AND IN EAST NY BROOKLYN, A 27 YR OLD PREGNANT BLACK WOMAN IS ATTACKED BY NYPD

IN ANOTHER CHOKEHOLD CASE

YUP ANOTHER WHITE ASS STUPID FUCKING DOUCHE BAG COP

TRYING TO STRANGLE A BLACK WOMAN

BECAUSE SHE WAS ILLEGALLY GRILLING HAMBURGERS ON A GRILL

BIG MAN HAD TO BRING HER DOWN!

WHITE COPS SHOULD STAY THE FUCK OUT OF BLACK HOODS

GIVE ME A FUCKING BREAK!?

AND I GUESS IT WAS IMPERATIVE THAT HE DO THIS IN FRONT OF HER KID?

WHY DID HE EVEN TOUCH THIS WOMAN!

IF I WERE HER I’D SUE HIM FOR ATTEMPTED RAPE ON A PREGNANT WOMAN

THAT’S WHAT I’D DO!

=========================================================

Pregnant Woman Allegedly Put In Chokehold By NYPD Officer

Posted: 07/28/2014 6:54 pm EDT Updated: 3 hours ago

A New York City police officer allegedly placed a 27-year-old pregnant woman in a chokehold Saturday after she was accused of illegally grilling in East New York, Brooklyn. The incident was captured on camera.

Photos first published by the New York Daily News appear to show an unidentified member of the New York City Police Department wrapping his arms around Rosan Miller’s neck and upper torso as her daughter watches nearby. Miller was uninjured but was given a summons for disorderly conduct, the outlet reported.

Advocacy group People Organizing and Working for Empowerment and Respect released images of the incident Monday to the Daily News.

“She was grilling in front of her home, not committing any crime,” former City Councilman Charles Barron told The New York Post of the incident. “We want these people out of our community.”

Use of the chokehold by New York police officers has been banned for more than 20 years, according to Reuters. Yet the outlet reports that the department has a “backlog” of chokehold complaints currently under investigation.

The latest chokehold incident comes just over a week after Staten Island man Eric Garner died while being placed in a chokehold by a member of the NYPD. At the time, Garner was being arrested on charges stemming from illegal cigarette sales. A bystander captured the incident on video.

After a meeting with Garner’s family and federal prosecutors in Brooklyn on Friday, activist Rev. Al Sharpton called for an end to the use of the chokehold nationwide.

“We cannot just depend — and this is important — on police policy to stop the choke hold,” Sharpton said, per Reuters. “We need a federal precedent.”

======================================================

An NYPD cop puts his arm around Rosan Miller's neck in an apparent chokehold, which is prohibited by the department.

Rosan Miller struggles against the cop over the weekend in Brooklyn.

Former city councilman Charles Barron points out the woman's daughter can be seen watching her mother's arrest.

The seven-months-pregnant Rosan Miller struggles over the weekend.

Rosan Miller (above), her husband Moses Miller and brother John Miller were all arrested.

MALAYSIA FLIGHT 17 BLACK BOX SAYS IT WAS A MISSILE – RUSSIA MAY BE TRIED FOR WAR CRIME

I HOPE THEY KICK RUSSIA AND PUTIN ASSHOLES

UNTIL THEY ARE BLOODY AND CAN’T SIT DOWN

AND THEN SANCTION THE SHIT OUT OF THAT COUNTRY

ISOLATING IT FOR YEARS TO COME.

RUSSIANS ARE ASSHOLES

AND I HOPE THEY ALL DIE FOR THIS

[==========================================================

STORYLINEComplete coverage of Malaysia Airlines Flight MH17, which was shot down near the Ukraine-Russia border with 298 people aboard on July 17, 2014.

THEN WHEN I THINK I’VE HEARD IT ALL-WHOOPI GOLDBERG DEFENDS HER BLACK BROTHER STEPHEN A SMITH

OF COURSE SHE DID

SHE WON’T SLEEP WITH HIM

NOR WILL SHE ACKNOWLEDGE HE’S ALIVE IN ANY WAY

BUT SHE WILL AGREE WITH HIM

BECAUSE ISN’T THAT WHAT ALL BLACK WOMEN DO

STAND BY THEIR MEN?

NOT ALL BLACK WOMAN ARE LIKE HER

AND NOT ALL BLACK MEN ABUSE THEIR WIVES

BUT WHEN THEY DO

THEY ARE LOW DOWN NIGGER SHIT IN MY BOOK

AND ANY OTHER MAN OF ANY OTHER COLOR

WHO BEATS ON HIS WIFE

NEEDS TO HAVE HIS PENIS RETRACTED THE HARD WAY!

Goldberg is a hypocrite – if she’s so black why does she always run after the white guys?

