Rodents, fleas may be getting bum rap on plague
By Noah Larsen
Small rodents and fleas have long been associated with outbreaks of plague among prairie dogs, but new research from a University of Colorado team has found no significant link between the local abundance of rodents and fleas and the occurrence of plague in prairie dog colonies.
This result is somewhat unexpected, researchers say.
Recent research confirms a correlation between grassland areas inhabited by prairie dogs and higher rodent and flea populations. It is also known that small rodents can be “reservoir hosts,” or carriers, of Yersinia pestis, the bacteria that causes the plague, and that fleas they carry can pass the disease to prairie dogs.
It is thus tempting to infer that when a prairie dog colony moves into a grassland area, small-rodent and flea populations may rise dramatically, passing the bacteria to prairie dogs, thereby inducing the plague.
That tidy explanation is undercut by new research published by Sharon Collinge, CU associate professor of biology and environmental studies. Her team included CU Research Associate Chris Ray, former graduate student Robert Jory Brinkerhoff and Ken Gage of the Centers for Disease Control. They found no significant correlation between small rodent and flea populations and plague outbreaks in prairie dog colonies.
The results of their research appear in an article published in the journal Vector-Borne and Zoonotic Diseases.
As the authors note of fleas and small rodents, “If such species do, in fact, serve as pathogen reservoirs, it is reasonable to presume that changes in their abundance or changes in the prevalence and abundance of their fleas could trigger epizootic events.”
In other words, it would seem logical that prairie-dog colonies saddled with the plague would have experienced an increase in small rodents and fleas prior to infestation.
“We wanted to understand the ecology and epidemiology of this important disease, and the interaction of ecology with epidemiology—especially how the structure of the ecological community may affect the occurrence and spread of disease,” explains Ray.
To better understand the dynamics of plague, the team tracked flea and rodent abundance on black-tailed prairie dog colonies at 24 sites in Boulder County before, during and after a plague outbreak. The goal was to confirm the prediction that prairie-dog colonies experiencing plague showed “increases in small-mammal, prairie-dog and flea abundance in the years preceding a plague event.”
In total, 3,237 small mammals, representing seven species, 1,865 prairie dogs, and 19,962 fleas were sampled. Plague outbreaks were recorded at six colonies during 2005 and 2006. Statistics from infected colonies were compared to statistics from colonies selected at random from the remaining, non-infected sites.
The team found no statistically significant evidence that there are substantial differences in rodents and flea occurrence between healthy colonies and those plagued with plague.
The study did detect a small increase in flea occurrence on small mammals at plague-positive sites, but the increase was not significant when compared to the randomly selected plague-negative sites.
The research “suggests that high abundance of prairie dogs and small mammals and high flea prevalence and abundance do not predispose a given prairie dog colony to plague.”
While changes in abundance were not significant, the researchers did find that the diversity of species was greatly affected by plague events. The data show that after a plague-caused prairie dog die-off, the diversity of small mammals increases toward the level of diversity commonly found in the absence of prairie dogs.
“These results suggest that small mammal species are affected by plague events, but that changes in mammal abundance or flea prevalence, abundance or intensity do not precede plague epizootics,” the authors say.
The authors note that, due to an inability to predict which colonies would become plague-positive, the samples sizes were fairly small. However, as Ray explains, “The evidence we present is based on the most intensive sampling ever done for this purpose.”
While the study doesn’t completely undermine the possibility that rodent and flea abundances have an impact in Y. pestis transmission, it suggests that other factors may play a stronger role in plague transmission.
“In our other studies, we found strong relationships between disease occurrence and climate plus land-cover variables—relationships that were similar even in very different landscapes,” says Ray, referring to work published in 2005 and 2008.
“We do not suggest that mammal abundance and flea prevalence and abundance are unimportant to Y. pestis transmission, but we believe other factors have equivalent or greater influence on the dynamics of plague-associate prairie-dog die-offs,” the authors conclude.
The team’s research was supported by the National Science Foundation and the National Institutes of Health, which maintain a joint program in the Ecology of Infectious Disease. It was also funded by the EPA’s National Center for Environmental Research.
