Black Death and HIV aids are the most infectious pandemics that have high fatality rates. While Yersinia pestis bacteria cause Black Death, a virus causes HIV. The Black Death causing bacteria and the HIV virus are known to develop and spread faster once they get into the human body as they can only survive inside the host within some temperature. The importance of this research is that it would help revisit the 13th century plague, compare its fatality with the present day HIV Aids, and educate the audience on the most effective control method and treatment. The purpose of this study is to compare and contrast the Black Death and HIV, their methods of infection, the anatomy and path physiology as well as the microbial characteristics of the virus and the Bactria, their genome, target cell, and finally examine their mode of transmission and the virulent factors. The paper will also cover the diseases signs and symptoms as well as the treatment and control goals of each disease. By examining the two diseases, the paper argues that without early detection and control, both Black Death and HIV aids can wipe a whole population within a short time.
Bacteria called Yersinia pestis, a rod-shaped bacterium; cause Black Death (bubonic plague). The plague has a very high fatality rate as can wipe out a population. As the fleas feed on the infected animals and spread the bacteria to the human population as was in the case of Black Death pandemic in the city of Messina in Sicily. Between October 1347 and July 1352, the disease killed over 23 million people. The bacteria were named after Aleixandre Person who discovered the gigantic bacteria in 1894 in Asia (Horrox, 2007). The French scientists realized that the dead people had similar symptoms. The disease is called Black Death because it caused gangrene in the hands and feet of the infected people. Black Death is a systemic invasive infectious disease that can spread rapidly. The virulent pathogen responsible for the Black Death caused severe illness and can result in death within hours if antibiotics are not administered promptly. This was the cause of many deaths observed in the Alps region, Europe, and China in the 6th century, 14th century, and 1855 respectively (Dennis, &, Mead, 2009).
The Black Death bacterium is Gram-negative, bipolar-staining coccobacillus from the enterobactriaceae family. The bacterium is an obligate intracellular pathogen that only survives within the host. It is only fermentative organism, motile and can leave layers of thick anty-phagocytic slime on its path. The bacteria spread faster and develop faster once it is inside the flea but cannot kill the fleas faster due to the difference in the physiologies and anatomy of the flea. The bacterium needs a warmer climate to breed and reproduce faster (Echenberg, 2010). The bacteria is transmitted by a rodent, pests, and humans but the primary carrier of the Yersinia pestis bacteria is the fleas that feed on the infected host such as rodents. As the fleas move from one place to another, the carry the infection as the bacteria reproduce inside the flea. The main carriers have always been the oriental rat flea also known as the Xenopsylla Cheopis of the genus Rattus. The bacteria reproduce and blocks the gut of the fleas and stops any gastrointestinal functional in the flea. As the flea feeds on the human being, the flea regurgitates the intestinal contents into the new hosts (Horrox, 2007).
The bacteria is known to encode two main antigenic molecules known as the faction one capsular antigen and the VW Antigen (von Willebrand Factor Antigen). It is important to note that the two pathogens are important for pathogenicity, but they cannot be expressed in lower temperatures bellow 37oC. The main reason why Yersinia pestis is not as virulent in the fleas as they are virulent in the human being is that the body temperature of the fleas is bellow 250C. According to Dennis, &, Mead, (2009), the translocation of Yersinia pestis outer protein blocks the ability of the host cells to communicate with its immune system cells, and in the process, the blockage down regulates the phagocyte host cells response to any infection. Catlin, (2003) argues that the Yersinia Protein Kinase a (YpkA) and the Yersinia over protein (YopH) are delivered through the type three-secretion systems (TTSS), and once they are in the host agent cell, they can subvert the signal traducing thereby inhibitive any form of oxidative bursts. Additionally, the rough lipopolyszccharide chain on the pathogen can mediate antibody resistances by causing the membrane attack complexes (Epstein, Pantaleo, Graziosi, & Fauci, 1993).