She couldn’t get a man with perfect vision if she tried. And I know that if Rosie O’Donnell were on that show

The day she said this shit – they’d be a fucking fight.

===================================================================

Whoopi Goldberg Defends Stephen A. Smith’s Controversial Comments On Domestic Violence

Posted: 07/28/2014 5:36 pm EDT Updated: 3 hours ago

Print Article

–“The View” co-host Whoopi Goldberg defends Stephen A. Smith’s controversial stance on domestic violence. (The View)

whoopi goldberg

I would love to give her a shot in her ugly face. I’m going to tell her off on Twitter.

Quick Poll

Do you agree with Whoopi’s comment?

Yes

72.83%

No

27.17%

NEW HORROR TV SHOW ‘THE STRAIN’ IS BALL DROPPING-LY HILARIOUS

SO IN THIS WEEK’S INSTALLMENT, SPTLY NAMED

EPISODE 3

OF PRODUCER GUILLERMO DEL TORO’S EPIC TRILOGY “THE STRAIN

THE GOTH ROCKER STANDS OVER THE TOILET AND PISSED

AND THEN WATCHES AS HIS PENIS FALLS INTO THE HOLE AND HE FLUSHES IT DOWN THE TUBES.

I WISH THAT COULD REALLY HAPPEN TO ALL THE PAEDOPHILES, RAPISTS AND MORONIC MEN

WHO THINK THEIR DICK IS GOD’S GIFT TO WOMAN.

NOTE TO MORONS:

NO

IT’S

NOT

====================================================

This article below says it’s shocking but I think it’s hilarious!

The Strain: A Haunting Glimpse of the Vampire Race

Original | Shawn S. Lealos, Originals

Published July 28, 2014 02:01AM EDT

This photo released by FX shows Cory Stoll, left, as Ephraim Goodweather, in a scene from the TV ser
This photo released by FX shows Cory Stoll, left, as Ephraim Goodweather, in a scene from the TV series, “The Strain.” (AP Photo/FX, Michael Gibson) (ASSOCIATED PRESS)

Last week’s episode of The Strain was a bit of a let down but things got rolling again on Sunday night. FX’s vampire series exploded off the blocks with the CDC team getting an up-close look at the scary phenomenon they are facing and viewers learned a lot more about vampire Thomas Eichorst (Richard Sammel).

The Strain starring Corey Stoll, Sean Astin and Mia Maestro airs on FX Sundays at 10 pm ET.

The Charade

The episode began with a vampire literally putting on his face. The vampire looked a lot like Lord Voldemort from the Harry Potter movies, a white smooth face missing the nose and ears. The man behind the mask turned out to be Thomas Eichorst and the scene displayed how he is able to look human while the others disintegrate and change into vampires. He then admitted that his charade will soon end. This was a great way to open the show and did a lot to explain the world of the vampires that will soon start to form.

The Survivors Continue to Change

Sunday night’s episode focused heavily on the survivors from the plane. While Captain Redfern (Jonathan Potts) remains in the hospital under observation, the other survivors started to see their lives fall apart. Missing in action this week was the lawyer Joan (Leslie Hope), but returning after not showing up last week was the fourth survivor Ansel (Nikolai Witschl), who is visibly sick and scared his with to death when he guzzled steak blood. Although that sounds creepy, it was the Goth rocker Gabriel Bolivar (Jack Kesy) who won the creepiest moment in this episode. Last week he bit a groupie during an orgy, and this week made certain he would never participate in an orgy again when he lost his manliest tool. It seems that vampires don’t only grow teeth, lose their hair and have blood-red eyes; they’re asexual too. This was a hugely shocking moment. (all they do is feed~!)

Beat that Marilyn Manson!!!

Jim Kent’s Two Bosses

In the premiere episode of The Strain, Jim Kent (Sean Astin) betrayed his team – and the human race – when he let the truck transporting a coffin pass through the security checkpoint. This week, The Strain showed why, as Jim’s wife Sylvia (Melanie Merkosky) has cancer and he betrayed his team for money to help her. Of course, he didn’t know what he was unleashing, so he can be forgiven. Unfortunately, his moral conflict is far from over. When he threatened to go to the police about the incident, Eichorst gave Jim great news, informing him that he could get Sylvia into an experimental drug program that could cure her cancer. As a result, Jim learned he now has two bosses, Eichorst being the second and the CDC being the first. Of course, he doesn’t know Eichorst is a vampire, so maybe his wife may not be going to the best place for her cure.

The Rats Are Scared

The exterminator Vasiliy Fet (Kevin Durand) was back this week and he got a huge clue as to the coming danger. The city is experiencing a rat infestation and the rats are attacking homes, schools and hospitals. Fet was sent to a large house to exterminate a rat that bit a little girl. After finishing the job, Fet stepped out the door and saw dozens of rats heading towards water, scurrying from tunnels and drainage ditches. It seems that Vasiliy Fet will become a very important part of The Strain’s storyline this season.

