Obama Brings Ebola Into America After Signing Executive Order to Detain Sick Americans
Officials are importing Ebola into the U.S. which doctors have failed to contain in Africa
Image Credits: Sebástian Freire / Flickr (Medical workers)
by Kit Daniels | Infowars.com | August 2, 2014
Despite the fact that doctors in Africa cannot keep Ebola from spreading, United States officials brought an affected patient into the country only days after President Obama signed an executive order mandating the detention of Americans who show signs of “respiratory illness.”
The first known Ebola patient on U.S. soil, Dr. Kent Brantly, was flown into Emory University Hospital in Atlanta, Georgia, today after contracting the disease in Liberia during the latest outbreak in West Africa which has claimed the lives of over 700.
“Video from Emory showed someone wearing a white, full-body protective suit helping a similarly clad person emerge from the ambulance and walk into the hospital early Saturday afternoon,” CNN reported.
This has stoked concerns among the American public that Ebola could now spread inside the U.S., especially since the virus has been difficult to contain in Africa.
“It sounds like the perfect script for a horror movie: A virus with no vaccine and no cure kills hundreds of people; despite containment efforts, it keeps spreading, but it’s actually all too real in West Africa, where doctors have said Ebola is now ‘out of control,’” wrote Sheila M. Eldred for Discovery News.
Hospitals in America may not fare any better considering that antibiotic-resistant “nightmare bacteria” spread from one medical facility in 2001 to 46 states by 2013.
“Allegedly the Ebola carriers will be quarantined in special rooms, but we already know that American hospitals cannot even contain staph infections,” columnist Paul Craig Roberts wrote. “What happens to the utensils, plates, cups, and glasses with which the ebola infected persons eat and drink and who gets to clean the bed pans?”
“One slip-up by one person, one tear in a rubber glove, and the virus is loose.”
This really highlights the reckless nature of the global elite and government officials for importing a virus into the country which has no specific treatment and a mortality rate of up to 90%.
Similarly, state-funded universities and other facilities across the U.S. are maintaining weaponized viruses for so-called “bio-defense” under the Project Bioshield Act passed by Congress in 2004, but because these facilities are only moderately secure for the most part, there is a real risk that a deadly virus could escape into the public and affect millions of Americans in an outbreak on the same level as the pandemics which killed 80% of Native American populations by the 19th century.
The National Research Council found that one of these laboratories in Kansas, for example, has a 70% chance that a virus will spread from its lab in the next 50 years, even though the facility is designated as “maximum security.”
And it should also be pointed out that this is just one lab out of many in the nation, a good percentage of which have even less security.
There is no doubt that an accidental or an orchestrated release of a virus from one of these labs could result in the deaths of millions as well as a draconian government response to the outbreak, including martial law, through both the Model State Emergency Health Powers Act drafted in 2001 and President Obama’s latest executive order which mandates the apprehension and detention of Americans who merely show signs of “respiratory illness.”
Simply put, instead of preventing Ebola and other viruses from spreading within the U.S., Obama is readying his administration for a power grab if a major pandemic breaks out throughout the country.
What Exactly is Ebola Virus
Ebola virus disease
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"Ebola" redirects here. For other uses, see Ebola (disambiguation).
Ebola virus disease
Classification and external resources
1976 photograph of two nurses standing in front of Mayinga N., a person with Ebola virus disease; she died only a few days later due to severe internal hemorrhaging.
Ebola virus disease (EVD) or Ebola hemorrhagic fever (EHF) is the human disease caused by the Ebola virus. Symptoms typically start two days to three weeks after contracting the virus, with a fever, sore throat, muscle pains, and headaches. Typically nausea, vomiting, and diarrhea follow, along with decreased functioning of the liver and kidneys. At this point, some people begin to have problems with bleeding.
The disease may be acquired upon contact with blood or bodily fluids of an infected animal (commonly monkeys or fruit bats). It is not naturally transmitted through the air. Fruit bats are believed to carry and spread the virus without being affected. Once human infection occurs, the disease may spread between people as well. Male survivors may be able to transmit the disease via semen for nearly two months. In order to make the diagnoses, typically other diseases with similar symptoms such as malaria, cholera and other viral hemorrhagic fevers are first excluded. Blood samples may then be tested for viral antibodies, viral RNA, or the virus itself to confirm the diagnosis.
Prevention includes decreasing the spread of disease from infected monkeys and pigs to humans. This may be done by checking such animals for infection and killing and properly disposing of the bodies if the disease is discovered. Properly cooking meat and wearing protective clothing when handling meat may also be helpful, as is wearing protective clothing and washing hands when around a person with the disease. Samples of bodily fluids and tissues from people with the disease should be handled with special caution.
