Australia - Measures Affecting Importation of Salmon Report of the Panel (Continued) Question 9. The 1996 Final Report (as well as its earlier drafts) only deals with wild ocean-caught adult Pacific salmon. In your scientific/technical opinion, do any imports of aquatic animals or aquatic animal products, other than salmonids, into Australia entail the same (or even higher) risks with respect to the introduction of the identified diseases as those that would arise from the import of uncooked salmon from Canada (either on a disease-by-disease basis or in an overall manner)? Please explain the basis for your opinion. 6.97 Dr. Rodgers replied that the importation of several other groups would pose a potential risk of disease introduction that would probably be at least as high, if not higher, than that posed by the importation of uncooked salmon from Canada. These groups would include any live ornamental fish, bait fish and trash fish for feeding aquacultured species. It was not possible to predict though, without an import risk analysis study, which of these represented the highest risk. However, importation of live fish for stocking of open waters containing indigenous fish, and the feeding of trash fish or bait fish directly to aquacultured species as a feed supplement or substitute would probably be the most important in terms of risk. Escapees from a closed system into an open waterway could also be a problem. The arrival of furunculosis into Australia via imported goldfish or into Norway via salmon smolts and the first reported outbreaks of VHS in turbot from Scotland and Ireland helped to support the hypotheses of live fish importation and feeding respectively. 6.98 A recent risk analysis report (October 1997), by the Western Australian Fishing Industry Council on the practice of importing frozen fish as bait, considered the possible introduction of viruses that could have an impact on the rock lobster industry. The resulting analysis was not able to distinguish between a very low risk of introduction and no risk at all. The report stated that the analysis could not conclude that there was no risk of introducing an exotic disease only that the risk of introducing an exotic disease that was capable of producing a large scale fish kill was either very low or did not exist at all. In conjunction with this conclusion the report identified a series of risk reduction measures that could be implemented for frozen bait. Question 10. Canada contends that for a given disease agent, the likelihood of disease establishment is higher for imports of whole, uneviscerated bait fish and for live fish known to host that disease agent than it is from imports of uncooked salmon for human consumption. In your view, are these contentions corroborated by scientific/technical evidence? If not, what factors would be needed to substantiate those views? 6.99 Dr. Burmaster responded that this seemed highly likely to him, but he had no independent information to support or refute such an opinion. 6.100 Dr. Rodgers replied that it was probably true to say that for a given disease agent, the likelihood of disease establishment was higher for imports of whole, non-eviscerated bait fish and for live fish than it was from imports of uncooked salmon for human consumption. However, the actual level of risk would be important and the opinion expressed in Question 9 was also relevant here. It was also a fact that there were complex processes that lead to disease establishment (see his response to Question 8). In addition, the final destination of a particular consignment would have an impact on potential disease establishment. For instance, a licensed, carefully controlled import of a live fish species destined to be confined for research purposes would entail a very much lower risk than open water stocking. The same considerations would apply to processing establishments, since uncontrolled waste discharges could be a factor in possible disease transmission (e.g. ISA in Norway). It was also worth noting that comprehensive controls that prohibited the importation of certain species and products or failed to differentiate adequately between an ornamental species and a wild fish with the same taxonomic name might promote an illegal, difficult to control, underground trade. This had probably been a factor, for instance, in the introduction and spread of spring viraemia of carp in the United Kingdom in recent years, although the elevated value of certain cyprinid species for sport fishing might also be important in such cases. Question 11. In their 7 October "Responses to Questions", Question 3, both Canada and Australia identify, for diseases subject to the dispute, non-salmonids which may also be carriers of these diseases. However, Australia seems to contend that a separate risk analysis may be necessary for these non-salmonids. In your view, can the risks represented by these non-salmonids be compared to those which arise from salmonids? If one presumes that the risks posed by salmonids are unacceptable, are there any scientific or technical reasons for not making the same presumption with respect to risks of the same diseases from non-salmonids? What factors should be taken into account in comparing the risks of entry, establishment or spread of a disease for one or several disease agents know to be carried by salmonids as well as non-salmonids? Can the data and findings contained in the Australian Final Report dealing with wild ocean-caught adult Pacific salmon be validly used in a risk assessment for the four other categories of salmon from Canada (see Question 7)? 