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Joshua Messinger
Faculty Advisor: Dr. Dave Gondek
Evaluation of Recombination across Chlamydia Species
Known in the United States primarily as a sexually transmitted disease,
Chlamydia is one of the most common bacterial infections worldwide and is the leading
cause of preventable blindness in developing nations. Tanzania still very much fights
trachoma (blindness due to Chlamydia trachomatis) and is hoping to eradicate this
problem by 2020. While treatments have been widely available for this disease, a
vaccine has not yet been discovered. This summer, I propose to do a research project in
the biology lab of Dr. Dave Gondek. Dr. Gondek’s lab explores how the Chlamydia
bacteria have come become a highly specialized intracellular (lives within your cells)
pathogen capable of manipulating the host organism. Due to the fact that it must live
within host cells in order to survive, its genome (genetic information) has become highly
specialized to specific hosts and has thus has reduced the size of its genome immensely.
Thus, it lacks the ability to activate a lot of its own proteins and therefore has adapted
Type III secretion methods in order to manipulate the host cell. Through Type III
secretion, the Chlamydia bacteria inject inactive, effector, proteins into the host cell
which the host then activates. In effect, the host has been manipulated into activating the
proteins that will inevitably lead to its own demise.
Chlamydia is highly host specific and thus many strains of the bacteria exist that
are capable of occupying unique hosts. For example, Chlamydia trachomatis occupies the
human host, while Chlamydia muridarum occupies mice. Due to the fact that Chlamydia
bacteria has made its genome smaller over time, it should not be able to cross into new
species and should thus be restricted to occupying just that native host. Our experiments
have shown that these strains of Chlamydia have been able to cross into new, non-native,
hosts at least to some limited degree. This provides evidence that this bacterial species is
capable, under the right conditions, of crossing into a new host therefore giving it the
potential to become an emerging disease in new organisms over time. Humanity has
encountered this before in the form of new versions of the flu ever year and how SARS
suddenly became a prominent disease. By continually studying how pathogenic bacteria
adapt to new hosts, humanity can become better equipped to cure new and emerging
diseases when they enter the population.
One particular strain of Chlamydia, Chlamydia muridarum (native to mice) has
shown particular versatility in crossing into a new host in the laboratory setting. This
provides evidence that there are additional genetic components that C. muridarum has
that the other strains of Chlamydia do not have. To assess what these differences may be,
the Gondek laboratory has begun examining what unique elements of C. muridarum may
exist and what these genetic components allow this strain to do that other strains are
unable to do. Having conducted this large screen of how these three strains of Chlamydia
adapt to non-native hosts, many potentially novel characteristics about these organisms
have been exposed that may lead to a better understanding of how new diseases emerge
and how we can cure them upon encountering them.
Figures and Results
1.00E+10
1.00E+09
1.00E+08
1.00E+07
1.00E+06
Trachomatis
1.00E+05
Caviae
Muridarum
1.00E+04
1.00E+03
1.00E+02
1.00E+01
1.00E+00
McCoy
Vero
HeLa
Cat Lung
Guinea Pig
Figure 1: Survey of Chlamydia Growth across 5 different species of hosts
This figure shows the degree to which the Chlamydia bacteria survive in
crossing into a new host. The x-axis represents different species of hosts. McCoy
corresponds to mice, Vero to monkeys, HeLa to humans and lastly cat and guinea pig
hosts were assessed. The y-axis demonstrates, on average across 4 experiments,
how many infectious units per milliliter of sample were obtained after a 24 hour
infection.