Hughes v Sydney Day Nursery
[2000] NSWSC 462
•30 May 2000
CITATION: Hughes & Anor v Sydney Day Nursery [2000] NSWSC 462 CURRENT JURISDICTION: Common Law FILE NUMBER(S): SC 20908/94 HEARING DATE(S): 7 February-15 February 2000, 17-23 February 2000 JUDGMENT DATE: 30 May 2000 PARTIES :
Linda Hughes (First Plaintiff)
Jacob Hughes by his tutor Linda Hughes (Second Plaintiff)
SDN Children's Services Inc (formerly known as Sydney Day Nursery & Nursery Schools Association Inc) (Defendant)
HIH Winterthur Workers' Compensation (NSW) Pty Limited (First Cross Defendant)
Mercantile Mutual Insurance (Australia) Limited (Second Cross Defendant)
CIC General Insurance Limited (Third Cross Defendant)
HIH Casualty and General Insurance Limited (Fourth Cross Defendant)
FAI General Insurance Company Limited (Fifth Cross Defendant)
GRE Insurance Limited (Sixth Cross Defendant)
Equitable General Insurance Company Limited (New Zealand) (Seventh Cross Defendant)
JUDGMENT OF: Studdert J
COUNSEL : S. Walmsley SC/M. Fordham (Plaintiff)
M. Cranitch SC/J. Simpkins (Defendant)
J. Poulos QC/S. Torrington (First Cross Defendant)
D. Davies SC (Second-Seventh Cross Defendants)SOLICITORS: McCourt Charlton (Plaintiff)
Clayton Utz (Defendant)
HIH Winterthur Workers Compensation (NSW) Pty Ltd (First Cross Defendant)
Phillips Fox (Second-Seventh Cross Defendants)CATCHWORDS: CLAIMS IN NEGLIGENCE - employer's duty of care to employee and to her unborn child - nature of duty - whether breach of duty - whether breach causative of harm - INSURANCE - liability of insurer under statutory workers' compensation policy - whether it extended to harm to child transplacentally as consequence of "injury" to mother LEGISLATION CITED: Workers' Compensation Act
Interpretation ActCASES CITED: Bankstown Foundry Pty Ltd v Braistina (1985-86) 160 CLR 301
Fleming: The Law of Torts, 9th ed. 181-183
X & Y (by her tutor X) v Powell (1991) 23 NSWLR 26
Lynch v Lynch (1991) 25 NSWLR 411
Bendix Mintex Pty Ltd v Barnes (1997) 42 NSWLR 307
ICI Australia Operations Pty Ltd v Walsh & Ors (1997) ATR 81-452
Wallaby Grip (BAE) Pty Ltd (In Liq) v Macleay Area Health Service 17 NSW CCR 355
Turner v State of South Australia (1982) 42 ALR 669
Ellis v Wallsend District Hospital (1989) 17 NSWLR 553
Papadopoulos v New South Wales Insurance Ministerial Corporation [1999] NSWCA 116
Cartledge v Jopling & Sons Ltd [1963] AC 758
Hume Steel Limited v Peart (1947) 75 CLR 242
Zickar v MGH Plastic Industries Pty Limited (1995-96) 187 CLR 310
E v Australian Red Cross Society (1991) 27 FCR 310
Paton v British Pregnancy Advisory Service Trustees [1979] 1 QB 276
Burton v Islington Health Authority [1993] QB 204
Attorney General for the State of Queensland v T (1983) 57 ALJR 285
Sutton - Insurance Law in Australia, 3rd ed. at 757-758
Kodak (A'asia) Pty Ltd v Retail Traders Mutual Indemnity Insurance Assoc (1942) 42 SR (NSW) 231
Dairy Farmers Co-op Pty Ltd v CIC Insurance Ltd (1991) 7 ANZ Ins Cas 61-093 (SC NSW)
Green v Windman [1964] VR 297
Davis & Young Pty Ltd v Assurance Compagnie Baltica etc [1986] VR 203 (FC)
Re Linsley & Co-op Insurance Assoc (1976) 62 DLR (3d) 408
Nigel Watts Fashion Agencies Pty Ltd v GIO General Ltd (unreported, NSWCA, 22 December 1994)
Rheem Australia v Manufacturers' Mutual Insurance (1984) 2 NSWLR 370
Manufacturers' Mutual Insurance Limited v Hooper (1998) 5 ANZ Insurance Cases 60-849
Cuckson Textiles Pty Ltd v Queensland Insurance Co. Ltd (1968) 88 WN Pt 1
The Workers' Compensation Board of Queensland v Technical Products Pty Ltd (1988) 165 CLR 643DECISION: See para 243
LINDA HUGHES & ANOR v SYDNEY DAY NURSERY & NURSERY
SCHOOLS ASSOCIATION INC.THE PLAINTIFFS’ ACTIONS
The first plaintiff was a child care worker employed by the defendant at the time of becoming pregnant. Three months after his birth the second plaintiff was diagnosed as suffering from CMV infection “acquired transplacentally” and became, and remains, seriously disabled. It was the plaintiffs’ case, disputed by the defendant, that the first plaintiff acquired primary CMV infection during her pregnancy as a consequence of the defendant’s negligence and that this infection was passed on to the second plaintiff in utero.The plaintiffs claimed damages.
HELD:
1. That the defendant was negligent in failing to warn the first plaintiff of the possibility that the CMV virus if acquired during pregnancy could damage the unborn child of a child care worker.2. Had the first plaintiff been warned of that possibility the first plaintiff would not have continued in her employment during her pregnancy.
3. The disabling condition from which the second plaintiff suffered was CMV “acquired transplacentally.”
4. However the first plaintiff’s age and occupation made it highly likely statistically that the first plaintiff would have had CMV before her pregnancy commenced in which event her infection passed on in pregnancy would not be primary.
5. The plaintiff’s case depended upon proof that the second plaintiff’s infection was a result of primary infection in the first plaintiff as distinct from reactivated infection.
6. It was not proved on the balance of probabilities that the first plaintiff’s infection passed on to the second plaintiff transplacentally was primary as opposed to reactivated infection.
7. Hence, there was no causative link between the defendant’s negligence and the harm suffered by the plaintiffs and their claims failed.
THE CROSS CLAIMS
The defendant had two policies of insurance, being:
(a) a statutory form of workers’ compensation policy;
(b) a community care policy.The insurers under both policies denied liability to indemnify the defendant and were joined in the proceedings as cross defendants. The community care policy excluded liability where indemnity was afforded under a workers’ compensation policy.
2. Assuming injury to the first plaintiff, the statutory workers’ compensation policy was to be construed as covering liability to the second plaintiff as a liability consequent upon the injury to the first plaintiff.
HELD:
1. Had it been proved that the first plaintiff suffered injury that arose out of or in the course of her employment by way of primary CMV infection which was then passed transplacentally to the second plaintiff, this would have attracted liability to the workers’ compensation insurer for both claims.----------------
IN THE SUPREME COURT
OF NEW SOUTH WALES
COMMON LAW DIVISIONSTUDDERT J
Tuesday 30 May 2000
20908/94 LINDA HUGHES & ANOR v SYDNEY DAY NURSERY & NURSERY SCHOOLS ASSOCIATION INC.
JUDGMENT
1 HIS HONOUR: In this cause the first plaintiff, Linda Hughes, and her son, the second plaintiff Jacob Hughes, are seeking damages from the defendant, Sydney Day Nursery and Nursery Schools Association Incorporated. On 6 August 1992 the first plaintiff gave birth to the second plaintiff who, tragically, was found shortly after his birth to be physically disabled. It is the plaintiffs’ case that the second plaintiff’s disabilities were due to congenitally acquired cytomegalovirus (which I shall refer to in this judgment as CMV), and that the first plaintiff acquired that condition in the course of her employment with the defendant and as a consequence of its negligence.
2 Liability has been strenuously resisted by the defendant. The defendant denies having been negligent, and there has been a very live issue at the trial as to whether the second plaintiff has suffered from CMV and, if so, how it was acquired. If it was congenitally acquired CMV, then there has also been a very live issue as to when and how his mother herself became a carrier of CMV.
3 The defendant has cross claimed against the first cross defendant HIH Winterthur Workers’ Compensation (NSW) Pty Limited, seeking indemnity in the event of the plaintiffs succeeding against the defendant. The defendant claims to be entitled to be indemnified by the first cross defendant under a statutory form of policy issued pursuant to the Workers Compensation Act.
4 The defendant has a second cross claim against Mercantile Mutual Insurance (Australia) Limited (second cross defendant), CIC General Insurance Limited (third cross defendant), HIH Casualty and General Insurance Limited (fourth cross defendant), FAI General Insurance Company Limited (fifth cross defendant), GRE Insurance Limited (sixth cross defendant), and Equitable General Insurance Company Limited (New Zealand) (seventh cross defendant). The defendant claims in the alternative to the claim against the first cross defendant that the second to the seventh cross defendants are liable to indemnify it pursuant to a policy which they issued to the defendant known as a community care policy.
5 Each cross defendant has denied liability under the relevant policies.
6 The plaintiffs’ claim against the defendant and the defendant’s cross claims have been heard together.
7 The second plaintiff is very seriously disabled, and agreement has been reached for the purposes of the plaintiffs’ claim against the defendant and the defendant’s claim against the first cross defendant that should the plaintiffs succeed damages should be awarded to the plaintiffs as follows:
(ii) on the claim of the second plaintiff, in the sum of $4,500,000 plus costs.
(i) on the claim of the first plaintiff, in the sum of $150,000 plus costs;
8 The remaining cross defendants as the insurers under the community care policy have not involved themselves in that agreement, but Mr Davies of Senior Counsel informed the Court that these insurers put forward no evidence on the issue of quantum concerning either claim.
9 The cause is one which has given rise to medical issues of much complexity, and it has called for close attention to the specialist witnesses whose evidence has been introduced. At the outset, however, it is important to determine what has been established as to the first plaintiff’s background, and the nature and conditions of her employment with the defendant. It is also important to address what has been proved concerning her pregnancy and the events that led up to her first seeking medical attention for Jacob, when the first plaintiff became concerned about her son’s development in October 1992.
10 The first plaintiff gave evidence about these various issues and impressed me as being a truthful and generally reliable witness. I am satisfied on the balance of probabilities that those matters which I am about to record under the heading “The first plaintiff’s history, the second plaintiff’s birth and the detection of his abnormality” have been established as facts.
The first plaintiff’s history, the second plaintiff’s birth and the detection of his abnormality
11 The first plaintiff was born on 22 January 1967 and after completing her Higher School Certificate attended the TAFE at Newcastle where she obtained her Child Care Certificate in November 1986. It will be necessary to examine the nature of the work the first plaintiff undertook in closer detail later but, for the present, I record the following outline. From May 1987 until July 1988 the plaintiff worked in a child care centre at Royal North Shore Hospital but then spent some two years overseas from August 1988 until September 1990. In that period overseas the plaintiff employed her occupational skills, doing day nursery work and also working as a nanny. Following her return to Australia the plaintiff obtained employment with the defendant in October 1990, and from that time until some six months after Jacob was born the first plaintiff worked for the defendant continually other than when on maternity leave.
12 The first plaintiff worked with two year old children in the course of her employment with the defendant at the defendant’s child care centre at Redfern until early 1992; there were two other carers working with her and there were seventeen to eighteen children under her care.
13 The plaintiff was not married but late in 1991 began a relationship with one Kevin Elder. That relationship began in about September 1991 and late in November 1991 it was confirmed that the first plaintiff was pregnant, an event of which she informed the director of the day care centre early in December 1991. The course of the pregnancy appeared uneventful, although the plaintiff described a period of some flu like symptoms in December 1991, being ill on Christmas Eve and Christmas Day. After the Christmas holidays the first plaintiff’s position at the day care centre was altered, and she was moved to care for children under two years of age. Whilst no explanation was given to her officially for this change in position, the plaintiff’s understanding was that there had been a child carer in the group looking after the under two year olds who was not getting on with other carers in that group, and the plaintiff and this other worker changed positions so as to eliminate the stress in the under two section.
14 The first plaintiff’s relationship with Jacob’s father did not last and by January 1992 the first plaintiff was aware that she was going to be raising the infant she was carrying as a single parent.
15 Whilst looking after the under two year olds, the plaintiff was one of four looking after fifteen children and she said that her hours varied. The work day commenced at 7.30 or 9.30 and finished at 3.30 or 5.30. There were two rooms for changing nappies on these infants, one of which had hand washing facilities and the other of which did not.
16 The plaintiff went on maternity leave on 17 June 1992 and Jacob was born on 6 August 1992. The plaintiff became concerned by October 1992 as to Jacob’s development. In particular he was arching himself backwards; so after speaking to the sister at the child care health centre the plaintiff consulted a general practitioner, Dr Honeyman, and was referred to Dr Grigor.
17 The plaintiff consulted Dr Grigor for the first time on 4 November 1992, when the doctor considered the infant was neurologically abnormal. By January 1993 Dr Grigor had made a diagnosis of CMV infection, “acquired transplacentally”.
18 There is no evidence that the first plaintiff was aware at any time up to the date of the first consultation with Dr Grigor that she had ever suffered from CMV.
19 A number of medical issues arise in this case as I have already mentioned. For the plaintiffs to succeed, they must prove that Dr Grigor’s diagnosis was correct, and further that the second plaintiff has been suffering from congenital CMV as a consequence of the acquisition of primary CMV by his mother during her pregnancy, in turn passed on to her son. Further they must prove that the infection resulted from the negligence of the defendant.
(a) To the first plaintiff
The duty of care owed by the defendant
20 In order to succeed against the defendant the plaintiffs must prove harm suffered by reason of breach of the defendant’s duty of care. There is, of course, no issue but that the defendant as the first plaintiff’s employer owed to her that duty of care that arose by reason of the employer/employee relationship, the common aspects of which are so well established.
21 Counsel have referred to Bankstown Foundry Pty Limited v Braistina (1985-86) 160 CLR 301 where, addressing a submission that the law as to the nature of an employer’s duty had changed, Mason, Wilson and Dawson JJ said:22 The above statement of principle is still applicable and it defines the duty which the defendant owed to the first plaintiff as she pursued her employment with the defendant.
“This is not the place for an examination of the reasoning in earlier decisions of this Court. What must be asserted is that the law has not changed. It is as accurate today as it was thirty years ago to say that the duty
‘is that of a reasonably prudent employer and it is a duty to take reasonable care to avoid exposing the employees to unnecessary risk of injury’: Hamilton v Nuroof (W.A.) Pty Ltd (1956) 96 CLR 18 at 25, per Dixon CJ and Kitto J.
We digress to remark upon the formulation preferred by Windeyer J, with whom McTiernan, Kitto, Taylor and Owen JJ agreed, in Vozza v Tooth & Co. Ltd (1964) 112 CLR 316 at 319, namely:
‘For a plaintiff to succeed it must appear, by direct evidence or by reasonable inference from the evidence, that the defendant unreasonably failed to take measures or adopt means, reasonably open to him in all the circumstances, which would have protected the plaintiff from the dangers of his task without unduly impeding its accomplishment.’
This passage has been repeated more than once in recent decisions of the Court: Raimondo v South Australia (1970) 23 ALR 513 at 518; McLean’s Roylen Cruises Pty Ltd (1984) 58 ALJR at 425; 54 ALR at 7. It seems right to us to caution the reader against interpreting the concluding phrase in the citation, that is, ‘without unduly impeding its accomplishment’, as furnishing an additional qualification to an employer’s liability independently of the question of what is reasonable in the circumstances. If protective measures are reasonably open to an employer then ordinarily they will not unduly impede the accomplishment of the task. The extent to which the proposed measures would unduly impede that accomplishment will bear directly on the question whether it was reasonable to expect them to be undertaken.
Furthermore, it has long been recognized that what is a reasonable standard of care for an employee’s safety is ‘not a low one’: O’Connor v Commissioner for Government Transport (1954) 100 CLR 225 at 230. Whether or not it will be found to have been satisfied is always a question of fact to be determined in the light of the circumstances of each case.”
23 The second plaintiff had not been born during the period when the defendant was allegedly negligent. However Mr Cranitch has not sought to argue that no duty of care towards Jacob existed. That Jacob had not been born when on the plaintiffs’ case the harm occurred does not negative the existence of a duty of care or preclude his pursuit of a claim following his birth for harm occasioned whilst en ventre sa mere: see Fleming: The Law of Torts, 9th ed. 181-183; X & Y (by her tutor X) v Powell (1991) 23 NSWLR 26 and in particular the judgment of Mahoney JA at 29-30 and of Clarke JA at 37-38; and Lynch v Lynch (1991) 25 NSWLR 411. Because of the concession made by Mr Cranitch it is not necessary to consider further the basis of a duty of care by the defendant towards the second plaintiff. Whether there was a breach of duty owed to either plaintiff is a different matter, and I turn to address this issue.
