Sasha Hardcastle and Comcare
[2015] AATA 46
•29 January 2015
[2015] AATA 46
Division GENERAL ADMINISTRATIVE DIVISION File Number
2013/4618
Re
Sasha Hardcastle
APPLICANT
And
Comcare
RESPONDENT
DECISION
Tribunal Dr M Denovan, Member
Date 29 January 2015 Place Canberra The Tribunal affirms the decision under review.
...........................[SGD].............................................Dr M Denovan, Member
CATCHWORDS
WORKERS’ COMPENSATION – chronic fatigue syndrome – Coxsackie B virus – water drunk – decision under review affirmed.
LEGISLATION
Safety Rehabilitation and Compensation Act 1988 (Cth) ss 5B, 14
CASES
Baranski v Comcare [2013] FCAFC 31
Sydney South West Area Health Service v Stamoulis [2009] NSWCA 153
EMI (Australia) Ltd v Bes [1970] 2 NSWR 238Makita (Australia) Pty Ltd v Sprowles [2001] NSWCA 305
REASONS FOR DECISION
Dr M Denovan, Member
29 January 2015
INTRODUCTION
Mrs Hardcastle, the applicant, was employed as a communications manager with the Commonwealth Scientific and Industrial Research Organisation (“CSIRO”). It is accepted by both parties that Mrs Hardcastle was diagnosed with chronic fatigue syndrome (“CFS”) in 2012. Mrs Hardcastle contends her employment at CSIRO significantly contributed to her contracting this condition. The basis of Mrs Hardcastle’s claim is that this condition was either caused or contributed to significantly by Coxsackie B virus infection, which she contracted when she attended a work approved course of study at the Rydges Capital Hill Hotel (“the Rydges Hotel”) on 20 to 22 March 2012. She claims faeces contaminated with Coxsackie B virus entered a water jug when it was filled from the tap located in the women’s toilets, and Mrs Hardcastle subsequently consumed water from that vessel.
The diagnosis of CFS is not in dispute, though Mr Woulfe for the respondent does not accept that Mrs Hardcastle contracted Coxsackie B virus during the conference, or that her CFS was caused or significantly contributed to by Coxsackie B virus or any other factor related to her employment with CSIRO.
I must decide whether Comcare is liable under s 14 of the Safety Rehabilitation and Compensation Act 1988 (Cth) (“SRCA”) for Mrs Hardcastle’s CFS. In order to make that decision, the issues I must consider are:
(a)Did Mrs Hardcastle contract Coxsackie B virus, or any other infection whilst in attendance at the course of study at the Rydges Hotel from 20 to 22 March 2012
(b)If so, did that infection significantly contribute to the cause of her CFS?
BACKGROUND
Mrs Hardcastle attended a course at the Rydges Hotel from Tuesday 20 to
Thursday 22 March 2012, inclusive. This course of study was approved by her work.
Mrs Hardcastle reported onset of flu-like symptoms on third day of the conference, that is 22 March 2012.
Mrs Hardcastle did not attend work on Friday 23 March 2012. Mrs Hardcastle emailed her supervisor that day and advised that she was unwell.
Mrs Hardcastle attended work on Monday 26 March 2012 and possibly
Tuesday 27 March 2012.[1]
[1] In her statement (Exhibit 1) Mrs Hardcastle claims she did not attend work this day, however in the statement made by her husband (T11), it is said that she did attend.
Mrs Hardcastle did not attend work on Wednesday 28 March 2012. On that day, she consulted her regular general practitioner Dr Ayres. Dr Ayres certified her unfit for duties until 30 March 2012.
Mrs Hardcastle did not attend work on Friday 30 March 2012. On that night she was taken by ambulance to Canberra Hospital. She complained of chest pain and was noted to have bradycardia (slow heart rate). She was sent home the same night; the cause of her chest pain was not determined.
Mrs Hardcastle returned to the medical clinic on several occasions in April and in early May. On each occasion her general practitioner provided her with medical certificates for short periods, ranging from two to seven days.
Mrs Hardcastle was reviewed by general physician Dr Terry Gavaghan on 14 June 2012. In a report dated 18 June 2012, Dr Gavaghan opined Mrs Hardcastle was suffering from ‘post infective fibromyalgia’, and ‘post infective chronic fatigue’. Dr Gavaghan ordered a number of blood tests.
