interesting that the title of the paper asserts that the contiguous cull did "help eliminate" the epidemic but does not prove it.  Actually, as has been noted by others, since the disease was already in the decline phase, the contiguous cull escalated the crisis.  It eliminated - not the disease - but literally millions of healthy animals and the last remaining vestiges of trust between farmers and MAFF.  All this could have been avoided if the Science Committee had listened to advice from those who understood the disease and the new technologies.
If Professor King were really able to defend the contiguous cull there would be convincing mathematical evidence. That there is not, and that he is left trying to blind us with science, speaks volumes. More eloquent by far are the numbers of healthy, terrified sheep slaughtered in their thousands at Great Orton. And of those thousands 9 animals returned blood tests for the disease that were not negative.

(Paper from the Government's Chief Scientific Adviser, Professor David King, to the Anderson Inquiry

and the scientific review by the Royal Society)

1. Objective

1.1  The overall objective was to bring the epidemic to a close as quickly as possible while minimizing the total numbers of livestock lost.

To suggest that one of the objectives was to minimize the total number of livestock lost is astonishing.  Why then did the CSA and his Scientific Group - being ignorant of foot and mouth -  fail so disastrously to listen to the veterinary and scientific advice of Dr Donaldson and Dr Kitching? These experts from Pirbright  told them all along that their model was flawed and the policy wrong.  More importantly,there were those internationally renowned experts with genuine field knowledge who urged vaccination from the start - but what can only be thought of as deliberate misinformation turned the country against it.

 In order to do this the first task was to bring the epidemic 'under control'. It is important to be able to quantify what is meant by 'under control'. It is the situation where each new case of FMD when introduced into a susceptible (=uninfected) group of animals generates, on average, less than one secondary case. This average (the case reproduction number or ratio) is referred to as the 'R' value. Over time an epidemic with an R value of less than one will eventually peter out. An epidemic with an R value greater than 1 will continue to increase. 

Absolutely right - but what Prof King failed to realise - because he sought the wrong advice - was that he was mistaken about the number of "new" cases

2. Bringing the epidemic under control

2.1 In early March 2001 the R value of the UK FMD epidemic was well above 1, and the epidemic was on an upward curve with the numbers of cases increasing daily.

He is mistaken.  Although the curve appeared to be rising steeply, what it was in fact showing - as will be evident when (if) the data is revealed publically - were previously undiscovered but already incubating pre-movement ban cases - and possibly some cases where, because of disastrously slow slaughter times on already established IPs - the virus was accumulating to such an extent that spread was possible. 

Slaughter times for this epidemic have been well hidden.  For the first 9 weeks of the epidemic 23% only of infected farms were put down within 24 hrs, 63% within 48 hrs. 
On  dangerous contact farms for the epidemic as a whole 4% were slaughtered within 48 hrs, 2% were slaughtered within 48 hrs in the first 9 weeks.  (Source Parliamentary Questions 5479)

The R value was 1.45 during the period before the contiguous cull took place.

This statement is unlikely to be backed up by analysed data - if it is ever made public.  It is now thought that these were not new outbreaks but  pre-ban previously undiscovered ones.  So IPs were not causing new outbreaks except where, as stated above, delays in slaughter times were allowing spread.

The Taiwan epidemic is of significance for the following reasons:- (see paper Howard and Donnelly 2000 )
1. The epidemic was out of control for several reasons - difficulty in stopping markets, no blanket movement restrictions delays in slaughter were up to 12 days, disease wasn't being reported quickly.
2. Simulations showed that had a policy of slaughter within 24 hrs been implemented the epidemic would have been  brought under control within 12 days and would have virtually died out within 26 days.
3. . Wind borne transmission was not thought to be a problem 

 Epidemiological modelling carried out in mid March suggested that action already implemented by MAFF (now DEFRA), ie movement controls, infected premises (IP) culling and dangerous contacts (DC) culling, should have had an effect in reducing the rate of increase in cases.

It did.  The spread of infection was halted by the movement ban, late though it was.  Tried and tested culling methods were working - but not as well as they should have.  Contingency plans were so poor that there were no effective emergency measures to ensure swift stamping out.  What was also obscuring things for the inexperienced modellers and scientists in King's group was that they assumed  that any case after the movement ban was a "new" case rather than one that had a link with a pre-movement ban outbreak - and, most importantly - they failed to realise the significance of the delays in slaughter times. By mid March, 90% of cases were confirmed by "clinical diagnosis" alone, not infallible in bovines and virtually impossible in sheep.  Blood tests (at this early stage clinical diagnosis was tested after slaughter) and analysis of data will reveal that many of these were not FMD at all.  The "rising graph" was misleading.