(b) To the second plaintiff
24 It is the plaintiffs’ contention that the defendant, as the first plaintiff’s employer, was negligent in a number of respects which exposed the first plaintiff, and the second plaintiff then in utero to unnecessary risk of harm. In the statement of claim the negligence was particularised as follows:
Has the defendant breached its duty of care to the plaintiffs?
“(a) allowing the first plaintiff to work with babies when it knew she was pregnant and when it knew or ought to have known that pregnant women working with babies had a substantially higher than usual rate of passing CMV to a foetus;
(b) failing to warn the first plaintiff that, as she was pregnant, she stood a greater than usual risk of passing CMV to her foetus;
(c) failing to ensure that the first plaintiff had a blood test to determine her immune status;
(d) failing to provide the first plaintiff with any or any adequate hand washing facilities;
(e) failing to provide sufficient staff so that the child carers working with babies could wash their hands immediately after changing nappies of children.”25 In the course of addresses, Mr Walmsley of Senior Counsel, for the plaintiffs, informed the Court that particulars (d) and (e) were not being pursued and those allegations accordingly do not call for attention.
26 The remaining particulars were refined during the trial and Mr Walmsley ultimately submitted, and this was the case to which Mr Cranitch directed his submissions, that the defendant was negligent:
(ii) in transferring the plaintiff during her pregnancy to work with children under two years of age.
(i) in failing to warn the first plaintiff of the risk of passing CMV to her foetus and of thereby causing harm to the unborn child;
27 It is necessary, in considering the alleged breaches of duty, to determine what has been proved to have been the defendant’s state of knowledge at relevant times. Did the defendant in one or other of the ways complained of expose the plaintiffs to a risk of harm which was reasonably foreseeable?
28 The relevant evidence as to the defendant’s state of knowledge is meagre. Mr Walmsley referred to an article by Stuart Adler published in the “New England Journal of Medicine” in 1989. That article contained a recommendation in these terms:
“Day-care workers, particularly those who care for children younger than two years of age and who are pregnant or anticipating pregnancy, should be given the option to be tested for immunity to CMV. Seronegative women may decide not to care for children during the first half of the pregnancy. If they continue caring for young children, they should be counseled to avoid ‘intimate contact’ with children during this period. Such counseling should recommend frequent hand washing and, if feasible, the use of gloves, especially when handling diapers or respiratory secretions, and the avoidance of mouth-to-mouth contact and unnecessary or excessive kissing of children. Whether such practices would reduce the risk of acquiring CMV infection is unknown. If rigorously maintained, however, they should be successful.”
29 The evidence does not establish either directly or by reasonable inference that the article above referred to came to the knowledge of the defendant at any time before the birth of Jacob.
30 One of the articles introduced into evidence by the plaintiffs (at pp 63G-J of Exhibit C) was an article entitled “A seroprevalence study of cytomegalovirus infection in child-care workers in the Eastern Sydney Area.” The research question for the study was identified in these terms: “Are child care workers at increased occupational risk of acquiring CMV infection?” The paper observed that to date no studies on the question had been carried out in Australia. In the background information set out in the article appeared the following:
“Overseas data suggest that CMV infection is common among children in child-care centres, and US studies have found 22-57% of children to be excreting virus in the urine [Demmler, 1991]. CMV can be detected in the saliva of many of these children as well [Hutto, 1986; Volpi, 1988]. Studies of the child-care centre environment confirm that CMV contaminated secretions are spread by infected children onto objects and surfaces in the centre. CMV was found on most toys which had been placed in children’s mouths and could be grown from the hands of children and teachers [Hutto, 1986]. The virus was able to survive on surfaces for up to 30 minutes, a long enough time to be picked up by other children or carers. Acquisition and thus excretion of CMV is age related, with higher rates found in under 3 year olds and lower rates in the over three year age group. The duration of excretion in these otherwise healthy children ranged from 3 to 41 months (mean 18 months) [Adler, 1991]. Given the high prevalence and the prolonged nature of CMV shedding by children in care and subsequent contamination of the child-care environment with CMV containing secretions, it is not surprising that adult contacts, including parents and child-care workers, are at increased risk of CMV acquisition.”
31 The article is not dated but Mr Cranitch pointed out that the references included a publication in 1992 so that it is appropriate to infer that the study was being undertaken no earlier than 1992. One of the two chief investigators identified in the article who was to undertake the study was Dr Mark Ferson.
32 Mr Cranitch relied upon this publication as affording some evidence of the limited nature of any relevant knowledge in Australia in the period with which the present case is concerned.
33 There is one article which I find on the balance of probabilities did come to the defendant’s notice. The evidence satisfies me that the defendant subscribed to a publication known as “Rattler”. In the winter 1990 edition of that publication, which I infer from records tendered was probably received by the defendant at or about the end of June 1990, there appeared an article by Dr Mark Ferson entitled “Preventing and controlling infection in the child care environment”. The author of the article was described at the foot of it as the Public Health Specialist with the Eastern Sydney Area Health Service and the article occupied three pages of the publication. It identified a number of viral infections spread by the respiratory route and these infections included CMV. Under the heading “Health consequences” in the body of the article appears the following:
“The health consequences of outbreaks of infection in the centre-based care may be considerable. For the children involved, infections and their complications can cause much misery and some risk of long-term effects. For example, viral gastroenteritis in young children can lead to hospitalisation, while measles and mumps are very much underestimated as causes of serious illness. Important complications include pneumonia and brain infection in the case of measles, and deafness in the case of mumps. Some infections are often more severe in adults than in children (eg measles, mumps, chicken pox),while the unborn baby may be placed at great risk of damage if pregnant women among carers or the family catch rubella (german measles) or cytomegalovirus (CMV).”
34 It seems to me from a reading of the article that this alerted the reader to the specific risk to the unborn child in the event that a pregnant child care worker caught CMV in her work environment. That risk was described as being a “great risk of damage”. There is no direct evidence as to what employee or employees of the defendant read the “Rattler” article, but it seems to me to be a reasonable inference that the article would have been considered by such person or persons who were then responsible for health care considerations at the defendant’s day care centre.
35 The defendant was interrogated in this case. Interrogatories were directed at the minutes of two committee meetings. The earlier committee meeting in point of time was a meeting of the “Train the Trainer’s Subcommittee of the Health Policy Committee”. The minutes record that that meeting took place in 24 April 1991 and it is recorded that one Marianne Grech was in attendance. In answer to an interrogatory the defendant disclosed that Marianne Grech was the Executive Officer of the defendant between the beginning of April 1991 and the end of June 1992. Although Mr Walmsley referred to the content of the minutes of this meeting, it does not seem to me that this document advances the plaintiffs’ case.
36 The next document the subject of interrogatories is a document headed “Minutes of the sub-committee meeting of the ‘Health Policy’ committee concerned with training held at Sydney Day Nurseries Head Office, Redfern, on May, 15th, 1991”. The minutes record that Marianne Grech, identified as the defendant’s Executive Officer, was present. So too were Margaret Barns and Janet Robinson. In answer to interrogatories it appears that Margaret Barns was an Area Coordinator for the defendant and that Janet Robinson was a Staff Development Coordinator for the defendant. So far as the answers to the interrogatories go, Margaret Barns was employed by the defendant “for the whole of the period commencing at the beginning of February 1991 and ending at the end of June 1992”; Janet Robinson was employed by the defendant “four days per week during the period commencing at the beginning of February 1991 and ending at the end of June 1992”. The minutes of the meeting of 15 May 1991 record, inter alia, the following:
“Terms of reference of Mark’s draft policy discussed, with a view to their being expanded. Mark did expand on risks to workers of CMV infection…no immunisation exists, status of susceptibility to the virus can change so routine screening on employment seems unfeasible. Duty of care may be covered by training and personal decision of a worker to continue to work in a particular area. The recommendation might be that a program might offer screening but that in practical terms, workers should be informed and take responsibility for their own status.
A pamphlet on CMV is in progress. Mark undertook to distribute it to committee members.”
37 It is a reasonable inference to draw that the reference to Mark is a reference to Mark Ferson who was the author of the “Rattler” article above referred to. The “draft policy” in the minutes has not found its way into evidence but it seems that the draft referred to risks to workers of CMV infection, to there being no immunisation available and to the impracticability of routine screening of workers. The minutes then specifically addressed the “duty of care”. In context I would take this as being a reference to consideration of the duty of care to child care employees. What was perceived relevant to the duty was training, but I infer from the remainder of the above passage that it was perceived that carers should be informed of the risk of infection so as to make an informed decision to continue to work in a particular area. The pamphlet referred to in the minutes did not find its way into evidence.
38 The minutes then recorded a number of recommendations, the first of which concerned “Sound training on hygiene should cover CMV in susceptible people”. Recommendation 12 concerned casual staff and students and it is recorded in this recommendation:
“…it is seen to be crucial that student awareness is raised to risks if they are not immunised. They should be encouraged to take responsibility for their immune status.”
39 In that recommendation the defendant addressed what it perceived to be a need concerning casual staff and students and recognised a foreseeable risk of infection and a need to inform the subject group of the risk. Inevitably the defendant must have perceived that the same need existed concerning permanent employees.
40 Dr Ferson was not called, so there was no direct evidence as to any instruction he gave to the defendant relevant to the present case, although the minutes to which I have referred invite the inference that he was providing assistance to the committees identified in those minutes in relation to problems associated with infectious diseases and in particular CMV.
41 I am, of course, alert to what Dr Ferson wrote in the winter edition of “Rattler” as well as to what is recorded in the minutes referred to above.
42 It was agreed between the plaintiffs and the defendant that a diary entry made by the solicitor formerly instructing for the plaintiffs recorded: “16/11/95, T/A Dr Mark Ferson confirmed approach by the other side.” This entry was relied upon by the plaintiffs to explain why the doctor had not been called by the plaintiffs and as a basis for drawing an inference, there being no explanation for the defendant’s failure to call Dr Ferson, that his evidence would not have assisted the defendant’s case. I remind myself, however, that the rule in Jones v Dunkel (1959) 101 CLR 298 does not permit me to convert suspicion into reasonable inference. However the defendant called no evidence at all on the issue of its knowledge concerning CMV at times relevant to this case, nor did it call any evidence on the issue of instruction of the plaintiff in relation to CMV. Rather, through Mr Cranitch, it relied upon what it was submitted were the shortcomings in the evidence introduced on behalf of the plaintiffs.
43 What has been proved on the evidence introduced?
44 The evidence I have reviewed satisfies me on the balance of probabilities of the following matters:
(i) that the defendant, through the winter 1990 publication of the “Rattler”, was made aware that child care workers were by their occupation placed at risk of infection by CMV;(ii) that the defendant, through the same publication, was made aware that if a child care worker was pregnant and “caught” CMV, her unborn child might be “ at great risk of damage ”;
(iii) three of the defendant’s officers are recorded in the relevant minutes (annexure A to Exhibit D) as having attended a meeting of a committee at the head office of Sydney Day Nurseries at Redfern on 15 May 1991 and it is admitted in an answer to an interrogatory that Janet Robinson, a Staff Development Coordinator for the defendant, was present at that meeting;
(iv) that at that meeting consideration was given to a policy document prepared by Dr Mark Ferson (the author of the “Rattler” article published in the winter of 1990) concerning the risk of CMV infection to which day care workers were exposed, and the need
(a) to train such workers on appropriate hygiene;
(b) to inform such workers of the risk of continuing to work in their particular area; and
(c) to inform such workers to assume responsibility for ascertaining their status of susceptibility to CMV.
45 Having reflected upon the relevant evidence, I am satisfied that by mid 1991 the defendant had such knowledge available to it of the risks of exposure of child care workers to the CMV virus as attracted a duty in the defendant to alert the plaintiff to the risk in her work environment of CMV infection, not only to her, but to any child she might be carrying. I find that the duty extended to requiring that a warning be given that the CMV virus could damage any such unborn child. The plaintiff informed the director of the defendant, Ms Nicholson, of her pregnancy early in December 1991, but the duty to warn the plaintiff also existed before Ms Nicholson was informed of the pregnancy because it was foreseeable that a young woman of child-bearing age might become pregnant.
46 Did the defendant discharge its duty of care in the circumstances of this case?
47 The defendant gave the following responses to the following interrogatories:
“8A. Did you, between 15 May 1991 and the end of June 1992, take any, and if so, what steps to tell the First Plaintiff that pregnant women were vulnerable to Cytomegalovirus (‘CMV’)?
8B. After making all reasonable enquiries, the Defendant is unable to answer this interrogatory other than to say that the First Plaintiff may have been given information regarding the risks of CMV to pregnant women on or about 19 August 1991 at an In House Staff Development Programme session on Infection Control Practices held between 12.30 and 1.30 pm at the Redfern Centre of the Defendant.
10A. During the period 15 May 1991 and the end of June 1992 did you request the First Plaintiff to:
(a) confirm her CMV status?
(b) take responsibility for her own CMV status?
10B. (a) No.
(b) On the assumption that interrogatory 10A(b) is directed at communications between the Defendant and the First Plaintiff, the substance of which was that the First Plaintiff was requested to take responsibility for ensuring that she did not contract CMV specifically, the Defendant’s answer is ‘No’. From time to time, however, the First Plaintiff was requested by staff members of the Defendant to take steps to protect her own health, for example but without limitation, following a handwashing procedure.”
48 I am satisfied that the defendant did give adequate instruction to the first plaintiff as to the need for handwashing. The plaintiff was also instructed as to the requirement that gloves should be worn when changing dirty nappies.
49 The first plaintiff’s area coordinator, Mrs Mitchell, gave the first plaintiff written instructions on 3 April 1991 which, inter alia, address the need for hygiene and for staff to wash their hands before and after various defined activities. Then various bulletins and posters made available to staff indicate an emphasis by the defendant on the need for handwashing: see Exhibits 7 and 8 and the paper prepared by Ms Robinson in June 1991, being part of Exhibit C. The plaintiff acknowledged in cross examination that regular bulletins were posted on the notice board in the staff room which addressed issues that included hygiene. Further there was a staff development day held on 19 August 1991 and Exhibit 9 records that the first plaintiff attended that programme. The exhibit records as the objective of the programme:
“By the end of the session staff attending will be able to list ways in which to stop transmission of certain diseases, they will be able to implement a handwashing programme and will understand that handwashing is a requirement of the association.”
50 On her part the first plaintiff acknowledged attendance at that programme and said that the emphasis was on washing hands and using diluted bleach to clean surfaces and also to ensure that toys were disinfected.
51 I find then that the defendant gave adequate instruction on matters of hygiene and, indeed, Mr Walmsley has not contended to the contrary.
52 However none of the documentary material to which I have referred specifically addressed the need to warn of the possibility that the CMV virus could damage the unborn child of a child care worker.
53 It is the plaintiffs’ case that the warning which I have determined was required was not given. I am asked to make such a finding having regard to the evidence which the first plaintiff gave. Mr Cranitch submitted that I would not be satisfied by such evidence that the first plaintiff was not given appropriate instruction and warning. The competing submissions about this demand close attention to the evidence which the first plaintiff gave on this issue.
54 The plaintiff gave evidence of her attendance at the lecture given by Ms Robinson in August 1991, and I take this to be the staff development programme referred to in Exhibit 9 to which I referred earlier. According to the first plaintiff the lecture was entitled “Warfare on Germs” or “Germ Warfare”. I observe that “Germ Warfare” was given prominence in the heading to Ms Robinson’s paper of June 1991 which comprises part of Exhibit C at pp 80-82. That June 1991 paper referred to CMV only as one of nine viral infections spread by the respiratory route, but the paper made no reference to any CMV hazard associated with pregnancy. Nor did it exhort readers to check their immune status. Concerning the instruction given in August 1991 the first plaintiff was asked these questions and gave these answers (T8):55 Then the first plaintiff gave evidence as to a conversation which she said she had with Ms Robinson after Dr Grigor had diagnosed that her son was suffering from congenital CMV (T17):
“Q. Do you recall what she talked about? At least, was there some title that her talk had?
A. I think it was called warfare on germs, or germ warfare.
Q. Do you recall her raising at that meeting, or at least during that lecture, cytomegalovirus, or CMV?
A. It may have just been mentioned in passing.
Q. You recall her telling you that pregnant women were vulnerable. That is, that their, pregnant women’s foetuses were vulnerable to CMV?
A. No.”56 Later, in cross examination, at T40:
“Q. At some stage in January/February 1993, did you have a discussion with somebody called Janet Robertson at the defendant’s child care centre?