Serology for Cytomegalovirus (“CMV”), Epstein Barr virus (“EBV”) VCA (serological test for anti EBV antibodies), enterovirus (CFT titre) and Lyme disease was performed on 18 June 2012.
The results were negative for Lyme disease. Mrs Hardcastle’s serology indicated past exposure to CMV, EBV and enterovirus.
Mrs Hardcastle was seen by rheumatologist Dr Suren Jayaweera, on 18 July 2012.
Dr Jayaweera diagnosed her with post viral fatigue and opined Coxsackie B virus was the likely virus that Mrs Hardcastle contracted, due to the history of bradycardia.
Dr Jawaweera indicated that there were other possible explanations for the bradycardia, for example, it could have been due to a fainting episode. Dr Jayaweera opined
Mrs Hardcastle’s chest pain was not typical of pericarditis. She noted that Coxsackie B virus can cause myocarditis and as a precaution, she recommended an ECG and echocardiogram.
Mrs Hardcastle was subsequently reviewed by cardiologist Dr Walter Abhayaratna. There is reference to that report in some of the other doctors’ reports however no report from Dr Abhayaratna was tendered.
General Practitioner Dr Ayres provided a reported dated 14 April 2013. In that report he referred to the report of Dr Gavaghan, and stated that there were no medical records or pathology results which suggest Mrs Hardcastle has been diagnosed with Coxsackie B virus. Dr Ayres said he could not define the relationship between her claimed condition and her Commonwealth employment.
On 10 May 2013 the respondent denied liability under s 14 of the SRCA for CFS, post viral fatigue, post infective fibromyalgia and post viral fibromyalgia. Comcare affirmed the decision on 17 July 2013, and on 11 September 2013 Mrs Hardcastle applied to the Administrative Appeals Tribunal for review.
Consultant Rheumatologist, Dr Kevat saw the applicant on 13 January 2014. He opined that, based on the symptoms Mrs Hardcastle reported and the usual incubation period for Coxsackie B virus, Mrs Hardcastle contracted the virus on the way to, or when she arrived at, the study course at the Rydges Hotel.
CONSIDERATION
The applicant’s case principally relies on the evidence of consultant microbiologist
Dr Crawford. Although Dr Jayaweera and Dr Kevat made comments in their reports that appear to support aspects of the applicant’s case, neither doctor was made available for cross examination, and I am not in a position to evaluate the reasons behind their comments. The respondent’s case principally relies upon the evidence of infectious disease physician and medical microbiologist Dr Korman. In addition to their written reports the tribunal had the benefit of both doctors appearing by video at the same time at the hearing.
Mr Woulfe submitted that I should prefer the evidence of Dr Korman. This is because of a number of reasons, not the least of which is that Dr Korman holds qualifications in science equal to that of Dr Crawford, and additionally, is a qualified medical specialist who has years of experience treating people. Dr Korman therefore has skills and experience relevant to the medical specialty discipline which are broader and more relevant than those of Dr Crawford, who is a research doctor, and has no medical qualifications nor clinical experience.
It is undeniable that Dr Korman has additional qualifications that are relevant, particularly when issues relating to clinical matters are being considered. It would be a mistake however, if I were to make a decision based solely on the basis that I preferred Dr Korman’s opinion because of his superior qualifications and experience. Mr Anforth referred to the decision of the Court of Appeal in Makita (Australia) Pty Ltd v Sprowles [2001] NSWCA 305. In that matter, the primary judge was criticized for accepting the opinion of an expert, without critically evaluating the basis of that opinion.[2]
[2] [2001] NSWCA 305 at [88], [102].
Mr Anforth submitted further that the standard of proof required by medical scientists to establish causation is very different to that required by decision makers under the Act. He referred me to the matters of EMI (Australia) Ltd v Bes [1970] 2 NSWR 238, and Sydney South West Area Health Service v Stamoulis [2009] NSWCA 153.
Mr Anforth contends that, using the reasoning in these cases, as long as the medical experts agreed it was possible that Mrs Hardcastle’s CFS was caused, or significantly contributed to, by Coxsackie B virus, and the virus was possibly contracted when she was at the Rydges Hotel attending the study course in March 2012, it is open for me to make a finding that the virus was the probable cause of Ms Hardcastle’s CFS.
