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From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.bio.food-science,sci.bio.microbiology
Subject: Re: IFST condemns UK Government's reported rejection of E.coli safety
recommendations
Date: Fri, 21 Mar 1997 06:51:54 +0000
In article <3332cea4.7422344@news.easynet.co.uk>, J Ralph Blanchfield
<jralphb@easynet.co.uk> writes
>Many butchers already segregate cooked and raw meats successfully.
>There is no reason why others should be allowed to fail to meet this
>necessary safety measure. Any butchers who cannot do so should not be
>allowed to handle cooked meats.
This is done in several small English country butchers that I know of
already, complete with (THEY claim) requisite washbasin between cooked
and raw. Does the law vary between Scotland and the England in this
respect already?
Please also note the very low (I have come across one case only) EC O157
infection in farmworkers which might suggest that an immunity is readily
produced with low level exposure.
I would also like to request if anyone knows in EC O157 is a new strain,
previously not seen in the UK, or an old strain that the human
population has currently low resistance to.
--
'Oz "Is it better to seem ignorant and learn,
- or seem wise and stay ignorant?"
From: Tim Williams <tim@microbes.demon.co.uk>
Newsgroups: sci.bio.food-science,sci.bio.microbiology
Subject: Re: IFST condemns UK Government's reported rejection of E.coli safety
recommendations
Date: Sat, 22 Mar 1997 22:01:26 +0000
In article <DkUZsJAKAjMzEwmU@upthorpe.demon.co.uk>, Oz
>Please also note the very low (I have come across one case only) EC O157
>infection in farmworkers which might suggest that an immunity is readily
>produced with low level exposure.
This may be the case, E coli O157 infections appear to be more common at
extremes of age. The same is very much true of the complications
associated with 0157 (Haemolytic uraemic syndrome and Thrombotic
thrombocytopaenia purpura) There have certainly been cases of infection
of children following contact with bovine faeces.
>I would also like to request if anyone knows in EC O157 is a new strain,
>previously not seen in the UK, or an old strain that the human
>population has currently low resistance to.
There is evidence to suggest that E.coli 0157:H7 is a relatively new
pathogen. The first known outbreak of haemorrhagic colitis was in 1982
in the North West United States and Canada. Retrospective studies that
looked at 3000 stored isolates at CDC in the States found only one
previous case (1975 in California). Using molecular typing methods, it
also appears that differences between different isolates of 0157:H7 are
much smaller than genetic differences between other strains of E.coli.
This would suggest a recent emergance of this organism.
--
Tim Williams
From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.bio.food-science,sci.bio.microbiology
Subject: Re: IFST condemns UK Government's reported rejection of E.coli safety
recommendations
Date: Sun, 23 Mar 1997 00:12:51 +0000
In article <$TsQFLA2aFNzEwL8@microbes.demon.co.uk>, Tim Williams
<tim@microbes.demon.co.uk> writes
>In article <DkUZsJAKAjMzEwmU@upthorpe.demon.co.uk>, Oz
>>
>>Please also note the very low (I have come across one case only) EC O157
>>infection in farmworkers which might suggest that an immunity is readily
>>produced with low level exposure.
>
>This may be the case, E coli O157 infections appear to be more common at
>extremes of age. The same is very much true of the complications
>associated with 0157 (Haemolytic uraemic syndrome and Thrombotic
>thrombocytopaenia purpura) There have certainly been cases of infection
>of children following contact with bovine faeces.
>
>>I would also like to request if anyone knows in EC O157 is a new strain,
>>previously not seen in the UK, or an old strain that the human
>>population has currently low resistance to.
>
>There is evidence to suggest that E.coli 0157:H7 is a relatively new
>pathogen. The first known outbreak of haemorrhagic colitis was in 1982
>in the North West United States and Canada. Retrospective studies that
>looked at 3000 stored isolates at CDC in the States found only one
>previous case (1975 in California). Using molecular typing methods, it
>also appears that differences between different isolates of 0157:H7 are
>much smaller than genetic differences between other strains of E.coli.
>This would suggest a recent emergance of this organism.
I have left all the quotes deliberately.
If this is a newly emerged strain then it becomes clearer. As I
understand it there are other strains of EC that produce the same, or at
least a very similar toxin. Similar enough to come out positive in the
recently developed test. However the other strains are not pathogenic,
or very rarely so. A new strain should, as far as I can see, attack
those members of the population that are susceptible and this would
typically be older people that didn't come across it in their youth, and
children. This may be compounded by the way food for children and old
people is prepared, ie often institutionally and in quantity, allowing
for mass infection which has, I believe, been a feature of the scottish
outbreaks.
On another tack this perhaps brings up another pointer for the future.
As hygeine has improved, both in the home and in the food chain,
exposure to 'environmental' bacteria must have been significantly
reduced. I would presume this would reduce the rapidity of the bodies
response to new infections, in some people to the point where toxins
could cause serious damage. One could endevour to improve hygeine still
further, but this opens one to the possibility of severe reactions where
this occasionally fails, as it must. It may be that inoculation to
emerging pathogens may be a better route. We see this with tetanus,
which was not required when dirty deep wounds were common, but as
hygeine has improved we may need to keep watch for other emerging
pathogens so as to be able to immunise the population rather than wait
for it to occur naturally, and perhaps on occasion fatally.
We are living in a society that is further and further removed, and
isolated, from the natural world. We cannot, however, divorce ourself
from nature completely. [End of sermon.]
--
'Oz "Is it better to seem ignorant and learn,
- or seem wise and stay ignorant?"
From: Tim Williams <tim@microbes.demon.co.uk>
Newsgroups: sci.bio.food-science,sci.bio.microbiology
Subject: Re: IFST condemns UK Government's reported rejection of E.coli safety
recommendations
Date: Sun, 23 Mar 1997 09:55:54 +0000
Please forgive me if I repeat things that have already been stated, or
show ignorance of some previously made point. This thread has only
recently appeared on sci.bio.microbiology.
In article <VQ3cRJADWHNzEwuH@upthorpe.demon.co.uk>, Oz
<Oz@upthorpe.demon.co.uk> writes
>If this is a newly emerged strain then it becomes clearer. As I
>understand it there are other strains of EC that produce the same, or at
>least a very similar toxin. Similar enough to come out positive in the
>recently developed test.
