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Author Topic: Foot And Mouth Disease Outbreak Due to U.K Wet Weather on the cards?  (Read 80001 times)

Offline Andrew K Fletcher

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ITN News:
Foot-and mouth is a devastating disease - but what do we know about its effects and how it spreads?
Source: http://cbc.ca/news/indepth/background/footandmouth.html
ITN's Nicholas Owen has been looking at a previous outbreak in 1967 and the issues involved:
Almost half a million animals were slaughtered as Britain struggled to contain its worst outbreak of foot- and-mouth.
It was a farming catastrophe. The total bill then was £150 million in slaughter costs and lost sales, plus £27 million paid in compensation to farmers.
From a single case in Shropshire, large areas of the country were eventually affected.
Foot and mouth is a disease that can affect all cloven hoof animals, like pigs, sheep, cattle, goats and deer.
Source: http://www3.itn.co.uk/news/20010221/britain/12footbcgrnd.shtm
Symptoms vary between species:
Cattle – Fever, dullness, off feed, shivering, reduced milk yield and sore teats in milking stock, tenderness of feet or lameness.
Sheep and goats – Fever, lameness, stiff legged walk, off colour, tendency to lie down.
Pigs – Fever, lameness, dullness, off feed.
(Comment When animals lay down, circulation is compromised further. A.K.F.)
A vaccine is available, but it is expensive, boosters are needed within a year and vaccinated animals endanger a country's disease-free status, which can take years to recover. Laboratory tests cannot distinguish between vaccinated animals and infected ones. There is no cure. It usually runs its course in two or three weeks, after which the great majority of animals recover naturally.
http://www2.warwickshire.gov.uk/Web/corporate/pages.nsf/Links/E708A22F2BC32BD480256A01004BE3E3
Warwickshire Web . Warwickshire County Council, Shire Hall, Warwick, CV34 4RA,
Q: Which animals are susceptible? Cattle, sheep, pigs and goats are susceptible and some wild animal such as hedgehogs, coypu, rats, deer and zoo animals including elephants.
Q: What are the symptoms? Vesicles (blisters) in the mouth or on the feet and other symptoms which vary somewhat but may be:
CATTLE - Fever, dullness, off feed, shivering, reduced milk yield and sore teats in milking stock, slavering, tenderness of feet or lameness.
SHEEP AND GOATS - Fever, lameness, stiff legged walk, off colour, tendency to lie down.
PIGS - Fever, lameness, dullness, off feed.
Q:What kinds of virus are there?
There are 7 main types: O, A, C, SAT.1, SAT.2, SAT.3, and Asia 1. Within each type there are many sub-types, e.g. O1 and A22. The average incubation period is 3-8 days but it can be shorter or may extend to 14 days or longer. It has been confirmed that the virus responsible for the present outbreak is the highly virulent pan-Asiatic O type. When animals recover from infection by one type of virus they have little or no protection against attacks by any one of the others.
Q: How is the virus destroyed?
It can be destroyed by heat, low humidity, or certain disinfectants, but it may remain active for a varying time in a suitable medium such as the frozen or chilled carcass of an infected animal and on contaminated objects.
SOURCE: http://www2.warwickshire.gov.uk/Web/corporate/pages.nsf/Links/E708A22F2BC32BD480256A01004BE3E3
Persistence of virus environment
AUSVETPLAN Foot-and-mouth disease
FMD virus may remain infective in the environment for several weeks and possibly longer in the presence of organic matter such as soil, manure, and dried animal secretions, or on chemically inert materials such as straw, hair and leather.
The virus has the following general properties (Donaldson 1987).
1 ) The virus is most stable at pH 7.4–7.6 but will survive at pH 6.7–9.5 if °C or lower. Below pH 5.0 or above pH 11.0the temperature is reduced to  inactivation is very rapid.
2) Raising the temperature reduces the survival time. At temperatures below °C for 30freezing point the virus is stable almost indefinitely. Exposure to 5 minutes is sufficient to destroy most strains although there is some variation between strains in resistance to temperature and/or pH stress.
3) Sunlight has little or no direct effect on infectivity; any loss is due to secondary drying
and temperature.
4) The survival of airborne virus is mainly influenced by relative humidity (RH) with good
survival above 60% RH and rapid inactivation below 60% RH (Donaldson 1972).
Source: http://www.aahc.com.au/ausvetplan/fmdfinal.pdf
OFFICE INTERNATIONAL DES EPIZOOTIES
Organisation mondiale de la santé animale World organisation for animal health Organización mundial de sanidad animal
Q: Which other countries have recently had FMD? (Foot and mouth disease)
Argentina : 6 April 2001 Bhutan : 10 November 2000 Brazil : 19 January 2001 Colombia : 29 December 2000 Egypt : 15 September 2000 France : 6 April 2001 Georgia : 23 June 2000 Greece : 2 February 2001 Iran : 15 October 1999 Ireland : 6 April 2001 Israel : 9 February 2001 Japan : 29 September 2000 Kazakhstan : 28 July 2000 Korea : 18 August 2000 Kuwait : 1 September 2000 Malawi : 23 March 2001 Malaysia : 11 February 2000 Mauritania : 8 December 2000 Mongolia : 23 March 2001 Namibia : 27 October 2000 Netherlands : 6 April 2001 Peru : 14 January 2000 Russia : 28 April 2000 Saudi Arabia : 14 April 2000 South Africa : 9 March 2001 Swaziland : 9 March 2001 Taipei China : 9 March 2001 Tajikistan : 25 August 2000 Turkey : 24 December 1999 United Kingdom / Great Britain : 6 April 2001 United Kingdom / Northern Ireland : 9 March 2001 Uruguay : 26 January 2001 Zambia : 1 September 2000 Zimbabwe : 4 February 2000 Source: http://www.oie.int/eng/info/hebdo/a_dsum.htm
COMMENT: How can we ever expect to contain foot and mouth when it is already established throughout the world? A.K.F.
Management control and prevention SOURCE: http://WWW.ThePigSite.Com
Vaccination (where applicable)
·   In endemic and high risk areas routine vaccination may be practised mainly to protect the breeding stock.
·   Most FMD vaccines are produced in cell suspension cultures and inactivated by ethylenamine derivatives. An adjuvant is added to make them more potent. Oily adjuvants are used in swine.
·   Vaccination in pigs is problematical. This is because protection is short-lived lasting only about six months. It is also partly because there are seven serotypes of FMD and protection against one leaves animals susceptible to the others. Vaccines must be multivalent (several serotypes) in most endemic regions. Since FMD is largely a winter disease, vaccination should be carried out in the autumn.
·   Serotypes - There are 7 main serotypes: A, O, C, SAT 1, SAT 2, SAT 3 and Asia 1. There are also many strains within serotypes. Careful selection of the strains for incorporation in vaccines is essential to ensure they are effective.
From: Martin Rowley(martinr@booty.demon.co.uk) Subject: Foot and Mouth Disease ... and the weather
Newsgroups: uk.sci.weather Date: 2001-02-24 09:50:28 PST

I note that there has not been one post yet in this newsgroup regarding what may turn out to be a major disaster for the farming community in the UK (and a major drain on the Exchequer) .. the current outbreak of Foot and Mouth Disease. (FMD). For those too young to remember, FMD has integral links with synoptic meteorology. For those who have them available, I recommend the edition of 'Weather' noted below. From that I quote the following:-

" The recent epidemic, in which over 2300 farms were infected between October 1967 and June 1968, was the most serious ever experienced in Britain. The Meteorological Office, in close collaboration with the Central Veterinary Laboratory, Weybridge, has investigated the possibility that meteorological factors were responsible for some of the spread. The results of this analysis suggest that most of the spread was due to the wind, and hence stricter controls on movement would have had little effect. Moreover, it appears likely that precipitation played an important part in spread over distances greater than a few kilometres .... " (my note: note the phrase ... 'most of the spread' etc.)

