Stace and Military Rehabilitation and Compensation Commission

Case

[2009] AATA 134

5 March 2009

No judgment structure available for this case.

Administrative Appeals Tribunal

DECISION AND REASONS FOR DECISION [2009] AATA 134

ADMINISTRATIVE APPEALS TRIBUNAL      )

)          No. N2006/0475

VETERANS’ APPEALS DIVISION

)

Re THE LATE ALLAN STACE

Applicant

And

MILITARY REHABILITATION AND COMPENSATION COMMISSION

Respondent

DECISION

Tribunal

Dr J D Campbell, Member

Date5 March 2009

PlaceSydney

Decision The decision under review is affirmed.

...................[sgd]...........................

Dr J D Campbell

Member

CATCHWORDS

VETERANS’ AFFAIRS – Military Compensation – Renal Disorder (Nephritis) – Injury Simpliciter – Causation – Disease – Material Contribution – Decision under review affirmed

Safety, Rehabilitation and Compensation Act 1988 - sections 4, 14

New South Wales t/a New South Wales Department of Agriculture v Allen [2000] NSWCA 141

Zickar v MGH Plastic Industries Pty Limited (1996)187 CLR 310

Treloar v Australia Telecommunications Commission (1990) 26 FCR 316

REASONS FOR DECISION

5 March 2009

Dr J D Campbell, Member

Background

1.     Mr Stace was born in 1982. Mr Stace enlisted in the Regular Army for a four year term on 23 May 2001. He completed basic training at Kapooka prior to corps allocation to Infantry and training at Singleton. Mr Stace transferred to Artillery, trained as a gunner at Puckapunyal and was posted to 4 Field Regiment in Townsville prior to his discharge on the grounds of “Not suited to be a soldier” on 21 June 2002.

2.     In December 2003 Mr Stace consulted his general practitioner because of tiredness, feeling ill and noting blood in his urine. Following many consultations, much investigation and hospitalisation, Mr Stace was diagnosed as suffering from mesangiocapillary glomerulonephritis (“MCGN”), immune complex nephritis and end-stage renal failure by Professor Nanra, a consultant nephrologist, in his report of 13 March 2005 (T46).

3.     On 25 January 2005 Mr Stace lodged a claim for rehabilitation and compensation for renal failure, with Mr Stace alleging that the Japanese B encephalitis vaccination received during his period of military employment contributed to the condition (T37).

4.     On 26 October 2005 the Respondent denied liability in respect of the claim for renal failure on the basis that the evidence did not show, on the balance of probabilities, that Mr Stace’s military employment had contributed in a material degree to the condition (T61).

5.     Following a request for review by Mr Stace on 28 November 2005 the Respondent issued a reviewable decision which affirmed the earlier determination on 6 April 2006 (T70).

6.     Mr Stace died following a motor vehicle accident while returning from renal dialysis on 2 June 2006.

Issues

7.     The relevant issues in this matter are:

(a)Whether Mr Stace suffered an injury simpliciter, with the injury arising out of, or in the course of, his employment, or

(b)Whether Mr Stace suffered an ailment or an aggravation of any such ailment, being an ailment or an aggravation that was contributed to in a material degree by his employment in the Army.

Medical Background History

8.     Dr Mahony, a consultant nephrologist, noted that Dr Wong, Mr Stace’s attending general practitioner, has records indicating that prior to his enlistment Mr Stace “had many attendances in early childhood with tonsillitis, oropharyngitis, otitis media, [upper respiratory tract infection] and one episode of right upper lobe pneumonia” (Exhibit R2).

9.     A pathology test report dated 10 January 2004 notes that on 13 November 2000 Mr Stace had a serum creatinine of 92, the normal reference range being 60-120umol/L (T18, p. 51).

10.   Army entry medical records dated 19 April 2001 note that Mr Stace had no history of previous kidney disease or other related issues, and there were no abnormalities detected of his genito-urinary system on examination. Blood pressure was recorded as 110/70 and urinalysis did not detect any abnormality (T3, pp. 11-17).

11.   On 3 May 2001 pathology reports note that neither Hepatitis B nor Hepatitis C were detected (T71, p. 52), with a further test confirming such results undertaken and reported upon on 4 June 2001 (T71, p. 55).

12.   A Medical Attestation form dated 29 May 2001 notes that Mr Stace had not received any medical treatment since 19 April 2001 (T5).

13.   A Medical Induction Declaration form dated 30 May 2001 notes that Mr Stace was not suffering from any illness and did not object to being inoculated with various vaccines (T6).

14.   An inoculation register (T71, p. 1) notes that the following inoculations/vaccinations were given during Mr Stace’s period of military service:

6 June 2001

ADT

23 July 2001

ADT

15 June 2001

Oral Sabin

28 February 2002

Oral Sabin

30 May 2001

Typhim Vi

6 June 2001

Twinrix

23 July 2001

Twinrix

7 February 2002

Twinrix

15 June 2001

MMR

6 February 2002

JEV (Jap. Encephalitis)

28 February 2002

JEV

15.   An Outpatient Clinical Record notes that Mr Stace presented with symptoms consistent with a diagnosis of upper respiratory tract infection on 12 June 2001 and a diagnosis of sinusitis on 26 June 2001 (T71, p. 3).