A. Yes.
Q. To the best of your recollection, what did you say and what did she say?
A. I asked her why she hadn’t told me about CMV and she said she did at the meeting on germ warfare.
Q. If you had known that CMV infection of the mother, when pregnant, could cause birth defects in the child she was carrying, would you have done anything?
A. Yes.
Q. What would you have done?
A. I would have had a blood test to see whether I was immune to CMV or not and then followed the medical advice which was not to have --
HIS HONOUR: Q. What you would have done, never mind, pursuant to advice or not. Apart from having a blood test, is there anything else you would have done if you had been aware of this risk?
A. I wouldn’t have worked with young children.”
“Q. I think eventually a staff development day was held in order to promote this germ warfare, as I think you described it yesterday, is that right?
A. Yes.
Q. And you attended the staff development session?
A. Yes.
Q. And it was a discussion on ways in which to stop transmission of certain diseases?
A. Yes.
Q. And CMV was one of the diseases discussed, wasn’t it?
A. I don’t recall specifically but I believe so.
Q. Do you recall the advice that was given to you or not?
A. Yes.
Q. And what was that advice do you say?
A. In regards to what specifically?
Q. To the diseases, and if you can recall in relation to CMV?
A. There was a list of diseases and Janet Robinson went through how individual diseases were - how cross infection occurred with various diseases. I don’t know if she went through all of them. She listed some. I don’t know if she went through each one individually or in groups or whatever. The emphasis was on washing hands and using diluted bleach to clean surfaces.
Q. And ensuring that all toys were disinfected?
A. I think that was included, yeah.
…………….
Q. And what was being promoted was a very strict regime of hygiene to prevent infection and cross infection wasn’t it?
A. Yes.
Q. You clearly understood that to be the case?
A. Yes.
Q. And you clearly understood, did you not, that many of the diseases including CMV were diseases which had dangers for both the child carer and for the children?
A. I don’t think there was that emphasis. It was more amongst the children, care of the children was the emphasis.
Q. But there was no doubt in your mind, was there, that these diseases were readily communicable?
A. Yes.
Q. And I take it you didn’t exclude yourself from the possibility that you might in fact catch one or other of the diseases mentioned?
A. I suppose not.”57 Mr Cranitch submitted, having regard in particular to the way the questions extracted from T8 were framed and the response Ms Robinson gave when confronted by the first plaintiff, asserting that the first plaintiff had been told at the meeting (the extract from T17 of the transcript) I would not find the relevant omission by the defendant. I do not accept that submission. Mr Cranitch did not put to the first plaintiff in cross examination that she had been given some specific warning and, having regard to the answer to interrogatory 8A, set out earlier, it seems clear that his instructions would not have permitted him to do so. Moreover, Ms Robinson has not been called.
58 I view the first plaintiff’s evidence as amounting to an assertion that she was not warned that pregnant women’s foetuses were vulnerable to CMV. It was the first plaintiff’s grievance that she had not been told about this which prompted her to speak to Ms Robinson after Dr Grigor had made his diagnosis. I accept the first plaintiff’s evidence that I have reviewed as being truthful and reliable.
59 I find that the defendant was negligent in failing to give the warning I have defined in paragraph 45.
60 I turn to consider the second allegation of negligence pursued by the plaintiffs, set out in para 26(ii) above.
61 In reviewing the first plaintiff’s working history I referred to the change that occurred after the first plaintiff returned to work in January 1992, when she was transferred to work with children under two years of age. It is clear that before the decision to place the first plaintiff with the under two year olds took effect, the defendant knew that the first plaintiff was pregnant. I find that the first plaintiff told not only the director of the centre, but also the mothercraft nurse at the centre, Ms Lumsdane (T10-11).
62 A considerable amount of evidence has been introduced which addresses the comparative risks of infection from working with children under two and children older than two years of age. Prof Isaacs expressed the opinion that the risk for women in child day care centres is “particularly high with workers looking after children under two years old.” (report dated 9 September 1993). Prof Rawlinson was questioned in his evidence at some length about this matter. His evidence was that the younger the child the greater the excretion of CMV. Prof Rawlinson was asked this question and gave this answer at T290:63 Then at T358:
“Q. So, in other words the younger the child the more virus there is likely to be in the environment, the more likelihood that the virus will be in the environment?
A. Depending upon the age. So if a child is very young, they pass more; a large amount of virus in their urine and also they tend to be in nappies and in a less controlled, situation than say a three or four year old where they can use the toilet themselves. The amount of virus in all children less than five years of age is very high and it is my opinion that the suggestion that spread of infection is more easy in the younger children is as dependent or possibly more dependent upon access of adult to that urine, that is because they are changing nappies or because they are soiling rather than the actual amounts of virus.”
“Q. First of all, you would expect, as listed here in the first column, working with babies you would be much more likely to have contact with the CMV?
A. Yes, the evidence is that if you work with children less than two, because babies very frequently acquire CMV they would be excreting higher amounts, as we discussed beforehand. Not only the fact that the baby has CMV, the amount of CMV and availability of, and access and presumably a baby of two who may not be able to typically be in nappies, there is also access. So, as you say there is a number of different features that add to the risk of infection.”64 Dr Hall gave evidence that the youngest children give rise to the greater opportunity for transmission of the virus because of the presentation of dirty nappies (T145).
65 The paper from Dr Adler to which I made earlier reference recorded the conclusion that the risk to workers in day care centres of acquiring CMV from children there was “significantly greater” amongst those workers caring for children under two years of age.
66 I find it to be more probable than not that the risk of acquiring CMV was greater for a worker placed in the environment into which the first plaintiff was transferred in January 1992 than it had been in the environment in which the plaintiff worked in 1991. The evidence which I find supports that conclusion is persuasive, but did the defendant have such knowledge at the relevant time? The absence of toilet training in the under two group is a very obvious risk factor present in the environment into which the first plaintiff was transferred. The “absence of toileting skills” was a particular factor addressed by Dr Ferson in the “Rattler” article and was identified as one of a number of factors greatly increasing the risk of transmission of infection and as placing carers at risk.
67 It seems to me that an awareness that the first plaintiff was in the early stages of pregnancy added emphasis to the need for the defendant to warn the first plaintiff of the risk of harm to the unborn child so as to afford her an opportunity to determine whether she would continue to work in the day care environment at all, and in particular whether she would work in the altered day care environment with the added exposure to dirty nappies. Absent any warning, I find that the defendant was negligent in transferring the first plaintiff in January 1992.
68 For the above reasons I find that negligence has been proved.
69 Contributory negligence was pleaded, but Mr Cranitch did not rely upon this defence.
70 Was such negligence as has been proved causative of harm? It is for the plaintiffs to prove that it was: see Bendix Mintex Pty Limited v Barnes (1997) 42 NSWLR 307 per Mason P at 311 and Beazley JA at 339; ICI Australia Operations Pty Limited v Walsh & Ors (1997) ATR 81-452; and Wallaby Grip (BAE) Pty Limited (In Liq) v Macleay Area Health Service 17 NSW CCR 355 and in particular the judgment of Beazley JA at 362-363.71 In the circumstances of this case the plaintiff must prove:
Causation
(i) on the assumption that the second plaintiff did acquire primary congenital CMV, that had the plaintiff been given the appropriate warning she would probably have avoided the risk of such acquisition.
The need to establish this causative link is clear. It may be emphasised by reference to Turner v State of South Australia (1982) 42 ALR 669 in which Gibbs CJ said at 670:
“When the employer does unreasonably fail to take a precaution against danger, the plaintiff cannot succeed unless he satisfies the court that if that precaution had been taken the injury would probably have been averted, or, in other words, that the safety measures would have been effective and that he would have made use of them if available; Duyvelshann v Cathcart & Ritchie Ltd (1973) 1 ALR 125.”
(i) Absent negligence, would the harm have been avoided?
(ii) Secondly, the second plaintiff’s disabling condition was primary congenital CMV acquired by reason of the defendant’s negligence;
72 As to (i), the first plaintiff’s evidence was, and this appears from an extract from T17 set out earlier (at para 55), that had she been aware of the risk, the plaintiff would have had a blood test to see whether she was immune to CMV or not, and that she would not have worked with young children.
73 I observe in considering this response that unless the plaintiffs satisfy me that the first plaintiff acquired primary CMV infection during pregnancy this action must fail, so for the present it is to be assumed that a blood test taken at the time warning and instruction ought to have been given would have proved negative. What then would the first plaintiff be likely to have done had the defendant discharged its obligation by warning and instruction?
74 Mr Walmsley submitted that even if the first plaintiff had decided to carry on working with the defendant after being given appropriate warning and instruction she could have avoided the risk of infection by greater attention to hygiene. I do not accept this submission because I accept the first plaintiff’s assertion that she was careful about hygiene and that she complied with the standards set by her employer in August 1991 to the best of her ability (T41).
75 Would the first plaintiff have declined to work with young children as she claimed she would have done?
76 I must exercise caution in assessing the first plaintiff’s evidence that she would not have continued to work with small children had she been given appropriate warning and instruction. Whilst I have assessed the first plaintiff as being an honest and reliable witness, and whilst I accept that the first plaintiff was being honest in stating what her reaction would have been to an appropriate warning, I must bear in mind that in giving her evidence the first plaintiff is equipped with the benefit of hindsight. The first plaintiff now knows of her son’s disability and entertains the belief, I have no doubt honestly, that his misfortune could have been avoided if his mother had not worked for the defendant, coming in contact with young children during her pregnancy. Her conviction that she would not have continued to work for the defendant is doubtless influenced by her belief. However, as Samuels JA observed in a decision to which Mr Walmsley very properly referred:
“…It is open to a court to disbelieve evidence found to be tainted by hindsight.”
See Ellis v Wallsend District Hospital (1989) 17 NSWLR 553 at 581.
77 In deciding whether the discharge by the defendant of its duty to warn would probably have avoided the harm suffered, I must apply a subjective test: see Ellis v Wallsend District Hospital (supra) per Samuels JA, again at 581. How would the first plaintiff have reacted to appropriate warning and instruction?
78 Mr Cranitch submitted that I would not be satisfied that appropriate warning and instruction, if given, would have altered the course of events. In considering that submission I must be mindful in particular of these matters:
(i) that the first plaintiff agreed that she was concerned that there were risks of various diseases in her continuing to work with small children at a day centre that may have affected her health in pregnancy (but which did not cause her to seek work elsewhere);(ii) that the first plaintiff was aware rubella was a major cause of foetal abnormality, especially in the first trimester;
(iii) that the first plaintiff was aware that hepatitis B was a disease which, if contracted, would probably mean that she would have not been healthy in her pregnancy and she did not think that she discussed this with her doctor;
(iv) that the first plaintiff’s qualifications were as a child care worker and she enjoyed the work, and wanted to continue in it during and after her pregnancy;
(v) that by the end of January 1992 the first plaintiff appreciated that because of the failed relationship with Jacob’s father she would be raising Jacob as a single mother. I would accept that would have involved a financial need for continued employment.
79 It is relevant in weighing the above matters that the first plaintiff said, and I accept, that the only disease of which she was aware that could cause foetal abnormality was rubella, and that when she discovered her pregnancy the first plaintiff underwent tests to ascertain her continued immunity to rubella. The first plaintiff said she was unaware that hepatitis B could cause complications in a pregnancy and that she did not know that any risks in the child care environment involved risk to her child. I accept that this was her belief until after she gave birth to Jacob.
80 The plaintiff said that had she not been working in day care there were other options such as working with older children out of school hours.
81 I regard it as significant that the first plaintiff made changes to her lifestyle after she became aware of her pregnancy and, I am satisfied, because of it. In the interests of her unborn child the first plaintiff gave up smoking and she ceased to be a vegetarian. The change in diet followed advice from the first plaintiff’s doctor that she had to improve her nutrition.
82 I formed the impression of the first plaintiff that she was a young lady who would have taken her responsibilities to her unborn child most seriously, and on balance I accept that she would have given up child care work had she been alerted by the defendant to the risk to her child as expressed by Dr Ferson in the “Rattler” article earlier mentioned.
83 Turning from the failure to alert and to warn the plaintiff, what was the significance, in a causative sense, of the further negligence I have found, namely in transferring the first plaintiff to work with the children under two years of age? The first plaintiff placed this event as having occurred in mid to late January 1992 (T11).
84 On the assumption that Jacob did acquire congenital CMV from primary infection in his mother, when did this occur? Evidence as to this has been given based upon neuroimaging of the second plaintiff. A cranial MRI was performed on 19 July 1994 and this disclosed abnormalities which were interpreted by Dr Kendall, a neuroradiologist specialising in paediatric neuroradiology, as supporting a diagnosis of CMV. I shall consider this evidence more closely when addressing the issue as to whether the second plaintiff has been proved to be suffering from congenital CMV as a result of primary infection in his mother.
85 However, in the present context it is necessary to consider and assess the evidence which was given as to when the abnormality shown by MRI developed. The report from Royal North Shore Hospital Department of Radiology, where the MRI scan of the brain was done, dated the insult “to at least the second trimester of pregnancy”. Dr Grigor was unable to express an opinion as to the stage at which the infection of the foetus had began when he was asked to consider the significance of the MRI in this context (T141). Prof Isaacs appears to have accepted that the infection process occurred in the second trimester of pregnancy, that is between weeks thirteen and twenty-six of gestation (T151). As I understand his evidence, Prof Isaacs adopted the available neuroradiological opinion about this; Prof Isaacs commented (T151):86 Later (T158), Prof Isaacs expressed his belief that the MRI was an indicator to the time of the occurrence of the infection and said that
“…Dr Kendall and I think all the neuroradiologists agree that it is in fact likely to be between the thirteenth and twentieth [weeks] of gestation”.
87 Dr Kendall stated in his report of 17 January 2000:
“If it was caused by CMV infection, Linda must have been infected at about that time, thirteen to twenty weeks gestation.”
88 In his oral evidence (T259) Dr Kendall said that he thought the damage to the foetus commenced
“I agree with Dr Boldt’s timings. The insult is most likely to have taken place over a period between fifteen and thirty weeks of gestation.”
“somewhere about sixteen to eighteen weeks gestation and that it continued until gliosis was occurring.”
89 He explained this would have meant it continued up to twenty-six weeks of gestation.
90 Jacob was a full term baby, so conception occurred about 14 November 1991. On the evidence reviewed, the infection process of the foetus began no earlier than the thirteenth week of the mother’s pregnancy, that is to say no earlier than 13 February 1992, and of course it could well have begun later in February. However Prof Isaacs gave evidence (T196) that the incubation period for the infection was “about two to four weeks”. The incubation period of a disease is generally defined as the time that elapses between the implanting of the organisms of an infective disease in the host and the appearance of the first clinical symptoms of the disease. What is meant by the incubation period in the present context has not been precisely defined, but as I understand it the significance of the incubation period in the present context is that it represents the period that would have elapsed between the entry of the organisms and the evidence indicating when damage to the brain commenced as detected radiologically. The evidence thus establishes that the incubation period could have begun as early as 16 January 1992.
91 Of course I am mindful that it is not possible to express times in the present context with certainty, and I must make allowance for this. However it follows from what I have recorded as to times, that I am unable to find that the CMV was acquired by the first plaintiff (assuming primary infection) after her transfer to the higher risk area working with the children under two years of age. The first plaintiff was not precise about the date of transfer, which could have been late in January 1992 (T11). It follows that the plaintiff has failed to establish that her transfer was significant in a causative sense.
92 However, that the first plaintiff did continue to work as a day care worker after she became pregnant I do regard as significant in a causative sense (assuming primary infection). I am mindful of course that the first plaintiff could have acquired CMV other than in her work environment. The evidence disclosed that CMV is commonly present in the community, although its incidence varies depending upon socio-economic factors. Without seeking to be exhaustive, the virus may be transmitted through contaminated secretions or by the respiratory route (Prof Isaacs T164); it may be transmitted in sexual activity (T164); or by intimate contact (Dr Grigor T103-104); and of course it may be transmitted to adults by young children in the day care environment. Allowing for the possibility that this disease may have been acquired by the first plaintiff away from her work environment, if this was a case of primary infection, I consider it to be more probable than not that the plaintiff acquired the disease at her workplace. I am mindful of the evidence Prof Isaacs gave about this (T162):
“Making the assumption that Jacob had congenital CMV infection…the odds were greatly in favour of [the first plaintiff] having acquired CMV in her work, rather than in the day to day normal activities.”
93 I accept the above expression of opinion by Prof Isaacs (assuming for the present the mother acquired primary infection in her pregnancy), and I am influenced by that in the finding I have stated.
94 It follows that if this was a case of primary infection of the mother in pregnancy causing the harm to the foetus, I consider such harm to be causally linked to the defendant’s negligence. This is because I am satisfied on the balance of probabilities that if the defendant had given the first plaintiff the appropriate instruction and warning as to the risk of harm to the unborn child should she acquire CMV, the first plaintiff would not have continued to work in the day care environment, even with two to three year old children. The appropriate warning should have been given before the first plaintiff advised the defendant of her pregnancy and again after such advice.