That these matters are possibilities only is not enough to make a finding in the applicant’s favour.
I must be persuaded, not simply that it was possible, but that it is more likely than not that Mrs Hardcastle contracted Coxsackie B virus during her attendance at the Rydges Hotel conference, and also, that it is more likely than not that that virus significantly contributed to her CFS.
Both doctors agree that on the basis of the symptoms Mrs Hardcastle reported, it is more likely than not she contracted a viral illness prior to developing CFS, and the clinical onset of the viral illness was on or about 20 March 2012. Consistent with this are the opinions of Drs Ayres, Gavaghan, Jayaweera and Kevat. All of these doctors expressed the view that the CFS Mrs Hardcastle was suffering from was post viral.
Did Mrs Hardcastle contract Coxsackie B virus or any other viral infection when she attended the work-approved study course at the Rydges Hotel from 20 to 22 March 2012?
Coxsackie B virus is one of the enterovirus family of viruses. There are more than 70 different strains of enterovirus, which include the group A and group B Coxsackie viruses, the echoviruses, the polioviruses, Hepatitis A virus, and several strains that go only by the name enterovirus. Even though there are many strains of enterovirus, about 12 enteroviruses cause most illnesses.
Coxsackie B infections are common in childhood. Most Coxsackie virus infections are mild and more than 90% do not even cause symptoms. Symptoms when experienced are usually mild. Dr Crawford explained that enteroviruses are so named because they infect the gastrointestinal system, and for this reason are often associated with vomiting and diarrhoea. They can also cause symptoms similar to those of the common cold. Because they infect the gut, these viruses usually spread through the faecal-oral route. A person generally contracts the virus when they eat or drink food or fluids contaminated by faeces from an individual who is infected with the virus.
Dr Crawford opined that on the balance of probabilities, Mrs Hardcastle contracted Coxsackie B virus during her course of study at the Rydges Hotel in March 2012, and that this virus was the cause of her CFS. Dr Korman does not agree.
During the hearing Dr Crawford said that the reason he felt Mrs Hardcastle contracted Coxsackie B virus at the Rydges Hotel was because of:
(1) the history of the water jug being filled from the hand basin in the ladies’ toilets which presented a likely source of the infection; and
(2) the incubation period for Coxsackie B virus was consistent with the clinical onset of Mrs Hardcastle’s illness; and
(3) Mrs Hardcastle’s initial symptoms were typical of Coxsackie B virus.
Dr Korman took issue with Dr Crawford’s logic for each of these reasons.
Mrs Hardcastle’s symptoms
Dr Crawford relied upon the symptoms Mrs Hardcastle claims to have been suffering from when he concluded she contracted Coxsackie B virus at the Rydges Hotel.
Mrs Hardcastle did not report gastrointestinal symptoms that Dr Crawford explained were typical of enteroviruses, such as vomiting or diarrhoea. Both Drs Korman and Crawford agree that the symptoms reported by Mrs Hardcastle were not specific and could have been caused by a large number of viruses, in addition to Coxsackie B virus.[3] Other viruses which are prevalent in the community and capable of causing such symptoms include rhinovirus, herpes viruses, abdoviruses, rhinoviruses, picornavirus, influenza and parainfluenza viruses. As with enteroviruses, there are many different strains of each of these groups of viruses. These viruses are commonly spread via secretions from an infected person’s mouth or nose and can enter via the eye, mouth or nose.
[3] Dr Crawford identified Mrs Hardcastle’s chest pain as indicative of Coxsackie B virus, which I discuss later.
Coxsackie B virus can sometimes cause problems associated with chest pain, such as pleurodynia (chest pain sometimes referred to as Bornholm disease) as well as pericarditis and myocarditis (inflammation of the heart), all of which cause chest pain.
