Volume 3: The Early Years, 1986-88
1. The identification of a new disease in cattle
The earliest confirmed case

1.7 The earliest case of BSE to be confirmed by the CPU was a cow owned by Mr Peter Stent of Pitsham Farm in Sussex (Cow 142). Brain samples from Cow 142 were first examined in September 1985. It was not, however, until June 1987 that Mr Gerald Wells, on review of the archives of the Pathology Department, confirmed this as a case of BSE.

1.8 The pathologist who carried out the original examination of the brain of Cow 142 from Pitsham Farm was Ms Carol Richardson. She told the Inquiry that she identified pathological changes in the brain as 'scrapie in a cow' and that colleagues at the CPU confirmed her diagnosis. This evidence conflicts with that given by other members of the Pathology Department, who said that BSE was first identified as a likely transmissible spongiform encephalopathy in cattle at the end of 1986. Ms Richardson's evidence has led to allegations in the media that MAFF became aware of the emergence of BSE in September 1985 and concealed this fact for over a year. The resolution of this issue calls for a detailed analysis of the evidence.

1.9 On 22 December 1984 Mr David Bee, a local private veterinarian, was called to examine Cow 133, owned by Mr Peter Stent of Pitsham Farm in Sussex. She had an arched back and had lost weight. ¹ Mr Bee visited the farm on several further occasions over the following months, and continued to see animals showing unusual symptoms. ² Cow 133 developed a head tremor and a lack of coordination before dying on 11 February 1985. ³ Mr Bee sought assistance from Mr J M Watkin-Jones, a veterinarian at the Winchester VIC.

1.10 By the end of April 1985 five more cows had died on the farm. Mr Bee and Mr Watkin-Jones coined the phrase 'Stent Farm Syndrome' to describe these cases. ⁴ A number of samples of body tissue were submitted to the CVL for pathological analysis. Various possible ailments were identified, but despite a wide range of tests no definite diagnosis proved possible. It was suggested that Mr Stent submit a live affected cow for slaughter and post-mortem. ⁵

1.11 Later in the summer of 1985, Mr Stent had two live cases of this apparent 'syndrome'. The first of these cows was sent for slaughter on 1 August, with the head and other tissues being sent on to the local VIC. Unfortunately, the brain of this animal had no diagnostic value as it had been slaughtered by being shot in the head. ⁶ The second animal, Cow 142, was sent live to the CVL on 2 September for euthanasia and a post-mortem examination. ⁷

1.12 Carol Richardson, the pathologist on duty at the CVL, received the samples of brain, spinal cord and kidney of Cow 142 on 10 September, and examined them on 13 September. ⁸

1.13 Ms Richardson recorded her observations on a Case Card (Form DL99). The case history recorded that Cow 142 was said to be typical of seven cows on the Stent farm over the previous five months, which were described as 'nervous'. ⁹ She transcribed her comments from the Case Card onto a Pathology Report dated 19 September 1985, addressed to Mr Watkin-Jones. They were as follows:

PATHOLOGY REPORT

Gross observations: Received in formalin a well preserved bovine brain, 2 pieces of spinal cord and pieces of kidney all grossly normal.

Microscopic observations:

Cerebrum - mild multifocal (4 foci) non-suppurative perivascular infiltration and focal gliosis.

Thalamus - NVL

Cerebellum - NVL

Corpora quadrigemina - mild neuropil vacuolation

Medulla - moderate neuronal and neuropil vacuolation of the reticular formation

Spinal cord - mild neuropil vacuolation of the lumbar dorsal horns.

Kidney - chronic mild/moderate non-suppurative interstitial reaction with tubular regeneration and fibrosis.

Also a mild peracute multifocal tubular necrosis with focal hyaline droplet change.

DIAGNOSIS:

1. Moderate spongiform encephalopathy - acute

2. Mild renal nephrosis - peracute

REMARKS: These acute changes suggest a toxicity of some description. The non-suppurative reactions are far more chronic, mild and non-specific. ¹⁰

1.14 Ms Richardson's Pathology Report was sent to Mr Watkin-Jones at the Winchester VIC on 19 September 1985, who forwarded the report to Mr Bee, Mr Stent's vet, with this comment:

I enclose a histological report carried out by my colleague Carol Richardson. I have discussed her findings with her at some length and she comments that the pathological changes found would be consistent with bacterial toxin. ¹¹

1.15 As to this comment, Mr Bee remarked in his statement to us:

I recall my disbelief at this statement at the time. I believed the problem had been associated with fungal contamination of feed and mycotoxin production. On 4/10/85 we received a laboratory report stating that a fungal toxin called citrinin had been found in the feed. In any case, by this time, new cases had ceased to develop. I imagined that the problem had run its course. ¹²

