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Although the word "chemotherapy" raises fear, if
not panic, in the hearts of all of us boomers, from a strictly
pharmacological point of view the term is much broader than the brutal
mode for treating cancer. Technically, chemotherapy refers to any
use of chemicals -- i.e., drugs -- to treat a disease. For instance,
this week I began chemotherapy with Clindamycin for an infected
tooth.
The dentist really stressed that I report back to him
immediately if I had
any diarrhea while taking the drug, and the pharmacist emphasized that
point even more. I didn't understand why these folks were so edgy about my
scatological future. Although I have a PhD in pharmacology, I had no
idea what they were going on about because the closest I've come to
pharmacology in the last 15 years has been getting that Clindamycin
prescription filled.
So out of a mixed sense of professional embarrassment, self-preservation,
and curiosity I dove for the books to refresh my memory of the side
effects of Clindamycin. If the truth be told here -- which, rest
assured, it is always told on this website -- I actually had no memory
of the side effects of Clindamycin to refresh. I was barely able to
recognize it as an antibiotic. But my good friend Richard Lehne
publishes the number one nursing pharmacology textbook in the world, and when every new
edition comes out he sends me a copy, gratis. So I cracked the latest
edition of Lehne's Pharmacology.
I found out Clindamycin can cause a condition known as
pseudomembraneous colitis (abbreviated, for obvious reasons, to "PMC")
or less often called "clostridial colitis." Colitis refers to inflammation of the colon. Clostridial
refers to a genus of germs -- Clostridium. Clindamycin-induced PMC is a nasty
colitis in which, if not
stopped, the colon
is sort of eaten away from the inside. Occasionally we hear about Staph
a or other bacteria attacking the skin of patients and eating it away
-- necrotizing fasciitis, it's called. Well, Clindamycin-induced PMC
is much the same kind of phenomenon on the inside. The culprit in
PMC is not Staph a., it is Clostridium
difficile.
Many of you will recognize Clostridium. The clostridium genus is
one of those
groups of bacteria that has been kicking Homo sapiens' butts for tens of
thousands, if not hundreds of thousands, of years. Gas
gangrene, tetanus, and food poisoning (botulinism) are all deadly diseases
caused by this group of nasties.
There are two traits of
this genus that are particularly important with respect to land-application of BS. The first is that
these organisms are all obligate anaerobes, which means that not only do
they not require oxygen to survive, but oxygen is toxic to them.
When exposed to oxygen, as when they enter the sewage stream and aeration
processes of sewage treatment systems, they hunker down into survival
mode.
The second BS-related trait of C. difficile, and
all clostridia, is that survival mode means forming spores. These
spores are called "endospores".
A number of bacteria can form endospores, and they are, in general, pretty
scary. For instance, it was anthrax endospores that killed 5 people
in the 2001 anthrax attack.
Within the context of Clostridium and land-applied BS, endospores are as scary as
Jason, the guy in the horror movies with the hockey mask, because, like
Jason, endospores keep coming back. You almost can't kill
them. One researcher has referred to them as the most durable form
of life known. Endospores are resistant
to UV radiation, boiling, extreme pH, and chemical disinfectants -- precisely the kinds of
"treatments" that are applied to raw sewage sludge to convert it
into . . .ha, ha, ha, . . . "biosolids."
Yeah. When you make biosolids, you are making clostridial endospores. Whenever
you have C. difficile flushed down a toilet -- and that is
happening virtually constantly in a moderately sized city -- you are
sending to the waste-treatment plant bacteria that will become the
endospores in the BS that is spread on the farmers' land. Hospitals
are huge sources of C. difficile.
Just the presence of these spores in the air are
indicative of bacterial contamination in the surrounding environment. A recent patent
application from UCLA uses endospore detection as a way to assess air
contamination by bacteria generally. Surely, you say, EPA regulations
protect us from these tiny endospore time-bombs. Ha!
EPA microorganism monitoring requirements for both Class A
and Class B are nil verging on none. You can meet the requirements,
even for Class A, simply by measuring either the so-called fecal
coliforms or Salmonella. This
requirement is based on the "logic" that these are
"indicator organisms;" i.e., if they're there it indicates the presence of trouble, and
if they're not there, then there's no trouble. Link
to the Part 503 rule.
