Repatriation Commission v Watson, E.n
[1995] FCA 578
•4 AUGUST 1995
CATCHWORDS
VETERANS' ENTITLEMENTS - Service in New Guinea - Creutzfeldt - Jakob disease - Whether reasonable hypothesis connecting disease with war service.
Veterans' Entitlements Act 1986
Bushell v. Repatriation Commission (1992) 175 CLR 408
Byrnes v. Repatriation Commission (1993) 177 CLR 564
Preston v. Repatriation Commission (1993) 45 FCR 214
East v. Repatriation Commission (1987) 16 FCR 517
McMahon v. Repatriation Commission (unreported, 21 July 1993)
REPATRIATION COMMISSION v ELSIE NANCE WATSON VG 160 of 1994
COURT:Sundberg J
PLACE:Melbourne
DATE:4 August 1995
IN THE FEDERAL COURT OF AUSTRALIA )
VICTORIA DISTRICT REGISTRY ) No VG 160 of 1994
GENERAL DIVISION )
BETWEEN:REPATRIATION COMMISSION
Applicant
AND:ELSIE NANCE WATSON
Respondent
COURT:Sundberg J
DATE:4 August 1995
PLACE:Melbourne
MINUTES OF ORDER
The Court orders that:
The appeal is allowed.
The decision of the Administrative Appeals Tribunal (Veterans' Appeals Division) is set aside and the decision under review by the Tribunal is affirmed.
Note:Settlement and entry of orders is dealt with in Order 36 of the Federal Court Rules.
IN THE FEDERAL COURT OF AUSTRALIA )
VICTORIA DISTRICT REGISTRY ) No VG 160 of 1994
GENERAL DIVISION )
BETWEEN:REPATRIATION COMMISSION
Applicant
AND:ELSIE NANCE WATSON
Respondent
COURT:Sundberg J
DATE:4 August 1995
PLACE:Melbourne
REASONS FOR JUDGMENT
SUNDBERG J:
Mr. Watson's war service
Evan Lawrence Watson served in the Australian Army from 1939 to 1945. His service included two periods of duty in New Guinea: from November 1944 to January 1945 and from March to September 1945. At the beginning of that period he was 25 years old. Mr. Watson served with the 2/8th Infantry Battalion as an infantryman. The nature and circumstances of his duty in New Guinea are not known, though while there he was hospitalised for eight days with gastroenteritis. He had a number of disabilities that were accepted as war-caused: malaria, clinical amoebiasis, psoriasis with puritis ani and scrotum, and retinal vein thrombosis.
Mr. Watson's health after his return
According to Mrs. Watson, after her husband's return from New Guinea he suffered memory, concentration and personality change, and because of this and recurrent bouts of malaria he had trouble settling down. However, significant memory problems did not develop until the late 1970s. Mr. Watson gave up his job in 1979 due to failing memory. Memory and other cognitive functions continued to deteriorate, leading to his hospitalisation in 1987. By late June 1992 he was no longer able to communicate and was then probably not aware of his surroundings.
1984-1992
Between 1984 and 1986 Mr. Watson was diagnosed by two medical practitioners in Bendigo, where he lived, as suffering from Alzheimer's disease. In June 1992 Dr. Simpkins diagnosed Mr. Watson as suffering from "a very advanced Alzheimer's disease". In July 1992 Dr. Koechne reported that "the correct diagnosis is Alzheimer's disease", and that "from the family history ... the cause is almost certainly genetic". The family history referred to is that Mr. Watson's brother and sister both suffered from some form of dementing disorder or disorders.
The pension claim
In July 1992 Mr. Watson made a claim for disability pension for Alzheimer's disease ("AD"). In August 1992 a delegate of the Commission determined that Mr. Watson's AD was not war-caused within the meaning of s.9 of the Veterans' Entitlements Act 1986 Act ("the Act"), and the claim was refused. This determination was affirmed by the Veterans' Review Board in March 1993. In May 1993 Mr. Watson applied to the Administrative Appeals Tribunal for review of the Board's decision. Shortly after the Tribunal commenced its review Mr. Watson died. His widow, Elsie Nance Watson, continued his claim pursuant to s.126 of the Act.
Dr. Bennett's report
In the Tribunal medical evidence was given for Mr. Watson by Dr. Bennett. He is a Fellow of the Royal Australian College of Physicians, a Fellow of the Royal College of Physicians of Edinburgh, and a Fellow of the Royal Australian College of Medical Administrators. He is a specialist in infectious diseases and for 35 years was a specialist in that area at Fairfield Hospital. He continues to practise in that field and chairs a number of committees of the Health Department of Victoria on that subject. He has published many papers on infectious diseases and for some 40 years has had a "great interest" in dementing diseases (Creutzfeldt-Jakob disease ("CJD"), Kuru, prion disease) though he has not published papers on them. He has advised the Health Department on CJD and has read as much about it as he could. His interest in CJD continues.
