Kabrovski v Telstra Corporation Ltd [2004] NSWDDT 35

Dust Diseases Tribunal of New South Wales

CITATION : Kabrovski v Telstra Corporation Ltd [2004] NSWDDT 35 PARTIES : Tony Kabrovski Telstra Corporation Ltd MATTER NUMBER(S) : 447 of 2002 JUDGMENT OF: Duck J at 1 CATCHWORDS: :- LEGISLATION CITED: CASES CITED: DATES OF HEARING: 19 & 20/07/04 DATE OF JUDGMENT: 07/21/2004

FOR PLAINTIFF: Mr A Leslie, QC instructed by Turner Freeman. LEGAL REPRESENTATIVES: FOR DEFENDANT: Mr T Rowles instructed by Sparke Helmore

JUDGMENT:

1. The plaintiff brings proceedings for provisional damages in respect of a condition of asbestos related pleural disease. 2. He is a man who was born in Macedonia on 8 January 1945. He went to school and to Teachers College in that country. He came to Australia on 9 May 1969 when he was 24. Within a couple of weeks he had obtained employment with the predecessors of Telstra Corporation Ltd, the defendant. The evidence suggests that initially he worked for the Postmaster General's Department, then for the Australian Telecommunications Commission and he remains now employed by Telstra Corporation Ltd. Initially he worked as a member of a conduit gang. He was engaged in the installation of telephone lines. He worked with materials referred to as "pits and pipes." It is not the subject of dispute that for a time the pits in which equipment was placed were constructed in part of asbestos cement. In the course of his work he was exposed to the inhalation of asbestos dust and fibre. 3. He remained working in the conduit gang through into 1970. This work was done in the Sutherland District. He then became a lineman and worked out in the field during the period from 1970 to 1977. Part of his work as a lineman required adjustment and repair of pits and pipes. In addition he worked beside other workers who were members of the conduit gang. In that way he continued to be exposed to asbestos dust and fibre. During the period 1971 to 1973 he worked in the Waverley area, part of that work involving the replacement of asbestos cement pits and pipes. Between 1972 and 1973 he worked in the Bonnet Bay area installing pits and pipes. 4. During the period up to 1977 he said no precautions were taken to prevent the inhalation of asbestos dust and fibre. From 1977 to 1989 he became a depot clerk. From time to time his work took him into the field to amend and check plans and this work placed him in the vicinity of workers working on the pits and pipes. In that period, that is from 1977 to 1989 no precautions were taken to protect workers from the inhalation of asbestos dust and fibre. Thereafter new pits were provided which were made of plastic, although there remained in the field many pits and pipes which were constructed of the old material containing asbestos. 5. The plaintiff now works as a team leader. That work takes him into the field. 6. He said, however, that from the late 1980s precautions have been taken at work so that dust does not arise from the asbestos pits and pipes. 7. His case in essence is that the exposure to asbestos at work has produced a condition of asbestos related pleural disease. It is propounded on his behalf that the symptoms attributable to that disease first manifested themselves in 1987 when he went to see his GP, Dr Khan. True it is that the nature of his illness was not then understood properly and a clearer picture did not emerge until the late 1980s. Nonetheless the case advanced on his behalf is that symptoms were present as early as 1987, that as a result of that fact the tort of negligence had been completed, that is, that there had been duty, breach and damage suffered by 1987 and hence he was then entitled to maintain proceedings for damages in respect of the tort. 8. The defendant raises a number of defences to which reference can be made in due course. The principal matter to which I wish to refer at this stage arises because of s 44 of what was the Commonwealth Employees Rehabilitation and Compensation Act 1988, now known as the Safety Rehabilitation and Compensation Act 1988. S 44 provides this: 1. Subject to s 45 an action or other proceedings for damages does not lie against the Commonwealth, a Commonwealth Authority, a licensed corporation or an employee in respect of: (a) An injury sustained by an employee in the course of his or her employment, being an injury in respect of which the Commonwealth Authority or licensed corporation would, but for this subsection, be liable (whether vicariously or otherwise) for damages; or (b) The loss of or damage to property used by an employee resulting from such an injury; whether that injury loss or damage occurred before or after the commencement of this section. 9. Subsection (1) does not apply in relation to an action or proceeding instituted before the commencement of the section. S 45 provides a limited exception to those provisions to which it is not necessary to go to at present. 