Crohn'sCanada
Addressing the alarming rise of the bacterium "Mycobacterium avium Paratuberculosis"
in the environment and the growing evidence linking this bacterium to Crohn's
disease.
   
History of Crohn's Disease, Johne's disease, Mycobacterium avium Paratubercuosis, and Koch's Postulates

 

Founders: Diane and Michael Fagen

Contact Info: dianef84@yahoo.com

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Does Mycobacterium Paratuberculosis cause Crohn's disease by Alan Kennedy  

(PARA) PARATUBERCULOSIS AWARENESS & RESEARCH ASS.,INC



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The Johne's Information Center

History of Early Research on Crohn's disease

Dr. B. Crohn

Got Milk? by Michael Greger, MD Updated January 2001

THE CROHN'S CONNECTION  by Lisa Chamberlain

Dire Warnings About Johne’s
Disease A wake-up call for the dairy industry?

Micobacteria and Crohn's Disease

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A Brief History On Crohn's Disease

www.crohnscanada.org ~ Crohnscanada~ dianef84@yahoo.com

Disclaimer:
MAP-Canada does not advocate a particular cause of Crohn's disease.  Our website is intended only to present evidence.  Our readers may draw their own conclusions.  We are not medical specialists and do not offer any treatment or nutritional advice.  Our mission is not to lay blame on any individual or industry, but rather to urge the Government of Canada to address the evidence presented on this site.

Mise au Point:
MAP-Canada ne recommande aucune théorie particulière sur la cause de la maladie de Crohn.L'intente de notre site Web est simplement de présenter certaineévidence mais vous pouvez arriver à vos propres conclusions.Nous ne pouvons donner de conseils de nature médicale ou alimentaire. Notre mission ne consiste aucunement à blâmer un individuou une industrie mais
plutôt à s'assurer que le Gouvernement du Canada aborde l'évidence que nous présenton

MAP-Canada would like to extend a very sincere thank you to Yanik Chicoine at www.mirweb.com for his generosity and assistance in the hosting and the mounting of this site.

MAP-Canada aimerait remercier sincèrement Yanik Chicoine a www.mirweb.com pour sons générosité et sons assistance pour l'hébergement et la programation du site.

Burrill Bernard Crohn

In 1932, Dr. Crohn and his two colleagues, Dr. Leon Ginzburg and Dr. Gordon D. Oppenheimer, published an important paper describing the features of the then relatively unknown condition. They described fourteen cases , characterizing Crohn's disease as "Terminal Ileitis: A new clinical entity"; the description was changed to "Regional ileitis" on publication. It is by virtue of alphabetization rather than contribution that Crohn's name appeared as first author: because this was the first time the condition was reported in a widely-read journal, and the disease has come to be known as Crohn's Disease for reasons of publicity rather than precedence.

At the time he described the disease, Crohn was a practitioner and usually admitted his patients to the Mount Sinai Hospital in New York for their operations. Crohn gradually became more attached to the Mount Sinai Hospital, where he worked with the neurologist Bernard Sachs (1858-1944). There he soon built a very large and successful reception for patients with granulomatous enterocolitis and eventually was made chief of the department of gastroenterology. As such he was highly respected through all of his professional career and received numerous patients from all over the USA, some even from Europe.

Some of his initial research into the causes of the disease was centered around his personal conviction that it was caused by the same pathogen, a bacterium called Mycobacterium paratuberculosis, responsible for the similar condition that afflicts cattle called Johne's disease. However he was unable to isolate the pathogen (most likely due to the fact that M. paratuberculosis sheds its cellular wall in humans and takes the form of a spheroplast, making it virtually undetectable under optical microscope)

 

A Brief History of Johne's Disease

Before "Johne's disease"

As early as 1826, a chronic debilitating intestinal disease of cattle was recognized. Its characteristics and cause (etiology) were not of any currently known disorder. It was not until 1894 that the ailment was recognized as an infectious disease with a unique etiology.