However, these indicator organisms are not even vaguely related to the Clostridium
species or any kind of endospores. You can count fecal coliforms in a BS sample until the cows
come home (of course McElmurray's cows aren't coming home because
Augusta's BS killed them) and you won't know a thing about how many C. difficile endospores are in the BS. So, C. difficile gets a free ride
as far as Part 503. John Walker, Alan Rubin and the other EPA
BS-promoters who concocted the Part 503 rules apparently could have cared
less about these deadly bacteria or their endospores.
What happens after the BS is not tested for these
little endospore devils? The BS is transported to
the farmers' fields in a semi-solid form, which means it still has a high
water content. The BS is slung out of a spreader machine and then it
dries. Once it dries the hydraulic adhesive forces between spores and the
organic matrix disappear. Now the spores are free to be picked up by
the wind and distributed all over the county -- or at least to those parts of
the county that are downwind of the sludged fields. Do you remember
the pods that were jettisoned when Darth Vader's death star was under
attack? That's exactly what's happening with the endospores being
blown away from the sludged fields. They escape certain death to live another day.
When they find themselves in a nice anaerobic environment with plenty of
nutrients, and perfect pH, and a perfect temperature, like a some a
person's intestine, they pop open and begin growing. They are microscopic time-bombs waiting to
go off.
These endospores have evolved over hundreds of thousands
of years to lie patiently dormant in an unfavorable environment until they are picked up by mammals,
reptiles, or birds and incorporated into their
gastrointestinal tracts. Wikipedia
says humans are mammals, and I believe it, mostly, although the ones
spreading BS are more like reptiles. And being
mammals, humans are targets for Clostridium difficile. Humans inhale the wind that carries these
endospores off of sludged fields. Humans eat vegetables whose
surfaces are covered with wind-borne endospores. Small, cute humans
wipe their hands across the exposed surfaces of playground gear upon which
endospores have settled and transfer the endospores to their mouths.
Once inside humans' digestive tracts, the spores find the ideal conditions
to revert to their bacterial state. Bingo! You have now
effectively transported C. difficile from the toilets of
Mount Sinai Hospital in Manhattan to Mrs. Brewster's first grade class
in Campbell County, Virginia, and everybody else downwind from Synagro's sludged fields.
But these infections will not be evident because the C.
difficile infection is asymptomatic. Mrs. Brewster's
kids who ingest
the C. difficile endospores by licking their slides and swings, or their parents who eat home-grown tomatoes coated with the spores will
not show a single symptom. C.
difficile just blends in with the rest of the normal bacteria that
populate the gut -- the so-called normal flora. For years and years
C. difficile can just hang out there and cause no problems.
It's growth is suppressed by the normal flora. . . but it survives.
Eventually, a fairly moderate proportion of folks with C.
difficile in their gut come down with completely
unrelated infections -- like my aching tooth. Many of these
infections will be treated with a
broad-spectrum antibiotic, probably Clindamycin or a cephalosporin.
"Broad-spectrum" means the antibiotic kills all sorts of germs
-- Gram positive, Gram negative, Strep, Staph, E. coli, you name it.
Of course, these antibiotics kill the normal gut flora, too. But
it's the normal gut flora that are holding the C. difficile in
check. So all hell breaks loose because without any competition from the normal bacteria, C.
difficile grows and grows, and in the growing it releases a couple of toxins that
produce the diarrhea and colitis.
The clinicians call the diarrhea "antibiotic-associated diarrhea," and it happens a lot, like in about 3
million Americans a year in hospital settings and in 20,000 in outpatient
settings. If the colitis develops into PMC, lesions can penetrate
the colon. Now you have bacteria entering the body cavity through
the holes in the colon. Septicemia it's called. The end for
this septicemic dude -- or kid -- may
not be far off. One
study found that of 200 hospital patients treated with clindamycin,
20% developed diarrhea and 10% developed PMC. These are huge numbers.
With respect to C. difficile infections from BS, it's a perfect storm sort of situation; all
of the right
conditions have to come together simultaneously. Because C.
difficile can lie dormant in the gut for years after it is acquired from
sludge-dust, the effects may not occur until years after the BS has been applied, or
the person has moved away from the place where they contracted the C.
difficile. This is one reason why going around knocking
on doors asking if the people who live near sludged fields feel OK,
is probably a worthless way to conduct the epidemiological studies.
The fact that someone says "I feel fine." doesn't mean
anything.
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