The Battle Begins

Abraham Setrakian (David Bradley) convinced a judge to release him by acting like a feeble old man. He left the courthouse and Nora (Mia Maestro) stopped him to ask for help. They had a chat and he realized that she was not willing to accept burning all the dead bodies. He told her she was not worth his time. Next we saw that Abraham had gotten ahold of a list of dead passengers’ addresses and it looks as if he’s off to exterminate the dead. Meanwhile, the one plane survivor who did the right thing after the plane incident, pilot Doyle (Jonathan Potts), escaped from his hospital room and headed to the basement and started to eat. In true horror fashion, this once-good man turned pure evil in an instant and attacked Jim Nora and Eph (Corey Stoll). Doyle is the first survivor to turn full-fledged vampire. The episode fades to black as Doyle’s head is smashed by a fire extinguisher-wielding Eph.

With that death, the war is officially on. Now, the question has to be how Eph and his team explain murdering the pilot. There is also the question of the rats, the loss of the rocker’s penis, Jim Kent’s morality, and the murders that Abraham has planned. There are a lot more questions than answers at this point, but The Strain has perfected the art of freaking out its audience.

 

 

t

The master

 

 

I WAS WRONG ABOUT HOW EBOLA VIRUS IS SPREAD

EBOLA

LIKED AIDS

IS SPREAD THROUGH BODILY FUNCTIONS

or the exchange of bodily functions

So it’s plausible that the two Aid Workers – one is a doctor – are sick

is because they came in contact with blood or a patient’s bodily fluid (piss/shit)

The Africans are not clean people

That is why this virus is so widespread there

But I still think that the uniforms that the doctors wear there are not good

HAZMAT would have been better and they should have had protection on even when NOT WITH

PATIENTS

SO IF THE DOCTORS WIFE AND TWO KIDS WERE NOT AT THE CLINIC AND DID NOT HAVE ANY PISS/SHIT OR CONTACT WITH ANYONE WHO HAS THIS DISEASE

THE CHANGES OF THEM GETTING IT OR SPREADING IT IS NIL

HOWEVER THE DOCTOR, THEIR 33 YEAR OLD FATHER, IS A DEAD MAN.

THERE IS NO CURE FOR THIS EBOLA VIRUS

===================================================================

Ebola virus disease

From Wikipedia, the free encyclopedia
“Ebola” redirects here. For other uses, see Ebola (disambiguation).
Ebola virus disease
Classification and external resources
7042 lores-Ebola-Zaire-CDC Photo.jpg

1976 photograph of two nurses standing in front of Mayinga N., a patient with Ebola virus disease; she died only a few days later due to severe internal hemorrhaging.
ICD-10 A98.4
ICD-9 065.8
DiseasesDB 18043
MedlinePlus 001339
eMedicine med/626
MeSH D019142

Ebola virus disease (EVD) or Ebola hemorrhagic fever (EHF) is the human disease caused by ebola viruses. Symptoms start two days to three weeks after contracting the virus with a fever, throat and muscle pains, and headaches. There is then nausea, vomiting and diarrhea along with decreased functioning of the liver and kidneys. At this point some people begin to have problems with bleeding.[1]

The disease is first acquired by a population when a person comes into contact with the blood or bodily fluids of an infected animal such as a monkey or fruit bat. Fruit bats are believed to carry and spread the disease without being affected by it. Once infection occurs, the disease may be spread from one person to another. Men who survive may be able to transmit the disease sexually for nearly two months. To make the diagnosis, typically other diseases with similar symptoms such as malaria, cholera and other viral hemorrhagic fever are excluded. The blood may then be tested for either antibodies to the virus, the viral RNA, or the virus itself to confirm the diagnosis.[1]

Prevention involves decreasing the spread of the disease from infected monkeys and pigs to humans. This may be done by checking these 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 be helpful, as may wearing protective clothing and washing hands when around someone sick with the disease. Samples from people with the disease should be handled with an extra degree of caution.[1]

There is no specific treatment for the virus with efforts to help people including giving the person either oral rehydration therapy orintravenous fluids.[1] The disease has a high death rate: often between 50% and 90%.[1][2] It typically occurs in outbreaks in tropical regions of Sub-Saharan Africa.[1] Between 1976, when it was first identified, and 2014, fewer than 1,000 people a year have been infected.[1][3] The largest outbreak to date is the ongoing 2014 West Africa Ebola outbreak, which is affecting Guinea, Sierra Leone,Liberia, and Nigeria. The disease was first identified in the Sudan and the Democratic Republic of the Congo. Efforts are ongoing to develop a vaccine; however, none exists as of 2014.[1]

Signs and symptoms[edit]

Manifestation of Ebola begins abruptly with a sudden onset of an influenza-like stage characterized by general malaise, fever with chills, sore throat, severe headache, weakness, joint pain, muscle pain, and chest pain.[4] Respiratory tract involvement is characterized by pharyngitis with sore throat, cough, dyspnea, and hiccups. The central nervous systemis affected as judged by the development of severe headaches, agitation, confusion, fatigue, depression, seizures, and sometimes coma.

