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Yersinia Pestis in Fleas
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).
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Genome
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
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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.
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Use in Bioterrorism
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Conclusion
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References
Edited by student of Joan Slonczewski for BIOL 238 Microbiology, 2009, Kenyon College.