16.   On 31 July 2001 Mr Stace presented with pain to his right lower leg having been unable to finish the challenge march. Mr Stace described a previous episode of shin splints some two and a half years earlier. Mr Stace was admitted and remained hospitalised until 6 August 2001. Clinical charts record blood pressure as 110/70 with urinalysis recorded as showing no abnormality, while clinical notes suggest a diagnosis of bilateral tibial periostitis, although the bone scan is reported as not being clinically significant (T71, pp. 4 - 5, 22 - 23, 38).

17.   On 5 September 2001 army medical records note Mr Stace presenting with symptoms of feeling unwell and vomiting. Blood pressure is recorded as 130/70 with urinalysis recorded as not detecting any abnormality (T71, p. 6).

18.   On 21 September 2001 army medical records note that Mr Stace complained of low back pain following his first pack march. The records indicate that Mr Stace was treated with physiotherapy and anti-inflammatory medications at Singleton (T71, p. 7).

19.   On 23 October 2001 army medical records note that Mr Stace reported to the Regimental Aid Post (“RAP”) at Puckapunyal complaining of a recurrence of low back pain over the previous four days. Mr Stace was admitted to hospital for bed rest with a suggested diagnosis of low back strain. The records indicate that Mr Stace’s lumbo-sacral spine was x-rayed, and on 25 October 2001 the x-rays were reported as showing “an old spondylosis defect at both pars intra-articularis” (T71, p. 102). Mr Stace is reported as having been discharged on 24 October 2001 with restrictions, namely, sedentary duties for six days, no heavy lifting, no prolonged standing, no sport and no physical training (T71, p. 25). Mr Stace was readmitted on 29 October 2001 having been in the field for three days with increasing back pain. The back pain experienced by Mr Stace is recorded as having settled with further physiotherapy and back exercises, with Mr Stace being returned to restricted duty (five days) on 31 October 2001 (T71, pp. 103-106). Blood pressure was recorded as 110/60, with no abnormalities recorded on urine testing (T71, p. 41).

20.   On 7 December 2001 the army medical records note that Mr Stace presented complaining of difficulty with sleeping the previous night, “feeling really hot”, “worn out”, “headache” and “queasy in [the] stomach”. Mr Stace was considered to be suffering from a heat illness, having not been long in Townsville (4 Fd Regt) (T10, p. 25). On 13 December 2001 Mr Stace is noted to complain of left shin pain and a burnt tip of right index finger (Zippo lighter), with the pain in the left shin commencing at about the three kilometre mark of a four to four and a half kilometre run (T10, p. 26). Mr Stace is noted to have sought treatment for tinea left foot on 16 January 2002, bilateral shin splints on 23 January 2002 (T10, p. 27), an allergic reaction to an insect bite on his right ankle on 13 February 2002, with symptoms of feeling “dizzy”, “squeamish in stomach”, “some vertigo”, “minor shakes” and “earlier seeing double”, although no difficulty with breathing (T10, pp. 28, 30), an injury to the lateral aspect of his left ankle on 25 February 2002, with an x-ray reported as showing no fracture or dislocation (T71, pp. 108 - 109).

21.   On 10 June 2002 the army medical records note that Mr Stace was admitted to hospital for petrol burn and injuries to his right hand, and right lower arm, which were described as superficial. The records note Mr Stace stayed in hospital until 18 June 2002, during which time his burns were dressed daily. There is no record of any complications arising from the burns in the army medical records (T10, pp. 31-35; T71, pp. 112-114). During his hospitalisation between 10 June 2002 and 18 June 2002, Mr Stace’s blood pressure was recorded at 142/82 and 125/65 and urine analysis on two occasions did not reveal any abnormalities (T71, p. 39).

22.   Army medical records note that Mr Stace underwent a comprehensive preventive health examination on 11 June 2002 (final medical board) (T12, pp. 37-45). This examination, in noting the burn to his right hand, concluded that Mr Stace remained “unfit for duty” and referred him for further assessment of his burns by Dr Tassen, a plastic surgeon, who concluded that the burns were superficial to his right hand and forearm (T13, p. 46).

23.   Dr Wong, Mr Stace’s treating general practitioner, in his report of 7 June 2005 (T51), details Mr Stace’s attendances to include:

23 May 2001

Upper respiratory tract infection – treated with Rulide and Seretide.

27 June 2002

Review of petrol burns to right hand and forearm – took until mid July 2002 before burnt areas were healed.

21 July 2003

Upper respiratory tract infection and review of injury to left ankle sustained during army service. On 4 August 2003 discussed result of x-ray performed on ankle.

15 December 2003

Mr Stace presented with a history of painless haematuria of recent onset.

24.   Dr Wong reports that Mr Stace’s haematuria was investigated. In the course of these investigations the following results were recorded:

11 December 2003 (T18)

Serum creatinine 128 (Normal range 60-120)

15 December 2003 (T18)

Urine analysis:

Blood ++++

Protein ++

12 December 2003 (T16)

X-ray abdomen:

“No radio-opaque calculi seen in the line of urinary tract.”

12 December 2003 (T17)

Renal ultrasound – “no obvious ultrasound evidence of cause for haematuria … Both kidneys appear within normal limits.”