Improving implementation of these measures during March should have further reduced the rate of increase of new cases. However, analyses show that such improvements alone would have been insufficient to bring the epidemic under control rapidly.

It seems now highly likely that they would have been sufficient.  There was NO big increase in the rate of new cases.  It just appeared to be so.  Animals were incubating the disease since before the ban (or, where slaughter times were allowing a huge increase in virus emission, being infected because of delays in preventing virus plumes to increase)  Animals with lesions developed produce between 100,000 and 500,000 times more virus.  Some unfortunate cattle farmers saw their entire herd infected between the time they reported the first signs to the time that the slaughter teams eventually arrived. The 24 hour target was reached very rarely.  Sheep flocks behaved quite differently from the"sentinel" animals, cattle, with only a very few affected at any one time.  The modellers made no distinction though and based their predictions on the likely spread to a hypothetical animal.


Part of the reason for this is that best estimates show that the fraction of DCs actually incubating FMD was not high.

This sentence appears to be saying that Dangerous Contacts hardly ever got infected - a fact borne out by the testing that was done.

Therefore, relying on IP+DC culling would have resulted in a larger epidemic and more livestock being lost.

This sentence does not make sense. There is no logical link here.

In other words, a larger epidemic would have occurred than that arising if further control measures had not been added to the existing policy.

The idea that more animals would have been killed if fewer animals had not been culled on contiguous premises is gobbledegook.  Can Professor King really imagine that anyone reading this will accept such a notion?  He is attempting to say that the policy of killing animals in big swathes around IPs worked - but what testing was carried out shows that contiguous premises themselves were very rarely - if ever - actually infected, except in Cumbria where the disease had evidently taken a strong hold before any tried and trusted policy was put into operation.


It was concluded, based on detailed epidemiological modelling, that the introduction of contiguous premises (CP) culling would bring about a more rapid decline in the incidence of new cases and significantly reduce the total numbers of livestock lost over the course of the epidemic.

He is repeating what he said above.  It still does not go any way to prove that the contiguous cull was justified but merely says again what he would like to have been the case.

2.2 However, the models themselves are simply a means of expressing the underlying basis of the effectiveness of the policy. The principles are as follows. Animals exposed to FMD infection themselves generally become infectious before the appearance of signs, although they become significantly more infectious around the time they display clinical signs. There is, inevitably, some further delay before the signs are observed and reported, during which time the animals are highly infectious. 

This states the blindingly obvious.  What it does not do is justify the contiguous cull  - which would have been effective only  if the premises surrounding the infected ones were at real risk.  The fact is that they were not.  Transmission of FMD is not like the dispersal of pollen, alighting on anything within a given radius.  FMD, as the Pirbright experts were at pains to point out,  has very limited airborn spread.  Animals do not go visiting neighbouring farms and rub noses with each other.  They remain in flocks and herds on their farms.  Testing and monitoring, as recommended by the Northumberland report, should have been quite sufficient.
2.3 The timing of clinical signs and increase in infectiousness depends on species, including livestock susceptibilities and excretion profiles, the mechanism of virus emission and survival, local topography and husbandry practises (sic). However, despite these variations, the general argument is robust.
Prof King is here hoping to pre-empt the criticism , already stated above, that the modellers' error in distinguishing the relative infectivity of the animals concerned was a grave one.
Removing animals in the early pre-clinical stage of infection removes them as a potential source of further infection.
No one would deny that this is true - but the modellers and the Science Group made some erroneous assumptions about the probablitity of animals on contiguous premises being in the early pre-clinical stage of infection.  They would like it to have been so in order to justify their policy perhaps but the experts in the disease argue that this strain of virus simply did not travel in new ways.  It was classic FMD and could have been controlled by 24 hour slaughter with the addition of testing and monitoring of dangerous contact premises.
It would be very helpful to have a test which could diagnose FMD in animals which are incubating but not showing symptoms, which is fast enough and reliable enough to allow their removal before the infection passes to other farms. However the use of such tests would mean testing a relatively large number of animals, ie until clinical signs appear, given there is no guidance as to which animals to sample.
An extraordinary statement, given what we know about the disease.  Professor King is saying that it was easier to guess and kill millions rather than test and monitor around the Infected Premises.  Had resources been concentrated on testing to ensure that an IP really did have (and two thirds approximtely did not) then the testing of dangerous contacts would have been perfectly feasible. 
Of course, the tragedy is that he himself was offered the Rapid Diagnosis Real Time PCR on-site test (he told the EFRA committee about this on April 25) but it was thought advisable not to use it for reasons best known to himself and perhaps to HMG.
Moreover, suitable tests have yet to be fully developed. An alternative means of identifying farms which may be incubating FMD has therefore to be used.
So they trusted a model, based on the spread of a human sexually transmitted disease, with data that even Professor Anderson has said was "appalling" in which a hypothetical animal was the supposed "at risk" species.  Locations were taken from three different and not compatible databases and out of date post codes were also fed into the model.

