In this edition of Clinical Infectious Diseases, Brechet et al have demonstrated that hospital wastewater is an important environmental source of extendedspectrum β-lactamase–producing Escherichia coli (ESBLEC). They analyzed wastewater samples from Besancon, France, including ones “downstream” from 2 hospitals, from unrelated wastewater sites independent of the hospitals and from the municipal wastewater treatment plant inlet and outflow. Hospital effluent was clearly identified as the major contributor to the waste stream ESBLEC burden. They also examined samples of river water upstream and downstream of the wastewater plant and of digested sludge (used to fertilize farm land), which allowed them to quantify how much ESBLEC is dispersed into the environment. They identify an important opportunity to dampen the spread of antibiotic resistance. In their study, hospital wastewater had 30-fold more ESBLEC per unit volume than did the nonhospital wastewater stream. This is consistent with the fecal excretion of ESBLEC from infected patients and selection for ESBLEC due to antibiotics in the wastewater stream. Wastewater treatment removed approximately 95% of the ESBLEC, yet the estimated amount of ESBLEC released into the river (6 × 10/day) and to farmland via sludge (2.6 × 10 ESBL/kg) remained high. Unlike drinking water, wastewater treatment is designed to decrease but not eliminate pathogens. Because downriver exposure to water-borne pathogens is mitigated by the natural die-off of bacteria in the river, and (at least in principle) eliminated by downriver drinking water treatment, this arrangement has been accepted as reasonable. However, this view may be overly optimistic. The practice of spreading raw cattle manure on agricultural land has come into question given the well-documented outbreaks of E. coli O157:H7 and Salmonella in food. Many studies have documented that E. coli O157:H7 persists in soil and water. The survival of the organisms is related to their physical environment (eg, temperature, oxygen, pH, energy sources, soil texture) and by biotic factors such as predation by protozoa and the diversity of the rest of the microbial community [1, 2]. If cow manure used as fertilizer can spread pathogens, why should one doubt that human sewage sludge can do the same? Indeed, in France, Hartmann et al have found that CTX-M ESBLEC genes were found in 20% of soil samples from farms in Burgundy, and that live ESBLEC could be cultured from soil last fertilized with manure a year before [3]. It is not hard to see how ESBLEC that has been spread on farm soil—either from animal manure or wastewater sludge—can be recycled into the human food chain, either on plants or via food animals. There should be little doubt that ESBLEC released into a river can easily enter the human population though water-borne spread. Recreational swimmers downstream of a sewage outlet will be exposed and can become unwitting reservoirs of ESBLEC and other resistant pathogens. In fact, the number of ESBLEC calculated by Brechet et al is likely to be a substantial underestimate of the amount released during periods of heavier rainfall. Their data were collected during a dry season. As in many cities, the wastewater system in Besancon collects both sewage and urban surface water (such as rain) in a combined sewer system. These systems are designed to overflow into rivers or streams when heavy rainfall threatens to overwhelm sewage treatment plants. On these occasions, a nasty mix of raw sewage and rainwater is discharged into the receiving water, putting people downstream at risk. In a landmark article by Curriero et al, it was shown that 68% of water-borne disease outbreaks in the United States were preceded by heavy rainfall in the same watershed [4]. Similar data exist for sites as diverse as Taiwan [5], Canada [6, 7], and India [8]. Once these organisms are Received 6 March 2014; accepted 9 March 2014. Correspondence: Michael Barza, MD, Department of Medicine, Steward Carney Hospital, 2100 Dorchester Ave, Boston, MA 02124 (michael.barza@steward.org). Clinical Infectious Diseases © The Author 2014. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals. permissions@oup.com. DOI: 10.1093/cid/ciu194
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