Black-tailed prairie dogs
Small rodents and fleas have long been associated with outbreaks of plague among prairie dogs, but new research from a University of Colorado team has found no significant link between the local abundance of rodents and fleas and the occurrence of plague in prairie dog colonies.
This result is somewhat unexpected, researchers say.
Recent research confirms a correlation between grassland areas inhabited by prairie dogs and higher rodent and flea populations. It is also known that small rodents can be “reservoir hosts,” or carriers, of Yersinia pestis, the bacteria that causes the plague, and that fleas they carry can pass the disease to prairie dogs.
It is thus tempting to infer that when a prairie dog colony moves into a grassland area, small-rodent and flea populations may rise dramatically, passing the bacteria to prairie dogs, thereby inducing the plague.
That tidy explanation is undercut by new research published by Sharon Collinge, CU associate professor of biology and environmental studies. Her team included CU Research Associate Chris Ray, former graduate student Robert Jory Brinkerhoff and Ken Gage of the Centers for Disease Control. They found no significant correlation between small rodent and flea populations and plague outbreaks in prairie dog colonies.
The results of their research appear in an article published in the journal Vector-Borne and Zoonotic Diseases.
As the authors note of fleas and small rodents, “If such species do, in fact, serve as pathogen reservoirs, it is reasonable to presume that changes in their abundance or changes in the prevalence and abundance of their fleas could trigger epizootic events.”
In other words, it would seem logical that prairie-dog colonies saddled with the plague would have experienced an increase in small rodents and fleas prior to infestation.
“We wanted to understand the ecology and epidemiology of this important disease, and the interaction of ecology with epidemiology—especially how the structure of the ecological community may affect the occurrence and spread of disease,” explains Ray.
To better understand the dynamics of plague, the team tracked flea and rodent abundance on black-tailed prairie dog colonies at 24 sites in Boulder County before, during and after a plague outbreak. The goal was to confirm the prediction that prairie-dog colonies experiencing plague showed “increases in small-mammal, prairie-dog and flea abundance in the years preceding a plague event.”
In total, 3,237 small mammals, representing seven species, 1,865 prairie dogs, and 19,962 fleas were sampled. Plague outbreaks were recorded at six colonies during 2005 and 2006. Statistics from infected colonies were compared to statistics from colonies selected at random from the remaining, non-infected sites.
The team found no statistically significant evidence that there are substantial differences in rodents and flea occurrence between healthy colonies and those plagued with plague.
The study did detect a small increase in flea occurrence on small mammals at plague-positive sites, but the increase was not significant when compared to the randomly selected plague-negative sites.
The research “suggests that high abundance of prairie dogs and small mammals and high flea prevalence and abundance do not predispose a given prairie dog colony to plague.”
While changes in abundance were not significant, the researchers did find that the diversity of species was greatly affected by plague events. The data show that after a plague-caused prairie dog die-off, the diversity of small mammals increases toward the level of diversity commonly found in the absence of prairie dogs.
“These results suggest that small mammal species are affected by plague events, but that changes in mammal abundance or flea prevalence, abundance or intensity do not precede plague epizootics,” the authors say.
The authors note that, due to an inability to predict which colonies would become plague-positive, the samples sizes were fairly small. However, as Ray explains, “The evidence we present is based on the most intensive sampling ever done for this purpose.”
While the study doesn’t completely undermine the possibility that rodent and flea abundances have an impact in Y. pestis transmission, it suggests that other factors may play a stronger role in plague transmission.
“In our other studies, we found strong relationships between disease occurrence and climate plus land-cover variables—relationships that were similar even in very different landscapes,” says Ray, referring to work published in 2005 and 2008.
“We do not suggest that mammal abundance and flea prevalence and abundance are unimportant to Y. pestis transmission, but we believe other factors have equivalent or greater influence on the dynamics of plague-associate prairie-dog die-offs,” the authors conclude.
The team’s research was supported by the National Science Foundation and the National Institutes of Health, which maintain a joint program in the Ecology of Infectious Disease. It was also funded by the EPA’s National Center for Environmental Research.