Yersinia pestis: Difference between revisions
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Describe the appearance, habitat, etc. of the organism, and why it is important enough to have its genome sequenced. Describe how and where it was isolated. | Describe the appearance, habitat, etc. of the organism, and why it is important enough to have its genome sequenced. Describe how and where it was isolated. | ||
Include a picture or two (with sources) if you can find them. | Include a picture or two (with sources) if you can find them. | ||
Yersinia pestis is a nonmotile, non–spore-forming, pleomorphic, gram-negative coccobacillus. The bacteria elaborate a lipopolysaccharide endotoxin, coagulase, and a fibrinolysin, which are the principal factors in the pathogenesis of this disease. | |||
==Genome structure== | ==Genome structure== | ||
Revision as of 18:16, 31 March 2008
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Classification
Higher order taxa
Domain: Eubacteria
Phylum: Proteobacteria
Class: Gamma Proteobacteria
Order: Enterobacteriales
Family: Enterobacteriaceae
Genus: Yersinia
Species: Yersinia Pestis
Species
Yersinia pestis
Description and significance
Describe the appearance, habitat, etc. of the organism, and why it is important enough to have its genome sequenced. Describe how and where it was isolated. Include a picture or two (with sources) if you can find them.
Yersinia pestis is a nonmotile, non–spore-forming, pleomorphic, gram-negative coccobacillus. The bacteria elaborate a lipopolysaccharide endotoxin, coagulase, and a fibrinolysin, which are the principal factors in the pathogenesis of this disease.
Genome structure
Describe the size and content of the genome. How many chromosomes? Circular or linear? Other interesting features? What is known about its sequence? Does it have any plasmids? Are they important to the organism's lifestyle?
The genome structure has been decoded for two of the three sub-species of Yersinia pestis, the KIM strain and the CO92 strain. The chromosome of the KIM strain contains 4,600,755 base pairs and the chromosome of the CO92 strain has 4,653,728 base pairs. There are 4,012 protein-coding genes, including 149 pseudogenes. The genome is rich in insertion sequences and displays anomalies in GC base-composition bias, which indicates frequent intragenomic recombination. Many genes seem to have been acquired from other bacteria and viruses, which suggests that Yersinia pestis is a pathogen that has undergone a large-scale genetic evolution. Yersinia pestis is also the host to the plasimds pCD1, pPCP1, and pMt1 which along with a pathogenicity island called HPI encode the proteins that cause the infamous pathogenicity of the bacteria. These virulence factors are essential for the invasion of the bacteria into the host, and the injection of its proteins into the cell.
Cell structure and metabolism
Describe any interesting features and/or cell structures; how it gains energy; what important molecules it produces.
Ecology
Describe any interactions with other organisms (included eukaryotes), contributions to the environment, effect on environment, etc.
Yersinia pestis is a gram negative bacteria that is a facultative anaerobe. During an outbreak the bacteria can survive for long periods of time in cool, moist areas such as the soil of rodent holes. Between outbreaks the bacteria is believed to circulate within populations of several rodent species without causing excessive death. Such groups of infected animals serve as silent, long-term carriers of the infection.
Pathology
How does this organism cause disease? Human, animal, plant hosts? Virulence factors, as well as patient symptoms.
Yersinia pestis is transmitted to people that have been bitten by infected fleas that are carried on rodents, most commonly which are rats, field mice, squirrel prairie dogs, rabbits and even animals such as cats and camels. The most common vector is the is the rat flea Xenopsylla cheopis, although ticks and human lice have been identified as possible vectors. Humans are accidental hosts in the natural cycle of this disease.
When the flea ingests blood that is infected with yersinia pestis, the blood begins to clot and the bacteria multiply to the thousands. These bacteria are inoculated in a host’s skin during subsequent blood feedings. The bacteris migrate to the lymph nodes where they are phagocytosed by the polymorphonuclear cells and mononuclear phagocytes, and multiply intracellularly. Afterwards with lysis the bacteria can invade distant organs and continue to multiply.
Application to Biotechnology
Does this organism produce any useful compounds or enzymes? What are they and how are they used?
Yersinia pestis is a very possible agent to be used in biological warfare. It is an optimum choice for a bioweapon, as it is very easy to spread and is resistant to multiple drugs. Because of the delay between exposure to the bacteria and signs of illness, people could travel over a large area before becoming contagious and possibly infect others. It is also possible to be employed as a bioweapon, because the bacterium occurs in nature and could very easily be isolated and grown in a labrotory. If used as an aerosol attack it could cause cases of the pneumonic form of the plague from one to six days after infection. However manufacturing such a weapon requires further advanced knowledge and technology.
Current Research
Enter summaries of the most recent research here--at least three required
Plague research is being conducted by several government agencies in an effort to help in the diagnosis, treatment, and prevention caused by Yersinia pestis, as well as addressing the need to defend against possible bioterrorist-caused disease outbreaks. Specifically this research focuses on developing a vaccine against the pneumonic plague, developing antibiotics to prevent and treat infection, and most importantly studying and identifying genes and proteins in Yersinia pestis that infect the digestive tract of fleas and enable them to grow and function in humans. Specifically, scientists at the National Institute of Allergy and Infectious Diseases (NIAID) Rocky Mountain Laboratories (RML), found that three genes in Yersinia pestis change it from a harmless, long-term inhabitant in the flea’s mid gut to one that migrates and accumulates in its foregut. As a result of this change, the flea begins to starve, causing it to fanatically feed, during which it regurgitates the bacteria and hence transmits the plague. Although it was known for quite some time that the bacterium’s transmission is dependant on the fleas as hosts, there was little understanding about the molecular and genetic mechanisms by which this colonization occurs. They began experiments on three hemin storage genes (hms), which are abundant in red blood cells, and acts as the iron-containing part of the hemoglobin molecule that binds oxygen. To understand the role of these genes in the host Dr. Hinnebusch conducted experiments with Oriental rat fleas, in which he injected the normal Yersinia pestis bacteria and a mutant form which was missing the hms genes. After four weeks, the scientists found that only those fleas infected with the normal bacteria developed the foregut blockage, which was accompanied by a high rate of mortality. These results indicated that the hms genes are required for Yersinia pestis to cause the foregut blockage. Next, they highlighted both forms of Yersinia pestis with fluoresce green and after dissecting the host fleas noted how the mutant bacteria remained in the midgut while the normal bacteria had migrated to the foregut in many fleas which eventually, became packed with bacteria. Now other genes are being studied that may affect the bacteria’s ability to transmit infection and it was observed that the blockage that develops in the flea foregut breaks down at temperatures above 80 to 85 degrees Fahrenheit. Scientists are trying to determine why this occurs and if such temperature changes might suppress the products of hms or other genes.