Leaf It to Us
Journal Club Review
April 2012
New Insights into the Effects of Temperature on Plague Transmission: A Review of
Two Articles
By Christine Bradley
Schotthoefer, A. M., Bearden, S. W., Holmes, J. L., Vetter, S. M., Montenieri, J. A., Williams, S.
K., . . . Gage, K. L. (2011). Effects of temperature on the transmission of Yersinia pestis by the
flea, Xenopsylla cheopis, in the late phase period. Parasites and Vectors, 4, 191. Doi:
10.1186/1756-3305-4-191
Gage, K. L., Burkot, T. R., Eisen, R. J., and Hayes, E. B. (2008). Climate and vectorborne
diseases. American Journal of Preventive Medicine, 35(5), 436-450. Doi:
http://dx.doi.org/10.1016/j.amepre.2008.08.030
At warm
Something interesting happens in the
temperatures
western United States when the temperature
exceeding 27̊C, the
increases in late summer. The number of
bacteria is unable
people infected by plague declines sharply.
to colonize the flea
Plague is the result of infection by the
gut, leading to a
bacterium, Yersinia pestis, and is transmitted
reduction in flea
by fleas. When fleas consume a blood meal
regurgitation and,
from an infected host, they also take up
we believed,
some of the pathogen. Once in the
plague
Image
courtesy
of
gastrointestinal tract of the flea, Y. pestis
transmission. New
Elsevier
Inc.
forms large aggregates that block the
evidence, however,
movement of material through the tract and
suggests that temperature does not have such
prevent the bacteria from being expelled.
an exacting effect on plague transmission.
The flea is forced to regurgitate the blockage
Instead, warmer temperatures worsen the
back into a host before the flea can take
survival rate of Y. pestis and the flea itself.
another blood meal, thus spreading the
Before I continue, a brief description
bacteria from one host to another.
of some epidemiology terms is necessary. A
Earlier studies demonstrated that the
reservoir of infection is an environment or
ability of Y. pestis to form aggregates within
population of animals in which a disease is
the flea gut was dependent on temperature.
normally present. The reservoir population
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is generally unaffected by the disease, but
can pass the disease on to other living hosts.
Vectors, such as fleas, are organisms that
carry the infectious bacteria from a reservoir
population to an outside host without
becoming infected.
Dr. Kenneth L. Gage is the chief of
the Flea-Borne Diseases
Activity at the National
Center for Emerging and
Zoonotic Infectious
Diseases and lead author of
the review article on vectorborne diseases. He is an
employee of the Centers for
Disease Control and
Prevention(CDC) and is
actively involved in the
study and control of plague.
Gage has done extensive
research on the topic and is
an expert in the field.
Dr. Anna M.
Schotthoefer is also an
employee of the CDC and
headed the study on plague
transmission. Schotthoefer
works under the Bacterial
Diseases Branch in the Division of Vector
Borne Diseases at the National Center for
Emerging and Zoonotic Infectious Diseases.
She has studied the mechanisms of plague
transmission for several years, recently
focusing on the relationship between
temperature and plague transmission rates.
Gage writes extensively on the
effects of climate on vectorborne diseases.
His article provides a strong background for
understanding Schotthoefer’s experimental
protocol and the significance of her findings.
April 2012
Gage’s review highlights the relationship
between temperature and the occurrence of
plague, explaining that plague outbreak rates
drop dramatically as temperatures rise above
27̊C. This sets the stage for Schotthoefer’s
study on the physiological effects of
temperature on Y. pestis and the diseasebearing flea, Xenopsylla
cheopis. Ultimately,
Schotthoefer concludes
that temperature plays a
more indirect role in
plague transmission, and
a quick review of Gage’s
work indicates bacteria,
vector, and reservoir
population survivorship
as the potential
determining factors of
plague transmission.
Gage proposed
that temperature could
directly affect plague
transmission by
inhibiting the ability of
Y. pestis to form
aggregates in the
digestive tract of fleas,
but Schotthoefer suggests that the effects of
temperature are much less direct. The study
by Schotthoefer found that plague
transmission occurred throughout the late
-Schotthoefer
phase
in a variety of thermal conditions.
Interestingly, while the scientists did not
observe Y. pestis blockages in the guts of
fleas housed above 27̊C, plague transmission
in this group of insects still occurred. The
results suggest that the formation of Y. pestis
aggregates is not required for transmission
of the bacteria as was previously thought. In
“. . . high
temperature
s alone do
not appear
to
significant
ly impair
the ability
of fleas to
transmit Y.
pestis
infections.
”
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light of these findings, Schotthoefer suggests
possible alternative mechanisms that explain
the relationship between temperature and
plague transmission.
In the review article by Gage, the
broad effects of climate on vectors and
reservoirs are discussed.
Gage indicates that the
observed changes in
plague transmission are
largely based on the effects
of climate on the
survivorship of the vector
and reservoir species. Mice
and rats, which harbor Y.
pestis, reproduce and
thrive in warm conditions
when food is plentiful and
improve conditions for
increased plague
transmission. As
temperatures continue to
increase past 27̊C, the flea
populations that spread Y.
pestis tend to decline due
to the thermal sensitivity of
their larvae.
Gage briefly
suggests that Y. pestis itself
is negatively affected by
rising temperatures, but Schotthoefer
indicates the more specific cellular impacts
of temperature on Y. pestis. One possibility
is that temperature reduces the ability of Y.
pestis to colonize certain regions of the gut.
Normally, the bacteria readily aggregate in a
stomach-like region of the flea known as the
proventriculus, but higher temperatures may
reduce colonization ability. In a second
theory, the authors suggest that high
April 2012
temperatures shorten the lifespan of Y.
pestis and vector fleas. The third and final
proposition considers the effects of
temperature on Y. pestis population density.
Although fleas kept at higher temperatures
housed fewer bacteria in their digestive
tract, the authors note
that currently no
correlations between
plague transmission rate
and bacterial load have
been determined. The
relationship between
temperature and plague
transmission depends on
a currently poorly
understood combination
of vector, reservoir, and
bacteria sensitivities to
heat.
For many years,
scientists thought that
plague transmission was
dependent on the ability
of Y. pestis to form
aggregates in the gut.
We assumed that
because Y. pestis
blockages are not
present in fleas when the
temperature exceeds 27̊C, fleas were unable
to transmit-Gage
the disease above that
temperature. New research by Schotthoefer
indicates that plague transmission is not that
simple. Instead, as mentioned by both Gage
and Schotthoefer, temperature indirectly
affects the transmission of plague by altering
the life cycle of the bacteria, vectors, and
reservoir species.
“. . .
threshold
temperature
s might be
important
because
excessively
high
temperature
s adversely
affect flea
survival .
. .”
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