6.101 Dr. Burmaster recalled his answers to Question 4. He believed that the risks represented by non-salmonids could be compared to those which arose from salmonids. With regard to making the same presumption of the acceptability of the risks posed by salmonids and non-salmonids for the same disease, he indicated that it all depended on the particular evidence. As discussed in his answer to Question 17, below, a risk assessor could answer this question by developing and combining probability distributions for the variables flowing from the seven conceptual steps identified by New Zealand. To identify what factors should be taken into account in comparing the risks of entry, establishment or spread of a disease for one or several disease agents known to be carried by salmonids as well as non-salmonids, a risk assessor must develop and combine probability distributions for the two (or more) scenarios. Dr. Burmaster did not believe that the data and findings contained in the Australian Final Report dealing with wild ocean-caught adult Pacific salmon could be validly used in a risk assessment for the four other categories of salmon from Canada because the 1996 Final Report did not meet the minimum standards for a risk assessment. New Zealand's final risk assessment did meet the minimum standards for a risk assessment and, as such, might contain an answer acceptable to the parties in this dispute. If the parties could not agree on the findings in New Zealand's Final Report, he did not think that the current dispute could be resolved without a new quantitative risk assessment using probabilistic methods. 6.102 Dr. Rodgers indicated that the basic underlying risk assessment would be the same but a good risk assessment model would be modular and therefore flexible enough to take account of any additional or different risks posed by non-salmonids. Although the risks might be compared, any additional risks, or those considered for salmonids that would be inappropriate for non-salmonids, would mean that a separate risk assessment would be necessary for each category of import. In addition, some of the diseases of concern are salmonid diseases and as such it would be inappropriate to transfer the data to a risk assessment of non-salmonids. However, non-salmonids could be carriers of some of the diseases of concern and therefore act as agents of dissemination. Essentially, although some data could be used to assess the risk factors, the outcome of an assessment might be different. This would apply to both qualitative and quantitative risk analysis. He noted that the points he made in response to Question 1 concerning the minimum requirements of a risk assessment were also valid here. 6.103 The same would be true for the four other categories of salmon from Canada, although these were closer in taxonomic concept and other considerations. Some of the data and findings contained in the Australian Final Report dealing with wild ocean-caught adult Pacific salmon could be validly used in a risk assessment for the four other categories of salmon. However, there were additional factors to consider for aquacultured species and wild freshwater-caught species, as opposed to wild ocean-caught fish. These would include the presence of known vectors (and alternative host species), the access of anadromous fish to water supplies, protected water sources, purchase of ova/fry/other fish/fish products, sharing equipment with other farms (vaccination, grading machines, etc.), sharing staff with other farms, density of farms locally, density of infected farms locally (introduction/reintroduction of fish), distance to sea, number of salmonid rivers locally, age of farm/hatchery, annual production, type of feed (cold processing, supplementation with trash/wild fish), the prevalence of residual infection in the area and the type of management practices undertaken. 