Brian Johns v Simon Blackwood (Workers' Compensation Regulator)
[2015] QIRC 110
•5 June 2015
QUEENSLAND INDUSTRIAL RELATIONS COMMISSION
CITATION: | Brian Johns v Simon Blackwood (Workers' Compensation Regulator) [2015] QIRC 110 |
PARTIES: | Johns, Brian v Simon Blackwood (Workers' Compensation Regulator) |
CASE NO: | WC/2014/110 |
PROCEEDING: | Appeal against a decision of Simon Blackwood (Workers' Compensation Regulator) |
DELIVERED ON: | 5 June 2015 |
HEARING DATES: | 5 September 2014 |
MEMBER: | Industrial Commissioner Black |
ORDERS : | 1. Appeal allowed 2. The decision of the Regulator dated 13 March 2014 is set aside and substituted with a decision that the appellant's claim is one for acceptance 3. The matter of costs is reserved |
| CATCHWORDS: | WORKERS' COMPENSATION - APPEAL AGAINST DECISION - worker sustained non-work related wound - wound subsequently infected by bacteria found in wet and muddy workplace environment - microbiology results show presence of two pathogens of which one is associated with work environment - employment found to be a significant contributing factor |
| CASES: | Workers' Compensation and Rehabilitation Act 2003, s 32, s 550 |
| APPEARANCES: | Mr R. Myers, Counsel, instructed by Shine Lawyers, for the Appellant. Ms D. Callaghan, Counsel, directly instructed by Simon Blackwood (Workers' Compensation Regulator), for the Respondent. |
Decision
Introduction
Brian Johns ("the appellant") appeals a decision of the Review Unit of the Workers' Compensation Regulator ("the regulator") to reject his application for workers' compensation.
The appellant lodged his application for compensation with WorkCover on 26 July 2013 in respect to an injury sustained while working for Civil Tec Pty Ltd on a construction site near Gladstone. On his claim form he referred to the injury as "right leg below knee amputation", alleged to have been sustained as a consequence of "wearing gum boots at work which led to a blister on my toe." A workers' compensation medical certificate was issued on 11 September 2013 and identified the appellant's injury as "below knee amputation R leg (2ᵒ diabetic foot)."
WorkCover Queensland rejected the application for compensation in a decision dated 26 November 2013. On 4 February 2014, the appellant sought a review of WorkCover's decision. On 11 March 2014 the regulator confirmed WorkCover's decision that the claim was one for rejection. It is this decision that is now subject to appeal to the Commission pursuant to s 550 of the Worker's Compensation and Rehabilitation Act 2003 ("the Act").
The appellant commenced employment with Civil Tec as a machine operator on 9 July 2012. He was involved in laying foundations for a gas piping project in Gladstone. The appellant described his work area as swampy and in order to access the machinery he was working on, he was required to walk through muddy water. The appellant stated that he was provided with gum boots which were a cause of irritation and blistering. He said that mud and water would often enter his boots while working in the muddy environment in which the machinery was situated. Despite initially attributing his infection to blisters, in the proceedings it was accepted that the wound that subsequently became infected was caused by a burn to the right toe sustained while riding a motorbike without shoes.
The appellant began feeling unwell on 31 October 2012. When his condition had not improved the next day he attended at the Emergency Department of the Gladstone Hospital before being admitted to hospital as an in-patient. While the appellant reported feeling generally unwell he also drew attention to a sore right toe. A swab taken from the burn on the appellant's right toe on 1 November 2012 grew two bacteria - a Staphylococcus aureus (Staph A) and an Acinetobacter baumannii (Acinetobacter). The appellant was diagnosed with septis caused by foot cellulitis. His right toe was subsequently amputated on 6 November 2012.
The appellant was discharged from Gladstone Hospital on 12 November 2012. He was subsequently re-admitted to the hospital for further treatment on 30 November 2012. Over time it became apparent that the treatment had not been successful and the appellant suffered a forefoot amputation in February 2013 and a below knee amputation on 28 June 2013.
Issue for Determination
The issue for determination in this appeal is whether the worker suffered an injury pursuant to s 32 of the Act which, for the purposes of this appeal, relevantly provides as follows:
"32 Meaning of injury
(1)An injury is personal injury arising out of, or in the course of, employment if the employment is a significant contributing factor to the injury."
…
(3)Injury includes the following-
(a) a disease contracted in the course of employment, whether at or away from the place of employment, if the employment is a significant contributing factor to the disease."
Nature of the Appeal
The appeal to the Commission is by way of a hearing de novo. To succeed with his appeal, the appellant must establish on the balance of probabilities that his injury arose out of, or in the course of, his employment and in circumstances where the employment was a significant contributing factor to the injury.