"Conclusions:
1. A large proportion of the spread during the 1967-8 epidemic was due to the wind.
2. On at least one occasion, the virus was carried over 100km by the wind.
3. During anticyclonic weather with calm or light winds, airborne spread it largely confined to a distance of about 4 km from a source.
4. Precipitation plays some part in increasing the amount of deposition.
5. It is possible that precipitation is essential for the occurrence of appreciable deposition beyond about 10 km."

If the origin of the *current* outbreak (as noted in today's news) is in fact at the farm in Northumberland, and that conditions were conducive to FMD viral generation at least a month ago, then the present stringent movement controls (although essential), may prove to give a false sense of security ... the viral agents may have long been dispersed by both dry and wet deposition over large areas of the country. Wet deposition being much more effective and the primary vector for infection in the 10's of km downwind range. Over the past couple of weeks, the wind over NE England has 'boxed the compass', albeit with a bias to drift towards the east or north-east (over the North Sea).
However, for a few days around the 8th/9th and again on the 18th/19th, winds had a high northerly component. We have also had south-ward moving frontal bands which could be agents to 'sweep up' the viral agents (minute droplets containing the disease), depositing them further south in precipitation. Also note that the otherwise prevailing west or SW winds would aid vectoring of the disease from, for example, the Isle of Wight farm.

There are some similarities with the present day meteorological situation. The outbreak in the late 60's came in the third year of a run of three 'wet' years (we have just had 3 wet years..  notably so in the case of 2000), and the September & October of 1967 had above average rainfall (using the EWP series), with October approaching twice-average rainfall. (Also, as an aside, the late 60's outbreak also started in pigs before crossing to other species).

The news media aren't making much of this aspect at the moment (just mentioning the wind as an aside), but I fancy that we may have a major problem here as the source was not identified soon enough, allowing what I believe to be acknowledged to be the major vector agents (wind & precipitation), to have full effect for over a month.
Reference:
'Weather', June, 1969 "Effects of wind and precipitation on the spread of Foot-and-mouth disease.
PB Wright, Meteorological Office, Bracknell. pp204-213 Martin Rowley  http://www.booty.demon.co.uk/metindex.htm

Received from HM Stationary Office on the 24th April 2001
 

Offline Andrew K Fletcher

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Relevant extracts from:
REPORT OF THE COMMITTEE OF INQUIRY ON
Foot-and-Mouth Disease
1968
By command of Her Majesty April 1969
PART 1: Command. 3999 SBN 10 139990 1 HM stationary Office
 
Factors involved in the introduction and spread of disease
Page15:
27. Since 1954 there has been further evidence in support of the theory that foot-and-mouth disease, (FMD), virus is transmitted in air currents. Recent evidence from Denmark suggests that the virus can be windborne for up to eighteen miles over sea and in exceptional circumstances, over twice that distance.
Danish veterinary officials thought that windborne infection, associated with darkness and damp weather, was the most frequent cause of primary outbreaks in Denmark.
28. In Great Britain much work has been done by the Meteorological Office, (MET Office), and the Ministry Of Agriculture to examine the general hypothesis that meteorological conditions could have favoured the spread of the virus from Continental sources on the occasions of past outbreaks of the disease in Great Britain- and to assess the effects of meteorological conditions on secondary spread in this country. An examination by MET, of all primary outbreaks since 1937, except minor ones, has shown that in every case of multiple and simultaneous outbreaks on the south and east coasts, suitable wind tracts could be found leading back to known infected areas in Europe. It was noted that in the area of the outbreaks, rain, which could have precipitated the virus, occurred at the relevant time.
An alternative interpretation by the Microbiological Research Establishment was that the outbreaks could be better accounted for by the favourable effects on the viability of the virus in the high humidity prevailing at the time.
29. The MET Office also examined the effect of meteorological conditions on secondary outbreaks of the disease. This was done in five areas: Cheshire (1952); Shropshire (1961); Northumberland (1966); Hampshire (1967), and Cheshire (1967). (The last of these studies had advanced to the point of examining those outbreaks during the initial stages of the epidemic for which there were very few possible authenticated sources; further work is in progress.)
The results of the examination suggested that wind and rain might have played a part in the spread of the disease.
In general the examination showed that-
i.   few outbreaks occurred upwind of any known source:
ii.   outbreaks were limited to about 2 ½ miles downward in dry weather;
iii.   Outbreaks extended further downwind in wet weather and even further in periods of light rain;
iv.   Most outbreaks were downwind of more than one possible source of infection on several occasions during rainy periods;
v.   Selecting the most likely sources of infection, the percentages of total outbreaks downwind, in relation to distance, were as follows- 33% within 1 ¼ miles; 60% within 3 miles 75% within 6miles; 85% within 12 ½ miles; 90% within 18 ½ miles 95% within 31 miles. (these percentages did not include the Cheshire 1967 epidemic);
One case might have been associated with airborne spread of the virus at a distance of fifty miles;
vi.   in all five areas there were a number of secondary outbreaks during the second week following primary infection; after dry weather the number was low and after wet weather it was high;
vii.   in all five areas there was a decline in the number of new outbreaks during a period of dry weather.
The MET Office concludes that the amount of spread due to meteorological causes could be as high as 95% and was unlikely to be less than 80%. They also concluded that spread did not occur unless favourable wind and rain conditions prevailed.
30. The evidence suggests that viruses contained in airborne particles will travel in a viable form in the air for distances of up to thirty miles or more depending upon their particle size, the strength of the wind and other factors.
Transmission of airborne virus by night appears to be a greater threat than by day because of the absence of ultraviolet light. The Microbiological Research Establishment suggested that there might be other influences at work in the survival of foot-and-mouth disease virus about which conclusive answers are not at present available. For example, some viruses are known to survive better in association with large particles rather than small ones. Atmospheric relative humidity is a very important factor; high relative humidity appears to prolong the survival of viruses in aerosols.
The salt and protein content of the material in which the viruses are conveyed and the extent of atmospheric pollution might exert an influence on survival. Although heavy rain may aid deposition of the viruses, experiments suggest that it may clear the atmosphere of noxious substances deleterious to the viruses and so prolong their survival.
31. The releases of foot-and-mouth-disease virus into the air may be brought about in many ways. Present work at the Animal Virus Research Institute on the presence of virus in the air of animal houses containing infected animals shows that the amount of excreted virus is fairly uniform, starting before the vesicles appear and continuing thereafter. Movement of infected animals or the disturbance of infected materials could create an aerosol containing the virus. Animals either housed or at pasture can be infected by inhalation of airborne virus. It has been suggested that the virus might be drawn up into the air and carried to other sites in thermal air currents generated when infected carcasses are burned. In this case the virus source might not be confined to the carcasses; contaminated dust particles from the ground surrounding the pyre might also be drawn up into the air and carried away by the wind.
During the 1967 /1968 epidemic in the West Midlands large volumes of air were sampled at points 100 and 300 yards down from fires used to destroy-(Page 25 same document)- carcasses on two farms. No virus was isolated from the samples but it was thought that the efficiency of the technique employed might not have been high enough to give significant results.
32. Airborne particles can be deposited by gravity, by downward diffusion of air, by impaction on a solid object or in falling raindrop. Large particles (greater than 10 microns) will be deposited close to the source of infection. Virus deposited on pasture or fodder can cause infection when ingested. Smaller particles, on the other hand, will travel in an aerosol and be little effected by gravity or rainfall (other than very heavy rainfall), The probability of infection by inhalation will depend on the concentration of virus-containing particles in the air. It will also depend on the viability of the virus which will be influenced by a number of factors, the most important probably being relative humidity.
43. It is possible that birds are responsible for the introduction of foot-and-mouth disease into countries and for its subsequent spread. It is known that foot-and-mouth disease virus can be conveyed on the feet or feathers of birds and can be excreted by them after ingestion of material contaminated with the virus, but there is no evidence that birds can become infected with the virus.
The Gowers Committee pointed out that the virus had been recovered from the feet and feathers of a bird contaminated experimentally as long as 91 hours after contamination. Also it was reported that starlings given the virus by mouth had excreted it in their faeces for a period of 10-26 hours. It is thus probable that birds may spread the virus and so cause secondary outbreaks.
They are likely to constitute a greater risk if they are carrion eaters such as crows and seagulls. In the recent past there has been considerable misgiving about attributing primary outbreaks with bird migration and it has been suggested that many of the outbreaks so attributed may have been due to windborne virus. Recent Danish research evidence suggests that some of the outbreaks previously presumed to have been associated with bird migration to that country cannot be related to migration patterns.