95 However has the evidence established that this is a case of congenital CMV due to primary infection of the mother in 1992? To a consideration of this most difficult issue I now turn.96 Has it been proved that Jacob is suffering from congenital CMV through the exposure of his mother to the virus in the course of her work with the defendant. This involves consideration of discrete issues:
(ii) The definition of the disorder of the second plaintiff
(a) Is his condition caused by congenital CMV?(b) If so, was this acquired in consequence of work related primary infection of his mother during her pregnancy, in turn passed on to Jacob?
(a) Is the condition due to congenital CMV?
97 In seeking to prove their case, the plaintiffs rely in particular upon the evidence of Dr Grigor, Prof Isaacs and Dr Kendall. Dr Hall was also called in the plaintiff’s case but his expertise is in occupational medicine and his focus was on the measures that would have been available to the defendant to minimise risk of exposure to CMV. Dr Hall did not profess to have any particular expertise in CMV and I do not understand Mr Walmsley to rely upon his evidence to support the diagnosis for which the plaintiffs here contend.
98 Dr Grigor is a specialist physician of long standing. He has specialised in paediatric internal medicine, having thirty-five years of clinical practice. In that time Dr Grigor said he had seen a lot of children suffering from intrauterine infection “of which CMV would have been the commonest” (T68).
99 At the first consultation Dr Grigor did not reach a positive diagnosis. His evidence as to the position following this consultation was as follows (T66):
“A. Well, I didn’t reach a definitive diagnosis but I was concerned that he had what I might have diagnosed as microcephaly. His head was pathologically small. He had features of cerebral palsy. He had increased tone in his limbs with abnormal movements. I might explain, it is extremely difficult, if not impossible, to confidently diagnosis cerebral palsy in the first year of life, because those sort of signs can go away, in the course of the first year of life. So one can see those features and suspect cerebral palsy but prudently, one would not conclude that that was so, until one watched the progress over a period. So I saw him as having those two major features.
Q. Is a small head and features suggestive of cerebral palsy?
A. They suggested to me that possibility that he had suffered an intrautero insult, most likely to be caused by some viral infection; some infection, not solely viral, and I instigated an investigation based on the proposition that that might be the cause of the trouble.
Q. What was it that suggested to you that it was something that had happened intrautero?
A. The failure of his head to grow, particularly in association with the neurological deficit, abnormal neurological features, which indicated to me that something had gone wrong with the growth of his brain; presumably something had in some way damaged his brain intrautero.”100 Dr Grigor arranged for a blood count and other investigations, known as TORCH status studies, which studies were designed to detect a range of infections including CMV. The blood count was normal and there were also negative results to the TORCH test including the complement fixation test for CMV. The urine sample taken from Jacob showed that he had the CMV virus but that sample analysis taken at three months did not prove the acquisition of the virus congenitally. It may have been a recent occurrence.
101 Dr Grigor explained that in reacting to a viral infection the body responds by forming antibodies, and in ordering tests for CMV Dr Grigor was looking for evidence of the presence of immunoglobulins. That evidence was not forthcoming because the test results were negative. Dr Grigor found that puzzling and ordered repeat testing to see if there had been a mistake made with the first tests. However the second set of tests again produced a negative result and Dr Grigor said he was surprised by this. Nevertheless he still suspected CMV. His view was strengthened by the emergence of evidence that Jacob was profoundly deaf. Tests detected this state of affairs in January 1993 and on 25 January 1993 Dr Grigor wrote to Prof Gibson for the purpose of having the hearing loss addressed. When writing to Prof Gibson, Dr Grigor said that the child “almost certainly has CMV infection acquired transplacentally.”
102 Addressing Jacob’s deafness, Dr Beckenham, a paediatric ear nose and throat specialist who was not required for cross examination, reported on 29 July 1993:
“The deafness is almost certainly congenital deafness related to cytomegalic virus.”
103 A CT brain scan was done was 1 February 1993. The result was an abnormal one and the test showed “extensive cerebral white matter abnormalities with poor white/grey inter-digitation.” Dr Grigor interpreted that as meaning that there had been some insult to the baby at an early stage of development. He said it was a very non-specific finding but it demonstrated some intrautero infection had taken place. The CT though showed no calcification.
104 Dr Grigor continued to see Jacob and his mother through 1993, 1994 and 1995 until he retired from private clinical practice. He did not see Jacob after that because he needed acute management and for this Jacob was passed to the care of Dr Delocry.
105 Notwithstanding (1) the absence of an enlarged liver and an enlarged spleen, (2) the absence of calcification shown on the CT, (3) absence of petechiae, and (4) the negative serology results, Dr Grigor expressed the following view in his report to the first plaintiff of 22 March 1993:
“Since I first saw Jacob on 4 November 1992 it has become evident that he has suffered intrauterine infection with cytomegalo virus (CMV) which has led to microcephaly secondary to damage to his brain, a spastic cerebral palsy and marked developmental delay.”
106 Dr Grigor did not later change that opinion, as his evidence before this Court demonstrated.
107 Commenting in his evidence upon the MRI report following the scan in July 1994, Dr Grigor gave this evidence (T75):108 In cross examination Dr Grigor acknowledged that by February 1993 he was fairly well persuaded with his diagnosis and did not look for other possible alternatives. He explained why in the following answer (T95):
“Q. When you read it, did it cause you to change your diagnosis in any way?
A. No, it didn’t.
HIS HONOUR: Q. Does it influence that diagnosis, one way or the other?
A. I think it indicates, your Honour, that Jacob clearly suffered some significant insult to his brain, in the second semester of pregnancy, in the middle of the pregnancy roughly, which I’d inferred, from the evidence previously available, had happened. I guess it leant formal conformation that that had taken place and confirmation such as was suggested in the less sophisticated CT scan at the earlier time. So it added to that conclusion. It added weight to that conclusion, without necessarily telling me that it was one thing or the other. But putting it with all the other evidence that I felt I had on clinical ground, it strengthened my conclusion that it was likely to be a CMV infection.”
“One, I believe the diagnosis was so probable, not certain but so probable that I was very comfortable with it clinically and, secondly, pursuing a diagnosis that doesn’t fit in with all those features and will not change the - which will not change any of the management or the prognosis for the patient I am treating is not particularly appealing as it involves invasive investigations of a little baby.”
109 Prof Isaacs is Clinical Professor of Paediatric Infectious Diseases at the University of Sydney. He is the former head of the Department of Immunology and Infectious Diseases at Royal Alexandra Hospital for Children and he is now a senior staff physician at Westmead Children’s Hospital.
110 Prof Isaacs was not called upon to treat Jacob but he wrote a number of reports about the case dated 9 September 1993, 17 December 1996 and 27 June 1999. His opinion, as expressed in the latest of these reports, reads:111 When Prof Isaacs wrote the last of his reports he was not aware of the second set of seronegative test results but, having considered these test results, Prof Isaacs stated his opinion in his oral evidence (T153):
“In my opinion, the constellation of clinical, laboratory and radiological findings make a diagnosis of congenital CMV infection highly likely. It is difficult for me to put an exact figure on the likelihood that Jacob’s disabilities result from congenital CMV infection, but I would certainly say it is more likely than not that they are a result of congenital CMV infection.”
112 In cross examination Prof Isaacs was, inter alia, asked the following questions and gave the following answers (T159):
“My opinion is that on clinical grounds and the balance of probabilities that Jacob had suffered from congenital (CMV) infection as the cause of his disability…”
“Q. And in the evidence, I think we have heard from another expert, the symptom complex that may result, commonly described as cerebral palsy, can be an obvious and often is undiagnosible in around about 80 percent of cases?
A. Jacob has combination of symptoms, not just cerebral palsy but also [sic] essentially neural deafness, nerve deafness that is suggestive but not diagnostic of congenital CMV infection.
Q. Again there are other infections, if I can use the word broadly, other insults to the foetus, which can result in that form of sensory neural deafness?
A. Yes, if they occurred earlier in the pregnancy. For example, congenital rubella syndrome, would have to have occurred, which is not possible in this case, would have to have occurred in the six to eight weeks it generally takes to damage the developing baby at that stage. CMV is different in a malformed brain that is already deformed, whereas those other infections you talk about rubella and toxoplasmosis and so on, they deform a brain as it is growing at a critical stage of development, which is much earlier than the second trimester.
Q. There are other unknown congenital deafness cases where the cause simply cannot be ascribed, aren’t there. It is not simply limited to the factors that you have indicated is it?
A. No, what I am saying is there is a combination of defects in Jacob, that pushes me very strongly towards this being caused by congenital CMV infection. There are two indicators --
Q. There are many contra-indicators in Jacob’s case aren’t there?
A. No. I would say that he has a small head and evidence of a neurapraxia disorder at 13 to 20 weeks. That is in the second trimester. He has cerebral palsy and sensory neural deficit and that he acquired the cytomegalo virus sometime between being a foetus to three months of age and that adds up to an enormous co-incidence if it is not due to congenital CMV infection. So if Jacob’s disabilities were not caused by congenital CMV infection, we have no good explanation for what has caused them and we have to say that his acquisition of CMV by three months of age was a coincidence and I think that is less likely than his whole condition is due to congenital CMV.”113 Dr Kendall was brought from the United Kingdom to give evidence. Dr Kendall’s impressive curriculum vitae was tendered and his expertise as a neuroradiologist was clearly established.
114 Dr Kendall considered the MRI films and reported that they showed abnormalities115 In his evidence in Court, and by reference to images, the doctor pointed to presentations on the images which he described (at T210) as
“typical of polymicrogyria associated with regions of gliosis and possible calcification. They are very consistent with congenital cytomegalic inclusion virus infection occurring in the second trimester and resulting in abnormal cortical organisation with dysplasia.
The corpus callosum, brain stem, cerebellum and cervical spinal cord are normal.
The Sylvian fissures are shallow but there is no other evidence of malformation.
The membranous labyrinths are normal.
High resolution CT scans of the temporal bones are of very good quality. The middle and inner ears are shown to be normal.
The imaging features strongly support the diagnosis of congenital cytomegalic virus infection acquired in the second trimester.”
“abnormalities…absolutely typical of cortical dysplasia…an abnormality in the development of the brain caused by interference with development of the cortex.”
116 A further abnormality reflected by damaged white matter was defined as gliosis. In the opinion of Dr Kendall, the combination of the cortical dysplasia and the gliosis was “highly suggestive of a foetal infection by [the cytomegalovirus]” (T212). As to the other abnormalities shown, Dr Kendall thought these were secondary.
117 Dr Kendall was asked this question and gave this answer (T214):
“Q. You say that you agree that the MRI findings are not diagnostic of congenital CMV. In that context, what did you mean by diagnostic?
A. Well, if I were shown those images with no information, except that the child had some kind of cerebral palsy, my report to the clinician would be the description that I have already given to you. And it would say that these appearances strongly suggest cytomegalic inclusion virus infection but that obviously we would need clinical and other input, to confirm that diagnosis. We wouldn’t leave it at that. But I would go so far as to say, they were highly suggestive of the diagnosis, even on its own, that image.”118 In the above review of the evidence of the specialists called by the plaintiffs, I have not attempted to do more than record in outline the opinions supporting the finding of congenital CMV. Each doctor was extensively cross examined by Mr Cranitch and by Mr Poulos and each of the doctors was criticised by Mr Cranitch and Mr Poulos. The cross examination and criticisms addressed contra-indications to the diagnosis advanced on the plaintiffs’ behalf and require close consideration.
119 The defendant called one witness, Prof Rawlinson. As with the experts called in the plaintiffs’ case, I am satisfied that Prof Rawlinson is highly qualified in his field. He is an associate professor in the School of Pathology at the University of New South Wales and as a medical virologist works in the Division of Virology in the Department of Microbiology and the Department of Infectious Diseases at the Prince of Wales Hospital. Prof Rawlinson has made a special study of CMV, particularly over the last six years, and he described his research unit as the largest unit in Australia studying the human side of CMV. Having been qualified to give evidence in this case, Prof Rawlinson provided a number of reports which were introduced into evidence. Whilst Prof Rawlinson accepted that the second plaintiff had the symptom complex of cerebral palsy and deafness, in his opinion these features did not justify a diagnosis of CMV. Prof Rawlinson said that a large number of children with cerebral palsy and/or deafness remain undiagnosed.
120 Prof Rawlinson identified as the principal reason for concluding that Jacob does not have CMV the negative serology results. Prof Rawlinson was asked this question and gave this answer (at T280):121 Other features which Prof Rawlinson identified as unusual in a sufferer of congenital CMV were the absence of an enlarged liver and an enlarged spleen and the absence of petechiae. Further there was the absence of intracranial calcification. These features Prof Rawlinson did not regard as ruling out congenital CMV but he said they were “unusual in a child with severe congenital CMV”. He went on to say (T 281):
“Q. You have, whilst conceding that his disabilities are consistent with cerebral palsy, you formed the view that this cerebral palsy was not the outcome of CMV infection. Is there is a primary reason why you espouse that view and I know you have given several in your report, what is the overriding feature that you believe that leads you to the conclusion that you formed?
A. When I wrote my initial report Jacob Hughes was described as having a complement fixation titre or CFT, as negative, less than one in eight: Which was taken at three months of age. I regarded that as very strong if not definitive evidence that he did not have congenital CMV despite the fact that he had CMV grown from his urine subsequently I think at four months of age. There is a subsequent test result that I saw yesterday - in fact I saw about a week ago. There is a subsequent test result that I was told about about a week ago and that I saw yesterday which indicated that a subsequent complement fixation test was also negative done at four months of age. It is not possible to diagnose congenital CMV in the absence of antibody in the child. It is possible for a test to be falsely negative and I gave the figures of three percent per test yesterday. It is unlikely as the CFT is a sensitive assay and when this was done, eight years ago the assay had been in use for some time and was well controlled. The occurrence of CMV growing in Jacob’s urine at four months of age, I regarded as an interesting finding but non diagnostic of CMV causing his malformation because of the reasons I have given previously.”
“What is as absolute as medicine gets is the absence of CMV antibody in his blood on two occasions within four months of birth.”
122 In Prof Rawlinson’s opinion the absence of antibodies to CMV when Jacob was three months of age and at four months of age “makes the diagnosis of congenital CMV untenable” (T330).
123 As with the doctors called by the plaintiff, I have not referred above exhaustively to the evidence Prof Rawlinson gave and again his evidence has called for close examination. I must also consider the criticisms which Mr Walmsley made of this witness.
124 Diagnosis in this case was made more difficult by the passage of time because on the evidence it would appear that no blood test was undertaken until Dr Grigor ordered his tests in the fourth month of Jacob’s life. The importance of testing soon after birth as a diagnostic tool is clearly established by the evidence. As Prof Isaacs proffered (T177):
“The diagnosis of congenital CMV infection is made by growing the virus from the baby in the first week of life or by finding IgM antibodies for CMV present in cord blood or in the baby at birth.”
125 Prof Rawlinson defined the critical period as being the first three weeks of life (p 9 of report of 3 September 1998). Prof Rawlinson also referred to consensus statements by experts to the effect that “the absence of IgG antibody to CMV in cord or infant blood rules out congenital infection”: see Prof Rawlinson’s report of 18 January 2000 at p 7.
126 It is plain that what Prof Isaacs referred to as “the window of opportunity” (T 177) for the most reliable diagnosis was lost in this case, because there was no analysis undertaken of cord or infant blood.
127 Apart from the negative serology results, other features of the case which are not typical of CMV have been identified in the medical evidence. There are absent in Jacob’s case features that may be found in congenital CMV, and in particular there has not been detected:
(i) an enlarged liver and an enlarged spleen;(ii) petechiae;
(iii) any evidence of intracranial calcification.
128 I have considered what each of the experts regarded as the diagnostic significance of these missing features.
129 Dr Grigor reported to Dr Honeyman on 22 March 1993 (Exhibit C, p 168) that Jacob had no enlarged liver or spleen, although earlier he had reported on 4 November 1992 that the spleen was then palpable, and that this was not a normal finding (T 73). What Dr Grigor said as to the significance of spleen enlargement was this (at T74):
“The spleen enlarges for many reasons, the commonest of which would be infection. It’s enlarged, as I have already explained, in children born, often but not always, in children born who have suffered an intrautero infection. The fact that he had an enlarged spleen at the age of three months and that hadn’t been recorded beforehand by anybody, made it hard to interpret what it meant. But it would have been consistent with him having had an intrautero infection. It could have been consistent with him having had an infection after he was born. That infection could, by inference, have been CMV, as he did have it in his urine.”
