The Death of Phar Lap

PHAR LAP DIED AT around 8.30am (Australian Eastern Standard Time) on April 6, 1932. This was around 2.30pm on April 5 in San Francisco, where the death occurred. For the next 68 years there was much conjecture as to the cause of the great horse’s death, until Peter Thompson and I released our biography, Phar Lap, in which we demonstrated that the cause of death was almost certainly a bacterial infection known as Duodenitis-Proximal jejunitis.
 
In 2006, a new argument was put that Phar Lap had succumbed to arsenic poisoning. This theory received much coverage, even though Phar Lap did not show the signs of a horse suffering from arsenic poisoning in the last 24 hours of his life and the champion’s post-mortem specifically ruled out arsenic as a possible cause of death.
 
Since then, there have many claims made that Tommy Woodcock was to blame for the wonder horse’s death.
 
This is wrong ...
 
 
THE VRC HANDICAPPER GAVE Phar Lap 10.10 (68kg) for the 1931 Melbourne Cup, which meant he would have smashed Carbine’s weight-carrying record had he won. However, he finished eighth as a 3-1 favourite. It was the first time the champion had started at odds that generous since September 1929, and the first time since February 1930 he’d finished worse than second in a race.
 
By Cup Day 1931, Phar Lap was a tired horse. Soon after, however, he was on a boat to New Zealand, on to California, and then down the long road to the Agua Caliente racetrack situated just on the southern side of the US–Mexican border. There, in the rich Agua Caliente Handicap, Phar Lap produced one of his greatest performances, sitting four or five wide until he took off five furlongs from home to win by two lengths. That one win was enough for some US racing historians to rate Phar Lap one of the greatest horses to race in North America.
 
Sixteen days later, Phar Lap was dead, in what many thought to be sinister circumstances. For 68 years, from 1932 to 2000, one of Australia’s enduring legends was that the great champion had been poisoned. He had lived a heroic life and Australians wanted to believe that he was extraordinary. When the famous racecaller Bill Collins described the finish of the 1986 Cox Plate with that wonderful phrase, ‘Bonecrusher races into equine immortality,’ he eloquently captured how we feel about our best-loved stars of the turf. Thus, when Phar Lap’s mortality was so tragically confirmed and remained unexplained, we had to believe that something sinister had occurred. Ignorance of bacteria and how they worked made it easy to blame the dark forces of evil that we knew ran amok in that crime-ridden society of North America.
 
In 2000, when Peter Thompson and I published our findings about the actual cause of death — a humble bacterial infection whose existence was unknown until 1982 — it was widely acclaimed as the solution to the mystery. Six years later, when scientists discovered two forms of arsenic in some hair from Phar Lap’s mane, sensationalists in the media and opportunists in politics resuscitated the prejudices of the past.
 
‘Australia’s greatest racehorse, the mighty Phar Lap, may solve the mystery of his own death,’ was how the then Minister for Innovation in Victoria, former premier John Brumby, began a media release in October 2006, ignoring the fact that in our book we had put forward a compelling case that the cause of death was a common bacteria, which produced an enterotoxin that caused a disease syndrome known as Duodenitis-Proximal jejunitis. Mr Brumby was alluding to analysis that was being undertaken using synchrotron technology, which had revealed traces of arsenic in hairs from the stuffed hide of Phar Lap — the famous exhibit at the Melbourne Museum. In June 2008 further analysis allegedly ‘proved’ Phar Lap died of arsenic poisoning, a contention that was again argued in an article published in the journal Angewandte Chemie in April 2010. However, in that article the authors conceded that ‘many complexities in the analysis (and interpretation of results) of arsenic in hair exist’. They also contended that Phar Lap’s symptoms and autopsy results ‘are consistent with ingestion of a large dose of arsenic just prior death’.
 
 
THE SYNCHROTRON ANALYSIS DETERMINED that arsenic found in the shaft of the hairs from Phar Lap’s mane had not been used in the taxidermy process. By making assumptions about the rate of growth of the hair, estimations were made that the horse ingested this arsenic anywhere between 10 and 40 hours before his death. From this came the superficial and hysterical reaction: ‘Arsenic is bad, there was arsenic in his system, so arsenic killed him.’
 
