillman  
594. We'll have lots of time to chat with the Par ties tomorrow.  Next question relates to Question 
120.  In your reply to Question 120 you state that:  the "unrestricted risk estimation" in the IRA 
"needs to be re-calculated for sever al reasons".  Does this imply th at in your view the conclusion in 
the IRA that the inspection of a 600 fruit sample fr om each import lot would not achieve Australia's 
accepted level of protection? WT/DS367/12 
Page 78  
 
  Dr Cross
 
595. I am unable to do the risk assessment...  Well, perh aps if I tried, I might have been able to do 
it, but I didn't attempt to do the risk assessment calcu lation.  I just note that some of these important 
factors had not been taken into account in the IRA.   Once we have been through the viability, the 
parasitism, the protracted emergence and the number of  apples that have to be disposed of within the 
range of female flight of apple trees, and the mode of trade.  All those things are very important 
factors and they haven't been taken into account in an adequate way in the IRA in my view.  If the 
IRA is re-done, it might be found that the unrestricted risk assessment comes out to below the ALOP, but I don't know whether that is the case or not.  Th e exercise needs to be done.  If the risk assessment 
shows there is a risk above the ALOP, then a samp ling procedure needs to be, the size of the sample 
needs to be, calculated to reach th e ALOP.  It should not be calculated to demonstrate that New 
Zealand apples have got apple-leaf midge.  It should start at the point of preventing the risk.  I didn't go through that exercise myself because I think th at is something that Australia needs to do. 
Australia
 
596. We should just like to ask a question following-up on your remarks, and in respect of your 
written replies where you did indicate that the probab ility of entry, establishment of spread for ALCM 
may be reduced if fruit waste was enclosed so that  adult midges could not escape and if all apples 
were held in cool chain conditions until sold to consumers.  Our understanding is that your comments 
about the reduction in probability were conditiona l on whether waste would be so enclosed and 
whether apples would not be distributed to orchard p acking houses.  It would be useful if you could 
clarify that point.  And, also, you would be aw are that Australia and New Zealand disagree about 
whether apples would be distributed to orchard pa cking houses and also as to how apple waste is 
managed in Australia.  Could you  expand on your written comment that the potential risks would be 
higher if large numbers of fruit were held in ambient temperatures in the vicinity of an apple orchard. 
Dr Cross  
597. Yes, I think that this is sort of self-evident, exactly that.  If large volumes of apples are packed 
or graded and there is waste fruit from that process and it is disposed of or held in the vicinity of apple 
orchards, within less than 200 metres of the site that  this is occurring, clearly those apple fruits could 
potentially have a low incidence of infested or occupied cocoons on them and a small number of 
midges may emerge and they would have a higher chance then of being able to make it to the nearby apple orchard.  Clearly, the way the fruit is handled  in Australia seems to me to have a very large 
effect on the risk.  If that happened, I think the risk as demonstrated in the IRA would be probably 
quite substantial.  If large numbers of fruit were disposed or held quite close to orchards and not in 
refrigerated conditions, then I think there would be a substantive risk.  But if that doesn't occur and 
fruit is retail-ready and sold in small quantities to i ndividual consumers, then the risk is, in my view, 
greatly reduced because it is unlikely that large numbers  of apples would be disposed of or held close 
to an apple tree. 
Chairman
 
598. Could I follow-up with a question more on transp arency, perhaps.  In commenting on your 
responses to Question 113,. Australia submits that " pursuant to the recommendations of the Final IRA 
Report, there will be no 600-unit inspection by AQIS on arrival  in Australia, because the 
consignments are to be pre-cleared  in New Zealand".  In your view is that fact clear from Australia's 
IRA? 
Dr Cross  
599. I was uncertain as to whether a second inspection would occur.  Clearly, that's an important 
point.  That's not something that I can really determine myself. 
Chairman  
600. But, from the IRA, it was not clear to you whether there was…  WT/DS367/12 
 Page 79 
 
