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Yersinia Pestis and Bioterrorism by Jada Swearingen

Introduction

Yersinia Pestis (also known as the Black Death) is a gram-negative coccobacillus that is transmitted by rodent fleas to animal hosts including humans. The bacterium is highly contagious, and humans can be infected by handling an infected animal, getting bitten by an infected rodent flea, or inhaling an aerosol from an infected animal or human (1).

To observe this bacterium, you can use a Wayson or Giemsa stain as well as Gram stain under light microscopy (1). In Wayson staining, Y. pestis appears as light blue bacilli with dark blue polar bodies. You can also use direct fluorescent antibody testing for observations of the bacteria. Identification of Y. pestis can be made by conducting a polymerase chain reaction assay (1).

There are three types of widespread plaques that Yersinia Pestis can cause: Pneumonic, bubonic, and septicemic. In the U.S. bubonic is the most common. Incubation period for bubonic plague is typically longer than for pneumonic plaque. Pneumonic starts as flulike illness but quickly progresses to high fever, chest pain, cough, dyspnea, and hemoptysis. Shock also often occurs, and white blood cell count is significantly elevated. In later stages pf the disease, disseminated intravascular coagulation can occur. Chest radiographs can be used in pneumonic plaque to reveal bilateral lower lobe alveolar opacities. Septicemic mostly involves patients showing signs of septic shock (1).


Electron micrograph of the Ebola Zaire virus. This was the first photo ever taken of the virus, on 10/13/1976. By Dr. F.A. Murphy, now at U.C. Davis, then at the CDC.


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Legend/credit: Electron micrograph of the Ebola Zaire virus. This was the first photo ever taken of the virus, on 10/13/1976. By Dr. F.A. Murphy, now at U.C. Davis, then at the CDC.
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Genome

The genome sequence of Y. pestis strain CO92, consists of a 4.65-megabase (Mb) chromosome and three plasmids of 96.2 kilobases (kb), 70.3 kb and 9.6 kb. The genome has many insertion sequences and displays anomalies in GC base-composition bias, indicating frequent intragenomic recombination. Y. pestis' ability to adapt to many different hosts could have developed from horizontal gene transfer. The genome also contains around 150 pseudogenes.

Immune system resistance comes from its established virulence factors. One crucial virulence factor is T3SS and Yersinia outer proteins. Both target phagocytosis cells and inhibit cell signaling pathways altering functions of phagocytosis and gene expression.


Include some current research in each topic, with at least one figure showing data.

Life Cycle

Y. pestis blocks digestive tracks of fleas by forming biofilms. This causes fleas to repeatedly bite other hosts to obtain food thus spreading the bacteria. Polymer of N-acetyl-D-glucosamine holds biofilm together. Capsule, F1 antigen, and type 3 secretions system injects antiphagocytic proteins into cells to avoid phagocytosis. Once in lymphatic system they are carried to lymph nodes and cause purulent adenitis (pus inflammation) called a bubo. Bacteremia is common and dissemination to various organs may occur quickly. Untreated plague bacteremia or sepsis results in a massive systemic inflammatory responses syndrome due to cytokines such as TNFα, and is associated with 80–100% mortality if left untreated. Dissemination causes necrosis and bleeding of many internal organs. Skin lesions called purpura may be found at the fingers, toes, and trunk. Their lesions progress from red to dark purple or black – giving rise to the term ‘Black Death.’ They are caused by a bleeding diathesis due to disseminated intravascular coagulation.


Include some current research in each topic, with at least one figure showing data.


Reproduction

The Y. pestis bacterium has a capsule, F1 antigen, and secretion systems that inject antiphagocytic proteins into the host’s cells to avoid destruction via phagocytosis. Find more on replication! One in the lymphatic system, the bacteria travel through the bloodstream and are carried to the lymph nodes causing purulent adenitis (pus inflammation) which is called a bubo. Bacteremia is common and dissemination to various organs often occurs rapidly. Bacteremia causes systemic inflammatory response syndrome due to cytokines such as TNFα. Y. pestis also causes skin lesions called purpura to form around the fingers, toes, and trunk. These lesions progress from red to dark purple/black which are the symptoms most recognized in a patient with the “Black Death” (1).

Use in Bioterrorism

Pneumonic plaque is the most likely to be used as a bioterrorist weapon because of its ability to spread quickly and cover a wide range of the population before medical intervention could occur. According to the Centers for Disease Control and Prevention, if a massive plague outbreak in the United States should ever occur, the best way to stay safe is to take shelter inside and do not go outside until local officials say it is safe to leave. Staying in touch with emergency contacts, listening to the radio/phone/television for updates, and preparing a first aid kit that can cover basic personal needs for at least 72 hours is highly recommended.



Include some current research in each topic, with at least one figure showing data.

Conclusion


Overall paper length should be 3,000 words, with at least 3 figures.

References

[Sample reference] Takai, K., Sugai, A., Itoh, T., and Horikoshi, K. "Palaeococcus ferrophilus gen. nov., sp. nov., a barophilic, hyperthermophilic archaeon from a deep-sea hydrothermal vent chimney". International Journal of Systematic and Evolutionary Microbiology. 2000. Volume 50. p. 489-500.

Edited by Jada Swearingen, student of Joan Slonczewski for BIOL 238 Microbiology, 2009, Kenyon College.