Dr Crawford indicated in his report that the chest pain Mrs Hardcastle experienced was possibly due to Bornholm disease. He is the only expert witness to make this suggestion. The possibility that Mrs Hardcastle’s chest pain was due to Coxsackie B virus was discounted by medically qualified experts Drs Jayaweera and Korman. Dr Jayaweera noted Mrs Hardcastle’s history of chest pain was not typical of pericarditis. Dr Korman explained that the chest pain Mrs Hardcastle described was not characteristic of pericarditis, myocarditis or myositis. Dr Korman explained that myocarditis is most unlikely. Had it been expected by medical staff that examined Mrs Hardcastle when she presented to the Canberra emergency department, confirmation of the diagnosis would have been made by blood test (elevated creatine kinase or troponin in the blood confirms the diagnosis). No such testing was performed. The only cardiac symptom or sign Mrs Hardcastle was observed to have that is possibly associated with Coxsackie virus was bradycardia. There are numerous possible causes of bradycardia. Dr Jayaweera indicated that the cause of Mrs Hardcastle’s bradycardia may have been the fainting episode. Mrs Hardcastle has been reviewed by cardiologist Dr Abhayaratna. Mrs Hardcastle has made statements to the effect that Dr Abhayaratna referred to Coxsackie B virus as “the smoking gun.” I can put no weight on such hearsay evidence. Comcare has made unsuccessful attempts to obtain a report from Dr Abhayaratna. I assume if Dr Abhayaratna’s report would have advanced the applicant’s case, it would have been tendered.
I find that Dr Crawford has erroneously concluded that Mrs Hardcastle’s chest pain was indicative of Coxsackie B virus. His error may well be because he is not a medical doctor, and has no clinical experience and knowledge. Mrs Hardcastle’s cardiac pains were not characteristic of Coxsackie B virus and the cause is unlikely to be from that virus. There is no medical evidence to support a conclusion that the temporary bradycardia she experienced was more likely than not due to Coxsackie B virus.
Pathology results
There is no general test that a doctor can order which will determine the type of viral infection a person is suffering from. Each virus must be specifically tested for.
Both Drs Korman and Crawford agree that evidence of a recent viral infection is detectable in the blood for short periods after the infection is contracted. Evidence of a recent infection usually is present in a person’s blood for some weeks. Both Dr Korman and Dr Crawford agree is possible that Mrs Hardcastle contracted a virus in March 2012, however by the time the first tests for specific viruses were ordered in June 2012, no evidence of the particular virus that she had suffered from remained in her blood.
Dr Korman explained that the test for enterovirus that was performed was non-specific, and was for the entire species. Even if there had been evidence of recent infection, which there was not, it could have been caused by one of the many different strands of enterovirus. To determine if Mrs Hardcastle had Coxsackie B virus, two blood tests separated in time would have needed to have been performed when she was initially unwell. A fourfold increase in the specific viral titre is necessary for a positive diagnosis. Unfortunately, by the time Mrs Hardcastle was diagnosed with CFS, it was too late to perform accurate testing for Coxsackie B virus.
Dr Jayaweera did not order testing for every possible viral infection. Rather, he ordered tests for cytomegalovirus, infectious mononucleosis, enteroviruses, and Lyme disease. Presumably he selected these viruses because he considered these viruses had a possible association with CFS.
The serology provided evidence of Mrs Hardcastle having been previously infected with enterovirus, cytomegalovirus and Epstein Barr virus. Both doctors agreed it was impossible to say when those infections occurred. It is possible that any one of these three viruses was responsible for her illness in March 2012. Mrs Hardcastle implied that EBV was unlikely to be the culprit for the March 2012 infection. She claims to have been quite unwell with a viral infection which she now attributes to EBV (also known as kissing virus, or infectious mononucleosis) when she was about 15 years old. It is impossible to know when Mrs Hardcastle contracted EBV as it is an extremely common viral infection and, like the enteroviruses, it can cause a spectrum of symptoms from no symptoms, to severe illness with fatigue, sore throat and fevers. EBV is not the only virus that can cause the symptoms Mrs Hardcastle describes as experiencing when she was 15, and to suggest an illness Mrs Hardcastle recalls she suffered at that age was due to EBV is speculative at best. EBV can be responsible for symptoms of the type Mrs Hardcastle suffered in March 2012. Like Coxsackie B virus, EBV has been suggested as having an association with CFS.
Dr Crawford had access to the serological results, and stated in his report that their results indicated a possible recent enterovirus infection. That statement is misleading; the pathology results indicate at some time in her life, Mrs Hardcastle has been exposed to one of the many enteroviruses. No tests specific to Coxsackie B virus were performed.