130 I do not find in Dr Grigor’s evidence, particularly in regard to his report to Dr Honeyman of 22 March 1993, any convincing evidence of abnormal enlargement of spleen or liver, and it would not appear that any such enlargement was detected in hospital following Jacob’s birth.
131 There was apparently no jaundice detected, and had this been detected this could have indicated liver malfunction, according to Dr Grigor. However babies are frequently jaundiced, so that the presence or absence of jaundice in Jacob’s case was not, as I understand Dr Grigor’s evidence, a useful indicator concerning CMV. Nor was absence of an enlarged spleen. Such absence was “wishy-washy” and was not persuasive one way or another diagnostically (Dr Grigor T 133).
132 Dr Grigor did say of one hundred babies born with CMV, ninety to ninety-five percent of those would show no features of jaundice or petechiae (T 94).
133 Dr Grigor said that intracranial calcification would be present in roughly forty percent of cases only (T 94).
134 Prof Isaacs was alert to the absence of an enlarged liver and an enlarged spleen; he was also aware that Jacob did not have petechiae or intracranial calcification, which calcification he said occurred in about fifty percent of cases. However he said that in making a clinical judgment it was necessary to evaluate that which was present and that which was not (T 181-182). The absence of those features did not dissuade Prof Isaacs from his diagnosis in Jacob’s case of congenitally acquired CMV.
135 Dr Kendall said, in relation to the CT scan and the radiologist’s report that there was no calcification, that calcification occurs (“according to the results of a very large study”) in about forty-three percent of children with congenital CMV. In his opinion its absence “certainly by no means excludes the diagnosis [of CMV] and is entirely consistent with it” (T216)
136 As to the absence of intracranial calcification, Prof Rawlinson said studies he had considered indicated that in cases of severe malformation the incidence of calcification was as high as seventy percent, and because of the severity of Jacob’s malformation the likelihood of his having calcification if he was suffering from congenital CMV was of the order of seventy percent. In earlier reviewing the evidence of Prof Rawlinson I recorded (at para 121) his opinion that the absence of intracranial calcification and petechiae and the fact that Jacob did not have an enlarged liver and a big spleen were unusual features in a child with congenital CMV.
137 As I assess the expert evidence, it seems to me that I should regard the absence of intracranial calcification, the absence of an enlarged liver and an enlarged spleen, and the absence of petechiae as rendering the diagnosis of congenital CMV less probable than it would have been had those features been present, but not impacting upon such diagnosis so as to make it an unlikely one. Prof Rawlinson, who is the only expert who does not consider that Jacob was suffering from congenital CMV, does not regard those absent features alone as excluding the diagnosis advanced on behalf of the plaintiffs.
138 However those are not the only features that stand in the way of such diagnosis. There are the negative serology results to be considered.
139 Prof Rawlinson considers that the results of the complement fixation tests which Dr Grigor arranged virtually ruled out the diagnosis of congenitally acquired CMV. I referred earlier to his evidence about this at paras 120-122. In cross examination by Mr Walmsley Prof Rawlinson said he no longer regarded it as possible that Jacob had congenital CMV (T346), and the strongest element in the case that ruled out such diagnosis was the absence of the antibodies in Jacob’s blood at three and four months of age (T347).
140 Prof Rawlinson was firm in his opinion rejecting the diagnosis advanced by Dr Grigor, Dr Kendall and Prof Isaacs. Indeed his conviction in rejecting such diagnosis was the subject of criticism by Mr Walmsley who urged that I should view this as an unsatisfactory feature of his evidence.
141 How do the doctors upon whom the plaintiff relies account for the absence of antibodies in Jacob at the time the relevant testing was undertaken?
142 As I observed earlier, Dr Grigor was “puzzled” by the first negative test results and he was “surprised” by the second negative test results. Plainly, since notwithstanding the negative test results, Dr Grigor felt “comfortable”; he did not attach the same importance to those results as Prof Rawlinson. It is equally clear that neither did Prof Isaacs. This, I suspect, is to be explained at least in part by reason of the differing specialities in which the three experts practise.
143 Dr Grigor recognised that the second negative result ruled out laboratory error. Given that Jacob was shedding CMV through his urine, Dr Grigor considered it unlikely that the child had a post natal infection, because he would have expected Jacob to have produced antibodies to the infection over the period between the two tests, had the infection occurred after birth. Dr Grigor reasoned that the child’s failure to manufacture antibodies was explicable on the basis that (because the infection was in utero), “his body recognised the [CMV] as itself and so did not see itself as a foreign antigen, a foreign stimulant to producing antibodies” (T87). Dr Grigor conceded he was not aware of other cases where a failure had been explained on this basis, and he also conceded a possible explanation for the absence of antibodies in the presence of the CMV post natally was that when the urine was tested the infection may have occurred so recently before that test that the child was still to develop antibodies to the virus (T88).
144 Prof Isaacs acknowledged that the first of the complement fixation tests did not support the diagnosis he made, but he did not think that it excluded it either (T153). He regarded the second test result as “confusing”. Prof Isaacs saw as the explanation for the absence of antibodies in Jacob’s blood that the child’s immune system “was deliberately not seeing the virus”. The professor went on (at T154):
“In other words, it’s a situation analogous to trying to vaccinate a baby at birth and sometimes you can’t do that because the baby thinks that the vaccine you are giving is the baby’s itself so refuses to recognise it. The baby gets mixed up between what is foreign and what is itself. So that would be my considered explanation. It’s an explanation I’ve discussed with a very learned colleague, Professor Lyn Gilbert at Westmead Hospital who is an authority on antenatal infection…”
145 Neither Dr Grigor nor Prof Isaacs resiled from the possible explanations each advanced for the seronegative test results during cross examination. Nor did Prof Rawlinson depart from his perception as to the definitive consequences of the absence of antibodies in Jacob’s system, namely that Jacob was not suffering from congenital CMV.
146 Prof Rawlinson, referring to the tolerance explanation advanced as accounting for the absence of antibodies, called it “a plausible hypothesis by one of my peers in the medical profession whom I respect” (T348) but he disagreed with both Dr Grigor and Prof Isaacs in the conclusions they reached. Indeed Prof Rawlinson regarded the margin for error in the conclusions which he, Prof Rawlinson, had reached as being “extremely low and in my opinion almost negligible.”(T349)
147 The disagreement between the medical experts in this case is clearly defined. On the one hand Dr Grigor, Prof Isaacs and Dr Kendall support the diagnosis for which the plaintiff contends; on the other hand Prof Rawlinson rejects it, and rejects it in the most emphatic of terms.
148 In the course of submissions both Mr Cranitch and Mr Poulos have been critical of the doctors called by the plaintiff and have submitted that I should view their evidence as unsatisfactory. It was submitted that the evidence of each doctor so called was flawed, and that I should regard each as sympathetic to the plaintiff. It was submitted that Dr Grigor made a diagnosis that fitted in with some symptoms consistent with his diagnosis, but that he did not consider other causes, albeit that he was aware of a very high percentage of cases in which what causes cerebral palsy remains undetected. It was submitted that Prof Isaacs was pro-plaintiff and lacked objectivity in reaching his opinion as to the cause of Jacob’s disabilities. This lack of objectivity was manifested inter alia, it was submitted, by a reluctance to consider the possibility that the first plaintiff acquired CMV through sexual exposure although such a route is a recognised one for infection by this virus. Further it was submitted that Prof Isaacs lacked objectivity in not giving due consideration to the first plaintiff’s complete history as a child care worker, when he was recalled to give evidence concerning the recent study conducted at the University of Alabama (see Exhibit 4), a study to which I shall later refer in some detail. Dr Kendall was criticised as expressing opinions outside his field as an expert in radiology. It was also submitted that Dr Kendall’s evidence was flawed because he had the wrong history; he had understood that TORCH tests undertaken on Jacob were positive for congenital CMV, and it was argued that this must have influenced the opinion the doctor expressed.
149 Prof Rawlinson was also the subject of critical submissions. Mr Walmsley submitted that his evidence had to be approached with caution because the witness was too uncompromising in his ultimate conclusion and his dismissal of the contrary views expressed. It was further submitted that he gave evidence which was plainly wrong concerning his source of knowledge about the mothers who were involved in the study the subject of Exhibit 4.
150 I have had regard to the various criticisms of all the experts who gave evidence in this case, but I am satisfied not only that each of them was highly qualified in his particular field of expertise but that each gave evidence of opinions genuinely held. This assessment has not, of course, simplified my task.
151 The symptoms of cerebral palsy and Jacob’s deafness could have causes other than CMV. There are those features of CMV absent in Jacob’s case such as those I considered earlier. Then there is the absence of antibodies to the virus. That Jacob had CMV when his urine was tested, and that his mother was seropositive when tested in March 1993 may be coincidental. Jacob may have become infected with the virus after birth, and his mother may well have carried the virus as a result of her exposure to it in the ordinary course of living, and in particular in her case as a result of exposure to the virus in her calling as a child care worker.
152 However I find myself impressed by the expert opinions expressed by Dr Grigor and by Prof Isaacs that Jacob’s condition is due to congenital CMV. I am impressed with their assessment of what they perceive supports the diagnosis of congenital CMV in this case. I have also been considerably assisted by the evidence of Dr Kendall. In evaluating his evidence I am mindful of Mr Cranitch’s criticism to the effect that this witness went outside his field of expertise when he ruled out ischaemia as a cause of the white matter damage. Mr Cranitch submitted that his evidence was contradicted about this by Dr Grigor and by Prof Rawlinson. This involves consideration of the evidence that Dr Grigor gave in point (see in particular at T129) and the evidence of Prof Rawlinson (see in particular at T271-272) and the evidence of Dr Kendall (see in particular at T222, 223 and 247). Having considered the evidence that bears upon this submission, it seems to me that what Dr Kendall said in expressing a view that this plaintiff had not had an ischaemic episode was an opinion based upon his interpretation of the images he had considered. I understand his evidence in this way. Dr Kendall’s evidence satisfies me that the combination of cortical dysplasia and gliosis was, as he expressed it, “highly suggestive” of the infection of the foetus by CMV. I observe that Dr Boldt, a consultant diagnostic radiologist, was qualified by the defendant and that Dr Kendall commented on what Dr Boldt wrote in Dr Kendall’s letter to the plaintiff’s solicitors dated 17 January 2000 (Exhibit C, pp 51-52). It emerged in cross examination of Dr Kendall that Dr Boldt wrote a report (T214), but the defendant did not seek to introduce that report into evidence, nor was that doctor called. No explanation was given as to why the doctor was not called and I draw the inference that had he been called the evidence would not have advanced the defendant’s case.
153 Ultimately, notwithstanding the evidence of Prof Rawlinson, I find myself persuaded by the medical evidence introduced in the plaintiff’s case that it is more probable than not that Jacob is suffering from congenital CMV and I so find. Is this condition one which was acquired by reason of primary infection of the first plaintiff during pregnancy?
Was the CMV acquired in consequence of work-related primary infection of the plaintiff during her pregnancy or in consequence of a process of reactivation?
154 Earlier I dealt with the evidence as to the time frame in relation to the acquisition by the foetus of congenital CMV (paras 84-91 above). On such evidence I consider it to be more probable than not that the relevant incubation period for the infection did not begin at the soonest before 16 January.
155 It does not automatically follow from this however that the first plaintiff herself acquired the virus at about that time. It is recognised that the virus may be reactivated, and that it is possible for a foetus to become infected by reason of reactivation of the virus in the mother during pregnancy. This is well established by the evidence, so I need refer only to what Prof Isaacs wrote in his report dated 27 June 1999 (Exhibit C, p 47):
“Cytomegalovirus (CMV) is a herpes virus and can persist and reactivate. Congenital CMV infection can follow primary maternal CMV infection (mother first infected in pregnancy) or maternal reactivation/secondary infection (mother infected in past, but reactivates in pregnancy)”
and to the evidence of Prof Rawlinson (T397):
“Reactivation is an extremely common event found during pregnancy occurring in something like one third to one half of all women.”
156 Whilst the evidence establishes that the first plaintiff was seropositive for CMV in March 1993, this establishes only that she had been infected in the past, but not when that infection occurred. There is no evidence as to the serological status of the first plaintiff before her pregnancy began.
157 As I observed earlier (para 92), the evidence disclosed that CMV is commonly present in the community, and may be acquired in various ways. Moreover, a person may carry the virus without knowing it, and may become infected by the virus, either mistaking the infection for influenza or not even becoming aware of its presence at all. Prof Rawlinson said that adults infected with CMV are asymptomatic in seventy percent of cases (T327).
158 What triggers reactivation during pregnancy is not known (Prof Isaacs, T308), although it would seem that a relevant factor is the compromise of the mother’s immunity system by reason of her pregnancy (Prof Isaacs, T203). Reactivation, when it occurs, is not, Prof Isaacs said, and I accept, in consequence of a further assault by CMV (T160). It follows that if the process of infection of the foetus in this case was due to reactivation of the virus in the mother, such occurrence cannot be linked on the evidence to any breach of duty by the defendant. If this is a case of reactivation, the evidence does not permit of a finding as to when or in what circumstances the virus first entered the mother’s system. Hence the plaintiffs’ claim cannot succeed unless, on the balance of probabilities, I find that what caused Jacob’s condition was work-related primary infection of the first plaintiff during pregnancy.
159 For this reason, it is of critical importance to consider whether it has been established that the first plaintiff first became infected by the virus, in the primary sense, after her pregnancy began, or whether the infection of Jacob resulted from reactivation of a virus acquired at some indefinite time in the past
160 Statistically, it appears on the evidence to be likely that the first plaintiff would have contracted CMV before her pregnancy commenced. Prof Isaacs wrote (report 27 June 1999) that “less than fifty percent of Australian women of child bearing age are CMV seronegative”. In cross examination he agreed that women working in child care centres are far more likely to become seropositive in the course of their working lives than persons not engaged in such work. The professor agreed that for day care workers working with older children there was an acquisition rate of about ten percent per annum so that in four years there was “a forty percent chance of [the first plaintiff] being seropositive at the end of four years if she began seronegative at the start” (T161). Moreover, the professor agreed that the rate of acquisition for day care workers was considerably higher working with babies or toddlers in nappies than if they worked with older children (T161).
161 Basing his opinion on what he described as a range of different studies made in a number of countries, Prof Rawlinson said that it was likely that the first plaintiff was infected with CMV by the time she started to work with the defendant. Indeed, statistically, Prof Rawlinson stated the likelihood as being as high as between eighty-five percent and ninety percent (T288). In his report of 3 September 1998 Prof Rawlinson wrote:
“Linda Hughes commenced employment at the Sydney Day Nursery in October 1990. It is documented that at the time of her pregnancy she had been working in child care for approximately 4 years. Given that day care workers have approximately a 15% per annum risk of acquiring CMV, and that Australian 15-20 year old women have a preexisting seropositivity rate to CMV of approximately 30-40%, the a priori risk of Linda Hughes being CMV immune (seropositive) in November 1992 was 85-95%. It is likely that Linda Hughes did not contract CMV for the first time while working at the Redfern Day Nursery.”
162 Prof Rawlinson was cross examined about a study made by Dr Adler published in the New England Journal of Medicine in November 1989 (Exhibit K). As that exhibit records, the conclusions expressed were based on a study of 610 women employed at thirty-four day care centres. The conclusion was that workers in day care centres may acquire CMV from the children there and that this risk is significantly greater among those who care for children less than two years of age (see concluding paragraph of the abstract).
163 There is a table (Table 2) in Exhibit K which compares findings concerning child care workers working with children under two years of age with those working with children over two years of age. According to this table, those working with children under two years of age tested seropositive in fifty percent of cases when they had been working up to five years in such an environment. Those working with children over two years of age for up to five years tested seropositive in forty percent of cases. The study did draw a conclusion (expressed in the abstract) that there was an annual seroconversion rate of eleven percent working with the younger children although how this conclusion is to be reconciled with the figures in Table 2 is not altogether clear.
164 Analysing the plaintiff’s working history, Prof Rawlinson assessed the plaintiff has spent over forty percent of her working life in the higher risk environment of children under two years (T390). He agreed that her prospects of having seroconverted were less than had she been working with babies all the time, but notwithstanding the Table 2 figures in the study, Prof Rawlinson still considered that the first plaintiff’s prospects of being seropositive were greater than fifty percent (T390). I confess to having difficulty in reconciling the figures in Table 2 with this conclusion. Viewing them at face value, what Table 2 figures appear to indicate is that for a person with the plaintiff’s working history her chances of being seropositive by December 1991 were greater than forty percent but less than fifty percent.
