The pathogen Y. Pestis is particularly good at surviving in both animals and insects, and does not require a human host to survive and thrive. [9]. Because it doesn’t necessarily have to inhabit a human to survive, Y. Pestis can survive for a very long period of time outside of a human host. [9]. In terms of pathogenic reservoirs, the bacteria rely on human and animal reservoirs, as well as environmental reservoirs (the bacteria can survive in soil for several months). [9]. Outside of humans, one of the major carriers of Yersinia Pestis is fleas, which can then live on and bite (infect) animals in the cases of bubonic and septicemic plague. The bacteria colonizes the midgut of the flea, and is able to do so by the actions of Yersinia Murine …show more content…
Toxin, a plasmid-encoded phospholipase D that is able to cause an enzyme-catalyzed hydrolysis of phosphodiester bonds) and by the HMS (Hemin Storage System), which synthesizes extracellular polysaccharides, a fundamental component of the production and structure of biofilm and the outer cell wall. [3]. In the midgut of the flea, more specifically the Proventriculus (a modification of the foregut, and a bulb-shaped organ that regulates the passage of food into the flea’s digestive system), the bacteria begin to secrete biofilm to both protect the colonies while replicating, as well as increase the likelihood of transmission when the flea bites an animal. [1/2].The biofilm produced by the bacteria will often grow to obstruct the esophagus of the flea, making it impossible for the flea to feed. [4]. Instead, when the flea bites an animal, that animal’s blood will flood the flea’s esophagus, mix with the biofilm, and return to the animal, thus infected the bitten animal. [4]. When the bacteria infect animals, Y. Pestis first attacks and inhabits the body’s macrophages, and essentially rides them along until they reach the lymph nodes, and other internal organs (liver, spleen). [3]. In the process, the bacteria can also cause the macrophages to lyse (rupture). [3]. In these organs, the bacteria (in the cases of all three categorizations of infection) create lesions, and are able to proliferate extracellularly (utilizing YOPs). [3]. YOPs proteins are virulence accessory factors that, when certain environmental cues are made, are able to be secreted by the bacteria. [9]. YOPs also further interfere with immune cell function by blocking the host cell from communicating with immune cells, and are able to cause the death of immune cells by apoptosis. [9]. Y.
Pestis is able to make a host sick in many ways. In the case of bubonic plague, Y. Pestis enters the body through a flea bite. [3]. Y. Pestis triggers an immune response from a human host by first colonizing the body’s macrophages, which it is able to gain access to by phagocytosis. [3]. Then, once the bacteria have reached the lymph nodes, it escapes the Macrophages (sometimes causing lysis or rupture of macrophages) and replicates extracellularly. [3]. From there, secondary infection by mass colonization of immune cells in blood stream can occur, otherwise known as septicemic plague. [3]. Y. Pestis is also able to, in some cases, colonize the lungs (Pneumonic plague) by inhalation of droplets containing bacteria.[3]. Pneumonic plague causes severe immune response, and has a mortality rate of nearly 100 percent. [3]. When Y. Pestis colonizes these regions of the body, the bacteria release a number of toxins to aid in both maintenance of the bacteria themselves as well as the evasion of the host’s immune system. [3]. One of these toxins is the Yersinia Murine Toxin, which is primarily useful in the proventriculus of the carrier fleas rather than in the body of an infected mammal. …show more content…
[3]. An infection of a human by Y. Pestis triggers a large-scale immune response. [10]. Firstly, the bacteria triggers an initial immune response when macrophages find the bacteria. [10]. Those bacteria that do not enter the macrophages are destroyed by granulocytes called neutrophils. [12]. After the bacteria enters the macrophages through phagocytosis and begin to proliferate, the lipopolysaccharides within the structure of the bacteria’s cell wall again play a large role in the virulence of Y. Pestis; the LPS structures in the bacteria’s cell wall allows the bacteria to become resistant to serum-mediated lysis during the flea-to-human transmission process. [3]. Thus, the bacteria that exit the macrophages are essentially immune to any further phagocytosis by phagocytic immune cells (like macrophages, neutrophils, and dendritic cells), and can also prevent the production of cytokines, effectively slowing down the host’s immune response. Following the bacteria’s exit of the macrophages after reproduction, Y. Pestis will then employ YOPs, by essentially sticking the proteins onto phagocytic immune cells to interfere with cell function. [10]. Because Y. Pestis primarily targets phagocytic cells (specifically dendritic cells, that play a large role in triggering both T-cell and B-cell activation within the immune system), the host’s body can no longer perform the normal immune response. [4]. Despite all that we now know about Yersinia Pestis, we are still fighting this pathogen today, especially in places with limited access to resources.
