Evolutionary Insights and Effective Invasive Steps of Yersinia spp.
Author: Malvi Prakash Golwala (U53409030)
Email address: malviprakash@mail.usf.edu
Course name: Cellular Microbiology
Course number: BSC6932.079F15
Semester year: 2015
Abstract
Yersinia is a gram-negative bacteria causing plague pandemics in humans. They are facultative intracellular organisms that can very efficiently survive and replicate inside cells (1). They cause fatal plague and have destroyed millions of lives since 541 A.D (2). This review will highlight how these organisms subvert the immune system. It will elaborate on all the mechanisms and proteins utilized for the same. The main are the Yops or Yersinia outer proteins. But, there are other factors as
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Introduction
“The effects of this natural and human disaster changed Europe profoundly, perhaps more so than any other series of events. For this reason, alone, the Black Death should be ranked as the greatest biological-environmental event in history, and one of the major turning points of
WesternCivilization.”
Gottfried, R. S. 1983. The Black Death. Natural and human disaster in medieval Europe.
Yersinia rod shaped, non-motile or motile by peritrichous flagella, facultative anaerobe that exhibits a bipolar staining with methylene blue, Giemsa, etc. leading to a safety pin (3). Their pathogenicity lies within mainly 3 plasmids namely, pMT1 (Murine toxin), pPCP1 (Pesticin coagulase plasminogen activator) and in some species pYV (Yersinia virulence) (4). The genus Yersinia consists of 19 species. But, this review will only focus on three of them.
Yersinia started with the Justinian Plague between 541 and 750 A.D., going to The Black Death (1347-1351), killing almost one-third of the European population eventually causing the third pandemic between 19th until mid-20th century
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Ivy mutants showed sensitivity to not only lysozyme but also PMNs. Ivy mutants were less virulent in OF-1 mouse models of bubonic and pneumonic plague (shown in figures below).
Sensitivity to lysozyme would mean the release of peptidoglycan fragments. These are known to induce inflammatory compounds. Ivy deficient Yersinia pestis were not shown to induce inflammation as well (38-39) (as shown in figure below).
While studies were carried out for Yersinia pestis, similar were done for Yersinia pseudotuberculosis as well. When Ivy deletion was tested in Yersinia pseudotuberculosis, it did not affect inhibition of lysozyme in M. luteus, nor did it affect the virulence in orally infected mice (38) (as shown in figure below).
Yersinia pseudotuberculosis uses an alternative technique which does not include O-acetyltransferase, peptidoglycan N-deacetylase or EpsC protein which helps to provide resistance against lysozyme. Its LPS is different than from that of Yersinia pestis as well (40-44). This is probably the difference between the two species due to which Yersinia pseudotuberculosis is known to have greater resistance against antimicrobial peptides (45-46). Lysozyme resistance mechanism still remains to be
The Black Death was the name given to a plague that occurred in the mid 13th century which caused at least a third of the world’s population to perish. During the years in which the plague spread across Europe, many aspects of life for the people that lived were altered forever. This epidemic was like no other in history and had an unprecedented outcome. The effects of the Black Plague on society were substantial resulting in great changes of social classes through role reorganization, changes in belief systems, and ways that society interacted.
The bacteria that was contained within Unknown tube #12 is believed to be Pseudomonas aeruginosa, Figure 1. The bacteria tested to be Gram Stain negative, producing a pink, red color retained from the staining process. When the species of bacteria was plated on nutrient media, the cells produced an irregular and spreading configuration as shown in Figure 2. This same plating test provided the margins and elevation, lobate and hilly, respectively. The specimen was stabbed in a Fluid Thioglycollate Medium (FTM) tube using an inoculated loop of the bacteria. The results of this experimentation indicate the type of oxygen requirement of the bacteria. The test found the bacteria to be aerobic as colonies of the bacteria began to form along the top of the FTM tube (Manual 2017).
The bacteria Yersinia Pestis is the cause of the black plague. Y. Pestis was discovered by Alexandre Yersin in 1849. The plague was the cause of one of the world's most horrific epidemics in the entire world. The plague is an infectious disease that first appeared in 1347 in China and made its way to Asia and then the Black Sea. The Black Plague has caused death to about 75 million lives. The plague is a deadly bacterial infection that can cause death if left untreated. The plague got its name the “Black Death” due to the fact that this disease caused black boils on the skin and that its victims were always on the verge of death when seen. The Plague would then soon arrive in Europe
This functions by deregulating the interactions between both the membrane-bound integrins of the focal adhesion complexes as well as the actin cytoskeleton via the dephosphorylation of numerous substrates, including paxillin, SKAP-HOM, Fyn-binding protein, and the focal adhesion kinase that are all existent in macrophages and neutrophils. By interrupting these interactions, phagocytic cells become incapable of consuming Y. pestis. YopH also appears to control many other effects, such as the subdual of the oxidative burst of macrophages (Aepfelbacher, 2004) and the prevention of early calcium signaling present that is present in neutrophils (Andersson et al., 1999). This Yop was also discovered to decrease the functionality of T and B cells as well as hinder the release of chemokines that attract monocytes during an inflammatory response (Cornelis, 2005). Overall, these effects aid Yesinia by disrupting the cells of the immune system which thwarts the initiation of a suitable immune
The Black Death was the world’s most disastrous disease. It killed 25% of the European population, 26 million people per 5 years. It also ruined families, businesses, and more. This was a tragedy that we will remember
In other news, the Bubonic Plague can be treated. Some treatments are wormwood, balm, and mint that were used to take care of sickness and nausea. The problems in the lungs could have been treated by using liquorice and comfrey. Headaches during having the illness were treated using bay, lavender, sage, and rose. Many other treatments were used to help treat the Bubonic
This essay discusses the Black Death, which was a fatal plague that killed millions of people across the world and how the Black Death was transmitted will be further explained in the essay. The Black Death disease commenced in China and it spread to Europe, which is also further explored. The long and short-term effects will be identified. There are three different known plagues that are known as the bubonic plague, pneumonic plague, and septicemic plague, but they were not all of them were transmitted in the same way. This plague commenced in the 1300's when symptoms began to appear and the outbreak was minimised a few years later.