Evidence
During the course of the proceedings, evidence was provided by four witnesses. The witnesses for the appellant were as follows:
· Brian Johns
· Associate Professor Rob Baird.
The witnesses for the Regulator were as follows:
· Larry Wells
· Dr Paul Bartley.
Chronology
A chronology of significant events is set out below:
9 July 2012 Appellant starts work at Gladstone 21 October 2012 Last day of work before time off 26 October 2012 Burn to toe from motorbike carburettor 28 October 2012 Appellant resumes work 31 October 2012 Appellant starts feeling unwell 1 November 2012 Appellant cannot complete work 1 November 2012 Appellant presents at Gladstone Hospital 1 November 2012 Blood cultures grow two bacteria: Staphylococcus aureus and an Acinetobacter baumannii 6 November 2012 Right toe amputation 12 November 2012 Appellant discharged from Gladstone Hospital 30 November 2012 Appellant presented to Gladstone Hospital for dressing change. Re-admitted to hospital with "open infected wound to toe post amputation" 30 November 2012 Culture swab grows Staphylococcus aureus 5 December 2012 Staphylococcus aureus isolated in bacterial culture 2 February 2013 Blood cultures grow a mixture of Staphylococcus aureus and Enterococcus faecallis February 2013 Forefoot amputation 28 June 2013 Below knee amputation
Underlying Condition
It was not in dispute that the appellant was a poorly controlled diabetic and that it was this condition that was a major contributing factor to the development of the infection that led to the amputations suffered by the appellant.
In his report Dr Baird effectively characterised the appellant's circumstances as high risk. He said that a poorly controlled diabetic, working in muddy tropical water, with an open wound to his foot, would directly and significantly contribute to the contraction of a poly-microbial infection. Dr Baird said that three main factors were implicated in the need for the toe amputation:
(i) Poorly controlled diabetes predisposed the appellant to infection;
(ii) The burn to the toe allowed bacteria to enter the foot; and
(iii) Bacterial contamination of the injury occurred when bacteria entered the open wound causing a local infection which had the potential to spread.
Dr Bartley's evidence was consistent with this. He said that the macro and microvascular disease and the poorly controlled diabetes were the "the big issues". The appellant's burn had breached the normal barrier to infection while his body's ability to respond both in terms of healing the breach and fighting off any secondary infection was impaired by his poorly controlled diabetes.
Dr Bartley's evidence at T1-74 was to the effect that the appellant's microvascular disease was a consequence of many years of poor diabetic control and that while "the wound and the subsequent superficial infection may have taken place over days to weeks, it’s the lead-up work from the poor diabetic control that’s contributed substantially to the subsequent events".
The effect of Dr Baird's evidence was very similar. He said that "the critical thing in Acinetobacter infections is that they occur in patients who have diabetes or some underlying problem". He said that persons in good health who get exposed to mud normally do not get infections. He also said that infections in diabetics from mud and water is common in tropical and sub-tropical areas.
In terms of the timing of events Dr Baird said that while infections can come on suddenly, they required the diabetes to be out of control, or not well controlled. He said that the speed of the infection and a requirement for medical treatment a few days after the burn was sustained could be regarded as typical for a poorly controlled diabetic.
The most likely scenario relevant to the appellant is consistent with Dr Baird's opinion. The appellant sustained a burn to his big right toe while riding his motorbike in Mackay on 26 October 2012, resumed work on 28 October 2012, and presented at the Gladstone Hospital on 1 November 2012. His great right toe was amputated on 6 November 2012.
The effect of Dr Bartley's evidence around timing was similiar. Dr Bartley proceeded on the basis that the time interval between the burn and the date of toe amputation was two weeks. He said that it would not have been significant if the time interval were longer and that the burn had been sustained in September 2012.
Gladstone Hospital
The appellant presented at the Emergency Department of Gladstone Hospital on 1 November 2012. The medical records disclose that, after admission, an examination of the appellant revealed a right big toe injury which was caused by a burn from a carburettor sustained while the appellant was riding his motorbike without boots. The pervasive clinical concern related to a secondary infection in the appellant's right toe. A diagnosis of "foot cellulitis as the cause of the sepsis" was entered.
Dr Baird's report indicates that swabs of the infected area were ordered because the medical officer "was worried about MRSA, a more resistant form of staphylococcus aureus becoming more prevalent in the community, and needing different antibiotics to those already prescribed". A few days after his admission to hospital acute osteomyelitis of the appellant's great right toe caused its amputation on 6 November 2012. This treatment however was not successful and subsequent surgical interventions were necessary involving a forefoot amputation in February 2013 and a below knee amputation on 28 June 2013.