REPORT OF THE COMMITTEE OF INQUIRY ON
Foot-and-Mouth Disease
1968
By command of Her Majesty December 1969
PART 2: Command. 4225 SBN 10 142250 4 HM stationary Office
Chapter V1: Postscript to part 1 of the Committee’s Report
Page 93: (a) General
223. Since the submission of Part1 of our report on 7th March, 1969 considerable advances have been made in research on foot-and-mouth disease. Many of which have followed the opportunity given to the staff of the Animal Virus Research Institute at Pirbright, Surrey in the 1967/1968 epidemic to go into the field for the first time. The Institute already had considerable epidemiological experience in countries overseas where the disease is both endemic and epidemic. However, the study of the disease in Great Britain, with its completely susceptible livestock population, presented entirely different problems which in the event were not solved by field investigations.
Nevertheless, the opportunities for study of the epidemiological problems presented by the epidemic made it possible to define a number of problems more clearly. They have since been studied intensively by the staff of the Institute in collaboration with veterinary staff of the Ministry of Agriculture, the Microbiological Research Establishment, the Meteorological Office, and the Atomic Energy Research Establishment. Some of the not inconsiderable results obtained so far are given in the following paragraphs. In general they reinforce the conclusions drawn in Part1 of our Report. It should be emphasised that the work provided information on how individual and small groups of animals behave under experimental conditions but could not show precisely how animals would react to the disease under normal farming conditions.
(b) Characteristics of Foot-and-Mouth Disease Virus
224. Strains of foot-and-mouth disease virus from the 1967/1968 epidemic were studied in susceptible animals under experimental conditions. In brief, the experiments indicated that:
(c) the strain of the virus isolated during the 1967/1968 epidemic was particularly stable under certain laboratory conditions.
225. Speculation arose as to whether these characteristics contributed to the serious nature of the 1967/1968 epidemic. Since then, however, other strains of foot-and-mouth disease virus have been similarly examined and it is clear that the early excretion shown by the 1967/1968 strain is common to a number of strains isolated both in the country and abroad. It was found that strains can nevertheless show considerable variation in such properties as stability under laboratory conditions and it may be that such characteristics will provide useful markers in future in identifying the origin of strains responsible for outbreaks.
Page 94: (c) Windborne Transmission of Foot-and-Mouth Disease virus
228. Naturally it has not been possible to carry out experiments in the field to investigate the transmission of foot-and-mouth disease virus by wind because of the obvious risks involved. However, experiments in the laboratory have shown that the virus in the aerosol form is very fragile when humidity is low and persists for long periods when the humidity is high.
There was evidence from the 1967/1968 epidemic to indicate that rain-bearing winds played an important part in spreading the disease. Furthermore retrospective studies have been made of previous outbreaks of the disease in relation to the meteorological conditions existing at the time and these support the important part played by wind and humidity in the spread of infection.
For example, in one of the studies made, of an outbreak, which occurred in East Keswick (between Wetherby and Leeds) in October 1960. Meteorological experts, without any knowledge of the pattern of the spread, on the basis of the wind tracts and humidity as well as other weather conditions prevailing at the time, indicated where the outbreaks should have occurred. Their indications were correct but of equal importance, they were also able to indicate correctly those areas, which remained free of disease. It is considered that the virus can be carried by wind, if the conditions are ideal, over distances of more than sixty miles. This approach will be valuable in dealing with future outbreaks particularly in indicating where to look for secondary outbreaks associated with wind spread once a primary outbreak is reported.
Signed: Northumberland (Chairman) Anthony Cripps; David G. Evans; Henry Plumb; Eric L. Thomas; David Walker; William L. Weipers; John N Jotcham (Secretary); Melba D. White (Assistant secretary) 3rd November, 1969
Foot & Mouth linked by weather patterns in 1967, 68 and this epidemic! (Does the evidence outweigh coincidence?)
 

Offline Bored chemist

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The word endemic also implies that the virus is maintained in the wild population of animals. Sorry if this was taken out of context.

However calling me a liar over something as minor as a misunderstanding tells people a lot more about you BC than it does about me.

I Bet you wouldnt say this to my face!
Smallpox essentially only had one host- humans.
It was still described as endemic in some areas before it was wiped out. Your deffinition of endemic isn't the usual one. It's essentially the opposite of the one given here.
http://en.wikipedia.org/wiki/Endemic_(epidemiology)
 Measles and chickenpox (ironicly, given the name) are only commonly found in humans. These diseases too are endemic in our population.

Even the common cold is an example that shows that you are simply wrong.

Foot and Mouth Disease is endemic in some places, not because there are wild hosts for it, but because it's endemic in the cattle heards. The virus is bad for animals but not usually fatal.

I called you a liar because you said something that wasn't true. What it says about me is that I don't accept people putting words in my mouth. I never said anything about wild animals. Your point was a total strawman. You ought to know better.
A preference for truth over falsehood is fairly common among people, particularly scientists.
I'd be less likely to say it to your face, but only because I doubt you would have made the claim you did if we were face to face.

Incidentally, this " FOOT & MOUTH IS LINKED IRREFUTABLY TO THE WEATHER!"
Is also untrue, because everyone here has seen the refutation.

Anyway, those papers say a lot about the spread of the virus- bad weather has an effect.
They don't say that the disease is caused by bad weather.


The simple fact is that we often have bad Summers, but we seldom have FMD so it's logically impossible for bad Summers to cause FMD.

If we get an outbreak this year it will be due to a breach of quarantine.
« Last Edit: 28/08/2008 19:15:55 by Bored chemist »
 

Offline Andrew K Fletcher

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I have never said that the virus is caused by bad weather anywhere. I refrain from calling you a liar. In fact it never entered my head to call you a liar over something so trivial.

The link to the weather is in how the weather lowers the circulation and body temperature making the animals more susceptible to infectious diseases. This explains why the infected animals recovered when they were housed in clean dry laboratory conditions.

The common cold shows exactly how this theory is correct. It is no coincidence that when the weather takes a turn for the worse, the UK population begins to suffer from colds, influenza, coughs, aches and pains with annual predictability.

