Woodman, James Stanley v Repatriation Commission
[1996] FCA 1100
•13 Dec 1996
IN THE FEDERAL COURT OF AUSTRALIA )
VICTORIA DISTRICT REGISTRY ) No. VG739 of 1995
GENERAL DIVISION )
On appeal from the Veterans' Appeal Division of the Administrative Appeals Tribunal constituted by Deputy President G.L. McDonald, Mr. R.C. Gillham and Dr. D.M. Sutherland, Members
BETWEEN: JAMES STANLEY WOODMAN
Applicant
AND:REPATRIATION COMMISSION
Respondent
CORAM: Jenkinson J.
PLACE: Melbourne
DATE: 13 December, 1996
MINUTES OF ORDER
THE COURT ORDERS THAT:
The appeal be dismissed.
The applicant pay the respondent's costs of the appeal.
(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. VG739 of 1995
GENERAL DIVISION )
On appeal from the Veterans' Appeal Division of the Administrative Appeals Tribunal constituted by Deputy President G.L. McDonald, Mr. R.C. Gillham and Dr. D.M. Sutherland, Members
BETWEEN: JAMES STANLEY WOODMAN
Applicant
AND:REPATRIATION COMMISSION
Respondent
CORAM: Jenkinson J.
PLACE: Melbourne
DATE: 13 December, 1996
REASONS FOR JUDGMENT
Appeal from a decision of the Administrative Appeals Tribunal that the rheumatoid arthritis contracted by the applicant was not "a war-caused disease" within the meaning of that expression in the Veterans' Entitlement Act 1986 ("the Act").
The applicant was born on 5 August 1921. At his medical examination upon joining the Australian Army in September 1941 he declared himself to be suffering from "backache". No significant medical abnormality was recorded at that time. During service in New Guinea in the Army, which was "operational service" within the meaning of that expression in the Act, the applicant experienced severe pain in his lower back while he was helping to lift a hospital
patient who was encased in a plaster cast. The onset of pain followed immediately upon a sensation of something snapping in his back. The only treatment in New guinea was by a ray lamp. Pain in the lower back has persisted ever since. In 1991 a delegate of the respondent determined that the applicant's "lumbar spondylosis" was war-caused, but that his rheumatoid arthritis, symptoms of which he had noticed in his limbs for many years, was not war-caused.
An eminent medical practitioner who specialises in immunology, Dr. I.R. Mackay, propounded the hypothesis that the lower back pain experienced by the applicant in New Guinea was "an early expression of rheumatoid arthritis, at that time mainly localized to the spine". A careful reading of the transcript of Dr. MacKay's evidence and of his written report, which was in evidence, makes it quite clear that he did not regard the exertion of lifting the patient, or any physiological event which occurred at that time, as making any causal contribution to the contraction of the disease of rheumatoid arthritis. Nor is there any indication that Dr. MacKay thought that the disease was aggravated by the lifting or by any such a physiological event. (See s.9(1)(e) and Repatriation Commission v. Yates (1995) 57 F.C.R. 241). The suggestion by counsel for the applicant that there was such an aggravation ignores the distinction between the manifestation of a disease by a symptom of the disease and aggravation of the disease (See Yates' Case at 248-250).
Dr. MacKay expressed the opinion that the contraction of the disease may have occurred during the applicant's adolescence, or shortly before the lifting incident during operational service. He seemed to regard each possibility as a not unreasonable hypothesis. Counsel for the applicant submitted that, if the contraction of the disease occurred while the applicant was rendering operational service, s.9(1)(a) operated to require that the disease be taken to be a war-caused disease. The contraction of the disease is to be regarded as itself the "occurrence" to which that paragraph refers, according to the submission. That is in my opinion an untenable submission.
During his service in New Guinea the applicant suffered from malaria and he continued to suffer malarial relapses for five or six years after the war. In his report Dr. MacKay, having dealt with the applicant's lower back symptoms and their possible significance in relation to rheumatoid arthritis, concluded with the following passage:
"It may be that it is sufficient for Woodman's case that the reasonable possibility is raised that his current rheumatoid arthritis began during his eligible army service, without the need to attribute provocative causes. Rheumatoid arthritis is, as stated in the 1993 determination (p 70), `an autoimmune problem'. What this means is that there is a malfunction of the immune system of such a type that an immunological attack is mounted on a normal body constituent, joint tissue such as synovium or cartilage in the case of rheumatoid arthritis. Why and how this particular malfunction occurs is unclear, although an infectious origin is often cited. Provocative infections could initiate autoimmunity in any one of at least three ways, as follows. (1) The infectious agent, virus, bacterium or parasite, could inflict damage at a target site sufficient to cause release of bodily constituents which, in a genetically predisposed individual, would act as autoantigens and generate an autoimmune response. (2) The infectious agent would present antigenic configurations (epitopes) that so resembled a bodily antigen that an autoimmune response would be initiated to the microbial antigen and perpetuated by the corresponding antigenic structure of the host, a process known as molecular mimicry. (3) A chronic infection by a persisting pathogenic organism could act as a source of continuing antigenic stimulation of B lymphocytes in the course of which there could arise `mutant' reactivities with native body autoantigens.