An explanation for the failure of the initial treatment to resolve the appellant's condition was canvassed in the medical evidence. One of the considerations was whether the appellant's infection at the time of admission to the Gladstone Hospital might have been more extensive than initially thought. Dr Baird opined at T1-32 that the "initial infection was obviously what led to the first amputation and, unfortunately, in diabetics there’s often a bit of a cascade, because when you cut into poorly viable tissue, secondary infection can develop and poor wound healing can develop and infect." He went on to explain that (T1-32):
"Unfortunately, the damage often occurs very early on in infection. The bacteria in a diabetic tend to act together in synergy and cause a lot of tissue damage, so in spite of the fact they can be killed reasonably quickly, the toxins they release are effectively burning or scalding the tissue from inside, and in a diabetic patient who often has very poor blood flow to the legs, that can be enough to tip an individual over into requiring an amputation, whereas if this was a fit and healthy man without diabetes, normally that wouldn’t be the outcome."
The effect of Dr Baird's evidence at T1-29 was that it was possible that the infection could have spread very quickly. He said that the speed of infection depended on the virulence of the bacteria, how poorly controlled the diabetes was and how much damage had already been caused to the leg by the diabetes. These variables meant that the speed of the infection would vary from individual to individual and periods of hours, days or weeks could be involved.
Dr Bartley accepted at T1-69 that it was possible that all the damage had been done by the time the appellant was admitted to hospital on 1 November 2012:
"Save, Doctor, that by the 1st of November of 2012, all of the damage that ultimately gives rise to the necessity for the above-knee amputation could have been done? ‑‑‑Possibly."
Dr Bartley had earlier opined in his written report that he was "suspicious for the presence of underlying neuropathy particularly one that is specific for lack of pain sensation. I am suspicious that in retrospect the patient may have had more extensive osteomyelitis and/or complex soft tissue infection (particularly tenosynovitis of the first toe extensor tendons) than was clinically apparent at the time of the initial amputation". His evidence in the proceedings at T1-69 is set out below:
"… my opinion is that the reason why he progressed to further infection later is that the actual infection had spread beyond the surgical field and that what he needed was probably a combination of more aggressive imaging to determine the true extent of the infection. So, in other words, more sophisticated X-rays or MRI scanning and probably more extensive surgery, possible even a transmetatarsal amputation at the start depending on what that showed to halt his infection and that happened because of his host defences being inadequate by virtue of his impaired -both phagocytic cells and also his impaired blood vessels -all from his diabetes."
Swabs collected from the burnt area of the appellant's right toe on 1 November 2012 isolated that Staph A bacteria and the Acinetobacter bacteria. The impact of the Staphylococcus aureus bacteria was not in dispute for two reasons. Firstly, it had no role to play in establishing a connection between the appellant's employment and his injury. Dr Baird said that the Staph A infection would not be directly related to the appellant's employment while Dr Bartley said that he would not regard the appellant's Staph A infection "as a particular occupational risk". Secondly, it was common ground that the Staph A was a significant contributing factor to the development of the infection in the appellant's right toe. Dr Bartley opined that the "clinical scenarion presented is consistent with Staphylococcus aureus infection in a patient with poorly controlled diabetes" while Dr Baird concluded that it was likely that both the Staph A and the Acinetobacter were "the significant cause of the infection".
Whether the appellant acquired the Acinetobacter bacteria in the course of his employment is a matter for determination. If this can be established the matter in contention is whether the Acinetobacter acted as a co-pathogen with the Staph A and contributed significantly to the development of the appellant's infection. This is the primary finding to be made.
Association with Work Environment?
The respondent advanced a number of reasons in support of a proposition that it could not be established with sufficient certainty that the appellant acquired the Acinetobacter bacteria in the course of his employment. In advancing this argument the respondent did not deny that it was possible that the bacteria was acquired at work, but said that there was a range of other options and that the mere possibility that the bacteria was acquired at work was not sufficient to support a balance of probabilities finding to this effect.
Dr Baird acknowledged that there was no way of knowing from the swab result how long the Acinetobacter had been present in the area from which the swab was taken. Dr Bartley gave the same evidence. Nor, on the evidence, could it be established with certainty where the Acinetobacter organism came from, or that the organism did exist in water or mud in the Gladstone area.