10 January 2004 (T20)

Renal and abdominal CT – “normal study.”

5 March 2004 (T21)

Dr Patterson, consultant urologist, to whom Dr Wong had referred Mr Stace on 22 December 2003, suggests that some renal pathology may have been present.

June 2004 (Dr Mahony’s report) (Exhibit R2)

Serum creatinine 176 (N 60-120)

16 July 2004 (T24)

Dr Patterson, in noting a further episode of macroscopic haematuria and an absence of any findings in a repeat ultrasound and intravenous pyelogram to explain the cause of the haematuria, suggested that Mr Stace was suffering from a “medical type problem” and recommended a “fairly urgent referral to a nephrologist.”

August 2004 (T31)

Admission to hospital under care of Professor Nanra. Investigations (renal biopsy) confirmed the diagnosis as MCGN, despite some atypical features.

Mr Stace’s renal function continued to deteriorate with dialysis commencing in September 2004.

25.   Mr Stace’s renal condition was treated with dialysis, with the course complicated by issues surrounding non-compliance and non-attendance (T47), and episodes of permacath infection requiring hospitalisation in 2005/2006 (Exhibit R2). Dr Wong noted that Mr Stace was “well when he left dialysis on 2nd June 2006, but had a fatal car accident later that day”.

26.   In a letter dated 25 February 2005 (T43) Mr Stace records that he was a champion boxer prior to his army service, that he “used to be very tired all the time in the army” and this continued after his army service ceased. Mr Stace repeated such history of symptoms in his letter of 9 January 2006 (T66).

Medical Evidence

Professor Nanra

27.   In a report dated 13 March 2005 (T46) Professor Nanra defined Mr Stace’s diagnosis as:

·Mesangiocapillary Glomerulonephritis (cause not defined by tests)

·Immune Complex Nephritis

·End-stage Renal Failure

28.   Further, Professor Nanra concluded that “the diagnosed condition, on the balance of probability, may have a causal relationship to the military employment (the Japanese Encephalitis vaccination that he received while in the Army), with, however, it being “possible that an alternate trigger such as infection may be responsible.” Professor Nanra, while noting that the diagnosed condition could be caused by other trigger factors, stated the opinion that it was “reasonable to incriminate the Japanese Encephalitis Vaccination”, as “vaccinations can induce Immune Complex Disease and can lead to Mesangio-capillary Glomerulonephritis.” At the time of writing this opinion, Professor Nanra did not have access to Mr Stace’s army medical records. His opinion that the probability was more than 50 per cent that Mr Stace’s army employment contributed to his condition was based on the Japanese Encephalitis Vaccination and any infection, if he had an infection during service, supported by Mr Stace’s complaints of being frequently tired both during and after service, shin splints and leg swelling as described by Mr Stace and raised blood pressure during service as described by Mr Stace. On the assumption that such facts were correct, Professor Nanra was of the opinion that the condition developed before Mr Stace’s discharge from the army (T46).

29.   In a further report dated 15 August 2005 (T53) Professor Nanra confirmed his opinion that “the diagnosed condition [MCGN], on the balance of probability, could have a causal relationship with the various vaccinations and inoculations that [Mr Stace] received during military employment,” with the possibility that “an alternate trigger such as an infection may also be the antigenic stimulus” (citing Army records referring to Mr Stace suffering a pustular infection right foot in February 2002, and burns to the right hand in June 2002). Professor Nanra concluded that it was “not possible to estimate when [the] kidney condition commenced”, although it developed after Mr Stace’s military discharge.

30.   In a further report dated 16 September 2006 (Exhibit A2) Professor Nanra continued to express the opinion that, on the balance of probabilities, there could be a causal relationship between Mr Stace’s military service (vaccinations, inoculations, infections and burns) and his nephritis, with the nominated events providing the antigenic stimuli giving rise to the Immune-Complex Nephritis. Professor Nanra stated that the scientific data in favour of a possible relationship is quite good, although the predisposing antigen stimulus leading to Immune-Complex Disease is usually not identifiable. Professor Nanra also observed that the time of identification of definite kidney disease some 18 months after having left military service “is totally in keeping with the onset of disease triggered by something during military service.” Professor Nanra reaffirmed that on the balance of probabilities there could be a causal relationship between the medical events during military service and the Immune-Complex Nephritis.

31.   In a further report dated 15 July 2007 (Exhibit A3) Professor Nanra detailed the various stages of immune complex disease, and noted that clinical evidence of kidney disease is usually not evident in Stages One to Three (exposure, immune response, deposition of immune complexes in the kidney). Professor Nanra also notes that the rate at which Stages One to Three develop is variable (gradual or rapid) and that the onset of nephritic syndrome is also variable (gradual or rapid). Professor Nanra considered that while the time for progress through the first three phases cannot be defined scientifically, the onset of Stage Four is recognised by the detection of mild blood and protein detected by a proper urine test. Professor Nanra observed that detection of disease is not the same as onset of disease, with the onset of disease in Mr Stace’s case being any time between 21 June 2002 and December 2003, with detection in December 2003.