6.104 Dr. Wooldridge observed that she had answered the majority of points in this question within her answers to other questions. Much of it concerned risk assessment technique. The risks from salmonids and non-salmonids could be compared by comparing available data pre-entry data plus potential exposure pathways. The decision on whether risk were acceptable or not depended on many factors but if the risks were assessed as being (or are otherwise believed to be) at a similar level then she believed they must be either equally acceptable or equally unacceptable regardless of the source. The comparison should take into account all available information. Any data used in one risk assessment which was valid in another assessment could be used in that assessment also. This would in such circumstances most probably include data from post-entry exposure onwards, and possibly pre-entry processing and inspection. Question 12. Is evisceration an effective means of reducing the risk to a negligible level of each of the identified diseases? (See summary table provided by Australia in its 7 October "Responses to Questions", Question 13.) Would the effects of evisceration in terms of reducing the risk of disease transmission be similar in all circumstances? Which of the disease agents can be found in flesh (muscle), remnant kidney tissue, bone, skin, gills, head, or blood? Do you know of specific cases where diseases have been transmitted from one area to another by imported eviscerated fish? From imported eviscerated salmonids? Please identify and describe these cases. 6.105 Dr. Burmaster doubted that evisceration alone reduced the risk to a "negligible" one, but New Zealand's Report showed that evisceration in combination with other factors reduced the risks to acceptable levels. 6.106 Dr. Rodgers responded that evisceration was probably an effective means of reducing the risk to an acceptable level in certain of the identified diseases. The level of reduction would largely depend on the tissue location of the disease causing agent and the effectiveness of the evisceration process. Many of the disease agents of concern had the potential to remain at some level after evisceration, particularly those that might be concentrated in the head, brain, gills, musculature, heart, kidney remains and skin or external surfaces. Different pathogens could target different organs, although since viruses were intracellular they were particularly difficult to remove. Certain of the bacterial disease agents could also remain, especially those that caused lesions in the musculature (e.g. Aeromonas salmonicida) or were harboured in the kidney (e.g. Renibacterium salmoninarum). Evisceration would not remove all the parasites either, particularly those that appeared in the blood, on external surfaces or as cysts (e.g. Loma salmonae, Henneguya salminicola and Kudoa thyrsites). In addition, infected host individuals might serve as "carriers" or "reservoirs" of a disease agent without being demonstrably affected themselves and they therefore acted simply as vehicles of agent transmission. At such low levels they were very difficult to detect and therefore to know which particular tissues are affected. 6.107 Dr. Rodgers added that he did not know of any specific cases where fish diseases had been transmitted from one area to another by imported eviscerated salmonids or other eviscerated fish. 6.108 Dr. Winton stated that the FDC was unanimous in its belief that evisceration was an effective method to greatly reduce the risk of transmission of the notifiable fish diseases regardless of their source (hatchery or wild). Certainly for very stable pathogens (e.g. those with spore stages), there might be some residual infectivity in the flesh or heads of highly infected animals (typically this would be more likely to happen in fish harvested from hatcheries where a disease outbreak with attendant mortality was occurring), but the level of infectivity in the eviscerated animal could usually be expected to be considerably less than that present in viscera. The FDC considered that the risk of transmission of fish diseases by movement of eviscerated fish products was probably lower than the risk from certain other activities (movement of aquarium fish, ballast water in ships, etc.) and thus did not justify trade restrictions. Recently, the US government changed its regulations to exempt eviscerated fish from requirements for certification under US Title 50 based upon this same concept. Several other countries (e.g. the European Union and New Zealand) had also adopted this approach and reduced or eliminated disease control requirements for aquatic animals destined for human consumption. 6.109 Dr. Winton indicated that he knew of no case (salmonids or otherwise) where eviscerated fish had been shown to result in the importation and establishment of an infectious disease in fish; however, Australia was correct in that it might be difficult to find such cases if they occurred in wild fish. Nevertheless, where expansions of the geographic range of a fish disease had been documented, they were most often associated with increased surveillance efforts or the application of more sensitive diagnostic methods. There were also several documented cases where a fish disease had been introduced into an area previously known to be free of the disease through importation of live fish or eggs for rearing in hatcheries (infectious hematopoietic necrosis virus was a good example) and even a few diseases that were introduced by importation of uneviscerated fish for use as food for fish reared in net-pens (viral hemorrhagic septicemia virus in turbot in the United Kingdom). 