Since the discovery of the pathogen in 1894 [6], we have learned a lot about the bacteria that was responsible for what was arguably the worst epidemic the modern world has ever seen. There are two other somewhat similar pathogens that both also belong to the Yersinia genus, both of which are mostly food-borne, and only really cause stomach pain and diarrhea. [14]. However, there are still many unknowns when it comes to both strains of the Yersinia Pestis bacteria (Strain KIM and Strain CO92). [11]. Current research occurring at the Indian Academy of Sciences, may suggest that Yersinia Pestis and its close relative of the same genus (and far less lethal symptoms), Yersinia Pseudotuberculosis may have evolved from a common ancestor thousands of years ago. [11]. It is not completely known if Y. Pestis is still evolving, as resources in countries where the pathogen is still present are thin.
[11]. References: “Digestive System.” ENT 425 - General Entomology, 2015, genent.cals.ncsu.edu/bug-bytes/digestive-system/. “Drosophila Gross Anatomy Ontology - Proventriculus - Classes | NCBO BioPortal.” NanoParticle Ontology - Polydispersity Index - Classes | NCBO BioPortal, bioportal.bioontology.org/ontologies/FB-BT?p=classes&conceptid=FBbt%3A00005752. “Yersinia Pestis (Pathogenesis).” Ignicoccus Hospitalis - Microbewiki, microbewiki.kenyon.edu/index.php/Yersinia_Pestis_(Pathogenesis). Ngo, Minh, et al. “The Plague.” Ignicoccus Hospitalis - Microbewiki, microbewiki.kenyon.edu/index.php/The_Plague. “Plague.” National Institute of Allergy and Infectious Diseases, U.S. Department of Health and Human Services, 14 June 2018, www.niaid.nih.gov/diseases-conditions/plague. “Plague.” Centers for Disease Control and Prevention, Centers for Disease Control and Prevention, 14 Sept. 2015, www.cdc.gov/plague/history/index.html. “CDC Laboratory Training.” Centers for Disease Control and Prevention, Centers for Disease Control and Prevention, 27 Oct. 2017, www.cdc.gov/labtraining/training-courses/biothreat-preparedness-sentinel/yersinia-pestis.html. “Lipopolysaccharides - Structure, Function and Application.” Sigma-Aldrich, The Journal of Pharmacy and Pharmacology, www.sigmaaldrich.com/technical-documents/articles/biology/glycobiology/lipopolysaccharides.html. “Yersinia Pestis.” Chlamydia Trachomatis, web.uconn.edu/mcbstaff/graf/Student%20presentations/Y.%20pestis/Yersinia%20pestis.html. “Yersinia Pestis.” Clostridium Botulinum | Pathway Medicine, pathwaymedicine.org/Yersinia-pestis. “Yersinia Pestis.” Ignicoccus Hospitalis - Microbewiki, microbewiki.kenyon.edu/index.php/Yersinia_pestis. “Granulocyte: MedlinePlus Medical Encyclopedia.” MedlinePlus, U.S. National Library of Medicine, medlineplus.gov/ency/article/003440.htm. Selvy, Paige E., et al. “Phospholipase D- Enzymology, Functionality, and Chemical Modulation.” Advances in Pediatrics., U.S. National Library of Medicine, 12 Oct. 2011, www.ncbi.nlm.nih.gov/pmc/articles/PMC3233269/. “Yersinia Pseudotuberculosis.” Ministry of Health NZ, www.health.govt.nz/your-health/conditions-and-treatments/diseases-and-illnesses/yersinia-pseudotuberculosis.