But there are alternative explanations for the arsenic found in Phar Lap’s hide, none of which carry a sinister undertone. It is true, for example, that hair absorbs substances via the blood supply to the follicle, but as research on other taxidermied museum specimens shows hair can also absorb arsenic from the environment. Dunnett and Lees, in a paper published in Research in Veterinary Science in 2003, proved that external contamination can cause the incorporation of drugs into all parts of the hair, including the follicle. The original theories about arsenic poisoning being the cause of Phar Lap’s death came about because trees adjoining the paddock in which he had been grazing were sprayed with a pesticide containing lead arsenate; there were fears that Phar Lap had eaten grass onto which the pesticide had fallen, and that this was his undoing. The autopsy refuted this notion, but it is still possible some or even most of the arsenic in Phar Lap’s hair came from the pesticide spray landing on Phar Lap’s skin and being absorbed into his hair, without causing him harm. Several other animals in the same paddock with Phar Lap were unaffected by that ‘contaminated’ grass.
 
It is also well recognised that the nature of hair, even its colour, can affect the amount of arsenic taken up from the blood supply and from the environment. Other variables include the rate of take-up from the blood and the pace of growth of the hair. So conclusions about how much arsenic Phar Lap had ingested, or when he had ingested it, must remain vague at best.
 
But for those so easily convinced arsenic was the culprit, the next question was obvious: ‘How was the great horse poisoned?’ And the most popular answer in the media was that Tommy Woodcock did it. For example, on June 19, 2008, the Melbourne Age reported: ‘It was probably strapper Tommy Woodcock who may have mistakenly put too much arsenic in one of his tonics for his beloved Phar Lap.’
 
Similarly, Agence France-Presse stated: ‘The latest theory surrounding Phar Lap’s demise was that the strapper that accompanied the gelding to the United States, Tommy Woodcock, used too much arsenic while making up a batch of tonic and accidentally killed his charge.’
 
At the same time, an old notebook, which once belonged to Harry Telford and contained a series of recipes for tonics, some of which included arsenic, was found (and then purchased by Museum Victoria for a reported $37,000). This was used as more evidence of Woodcock’s guilt, even though it is common knowledge that most trainers of the 1930s safely used arsenic-based tonics; some trainers were still doing so as recently as the early 1980s. To compare the amount of arsenic in such tonics against that needed to kill a thoroughbred is akin to comparing a test tube to a bucket.
 
 
CRUELLY, THE PEOPLE ACCUSING Tommy Woodcock of making a colossal, grievous and stupid error never stopped to think there are alternative explanations for the synchrotron’s findings. Much worse, they did not consider the known and unchallenged facts: that at the time of Phar Lap’s death, university experts specifically searched for evidence of arsenic poisoning and could only find small amounts, more likely to be beneficial than detrimental to the horse; and that the clinical signs and progress of Phar Lap’s rapidly deteriorating condition were a text book presentation of Duodenitis-Proximal jejunitis and entirely inconsistent with arsenic poisoning.
 
First, the clinical signs. In 2001, Dr Stan Casteel, Professor in Research Toxicology at the University of Missouri-Columbia in the United States, published a paper entitled Metal Toxicosis in Horses in which he wrote, ‘Clinical signs of acute inorganic arsenic toxicosis in horses include drooling, trembling, ataxia, depression, colic, recumbency and green-to-black watery diarrhoea.’ Six years later, Dr Sally Church, a senior lecturer in equine medicine and surgery at the University of Melbourne, told Graeme Putt, co-author with Pat McCord of the 2009 book Phar Lap: the Untold Story, that acute severe arsenic poisoning in horses is reported to cause severe haemorrhagic diarrhoea.
 
It is a natural reflex, when a horse is sick, for a veterinary surgeon to examine the horse’s droppings. According to Tommy Woodcock’s account, in the hours before Phar Lap died, the champion’s vet, Bill Nielsen, did so and then stated, ‘Gee, he don’t seem bad.’ This strongly suggests Phar Lap was not suffering from any form of diarrhoea.
 