Both doctors agreed that enterovirus infections are very common in childhood. They both agreed that if a random test was performed, 50 – 80 % of the population would have serology the same as that of Mrs Hardcastle; that is evidence of previous exposure to EBV and to one or more of the enteroviruses.
Mrs Hardcastle’s serological results do not advance her case. Dr Korman and
Dr Crawford agreed that there is no serological evidence which proves Mrs Hardcastle has ever having been infected with Coxsackie B virus. Serology results demonstrate
Mrs Hardcastle was exposed at some time in her life to one of the many types of enterovirus, as well as CMV and EBV. Mrs Hardcastle may have also been infected with other types of viruses; not all possible viruses were tested for.Contamination of water in drinking jug
Mr Woulfe drew my attention to inconsistencies in the history provided by
Mrs Hardcastle over time. In her initial claims she suggested she contracted an infection from other attendees at the conference who she observed were suffering from upper respiratory tract symptoms. From the reports of Dr Gavaghan and Dr Jayaweera, it appears she expressed a belief this was the likely aetiology of her illness.
After Mrs Hardcastle saw Dr Gavaghan on 14 June 2012, she contacted her supervisor, Mr Owen Craig at CSIRO and made definitive statements about having been told by the specialist that she had Coxsackie B virus. This is of concern, because the blood tests
Dr Gavaghan ordered, looking for a number of possible viruses, were not performed until 18 June 2012. Of further concern is the fact that in his report, Dr Gavaghan did not express an opinion as to the likely cause of her recent illness, and from reading his report I infer it was his view that no infectious agent was likely to be identified.[4]
[4] Dr Gavaghan stated in that report (T3) that there was no point referring Mrs Hardcastle to an infectious diseases physician unless the infectious agent could be identified.
Dr Gavaghan stated in his report that he had advised Mrs Hardcastle to research CFS, and it was Mrs Hardcastle’s oral evidence that she had followed that advice.
Of more concern is that Mrs Hardcastle emailed Mr Craig and told him that recent blood tests confirmed that she had Coxsackie B virus. As discussed above, the serology did not confirm Coxsackie B virus. Dr Ayres made it very clear that there had been no confirmation of the infection.
The applicant’s husband, Mr Hardcastle, also made erroneous statements to the same effect, in relation to an infection of Coxsackie B virus.[5]
[5] T11.
In July 2012, Mrs Hardcastle asked Mr Craig to inform the HR department at CSIRO that she had a confirmed diagnosis of Coxsackie B virus, which was spread via contaminated utensils and food.
It was not until after her claim was rejected by Comcare that Mrs Hardcastle first mentioned having been exposed to potentially contaminated water.[6] Mr Woulfe contends that Mrs Hardcastle has taken the advice of Dr Jayawerra, has undertaken some research on the subject of Coxsackie B virus, and has modified her history, accordingly.
[6] However I note that Mr Hardcastle makes reference to filling of the jugs prior to the initial determination by Comcare (T11).
Dr Crawford and Dr Korman both agreed that the possibility of contracting Coxsackie B virus from a jug filled from the tap in a hand basin located a women’s toilet facility was so low that they would both be comfortable drinking water from a jug so filled.
Dr Crawford said that faeces could have entered the drinking water without anyone noticing. He said that the amount of faeces necessary to contaminate the water need not have been visible to the naked eye; it may have been a microscopic amount. Dr Korman said that the amount of faeces that would have been necessary to contaminate the water was such that it was unlikely a sufficient amount would have entered the water when a jug was filled in the manner described by Mrs Hardcastle. Dr Korman said contamination of the drinking water with faeces infected with Coxsackie B virus, in the manner suggested by Mrs Hardcastle was most unlikely. On this point, Dr Crawford maintained it was possible, although when questioned, he raised his opinion of the likelihood to “probable”.
Dr Korman explained, and Dr Crawford agreed, not all faeces carry viruses or diseases. It is only when the faeces is from an infected individual that it could be contaminated with Coxsackie B virus. Dr Korman explained that even if there was some faeces on the basin in the women’s toilets, and even if those faeces was infected, and even if that infected faeces entered the water jug when it was being filled, a very large amount would need to enter the water. He said sufficient infected faecal material was unlikely to enter the water merely by the jug being filled in the manner described. Dr Korman opined that passage of infection by that mechanism was most unlikely.
