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Colitis
Colitis is inflammation of the bowel that can be acute
or chronic. Acute inflammatory changes are usually self-resolving
and are caused by specific infections such as shigella,
salmonella, amoebae or Campylobacter jejuni to give few
examples. These do not require any treatment with human
probiotics since they are self-limiting or can be treated
with specific antibiotics. Chronic inflammation can also
be caused by chronic infections eg C difficile, Dientamoeba
fragilis, and E. histolytica.26
In patients with chronic colitis of unknown origin various
subdivisions of the condition have been made. Patients
can have a microscopic colitis, which presents as chronic
diarrhoea and cramping but colonoscopically there are
no areas of inflammation until one takes a biopsy and
then typical inflammatory cells are visible under the
microscope. Other patients have classic distal where colonoscopically
inflammatory changes begin at the rectum and can extend
to a variable distance up the bowel. In some patients
the entire bowel is involved in colitis and this is called
pan-colitis. Crohn's and collagenous colitis make up other
subdivisions.
The treatment of colitis has been generally standardised
throughout the world and usually requires anti-inflammatory
drugs such as corticosteroids (eg. prednisone), 5-aminosalicylic
acid (5-ASA) compounds (eg. sulfasalazine, olsalazine,
mesalazine), azathioprine, 6-mercaptopurine, cyclosporin,
and antibiotics such as metronidazole, ciprofloxacin and
vancomycin. Most of these agents, except for prednisone,
also have anti-microbial actions, which points to the
fact that colitis is almost certainly a chronic infection
with a hitherto undescribed pathogen or pathogens. Among
theories on causation of colitis it is generally thought
that a passing bowel infection initiates an ongoing autoimmune
response. The basis for this is - in part - the observation
that we cannot find a pathogenic organism that causes
colitis, and that it appears to respond to immunity-modifying
drugs. Yet colitis may also follow an acute bowel infection-like
episode. Other chronic infections such as Helicobacter
pylori, hepatitis B or C, bronchiectasis, or fungal infections
of the skin do not set up an ongoing 'autoimmune' condition.
Hence, from the observation of other infections in the
body it is highly unlikely that colitis is anything more
than a chronic infection causing chronic inflammation
and the infection has simply not been found. A similar
situation has been operating in Crohn's disease where
an immune reaction to an unknown pathogen has been invoked
as the mechanism. It is now unlikely that this is the
mechanism operating but rather that Mycobacterium avium
ssp. paratuberculosis (Map) is the ongoing infection that
starts up and maintains the inflammation. ( www.crohns.org
)
From these simple observations it is likely that ulcerative
colitis, along with microscopic colitis, represents the
visible effects of a chronic infection of the gut flora
which science has not yet identified. It is likely that
this infection through the release of various cytokines
produces the clinical picture we call colitis. Although
HPI has been successful in reversing colitis24,
25 this treatment
is less successful in colitis than it is in C. difficile
diarrhoea and pseudomembranous colitis. The reason for
this is unclear but we may be dealing with a pathogen
or pathogens which are not as easily destroyed by the
influx of normal human bacterial flora. Furthermore, in
C. difficile diarrhoea and in patients with diarrhoea-predominant
IBS the bowel is generally not inflamed and this may allow
for easier implantation of a new bacteria onto the bowel
mucosa than it is in colitis. In chronic colitis the implantation
of the flora may be less likely on the inflamed tissues.
We have noticed that if patients are given standard anti-inflammatory
therapy until their bowel wall is completely healed, HPI
can achieve long term reversal of colitis in more than
50% of patients in our experience, but the result is still
unpredictable in the individual case. In addition if C.
difficile co-exists in patients with chronic ulcerative
colitis HPI can eradicate C. difficile and reduce the
severity of the condition in such patients. Furthermore,
the removal of associated parasites, especially D. fragilis
which in itself can cause colitis,26,
27 can also
reduce the severity of colitis. We have patients who have
had co-existing D. fragilis, Blastocystis hominis and
C. difficile and whose severity of ulcerative colitis
could be dramatically improved simply by removing the
co-existing pathogens by either specific anti-parasitic
agents or by human probiotic infusion. C. difficile is
typically 'impossible' to remove by the use of vancomycin,
metronidazole or rifampicin in patients with chronic colitis.
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