6.110 Conversely, there were also examples where fish that potentially contained high levels of an infectious agent had not resulted in transmission of disease if eviscerated. For example, approximately 80 per cent of all rainbow trout produced in the United States came from the Hagerman Valley of Idaho where fish in virtually 100 per cent of the farms had been exposed to, or were infected with, infectious hematopoietic necrosis virus (IHNV). While there were perhaps more than a dozen documented cases of IHNV being spread by movement of infected fish or contaminated eggs, there was not a single case where transmission of IHNV was associated with fresh eviscerated fish for human consumption in spite of the fact that large numbers of these were sold in supermarkets throughout the United States within 24-48 hours of slaughter. Similarly, Piscirickettsia salmonis was present in many farmed salmon in Chile and infectious salmon anaemia was present in several salmon farms in Norway. No case of transmission of either agent to fish in any other part of the world had been documented in spite of the fact that thousands of metric tons of such products were shipped fresh throughout the world each year in the form of iced, eviscerated product. 6.111 While there were few actual studies on efficiency of transmission of a fish disease by various types of products, an unpublished study was conducted in Dr. Winton's laboratory in collaboration with the Clear Springs Trout Company in Idaho where nearly all fish were infected with IHNV at some level during various stages of rearing. Fresh fish were removed directly from the processing area and sampled for virus. They found no evidence of virus in the flesh of processed fish by either cell culture or by the polymerase chain reaction assay. Some of his colleagues had also conducted tests looking for IPN virus in Atlantic salmon imported fresh into the United States. These studies remained unpublished as no virus was found. In a few limited surveys of ocean-caught salmon, both the incidence and intensity of infection of a given disease was typically lower than found among fish reared at hatcheries where the disease was enzootic. Question 13. With respect to the diseases at issue, what is the difference in effectiveness, with regard to reducing the risk of disease transmission, of evisceration as compared to heat treatment of the product? as opposed to full cooking of the flesh of the product? 6.112 Dr. Burmaster observed that no method was risk free. Cooking reduced the risk as a function of time, temperature, and pressure. Long ago, food technologists prepared and published tables showing the logarithmic efficiencies of different heat treatments (such as blanching, parboiling, or canning). He was unaware of any "hard" data to compare the effectiveness of evisceration to the effectiveness of cooking or canning. New Zealand's risk assessment concluded that a regulatory program that included evisceration as one step reduced risks to de minimis values. 6.113 Dr. Rodgers responded that he could not provide a complete answer to this question because comparative data for evisceration, heat treatment and full cooking were scarce. However, a published study (Whipple and Rohovec, 1994) on the effect of heat and low pH on selected viral and bacterial fish pathogens had been undertaken. The study concluded that A. salmonicida, Mycobacterium cheloni and the IHN virus were sensitive to a heat treatment of 65ºC for 15 minutes and 82ºC for 5 minutes. They were also sensitive to the fish silage process which used a pH of 4. In addition, although more heat resistant, the IPN virus and R. salmoninarum would also be killed when incorporated into fish silage and heated to 82ºC for 5 minutes after a 15 minute period at 65ºC. The study was carried out in order to test the efficacy of procedures used for processing fish viscera to be incorporated into fish diets. Full cooking should, of course, completely eliminate such pathogens providing the process was properly carried out. The only possible exception would possibly be a spore-forming organism, such as Myxobolus cerebralis, the causal agent of whirling disease, although there was some suggestion from the literature that this would not survive at a temperature of 100ºC for 10 minutes. Most of the other studies related to inactivation by heat were largely concerned with incubation and cultivation temperatures in artificial media, not to reduction of pathogen levels in tissue. Question 14. Which of the disease(s) or disease agents of concern, if carried by live fish, can be detected by organoleptic examination? Which of the disease(s) of concern, if carried by uncooked salmon, can be detected by organoleptic examination? 6.114 Dr. Rodgers replied that in many cases the success of determining the presence of a particular disease agent and subsequent diagnosis relied on an interpretation of all the available information, including historical data, visual examination and tissue sampling. Unfortunately, no single sign was indicative of a specific individual disease condition. Similarly, not all reported clinical signs were present in every case of the disease. 