 
  Dr Cross  
601. I was in doubt as to whether or not it would occur, or not, and how effectively it would be 
done;  whether it would just be a cursory inspec tion or whether it would be a thorough 600 randomly 
drawn sample, that it's supposed to be, if it's a proper inspection… 
Chairman  
602. Maybe just a related question.  In your view , is the IRA clear on the relationship between 
pre-clearance and the procedures to be applied to New Zealand apple fruit? 
Dr Cross  
603. Sorry, say the last bit again. 
Chairman  
604. Is the IRA clear on the relationship between pre- clearance and generally the procedures to be 
applied to New Zealand apple fruit? 
Dr Cross  
605. It may be clear, but I may not have understood it fully. 
Chairman  
606. Okay.  Let me move on to a question related to importation step 2.  According to Australia, 
cocoon viability is taken into account through its  use of a triangular distribution for importation 
step 2.  In its rebuttal submission, New Zealand argues that taking viability into account should have 
shifted the entire distribution.  Would you have any comment on this statement? 
Dr Cross  
607. Yes.  I believe that's the case.  I think the most likely value for the importation step 2 should 
perhaps be the one that is given as the general mean  in the August 2005 data, which is .16 per cent.  
So we do have this quite good estimate for this ce ntral value.  Maybe the minimum value is very 
small, perhaps negligible.  And perhaps the maximum value should be the greatest level of infestation 
that has been detected in lots in  recent years.  I think there's some data from New Zealand exports to 
California, which shows some values of about 5 per cent infestation in some of those lots.  I'd have to 
check the data.  That would appear to be the sort of range of data values that should be used, in my 
view.  Clearly, if you had a viability of 50 per cent, it would shift the whole lot, you know, one way.  
It wouldn't just alter the upper value or the lower.  It would shift the whole lot.  And similarly with 
parasitism.  And I don't think that that c hoice of values has reflected that properly. 
Chairman  
608. Let me move on to another question, in the light of your response to question 111.  And this is 
more relating to step 3.  Is it your view that the IRA over-estimates the probability that apples are 
contaminated during picking and transport to the packing house? 
Dr Cross  
609. I think we don't know what proportion of the contamination of the fruit arises at different 
stages in the growing process.  I personally believe th at the amount of contamination that would occur 
during the harvest process would be a rather sma ll proportion of the amount that would arise during 
the earlier part of the whole growing season.  But th ere is clearly a low probability that larvae could, 
when the fruit is picked, that they could fall onto th e fruit as the fruit is picked, and that would slightly 
increase the risks.  But I don't know how you woul d quantify those values an d the values chosen, I 
don't know on what basis.  Here, (10-3, 5 x 10-2) uniform, I don't know how those were chosen, those 
values, or whether there's any study that shows what would be appropriate values.   But all this is in a 
way taken into account, because of the end point in spections data actually includes both components 
anyway. WT/DS367/12 
Page 80  
 
  William Ehlers
 
610. There is something that is baffling me a little b it.  That's probably because I don't understand.  
So I'd like to just quickly go back to one of th e earlier questions, which is the range of flight.  
Because, if I understood correctly, even though there is  very little study that can really confirm all of 
this, at least one study that you have done had a limi t of about 50 metres for males being attracted by 
pheromones. 
Dr Cross  
611. It wasn't a limit.  It showed that the midg es could fly 50 metres, but that was the longest 
distance investigated.  And that was attracted by  a pheromone source, which is different from the 
female being attracted to its host plant.  And we  don't know whether males and females have a similar 
flight range. 
William Ehlers  
612. And which is the stronger of the two, do we know? 
Dr Cross  
613. Well, I think it's a powerful life force, the fema le finding where to lay its eggs is pretty 
important to it.  You know, I don't know that we have any evidence to say that the flight range of the 
females is shorter or longer than the males.  We don't have information on th at.  They have a bigger 
body weight, but then again they are stronger insects.  They are slightly larger, stronger insects. 
William Ehlers  
614. So these factors, then, help me to understand better why your estimation of 200 metres is 
reasonable, because of the stronger attraction to find ing a place to leave the eggs, and because they are 
stronger animals… 
Dr Cross  
615. No, not necessarily a stronger attraction, it's that we don't know how far the females can fly.  
There is no good data that gives you some sort of statistical distribution of how far a midge can fly in this particular instance.  We have very little data.  All we can do is sort of observe the midge's habits, 
and the way it lives, and think that probably long range dispersal of this midge is rather unlikely.  It's 
a weak flyer.  But the 200 metres assumption of the Australian IRA seemed to me to be reasonable…  
It wasn't out of court.  It might be wrong, of course.  It might be wrong by a factor of several fold.  It could be that they can fly 500 metres, or something, but we don't have any better data. 
William Ehlers
 
616. I was trying to contrast, you know, the 200 with the 50 and the fact that they stay on the 
ground a lot and rise according to how the wind help s them and that.  But now I understand better, 
with what you've said.  So let me go back to our list of questions.  In the light of your response to question 112, is it your view that the IRA's analys is at importation step 3 appropriately takes into 
account the potential availability of sufficient flushe s of leaf growth suitable for ALCM infestation 
during harvest in New Zealand, given that later grow th flushes may be stimulated by irrigation or wet 
seasonal conditions? 
Dr Cross
 
617. Well, I think that, clearly, apple trees can be gr owing at harvest.  It depends on the weather 
conditions, how much rainfall there has been, how vi gorous the orchard, how many shoots there are.  
But apple leaf midge infestations can go on beyond harvest.  And it tends to drop off because, as the 
fruit gets bigger, the shoot growth of the trees tends to shut down.  So, the probability decreases, but it 
most certainly can happen that there is shoot growth  in apple trees at harvest, which is attacked by 
apple leafcurling midge, which is reaching its mature state larva stage, ready to go, fall from the tree,  WT/DS367/12 
 Page 81 
 
 
  and then infest the apple.  And that's certainly the case.  I don't think either Party disputes that.  So 
what is the angle that you're trying to elucidate? 
William Ehlers  
618. I think you've covered it with your answer.  In  your reply to question 101, you indicate that 
the basis for the values given in  the IRA at infestation step 3 for the likelihood that clean fruit 
contaminated by ALCM during the picking and transport to the packing house, is not clear. 
Dr Cross  
619. So this is the risk that clean fruit maybe th en subsequently infested from leaf material 
attached to that fruit at harvest? 
William Ehlers  
620. Yes, if you…  The question originally said  please comment on whether the consideration in 
Australia's IRA of the likelihood of entry and establishment of ALCM, through mature apple fruit 
from New Zealand, was objective and credible, relyi ng on respected and qualified scientific sources 
with respect to the possibility that clean fruit could be contaminated by ALCM during picking and transport through any leaf material. 
Dr Cross
 
