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 Left behind | Back to blogs for industry | Another micriobial pathogen in the news | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Clostridium difficile causes a nasty form of diarrhea, which in severe cases can become pseudomembranous colitis. I've been interested in "C. diff" since it almost killed my mother-in-law a few years ago. The Wapo reports a troubling trend: Adding to the alarm is evidence that the infection is occurring outside of hospitals. When the CDC began looking for such cases earlier this year, investigators quickly identified 33 cases in New Hampshire, New Jersey, Ohio and Pennsylvania, including 23 people who had never been in the hospital and 10 women who had been hospitalized only briefly to deliver a baby, the agency reported this month. Eight of the patients had never taken antibiotics.The story suggests a connection with acid reflux drugs such as Prilosec or Prevacid...which is discussed in this JAMA paper. By suppressing stomach acid, the drugs may inadvertently help the bug, the researchers said.Earlier, I noted two papers describing Clostridium difficile in Canadian and US outbreaks. This story stimulated me to go back and look at those and wonder what is known about how Clostridium difficile gets around. In addition, I'm wondering what the cases that are not associated with antibiotic treatment mean. Spread First, I note that I misread one the papers in the earlier post [corrected now]...the Quebec outbreak is described as "predominantly clonal". The US strains have clearly diverged from each other and from the Canadian strain, but they're related based on DNA markers, including the presence of the binary form of the toxin and characteristic deletions in the tcdC gene (I read the figure legend without looking at the enlarged figure...I thought the Canadian strain had an 18bp deletion while the US strains had a 39 bp deletion. Actually both deletions are found in both populations, and the 18 bp deletion is more frequent among outbreak patients. Related strains are found in historical samples from the US going back to the late 1980s. The strain is also thought to be in Europe, if I'm reading the papers right this time. Loo et al. discuss how the same strain could spread between so many hospitals. Transmission of this predominant strain among hospitals could have occurred as the result of transfers of colonized or infected patients or, perhaps, from colonized health care workers who worked at multiple institutions. In these institutions, the majority of rooms have multiple beds, with shared toilets, facilitating transmission within hospitals. It has been demonstrated that patients housed in single rooms have a lower incidence of C. difficile-associated diarrhea than patients accommodated in double rooms.30This 2001 review by Farbut and Petit link points to how easy it is to spread C. difficile Transmission of C. difficile is thought to occur via the oro-fecal route. Outbreaks in hospitals and typing of strains suggested that transmission is probably via staff hands. A study documented positive hand cultures in 59% of hospital personnel caring for patients with positive culture [3].Contaminated rectal thermometers are also implicated - the spores are alcohol resistant. Still how does a strain spread over multiple continents?Farbut and Petit also cite this: McFarland et al. [3] compared the rate of environmental contamination in rooms of patients with C. difficile-associated diarrhea to that of contamination in rooms of C. difficile asymptomatic carriers. They showed that contamination was significantly higher in rooms of patients with diarrhea compared to asymptomatic carriers (49 vs. 29%). They also analyzed contamination in rooms without C. difficile-positive patients and found a contamination rate of 8%, showing that spores of C. difficile can persist, despite routine cleaning of rooms.What jumps out at me is that so many asymptomatic patients are shedding spores. Although C. difficile was only found in 3% of healthy adults in previous studies, perhaps the role of carriers is underappreciated. There are also reports of possible exchange with domestic animals. Antibiotic-independent cases That there could be more C. difficile outside of hospitals and nursing homes than previously thought is unfortunately consistent with the cases reported in the WaPo story, as well as with the cases described in MMWR(the CDC report cited above) involving pregnant women and children who had not recently taken antibiotics. The association of antibiotic treatment with symptomatic C. difficile infections is based on the idea that competing bacteria normally keep C. difficile levels too low to allow it to enough toxin to make the patient sick. After antibiotics, C. difficile, which has been able to persist as spores, gets a head start on the other bacteria that will recolonize the gut. The strain being found in the outbreaks makes a lot more toxin, so it could be that is sufficient to lead to symptoms when a susceptible person ingests spores. Alternatively, higher toxin levels could just change the threshold of how much disruption of the normal flora is needed to get diarrhea. This could vary due to variation in the resident microflora from individual to individual. There is likely to be a genetic component to this, but it would not be surprising if things like pregnancy or proton-pump inhibitors affected the ecology of the gut. But I find myself wondering about an environmental factor that could mimic antibiotic treatment. Could things like changes in stomach acid affect the ecology of the bacteriophage that are in the gut? Phage blooms could decimate the normal competitors for C. difficile, allowing it to bloom in turn, just as it does after antibiotic treatment. We know very little about the bacteria in the gut, and perhaps even less about their most important predators, the phage.
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