165 Of course Exhibit K is only one study and Prof Rawlinson did not base his opinion as to the chances of the first plaintiff being seropositive prior to pregnancy only on Exhibit K. and I am mindful of Prof Isaacs’ opinion earlier referred to as based upon statistics. Notwithstanding Exhibit K, the evidence of Prof Isaacs and of Prof Rawlinson satisfies me that, statistically, there was a high likelihood that the first plaintiff would have been seropositive before her pregnancy.
166 The Adler study seems to me to add emphasis to the need to which I adverted in addresses for extreme caution to be exercised in evaluating statistics.
167 Nor do I dismiss as irrelevant the first plaintiff’s training and approach to matters of hygiene. The first plaintiff said that she received theoretical and practical training in hygiene in her course at TAFE and on my assessment of the first plaintiff I consider it more probable than not that she would have been conscientious about matters of hygiene in the course of her work. Certainly the evidence as to the period of her employment with the defendant does not indicate otherwise. However, I am mindful of Prof Rawlinson’s evidence about the significance of the TAFE training. His view was that education on a regular basis as to the need for handwashing and care in handling soiled articles was what was important rather than formal training. It seems to me though that the first plaintiff’s formal training is a matter to be given some weight, albeit slight, in evaluating the possibility that the first plaintiff was seropositive before her pregnancy.
168 Whilst the first plaintiff’s working history is a very important consideration in endeavouring to determine whether or not Jacob’s condition resulted from primary infection in the mother, it is not the only one.
169 In his report of 27 June 1999 Prof Isaacs wrote:
“Although severe congenital infection can occur following either primary or secondary maternal infection, it is far more likely to follow primary infection. Unlike congenital rubella, severe congenital CMV infection can follow primary maternal infection in any trimester.
If Jacob Hughes did indeed have congenital CMV infection, the severity of his disease means that it is far more likely to have been a result of primary maternal CMV infection than reactivation.”
170 Prof Isaacs adhered to that view in his oral evidence and in cross examination (T201). After considering the first plaintiff’s full working history, he said (T201) that it was “highly unlikely this is secondary or reactivation CMV. It is likely to be primary.”
171 The defendant introduced into evidence a paper dated July 1999 recording the results of a study carried out at the University of Alabama (I shall refer to it as the Alabama study). That study aimed to determine the frequency of CMV infection in the infants of women with recurrent CMV infection. The range of severity of clinical abnormalities in the newborn did not differ in the cases identified as resulting from primary infection in the mother and recurrent infection in the mother. I shall return to this study later.
172 Dr Isaacs was recalled after being given the opportunity to consider the Alabama study so as to give evidence concerning it. He remained of the opinion that the most likely cause of Jacob’s disabilities was primary maternal CMV infection. In response to a question at T293 the professor gave this evidence:173 Then later at T295:
“Q. Does it change your views in any way, that you have expressed to his Honour, about Jacob Hughes and the cause of his physical and mental difficulty?
A. My feeling is still that the most likely cause is primary maternal cytomegalo virus infection. This is a matter of degree about the possibility of it being due to non-primary maternal infection. That is to say, reinfection, or infection with a secondary strain, a new strain of cytomegalo virus, or reactivation of her own strain. That is a possibility. I have always said that was a possibility. My own feeling is that this paper is an interesting one, one which suggests that at least in Alabama, which is a very different situation from Sydney, that secondary, or reactivation infection, or non-primary I should call it, I think, is more common than we had previously thought.
It’s rather a stunning paper in that, exactly the same group had previously published in the New England Journal of Medicine in 1992, a paper which Fowler was the first author and it’s in the papers here, a paper in which they’d looked in the same Alabama population and they had found 24 babies who were born with symptomatic congenital CMV infection and all 24 were thought to be the result of primary maternal CMV. So now suddenly, this same group has changed their minds and is saying between 1991 and 1997 we had as many proven non-primary, as proven primary.”
174 In cross examination Prof Isaacs expressed the opinion that Jacob’s tolerance, explaining his lack of antibodies, could only have occurred with primary maternal infection, not reactivated infection. I refer to the evidence given by Prof Isaacs at T303-304:
“Q. What’s your comment, or view, about the findings in regard to this, the severity of the disorder, when the infection came from a reactivated source in the mother?
A. I still think that in a Sydney setting, it’s by far the most likely that it would be primary doing. I’ve never said that this couldn’t be non-primary. It certainly can be non-primary. There have been nasty symptomatic congenital CMV infections due to non-primary infections in mothers. As I say, they have been written up before but they are small numbers, compared with the primary cases causing it. So what they have done in Alabama here, is just take the symptomatic babies and then see whether they were primary, or non-primary in the mother by looking back at its serum that they had stored in the previous six years. But you are quiet right in saying, you can have non-primary infection causing nasty disease in a baby. That’s absolutely right. When that does occur, I mean the authors themselves say that we really need to look at this further. That probably out in the wide world away from the University of Alabama, it may well be that by far the most likely cause of symptomatic congenital CMV is primary. That’s what they concluded at the end. But more study is needed. As I say this is an interesting study but one that does not materially alter the balance of probabilities in our case, in this case of Jacob Hughes.”175 I did not find that evidence that the absence of antibodies ruled out reactivated infection to be persuasive and I am mindful of the concession in the last answer above. Elsewhere (T300) Prof Isaacs made it clear that the type of infection in the child could not be categorised by reference to the severity of such infection:
“…Tolerance is a phenomenon whereby it’s the very first time that a virus gets into your system.
CRANITCH: Q. As a matter of logic, the reason why Jacob was injured, was because he had a viral attack, on your thesis. Is that right?
A. As a result of a viral infection, yes.
Q. So that is the first time when he has seen the virus, on your thesis. Is that right?
A. Yes.
Q. So whether or not that virus is a result of mother’s reactivation virus, or alternatively a primary infection, it matters not a wit, in terms of your thesis, does it, because for Jacob to be infected and allowing some credit to this study in paediatrics, that the damage can be just as severe with reactivation, if it is the first time he sees it. It doesn’t matter a wit whether it’s primary or secondary, because it was the first time that he comes into contact with the virus that is important, not when the mother comes into contact with the virus?
A. You may be correct.”
“Q. What I want to be clear on, what is your view now, having regard to this study, as to whether you can categorise the type of infection, by reference to the severity of the infection in the child?
A. No, I don’t believe you can. I never did believe you could.”
176 The last response does not seem to rest altogether comfortably with Prof Isaacs’ response recorded at para 169 above. Be that as it may, ultimately, as I understand Prof Isaacs, it was not the severity of the disabilities in Jacob which led him to decide upon primary infection as opposed to reactivation, but rather that there was much less chance of the foetus becoming symptomatically infected by a process of reactivation.
177 Dr Kendall was of the opinion that the infection was primary in the mother. He was of this view because the abnormality as shown on the MRI was very extensive. He said (T216):178 He agreed that if it was demonstrated by studies that reactivated infection caused severe dysfunction in the same way that primary CMV did his view might change: I refer to the transcript at pp 216-217:
“Secondary infection usually gives rise to a much milder condition and it is said to be very infrequent, whereas primary infection tends to be severe and is far more common as a cause of congenital CMV.”
179 Dr Kendall did not hold himself out to be an expert in distinguishing primary and reactivated infection. At T217:
“Q. I take it, if the emerging research indicated that indeed reactive CMV is firstly, more prevalent than originally thought and secondly, can cause exactly the same degree of deformity and dysfunction in the brain, your view might well change?
A. I know that secondary CMV is common but for it to reactivate and cause that type of damage, to the extent of my knowledge, is certainly very infrequent, if it does occur at all.
Q. But if it is demonstrated, by studies, to be causative of severe dysfunction, in the way that the primary CMV is, then your view might well change?
A. If I was provided with evidence that that was the case.”
“Q. But you don’t hold yourself out, doctor I take it, to be an expert on primary and secondary CMV?
A. No, I don’t hold myself out as being an expert on that type of thing.
Q. It is your understanding --
A. Yes.
Q. -- that there is a body of thought which holds, that secondary CMV infection is rare and that the side effects of it, in terms of the way in which it affects the developing foetus, is usually less severe than primary infection. Is that correct?
A. That is true. Until a few years ago it was thought never to infect the foetus.
Q. When you say a few years ago, what are we talking about in terms of time?
A. I suppose somewhere in the region of ten years ago, there was then doubt expressed as to whether secondary CMV did, in fact, cause exacerbations of the foetus and since that time it has been accepted that it can do so.”180 Dr Kendall was not cross examined about the Alabama study. I accept that Mr Cranitch did not have access to the study at the time Dr Kendall was in the witness box. Although opportunity was given for Dr Kendall’s recall after the introduction of the evidence of the study, Dr Kendall was not recalled.
181 Dr Grigor did not express a view as to whether the CMV was primary or the result of a reactivated virus when he was first called. However like Prof Isaacs, he was recalled after considering the Alabama study. That study did not cause Dr Grigor to alter his diagnosis but when asked specifically (T312) whether he categorised the nature of the infection that was passed on to the child as being primary or reactivated, Dr Grigor said he did not have a view about that “one way or the other.” I take that response as indicating that Dr Grigor was undecided on this issue. Because of the obvious importance of the question, I would infer that Dr Grigor would have been asked to consider this issue before he was called, and to express an opinion if he was able to do so. Whether this be so or not, Dr Grigor’s evidence does not assist the plaintiffs on this critical issue.
182 Prof Rawlinson, in his report of 3 September 1998, said (para 6):
“Jacob Hughes suffers from severe disability, which never results from the rare instances of reactivation infection or reinfection during pregnancy.”
183 Given the finding I have made of CMV infection, that opinion would tend to support the plaintiffs’ contention that this CMV was primary in the sense being considered.
184 However, when alerted to the Alabama study, Prof Rawlinson regarded that study as revealing that the incidence of infection of babies from the reactivated process was much higher than previously appreciated, and after considering the study, he said that the sentence set out above from his report required correction and should read:185 In cross examination, Prof Rawlinson was asked this question and gave this answer (T362):
“Jacob Hughes suffers from severe disability which can result from reactivation infection or reinfection during pregnancy.”
“Q. It is still the position, is it not, that if it was, contrary to your views, congenital CMV, then on the very strong probabilities it was a primary infection?
A. No, on the basis of the publication evidence from last year, the possibility - looking at a child who is severely affected rather than looking from the other direction, taking a child and saying what is the likelihood of this child having acquired congenital CMV on the basis of primary or reactivation infection, it’s approximately one in two. There were a significant number of - there was forty-seven babies in the Boppana studies I understand, about half of those, I think twenty-two, had CMV, which it was uncertain whether it was primary or reactivation. The authors felt that a significant number of those were reactivation, but they did not know.”
186 If Prof Rawlinson was intending by the above answer to indicate that the Alabama study established that severe abnormality occurs just as frequently following reactivation as following primary infection, it does not seem to me that the Alabama study resulted in any such conclusion. In fairness to the witness, I doubt that this was what was intended to be conveyed by his answer, particularly having regard to his later cross examination to which I shall refer presently.
187 I return to the Alabama study itself (Exhibit 4). It seems that the study was conducted between 1991 and 1997 and the study subjects included 246 children with congenital CMV infection. Forty-seven of these children had clinical abnormalities following birth and of those infants, eight were born to mothers with confirmed reactivated infection. Another eight cases were cases of abnormalities following primary maternal infection. The study findings were that the range of severity of clinical abnormalities during the newborn period did not differ in the cases determined to be primary infection cases and those that were not. It is stated in the paper following the Alabama study:188 The concluding paragraph of the report contained the following expression of reservation:
“A previous study from this laboratory has thoroughly investigated the association between maternal antibody status and outcome in 197 children with congenital CMV infection born between 1972 and 1990. None of the 64 congenitally infected children who were born to women with recurrent CMV infection and were included in the study had clinical abnormalities at birth, and all 24 infants with symptomatic infection were born after a primary maternal infection. An earlier publication from this laboratory by Stagno et al also reported that none of the congenitally infected children born to women with preexisting immunity had symptomatic infection. Based on these findings, it has been believed widely that symptomatic congenital CMV infection almost always occurs after a primary maternal infection. However, the results of the present study clearly document that symptomatic congenital CMV infection after a recurrent maternal infection occurs more frequently than has been thought previously…”
“A major limitation of the present study is our inability to categorize the type of maternal infection in more than half of the children with symptomatic congenital CMV infection born during the study period. It is possible, and perhaps likely, that the vast majority of symptomatic infections occur after a primary CMV infection during pregnancy. It is also possible that categorization of most maternal infections will lead to identification of an increased proportion of children who were born to mothers with preexisting immunity among infants with symptomatic congenital CMV infection…”
189 I do not read the authors of the report as conveying in the above passage that they regarded it as unlikely that the vast majority of symptomatic infections occur after a primary CMV infection during pregnancy. Indeed they say this is “perhaps likely”, and this in the expression of medical as opposed to legal opinion . Before this most recent Alabama study, the same laboratory had made the finding that 100% of infants symptomatically infected with CMV were born to mothers whose infection was primary, and then there was the earlier study by Stagno leading to the same conclusion. Having considered the Alabama study, (and allowing for the major limitation to which the report refers (para 186 above)), the earlier studies to which Exhibit 4 refers and the evidence of Prof Isaacs to which I have referred (at paras 172-173), it seems to me to be more probable than not that the majority of symptomatic infections in infancy occur after primary CMV infection in the mother during pregnancy.
190 What the study indicates is that the effects of the reactivation of the virus can be just as severe as the effects from a primary infection. This feature of the study appears to have influenced Prof Rawlinson to change his mind in the respects indicated, but Prof Isaacs had considered before he saw the report that severe congenital infection could follow reactivated maternal infection (indeed he indicated this in his report of 27 June 1999), and the Alabama study has not altered his opinion.
191 I find on the evidence that the incidence of reactivation of CMV in the mother causing severe abnormality in the infant is very much less than the incidence of primary infection in the mother resulting in severe abnormality in the infant.
192 I am assisted in making this finding by the evidence of Prof Rawlinson concerning a paper which he wrote “a couple of years ago” (T393). This paper was entitled “Diagnosis of human CMV infection and disease”. The professor wrote that congenital infection occurred mainly in the babies of women who had primary infection during pregnancy, and in cross examination (T394) the professor agreed this remained the position notwithstanding the Alabama study. Prof Rawlinson was asked the following questions about the paper (T394):
“Q. Then you go on to say:
‘Primary maternal infection is much more likely to result in intrauterine transmission than maternal reactivation of CMV.’
A. Yes.
Q. That is still your position isn’t it?
A. Yes, it is.
Q. Then you say that:
‘The maternofoetal transmission rate in primary infection is approximately 50 per cent’
and that is still your understanding?
A. Yes.
……………….
Q. Then you say that for those people who have had it before, there is a 0.5 to 1.5 percentage possibility that they will have a foetal infection during what you call a reactivation infection?
A. Yes.
Q. And leading to clinically apparent disease in 0 to 0.5 per cent of cases?
A. Yes, these are ranges based - they are consensus figures to convey the general impression of the transmission rate.
Q. Then in the other column you deal with women who start off their pregnancy with no immunity?
A. Seronegative.
Q. And of those you say 50 per cent - what are the 50 percent and 10 per cent figures referred to there? First of all you have 50 per cent higher SES, what does that mean?
A. That is 50 percent are immune and 50 percent are non-immune, and for lower socioeconomic status, 90 percent are immune and 10 percent are non-immune to CMV. That is 50 percent of higher SES are seronegative to CMV and 10 percent of lower SES are seronegative to CMV.
Q. Then in the maternal infection box, which is the next one, you have got 1 to 5 percent?
A. Yes.
Q. What are you saying about that?
A. That something like the average of that, 3 percent of women are infected during pregnancy from both of those groups.
Q. Women who have not had CMV before?
A. Yes, that is developed primary infection during pregnancy.
Q. And then the next box is obvious, that of those who do get it in pregnancy, 50 percent of them or thereabouts suffer some primary infection?
A. 50 percent of those mothers will pass the virus to their unborn child, across the placenta.
Q. Leading to clinically apparent disease in 10 to 15 per cent of cases?
A. Yes.
Q. So that the net result is that on percentage basis, women who had some immunity have extraordinarily small prospect of passing on clinically apparent disease to the foetus, than those who have not?
A. Percentage wise, yes.
Q. That is still the position, isn’t it?
A. Well the position percentage wise is still that, but the difference now is that the absolute numbers appear to be similar, of a similar order.”
193 The above evidence emphasises, statistically, how rare is the chance of reactivated infection leading to clinically apparent disease in the child. It is, Prof Rawlinson, agreed “an extraordinarily small prospect”.