Kirsten I. Bos, Verena J. Schuenemann, et al, “A draft genome of Yersinia pestis from victims of the Black Death,” Nature, 7370, (2011): 506-510
After a series of biochemical tests and evaluation to determine several unknown bacteria, the bacterium Yersinia pestis was chosen to report. The discovery of Y. pestis dates back to 1894 by French/Swiss physician and bacteriologist named Alexandre Yersin. The name Yersinia pestis is synonymous with its more common name, the plague. Y. pestis is known to infect small rodents such as mice and rats, but is transmitted to humans through the bite of an infected animal or flea. Although this bacterium is known to still cause illness today, it is infamous for three pandemics that occurred in earlier centuries. According to the Centers for Disease Control and Prevention, the first recorded pandemic occurred in 541 A.D. and is known as the Justinian Plague. The second pandemic originated in China in 1334 and has received the egregious name the “Black Death.” Finally, the third outbreak took place in the 1860’s and is known as the Modern Plague. It wasn’t until the end of the Modern Plague that scientists discovered the causative agent and mode of transmission of the Yersinia pestis bacterium.
The disease was caused by a bacteria called Yersinia Pestis which was carried by fleas that lived on the black rats. These rodents helped spread the plague. The diseases spread one of two ways. The first was through human contact and the second was through the air, people were infected with the disease just by inhaling it. The symptoms and characteristics of the disease included fever, fatigue, muscle aches and the formation of buboes which is swollen lymph nodes. These buboes were usually found under the arm, on the neck or in the groin area. It is caused by internal bleeding which eventually forms black spots or boils under the skin (which is why it is called the black death). Death usually followed shortly after these symptoms
Ever wonder who broke way for women in the graphic design industry in the 1930s-50s? The answer is Cipe Pineles , in this era women was thought to only obtain a certain job in a males eyes. Her style and way of work soon grabbed the attention of Vogue, Seventeen magazine, Glamour , and Charm just to name a few. Its amazing how quick her life flipped around from selling her work on the streets of New York to working with big time directors. Living out your dreams.
Do you have a love for a sport or hobby that you been playing since you were very young? Well, Simone Biles had been having a love for gymnastics since she was just six years old and she started training at eight years old with her coach Aimme Boorman. Simone Biles had the best Olympics because she won the most medals out of all the gymnasts that competed and she dedicates 300 days out of the whole year training. However, people think Michael Phelps did the best because he won the most gold medals out of all USA Olympic medalist.
Many say that history repeats itself, and throughout history, the spread of food-borne diseases has been constantly threatening humans. Salmonella, a disease which attacks numerous people a year, has returned, infected, and put people under panic of what they are eating. According to Foodborne Diseases, it is stated that “Salmonella comprises a large and diverse group of Gram-negative rods. Salmonellae are ubiquitous and have been recovered from some insects and nearly all vertebrate species, especially humans, livestock, and companion animals” (Gray and Fedorka-Cray 55). Because of the flexibility and the ability to reproduce rapidly, this infamous disease still remains as one of the most common threats in our society as well as an unconquerable problem that humans face these days.
Disease and parasitism play a pervasive role in all life. Many of these diseases start with microparasites, which are characterized by their ability to reproduce directly within an individual host. They are also characterized by their small size, short duration of infection, and the production of an immune response in infected and recovered individuals. Microparasites which damage hosts in the course of their association are recognized as pathogens. The level of the interaction and the extent of the resultant damage depends on both the virulence of the pathogen, as well as the host defenses. If the pathogen can overcome the host defenses, the host will be damaged and may not survive. If on the other hand the host defenses overcome the pathogen, the microparasite may fail to establish itself within the host and die.