32.   In developing the possible association between army service and exposure to antigenic stimuli and causation of immune complex nephritis, Professor Nanra stated that “it is not possible to give a clear cut opinion” and considered the relationship in terms of a reasonable hypothesis with antigenic exposure between February 2002 and 10 June 2002, development of antibodies and immune complexes over a period of weeks and months, with development of immune complex mediated glomerulonephritis between 21 June 2002 and December 2003 (Exhibit A3).

33.   In his report of 20 August 2008 (Exhibit A6) Professor Nanra reiterated that it was his opinion that Mr Stace’s employment was more probable than not the trigger for the disease Mr Stace suffered from. Professor Nanra, in his report dated 2 July 2008 (Exhibit A5), noted that “chickenpox has been associated with different forms of kidney diseases including glomerulonephritis”, but that the association is with “acute disease as opposed to delayed or chronic disease.”

34.   In oral evidence, Professor Nanra detailed the following observations:

·Renal nephritis is a disease of kidney filters, with the triggering factor which initiated the nephritis unable to be detected in more than 95 per cent of cases – the trigger having occurred in the past and no longer identifiable, or where medical science has not been able to identify the triggering factors. In summary, Professor Nanra stated that it is very unusual to detect the triggering factor.

·He was certain that an antigen triggered the disease process, and that it was possible that certain happenings in the army may have been the initial trigger in Mr Stace’s case. In further comment, Professor Nanra spoke in terms of not knowing what the antigen was that triggered the process, but there were a number of events associated with Mr Stace’s employment (vaccinations, infections, etc) which could possibly trigger the disease process, with it not being unreasonable for him (Professor Nanra) to think that it was a possibility one or all of these events could have acted as a trigger, but he could not be certain. In summary terms, Professor Nanra agreed to his evidence meaning that it was possible that one of the triggering mechanisms occurred during Mr Stace’s army service and if that possibility did occur (that is, the presence of a triggering mechanism), then it was probable a causal relationship with employment exists, but Professor Nanra was specific in nominating that it was only a possibility that events associated with Mr Stace’s army service may have been a triggering mechanism, as there may have been something totally different, which cannot be identified, which constituted the triggering mechanism.

·That the antigen trigger may be endogenous (something within the body) or exogenous (something outside the body), while the term idiopathic is used to describe cases where it is unknown whether the trigger is endogenous or exogenous.

·That because of the multifactorial nature of renal disease, once the triggering mechanism has set off the immune response with the disease process initiated, the progress of the disease is one of self perpetuation with progression depending on further antigenic stimuli.

·That between November 2000 and December 2003 Mr Stace’s kidney function came down from 108 per cent to 76 per cent, with the exposure to an antigen having to occur prior to the onset of the immune complex disease process, with failure of the normal defence mechanisms leading to immune complexes being deposited in the kidney and the commencement of the nephritic disease process, all of which can occur over periods ranging from weeks to sometimes years.

·For there to be no evidence of kidney disease there must be evidence of normal kidney function tests, the urine test must not show any abnormality and the blood pressure must be normal.

·That there may have been other exogenous triggering factors in Mr Stace’s pre-service environment, for example, tonsillitis. If indeed the immune complex disease process had been initiated by an earlier triggering mechanism, the inflammation arising from the burns in June 2002 could have reactivated or precipitated an ongoing immune problem, with the potential for the burns process to be a significant contributor.

·That, in his opinion, it was “more likely that a vaccination could have triggered [the] whole cascade”, with the burns activating a process that may have been started by an initial trigger.

·That he was unable to suggest which of the various vaccinations/inoculations was more likely to be the culprit (that is, triggering mechanism).

·That in Mr Stace’s case there had been a fairly rapid deterioration in his kidney function between December 2003 and June 2004 (76 per cent to 55 per cent), with the indication of rapidly progressing kidney disease. Further, no assumptions as to the underlying nature of the progression of a kidney disease at the time of onset can be drawn from the rate of progression in its later stage because of the very nature of the disease process.

·That in Mr Stace’s case the triggering mechanism was more likely to have occurred months or up to two or three years prior to the clinical onset of the nephritic disease, sometime between 21 June 2002 and December 2003, with the exact time not able to be determined.

·That during Mr Stace’s period of army service, while acknowledging that one could not be certain in the absence of renal function tests, it was more likely than not that the kidneys were functioning normally (assuming no abnormality in urine tests and normal blood pressure).

·That in the absence of knowledge concerning Mr Stace’s antigenic challenges pre-service and post-service, on the assumption that the vaccinations and burns were possible antigenic stimuli, the most that can be said is that the kidney disease may have been contributed to by the vaccinations or the burns.

·That vaccination involving an antigen does not necessarily result in a spontaneous response with the immune complex disease process comprising various stages, occurring over weeks, months or years.

·That, in his view, after examination of the army medical records, Mr Stace was unwell throughout his army service.

·That it is entirely speculative as to whether any of the particular events in Mr Stace’s case caused or exacerbated his kidney disease.

Dr Gorman – Consultant Physician

35.   In a report dated 21 September 2005 (T58) Dr Gorman, a consultant physician and pain management specialist, detailed a clinical history and examination of Mr Stace. Dr Gorman concluded that:

·The diagnosis was mesangiocapillary glomerulonephritis.

