Ebola Hemorrhagic Fever - Essay Example

?Introduction Highly contagious and infectious diseases are continually emerging throughout the world, some we have been able to control and conquer,like smallpox. However there are more out there, one that we have yet to come to understand fully is the Ebola Hemorrhagic Fever caused by the Ebola virus. The Ebola virus is a distinct, rod-shape virus in the family of Filoviridae. They produce acute hemorrhagic fever in mankind. Some of the clinical manifestations of the virus might be similar to the Lassa fever or yellow fever but if cluster of these cases occurs, one can identify the unique, approximately 6 days following bloody diarrhea, a maculopapular may appear accompanied by substantial bleeding at needle sites and bodily orifices characteristics of the Ebola virus. The continued outbreak of Ebola in Africa has drawn worldwide attention because of its explosive emergence, high mortality, nosocomial secondary transmission, and ecological mystery. The worst outbreak occurred in the Democratic Republic of the Congo (formerly Zaire) and killed 250 out of 315 who contracted it, while one of the latest outbreaks, lasting through February of 2009, had a 47% mortality rate, killing 15 of the 32 infected (CDC). Safety measures recommended to avoid the contraction of the Ebola virus include the use of personal protective equipment (PPE, including masks, gloves, gowns, and goggles) and, infection control measures including isolation, and complete sterilization of equipment. There is little research at this time regarding control of the infection since there is absence of significant knowledge about Ebola’s ecology. Thus, Ebola hemorrhagic fever (EHF) is perhaps the most virulent virus known to mankind. Background In central Africa, the Ebola virus was found to be the cause of a hemorrhagic fever with a high mortality rate in the mid-1970s and reemerged there in the mid-1990s (Waigmann, 2003, p. 6). In 1976, epidemics of hemorrhagic disease with very high mortality, up to 90%, broke out simultaneously in a remote area of Northern Zaire, now the Democratic Republic of the Congo, (DRC) and Southern Sudan (Zuckerman, 2009, p. 755). The outbreaks in these areas were found to be due to two separate but antigenically related filovirus strains, distinct from Marburg virus. After some tests, these viruses were grouped under the name Ebola virus, after a river in Zaire (Zuckerman, 2009, p. 755). Among 318 probable cases, 280 died, a mortality rate of 80% (Zuckerman, 2009, p. 759). A smaller Ebola outbreak occurred in Sudan in 1979 with 34 patients and 22 deaths. There were outbreaks in 1989, when a shipment of monkeys with Ebola virus was imported from the Philippines by a commercial biological supply company in the United States. The 1989 outbreak was focused in Reston, Virginia, and was thus called Ebola Reston strain. Hundreds of monkeys were killed in 1989 Ebola Reston outbreak to avoid spread of infection to humans. Animal handlers showed signs of infections, but not clinical manifestation. Because of this, it was believed that Philippine monkey strain of Ebola was less virulent for man. In 1992, there was a small monkey outbreak in Italy, and a single case of a Swiss technologist who did an autopsy on a chimpanzee in the Tai forest area of the Ivory Coast. In the early part of May 1995, health authorities noticed a cluster of Ebola cases in Kikwit Hospital, in Democratic Republic of Congo. Most of the cases resulted from close contact with patients and aerosol transmission, the mechanism by which Ebola virus is spread from a reservoir to a human being by means of aerosols (Ebola virus suspensions in air) and usually enters through the respiratory tract. The outbreak was controlled by limiting contact transmissions. In June 1995, 315 cases were detected and 77%, or 244, of these died (Evans, 1997, p. 140). In early 1996, an isolated outbreak occurred in Gabon with 37 cases and 21 deaths (Evans, 1997, p. 140). At the same time, a limited monkey outbreak occurred in a colony in Texas after importation of Philippine monkeys. The virus did not reappear until October 2000, when massive epidemic in the Uganda occurred (Zuckerman, 2009, p. 760). The origins were unknown. The epidemic was not brought under control until mid January 2001. There were a total of 425 cases and 224 deaths reported countrywide. As of December 2002, 30 confirmed cases, in additional, were reported. In May 2005, 11 confirmed cases still continue to occur. The origin of the Ebola virus outbreak is still unknown but control measures such as use of barrier techniques, surveillance, and early detection stopped further spread of infection. As of August 30, 2007, 103 people, one hundred adults and three children, were infected by a