Antibiotic resistant genes should be recognised as environmental
21 Dec 2010
Even small concentrations of antibiotics leaked into the
environment from human and animal consumption can result in
selection of antibiotic resistant genes in bacteria and ultimately
reduce the effective life of antibiotics.
Drug development cannot keep up with the spread of antibiotic
resistance, therefore it is important to take effective measures to
restrict the spread of resistance.
When an antibiotic is consumed, up to 90% passes through a body
without metabolizing. This means the drugs can leave the body almost
intact through normal bodily functions.
In the case of agricultural areas, excreted antibiotics can then
enter stream and river environments through a variety of ways,
including discharges from animal feeding operations, fish
hatcheries, and nonpoint sources such as the flow from fields where
manure or biosolids have been applied. Water filtered through
wastewater treatment plants may also contain used antibiotics.
Consequently, these discharges become “potential sources of
antibiotic resistance genes,” said Amy Pruden, a National Science
Foundation CAREER Award recipient, and an associate professor of
civil and environmental engineering at Virginia Tech.
“The presence of antibiotics, even at sub-inhibitory
concentrations, can stimulate bacterial metabolism and thus
contribute to the selection and maintenance of antibiotic resistance
genes,” Pruden explained. “Once they are present in rivers,
antibiotic resistance genes are capable of being transferred among
bacteria, including pathogens, through horizontal gene transfer.”
The World Health Organization and the Centers for Disease Control
recognize antibiotic resistance “as a critical health challenge of
our time,” Pruden wrote in a paper published in a 2010 issue of
Environmental Science and Technology.
Pruden said reducing the spread of antibiotic resistance is a
critical measure needed to prolong the effectiveness of currently
available antibiotics. This is important since “new drug discovery
can no longer keep pace with emerging antibiotic-resistant
infections,” Pruden said.
Pruden who has developed the concept of antibiotic resistance
genes as environmental pollutants has an international reputation in
applied microbial ecology, environmental remediation, and
environmental reservoirs of antimicrobial resistance.
In her work outlined in the Environmental Science and Technology
article, she and her co-authors, H Storteboom, M Arabi and JG Davis,
all of Colorado State University, and B. Crimi of Delft University
in The Netherlands, identified specific patterns of antibiotic
resistance gene occurrence in a Colorado watershed. Identification
of these patterns represents a major step in being able to
discriminate between agricultural and wastewater treatment plant
sources of these genes in river environments.
They assert that such unique patterns of antibiotic resistance
gene occurrence represent promising molecular signatures that may
then be used as tracers of specific manmade sources.
In their study they identified three wastewater treatment plant
sites, six animal feeding operation locations, and three additional
locations along a pristine region of the Poudre River, in an
upstream section located in the Rocky Mountains. They compared the
frequency of detection of 11 sulfonamide and tetracycline antibiotic
Their findings showed detection of one particular antibiotic
resistance gene in 100% of the treatment plant and animal feeding
operations, but only once in the clean section of the Poudre River.
As they are able to differentiate between human and animal
sources of the antibiotic resistance genes, Pruden and her
colleagues believe they can “shed light on areas where intervention
can be most effective in helping to reduce the spread of these
contaminants through environmental matrixes such as soils,
groundwater, surface water and sediments.
“This study advances the recognition of antibiotic resistance
genes as sources to impacted environments, taking an important step
in the identification of the dominant processes of the spreading and
transport of antibiotic resistance genes.”