RE Endemic:

Endemic according to your reference means it belongs there and is also said to be exclusive to the area. In the case of foot and mouth diseases and all virus that have the ability to mutate and be transmitted by air or by birds and wildlife, it can hardly fit in this case.

Endemic therefore as used in reference to a pathogen fits more with my interpretation than it does with the ones on Wiki.
 

Offline rosalind dna

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This Bluetongue disease has come over from a "protected" area in
France to the Uk and it can be a fatal disease in sheep also in goats:

http://news.bbc.co.uk/1/hi/uk/7583948.stm

BBC News:
Bluetongue cases discovered 
 
Bluetongue was first reported in the UK in 2007
Two cases of animal disease bluetongue have been detected in imported rams, the Department for Environment,
Food and Rural Affairs (Defra) has said.

The rams were imported from the same premises in the bluetongue-restricted zone in France.
The cases were found on premises near Lewes, East Sussex, and Hemel Hempstead, Hertfordshire.
Defra said there was no evidence the disease was being circulated by midges in the areas where cases were found.

The cases were detected as a result of post-import testing on all animals coming from the Continent which are susceptible to the disease, according to Defra.

Bluetongue, which can be fatal to animals, is transmitted between animals such as cows and sheep by midges.

Farmers throughout the protection zone should vaccinate as soon as vaccine is available to them

Alick Simmons
Deputy chief vet
______________________________________

The first outbreak of the disease in the UK hit the country in summer 2007.
A mass vaccination campaign against the disease began in April.
Some 21.5 million doses of vaccine have been made available to farmers.

Deputy Chief Vet Alick Simmons said the disease "has recently been confirmed as circulating this year in the Netherlands and large areas of France, despite vaccination programmes being undertaken".

"Similar re-emergence of the disease in the UK would also not be unexpected in the coming weeks," he said.

The bluetongue protection zone, which has kept in place to allow for vaccination, covers most of England.
It is legally permissible to import animals from France's protection zone.
Mr Simmons said the latest cases emphasised the need for farmers to be aware of the risks of importing animals from within restricted zones and the importance of vaccination.

"Farmers throughout the protection zone should vaccinate as soon as vaccine is available to them," he said.

http://news.bbc.co.uk/1/hi/england/cumbria/7581613.stm

It seems that it's the wet weather that's re-produced this animal disease and not FMD but just as worrying for the
farmers I'd guess.

 

Offline Bored chemist

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Wiki's example is
"In epidemiology, an infection is said to be endemic (from Greek en- in or within + demos people) in a population when that infection is maintained in the population without the need for external inputs. For example, chickenpox is endemic (steady state) in the UK,"

Nothing to do with places. FMD is the same in farm herds in some parts of the world. No need for wild animalss to be involved- they might be, but it's not a requirement.

Anyway, we just have to wait. If there's another outbreak without a breach of quarantine then you are right.
 

Offline Andrew K Fletcher

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endemic
1. Relating to a disease or pathogen that is found in or confined to a particular location, region, or people. Malaria, for example, is endemic to tropical regions.

http://www.thefreedictionary.com/endemic

 

 

Offline Bored chemist

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Take the particularly nasty disease "made-up-itis" as an example.
Wherever you find it, it found in that location or region. It is therfore endemic by the definition above. Interestingly, it remains endemic even if there's only one case ever in the world.
None of this relates to your original point about wild animals because they are not needed as a reservoir of the virus where there are infected farm animals. Where there are no such infected animals (such as in the UK at the moment) there are no outbreaks.

Anyway, we just have to wait. If there's another outbreak without a breach of quarantine then you are right.


Re bluetongue
"It seems that it's the wet weather that's re-produced this animal disease "
No, it seems that importing infected animals from France did that.
"Two cases of animal disease bluetongue have been detected in imported rams"
Of course a disease with a mobile vector  (the midge) could cross the channel anyway if the wind blew strongly). The weather will affect the spread of that disease of course.
« Last Edit: 29/08/2008 18:36:14 by Bored chemist »
 

Offline Andrew K Fletcher

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RE Bluetongue: midges live by shallow water and breed prolifically in wet weather where lots of stagnant shallow water benefits the larvae. So in this case the weather can be responsible for providing the stepping stones / puddles for the infected midge to move rapidly over many miles. Therefore the weather. The barrier in this case was the sea and bad policies have enabled the infection to cross the expanse of salty water to our land.

In the F&M outbreaks we see vets, farmers, soldiers, police, politicians, press and the public having to wash their footwear and hose down vehicles from infected areas. This says something about the virus having a mechanism to transfer from one source to infect another without the need for an animal. Why can’t this happen in the wild animal populations and among the bird and insect populations? It can and does, otherwise these disinfection controls would be deemed useless. (They may or may not be useless) But for now lets assume they are useful in containing the virus.

This would then show that the virus can no longer be considered as either indigenous or endemic as carriers, be it footwear or a hoofed or clawed foot the virus finds a way to move around. Why else would we need 2.5 million antiviral injections for bluetongue. Which incidentally it was also predicted in the theory that other more serious virus will show up in the UK sooner rather than later due to the weather patterns. Admittedly the virus has been traced back to a source. But should we experience severe weather this winter the contamination area is likely to expand rapidly.

You say the wild animals are not required. Maybe they are not, but they are among us and we are never more than a few yards from a rodent and rodents like many other creatures carry their own hosts like fleas and ticks.

I suspect that the UK is not as free from infections like foot and mouth disease as politicians would have us believe.

IA few days ago someone informed me of truck loads of carcases being driven along lanes in the farming community dripping fluids along the tarmac that sheep and cattle use to move from field to field. This happened before a major outbreak. It does not take much thought to realise that should these slaughtered animals have been infected prior to the media being informed about a F&M outbreak this careless act probably contributed and compounded the cross contamination. The person that told me this did not mention that these animals came from a farm close by. Which leaves us with some serious questions about what these animals were infected with and why were they being transported through countryside that was as yet unaffected?
 

Offline Andrew K Fletcher

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> News
Wales gets go ahead for bluetongue vaccination
29/08/2008 17:23:00
FWi
Welsh farmers have been called on to vaccinate their livestock at the earliest opportunity following conformation that the whole of Wales will be declared a bluetongue protection zone from Monday 1 September.

Farmers' Union of Wales president Gareth Vaughan urged farmers to vaccinate stock after DEFRA announced that eight cases of bluetongue  had been confirmed in imported cattle in Tiverton, Devon.

Mr Vaughan said: "For the first time this year we have seen cases of BTV8 in the UK, with three infected premises confirmed in the past week. The disease is now on our doorstep and from Monday Welsh farmers will be able to take action to minimise the risk to their livestock.

"I therefore urge farmers who have not yet ordered vaccine from their vets to do so immediately. It is expected that vaccine supplies will become available within days, with further batches arriving over the coming weeks."

The announcement coincides with Wales’ busiest time in terms of crucial livestock sales, which are desperately needed after the disruption caused by foot and mouth disease last year.
http://www.fwi.co.uk/Articles/2008/08/29/111891/wales-gets-go-ahead-for-bluetongue-vaccination.html

DELAWARE: Insect-borne virus found in deer
http://www.delmarvanow.com/apps/pbcs.dll/article?AID=/20080826/DW01/80826024/-1/DW

« Last Edit: 30/08/2008 08:53:54 by Andrew K Fletcher »
 

Offline Bored chemist

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Oh look! A conspiracy theory.
"I suspect that the UK is not as free from infections like foot and mouth disease as politicians would have us believe."
FMD is a contageous notifiable disease with clearly defined symptoms which are known to all farmers and vets. But Andrew thinks it is kept a secret.
Does anyone agree with him?
Cosmored, perhaps?