I am not sure what tests are being referred to here. It may be a
verotoxin detection method. If this is the case , then yes, it may pick
up 'non pathogenic strains' but these types tend to produce toxin in
much smaller quantities (I believe I have read that O157:H7 produces at
least 1000x the toxin levels of other , non enterohaemorrhagic E.coli)
>However the other strains are not pathogenic, or very rarely so.
To be pedantic, I should make the point (probably made previously) that
E.coli O157:H7 is only one (albeit probably the most common) of a group
of organisms termed the enterohaemorrhagic E.coli (EHEC). These are the
organisms which cause the bloody diarrhoea and complications such as HUS
and TTP. O157:H7 appears responsible for most recorded outbreaks in the
UK and North America. Other strains of EHEC (notably O111 and O26) have
been implicated in causing Haemorrhagic colitis in other countries.
It is possible that O157:H7 is more widely reported as it is easier to
detect in routine clinical laboratories because of it's non fermentation
of sorbitol. A German team has published data showing that non O157:H7
strains were associated with more cases of HUS in Eastern Europe.
--
Tim Williams
From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.bio.food-science,sci.bio.microbiology
Subject: Re: IFST condemns UK Government's reported rejection of E.coli safety
recommendations
Date: Sun, 23 Mar 1997 12:16:13 +0000
In article <fZr43CAq4PNzEwvn@microbes.demon.co.uk>, Tim Williams
<tim@microbes.demon.co.uk> writes
OK, we have some microbiologists on the thread, which is very nice.
I have some questions:
1) In their view is the increase in EC O157 a real one, ie is it due to
better reporting or is it an actual significant increase?
2) Whilst it would seem reasonable that at least some of the infection
derives from surface contamination of carcasses, I find it very hard to
believe that standards are markedly worse than ten or twenty years ago.
Indeed as far as farmers are concerned the standards have vastly
improved over that time and I would genuinely be astonished if that were
not also the case in abattoirs too. However I do sometimes wonder if
food preparation and hygeine has kept pace. I find it hard to see how
one can ever be confident of reducing surface bacterial contamination
such as to be certain that there are not a few hundred pathogenic
bacteria on a carcass (quoted bacterial loadings for EC O157). One
wonders if education further down the food chain is not more appropriate
if outbreaks are not to be reduced.
3) I saw quoted on the net that a large outbreak in the US was caused by
organic lettuce been irrigated using diluted cattle slurry so as to
provide nutrients (probably for improved colour as well as growth). Can
anyone confirm or deny this quote. This (as a farmer) is suspiciously
plausible but indicates the problem of locating sources of contamination
since even vegetables, particularly organic ones, may well come into
contact with animal excrement. Vegetables are often consumed raw, are
unrefrigerated and must on reflection be a significant risk.
4) I really do find it odd that farmers (many of whome are old),
farmstaff and their children, that inevitably come into very significant
contact with animal excreta have not been subject to considerably higher
infection rates. I would be interested in comments as to why this should
be so.
5) Is it indeed true that a few hundred EC O157 bacteria are enough to
instigate a clinical infection.
6) To what extent do antibodies to the TOXIN protect one from the more
serious effects of infection? Would one expect cross resistance since I
understand that the toxin is also produced in lesser amounts by other
strains?
7) There has been a steady reduction in additives originally designed to
improve shelf life in all foods. For example I believe that sodium
nitrite was routinely added to mince and that this reduced bacterial
numbers as well as improving the colour. Whilst I am not enthusiastic on
additives for cosmetic reasons there was much made at the time these
reductions were taking place that one should expect an increase in food
poisoning as a direct result of the reduction in bacteriostats. I find
it hard not to relate this to the steady increase in these problems over
the last decade. What is the microbiologists view?
That's probably enough for now, but I would be most interested in your
answers.
--
'Oz "Is it better to seem ignorant and learn,
- or seem wise and stay ignorant?"
From: Tim Williams <tim@microbes.demon.co.uk>
Newsgroups: sci.bio.food-science,sci.bio.microbiology
Subject: Re: IFST condemns UK Government's reported rejection of E.coli safety
recommendations
Date: Sun, 23 Mar 1997 16:14:04 +0000
In article <9m02sBAN8RNzEwIR@upthorpe.demon.co.uk>, Oz
<Oz@upthorpe.demon.co.uk> writes
>I have some questions:
>
>1) In their view is the increase in EC O157 a real one, ie is it due to
>better reporting or is it an actual significant increase?
Still open to debate: The PHLS has recently reported in the CDR
(Communicable disease report) that the recent increase in isolates from
Human faeces is a result of a change in policy. Untill recently only
specimens showing blood were investigated for EC O157 (By which I mean
E.coli O157:H7). Following changes to laboratory protocols, all samples
are tested. Also lab methods have changed, with introduction of an
enrichment media.
My personal belief is that numbers are steadily increasing. This would
be borne out by the steady rise in numbers of isolates of EC O157 in
England and Wales between 1985 and the present time. This , I believe,
would also be consistent with a recently evolved pathogen. Numbers will
continue to increase as the organism becomes more widespread (An article
in a recent New Scientist has linked possible spread to seagulls) . I
believe that cases of HUS have also increased over this period, which
would reflect such a rise in O157 infections.
>2) Whilst it would seem reasonable that at least some of the infection
>derives from surface contamination of carcasses, I find it very hard to
>believe that standards are markedly worse than ten or twenty years ago.
I have no experience of such matters, but would think that the standards
10 years ago would not be as relevant if carriage was lower.
>One
>wonders if education further down the food chain is not more appropriate
>if outbreaks are not to be reduced.
I agree, but it is not enough. If anybody thinks that Mrs Curry's
Salmonella in Eggs crisis is over, just look any recent CDR report.
People have short memories - if a problem is not constantly on the news,
it doesn't exist.
>3) I saw quoted on the net that a large outbreak in the US was caused by
>organic lettuce been irrigated using diluted cattle slurry so as to
>provide nutrients (probably for improved colour as well as growth).
No idea. I have certainly read eight cases of HUS in Germany linked to
parsley butter which was organically grown and fertilised with slurry.
This case is strange in that the causitive organism was a verotoxin
producing Citrobacter - not an E.coli
>4) I really do find it odd that farmers (many of whome are old),
>farmstaff and their children, that inevitably come into very significant
>contact with animal excreta have not been subject to considerably higher
>infection rates. I would be interested in comments as to why this should
>be so.