194 However, it is to be observed in the answer of Prof Rawlinson last set out above that he referred to the “absolute numbers” appearing to be similar. Prof Rawlinson was then asked to explain what he meant by absolute numbers and his evidence proceeded (T396-397):
“A. As Boppana did, if you take - and in fact as unpublished data have suggested - if you take a group of children with congenital CMV and you carefully look at, retrospectively - so you collect the children as they are affected and you retrospectively and diligently seek out the characteristics of their mothers - then the absolute numbers of congenital CMV cases that are resulting from reactivation appears to be much higher than we previously believed, and that is the thrust of the Boppana article; that even though percentage wise, because primary infection is a relative rare event during pregnancy --
Q. But it is still the position that although there are more cases that have been found and documented, on a percentage basis primary infection is vastly more likely to have caused birth defects, isn’t it?
A. Percentage wise. But in a sense what you are looking at is, if I can express it differently, if you look at all symptomatic children, not just severely symptomatic children - and again, I don’t think this is in this paper but we have published this - if you look at all children with some type of symptom due to CMV acquired congenitally - and that goes from a relatively mild form with perhaps low platelets, petechiae and evidence at birth of excretion of the virus, who are developmentally normal and not distinguishable from normal children, all the way through to the most severe manifestation of CMV which is cytomegalic inclusion disease which often results in death of the baby - then percentage wise the number of, the percentage of recurrent infections that result in disease is extremely low. But reactivation is an extremely common event during pregnancy, occurring in something like a third to one half of all women and so that is a vast number compared to the number of primary maternal infections during pregnancy.
So even though the percentage is very small, the absolute numbers of any malformation, all the way through from mild to very severe, the absolute numbers due to reactivation infection are very similar to the primary, those due to primary maternal infection, and we have known that for many, many years. The difference with the Boppana article is that it suggests that the severe spectrum, the more severe end of the spectrum of disease, can also result from reactivation infection. So the percentage in a sense has to be seen in the perspective of the number of women who are suffering or who are undergoing this event of reactivation and so the absolute numbers are very - are relatively the same between primary and reactivation infection. That is well established. There is no question about that. And the papers I have referred to all indicate that in Australia as well as elsewhere, although it has been studied better elsewhere.
The difference that the Boppana article is suggesting is that the more severe spectrum can also be due to reactivation because, as you would expect with a disease with spectrum like congenital CMV, there is a lot of children who are born with fairly mild manifestations: A big liver which gets better; petechiae, which are the most common presentation; low platelets which get better as they cope with the infection.”
195 I did not overlook what Prof Rawlinson said in the answer last cited when expressing my finding in para 189 above, but it seems to me that the professor’s response under immediate consideration does not allow for the qualification expressed in the report of the Alabama studies (para 186 above), because of the inability in that study to determine in more than fifty percent of the cases studies whether the mother had primary or reactivated infection.
196 I have found it to be extremely difficult to reach a conclusion on the evidence I have reviewed as to whether the injury to the second plaintiff was due to primary or reactivated infection in the mother. The severity of Jacob’s presentation does not rule out the possibility of reactivated infection as the source of his disabilities, but, subject to the qualification I have expressed, I accept the evidence given by Prof Rawlinson above (paras 192-193) stating his opinion based upon his studies. That evidence inevitably reflects statistical material. Although I have expressed the need for caution in evaluating statistics, since there is no direct evidence as to whether the first plaintiff was seropositive or seronegative immediately before her pregnancy, I am compelled to approach this matter evaluating the statistically based evidence. Statistics may be used in an appropriate case to support a conclusion: see, for example, Papadopoulos v New South Wales Insurance Ministerial Corporation [1999] NSWCA 116, in particular at para 34. The statistics must be weighed with all the evidence in the case, and here in particular, those statistics have to be considered with the medical evidence.
197 I now draw together the following findings:198 On the other side of the scales must be weighed these findings:
(i) that the occurrence of reactivated infection in pregnancy is common, happening in one in three to one in two women;(ii) that the chance of reactivated infection in the mother leading to severe disabilities in the child however is very low, and very much less than the incidence of primary infection in the mother leading to severe abnormality in the child, as the statistics below indicate;
(iii) that reactivation rarely leads to foetal infection, there being only one chance in 100 of this happening (taking Prof Rawlinson’s mid point);
(iv) that such reactivation leads to clinically apparent disease (not necessarily severe) even less frequently, there being only one chance in 250 of this happening (again taking Prof Rawlinson’s mid point);
(v) that, whilst reactivated infection in the mother is much more common than primary infection in the mother, it is more probable than not that the majority of symptomatic infections in infancy occur after primary CMV infection in the mother during pregnancy;
(vi) that primary infection when it occurs in pregnancy is much more likely to result in foetal infection than is reactivated infection, the incidence being one in two cases of primary maternal infection;
(vii) that such occurrence leads to clinically apparent disease in ten to fifteen percent of cases.
(i) that the very nature of the first plaintiff’s occupation made it highly likely, statistically, that the first plaintiff would have had CMV before her pregnancy commenced;(ii) that primary infection occurs in mothers in pregnancy relatively rarely, in only three percent of seronegative women (compare the incidence of the occurrence of reactivated infection: para 197(i) above)
(iii) that the severity of the disease in the second plaintiff does not exclude reactivated infection in his mother as its source;
199 Whilst I must give due weight to the findings recorded in para 197 above, the severity of the disease in Jacob does not exclude reactivated infection, as Dr Isaacs acknowledged, and it is for the plaintiff to prove that her infection was primary. The statistically high probability that the first plaintiff would have had CMV before her pregnancy stands in her way. I have reflected upon the support expressed by Prof Isaacs and by Dr Kendall (and which I have reviewed in this judgment) that the infection process was primary. I am not persuaded that Prof Isaacs’ opinion as to this makes adequate allowance for the statistically high probability that at her age and with her working history the first plaintiff would have been seropositive prior to the commencement of her pregnancy. Dr Kendall acknowledged that he was no expert in determining whether this was a case of primary or reactivated infection and he was not recalled to give further evidence in the circumstances I earlier outlined. I bear in mind Dr Grigor, by whose evidence generally I was particularly impressed, did not opine that the infection was primary.
200 Whilst it is possible that the first plaintiff had not had CMV before her pregnancy commenced, after much anxious consideration of all the evidence in this extremely sad case, I find myself unable to determine on the balance of probabilities that the first plaintiff did contract primary infection by reason of her employment by the defendant during her pregnancy. The inevitable consequence of the plaintiff’s failure to discharge the burden of proof on this issue is that the claims of the plaintiffs must fail and there will be verdict and judgment for the defendant on each claim.
The cross claims
201 Whilst the plaintiffs have failed against the defendant, the cross claims still assume relevance because of the issue of costs. The defendant seeks to be indemnified for its costs of defending this cause and for any other liability for costs in this cause.
202 Each of the policies contained provision for the insurer to protect the defendant against costs and it was submitted by counsel for the defendant that the failure of the plaintiffs to establish their claims would not deprive the defendant of an entitlement to recover its costs under the appropriate policy. Hence, it was submitted, there is a need to determine which of the policies upon which the cross claims were based would have been attracted had the claims of the plaintiffs succeeded, because it is to that insurer (or those insurers) that the defendant is entitled to look for relief for its costs incurred in defending the claims of the plaintiffs.
203 The claim made against the second to seventh cross defendants on the Community Care Policy was denied under Special Exception 1 of that policy, which provides:
“The insurance afforded by this Section does not apply to:
1. (a) Personal injury to any of YOUR Workers arising out of or in the course of their employment;
(b) ……..
(c) Liability for which YOU are entitled to seek indemnity under any policy of insurance required to be taken out pursuant to any legislation relating to workers or workmen compensation whether or not YOU are a party to such contract of insurance;
…….…”
204 Mr Davies, on behalf of the insurers named in the second cross claim, indicated that in the event that the plaintiffs succeeded against the defendant their claims would fall within the insuring clause of the Community Care Policy unless excepted by the exception provision above set out. It is appropriate to determine whether, had the plaintiffs succeeded, the policy of the first cross defendant would have afforded indemnity to the defendant for its liability to the plaintiffs. Plainly if the defendant is entitled to succeed under the cross claim against the first defendant, it cannot succeed under its Community Care Policy as well.
205 The Workers’ Compensation Policy was in statutory form and incorporated the amendments introduced by the legislation gazetted on 22 December 1989 as effective from 1 February 1990. Relevantly the policy provided:206 Where “injury” appears in the above policy it is to be given the same meaning as it is given in the statute creating the requirement for it. To give it a narrower meaning in the policy than in the statute itself would defeat the purpose of the statute which makes it compulsory for employers “to obtain and maintain” a policy of insurance complying with the insurance provisions of the statute. It would also ignore the combined effect of ss 3 and 11 of the Interpretation Act of 1987. In s 3 “instrument” is defined as meaning “an instrument (including a statutory rule) made under an Act and includes an instrument made under any such instrument”. Section 11 provides:
“WHEREAS section 155 of the Workers’ Compensation Act, 1987 (in this Policy called ‘the Act’) provides that an Employer shall obtain from a licensed insurer, and maintain in force, a Policy of Insurance that complies with Division 1 of Part 7 of the Act for the full amount of the Employer’s liability under the Act in respect of all workers employed by the Employer, and for an unlimited amount in respect of the Employer’s liability independently of the Act (being a liability under a law of New South Wales) for any injury to any such worker.
……..
NOW THIS POLICY WITNESSES that in consideration of the payment by the Employer to the Insurer of the premium for this Policy, IF,…the Employer becomes liable to pay compensation under the Act to or in respect of any person who is or is deemed by the Act to be a worker of the Employer (including any person to whom the Employer is liable by force of section 20 of the Act to pay compensation) or becomes liable to pay any other amount in respect of the Employer’s liability independently of the Act (being a liability under the law of New South Wales) for any injury to any such person (not including liability for damages in respect of a motor accident as defined in the Motor Accidents Act, 1988 or liability in respect of an injury, suffered by a person other than such a worker or deemed worker, arising out of any rescue or attempted rescue).
THEN, and in every such case, the Insurer will indemnify the Employer against all such sums for which the Employer shall be so liable; the Insurer will also pay all costs and expenses incurred with the written consent of the Insurer in connection with the defence of any legal proceedings in which any such liability is alleged.
……………….
AND is [sic] is hereby further agreed that the above indemnity is made subject to the due and proper observance and fulfilment by the Employer of the conditions hereunder, and the Insurer shall be (a) directly liable to any Worker and in the event of a Worker’s death, to the Worker’s dependants or other persons, to pay the compensation under the Act or other amount independently of the Act for which the Employer is liable and in respect of which the Employer is indemnified under this Policy; and (b) bound by and subject to any judgment, order, decision or award given or made against the Employer in respect of the injury for which the compensation or other amount is payable and in respect of which the Employer is indemnified under this policy…”
“Words and expressions that occur in an instrument have the same meanings as they have in the Act, or in the relevant provisions of the Act, under which the instrument is made.”
207 The statutory form of policy is prescribed by an instrument made under the statute itself.
208 “Injury” is defined in s 4 of the Workers’ Compensation Act 1987:
“Injury
(a) means personal injury arising out of or in the course of employment;
(b) includes -
(i) a disease which is contracted by a worker in the course of employment and to which the employment was a contributing factor; and
(ii) the aggravation, acceleration, exacerbation or deterioration of any disease, where the employment was a contributing factor to the aggravation, acceleration, exacerbation or deterioration;…”
209 I am satisfied that that same definition applies to the policy for the purposes of the cross claim under consideration.
210 Had the plaintiffs succeeded, it would have been upon the basis that the first plaintiff acquired a primary infection during her pregnancy. Hence the assumption has to be made for present purposes that this was an event that occurred, in considering whether it would have amounted to “injury” within the meaning of the statutory policy.
211 The evidence did not establish that the first plaintiff was unwell or any time in her pregnancy by reason of the CMV. I am not satisfied that the malaise the first plaintiff described such as affected her on Christmas Eve and Christmas Day (T11) was symptomatic of CMV, and I do not find that the first plaintiff was unwell at any stage because she had contracted CMV. However, it would not necessarily follow that no “injury” was suffered under the policy.
212 The existence of injury is not determined by the presence or absence of symptoms. In Cartledge v Jopling & Sons Ltd [1963] AC 758 Lord Pearce said at 778-779:213 Professor Issacs gave evidence which, assuming primary infection, would have explained the process that occurred with the mother. Professor Isaacs was asked the following questions (T204):
“In my opinion, it is impossible to hold that a man who has no knowledge of the secret onset of pneumoconiosis and suffers no present inconvenience from it cannot have suffered any actionable harm. So to hold might possibly on the wording of the Fatal Accidents Act deprive of all remedy a widow whose husband dies of pneumoconiosis without having had any knowledge or symptoms of the disease. And it would be wrong to deny a right of action to a plaintiff who can prove by x-ray photographs that his lungs are damaged but cannot prove any symptom or present physical inconvenience. Nor can his knowledge of the state of his lungs be the deciding factor. It would be impossible to hold that while the x-ray photographs are being taken he cannot yet have suffered any damage to his body, but that immediately the result of them is told to him, he has from that moment suffered damage. It is for a judge or jury to decide whether a man has suffered any actionable harm and in borderline cases it is a question of degree.”
“Q. Doctor, what actually happens when the CMV virus enters an adult host in the physiological terms?
A. What is thought to happen is that it enters, it connects to cells, infects those cells, and then causes an infection that may be quite localised or may spread to the lymph glands, and then finally localises in nerve cells, much like the Herpes Simplex virus or chicken pox virus. That is what is thought to happen.
Q. When you say ‘infects the cells’ what physically takes place within the cell?
A. The virus attaches to the host cell, injects its nucleic acid, which becomes incorporated into the host cell DNA, and that host cell is then induced to produce virus as well as its own proteins. The amount of virus produced may vary and the ability for the virus to remain latent is a particular characteristic of the Herpes virus group.
Q. When you say the cell becomes infected by the injection of the nucleic acid?
A. Yes.
Q. Does that damage the cell in the short term or the long term?
A. In the long term the cell will produce lots of virus and rupture and die, that particular cell, yes.
Q. At what stage do antibodies become produced?
A. The so called IgM antibodies are produced within about two weeks of infection and persist for about six to eight weeks usually, although longer in a foetus. IgG antibodies are produced within two to four weeks and persist indefinitely.
Q. And what do the antibodies do once they are produced?
A. Well, IgM antibodies, which are produced in response to an acute infection, are rather non-specific and they try and mop up the virus, although that is not the only way that one recovers. IgG antibodies are usually thought to prevent reinfection generally, but because CMV can go latent and remain there, those IgG antibodies are actually almost for show. They are not working very well.
Q. But now when you say ‘mop up the virus’, in what way do they do that relative to its being within the cell?
A. They can’t mop up a virus that is actually within a cell. Antibodies cannot attach to the virus if it is inside the cell, but when the cell ruptures and lets the virus out into the rest of the body, so that it is loose in blood or tissues, then antibodies can attach to the virus and neutralise it, mop it up.
Q. And the antibodies don’t operate by destroying the cells in which the virus is?
A. No, they don’t, no.
Q. They wait for the cell to rupture?
A. The antibodies will neutralise, they are proteins, and they are just floating there, but they will actually be attracted to free virus and attach to it and neutralise it.
Q. The virus is passed from a pregnant host to the foetus across the placenta.
A. In the bloodstream, yes.
Q. In the bloodstream?
A. Yes.
Q. What does it then do when it reaches the foetus? Does it react in the same way as in the adult host?
A. Yes, but the foetus is more immunologically immature or more at risk from a severe risk infection with the virus disseminating throughout the foetus’ body.
Q. Does it attack the cell and deposit the same thing to the cell in the foetus as it does in the adult host?
A. The basic principle of the infection is the same but the extent of the infection is greater in the foetus, or can be greater in the foetus.”214 It seems to me that had I found primary infection, the process described by Prof Isaacs would have amounted to “injury”, notwithstanding the absence of symptoms, because of changes harmful to the first plaintiff’s normal physiological state.
215 In Hume Steel Limited v Peart (1947) 75 CLR 242 Latham CJ said at 252-253:
“There is a distinction according to the common usage of language between getting hurt and becoming sick. The former would be described as an injury and the latter would generally not be so described. But it requires little analysis to show that an injury may be either external or internal. It appears to me to be difficult to draw any satisfactory distinction between the breaking of a limb and the breaking of an artery or of the lining of an artery. One is as much an injury to the body, that is, something that involves a harmful effect on the body, as the other. Each is a disturbance of the normal physiological state which may produce physical incapacity and suffering or death . Accordingly, in my opinion, the detachment of a piece of the lining of the artery in the present case should be held to be an injury.”
(Emphasis added)
216 See also Zickar v MGH Plastic Industries Pty Limited (1995-96) 187 CLR 310 and in particular the joint judgment of Toohey, McHugh and Gummow JJ at 332; and E v Australian Red Cross Society (1991) 27 FCR 310 per Wilcox J at 351.