There is no specific treatment for the disease; efforts to help persons who are infected include giving either oral rehydration therapy or intravenous fluids. The disease has high mortality rate: often killing between 50% and 90% of those infected with the virus. EVD was first identified in Sudan and the Democratic Republic of the Congo. The disease typically occurs in outbreaks in tropical regions of Sub-Saharan Africa. Between 1976, when it was first identified, through 2013, fewer than 1,000 people a year have been infected. The largest outbreak to date is the ongoing 2014 West Africa Ebola outbreak, which is affecting Guinea, Sierra Leone, and Liberia. As of July 2014 more than 1320 cases have been identified. Efforts are ongoing to develop a vaccine; however, none yet exists.
Signs and symptoms
Symptoms of Ebola.
Signs and symptoms of Ebola usually begin abruptly with an influenza-like stage characterized by feeling tired, fever, headaches, and joint, muscle, and abdominal pain. Vomiting, diarrhea and loss of appetite are also common. Less common symptoms include: sore throat, chest pain, hiccups, shortness of breath and trouble swallowing. The average time between contracting the infection and the start of symptoms is 8 to 10 days, but can occur between 2 and 21 days. Skin manifestations may include a maculopapular rash (in about 50% of cases). 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.
In the bleeding phase internal and subcutaneous bleeding may present itself through reddening of the eyes and bloody vomit. Bleeding into the skin may create petechiae, purpura, ecchymoses, and hematomas (especially around needle injection sites).
All people infected show some symptoms of circulatory system involvement, including impaired blood clotting. Bleeding from puncture sites and mucous membranes (e.g. gastrointestinal tract, nose, vagina and gums) is reported in 40–50% of cases. Types of bleeding known to occur with Ebola virus disease include vomiting blood, coughing it up or defecating it. Heavy bleeding is rare and is usually confined to the gastrointestinal tract.
In general, the development of bleeding symptoms often indicates a worse prognosis. However, contrary to popular belief, bleeding does not lead to hypovolemia and is not the cause of death (total blood loss is low except during labor). Instead, death occurs due to multiple organ failure (MOF) due to fluid redistribution, low blood pressure, disseminated intravascular coagulation, and focal tissue death.
Life cycles of the Ebolavirus
EVD is caused by four of five viruses classified in the genus Ebolavirus, family Filoviridae, order Mononegavirales. These four viruses are Bundibugyo virus (BDBV), Ebola virus (EBOV), Sudan virus (SUDV), Taï Forest virus (TAFV). The fifth virus, Reston virus (RESTV), is not thought to be disease-causing in humans. During an outbreak those at highest risk are health care workers and close contacts of those with the infection.
It is not entirely clear how Ebola is spread. EVD is believed to occur after an ebola virus is transmitted to an initial human by contact with an infected animal’s bodily fluids. 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 contaminated medical equipment, particularly needles and syringes. Transmission through oral exposure and through conjunctiva exposure is likely and has been confirmed in non-human primates. The potential for widespread EVD infections is considered low as the disease is only spread by direct contact with the secretions from someone who has symptomatic disease. The quick onset of symptoms makes it easier to identify sick individuals and limits a person’s ability to spread the disease by traveling. Because bodies of the deceased are still infectious, some doctors had to take measures to properly dispose of dead bodies in a safe manner despite local traditional burial rituals.
Medical workers who do not wear appropriate protective clothing may also contract the disease. In the past, hospital-acquired transmission has occurred in African hospitals due to the reuse of needles and lack of universal precautions.
EVD is not naturally transmitted through the air. They are, however, infectious as breathable 0.8–1.2 micrometre laboratory generated droplets; because of this potential route of infection, these viruses have been classified as Category A biological weapons. Recently the virus has been shown to travel without contact from pigs to non-human primates.
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 have 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.
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.
Bats are considered the most likely natural reservoir; plants, arthropods, and birds have also been considered. Bats were known to reside in the cotton factory in which the first cases for the 1976 and 1979 outbreaks were employed, and they have also been implicated in Marburg virus infections in 1975 and 1980. Of 24 plant species and 19 vertebrate species experimentally inoculated with EBOV, only bats became infected. 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. 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.
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. 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.
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. Fruit bats are also eaten by people in parts of West Africa where they are smoked, grilled or made into a spicy soup.
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. 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. The genomes of the five different ebolaviruses (BDBV, EBOV, RESTV, SUDV, and TAFV) differ in sequence and the number and location of gene overlaps.