621. I think there is a rather small risk that this coul d occur.  Most of the leaf material attached to 
fruits would not be growing shoots that harbour the leaf galls.  They would probably be too old and 
would be unlikely to harbour apple leaf midge.  Bu t you can't exclude the possibility that there might 
be some young shoot material amongst that at harvest.   So there is a risk, but I would think the risk 
was rather small.  But particular values have been chosen here, (10-3 to 5 x 10-2), so particular values 
have been chosen, and I was just questioning what was the basis for those values and how they were 
chosen.  I don't understand how they were chosen. 
William Ehlers  
622. We were following exactly that line.  So would that mean that, in your view, the analysis is 
not sufficiently supported by the scientific evidence? 
Dr Cross  
623. Well, the choice of values, I would say, is not supported by scientific evidence, because the 
basis for the choice is not clear.  There has been no study of what the likelihood is going to be.  So 
these values appear to have been picked to help making the calculation as a whole.  I don't know what 
basis on which they've been picked, the particular valu es.  All I can say is that I believe that the risk 
will be rather low from this step. 
William Ehlers  
624. Okay.  I don't see anybody asking for the floor, so  I'll move on.  Does – and this refers to 
importation step 6, that's the likelihood that AL CM will survive palettisation, quality inspection, 
containerization and transportation – does the pape r by Rogers et al (2006) support New Zealand's 
contention that only 15 per cent of ALCM cocoons contain live pupae? 
Dr Cross  
625. Why is this particularly relevant to importation step 6? 
William Ehlers  
626. Yes.  The reference was to Australia's second s ubmission, paragraph 622, so I'd have to look 
for that. WT/DS367/12 
Page 82  
 
  Dr Cross
 
627. This is back to the question of the viability of  the larvae, in the cocoons.  We have this one 
study of Rogers et al, which shows – I have to get the exact figures out – I think it's 25 per cent of occupied cocoons contained viable larvae.  So this particular study showed that three-quarters of the 
larvae were not viable.  So we have this one snap s hot of viability, and we have very little data to go 
on.  But I believe it is a very significant factor, looking at the different lots of apples in the Rogers 
paper, there was quite a range of values given for the different lots.  And the highest viability among 
those different samples was 50 per cent.  In the ab sence of any other information on this factor, one 
would think that perhaps a conservative estimate of 50 per cent would be a sort of reasonable 
compromise.  But we need more data.  I notice th at in the recent papers from New Zealand, again 
there is some information on this Sandanayaka an d Rogers paper of 2009, which does again seem to 
support this rather low viability percentage of…  If you look at the data itself, I'd have to go back to it, 
but I think only about 20 per cent of the larvae in co coons, having been stored for at least ten weeks, I 
have to say, in cold store, were actually viable.  So we do have perhaps two or three sources of data 
that show that not all the larvae in these, all th e insects in these cocoons, are viable, and that a 
substantial proportion of them are not.  And clearly that needs to be factored in. 
William Ehlers
 
628. Okay.  But I notice that all the numbers you are using are above the 15 per cent. 
Dr Cross  
629. Yes.  I have to go back.  There is a difference between the percentage of the whole sample 
and the percentage of the ones that were occupied.  I' d have to get out the paper by Rogers et al., but it 
is clear in there that, I think I've got it the right way round, that the 25 per cent is the viability of the 
occupied cocoons.  And it's occupied cocoons that ar e the – the incidence of occupied cocoons – that 
occurs in the August 2005 data.  So perhaps we should just think about the viability in occupied 
cocoons. 
William Ehlers  
630. Okay.  Let's move on.  Question 94(i).  Regarding the conditions for adult emergence of 
ALCM, you wrote:  "Unless evidence to the contrary  is produced, Australia's IRA relating to this 
issue was objective and credible and relied on limited  scientific evidence available.  However, an 
important point is that longer period of adult em ergence would substantially reduce the likelihood of 
small numbers of individuals in a consignment emerging within a few days of each other, and being able to mate and lay eggs to start an infestation. "  So does this last sentence imply that the IRA has 
overestimated the risk, as New Zealand implies in its rebuttals submission? 
Dr Cross
 
631. Yes, it does.  Clearly, that long protracted period of emergence with a short life span 
substantially reduces the risks.  If they all emerge d on one day, there would be a much higher chance 
of them being able to find each other and mate and go off and find their host plant.  But a male 
emerging on day one is most unlikely to meet a female emerging on day seven, say.  So, no 
calculation has been done.  I believe it would be pos sible to make a reasonable statistical calculation 
of the factor by which this risk is reduced.  Bu t I believe that this prolonged emergence period does 
reduce the risk several fold.  A simple consider ation of a three day life span and a three week 
emergence period would clearly reduce the likelihood of small numbers of males and females being 
able to meet for the purposes of mating, it would be  substantially reduced sev eral-fold, even in that 
rather narrow consideration of just  a three week emergence period. 
William Ehlers  
632. All right.  Getting back to climatic conditions.  In question 94(v), you wrote that "Climatic 
conditions in SE Australia, which have been exceptiona lly hot and dry, have been quite unsuitable for 
ALCM survival".  WT/DS367/12 
 Page 83 
 
