Your English is fine.
This is how my IBS started 40 years ago from an enteric infection from Amoebic dysentery.
Its a must to reduce stress, that can actually contribute to PI IBS becoming IBS. There are a lot of ways to do this, but again I also recommend the HT for IBS.
Some things to read.
An infection can start IBS, but the initial infection goes away and a person is left with PI IBS that can lead to IBS.
One of if not the top doctor in PI IBS is DR Spiller in the UK.
Post-infectious irritable bowel syndrome
Post-infectious irritable bowel syndrome (PI-IBS) is a common disorder wherein symptoms of IBS begin after an episode of acute gastroenteritis. Published studies have reported incidence of PI-IBS to range between 5% and 32%. The mechanisms underlying the development of PI-IBS are not fully understood, but are believed to include persistent sub-clinical inflammation, changes in intestinal permeability and alteration of gut flora. Individual studies have suggested that risk factors for PI-IBS include patients’ demographics, psychological disorders and the severity of enteric illness. However, PI-IBS remains a diagnosis of exclusion with no specific disease markers and, to date, no definitive therapy exists. The prognosis of PI-IBS appears favorable with spontaneous and gradual resolution of symptoms in most patients.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2721231/
and
http://www.ibs-irritable-bowel-syndrome.com.au/downloads/Post_Infectious_IBS_Spiller.pdf
They have found Important cellular structural changes after the intial infection in IBS.
"Post-infectious Irritable Bowel Syndrome
Robin Spiller; Eugene Campbell
Curr Opin Gastroenterol. 2006;22(1):13-17. ©2006 Lippincott Williams & Wilkins
Posted 12/08/2005
Abstract and Introduction
Abstract
Purpose of Review: Irritable bowel syndrome patients form a heterogeneous group with a variable contribution of central and peripheral components. The peripheral component is prominent in irritable bowel syndrome developing after infection (post-infectious irritable bowel syndrome) and this has proved a profitable area of research.
Recent Findings: Recent studies have overthrown the dogma that irritable bowel syndrome is characterized by no abnormality of structure by demonstrating low-grade lymphocytic infiltration in the gut mucosa, increased permeability and increases in other inflammatory components including enterochromaffin and mast cells. Furthermore, increased inflammatory cytokines in both mucosa and blood have been demonstrated in irritable bowel syndrome. While steroid treatment has proved ineffective, preliminary studies with probiotics exerting an anti-inflammatory effect have shown benefit.
Summary: The study of post-infectious irritable bowel syndrome has revealed the importance of low-grade inflammation in causing irritable bowel syndrome symptoms. It has suggested novel approaches to irritable bowel syndrome including studies of serotonin and histamine metabolism which may be relevant to other subtypes of of the disease.
http://www.medscape....le/518355_print
Both serotonin and histimine are implicated in IBS and can cause the symptoms.
Post infectious IBS was recently "demonstrated as a brain gut axis disorder." As is IBS, because both the brain and the gut are operational to cause the symptoms.
So I will post more but read these.
enterochromaffin cells and serotonin and IBS
http://www.ibsgroup....showtopic=80198
Mast cells
Jackie (Jack) D. Wood "
FYI
"You have two brains: one in your head and another in your gut. Dr. Jackie D. Wood is a renowned physiologist at The Ohio State University. He calls the second brain, "the-little-brain-in-the-gut." This enteric nervous system is part of the autonomic nervous system and contains over one hundred million neurons, which is as many as are in the spinal cord. This complex network of nerves lines the walls of the digestive tract form the esophagus all the way down to the colon. This little brain in the gut is connected to the big brain by the vagus nerves, bundles of nerve fibers running from the GI tract to the head. All neurotransmitters, such as serotonin that are found in the brain are also present in the gut.
Dr Wood has discovered that this little-brain-in-the-gut has programs that are designed for our protection and which are very much like computer programs. They respond to perceived threats in the same way that the limbic system or the emotional brain does. So the threat of a gastrointestinal infection can activate the program that increases gut contractions in order to get rid of the infection. The symptoms are abdominal cramping and diarrhea.