Like all filoviruses, ebolavirions are filamentous particles that may appear in the shape of a shepherd’s crook or in the shape of a "U" or a "6", and they may be coiled, toroid, or branched. 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.
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.
Endothelial cells, mononuclear phagocytes, and hepatocytes 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.
The presence of viral particles and cell damage resulting from budding causes the release of cytokines (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 coagulopathy.
The most important method of diagnosis EVD is the medical history, especially travel and occupational history and the person’s exposure to wildlife. EVD can be confirmed by isolating ebolaviruses from or by detection of ebolavirus antigen or genomic or subgenomic RNAs in patient blood or serum samples during the acute phase of EVD. Ebolavirus isolation is usually performed by inoculation of grivet kidney epithelial Vero E6 or MA-104 cell cultures or by inoculation of human adrenal carcinoma SW-13 cells, all of which react to infection with characteristic cytopathic effects.
Filovirions can easily be visualized and identified in cell culture by electron microscopy due to their unique filamentous shapes, but electron microscopy cannot differentiate the various filoviruses alone despite some overall length differences. Immunofluorescence assays are used to confirm ebolavirus presence in cell cultures. During an outbreak, virus isolation and electron microscopy are most often not feasible options. The most common diagnostic methods are therefore RT-PCR in conjunction with antigen-capture ELISA, which can be performed in field or mobile hospitals and laboratories. Indirect immunofluorescence assays (IFAs) are not used for diagnosis of EVD in the field anymore.
Phylogenetic tree comparing the Ebolavirus and Marburgvirus. Numbers indicate percent confidence of branches.
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 today’s Ebolavirus and Marburgvirus.
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. However, paleoviruses (genomic fossils) of filoviruses (Filoviridae) found in mammals indicate that the family itself is at least tens of millions of years old. Fossilized viruses that are closely related to ebolaviruses have been found in the genome of the Chinese hamster.
The symptoms of EVD are similar to those of Marburg virus disease. 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. 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.
A researcher working with the Ebola virus while wearing a BSL-4 positive pressure suit to avoid infection
Ebola viruses are contagious with prevention predominantly involves behavior changes, proper personal protective equipment, and disinfection. Governments and individuals often quarantine the area where the disease is occurring; while the lack of roads and transportation may help.
Techniques to avoid infection involve not contacting infected blood or secretions, including from those who are dead. This involves suspecting and diagnosing the disease early and using standard precautions for all patients in the healthcare setting. Recommended measures when caring for those who are infected include: wearing protective clothing including: masks, gloves, gowns and goggles, equipment sterilization and isolating them.
Due to lack of proper equipment and hygienic practices, large-scale epidemics have occured mostly in poor, isolated areas without modern hospitals or well-educated medical staff. Traditional burial rituals, especially those requiring embalming of bodies, should be discouraged or modified. Airline crews who fly to areas of these areas of the world are taught to identify Ebola and are to isolate anyone who has symptoms.
No vaccine is currently available for humans. The most promising candidates are DNA vaccines or vaccines derived from adenoviruses, vesicular stomatitis Indiana virus (VSIV) or filovirus-like particles (VLPs) because these candidates could protect nonhuman primates from ebolavirus-induced disease. DNA vaccines, adenovirus-based vaccines, and VSIV-based vaccines have entered clinical trials.
Vaccines have protected nonhuman primates. Immunization takes six months, which impedes the counter-epidemic use of the vaccines. In 2003, a vaccine using an adenoviral (ADV) vector carrying the Ebola spike protein therefore was tested on crab-eating macaques. The monkeys twenty-eight days later were challenged with the virus and remained resistant. A vaccine based on attenuated recombinant vesicular stomatitis virus (VSV) vector carrying either the Ebola glycoprotein or the Marburg glycoprotein in 2005 protected nonhuman primates, opening clinical trials in humans. The study by October completed the first human trial, over three months giving three vaccinations safely inducing an immune response. Individuals for a year were followed, and, in 2006, a study testing a faster-acting, single-shot vaccine began; this new study was completed in 2008. Trying the vaccine on a strain of Ebola that more resembles the one that infects humans is the next step.
On 6 December 2011, the development of a successful vaccine against Ebola for mice was reported. Unlike the predecessors, it can be freeze-dried and thus stored for long periods in wait for an outbreak. An experimental vaccine made by researchers at Canada’s national laboratory in Winnipeg was used in 2009 to pre-emptively treat a German scientist who might have been infected during a lab accident. However, actual EBOV infection could never be demonstrated without a doubt. Experimentally, recombinant vesicular stomatitis Indiana virus (VSIV) expressing the glycoprotein of EBOV or SUDV has been used successfully in nonhuman primate models as post-exposure prophylaxis.[clarification needed]
Ebola viruses are World Health Organization Risk Group 4 pathogens, requiring biosafety level 4-equivalent containment. Laboratory researchers must be properly trained in BSL-4 practices and wear proper personal protective equipment.