It was Dr Baird's evidence that Acinetobacter is a water-borne bacteria which is commonly found in wounds associated with contamination by environmental water including creeks, rivers, streams and estuaries. The estuarine environment within which the appellant worked was consistent with such an environment. In his report Dr Baird said that "there is a strong association with water as a causative agent" of infections such as those contracted by the appellant. Dr Baird said that the volume of water encountered did not change the likelihood of infection but that mud was a different consideration. He described mud as "bacterial soup".
It was Dr Bartley's evidence that "on the balance of probabilities, the microbiological culture results (from 01/11/2012) did reflect Mr Johns' work environment. The burn could have been acquired elsewhere and then become colonised or infected with Staphylococcus aureus (from the patient's own skin) and Acinetobacter baumannii (from the estuarine water) at a later time point". In his evidence at T1-66 he accepted that the Acinetobacter could have come from the appellant's work environment. While however Dr Bartley said that the Acinetobacter was present at the start and may have reflected the appellant's work environment, he opined that subsequent events suggested that it was not as significant a factor as may have appeared to have been the case in the first instance.
The weight of the medical evidence was tilted toward a finding that it was more probable than not that the bacteria was acquired at work. This is not to say that other conclusions were not possible. However having regard to areas of common ground in the evidence of Dr Baird and Dr Bartley a balance of probabilities finding is able to be entered that it was more likely than not that the Acinetobacter organism would be found in the appellant's work environment and that the presence of the Acinetobacter bacteria shown on the 1 November 2012 swab was attributable to the work environment. However whether the Acinetobacter bacteria significantly contributed to the development of the infection is a separate question to be answered.
Microbiology Results
A culture result of a swab taken from the burn site on 1 November 2012 disclosed the presence of both the Acinetobacter and the Staph A bacteria. However a subsequent swab taken on 30 November 2012 isolated only the Staph A bacteria. Exhibit 6 discloses that swabs were also taken at the request of Dr Dammalapati in Mackay on 5 December 2012, 14 December 2012, and 2 February 2013. The test results showed that Staph A was isolated in the 5 December 2012 and 2 February 2013 swabs.
Had both the Staph A and Acinetobacter bacteria been isolated in some or all of the swabs taken after 1 November 2012 swab, the grounds for rejection of the appellant's claim for compensation would have narrowed. As it was however only the Staph A bacteria was present in the subsequent swabs. While it was accepted by both specialists that there was no way of knowing whether the Staph A isolated in the 1 November 2012 swab was the same organism that was isolated in subsequent swabs, Dr Bartley considered that it was likely that the organisms were the same.
The microbiology report relating to the swab taken on 1 November 2012 was in the evidence as page 122 of Exhibit 3. The exhibit discloses that the gram stain report identified gram-positive cocci resembling Staphylococcus and gram-negative bacilli. The culture report identified "Staphylococcus aureus 2+" and "Acinetobacter baumannii complex 2+".
Dr Baird explained that the laboratory analysis of a swab involved the production of an initial "gram stain" result followed by "culture" result. Dr Baird said that in the first instance the swab is rolled out onto a culture plate and subject to inspection under a microscope. This analysis produces a "gram stain" result. The "culture" results take up to 48 hours to become available because the bacteria have to be given time to grow. Dr Baird said that if bacteria is seen on the gram stain, it means that the bacteria is present in very high numbers. He said the differentiation, at this point, between very high numbers and low numbers, was important. Low numbers are indicative of "on skin colonisers" while high numbers are indicative of an infection.
In terms of the swab taken from the appellant on 1 November 2012, Dr Baird said that the gram stain result showed that high numbers of Acinetobacter bacteria were present on the gram stain. He said that the high numbers of the bacteria seen on the gram stain "were very suggestive evidence that the Acinetobacter was there as a co-pathogen, rather than a colonizer" (T1-37). Further at T1-38 he said that "the wonderful thing about a gram stain is that you don’t see bacteria until they’re there in high numbers, which is normally 50 to 100,000 bacteria per mil."
Dr Bartley however questioned whether the gram stain result did disclose high numbers of the Acinetobacter bacteria. While Dr Baird had said that the "gram negative bacilli" shown on the gram stain result was "consistent" with Acinetobacter, Dr Bartley pointed out that the gram-negative bacilli included both "mixed coliforms" and the Acinetobacter organisms. He therefore challenged the conclusion that high numbers of gram negative bacilli should be read to equate to high numbers of Acinetobacter. It followed that Dr Bartley did not accept that the gram stain results were indicative of an Acinetobacter infection and he was reluctant to dismiss the Acinetobacter as a coloniser.