2.4 Analysis has shown that some 30% of new cases of FMD were found within 1 km of previously infected premises, and 70-80% within 3km. (This is based on statistical evidence from the recorded cases and does not rely on establishment of a causal link between cases, since we still do not know the transmission routes of the virus in this outbreak. Nor does it rely on the mathematical modelling.)
Professor King does not define "new cases" here.  Does he refer to cases that were blod tested and shown to be positive? If so, the data would seem to have been taken from Cumbria, the area where the greatest number of genuine cases were found.  To suggest that this analysis holds true for the rest of the country is misleading. 
 Therefore culling of susceptible animals on contiguous premises removed a significant proportion of cases which had yet to be identified (because the animals were not showing clinical signs). These cases would have been expected to be reported as infected within the next five to ten days if they had been allowed to develop. And if those cases had been allowed to develop, they would in turn have given rise to further cases. 
The use of the word "therefore" is quite misplaced.  Again, the fallacy in Professor King's argument is self-evident.  Animals that are not showing clinical signs are healthy animals.   They may be "susceptible" ( a word rather favoured by the government at the moment in erroneously suggesting animals that are about to fall ill) but they are not incubating disease unless they have been in direct contact with disease.  The county statistics show such a discrepancy between animals culled and animals found to have been  diseased that there can be little doubt in the minds of anyone that a huge number of animals were killed "in error".  The farmers knew their animals.  They knew they were healthy.  Not a single farmer objected to having diseased animals culled - eiher in this outbreak or in 1967.  The difference this time is the extreme trauma - and that was a result of a policy that forced farmers and stckholders against their will to give up for slaughter animals they knew perfectly well were not diseased nor  had they ever been in contact with animals that were.

2.5 The contiguous cull helped effectively to arrest what had been an upward trend in the daily case numbers. This had the effect of turning the rising curve of daily case numbers into a declining curve more quickly, reducing both the overall number of cases and the total number of animals slaughtered over the full course of the epidemic.
It is no use simply repeating this.  The graph may have started to come down at the end of March - but that was because the old pre-movement ban incubating cases were all being found.  After movement was stopped the cases stopped - except that in Cumbria there were more "occult" cases than had been realised.  We still do not knmow the date of the first case, nor can we be sure of anything until the analysis of available data is put into the public arena. 
 If it is not made public the inference will be that the data is an embarrassment.

2.6  The contrary argument has been put forward that the advantage in culling pre-symptomatic animals is small, since vastly more virus is liberated around the time animals display clinical signs of infection than when they are incubating the disease. However, this does not alter the fact that the time taken to identify symptoms and to slaughter means that animals would in practice be infectious for a significant period before being culled. Data from DEFRA suggests that intervals of around 8 days between infection and reporting were typical, with the implication that three-quarters of secondary infections had already happened before the primary case was reported. Consequently, without a CP cull policy, there was a very real risk that most of the viral transmission would already have occurred by the time the animals were slaughtered.
Again, Professor King is ludicrously missing the point.  He seems to be suggesting that diseased animals  were all going to be wandering about infecting other premises. This  is just not so.  He is still assuming that secondary infection would happen between farms contiguous to each other - whereas in reality, as has been pointed out many times over the past months, direct animal to animal contact or the spread by fomites is what gets infection onto secondary farms.  Only "dangerous contacts" should have been strictly monitored.
It is logical to carry out pre-emptive culling only where you can be convinced that spread is likely.  They were told that spread was not likely at any distance.  They were not prepared to listen, it seems.

2.7  It has also been argued that resources taken up by the CP cull were considerable and would have been better deployed in identifying and culling infected herds and flocks. It is true that there were significant pressures on resources in the early days, which led to at least one CP farm being culled up to 21 days after animals in the IP had been slaughtered.
This is true.  Lack of contingency planning made emergency slaughter very slow indeed. Once this was realised, vaccination was the only humane way forward.  The vaccine was available.  Only politics prevented a civilised and timely end to the crisis in April.
However, it needs to be noted that the CP cull was responsible for only 20% of the total cull;
A disingenuous statement.  Had there been no CPs  - which muddied the water with panic measures and bullying coercion the disease would have been seen to be in its decline stage by mid April
local/3KM and welfare culls contributed much to the pressure on resources during this period.
There would have been no need to the absurdly draconian restrictions that resulted in such animal welfare problems that slaughter was the only way out. What were "local" culls if not caused by slipshod spread of infection  as a result of such widespread chaos and what were  "3km" culls  if not contiguous culls?
And none of this alters the conclusion that without the CP cull the epidemic would have been significantly more severe. 

