this is why people should worry about the ebola virus here are just some of the symptoms.................Signs and symptoms Signs and symptoms of Ebola.[8] Signs and symptoms of Ebola usually begin suddenly with an influenza-like stage characterized by fatigue, fever, headaches, joint, muscle, and abdominal pain.[9][10] Vomiting, diarrhea, and loss of appetite are also common.[10] Less common symptoms include the following: sore throat, chest pain, hiccups, shortness of breath, and trouble swallowing.[10] The average time between contracting the infection and the start of symptoms (incubation period) is 8 to 10 days, but it can vary between 2 and 21 days.[10][11] Skin manifestations may include a maculopapular rash (in about 50% of cases).[12] Early symptoms of EVD may be similar to those of malaria, dengue fever, or other tropical fevers, before the disease progresses to the bleeding phase.[9] In 40–50% of cases, bleeding from puncture sites and mucous membranes (e.g., gastrointestinal tract, nose, vagina, and gums) has been reported.[13] In the bleeding phase, which typically begins five to seven days after first symptoms,[14] internal and subcutaneous bleeding may present itself in the form of reddened eyes and bloody vomit.[9] Bleeding into the skin may create petechiae, purpura, ecchymoses, and hematomas (especially around needle injection sites). Sufferers may cough up blood, vomit it, or excrete it in their stool. Heavy bleeding is rare and is usually confined to the gastrointestinal tract.[12][15] In general, the development of bleeding symptoms often indicates a worse prognosis and this blood loss can result in death.[9] All people infected show some signs of circulatory system involvement, including impaired blood clotting.[12] If the infected person does not recover, death due to multiple organ dysfunction syndrome occurs within 7 to 16 days (usually between days 8 and 9) after first symptoms.[14] Causes Main articles: Ebolavirus (taxonomic group) and Ebola virus (specific virus) Life cycles of the Ebolavirus EVD is caused by four of five viruses classified in the genus Ebolavirus, family Filoviridae, order Mononegavirales. The four disease-causing viruses are Bundibugyo virus (BDBV), Sudan virus (SUDV), Taï Forest virus (TAFV), and one called, simply, Ebola virus (EBOV, formerly Zaire Ebola virus)). Ebola virus is the sole member of the Zaire ebolavirus species and the most dangerous of the known Ebola disease-causing viruses, as well as being responsible for the largest number of outbreaks.[16] The fifth virus, Reston virus (RESTV), is not thought to be disease-causing in humans. These five viruses are closely related to the Marburg viruses. Transmission Human-to-human transmission can occur via direct contact with blood or bodily fluids from an infected person (including embalming of an infected dead person) or by contact with objects contaminated by the virus, particularly needles and syringes.[17] Other body fluids with ebola virus include saliva, mucus, vomit, feces, sweat, tears, breast milk, urine, and semen. Entry points include the nose, mouth, eyes, or open wounds, cuts and abrasions.[18] The potential for widespread EVD infections is considered low as the disease is only spread by direct contact with the secretions from someone who is showing signs of infection.[17] The symptoms limit a persons ability to spread the disease as they are often too sick to travel.[19] Because dead bodies are still infectious, traditional burial rituals may spread the disease. Nearly two thirds of the cases of Ebola in Guinea during the 2014 outbreak are believed to be due to burial practices.[20][21] Semen may be infectious in survivors for up to 7 weeks.[1] It is not entirely clear how an outbreak is initially started.[22] The initial infection is believed to occur after ebola virus is transmitted to a human by contact with an infected animals body fluids. One of the primary reasons for spread is that the health systems in the part of Africa where the disease occurs function poorly.[23] Medical workers who do not wear appropriate protective clothing may contract the disease.[24] Hospital-acquired transmission has occurred in African countries due to the reuse of needles and lack of universal precautions.[25][26] Some healthcare centers caring for people with the disease do not have running water.[27] Airborne transmission has not been documented during EVD outbreaks.[2] They are, however, infectious as breathable 0.8– to 1.2-μm laboratory-generated droplets.[28] The virus has been shown to travel, without contact, from pigs to primates, although the same study failed to demonstrate similar transmission between non-human primates.[29] Bats drop partially eaten fruits and pulp, then land mammals such as gorillas and duikers feed on these fallen fruits. This chain of events forms a possible indirect means of transmission from the natural host to animal populations, which has led to research towards viral shedding in the saliva of bats. Fruit production, animal behavior, and other factors vary at different times and places that may trigger outbreaks among animal populations.