No ebolavirus-specific treatment exists. Treatment is primarily supportive in nature and includes minimizing invasive procedures, balancing fluids and electrolytes to counter dehydration, administration of anticoagulants early in infection to prevent or control disseminated intravascular coagulation, administration of procoagulants late in infection to control hemorrhaging, maintaining oxygen levels, pain management, and administration of antibiotics or antimycotics to treat secondary infections. Early treatment may increase the chance of survival.
The disease has a high mortality rate: often between 50 percent and 90 percent. If an infected person survives, recovery may be quick and complete. Prolonged cases are often complicated by the occurrence of long term problems, such as inflammation of the testicles, joint pains, muscle pains, skin peeling, or hair loss. Eye symptoms, such as light sensitivity, excess tearing, iritis, iridocyclitis, choroiditis and blindness have also been described. EBOV and SUDV may be able to persist in the semen of some survivors, which could give rise to infections and disease via sexual intercourse.
For more about specific outbreaks and their descriptions, see List of Ebola outbreaks.
CDC worker incinerates medical waste from Ebola patients in Zaire in 1976
While investigating an outbreak of Simian hemorrhagic fever virus (SHFV) in November 1989, an electron microscopist from USAMRIID discovered filoviruses similar in appearance to Ebola in tissue samples taken from crab-eating macaque imported from the Philippines to Hazleton Laboratories Reston, Virginia.
Blood samples were taken from 178 animal handlers during the incident. Of those, six animal handlers eventually seroconverted. When the handlers did not become ill, the CDC concluded that the virus had a very low pathogenicity to humans.
Because of the virus’s high mortality, it is a potential agent for biological warfare.
Given the lethal nature of Ebola, and since no approved vaccine or treatment is available, it is classified as a biosafety level 4 agent, as well as a Category A bioterrorism agent by the Centers for Disease Control and Prevention. It has the potential to be weaponized for use in biological warfare. The BBC reports in a study that frequent outbreaks of Ebola may have resulted in the deaths of 5,000 gorillas.
2007 to 2011
As of 30 August 2007, 103 people (100 adults and three children) were infected by a suspected hemorrhagic fever outbreak in the village of Kampungu, Democratic Republic of the Congo. The outbreak started after the funerals of two village chiefs, and 217 people in four villages fell ill. The World Health Organization sent a team to take blood samples for analysis and confirmed that many of the cases were the result of Ebolavirus. The Congo’s last major Ebola epidemic killed 245 people in 1995 in Kikwit, about 200 miles (320 km) from the source of the August 2007 outbreak.
On 30 November 2007, the Uganda Ministry of Health confirmed an outbreak of Ebola in the Bundibugyo District. After confirmation of samples tested by the United States National Reference Laboratories and the Centers for Disease Control, the World Health Organization confirmed the presence of a new species of Ebolavirus, which was tentatively named Bundibugyo. The epidemic came to an official end on 20 February 2008. While it lasted, 149 cases of this new strain were reported, and 37 of those led to deaths.
An International Symposium to explore the environment and filovirus, cell system and filovirus interaction, and filovirus treatment and prevention was held at Centre Culturel Français, Libreville, Gabon, during March 2008. The virus appeared in southern Kasai Occidental on 27 November 2008, and blood and stool samples were sent to laboratories in Gabon and South Africa for identification.
On 25 December 2008, it was reported that the Ebola virus had killed 9 and infected 21 people in the Western Kasai province of the Democratic Republic of Congo. On 29 December, Doctors Without Borders reported 11 deaths in the same area, stating that a further 24 cases were being treated. In January 2009, Angola closed down part of its border with the Democratic Republic of Congo to prevent the spread of the outbreak.
On 12 March 2009, an unidentified 45-year-old scientist from Germany accidentally pricked her finger with a needle used to inject Ebola into lab mice. She was given an experimental vaccine never before used on humans. Since the peak period for an outbreak during the 21-day Ebola incubation period had passed as of 2 April 2009, she had been declared healthy and safe. It remains unclear whether or not she was ever actually infected with the virus.
In May 2011, a 12-year-old girl in Uganda died from Ebola (Sudan subspecies). No further cases were recorded.