6.115 Disease conditions were diverse and might elicit very varied response patterns in fish. The pathology and outcome of individual infections were the result of several factors including the physiological and immunological status of the host, species, age, stage of sexual development and nutritional status. Other properties included the water temperature, salinity, pH, pathogen numbers and their location within the host. Under certain circumstances fish might act as symptomatic carriers and pass the infective agent to susceptible animals. Unfortunately, the symptoms and gross pathology of many fish diseases were similar, and it could be difficult for even experienced fish pathologists to distinguish between the different pathological conditions, notably when two or more diseases might be present. Common visual signs of disease among salmonids included dark skin colour, excess mucus production (skin or gills), exophthalmia, distended abdomen, skin ulcers and petechial haemorrhages at the base of fins, skin, gills or muscle. These might be encountered to varying degrees in several disease conditions. In addition, spoilage organisms such as Alteromonas spp. and Pseudomonas spp. (and others) produced distinctive odours following contamination during storage and filleting operations. For these reasons, diagnosis should not be made solely on the basis of disease signs. 6.116 By way of example, Dr. Rodgers observed that the following disease signs could be indicative of several possible causal agents: (a) Exophthalmia (many viral diseases such as IPN and IHN; bacterial diseases such as BKD, ERM; parasitic diseases such as PKD; nutritional deficiency such as lack of certain vitamins); (b) Dark skin colour (viral diseases such as VHS; bacterial diseases such as ERM, furunculosis; nutritional deficiency such as lack of certain vitamins; stress due to poor water quality); (c) Excess mucus production (skin or gills: parasitic infections in general; environmental irritant); (d) Distended abdomen (virus diseases in general; several bacterial conditions; fungal infection; kidney malfunction; intestinal cestodes; nutritional imbalance); (e) Skin ulcers (many different disease conditions); (f) Petechial haemorrhages (skin or muscle: viral diseases such as VHS; bacterial diseases in general; protozoan or crustacean parasites). It was possible to isolate specific fish pathogens from apparently healthy fish without evidence of any clinical disease. There were also many facultative fish pathogenic bacteria and viruses whose pathogenicity depended directly on environmental quality and which in cases of decreasing quality could lead to similar septicaemias to those caused by specific fish pathogenic agents. Therefore the identification of the pathogen was important, with disease diagnosis being a step-wise procedure divided into a consideration of archival information, general examination, collection of samples and subsequent analysis for pathogen identification. Organoleptic tests might be a part of the general examination but could not be relied on solely for disease identification, although a visual examination for grading purposes would identify unsightly looking fish (e.g. superficial damage, ulcers and possibly extensive haemorrhaging). Such fish might not then enter the supply chain as a quality product. Question 15. Are you aware of any evidence of major disease spread with a significant impact on salmon production (wild or cultured, including recreational fisheries)? In regard to new introductions, to what extent is it feasible to identify the means/pathway of the introduction of the disease? 6.117 Dr. Rodgers replied that there had been several occurrences of disease spread with a significant impact on salmon production. The most notable documented incidences concerned the introduction of furunculosis in Atlantic salmon smolts and Gyrodactylus salaris on smolts into Norway, from Scotland and Sweden, respectively. 6.118 A recent graphic example of possible disease spread in non-salmonids concerned the large mortalities experienced in wild pilchards along the coast of South Australia and New Zealand. Frozen pilchards imported from California, Chile, Peru and Japan were fed to sea cage tuna in Australia, resulting in an epizootic among pilchards that eventually spread along 6,000 km of coastline. A herpesvirus was thought to be the cause of the mortalities, although this had not been proved definitively. The involvement of imported baitfish had also been suggested as a cause of disease introduction of enteric redmouth in France from minnows. The isolated cases of VHS in turbot recorded in Scotland and Ireland, linked to the feeding of marine fish as a feed supplement, should also be noted. Although these incidences referred to non-salmonids they served to indicate the potential for disease spread in certain circumstances. The importation of ova had also been blamed for the spread or introduction of diseases such as furunculosis, IHN, BKD and IPN into countries as diverse as Sweden, Japan, China, Chile, Germany and Taiwan. 