UPDATE: I haven’t had much spare time to work on this site recently, but I am creating a new irritable bowel syndrome/Crohn’s blog very soon… it will include many new startling (perhaps ground-breaking) insights into IBS/CD.

For now consider this:

"Researchers in London have discovered that a weak immune response instigates Crohn's disease, possibly laying to rest the popular belief that an auto-immune condition is to blame”. (Link.)

The conclusions of this study do not seem to support auto-immunity or an overly aggressive response to MAP as the underlying cause of CD. However, the conclusions do FULLY support my hypothesis below.

For many years there have been generally two camps for Crohn’s researchers/experts: those who support auto-immunity (genetic predisposition) and those who support MAP-infection as the primary causative factor of CD… but, perhaps it’s a combination of MAP, genetic predisposition (a weak immune response to MAP) and diet that leads to Crohn's??? More details on my new blog!

Additionally, I’d like to say many thanks for all your supportive emails and kind words!

Mycobacterium avium subspecies paratuberculosis, or MAP for short, is the organism responsible for a chronic, intestinal inflammatory disease found mainly in domestic livestock, including cattle, deer, sheep and goats.

MAP was first described in 1895 by Dr H. A. Johne and Dr L. Frothingham after they observed the bacteria throughout the inflamed intestinal-tissues of a cow that failed to gain weight or produce milk. And the disease has since become known as Johne’s disease (JD) or paratuberculosis.

Even though a herd of cattle may become infected with Mycobacterium avium subspecies paratuberculosis (MAP), usually only a small percentage develop clinical signs of the disease, which is often characterized by profuse diarrhoea and severe weight loss. And, as the disease advances, animal death inevitably follows.

Paratuberculosis was long considered a disease of domestic ruminants only. But significant research over the last decade or so has seen MAP isolated from many different animals and numerous species. However, observation and study data suggests MAP primarily expresses clinical disease in domestic livestock (especially dairy cattle).

If you are new to MAP and Johne’s disease, and want to learn more about them, visit one or more of the pages listed below.

• Johne’s FAQs
• History of Johne’s disease
• Articles and brochures
• True cases and stories
• Biology of MAP

A growing number of studies have found MAP in the intestines Crohn’s disease (CD) patients. And therefore it’s been proposed that MAP may be a major cause CD too. If you are unfamiliar with Crohn’s disease, one or more of the sites below will provide a brief introduction to the disease.

• National Digestive Diseases Information Clearinghouse
• Crohn’s and Colitis Foundation of America
• Crohn’s and MAP infection

How MAP causes disease is simply unknown, but, it’s assumed MAP somehow initiates an immune-system response from susceptible hosts (cattle, sheep, deer, etc) and their immune responses may, in some way, lead to inflammation, pathological lesions and ulceration. In other words, it’s assumed that susceptible hosts’ immune responses to MAP cause gut inflammation by erroneously ‘attacking’ their own intestinal tissues.

However, I’m proposing the above assumption is wrong. I’m proposing MAP directly causes tissue damage observed in MAP-infected hosts, and their immune systems respond to the tissue damage, and not the other way round!

Below is a hypothesis which details my personal view of how Mycobacterium avium subspecies paratuberculosis may cause disease including:

• How MAP may survive the antibacterial compounds of and kill macrophages. (It’s very unlikely to be related to extra-cellular toxins because none have ever been discovered.)
• Why MAP almost exclusively expresses clinical disease in domestic ruminants. There have been a small number of documented cases of clinical paratuberculosis in wildlife but that number is insignificant in contrast to the potentially vast number of cattle that have developed clinical Johne’s disease over the last few decades.
• Why dietary calcium may reduce MAP infection in Beige mice.
• Why acidic soil-types seem to favour Johne’s disease expression in cattle, and alkaline soil-types seem to retard disease expression. And, why the application of lime to grazing pastures may limit Johne’s disease infection/expression as well.
• How MAP may cause disease in Crohn’s sufferers.

So how does MAP cause disease? How does this enigmatic bacterium kill certain immune cells and cause severe inflammation?

I’m proposing MAP is acidogenic! I’m proposing MAP causes disease by penetrating a potential host’s intestinal mucosal layer, attaching itself to the intestinal lining and, if a colony or colonies of MAP eventually become large enough, fermenting a wide-range of sugars (inc. starch or partially digested starch) to produce enough organic acid(s) at such a low ph to burn its host’s gut lining leading to various levels of inflamed tissues. The inflamed tissues then produce macrophage-colony stimulating factor (M-CSF) which cause macrophages to migrate to the site of inflammation where MAP invades them, replicates inside them and inevitably kills them, and a complex immune-system response follows possibly involving CD4+ T cells, IL-16, IL-18, etc. Over a period of time, with significant carbohydrate consumption, MAP colonies increase in size leading to greater levels of inflammation and, potentially, gross lesions and multiple ulcerations.