 

The discovery by Johne and Frothingham

The discovery by Johne and Frothingham On October 23, 1894, in the Oldenburg region of Germany, a farmer purchased a cow that failed to produce milk or gain weight satisfactorily. A local veterinarian by the name of Herr Frederick Harmes examined the cow and, noting the diarrhea and weight loss, suspected intestinal tuberculosis. The cow tested negative by the tuberculin skin test however. It died the following spring and Dr. Harmes sent its intestines, stomach, and omentum for examination to the Veterinary Pathology Unit in Dresden. There the tissues were examined by Dr. H.A. Johne and Dr. L. Frothingham, a visiting scientist from the Pathology Unit in Boston, Massachusetts. They noted the thickened intestinal mucosa and enlarged mesenteric lymph nodes. On histologic examination, they found that the intestinal wall was heavily infiltrated with leukocytes and epithelioid cells and occasional giant cells. Using an acid-fast stain, abundant acid-fast (red staining) bacteria were seen throughout the inflamed tissues. Although the organisms resembled the bacteria that caused tuberculosis, a sample of the infected tissue containing the organisms failed to cause disease when injected into guinea pigs. Johne and Frothingham concluded that the disease observed in the cow was caused by the bacterium that causes tuberculosis in birds (Mycobacterium avium) and, in recognition of the pathologic similarity to intestinal tuberculosis(normally caused by the bacterium that causes tuberculosis in cattle, Mycobacterium bovis), proposed the name "pseudotuberculous enteritis" for the disease.

 

Baillieres Clin Gastroenterol 1990 Mar;4(1):23-42.
Molecular biology of Crohn's disease mycobacteria. Hermon-Taylor J, Moss M, Tizard M, Malik Z, Sanderson J.

A Glasgow surgeon, T.K. Dalziel, published a detailed description of chronic enteritis in humans in 1913. He proposed that the disease was caused by the same organisms as those responsible for chronic enteritis, Johne's disease, in animals described a few years earlier (1895). Dalziel's dilemma was that he could see acid-fast bacilli in the diseased animal tissues but not in the diseased human tissues. Little real progress in the medical understanding of the causes of chronic enteritis in humans occurred over the next half a century or more. From 1978, a decade of research in many laboratories using improved methods for the culture of environmental mycobacteria showed that these could be grown in bacillary form from about one in five cases of Crohn's disease, from the same proportion of cases of ulcerative colitis, and rom about one in ten control tissues. Spheroplasts were grown from two in five cases of Crohn's disease, one in five cases of ulcerative colitis, and rarely from control tissues. The nature of these agents was often uncertain. We describe work which began in 1985 and led rapidly to the identification of IS900, a DNA repetitive element in an uncharacterized Crohn's disease mycobacterial isolate. With other solates, these were then shown by DNA fingerprinting to be indistinguishable from Mycobacterium paratuberculosis, Johne's bacillus. Similar techniques also demonstrated the wood-pigeon strain of M. vium in some Crohn's disease cultures. This bacillus can also cause chronic enteritis in calves. IS900 is he first of a family of unusual DNA insertion sequences which extend widely throughout environmental mycobacteria. Use of assays based on PCR amplification of highly specific DNA sequences from these insertional elements, and recombinant and synthetic peptides from their predicted proteins, will evolutionize the detection and characterization of these agents. These methods, applied to animal, human and environmental samples, will indicate new ways for the prevention and treatment of chronic enteritis, as well as other disorders associated with infections by environmental mycobacteria.

 

A complex and controversial question: can M. paratuberculosis infect and cause disease in humans? Johne's Information Center, University of Wisconsin:

How can humans be exposed to MAP?
Before listing potential routes of human exposure, it is useful to recap MAP’s life history. The main reservoir for MAP in nature is infected animals. MAP is considered an obligate pathogen, meaning that it replicates in infected animals. Among animals, MAP is found primarily in ruminants such as cattle, sheep, and goat. (Non-ruminant animals such as omnivores and carnivores are infrequently infected with MAP and the infection rarely progresses to disease.) Ruminant infections begin when MAP is swallowed.......please follow link to read the full article.

 

Does MAP infect humans?
Two studies, one authored by Abubakar et al. and the other by Feller et al., have assembled publications on studies searching for MAP, or immune responses to MAP, in humans -to establish whether MAP ever infects humans (see publications listed below). Both have concluded that MAP has infected humans although whether these infections subsequently were the direct cause of disease is an open question. In the cases when MAP could be isolated from humans, the genetic fingerprints of the organism were the same as those cultured from animals.