Both Drs Crawford and Korman agreed the source of most Coxsackie B virus infections is usually not identifiable. Both agreed the most usual route is when a person eats food contaminated with faeces from an infected individual. This may happen in many ways: a person may, for example, buy contaminated take away food, eat contaminated food at a restaurant, touch infected furniture or shake hands with an infected individual.
Dr Korman said that it would only be when there was an identifiable, unusual event that carried a significant risk of infection that he would be comfortable in stating it was the likely source of infection. Dr Korman gave the example of a person having changed the nappy of a sick baby in the days prior to contracting Coxsackie B virus as such an event. Dr Korman said that he did not regard drinking water from a jug filled from the basin located in a woman’s toilet cubicle as sufficiently unusual or out of the ordinary to be likely to cause an infection. That only Mrs Hardcastle claims to have symptoms is also significant.
Mrs Hardcastle gave evidence to the effect that she was fastidious with personal hygiene, that she avoided personal contact with persons whom she was aware had children in day care, and that she always used hygiene wipes on computers prior to using them.
Mrs Hardcastle also said that she had checked her credit card and other bank records and concluded that she did not eat out around the period in question, prior to developing symptoms or a viral illness. Dr Woulfe submitted that this and many other aspects of the applicant’s evidence were ‘too perfect’, and was likely the result of her undertaking research either independently, or at the suggestion of Dr Jayaweera.
I do not believe it is possible for Mrs Hardcastle, or anyone else, to illuminate all possible causes of an infection. Mrs Hardcastle initially believed she contracted an infection via the respiratory route. It was not until some weeks had passed that she learned of the possibility of Coxsackie B virus. After the passage of such time, it is unlikely that the applicant could recall everything she touched, every person she had contact with or everything she ate. If Mrs Hardcastle was suffering from a virus spread by the faecal-oral route, then the potential sources of infection would have been numerous, and identification of a particular source would be nearly impossible, unless, as Dr Korman said, there had been an unusual occurrence. That Mrs Hardcastle cannot recall of any other possible source of infection, does not equate to no other possibility existing.
Incubation time
Mr Crawford advised the tribunal that the average incubation time for Coxsackie B virus and indeed for most viruses is two to five days. Dr Korman agreed. Both Drs Korman and Crawford agreed that the incubation period for Coxsackie B virus is often quoted as two to ten days. Dr Korman pointed out that the incubation period is not always the same; the reason the incubation period is quoted to have a large range, of two to ten days, is because it can be altered by a number of factors, such as the health of the individual and environmental factors. Many viruses have incubation periods that are longer than five days.
Dr Ayres, when asked to provide a report on her background medical history, stated that Mrs Hardcastle had suffered a reactive anxiety episode in 2009 and injuries from a minor RTA (road traffic accident) in August 2010, and her recovery had been protracted with greater than one year persistent neck and shoulder pain.
Although Dr Korman conceded that it was possible that Mrs Hardcastle could have contracted Coxsackie B virus whilst she attended the study course at the Rydges Hotel, he said that this was just one of many possible viruses and sources of viral infection.
Dr Korman opined that Mrs Hardcastle could have contracted a virus during the study course at the Rydges Hotel, but given the usual incubation period of two to five days, and possibly longer, it was more likely she had contracted a virus prior to the conference.
Although not all people who contract Coxsackie B virus develop symptoms, if
Mrs Hardcastle had contracted Coxsackie B virus at the Rydges Hotel, it is likely that at least some other participants and staff would have been unwell.
Dr Crawford in his report placed reliance upon some conference participants and Rydges Hotel staff members being unwell. I note enquiries were made in that regard by CSIRO’s human resources staff, and there is no evidence of any attendees being unwell with symptoms consistent with Coxsackie B virus. There is no mention of staff members being unwell. The only suggestion of others being unwell is a reference to the coughing individual Mrs Hardcastle first identified as the potential source of her illness, and a CSIRO staff member reported to have been suffering from a totally unrelated respiratory illness following the conference (low levels of mycoplasma pneumonia – a bacterial, not viral infection). No suggestion of a causal link between the mycoplasma pneumonia and the conference has been suggested.
