Yersinia pestis
A draft genome of Yersinia pestis from victims of the Black Death maps the genome from the plague of 1347-8. Researchers obtained DNA from the teeth of plague victims buried in a mass grave in East Smithfield, (originally the Churchyard of the Holly Trinity) near the Tower of London.
Alexander Yersin linked Y. pestis to bubonic plague in 1894. However, controversy and doubt exist over the identity of the plague organism in part because today’s plague does not match the virulence of the Black Death that ravaged Europe in the 1300s. The sequencing by an improved technique (molecular capture assay) apparently establishes that the organism of the Black Death is the same as today’s plague with minor differences.
The bubonic plague existed in Asia with appearances in the Middle East and the Justinian plague in Rome and Constantinople in 541-542. Hippocrates describes a plague in Athens in 430-426 BC. Sanskrit tablets describe plague in Asia as early as 600 BC. Jewish physicians even associated plague with rats in the Tara also about 600 BC. Neither ancient plague, nor modern plague, 19th century to the present time manifested the virulence and devastation of the Black Death of 1347.
The diversity of today’s plague in China suggests that the Far East may have been the reservoir with appearances in Europe carried down the Silk Road and through the Mediterranean by rats aboard ship. The configuration of large Phoenician trading ships may have further enabled the spread
Doubters question whether the plague prior to 1347 was even the same organism. One researcher suggests that the ancient plague in Athens was Salmonella. A look to the history of clinical medicine could end the controversy at least from a practical standpoint. The clinical acumen of Hippocrates in 450 BC was sufficient to distinguish Typhoid from the plague as well as small pox, malaria and TB. There may be historical confusion and laboratory doubt but the clinical picture of plague was and is so distinctive that physicians of that day should not have confused plague with other infections.
The issue of virulence in the case of the Black Death seems explainable by the minor differences in the genome then and now. It would be interesting to see which changes correlated with the change in virulence. With its rapid spread, Y. pestis had an ideal environment in which to evolve taking advantage of weaknesses in the host population. With that evolution, came increased virulence, which shortened the duration between onset and death. The shorter time of infectiousness inhibited the further spread of the epidemic. Thus, the epidemic faded away. Furthermore, the population at risk diminishes as those most susceptible to the infection die off leaving those with minor expositors and resulting mobilized immune systems -- and those with genetic resistance to the disease in the first place -- in greater numbers relative to the further spread of the disease.
One might further speculate that faced with a diminished population, it was to the organism's advantage to devolve into a less virulent form in order to give greater expositor to others and thus a greater chance of continuing its presence and preserving its DNA. I would suppose that process of devolving to be the mechanism of dormancy in China or elsewhere in East Asia.
I do not think that it would have been essential that Y. pestis devolve along the exact genetic lines that it used in achieving greater virulence. The change in strategy might explain the dichotomy in the sequencing of today’s Y. pestis DNA with that of ancient DNA.
My epidemiology professor speculated that the Black Death Y. pestis achieved a level of virulence in which it spread pneumatically, thus the name pneumonic plague. One might further imagine that with a pneumonic form, the cyanosis would turn the victim black in death.
If indeed the above considerations proves relevant, it would not be surprising to find today's Y. pestis devolved to a less virulent form than the Black Death which so devastated Europe.
http://www.nature.com/nature/journal/v478/n7370/full/478465a.html
Alexander Yersin linked Y. pestis to bubonic plague in 1894. However, controversy and doubt exist over the identity of the plague organism in part because today’s plague does not match the virulence of the Black Death that ravaged Europe in the 1300s. The sequencing by an improved technique (molecular capture assay) apparently establishes that the organism of the Black Death is the same as today’s plague with minor differences.
The bubonic plague existed in Asia with appearances in the Middle East and the Justinian plague in Rome and Constantinople in 541-542. Hippocrates describes a plague in Athens in 430-426 BC. Sanskrit tablets describe plague in Asia as early as 600 BC. Jewish physicians even associated plague with rats in the Tara also about 600 BC. Neither ancient plague, nor modern plague, 19th century to the present time manifested the virulence and devastation of the Black Death of 1347.
The diversity of today’s plague in China suggests that the Far East may have been the reservoir with appearances in Europe carried down the Silk Road and through the Mediterranean by rats aboard ship. The configuration of large Phoenician trading ships may have further enabled the spread
Doubters question whether the plague prior to 1347 was even the same organism. One researcher suggests that the ancient plague in Athens was Salmonella. A look to the history of clinical medicine could end the controversy at least from a practical standpoint. The clinical acumen of Hippocrates in 450 BC was sufficient to distinguish Typhoid from the plague as well as small pox, malaria and TB. There may be historical confusion and laboratory doubt but the clinical picture of plague was and is so distinctive that physicians of that day should not have confused plague with other infections.
The issue of virulence in the case of the Black Death seems explainable by the minor differences in the genome then and now. It would be interesting to see which changes correlated with the change in virulence. With its rapid spread, Y. pestis had an ideal environment in which to evolve taking advantage of weaknesses in the host population. With that evolution, came increased virulence, which shortened the duration between onset and death. The shorter time of infectiousness inhibited the further spread of the epidemic. Thus, the epidemic faded away. Furthermore, the population at risk diminishes as those most susceptible to the infection die off leaving those with minor expositors and resulting mobilized immune systems -- and those with genetic resistance to the disease in the first place -- in greater numbers relative to the further spread of the disease.
One might further speculate that faced with a diminished population, it was to the organism's advantage to devolve into a less virulent form in order to give greater expositor to others and thus a greater chance of continuing its presence and preserving its DNA. I would suppose that process of devolving to be the mechanism of dormancy in China or elsewhere in East Asia.
I do not think that it would have been essential that Y. pestis devolve along the exact genetic lines that it used in achieving greater virulence. The change in strategy might explain the dichotomy in the sequencing of today’s Y. pestis DNA with that of ancient DNA.
My epidemiology professor speculated that the Black Death Y. pestis achieved a level of virulence in which it spread pneumatically, thus the name pneumonic plague. One might further imagine that with a pneumonic form, the cyanosis would turn the victim black in death.
If indeed the above considerations proves relevant, it would not be surprising to find today's Y. pestis devolved to a less virulent form than the Black Death which so devastated Europe.
http://www.nature.com/nature/journal/v478/n7370/full/478465a.html
posted by Clancy Hughes | 12/18/2011 01:59:00 PM
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