6.119 Scientific "detective work" was often the only solution available to identify the means or pathway of introduction for a disease. However, the main problem was normally that the manifestation of a new disease condition occurred after the initial causal event. This meant that there was no source material to work with and an educated assumption, based on corroborative evidence or circumstantial detail, was often necessary. Nevertheless, such conclusions were decided only after collecting all the necessary data and eliminating unlikely scenarios. This type of investigation would normally be carried out by experienced teams and would be very time consuming. The proportions and causes of the problem would have to be determined in order to discover whether there were any external influences that could be assigned to any particular introduction. The identification of the pathway of an introduction might be a complex diagnostic problem that would involve collecting information on environmental conditions, clinical signs, aetiological factors, possible transmission routes, identification of any potential pathogen, authorised movement records and the possible existence of illegal imports. 6.120 Dr. Wooldridge noted that risk assessments were originally developed precisely for the assessment of potential risks which had not yet occurred and for which the potential pathways from hazard to outcome had not been observed; for example, the risk of radiation release from new designs of nuclear power station and, on the biological side, the risks of new pathogenic bacteria returning to earth from space travel. In such cases identification of potential pathways from hazard to outcome was thus an integral part of the assessment. Therefore, with regard to new disease introductions, it was perfectly feasible, and an integral part of the risk assessment, to identify potential pathways for the introduction of disease. And in the assessment being undertaken here, this part was likely to have access to more relevant available information than in the "exotic" examples just quoted. Question 16. Australia (in its 7 October response to Question 10) has stated that there are no reports on introduction of unwanted exotic diseases of fish through imports of product for human consumption. Australia has suggested, inter alia, that this can be explained because of the difficulty of recognizing -or establishing - any such occurrence, because many or all of the diseases of concern occur endemically and because of lack of research. What is your view on these points? To what extent, if any, are examples of disease transmission in terrestrial animals relevant to this case? 6.121 Dr. Burmaster agreed that there were no reports of introductions via imports of fish products for human consumption. While it was usually not possible to "prove the negative" from the "condition of no reports", the "condition of no reports" did allow one to put statistical bounds on the probability of the unwanted event. In other words, the "condition of no reports" did contain information that a risk assessor could use to put bounds on the probability. He thus disagreed with Australia's implicit argument that a "condition of no reports" supplied no evidence to a risk assessment. Question 17. What chain of events must be met for uncooked salmon products to cause the entry, establishment and spread of the identified diseases into Australia? 6.122 Dr. Burmaster broadly agreed with the seven conceptual steps identified in the Summary (page 1) and again in the Introduction (page 3) of New Zealand's 1994 risk assessment report: - the disease must be present in the waters of origin; - the disease must be present in the particular fish caught (or the flesh mush have become contaminated during processing); - the pathogen must be present in the imported tissues; - the diseased fish must pass inspection and grading procedures; - the pathogen in the flesh must survive storage and processing and be present in an infectious dose; - the pathogen must be able to establish infection by the oral route or by the host being bathed in it; - scraps of the flesh product must find their way into a susceptible fish host in New Zealand or an infectious dose of pathogen must find its way into contact with a susceptible fish host by some other means. 