WCRA: Rooster Booster & causation for pneumococcal meningitis, encephalitis and septicaemia

Cowen v Bunnings Group Limited [2014] QSC 301

The plaintiff claimed against her employer Bunnings for her exposure to opened bags of Rooster Booster chicken manure. The bags of fertiliser had broken and the contents, which were ordinarily moist became dusty in the exposed sunlight and heat. The plaintiff was required to clean up the open bags, sweep, dust and repackage the bags. By the end of doing the task the plaintiff was covered in the manure dust. The exposure initially caused watery eyes, sneezing and coughing. The plaintiff  went home and subsequently developed headaches. The plaintiff went to bed and come to work the following day and subsequently collapsed and was taken to hospital, where she went into a coma a developed with pneumococcal meningitis, encephalitis and septicaemia.

Damages were agreed at $700,000 clear of the refund to WorkCover Queensland.

Wilson J:

[8] Bunnings admits a breach of its duty of care to Ms Cowen as her employer, and that it was foreseeable that the work she performed on this occasion might cause her some injury.

[9] Bunnings denies, however, that its breaches caused Ms Cowen’s serious illness which, it says, was simply coincidental with the work she did that day. Other causes – a pre-existing respiratory illness, smoking, the presence of atmospheric sulphur dioxide in Mt Isa (or some combination of these factors) – are, Bunnings says, at least equally likely to have caused the illness. Those other possible causes mean, Bunnings argues, that Ms Cowen cannot prove that it is more probable than not that her exposure to Rooster Booster dust was causative. That, it happens, is the question upon which the case turns.

[10] The physical process by which Ms Cowen came to develop her illness is not in dispute. It is common ground that the illness was caused by a streptococcus pneumoniae, and that she presented with a severe manifestation of infection with that organism. The likely course initially involved the colonisation, by this bacterium, of Ms Cowen’s upper respiratory tract – a very common event, such that 10-40% of the population have a similar colonisation at any given time. What made her condition dangerous was the relatively rare event that the bacterium descended into her lungs and thence, via her bloodstream, to her meninges and brain, and made her very ill.[5]

[11] As her case is pleaded she accepts that, before she began cleaning up the fertiliser, the offending bacterium was already colonised in her upper respiratory tract. Its presence is plainly probable, in light of the subsequent nature and progress of the illness she developed. Secondly, she alleges that the dust she inhaled caused irritation of her respiratory tract mucosa, and that irritation lead to the introduction of the bacterium into her blood stream, and brain. Thirdly, she alleges that this process lead to her severe illness.

[12] Neither the defendant nor any of the expert medical witnesses called in the case dispute the first proposition: i.e., that the bacterium was present in Ms Cowen’s upper respiratory tract when she did the work of cleaning up the fertiliser dust. Nor is there any dispute that once the bacterium reached her blood stream, and then her meninges and brain, she became very ill with the disease which required her admission to hospital, and intensive care there.

[13] Rather, it is the second part of the process – what it was that caused the bacterium to travel from her upper respiratory tract to her bloodstream and, thence, her brain – which is in issue. Was it caused by her exposure to the dust or was it coincidental, with other possible causes outweighing or negating the possible effects of the dust exposure such that it cannot properly be categorised as causative, in law?

[14] Four eminent medical specialists gave evidence upon the point. Three are consultant physicians specialising in infectious diseases, and the fourth is a thoracic physician specialising in respiratory and sleep disorders. Two, Drs Clarke and McCormack, thought there was a causal connection on the balance of probabilities; the other two, Drs Mitchell and Bartley, agreed it was ‘certainly not implausible’,[6] but were not persuaded to a level which would allow them to concede causation on the ‘probability’ test.

[15] In undertaking that exercise the medical practitioners were applying a legal test, not one that was scientific in the traditional sense or of a kind usually associated with epidemiology (which is the study of the incidence and distribution of diseases, and of their control and prevention). That implies no criticism of the doctors – they were invited, by the lawyers, to undertake the exercise and proffer an opinion.

[16] The scientific approach to causation, using what the Macquarie Dictionary calls the ‘scientific method’, customarily involves the identification of a problem; the collection of relevant data; the formulation of a hypothesis on the basis of this data; and, finally, empirical testing of the hypothesis to prove its validity.