While the evidence around the gram stain results was in dispute, generally consistent evidence was given by both specialists about the culture results which reported the presence of "Staphylococcus aureus 2+" and "Acinetobacter baumannii complex 2+". When asked whether the designation of "2+" associated with the Acinetobacter cultured identified it as a coloniser or an infector, Dr Bartley opined as follows (T1-61):
"Look, it’s not hard and fast. It makes it -it makes it harder to disregard it from a treating physician point of view. The literature on comparing superficial swabs versus tissue specimens would indicate that, particularly for coliforms and environmental organisms like these on a surface swab, their presence there doesn’t correlate well with their presence in deep tissue cultures where you use a deep tissue culture as the gold standard. Having said that, sometimes these organisms in the setting of burns can be pathogens, or, at least, co-pathogens, so it’s hard to dismiss them completely, particularly when they’re, you know, reasonably heavy like this."
It was Dr Baird's evidence (T1-31) that the designation of "2+" associated with the Acinetobacter and Staph A bacteria on the culture report meant that both bacteria were present in substantial numbers:
"So then moving down to the culture, the two bacteria that were seen were subsequently cultured. The gram positive cocci resembling Staph aureus was grown, and those three-letter acronyms are purely for which antibiotics it was susceptible to. And the second bacterial grown was the Acinetobacter baumannii complex. The two pluses after those Staph aureus and Acineto baumannii refer to the amount of growth on the culture plates, and they were both there in good solid numbers."
It was Dr Bartley's evidence that the sequence of events relevant to the appellant's infection "can be accounted for completely by the presence of microvascular diabetic disease along with Staphylococcal aureus infection and poor compliance with treatment". He said that the Staph A bacteria was "a lethal human pathogen and a well described pathogen in the setting of diabetic foot infections" His evidence at T1-69 is relevant:
"And you certainly can’t say that it was the staph bacteria that caused the infection? ‑‑‑No, I think I can. Yeah. They can be fairly confident -staph aureus has go a well-earned reputation for association with skin and soft tissue infection and septicaemic and other life-threatening complications, both in the presence and absence of diabetes, and it is certainly, again, a significant pathogen in the setting of burns and neuropathic ulcers and other breaches in skin integrity. So staph aureus could easily do all of this.
All right. I appreciate that and I perhaps put it badly. You can’t exclude the fact that the staph was a co-pathogen? ‑‑‑I think the staph was the driver."
Dr Bartley's view was that if the Acinetobacter had been a significant factor and had acted as a co-pathogen to cause the infection, then it would have continued to be isolated in subsequent microbiological results on 30 November 2012 and 2 February 2013. Dr Bartley's conclusion on this aspect is recorded at T1-69:
"… So if the staph was going to go in and do it and you’re arguing the staph is the pathogen then if the Acinetobacter was the pathogen it should have followed the staph as well and subsequent events have shown that it hasn’t been found. So it was there -it was taken reasonably seriously at the start -quite appropriately, I think -but, again, on reflection, I don’t think it was significant. It was there on the surface."
Dr Baird however maintained that the sequence of events in which only the Staph A continued to be isolated was to be expected. His explanation was on the record at T1-39:
" … I believe it was a co-pathogen, in terms of causing the initial injury, and I believe the antibiotics Mr Johns was given would have killed the Acinetobacter very quickly.
But it didn’t kill the Staphylococcus aureus? ‑‑‑Don’t always -there’s a difference between Acinetobacter and staph aureus. If I could explain.
Certainly? ‑‑‑Acinetobacter is an uncommon coloniser of a human, so even in the wet season in Darwin, it’s uncommon to be colonised on a human. So normally, for it to cause infection, you have to have got it from somewhere else, like mud. Staph aureus is quite different, and 20 per cent of everybody in the room around you will be carrying staph aureus in their nose, groin, and between their toes, if we went swabbing for it, so it means when there’s an open wound, it’s very easy for the staph to get back in there, whereas Acinetobacter you can kill quite quickly, if you get the correct antibiotics, and unless you’re exposed to Acinetobacter again, it won’t come back, but it will have done its damage."
The effect of Dr Baird's evidence was that the absence of the Acinetobacter bacteria in the swab results of 30 November 2012 was consistent with the positive effects of the antibiotics which he said would normally kill off the bacteria within 48 hours. Dr Bartley provided qualified agreement with this view. Firstly he accepted this view on the condition that the Acinetobacter was actually a cause of the infection. Secondly he said that the bacteria could have been removed when the toe was amputated.
Dr Baird explained the continuing presence of the Staph A bacteria by saying in effect that the Staph A bacteria was "notoriously difficult" to treat and that the antibiotics administered may not have been effective. He also said that it was possible that the Staphylococcus organism that was present on admission had been successfully treated but that the appellant had acquired a different form of the Staphylococcus bacteria while in hospital (T1-31).