·There was no causal relationship between Mr Stace’s condition and his military service as “there is no documented relationship between vaccination and the onset of glomerulonephritis.” Dr Gorman acknowledged that there is a documented relationship between hepatitis and MCGN, but opined that “pustular infection of the right foot and burns to the right hand would have introduced foreign proteins, but to then state that they were the likely source of immune complex disease is … too conjectural to be valid.”

·Mr Stace would have suffered from his nephritic condition “regardless of his military employment” as the cause of the condition is not known and that “it is far too conjectural to hypothesise that the minor skin infections, the burns or the inoculations were the source of the antigenic stimulus.”

·In his view Mr Stace “was developing his renal disease during his Army service” as evidenced by his levels of physical activity (poor performance) both during his army service and post service as a labourer. Dr Gorman did not believe that his army service caused the condition to worsen.

Dr Mahony – Consultant Renal Physician

36.   In a report dated 4 June 2007 (Exhibit R2) Dr Mahony detailed a summary analysis of Mr Stace’s army medical records, including inoculations and vaccinations received and details of any urinalysis undertaken during his army service. Dr Mahony also summarises briefly the clinical history of Mr Stace post-army service.

37.   Dr Mahony concludes that the diagnosis of Mr Stace’s kidney condition was MCGN. Dr Mahony notes that the first symptom referable to the disease was the macroscopic haematuria in December 2003. Further, Dr Mahony concluded that “normal urinalyses on 10 and 15 June 2002 are incompatible with [the presence of] renal disease and especially glomerulonephritis, at that time.”

38.   Dr Mahony noted that “the aetiology of MCGN is not clear” and “it is most often idiopathic”, with “circulating immune complexes … detectable in about 1/3 of cases.” Dr Mahony noted that “the histological appearances had been described in a number of other systemic conditions,” hepatitis being the most common association. Dr Mahony noted that Mr Stace had no evidence for any of these nominated conditions being present, and in such circumstances the aetiology is idiopathic.

39.   Dr Mahony did not consider that Mr Stace suffered an injury or an aggravation of an injury that arose out of, or in the course of, his employment. Further, Dr Mahony concluded that “Mr Stace did not suffer from a renal disorder arising out of his employment [as] his urinalysis and blood pressure were entirely normal in the week that he left the Army, and some four months after his vaccination and insect bite,” with the burns suffered one week prior to discharge, being “apparently not infected and clearing spontaneously.”

40.   Dr Mahony in noting that “Mr Stace had no immediate reaction to his Japanese encephalitis vaccinations” observed that “the normal urinalyses some three to four months later precludes any glomerular complication of these vaccinations.” Dr Mahony in further noting that there is some literature regarding vaccinations and glomerulonephritis observes that “it does not include any strong evidence for an association for Japanese encephalitis vaccinations.”

41.   Dr Mahony was of the opinion that “burns themselves do not cause glomerular disease,” and that “the normal urinalyses precludes any evidence of glomerulonephritis related to infections” prior to 15 June 2002 (the time of last in-service urinalysis).

42.   Dr Mahony was of the opinion that “Mr Stace did not have an underlying or pre-existing condition to which his military employment contributed.”

43.   In a further report dated 26 March 2008 (Exhibit R4) Dr Mahony comments on two journal articles. The first article is Wraith DC, Goldman M and Lambert P, “Vaccination and Autoimmune disease: What is the evidence?” (2003) 362 The Lancet, 1659-1666 (Exhibit R6). Dr Mahony notes that the article “describes mechanisms but lists only 3 autoimmune diseases proven to be due to vaccines [namely] rabies, influenza and measles,” with no renal diseases noted as arising.

44.   Dr Mahony also observes that this article lists criteria for assessing adverse events due to vaccines. These criteria include:

·Consistency and strength of association;

·The specificity (association to be distinctive and the adverse event linked uniquely or specifically to the vaccine concerned); and

·Temporal relation (clear temporal relation between the vaccine and the adverse event).

Dr Mahony notes that “these criteria deny any current vaccinations as causing an autoimmune disease.”

45.   In commenting upon a second article, Lambert E, Liebling A, Glusac E and Antaya R, “Henoch-Schonlein Purpura following a Meningococcal Vaccine” (2003) 112 Pediatrics, e491-e494 (Exhibit R6) which describes one of the two cases arising from the six million doses of the vaccine given, Dr Mahony notes that “urinalysis was negative one week after the vaccination”, while “two weeks later repeat urinalysis revealed a large amount of blood and three months after immunisation the patient developed 3+ proteinuria and 3+ haematuria.”

46.   Further in this report, Dr Mahony concurs with Professor Nanra that Mr Stace’s kidney disease became evident in December 2003, with it being “more likely that the onset of [Mr Stace’s] renal disease was later in the period June 2002 - December 2003,” as normal urinalysis and blood pressure were noted in June 2002 some four months after the vaccinations. Dr Mahony agrees that Mr Stace’s glomerulonephritis may have commenced many months, but not years, prior to December 2003.

47.   Dr Mahony in his report of 26 March 2008 debates Professor Nanra’s assertion that “urine was tested by dipsticks that are not as accurate and reliable as a proper urine examination by microscopy and protein quantification” in the circumstances of the absence of any symptoms. Dr Mahony, in noting an article attached to his report, observed that “dipstick testing for microhaematuria is quite sensitive and false negatives are … rare”, while dipstick testing for protein has “occasional false positives … and does not detect the Bence-Jones protein of myeloma; otherwise false negatives are rare.”

