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The Worlds Fight Against Microbes Many infectious diseases that were nearly eradicated from the industrialized world, and newly emerging diseases are now breaking out all over the world due to the misuse of medicines, such as antibiotics and antivirals, the destruction of our environment, and shortsighted political action and / or inaction. Viral hemorrhagic fevers are a group of diseases caused by viruses from four distinct families of viruses: filo viruses, arena viruses, flaviviruses, and bunyaviruses. The usual hosts for most of these viruses are rodents or arthropods, and in some viruses, such as the Ebola virus, the natural host is not known. All forms of viral hemorrhagic fever begin with fever and muscle aches, and depending on the particular virus, the disease can progress until the patient becomes deathly ill with respiratory problems, severe bleeding, kidney problems, and shock. The severity of these diseases can range from a mild illness to death (CDC I). The Ebola virus is a member of a family of RNA (ribonucleic acid) viruses known as filo viruses.
When these viruses are magnified several thousand times by an electron microscope they have the appearance of long filaments or threads. Filo viruses can cause hemorrhagic fever in humans and animals, and because of this they are extremely hazardous. Laboratory studies of these viruses must be carried out in special maximum containment facilities, such as the Centers for Disease Control (CDC) in Atlanta, Georgia and the United States Army Medical Research Institute of Infectious Diseases (USAMRIID), at Fort Detrick in Frederick, Maryland (CDC I, II). The Ebola hemorrhagic fever in humans is a severe, systemic illness caused by infection with Ebola virus. There are four subtypes of Ebola virus (Ebola-Zaire, Ebola-Sudan, Ebola-Ivory Coast, and Ebola-Reston), which are not just variations of a single virus, but four distinct viruses. Three of these subtypes are known to cause disease in humans, and they are the Zaire, Sudan, and Ivory Coast subtypes.
Out of all the different viral hemorrhagic fevers known to occur in humans, those caused by filo viruses have been associated with the highest case-fatality rates. These rates can be as high as 90 percent for epidemics of hemorrhagic fever caused by Ebola-Zaire virus. No vaccine exists to protect from filo virus infection, and no specific treatment is available (CDC II). The symptoms of Ebola hemorrhagic fever begin within 4 to 16 days after infection. The patient develops chills, fever, headaches, muscle aches, and a loss of appetite. As the disease progresses vomiting, diarrhea, abdominal pain, sore throat, and chest pain can occur.
The blood fails to clot and patients may bleed from injection sites as well as into the gastrointestinal tract, skin, and internal organs (CDC I). The Ebola virus is spread through close personal contact with a person who is very ill with the disease, such as hospital care workers and family members. Transmission of the virus can also occur from the reuse of hypodermic needles in the treatment of patients. This practice is common in developing countries where the health care system is under financed (CDC I). Until recently, only three outbreaks of Ebola among people had been reported. The first two outbreaks occurred in 1976.
One was in western Sudan, and the other in Zaire. These outbreaks were very large and resulted in more than 550 total cases and 340 deaths. The third outbreak occurred in Sudan in 1979. It was smaller with only 34 cases and 22 deaths. Three additional outbreaks were identified and reported between 1994 and 1996: a large outbreak in Kikwit, Zaire with 316 cases and 244 deaths; and two smaller outbreaks in the Ivory Coast and Gabon. Each one of these outbreaks occurred under the challenging conditions of the developing world.
These conditions including a lack of adequate medical supplies and the frequent reuse of needles, played a major part in the spread of the disease. The outbreaks were controlled quickly when appropriate medical supplies were made available and quarantine procedures were used (CDC I). Ebola-Reston, the fourth subtype, was discovered in 1989. The virus was found in monkeys imported from the Philippines to a quarantine facility in Reston, Virginia which is only about ten miles west of Washington, D. C. (Preston 109). The virus was also later detected in monkeys imported from the Philippines into the United States in 1990 and 1996, and in Italy in 1992.