10. The plaintiff's approach to this case has been that s 44, if it otherwise applies to the plaintiff, is invalid in conformity with the High Court decision in Georgiadis v Australian and Overseas Telecommunications Corporation 1993-1994 179 CLR 297. Stated shortly the thrust of the decision is that if a right of action had accrued in a plaintiff, the provisions of s 44 which commenced in force on 1 December 1988 effected an acquisition from such a prospective plaintiff of his rights to sue other than on just terms, and hence infringed s 51 (xxxi) of the Constitution. 11. It is necessary then to examine what happened. Before setting off on a review of the evidence I wish to say that the plaintiff has made it clear that unless he can demonstrate that on the balance of probabilities the tort giving him the right to sue had been completed prior to 1 December 1988 his right to bring these proceedings has been barred by the provisions of s 44. 12. While he was giving his evidence the plaintiff was asked whether he had noticed something about this respiratory health, and he said he had. As a result of it he went to see his GP, Dr Khan. The plaintiff said that he told the doctor about his breathing. The complaints about which he testified were that he suffered tightness of chest and shortness of breath. He was asked what he noticed about breathing deeply and he said it was difficult. The plaintiff said that chest tightness and shortness of breath were the first symptoms that he had noticed. 13. Dr Khan sent him for x-rays and sent him to Professor Schonnell for tests. The plaintiff's evidence was that when these steps had been taken he went back to Dr Khan, who could not see anything specifically wrong. The plaintiff was asked whether the doctor advised him that he thought that he, the plaintiff, was over anxious about his chest symptoms and the plaintiff agreed. The plaintiff said that from that time to this he has suffered from tightness in his chest and breathlessness. The evidence discloses that in 1991 he went back to Dr Khan and then commenced to see other specialists including Professor Schonnell, Dr Moses, Dr Hamor and ultimately Dr Loblay and Dr Rimmer. It became apparent over the years that the plaintiff was suffering from a condition described as hypereosinophilic syndrome, a disorder of the white blood cells. He was asked whether he had noticed anything about his own nose and throat and he said, yes, he had a condition similar to sinus. He was given medication for it which worked. He obtained relief from the medication. He said, however, that the medication did not relieve the tightness in his chest, it was still the same. 14. The plaintiff was then asked about being sent for x-rays and CT scans, which he said that he did have. It was suggested to him that they had revealed pleural plaques and pleural thickening, which he said was correct. It was then led without objection that the tests had revealed that he had been exposed to asbestos and may have asbestos related disease. He said, yes, that was so. The plaintiff then made a claim on Telstra which was administratively rejected by an officer from the Government Insurance Office who had apparently been appointed to administer these claims. He then objected to that determination and the matter was reviewed by another official administratively who confirmed that the plaintiff's application should be rejected. These matters have a bearing on one of the defences the defendant wishes to raise in the proceedings. 15. The rest of the plaintiff's evidence-in-chief consisted of an account of the various doctors on whom he has attended and finally two questions to this effect: he was asked whether since April 1987 he had noticed any improvement in the tightness in his chest on deep breathing, to which he said, "no." He was asked what had been the position in that period on exertion or sustained effort and he said, "Still shortness of breath and tightness." It will be seen clearly enough how the plaintiff's case is made. 16. In cross-examination a number of things were put to the plaintiff about his exposure to dust at work, and I do not think it is necessary to go over them. It was suggested to him that he did not go back to see Dr Khan for any chest problems in the period 7 July 1987 until 1990. The plaintiff would not accept that that was so, although Dr Khan makes it clear that he thought that was correct. It was further suggested that he did not see Dr Khan again until 15 January 1991 about chest problems, which seems to follow from the doctor's report, but the plaintiff would not accept that either. The plaintiff said that his breathing difficulties were significant but not enough to cause him to go off work. He was asked about whether he had had time off and his answers were not conclusive. He said that he had not had many days off. It was suggested to him in terms that he had had no time off work at all and he said he probably used his holidays. 17. It was then suggested that he had been to the doctor many times, that is to Dr Khan, during the period up until 15 January 1991 but that on none of those visits did he make any complaint about his chest problems, a matter with which the plaintiff would not agree. 