Dr. Bennett did not examine Mr. Watson. Indeed in his report dated 14 September 1993 he described Mr. Watson as "the deceased", though he did not die until 15 February 1994. In his report, Dr. Bennett said that although Mr. Watson had been diagnosed as suffering from AD, it was in fact impossible to distinguish AD on clinical grounds from other dementias, such as CJD, except by a microscopic examination of brain tissues obtained at autopsy. No such autopsy had been carried out on Mr. Watson.
The following account of Dr. Bennett's report (taken largely from the Tribunal's reasons for decision) accurately renders the effect of the report.
Dr. Bennett said that amongst the specific changes found in the brain are some which have been labelled "spongiform changes". There are a number of similar brain diseases in man which have these pathological findings in common, for example CJD, Kuru (Laughing disease) and other brain diseases which occur in animals, for example Scrapie and Bovine Spongiform-encephalopathy (Mad Cow disease). These diseases have therefore been grouped under the heading of "Spongiform encephalopathies".
Spongiform encephalopathies have also been called "transmissible dementias". Dr. Bennett said the evidence that these diseases are transmissible comes from two main sources. In 1957 a dementing disease was described in New Guinea by C.D. Gajdusek and Zigas which was called Kuru disease. In 1966 Gajdusek was able to transmit a disease resembling Kuru disease to chimpanzees by inoculating them with material from fatal cases of human Kuru disease. Disease did not become apparent in these animals until after 18-21 months. In New Guinea the transmission of Kuru disease from person to person seemed to be related to cannibalism as the disease ceased when that practice ended. In 1968 Gajdusek succeeded in transmitting another human spongiform encephalopathy, namely CJD, to chimpanzees after a similar long latent period. It was found that CJD could be transmitted to these animals not only by inoculation with extracts of brain, but also by inoculation with extracts of various other tissues taken from patients who had died from CJD. Because of the slow development of disease in
animals after inoculation, and because they were assumed to be caused by viruses, a new term was coined for the diseases, namely "slow virus disease".
The other evidence that indicated CJD was transmissible came from observations that the disease could be accidentally transmitted by one person to another. Dr. Bennett said that patients who had received corneal or dural grafts from persons who had died with CJD developed CJD themselves, after a latent period. Also, human pituitary hormone derived from patients dying of CJD had resulted in CJD in recipients of the hormone. The "agent" causing CJD is very resistant to disinfection, boiling water and formalin. Because of this CJD, has been transmitted to patients undergoing neurosurgery by instruments which had previously been used on patients with CJD. Dr. Bennett said that it is particularly noteworthy that the "incubation period", being the period between accidental inoculation and the appearance of the disease, varies from months to many years, and that the clinical features of the resultant neurological disease often differ according to the route by which the patient was accidentally inoculated.
Another feature of the spongiform encephalopathies is that the brain of patients with these diseases always contains an aberrant form of a normal cell protein - this abnormal protein was named "prion protein" by Prusiner in 1982, to designate a small proteinaneous infectious particle. In 1990 Prusiner and his colleagues in America succeeded in transplanting prion protein into mice which then developed typical pathological changes of spongiform encephalopathy in their brains. Accordingly, it appears that the prion protein is the key factor in the diagnosis and transmission of the spongiform encephalopathies. This has been further emphasised by the finding that
some individuals who die from a dementing or ataxic illness may have prion proteins present in their brains in the absence of the typical microscopic changes indicating a spongiform encephalopathy. The key pathological finding in the brain of patients with these diseases is the presence of prion protein. Therefore, the new name which has been given to the spongiform encephalopathies of humans [CJD and Kuru] and to similar diseases of animals is "prion disease".
Dr. Bennett raised the question whether prion protein is an infectious agent, stating that this has been doubted because prion protein is devoid of nucleic acid and is thus different from viruses and viroids. Also, some cases of CJD occur in families, that is, they are familial. He said it has been suggested that prion disease may be caused by a cytotoxic metabolite, that is, some substance which kills specific cells in the brain. S.B. Prusiner has suggested that prion diseases are both genetic and infectious.
It was Dr. Bennett's view that it may be some time before the exact nature of prion protein is determined. However, he said there is no doubt prion protein disease can be transmissible from person to person by various unusual ways, and that the resultant disease can be diverse in manifestation according to the route of inoculation.
