Researchers in two states have reported moving closer to stopping infections of the dreaded clostridium difficile bacteria commonly known as C. diff. Their findings are intriguing to patients such as myself who have suffered from repeated bouts of this intestinal infection.
Scientists at Boston's Massachusetts General Hospital used an oral medication made from an intestinal enzyme to prevent C. diff in mice, Medical News Today reports. Surgeons at the Penn State University College of Medicine have detected a human genetic mutation that could create treatments to prevent repeat infections.
C. diff is a bacterium that typically strikes hospitalized or institutionalized patients or those who have had a course of antibiotics. Among those at risk are individuals with ulcerative colitis or Crohn's disease, both types of inflammatory bowel disease (IBD). Even healthy individuals sometimes contract the infection, which is becoming more severe and more difficult to treat in the United States, the Mayo Clinic says.
The infection causes diarrhea, fever, abdominal pain, and inflammation and swelling of the colon. Ironically, the treatment for C. diff is an antibiotic, typically Flagyl. Experts estimate that the illness strikes around 336,000 people yearly and link it to 14,000 deaths and $1 billion in costs. ScienceDaily reported that C. diff is four times more likely to kill IBD patients than those without the condition.
The Massachusetts scientists gave mice four days of an antibiotic treatment. One of the two groups treated received oral doses of a purified intestinal enzyme, intestinal alkaline phosphate (IAP). Those in the other group received only standard antibiotic therapy.
Mice in the first group had cleared C. diff from their guts by day five, while the others still tested positive for the toxin it produces. Researchers also noted fewer symptoms like diarrhea and overall improvement of the colon. The next step is learning whether similar IAP treatments can prevent C. diff in humans.
Patient recurrence rates range from 20 to 50 percent. The Penn State team studied a human gene called tcdC. It signals C. diff bacteria to shut off production of the toxin that makes people sick. Over time, this gene sometimes mutates and boosts recurrence rates.
After following 73 subjects, researchers concluded that mutations on two base pairs within the tcdC gene were linked to higher toxin production. A mutation in either pair upped the risk of a recurrent infection by 80 percent. The team concluded that patients with mutations need an extended period of antibiotics.
While a patient with Crohn's disease, I have had four C. diff infections. Like many Crohn's patients, I take drugs to reduce disease activity by suppressing my immune system. I sometimes need antibiotics for common infections that most can overcome without treatment, putting me at risk for C. diff. It's encouraging to see both teams of researchers moving closer to stopping this serious infection.
Vonda J. Sines has published thousands of print and online health and medical articles. She specializes in diseases and other conditions that affect the quality of life.