CA-CDI was first described in the 1980s in patients receiving outpatient antimicrobial drug treatments (27–29
). In 2005, the emergence of the NAP1 epidemic strain was associated with an increase in the incidence of HA-CDI and an increase in reports of CDI in low-risk populations, such as persons living in the community, children, and peripartum women (4
). Our laboratory surveillance showed that 18% of the CDI cases were CA, a finding that is similar to other surveillance studies reporting percentages of 20%–30% (9,30–32
). CA-CDI case-patients were younger and healthier than those with HA exposure (median age 53 vs. 72 years). Although 20% of CA case-patients had illness severe enough to require hospitalization, no CDI-related complications or deaths were reported.
In a population-based surveillance study in Durham North Carolina, USA, in 2005 (9
), 59% of the CA-CDI case-patients required hospitalization, and 15% reported an emergency department visit. Similar to our findings, none of those case-patients required admission to intensive care units or surgical interventions, such as colectomy. Surveillance findings for CA-CDI in Connecticut, USA, in 2006 (13
) showed that 111 (46%) of 241 CA-CDI case-patients required hospitalization, 29 (12%) required admission to intensive care units, 5 (2%) had toxic megacolon or colectomy, and 5 (2%) died of CDI complications. However, surveillance in Connecticut was conducted on the basis of preferential reporting by physicians and infection prevention specialists, which may have resulted in identification of the most severe disease and hospitalized case-patients. In addition, interviews were not performed to confirm lack of health care exposure.
We observed that 76% of CA-CDI case-patients were exposed to antimicrobial drugs in the 12 weeks before diagnosis. This percentage is higher than previously reported estimates of 40%–61% (9,10,13,14,31,33,34
) and may reflect more complete information obtained during detailed case interviews. For example, several patients received antimicrobial drugs from their dentist, and such information is likely unavailable in outpatient medical records. These drugs were prescribed for common outpatient indications, and several patients received clindamycin for dental prophylaxis or infection. The role of PPI in CA-CDI remains controversial. Some studies have reported increased risk for disease associated with their use (12,35
). Twenty-six percent of CA-CDI case-patients interviewed reported PPI use. However, it is difficult to assess if this is a major risk without a control group comparison.
Molecular testing showed a similar distribution of strains between HA and CA cases, and the percentage of cases with the NAP1 epidemic strain ranged from 46% in HA cases to 32% in CA-CDI cases. The percentage of CA cases with the NAP1 strain was similar to that in other reports (18%–37%) (8,36–38
). Similar strain distribution in health care facilities and the community suggests that in contrast to the emergence of CA-methicillin-resistant S
strains, there was no preferential transmission of particular strains within or outside the health care setting. Health care facilities might act as a reservoir for CA disease or that the community might act as a reservoir for HA-associated disease.
Our study examined potential exposure routes for C. difficile
acquisition in the community. There are 4 postulated sources for exposure to C. difficile
): consumption of contaminated food and water, animal-to-person contact, person-to-person contact, and environment-to-person contact. Foodborne acquisition has been hypothesized as a source of CA infections on the basis of recovery of C. difficile
spores from food products and similarities between strains recovered from animals and those known to cause disease in humans (15–19
). However, there is currently insufficient evidence to support foodborne acquisition as a common source of CA-CDI (7
We assessed food and animal exposure during interviews with CA-CDI case-patients and did not find any specific association. However, we were unable to compare our observations with food and animal exposure patterns among persons in the community without CDI. Other possible sources of exposures include environments contaminated by C. difficile spores, such as hospitals and long-term care facilities; 21% of CA-CDI case-patients reported visiting or accompanying a family member to a health care facility in the 12 weeks before diagnosis. Contact with an ill or C. difficile–colonized family member or a household member who worked in a health care setting (i.e., someone who might have carried C. difficile spores on their hands or clothes) is another possible exposure. Two case-patients reported that a family member had diarrhea or was given a diagnosis of CDI, and several had a household member who worked in a health care setting. We also observed an excellent C. difficile recovery rate from refrigerated stool swabs, indicating that this method could be used in epidemiologic studies in which storage and processing of C. difficile specimens are required.
Our findings need to be interpreted in light of several limitations. We were unable to calculate the incidence of CA-CDI because surveillance did not include all laboratories servicing the Monroe County population. This study is descriptive, and the lack of a control group prevents us from estimating the risk for various exposures in development of CDI. At the time of this study, diagnosis of C. difficile
relied on testing with the toxins A and B enzyme immunoassay, which has a sensitivity of 60%–90% and specificity of 90%–95%. In low- prevalence populations, such as outpatients, the positive predictive value is low and the likelihood of false-positive results is higher, which might have biased some results by including patients who did not have CDI (40
). However, this bias was minimized by laboratory refusal of formed (i.e., nondiarrheal) fecal specimens and exclusion of cases without diarrheal symptoms. We did not review medical records from physician and dental offices. Therefore, patient-reported antimicrobial drug and PPI use was not confirmed. We attempted to interview all persons with potential CA-CDI but were unable to do so in 29% of the cases. These cases were defined as probable CA and included in our clinical summary. The small number of CA-CDI cases and isolates also limited our capacity to assess difference between NAP1 and other strains in severity and outcome of CDI.
In conclusion, CA-CDI represented 18% of CDI cases in Monroe County. CA-CDI case-patients were younger and healthier than HA-CDI case-patients. Use of antimicrobial drugs in outpatient settings remains a serious exposure, and even limited exposure to the health care environment or to persons in contact with health care facilities might play a crucial role in acquisition of CDI in the community. Prevention of CA-CDI will require further studies to understand risk factors leading to CDI in patients not exposed to antimicrobial drugs and the role of various potential exposures to C. difficile, such as food, animals, and household environment. Our results suggest that educating outpatient clinicians, including dentists, about the risk for community-associated CDI following use of oral antimicrobial drugs and that promoting judicious use of these drugs are potentially important interventions for the prevention of CDI in the outpatient setting.