KA-2024-BHM-000008 - [2025] EWHC 2093 (KB)

The judge’s review of the expert evidence

On 6 September 2016, the Appellant presented at her GP with a history of diarrhoea. On 7 September a regional laboratory reported a finding of cyclospora oocytes in her stool sample. Seven days later, the national reference laboratory (at the National Hospital for Tropical Diseases) carried out a second test. No cyclospora oocytes were found, and the national reference laboratory concluded therefore that cyclospora was not present in the stool sample.

Dr Bowling, the Appellant’s expert gastroenterologist, said:

“Stool samples in the UK identified cyclospora. Given this result, it is highly unlikely that the claimant’s gastroenteritis was caused by an unrelated pathogen. On the balance of probabilities, the enteritis was caused by cyclospora.”

Though Dr Bowling took the view that on the balance of probabilities the Appellant’s illness was caused by cyclospora acquired in Mexico, he deferred entirely to the microbiologists. Dr Bowling was unable to assist with when it is that patients present with symptoms of cyclospora as very few people present with cyclospora in clinic. The relevance of this last observation was that it had been contended by the Respondent that most people who ingest cyclospora do not show symptoms until a number of days afterwards. The Appellant had first shown symptoms on her third day in Mexico.

Professor Bjarnason, the Respondent’s expert gastroenterologist, said, “It is impossible to be dogmatic about the precise cause of this case.” Professor Bjarnason said,

“We agree many aspects of this illness are described (inaudible) Ms Rawson to cyclospora that she acquired the infection on the balance of probability in Mexico during the holiday and that she has developed IBS.” [My guess is that the missing word is something like “link”]

Professor Bjarnason pointed out that the symptoms appeared three days after the Appellant’s arrival and said that very few patients indeed would be symptomatic of cyclospora infection within three days of arrival. He said that it was possible that the Appellant’s original symptoms on 11 July were caused by any of the other 30 or so enteropathogens that cause travellers’ diarrhoea.

Professor Bjarnason said that in his first report he had accepted the presence of cyclospora in the stool sample, but that he must have missed the second laboratory report, because, if he had read it, he would not have accepted the presence of cyclospora.

The joint statement of the gastroenterologists said that it was agreed that stool microscopy described cyclospora oocysts (i.e oocytes) in the Appellant’s stool, though it was noted that the stool sample was submitted six weeks after the Appellant’s return from Mexico.

Professor Threlfall, the Appellant’s microbiology expert, said that, on the balance of probabilities, he considered it extremely likely that the microbiological cause of the Appellant’s illness was an infection of cyclospora, which was contracted whilst she was a guest at the hotel, and within 48 hours of arrival.

Professor Threlfall addressed the fact that the regional laboratory had recorded cyclospora oocytes in the Appellant’s stool sample, but the national reference laboratory did not. He said:

“The sample tested by the reference laboratory was reported as normal, no action. It should be realised that testing for cyclospora is notoriously difficult. At the time of the claimant’s illness, the most common method for testing for the presence of cyclospora was concentrate microscopy, where the presence of only a small number of oocytes or even a single oocyte is regarded as indicative of cyclosporiasis [the disease caused by cyclospora]. The test undertaken by the reference laboratory and referred to by the solicitors for the defendant were similarly concentrate microscopy. Thus, a negative result as recorded by the reference laboratory is not necessarily absolutely confirmatory evidence of what has been described as a false positive.”

Professor Threlfall suggested that the second sample, seen by the national reference laboratory, could have deteriorated over the seven days [in fact it was nine days] between the regional test and the national test.

Dr Gant, the Respondent’s microbiology expert, was the Clinical Director for Infection at the Hospital For Tropical Diseases at UCLH NHS Foundation Trust. This is the UK’s specialty referral hospital for infectious diseases acquired abroad. The Hospital For Tropical Diseases contains the national reference laboratory to which the Appellant’s stool sample was taken. He did not agree that the evidence showed that the Appellant had been infected by cyclospora. He dealt in his report with the fact that the regional laboratory had recorded cyclospora oocytes in the Appellant’s stool samples, and the national reference laboratory had not, as follows:

“Because laboratory technicians around the UK are not highly experienced in detecting cyclospora, UK public health authorities have designated a national reference laboratory in each country. The National Reference Laboratory for England is the Hospital for Tropical Diseases, where staff have specific experience and training in identifying the organism. The stool sample provided by the claimant was, on the balance of probabilities, one of those false positives; the local lab thought they had seen it but the more experienced lab did not identify cyclospora.”

Dr Gant did not agree that the sample would have deteriorated and become free of cyclospora oocytes between the first test and the second. He said:

“This is speculative and highly unlikely from a biological perspective, as oocytes will remain detectable in a stool sample for extended periods of time, far exceeding the time elapsed in confirmatory testing by the reference laboratory.”

Dr Threlfall said in evidence that the regional laboratory would test for oocytes via concentrated microscopy, whereas the national reference laboratory would use an extenuated stain system. He accepted that the national reference laboratory was the gold standard. Dr Threlfall said that he would defer to Dr Gant’s testing experience. Dr Threlfall also accepted that there were no academic papers to support the theory that a stool sample could degrade, in the sense that cyclospora oocytes which were previously there would disappear, in seven days.

The judge said that, in his evidence, Dr Gant said that there were no antibodies for the cyclospora, and that the fluorescing was naturally occurring and not relied upon antibodies to do so. He said that the national reference laboratory is the gold standard for the test of this type, and agreed in cross-examination that the regional laboratory was justified in treating the test results as a probable cause of cyclospora and that the NHS were right to likewise treat it as a probable cause of cyclospora. At the very end of his cross examination, when being pressed as regards whether cyclospora was the probable cause, Dr Gant said:

“So it’s epidemiological, it’s to do with pragmatism, limited resources, and it allows for definition to be put in place, and it’s probable and you’re right that’s how it is. So for the court that is what the particular specimen or this particular case might be described as.”

In re-examination, however, the judge said that Dr Gant clarified that last remark and he said that what he was saying was that on the papers there was a probable finding of cyclospora oocytes, but not once a full examination of all the features of the case were taken into account.

I interrupt my review of the judge’s findings to say that I will return to what was said by Dr Gant on this issue in cross-examination and in re-examination, because it was a central plank of Mr Pennock’s submissions that Dr Gant had conceded in cross-examination that the court should proceed on the basis that the probable cause of the Appellant’s illness was cyclospora, and so the Respondent’s own microbiology expert had conceded that, on the balance of probabilities, the cause was cyclospora. That was why Mr Pennock had stopped his cross-examination there: he took the view that the case was effectively won, as the Respondent’s key witness had accepted that the cause was cyclospora, and such a finding meant that, in reality, the causation issue would also be resolved in the Appellant’s favour. Mr Pennock further submitted to me that, properly understood, the answers given by Dr Gant in re-examination did not resile from this concession. Mr Saxby submitted that this was a misinterpretation of Dr Gant’s evidence. I will deal with these submissions when I deal in turn with the grounds of appeal.