While we are at it, this
"In the F&M outbreaks we see vets, farmers, soldiers, police, politicians, press and the public having to wash their footwear and hose down vehicles from infected areas. This says something about the virus having a mechanism to transfer from one source to infect another without the need for an animal. Why can’t this happen in the wild animal populations and among the bird and insect populations? It can and does, otherwise these disinfection controls would be deemed useless. (They may or may not be useless) But for now lets assume they are useful in containing the virus.

This would then show that the virus can no longer be considered as either indigenous or endemic as carriers, be it footwear or a hoofed or clawed foot the virus finds a way to move around. Why else would we need 2.5 million antiviral injections for bluetongue."

is a non sequiteur. It starts off by making observations about FMD, then uses thenm to try to prove something about bluetongue.
FMD is a virus, it's small and so it can be accidentally carried about by birds other aniimals and people.  Of these peiople are by far the most mobile (people often travel hundreds of miles in a day- animals generally don't).
That makes cleaning boots and such a good idea. We can't do a lot about the birds but we can reduce the likelihood of infection buy restricting the movement of cattle. We can also make sure that farms near the infected animals are kept under close observation. If there's any infection there the cattle are destroyed.

What Andrew seems not to understand is that there is a difference between a host and a vector.
Birds can transmit the virus, carried on their feet. However if the virus isn't taken to another cow it dies out. Imagine that we had wild cows - these too could get the virus and it would circulate among them in much the same way as measles does in people. Contact between these animals and farmed cows would mean that the farm animals would keep getting infected.
The wild cows would act as a reservoir for the disease because it infects them. It doesn't infect birds so there's no reservoir of infection.
That's why the disease is not endemic in the UK.

 

Offline Andrew K Fletcher

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Don't be silly BC. Conspiracy theory? I am stating that the virus probably has other hosts that maintain it until the climate takes a turn for the worse. If this were not the case, then Foot and mouth would have become extinct a long long time ago. The view that politicians probably kept the lid on the previous outbreaks until the evidence overwhelmed them is not a conspiracy theory but a probability.

The Blue tongue outbreak was used to show how weather affects animals and animal health and how it can affect a known or unknown disease / pathogen / parasite.

This is about how the body behaves under the stress of high humidity and how it prevents us from fighting infections, but more to the point how it prevents cattle, pigs and sheep from remaining healthy.

There was a chemist on the F&M team that screwed up big style. So climb down off your degree for a while and read the text with an open mind.



Oh look! A conspiracy theory.
"I suspect that the UK is not as free from infections like foot and mouth disease as politicians would have us believe."
FMD is a contageous notifiable disease with clearly defined symptoms which are known to all farmers and vets. But Andrew thinks it is kept a secret.
Does anyone agree with him?
Cosmored, perhaps?

While we are at it, this
"In the F&M outbreaks we see vets, farmers, soldiers, police, politicians, press and the public having to wash their footwear and hose down vehicles from infected areas. This says something about the virus having a mechanism to transfer from one source to infect another without the need for an animal. Why can’t this happen in the wild animal populations and among the bird and insect populations? It can and does, otherwise these disinfection controls would be deemed useless. (They may or may not be useless) But for now lets assume they are useful in containing the virus.

This would then show that the virus can no longer be considered as either indigenous or endemic as carriers, be it footwear or a hoofed or clawed foot the virus finds a way to move around. Why else would we need 2.5 million antiviral injections for bluetongue."

is a non sequiteur. It starts off by making observations about FMD, then uses thenm to try to prove something about bluetongue.
FMD is a virus, it's small and so it can be accidentally carried about by birds other aniimals and people.  Of these peiople are by far the most mobile (people often travel hundreds of miles in a day- animals generally don't).
That makes cleaning boots and such a good idea. We can't do a lot about the birds but we can reduce the likelihood of infection buy restricting the movement of cattle. We can also make sure that farms near the infected animals are kept under close observation. If there's any infection there the cattle are destroyed.

What Andrew seems not to understand is that there is a difference between a host and a vector.
Birds can transmit the virus, carried on their feet. However if the virus isn't taken to another cow it dies out. Imagine that we had wild cows - these too could get the virus and it would circulate among them in much the same way as measles does in people. Contact between these animals and farmed cows would mean that the farm animals would keep getting infected.
The wild cows would act as a reservoir for the disease because it infects them. It doesn't infect birds so there's no reservoir of infection.
That's why the disease is not endemic in the UK.


 

Offline Bored chemist

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In order for there to be a background level of FMD in this country the politicians, the farmers and the vets would all have to agree to keep it a secret. That's a conspiracy.

"I am stating that the virus probably has other hosts that maintain it until the climate takes a turn for the worse. If this were not the case, then Foot and mouth would have become extinct a long long time ago. "

This is England- our climate always takes a turn for the worse. As I write this the papers are discussing whether or not this is the wettest August on record- but there is no outbreak.

If there were any wild host for the disease we would have an outbreak of FMD now and there isn't one.
As you steadfastly reuse to believe (in spite of the evidence) in this country FMD is extinct so your own reasoning shows that your hypothesis is false.

Incidentally, since I don't have a degree it's a rather pointless ad hom attack to say that I should climb down off it.
Even if I had one, this sentence "There was a chemist on the F&M team that screwed up big style. So climb down off your degree for a while and read the text with an open mind." makes no sense- just because one chemist screwed up doesn't mean anything about the performance of other chemists.
 

Offline Andrew K Fletcher

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Please explain how the deer managed to avoid the virus? Did they slaughter them all? Have they antibodies now and who inocculated the deer population? What about the wild boar population?


Foot and mouth virus spreads to wild deerProtesters march to halt mass slaughter

Special report: foot and mouth diseaseAnthony Browne, environment correspondent The Observer, Sunday April 22 2001 Article historyThe foot and mouth virus has passed into Britain's wild deer population, making the Government's policy of mass slaughter of farmyard livestock futile.
There have been several cases of vets clinically identifying the disease in wild deer, some of which have died from it. There have also been many reports from Devon, Cumbria and Northumberland of deer limping and exhibiting other unusual behaviour linked to the disease.

Veterinary experts say it is impossible to vaccinate or cull wild deer and once infected they will act as a reservoir for the virus, repeatedly re-infecting livestock. It will make it almost imposs-ible for Britain to rid itself of the virus, until it dies out naturally in wild deer, which could take years.

Last week a roe deer was found dead at Kirk House Farm near Penrith, which had already been confirmed as having foot and mouth in livestock. Local vet Matt Coulston, of Frame Swift and Partners, identified lesions on all four feet and in its mouth. 'It had signs consistent with foot and mouth disease,' he told The Observer. 'There have been loads of people round here reporting dead deer and sick deer. People suspect that Maff [the Ministry of Agriculture, Fisheries and Food] are ignoring it because it is difficult to deal with.'

The British Deer Society has been flooded with reports from deer experts reporting the animals limping and being covered with lumps. Mike Squire, secretary of the society, said: 'We find it difficult to believe that deer exposed to the same pastures as infected cattle and sheep have not been exposed to foot and mouth disease.'

A Maff spokesman said yesterday that government vets had tested nine deer for foot and mouth and none had been found positive: 'So far there have been no confirmed cases of foot and mouth in deer.'