Chronic malarial infection is an example of mechanism (3). A survey of the medical literature for evidence of malaria being a factor in autoimmunity disclosed a report as early as 1952 by Moore and Mohr (Journal of the American Medical Association 150: 467-473, 1952) in which infections such as malaria were associated with `falsely positive' tests for syphilis. The nature of the test system for the serological diagnosis of syphilis is such that a `false positive' reaction can occur when serum reacts with normal tissue constituents in the antigenic preparation rather than with constituents of spirochaetes, the causal microorganism of syphilis. False positive reactions for syphilis are therefore taken to be a marker for autoimmune reactivity. More recently Abu-Shakra and Shoenfeld (Autoimmunity 9: 337-344, 1991) reviewed the subject of parasite infections including malaria and autoimmunity (copy herewith). This review draws attention to the frequency of autoantibodies, and particularly the antinuclear antibodies seen in the autoimmune disease, systemic lupus erythematosus, in subjects with chronic parasitic infections including malaria. The review describes the various mechanisms by which this might occur, and include chronic mitogenic stimulation of B lymphocytes by the infectious process, thus predisposing to somatic mutations among B lymphocytes of a type predisposing to autoimmune reactivity.
In conclusion the `reasonable hypothesis' of a war-serviced (sic) connected basis for rheumatoid arthritis in the case of Woodman subsumes the two considerations of the known long latent period between the initiating stimulus for an autoimmune reaction and the eventual clinical expression, and the possibility of a persistent infectious process, in this case malaria, causing a derangement of immunological function that predisposes to autoimmunity. There are of course required added causal factors for overt disease including the important contribution of the genetic constitution of the affected individual."
Both in the first sentence of that passage and in the transcript of Dr. MacKay's oral evidence there are indications that he supposed that entitlement to a pension under the Act might be established by the existence of a reasonable hypothesis that the contraction of the rheumatoid arthritis occurred during operational service. That must be borne in mind when considering the following passages of his oral evidence:
"In summary then. Doctor, are you suggesting that there are two possible hypotheses as far as the veteran is concerned; the first one in that some of the earlier symptoms might in fact have indicated rheumatoid arthritis very early during his war service, and secondly that there may be some possible stimulation of the immune system which later made him more susceptible to the condition?---Taking the two questions separately, there is evidence even during his period of service that he had what we call articular pain; that is pain in the back, and I will concede that rheumatoid arthritis beginning with back pain is not usual, but not entirely excluded by the evidence. The back pain is attributed to the lifting of a heavy patient. Of course we have to bear in mind that when people do have musculo skeletal pain, or even when there is an onset of - this is with the onset of rheumatoid arthritis, there is always a natural search for a cause. Perhaps it was because of lifting this or doing that or striking this part of the body or that. So that it may well be that the lifting did cause a muscular sprain, or it may be that this was one of the first expressions of the rheumatoid arthritis. Even during his period of service - and we can note that he is talking of - there are discussions in the transcripts of spreading pains and fibrositis in the late 1940s, so there does seem to be some sort of continuum. The second point, and I do not think this point is essential for the development of a supportive case, that he was exposed to possible rheumatoid triggers during his period of service, and it may be that in the totality of the case his exposure to these triggers can be taken into consideration as facilitating his development of rheumatoid arthritis.
Doctor, do you - you do not specifically say, sir, in your report but I take it from the evidence that you have given you regard that there is a reasonable hypothesis linking the service with the rheumatoid arthritis?---Yes. I think there is a reasonable hypothesis.
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And so do you say then that the malaria or the episodes of malaria strengthens a service link?---Perhaps that might not be for me to judge. I take my responsibility as to impartially provide the current thinking in relation to these diseases, and there is current thinking that parasitic infections of which malaria is an example might be a triggering event for an auto-immune disorder.
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And how would you apportion the cause between the two circumstances, that is, the stimulation of the auto immune system by malaria and some other stimulation which - - -?---We don't know about. Again I would have to cite what I would think would be the opinion of the majority of skilled Rheumatologists and that would be that although malaria would be a candidate, the majority of Rheumatologists would be looking for something other than malaria simply because documented examples of rheumatoid arthritis after malarial infection is uncommon, so that when you pick up a text of rheumatology and look up the causes of rheumatoid arthritis, you would probably not see listed among the possible causes an attack of malaria. This may
be because rheumatoid arthritis is predominantly a Caucasian disease and in non-malarial so I'm simply putting it as a non inconceivable possibility with the attributable reference here in a scientific journal that concedes the possibility that malaria could be one of the triggers."