I cannot answer this one, but at a recent meeting of the Chartered
Institute of Environmental Health, a speaker mentioned that he believed
that O157 infection in children , following contact with animals, was
greatly under reported. (I believe that he meant that the infection was
noted, but the connection with the animals not taken into account.)
>5) Is it indeed true that a few hundred EC O157 bacteria are enough to
>instigate a clinical infection.
Almost certainly. Most papers I have read put the infectious dose at
less than one hundred. Some put it at significantly lower than this.
>6) To what extent do antibodies to the TOXIN protect one from the more
>serious effects of infection? Would one expect cross resistance since I
>understand that the toxin is also produced in lesser amounts by other
>strains?
A very good question. I believe that the central Public Health Lab at
Colindale is investigating this at the moment.
>
>7) There has been a steady reduction in additives originally designed to
>improve shelf life in all foods. For example I believe that sodium
>nitrite was routinely added to mince and that this reduced bacterial
>numbers as well as improving the colour. Whilst I am not enthusiastic on
>additives for cosmetic reasons there was much made at the time these
>reductions were taking place that one should expect an increase in food
>poisoning as a direct result of the reduction in bacteriostats. I find
>it hard not to relate this to the steady increase in these problems over
>the last decade. What is the microbiologists view?
This may well be (I cannot answer with any great confidence - this is
outside of my experience). It may be that consumers will just not accept
these preservatives any longer.
--
Tim Williams
From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.bio.food-science,sci.bio.microbiology
Subject: Re: IFST condemns UK Government's reported rejection of E.coli safety
recommendations
Date: Sun, 23 Mar 1997 17:38:02 +0000
Many thanks indeed for your replies. I hope others on your newsgroup can
fill in the few areas you were not confident about, or indeed add their
views.
In article <8jSQpAAMbVNzEwpO@microbes.demon.co.uk>, Tim Williams
<tim@microbes.demon.co.uk> writes
>In article <9m02sBAN8RNzEwIR@upthorpe.demon.co.uk>, Oz
><Oz@upthorpe.demon.co.uk> writes
>>1) In their view is the increase in EC O157 a real one, ie is it due to
>>better reporting or is it an actual significant increase?
>
>My personal belief is that numbers are steadily increasing. This , I believe,
>would also be consistent with a recently evolved pathogen. Numbers will
>continue to increase as the organism becomes more widespread. I
>believe that cases of HUS have also increased over this period, which
>would reflect such a rise in O157 infections.
So we are seeing a transition between a population susceptible to this
strain, but in the process of becoming (largely) immune. Doubtless this
has happened before, but probably not as well documented.
>I agree, but it is not enough. If anybody thinks that Mrs Curry's
>Salmonella in Eggs crisis is over, just look any recent CDR report.
>People have short memories - if a problem is not constantly on the news,
>it doesn't exist.
Agreed. However the swing from one extreme to another is very damaging
to all concerned. Currently at least some people think that it's now OK
to leave mayonnaise and indeed many other rapidly perishable foods at
room temperatures for many hours awaiting consumption. At least part,
and maybe a major part, of the problem is the inability to appreciate
that bacteria can multiply, sometimes rather rapidly.
>>3) I saw quoted on the net that a large outbreak in the US was caused by
>>organic lettuce been irrigated using diluted cattle slurry so as to
>>provide nutrients (probably for improved colour as well as growth).
>No idea. I have certainly read eight cases of HUS in Germany linked to
>parsley butter which was organically grown and fertilised with slurry.
>This case is strange in that the causitive organism was a verotoxin
>producing Citrobacter - not an E.coli
Cattle have plenty of resident bugs that most of the population will not
have been exposed to. One wonders if a short rinse in chlorinated water
would significantly reduce the bacterial load for fresh vegetables (of
course at a risk of increasing the intake of organochlorine compounds).
I have also wondered for some years if the acidic nature of a french
dressing has a similar, if lesser, bacteriocidal effect (with or without
garlic :-).
>>4) I really do find it odd that farmers (many of whome are old),
>>farmstaff and their children, that inevitably come into very significant
>>contact with animal excreta have not been subject to considerably higher
>>infection rates. I would be interested in comments as to why this should
>>be so.
>I cannot answer this one, but at a recent meeting of the Chartered
>Institute of Environmental Health, a speaker mentioned that he believed
>that O157 infection in children , following contact with animals, was
>greatly under reported. (I believe that he meant that the infection was
>noted, but the connection with the animals not taken into account.)
Are we talking about pets as well as bovines here? One might presume
that the spread of EC O157 (and indeed others) would include it's spread
to other mammals. One has to say that, loveable as they are, dogs do
have (to human eyes) a strange veiw of suitable things to eat. :-)
>>5) Is it indeed true that a few hundred EC O157 bacteria are enough to
>>instigate a clinical infection.
>>
>Almost certainly. Most papers I have read put the infectious dose at
>less than one hundred. Some put it at significantly lower than this.
Forgive me for asking but to me this level is such that realistic
prevention of contamination for uncooked foods is essentailly
impossible. Indeed human to human contact should, I would have thought,
be a major source of spread particularly in institutions or indeed
anywhere where significant numbers are in contact for a significant
time. I doubt that washing your hands would reduce the levels to under a
hundred bacteria.
>>7) There has been a steady reduction in additives originally designed to
>>improve shelf life in all foods. For example I believe that sodium
>>nitrite was routinely added to mince and that this reduced bacterial
>>numbers as well as improving the colour. Whilst I am not enthusiastic on
>>additives for cosmetic reasons there was much made at the time these
>>reductions were taking place that one should expect an increase in food
>>poisoning as a direct result of the reduction in bacteriostats. I find
>>it hard not to relate this to the steady increase in these problems over
>>the last decade. What is the microbiologists view?
>
>This may well be (I cannot answer with any great confidence - this is
>outside of my experience). It may be that consumers will just not accept
>these preservatives any longer.
Ahh. Like so many things in life, and particularly in nature, it may be
that to refuse to accept one thing because of risks simply opens one to
a different risk. Life was ever so. It would be nice to be able to put
some figures on the risk of preservatives verses the risk of infections.
In passing, does anyone know the mortality due to preservatives for a
comparison?
Not that anyone would take any notice, preservatives are not politically
correct.
--
'Oz "Is it better to seem ignorant and learn,
- or seem wise and stay ignorant?"