Is it more likely than not, that the viral infection Mrs Hardcastle suffered from in March 2012 was causally associated with her CFS?
A syndrome, Dr Korman explained, is a condition that is characterised by a group of symptoms that consistently occur together. Chronic fatigue syndrome, like all syndromes, is a collection of symptoms that commonly occur together. There is no diagnostic test for CFS, the diagnosis is made by a process of elimination; that is, when no other cause for the set of characteristic symptoms can be identified, the diagnosis of CFS is made. As I have already indicated, both parties agree that Mrs Hardcastle has been correctly diagnosed as having CFS.
Drs Crawford and Korman agree that the cause of CFS is not known. Dr Crawford said that many doctors regard the diagnosis as controversial. Dr Korman explained that consensus in the medical community is that the cause of CFS is likely to be heterogeneous, and less likely to have a simple or single aetiology. He said that several factors have been suggested as possible causes, including immunological, genetic, viral, neuroendocrine and psychological, and CFS is best regarded as a spectrum of illness that is triggered by a variety of factors in people who have an underlying predisposition.
A possible link between Coxsackie B virus and Mrs Hardcastle’s CFS was suggested by Dr Jayaweera. Drs Kevat and Crawford also indicated there was a possible link. Other than Dr Crawford, none of these doctors were made available at the hearing, and so I am not in a position to appraise the reasoning of these doctors.
Both Dr Korman and Dr Crawford agree that a number of viruses have been suggested as possibly associated with CFS. According to Dr Korman, these viruses include
Epstein–Barr virus (EBV), xenotropic, murine leukaemia virus related virus CMV,
Q fever, Ross River virus and enteroviruses. Dr Crawford also mentioned parvovirus B19 as a possible cause.
Dr Crawford referred to two studies which he said linked CFS to Coxsackie B virus.[7]
Dr Korman said that none of the above mentioned viruses have been proven to cause CSF, and, quoting other experts, noted that the role of enterovirus infection in CSF is ‘“really speculative.”’[8] He referred the tribunal to a large number of reference papers, and in particular to a study published in 2008,[9] in which the author, Abzug, critically analysed the relevant literature on the subject and concluded that the role, if any, is uncertain.
[7] Exhibit 6.
[8] Exhibit 7.
[9] Ibid.
Dr Korman explained that the reason a possible causal link has been suggested between CFS and Coxsackie B virus (as well as other viruses mentioned) is because of the erroneous conclusions made by those who first investigated and wrote papers on the subject. He explained that tests were performed on a number of people thought to be suffering from CSF. A large number of those tested were noted to have serology positive for Coxsackie B virus, and/or the other viruses mentioned. Dr Korman explained there was a simple explanation for this apparent association. The viruses that are thought to have an association with CFS are very common in the community; partly because many of those infected do not develop symptoms and as a result tests for these viruses are not routinely carried out. It was found that the viruses are common in the community, and later studies identified the same viruses in roughly the same proportion of patients who did not have CFS.
Dr Korman explained that Dr Abzug was a world expert in enteroviruses, and in
Dr Korman’s words, would ‘love to find a link between enteroviruses, and CFS.’ The fact that Dr Abzug was unable to find such a link was significant, as had there been any evidence of a link, Dr Abzug would have been keen to say so.
Dr Crawford said that where there is a history of a flu-like illness at the onset of what then becomes persistent illness, an infectious aetiology for CSF is suggested. Dr Korman said the temporal association does not necessarily imply aetiology. He explained that the association could be explained due to a number of possibilities. For example, it has been suggested that there could be an abnormality in a person’s immune system, which predisposes that person to both viral infections and CFS. This theory is supported by the fact that many persons who develop CFS have also recently suffered from a flu-like illness due to a virus, yet the same virus causes no symptoms in the majority of people. Mrs Hardcastle was involved in a motor-vehicle accident in 2010, and there is evidence that her recovery was somewhat protracted. Dr Korman suggested this is consistent with a conclusion that her immune system may have been compromised prior to her contracting a viral infection in March 2012. Mrs Hardcastle claims to have been well prior to the onset of her illness in March 2012. She gave evidence to the effect that she suffers less flu-like illnesses than most of her colleagues, and she claims that on one occasion her general practitioner commented on how infrequently she attends the surgery. It is beyond the scope of this decision to determine the state of Mrs Hardcastle’s immune system. I accept that it is possible that that she contracted a viral infection in March 2012 because her immune system was somewhat compromised. That may explain why she had an infection that she claims her doctor described as ‘severe,’ even though the likely causative agent usually causes no, or only mild symptoms in most people.