18. The plaintiff confirmed that he continues to work for the defendant full time, even up to the present day. 19. The plaintiff was then asked a series of questions about histories he had given to various doctors as to when his breathing difficulties commenced. The thrust of the questions was to the effect that the doctors had all reported that his complaints commenced in 1991 or 1992, did he agree that that is what he told them. The plaintiff broadly speaking would not accept that that was the history that he had provided. He insisted that he had told Dr Kwok Yan that his problems were ongoing since 1987. Similarly he disagreed that he told Dr Bryant that his problems had commenced eight years before the doctor's report. The plaintiff insisted that he had told him that his problems had commenced in 1987. His evidence in this respect is in conflict with the doctor's letters. 20. Some questions were asked about whether he had changed his story during the course of 2004 about when his symptoms commenced, those questions being formulated by reference to the Pt 33 particulars which were amended during that year. I do not think anything really turns on that aspect of the case. 21. In re-examination the question was asked about instructions furnished to his solicitors as to when he first noticed breathlessness, that elicited a letter from the solicitors to the plaintiff and a printout of an email reply, which became PX.3, in which the plaintiff maintained that his symptoms had persisted from the middle of April 1987. He mentioned fixing the date by reference to the Macedonian Orthodox Easter in that year. 22. It is convenient then I think to look at the medical material. Dr Khan has reported, his letter bears date 1 March 2002 and it is PX.1 in the proceedings. There is no doubt that the plaintiff attended on the doctor on 26 May 1987 complaining of the recent onset of dyspnoea and difficulty with breathing. The doctor arranged for tests, as the evidence I mentioned had suggested. The Histomine Challenge Test excluded asthma at that stage. Spirometry was normal. One test was described this way: His IgE levels grew moderately elevated. 23. Dr Khan thought that that test result related to his dermatitis rather than his chest. The doctor advised the plaintiff, he said that he thought he had an anxiety problem which resulted in the plaintiff, according to the doctor, feeling better, feeling reassured and breathing easier. The doctor then reported that he did not see the plaintiff again for any difficulties associated with breathing until 15 January 1991. He added, "Interestingly he was seen on many occasions in the interim but he did not complain specifically of chest problems including a cough or wheezing." In 1991 various tests were administered. Nothing was detected clinically. He was offered inhaled steroids but refused them. It should be noted that the doctor described the plaintiff's symptoms in early 1991 as "a flu like illness." In March 1992 the doctor reported that the plaintiff returned, again with symptoms compatible with flu and a lower respiratory tract infection, for which he was given antibiotics. Medications were given and altered. The doctor records that in August 1992 the plaintiff reported a cessation of his coughing. In March 1993 the plaintiff saw Dr Schonnell again. He had by that time ceased his treatment on his own accord and was advised to recommence it. 24. A second opinion was sought by the plaintiff. Dr Khan referred him to Dr Kwok Yan, another respiratory consultant. He saw Dr Yan through 1996 and 1997. In June 1996 he saw also Dr George Hamor, who agreed with Dr Yan's assessment. In March 1997 Dr Khan reports, a pleural effusion was found by Dr Loblay. Dr Khan provided no diagnosis, he said it was difficult to provide even a working diagnosis. He disclaimed expertise in the field of respiratory medicine. 25. The plaintiff was sent to Dr David Bryant for medico-legal purposes. Professor Bryant has furnished several reports, the first of them bears date 18 December 2001. The bundle of reports constitutes PX.2 in the proceedings. The doctor thought, firstly, that the history of asbestos exposure in the plaintiff was confirmed by the finding of bilateral calcified pleural plaques. I interpolate that I do not think any dispute arises about that. The doctor accepts the diagnosis made by others of hypereosinophilic syndrome in the plaintiff. It is a syndrome of unknown aetiology and a variable prognosis. That syndrome is unusual. The doctor said that pleural thickening and pleural effusions are in his experience an uncommon manifestation of the hypereosinophilic syndrome and he enclosed an article from a medical publication significant because he said the author did not mention them as a manifestation of it. By reasoning of exclusion he then said it was more probable than not that the pleural changes in the patient were due to previous asbestos exposure. He spoke of the increased risks of developing mesothelioma or bronchogenic carcinoma. He disclaimed any relationship between hypereosinophilic syndrome and asbestos exposure. 26. The second of the doctor's letters bears date 25 July 2002. The report contains a short historical review of the plaintiff's attendances on medical practitioners leading to the observation in these terms: "….but I understand that no evidence of pleural disease was found until March 1997. I therefore have no objective evidence of any pleural disease prior to 1997. Indeed, clinical examination and chest x-rays prior to that time apparently did not show any pleural disease and it is therefore more probable than not that his breathlessness prior to 1997 was due to his emerging hypereosinophilic syndrome rather than due to asbestos related pleural disease." 