Infection caused by this subtype can be fatal in monkeys; however, the only four Ebola-Reston virus infections confirmed in humans did not result in the disease. These four documented human infections resulted in no clinical illness. Therefore, the Ebola-Reston subtype appears less capable of causing disease in humans than the other three subtypes. Due to a lack of research of the Ebola-Reston subtype there can be no definitive conclusions about its pathogenicity (CDC II). Staphylococcus is a genus of nonmotile, spherical bacteria. Some species are normally found on the skin and in the throat, and certain species can cause severe life-threatening infections, such as staphylococcal pneumonia (Mosby 1477).
Despite the age of antibiotics, staph infections remain potentially lethal. By 1982 fewer than 10 percent of all clinical staph cases could be cured with penicillin, which is a dramatic shift from the almost 100 percent penicillin susceptibility of Staphylococcus in 1952. Most strains of staph became resistant to penicillins by changing their DNA structure (Garrett 411). The fight against staph switched from using the mostly ineffective penicillin to using methicillin in the late 1960 s. By the early 1980 s, clinically significant strains of Staphylococcus emerged that were not only resistant to methicillin, but also to its antibiotic cousins, such as naficillin.
In May 1982 a newborn baby died at the University of California at San Francisco's Moffit Hospital. This particular strain was resistant to penicillins, cephalosporins, and naficillin. The mutant strain infected a nurse at the hospital and three more babies over the next three years. The only way further cases could be prevented was to aggressively treat the staff and babies with antibiotics to which the bacteria was not resistant, close the infected ward off to new patients, and scrub the entire facility with disinfectants. This was not an isolated case, unfortunately.
Outbreaks of resistant bacteria inside hospitals were commonplace by the early 1980 s. The outbreaks were particularly common on wards that housed the most susceptible patients, such as burn victims, premature babies, and intensive care patients. Outbreaks of methicillin resistant Staphylococcus aureus (MRSA) increased in size and frequency worldwide throughout the 1980 s (Garrett 412). By 1990, super-strains of staph that were resistant to a huge number of drugs existed naturally. For example, an Australian patient was infected with a strain that was resistant to cadmium, penicillin, kanamycin, neomycin, streptomycin, tetracycline, and trimethoprim. Since each of these drugs operated bio mechanically the same as a host of related drugs the Australian staph was resistant, to varying degrees, some thirty-one different drugs (Garrett 413).
A team of researchers from the New York City Health Department, using genetic fingerprinting techniques, traced back in time over 470 MRSA strains. They discovered that all of the MRSA bacteria descended from a strain that first emerged in Cairo, Egypt in 1961, and by the end of that decade the strains descendants could be found in New York, New Jersey, Dublin, Geneva, Copenhagen, London, Kampala, Ontario, Halifax, Winnipeg, and Saskatoon. Another decade later they could be found world wide (Garrett 414). New strains of bacteria were emerging everywhere in the world by the late 1980 s, and their rates of emergence accelerated every year. In the U.
S. alone, an estimated $ 200 million a year was spent on medical bills because of the need to use more exotic and expensive antibiotics, and longer hospitalization for everything from strep throat to life-threatening bacterial pneumonia. These trend, by the 90 s, had reached the level of universal, across-the-board threats to humans of all ages, social classes, and geographic locations (Garrett 414). Jim Henson, famed puppeteer and inventor of the muppets, died in 1990 of a common, and supposedly curable bacterial infection. A new mutant strain of Streptococcus struck that was resistant to penicillins and possessed genes for a deadly toxin that was very similar to a strain of S. aureus discovered in Toxic Shock Syndrome.
This new strain of strep was later dubbed strep A-produced TSLS (Toxic Shock-Like Syndrome). Only a year after its discovery lethal human cases of TSLS had been reported from Canada, the U. S. , and several countries in Europe. Streptococcal strains of all types were showing increasing levels of resistance to antibiotics.
According to Dr. Harold Neu, who is a Columbia University antibiotics expert, a dose of 10000 units of penicillin a day for four days was more than adequate to cure strep respiratory infections in 1941. By 1992 the same illness required 24 million units a day, and could still be lethal (Garrett 415). The emergence of highly antibiotic resistant strains Streptococcus pneumoniae, or Pneumococcus, was even more serious.