48.   Finally, in his report Dr Mahony concludes that there is little evidence to support Professor Nanra’s hypothesis linking Mr Stace’s glomerulonephritis with his army service namely:

a)There is little if any evidence for vaccinations causing glomerulonephritis

b)There was no specific infection in Mr Stace’s attendances on 13 occasions between June 2001 and June 2002

c)Burns per se are not related to glomerulonephritis

d)The longest gap between vaccination time and renal expression is of the order of 3 months

e)There is no proven renal disorder, experimental or clinical, with a latent period of greater than 12 months from exposure to expression

49.   In oral evidence Dr Mahony confirmed the following:

·The methodology he used in arriving at the opinions expressed in his first report.

·His opinion as regards the clinical usefulness of dipstick urinalysis.

·That in the light of the earlier pre-service normal renal function test and with normal blood pressure readings and no abnormal urinalyses during his army service Mr Stace’s “renal function was normal throughout his army service.”

·That his renal disease became evident in December 2003 with, in his view, clinical onset some six to 12 months earlier in the light of the progressive, aggressive course from December 2003 to August 2004.

·That it is unlikely that the vaccination materially contributed to his MCGN, as they were given at least four months prior to discharge, with most renal responses to whatever stimuli occurring well within that time frame.

·That burns per se do not give rise to this form of nephritis.

·That Mr Stace did experience an insect bite on 13 February 2002 on his right foot which was red, inflamed with some pus, which may be an indication of infection. It was noted that it was the medical assistant Sgt Hall who wrote the comment about the presence of pus, while the medical officer, Capt Johnston, considered the bite was “not infected at this time.” Dr Mahony concluded that in such circumstances there was no evidence of infection.

·That there was no clear evidence of an infection sustained during service at any time which might be related to any subsequent renal disorder.

·That the cause of MCGN is more often not known than known.

·That the possibility of the inoculations producing antigens or contributing to the disease is “remote”, as evidenced by the literature review undertaken, including the articles nominated in Exhibits R6 and R7.

·That the burn injury to the right hand was painful as evidenced by the record at T10, p. 31 where pain is recorded as “now in pain +++” and with morphine being prescribed for pain relief. Similarly, on 11 June 2002 the entry records “Blisters ++ forearm hypothenar and thenar – macerated palm.” Dr Mahony observes that no antibiotics were prescribed for the burns.

·That in some cases the disease can be said to be multi-factorial, the proposition being that genetic susceptibility makes some people likely to get the disorder while other people are unaffected. Dr Mahony stated that while “there are some genetic predispositions which are known for some renal disorders,” MCGN is not one of them to the best of his knowledge.

·That despite clinical records suggesting that Mr Stace presented to the doctor as a child on numerous occasions there is no evidence of a compromised renal system up until and to some time after June 2002.

Consideration and Findings

50.   The medicine in this matter is complex. Both consultant nephrologists agree that the diagnosis is MCGN, albeit with some atypical features. I note that both nephrologists consider that the resulting kidney disease (nephritis) arises as a consequence of an exposure to an antigen (the trigger), the immune response, deposition of immune complexes in the kidney and the onset of the nephritic syndrome. Professor Nanra notes that the rate of development of the first three phases of the disease process is variable (gradual or rapid) with the onset of the fourth phase (nephritic syndrome) also variable (gradual or rapid) with further progression to renal failure also being variable. I accept the diagnosis as nominated by both nephrologists and, indeed, that given by Dr Gorman on the balance of probabilities.

51.   Before I proceed further with my detailed findings I must address the medical report by Dr Gorman. I note that he is a general physician specialising in pain management. I note that in his report there is reference to seeking information from unnamed renal physicians. In the circumstances of this matter, namely, the complexity and specificity of the disease in question, I consider that Dr Gorman’s report is born of lesser clinical knowledge in the narrow context of super speciality medicine. In such circumstances, I place considerably less weight on his opinion to that given by the two nephrologists. I also note that neither party pursued aspects of his opinion in support of their respective positions.

52.   From the detailed analyses of the two nephrologists’ opinions it is evident, and I also find, that there was no clinical evidence of Mr Stace suffering from renal disease prior to his military service and during his army service. It is agreed by both specialists that the first clinical evidence of renal disease was in December 2003, when Mr Stace presented with a short history of haematuria. I note that the two nephrologists disagreed as to when the renal disease had its clinical onset, with Dr Mahony considering the onset to have been in the months prior to presentation, while Professor Nanra believed it could have been earlier. Both nephrologists agreed that, on the balance of probabilities, Mr Stace’s renal disease (that is, the nephritis) did not commence until after the completion of his army service, namely 21 June 2002. I concur with such a finding and for the reasons expressed by the two nephrologists, that there was no clinical evidence of renal disease either before or during Mr Stace’s service or at the time of his discharge on 21 June 2002. I note, but do not accept, Dr Gorman’s opinion, that the renal disease (nephritis) came on during his army service as evidenced by Mr Stace’s tiredness during service and when undertaking general labouring jobs after his service, for the very reason that there is no clinical evidence of compromised renal function either pre-service or during service – this being the agreed evidence of the two nephrologists.

