Yersinia pestis CO92: Difference between revisions

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Most of the spreading occurs between rodents and fleas. Every infected animal can transmit the infection to humans through contact with skin tissue. Humans can also spread the bacteria to other humans through sneezing, coughing, or direct contact with infected tissue. In the United States, several species of rodents are thought to maintain Y. pestis (Inglesby). It is known that rodent populations will have a variable resistance, which could lead to a carrier status in some individuals (Meyer). There is evidence that fleas from other mammals have a role in human plague outbreaks. Initial acquisition of Y. pestis by the vector occurs during flea feeding on an infected animal. Several proteins then contribute to the maintenance of the bacteria in the flea digestive tract, among them the hemin storage (Hms) system and Yersinia murine toxin (Ymt). it has been demonstrated that Ymt is important for the survival of Y. pestis in fleas. The Hms system plays an important role in the transmission of Y. pestis back to a mammalian host. While in the insect vector, proteins encoded by Hms genetic loci induce biofilm formation in the proventriculus, a valve connecting the midgut to the esophagus. Aggregation in the biofilm inhibits feeding and causes the flea to regurgitate blood. Transmission of Y. pestis occurs during the futile attempts of the flea to feed. Ingested blood is pumped into the esophagus, where it dislodges bacteria growing there and is regurgitated back into the host circulatory system (Hinnebusch).   
Most of the spreading occurs between rodents and fleas. Every infected animal can transmit the infection to humans through contact with skin tissue. Humans can also spread the bacteria to other humans through sneezing, coughing, or direct contact with infected tissue. In the United States, several species of rodents are thought to maintain Y. pestis (Inglesby). It is known that rodent populations will have a variable resistance, which could lead to a carrier status in some individuals (Meyer). There is evidence that fleas from other mammals have a role in human plague outbreaks. Initial acquisition of Y. pestis by the vector occurs during flea feeding on an infected animal. Several proteins then contribute to the maintenance of the bacteria in the flea digestive tract, among them the hemin storage (Hms) system and Yersinia murine toxin (Ymt). it has been demonstrated that Ymt is important for the survival of Y. pestis in fleas. The Hms system plays an important role in the transmission of Y. pestis back to a mammalian host. While in the insect vector, proteins encoded by Hms genetic loci induce biofilm formation in the proventriculus, a valve connecting the midgut to the esophagus. Aggregation in the biofilm inhibits feeding and causes the flea to regurgitate blood. Transmission of Y. pestis occurs during the futile attempts of the flea to feed. Ingested blood is pumped into the esophagus, where it dislodges bacteria growing there and is regurgitated back into the host circulatory system (Hinnebusch).   
Pathogenesis due to Y. pestis infection of mammalian hosts is due to several factors including an ability of these bacteria to suppress and avoid normal immune system responses such as phagocytosis and antibody production. Flea bites allow for the bacteria to pass the skin barrier. Y. pestis expresses the yadBC gene, which is similar to adhesins in other Yersinia species. Y. pestis expresses a plasminogen activator that is an important virulence factor for pneumonic plague and that might degrade on blood clots in order to facilitate systematic invasion. Many of the bacteria's virulence factors are anti-phagocytic in nature. Two important anti-phagocytic antigens, named F1 (Fraction 1) and V or LcrV, are both important for virulence(Collins). These antigens are produced by the bacterium at normal human body temperature. Furthermore, Y. pestis survives and produces F1 and V antigens while it is residing within white blood cells such as monocytes, but not in neutrophils. Natural or induced immunity is achieved by the production of specific opsonic antibodies against F1 and V antigens; antibodies against F1 and V induce phagocytosis by neutrophils. In addition, the Type III secretion system (T3SS) allows Y. pestis to inject proteins into macrophages and other immune cells. These T3SS-injected proteins are called Yops (Yersinia Outer Proteins) and include Yop B/D, which form pores in the host cell membrane and have been linked to cytolysis. The injected Yop proteins limit phagocytosis and cell signaling pathways important in the innate immune system. Yersinia pestis proliferates inside lymph nodes where it is able to avoid destruction by cells of the immune system such as macrophages (Bliska). A timeline is shown below illustrating the symptoms that occur with infection.
Pathogenesis due to Y. pestis infection of mammalian hosts is due to several factors including an ability of these bacteria to suppress and avoid normal immune system responses such as phagocytosis and antibody production. Flea bites allow for the bacteria to pass the skin barrier. Y. pestis expresses the yadBC gene, which is similar to adhesins in other Yersinia species. Y. pestis expresses a plasminogen activator that is an important virulence factor for pneumonic plague and that might degrade on blood clots in order to facilitate systematic invasion. Many of the bacteria's virulence factors are anti-phagocytic in nature. Two important anti-phagocytic antigens, named F1 (Fraction 1) and V or LcrV, are both important for virulence(Collins). These antigens are produced by the bacterium at normal human body temperature. Furthermore, Y. pestis survives and produces F1 and V antigens while it is residing within white blood cells such as monocytes, but not in neutrophils. Natural or induced immunity is achieved by the production of specific opsonic antibodies against F1 and V antigens; antibodies against F1 and V induce phagocytosis by neutrophils. In addition, the Type III secretion system (T3SS) allows Y. pestis to inject proteins into macrophages and other immune cells. These T3SS-injected proteins are called Yops (Yersinia Outer Proteins) and include Yop B/D, which form pores in the host cell membrane and have been linked to cytolysis. The injected Yop proteins limit phagocytosis and cell signaling pathways important in the innate immune system. Yersinia pestis proliferates inside lymph nodes where it is able to avoid destruction by cells of the immune system such as macrophages (Bliska). A list is shown below illustrating the symptoms that occur with Y. pestis CO92 infection.
Bubonic plague