Dr Bartley said that the particular identification of the Staph A and Acinetobacter bacteria in the 1 November 2012 microbiology report was "probably because they were predominant and are both recognised as either actual pathogens or potential pathogens if the appropriate clinical signs and symptoms suggest there's infection there" (T1-60). The effect of this evidence was that the identification of both bacteria in the report did not mean that, as a matter of fact, both were pathogens. Despite this, both Dr Bartley and Dr Baird agreed that, given the 1 November 2012 microbiology results, it was appropriate for medical staff at the Gladstone Hospital to conclude that the Acinetobacter and the Staph A bacteria were co-pathogens, and to treat the appellant's infection with polymicrobial antibiotics.
Notwithstanding the appropriateness of the initial treatment, it was Dr Bartley's evidence that, some retrospective explanation had to be found for the failure of the initial treatment and the continuing and worsening infection. It was in this context that he opined that the absence of Acinetobacter in the 30 November 2012 swab and beyond meant that the first swab result should be construed to mean that the Acinetobacter bacteria should be regarded as either a "limited local stage infection that was dealt with by the amputation of the great toe or it was a surface coloniser and really wasn’t an invasive organism."
Dr Bartley concluded that the second microbiology result on 30 November 2012 was consistent with a view that the Acinetobacter was not a critical factor in the development of the appellant's infection and that the overwhelming issue confronting the appellant was his diabetes and the Staph A infection. While he conceded that the appellant's treatment by antibiotics on admission to the Gladstone Hospital, or the surgery to remove the toe, may have killed off the Acinetobacter bacteria, he said that the exclusion of the Acinetobacter did not stop the infection.
Dr Baird did not accept that the Acinetobacter bacteria isolated in the 1 November 2012 swab was a coloniser rather than an infection. In his report Dr Baird stated that that "Acinetobacter baumannii are not normally present in humans as colonising bacteria". Further his evidence in the proceedings (T1-39) was to the effect that it was uncommon for Acinetobacter to be colonised on a human and that for it to cause an infection it normally had to be acquired in some other way, for example from contact with mud. It was Dr Baird's evidence that both the Acinetobacter and Staph A bacteria were known causes of skin and soft tissue infection and that it was likely that they both were significant causes of the appellant's injury, particularly given the association between Acinetobacter and diabetes (T1-32):
"… So Acinetobacter often goes along with diabetes. So they go hand in hand, because Acinetobacter isn’t a particularly virulent pathogen always outside diabetes, unless it’s infected into a wound in very, very high numbers."
Factors Supporting the Respondent's Case
The following propositions supported the respondent's defence of the appeal:
(i) Acinetobacter was not a significant pathogen in the development of the appellant's infection;
(ii) While the presence of the Acinetobacter bacteria reflected the appellant's working environment, the appellant could also have acquired the Acinetobacter bacteria through contact with water or mud outside the workplace and/or during his visit to Mackay;
(iii) The sequence of events arising from the appellant's presentation at hospital on 1 November 2012 can be accounted for completely by a deep Staph A infection in a poorly controlled diabetic. While it was appropriate to treat the Acinetobacter as if it were a co-pathogen in the initial phase, beyond that point the Staph A bacteria was the consistent theme and the Acinetobacter was not as significant as first thought;
(iv) That had the Acinetobacter not been present, or if its presence were simply as a coloniser, neither the progress of the infection nor the outcomes would have been different. The presence of the Acinetobacter bacteria was not a prerequisite to the development of the infection. The Staph A bacteria could have done all the damage on its own. An Acinetobacter infection was not necessary to explain the progress of the infection or the outcomes (three amputations);
(v) If the Acinetobacter were a significant contributor to the appellant's morbidity subsequent to his toe amputation, the bacteria should have been cultured along with the Staph A from the swabs taken on 30 November 2012, 5 December 2012 and 2 February 2012;
(vi) While the Acinetobacter bacteria may have been removed by the polymicrobial antibiotics, the infection was not removed;
(vii) If the Acinetobacter organism was a surface coloniser it could be expected to have disappeared in the surgical process associated with the amputation of the appellant's great toe;
(viii) That if the full damage had been done on presentation to Gladstone Hospital, then on Dr Bartley's evidence, it may mean that the infection had progressed up the appellant's foot or the infection was present in the bones of his foot, and in these circumstances the Acinebacter should have been cultured at later dates (noting that the forefoot was amputated in February 2013 and the leg amputation occurred in July 2013).