However, the Maff vets use the Elisa test, which was developed on cattle and sheep and is not thought to be so effective on deer. Research from Russia also suggests it is very difficult to test whether deer have been infected with foot and mouth from blood samples.

In 1974 the government Animal Health Institute in Pirbright kept a number of deer in proximity to sheep with foot and mouth for two hours in a controlled experiment. The scientists found all six native species of deer contracted the disease, and several died.

In an outbreak of foot and mouth in California in 1924, the outbreak spread rapidly to deer. Slaughtermen culled 22,000 deer in the Stanislav National Park and found that, of those, 2,279 were infected.

Dr John Fletcher, past president of the Veterinary Deer Society, said: 'It's highly likely the virus has entered the wild deer population - the deer are in abundance and graze in close contact with sheep and cattle. Nothing has been confirmed, but there is an abundance of anecdotal evidence, and it would be quite surprising if it hasn't entered the population.'

Simon Booth, director of the Deer Inititiative, the government advisory body on deer in England, said: 'There have been unconfirmed cases of it appearing in deer.'

Deer experts have been calling on Maff for weeks to conduct a selective deer cull to ascertain the extent of the disease and to draw up contingency plans. However, Maff ignored their warnings until it called an emergency meeting on Friday. It is now considering lifting the ban on deer-stalking to provide the carcasses for tests.

The existence of the disease in Britain's 1.5 million wild deer population means the policy of mass slaughter of more than a million farm animals and the closure of most of the British countryside has been pointless. Wild deer are so evasive and diffi cult to track down that it is impossible to vaccinate or cull them. Shooting at herds of deer will simply cause them to run, spreading the disease further.

The deer population will harbour the disease before building up resistance and it eventually dies out. This could take years. Until then the deer will repeatedly re-infect livestock and, with the disease endemic in Britain, meat exports will continue to be banned.

Squire said: 'We're looking at a huge slaughter and cost to the taxpayer for no purpose. How do you think the public will react when they know that?'

Booth said: 'If it's in the deer population, it will mean the mass slaughter policy will not work.' Confirm-ation of foot and mouth among deer will force the Government to abandon the mass slaughter programme, a move that has been steadfastly resisted by the National Union of Farmers. 'It will force their hand into vaccination,' said Fletcher.


www.bds.org.uk British Deer Society http://www.guardian.co.uk/uk/2001/apr/22/politics.footandmouth



http://www.thedeerinitiative.co.uk/pdf/fmdguide.pdf

From The TimesAugust 7, 2007

Finding the real culprit for foot-and-mouth
Sir, In all the speculation about how the foot-and-mouth virus might have been transmitted from the facilities at Pirbright to the cattle in Normandy (report, August 6 ), one possible vector seems to have gone unmentioned. Holders of allotments, adjacent to the field where the affected cattle were kept, find they are plagued by wild deer. Not only do the cultivators see deerslots everywhere and find their crops chewed, but they also need to check after each visit that they have not picked up ticks.

All species of deer in Britain, particularly roe and muntjac, are susceptible to the foot-and-mouth virus and excrete it at much the same levels as sheep and cattle (Gibbs et al, The Veterinary Record, Vol 96, Issue 26, 558-63, 1975). Between Pirbright and Normandy, the countryside is heavily wooded and there are plenty of woodland corridors, ideal for deer, between more open fields. Is this aspect of biosecurity being addressed?
http://www.timesonline.co.uk/tol/comment/letters/article2210565.ece
« Last Edit: 31/08/2008 20:13:40 by Andrew K Fletcher »
 

Offline Bored chemist

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"Please explain how the deer managed to avoid the virus?"
They are not generally found on cattle or sheep farms where the virus was which helps; of course there were exceptions.
"Veterinary experts say it is impossible to vaccinate or cull wild deer and once infected they will act as a reservoir for the virus, repeatedly re-infecting livestock. It will make it almost imposs-ible for Britain to rid itself of the virus, until it dies out naturally in wild deer, which could take years. "
It clearly didn't take years, but the disease died out just as the experts predicted.

"Booth said: 'If it's in the deer population, it will mean the mass slaughter policy will not work.' "
The mass slaughter policy worked so either this guy was wrong or the disease didn't reach the general deer population.
"A Maff spokesman said yesterday that government vets had tested nine deer for foot and mouth and none had been found positive: 'So far there have been no confirmed cases of foot and mouth in deer.' "
Looks like that's the reason.
Perhaps it's related to this fact
"In an outbreak of foot and mouth in California in 1924, the outbreak spread rapidly to deer. Slaughtermen culled 22,000 deer in the Stanislav National Park and found that, of those, 2,279 were infected."
 so 90% of the deer didn't get the disease.

The other way to look at this is to hypothesis that there is a reservoir of infection in the UK- lets say in deeer for the sake of a concrete example.
OK this is known to be a virrulent disease- it has clear symptoms which, at least since the 2 recent outbreaks, anyone involved in farming would recognise. Even if they didn't spot that it was FMD they would certainly see that the animals were ill and some would proably die.
While it's not very common for deer and cattle or sheep to share pastures it not unheard of.
The experiment you mention shows that deer can catch FMD from other animals so it's fair to assume that the cattle or sheep would catch it from deer if the deer were infected.

If there is a stock of deer carrying the virus in the UK and given that this wet summer has been as good a set of conditions for the spread of the virus as you are likely to ghet, why hasn't there been an outbreak.

Let's be clear about this- if the virus is there you are going to get infected farm animals- the infection spreads like wildfire. It spread quickly even wnen ther are precautions in place to reduce the spread.
In a very short time there would be a massive outbreak. Sick animals would produce little or no milk and they would not get passed as fit for use as food.

How in the name of all that's holy do you think that this could happen and that we wouldn't notice?

Or are you going to say that the outbreak has been covered up by the men in black?
 

Offline Andrew K Fletcher

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Yes they were found on the farms where cattle and sheep are kept! Deer are everywhere where there is woodland. My wife and I regularly see them in Devon and have noticed their marks on trees in other areas.

Remember it is being said that it takes widespread prolonged flooding or prolonged high humidity to bring the animals down to the point that their own immune system fails and the virus becomes a problem. Under dry conditions the virus quickly retreats, presumably because the animals become more efficient at fighting the infection.

Testing a small group of deer to see if the whole population of deer may be harbouring this virus is unscientific and destined to produce a convenient null effect given the ratio of the deer that were culled in California this would appear to be correct as 9 dead deer could have easily shown that the Californian deer population did not have F&M.

If the disease naturally dies out, how come the World still has this disease? Note the pattern in the rainy season below. And the mention of floods in the South African Extract.l


http://www.fao.org/News/2001/011207-e.htm
Foot-and-mouth disease -- the Maasai caught between two worlds
But East Africa's cattle-raising Maasai people don't kill their infected cattle. For them, foot-and-mouth disease has almost become a part of everyday life -- it's so common they refer to it using the same word they use for the common cold: oloirobi. It occurs almost every rainy season with minimal loss of life.



