Hospitals and Antibiotics Help Create a Dangerous Epidemic

Thirty years ago in Boston, I worked as a research assistant in a local hospital. Each

morning on my way up to my lab, I passed another lab where an infection called “antibiotic-

associated psueodmembranous colitis” was being studied. It sounded exotic, and the lab’s

complex culture media, gas cylinders, and clear plastic chambers for growing oxygen-sensitive

organisms added to that sense of the exotic. But that infection did not remain exotic. Thirty

years later, it has become a major threat to hospitalized patients and community residents.

That complicated name, antibiotic-associated psueodmembranous colitis, has been

replaced by something slightly more pronounceable, Clostridium difficile-associated disease, or

CDAD. By any other name, the agent of this illness is a bacterium called, C. difficile. It is a

cousin of the two bacteria that cause tetanus and botulism, and like them it produces disinfectant-

resistant spores and dangerous toxins.

C. difficile infections usually begin in the colon. The bacteria’s toxins (A and B)

produce diarrhea and colitis (i.e., inflammation of the colon). There may be abdominal pain,

fever, nausea, dehydration and sometimes blood in the stool. Sepsis, intestinal perforation and

death can occur in severe cases.

How do you get CDAD? Odd as it may seem, you get from taking antibiotics. That may

seem like a paradox because antibiotics are taken to kill bacteria. If you take certain antibiotics

(clindamycin, for example) for long periods of time the normal, harmless bacteria living in your

intestine will be killed, leaving room for C. difficile to move in.

So-called “broad-spectrum” antibiotics and fluoroquinolone antibiotics are risk factors

for developing CDAD. Other risk factors include, age (65 and up), underlying illness, long

hospital stays, and facilities with poor infection control practices such as patient isolation and

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staff hand-washing.

There is some evidence that common medications also may increase the risk of CDAD.

These common drugs include proton pump inhibitors (such as Prilosec and Nexium), and H2

receptor antagonists (such as Pepcid and Zantac), for treating ulcers; and non-steroidal anti-

inflammatory painkillers.

So where does C. difficile come from? The bug can be passed from person to person or

picked up in contaminated environments. The ideal environment is a crowded hospital or long-

term care facility with large numbers of ill and elderly patients taking antibiotics and being

treated by the same doctors and nurses. In addition, three to ten percent of healthy people may

be asymptomatic carriers of C. difficile.

Treatment for most cases also may seem like a paradox. First, the original antibiotics that

probably initiated CDAD are stopped. Then another antibiotic, such as metronidazole or

vancomycin, is started. Yet, even after appropriate treatment, some patients may experience a

recurrence of CDAD, either from re-infection from another source or relapse from their first

infection.

Severe cases involving sepsis or peritonitis may require surgery. A recent report in the

journal, Clinical Infectious Diseases, notes that “total colectomy [removal of the colon] appears

to be the procedure of choice to save these patients’ lives.”

Prevention is always better than treatment, especially when treatment might involve

radical surgery. Effective prevention requires rigorous infection control practices in hospitals

and other health care facilities. Gloves and gowns, regular hand washing, and isolation of

infected patients are all important techniques for stopping person-to-person transmission of C.

difficile. Washing down common surface areas with bleach also is critical to destroying the

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bacteria’s tough, long-lasting spores.

CDAD usually is a problem associated with hospital settings, but that may be changing.

A few years ago, scientists at the Centers for Disease Control and Prevention began to notice

cases of CDAD that were community-acquired, involved younger people, and people who were

not taking antibiotics. The community cases tended to be more severe and appeared to be the

work of a new strain of epidemic or hypervirulent C. difficile.

By early 2007, a strain (NAP-1) had been identified in cases in 24 states, including

Maryland. The NAP-1 strain produces sixteen times more toxin A and 23 times more toxin B

than typical hospital strains and has a third toxin of uncertain importance. NAP-1 is also

resistant to common fluoroquinolone antibiotics. Equally worrisome, is a March 2007 report

describing strains of C. difficile (including NAP-1) from various types of ground meat in Canada

and parts of the U.S.

Are domestic animals and meats a source of many community-acquired infections? It’s

not clear, but scientists are trying to establish connections between epidemic strains of C.

difficile and domestic animals, asymptomatic human carriers, and hospitalized patients.

It’s not a pretty picture, but it is a reminder of how the dangerously exotic can become the

dangerously common.