     Incubation period of 2–6 days, when the bacteria is actively replicating.
     Incubation period of 2–6 days(bacteria is actively replicating)
     Universally a general lack of energy
     Lethargy
     Fever
     Fever
     Headache and chills occur suddenly at the end of the incubation period
     Headache and chills occur suddenly at the end of the incubation period
     Swelling of lymph nodes resulting in buboes, the classic sign of bubonic plague. The inguinal nodes are most frequently affected
     Swelling of lymph nodes resulting in buboes, the classic sign of bubonic plague. The inguinal nodes (groin) are most frequently affected
The traditional first line treatment for Y. pestis has been streptomycin,[44][45] chloramphenicol, tetracycline,[46] and fluoroquinolones.
The traditional first line treatment for Y. pestis has been streptomycin,[44][45] chloramphenicol, tetracycline,[46] and fluoroquinolones.



Revision as of 21:44, 29 December 2011

This student page has not been curated.

A Microbial Biorealm page on the genus Yersinia pestis CO92

Classification

Domain; Phylum; Class; Order; family; genus; species [Others may be used. Use NCBI link to find]

Bacteria; Proteobacteria; Gammaproteobacteria; Enterobacteriales; Enterobacteriaceae; Yersinia; Yersinia pestis

Description and significance

Describe the disease caused by this organism if it is a pathogen, or the natural macroscopic "field guide" appearance and habitat of your organism if it is not. What is or has been the impact your organism on human history or our environment?. How does it do this? How have we harnessed this power, or tried to prevent it? In other words, how do you know it if you see it, and how does its presence influence humans in the present, and historically?

The Gram-negative bacterium Yersinia pestis CO92 is the causative agent of the systemic invasive infectious disease classically referred to as the plague and it has been responsible for human pandemics. It was the causative agent of the Black Death, or the bubonic plague. The Black Death is estimated to have killed 30 to 60 percent of Europe's population between 1348 and 1350 (Abdoudharm). The aftermath of the plague consisted of religious, economic and social upheaval. The population of Europe did not recover for nearly 150 years. The appearance of the disease caused by Yersinia pestis is often characterized by buboes, swollen lymph nodes in the groin, underarm, and neck. Y. pestis often leads to necrotic tissue that is black in color which is where the name the Black Death originated. The animal reservoirs that carry Y. pestis are fleas and rodents. These animals can pass the bacteria onto humans directly or indirectly (Meyer). The pathway for infection is described in detail in the ecology section. The specific strain of Yersinia pestis CO92 has been studied for its possible role in biological warfare. An aerosolized plague weapon could cause fever, cough, chest pain, and hemoptysis with signs consistent with severe pneumonia 1 to 6 days after exposure. Rapid evolution of disease would occur in the 2 to 4 days after symptom onset and would lead to septic shock with high mortality without early treatment (Inglesby). Y. pestis CO92 is a very dangerous bacteria and if used in biological warfare it could be catastrophic for the entire global population.