Furthermore, I’m proposing that gross lesions and ulcerations observed in MAP-infected CD patients and JD-inflicted animals are caused by an accumulation of microscopic intestinal-tissue burns, and, their immune systems try to prevent gut ulceration by thickening their intestinal walls.

Indeed, a Crohn’s study by Lee, DeSchryver-Kecskemeti and Stenson, noted “a statistically significant thickening of the muscularis mucosae when compared with disease controls”, and “similar findings were also present in a previously characterized experimental model of CD (trinitrobenzene sulfonic acid-induced colitis in rats), particularly in what appeared to be grossly strictured areas”. In addition, a study by Graham and colleagues noted an accumulation of collagen in the strictured intestines of Crohn’s patients. This was also observed by Patterson et al in cattle with Johne’s disease. Likewise, collagen accumulation was also found during an experimental study involving esophageal burns in rats.

I’m proposing that the source of sugars/starches, fermented by MAP to produce acid in JD-inflicted ruminants, is manufactured cattle feed - which is typically 65% carbohydrates. Indeed, Newman Turner, a cattle farmer from the UK, documented in his book, Fertility Farming (1951, Faber & Faber, London), that he believed “the widespread incidence of Johne’s disease coincided with the general use of manufactured cattle foods”. And, some farmers have observed cattle with clinical JD still seem to feed ‘well’ or even excessively.

(Source: http://www.crohns.org/map_food/photo.htm)

If carefully considered, a startling insight arises from my hypothesis: if it’s proven that MAP causes disease via acid production, like Streptococcus mutans the major cause of dental disease, it almost certainly proves MAP is a major cause Crohn’s! In other words, the first scientists to demonstrate that MAP causes disease by microscopically burning its hosts’ intestinal tissues, are also the first scientists to provide near overwhelming evidence that MAP is a major of Crohn’s disease! Read on…

As mentioned, I’m proposing MAP causes intestinal disease by producing acids that microscopically burn its host’s gut lining. So:

• Does MAP counter the antibacterial compounds of and kill macrophages by organic acid production? (In the same way I’m proposing it causes disease.)
• Does MAP almost exclusively express clinical disease in domestic ruminants because of the rich supply of carbohydrates in manufactured cattle feed? (Which are generally unavailable to wild animals and wildlife.)

• Did dietary calcium reduce the level of MAP infection in Beige mice by neutralizing some of the acids produced by MAP and therefore limited infection and disease expression? A recent study by Chata et al, noted that calcium gluconate was effective for relief of severe pain in 7 cases of hydrofluoric acid burn; evidently, the calcium gluconate reduced the effects of the acid burns.
• Do alkaline soil-types retard JD expression by buffering acids produced in MAP-infected ruminants? Does applying lime (calcium oxide) to pastures, which is used in the water and sewage industry to reduce acidity, hinder MAP’s ability to cause intestinal disease by neutralizing some of its acid production?
• Does MAP cause Crohn’s disease, in the same way I’m proposing it causes JD, by fermenting a wide-range of sugars (inc. starch or partially digested starch) to produce enough organic acid(s) at such a low ph to burn its human host’s gut lining, leading to various levels of low-grade intestinal inflammation and, potentially, gut lesions and ulceration? Many studies have noted high sugar/carb consumption in CD sufferers. And a number of studies have noted disease improvement or even remission in CD patients on low-carb (sugar restricted) diets.

  Additionally, Lee et al, as mentioned above, observed significant thickening of the intestinal wall in CD patients during a study which he noted was similar to acid-induced colitis in a previous experimental model of Crohn’s in rats. This is further supported by collagen accumulation noted in CD, JD and an experimental study involving esophageal burns in rats.

If MAP needs a supply of carbohydrates to produce acid and cause disease, how can my hypothesis explain the small number of documented cases of clinical Johne’s disease in wildlife? A study by Daniels and colleagues observed that ruminants will try to avoid but inevitably consume feed contaminated by wildlife faeces. Consequently, they suggested that contaminated feed may be potential source of bacterial infection for livestock. Likewise, did the documented cases of wildlife with clinical JD develop the disease as a result of consuming partially digested, MAP-infected cattle feed from pastures where clinically-infected ruminants with diarrhoea were grazed?

Streptococcus mutans, the major cause of dental carries, also causes disease by producing acids. The genomes of MAP and Streptococcus mutans have been sequenced. A comparison of their genomes may reveal similar virulence genes. Indeed, Tizard and colleagues conducted a study to find genes specific to MAP, and they identified “a low G+C content genetic island” which they associated with “LPS or extracellular polysaccharide biosynthesis”. A number of genetic islands have been identified in Streptococcus mutans' UA159 genome, including some with a low G+C content.