Dr. Bennett stated that another important question was whether all prion diseases are different disease entities or variants of the one disease. The fact that clinical manifestations of CJD vary according to the route by which a patient is accidentally inoculated with the agent could mean that there is only one prion disease of humans, and the resultant disease state (given various names such as CJD and Kuru according to certain clinical features) varies only because of the different ways the agent has been transmitted. If this is shown to be true, then there is no doubt that Australian troops were very likely to have been exposed to prion disease in the form of Kuru which was prevalent in New Guinea during the war. Moreover, during the war there were great population dislocations amongst the indigenous people of New Guinea, so that troops could have come in contact with remote tribes some of whom could have been carrying the prion agent in the latent period before they developed disease. There are plenty of precedents in infectious disease history to justify such an argument - to wit the latent period in AIDS.
It was Dr. Bennett's view that inoculation or ingestion of human tissue containing the prion agent are unlikely to be the only methods of transmission to explain the occurrence of sporadic cases of CJD or other human prion disease. All the known methods of transfer of infectious diseases and of diseases transmitted by some toxin or poison remain possibilities.
Dr. Bennett then applied the foregoing exposition to Mr. Watson's case. His conclusions can be summarised as follows:
(a)Since no post-mortem examination of the brain was made, "it is an undeniable fact that Mr. Watson may have had CJD".
(b)Prion diseases such as Kuru and CJD were known to occur in New Guinea during the war, and in the case of Kuru were known to be prevalent.
(c)Prion diseases are transmissible between humans in the ways described above. However most cases of CJD occur sporadically, and the mode of transmission is unknown. "All possibilities remain for this unknown mode of transmission, such as ingestion or inhaling the agent, transmission by blood or venereally, inoculation by the agent through skin abrasions, transmission by insect bite or transmission by some contact with animals".
(d)Clinical features of prion disease, such as CJD, do not become evident for many months or many years after transmission.
(e)Because he contracted malaria and dysentery in New Guinea, he may have been more susceptible to contracting prion disease.
(f)Dr. Bennett concludes by summarising the "undeniable, very reasonable and quite probable hypothesis linking Mr. Watson's dementing disease with his war service":
While serving in PNG during WW2, Mr. Watson contracted by some at present unknown method, prion disease in the form of CJD. It is more likely that he contracted the disease in PNG than in Australia, because of the known high prevalence of prion disease [Kuru in particular] as well as CJD in PNG. After a typically long latent period of years, Mr. Watson developed features of CJD. His disease was labelled as Alzheimer's disease, but this was not substantiated by definitive pathological testing and, therefore, because of the overlapping clinical features of this disease with CJD, it is an undeniable and probable possibility that he had CJD.
Dr. Whyte's report
Dr. Whyte gave evidence for the Commission. He is a Fellow of the Royal Australian College of Physicians. He is a consulting physician at Mount Royal Hospital. He is currently undertaking a Ph.D. at Melbourne University and for several years has been studying biochemical issues relating to AD. He has presented papers at a number of world conferences on these issues and has contributed to text books dealing with AD. The following account of Dr. Whyte's report (taken from the Tribunal's reasons for decision) accurately renders the effect of the bulk of the report, though it will be necessary to supplement the Tribunal's account later in these reasons.
Dr. Whyte discussed the epidemiology of AD, noting that the disease is characterised by a steadily progressive intellectual deterioration. The duration of the illness is usually five to twelve years following the onset of clinical symptoms. However, more rapid clinical courses with death under one year, or protracted clinical courses with survival up to 25 years following onset of the disease, are possible.
There are a number of risk factors for the development of AD, age being the most important. It is not, however, a feature of normal ageing. Other factors are genetic factors, head injury, increased aluminium intake and depressive illnesses. Studies have demonstrated an increase in risk for the development of AD where there is a first degree relative with dementia. The risk is increased 2.6 times for one first degree relative and 7.5 times for two first degree relatives with dementia.
Dr. Whyte said that it has been hypothesised that the pathological process of AD begins approximately 30 years prior to the onset of clinical features. The main pathological hallmark of the disorder is the deposit of a specific form of amyloid between nerve cells, within nerve cells, and within the walls of blood vessels. Amyloid is seen in diseases with a clearly infectious basis, such as Kuru, or in disorders that do not have an infectious aetiology, such as AD. Case reports of CJD deposits co-existing with AD amyloid deposits are not infrequent and are totally in keeping with a chance occurrence of the two diseases. This is not unusual considering that approximately 20 per cent of brains of people 60 years of age will have AD amyloid deposits, despite the absence of clinical disease.
