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Helminthotherapy is being used by Dr. Joel Weinstock and his colleagues from the University of Iowa, who reported recently (New Scientist, August 7, 1999), that regular doses of worms which normally do not infect humans, might cure people with inflammatory bowel diseases such as ulcerative collitis and Crohn’s disease. They believe that these distressing conditions (diarrhea, abdominal pain, bowel obstruction and bleeding) are increasingly common in the developed world because the absence of intestinal parasites. Dr. Weinstock has treated six patients with eggs, which hatched, developing to parasitic worms. The results were very encouraging and he is planning a larger trial. According to this research, between the second and third week after treatment, five of the six patients went into complete remission. Weinstock and his colleagues believe that the immune system is more likely to produce powerfull inflammatory agents such as gamma-interferon, which stimulate macrophages activity. The six patients in the initial trial were chosen because steroids and other drugs which diminish the immune system had not helped.

To induce chronic and continuous intestinal blood loss as therapy for congenital polycythemia in a 3 year old child, adult Ancylostoma duodenale were transferred directly from a dog to the patient via a nasoduodenal tube. By transferring adult worms, larval migration via the skin, blood and lungs –with possible attendant undesired side effect- was avoided. Furthermore, by eliminating larval migration with associated intimate tissue contact, immunogenicity was presumably reduced, and a known number of adult worms could be delivered directly to the final predilection site, the small intestine. An eosinophilic reaction op up to 23,000 cells/mm 3 was observed, which may have adversely affected attempted superinfection. The relatively small numbers of parasites given on three separate occasions did not result in blood loss to a degree sufficient to eliminate the need for other forms of therapy (Walterspiel, JN, Schad, GA and Buchanan GR. Direct transfer of adult hookworms (Ancylostoma duodenale) from dog to child for therapeutic purposes. J. Parasit. 1984; 70: 217-219).

British research has revealed that the parasites responsible for the common tropical disease schistosomiasis (bilharzias) hold the key to the prevention of insulin dependent diabetes, also known as Type A diabetes. Research has shown that mice bred to develop Type 1 diabetes do not do so if they are infected with the eggs of schistosome parasites.

The scientists responsible for the discovery believe that within three years they will have identified the substance in the egg that is responsible for preventing diabetes. It should then be possible to test it, or a drug based on it, as a means of preventing the onset of Type 1 diabetes. A similar treatment may also be effective in preventing other diseases caused in the same way as Type 1 diabetes, including rheumatoid arthritis and inflammatory bowel disease, and possible asthma.

The breakthrough discovery was made when Dr. Anne Cooke of the Pathology Department of Cambridge University, who is studying diabetes using mice, which are genetically predestined to develop the Type 1 form, moved from London to Cambridge taking a colony of mice with her. The mice became accidentally exposed to parasitic and other infections. As a result only 50% instead of the normal 80% of the mice developed Type 1 diabetes.

Type 1 diabetes is rare in the developing world where tropical parasitic diseases such as schistosomiasis are rife. In contrast, it is on the increase in the developed world where vaccination and improved hygiene have virtually eliminated parasitic infections. This led Anne Cooke and her colleague parasitologist Dr. David Dunne to consider whether such infections might be preventing the development of Type 1 diabetes, as they had to some extent in her mice.

To test the hypothesis they infected mice genetically programmed to develop Type 1 diabetes with schistosome eggs and larvae. Dr. Cooke and Dr. Dunne found that these reduced the incidence of diabetes. When the mice were infected early in life so they had not had time to begin to develop diabetes, then none of them went on to develop the disease. They were totally protected by the infection. Further research showed that it is some component of the egg, rather that later stages of the parasite’s development that confers protection.

The way in which Type 1 diabetes is caused suggests how the infection may be having its effect. The disease is caused by an autoimmune reaction, in which the human immune system attacks some part of its own body as if it were a microorganism that had gained access to the body. In Type 1 diabetes the targets for attack are the cells in the pancreas, which produce insulin.

It is known that in people chronically infected with schistosome, the nature of the immune response to infections becomes altered, in a way, which reduced the strength of the part of the response which, if misdirected, can cause autoimmune diseases. This is probably why Type 1 diabetes, as well as rheumatoid arthritis, are relatively rare in developing countries in the tropics, where chronic infection with schistosomes is very widespread.

The low prevalence of human schistosome infections in the developed world is a relatively recent phenomenon. On an evolutionary timescale, infection with parasites is the normal human condition. So the current increase in the incidence of Type 1 diabetes in developed countries may be due to the new (on an evolutionary time scale) absence of parasitic infections, revealing a susceptibility to autoimmune diseases, which previously would have been hidden and so would not have been eliminated by evolutionary proceses.

Dr. Cooke, Dr. Dunne and their Cambridge colleagues are now working to identify the antigen or antigens in the schistosome egg, which are responsible for altering the immune response and preventing the autoimmune destruction of insulin-producing pancreatic cells. They estimate that this may take about three years, after which it would be possible for a pharmaceutical company to begin the work of developing a drug upon the vital egg component.

At present Type 1 diabetes is usually diagnosed only after the majority of the insulin producing cells have already been destroyed. But much work is going into finding ways to identify those at risk earlier. When such diagnostic techniques are available, then a drug developed from Dr. Cooke’s work could be given prophylactic to protect those at risk. If the same drug could be given to people already affected by Type 1 diabetes, but with insulin producing cells still surviving, then research suggests it may be possible to cause such cells to regenerate, once the autoimmune reaction destroying them has been terminated.

Other autoimmune conditions as well as Type 1 diabetes may be prevented and possible treated in the same way. Rheumatoid arthritis, inflammatory bowel disease and asthma are among the possibilities.

NOTE: For more information contact Dr. Anne Cooke, Department of Pathology, Tennis Court Road, University of Cambridge CB21 QP, UK, Tel.: ++ 44 1223 337733 or Emma Wilkinson, Wellcome Trust, Tel.: 0171 6118846, Facsimile: 0171 6118416.



Copyright © 2007 Hebrew University, Jerusalem, Israel
Last modified: 01/01/07