In July 2012, the Ugandan Health Ministry confirmed 13 deaths due to an outbreak of the Ebola-Sudan variant in the Kibaale District. On 28 July, it was reported that 14 out of 20 (70% mortality rate) had died in Kibaale. On 30 July, Stephen Byaruhanga, a health official in Kibaale District, said the Ebola outbreak had spread from one remote village to several villages.
The World Health Organization‘s (WHO) global and alert response network reported on August 3 that the suspected case count had risen to 53, including 16 deaths. Of these cases, five were confirmed by UVRI as Ebola cases. There were no confirmed cases outside of Kibaale District except for a patient who was medically evacuated to Kampala District and then died. WHO and CDC support was on the ground in Uganda supporting the government response. There were no confirmed cases outside of Uganda. Included among populations confirmed to be affected were prisoners in Kabbale prison.  Dr. Joaquim Saweka, the WHO representative to Uganda, reported that the outbreak was under control and that everyone known to have had contact with a known Ebola patient was in isolation.
On 8 August, the Ugandan Ministry of Health recorded 23 probable and confirmed cases, including 16 deaths. Ten cases were confirmed by the Uganda Virus Research Institute as Ebola. 185 people who came into contact with probable and confirmed Ebola cases were followed during the incubation period of 21 days.
On 17 August, the Ministry of Health of the Democratic Republic of the Congo reported an outbreak of the Ebola-Bundibugyo variant in the eastern region. By 21 August, the WHO reported a total of 15 cases and 10 fatalities. No evidence suggested that this outbreak was connected to the Ugandan outbreak. By 13 September 2012, the WHO revealed that the virus had claimed 32 lives and that the probable cause of the outbreak was tainted bush meat hunted by local villagers around the towns of Isiro and Viadana.
Main article: 2014 West Africa Ebola outbreakpIn February 2014, a strain of the Ebola Virus appeared in Guinea. This is the first Ebola virus outbreak registered in the region. As of April 10, 157 suspected and confirmed cases and 101 deaths were reported in Guinea, 22 suspected cases in Liberia including 14 deaths, 8 suspected cases in Sierra Leone including 6 deaths, and 1 suspected case in Mali. Investigations on these are under way.By late June 2014 the death toll had reached 390 with over 600 cases reported. By 23 July 2014, the World Health Organization had reported 1201 confirmed cases including 672 deaths since the epidemic began in March. On July 31 2014, WHO reports the death toll has reached 826 from 1440 cases. 
Emory University Hospital was the first US hospital to care for patients exposed to Ebola. Two American medical providers, Kent Brantly and Nancy Writebol, were exposed while treating infected patients in Liberia. Arrangements were made for them to be transported to Emory via speciality aircraft. Emory Hospital has a specially built isolation unit set up in collaboration with the CDC to treat patients exposed to certain serious infectious diseases. On 2 August 2014 Brantly was flown in to Dobbins Air Force Base in Marietta, Georgia, and transferred to Emory Hospital.
For more about the outbreak in Virginia, see Reston virus.
Cases of ebola fever in Africa from 1979 to 2008.
Ebola virus first emerged in 1976 in outbreaks of Ebola hemorrhagic fever in Zaire and Sudan. The strain of Ebola that broke out in Zaire has one of the highest case fatality rates of any human virus, roughly 90%.
In 1990, Hazelton Research Products’ Reston Quarantine Unit in Reston, Virginia suffered a mysterious outbreak of fatal illness among a shipment of Crab-eating Macaque monkeys imported from the Philippines. The company’s veterinary pathologist sent tissue samples from dead animals to the United States Army Medical Research Institute of Infectious Diseases (USAMRIID) at Fort Detrick, Maryland, where a laboratory test known as an ELISA assay showed antibodies to Ebola virus.
Shortly afterward, a US Army team headquartered at USAMRIID went into action to euthanize the monkeys which had not yet died, bringing those monkeys and those which had already died of the disease to Ft. Detrick for study by the Army’s veterinary pathologists and virologists, and eventual disposal under safe conditions.
The Philippines and the United States had no previous cases of Ebola infection, and upon further isolation researchers concluded it was another strain of Ebola, or a new filovirus of Asian origin, which they named Reston ebolavirus (REBOV) after the location of the incident.
Some scientists also believe that the Plague of Athens, which wiped out about a third of its inhabitants during the Peloponnesian War, may have been caused by Ebola. However, these studies are conflicting, and point to other possible diseases such as typhoid.