 
  Dr Cross  
633. Yes.  I understand there's been a period of drought  in the South-East part of Australia, maybe 
for up to a decade.  And there have been long periods without regular summer rainfall.  The apple leaf curling midge does need summer rainfall to survive, to  thrive.  We know that in my country that we 
get dry periods, the population of the midge reduces  greatly.  I think the same experience has been 
found in New Zealand, that the midge is favoured by  wet weather.  It's most troublesome in areas 
where there is a wet climate.  Northern Ireland is one of its worst epicentres.  And the places where it 
is truly a serious pest problem tend to be wetter ar eas.  So I question whether an area where there has 
been a prolonged period of drought could support, or the apple leaf midge could survive in those 
areas.  But maybe that's in the last ten years.  And then there's the longer term considerations over 
what period should we consider the risk.  If y ou looked at the long-term data, for 25 years or 
something, it may be that there is adequate rainfall in many of these areas. 
William Ehlers
 
634. Yes.  Well, in that context, New Zealand says in its rebuttal submission that the only area in 
Australia that is prone to the es tablishment of apple leaf curling midge is Tasmania.  Would you agree 
with that? 
Dr Cross  
635. Well, I haven't done the climatic analysis and I think it is important that a proper climatic 
analysis is done to look at maybe the ten year av erage, which is the drought period, and the longer 
term.  Who knows what the future climate is going to be like, but that has a profound bearing on the risk.  I haven't done a climatic analysis, and a clim atic analysis hasn't been done of other areas of 
Australia, in the South, where there may be adequa te rainfall, and cooler conditions, where it could 
survive.  Maybe in the southerly areas.  So, yes, my limited knowledge of the climate of Australia would lead me to believe it could survive in Tasmania .  I think an analysis needs to be done to see, to 
demonstrate whether it could, what other areas it coul d occur in.  I think, overall, the vast bulk of the 
territory of Australia has an unsuitable climate fo r apple leaf curling midge.  And it's only in these 
very southerly areas where there's adequate rainfall, that it poses a risk.  And that clearly should have 
quite a big effect on the risk assessment. 
William Ehlers
 
636. I think Ms Hillman will take it up now. 
Chairman  
637. May I ask of the Parties, because we are now at 7 p.m.  Do you have a number of questions to 
Dr Cross?  We have another four.  One qu estion from New Zealand.  Would you have many 
questions?  I am just wondering whether we could spe nd a little bit more time and just finish it.  The 
alternative is to come round tomorrow morning.  I understand New Zealand has one question.  We 
have another four or five questions. 
Australia  
638. In that case, Mr Chair, we may well be able to fi nish in another half an hour.  I don't think we 
have very many on our side. 
Chairman  
639. Are you willing to continue for another half an hour?  Seems so.  Are we happy to continue?  
I should just also note, remember there is a final section, called "Other".  Do you have other questions, beyond this area, because we'd just have  to check whether…  We don't, but you might.  
And New Zealand says no. 
Australia
 
640. We may have one or two, but that would be the maximum. WT/DS367/12 
Page 84  
 
  Chairman
 
641. Shall we give it a shot? 
Australia  
642. I'd like to, if that's all right with New Zealand. 
Chairman  
643. Dr Cross, are you satisfied if we continue for another half an hour? 
Kirsten Hillman  
644. This is a question regarding Question 115.  Th is question addresses the IRA's consideration of 
the likelihood of entry and establishment of ALCM  with respect to whether adult emergence from 
diapause may take place in seasons other than spring.  Now, Australia has interpreted your response to 
that question as largely confirming – and that's a quote from Australia's comments – its position "in 
respect to suitable environmental conditions and emer gence".  Do you agree that  your answer to that 
question largely confirms Australia's position? 
Dr Cross  
645. Clearly, if apples are brought into an environmen t, apples which have cocoons in them, that 
contain post-diapausing larvae, are brought into wa rm conditions, indoors, in a supermarket, in a 
house, or whatever, in winter, or at times when apple trees are not growing out of doors, clearly the apple leaf curling midge could emerge fairly quickl y.  If apples were introduced into Australia in the 
winter in the outdoor environment, the conditions wo uldn't be suitable for emer gence at that time, but 
they would be subsequently, when the conditions  warmed up, the cocoons would still be there 
subsequently.  So can you just rep eat exactly what you want from me? 
Kirsten Hillman
 