[17] As Spigelman CJ observed in Seltsam Pty Ltd v McGuiness & Anor,[7] a number of well-known High Court decisions[8] show how, and why, the way the common law approaches causation is quite different from accepted, and customary, scientific methods. He said:

The common sense approach to causation at common law is quite different from a scientist’s approach to causation …. An inference of causation for the purposes of the tort of negligence may well be drawn when a scientist, including an epidemiologist, would not draw such an inference.[9]

[18] The task confronting a court, adopting this legal approach to causation, had earlier been explained by Mahoney JA in Fernandez v Tubemakers of Australia Ltd:[10] medical science may say in individual cases that there is no possible connection between the alleged causative event and the injury, and in that event the court cannot act as if there were a connection; but, if medical science is prepared to say the connection is possible then it is up to the court to decide if it is probable, to the requisite degree.[11]

[19] This emphasis in the law of tort upon the process of making findings about causation based upon degrees of probability rather than scientific precision has a long and respectable pedigree. As Dixon CJ and others[12] explained in Ramsay v Watson,[13] a medical expert may express an opinion as to the nature and cause, or probable cause, of an ailment, but it is for the jury to weigh and determine the probabilities; and, in undertaking that exercise, the Court is not to transfer the task to the experts but, rather, to ask itself: ‘Are we on the whole of the evidence satisfied on a balance of probabilities of the fact?’.[14]

[20] So it has been said, for example, that a finding of a causal connection may be open even if there is no medical evidence to support it,[15] or when the medical evidence does not rise above the opinion that a causal connection is possible.[16]

[21] More recently the High Court again both explained this approach to causation, and confirmed its continuing validity, in Tabet v Gett.[17] Kiefel J (with whom Hayne, Crennan and Bell JJ agreed) said that the purpose of proof at law, unlike science or philosophy, is to apportion legal responsibility – and that requires the courts, by a judgment, to ‘reduce to legal certainty questions to which no other conclusive answer can be given’.[18]

[22] Earlier, Kiefel J had spoken of the way the courts undertake this exercise. The common law, her Honour said, requires proof by the person seeking compensation that the negligent act or omission caused the loss or injury constituting the damage; but all that is necessary for that purpose is for the plaintiff to show that, according to the course of common experience, the more probable inference arising from the evidence is that the defendant’s negligence caused the injury or harm. ‘More probable’ means, she said, no more than that upon a balance of probabilities such an inference might reasonably be considered to have some greater degree of likelihood. But it does not, as Kiefel J emphasised, require certainty.[19]

[37] The absence of any support in the medical/scientific literature is also not determinative. It does suggest that this event, if it occurred, was unusual and may have been rare or, even, surprising and unanticipated. That is, again, a material factor in determining causation but it is not determinative.

[38] As Spigelman CJ observed in Seltsam, the legal concept of causation requires the court to approach the matter in a distinctly different manner from that which may be appropriate in either philosophy or science, including the science of epidemiology.[25] The fact that medical science has not recorded a similar course of infection does not mean that it has not happened – or, importantly for present purposes, in a case where there is medical evidence indicating it is on one view quite possible and, on another, that it is not impossible or implausible, that it could not have occurred.

[39] The compelling features pointing to a causal connection are, firstly, the strong relationship in time between one event, and the other. The second is the nature of the material to which the plaintiff was exposed and the duration of exposure which, on any view, was serious and unpleasant and, in particular, caused immediate and prolonged upper respiratory tract symptoms. Dr McCormack thought the temporal connection weighed against coincidence, and that is also, again compellingly, the common-sense conclusion. The absence of similar examples in the literature cannot mean, as Drs Mitchell and Bartley had to concede, that the internal physical process he postulated is improbable or, in their words, implausible.


[66] This is a case in which the plaintiff suffered a serious illness shortly after a severe exposure to dust which, I am satisfied, led her to develop symptoms which can instigate the internal physical process of infection accepted by two of the four medical experts called in the case as providing an explanation for her subsequent serious illness.

[67] While the event is unusual, the close relation in time between exposure and the development of the illness means that explanation accords with common sense and provides an acceptable causative pathway, according to the appropriate legal test.

[68] While other causes had been advanced as possibilities, one (a pre-existing illness) is exploded by the evidence, and all the others involve such a high degree of coincidence – and, indeed, awfully bad luck – that they are considerably less plausible, to a degree which means that the attribution of causation to them would, with respect to the doctors, defy common sense.

[69] The plaintiff, for these reasons, must succeed in the case and have judgment against the defendant.


David Cormack – Brisbane Barrister & Mediator

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