53.   I observe that both nephrologists were of the opinion that the cause of MCGN was idiopathic (that is, unknown) in a high percentage of cases. Further, I note that both nephrologists were of the opinion that there was no clinical evidence of particular systemic conditions, such as hepatitis, which are associated with similar renal histological appearance.

54.   The difference in clinical opinion between the two clinical specialist nephrologists is, essentially, that Dr Mahony is unable, in this matter, to move beyond the cause being unknown. In his analysis of the clinical material in evidence he concluded, on the balance of probabilities, that there was no evidence of infection during Mr Stace’s military service; that while there was evidence of many childhood infectious episodes there was no evidence to suggest impaired renal function either prior to or during service; that burns suffered by Mr Stace at the end of his army service were not infected (no evidence of antibiotic medication) and that burns per se were not associated with the nominated condition. In relation to vaccinations and inoculations during Mr Stace’s service, Dr Mahony noted from the clinical articles in evidence (Exhibits R6 and R7) that there was a very small, almost negligible, association between inoculations and vaccinations and the nominated condition; that such evidence does not include any strong evidence of an association with Japanese encephalitis vaccine, and that further the clinical articles suggest any glomerular complications arising from vaccination/inoculation occur within a four month period.

55.   I note that in summary refutation of Professor Nanra’s opinion linking Mr Stace’s MCGN with his army service, Dr Mahony nominates the following:

·There is little evidence of vaccinations/inoculations causing glomerulonephritis.

·There was an absence of any specific infection in Mr Stace’s attendances on 13 occasions between June 2001 and June 2002, with the army medical records in relation to a bite to the ankle in February 2002 demonstrating no clear evidence of an infection with the material recorded by the doctor, as opposed to the sergeant, suggesting the bite was not considered to be infected.

·That burns per se are not related to glomerulonephritis.

·That the longest gap between vaccination and renal expression is in the order of three months.

·That there is no proven renal disorder, experimental or clinical, with a latent period of greater than 12 months from exposure to clinical expression.

56.   In addressing Professor Nanra’s opinion I observe that his first report and opinion was made after consultation with Mr Stace and without relevant access to Mr Stace’s army medical records. In his report of 13 March 2005 Professor Nanra concluded that the diagnosed condition could have a causal relationship with his army service by way of the trigger being Japanese encephalitis vaccination or perhaps by way of an alternate trigger such as an infection during service. Professor Nanra in this report considered that the probability that Mr Stace’s army service contributed to the causation of the condition was more than 50 per cent. His opinion was based upon Mr Stace receiving Japanese encephalitis vaccination, Mr Stace feeling frequently tired during service and after service, and symptoms of shin splints, leg swelling and raised blood pressure described to him by Mr Stace.

57.   In a further two reports dated 15 August 2005 and 16 September 2005 Professor Nanra confirmed his earlier opinion that the diagnosed condition, on the balance of probabilities, could have a causal relationship with Mr Stace’s army service, with the antigenic triggering mechanism being either the inoculations/vaccinations or an infection. In support of his opinion Professor Nanra stated that the identification of the disease in December 2005 “was in keeping with the onset of the disease [being] triggered by something during military service.”

58.   In a report dated 15 July 2007 Professor Nanra stated that it was “not possible to give a clear cut opinion” of the possible association between army service and exposure to antigenic stimuli and causation of nephritis, and preferred to consider the relationship in terms of a “reasonable hypothesis”.

59.   In oral evidence Professor Nanra confirmed that:

·It was very unusual to detect the triggering factor.

·He was certain that an antigen triggered the disease process in this matter, with there being a number of events in Mr Stace’s army employment that may have been the trigger, with it not being unreasonable for him to think that it was a possibility.

·It was possible for one of the triggering events to occur during his army service and if it did occur (that is, the presence of a triggering mechanism) then the probability of causal relationship exists.

·It was only a possibility that events during his army service may have been a triggering mechanism, for it may have been something totally different which cannot be identified which constituted the triggering mechanism.

·Vaccination could have triggered the whole cascade, with the burns activating a process started by an initial trigger.

·He was unable to suggest which of the various inoculations/vaccinations was more likely to be the culprit.

·The exact time of when the triggering mechanism occurred cannot be determined.

·On the assumption that the vaccinations and burns were possible antigenic stimuli the most that can be said is that the kidney disease may have been contributed to by the vaccinations or the burns.

·Vaccinations involving an antigen do not result in a fairly spontaneous response.

·In this case it is entirely speculative as to whether any of the particular events in this case caused or exacerbated his kidney disease.

60.   In his report dated 20 August 2008 Professor Nanra asserted that it was his opinion that Mr Stace’s “employment was more probable than not, the trigger for the disease” from which Mr Stace suffered. I note that this opinion was rendered after Professor Nanra’s opinion was sought by way of a direct question by Mr Stace’s solicitors, and that Professor Nanra’s opinion was provided after all notes and evidence available to him had been reviewed.