1.16 When giving evidence, Ms Richardson was categoric that she did not discuss Cow 142 with Mr Watkin-Jones. ¹³ Nor would she have ascribed the pathology that she saw to bacterial toxins. She would have expected bacterial toxins to result in neuronal necrosis. ¹⁴ In her written statement to the Inquiry Ms Richardson said:

Although I had never seen this type of lesion before in a cow I had frequently seen the combination of neuronal and neuropil vacuolation with this distribution in Scrapie. To me, this was Scrapie in a cow. ¹⁵

1.17 She went on to explain her diagnosis:

From the history of the case on the Stent farm, it seemed as if the clinical course of the disease was fairly rapid in that metabolic disorders of short duration and heavy metal toxicities were being considered on the farm. Therefore, it seemed likely that the cause(s) of the spongiform changes were a result of an acute clinical disease (rather than a chronic illness) and in the absence of a more likely aetiology, toxicity seemed to be the most appropriate category that fitted both symptoms and findings.

I dismissed the possibility that a bacterial toxaemia had caused the spongiform change; in my limited experience of ruminant neuropathology, toxaemia was likely to produce frank neuronal necrosis rather than degenerative vacuolation (cf. Clostridial toxaemia). ¹⁶

1.18 Ms Richardson added that she sought a second opinion from a ruminant neuropathologist colleague, Dr Martin Jeffrey, before writing her report on 19 September, leaving the brain sections, her findings, and a request for a further examination, on Dr Jeffrey's bench. 'I was eager to hear his opinion and immediately after lunch went to collect the slides. Martin had left a note on which was written "Bovine scrapie".' She met Dr Jeffrey as she left the room. Dr Jeffrey told her this was the first case that he had seen, but that Mr Wells, Head of the CPU, had examined two cases, and was expecting another two cases. ¹⁷

1.19 When giving oral evidence to the Inquiry, Dr Jeffrey said that he had no recollection of the discussion of the samples that Ms Richardson left for him. It was not uncommon for a pathologist to leave samples for a colleague to look at, but he did not recall this discussion or the leaving of a note stating 'Bovine scrapie'. Further, he did not remember mentioning that Mr Wells had two earlier cases of a similar condition. He added that there had been searches of CVL archives, and that these cases did not exist. ¹⁸ He thought that had these two cases been mentioned to him, with the prospect of two more, then it would have stuck in his memory: 'One is a novelty, two is a coincidence, three is a problem.' ¹⁹

1.20 In his written statement to the Inquiry, Mr Wells told us that he was attending a meeting in Cheshire at the time Ms Richardson examined the samples. He said that she had left the samples and a copy of her Pathology Report for him to examine on his return. It was common practice for an examining pathologist to leave sections for a colleague to express a view on. ²⁰

1.21 Mr Wells said that on his review of Ms Richardson's Report:

I agreed with her overall observations and that such observations were not artefactual i.e. caused as a result of post-mortem changes or in the preparation of sections. My conclusion was that the brain lesions observed in this case could not in my experience be attributed to a specific disease, but a speculative comment was made that they could possibly be the result of chronic bacteraemia or an endotoxaemia (the production of poisons in the blood due to infection). ²¹

1.22 Mr Wells made a manuscript note on the foot of Ms Richardson's Report:

. . . lesions probable sequel to chronic bacteraemia or endotoxaemia. ²²

1.23 He was, however, uncertain whether he made that note on the occasion of his first review of her Report. ²³ This was because he reviewed her Report on two further occasions. The second review was on 26 September 1985 when, at Mr Watkin-Jones's request, he reviewed the four casualties on the Stent farm whose samples had been submitted to the CVL. ²⁴ On that occasion he made a note: 'No conclusion drawn regarding common aetiology.' ²⁵ The third review was in June 1987, as part of the review of brain sections in the CVL archives, when he concluded that Cow 142 had been suffering from BSE. ²⁶

1.24 The manuscript note referred to above was but one of a number of annotations made by Mr Wells to the Report, and he could not recollect precisely when each was made. ²⁷

1.25 Mr Wells had no recollection of any reference being made to bovine scrapie. ²⁸ He commented that had Ms Richardson felt strongly that the observations she had made were of scrapie in cattle, he would have expected her to come back to him to discuss the matter subsequently, or to take the matter further herself. ²⁹ For her part Ms Richardson said that she had not sought a second opinion from Mr Wells. ³⁰ She had sought a second opinion from Dr Jeffrey. She had simply left the sections for Mr Wells to look at as she thought he might be interested, having already had two similar cases himself.