Newsgroups: sci.bio.food-science,sci.bio.microbiology
Subject: Re: IFST condemns UK Government's reported rejection of E.coli
safety recommendations
From: Oz <Oz@upthorpe.demon.co.uk>
Date: Mon, 24 Mar 1997 16:30:14 +0000
In article <5h64aa$ndg@panix2.panix.com>, Pierre Jelenc <rcpj@panix.com>
writes
>Oz <Oz@upthorpe.demon.co.uk> writes:
>>
>> Cattle have plenty of resident bugs that most of the population will not
>> have been exposed to. One wonders if a short rinse in chlorinated water
>> would significantly reduce the bacterial load for fresh vegetables (of
>> course at a risk of increasing the intake of organochlorine compounds).
>
>FWIW, I always soak _all_ my raw vegetables, fruit, and salads in dilute
>potassium permanganate (enough to turn the water decidedly pink purple)
>for 5-10 minutes.
Does this affect the flavour? Or indeed, by oxidation, the colour?
Me, I hope to get lots of multiple low doses of nearly everything and
trust in immunity. Call me a throwback or primitive if you will.
However it is a point for supermarkets where they *might* get sued for
supplying contaminated food. This will become more important if the
production of 'organic' food extends to africa and asia where there are
a number of rather nasty gastrointestinal diseases. In some areas human
sewage is the biggest and cheapest source of 'organic' fertiliser and
it's treatment may (!) not always have been, er, perfect.
--
'Oz "Is it better to seem ignorant and learn,
- or seem wise and stay ignorant?"
Newsgroups: sci.bio.food-science,sci.bio.microbiology
Subject: Re: IFST condemns UK Government's reported rejection of E.coli
safety recommendations
From: Oz <Oz@upthorpe.demon.co.uk>
Date: Mon, 24 Mar 1997 20:55:33 +0000
In article <5h6fqa$gpa@panix2.panix.com>, Pierre Jelenc <rcpj@panix.com>
writes
>Oz <Oz@upthorpe.demon.co.uk> writes:
>> In article <5h64aa$ndg@panix2.panix.com>, Pierre Jelenc <rcpj@panix.com>
>> writes
>> >
>> >FWIW, I always soak _all_ my raw vegetables, fruit, and salads in dilute
>> >potassium permanganate (enough to turn the water decidedly pink purple)
>> >for 5-10 minutes.
>>
>> Does this affect the flavour? Or indeed, by oxidation, the colour?
>
>No problem with the taste (I rinse it first, of course). A few things have
>a tendency to get oxidised a bit, e.g. endives and escarole. Those I soak
>briefly, about 1 minute.
Well, I suppose microbiologists are likely to have a 'thing' about bugs
and infection. I would strongly suggest that you ever avoid working on
an animal farm, in particular milking cows. :-)
You will forgive me if I comment that I find your procedure somewhat
excessive, however to each his own.
--
'Oz "Is it better to seem ignorant and learn,
- or seem wise and stay ignorant?"
Newsgroups: sci.bio.food-science,sci.bio.microbiology
Subject: Re: IFST condemns UK Government's reported rejection of E.coli
safety recommendations
From: Tim Williams <tim@microbes.demon.co.uk>
Date: Mon, 24 Mar 1997 21:03:01 +0000
In article <oRpDxCA6pWNzEwZ5@upthorpe.demon.co.uk>, Oz
<Oz@upthorpe.demon.co.uk> writes
>So we are seeing a transition between a population susceptible to this
>strain, but in the process of becoming (largely) immune. Doubtless this
>has happened before, but probably not as well documented.
I don't know if I agree with this, but I am unable to find any data to
support or refute this (But I'll keep looking).
>Are we talking about pets as well as bovines here? One might presume
>that the spread of EC O157 (and indeed others) would include it's spread
>to other mammals. One has to say that, loveable as they are, dogs do
>have (to human eyes) a strange veiw of suitable things to eat. :-)
Yes. Certainly one case quoted at the Environmental Health seminar
involved a child with no direct contact with cattle, but whose pet dog
frequently found in a field containing cattle manure. Swabs of the dogs
coat yielded O157. Other cases were linked to 'Childrens farms' (Areas
where children were able to play with young lambs, calves etc).
I must stress that all the above is anecdotal, being my memories of a
lecture.
>Forgive me for asking but to me this level is such that realistic
>prevention of contamination for uncooked foods is essentailly
>impossible. Indeed human to human contact should, I would have thought,
>be a major source of spread particularly in institutions or indeed
>anywhere where significant numbers are in contact for a significant
>time.
Person to person spread has certainly been implicated in outbreaks,
particularly in nursery schools and old Age homes.
--
Tim Williams
Newsgroups: sci.bio.food-science,sci.bio.microbiology
Subject: Re: IFST condemns UK Government's reported rejection of E.coli
safety recommendations
From: Oz <Oz@upthorpe.demon.co.uk>
Date: Tue, 25 Mar 1997 08:05:29 +0000
In article <XIgqDAAFwuNzEw$s@microbes.demon.co.uk>, Tim Williams
<tim@microbes.demon.co.uk> writes
>In article <oRpDxCA6pWNzEwZ5@upthorpe.demon.co.uk>, Oz
><Oz@upthorpe.demon.co.uk> writes
>>So we are seeing a transition between a population susceptible to this
>>strain, but in the process of becoming (largely) immune. Doubtless this
>>has happened before, but probably not as well documented.
>
>I don't know if I agree with this, but I am unable to find any data to
>support or refute this (But I'll keep looking).
On reflection whether this is the case with EC O157 or not, it strikes
me that there may be a problem of immunity to potential pathogens as
lifestyles change. This may be of general importance since we may well
see other pathogens causing significant mortality that heretofore were
not considered pathogens at all.
There is no doubt in my mind that hygeine in food has improved very
drastically over the last couple of decades. Although this has
presumably reduced levels of salmonella and other known gastrointestinal
pathogens we see (in the press at least) if anything an increase in
serious cases. This may just be an effect of reporting of course but let
me just compare human populations with animal ones for a moment.
In pigs there is a common technique called the minimal disease herd.
Here animals are rigorously separated from outside contact and entry is
forbidden except by staff members who are contractually obliged to keep
away from other pigs. Incoming animals (eg for breeding) are brought by
specialist transport only from other minimal disease herds. The herd is
in biological isolation. The idea is to have healthier pigs and use less
medication. The problem is that when disease does get in the effects on
the animals is truly devastating.