27. The third of Dr Bryant's reports bears date 9 November 2002. The substantial thrust of the report appears, I think, in the fifth paragraph where the doctor said, "I am not aware of pleural effusions occurring as a part of this syndrome." A reference to a 1982 publication is quoted. "It is therefore my opinion that it is more probable than not that the pleural plaques and pleural effusions that have been detected in Mr Kabrovski's case are due to previous asbestos exposure rather than being due to a manifestation of his idiopathic hypereosinophilic syndrome." That opinion is contradicted by other evidence in the case and the resolution of the conflict between the experts I think becomes important. The doctor completed that report by saying in effect that there is a time lag between exposure and the development of symptoms of asbestos related pleural disease and he believed that exposure prior to 1989 resulted in the development of his subsequent symptoms. He said that the changes were likely to have gradually evolved over a period of many years and that such change is likely to have been present prior to 1988 even though the first clinical evidence of pleural effusions was not detected until 1997. 28. There is a report from the professor of 18 August 2003. He had no evidence, he wrote, that the plaintiff has asthma, although that is the subject of a dispute as well. There was no evidence, the doctor wrote, of asbestosis. Lung function testing carried out on 4 June 2003 showed evidence of restrictive disease. Diffusing capacity was within normal limits. The extent of the impairment of the plaintiff he thought was 10 per cent of the whole person. He thought there was due to benign asbestos related disease alone. He thought there was unlikely to be rapid worsening of lung function but whether or not deterioration might occur over a 10 to 15 year is conjectural. 29. The last of the doctor's reports is dated 14 April 2004. The opinions he expresses remain consistent. He thought it probable that the current level of impairment would persist indefinitely. There was a small chance, he wrote, that the impairment might increase over time, but the likelihood of that cannot be estimated with any certainty. He repeated his view that it was more probable than not that his pleural changes were due to previous asbestos exposure rather than his hypereosinophilic syndrome. He then provided an estimate of future medical expenses resulting from pleural thickening. 30. The other medical material in the plaintiff's case which provides support for his claim comes from Dr Julian Lee, whose opinion was obtained by the defendant. The doctor's report is PX.4. He thought that the radiology of the plaintiff's person was characteristic of asbestos related pleural disease. He thought work materially contributed to the contraction of his pleural condition and there was no limitation, he wrote, on the plaintiff's fitness for full-time employment. At the end of his report he wrote this: On balance asbestos exposure is the probable cause of the claimant's bilateral pleural effusions for which surgical drainage was performed in 1997. It would be particularly helpful to receive clarification of the diagnosis and management from his treating physician Dr Loblay. 31. The doctor said that he would be pleased to amplify his remarks should this information become available. But there is no evidence to suggest that such material was made available to him at any stage. 32. Dr Loblay and Dr Rimmer have had the care of the plaintiff and the administration of his treatment for a number of years. Dr Loblay has been involved in his management since early 1997. That doctor's report bears date 10 August 2001 and forms part of DX.1. The doctor wrote: He [that is the plaintiff] initially presented with involvement of his sinuses upper airways and lungs with pleural effusion and early cardiac involvement. Once the diagnosis was made, [that is idiopathic eosinophilic syndrome] he responded rapidly to cortico steroid therapy and he has been maintained on Azathioprine and low dose Prednisone since that time. 33. The doctor wrote: Although his disease has been well controlled there have been episodic grumbling relapses which have required increased steroid doses. Earlier this year he experienced an exacerbation of symptoms and an increase in eosinophilia following what appeared to be a respiratory infection. This has been settling gradually over the past few months. 34. In the course of monitoring his disease activity the doctor wrote: An x-ray and subsequently a CT scan of the chest showed the presence of pleural plaques typical of asbestos exposure. I arranged for him to be reviewed by Dr Janet Rimmer, the respiratory physician who has been seeing him intermittently for ongoing advice about his eosinophilic syndrome. 