People who are interested in infections that are transmitted in hospitals (umm, ghouls like me) have a special sick relish for Clostridium difficile, or in its short form, C. diff. C. diff lives in the intestines, part of a complex population of many bacteria — you did know there are more bacteria in your body than there are cells that belong to you, right? — but it roars out of control if those other bacteria are wiped out by a course of antibiotics, especially clindamycin. Removing the other bacteria clears out space for C. diff to reproduce in much greater numbers; the toxins it produces irritate the lining of the intestine, producing colitis, and triggering fever, cramps and diarrhea, and in the worst cases, sepsis. miscarriage and death.
C. diff colitis is one of the most common and serious hospital-acquired infections because — if you’re reading this over breakfast, you might want to stop eating now — severe diarrhea in a hospital patient who is confined to a bed and using a bedpan tends to get everywhere. Really, everywhere: bed linens and bedrails, floors and walls, stethoscopes, telephones, computer keyboards, and the hands of the healthcare personnel who operate those devices and then touch another patient.
C. diff persists so spectacularly because in the outside air, it forms a hard-shelled spore that protects its genetic material from assault — including from the alcohol in the hand gel that most healthcare workers use to clean their hands in between patients, and from the stomach acid of patients who swallow it. (See, I told you to stop eating.) Because of that, and because it’s such a devastating infection, hospitals toil incredibly hard at sanitizing to get rid of it.
C. diff colitis is a stubborn and ugly infection. Earlier this summer, an Illinois man named Ed Corboy Jr. described his mother Joan’s experience with it to the Infectious Diseases Society of America:
I watched helplessly as [she] grew weaker, more dehydrated, and nearly died. She was started on intravenous fluids and standard antibiotics while in the hospital two different times that December. Her blood pressure dipped dangerously low on many occasions. She had lost almost 55 pounds in the previous five months, and she was so profoundly exhausted, tired, and wasting away that it became apparent in early January she might die from this. She could hardly get to a bedside commode without two people helping her. Prior to this she was able to walk to her bathroom with her walker on her own for years.
Starting about 10 years ago, C. diff got dramatically more problematic: more virulent, more resistant to treatment, and more commonly occurring in people who would not have been expected to have it — often, healthy young people who had not been in hospitals, who seemed to be developing the illness in the outside world. Two CDC researchers said in 2008:
In the United States, the number of hospital discharges where (C. diff associated diarrhea, CDAD) was listed as any diagnosis doubled between 2000 and 2003, with a disproportionate increase for persons aged > 64 years. By 2003, regional reports of CDAD outbreaks from hospitals throughout the US and in Quebec, Canada emerged, describing severe disease associated with greater numbers of complications, including colectomies, treatment failures, and deaths. In 2004, the attributable mortality rate of nosocomial CDAD in Quebec hospitals was 6.9%, compared to 1.5% among Canadian hospitals in 1997. In the US, death certificate data suggest mortality rates due to CDAD increased from 5.7 per million population in 1999 to 23.7 per million in 2004. (Gould, Critical Care, 2008)
The reason for the surge has been understood to be the emergence of a new, hypervirulent strain of C. diff that produces up to 20 times more toxin than earlier ones. (C. diff nomenclature will make your brain hurt, but the strain is generally known as NAP1/027/BI, toxinotype III.) But increased virulence doesn’t explain the increased incidence, and the transmission patterns of the new strain have been murky.
An emerging line of inquiry suggests that the transmission patterns become much more clear if you look in a different place for the bacterium’s origin: not in hospitals, but in food.
C. diff has been identified in live pigs, cows and chickens. The bacterium has been found in retail meat in the United States and in Canada (in three separate studies), and in salad greens in Scotland. And in a paper published this month, the main authors from those Canada studies establish that minimum recommended cooking temperatures for ground beef don’t kill C. diff spores.
(You’re really not eating now, right?)
So, OK: But are the C. diff strains found in animals the same ones that are causing human disease? The answer turns out to be Yes. Several researchers have found overlaps, in 2007, 2009 and earlier this year, in a study with the perfect title: “Innocent bystander or serious threat?”.
And in what looks certain to be a provocative presentation, a team of researchers from Houston is going to present a paper at the annual meeting of the Infectious Diseases Society of America in a few weeks, titled: “Potential Foodborne Transmission of Clostridium Difficile Infection In a Hospital Setting.” (Uh-oh.)
The case for C. diff as a foodborne illness still isn’t made. In an excellent paper published last month, L. Hannah Gould and Brandi Limbago of the CDC go over the findings so far, and detail what evidence and further research are still needed.
It is reasonable to assume that the general public is and has been often exposed to low numbers of potentially infectious C. difficile spores. There is currently limited epidemiologic evidence to support or refute the hypothesis that C. difficile is transmitted by the foodborne route; the presence of C. difficile on retail foods suggests but does not prove that some proportion of infections is acquired this way. The food supply may thus serve as a source of new strains causing human infections; alternatively, food could be another constant and normally innocuous exposure. (Gould, Emerging Infectious Diseases, 2010)
What’s really interesting, though, is that microbiologists aren’t the only ones noticing this accumulation of evidence. C. diff as a possible foodborne pathogen caught the attention of foodborne-illness attorney Bill Marler early last year. If Marler — the most aggressive and, I suspect, successful foodborne-injury lawyer on the planet, dating back to the 1993 Jack-in-the-Box outbreak — is starting to notice the evidence tying C. diff outbreaks to food, there might be a lot more attention paid to this connection fairly soon.
Image of C. diff by Janice Carr, courtesy of Public Health Image Library, CDC.