[30] Reservoir Bushmeat being prepared for cooking in Ghana, 2013. Human consumption of equatorial animals in Africa in the form of bushmeat has been linked to the transmission of diseases to people, including Ebola.[31] Bats are considered the most likely natural reservoir of the EBOV. Plants, arthropods, and birds were also considered.[1][32] Bats were known to reside in the cotton factory in which the first cases for the 1976 and 1979 outbreaks were observed, and they have also been implicated in Marburg virus infections in 1975 and 1980.[33] Of 24 plant species and 19 vertebrate species experimentally inoculated with EBOV, only bats became infected.[34] The absence of clinical signs in these bats is characteristic of a reservoir species. In a 2002–2003 survey of 1,030 animals including 679 bats from Gabon and the Republic of the Congo, 13 fruit bats were found to contain EBOV RNA fragments.[35] As of 2005, three types of fruit bats (Hypsignathus monstrosus, Epomops franqueti, and Myonycteris torquata) have been identified as being in contact with EBOV. They are now suspected to represent the EBOV reservoir hosts.[36][37] Antibodies against Zaire and Reston viruses have been found in fruit bats in Bangladesh, thus identifying potential virus hosts and signs of the filoviruses in Asia.[38] Between 1976 and 1998, in 30,000 mammals, birds, reptiles, amphibians and arthropods sampled from outbreak regions, no ebolavirus was detected apart from some genetic traces found in six rodents (Mus setulosus and Praomys) and one shrew (Sylvisorex ollula) collected from the Central African Republic.[33][39] Traces of EBOV were detected in the carcasses of gorillas and chimpanzees during outbreaks in 2001 and 2003, which later became the source of human infections. However, the high lethality from infection in these species makes them unlikely as a natural reservoir.[33] Transmission between natural reservoir and humans is rare, and outbreaks are usually traceable to a single case where an individual has handled the carcass of gorilla, chimpanzee or duiker.[40] Fruit bats are also eaten by people in parts of West Africa where they are smoked, grilled or made into a spicy soup.[37][41] Virology Main articles: ebolavirus (taxonomic group) and Ebola virus (specific virus) Genome Electron micrograph of an Ebola virus virion Like all mononegaviruses, ebolavirions contain linear nonsegmented, single-strand, non-infectious RNA genomes of negative polarity that possesses inverse-complementary 3 and 5 termini, do not possess a 5 cap, are not polyadenylated, and are not covalently linked to a protein.[42] Ebolavirus genomes are approximately 19 kilobase pairs long and contain seven genes in the order 3-UTR-NP-VP35-VP40-GP-VP30-VP24-L-5-UTR.[43] The genomes of the five different ebolaviruses (BDBV, EBOV, RESTV, SUDV, and TAFV) differ in sequence and the number and location of gene overlaps. Structure Like all filoviruses, ebolavirions are filamentous particles that may appear in the shape of a shepherds crook or in the shape of a U or a 6, and they may be coiled, toroid, or branched.[43] In general, ebolavirions are 80 nm in width, but vary somewhat in length. In general, the median particle length of ebolaviruses ranges from 974 to 1,086 nm (in contrast to marburgvirions, whose median particle length was measured at 795–828 nm), but particles as long as 14,000 nm have been detected in tissue culture.[44] Replication The ebolavirus life cycle begins with virion attachment to specific cell-surface receptors, followed by fusion of the virion envelope with cellular membranes and the concomitant release of the virus nucleocapsid into the cytosol. The viral RNA polymerase, encoded by the L gene, partially uncoats the nucleocapsid and transcribes the genes into positive-strand mRNAs, which are then translated into structural and nonstructural proteins. Ebolavirus RNA polymerase (L) binds to a single promoter located at the 3 end of the genome. Transcription either terminates after a gene or continues to the next gene downstream. This means that genes close to the 3 end of the genome are transcribed in the greatest abundance, whereas those toward the 5 end are least likely to be transcribed. The gene order is, therefore, a simple but effective form of transcriptional regulation. The most abundant protein produced is the nucleoprotein, whose concentration in the cell determines when L switches from gene transcription to genome replication. Replication results in full-length, positive-strand antigenomes that are, in turn, transcribed into negative-strand virus progeny genome copy. Newly synthesized structural proteins and genomes self-assemble and accumulate near the inside of the cell membrane. Virions bud off from the cell, gaining their envelopes from the cellular membrane they bud from. The mature progeny particles then infect other cells to repeat the cycle. The Ebola virus genetics are difficult to study due to its virulent nature.