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Faculty Publications and Presentations Department of Biology and Chemistry

4-2006

The Origin of Bubonic

Alan L. Gillen Liberty University, [email protected]

Frank Sherwin

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Recommended Citation Gillen, Alan L. and Sherwin, Frank, "The Origin of " (2006). Faculty Publications and Presentations. 147. https://digitalcommons.liberty.edu/bio_chem_fac_pubs/147

This Article is brought to you for free and open access by the Department of Biology and Chemistry at Scholars Crossing. It has been accepted for inclusion in Faculty Publications and Presentations by an authorized administrator of Scholars Crossing. For more information, please contact [email protected]. Perspectives

The origin of viruses and other . A few amino-acid metabolism. This reduction plasmid genes for toxins (table 1) have of metabolic pathways may have bubonic plague been acquired from another existing allowed the bacterium to conserve , but many chromosomal genes energy. The newly emerged strains Alan Gillen and Frank Sherwin have been lost. It takes only a few (variants) were thus streamlined, such genetic changes to produce a new, which might have contributed to the lthough some forms of the extremely infectious variant,4 so it may development of pathogenicity (i.e. Abacterium are harmless, have taken only hundreds or a few plague) due to the genes they lacked. other forms have devastated thousand years to produce the current The absence of important biosynthetic populations, causing a plague of bubonic plague strain that has existed genes is believed to be a hallmark of biblical proportions (Psalm 91:3–7, 9, for about the last 500 years. decay. 10). Bubonic plague, also known as the ‘’ that killed one fourth Loss of chromosomal DNA Genes added and moved of Europe’s population in the 1300s, Researchers hypothesize that key The corruption by three genes of appeared as a great pestilence several chromosomal genes (i.e. involved in a relatively benign recent ancestor of times in the Old Testament, including metabolic pathways) were inactivated/ Y. pestis may have played a key role in Psalm 91 and in 2 Sam 24:14– lost in changing from a soil inhabiting in the emergence of bubonic plague. 25. Perhaps the clearest example of Yersinia to a pathogenic Yersinia Hinnebusch and colleagues, a plague such a plague is recorded in 1 Sam. species.2 Pathogenic Yersiniae have expert team at the National Institutes 6:4–19, where there is a specific lost structural information and function for Health,8 maintains that the acquisi- reference to the tumors on people in about 149 genes. Of these, 58 are tion of two plasmid genes (i.e. just a ( = the tumors of lymph glands) the result of frameshift ,5 few discrete genetic changes) in recent and to (the that 32 have undergone deletions, and times changed the fairly harmless, Y. carried the plague bacterium, Yersinia the rest are nonsense mutations.6 pseudotuberculosis, that causes mild pestis.) The biblical time frame for These incomplete/inactivated genes or food poisoning, to the agent of the the plagues described in 1 Samuel was ‘pseudogenes’ are an important feature ‘Black Death’. A third gene (carried about 3,000 years ago.1 Interestingly, of the Y. pestis genome.7 on plasmid pMT1) produces murine experts on plague ‘evolution’ estimate Wren2 suggests that the genes toxin, an enzyme required for the initial the emergence of Y. pestis at about lost in Y. pestis affected bioenergetic survival of Y. pestis in the 1,500–20,000 years ago (within an functions, including dicarboxylic midgut (table 1).7 By acquiring this last evolutionary timeframe, of course).2

Plague’s origin is multifaceted Many infectious can be traced back to the decay and corruption of the original created design of as a result of the Fall. Corruption literally means to destroy (from the Latin corruptus). The origin of pathogenic ( causing) bacteria such as Y. pestis is complex and multifaceted, and may be explained by a combination of genes Genome Size that were lost, added and moved. The story of Yersinia’s degeneration into the plague may serve as a model of ‘fast’ genomic decay and corruption.2 It appears that the beginning of pathogenicity in the genus Yersina started with a net loss of chromosomal DNA from its original ‘kind’ (figure 1). Later, there were minor additions of Figure 1. Origin of plague: the decay and corruption of nonpathogenic Yersinia to plasmid DNA3 as well as DNA from highly virulent Y. pestis in a few thousand years.