In general, outbreaks of EVD among human populations result from handling infected wild animal carcasses. In general, declines in animal populations precede outbreaks among human populations. Since 2003, such declines have been monitored through surveillance of animal populations with the aim of predicting and preventing EVD outbreaks in humans. Recovered carcasses from gorillas contain multiple Ebola virus strains, which suggest multiple introductions of the virus. Bodies decompose quickly and carcasses are not infectious after three to four days. Contact between gorilla groups is rare, suggesting transmission among gorilla groups is unlikely, and that outbreaks result from transmission between viral reservoir and animal populations.
Outbreaks of EVD may have been responsible for an 88% decline in tracking indices of observed chimpanzee populations in 420 square kilometer Lossi Sanctuary between 2002 and 2003. Transmission among chimpanzees through meat consumption constitutes a significant 5.2 (1.3–21.1 with 95% confidence) relative risk factor, while contact between individuals, such as touching dead bodies and grooming, do not.
Hyperimmune equine immunoglobulin raised against EBOV was used in Russia to treat a laboratory worker who accidentally infected herself with EBOV. The treatment, however, was unsuccessful in saving her life.[clarification needed] Other promising experimental therapeutic regimens rely on antisense technology. Both small interfering RNAs (siRNAs) and phosphorodiamidate morpholino oligomers (PMOs) targeting the EBOV genome could prevent disease in nonhuman primates.
Researchers from the U.S. Army Medical Research Institute of Infectious Diseases also found that FDA-approved estrogen receptor drugs used to treat infertility and breast cancer (clomiphene and toremifene) inhibit the progress of Ebola virus in infected mice. Ninety percent of the mice treated with clomiphene and fifty percent of those treated with toremifene survived the tests. The authors of the study concluded that given their oral availability and history of human use, these drugs would be excellent candidates for repurposing efforts to treat Ebola virus infection in remote geographical locations, either on their own or together with other antiviral drugs.
During an outbreak in the Democratic Republic of the Congo in 1995, seven of eight patients having received blood transfusions from convalescent individuals survived. However, this potential treatment is considered controversial.
Why Experts Were Surprised That Ebola-Infected Doctor Could Walk Into a Hospital
Aug 2, 2014, 5:16 PM ET
By GILLIAN MOHNEY via World News
Plane Carrying American Ebola Victim Lands in Georgia
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The fact that an Ebola-infected American was able to walk into a Georgia hospital today after his return to the United States surprised even medical experts familiar with the ravages of the deadly disease.
Dr. Kent Brantly arrived at Emory University Hospital today after being evacuated from Monrovia, Liberia where he was being treated for Ebola. Although Brantly had shown signs of the disease for the past week, he managed to walk into the hospital with the support of medical personnel.
All three wore protective gear to contain the deadly virus.
Brantly, along with missionary Nancy Writebol, was infected with the disease after working with Ebola-infected patients in Liberia’s capital city. This current Ebola outbreak is the worst on record and has killed more than 700 in three countries in West African and infected more than 1,300.
Before Brantly arrived in Atlanta, not much about his condition had been made public. According to Samaritan’s Purse, the aid organization he was working for, Brantly was in "serious but stable" condition before being flown to the U.S.
When the doctor was able to walk into the hospital, at least two experts said they were surprised but pleased that the doctor seemed to be doing well.
This strain of the Ebola virus has a fatality rate of approximately 60 percent and past outbreaks had fatality rates as high as 90 percent.
Dr. William Schaffner, an infectious disease specialist at Vanderbilt University School of Medicine, said he felt "guardedly optimistic," since Ebola usually advances quickly and Brantly had shown signs of the disease for at least a week.
"The first thing we all said ‘Whoa he’s not on a vent,’" Schaffner said of realizing that Brantly did not need a ventilator to help him breathe. "In general [with] Ebola is … you progress on a downhill course. If you’re at this point and you’re holding your own you’re entitled to be optimistic."
Courtesy Samaritans Purse
PHOTO: Dr. Kent Brantly speaks with a worker outside the ELWA Hospital in Monrovia, Liberia
While the incubation period can last from eight to 21 days, once someone develops symptoms they can be sick for a wider range of time. Schaffner explained that when someone shows signs of Ebola they tend to go downhill fairly rapidly and consistently.
Scaffner explained that once a person shows signs of Ebola the symptoms don’t usually disappear until the person overcomes the virus. As a result, they don’t usually have periods where they could appear healthy and relapse.
Schaffner said the fact that Brantly appeared to be well enough to walk, indicates that at least for the moment his heart rate, respiratory rate and other vital signs were not critical.
Dr. Stephen Morse, a professor of Epidemiology at the Columbia University Mailman School of Public Health, said although it does not guarantee Brantly will fully recover, the fact that he could walk 10 days after showing Ebola symptoms is a "good sign."