The Tribunal dealt with the possible relationship between malaria and rheumatoid arthritis in the following passages:
"9. Dr MacKay also advanced a second hypothesis which he said was not essential for the development of a supportive case in relation to the first hypothesis. He said that there is quite substantial and convincing evidence that rheumatoid arthritis is an autoimmune disease (the body's own immune system attacks the body itself) and that the applicant may have been exposed to possible rheumatoid triggers during his period of service as a consequence of his malaria. Dr MacKay said that it may be that `in the totality of the case his exposure to these triggers can be taken into consideration as facilitating his development of rheumatoid arthritis' (trans, p.5). In his report (exh B), Dr MacKay identifies three ways in which provocative infections could initiate autoimmunity. One way was through a person suffering from a chronic infection caused by a persisting pathogenic organism. Malaria was such an organism which, in the instant case, since it occurred over a number of years, could be regarded as being persistent and could have caused a derangement of the applicant's immunological function predisposing him to autoimmunity. Dr MacKay referred to literature on the subject (including an article by Abu Shakra and Shoenfeld in Autoimmunity 1991; 9:337-44), which led him to conclude that there may be the possibility of a connection between autoimmune disease and malaria. He did not state that the literature established a direct connection between malaria and rheumatoid arthritis. A copy of the article was provided to the Tribunal by Mr De Marchi after the hearing. The Tribunal notes that the authors discuss mainly the association between autoimmunity and infections with five diseases including malaria. In the section devoted to malaria, they refer specifically to only one - systemic lupus erythematosus - of the many autoimmune diseases. The authors state that `the clinical significance of the antibodies in malaria is not known'. They conclude by saying, inter alia, that the specific association between infection and autoimmunity is still obscure.
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12. With respect to the second hypothesis Dr MacKay has stated a general principle (a chronic persisting infection could prompt an autoimmune reaction) and then sought to apply it to the specific circumstances of the applicant (the applicant has had such a disease, malaria, and subsequently suffered from an autoimmune disease, rheumatoid arthritis). However, Dr Hall's evidence:
(a) distinguishes between the type of auto-antibody profile seen in systemic lupus erythematosus, and the profile of the antibody appearing in rheumatoid arthritis. In the former, the patient may suffer inflammation of the joints but never the type of joint damage suffered from those who have rheumatoid arthritis. According to Dr Hall's evidence, this is a fundamental difference in the way in which the autoimmune diseases, studied by Dr Shoenfeld, operate, compared to the operation of rheumatoid arthritis and, consequently, the two are not comparable in any, or any meaningful, way; and
(b) does not support an hypothesis connecting malaria with the onset of rheumatoid arthritis. In areas of high malarial infection (e.g. New Guinea) rheumatoid arthritis is `extraordinarily uncommon' (trans, p.16). Accordingly, the possibility of a connection raised by Dr MacKay is positively excluded on the evidence Dr Hall.
The evidence of Dr MacKay is based on a survey of the literature from which he has drawn
general conclusions and then sought to apply them to the applicant's case. Moreover, his comment that he did not think his second hypothesis was essential for the development of a supporting case and his statement that `it may be that in the totality of the case his exposure to these triggers can be taken into consideration as facilitating his development of rheumatoid arthritis' suggest to the Tribunal that Dr MacKay was putting forward the hypothesis in a rather tentative way. On the other hand, Dr Hall's evidence expressly excludes the possibilities raised by Dr MacKay. On the basis of the evidence before the Tribunal, it is of the view that Dr MacKay's conclusions are too remote to be regarded as `reasonable'."
Dr. Hall was also a specialist in rheumatology.
In Bushell v. Repatriation Commission (1992) 175 C.L.R. 408 at 415 Mason C.J., Deane and McHugh JJ. observed:
"Conflict with other medical opinions is not sufficient to reject a hypothesis as unreasonable. As we have earlier pointed out, it is not the function of s.120(3) to require the Commission to choose between competing hypotheses or to determine whether one medical or scientific opinion is to be preferred to another. This does not mean, however, that in performing its functions under s.120(3) the Commission cannot have regard to the medical or scientific material which is opposed to the material which supports the veteran's claim. Indeed, the Commission is bound to have regard to the opposing material for the purpose of examining the validity of the reasoning which supports the claim that there is a connexion between the incapacity or death and the service of a veteran. But it is vital that the Commission keep in mind that that hypothesis may still be reasonable although it is unproved and opposed to the weight of informed opinion."
If (as may I think be doubted) Dr. MacKay was propounding what he called "a non-inconceivable possibility" as a "reasonable hypothesis", within the meaning of that expression in s.120(3) of the Act, the "opposing material" to which the Tribunal referred to paragraph 12 of its reasons for decision in my opinion justified its factual conclusion that the hypothesis was too tenuous to be accepted as reasonable. It is perhaps regrettable that Dr. MacKay was not given the opportunity to express in evidence his opinion upon the evidence summarised in sub-paragraph 12(a) of those reasons. But there was no suggestion that the applicant's counsel was denied the opportunity to adduce that evidence by re-calling Dr. MacKay.
In my opinion the appeal should be dismissed with costs.
I certify that this and the 9 preceding pages are a true copy of the Reasons for Judgment of the Honourable Justice Jenkinson.
Associate
Dated: 13 December, 1996
Counsel for the Applicant : Mr. D. De Marchi
Counsel for the Respondent : Mr. N. Green
Solicitors for the Applicant : De Marchi & Associates
Solicitors for the Respondent : Australian Government Solicitor
Date of Hearing : 30 August, 1996
Date of Judgment : 13 December, 1996
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