In my own herd diseases that are endemic at low level rarely cause
problems, and indeed may never be seen clinically. It is new diseases
from outside that cause mortality. We have consciously located calf
accommodation so they are in close contact with the cows. Apart from IBR
introduced by a bull, we have never had to treat, or had a significant
problem, with cow diseases in 20 years (fingers crossed). The herd was
Brucellosis and TB free when we took it over.
Now human populations used to receive regular doses of bacteria from the
countryside outside the cities on their food, generally at low level but
occasionally at high level usually due to a gross failure of hygeine.
Consequently the population in cities generally had a relatively high
level of immunity to most of the environmental bacteria. The very
considerable improvements in food hygeine over the last 20 years may
well have been enough to break this connection, at least for a minority
of the population. If this is the case we must consider that previously
non-pathogenic, or rarely pathogenic, bacteria may now become capable of
causing serious illness in at least a subset of the isolated (city)
population.
How one deals with this is not that straightforward. I very much doubt
that permanent isolation of the population from these bacteria is
possible, they are common in the environment. Equally a reduction in
food hygeine is probably not acceptable either although effort might be
directed in preventing gross contamination and multiplication rather
than sterility. Perhaps a regular (annual?) innoculation may need to be
considered, although this may be available over the counter.
Or perhaps (as has been known) I am talking rubbish.
--
'Oz "Is it better to seem ignorant and learn,
- or seem wise and stay ignorant?"
Newsgroups: sci.bio.food-science,sci.bio.microbiology
Subject: Re: IFST condemns UK Government's reported rejection of E.coli
safety recommendations
From: Tim Williams <tim@microbes.demon.co.uk>
Date: Tue, 25 Mar 1997 20:55:22 +0000
In article <cPlu2BAJd4NzEw+$@upthorpe.demon.co.uk>, Oz
<Oz@upthorpe.demon.co.uk> writes
>Now human populations used to receive regular doses of bacteria from the
>countryside outside the cities on their food, generally at low level but
>occasionally at high level usually due to a gross failure of hygeine.
>Consequently the population in cities generally had a relatively high
>level of immunity to most of the environmental bacteria. The very
>considerable improvements in food hygeine over the last 20 years may
>well have been enough to break this connection, at least for a minority
>of the population. If this is the case we must consider that previously
>non-pathogenic, or rarely pathogenic, bacteria may now become capable of
>causing serious illness in at least a subset of the isolated (city)
>population.
>
>Or perhaps (as has been known) I am talking rubbish.
I don't think you are talking rubbish. Anecdotal evidence suggests that
many councillors who take trips to the continent return with diarrhoea.
It has been suggested that this is a result of lack of exposure to
common food borne organisms (I believe , but am open to correction, that
the problem is often the nicely named Small Round Virus). The theory
goes that the Continentals , with less processed foodstuffs (Real Food?)
are exposed to a higher number of organisms as children, and
subsequently develop immunity.
--
Tim Williams
From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.bio.food-science,sci.bio.microbiology
Subject: Re: E.coli O157 outbreak in Scottish hospital
Date: Wed, 28 May 1997 11:29:16 +0100
In article <338f697f.6537283@news.easynet.co.uk>, J Ralph Blanchfield
<jralphb@easynet.co.uk> writes
>But is it a "secondary" infection, or is it a new infection occurring,
>by coincidence, in the hospital where many of the victims of the
>Wishaw outbreak were cared for?
Could be either, but perhaps most likely a secondary infection.
Ralph will doubtless remember a thread on ProMed discussing ECO157. I
commented that it was said that it appeared that only a few hundred
(yes) microbes were needed to cause an infection. A highly qualified
poster said that it was worse than this and only 50 to 100 were
required.
I pointed out that to reduce infection levels to this amount would be
unattainable in an operating theatre and indeed probably exceeds the
capability of any reasonable disinfection regime. (How one would even
contemplate doing so in food, or in abattoir premises, beggars belief.)
Also on that thread was the comment that due to the very low levels of
bacteria required the disease was effectively contagious and was readily
transmitted by, say, hand to hand contact.
So basically the only way to ensure that you are safe from danger of
this bacterium is to ensure that you regularly come across it and are
thus immune to it (probably more importantly it's toxin). Whatever you
do you aren't going to be able to avoid exposure to it for your
lifetime.
It is worth noting that those people who handle cattle, and are
inevitably heavily exposed to their pathogens (which must include ECO157
since about 0.25% of cattle carry it) are prominant in NOT succumbing to
the disease. I know of only one case and that was of a sheep farmer.
--
'Oz "Is it better to seem ignorant and learn,
- or seem wise and stay ignorant?"
From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.bio.food-science
Subject: Re: E.coli O157 outbreak in Scottish hospital
Date: Sat, 31 May 1997 21:08:13 +0100
In article <2807@purr.demon.co.uk>, Jack Campin <jack@purr.demon.co.uk>
writes
>jackmowbray@delphi.com writes:
>> Oz <Oz@upthorpe.demon.co.uk> writes:
>>> So basically the only way to ensure that you are safe from danger of
>>> this bacterium is to ensure that you regularly come across it and are
>>> thus immune to it (probably more importantly it's toxin).
>> So, are you suggesting to the readers of your post that they intentionally
>> ingest or otherwise expose themselves to foodborne pathogens, specifically
>> E. coli 0157:H7 ?
>
>And given that some of the cases have been in infants, it looks like Oz is
>suggesting these organisms ought to be added to baby food...
An interesting suggestion. Funnily enough there is a folklore saying
about eating a peck of dirt before you die. A peck is (if I remember
correctly) about 100kg (2 cwt). Anyone who has had infants knows their
propensity (enthusiasm even) for eating dirt, particularly when they
first become 'mobile'.
No, I jest a little. The fact is that infants must become immune to the
bacteria (and even viruses) in their environment, or else they will die.
Of course it helps greatly if they get a non-lethal dose to start with.
However, what are regarded as non-pathogenic strains of bacteria
commonly resident in the human gut do indeed vary from place to place.
Most people who have travelled abroad have had an upset stomach, usually
within a week (or day) of arriving in a significantly different country.
These can be accompanied by vomiting. However usually you just get the
one attack (3-24 hrs duration) and have no further problem since you are
then immune (at least from the assorted toxins). My family have noted
this on each occasion we have travelled abroad, we all get one nasty
attack and then no problem. Others I have mentioned this to have
reported the same situation.