Genome structure

Describe the size and content of the genome. How many chromosomes and plasmids? Circular or linear? Other interesting features? What is known about its sequence?

The complete genome sequence of Y. pestis strain CO92 consists of a 4.65-megabase chromosome and three plasmids of 96.2 kilobases (kb), 70.3 kb and 9.6 kb. The genome is unusually rich in insertion sequences and displays anomalies in GC base-composition bias, indicating frequent intragenomic recombination. Many genes seem to have been acquired from other bacteria and viruses (including adhesins, secretion systems and insecticidal toxins). The genome contains around 150 pseudogenes, many of which are remnants of a redundant enteropathogenic lifestyle. The evidence of ongoing genome fluidity, expansion and decay suggests Y. pestis is a pathogen that has undergone large-scale genetic flux and provides a unique insight into the ways in which new and highly virulent pathogens evolve (parkhill). Y. pestis is host to the plasmid pCD1. In addition, it also hosts two other plasmids, pPCP1 (also called pPla or pPst) and pMT1. Together, these plasmids, and a pathogenicity island called HPI, encode several proteins that cause the pathogenesis, for which Y. pestis is famous (Hixon).

Cell structure, metabolism & life cycle

Provide a physical and biochemical description of the organism. What kind of organism is it, what does it look like, how is it built, what are its metabolic properties, how can it be identified, what is it's life cycle, &c. In other words, describe the organism from its perspective.

Ecology (including pathogenesis)

Describe its habitat, symbiosis, and contributions to environment. If it is a pathogen, how does this organism cause disease? Human, animal, plant hosts? Describe virulence factors and patient symptoms.

Most of the spreading occurs between rodents and fleas. Every infected animal can transmit the infection to humans through contact with skin tissue. Humans can also spread the bacteria to other humans through sneezing, coughing, or direct contact with infected tissue. In the United States, several species of rodents are thought to maintain Y. pestis (Inglesby). It is known that rodent populations will have a variable resistance, which could lead to a carrier status in some individuals (Meyer). There is evidence that fleas from other mammals have a role in human plague outbreaks. Initial acquisition of Y. pestis by the vector occurs during flea feeding on an infected animal. Several proteins then contribute to the maintenance of the bacteria in the flea digestive tract, among them the hemin storage (Hms) system and Yersinia murine toxin (Ymt). it has been demonstrated that Ymt is important for the survival of Y. pestis in fleas. The Hms system plays an important role in the transmission of Y. pestis back to a mammalian host. While in the insect vector, proteins encoded by Hms genetic loci induce biofilm formation in the proventriculus, a valve connecting the midgut to the esophagus. Aggregation in the biofilm inhibits feeding and causes the flea to regurgitate blood. Transmission of Y. pestis occurs during the futile attempts of the flea to feed. Ingested blood is pumped into the esophagus, where it dislodges bacteria growing there and is regurgitated back into the host circulatory system (Hinnebusch). Pathogenesis due to Y. pestis infection of mammalian hosts is due to several factors including an ability of these bacteria to suppress and avoid normal immune system responses such as phagocytosis and antibody production. Flea bites allow for the bacteria to pass the skin barrier. Y. pestis expresses the yadBC gene, which is similar to adhesins in other Yersinia species. Y. pestis expresses a plasminogen activator that is an important virulence factor for pneumonic plague and that might degrade on blood clots in order to facilitate systematic invasion. Many of the bacteria's virulence factors are anti-phagocytic in nature. Two important anti-phagocytic antigens, named F1 (Fraction 1) and V or LcrV, are both important for virulence(Collins). These antigens are produced by the bacterium at normal human body temperature. Furthermore, Y. pestis survives and produces F1 and V antigens while it is residing within white blood cells such as monocytes, but not in neutrophils. Natural or induced immunity is achieved by the production of specific opsonic antibodies against F1 and V antigens; antibodies against F1 and V induce phagocytosis by neutrophils. In addition, the Type III secretion system (T3SS) allows Y. pestis to inject proteins into macrophages and other immune cells. These T3SS-injected proteins are called Yops (Yersinia Outer Proteins) and include Yop B/D, which form pores in the host cell membrane and have been linked to cytolysis. The injected Yop proteins limit phagocytosis and cell signaling pathways important in the innate immune system. Yersinia pestis proliferates inside lymph nodes where it is able to avoid destruction by cells of the immune system such as macrophages (Bliska). A list is shown below illustrating the symptoms that occur with Y. pestis CO92 infection.