The disease occurs in three phases, the bubonic, septicemia, and pneumonic. Then bubonic plague is characterized by the swollen and tender lymph nodes in the neck, groin, and the armpits and this is mainly within two days after the host is infected (Brubaker, 2007). The other symptoms at this phase include fever, chills as well as a headache and malaise. After this, the gangrene develops in the extremities accompanied by bacteremia and death (Echenberg, 2010). The gram-negative bacteria can induce shock if not treated in time. Secondly, the septicemia plague occurs after the bloodstream is invaded directly without the lymph nodes being affected. At the onset, the symptoms can be associated with flu and treated as flu, but complication such as severe seizure and shock occurs. Inlay, the pneumonic plague occurs when the patient inhales droplets of the infected materials that go directly to the lung and colonize the lung tissues. The patient may present symptoms such as a severe cough, sputum with bloodstains as well as chest pains, as well as cyanosis.
On the other hand, HIV is a member of the human retroviruses family (retro viridine); the subfamily of the HIV is the lentiviruses. Being an RNA virus, it can reverse transcribe the viral RNA to DNA through reverse transcriptase enzyme. Both HIV-1 and HIV-2 are common by the HIV is predominant in almost all parts of the world (Cheepsattayakorn, 2014). The virus can detach from the surface of the cell membrane of the hosts through budding with the cell membrane of the host forming the envelope of the reproduced virion thereby incorporating the host cell protein. The glycoprotein in the envelope helps in the attachment and injection process of the virus into the new host cell membrane. The common attachment glycoprotein on the envelope includes the glycoprotein 120, and the transmembrane glycoprotein while on the inner side, the environment is cover by a matrix protein (p17) with the capsid protein forming a cone shaped cover around the center of the vision. It is important to note that the core is made up of two enzymatic proteins. Single-stranded RNA molecules, reverse transcriptase as well as integrae and protease.
The immune deficiency system
The surface glycoprotein attaches to the viral membrane through the transmembrane glycoprotein. The GP 120 can identify the CD4 receptors from the surface of the target cells. On the other hand, the transmembrane glycoprotein can traverse the virion membrane as well as mediate the fusion of the host with the viral membrane to permit the entry of the HIV into the host cell. The HIV genome (Gag-Pol-Env genes) can encode the protein of the virus thereby encoding the protein to form the core of the virion that encodes the viral enzymes. The HIV targets the CD4 receptors cells and their co-receptor molecules. For example, the CD4 lymphocyte cells, the monocytes as well as the macrophage lineage cells and the follicular dendritic cells are targeted by the HIV.
The immune systems may be either the normal immune systems or the immune deficiency system. The normal immune systems may be innate immune systems or the adaptive or acquired immune systems. The innate immune system is composed of the natural killer cell lymphocytes produced to kill the target cells through an antibody-dependent- cellular cytotoxicity. Innate immunity also includes dendritic cells, the monocytes, the macrophages, as well as the tissue mast cells such as the neutrophils and the eosinophils. The adaptive immune systems, on the other hand, are composed of the antigen-specific responses usually ignited by the foreign antigens. Any form of cellular and humoral immunity mediated by the T cells is called adaptive immunity. The CD8 cytotoxic T cells mainly search for the virus-infected cells while the CD4 T cells primarily regulate the cellular and humoral immunity
The CD4 cells target the HIV through direct cell contact or by releasing the regulatory cytokines to act as the chemical messengers. The cytokines activate the CD8 t cells, or the monocytes and macrophages. The monocytes are the key effectors of humoral immunity that trigger specific antibody production after they are activated. The innate and the humoral immunity work together to protect the HIV infection
Pathogenesis of the HIV
In the event of an immune deficiency, the HIV can cause a complex chain of immunopathogenic mechanisms leading a vicious cycle starting with pathogenesis then into excessive immunosuppressant. HIV infection involves widespread dissemination of the HIV, which rapidly replicates in the host body triggering immune response specific to the HIV. At the onset, the immune response reduces the initial viremia significantly. However, as the immunity of the body reduces, it partially reduces the virus from the body, and the remaining viruses continue to colonize the host body. Even though the virus load is low, the clinical latency may be dormancy by asymptomatic latency develops as the viral replication continues and this leads to a gradual deterioration of the host's immune system clinically the manifestation of various clinical diseases