hemorrhagic fever outbreak in the village of Kampungu, within the Democratic Republic of the Congo. In November 30, 2007, an outbreak occurred in Bundibugyo District of the DRC. The last recorded epidemic of Ebola virus ended on February 20, 2009 with a death rate of 47%. These outbreaks, as well as the lack of medical cure to combat Ebola virus infection proved that Ebola virus is difficult to detect and control. Disease Description Ebola is a lipid-enveloped RNA virus belonging to the Filoviridae family. The virus is pleomorphic, usually seen as large rods. Ebola viruses are usually thermolabile. There are four known Ebola strains that cause illness namely, Ebola Zaire strain (EBO-2) which has unknown origin and easily transmitted through close contact and needles, Ebola Sudan strain (EBO-5) which is transmitted through nosocomial contact and has also unknown origin, Ebola Reston strain (EBO-R) which came from infected monkeys in the Philippines, and Ebola Zaire strain which infect humans through contacts with chimpanzees, monkeys, and primates (Nelson, 2007, p. 455). Most of the human epidemics have been initiated by contact with monkeys or other non-human primates, but it is unlikely for them to be the primary reservoir because they also have experienced high mortality from infection. The disease is characterized by an abrupt onset with fever, diarrhea, dysphagia (difficulty in swallowing), severe weakness, and hemorrhagic episodes. Most cases occurred from transmission from monkeys but, human-to-human transmission is also possible. People who survived Ebola virus infections do not develop high titers of neutralizing antibodies. The infected cynomolgus monkeys, that were found in Reston, Virginia, had been imported from the Philippines, an area not known to be endemic for Ebola. The monkeys were co-infected with Simian Hemorrhagic Fever (SMF) virus as well as the Ebola virus. Researchers of the Reston Research laboratory observed evidence of aerosol transmission among monkeys. The laboratory workers who had used barrier protections also developed serologic effects of infection but remained asymptomatic. Because of this, the four sub-types of Ebola virus were identified depending on the infectivity and pathogenecity. Clinical Manifestations Persons infected with the Ebola virus suffered from abrupt onset of fever, myalgia, headache, nausea, vomiting, abdominal pain, photophobia, diarrhea, chest pain, cough, and pharyngitis. By the fourth or fifth day, a maculopapular rash appeared on the trunk. Soon after the person begins having a fever, bleeding from different gastrointestinal orifices, and there is evidence of chemical hepatitis. Shock and circulatory collapse may be present in a short period, usually two to three days but if bleeding continues, patient rarely survived beyond nine days. Ebola virus infection can cause ghost-like appearance and the infected person will soon be critically ill (London, 1344). Diagnosis Ebola infection can be diagnosed through several measures. Electron microscopy has been used to reveal liver damage and if the Ebola infection is fatal. Virus antigen detection is also used to diagnose development of specific IgM and IgG antibodies 7 to 10 days after the onset of symptoms. During the acute phase, viremia and antigenemia is very high and virions in the blood can be measured by electron microscope. Antigen at titers contained in acute serum samples revealed 1:256 ratios using the rapid-antigen capture ELISA (antigen-capture enzyme-linked immunosorbent assay). Reverse transcriptase polymerase chain reaction assays provided useful information in the study of molecular epidemiologic strain in Kikwit. Pathogens are divided into Biosafety Levels (1-4) based on multiple factors such as virulence, transmissibility, environmental effect, and treatment availability. The Ebola virus belongs to BSL-4. Pathogens at each of the 4 BSLs must be handled in equivalently physically contained laboratory facilities, graded P1-4. The possibility exist that Ebola virus may be brought into the country unintentionally by those infected in endemic areas or intentionally by bioterrorists that having a BSL facility prevents further disease transmission. Reservoir, Transmission, Incubation Period, and Duration Transmission of infection is done through person-to-person contact. Infection may also occur through contaminated materials, preparation of victims for burial, or occasionally sexual contact. Injury or injection with needles posses the highest risk. Ebola virus infection’s incubation period is 2-21 days with duration of 6-9 days. Airborne transmission is also possible, as is highlighted by the case in Reston, Virginia where the Ebola virus remained suspended in the air environment (Nelson, 2007, 455). Epidemiology Read More