The bacteria normally inhabited human lungs without causing harm; however, if a person were to inhale a strain that differed enough from those to which ho or she had been previously exposed, the individuals immune system might not be able to keep in check (Garrett 415). By 1990, a third of all ear infections occurring in young children were due to Pneumococcus, and nearly half of those cases involved penicillin resistant strains. The initial resistances were incomplete. This means that only some of the organisms would die off and the childs ears would clear up, and both parents and doctor would believe the illness gone. The organisms that did not die off would multiply, and in a few weeks the infection would be back. Then if the parents used any leftover penicillins, they would possible see another apparent recovery, but this time the organisms were more resistant, and the ear infection returned quickly with a vengeance (Garrett 415 - 16).
In poor and developing countries the prevention of pediatric respiratory diseases had to be handled with scarce resources, available antibiotics, and little or no laboratory support to identify the problem. Health officials then defined the disease process not in terms of the organisms involved but according to where the infection was taking place, and the severity of the infection. In general, upper respiratory infections were milder and usually viral, while deep lung involvement indicated a potentially lethal bacterial disease. In 1990 the World Health Organization (WHO) said that the best policy for developing countries was to assume that pediatric pneumonia's were bacterial, and treat with penicillin in the absence of laboratory proof of a viral infection. This process was shown to have reduced the number of child deaths in the test areas by more than a third, and even more surprising was that there was a 36 percent reduction in child deaths due to all other causes. This was only the good news.
The bad ne ws was that penicillins and other antibiotics offered no more benefit to children with mild and usually viral respiratory infections than not taking any drugs at all and staying home. This was due to the fact that antibiotics have no effect on viruses. Another key danger was that village doctors, who lacked training and laboratory support, would overuse antibiotics, which would in turn promote the emergence of new antibiotic resistant S. pneumoniae (Garrett 417).
Because of drug use policies in both wealthy and poor countries, antibiotic resistant strains of pneumococcal soon turned up all over the world. Some of these strains were able to withstand exposure to six different classes of antibiotics simultaneously. This emergence of drug resistance usually occurred in communities of social and economic deprivation. Poor people were more likely to self-medicate themselves using antibiotics purchased off the black market, or borrowing leftovers from relatives (Garrett 417 - 19). " Whether one looked in Spain, South Africa, the United States, Romania, Pakistan, Brazil, or anywhere else, the basic principle held true: overuse or misuse of antibiotics, particularly in small children and hospitalized patients, prompted emergence of resistant mutant organisms" (Garrett 419).
Infectious diseases thought to be common, and relatively harmless are now becoming lethal to people of all ages, race, and socioeconomic status because of the misuse of medicines, which make the diseases ever more drug resistant, and short sighted political policies. It now seems that the microbes now have the microbes on the run. Consider the difference in size between some of the very tiniest and the very largest creatures on Earth. A small bacterium weighs as little as 0. 00000000001 grams.
A blue whale weighs about 100000000 grams. Yet a bacterium can kill a whale Such is the adaptability and versatility of microorganisms as compared with humans and other so called " higher" organisms, that they will doubtless continue to colonize and alter the face of the Earth long after we and the rest of our cohabitants have left the stage forever. Microbes, not microbes, rule the world. - Bernard Dixon, 1994 WORKS CITED CDC (I). Ebola Virus Hemorrhagic Fever: General Information.
web November 20 ]. CDC (II). Filo viruses in Nonhuman Primates: Overview of the Investigation in Texas. web November 20 ]. Garrett, Laurie. The Coming Plague.
Farrar, Straus. and Giroux: New York, 1994. Mosby's Medical, Morning, and Allied Health Dictionary 4 th Ed... Mosby-Year Book, Inc. : St. Louis, 1994. Preston, Richard.
The Hot Zone. Random House Inc. : New York, 1994. Roman, Bernard. Infectious Diseases in an Age of Change. National Academy Press: Washington, D. C. , 1995.
Top, Franklin H... Communicable and Infectious Diseases. C. V. Mosby Company: St. Louis, 1964.
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Research essay sample on Ebola Hemorrhagic Fever Washington D C