Professor King forgets that he has, as yet,  said nothing to prove this.  The crisis involved millions more animals caught up in the contiguous culls than would have been if the advice of the experts to continue with 24 hr (but prompt) slaughter on IPs and testing and monitoring elsewhere had been listened to in March.

3. Analyses based on dates of confirmation and on date of infection

3.1 The course of the epidemic can be recorded on the basis of the case confirmation date or the estimated infection date. The Chief Veterinary Officer of DEFRA has produced a curve showing the development of the epidemic as a function of estimated infection dates, and this seems to show that the epidemic was brought under control before implementation of the CP cull policy.
Yes.  It does.
This would be an incorrect conclusion from the data. The difference between the case confirmation and estimated infection dates may be accounted for by a number of factors and is not therefore a constant. In this epidemic the average was 8 days but the range was wide.
"An incorrect conclusion"?  Professor King seems to have confidence in what correct conclusions the data  allow one to make.  The "data" is not yet in the public domain so once again one wonders why  secrecy has been such a feature of this crisis.  One wonders too how it is that he is now suggesting a thorough acquaintance with incubation times and in what way he feels these to be significant.
Two other factors are relevant. Farms remained capable of transmitting infection after clinical signs had been reported during the 1 to 2 days before the animals were slaughtered.
This is true.  The slaughter times were poor and virus was able to proliferate. n But it must be remembered too that many so-called IPs were not infected at allSplitting IPs in to positive, negative and untested will reveal a lot.  How can you justify a contiguous cull around a negative  IP? The rate of false clinical diagnosis was very high - and vets were rarely told whether their diagnosis had been confirmed or not by Pirbright.  Therefore they  had to continue to rely on guesswork rather than improve as a result of quality control.
Also, infections which had already occurred would not have been reported as infected if the farms were removed by the contiguous cull, resulting in an immediate drop in the incidence of reported cases when contiguous culling was introduced.
But this must be guesswork only!  Because the majority of contiguous farm animals were killed without benefit of blood testing we cannot know for sure whether there was or was not infection there. And with the statistics we do have it seems likely that this was rare.  It is pure speculation.
Implementation of the contiguous cull also had an immediate effect on the curves of estimated date of infection against time. The turning point on that curve is therefore close to the date on which the CP cull was first being effectively implemented. (This is, of course, not the same as 100% achievement of the CP cull within 48 hours; even a lower level of achievement would have had an immediate effect.) When these factors are properly taken into account it is clear that the timings of the observed peaks in the incidence of estimated new infections or of newly reported cases are both entirely consistent with a significant impact of the contiguous cull on the transmission of FMD.
Is the Professor trying to blind us with science here?  Why does he assert that it was the implementation of the contiguous cull which affected "curves of estimated infection against time" when what any inquiry would want to know is whether he can produce evidence that the contiguous cull stopped the disease in its tracks. Since FMD has been shown not to travel any distance through the air, and since blood tests were not allowed in the majority of cases this seems a forlorn hope. 

3.2 Epidemiological modelling conducted by each of the Cambridge, Edinburgh and Imperial College teams demonstrated very clearly the importance of CP culling. The agreement between the predicted outcome of the epidemic with CP culling and the actual outcome of the epidemic was good; these calculations already included the period between date of infection and date of reporting (amongst other key parameters), so it was no coincidence that the date of the predicted turning point of the epidemic matched the actual date of the turning point of the epidemic. To some extent this agreement was a balancing of two factors: on the one hand the CP cull was not always fully implemented within 48 hours; and on the other the 3km cull of sheep in Cumbria was not included in the early modelling.
The data in all three models came from the same source and all three contained the same flaws.  The Cambridge/Edinburgh team states that ' over-reporting (ie misdiagnosis) was 25% shortly after the  
 The date of infection could not be accurately calculated since

