Targeting Of Host Organelles By Pathogenic Bacteri A Sophisticated Subversion Strategy

Imagine the bacteria as robbers trying to invade a house, the body in this analogy. The immune system is the police officers in charge of the house, and the meninges are the alarms around the point of the house that the robbers want to come in through. The robbers trick the police officers into helping them rob the house. The robbers used the police officers, originally intended to do good.

To attack its host, the bacterium needs multiple bacteria to disable victim’s cells so it can reproduce. It attacks the cells because it cannot survive outside of a host organism (Plague p7). The lethality of the disease is high but it can be treated if it is noticed before the symptoms become deadly (Newquist 240).

Tularemia, a severe disease that has a death rate up to 60 percent, is caused by the bacterium, Francisella tularensis. This bacterium is spread through vectors or consumption of infected meats. It has been discovered by the scientists from National Institute of Allergy and Infectious Disease that within the first eight hours of infection, F. tularensis tricks the host cell into increasing its mitochondrial function, thus obviating the cell’s inflammatory response. In the following twenty-four hours, the infectious bacteria now will cause the mitochondrial function to be impaired, providing the opportunity for F. tularensis to experience rapid replication. Although these findings may seem basic, they could play a crucial part of uncovering promising treatment strategies.

The coincidental phylogenesis hypothesis suggests some forms of pathogenic virulence did not co-evolve with the host . After, C. tetani bacteria enter a person wound, the bacteria may grow and divide rapidly, even though the human body is not their natural habitat. C. tetani produce neurotoxin that is lethal to the human race . Bacterium's normal aliveness cycle is in the soil not in a human body which that leads it to produce this toxin (Farrar, 2000). The bacterium gets inside a human instead of in the soil by mere coincidence . The neurotoxin is not coordinated at the human host. The harmfulness of numerous pathogens in people may not be an objective of determination itself, but instead an unplanned by-result of choice that works on different attributes. Broadening into new surroundings is a

A pathogen can be defined as a microorganism or a biological agent that causes disease. Pathogen’s sole aim is to replicate and produce progeny to pass its genes on to; therefore the notion of a perfect pathogen would be an organism that has the capacity to carry out this task. The major classes of infectious agents are bacteria, virus, protozoa, fungi and even prions (Albert B, 2002) . In order to be considered perfect a pathogen would have to possess many characteristic such as being highly contagious, rapidly shed, evoking limited immunity, constantly evolving and only moderately virulent, allowing most of the infect to recover, which means a larger pool of susceptible host (J.Hall, 2012). The host immune system protects us from most infection. However pathogens must overcome this in order to survive, and they have developed many adaptations to achieve this.

Often termed an “evolutionary arms-race,” the enduring battle between bacterial and phage defenses against one another has shed insight into the mechanisms behind coevolution, and how these adaptations have led to diversification and speciation within both populations. Research into the relationship has yielded evidence that antagonistic coevolution can be advantageous for both phage and bacteria, often resulting in adaptations that would not have evolved by mutation through natural selection alone.

This journal article was over how our bodies protect us from the internal and external environments. The host has three main “fences” that help with that protection, the skin, the gastrointestinal tract, and the respiratory tract. We are really interesting subjects, the internal and external surfaces of our bodies are constantly being introduced to new bacteria, microbes, and pathogens and yet we do not get sick. The barriers or fences protect us and are crucial for our immune response. There is still much not understood about the immune system but we do know with certainty that when a child is born he or she acquires around two thousand different species of bacteria that really help to get the child immune system started and running. The researchers also know that there is four dominate groups of bacteria phyla’s in the “intestinal niche”, Firmicutes, bacteroidetes, Actinobacteria, and proteobacteria. We are able to have our normal bacteria’s in and on us because our immune system has learned to co-exist with its symbiotic species. As one may wonder or even certainly expect, competition does occur between the host symbiotic organisms and potentially harmful bacterial cells. They compete mainly for nutrients but also for space, some microbes even engage in “chemical warfare” and possibly even killing its rivalry. Inflammatory disorders can possibly arise from the internal and superficial wars going on, that is why the immune system is constantly being monitored for comprises

T6SS is believed to resemble the tail of a bacteriophage. TssJ, TssL and TssM proteins combine to form a complex which anchors it to the cell membrane, stretching from outer to inner membrane. A baseplate, created by TssA, E, F, G and K resides within the inner membrane. VgrG resides within the baseplate and supports the tube of Hcp hexamers extending into the cytoplasm. TssB and TssC combine to form a sheath-like structure supporting the Hcp hexamer tube. Their interlacing construction provides strength to the barrel during contraction and effector release. At the tip PAAR and VgrG combine to create the “spike” at the end of the tube, which serves to puncture the membrane of the target cell, so that the effector proteins can be delivered. PAAR repeat containing proteins have been found to play an important role in the formation of the puncturing structure at the top of the tube, as their omission in certain bacteria result in loss of virulence. Once the effector proteins have been successfully delivered to the target cell, ClpV attaches to TssC to promote disassembly of the TssBC sheath. A specific defensive strategy, termed ‘Tit for tat’ has been described in Pseudomonas aeruginosa. This is made possible by TPP (threonine phosphorylation pathway) accessory proteins during cell to cell connection. PpkA and PppA act upon Fha1. Accessory proteins TagQ, R, S and T lead to a change in conformation and a firing event. All accessory proteins are necessary for activation. This strategy is activated in response to aggression from another cell. Not all P. aeruginosa organisms contain the necessary components for this defense

Summary Citation: Madigan, M.T., J.M. Martinko, K. S.Bender, D.H. Buckley, D.A.Stahl. 2014. Brock: Biology of Microorganisms. 14th edition. Benjamin Cummings, New York.

coli and other gram negative bacteria also employed this mechanism to play other roles in pathogenicity of bacteria such as colonization, infection, and the persistence of microorganisms in the host. The antibiotic resistance gene cluster mechanism we found in S. aureus strains have been investigated in Vibrio cholerae O139 and O1 SXT by Hochhut et al. [34] and other bacteria pathogens.

Prokaryotic and bacterial cells contain flagella unlike eukaryotic cells. Flagella is like gas in a car that allows bacterial cells to move in their environment. Targeting would result in a decrease of Pathogenicity.

Bacterial pathogens have the unique ability to survive by directly changing the host cell response to the infection. Activating pathways in the nucleus

N. Gonorrhoeae posse piliated gonococci that adhere to a host by synthesis of dense microcoloniess on the cell’s surface. The Opa proteins as well as lipopolysaccharides bind closely through cell surface receptor epithelial host, subsequently allowing bacterial subjugation and trancytosis of the epithelial cell host.

Population evolution and microbial life are a major component in biological applications today. Microbial life is being discovered everywhere and these microbes can have major positive and impacts on society. Some microbes can promote increased human immunity to certain diseases like Cancer (Green and Ariyan 2014) or can potentially decrease the human aging process (Ghose 2014). For example, current clinic trials are now using microbes to help increase the rate at which T-cells can respond to the presence of cancer cells (Green and Ariyan 2014). We are also discovering how microbes contribute to our ocean animal populations and how they influence ocean health (Woods Hole Oceanographic Institution 2014), both positively and negatively. Some microbes can actually aid in the clean-up of oil spills as they ingest and breakdown parts of oil, and others can help us determine how climate change is altering how water quality (Woods Hole Oceanographic Institution 2014).

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