The Black Plague, also known as the Black Death, started spreading in the early 1300’s when the climate in Western Europe became colder and wetter. The outcome of the climate change was
It would have been hard for anyone to try and keep from getting this disease. It was taking over Europe. The Bubonic Plague symptoms included enlarged or swollen lymph nodes, chills, headaches, fever, and the feeling of weakness. The symptoms do not seem like anything much different than a little modern virus, but it did much more effect. There were a few different symptoms that went along with the Septicemic Plague such as abdominal pain and shock. The tissue bleeding and death sometimes caused the tissue to appear black. The Pneumonic was a little worse, with chest pain, shortness of breath, cough, and
The bubonic was the first strain and was mentioned in the paragraph above. The pneumonic was more contagious, it was spread through the air- airborne. The plague is spread when the infected coughs up blood and the bacteria spreading it back into the air. The victim will develop a high fever and cough up blood, then the infected will go into a coma and most likely die. The third and most deadly strain is the septicaemic. The septicaemic is the rarest form and once in the bloodstream the infected will develop a rash. Within 24 hours of becoming infected the victim will die. This is the most fatal form of the plague because the victim could go to sleep perfectly fine and then never wake up. Many people at the time of the pandemic could not differentiate between the three strains, making it seem as though they were all one disease, this was part of the cause for mass confusion and panic
The prevalence of disease in the thirteenth century was very common in Europe,and Africa, later on spread to parts of Asia. Currently the bubonic is not that common but is still infecting a small portion of the earth. The Bubonic Plague is an infectious disease caused by the bacteria Yersinia Pestis, a zoonotic bacteria, usually found in small animals and their fleas. It is transmitted between animals and humans by the bite of infected fleas, direct contact, inhalation and rarely, ingestion of infective materials.
The lymph or lymphatic system is a major component of your body’s immune system. Then finally your lymph system becomes inflamed. Most of the time the Bubonic Plague is spread by a bite from an infected rodent or flea. It is very rare but it can also be spread from person to person contact. Another way it can be spread is from a piece of clothing that is contaminated or other material used by a person that has the plague. The bacteria enters the body through an opening in the skin.
The bacteria found in the Black Plague is known as Yersinia pestis that is a bipolar and plump, lightly-staining, coccobacillus. Remaining a dangerous threat even today as well as what was previously stated that it is a plausible agent for bioterrorism. And as stated, areas such as America, Asia, and Africa are foci endemic areas. Where wild rodents, such as squirrels and rats, are the sustenance pushing for the spread and infection of the disease. The transmission being from animal-to-animal through fleas and infection to humans through contact or bites. Instances of human-to-human infection are uncommon except for the pneumonic plague, the disease caused by plague bacillus also known as Y pestis. The germ was named after Alexander Yersin who had discovered it in 1894 during a pandemic in China that started in1860. Causing numerous casualties by how fast and effective the disease was spreading, it had seemed that there was no end in
Pathogenic L. monocytogenes go through an intracellular life cycle involving early escape from the phagocytic vacuole, rapid intracytoplasmic multiplication, bacterially induced actin-based motility, and direct spread to neighboring cells, in which they reinitiate the cycle. The bacterium is first phagocytosed by these cells and secretes a pore-forming toxin called listeriolysin, which allows the bacterium to escape from the phagosome. All virulent strains of L. monocytogenes synthesize and secrete listeriolysin. Phospholipase A and B are other virulence factors that facilitate escape of L. monocytogenes from the phagosome. Once out of the phagosome L. monocytogenes is capable of rapid division in the cytoplasm, evading the immune response and moving throughout the cytoplasm from cell to cell. L. monocytogenes is well known for its ability to propel itself like a rocket through the cell cytoplasm. This is the result of the bacterium’s ability to polymerize actin filaments at its tail end. Actin is arranged in subunits to form microfilaments that are capable of directing cell movement. L. monocytogenes accomplishes cell motility through a virulence factor called ActA that takes advantage of normal actin polymerization going on in the cell. The ActA protein shares sequence homology with a protein called WASP that is found in virtually all eukaryotic cells. WASP is responsible for recognizing and
The bacterium evolved by loosing its genes converting it from a free-living microbe into a pathogen. It needs the host’s nutrients in order to survive. The bacterium latches itself onto the host epithelial cells by a 160 kDa type 1 pilli. The pilli, located on a specific organelle on the polar region of the