646. I think you may have…  et's just have a l ook at Australia's comments…  Australia's 
comments actually don't go into very much more deta il than that, but the question had to do with the 
likelihood of entry and establishment of ALCM through mature apple fruit in seasons other than 
spring.  For example, if the cool chain is broke n and day length and temperatures replicate spring, 
such as in a controlled environment like a supermarket or a packing house, etc. 
Dr Cross  
647. Yes. I agree that that would occur if, you know, that could definitely occur in winter, the 
conditions for emergence could occur.  Or the fruit ma y be disposed of, and they would occur later, if 
the fruit was disposed of out of doors, then when  spring came along the cocoons would still be there 
and they could emerge then. 
Kirsten Hillman  
648. They could emerge, okay. 
Dr Cross  
649. They don't necessarily die after a short period.   They can hang on for a long time in cool 
conditions. 
Kirsten Hillman  
650. That answers our question.  Thank you.  The next question would be in respect of your 
response to question 117, where you stated that Au stralia's IRA was objective and credible in its 
treatment of climatic conditions for the spread of  ALCM in Australia, but then you identified some 
shortcomings.  Both Parties argued in their comments that your reply supported their respective positions.  So we'd be interested in your views on your answer.  WT/DS367/12 
 Page 85 
 
 
  Dr Cross  
651. I think I've already sort of answered this.  Obviously, apple leaf curling midge will only 
spread and cause a problem in areas of Australia wher e the climate is suitable for its existence.  And 
it's only going to be successful where the climate is  well suited.  I mean, there may be marginal areas 
where it can sort of hang on, but not do very well.  And I think that those areas have not clearly been 
established, these geographic and climatic boundary conditions haven't been established, of where 
exactly in Australia this could occur.  As I sai d, this business of latitudes less than 38 degrees in 
Europe, the climate is generally too warm for it.  That  needs to be taken into account in the analysis.  
And I think that that's what I gave in my reply to 117.  And I think I spelt out earlier. 
Kirsten Hillman  
652. Thank you, Dr Cross.  I think that's actually very helpful. 
Australia  
653. Sorry.  Ms Hillman, would you mind if Au stralia asked a question on that point. 
Kirsten Hillman  
654. Not at all.  Please, Australia. 
Australia  
655. Professor Cross, you have indicated that there may have been some shortcomings in the IRA 
in respect of climate and spread, but in your answ ers you did indicate that Australia's IRA on this 
point was objective and credible, and you concluded that the overall assessm ent is correct.  Is that still 
your position? 
Dr Cross  
656. I may have …  Yes, there's a difference betw een agreeing with the conclusions based on the 
methodology used, and thinking that the methodology itself was correct.  I wasn't, perhaps, sufficiently aware;  I didn't comment or I didn't c onsider, I think there's some instances where using 
the methodology used, the conclusions seem to be  reasonable, but I question whether the actual 
methodology was correct overall.  And I think in one  or two cases I may have come to the conclusion 
that, using the methodology, the conclusions draw n were correct, but maybe the methodology used 
was not really itself quite correct.  Perhaps I ought to come to an example of this.  A good example 
would be the impact of apple leaf curling midge, where I think the IRA considered that the impact 
would be severe, or not severe, highly significant loca lly, and this led to a certain score being drawn, a 
C-score if I remember correctly, yet if the conclu sion was different and a D-score was drawn, the 
overall conclusion reached would be the same becau se the methodology used didn't allow for, didn't 
reflect differences adequately in, the methodology di dn't reflect these differences very well.  I haven't 
explained myself very well.  But there could be instances where the methodology used – I concluded 
that using that methodology, the conclusion was good, but maybe I didn't sufficiently draw that there were areas where the methodology perhaps wasn't ta king in the factors into consideration properly. 
Chairman
 
657. Okay.  Dr Cross, in your response to Question 96, in the penultimate paragraph you write that 
the effects of ALCM infestation on skin finish or fruit quality are rare, and that the type of damage 
reported from New Zealand is extraordinary.  Coul d you explain the word "extraordinary"?  We 
weren't quite sure what you meant by that. 
Dr Cross  
658. I have seen photographs – I think quite old photographs of damage – where very heavy 
infestations of apple leaf midge that occurred durin g blossom led to some distortion or effects on the 
fruit quality.  I've never seen or heard of that occurring anywhere else.  And I think it's a highly 
unusual event.  Certainly it does not normally occur in Europe, where the apple midge has been WT/DS367/12 
Page 86  
 
  around for a long time.  So I think that effects of the apple leaf midge on fruit quality would be pretty 
unusual.  And I don't know whether it's been recorded in New Zealand in recent years at all.  It may 
be varietal as well. 
Chairman
 