I suppose we could render all bacteria extinct, but this has unfortunate
ecological side-effects. Maybe better to live with them where we can.
--
'Oz "Is it better to seem ignorant and learn,
- or seem wise and stay ignorant?"
Newsgroups: sci.bio.food-science
Subject: Re: E.coli O157 outbreak in Scottish hospital
From: Tim Williams <tim@microbes.demon.co.uk>
Date: Tue, 3 Jun 1997 22:44:59 +0100
Sorry to burst into this thread like this, but E.coli O157:H7 is a pet
subject of mine
I have tagged on various comments to selections from previous posts.
>If there was an antibody titre test for the bacteria (or it's toxin) it
>would only be recessary to sample a few thousand cattle workers compared
>to a few thousand central city dwellers.
A project has just started at the central PHLS lab at Colindale, London
to determine the rate of carriage of, and exposure to, EC0157 in farm
workers.
>E. COLI-CONTAMINATED WELL WATER LINKED TO GASTROINTESTINAL ILLNESS
>May 22, 1997
>(from a University of Guelph press release)
> For the first time in North America, a study has shown a link between
> gastrointestinal illness and the drinking of private well water
Similar reports appeared on Promed a couple of months ago about an
outbreak of ECO157 in hotels in the Canary Islands associated with water
from a contaminated borehole.
>O157:H7 looks as if it has been produced from another pathogenic
>(but not a verocytotoxin producing) E. coli, by a simple
>introduction of a virulence plasmid with genes for those
>shigella and shigella-like toxins.
>Recent posts elsewhere (Promed?) stated that other non-pathogenic
>strains of EC produce the same toxin, but in much smaller amounts.
>Interestingly these are NOT considered pathogenic
The pathogenesis of ECO157 is believed to be a result of the combination
of VT production (Encoded by a phage) and an adherance factor encoded by
plasmid DNA. So apart from the amount of VT produced (Which is far
higher in Enterohaemorrhagic E.coli ) lack of the adhesion plasmid would
result in non pathogenic strains.
>It only takes 60 bacteria to cause infection (although personally I find
>this hard, very hard, to believe).
At a recent meeting on ECO157 at the University of Birmingham, it was
stated that the infectious dose may be <10 organisms and may even be one
bacterium.
>I suppose we could render all bacteria extinct, but this has unfortunate
>ecological side-effects.
Not to mention putting me out of a job :-)
--
Tim Williams
Newsgroups: sci.bio.food-science
Subject: Re: E.coli O157 outbreak in Scottish hospital
From: Oz <Oz@upthorpe.demon.co.uk>
Date: Wed, 4 Jun 1997 07:39:01 +0100
In article <tG7J$AAbBJlzEwoW@microbes.demon.co.uk>, Tim Williams
<tim@microbes.demon.co.uk> writes
>
>Sorry to burst into this thread like this,
Pleased to have you post. Nothing like a specialist to sort our
ramblings out.
>but E.coli O157:H7 is a pet
>subject of mine
>I have tagged on various comments to selections from previous posts.
Excellent!
>>If there was an antibody titre test for the bacteria (or it's toxin) it
>>would only be recessary to sample a few thousand cattle workers
>compared
>>to a few thousand central city dwellers.
>
>A project has just started at the central PHLS lab at Colindale, London
>to determine the rate of carriage of, and exposure to, EC0157 in farm
>workers.
Well, they are keeping it very quiet from farmers. I haven't seen it
mentioned in the UK farming press. I hope they will also have a control
of 'unexposed' city dwellers.
>>E. COLI-CONTAMINATED WELL WATER LINKED TO GASTROINTESTINAL ILLNESS
>>May 22, 1997
>>(from a University of Guelph press release)
>> For the first time in North America, a study has shown a link between
>> gastrointestinal illness and the drinking of private well water
>
>Similar reports appeared on Promed a couple of months ago about an
>outbreak of ECO157 in hotels in the Canary Islands associated with water
>from a contaminated borehole.
Yup. I should have remembered this, Fuentaventura?. I believe that the
well was specifically known to be contaminated and was NOT supposed to
have been used for human consumption. OTOH water is expensive there, I
thought it all came from desalination anyway.
>At a recent meeting on ECO157 at the University of Birmingham, it was
>stated that the infectious dose may be <10 organisms and may even be one
>bacterium.
Well, this effectively means that standard farm, abattoir and food
processing (not to mention domestic) hygeine procedures are unlikely to
prevent spread, even if taken to extremes. So doing all the usual things
that one does for the prevention of enterobacterial infection are
unlikely to be effective.
We could slaughter all our livestock and go vegetarian, but then how
would we fertilise our organic produce? What would we do with our sewage
sludge (incinerate it?) and sewage effluent (chlorinate it?). Are we to
aim for a sterile world?
>>I suppose we could render all bacteria extinct, but this has
>unfortunate
>>ecological side-effects.
>
>Not to mention putting me out of a job :-)
I expect the ecological effects would be a tad more far reaching than
this. Just for fun consider legumes would aso be extinct as would the
surprisingly large number of organisms that rely on bacteria, ruminants
(probably most herbivores in fact) would soon be extinct too. If we were
to include the fungi then many other plants and insects would also no
longer be with us. :-(((
--
'Oz "Is it better to seem ignorant and learn,
- or seem wise and stay ignorant?"
From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.bio.food-science
Subject: Re: E.coli O157 outbreak in Scottish hospital
Date: Mon, 9 Jun 1997 20:16:47 +0100
In article <5nhfo1$l0p$2@news.uni-c.dk>, Torsten Brinch <iaotb@inet.uni-
c.dk> writes
>So where did O157:H7 hide in the decade before 1982? CDC had detected only
>_one_ single O157:H7 in >3,000 isolates serotyped between 1973 and 1982;
>the E.coli Reference Center reported _no_ O157:H7 in >20,000 serotyped
>cultures from animals; and in the UK, out of 15,000 strains serotyped
>before 1985, only _two_ O157:H7 were found.
>
>There is a severe contrast to the frequency by which O157:H7 has been
>found after 1985.
Some real information at last. OK, your input strongly suggests that
EC0157 is a new strain, nothing strange about that. Nice to know.