Factors Supporting the Appellant's Case
The appellant's case was supported by the following propositions:
(i) Dr Bartley acknowledged in his report that Acinetobacter is a well described pathogen or co-pathogen particularly in wounds associated with contamination by environmental water which was consistent with the appellant's working environment. He said in his evidence that the appellant's work environment posed a "reasonable risk" of infection;
(ii) Despite the difference in interpretation around the gram stain results, Dr Baird said that the culture result showed that both the Acinetobacter and the Staph A bacteria were grown in "good solid numbers", while Dr Bartley described the presence of both organisms as either "reasonably heavy" or "moderate", if a scale of "scant, moderate or heavy" were used;
(iii) Dr Bartley's evidence that both bacteria were specifically referenced in the microbiology report of 1 November 2012 because they were "predominant" and "both recognised as either actual pathogens or potential pathogens if the appropriate clinical signs and symptoms suggest there's infection there";
(iv) Dr Baird said that the usual conclusion from any microbiologist on the 1 November 2012 report would be that the culturing of Acinetobacter and Staph A would mean that there is a co-infection with co-pathogens. The treatment specifically for polymicrobial infection reflected this diagnosis;
(v) Dr Bartley agreed that it was appropriate to treat the Acinetobacter as a co-pathogen after evaluation of the 1 November 2012 microbiology result;
(vi) Dr Bartley said that it would be hard for the treating physician at Gladstone Hospital to disregard the presence of the Acinetobacter bacteria because these "organisms in the setting of burns can be pathogens, or, at least co-pathogens";
(vii) The removal of the Acinetobacter bacteria (between swabs on 1 November 2012 and 30 November 2012) was consistent with Dr Baird's evidence that antibiotics were very effective. It was also Dr Bartley's evidence that if the Acinetobacter bacteria were a cause of the infection and if it were correctly treated (which he accepted) on the appellant's admission to hospital, it could be expected that the Acinetobacter would no longer be present. Therefore while the Acinetobacter did not have a continuing role, it is likely that the Acinetobacter bacteria was removed by antibiotics soon after the appellant's admission at Gladstone Hospital;
(viii) Dr Bartley's evidence that it was "possible" that all the damage that ultimately led to all three amputations could have been done by the time of admission to Gladstone Hospital on 1 November 2012;
(ix) Dr Bartley's acknowledgement that in defined circumstances the Acinetobacter bacteria may have caused a "limited local stage infection that was dealt with by the amputation of the great toe" or that the Acinetobacter bacteria "would have been just limited to infection in and around his toe rather than more proximally in his foot".
Reasoning
A swab taken from the appellant's wound soon after his admission to Gladstone Hospital isolated both the Acinetobacter bacteria and Staph A bacteria. The swab result informed a treatment for a polymicrobial infection in which the Acinetobacter was regarded as a co-pathogen. The evidence of both Dr Bartley and Dr Baird was to the effect that it was more probable than not that the appellant had acquired the Acinetobacter bacteria during the course of his employment. The infection initially caused the amputation of the appellant's great right toe and subsequently led to the forefoot and below knee amputations. These circumstances give rise to a prima facie conclusion that the appellant's injuries were attributable to an infection which was caused in part by the Acinetobacter organism derived from the appellant's work environment.
Notwithstanding the prima facie position, the respondent advocated an outcome wherein the Acinetobacter bacteria did not make any significant contribution to the development of the appellant's infection, nor to the progress of the infection and the outcomes of the infection. The respondent relied on Dr Bartley's opinion to submit that the appellant's infection and the consequential amputations could be accounted for entirely by the presence of Staph A in a poorly controlled diabetic. It followed that Dr Bartley dismissed the Acinetobacter bacteria as playing any significant role in the development of the appellant's infection.
The appellant submitted that the weight of the evidence favoured a conclusion that the Acinetobacter was acquired through contact with wet and muddy conditions at work and then acted as a co-pathogen with Staph A to cause the appellant's burn to become infected. For the appellant that was largely the end of the matter and this evidence was sufficient to satisfy the test of sufficiency of association between the workplace and the injury.
The significance of Staph A in the development of the infection was not disputed by the appellant. It was also common ground that a major contributing factor to the development of the infection was the appellant's underlying condition of poorly controlled diabetes. The resolution of the appeal is to be found in a determination about whether the Acinetobacter bacteria, having regard to its association with the appellant's employment, could be held to be a significant factor in the development of the infection and the subsequent injuries sustained by the appellant.