35. It is proper to observe, I think, that the whole thrust of the doctor's report is that the plaintiff's condition results from - leaving aside the question of plaques - results from the eosinophilic syndrome, which he has been treating. 36. Dr Rimmer's report bears date 7 September 2001. I wish to observe in passing that both Dr Loblay and Dr Rimmer are extremely highly qualified practitioners. Dr Loblay holds a Phd and Dr Rimmer a Doctorate in Medicine. Dr Rimmer's report commences in a blunt fashion. She said: Mr Kobrovski suffers from the following conditions - (1) hypereosinophilic syndrome (pleural, lung, pericardial, oral, bone marrow and peripheral blood involvement). (2) Osteoporosis. (3) Asthma. (4) Rhinosinusitis. (5) Pleural plaques. 37. As to the pleural plaques the doctor wrote that they normally result from asbestos exposure as a result of occupation. Some discussion then ensues. At p 2 she wrote: It is important to note that Mr Kabrovski also has asthma and rhinosinusitis. 38. She observed that she first saw him in 1997 and reviewed him in April 1999 when his cortico-steroids were reduced. It was observed that there was a recurrence of symptoms including shortness of breath and exercise induced cough. These symptoms responded to Ventolin, suggesting that there was a recurrence of his asthma which was coincident with a reduction of cortico-steroid usage. The doctor describes her review of a CT scan of 3 July 2001. She then wrote a sentence which is difficult to construe and which may be important. The sentence is: These appearances would be consistent with pleural plaques secondary to asbestos exposure or thickened pleura basally, which is probably a residual of the pleural effusions associated with the hypereosiniphilic syndrome. 39. The doctor was not called and the report will have to stand as it is. It may be observed, however, that the doctor's opinion at the commencement of her report described a number of conditions from which he was suffering which did not include asbestos related pleural disease. 40. There is a report from Dr Moses, part of DX1, the report bears date 18 February 1991. It is significant because when he saw the plaintiff the plaintiff denied shortness of breath and wheeze. It was the doctor's opinion in 1991 that what was then troubling the plaintiff was a post viral cough. 41. There are reports too from Professor Breslin, who gave evidence in court. The second of his reports is the more useful because by then he had been provided with a lot of material about the plaintiff. He details the material which had been made available to him under the heading "Background Notes." At p 5 he summarises his position this way: He does have some pleural plaques which are almost certainly asbestos induced but the evidence is overwhelmingly in favour of the fact that the remainder of his pleural disease, that is the thickening and the pleural effusions, are due to the hypereosinophilic syndrome. 42. Also tendered are the results of x-rays of the plaintiff undertaken in the earlier years. There is a report from Dr Light of 18 February 1991 showing no abnormality of the heart, mediastinum or lung fields. There is a report from Dr E Broadfoot which bears date 10 June 1992 in which the doctor's comment is, "No intrapulmonary abnormality is seen at this examination." There is a report of 1 September 1995 by Dr R A Murray-Nobbs. The report is in these terms: Chest - the previously demonstrated right upper zone shadowing has resolved. No focal abnormality is seen in relation to the right upper lobe on the PA,( that is postero antero) projection or apical views. I understand the patient has clinically improved. No further assessment by CT has been arranged at this stage in view of these findings. 43. A report of 28 April 1996 signed by Dr Julian Adler includes: Bilateral pleural effusions were observed to be present. Further, there was some thickening of the pericardium and a fluid density focus lies [the doctor wrote] in the anterior mediastinum.. 44. How is one to resolve the differences of opinion between the experts? No matter the obvious inadequacies of those entrusted with making these decisions the system requires that we do our best. As I indicated when recounting the evidence it seems to me that Dr Bryant has approached the matter by saying in effect it is unusual in a person suffering from hypereosinophilic syndrome to have pleural effusions. He enclosed a text, to which I will go in a moment, "Therefore" he said "I believe it's more probable that his pleural condition results from the asbestos exposure." I think, having regard to the whole of the evidence, there are problems with that approach. 45. Firstly, those treating the plaintiff do not share the view. In particular I speak of Dr Loblay and Dr Rimmer. Secondly, they are supported in their approach, as was pointed out by Dr Breslin, by biopsies of the right lung and pleura, undertaken in 1997 and by the histopathological analysis of the fluid extracted from the plaintiff. In one sense one might say it does not matter how rare it is, the examination of those materials in this man has demonstrated that he has been affected by the hypereosinophilic syndrome, and that on balance it has produced the effusions and thickening of the pleura. 