3.3 This effect can be explained in a way which does not rely on modelling. If animals on a CP were incubating the disease on, say, March 28th and were not culled, as was the policy prior to March 24th, they would go on to develop symptoms on, say, 30th March and would be assigned a date of infection, say March 25th; these cases would appear on the estimated infection date curve and be assigned to March 25th. But if they were culled as a CP on March 28th, they would not contribute to the cases counted as having been infected on March 25th, because they would not have been showing symptoms on the date of culling. Subsequent serological tests on the culled animals are unlikely to pick up antibodies at this stage. The implementation of the CP policy on a given date would therefore begin to affect the plot of date-of-infection against time at an earlier date.
Prof King appears to forget that testing was  done for  more than antibodies.  Alex Donaldson's view of laboratory testing, as presented in his letter to the Vet record May 19

That is-

- diagnostic material was good, particularly as blood samples were often submitted along

with epithelium

- material submitted was tested for virus, viraemia and/or antibody as appropriate

- preclinical signs- viraemia and/or antibody can generally be isolated

- animals with FMD will have either virus or antibody or both in their blood.

-'While it is never the intention that laboratory diagnosis would replace clinical diagnosis,

we believe that laboratory support for a diagnosis of FMD in sheep, in particular, is


-'The extreme difficult of making a clinical diagnosis of FMD in sheep is, in our opinion, the

explanation for the discrepancy between the field and laboratory diagnoses'.

3.4 Full analyses of these factors have been published in Nature (Mark Woolhouse and others: "FMD under control in the UK", Nature 2001; 411: 258-9, in Science (Matt J Keeling and others: "Dynamics of the 2001 UK Foot & Mouth Epidemic - stochastic dispersal in a heterogeneous landscape", Science 2001; 294: 813-817) and in Nature (Neil M Ferguson, Christl A Donnelly & Roy M Anderson: "Transmission intensity and impact of control policies on the foot and mouth epidemic in Great Britain", Nature 413: 542-547).

4. Conclusions

4.1 The analyses have shown that, whether based on report date or adjusted for estimated infection date, although the CP cull policy was not the only measure responsible for eliminating the disease, it was a key one. It is possible that traditional measures, if implemented much more rigorously than was achieved in practice, could have brought the epidemic under control eventually, but the fall in the number of cases would be unlikely to have occurred as early as it did without the CP cull. Indeed, implementation of the CP cull would have been beneficial at any stage of the epidemic because it would have helped speed up the decline in daily case numbers, thereby reducing the 'tail' and leading to the loss of fewer animals overall.
We just find it mind-boggling that, having admitted that traditional measures "could have brought the epidemic under control " Professor King should say that the CP led to "the loss of fewer animals overall".  It led to the loss of a further nine million animals overall - and after the peak when cases, according to Dr Kitching, were already coming down.  

4.2 Conversely, universal adoption of a 3km cull would have removed even more of the potentially infected animals, which would have brought the epidemic to an end more quickly. However, this would have resulted in more animals being culled overall, and was not an approach advised by the Science Group.
UNIVERSAL adoption of the 3km cull! When data is showing clearly that there was little live-virus  infection in the country outside Cumbria?    Is Prof King really serious? "....this would have resulted in more animals being culled overall"  Yes  - and it is clear that the Professor sees the crisis in terms of interesting sets of numbers rather than a calamity of fear, pain and disillusionment on an unprecedented scale.

4.3 It must be borne in mind that the CP cull was introduced as an emergency measure to control an unprecedented outbreak of FMD. At the time the CP cull was introduced, the outbreak was out of control. As part of the control measures, the CP cull proved to be very effective in helping to bring the disease under control rapidly. It also had the distinct advantage of being administratively relatively straightforward to implement and control and, having an unambiguous definition, led to quicker culling. 
Again, we are speechless at the bare-faced nonsense of this.  "very effective"?  "administratively relatively straightforward"? "unambiguous definition"?  He means, in other words, when you go in killing, paying unskilled men by piece-work, asking no questions and allowing none to be asked you can reduce the number of animals likely to catch the disease - because they will all be dead.

4.4 Further studies need to be made as to whether a CP cull would be necessary for all types of FMD outbreak. Much would depend on the density, pattern or susceptibility of farms in the area of the outbreak. The views of the two Inquiries will be a vital input to future contingency planning.

This is like the Witchfinder General speculating upon whether, in future threats from the forces of darkness,  widespread burning at the stake is necessary.  He forgets that in future outbreaks NO farmer will allow the cruel and unnecessary policies of 2001 to be repeated.  Nor will it be necessary since the new marker vaccines will remove the last possible objections from the humane vaccination policy that was recommended in 1968 by the Lord of Northumberland's report.  On farm rapid diagnosis will have been validated.  All this inexplicable carnage will be looked back on with horror.