CONCLUSION
In order to be entitled to compensation under the SRCA, an employee must suffer an ailment or aggravation that was contributed to, to a significant degree, by the employee’s employment.[10] A ‘significant degree’ means a degree that is substantially more than material.[11]
[10] Safety Rehabilitation and Compensation Act 1988 (Cth) s 5B(1).
[11] Ibid s 5B(2).
There is a large amount of authority as to what ‘material’ is and what is a ‘significant degree.’
The cause of CFS is unknown. This is not a case where the exact cause of CFS is not proven but the medical and scientific experts agree on what the likely cause is.
Dr Korman was able to provide a detailed explanation about why viruses were once thought to play a role in the condition, and why now this is not the case.
Dr Crawford disagreed, however he did not offer any reasoned explanation as to why, and was not able to tender any scientific journal articles that refuted the conclusions in those put forth by Dr Korman.
Dr Crawford even pointed out that some doctors consider the diagnosis of CFS controversial.
I accept Dr Korman’s evidence, which was that the cause of CFS is likely to be heterogenic and that the frequency of viral infection in those with CFS is no higher than that of the general community. This was not contradicted by Dr Crawford.
Dr Crawford’s conclusions were often made on the basis of inaccurate assumptions (such as that other delegates and Rydges Hotel staff was also unwell). Dr Crawford’s opinions were less robust than those of Dr Korman, who supported his opinions with a wealth of scientific journal material. Dr Crawford frequently changed the weight of his opinions; often saying something was ‘possible’ before changing to ‘probable’ when requestioned.
Dr Korman considered all possibilities and gave a very balanced account of the possible explanations for Mrs Hardcastle’s symptoms, and was able to explain why Coxsackie B virus was not more likely to be the culprit in Mrs Hardcastle’s case than any other virus. Dr Crawford appeared to approach the situation from an adversarial position. I felt that he had already made up his mind that Mrs Hardcastle contracted Coxsackie B virus, subsequently causing her CFS, because that is what he was asked to say. He did not appear to have contemplated other possible viral causes of Mrs Hardcastle’s illness. Further, he seemed to make his conclusions by selectively focusing on aspects of the history and pathology results that supported the applicant’s case, without giving a balanced account of all possibilities. Dr Crawford does not treat patients because he is not a medical doctor. Perhaps that is why he did not turn his mind to the many other causes of chest pain and bradycardia. Dr Crawford did not appear to have the depth of academic knowledge that Dr Korman had. Dr Korman was able to speak in depth about the articles he presented to support his report.
I am satisfied on balance that Mrs Hardcastle suffered a viral infection, the clinical onset of which began on or about March 2012. I am not satisfied on the balance of probabilities that the virus Mrs Hardcastle suffered was Coxsackie B virus. I am not satisfied on the balance of probabilities that the viral infection Mrs Hardcastle experienced in
March 2012 was contracted when the she attended the Rydges Hotel, or at any other time during her employment.
There are numerous possible viruses that could explain Mrs Hardcastle’s symptoms, and there are numerous possibilities as to where and when such a virus was contracted.
I find that Mrs Hardcastle’s Commonwealth employment did not contribute, to a significant degree, to her suffering an ailment or any aggravation of such an ailment. Accordingly I find that Comcare is not liable to pay the applicant compensation under
s 14 of the SRCA.
DECISION
I affirm the decision under review.
I certify that the preceding 82 (eighty -two) paragraphs are a true copy of the reasons for the decision herein of Dr M Denovan, Member ..............................[SGD]..........................................
Associate
Dated 29 January 2015
Date of hearing 14 November 2014 Counsel for the Applicant Allan Anforth Solicitors for the Applicant Daniel Steiner, Capital Lawyers Counsel for the Respondent Peter Woulfe Solicitors for the Respondent Loretta Tolland, Comcare
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