"Micro-Organisms in Milk Cause Crohn's Disease" at:
For a refresher course here are Koch's postulates distinguishing a pathogen
from an adventitious organism:
1. The organism is regularly found in the lesions of the disease.
(this is from the article: MAP can now be detected by improved culture
systems and DNA tests in the inflamed gut of a high proportion of people
with Crohn's disease.) Comment-A "high proportion" is not statistically
valid to fulfill this postulate.
2.It can be isolated in pure culture on artificial media
3. inoculation of this culture produces a similar disease in experimental
4. the organisms can be recovered from the lesions in these animals.
These of course do not hold true for microbes that cannot be grown on
artificial media-viruses and ones that are only pathogenic in man.
This 1989 paper refutes the article entirely.
Kobayashi, K., M. J. Blaser, et al. (1989). “Immunohistochemical examination
for mycobacteria in intestinal tissues from patients with Crohn's disease
[see comments].” Gastroenterology 96(4): 1009-15.
We conducted an immunohistochemical search for mycobacteria in the
intestinal tissues of patients with Crohn's disease. Tissues obtained by
biopsy or surgical resection and fixed by a variety of methods (formalin,
periodate-lysine-paraformaldehyde, fresh-frozen) were reacted by an
immunoperoxidase method with antibodies to (a) Mycobacterium
paratuberculosis strain linda, (b) M. tuberculosis, and (c) the common
mycobacterial antigen, lipoarabinomannan. Each of the antibody preparations
was shown capable of detecting a variety of typical and atypical
mycobacteria (M. tuberculosis, M. kansasii, M. fortuitum, M. chelonei, M.
paratuberculosis, and cell wall-defective as well as cell wall-intact forms
of M. avium intracellulare) under conditions identical to those used for
staining the patients' tissues. We did not detect mycobacteria in any of the
67 specimens from 30 patients examined. These results, in conjunction with
those of our previous serologic studies, do not support the hypothesis that
infection with a Mycobacterium causes Crohn's disease.
According to this abstract sugar consumption could be implicated as the
cause of Crohn's:
Penny, W. J., J. F. Mayberry, et al. (1983). “Relationship between trace
elements, sugar consumption, and taste in Crohn's disease.” Gut 24(4):
Seventy patients with Crohn's disease, 50 with ulcerative colitis, and 58
control subjects were questioned about their sugar consumption, measurements
were made of their taste acuity, and blood levels of various trace elements
including zinc and selenium were estimated. Sugar consumption was
significantly increased in Crohn's disease (p less than 0.01). There was
only a minor reduction in taste acuity for acid taste in Crohn's disease.
Plasma zinc and whole blood selenium were reduced in Crohn's disease. No
relationship was found between sugar consumption, plasma zinc, and taste
acuity in Crohn's disease.
Here it is clearly Candida that is the cause:
Armstrong, N., M. Schurr, et al. (1998). “Fungal sacral osteomyelitis as the
initial presentation of Crohn's disease of the small bowel: report of a
case.” Dis Colon Rectum 41(12): 1581-4.
We report a unique case of Candida albicans sacral osteomyelitis in a 48
year-old female with previously undiagnosed Crohn's disease. The patient was
ill for one year with fatigue, weakness, and a 60-lb weight loss. At the
time of presentation, she developed chills, fever, right lower quadrant
abdominal pain, and right knee pain. Physical examination was significant
for a palpable right lower quadrant abdominal mass. A computed tomographic
scan of the abdomen and pelvis identified a large right-sided
retroperitoneal mass, severe right hydronephrosis, and air within the right
sacrum. Findings at laparotomy included small-bowel changes consistent with
Crohn's disease, a multiloculated retroperitoneal abscess, and evidence of
sacral osteomyelitis. A right hemicolectomy with sacral debridement and
placement of presacral drains was performed. Bone cultures from the sacrum
demonstrated a predominance of C. albicans, in addition to coliforms and
enterococcus. The patient was placed on amphotericin B and intravenous
antibiotics. Because serial computed tomographic scans of her pelvis
demonstrated progression of her pelvic osteomyelitis to include the sacrum,
right ilium, right acetabulum, and right femoral head, a repeat debridement
with resection of the right femoral head was performed. After 12 months of
follow-up, she was doing well without medications and had no constitutional
symptoms or radiographic evidence of disease progression. This report
illustrates a unique case of Crohn's disease presenting as sacral
osteomyelitis secondary to small- bowel fistulization. Aggressive
multidisciplinary surgical and medical management were the key to the
successful management of this difficult case.
Well, maybe other yeasts are a problem too! Here it looks like an allergic
McKenzie, H., J. Main, et al. (1990). “Antibody to selected strains of
Saccharomyces cerevisiae (baker's and brewer's yeast) and Candida albicans
in Crohn's disease.” Gut 31(5): 536-8.
IgG serum antibody was measured by ELISA in patients with Crohn's disease
(15), ulcerative colitis (15), and in normal controls (15) to 12 strains of
Saccharomyces cerevisiae (baker's and brewer's yeast) and to the two major
serotypes of the commensal yeast Candida albicans. Antibody to 11 of the 12
strains of S cerevisiae was raised in patients with Crohn's disease but not
in patients with ulcerative colitis when compared with controls (p less than
0.001). The pattern of antibody response to these 11 strains was variable,
however, suggesting the likelihood of antigenic heterogeneity within the
species. Antibody to C albicans was not significantly different in patient
and control groups. The specificity of this unusual antibody response in
Crohn's disease for S cerevisiae suggests that it is not simply the result
of a generalised increase in intestinal permeability. Furthermore, because
brewing and baking strains detected the response, the relevant antigen(s)
are presumably common in the diet. Hypersensitivity to dietary antigens may
be involved in the pathogenesis of Crohn's disease, and the role of S
cerevisiae requires further investigation.
Antibiotics are used to speed growth in animals. Simply by decreasing the
microbial load and accelerating healing may be why they see a positive
I have been down this road with my rheas. The experts said E.coli,
clostridium, and parasites like giardia and trichomonas as a result of
immunosuppression were causing the world-wide red gut diarrheal syndrome in
rheas and ostriches. Well, they were worng. By removing hexane extracted
soy from the diet and adding EFA's and antioxidants I completely abolished
all these problems in the infant rheas. At this point I believe the
organisms were the clean-up crew enjoying a free lunch from the toxin
induced cell breakdown. Just killing the organisms did not heal the
This is a case of justifying their grants.
From: email@example.com [mailto:firstname.lastname@example.org]On
Behalf Of Loren Muldowney
Sent: Tuesday, February 01, 2000 10:58 AM
To: Bluestem Associates
Cc: sanet; email@example.com
Subject: Re: "Pasteurized" milk and Crohn's Disease
In a conversation about the reasoning behind the mandatory
pasteurization, and having read the article entitled
> > This is scientific garbage. If this were true then Crohn's would be
> > common than allergies or the common cold in the UK.
Donna also said:
> > the weakened immune system and the altered
> > biochemistry of the gut of people with Crohn's disease provides a
> > environment for the growth of the mycobacterium.
to which Bart replied: (after making loads of good points)
> The ... statement here implies that the Crohn's article misses the
> truth, yet as I read things the question of immune systems and gut
> chemistry actually *reinforces* the general approach of the article.
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