659. So, the sense you are using it in, it's unusual, extr aordinary in the sense of unusual, rare to 
occur. 
Dr Cross  
660. Yes. 
Chairman  
661. Well, I'd like to come to the Question 120.  There is a disagreement among the Parties as to 
the correct interpretation of your response to Question 120 on the inspection of a 600 versus a 3,000 
fruit sample from each import lot.  There are two qu estions here.  One, does your response imply that 
in your view Australia could achieve its appropriate  level of protection through another measure that 
would be less trade restrictive than requiring a 3, 000 fruit sample from each lot, with a detection 
resulting in mandatory treatment or rejection for export?  And, secondly, does, in your view, the 
alternative measure, i.e. the inspection of a 600 fru it sample from each import lot achieve Australia's 
appropriate level of protection, either by itsel f or only in combination with other measures? 
Dr Cross  
662. Without recalculating the risk assessment incor porating these additional factors, it is very 
difficult to know what sort of size of population would lead to a risk, but exceeds the ALOP.  So I think, in order to answer that question, the IRA need s to be sort of recalculated to determine what size 
of population, what instance of occupied cocoons  would pose a risk above the ALOP and then the 
sample size should be adjust ed to address that risk. 
663. So, I mean, if a 600-fruit sample showed that th ere is a 95 per cent chance of the 0.5 per cent 
of fruit being infested, if half of those fruit are non-viable, another 30 per cent parasitized and, in any 
case, there is only a 1 in 5 chance that the male and female would mate and meet each other in their 
life, then that effective infestation level is reduced by a factor of 10, 20, 30 times, whatever the factors 
are that are determined by doing this risk assessment and then that needs to be applied to the sample 
sizes that are needed.  And I find it difficult to pr ejudge what those sample sizes should be.  Clearly 
one factor that I believe would make quite a big difference to the risk is the mode of trade question.  If 
the apples were retail-ready, ready-packed in smal ler packs, that were not handled at the seven 
wholesalers, that would greatly reduce the risk, mayb e that would overcome the risk all together, but 
until that calculation is redone, it's difficult to decide what the sample size should be.  3,000 fruits, to 
inspect 3,000 fruits is a big requireme nt and would be, I think, quite a restriction on the possible trade.  
It would be very difficult to do, in my view – expensive to do, if it was done for every orchard. 
Chairman
 
664. Let me ask you our ultimate question.  And maybe it has been responded to, but in a more 
general sense.  Assuming that the semi-quantita tive method could be considered a legitimate 
methodology, and you have had some comments about that in one or two of your questions, do you 
believe that the way that the IRA applied this risk assessment methodology to ALCM is objectively 
justified? 
Dr Cross  
665. Could you repeat the question again, so that I can just think about it a bit more.  WT/DS367/12 
 Page 87 
 
 
  Chairman  
666. Sure.  More in a sort of overall sense, if one  assumes that the semi-quantitative method can be 
considered a legitimate methodology.  Okay.  If th at's the case, do you believe that the way in which it 
was applied is, as it has been applied to ALCM, is objectively justifiable? 
Dr Cross  
667. I think the general methodology seems to be okay,  with some problems in it.  And if it's 
applied, including the different factors that have n't been included properly, I believe it will give a 
better and more objective assessment of the risks and s hould then lead to a good consideration of what 
measures would be needed to reduce or mitigate those risks. 
Chairman  
668. Fair enough.  That exhausts our questions.  Not the Panel, but the questions from the Panel.  I 
saw no one wanting to specifically latch onto any of  our questions, but certainly New Zealand if you 
have any questions, please you are welcome to pose them. 
New Zealand  
669. We just have one question and it does actually re late to one of the earlier questions put, it's a 
follow on. 
670. We just have one question, which relates to your  response to 94(v), where you state that  "A 
weakness in the IRA is that Australia failed to quantify (or at least delimit) the geographic range and range of conditions which are necessary for establis hment and spread of ALCM, both in terms of 
temperature and rainfall and their seasonal occurrence.  The geographic and climatic limits were not established."  Can you confirm that is still your position? 
Dr Cross
 
671. Yes.  I haven't yet seen a climatological analysis in relation to where apple leaf curling midge 
could exist in southern Australia.  I don't think the delimiting parameters have been established.  What 
is the winter chill requirement?  It could be some thing like days or hours below 5 degrees centigrade.  
I don't think that has been established and I don't thi nk the number of days of rainfall, or maybe even 
something like monthly seasonal tota ls of rainfall, I don' t think that those parameters have been 
established.  And then, based on that, where those necessary conditions occur for apple leaf curling 
midge to exist in Australia.  I realize that any assessment is probably going to be a crude one, based 
on where the midge occurs elsewhere in the world.  But I haven't seen that analysis, an attempt done 
at that analysis.  And I think that that's quite  an important thing to do for the risk assessment. 
Chairman  
672. Satisfied, New Zealand?  Australia. 
Australia  
673. Australia just has four questions on ALCM if everybody wouldn't mind staying a little bit 
longer.  My colleague, Mr Heinrich, will ask the first question. 
674. Dr Cross, in your written response on ALCM, you commented that there is significant lack of 
data in respect of a number of key matters.  Do yo u think it's fair to stay that there have been 
relatively few studies and reported reliable data on th e ALCM generally, in comparison to many other 
pests of phytosanitary concern? 
Dr Cross  
675. It is surprising that this creature is being th e subject of this concern between the Parties and 
that more good quality studies haven't been done.  For instance, in the 2005 data it would have been 
very good if we'd had some data on the viability of those larvae.  We've only had the Rogers study on WT/DS367/12 
Page 88  
 
  viability.  We have no study on the flight range of females.  There's opportunity to do a great deal 
more good quality studies to elucidate these factors.  And a lot of this would help take some of the guesswork out of the analysis.  So yes, I agree.  I mean, some insects have been quite extensively 
studied, in depth.  Apple leaf curling midge is not one of those.  And it's probably been less well 
studied than some of the other similar members of  the same genus, such as the Brassica pod midge or 
some of the other species. 
Australia
 