Foot and mouth disease: the experience of South Africa
http://www.oie.int/eng/publicat/rt/2103/A_r21334.htm
G.K. Brückner, W. Vosloo, B.J.A. Du Plessis, P.E.L.G. Kloeck, L. Connoway, M.D. Ekron, D.B. Weaver, C.J. Dickason, F.J. Schreuder, T. Marais & M.E. Mogajane
Rev. sci. tech. Off. int. Epiz., 2002, 21 (3), 751-764 http://www.oie.int/eng/publicat/rt/2103/4.2.Bruckner.pdf
Summary
Foot and mouth disease (FMD) is endemic in African buffalo (Syncerus caffer) in the Kruger National Park (KNP) and surrounding game parks in South Africa. The last outbreak of the disease in domestic stock outside the FMD control zone occurred in 1957. Due to the success in containing the disease, the country was accorded zone freedom from FMD without vaccination by the Office International des Epizooties (OIE: World organisation for animal health) in 1995. This status was lost in September 2000 when the first-ever recorded case of serotype O in South Africa was diagnosed in a piggery in KwaZulu-Natal after the illegal feeding of untreated swill. In November 2000, an outbreak of FMD caused by serotype South African Territories (SAT) 1 was diagnosed in a feedlot within the free zone of Mpumalanga Province. The SAT 1 outbreak was traced to cattle in the FMD control zone south of the KNP after the game-proof fence surrounding the KNP was severely damaged by floods. This enabled buffalo to come into direct contact with cattle outside the KNP. A further outbreak caused by SAT 2 was diagnosed within the FMD control zone in February 2001, also as a result of buffalo having escaped from the KNP. All these outbreaks were successfully contained, with the re-instatement of zone freedom from FMD without vaccination by the OIE in May 2002.
These outbreaks made it necessary to re-examine the methods of control and containment of FMD that have been practised for many years and which are in line with accepted international practices. The authors describe the rationale for the different control strategies that were followed, the need for a multidisciplinary approach to disease control, the interface between control and technological and diagnostic support and the lessons learned. Some suggestions for future control strategies are also offered.
Keywords
African buffalo – Control strategies – Feedlots – Foot and mouth disease – Logistic support – Multidisciplinary approach – Office International des Epizooties – South Africa – Zones.

Take a good look at the South African experience with F&M here we have an area that has long periods without infection, yet there is a known population of wild animals that carry the disease. The mention of floods again rears its ugly head yet they blame a broken fence for cross contamination when there are ample carriers both predatory and passive and no restrictions on vehicles moving in and out of the infected areas. But the virus remains dorment for long periods. So your argument that we don’t have it so we must be clear of it does not fit with the reality of F&M.
« Last Edit: 31/08/2008 23:24:49 by Andrew K Fletcher »
 

Offline Bored chemist

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"Testing a small group of deer to see if the whole population of deer may be harbouring this virus is unscientific and destined to produce a convenient null effect given the ratio of the deer that were culled in California this would appear to be correct as 9 dead deer could have easily shown that the Californian deer population did not have F&M.
"
Testing only the sick deer is a much better test that you seem to think.

When there's an outbreak it doesn't just affect animal d that have been kept in flooded fields- it spreads out much like fire.
It keeps not happening even though we have bad Summers.
Why not?

You keep not really answering that question.
 

Offline Andrew K Fletcher

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I have answered it, it is not the flooded fields but the humidity and dampness that follows the floods as the water returns to the atmosphere.

You fail to understand that if the virus in South Africa can lull for years then re-emerge without an alien introduction other than birds and insects and wild animals, you have to explain how the virus knows it is in Africa, UK,France, or any other country and why it behaves different in the UK than it does in other countries.

The fact of the matter is that it does not behave any different, we also have lulls of often many years.

When I researched this during the 2001 pandemic I learned that there are indeed smaller outbreaks that go unreported over the years.

But lets take a look to see if unusually high humidity plays a roll in perpetuating the disease. Hong Kong is a good start being 2001 and 2002

The Weather of January 2001
    January 2001 was warmer and wetter than usual. The mean temperature of 17.3 degrees was 1.5 degrees above normal and the ninth highest for January. The monthly total rainfall of 47.6 millimetres was more than double the normal value of
November01: http://www.hko.gov.hk/wxinfo/pastwx/metob200111.htm

December 01:  http://www.hko.gov.hk/wxinfo/pastwx/metob200112.htm

February  02:  http://www.hko.gov.hk/wxinfo/pastwx/metob200202.htm

March 02:  http://www.hko.gov.hk/wxinfo/pastwx/metob200203.htm

April 02: http://www.hko.gov.hk/wxinfo/pastwx/metob200204.htm

May 02 : http://www.hko.gov.hk/wxinfo/pastwx/metob200205.htm

June: 02: http://www.hko.gov.hk/wxinfo/pastwx/metob200206.htm

July 02: http://www.hko.gov.hk/wxinfo/pastwx/metob200207.htm

August 02: http://www.hko.gov.hk/wxinfo/pastwx/metob200208.htm

September 02  http://www.hko.gov.hk/wxinfo/pastwx/metob200109.htm

October 02: http://www.hko.gov.hk/wxinfo/pastwx/metob200210.htm

November 02: http://www.hko.gov.hk/wxinfo/pastwx/metob200211.htm

December 02: http://www.hko.gov.hk/wxinfo/pastwx/metob200212.htm



http://www.hko.gov.hk/wxinfo/pastwx/mws200201.htm  Weather January 02


Foot-and-mouth disease under control
Monday, January 26, 2004
There is no evidence to suggest that foot-and-mouth disease in Hong Kong is more serious this year than in previous years, the Agriculture, Fisheries and Conservation Department (AFCD) said today (January 26).
Some 1,200 pigs were confirmed to have been infected with foot-and-mouth disease in 2003, compared with some 2,200 and 4,100 for 2002 and 2001 respectively. Most of the pigs were infected in the winter months. In January this year about 900 pigs were reported to have been infected.
"Farmers should report foot-and-mouth disease cases to the AFCD as soon as possible. It is in their best interests to do so as this allows the AFCD to provide farmers with veterinary diagnostic services. It also enables us to monitor the serotype of the virus so that an appropriate vaccine could be chosen if a new serotype is found," AFCD's Assistant Director (Inspection and Quarantine) Mr Lai Ching-wai said.
"The AFCD has started inspecting pig farms again to look for any unreported foot-and-mouth disease cases. An operation has also been mounted by the Food and Environmental Hygiene Department to check for any illegal dumping of dead pigs," he said.
Foot-and-mouth disease is a common viral disease occurring in pigs in the region including in Hong Kong. The disease does occur in pigs in Hong Kong during the winter months. Farmers control the disease by vaccination.

Now lets take a look at the weather of 2003 in Hong Kong. The report above states F&M under control Jan 2004. So we should see a significant drop in humidity from September 2003 to January 2004.

Early September follows the high humidity trend which falls to lower levels towards the end of the month. October humidity is much lower November lower still and December lower again.