46. Further, when one looks at the material provided with Dr Bryant's letter, that is an extract from an article by Peter F Weller MD, which bears date May 26 2000, under the heading "Clinical Features" the following observation is made: The involvement of the heart, skin, nervous system, lungs and spleen each occurs in 45 to 60 per cent of cases. 47. Precisely what that means, of course, we do not know, but that is what it says. Later at p 3 of the extract under the subheading "Pulmonary Disease" the following appears: Approximately 40 per cent of patients with HES develop pulmonary involvement. The most common respiratory symptoms is a chronic persistent non productive cough. 48. The duel of the non present experts was carried on by the production by Dr Breslin of material which became DX2, an extract from a publication by Crofton and Douglas, Seeton and Ors published in 2001 in which the following appears: Pulmonary involvement, typically presenting as a cough that is worse at night, may be seen in up to 40 per cent of patients. Chest radiographics may show interstitial infiltrates and pleural effusions are common. 49. I have come to the view that on this occasion Dr Bryant's view is less probable than the view propounded ultimately by Dr Breslin, which is supported by other material from Drs Loblay and Rimmer. I think it more probable than not that the pleural effusions from which the plaintiff has suffered and for which he has been treated and the pleural thickening which is present result from the hypereosinophilic syndrome rather than from the exposure to asbestos. I think the bulk of the medical opinion, firstly, is to that effect. Secondly, Drs Rimmer and Loblay have had the care of the plaintiff's treatment for years and their qualifications are very high. Thirdly, the premise on which Dr Bryant has proceeded, that is that it is rare to have pleural effusions caused by the syndrome and resultant thickening, does not seem to be borne out by the whole of the publications, extracts of which have been made available. Further, his approach seems to be contradicted by the biopsies and histopathology from the pleural effusions. (See in this regard Dr Breslin). 50. That being so I prefer Dr Breslin's opinion on this occasion to Dr Bryant's. In a sense, having come to that view I think it is difficult for the plaintiff to succeed. I do not accept that at the time he attended in 1987 on Dr Khan he was suffering from the effects of exposure to asbestos in the workplace. I note that all the tests showed nothing. The doctor was unable to make a diagnosis and in light of the conclusion that I have come to, whether or not the condition may have reflected the developing asthma or a developing hypereosinophilic syndrome or whether it was simply the flu and its after effects, it may have been any of those things, but what it was not I think is a manifestation of the effects of exposure to asbestos. 51. The assertion by the plaintiff that he has been troubled continuously by chest tightness and coughing is an assertion easily made, but whenever one attempts to test it by reference to other existing material it does not stand up. The histories recorded by all of the doctors speak of troubles commencing in 1991 and 1992. Those doctors include Dr Bryant. The plaintiff, it may fairly be said, could not know what was causing his trouble in a circumstance in which the doctors were unable to diagnose him in 1987. It requires no great criticism of the plaintiff to say that whatever caused his sickness then I do not accept his evidence that he has continued to experience chest tightness and breathing difficulty from that time onwards. In particular he is contradicted in that respect by his own GP, Dr Khan. 52. On balance I am not satisfied that the plaintiff suffers, other than by way of having pleural plaques, from the after effects of the exposure to asbestos in the workplace. It is more probable than not, it seems to me, that his symptoms are to be explained by reference to the hypereosinophilic syndrome, from which he undoubtedly suffers and for which he has been treated since 1997. That being so I think it is sufficient now to say that I do not believe his claim can succeed and there should be a verdict for the defendant. 53. I mentioned at the outset that there were some other defences relied upon. The defences included an analysis of whether the plaintiff could possibly bring himself within the provisions of s 45 of the Safety Rehabilitation and Compensation Act 1988. Another defence which was raised was that having embarked upon the appeal process provided for by the Commonwealth Act the plaintiff was bound to pursue the rights thus conferred and was not at liberty to bring these proceedings. In light of the findings that I have made I do not see that it is necessary to deal with either matter further. 54. In all of the circumstances there will be a verdict for the defendant. 55. Plaintiff should pay defendant's costs but they should not include the costs of the strike out application. Mr A Leslie, QC instructed by Turner Freeman appeared for the plaintiff Mr T Rowles instructed by Sparke Helmore appeared for the defendant