676. I have a question in relation to the IRA's evaluation of importation steps 1 to 8 and the August 
2005 data.  Do you agree that the IRA team effectivel y arrived at two entirely separate conclusions as 
to the unrestricted risk on the basis of its two est imates for probability of importation?  That is, one 
based on the analysis of importation steps 1 to 8.   And the other based on the August 2005 data 
provided by New Zealand.  And if you do agree, th erefore, that it made no difference to the overall 
outcome, that the IRA team chose to retain its analysis of the older published data set out in 
importation steps 1 to 8, given that Australia's 3,000 unit measure is ultimately based on the August 2005 data conclusion. 
Dr Cross
 
677. I do appreciate that the IRA did consider those two different data sets.  I find it slightly 
surprising, or rather surprising, that the conclusions  reached were broadly the same given the fact that 
the parameters, I think, varied by a factor of 30 -fold in the central infestation level in the two 
considerations.  So yes, I appreciate that was done.  Could you repeat the latter part of your 
statement/question? 
Australia  
678. I think you've mostly answered the question, but my question related to the fact that the 
measure that was ultimately selected by the IRA team, well, its decision that a 600-unit inspection 
would not be sufficient, was based on its analysis  of the August 2005 data and the infestation level 
that that data provided, as opposed to the infest ation level that they estimated on the basis of 
importation steps 1 to 8. 
Dr Cross  
679. Yes, I appreciate that.  But neither analysis  took into account adequately the viability, the 
parasitism, or the extended period of emergence rela tive to the short life span, and some other factors 
as well. 
Australia  
680. Now my colleague, Dr Barry, has some questions for Dr Sgrillo. 
681. Dr Sgrillo.  I'd like to ask you a question about determining an appropriate inspection rate for 
a consignment in circumstances where it has been dete rmined that the unrestricted risk is above the 
appropriate level of protection, and therefore that  risk management measures are required.  Would 
you agree that the relevant factor for determining the appropriate rate of inspection for ALCM is the 
underlying level of infestation? 
Dr Sgrillo  
682. Yes, I agree.  The infestation will tell you how much you have to decrease this infestation to 
reach your appropriate level of risk.  And also how sensitive has to be your inspection system to catch 
any infestation above this level. 
Australia  
683. Sorry, one more question, for Dr Sgrillo again.  Would you agree that in order to have 
confidence in detecting a pest within a consignment that has low levels of underlying infestation, a  WT/DS367/12 
 Page 89 
 
 
  higher rate of inspection may be required, compar ed to a consignment which had a higher level 
infestation, if so could you explain why? 
Dr Sgrillo  
684. Usually, considering the same population size, if the infestation is higher you have to sample 
less, because …  I mean, if you have more units inf ested in the population, this will require a smaller 
number of samples to catch this infestation.  Howeve r, if you have a very low number, a very low per 
cent of infestation, you have to increase your sample size to catch it. 
Australia  
685. And when you're doing the sampling, what is th e standard statistical level of confidence you 
would consider appropriate when selecting an inspecti on rate?  Is there a typical level of confidence 
that is typically used? 
Dr Sgrillo  
686. I'm not sure if in the IPPC Standard on Inspection Methodology it is specified.  I would say 
that the majority of service that use, I mean a plant sampling technique, will use 95 per cent of confidence level.  But I'm not sure if this  is an international standard or not. 
Australia
 
687. That's all of Australia's questions on ALCM. 
Chairman  
688. New Zealand. 
New Zealand  
689. Just got one final question, and this is a question for Dr Cross.  In your response to Question 
120, on page 22, you state that, in determining the appropriate measure for ALCM, "the sample size 
should not be adjusted to fit the infestation rate whic h appears to be the case in the current analysis.  It 
should be set to meet Australia's ALOP."  Ca n you confirm that this is still your position? 
Dr Cross  
690. Yes, I think it is.  Logically, to me, it seems that  Australia wants to ensure that the amount of 
apple leaf curling midge on the lots of apples that  are coming from New Zealand have lower than its 
ALOP.  And so the sampling should be devised to m eet that requirement and not devised to detect the 
pest on the majority of New Zealand apple samples, which is a different process. 
Chairman  
691. All right.  Done with ALCM?  Well done.  "Oth er".  I think Australia… or have you included 
your other already in that batch of questions? 
Australia  
692. We have one question.  And if I can just go briefly back to the risk assessment process.  And 
this is just a question for Dr Schrader.  Just wanted to ask, would it be fair to say – and this is taking 
into account ISPM No. 11 – would it be fair to say th at, as part of the risk assessment process, there is 
no need to take into account or assess the risk for a pest or disease that does not occur in the 
geographical area for which the ri sk assessment has been conducted? 
Dr Schrader  
693. So you mean, whether you should not assess the risk of an organism which is not present in 
the area you are assessing?  No, of course not, because there is no need to do that. WT/DS367/12 
Page 90  
 
  Australia
 
694. We have no other questions on this. 
Chairman  
695. It would seem to me that we have reached th e end of today's meeting.  And I think what 
certainly – certainly from the Panel's perspective, and I'm sure also from the Parties – today has been 
very enlightening and has assisted us, I believe, greatly .  And it remains, therefore, I think, from the 
Panel's side, just to thank the experts for the work  that they have done up until this point and also 
today engaging with us.  I think it has been certainly very, very useful.  And we'd like to thank you for 
being here.  And for the Secretariat and the Parties fo r continuing until now.  I think it has been useful 
to actually conclude this session today.  It will a llow us a little bit of preparation for what happens 
tomorrow.  And if I understand it correctly we'll be in this room tomorrow at 3 p.m. for the second 
meeting with the Parties.  With that, the meeting is adjourned. 
  WT/DS367/12 
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  Annex 1 
 