Dr. Wood has determined that a type of cell found in the body and the gut, called the mast cell, is a key to understanding the connection of the big brain in the head with the little-brain-in-the-gut. Mast cells are involved in defense of the body. In response to certain threats or triggers, such as pollen or infection, mast cells release chemicals, such as histamine, that help to fight off the invader. Histamine is one of the chemicals that causes the symptoms of an allergy or a cold. When an infection of the gut occurs, such as food poisoning or gastroenteritis, the mast cells of the gut release histamine. The little-brain-in-the-gut interprets the mast cell signal of histamine release as a threat and calls up a protective program designed to remove the threat – at the expense of symptoms: abdominal pain and diarrhea.
The brain to mast cell connection has a direct clinical relevance for irritable bowel syndrome and other functional gastrointestinal syndromes. It implies a mechanism for linking allostasis and the good stress response to irritable states (e.g., abdominal pain and diarrhea) of the gut. Mast cells can be activated to release histamine in response to perceived psychological stress, whether the stressor or trigger is consciously perceived or not. So the end result is the same as if an infection activated the program in the-little-brain-in-the-gut: abdominal pain and diarrhea."
http://www.parkviewp...nuggets/n5.html
J Food Prot. 2007 Jul;70(7):1762-9.
Postinfectious irritable bowel syndrome: a long-term consequence of bacterial gastroenteritis.Smith JL, Bayles D.
Microbial Food Safety Research Unit, Eastern Regional Research Center, Agricultural Research Service, US Department of Agriculture, 600 East Mermaid Lane, Wyndmoor, Pennsylvania 19038, USA.
[email protected]Irritable bowel syndrome (IBS) is a commonly diagnosed disease characterized by gastrointestinal symptoms that may be associated with psychological illness and emotional problems. The prevalence rate worldwide for IBS ranges from 10 to 20% and is higher for women than for men. IBS imposes a substantial financial burden on both patients and employers because of increased medical costs and decreased work productivity. Recent studies indicate that inflammatory processes involving the gastrointestinal tract are strongly correlated with IBS. Acute bacterial gastroenteritis has been linked with the onset of symptoms in approximately 15% of patients diagnosed with IBS; these cases have been called postinfectious IBS. Organisms commonly associated with postinfectious IBS include the foodborne pathogens Campylobacter, Escherichia coli, Salmonella, and Shigella. The pathologic changes associated with postinfectious IBS are likely due to inflammatory reactions induced by the infecting organisms. Postinfectious IBS should be recognized as a potential long-term consequence of foodborne gastroenteritis.
PMID: 17685356
as you can see there are a few differ3nt pathogens here.
It is important to keep inflammation in perspective with IBS.
J Gastroenterol. 2007 Jan;42 Suppl 17:41-7. Links
Role of infection in irritable bowel syndrome.Spiller RC.
Wolfson Digestive Diseases Centre, University Hospital, Nottingham, NG7 2UH, UK.
Infection by pathogenic organisms leads to mucosal damage and disruption of the gut's extensive commensal flora, factors which may lead to prolonged bowel dysfunction. Six to 17% of unselected irritable bowel syndrome (IBS) patients believe their symptoms began with an infection, which is supported by prospective studies showing a 4%-31% incidence of postinfectious IBS-(PI) following bacterial gastroenteritis. The wide range of incidence can be accounted for by differences in risk factors, which include in order of magnitude; severity of initial illness > bacterial toxigenicity > hypochondriasis, depression and neuroticism, and adverse life events in the previous 3 months. PI-IBS has been reported after Campylobacter, Salmonella, and Shigella infections. Serial biopsies after Campylobacter jejuni gastroenteritis show an initial inflammatory infiltrate, with an increase in enterochromaffin (EC) cells, which in most cases subsides over the next 6 months. Those who go on to develop IBS show increased numbers of EC and lymphocyte cell counts at 3 months compared with those who do not develop IBS. Interleukin-1beta mRNA levels are increased in the mucosa of those who develop PI-IBS, who also show increased gut permeability. Recover can be slow, with approximately 50% still having symptoms at 5 years. Recent studies suggest an increase in peripheral blood mononuclear cell cytokine production in unselected IBS, an abnormality that may be ameliorated by probiotic treatment. The role of small-bowel bacterial overgrowth in IBS is controversial, but broad-spectrum antibiotics do have a temporary benefit in some patients. More acceptable long-term treatments altering gut flora are awaited with interest.
PMID: 17238025
Your long term antibiotic use may have upset your gut flora and it would be good if after your not taking them to take a good probotic, one with bifidobacteria in it.