217 What Prof Isaacs described as having occurred transplacentally would have involved further injury. I considered the time at which that harm occurred earlier (paras 85-90). Dr Grigor said that the earliest time at which a foetus could survive outside its mother’s body was about twenty-four weeks (T139), so that it seems that the harm that occurred to the foetus before that could be considered as further injury to the first plaintiff. In support of a submission to this effect, which submission I accept, Mr Davies referred me to Paton v British Pregnancy Advisory Service Trustees [1979] 1 QB 276 and to dicta of Sir George Baker P at 279; and to Burton v Islington Health Authority [1993] QB 204 at 226. I add a reference to Attorney General for the State of Queensland v T (1983) 57 ALJR 285 where the dicta of Sir George Baker P were cited with approval by Gibbs CJ at 286.
218 If the first plaintiff had acquired a primary infection in the employment environment, Prof Rawlinson’s evidence of the disease process which occurred, notwithstanding absence of symptoms, assumes relevance:219 And later (T284):
“Q. If it was, primary infection, that is: Incurred by Mrs Hughes during the period of Jacob’s gestation, how would it be classified in a medical sense?
A. Somewhere around 70 percent of CMV during pregnancy are asymptomatic. That is there are no clinical signs. If Mrs Hughes acquired CMV during pregnancy and had a primary infection she has an infection by definition. It’s a primary infection as she is antibody negative towards CMV. That is, it is the first time she has been infected with the virus in her life and the usual course is that she would have no symptoms and feel well. So, she does not have disease in the sense that she is affected in some way. However, if we measure her liver tests or we measure her full blood count then you will usually see manifestations within that of the infection, such as elevations in her tests that are commonly called liver function tests that is her transaminasers which indicate that her liver has been inflamed so she does have disease in that sense however she does not have clinical disease because we cannot detect it clinically.”
“Q. So, there is a reaction of the body to the invasion of the virus is that it?
A. Yes, that’s correct and that reaction is measured in what we call endorphin damage such as the liver inflames or in the most severe case in encephalitis and it is also measured by the body’s immune response and we measure antibodies and Mrs Hughes has blood tests that I have seen that indicates she is IgG positive and IgM negative: that is she has had previous infection.
Q. At some time in the past?
A. At some time.”220 Had this been a case of primary infection acquired by the mother in the employment environment, Prof Rawlinson’s evidence above referred to would meet the definition of injury by way of disease “contracted in the course of employment to which the employment was a contributing factor.”
221 I am satisfied therefore that had the plaintiffs proved that the first plaintiff acquired primary infection during her pregnancy this would have amounted in each of two ways to “injury” within the definition in the Workers’ Compensation Act. and within the policy issued by the first cross defendant. I am satisfied, consistent with authority and having regard to the findings of fact I have expressed, that the injury defined in the evidence I have reviewed would have been injury that arose “out of” the employment of the first plaintiff and “in the course of” it.
222 It has been submitted that the findings identified above are such as would have attracted the liability of the first cross defendant under the workers’ compensation policy in respect of the claims of the first plaintiff and of the second plaintiff. Mr Poulos of Queen’s Counsel argued that the words of the policy should not be read as extending to harm to others that results from injury to the worker. Mr Poulos submitted that the only liability to be covered was a liability to the employee herself. Mr Poulos submitted that since the form of the policy was prescribed by regulation under a statute there is no reason to read the policy in favour of the insured rather than the insurer. He referred to the statement of principle to this effect in Sutton - Insurance Law in Australia, 3rd ed., at 757-758:
“…both the New South Wales Full Supreme Court and the Supreme Court of Victoria have held that, where the form of insurance policy is prescribed by statute or regulation, as in the case of the workers’ compensation legislation, there is no reason why any particular provision of it should be read in favour of one party rather than the other, for neither is responsible for the drafting of a form that is imposed upon both by law.”
223 Cases cited in support of that statement of principle by the author were the following: Kodak (A’asia) Pty Ltd v Retail Traders Mutual Indemnity Insurance Assoc (1942) 42 SR (NSW) 231 at 233; Dairy Farmers Co-op Pty Ltd v CIC Insurance Ltd (1991) 7 ANZ Ins Cas 61-093 (SC NSW) at 77,369; Green v Windman [1964] VR 297 at 298; Davis & Young Pty Ltd v Assurance Compagnie Baltica etc [1986] VR 203 (FC) at 210; see also Re Linsley & Co-op Insurance Assoc (1976) 62 DLR (3d) 408.
224 Mr Poulos also drew attention to the Second Reading Speech when, in 1953, the counterpart under the earlier statute to s 155 of the current Workers’ Compensation Act was introduced into the earlier Act. What Mr Landa said on that occasion was:
“In order to ensure, to some extent at least, that such common law judgments will be readily satisfied and moreover, that the employer will have some measure of financial protection in the event of such judgments being given against him, it is proposed to require all employers to insure against common law liability for injuries…in respect of each of their workers. It will protect both the employer and the employee …”
(Emphasis added)
225 Thus the legislative intention was conveyed, Mr Poulos submitted, that it was proposed to require all employers to insure against common law liability for injuries in respect of each of their workers. The intention was not conveyed to provide for insurance on a broader scale such as that for which the defendant contends here.
226 Mr Poulos drew attention to the unreported decision of the Court of Appeal in Nigel Watts Fashion Agencies Pty Limited v GIO General Limited (22 December 1994). This was a case in which an employer leased premises and an employee was injured in a fall there. He sued the occupier claiming damages for negligence and the occupier joined the employer as third party in those proceedings. The employee succeeded against the occupier and the occupier succeeded against the employer because of a widely drawn indemnity provision in the lease entered into between the occupier and the employer. The employer sought indemnity from its workers’ compensation insurer for the judgment sum payable to the occupier. That claim failed at first instance and the appeal against that decision was unsuccessful. In the course of his judgment, with which the other members of the court agreed, Kirby P considered the argument addressed to the court that the statutory policy whereunder the insurer promised “to pay any other amount in respect of [the employer’s] liability independently of the Act for any injury to [a worker]” was wide enough to cover the liability in respect to the injury to the worker for which the employer was liable as third party. The President said of this claim:
“This claim must be rejected. The phrase in the policy is of long standing. Its purpose is plain. It is to provide indemnity to an employer for common law liability to a worker qua worker. It is not to provide indemnity to the employer in respect of every other way in which the employer might be liable to other persons, as by a promise in a contract of lease. The judgment against the employer as third party rested entirely upon the employer’s contractual liability under the lease. It was based on the exceptional provisions of that document. The workers’ compensation policy issued by the insurer to the employer did not respond to such a liability.”
227 The remarks of the learned President were made in the course of the consideration of a case which is quite different from the present one and there are two earlier decisions of the Court of Appeal upon which the defendant relied on its cross claim against the first cross defendant: Rheem Australia v Manufacturers’ Mutual Insurance (1984) 2 NSWLR 370 and Manufacturers’ Mutual Insurance Limited v Hooper (1998) 5 ANZ Insurance Cases 60-849.
228 In Rheem the statutory form of policy complying with the requirements of the 1926 Workers’ Compensation Act required that the insurer indemnify:229 It was held in this case that the policy was wide enough to include liability to indemnify in respect of a claim by a spouse for loss of consortium. In so holding the Court of Appeal overruled a longstanding decision of MacFarlan J in Cuckson Textiles Pty Limited v Queensland Insurance Co. Limited (1968) 88 WN Pt 1 474. In Cuckson it had been held that liability for injury to a worker in the statutory policy was limited to liability to the worker and did not extend to a claim at common law by anyone else. However in Rheem, Glass JA, with whose judgment Samuels JA agreed, said (at 375):
“if…the employer shall be liable to pay compensation under the Act to or in respect of any person who is or is deemed by the Act to be a worker of such employer, or to pay any other amount…in respect of his liability independently of the Act for any injury to any such person…”
230 Mahoney JA also agreed with Glass JA but in stating his own reasons said (at 377):
“The phrase in the statutory indemnity ‘liability…for any injury to’ a worker means on its proper construction ‘liability to any person consequent upon or in respect of injury to’ a worker.”
231 Rheem was followed in Hooper. In this later case it was held at first instance, applying Rheem, that the statutory policy gave indemnity to the employer for its liability to a person not its employee who was injured when he went to the rescue of employees of the employer. An appeal against the decision of the trial judge failed. In his judgment in Hooper, Hope JA, with whom Priestley JA agreed, remarked upon the history of the section that required statutory insurance cover. His Honour said (at 75,305):
“I am conscious that in a compensation to relatives claim, the claim is made by the dependants as such, whereas in the loss of consortium case, the claimant's spouse may not be a dependant of the worker. But I do not think that this requires the words of the policy to be read otherwise than as I have suggested. Section 18(3) refers to ‘dependants’ but s 18(1) is not so confined. It requires that there be a policy ‘in respect of his (the employer's) liability independently of this Act for any injury’ and the requirement is not, I think, limited so as to require the policy to be limited in this regard to dependants.
I am conscious also that, if this be the ambit of the words of the prescribed policy, it may comprehend, eg, claims by third parties for nervous shock arising from injury to the worker. But, once the words of the policy are seen as extending to liability to third parties, eg, dependants, and are not restricted to liability to dependants as such, then there is no basis in the wording of the legislation for restricting what would otherwise be the ordinary effect of the language of the policy. If the ambit of the prescribed policy is to be limited either by considerations of public interest or (if it be permissible) by the terms of the regulations, such a restriction should, I think, be imposed otherwise than by this Court.
232 Later, at 75,309 McHugh JA expressed the ratio decidendi of Rheem in the following passage:
“The requirement for insurance in respect of liability independently of the Act was not to be found in sec. 18 until 1953 when subsec. (1) was amended by the Workers’ Compensation (Amendment) Act 1953 to impose this obligation on employers. From at least 1972 there have been decisions, including reported decisions, construing the language of the subsection and of policies of insurance in the prescribed form so as to give employees an indemnity in respect of claims by persons other than a worker, or, where he is deceased, his dependants. The most recent of these decisions was that of this Court in Rheem Australia Ltd v Manufacturers’ Mutual Insurance Ltd (1984) 3 ANZ Insurance Cases 60-585; (1984) 2 NSWLR 370 where it was held that the insurer under such a policy was bound to indemnify an employer in respect of a claim by the spouse of an injured worker for loss of consortium. Notwithstanding this chain of decisions, no amendments were made to sec. 18(1) to impose any limits to the relevant indemnity other than those which, upon the proper construction of the subsection and of the prescribed form of policy, were already there. The Workers’ Compensation Act was an Act which was under continuous review and in respect of which amendments were made annually and sometimes more than once a year. In particular there were regular amendments of the Act from 1972 under the Workers’ Compensation Act 1987, significantly changing this area of the law, came into force on 30 June 1987. This absence of legislative concern about decision as to the extent of the indemnity is surely relevant when it is sought to limit that indemnity by reference to questions of policy to be inferred from the circumstances that the Act is a workers compensation Act.”
“Counsel for the appellant formally submitted that Rheem Australia Ltd v Manufactures’ Mutual Insurance Ltd (1984) 3 ANZ Insurance Cases 60-585; (1984) 2 NSWLR 370 was wrongly decided. But he did not seek leave to re-argue its correctness. The ratio of that decision is that the policy covers any liability to any person consequent upon or in respect of injury to a worker. If that ratio is applied to this case, then I think the ‘liabilities’ of the appellant are covered by the indemnity.”
233 The language of the policy under the 1926 Act which required consideration in Rheem and Hooper was essentially the same as the language in the policy with which the present case is concerned. Section 18(1) of the 1926 Act, making it compulsory for an employer to have insurance cover, is expressed in terms that do not differ from s 155(1) of the 1985 statute. The language in the present form of statutory policy and the language of s 155(1) was chosen no doubt with the history of the construction by the courts of the policy under the 1926 Act in mind. The legislature must have been aware that the policy under the 1926 Act had been construed to cover “any liability to any person consequent upon or in respect of injury to a worker”: per McHugh JA in Hooper.
234 Rheem was considered in the High Court in The Workers’ Compensation Board of Queensland v Technical Products Pty Limited (1988) 165 CLR 643. That case concerned the construction of provisions of the Queensland Workers’ Compensation Act. A worker had sustained serious injury and in consequence his wife claimed to have suffered nervous shock. The wife sued the employer which joined the Workers’ Compensation Board of Queensland. It demurred to the statement of claim on the ground that the plaintiff had no entitlement under the statute and the demurrer was upheld in the High Court. The decision is distinguishable because the statutory language in Queensland differs from that in New South Wales. However, commenting upon Rheem, Deane, Dawson and Toohey JJ said at 657:
“And in Rheem Australia Ltd v Manufacturers' Mutual Insurance Ltd. [1984] 2 NSWLR 370. a policy of insurance required by the Workers' Compensation Act 1926 (NSW) provided that the insurer would indemnify the employer in any case where ‘the employer shall be liable to pay compensation under the Act to or in respect of any person who is or is deemed by the Act to be a worker of such employer, or to pay any other amount...in respect of his liability independently of the Act for any injury to any such person’. The Court of Appeal held that the phrase ‘liability...for any injury to a worker’ meant ‘liability to any person consequent upon or in respect of injury’ to a worker and that such an indemnity included a claim by the spouse of an injured worker for loss of consortium. It is sufficient for present purposes to say of that decision that it depended upon the form of the policy in question. In particular, reliance was placed upon a specific clause in the policy providing that the insurer should be directly liable to any worker, and in the event of his death to his dependants, to pay the compensation or other amount for which the employer was liable and should be bound by and subject to any judgment given against the employer in respect of his liability independently of the Act and in respect of which the employer was indemnified under the policy. That provision was said to encompass liability pursuant to the Compensation to Relatives Act 1897 (NSW) and to require the conclusion that the phrase "liability for any injury to any worker" extended beyond liability to the injured worker himself.
235 I observe that those features of the policy in Rheem referred to in the Court of Appeal and in Technical Products are features retained, albeit with some difference in language, in the form of statutory policy requiring consideration in the present case. Indeed they are required by s 159(2) of the Workers’ Compensation Act 1987.
236 The narrower construction of the Queensland scheme in Technical Products does not bear upon the correctness of the decision in Rheem or how the form of statutory policy in New South Wales should be construed.
237 Mr Poulos submitted that Rheem and Hooper were wrongly decided, but that submission, if it is to be pursued, must be pursued at appellate level. It seems to me that the ratio of those cases applies to the statutory policy under the present Act and that I must follow these earlier decisions of the Court of Appeal.
238 In the result a finding that the first plaintiff acquired primary infection during her pregnancy arising out of and, in addition, in the course of her employment, would have amounted to “injury” within the meaning of the policy so as to expose the first cross defendant to a liability for the claims of both the first plaintiff and the second plaintiff. This is because the policy is to be construed as a policy that would have covered liability to the second plaintiff as a liability consequent upon the injury to the first plaintiff. The second plaintiff’s injury would have been a direct consequence of the injury to the mother.
239 Thus had the plaintiffs succeeded against the defendant, the defendant would have been entitled to indemnity by the first cross defendant for its liability to both plaintiffs for damages recovered against it, and the first cross defendant would also have been obliged (as the policy provided) to “pay all costs and expenses incurred with the consent of the insurer in connection with the defence of [these] proceedings.”
240 Since the plaintiffs’ claims have been unsuccessful it is inappropriate to make any of the declarations sought against any of the cross defendants in the cross claim. Nor is it appropriate to grant relief by way of judgment in the terms sought in the defendant’s cross claim.
241 Whilst the statutory policy required the first cross defendant to pay all costs and expenses in connection with the defence of legal proceedings “incurred with the written consent” of the first cross defendant, since the first cross defendant declined liability under its policy, I do not consider that the absence of written consent should in the circumstances disqualify the defendant from the benefit of an appropriate order as to costs as against the first cross defendant for costs properly incurred by it in this cause.
242 However, I do not propose to make any orders as to costs until the parties to this litigation have had the opportunity of considering these reasons for judgment on the plaintiffs’ claim and my findings referable to the defendant’s cross claims. If the parties, having considered my judgment, are unable to agree upon suitable costs orders on the claims of the plaintiffs and on the cross claims, I will entertain relevant submissions on a date to be fixed.243 For the present, I make formal orders as follows:
Formal orders
1. Verdict and judgment for the defendant on the claim of each plaintiff.2. Costs of the parties on such claims are reserved.
3. Orders in and costs on each of the cross claims reserved.
4. The matters to be relisted at 9.30 am on 6 June 2000 for the purpose of making orders in accordance with short minutes then presented as to costs on the plaintiffs’ claims, and as to each of the cross claims and costs thereon, or, failing agreement, for the appointment of a date for argument on any outstanding issues.
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