Corrections Suggested by Experts 
 
Paragraph 103, Dr. Schrader: 
 
 “Pest free area” should be replaced by “pest free place of production”, as this would be the correct term.   
Paragraph 581, second sentence, Dr. Cross: 
 This is a mistake. Actually the Sandanayaka and Rogers (2009) data appende d in NZ 2nd submission 
do not show that cold storage kills pupae. The apples were artificially infested with mature larvae then 
exposed to 10 weeks + cold storage. There were no pupae. It shows that adult emergence is delayed 
by at least 13 days after cold storage. 
 
Paragraph 589, Dr. Cross: 
 
The first sentence should read: "I think we are fortuna te there is some data on the incidence of apples 
that are infested with  the apple-leaf curling midge cocoons that are occupied by larvae or pupae."  
Otherwise the sentence and the whole section don't really make sense. 
 
Paragraph 654, last sentence, Dr. Cross: 
 
I did not explain this at all well and my answer is perhaps confusing. What I was trying to explain is 
that I assumed that the overall methodology was a recognized /generally accepted one, and the 
conclusions drawn were reasonable.  But there we re clearly problems with the overall methodology. 
 
Paragraph 688, Dr. Cross: 
 
The last sentence should read:  "And so the sampling should be devised to meet that requirement and 
not devised to detect the pest on the majority of New Zealand apple samples, which is not what is 
required ." 
  
_______________ 
  
 WT/DS367/12 
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  Annex 2 
 
Slides Shown by Australia at the Panel's Meeting with the Experts 
 
 
 
 
Aus SWS Annex 2 BRS Figure 
6
Figure 6 Australian autumn (March, April, May) data for wettest and driest years 
between 1998 and 2007.
 
 
 
   WT/DS367/12 
 Page 93 
 
 
  Aus FWS Annex 2 BRS Figure 
10A. Spring
024681012141618
03 0 6 0 9 0
Percentage of days with rainDaily average hours between 11 and 16 degrees Ctemperature = 8 hoursrain day = 30%
Nel10
Ne
Nel9
Mel11Mel10Mel9
Syd9
Syd11Syd10B. Summer
024681012141618
03 0 6 0 9 0
Percentage of days with rainDaily average hours between 11 and 16 degrees C
temperature = 8 hoursrain day = 30%
Nel2Nel12
Nel1
Mel1Mel2Mel12
Syd1Syd12Syd2
D. Winter
024681012141618
03 0 6 0 9 0
Percentage of days with rainDaily average hours between 11 and 16 degrees C
temperature = 8 hours
rain day = 30%Nel6
Nel7Nel8Mel8Mel6
Mel7Syd7Syd8Syd6
Figure 10.  Climatic suitability for European canker establishment in Melbourne, Sydney and 
Nelson using the rainfall and temperature criteria cited by Beresford and Kim (derived from Dubin 
and English 1975). The first three letters of each plotted point represent the locality name (Mel = Melbourne, Syd = Sydney, Nel = Nelson) and the numeric postfix represents the month of the year (where January is ‘1’) for: A. Spring; B. Summer; C. Autumn; and D. Winter.C. Autumn
024681012141618
03 0 6 0 9 0
Percentage of days with rainDaily average hours between 11 and 16 degrees C
temperature = 8 hoursrain day = 30%
Nel5Nel4
Nel3
Mel3Mel4Mel5
Syd5
Syd4
Syd3
 
 
 
Aus SWS Annex 2 BRS Figure 
8
Figure 8 Australian spring (September, October, 
November) data for wettest and driest years between 1998 and 2007
 WT/DS367/12 
Page 94  
 
   
Aus SWS Annex 2 BRS Figure 
10
Figure 10 Australian summer (December, January, February) data for wettest
and driest years between 1998 and 2007
 
 
 
 
  
Aus SWS Annex 2 BRS Figure 
12
Figure 12 Australian winter (June, July, august) data for wettest and driest years 
between 1998 and 2007
  WT/DS367/12 
 Page 95 
 
 
   
   
NZ FWS Annex 3 Figure 3B
 WT/DS367/12 
Page 96  
 
   
Annex 2 BRS figure 6
Figure 6 Australian autumn (March, April, May) data for wettest and driest years between 1998 and 2007 for two 
major trade centres (Sydney and Melbourne) and two major commercial pome fruit regions (Lenswood and 
Tumbarumba, near Batlow)). Sydney wettest = SW, Sydney driest = SD, Melbourne wettest = MW, Melbourne driest = MD, Lenswood wettest = LW, Lenswood driest = LD, Tumbarumba wettest = TW, Tumbarumba driest = TD; month of the year for each location indicated by numeric postfix (eg. Tumbaruma’s driest March between 
1988 and 2007 is ‘TD3’).
 
 
 
__________