[45] Pathophysiology Pathogenesis schematic Endothelial cells, macrophages, monocytes, and liver cells are the main targets of infection. After infection, a secreted glycoprotein (sGP) known as the Ebola virus glycoprotein (GP) is synthesized. Ebola replication overwhelms protein synthesis of infected cells and host immune defenses. The GP forms a trimeric complex, which binds the virus to the endothelial cells lining the interior surface of blood vessels. The sGP forms a dimeric protein that interferes with the signaling of neutrophils, a type of white blood cell, which allows the virus to evade the immune system by inhibiting early steps of neutrophil activation. These white blood cells also serve as carriers to transport the virus throughout the entire body to places such as the lymph nodes, liver, lungs, and spleen.[46] The presence of viral particles and cell damage resulting from budding causes the release of chemical signals (to be specific, TNF-α, IL-6, IL-8, etc.), which are the signaling molecules for fever and inflammation. The cytopathic effect, from infection in the endothelial cells, results in a loss of vascular integrity. This loss in vascular integrity is furthered with synthesis of GP, which reduces specific integrins responsible for cell adhesion to the inter-cellular structure, and damage to the liver, which leads to improper clotting.[47] Diagnosis The travel and work history along with exposure to wildlife are important to consider when the diagnosis of EVD is suspected. The diagnosis is confirmed by isolating the virus, detecting its RNA or proteins, or detecting antibodies against the virus in a persons blood. Isolating the virus by cell culture, detecting the viral RNA by polymerase chain reaction (PCR) and detecting proteins by enzyme-linked immunosorbent assay (ELISA) works best early and in those who have died from the disease. Detecting antibodies against the virus works best late in the disease and in those who recover.[48] During an outbreak, virus isolation is often not feasible. The most common diagnostic methods are therefore real-time PCR and ELISA detection of proteins, which can be performed in field or mobile hospitals.[49] Filovirions can be seen and identified in cell culture by electron microscopy due to their unique filamentous shapes, but electron microscopy cannot tell the difference between the various filoviruses despite there being some length differences.[44] Phylogenetic tree comparing the Ebolavirus and Marburgvirus. Numbers indicate percent confidence of branches. Classification The genera Ebolavirus and Marburgvirus were originally classified as the species of the now-obsolete Filovirus genus. In March 1998, the Vertebrate Virus Subcommittee proposed in the International Committee on Taxonomy of Viruses (ICTV) to change the Filovirus genus to the Filoviridae family with two specific genera: Ebola-like viruses and Marburg-like viruses. This proposal was implemented in Washington, DC, on April 2001 and in Paris on July 2002. In 2000, another proposal was made in Washington, D.C., to change the -like viruses to -virus resulting in todays Ebolavirus and Marburgvirus.[50] Rates of genetic change are 100 times slower than influenza A in humans, but on the same magnitude as those of hepatitis B. Extrapolating backwards using these rates indicates that Ebolavirus and Marburgvirus diverged several thousand years ago.[51] However, paleoviruses (genomic fossils) of filoviruses (Filoviridae) found in mammals indicate that the family itself is at least tens of millions of years old.[52] Fossilized viruses that are closely related to ebolaviruses have been found in the genome of the Chinese hamster.[53] Differential diagnosis The symptoms of EVD are similar to those of Marburg virus disease.[54] It can also easily be confused with many other diseases common in Equatorial Africa such as other viral hemorrhagic fevers, falciparum malaria, typhoid fever, shigellosis, rickettsial diseases such as typhus, cholera, gram-negative septicemia, borreliosis such as relapsing fever or EHEC enteritis. Other infectious diseases that should be included in the differential diagnosis include the following: leptospirosis, scrub typhus, plague, Q fever, candidiasis, histoplasmosis, trypanosomiasis, visceral leishmaniasis, hemorrhagic smallpox, measles, and fulminant viral hepatitis.[55] Non-infectious diseases that can be confused with EVD are acute promyelocytic leukemia, hemolytic uremic syndrome, snake envenomation, clotting factor deficiencies/platelet disorders, thrombotic thrombocytopenic purpura, hereditary hemorrhagic telangiectasia, Kawasaki disease, and even warfarin poisoning.[56][57][58][59]
Posted on: Wed, 08 Oct 2014 00:26:30 +0000
Trending Topics
Recently Viewed Topics
© 2015