"If you can walk in, that’s a very good sign. I was surprised but pleasantly," Morse said of seeing Brantly walk to the hospital entrance.
Jack Kearse/Emory University
PHOTO: The Ebola-stricken Americans will be treated this isolation rooms and others similar to it.
Morse said that Brantly was obviously not out of the woods and that he would be under constant monitoring to ensure his blood pressure, lung function, kidney function and other vitals remained steady.
"If he really does get better, we want to know his secret," Morse said.
After Brantly’s arrival, his wife Amber Brantly released a statement saying she is relieved her husband has arrived in the U.S.
"It was a relief to welcome Kent home today," Amber Brantly said in a statement. "I spoke with him, and he is glad to be back in the U.S. I am thankful to God for his safe transport and for giving him the strength to walk into the hospital."
2nd American With Ebola Expected to Arrive in U.S. Tuesday
Odd of a pandemic in America increases
Image Credits: Public domain
by ABC News | August 3, 2014
The plane carrying the second American patient who contracted Ebola while working in Liberia will leave the U.S. for the West African country later today and is expected to return Tuesday, a U.S. official told ABC News.
The private air ambulance is scheduled to take off today and arrive in Liberia after one stopover, the official said. The plane will then bring aid worker Nancy Writebol to Dobbins Air Reserve Base in Marietta, Ga., and is expected to land midday Tuesday.
The same plane brought Dr. Kent Brantly to Georgia on Saturday. He’s undergoing treatment at Emory University Hospital, where Writebol will be treated after she arrives in the U.S.
Ebola outbreak: Western drugs firms have not tried to find vaccine ‘because virus only affects Africans’, says UK’s top public health doctor
Professor John Ashton accuses pharmaceutical industry of ‘moral bankruptcy’
Sunday 03 August 2014
Britain’s leading public health doctor today blames the failure to find a vaccine against the Ebola virus on the "moral bankruptcy" of the pharmaceutical industry to invest in a disease because it has so far only affected people in Africa – despite hundreds of deaths.
Professor John Ashton, the president of the UK Faculty of Public Health, says the West needs to treat the deadly virus as if it were taking hold in the wealthiest parts of London rather than just Sierra Leone, Guinea and Liberia. Writing in The Independent on Sunday, Professor Ashton compares the international response to Ebola to that of Aids, which was killing people in Africa for years before treatments were developed once it had spread to the US and UK in the 1980s.
He writes: "In both cases [Aids and Ebola], it seems that the involvement of powerless minority groups has contributed to a tardiness of response and a failure to mobilise an adequately resourced international medical response.
"In the case of Aids, it took years for proper research funding to be put in place and it was only when so-called ‘innocent’ groups were involved (women and children, haemophiliac patients and straight men) that the media, politicians, scientific community and funding bodies stood up and took notice."
The Ebola outbreak has so far claimed the lives of at least 729 people across Liberia, Guinea, Sierra Leone and Nigeria, according to the latest figures from the World Health Organisation (WHO), although the number is likely to be far higher.
Yesterday, a US relief organisation confirmed that two US aid workers who contracted the disease in Liberia had left the country. Dr Kent Brantly was being treated in a specialised hospital unit in Atlanta, Georgia, after becoming the first person with the disease to arrive on US soil yesterday evening. The second aid worker, Nancy Writebol, was due to land on a separate private flight.
On Friday, the WHO warned that the outbreak in West Africa was "moving faster than our efforts to control it". The organisation’s director general, Dr Margaret Chan, warned that if the situation continued to deteriorate, the consequences would be "catastrophic" to human life. Professor Ashton believes that more money must be funnelled into research for treatment.
"We must respond to this emergency as if it was in Kensington, Chelsea and Westminster. We must also tackle the scandal of the unwillingness of the pharmaceutical industry to invest in research [on] treatments and vaccines, something they refuse to do because the numbers involved are, in their terms, so small and don’t justify the investment. This is the moral bankruptcy of capitalism acting in the absence of a moral and social framework."
Western countries are on high alert after Patrick Sawyer, a civil servant for the Liberian government, died last week after arriving at Lagos airport – the first known case in Nigeria. International airline hubs are the focus of attention because of the high volume of passengers flying into and out of West Africa every day. Dubai’s Emirates airline began a ban yesterday on its flights in Guinea over the crisis, with the suspension lasting until further notice.
Professor Ashton welcomed the decision by the Foreign Secretary, Philip Hammond, to convene a meeting of the Government’s crisis committee, Cobra, last week to discuss the UK’s preparedness for cases of Ebola in this country.