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Table 1. Virulence-associated plasmids of .8–10 4. Lorange, E.A., Race, B.L., Sebbane, F. and Hinnebusch, B.J., Poor vector competence of and the evolution of hypervirulence in Plasmid (size) Transferred Factor Action Yersinia pestis, J. Infect. Dis. 191:1907–1912, 2005. activates plasminogen 5. Frameshift mutations are changes in DNA pPla (9.6 kb) Pla surface (protease) activator; destroys C3B; C5A where insertions or deletions of sequence occur (i.e. complement factors) that are not a multiple of three base pairs, thus interferes with phagocytosis disrupting the gene/protein normal code. pYV (70.3 kb) Yops (proteins) and 6. A nonsense is any alteration of DNA that causes a codon representing an amino acid bacterial in to be replaced by a termination codon. pMT1 (96.2 kb) phospholipase D fleas (Murine toxin) 7. Hinnebusch, B.J., Rudolph, A.E., Cherepanov, P., Dixon, J.E., Schwan, T.G., and Forsberg, A., Role of Yersinia murine toxin in survival of Yersinia pestis in the midgut of the flea vector, gene from another organism, Y. pestis Genes, germs and Genesis Science 296:733–735, 2002. made a crucial shift in its range, Plague bacteria are not the only 8. Nester, E.W. et al., : A Human allowing it to survive in fleas, and Perspective, 4th ed, WCB McGraw-Hill Pub- microorganisms that have degenerated devolved to relying on its blood-feed- lishers, Boston, MA, 2004. into disease-causing organisms. A more ing host for transmission. This is just 9. Parkhill, J. et al., Genome sequence of Yersinia another example of the flexibility of common recent example of a harmless pestis, the causative agent of plague, Nature many microbes in sometimes repack- bacteria ‘devolving’ into a pathogenic 413: 523–527, 2001. aging themselves into more dangerous one is the intestinal coli 10. Hinnebusch B.J., Perry R.D. and Schwan T.G., Yersinia pestis hemin storage (hms) locus in agents of infectious disease. O157H7 strain that occasionally causes 12 the transmission of plague by fleas, Science This last corruption is one that fatalities. Other 273:367–370, 1996. that have undergone genomic decay distinguishes Yersinia pestis from all 11. Lateral gene transfer is any process in which closely related, more benign bacteria include various (e.g. an organism transfers DNA to another cell that such as Y. pseudotuberculosis and other genitalium and M. pneu- is not its offspring. Yersinia (e.g. Y. entercolitica).7 In turn, monia, the later causing ), 12. Pommerville, J.C., Alcamo’s Fundamentals of as Y. pestis adapted to rely on its new and leprae (the Microbiology, Jones and Bartlett Publishers, Sudbury, MA, 2004. blood-feeding host for transmission, ).13,14 the emergence of more deadly bacterial As we study the origin of infec- 13. Wood, T.C., Genome decay in the Mycoplas- mas, Acts and Facts Impact 340:1–4, 1981. strains would have been favoured. It tious disease from a creationist, biblical 14. Eiglmeier, K., The decaying genome of My- appears that these minor plasmid addi- perspective, bacteria provide us with cobacterium leprae, Lepr. Rev. 72:387–398, 10 tions were the last changes made in an a model of what may have happened 2001. otherwise long series of genetic losses to living things over time in a fallen, in Y. pseudotuberculosis’ chromosome cursed and corrupted world. Many ill- (figure 1). nesses can probably be traced back to One pathogenicity island was a loss of genetic information, plasmid acquired by Yersinia pestis from acquisition, and gene translocation in 2 a different bacterium. This cas­ organisms such as bacteria, fungi, etc. sette of genes was not the result For those who know the Creator, we of evolution of new chromosomal can rejoice that someday the Great DNA, but was an acquisition through Physician will restore all plagued bod- lateral gene transfer.11 It produced ies to a very good condition once again a corrupted message that gave (Rev. 22:2–3). bacteria a new ‘position’ in the gut. Y. pseudotuberculosis, which lacks the References hms locus gene inhabits harmlessly the midgut of the flea. Plague bacilli, 1. Ryrie, C., Ryrie Study Bible (KJV), Moody by contrast, have this inserted locus Press, Chicago, IL, 1994. gene. Free from their original control, 2. Wren, B.W., The Yersiniae—a model genus to causing a lack of ‘good’ ‘direction’ study the rapid evolution of bacterial patho- information, the bacteria migrate from gens, Nature Micro. Rev. 1:55–64, 2003. the midgut to the foregut, forming a 3. Plasmids are circular, double-stranded units of plug of packed bacilli which is passed DNA that replicate within cells independently on to the victim when the flea feeds. of the chromosomal DNA.

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