Dr. Whyte then discussed the "prion diseases" Kuru and CJD, reporting that the former disease has a 30 or more year period between infection and the onset of clinical disease. The disease is remarkable in its confinement to highland New Guineans. However in 1990 D.C. Gajdusek reported as follows: "No cases of the disease were seen in natives from elsewhere in New Guinea, eating and living together in schools or labour compounds with kuru-region persons in whom kuru developed while they were away from home. Furthermore, hundreds of native peoples from elsewhere in New Guinea and from surrounding Melanesian islands and Caucasians have now been resident for long periods in the kuru region since early government penetration almost half a century ago. In spite of the many thousands of man-years of close contact of these immigrants with the flora, fauna, food and people of the region, no case of kuru has occurred among them. Continued surveillance has revealed no alteration in the unusual pattern of kuru disappearance, which indicates the artificial man made nature of the epidemic. Kuru virus clearly has no reservoir in nature and no intermediate biological cycle for its preservation except in humans". Gajdusek further reported that, in contrast to the slow incubation period of the disease, the clinical period is characterised by a remarkably uniform clinical course, with death usually occurring within three to nine months.
Dr. Whyte described CJD as a rare disorder, which typically presents with a rapidly progressive dementia associated with a variety of other significant neurological abnormalities, including jerking movements and progressive motor dysfunction. Death usually occurs within one year following the commencement of clinical symptoms.
As to its epidemiology, Dr. Whyte said that the incidence of CJD is about one in a million people, although there has been a tendency for increased diagnosis as awareness of the disease has increased. Transmission of CJD from man to man has been demonstrated clearly, but only by direct inoculation of infected material into the body, for example in recipients of infected human pituitary gland extracts or infected tissue grafts. There was no evidence to suggest that transmission may occur by any other method. Wide scale reviews of CJD cases have failed, except in one or two rare cases, to show any prior contact of patients with other CJD sufferers. Dr. Whyte said that some CJD patients have also lived in isolated communities where contact with CJD sufferers is extremely unlikely. There is no evidence of transmission by contact with food or animals. CJD has always been a rare and in the main sporadic disease which, with the exception of a handful of iatrogenic cases, has defeated every attempt to identify a mechanism by which it might be spread.
While the incubation period of CJD is protracted (up to 30 years), the clinical course is almost always rapid, with a mean duration to death from onset of clinical symptoms of less than eight months. Rare patients may survive up to five to eight years and even fewer have been known to have survived up to a maximum of thirteen years. The most common clinical presentation is with physical neurological symptoms (60 per cent), with the remaining 40 per cent presenting with gradually progressive mental deterioration without initial physical neurological symptoms.
Dr. Whyte explained that the use of the term "virus" for the prion disease agent is misleading, because no true virus has ever been discovered and the infectious particle is capable of withstanding conditions which would destroy any presently known virus. Most authorities consider a small peptide called the prion protein to be the infectious particle. It is therefore not reasonable to assume that this same particle will behave like a totally dissimilar infecting agent because they share the same name. There is strong evidence that these agents are not transmitted by a mosquito vector. Kuru does not have an intermediate vector and the evidence of CJD does not increase in regions which have such vectors. Dr. Whyte went on to say that P. Brown had described the apparent outbreaks of CJD (in areas without such mosquito vectors) as being related more to a genetic abnormality than to a geographical one. In the review in 1990, Gajdusek commented upon his experience with a number of patients who had CJD and were professional blood donors, after which no reported case of CJD had arisen. He also described extensive experiments which attempted to transmit CJD through large blood transfusions to susceptible animals, without any success. This lack of transmission of CJD through blood transfusion and the "positive" absence of epidemiological data supporting the potential for a mosquito vector, effectively rules out this possibility. Dr. Whyte said that while different means of inoculation of CJD have been demonstrated to vary in their clinical presentation, there is no history in the case of Mr. Watson to suggest that accidental medical inoculation is of significance. He said that to imply that spontaneously acquired CJD is purely an infective illness is to ignore considerable increasing medical opinion that spontaneous CJD is due to a spontaneous aberration of a normal brain protein, which does not require an infectious agent for its commencement. Variation of the clinical features of prion dementias has also been linked to a variety of mutations in the prion proteins. There are therefore a range of theories to describe the clinical variation in prion diseases. It is clear though, with Kuru, that there is a large degree of consistency in clinical presentation of the disease, and strong evidence that simple exposure to people with the disease (whether latent or not) is insufficient to transmit the disease. This is true also for Caucasians living with at risk or infected people (Gajdusek 1990). There is no evidence, despite extensive studies of both people with Kuru and those in proximity or close contact with Kuru sufferers, that there is an increased incidence of other forms of prion disease. There is therefore no justification for believing that servicemen were at any increased risk of developing prion disease because of the presence of Kuru in New Guinea. Nor is there any justification for believing that they would be at an increased risk of developing CJD because of war service in New Guinea. He said there is no evidence that infectious illnesses may predispose to developing prion dementias.
