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More evidence has been published demonstrating that alterations of
intestinal microflora (such as by infection) can trigger bowel dysfunction
and illness.  This time a shigella infection (dysentery) has been shown to
be causative of IBS, with IBS occurring following recovery from dysentery.
A Reuters Health report appears today on Medscape.com.  (You may need to
register (free) with Medscape to read the article.)

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Bacillary Dysentery Linked to Irritable Bowel Syndrome

"NEW YORK (Reuters Health) Jul 27 - Bacillary dysentery plays a causative
role in irritable bowel syndrome (IBS), according to a report in the August
issue of Gut."

http://www.medscape.com/viewarticle/484283

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Shigellosis
http://www.cdc.gov/ncidod/dbmd/diseaseinfo/shigellosis_g.htm

"What sort of germ is Shigella?

The Shigella germ is actually a family of bacteria that can cause diarrhea
in humans. They are microscopic living creatures that pass from person to
person. Shigella were discovered over 100 years ago by a Japanese scientist
named Shiga, for whom they are named. There are several different kinds of
Shigella bacteria: Shigella sonnei, also known as "Group D" Shigella,
accounts for over two-thirds of the shigellosis in the United States. A
second type, Shigella flexneri, or "group B" Shigella, accounts for almost
all of the rest. Other types of Shigella are rare in this country, though
they continue to be important causes of disease in the developing world.
One type found in the developing world, Shigella dysenteriae type 1, causes
deadly epidemics there."

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Gut Aug 2004;53:1096-1101

Bacillary dysentery as a causative factor of irritable bowel syndrome and
its pathogenesis

L-H Wang, X-C Fang and G-Z Pan
Department of Gastroenterology, Peking Union Medical College Hospital,
Chinese Academy of Medical Sciences, Beijing 100730, China

ABSTRACT

Background and aims: The incidence of irritable bowel syndrome (IBS) or
functional bowel disorders (FBD) after bacillary dysentery (BD) has not
been extensively evaluated, and little is known of the pathogenesis of post-
infective (PI) IBS. Therefore, we investigated the incidence of IBS and FBD
in a Chinese patient population who had recovered from BD. To further
elucidate its pathogenesis, neuroimmunological changes, including
interleukins (IL), mast cells, neuropeptides, and the relationship between
mast cells and intestinal nerves, were investigated.

Methods: A cohort study of 295 patients who had recovered from BD (shigella
identified from stool in 71.4%) and 243 control subjects consisting of
patient siblings or spouses who had not been infected with BD were included
in the study. All subjects were followed up using questionnaires for 1-2
years to explore the incidence of FBD and IBS, as defined by the Rome II
criteria. In 56 cases of IBS (PI and non-PI) from another source, the
number of mast cells in biopsy specimens from the intestinal mucosa were
stained with antitryptase antibody and counted under light microscopy.
Also, the relationship of mast cells to neurone specific enolase (NSE),
substance P (SP), 5-hydroxytryptamine (5-HT), or calcitonin gene related
peptide positive nerve fibres was observed using double staining with
alcian blue and neuropeptide antibodies. In 30 cases of IBS (PI-IBS, n =
15) taken at random from the 56 cases, expression of interleukin (IL)-1, IL-
1ß, and IL-1 receptor antagonist (IL-1ra) mRNAs in intestinal mucosa were
identified using reverse transcription-polymerase chain reaction. The above
results were compared with 12 non-IBS controls.

Results: In the BD infected cohort, the incidences of FBD and IBS were
22.4% and 8.1% (in total)-10.2% (among those in who shigella were
identified) respectively, which were significantly higher (p<0.01) than the
incidences of FBD (7.4%) and IBS (0.8%) in the control cohort. A longer
duration of diarrhoea (7 days) was associated with a higher risk of
developing FBD (odds ratio 3.49 (95% confidence interval 1.71-7.13)).
Expression of IL-1ß mRNA in terminal ileum and rectosigmoid mucosa was
significantly higher in PI-IBS patients (p<0.01). The number of mast cells
in the terminal ileum mucosa in PI-IBS (11.19 (2.83)) and non-PI-IBS
patients (10.78 (1.23)) was significantly increased compared with that
(6.05 (0.51)) in control subjects (p<0.01). Also, in the terminal ileum and
rectosigmoid mucosa of IBS patients, the density of NSE, SP, and 5-HT
positively stained nerve fibres increased (p<0.05) and appeared in
clusters, surrounding an increased number of mast cells (p<0.01 compared
with controls).

Conclusions: BD is a causative factor in PI-IBS. The immune and nervous
system may both play important roles in the pathogenesis of PI-IBS.

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