Dr Baird's opinion was developed from a basis where he said that Acinetobacter infections normally occur in patients who have an underlying condition such as diabetes. His view was that it was not common for the Acinetobacter bacteria to be colonised on a human and for this bacteria to cause an infection it had to be acquired elsewhere than on the patient's skin. Given the appellant's working environment it was likely that he had acquired the bacteria from contact with water or mud at work. Dr Baird acknowledged that Staph A was a common cause of infection following colonisation on a person's skin. He accepted that, in the appellant's case, this bacteria would have acted as a co-pathogen. He also said that polymicrobial infections are more serious, as the bacteria can combine to cause a more virulent infection. Dr Baird's conclusion was that it was likely that both bacteria were "the significant cause of the infection to the foot occurring, and the subsequent skin and soft tissue infection, which was a direct cause of the need for toe amputation, and the temporally related forefoot amputation".
In arriving at a balance of probabilities finding having regard to all the evidence, I prefer the explanations provided by Dr Baird. I consider that it was more likely that both bacteria had a significant role to play in the development of the appellant's infection at the time of his admission to Gladstone Hospital on 1 November 2012. In distinguishing between the medical evidence I am reluctant in particular to dismiss the Acinetobacter bacteria as a coloniser and I am not satisfied that Dr Bartley adequately explained the impact on his reasoning of the probable removal of the Acinetobacter bacteria by polymicrobial antibiotics soon after the appellant's admission to Gladstone Hospital. In this regard there is a difficulty in reconciling this probability with Dr Bartley's opinion that the Acinetobacter had no role to play in the development of the appellant's infection.
The 1 November 2012 microbiology report provides a sound basis for the appellant's claim that the Acinetobacter bacteria should be regarded as a co-pathogen. While there was a difference in the evidence about the significance of the gram stain results, both specialists agreed that the culture report established the presence of the Acinetobacter bacteria in strong numbers. Dr Baird said that culture report indicated which bacteria were present and a cause of the infection on admission. He also said that the "usual conclusion from any microbiologist on that report would be it's a co-infection and with co-pathogens, as commonly occurs in diabetics, and he would be treated accordingly" (T1-32).
While Dr Bartley contested Dr Baird's view that the gram stain result was evidence that the Acinetobacter was not a coloniser, he did not adequately explain why the reasonably heavy presence of the cultured Acinetobacter was consistent with the Acinetobacter's role being limited as a coloniser. Nor did he address Dr Baird's view that it was not usual or common for the Acinetobacter organism to colonise on humans.
It seems to me that on the balance of probabilities it was more likely than not that the 1 November 2012 microbiology report established that the Acinetobacter was a co-pathogen. In these circumstances I am not inclined to accept Dr Bartley's reasoning where he concludes that the presence of the Acinetobacter bacteria in the microbiology report should be dismissed as a relevant consideration. In explaining his reasons Dr Bartley outlined two options, but the difficulty is that the options are competing options. That is, on the one hand he opines that the Acinetobacter was a coloniser, but on the other hand, in acknowledging that antibiotics may have removed the Acinetobacter soon after admission, he said that if the Acinetobacter were an infector its impact would have been limited to the toe amputation stage. The effect of the latter option is to accept that the Acinetobacter bacteria was a co-pathogen at the time of the appellant's admission to hospital and to transform the argument into one of degree. That is, in a circumstance where both bacteria were co-pathogens, the central consideration became which of the two contributed the most to the amputation injuries sustained. All that needs to be resolved however is that the bacteria derived from the appellant's workplace was a significant contributing factor to the infection and subsequent injuries.
If it is accepted that the Acinetobacter may have been an infector that was removed after treatment by polymicrobial antibiotics, it is inconsistent to argue that the Staph A was the only significant factor and that the Acinetobacter had no role to play in the appellant's condition. Both specialists accepted that if the Acinetobacter bacteria did act as a co-pathogen and contribute to the severity of the infection, but was subsequently successfully treated by antibiotics, it would not be expected to be isolated in the swab of 30 November 2012 and thereafter. Dr Baird's evidence in this regard was that it was the norm that once the Acinetobacter bacteria is isolated and treated, it will not return. On the other hand it was not uncommon that the Staph A bacteria may continue to infect. It follows that it is reasonable to conclude that the fact that the Staph A bacteria had a continuing role does not establish that the Acinetobacter was not a co-pathogen at the start and a significant cause of the initial infection.
Conclusion
In my view it was more probable than not that the Acinetobacter bacteria did act as a co-pathogen and was causally connected with the development of the infection and the subsequent injuries sustained by the appellant.
The appeal is upheld and the decision of the regulator dated 13 March 2014 is set aside and substituted with a decision that the appellant's claim for compensation is one for acceptance. The matter of costs is reserved.
I order accordingly.
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