PrepTest 88, Section 4, Question 17

For nearly a century after the discovery in the 1880s that a bacterium, Vibrio cholerae, causes cholera, scientists believed that it traveled to new geographic regions only via human hosts and that epidemics typically occurred when the bacteria spread through contamination, by human waste, of food and unchlorinated water supplies. But scientists wondered where the bacteria went during the many years between epidemics. How could the disease arise seemingly spontaneously around the world, often where it was thought to have been eradicated?

In the 1970s, microbiologist Rita Colwell's claim that she had isolated V. cholerae from the Chesapeake Bay in the eastern United States met with great skepticism, as no biologists believed V. cholerae could persist without a human host, and no cholera outbreaks were occurring anywhere near the Chesapeake. Indeed, there had been no cholera epidemics anywhere in the United States since 1911. But, noting that most historic cholera outbreaks have happened along seacoasts, Colwell suspected that V. cholerae could somehow survive in seawater and that perhaps the bacteria were not always detectable by traditional culture methods—that is, that they could not always be cultured (i.e., grown) in a petri dish. Later that decade, a small cholera outbreak near New Orleans in the southern United States allowed Colwell to test this hypothesis. She used a new detection method on water from the local bayous from which people with cholera had eaten crab. This method uses an antibody that latches onto a key component of the bacterium's cell membrane. Linked to that antibody is a molecule that fluoresces bright green under ultraviolet light if the V. cholerae bacterium is present. Her tests showed that the bacteria were in the bayous. Furthermore, in a study in Asia, Colwell's antibody test detected the bacteria in 51 of 52 suspect water samples, whereas culture techniques found them in only 7 of the same 52 samples.

Colwell's further studies revealed that V. cholerae, like some other bacteria, goes into a dormant, sporelike state when environmental conditions do not favor reproduction; in this state, the bacterium's metabolic rate plummets and the bacterium shrinks some 15- to 300-fold. It stops reproducing and therefore cannot be cultured. This "viable but nonculturable" state, says Colwell, functions as a survival mechanism, enabling V. cholerae to persist in a wide range of conditions and habitats far from human hosts. Though no one knows exactly what conditions awaken V. cholerae from dormancy, Colwell notes that seasonal peaks in sea-surface temperatures in the Bay of Bengal in south Asia correlate closely with peaks in that region's cholera cases. If, as Colwell believes, the bacteria are persisting in the water all along, it is possible that changes in seawater temperature or salinity are what enable them to spread among humans again.

For nearly a century after the discovery in the 1880s that a bacterium, Vibrio cholerae, causes cholera, scientists believed that it traveled to new geographic regions only via human hosts and that epidemics typically occurred when the bacteria spread through contamination, by human waste, of food and unchlorinated water supplies. But scientists wondered where the bacteria went during the many years between epidemics. How could the disease arise seemingly spontaneously around the world, often where it was thought to have been eradicated?

In the 1970s, microbiologist Rita Colwell's claim that she had isolated V. cholerae from the Chesapeake Bay in the eastern United States met with great skepticism, as no biologists believed V. cholerae could persist without a human host, and no cholera outbreaks were occurring anywhere near the Chesapeake. Indeed, there had been no cholera epidemics anywhere in the United States since 1911. But, noting that most historic cholera outbreaks have happened along seacoasts, Colwell suspected that V. cholerae could somehow survive in seawater and that perhaps the bacteria were not always detectable by traditional culture methods—that is, that they could not always be cultured (i.e., grown) in a petri dish. Later that decade, a small cholera outbreak near New Orleans in the southern United States allowed Colwell to test this hypothesis. She used a new detection method on water from the local bayous from which people with cholera had eaten crab. This method uses an antibody that latches onto a key component of the bacterium's cell membrane. Linked to that antibody is a molecule that fluoresces bright green under ultraviolet light if the V. cholerae bacterium is present. Her tests showed that the bacteria were in the bayous. Furthermore, in a study in Asia, Colwell's antibody test detected the bacteria in 51 of 52 suspect water samples, whereas culture techniques found them in only 7 of the same 52 samples.

Colwell's further studies revealed that V. cholerae, like some other bacteria, goes into a dormant, sporelike state when environmental conditions do not favor reproduction; in this state, the bacterium's metabolic rate plummets and the bacterium shrinks some 15- to 300-fold. It stops reproducing and therefore cannot be cultured. This "viable but nonculturable" state, says Colwell, functions as a survival mechanism, enabling V. cholerae to persist in a wide range of conditions and habitats far from human hosts. Though no one knows exactly what conditions awaken V. cholerae from dormancy, Colwell notes that seasonal peaks in sea-surface temperatures in the Bay of Bengal in south Asia correlate closely with peaks in that region's cholera cases. If, as Colwell believes, the bacteria are persisting in the water all along, it is possible that changes in seawater temperature or salinity are what enable them to spread among humans again.