Development of a vaccine is in the early stages in the US, but this is on a small scale and there is little hope of one being ready to treat the current outbreak in West Africa. Dr Anthony Fauci, the director of the National Institutes of Health, an agency of the US Department of Health and Human Services, has said it has plans possibly to begin testing an experimental Ebola vaccine on people in mid-September, following encouraging results in pre-clinical trials on monkeys. Earlier this month, the US Food and Drug Administration put a hold on a trial upon healthy volunteers by Tekmira Pharmaceuticals Corporation to ensure their potential Ebola treatment has no ill-effects, as it sought more information to ensure the safety of volunteers.
Professor Ashton said: "The real spotlight needs to be on the poverty and environmental squalor in which epidemics thrive and the failure of political leadership and public health systems to respond effectively. The international community has to be shamed into real commitment… if the root causes of diseases like Ebola are to be addressed."
Ebola: covert op in a hypnotized world
Image Credits: YouTube
by Jon Rappoport | August 3, 2014
You show people a germ and you tell them what it is and what it does, and people salute. They give in. They believe. They actually know nothing. But they believe.
The massive campaign to make people believe the Ebola virus can attack at any moment, after the slightest contact, is quite a success.
People are falling all over themselves to raise the level of hysteria.
This is what is preventing a hard look at Liberia, Sierra Leone, and the Republic Guinea, three African nations where poverty and illness are staples of everyday life for the overwhelming number of people.
The command structure in those areas has a single dictum: don’t solve the human problem.
Don’t clean up the contaminated water supplies, don’t return stolen land to the people so they can grow food and finally achieve nutritional health, don’t solve overcrowding, don’t install basic sanitation, don’t strengthen their immune systems so they can ward off germs, don’t let the people have power—because then they would throw off the local and global corporate juggernauts that are sucking the land of all its resources.
In order not to solve the problems of the people, a cover story is necessary. A cover story that exonerates the power structure.
A cover story like a germ.
It’s all about the germ. The demon. The strange attacker. (See, for example, this March 27th, Reuter’s article entitled “Beware of bats: Guinea issues bushmeat warning after Ebola outbreak”.)
Forget everything else. The germ is the single enemy.
Forget the fact, for example, that a recent study of 15 pharmacies and 5 hospital drug dispensaries in Sierra Leone discovered the widespread and unconscionable use of beta-lactam antibiotics.
These drugs are highly toxic. One of their effects? Excessive bleeding.
Which just happens to be the scary “Ebola effect” that’s being trumpeted in the world press.
(J Clin Microbiol, July 2013, 51(7), 2435-2438), and Annals of Internal Medicine Dec. 1986, “Potential for bleeding with the new beta-lactam antibiotics”)
Forget the fact that pesticide companies are notorious for shipping banned toxic pesticidesto Africa. One effect of the chemicals? Bleeding.
Forget that. It’s all about the germ and nothing but the germ.
Forget the fact that, for decades, one of the leading causes of death in the Third World has been uncontrolled diarrhea. Electrolytes are drained from the body, and the adult or the baby dies.
Any sane doctor would make it his first order of business to replace electrolytes with simple supplementation—but no, the standard medical line goes this way:
The diarrhea is caused by germs in the intestinal tract, so we must pile on massive amounts of antibiotics to kill the germs.
The drugs kill off all bacteria in the gut, including the necessary and beneficial ones, and the patient can’t absorb what little food he has access to, and he dies.
Along the way, he can also bleed.
But no, all the bleeding comes from Ebola. It’s the germ. Don’t think about anything else.
Forget the fact that adenovirus vaccines, which have been used in Liberia, Guinea, and Liberia (the epicenter of Ebola), have, according to vaccines.gov, the following adverse effects: blood in the urine or stool, and diarrhea.
No, all the bleeding comes from the Ebola germ. Of course. Don’t think about anything else.
Reporter Charles Yates uncovered a scandal in Liberia centering around the Firestone Rubber Plantation—chemical dumping, poisoned water.
And skin disease.
“Rash” is listed as one of the Ebola symptoms.
So is diarrhea.
Liberia Coca Cola bottling plant: foul black liquid seeping into the environment—animals dying.
Chronic malnutrition and starvation—conditions that are endemic in Liberia, Sierra Leone, and Guinea—are the number-one cause of T-cells depletion in the world.
T-cells are a vital component of the immune system. When that system is compromised, any germ coming down the pipeline will cause epidemics and death.
Getting the picture?
Blame it all on the germ.
Allow the corporate-government domination to continue.