Dr. Whyte concluded that the evidence supported the view that Mr. Watson had AD, that there was no evidence that war service or illness suffered during the war would have predisposed him to AD, and that it was extremely improbable that he had prion disease.
The report contained the following passages which are not reflected or fully reflected by the Tribunal's account of his report. After referring to the fact that Mr. Watson had retired from work due to failing memory in 1979, Dr. Whyte said:
It is likely that clinical symptoms would have been present for at least one to two years prior to him needing to retire from work, which would place the clinical disease onset in the late 1970's. The duration of the illness is therefore 14-16 years, which effectively rules out the possibility that Mr. Watson has CJD (see summary CJD).
The summary referred to is:
While the incubation period for CJD is protracted (~20-30 years), the clinical course is almost always rapid, with a mean duration to death from onset of clinical symptoms of ~8 months. Rare patients may survive up to 5-8 years and even fewer have been recorded to have survived up to a maximum of 13 years.
Dr. Bennett's oral evidence
In his evidence in chief Dr. Bennett accepted the probability that Mr. Watson had AD and not CJD, but said that nobody could be sure that he did not have CJD until a post-mortem was done. Until then "nobody can deny that possibility". He then referred to how easily CJD is transmitted. No doubt Mr. Watson had injections in New Guinea.
During the war it was common to inject one person, flame the needle and use it on another. The disease could have got into his bloodstream as a result of being tattooed in New Guinea. Or by being bitten by monkeys or dogs. After canvassing these and other possibilities he said: "Now if anyone says, all these things can't happen, how do you know they can't happen? We don't know how the disease is transmitted. Nobody knows how it is transmitted."
In cross-examination he repeated that on the available evidence nobody could deny the possibility that Mr. Watson may have had CJD until he had had an autopsy. He said later that there was an abysmal lack of knowledge on transmission of CJD - "we do not know what the organism is, how it is transmitted so no one cay say, one in a million. No one knows anything yet." Asked about the different clinical signs a CJD sufferer would have depending on the mode of transmission, he referred to an article in Lancet and said:
it points out that when people received the transmitted CJD to them by this particular way by the peripheral way, by blood, that was not directly into say an eye, or into a brain dural covering, that - contracted via the peripheral route, impaired voluntary movement and the absence of dementia. In other words they were not stupid. Subsequent myoclonia, shaking and death within a three or six month period, a quite different thing in that case to the ones that had acquired the disease say by a corneal graft. ... it is recorded in many places that the clinical features do vary in Creutzfeldt-Jakob according to the known ways in which it can be transmitted ....
Dr. Whyte's oral evidence
Dr. Whyte's examination in chief includes the following passages amplifying his report:
This gentleman does not have disease for one year; this gentleman has disease for 15 to 17 years. So, we can't just blithely just go along and say that his chance of having CJD is going to be .006 per cent, because that is the CJD in people who have had disease for one to two years.
Speaking of transmission Dr. Whyte said:
So, transmission has only been shown by direct inoculation of tissue. Now, that's a very important thing and again, as I mentioned, it gives different clinical presentations depending upon where you put the tissue. If you put the tissue outside of the brain you get motor dysfunction and if you put the tissue into the brain, you get dementia.
He then dealt with the short life-span of most CJD sufferers and continued:
The clinical presentation of CJD most often is with neurological symptoms, 60 per cent. Only a minority, 40 per cent, would present with a dementing illness. This is people with sporadic disease but there is a very important difference in people who present with an infective transmitive form of CJD.
He then referred to an article in Lancet and said that the authors
looked at the clinical onset of people who had known infective aetiologies and they found that at onset none presented with dementia, zero presented with dementia. So this is a
fairly tight clinical presentation of people who have been infected by a peripheral disease, by say tissue or something like that. And, as you would expect if you are going to believe that blood can do it, by blood. But what do we find in our patient's case Mr. Watson, he presented with dementia.
Later he mentioned the case of a CJD case study he had discovered since his report: a 46 year old man with a sixteen year illness duration. Dr. Whyte said:
And in many ways typical CJD clinical history; he had marked motor dysfunction from an early stage .... There's quite definite marked physical clinical findings and then a dementing illness. And then just before his death, generalised rigidity, cogwheeling, miclonis which is a jerking movement and course tremors. And that's been a feature of even the long duration CJD. So, prior to the death - in the terminal phase - they have this marked motor dysfunction of obvious jerking movements. And then a rapid terminal phase, even if some of the long durations have reported at say 11 or 13 years, appear to have little motor dysfunction - the terminal phase by the time they were really hospital bound, they had major motor dysfunction. And that's not something that's been reported on in this gentleman's case.