What are the arguments for MAP as a cause of Crohn’s disease?
Borrowing from the publication by Sartor in 2005 (see reference list below), the following observations based on several studies support the hypothesis that MAP is one of the causes of Crohn’s disease: Crohn’s disease in humans is similar to Johne’s disease in animals both clinically and pathologically. MAP has been documented to infect nonhuman primates. Human exposure to MAP is plausible by multiple routes (see #1 above). Evidence of MAP is detected in tissues of Crohn’s disease patients more often than controls (see #2 above). Evidence MAP is detected in the blood of patients with Crohn’s disease more often than controls. The genotypes of MAP found in animals are the same as those found in humans. Crohn’s disease patients have antibody to MAP in their blood more often than controls. Some Crohn’s patients have clinically improved when treated with antibiotics effective against a broad range of bacteria, including MAP.

 

Koch's Postulates

Koch was one of the original researchers into tuberculosis, in the 19th century. In an attempt to define what an infectious disease actually is, he formulated his famous postulates, which now bears his name.

Basically, if

1. An organism can be isolated from a host suffering from the disease and

2. The organism can be cultured in the laboratory and

3. The organism causes the same disease when introduced into another host and

4. The organism can be re-isolated from that host then

The organism is the cause of the disease and the disease is an infectious disease. There is an implicit
assumption in step three, namely that the other host must have a genetic make-up that causes it to react to the organism in the same way as the original host. Also, these steps do not apply to all infectious disease. Notably, the bacterium causing leprosy, Mycobacterium leprae, cannot be cultured in the laboratory. However, leprosy is still recognised as an infectious disease. -------------------------------------------------------------------------------- Source: http://alan.kennedy.name/crohns/PRIMER/koch.htm This page written and maintained by Alan Kennedy Follow this link to the top level page. Related Information -------------------------------------------------------------------- ------------ Some Bacteria of Medical Importance

 

The History of Vaccines by The College of Physicians of Philadelphia: This is an excellent website, giving an overview of Koch's Postulates, with an animated deminstration of Koch's Postulates.

 

Koch's Postulates have been met.

As you read the following articles, the connection between Johne's disease in cattle and Crohn's disease in humans will become very clear.

The evidence below is really very disturbing, Dr. Kennedy Dalziel, a Crohn's surgeon recognized in 1913, the similarity between Johne's disease in cattle and crohn's disease in humans. Quoting his words" Dr. Dalziel pointed out in his paper that though to the naked eye the diseases were identical, the lack of bacilli made them very different." In otherwords the only difference was the fact that he could not see the bacilli in humans as he could in cattle.

Once again in 1932. Dr. Burrill Bernard Crohn also believed that the two diseases, Johne's in cattle and Crohn's in humans were caused by the same pathogen, but he was unable to isolate the pathogen, as Mycobacterium paratuberculosis sheds its cellular in humans and takes the form of a spheroplast.

Considering in 1913, Dr. Kennedy Dalziel and Dr. Burrill Crohn in 1932 could not see this pathogen, called
mycobacterium paratuberculosis, due to the lack of technology,. Dr Dalziel and Dr. Crohn could not possibly have met the criteria for Koch's postulates, hence, Dr. Crohn ruled crohn's an autoimmune disease, not an infectious one.

In 1984, a microbiologist, Dr. Rodrick Chiodini, demonstrated that mycobacterium . paratuberculosis sheds its cell wall in humans, and takes a new form, called a spheroblast. In a landmark study, Dr. Chiodini cultured Mycobacteria from children infected with Crohn's.

Since that time, many renowned crohn's researchers have isolated and grown the same bacterium,
mycobacterium paratuberculosis, and over the years doctors have met Koch's Postulates over, and over again. Now the question is, when is this situation going to be resolved. When is this crisis going to be put on the front burner.

Millions of people are suffering everyday. They wake up every morning and have to struggle through another day. , Please email me at dianef84@yahoo.com, please help!!!

The Government is there, because we put it there, we have to wake them up. Pressure is the only way. Our Government has to know that we want something done, or nothing will get done.

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