61.   It is my opinion that a careful analysis of Professor’s Nanra’s written and oral evidence does not lay a foundation for the opinion expressed in his final report of August 2008. It is my finding that such an analysis clearly defines that throughout his written and oral evidence, with the exception of the report of 13 March 2005 (based on incomplete and not necessarily accurate material) and the August 2008 report, Professor Nanra has described a relationship between a triggering event (antigen) during Mr Stace’s service and his nephritis in terms of possibility (may, could) and/or a hypothesis. There is nothing in Professor Nanra’s evidence, apart from the assertion in his last report, that take the matter any further, nor are there any clinical articles from any peer reviewed journal nominated to support and substantiate the opinion he has expressed. Further, I note that during his oral evidence Professor Nanra confirmed that any contention of probability only arose if acceptance of the possibility that a triggering mechanism (inoculation, infection) was present and had indeed initiated the disease process. Finally, I find the final report of Professor Nanra not helpful for it contains an opinion given both without reasoning or recognition of assumptions previously defined and detail an opinion which is inconsistent with a detailed and particular analysis of his earlier written and oral evidence. Further I note an absence of learned articles underpinning either the nature of the hypothesis he has proposed or detailing factual, as opposed to theoretical circumstances, which associate events during Mr Stace’s service (inoculation, vaccination, infection) with the nephritic disease of which clinical evidence first occurred in December 2003.

62.   In summary conclusion I find that:

a)Mr Stace suffered from MCGN with the first clinical evidence of that disease being in December 2003.

b)That there is no material before me which could permit me, on the balance of probabilities, to find that Mr Stace’s renal function was compromised prior to or during his service.

c)That the cause of MCGN in greater than 95 per cent of cases is unknown, and that in this case the cause is unknown.

d)That the hypothesis that triggering mechanisms (inoculations, vaccinations, infections) experienced by Mr Stace during service is at best a possibility and at a minimum speculative in the causation of Mr Stace’s nephritic disease.

63.     In reaching my conclusions I have preferred the opinion of Dr Mahony. In so doing I note his opinion is drawn after a consideration of the factual evidence available, an analysis of such material and reasoning to support his opinions as well as detailing material from refereed journal articles tendered in the context of issues raised by Professor Nanra. Earlier in this decision, at paragraph 62, I discussed and detailed the difficulties and shortcomings inherent in Professor Nanra’s evidence. I shall not repeat these.

64.   Mr Perry, counsel for Mr Stace, contended that Mr Stace suffered either an injury, being an injury simpliciter arising out of, or in the course of, his employment or, in the alternate, suffered a disease, being an ailment or the aggravation that was contributed to in a material degree by his employment. Also I would note that Mr Perry was particular in submissions to draw attention to the issues of scientific proof and varying legal standards of proof and, in so doing, drew attention to the NSW Court of Appeal judgement, New South Wales t/aNew South Wales Department of Agriculture v Allen [2000] NSWCA 141.

65.   In addressing the evidence I have before me in this matter I observe the contention that Mr Stace received some inoculations/vaccinations during service. I observe that there is no evidence before me that amounts to Mr Stace experiencing a sudden and ascertainable or dramatic physiological change or disturbance of the normal physiological state, as a consequence of receiving such inoculations/vaccinations. Indeed, on the material before me there is no evidence of such during Mr Stace’s service. In such circumstances I find that the factual situation does not permit that an injury simpliciter has occurred in this matter (Zickar v MGH Plastic Industries Pty Limited (1996) 187 CLR 310 considered and applied).

66.   In addressing the issue of disease I note that such includes an ailment or an aggravation of an ailment that was contributed to in a material degree by Mr Stace’s employment. In the light of my earlier findings, namely that Mr Stace’s nephritic condition was not in evidence either prior to or during his army service, any issues surrounding aggravation do not arise in this matter.

67.   Earlier in this decision I concluded that the triggering antigen mechanisms postulated as being expressed by Mr Stace during his army service were, on the balance of probability, at best a possibility and at a minimum speculative, in the causation of Mr Stace’s nephritic disease. I would note that the triggering mechanisms referred to include the inoculations, vaccinations and infections experienced by Mr Stace during service. While I observe that the word infection was used I am satisfied, on the balance of probabilities, that while there was evidence of inflammation in the army medical records there was no evidence of infection requiring antibiotic therapy in the same records. In so stating I rely on examination of the army medical records and the opinion of Dr Mahony.

68.   In the light of such findings I find that, on the balance of probabilities, that Mr Stace’s army service made no material contribution to the ailment from which Mr Stace was later found to suffer. In so finding I note what the Full Federal Court stated in Treloar v Australian Telecommunications Commission (1990) 26 FCR 316 at 323 “that the section is not brought into play unless it is established by evidence that features of the employment did in fact and in truth contribute to the condition complained of. The causal connection must be established on the probabilities and not left in the area of possibility or conjecture. Once the link is established, however, it matters not that the contribution be large or small.”

69.   As a consequence of my findings in this matter I conclude by determining that the decision under review be affirmed.

I certify that the 69 preceding paragraphs are a true copy of the reasons for the decision herein of Dr J D Campbell, Member.

Signed:         .............[sgd]...................................................................
  Associate

Dates of Hearing  27 and 28 March 2008, 4 November 2008
Date of Decision  5 March 2009
Counsel for the Applicant         Mr M Perry
Solicitor for the Applicant          Mr Martin Kelly, MRM Lawyers
Counsel for the Respondent     Mr G T Johnson
Solicitor for the Respondent     Mr B O'Brien, DLA Phillips Fox

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