He then said that if the "fanciful idea" that Mr. Watson had CJD were to be accepted, then he had it in a way that has not been shown to occur. If he did get it from blood transfusion, he didn't present in the expected way. None of those who had hormone therapy presented with dementia, but Mr. Watson did. If Mr. Watson had CJD, then because he had a dementing onset, it would have to be spontaneous (i.e. non-infective). Then he returned to Mr. Watson's clinical signs, and said that his opinion that he had AD and not CJD was not based primarily on the length of the illness but
upon this gentleman's clinical course; a course of dementia without motor impairment and a terminal phase characteristic of Alzheimer's disease with no description whatsoever of the usual features of CJD, which are usually marked enough for anyone to notice them from the end of the room - jerking movements and the other features. So, really, it's not just the duration of the illness it's the clinical progression of the disease as well.
He then said that in Mr. Watson's case pathological confirmation (i.e. post mortem) was unnecessary, because the clinical differential diagnosis, clinical history and clinical features "very effectively" excluded CJD. Dr. Whyte was cross-examined on various parts of his testimony, but not about the different clinical features depending on the known ways in which CJD can be transmitted.
The legislation
Section 120(1) of the Act is in part as follows:
Where a claim under Part II for a pension in respect of the incapacity from ... disease of a veteran ... relates to the operational service rendered by the veteran, the Commission shall determine ... that the disease was a war-caused disease ... unless it is satisfied, beyond reasonable doubt, that there is no sufficient ground for making that determination.
Sub-section (3) provides in part:
In applying sub-section (1) ... in respect of the incapacity of a person from ... disease ... related to service rendered by the person, the Commission shall be satisfied, beyond reasonable doubt, that there is no sufficient ground for determining -
...
(b)that the disease was a war caused disease ...
...
... if the Commission, after consideration of the whole of the material before it, is of the opinion that the material before it does not raise a reasonable hypothesis connecting the ... disease ... with the circumstances of the particular service rendered by the person.
Under s.9(1) a disease contracted by a veteran is a "war-caused disease" if it
(a)... resulted from an occurrence that happened while the veteran was rendering operational service;
(b)... arose out of, or was attributable to, any eligible war service rendered by the veteran.
Mr. Watson's service in New Guinea was "operational service" as defined in s.6 and "eligible was service" as defined in s.7, and he was a veteran within the meaning of s.5.
Relationship between sub-ss.(1) and (3) of s.120
In Byrnes v. Repatriation Commission (1993) 177 C.L.R. 564, at p.571 Mason C.J., Gaudron and McHugh JJ. said:
The position may be summarised as follows:
(1)First, sub-s.(3) of s.120 is applied: do all or some of the facts raised by the material before the Commission give rise to a reasonable hypothesis connecting the veteran's injury with war service? The hypothesis will not be reasonable if it is contrary to known scientific facts or is obviously fanciful or untenable. If the
hypothesis is not reasonable, the claim fails. Proof of facts is not in issue at this point.(2)If a reasonable hypothesis is established, sub-s.(1) of s.120 is applied. The claim will succeed unless:
(a)one or more of the facts necessary to support the hypothesis are disproved beyond reasonable doubt; or
(b)the truth of another fact in the material, which is inconsistent with the hypothesis, is proved beyond reasonable doubt, thus disproving, beyond reasonable doubt, the hypothesis.
Reasonable hypothesis connecting disease with service
In East v. Repatriation Commission (1987) 16 F.C.R. 517, at p.532 the Full Court approved the following exposition of the meaning of "reasonable hypothesis":
A hypothesis may be conveniently defined as: ‘proposition made as basis for reasoning, without assumption of its truth; supposition made as starting point for further investigation from known facts; groundless assumption’: The Concise Oxford Dictionary
...
The addition of the word ‘reasonable’ would however seem to imply that what is required is more than a mere hypothesis. In the opinion of the Board, to be reasonable, a hypothesis must possess some degree of acceptability or credibility - it must not be obviously fanciful, impossible, incredible or not tenable or too remote or too tenuous. For a reasonable hypothesis to be ‘raised’ by material before the Board, we think it must find some support in that material - that is, the material must point to, and not merely leave open, a hypothesis as a reasonable hypothesis. At the same time, however, a hypothesis may be reasonable without having been proved (either on the balance of probability or beyond reasonable doubt) to be correct as a matter of fact. Were it
otherwise, it would no longer be a hypothesis but would have been elevated to some higher status. Accordingly a connection asserted by a hypothesis to exist between death or incapacity and service may still be reasonable even though theoretical, and it may be theoretical in either or both of a least two senses: by postulating a known medical fact but in circumstances not known to have definitely existed in the instant case; or by postulating a medical principle which science is not yet able to definitely prove but is unable to describe as unreasonable.