6.123 Dr. Rodgers observed that for uncooked salmon products to cause the entry, establishment and spread of the identified diseases into Australia the following criteria would have to be met: - infection occurring in source stock; - the presence of significant numbers of pathogens; - no detection of disease on routine sampling of source stock; - survival of the pathogen in processed fish (e.g. after evisceration and/or heat treatment); - survival of the pathogen in transit (presumably chilled or frozen); - processing plant with drain to water source (in the destination country); - susceptible host fish at destination; - interaction with susceptible host fish; - pathogen to overcome host defences, possibly in a stressed host; - subsequent pathogen reproduction (possible necessity for intermediate vector); - favourable environmental conditions; - local and national dissemination of disease. Essentially, the disease agent must be present in the particular fish caught for processing, although contamination during processing was also a possible but unlikely factor, and the pathogen must be present in the imported tissues or products. In addition, the diseased fish/flesh must pass grading, inspection and testing procedures. After harvesting, the pathogen in the flesh must survive the death of the host, subsequent storage and processing, then still be present in an infectious dose. Finally, sufficient infected flesh must find its way into the local environment or a susceptible fish host and the pathogen must be able to establish an infection by the oral route or by contact. 6.124 Dr. Wooldridge noted that this question defined three potential outcomes; the entry of the identified diseases into Australia; their subsequent establishment; and their spread. The question (and therefore the answer given here) addressed only possibility, not probability. Entry into Australia 6.125 For each of the diseases identified as a hazard, in order for it to enter Australia in uncooked salmon products, either the disease agent must originate from the fish harvest or it must be introduced as a contaminant at some point in the preparation and processing. If contamination occurred at any point before processing which would render the probable total amount of agent non-viable, then it need not be considered separately at the next stage. 6.126 Therefore, for entry to Australia, either: (a) the fish must contain the disease agent at the point of harvest; and (b) the disease agent must then remain present within the tissues selected for the imported product, at the point of import. If only part of the fish were selected for import (e.g. headless, eviscerated) then the agent must be present in that part selected. If any examination of the fish were undertaken, either visual or otherwise, any agent present must escape detection (detection assumed to lead to rejection). or (c) the fish must become contaminated during the processing so far. Then: (d) the agent must remain viable within the tissues selected for the imported product, at the point of import. Therefore any processing (e.g., freezing, thawing, chemical application) must fail to render the agent non-viable. or (e) the product must become contaminated with the disease agent after any final processing before import. Dr. Wooldridge noted that assessment of the probability of this occurring comprised a release assessment, of which the elucidation of the chain of necessary events was an essential component. Establishment 6.127 For each of the diseases identified as a hazard, in order for it to become established in Australia from the import of uncooked salmon products the agent must first enter Australia in imported uncooked salmon products. That is, it must be present and viable at the point of import of the product. However this was not in itself enough to enable establishment. 6.128 Given entry, then the chain of events necessary for establishment of the disease in Australia required: (a) the presence of susceptible animals (including fish); and (b) the existence of possible exposure pathways from the product at the point of entry to agent contact with a susceptible species. There might be many potential exposure pathways; and (c) for at least one of the potential pathways the disease agent must remain present and viable all the way through that potential exposure pathway. Therefore for at least one pathway all the following conditions must be met: (i) any processing in the pathway (e.g., freezing, thawing, chemical application, cooking) must fail to render the agent non-viable; and (ii) any regulatory activity in the pathway designed to reduce the potential for exposure (e.g. disposal method, siting of processing plant) must fail to render the agent non-viable; and (iii) any natural occurrence in the pathway which by its nature would tend to reduce the potential for exposure (e.g. dilution, exposure to sunlight, lack of necessary intermediate host) must fail to render the agent non-viable; and (d) At the point of exposure, conditions must be appropriate to enable successful transmission of agent in an infectious form into the susceptible species. This would be agent- and host-dependent; and (e) At the point of exposure there must not only be viable agent present, but it must be in a sufficient quantity to result in infection. This would be agent- and host- dependent. Spread 6.129 For each of the diseases identified as a hazard, in order for it to spread within local fauna, it first had to become established locally. However, this was not, in itself, enough