Jan 03: http://www.hko.gov.hk/wxinfo/pastwx/metob200301.htm
Feb 03: http://www.hko.gov.hk/wxinfo/pastwx/metob200302.htm
Mar 03: http://www.hko.gov.hk/wxinfo/pastwx/metob200303.htm
Apr 03: http://www.hko.gov.hk/wxinfo/pastwx/metob200304.htm
May 03: http://www.hko.gov.hk/wxinfo/pastwx/metob200305.htm
June 03: http://www.hko.gov.hk/wxinfo/pastwx/metob200306.htm
Jul 03: http://www.hko.gov.hk/wxinfo/pastwx/metob200307.htm
Aug 03: http://www.hko.gov.hk/wxinfo/pastwx/metob200308.htm
Sep 03: http://www.hko.gov.hk/wxinfo/pastwx/metob200309.htm
Oct 03: http://www.hko.gov.hk/wxinfo/pastwx/metob200310.htm
Nov 03: http://www.hko.gov.hk/wxinfo/pastwx/metob200311.htm
Dec 03: http://www.hko.gov.hk/wxinfo/pastwx/metob200312.htm
« Last Edit: 01/09/2008 09:33:13 by Andrew K Fletcher »
 

Offline Bored chemist

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"you have to explain how the virus knows it is in Africa, UK,France, or any other country and why it behaves different in the UK than it does in other countries."
OK, that looks like an interesting challenge.
A virus cannot really "know" anything, but it does carry information. For example the virus carries information about what strain it is.
In particular, the virus that caused the 2007 outbreak was the same one that had caused the 1967 outbreak- hardly suprising since that's the strain that pirbright dealt with. The report into that outbreak points out that this particular strain is no longer found in the wild. there's a link to the report here.
http://www.hse.gov.uk/news/archive/07aug/footandmouth.htm
and this is what it says "Defra identified the strain of FMDV involved in the outbreak as Type O1 BFS67,
which is the strain recovered from the 1967 FMD epidemic in Great Britain. This strain
is used in FMD reference laboratories and pharmaceutical manufacturing plants and
is not known to be currently in circulation anywhere in the world. Hereafter this will be
referred to as the O1 BFS strain."

OK, so that's one thing this virus can be said to "know" it "knows" that it came from a research facility- not the wild..

The other question is how the virus can know it's in the UK rather than in Africa.
Again, of course, it can't- but it doesn't need to.
All it needs to do is infect the local cattle (and, lets face it, it will do that).
In Africa it will meet cattle that have often been infected before so it will not cause any infection. The animal's immune system will wipe it out.
Sometimes it will meet a young animal that has never been infected before- in this case it will cause disease but, like the different strains of the virus, there are different bloodlines in the cattle. The cattle in Africa are those whose parents and grandparents etc for many generations have withstood the virus.

In the UK it faces a different world. None of the cattle have been infected with FMD before- so they are all fully susceptible. Also, while cattle have been deliberately bred for many characteristics, FMD resistance hasn't been a factor for generations.

You might think that this difference isn't big enough to explain the observed difference between outbreaks in the UK and the endemic disease in Africa.
Have you read what happened when the first Europeans traveled to South America and introduced viruses like measles, flu etc.?
They often wiped out the local population.
http://www.millersville.edu/~columbus/papers/orlow-e.html

There's yet another thing that viruses "know" - that it doesn't help to be too virulent. If a virus causes a massive infection the host dies out before the virus spreads very far. That's not good for the virus. It makes sense for the virus to evolve into a version that causes relatively mild symptoms (or even none at all) in the host.

In the decades since the older outbreaks in the UK the wild virus will have "calmed down". The stocks maintained in labs are under no such evolutionary pressure and will Therefore be more vigorous than the current wild forms.

Since the recent outbreak was an old virus, it's not that odd that it did more damage than the current wild strains.

Incidentally, re. "When I researched this during the 2001 pandemic I learned that there are indeed smaller outbreaks that go unreported over the years."
Not in the UK there aren't.

Thanks for the Hong Kong weather reports, but the fact is that you don't have any evidence to back your conspiracy theory.

and, just to reiterate the point,
"I have answered it, it is not the flooded fields but the humidity and dampness that follows the floods as the water returns to the atmosphere. "
In much the same way that the UK often has wet Summers, it often has high humidity.
The wet (or humid) conditions are common, but outbreaks are not.
You still need to explain the lack of outbreaks in other wet Summers. The difference between "wet" and "humid" isn't that big really.



 

Offline Andrew K Fletcher

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http://ukpress.google.com/article/ALeqM5guxWtyfYWpqQXW0pO97c-Wi7iiXQ
New outbreak of bluetongue found
1 day ago
A fresh outbreak of bluetongue has been detected in livestock imported to the UK, the Department for Environment, Food and Rural Affairs (Defra) has said.
The disease, which can be fatal to animals such as cows and sheep, was identified in 18 cattle on premises near Bishop Auckland, County Durham.


http://www.thenorthernecho.co.uk/news/3664233.Disease_outbreak_blow_to_farmers/
Disease outbreak blow to farmers
9:13am Thursday 11th September 2008
Farming leaders said last night that the latest outbreak, coming after the summer’s poor weather, which has wrecked crops, was further “dreadful news”.
Country Land and Business Association’s (CLA) regional director Dorothy Fairburn said: “This will be a blow to the whole industry.
“I would urge farmers to contact the National Farmers’ Union and the CLA for further information. It won’t have the same sort of serious effects as foot-and-mouth, but it couldn’t have come at a worse time of year for the sales of sheep and store cattle.
“It is absolutely dreadful news.”
Despite the threat from bluetongue – which has ravaged livestock across Europe – only one in five farmers have vaccinated their animals.
The disease is spread by midges that thrive in late summer weather. There are no cases of it being transferred to humans, but the illness can be fatal for cows and sheep.
The outbreak prompted warnings about importing cattle from the Continent where the NFU says the virus is virulent.
More than 30,000 cases were confirmed in France in one week last month.
NFU president Peter Kendall said: “Farmers need to be confident that either the animals have been correctly vaccinated and met all the appropriate conditions of the vaccine or they must be sure that the animals are not carrying the bluetongue virus through thorough testing.
 

Offline Bored chemist

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I'm sorry, but not suprised to hear that.
What has it got to do with the thread?
Bluetongue isn't foot and mouth disease.
FMD is not spread by biting midges which can be carried accross the channel on the wind.
FMD isn't widespread in Europe.
 

Offline Andrew K Fletcher

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Included Blue Tongue on the original post to show close relationship with weather and yes I agree that midges are responsible for infecting the herds, but suspect that the weather also plays a part in lowering the animals immune system and body temperature assisting the infection rates.
 

Offline Bored chemist

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Bluetongue outbreaks die out in Winter when it's cold and wet.
 

Offline Andrew K Fletcher

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Bluetongue outbreaks die out in Winter when it's cold and wet.

Bluetongue surviving winter by infecting livestock foetuses
Tuesday, 26 Aug 2008 12:13
Scientists have come up with a number of hypotheses for explaining how the Bluetongue virus survives winter.

When it first reached livestock in northern Europe in 2006 it was thought that the virus would be killed off during the winter and thereby prevent it from spreading.

However, the virus did survive the winter and in fact escalated the following year.

Scientists from the Institute for Animal Health looked into how the virus survived in the open access journal PLoS Biology.

They claim that the survival may be due to a number of different reasons. In mild winters, such as that of 2006/07 for example, the infected midges may have survived in livestock barns before becoming active again in spring.

Another possibility is that Bluetongue is in fact spread by some susceptible species of long-lived ticks and by the simple mechanical transmission by Melopagus ovinus, a wingless parasite that lives in sheep.

Evidence from Australia also points to the fact that the Bluetongue virus can survive inside midges and cattle for three to four months, enough time to survive the majority of winter.

In northern Europe, it seems that the virus can survive by transplacental infections – spreading from an infected pregnant animal to its foetus. This is a significant phenomenon in cattle due to its nine month gestation period.

Dr Mellor, of the Institute for Animal Health, concludes: "Experiments have revealed a toolbox of possible mechanisms, with the potential to interact with and complement one another..
http://www.inthenews.co.uk/news/science/
« Last Edit: 13/09/2008 21:33:16 by Andrew K Fletcher »
 

Offline Bored chemist

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Many bluetongue outbreaks die out in Winter when it's cold and wet.
 

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