The Full Court added:
A reasonable hypothesis requires more than a possibility, not fanciful or unreal, consistent with the known facts. It is an hypothesis pointed to by the facts, even though not proved upon the balance of probabilities.
See also Gilbert v. Repatriation Commission (1989) 86 A.L.R. 713, at pp.718-721. In McMahon v. Repatriation Commission (unreported, 21 July 1993) Burchett J. said:
In one sense, the less there is known about a particular question, the greater the number of competing hypotheses which may be suggested in relation to it. But that is not what s.120(3) contemplates. Its very purpose, the joint judgment in Bushell emphasises ... "is to ensure that a claim to which s.120 applies is not met unless there is some material which raises the relevant causal hypothesis". ... It will be noticed that s.120(3) requires the Tribunal to give "consideration [to] the whole of the material before it". Although, as was pointed out in Bushell, the sub-section is not concerned with the making of choices between competing hypotheses, it is concerned with whether a reasonable hypothesis of the requisite kind is raised, not by some part of the material taken alone, but by the whole of the material before the Tribunal.
Tribunal's decision
The Tribunal first found that the form of dementing illness suffered by Mr. Watson, from which he died, was CJD. It then concluded that the material gave rise to a reasonable hypothesis connecting the disease and death with war service. The Tribunal enumerated the facts which gave rise to the reasonable hypothesis: (i) Mr. Watson served in New Guinea as an infantryman in circumstances where it is reasonable to assume he had a degree of close contact with indigenous people, including highland people. (ii) At the time Mr. Watson served in New Guinea, prion diseases such as Kuru and CJD were known to occur and to be prevalent. (iii) Prion diseases are transmissible. (iv) In the case of CJD, transmission can be by certain medical procedures and familial relationship. (v) In most cases, however, CJD occurs sporadically, the mode of transmission being unknown. Various modes of transmission have been suggested, including: (a) ingesting or inhaling the agent; (b) by blood or venereal contact; (c) by inoculation of the agent through skin abrasions; (d) by insect bite; (e) by contact with animals. (vi) Clinical features of prion disease, such as CJD, do not become evident for perhaps many years after transmission of the agent to the patient. (vii) Mr. Watson developed dementia many years after his service in New Guinea. (viii) During his service in New Guinea Mr. Watson contracted malaria and dysentery. The Tribunal then said that Dr. Whyte's evidence did not disprove beyond reasonable doubt any one or more of the facts, and that it was therefore not satisfied beyond reasonable doubt that there was no sufficient ground for determining that Mr. Watson's dementia was war-caused, or that his death was war caused. The Tribunal set aside the decision under review and substituted for it the decision:
(a)That the diagnosis Alzheimer's disease ("AD") in respect of the late Evan Lawrence Watson, ("the veteran") claimed on 23 July 1992 as war-caused, be amended to Creutzfeldt-Jakob disease ("CJD");
(b)that the disease CJD contracted by the late veteran was a war-caused disease within the meaning of section 9 of the Veterans' Entitlements Act 1986 ("the Act").;
(c)that the death of the late veteran was war-caused within the meaning of section 8 of the Act; and
(d)that pursuant to section 13 of the Act the Commonwealth is liable to pay pension to the applicant Elsie Nance Watson, from 16 February 1994.
The appeal
The Commission has appealed to this Court under s.44 of the Administrative Appeals Tribunal Act 1975. The respondent accepted that pars.(c) and (d) of the Tribunal's decision were not supportable. Counsel for the Commission's first attack on the balance of the Tribunal's decision concerned its finding that Mr. Watson suffered from CJD. The Tribunal made this finding applying the test espoused in Doolette v. Repatriation Commission (1990) 21 A.L.D. 489 - "something less than the ‘balance of probabilities’." Section 120(6) provides that neither party has "any onus of proving any matter that is, or might be, relevant to the determination of the claim or application". Sub-section (4) provides:
Except in making a determination to which subsection (1) ... applies, the Commission shall, in making any determination or decision in respect of a matter arising under this Act or the regulations, including the assessment and re-assessment of the rate of pension granted under Part II or Part IV, decide the matter to its reasonable satisfaction.