   Incubation period of 2–6 days(bacteria is actively replicating)
   Lethargy
   Fever
   Headache and chills occur suddenly at the end of the incubation period
   Swelling of lymph nodes resulting in buboes, the classic sign of bubonic plague. The inguinal nodes (groin) are most frequently affected

The traditional first line treatment for Y. pestis has been streptomycin,[44][45] chloramphenicol, tetracycline,[46] and fluoroquinolones.

Interesting feature

Describe in detail one particularly interesting aspect of your organism or it's affect on humans or the environment.

==References

Bliska J.B., Mejía E., Viboud G. 2009. Yersinia Controls Type III Effector Delivery into Host Cells by Modulating Rho Activity. PLoS ONE. 4(2): e4431.


Aboudharam, G., Crubezy, E., Drancourt, M., Larrouy, G. 2001. Raoult, D. Molecular identification by “suicide PCR” of Yersinia pestis as the agent of Medieval Black Death. PNAS. 97(23) 12800-12820.

Bliska J.B., Mejía E., Viboud G. 2009. Yersinia Controls Type III Effector Delivery into Host Cells by Modulating Rho Activity. PLoS ONE. 4(2): e4431.

Collins F. M. 1996. Pasteurella, Yersinia, and Francisella. Baron's Medical Microbiology. 4th edition.

Hinnebusch, B. J., R.D. Perry and T.G. Schwan. 1996. Role of the Yersinia pestis hemin storage (hms) locus in the transmission of plague by fleas. Science. 273(5237): 367–70.

Hixson K. 2006. Biomarker candidate identification in Yersinia pestis using organism-wide semiquantitative proteomics. Journal of Proteome Research. 5(11): 3008–3017.

Inglesby, T., D. Dennis, D. Henderson, J Bartlett, M. Ascher, E. Eitzen, A. Fine, A. Friedlander, J. Hauer, J. Koerner, M. Layton, J. McDade, M. Osterholm, T. O'Toole, G. Parker, T. Perl, P. Russell, M. Schhoch-Spana, K. Tonat. 2000. Plague as a biological weapon: Medical and public health management. Journal of the American Medical Association. 283(17):2281-2290.

Meyer, K.F. (1957). The natural history of plague and psittacosis: The R. E. Dyer Lecture. Public Health Rep 72 (8): 705–19.

Parkhill, J., Wren, B.W., Thomson, N.R., Titball, R.W., Holden, M.T., Prentice, M.B., Sebaihia, M., James, K.D., Churcher, C., Mungall, K.L., Baker, S., Basham, D., Bentley, S.D., Brooks, K., Cerdeno-Tarraga, A.M., Chillingworth, T., Cronin, A., Davies, R.M., Davis, P., Dougan, G., Feltwell, T., Hamlin, N., Holroyd, S., Jagels, K., Karlyshev, A.V., Leather, S., Moule, S., Oyston, P.C., Quail, M., Rutherford, K., Simmonds, M., Skelton, J., Stevens, K., Whitehead, S., and Barrell, B.G. 2001. Genome sequence of Yersinia pestis, the causative agent of plague. Nature. 413:523-527