Even more importantly, all reported cases of arsenic poisoning in horses are consistent on one critical point: the time from the appearance of clinical signs to death is always a minimum of 24 hours.
 
Woodcock slept in the stall opposite Phar Lap. When he went to sleep on the night of April 4 1932, the horse was okay. The next morning, Phar Lap’s breath was hot, he was sweating and he wouldn’t accept the sugar cube Woodcock offered him first thing every sunrise. Not long after 2 pm, just nine hours later, the great horse was gone. This would not have been enough time for arsenic poisoning to have killed the champion.
 
Four days after his death, Phar Lap’s organs were examined by chemists from the University of California, who tested for a number of poisons. They specifically analysed samples of liver, lung, spleen, stomach and kidney, searching for ‘common volatile poisons, alkaloidal poisons, arsenic and mercury’, and claimed afterwards that they found nothing untoward.
 
In Phar Lap, The Story of the Big Horse, published in 1964, Isobel Carter reports the findings of R.U. Bonnar, a chemist with the United States Food and Drug Administration. Bonnar examined Phar Lap’s organs in advance of the post-mortem and found the concentration of arsenic trioxide in Phar Lap’s liver was 1.143 parts per million, less than one-eighth of the concentration required to diagnose arsenic poisoning of a horse.
 
On the basis of what he had seen as Phar Lap died and then during the autopsy, Bill Nielsen initially suspected that the cause of death was acute gastric enteritis (inflammation of the intestines), brought about by a toxic substance, but because he and others couldn’t identify what that toxin was, in the years that followed observers and gossip merchants were left to concoct their own poisons. For our book Phar Lap, we sought the advice of Dr John van Veenendaal, one of Australia’s leading equine surgeons. Dr van Veenendaal, a man who has worked for many of the country’s leading trainers and who treated some horses trained by Tommy Woodcock in the late 1970s and early 1980s, was shown the post-mortem reports of Phar Lap’s death. In response, he stated:
 
‘Phar Lap did die of poisoning but not a poison that was given maliciously or intentionally. The poison was an enterotoxin that caused Anterior Enteritis or more correctly Duodenitis-Proximal jejunitis. The clinical features that Tommy described to me and the reports you have supplied me with indicate that this was the most probable cause of death ... The disease syndrome now known as Duodenitis-Proximal jejunitis was not described in the literature until the early 1980s. Nielsen would not have been aware of this disease but his summation of the cause of death was correct.’
 
In 2008, after the synchrotron analysis made the papers, we sent copies of all the information we had on Phar Lap’s death, including the post mortem and the published reports from the team behind the synchrotron analysis, to Dr Tam Garland from Texas A&M University and the American Board of Veterinary Toxicology. Her response in part reads:
 
‘I do not believe arsenic was involved. There may be a background level or a very low level from some solutions in use then. I am convinced the cause of death was Duodenitis-Proximal jejunitis …’
 
Veterinary surgeons today know that horses can be quickly killed by Duodenitis-Proximal jejunitis. Bacteria in the gut of the horse produce a toxin that attacks the lining of the small intestine close to the stomach, causing a functional obstruction. The walls of the small intestine are severely damaged and acutely inflamed. The intestine is blocked, not by a physical barrier but by a length of intestine that refuses to function
 
The textbook description of Duodenitis-Proximal jejunitis is a list of the signs Phar Lap exhibited before his death: elevated temperature, increased pulse rate, acute colic, distention of the small intestine, a build-up of fluid in the stomach leading to perforation and rapid death. In almost all cases of Duodenitis-Proximal jejunitis, the horse has travelled significant distances in the preceding weeks. The fact that the disease was not identified until 50 years after Phar Lap’s died is important. Those performing the autopsy in 1932 would have looked first for a physical blockage in the intestine, and were probably astonished when they did not find one.
 
Only then would they have joined others in thinking seriously about less logical causes of death.

---