to enable spread. Spread might mean spread to other species than those initially infected or other geographical areas or both. 6.130 Given local establishment, the chain of events necessary for the spread of disease required: (a) that the initial establishment of disease did not only occur within a dead-end-host species (i.e. that transmission was possible from those initially infected at exposure). For spread across species, requirements were: (b) other susceptible species in Australia; and (c) the existence of possible exposure pathways from the initially infected species to others. These exposure pathways were subject to the same kinds of considerations as in the previous section, though they would be different in detail; and (d) at the point of exposure, conditions must be appropriate to enable successful transmission of agent from the initially infected to another susceptible species. This would be agent- and species-dependent; and (e) at the point of exposure viable agent must be in a sufficient quantity to result in infection of the host second species. This would be agent- and species- dependent. A particularly susceptible initially infected species might allow for agent multiplication thus allowing infection of a second, less susceptible species. For geographical spread, requirements were: (f) the presence of susceptible animals to be more than just locally present; and (g) the presence of exposure pathways from locally infected animals to those in other areas, with all the usual considerations plus, for waterway spread, the lack of natural geographical barriers; and (h) the ability of the agent to survive in the environment encountered in other geographical conditions (e.g. climate, presence of intermediate hosts, etc.). Question 18. In the period between May 1995 and December 1996, were there any advances in scientific knowledge that would justify a change in the conclusions from the 1995 Draft Report to the 1996 Final Report? 6.131 Dr. Burmaster replied that he did not think so. Question 19. Canada contends (First Submission of Canada, para. 175, Oral Argument of Canada, 9 September 1997, para. 92) that in the 1996 Final Report, Australia omitted significant information for the estimation of risk that was in its 1995 Draft Report, including data on which to base estimates of volumes of fish, prevalence of disease agents, quantities of waste and concentrations of waste. What is your view on this point? 6.132 Dr. Rodgers responded that in parts the 1996 Final Report was less detailed than the 1995 Draft Report and to a certain extent the specific section on qualitative risk analysis appeared to have been largely replaced by a straightforward textual summary. There also seemed to be more detail in the 1995 Draft Report in areas such as disease agent viability and infectious dose, although conversely it lacked some information contained in the 1996 Final Report (e.g. import country presence of infection data). In addition, the 1995 Draft Report presented some data in the form of a simple literature review for sections such as histopathology and diagnosis. On balance the best features of both draft reports should possibly have been combined to create a final analysis dealing with the aspects of a qualitative risk analysis, leading to an estimation of the possibility of each risk factor occurring. The 1996 Final Report put most emphasis on the unknown, or poorly understood, factors and the unique position of Australia, rather than accepting a low risk in conjunction with risk management (reduction) factors. Accurate data on prevalence of infection, fish weight and waste statistics, leading to an estimation of the disease risk per tonne of imported product, used particularly in combination with actual historical data that showed no disease introduction for similar importations elsewhere, was mainly valuable for a quantitative risk assessment. The more subjective approach of a qualitative risk assessment did not necessarily make full use of such detail. Nevertheless, the availability of such information, whether detailed or not, should warrant its inclusion in either scenario. 6.133 Dr. Wooldridge replied that it was precisely to facilitate the comparison of the information used that in her opinion the layout of the risk assessment should have been similar in both the draft and final document, and any change of data specifically indicated with the reason for the change. The change in format and order made comparison much more difficult and time consuming. Nevertheless, it was possible to identify data given in the 1995 Draft Report (for example the tables on pages 17, 24, 27, 29 giving data on fish, municipal waste water, etc.) which she was unable to find in the final assessment, and which was potentially relevant to the conclusions from the qualitative assessment and of potential use in a quantitative assessment. To continue with Australia - Measures Affecting Importation of Salmon: OIE Procedures and Recommendations

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