Too much calcium prevents the body from fighting a dangerous hospital infection

Clostridium difficile is a bacterium that causes diarrhea and intestinal infection. The infection may even be life-threatening. A new American study that is published in PLoS Pathogens shows that this bacterium can only thrive with an overload of calcium in the intestinal system. Such a calcium excess can be caused by overconsumption of calcium, lack of vitamin D, and regular use of antacids.

Clostridium difficile is a sporogenous bacterium that typically affects older people and chronically ill individuals who take antibiotics. It is widely represented in nature and is a particularly big problem in hospitals and nursing homes. Millions of people suffer from the stubborn intestinal infection. In the United States alone, it accounts for around 30,000 deaths annually. The new study reveals that Clostridium difficile cannot thrive in the intestines without calcium, which leads the scientists to assume this this knowledge may pave the road to better prevention and treatment in the future, especially in the most vulnerable patients.

Too much calcium is the key to solving the mystery

Clostridium difficile gains access to the body when its spores enter the oral cavity. Most people get exposed to the spores without ever finding out, simply because their immune system and gut flora take care of the problem. Science has not managed to find out what causes the stubborn spores to develop into bacteria in the oxygen-deprived environment of the intestinal system.
With help from mouse studies, scientists from the University of Michigan and the FDA (Food and Drug Administration) have found out why, in some patients rather than in others, the Clostridium difficile spores are much more likely to develop into the bacteria that cause the actual intestinal infection. Apparently, this happens with the presence of too much calcium in the intestines.
Under normal circumstances, calcium is carried from the small intestine to the bloodstream with help from vitamin D, but if a person lacks vitamin D, calcium stays in the intestinal system. Lack of gastric juice, the use of antacids and corticosteroids, and having various intestinal ailments such as Crohn’s disease may also inhibit the uptake of calcium. Moreover, consuming too much calcium may also result in excess calcium in the intestines. The problem especially seems to affect older people, who get plenty of calcium from dairy products and calcium supplements, but who lack vitamin D, take antacids, and have too little gastric juice. The combination of these factors increases the risk of Clostridium difficule developing into the stubborn bacterial infection in the intestinal system.

The Clostridium spores are major consumers of calcium

According to the new study, the presence of excess calcium in the intestinal system is what triggers the spores, causing them to break out of their dormant state and erupt from their shell. Earlier studies have shown that the Clostridium difficile spores need the amino acid, glycine, to help them develop into bacteria, but according to the recent study, calcium alone is enough. It showed that in mice whose intestinal system had been cleared of calcium, there was a 90% lower risk that the spores developed into bacteria.
Professor Philip Hanna likens the spores to armed seeds that are able to travel through the stomach acid without being harmed. Some of the spores consist of calcium, and the scientists have managed to demonstrate that additional calcium in the intestinal system can activate the spores and make them turn into bacteria.
In fact, it was one of Philip Hanna’s former students, Travis Kochan, who made the groundbreaking discovery. He noticed that researchers typically used a calcium-rich growth medium when cultivating Clostridium difficile in vitro. That way, they were able to make the spores develop rapidly in an artificial manner. Using a chemical agent, Travis Kochan managed to remove calcium from the original growth medium. As a result, none of the spores turned into bacteria. The bacterial growth had come to a full stop.
Travis Kochan says that the Clostridium difficile spores have specialized in such a way that they can only develop under the right conditions. Also, he appears to have found the explanation to why his own grandfather suffered from the serious intestinal infection that eventually killed him. Professor Philip Hanna does not believe that this new discovery should discourage patients from taking their prescribed medicine or supplements. However, he hopes that it will lead to better future treatments for this stubborn infection.

Elevated calcium makes the bacterium increasingly sensitive towards antibiotics

According to the scientists, it is a paradox that we can now help patients by adding more calcium to their intestinal system. That way, it possible to help the slumbering Clostridium difficile spores break out of their dormant state and turn into bacteria, which makes them increasingly sensitive towards antibiotics. This may also help prevent the spores from spreading in the environment from the patients’ diarrhea. The scientists hope that this new treatment may contribute to stopping the dangerous cycle and the spreading of spores in hospitals and nursing homes, where extra hygiene and antibiotics alone is not enough. It is important to focus on optimal calcium uptake to prevent the Clostridium difficile spores from having ideal growth conditions. After all, calcium is needed for the maintenance of strong bones in combination with vitamin D, magnesium, and vitamin K2.

References

Travis J Kochan et al. Intestinal calcium and bile salt facilitate germination of Clostridium difficile spores. PLOS Pathogens 2017 http://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1006443
Michigan Medicine - University of Michigan. Could calcium hold the key to fighting a dangerous hospital infection? Science Daily 2017

https://www.sciencedaily.com/releases/2017/07/170713155005.ht

https://www.ssi.dk/Service/Sygdomsleksikon/C/Clostridium%20difficile%20infektion.aspx

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2805518/