Pathogenesis of the HIV is affected by main factors such as the host factors, viral factors. The host factors including the cell mediated immunity, and the humoral immunity reduces the pathogenesis o the HIV, the viral factors such s the immune responses may also affect the rate of pathogenesis (Cheepsattayakorn, 2014). According to Pantaleo, Graziosi, &, Fauci (1993), the CD4 T lymphocyte may also be depleted or dysfunction when he HIV infection persists at this moment contributing to the pathogenesis. There are also some of HIV cytopathic effects that can cause single cell killing and total cell fusion forming the syncytia. The remaining unaffected CD4 cells can join with the single HIV-infected cell through their interaction with the gp120 to form a short-lived syncytium. Single cell cytotoxicity is associated with the accumulation of viral DNA that was not integrated. They also associated with the excessive inhibition of protein synthesis at the cellular level. The inhibition occurs when the cellular RNA processing is impaired. Additionally, when the gp120 is overproduced and accumulated, they accelerate the cytopathic effects. Finally, the inhibition of the lymphopoiesis can also accelerate cytopathic effects as the lymphoid precursor cells are destroyed and depleted (Cheepsattayakorn, 2014)
Bubonic plague is treated using antibiotics. For example, amino glycosides such s streptomycin, and fluoroquinolone ciprofloxacin. IV should be administered within hours of infections. A broad-spectrum antibiotic such as streptomycin is recommended for prophylaxis purposes (Echenberg, 2010). On the other hand, HIV cannot be treated but the HIV infection is fought using a combination of medicine. The antiretroviral therapy (ART) only controls the Virus load in the body to enable the patient livelonger and healthier. The ART also helps in reducing the risk of HIV transmission to the others. The combination of HIV medicines is taken on a daily basis to prevent the replication of the HIV reduces the viral load in the blood thereby enabling the body's immunity to improve its immunity. However, if the viral load is not reduced the HIV may proceed into AIDS (Epstein, Pantaleo, Graziosi, & Fauci, 1993).
Black Death changed the social structure of the medieval Europe as it eliminated more than a third of the medieval Europe population. The Black Death plagues lead to the alteration of the military campaigns. The Yersinia pestis is associated with the multiplication of microbes in the host tissue and eventual death of the human hosts if not treated in time. In the same way, HIV also multiply in the human body, weakens the body’s immune system for the other opportunistic diseases to attack the body. However while the Black Death is treated using antibiotics, there is a wide range of drugs that can be used to fight HIV. The drugs are categorized into six classes include those drugs that reverse transcriptase (these are non-nucleoside reverse transcriptase inhibitor), the second class is the nucleoside reverse transcripts inhibitors while the third class is the protease inhibitors. The others include the fusion inhibitors, the CCR5 antagonist, and finally the integrase strand transfer inhibitors. Right now, a number of HIV-Aids vaccines are under trial, but none is promising to treat the infection. The infected and the uninfected individuals can protect themselves from further infection by other ways. For example, the use of protection during sexual intercourse is recommended.
Dennis T &, Mead P. (2009). Yersinia species, including plague. In: Mandell GL, Bennett JE, Dolin R, eds. Principles, and Practice of Infectious Diseases. Seventh ed. Philadelphia, Pa: Elsevier Churchill Livingstone.
Gage L. (2007). Plague and other Yersinia infections. In: Goldman L, Ausiello D, eds. Cecil Medicine. 23rd ed. Philadelphia, Pa: Saunders Elsevier. : chap 333.
Catlin, K. (2003). Yersinia Pestis. American Society for Microbiology. American Society for Microbiology.
Cheepsattayakorn, A. (2014). Human Immunodeficiency Virus Infection (HIV)/Acquired Immunodeficiency Syndrome (AIDS): The Frontiers and Global Challenges. Journal of Human Virology & Retro virology, 1(2).
Epstein, F., Pantaleo, G., Graziosi, C., & Fauci, A. (1993). The Immunopathogenesis of Human Immunodeficiency Virus Infection. New England Journal of Medicine, 328(5), 327-335.
Brubaker, R. (2007). How the structural gene products of Yersinia pestis relate to virulence. Future Microbiology, 2(4), 377-385.
Horrox, R. (2007). The Black death (1st Ed.). Manchester: Manchester University Press.
Echenberg, M. (2010). Plague ports (first Ed.). New York: New York University Press.
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