E. coli

jsd at infi.net jsd at infi.net
Sun Nov 13 05:26:56 EST 1994


     Preston's "The Hot Zone" intrigued me enough to search out
bionet.virology and whatever reading material was immediately accessible
to a layman. Accordingly, I am able to relate to some of the comments made
here. i.e...

     JARDINE  P <F3CM at UNB.CA> says:
>This whole deal about lethal viral strains shows our ignorance about the
>biology of these bugs in the first place. In the absence of real
>understanding or at least respectful understanding of these pathogens, we
>allow the media and ourselves to make these events seem drastic and
exciting.

> There have been a number of postings lately about emergent viral strains and
> how they threaten us. Concern over this subject bothers me for two reasons.
> 1) It shows how biased we are in Western culture regarding how disease
> is working in the world. Every year 2.5 million people contract malaria
> and of these 250,000 die. Emerging strains of influenza, a nuisance to
> us in the "modern" world, kill thousands on there trip from China or
> Indonesia. But we put emphasis on a few deaths from hanta or Ebola?
> I think our priorities are a little screwy. Selfish at best.

     Now, I am no scientist, and I hope you guys don't mind me
intruding...but it's just a little bit hard not to be alarmed at
Marburg/Ebola/Hantaan et al. When people start dropping dead within
twenty-four hours after infection, as was the case with the Hanta virus in
the Four Corners area of the U.S., and when people hear of the horrendous
progressions of filoviruses laymen tend to view such occurrences as
horrifying. In truth, I believe the CDC has felt the same way.

     If I read what follows below accurately E. coli 0157:H7 is just a
hop, skip, ana jump away from wreaking havoc, major havoc in the U.S.
Comments regarding this, and anything else posited here are encouraged.

     Re E. coli 0157:H7 taken from The Coming Plague, Newly Emerging
Diseases In A World Out Of Balance, authored by Laurie Garrett...

               excerpt start:

One of the clearest and most troubling examples of animal/human
cross-species transmission of mutant bacteria was Escherichia coli. The
bacteria were ubiquitous, rod-shaped microscopic creatures found in the
intestines of all human and many other mammalian species. Most of the
time, in most people, they were harmless. And there was no microscopic
organism that was better understood than E. coli, as it had been the focus
of the majority of the world's molecular and cellular biology research
since the 1940's. Scientists liked to work with E. coli because all the
complex machinery of life was there to study, packaged inside a
predictable tubular structure which, almost like clockwork, stretched
itself out every 120 minutes, duplicated its DNA, divided down its middle,
and - voila - there were two E. coli. The hearty bacteria would readily
perform this feat of reproduction in the laboratory, always doubling their
total population every two hours. 

     Of course, the bacteria were capable of similar feats of reproduction
inside human intestines. If unchecked by the host's immune system, or if
of a particularly virulent strain prone to producing tough toxins, the
bacteria would cause diarrhea and vomiting. Typically, this occurred in
small children whose immune systems weren't fully developed, and the
ailment was particularly dangerous in malnourished or otherwise seriously
ill infants. 

     In 1982 something new showed up: E. coli 0157:H7. It was an
apparently novel organism that was capable of causing dangerous
hemorrhages of the colon, bowel, and kidneys of human beings of all ages.
And it hit suddenly in several U.S. states, as if out of nowhere. 

     Ten years later the details of 0157:H7 emergence would remain
obscure, but it's source would not: most cases came from contaminated
meat. Like most E. coli strains in the 1980's, it was moderately resistant
to ampicillin and tetracycline. More important, the mutant bacteria
appeared to have acquired the ability to produce Shigella-like toxins.
Studies of dozens of emergent bacterial species showed that genes for
antibiotic resistance and virulence often resided in the same regions of
the microbes' DNA, and could move together from one organism to another.
Thus, the same selection pressures that led to the emergence of the
resistance - in the case, use of antibiotics on livestock - also promoted
greater virulence. 

     Because of both agricultural and medical misuse of antibiotics, E.
coli strains of all kinds were rapidly acquiring broad ranges of
resistance during the 1970s and 1980s.

     [From the New Yorker - Apart from new invaders, established microbes
are developing resistance to standard remedies faster than new drugs can
be developed. The organism of gonorrhea has learned to outwit penicillin,
Staphylococcus to defy methicillin and malaria to evade chloroquine. If
there is anyone doctors and nurses trembled to treat, it's not AIDS
patients but those infected with multiple drug-resistant strains of
tuberculosis. The bacillus is spread through the breath, though not
easily. Seven of the 10 victims may die. A long-vanquished disease has
returned with vigor.]

     Stuart Levy showed in 1989 that E. coli rapidly spread from pigs and
cows to people living and working on a farm. And the resistance factors
themselves could move from E. coli that were inhabiting a pig, for
example, to bacteria that were infecting other higher animals, including
humans. 

     [From one of the book's notes: Some remarkable E. coli strains
emerged in the early 1990s. For example, outside Cambridge, England, two
strains appeared on a hospital transplant ward that were resistant to the
antibiotic imipenen, as well as cefotaxime, ceftazidime, ciprofloxacin,
gentamicin, ampicillin, azlocillin, coamoxiclav, timentin, cephalexin,
cefuroxime, cefamandole, streptomycin, neomycin, kanamycin,tobramycin,
trimethoprim, sulfamethoxazole, chloramphenicol, and nitrofurantoin. Only
one commonly used antibiotic remained effective: amikacin. If the strains
become resistant to that drug, they would be invulnerable to human
treatment. Lancet 341 (1993)] 

     In 1991 in the apple-growing region of Massachusetts there was a
small outbreak of E. coli 0157:H7 infection, producing serious illness in
twenty-seven people, ten of whom required hospitalization. All the cases
occurred during the fall apple harvest months. It turned out that the
bacteria were in local apple cider. And the cider was made from apples
plucked from trees that were fertilized with livestock manure. Presumably,
then, the manure was the excreta of 0157:H7-infected animals. 

     The stage was set for public health disaster.In January 1993 more
than 500 people from Washington State became seriously ill after eating
hamburgers prepared in ninety-three Jack-in-the-Box fast-food restaurants.
Fifty of the hamburger consumers developed the E. coli hemorrhagic
syndrome, and four of them - all small children - died. The culprit was E.
coli 0157:H7, which had arisen in the cattle and was in the hamburger. 

     Three months later a smaller outbreak occurred in a Sizzlers
restaurant in Grants Pass, Oregon. Five diners were hospitalized in that
E. coli 0157:H7 incident. 

     Politics immediately entered the picture, as consumer and legal
groups demanded that the U.S. government takes steps to ensure public
safety. They claimed that upward of 25 million American suffered food
poisoning each year, 6,000 of whom were victims of E. coli 0157:H7. The
Clinton administration responded by ordering increased meat inspections.
But the administration took no steps to get to the source of the problem:
the unregulated use of antibiotics on livestock. 

               excerpt end

     So, what happens if E. coli 0157:H7 figures out a way to get around
amikacin? What might have happened if the Reston Ebola strain had been
human hungry? Shouldn't we be alarmed. Rhetorical question as far as I am
concerned?

     Any comments from you specialists would be much appreciated.

     Peace...Jordan



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