Do we have any evidence of pathogenicity of EC0157 in cattle? Now the
only really pathogenic EC in cattle I have heard mention of is a rather
nasty, and almost invariably fatal, EC mastitis. I have no idea if this
was EC0157 or not, but I would be surprised if nobody had typed it (or
more likely, them).
Or is EC0157 'just another strain' that gives an enteritis of variable
severity that in some susceptible people is particularly severe? Will
the problem go away in a period of time when all humans have become
exposed and immune to either the disease or the toxin and it becomes
nothing more than another now non-pathogenic EC normally found in the
human gut (until pushed out by others)? One presumes that this is what
has happened in cattle since if we don't see it in humans when we look
back to the past, and it only takes a handful of bacteria to cause
disease, then one must presume that it was a new strain to cattle in the
recent past.
In short we ought perhaps to expect a continual stream of bacterial
varients that will cause severe reactions in susceptible people as they
pass through the human population, but most people shrug off after a
mild(ish) bought of illness? Given the propensity of nature to produce
mutants at fairly regular intervals are food scares going to be an
ongoing problem? One might ponder if regular exposure to new bacteria
might be essential to an effective and active immune system. Some of us
will suffer badly, this is true, but can we live in a sterile world?
Now, where was that really ripe farmhouse brie?
--
'Oz "Is it better to seem ignorant and learn,
- or seem wise and stay ignorant?"
From: Tim Williams <tim@microbes.demon.co.uk>
Newsgroups: sci.bio.food-science
Subject: Re: E.coli O157 outbreak in Scottish hospital
Date: Thu, 12 Jun 1997 07:35:56 +0100
In article <9S8sSBAb7xnzEw7Z@upthorpe.demon.co.uk>, Oz
<Oz@upthorpe.demon.co.uk> writes
>>It is believed that between 2 and 7% of EC O157 infected people will
>>develop complications. Aprox 30% of these will be left with permanent
>>damage (such as chronic renal failure, hypertension, neurological
>>defect).
>
>Hang on a tick. Are you saying that 93% to 98% of humans are immune, or
>are you defining 'infected' people as those ill enough to require
>medical attention to the extent that tests are done?
no - I was only commenting on complications. It was originally thought
that all people who ingested the bacteria developed diarrhoea. Somewhere
between 70 and 90% of these develop a grossly bloody diarrhoea (Sorry to
talk about such things on a food newsgroup !). The PHLS now screens all
faecal samples for E.coli. The lab at which I work processes about 50
samples a day - in the year since we began testing , we have picked up
only one case where an 'Asymptomatic' person carried the organism,
although provisional reports from the Lanarkshire butcher involved in
the Scottish outbreak suggest a high rate of asymptomatic carriage.
So - the current thinking is that the majority of people ingesting the
bacteria will develop diarrhoea - most with bloody diarrhoea. Of these
cases (About 700 last year in England and Wales) 2 - 7% will develop
complications such as Haemolytic uraemic syndrome. Of the people who
develop complications , 5-10% will die. (The high mortality rate in
Scotland is probably due to the high number of elderly people infected.)
Here endeth the lecture :-)
--
Tim Williams
Newsgroups: sci.bio.food-science
Subject: Re: E.coli O157 outbreak in Scottish hospital
From: Oz <Oz@upthorpe.demon.co.uk>
Date: Fri, 13 Jun 1997 06:30:24 +0100
In article <PGcBPBAMj5nzEw94@microbes.demon.co.uk>, Tim Williams
<tim@microbes.demon.co.uk> writes
>no - I was only commenting on complications. It was originally thought
>that all people who ingested the bacteria developed diarrhoea.
Not surprising, but not that unusual. The majority would not be reported
unless seriously acute which makes estimates of the complication rate
difficult.
>Somewhere
>between 70 and 90% of these develop a grossly bloody diarrhoea (Sorry to
>talk about such things on a food newsgroup !).
How do you know? We don't have millions of people reporting this
annually and certainly one ought to expect this to have been picked up
in the ag. press and we haven't. The main problem areas seen to
basically be old people's homes and the odd restaurant where one might
imagine poor hygeine might result in a high bacterial levels causing
particularly acute disease.
>The PHLS now screens all
>faecal samples for E.coli. The lab at which I work processes about 50
>samples a day - in the year since we began testing , we have picked up
>only one case where an 'Asymptomatic' person carried the organism,
>although provisional reports from the Lanarkshire butcher involved in
>the Scottish outbreak suggest a high rate of asymptomatic carriage.
Surely it might be expected that the typical healthy human would go down
with a short and mildly uncomfortable stomach ache, become immune and
cease to be a carrier. This would correlate with the 0.25% of cattle
found to be excreting the organism. Although some may be carriers (ie
the bug has become a commensal in them) one might presume that the rest
cleared the EC0157 from their system otherwise we would be seeing
massive cattle mortality or most cattle being carriers, which we do not
see.
>So - the current thinking is that the majority of people ingesting the
>bacteria will develop diarrhoea - most with bloody diarrhoea. Of these
>cases (About 700 last year in England and Wales) 2 - 7% will develop
>complications such as Haemolytic uraemic syndrome. Of the people who
>develop complications , 5-10% will die. (The high mortality rate in
>Scotland is probably due to the high number of elderly people infected.)
>
>Here endeth the lecture :-)
I don't think this is supported by the evidence very well.
--
'Oz "Is it better to seem ignorant and learn,
- or seem wise and stay ignorant?"
From: Tim Williams <tim@microbes.demon.co.uk>
Newsgroups: sci.bio.food-science
Subject: Re: E.coli O157 outbreak in Scottish hospital
Date: Fri, 13 Jun 1997 20:37:26 +0100
In article <sepoBEAwrNozEwBY@upthorpe.demon.co.uk>, Oz
<Oz@upthorpe.demon.co.uk> writes
>We don't have millions of people reporting this
>annually and certainly one ought to expect this to have been picked up
>in the ag. press and we haven't. The main problem areas seen to
>basically be old people's homes and the odd restaurant where one might
>imagine poor hygeine might result in a high bacterial levels causing
>particularly acute disease.
Only the Outbreaks are associated with old peoples homes and restaurants
- the majority of cases are sporadic or small family outbreaks
of the 233 cases in England between July 1996 and March 1997 only 18
were part of general outbreaks. (Communicable disease report May 9th
1997)
>>So - the current thinking is that the majority of people ingesting the
>>bacteria will develop diarrhoea
>> - most with bloody diarrhoea.
based on studies where outbreaks occurred in institutions and all people
who may have been exposed were screened presence of the organism. The
interim report on the PHLS study indicates that about half of all
patients from whom E.coli O157 was isolated did not have blood in their
stools.