Counsel for the Commission submitted that whether a veteran suffered from a disease, or whether he suffered from disease A or disease B, was to be determined in accordance with sub-s.(4), and that sub-ss.(1) and (3) were concerned only with the link between disease and war service. He conceded that Brennan J. in Bushell v. Repatriation Commission (1992) 175 C.L.R. 408, at p.425 took a different view. His Honour said:
Sub-section (1) governs the finding of each of the relevant facts on which entitlement depends: the circumstances of the veteran's operational service, the veteran's morbid condition and, relevantly, the causal connexion between the two: "a reasonable hypothesis connecting the injury, disease or death with the circumstances of the particular service rendered by the person".
Later his Honour repeated that the finding of the morbid condition and the circumstances of the veteran's operational service "is governed solely by sub-s.(1)": p.426. Though Brennan J. set out sub-s.(4) when he quoted the whole of s.120, he did not refer to that sub-section when dealing with the proof of morbid condition and operational service. Brennan J.'s view has been followed by Beazley J. in this Court: Preston v. Repatriation Commission (1993) 45 F.C.R. 214. Counsel for the Commission urged me not to follow Preston and to deal with the AD/CJD issue under sub-s.(4). According to Byrnes, the first matter that has to be determined under s.120 is whether the facts raised by the material give rise to a reasonable hypothesis connecting Mr. Watson's disease with war service. The Commission's submission concerning the correctness of the Tribunal's finding of CJD rather than AD is directed to proof of facts, and that is "not in issue at this point": Byrnes, p.215. It is "not the function of s.120(3) to require the
Commission to ... determine whether one medical or scientific opinion is to be preferred to another": Bushell, p.415.
Section 120(3) required the Tribunal first to identify the facts raised by the material. The "facts" raised by the material (which do not have to be proved by it) include that CJD exists, and Kuru is prevalent, in New Guinea; that indigenous people in New Guinea during the war were serving with and were in contact with Australian troops; that CJD and Kuru are transmissible by an injection; that if an injection were given to one of the indigenous people who suffered from CJD or Kuru and the same needle later used on an Australian soldier, that could transfer to the soldier a dementing disease; that CJD has a lengthy incubation period; that Mr. Watson was in New Guinea; that he was in hospital there; that he received an injection there; that in that way he had CJD transmitted to him; and that he developed dementia. These are the facts raised by the material. They do not have to be proved, though some of them were. The question then is whether those facts gave rise to a reasonable hypothesis connecting the CJD with Mr. Watson's war service. Various parts of the evidence give rise to a reasonable hypothesis in the sense described by the authorities. Thus Dr. Bennett's report would satisfy the requisite test. But the Tribunal is enjoined by McMahon to look at the whole of the material before it. That material includes Dr. Whyte's evidence about the clinical features of different modes of transmission of CJD. His evidence was that if CJD could be transmitted by any of the modes by which Dr. Bennett thought it possible that Mr. Watson became infected, such as injection with a contaminated needle, the clinical features would have involved motor dysfunction - obvious jerking movements. But Mr. Watson did not exhibit those clinical features, only dementia. As I have said, Dr. Whyte was not cross-examined on this issue. And Dr. Bennett agreed that someone who received CJD by the peripheral way, by blood, that was not directly into an eye or into the brain dural covering, would present with impaired voluntary movement and the absence of dementia. In the light of Dr. Whyte's evidence about the clinical features of peripherally transmitted CJD (and Dr. Whyte is a geriatric clinician), and Dr. Bennett's acceptance of those features (though he is not a geriatric clinician), the hypothesis initially raised by Dr. Bennett is seen to be contrary to known scientific facts, and obviously untenable. It was therefore not a reasonable hypothesis for the purpose of s.120(3). Because both medical experts accepted that peripherally transmitted CJD (the only suggested mode of transmission) resulted in motor dysfunction, and that Mr. Watson did not suffer from motor dysfunction, there was no evidence on the basis of which the Tribunal could have concluded that Mr. Watson's CJD was war-caused. That is an error of law which brings the Commission's appeal within s.44 of the Administrative Appeals Tribunal Act. It follows that the fact finding exercise (whether under sub-s.(1) or sub-s.(4)) does not arise, and I do not have to deal with the submission that I should not follow Preston.
The appeal is allowed. The decision of the Tribunal is set aside and the decision under review by the Tribunal is affirmed. The Commission did not seek an order for costs, and I make no order as to costs.
I certify that this and the preceding 26 pages are a true copy of the reasons for judgment of the Honourable Justice Sundberg
........ ........ ........ ........ ........ ........ ........ ........ .
Associate
4 August 1995
Counsel for the Appellant: P J Hanks
Solicitor for the Appellant: Australian Government Solicitor
Counsel for the Respondent: H C Berkeley QC / G K Moore
Solicitors for the Respondent: Geoffrey Tobin
Date of Hearing: 18, 19 July 1995
Place of Hearing: Melbourne
Date of Judgment: 4 August 1995
0
4
0