Even though the bubonic plague can not be transmitted among humans, it was the most common of the three plagues. The bubonic plague occurs when fleas feed on the blood of infected rodents, which are usually rats (Poland 1). The bacterium that causes the infection is known as Yersenia Pestis. The fleas then pass the bacteria when they bite a human or when materials infected with Yersenia pestis directly enters the body through a wound. The names of this plague come from the swellings, also known as buboes, that appeared on a victim’s neck, armpits, or groin (Gottfried,1).The lymph nodes suddenly become painful and swollen with pus especially in the groin. Later, the skin splits and oozes pus and blood. Blood also comes out of the victim’s urine which, like the rest of the symptoms, smells horribly. These swellings (also known as tumors) could be as small as an egg or as big as an apple. Even though some people survived this disease, others would have a life expectancy of a week.
There was killer called a Jimmy Himmy. She was a serial killer of older males. This killer wore a mask and eye patch with a black shroud getup (assassin). Jake and his brother tyrone,older teengers, and his adult friends Pablo, Hibbert and Jackeln go to the castle where she lives. She sneaks behind hibbert and kills him. They run in horror but the iron doors to escape are all locked. Then Pablo gets separated and gets killed in cold blood. They then calmed down and look for ways to get out of their. On the way they find a book and find out there is another serial killer. The killer other is crazy evil and is coming here to kill Jimmy Himmy as a challenge and his Black Raven. Right as they feel safe, the Black Raven kills Tyrone. Jake
The Great Plague was an outbreak that killed a third of population in Europe. It was a scourge that originated in the arid plains of central Asia and traveled along the Silk Road. From then on, fleas living on rats, which were typically found on merchant ships, carried it. There were three types of the plague: bubonic plague, this was an infection of the lymph glands and the symptoms were muscle cramps, fevers, swellings and seizures; pneumonic plague, which was known for coughing, often with blood and the symptoms were fevers, chest pains and shortness of breath; septicemic plague, this plague was an infection of blood, and some of the symptoms were low blood pressure, vomiting, diarrhea, abdominal pain, bleeding fro...
The septimic plague is transmitted through direct fleabite. With there being no incubation period the infection infects the bloodstream directly and immediately. In reaction the victim’s circulatory system collapses, they have a high internal bleeding rate, and are dead within the next twenty-four to thirty-six hours.
Andreas Vesalius was well known for his dissections in the 1500’s. Growing up in Brussels he was captivated by the anatomy of animals. Throughout his childhood Andreas dissected many small animals trying to uncover life’s mystery. This curiosity regarding anatomy came very naturally, due to the fact that he was born into a family of physicians. Vesalius started his formal education at the University of Louvain; then traveled to Paris to continue his studies in medicine. During his life time, Vesalius was an accomplished physician, and professor of anatomy. He also received his degree as a doctor of medicine at the age of twenty-two. Vesalius writings and teachings set the foundation of anatomy we know today, hence why he received the title; founder of modern anatomy.
6. Inglesby, Thomas V., David T. Dennis, Donald A. Henderson, John G. Bartlett, Michael S. Ascher, Edward Eitzen, Anne D. Fine, Arthur M. Friedlander, Jerome Hauer, John F. Koerner, Marcelle Layton, Joseph McDade, Michael T. Osterholm, Tara O'Toole, Gerald Parker, Trish M. Perl, Philip K. Russell, Monica Schoch-Spana, Kevin Tonat, for the Working Group on Civilian Biodefense. "Plague as a Biological Weapon." JAMA. Vol. 283 no. 17. 3 May 2000. http://jama.ama-assn.org/issues/v283n17/ffull/jst90013.html(17 Oct 2001).
The Plague is caused by a bacterium known as Yersinia Pestis. Which “was discovered by Yersin (a french physician) in 1894” as stated by the Journal La Peste Bubonique. Yersinia Pestis is a gram negative bacterium which is a rod shaped coccobacillus.
The most commonly recognized food borne infections are those caused by the bacteria Campylobacter, Salmonella, and E. coli 0157:H7, and by a group of viruses called Calicivirus, also know as the Norwalk viruses. “Thousands of types of bacteria are naturally present in our environment, but not all bacteria cause disease in humans.” (Schmutz 1)