(Griffen PM, Tauxe RV.The epidemiology of infections caused by
Escherichia coli 0157:H7, other enterohaemorrhagic E. coli, and the
associated haemolytic uremic syndrome.
Epidemiol Rev 1991;13: 60-98.
Cohen M, Gianella R.
Haemorrhagic colitis associated with Eschericia coli O157:H7.
Advances in Internal Medicine 1991; 37 :173-195.)
>>Of these
>>cases (About 700 last year in England and Wales) 2 - 7% will develop
>>complications such as Haemolytic uraemic syndrome. Of the people who
>>develop complications , 5-10% will die.
>I don't think this is supported by the evidence very well.
Moake J. Haemolytic-uraemic syndrome: basic science
The Lancet 1994; 343 :393-97.
Kovacs M, Roddy J, Gregoire S, Cameron W, Eidus L, Drouin J..
Thrombotic Thrombocytopenia Purpura following Haemorrhagic colitis due
to E.coli O157:H7.The American Journal of Medicine 1990 ;88 :117-179.
Advisory Committee on the Microbiological Safety of Food.
Report on Verocytotoxin-producing Escherichia coli.
London: HMSO 1995
I agree with you that we are not fully aware of the epidemiology of the
organism. It is hoped that studies such as the screening of agriculture
workers currently being set up at the central PHL lab will add to this
knowledge.
--
Tim Williams
Newsgroups: sci.bio.food-science
Subject: Re: E.coli O157 outbreak in Scottish hospital
From: Oz <Oz@upthorpe.demon.co.uk>
Date: Sat, 14 Jun 1997 07:22:52 +0100
In article <iM5nSCA2FaozEwx8@microbes.demon.co.uk>, Tim Williams
<tim@microbes.demon.co.uk> writes
A fund of useful knowledge. Many thanks.
However .... (as you probably expect)
>In article <sepoBEAwrNozEwBY@upthorpe.demon.co.uk>, Oz
><Oz@upthorpe.demon.co.uk> writes
>
>
>>>So - the current thinking is that the majority of people ingesting the
>>>bacteria will develop diarrhoea
>> - most with bloody diarrhoea.
>
>based on studies where outbreaks occurred in institutions and all people
>who may have been exposed were screened presence of the organism. The
>interim report on the PHLS study indicates that about half of all
>patients from whom E.coli O157 was isolated did not have blood in their
>stools.
The problem with followups where an *outbreak* has taken place would, I
suspect, be that the level of exposure is likely to have been very high
(say millions++ of bacteria) rather than tens or hundreds that one might
hope for where hygeine was quite good and initial bacterial loading
quite low. So many of the 'general public' might well have markedly
lower levels of 'blood in stools' and become immune asymptomatically
(well, nearly).
Anyway, let's face it, there is no way we are going to stop this
organism spreading through the human population given it's low infective
dose, and the recent work showing several months persistance in cattle
dung and on clean ss surfaces and other 'clean' areas. H. Sap is beat
and we just gotta get immune as symptom-free as possible.
>I agree with you that we are not fully aware of the epidemiology of the
>organism. It is hoped that studies such as the screening of agriculture
>workers currently being set up at the central PHL lab will add to this
>knowledge.
Me too. They are keeping it mighty secret though.
--
'Oz "Is it better to seem ignorant and learn,
- or seem wise and stay ignorant?"
From: Oz <Oz@upthorpe.demon.co.uk>
Newsgroups: sci.bio.food-science
Subject: Re: E.coli O157 outbreak in Scottish hospital
Date: Sun, 15 Jun 1997 09:34:28 +0100
In article <5nufdo$36e$2@news.uni-c.dk>, Torsten Brinch <iaotb@inet.uni-
c.dk> writes
>Oz wrote:
>
>>Do we have any evidence of pathogenicity of EC0157 in cattle?
><..>
>
>I've seen no evidence of pathogenicity in cattle during a
>quick lookaround for it.
I agree. Were it to be significant then it would have been found by now.
The drop in milk output from a dairy herd would result in megabucks
being spent to find the cause.
>The adhesion to human intestinal cells and subsequent
>systemic transfer of shigella toxin to the victim,
>are both important elements of E. coli serotype O157:H7 disease.
Since EC0157 has been identified in 0.25% of scots cattle one presumes
that it is able to adhere to cattle intestines. However it is not
unlikely that the shigella toxin is one known to the immune system of
most cattle (indeed possibly of many humans) and thus produced no
symptoms.
>Possibly O157:H7 does not transfer shigella toxins
>effectively to cows, because the plasmid coded protein
>O157:H7 has acquired for adhesion does not function
>well with cattle intestinal cells.
Could be. Given it's ability to survive in the environment for many
months I suspect immunity is more likely though.
>I think it could be argued, that O157:H7 was
>never a cattle pathogen, i.e. that cattle immunity
>towards O157:H7 disease is not acquired (see above).
We don't really know, I suspect. However we should also consider pigs,
where the same argument applies. I wonder if any screeing has been done
on pigs? Again, were it to be able to infect pigs in an epidemic fashion
then I would expect full megabucks to be spent on identification and
control were a herd to succumb.
>:-) We can't, we won't. There is some indication that O157:H7 is
>in a process of evolving into several closely related strains
>(the plasmid content seems to be unstable, but also genomic
>mutants have been reported; the lysogenic bacteriophage vector
>for the shigella toxine gene is now part of the O157:H7 genome,
>but it can change when/if it is transferred to other strains of EC).
>So we certainly should expect a continual stream of variants.
>Maybe we can hope for a suitable 'dilution' of the particularly
>nasty O157:H7 genomic setup in time? Or if we are so inclined:
>we could fear a mess of more or less pathogenic strains, with
>some of them starting to elude our diagnostic tools for O157:H7.
If reports of it's pathogenicity at the 10 bacteria level and it's
persistance on surfaces for months are true, then the entire human
population will be immune to the toxin long before that. Indeed this may
already be the case except for situations where the exposure to many
millions of bacteria temporarily overwhelms the immune response.
Still, nothing like closing the door after the horse has bolted, is
there?
--
'Oz "Is it better to seem ignorant and learn,
- or seem wise and stay ignorant?"
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