Cutaneous presentation may include: maculopapular rash, petechiae, purpura, ecchymoses, and hematomas (especially around needle injection sites). In general, development of hemorrhagic symptoms is indicative of a negative prognosis. However, contrary to popular belief, hemorrhage 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 dysfunction syndrome (MODS) due to fluid redistribution, hypotension, disseminated intravascular coagulation, and focal tissue necroses.

The average time between contracting the infection and the onset of symptoms is 13 days, but can be as long as 25 days.[5]

Hemorrhage[edit]

All people infected show some extent of coagulopathy and impaired circulatory system symptomology.[6] Bleeding from mucous membranes and puncture sites is reported in 40–50% of cases,[7] while maculopapular rashes are evident in approximately 50% of cases.[6] Sources of bleeds include hematemesis, hemoptysis, melena, and aforementioned bleeding from mucous membranes (gastrointestinal tract, nose, vagina and gingiva). However diffuse bleeding (i.e. heavy) is rare; occurrence is usually exclusive to the gastrointestinal tract.[6][8]

Causes[edit]

Main article: Ebolavirus

EVD is caused by four of five viruses classified in the genus Ebolavirus, family Filoviridae, order Mononegavirales: Bundibugyo virus (BDBV), Ebola virus (EBOV), Sudan virus(SUDV), Taï Forest virus (TAFV). The fifth virus, Reston virus (RESTV), is thought to be not disease causing for humans and therefore not discussed here.

Transmission[edit]

EVD is believed to occur after an ebola virus is transmitted to a human index case via contact with an infected animal host.[citation needed] Human-to-human transmission occurs 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 such as needles.[citation needed] In the past, explosive nosocomial transmission has occurred in under-equipped African hospitals due to the reuse of needles and lack of implementation ofuniversal precautions.[citation needed] Aerosol transmission has not been observed during natural EVD outbreaks.[citation needed] The potential for widespread EVD epidemics is considered low due to the high case-fatality rate, the rapidity of demise of patients, and the often remote areas where infections occur.[citation needed]

Risk factors[edit]

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.[9]

Between 1976 and 1998, in 30,000 mammals, birds, reptiles, amphibians, and arthropods sampled from outbreak regions, no ebolaviruswas 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.[10][11] 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.[10]

Plants, arthropods, and birds have also been considered as possible reservoirs; however, bats are considered the most likely candidate.[12] Bats were known to reside in the cotton factory in which the index cases for the 1976 and 1979 outbreaks were employed, and they have also been implicated in Marburg virus infections in 1975 and 1980.[10] Of 24 plant species and 19 vertebrate species experimentally inoculated with EBOV, only bats became infected.[13]

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.[14] As of 2005, three types offruit 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.[15][16]

The existence of integrated genes of filoviruses in some genomes of small rodents, insectivorous bats, shrews, tenrecs, and marsupials indicates a history of infection with filoviruses in these groups as well.[17] However, it has to be stressed that infectious ebolaviruses have not yet been isolated from any nonhuman animal.

Bats drop partially eaten fruits and pulp, then terrestrial 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.[18] Transmission between natural reservoirs and humans are rare, and outbreaks are usually traceable to a single index case where an individual has handled the carcass of gorilla, chimpanzee, or duiker.[19] Fruit bats are also reported to be a treat eaten by people in parts of West Africa where they are smoked, grilled or made into a spicy soup.[16] The virus then spreads person-to-person, especially within families, hospitals, and during some mortuary rituals where contact among individuals becomes more likely.[20]

The virus has been confirmed to be transmitted through body fluids. Transmission through oral exposure and through conjunctiva exposure is likely[21] and has been confirmed in non-human primates.[22] Filoviruses are not naturally transmitted by aerosol. They are, however, highly infectious as breathable 0.8–1.2 micrometre droplets in laboratory conditions;[23] because of this potential route of infection, these viruses have been classified as Category A biological weapons.[24]

All epidemics of Ebola have occurred in sub-optimal hospital conditions, where practices of basic hygiene and sanitation are often either luxuries or unknown to caretakers and where disposable needles and autoclaves are unavailable or too expensive. In modern hospitals with disposable needles and knowledge of basic hygiene and barrier nursing techniques, Ebola has never spread on a large scale. In isolated settings such as a quarantined hospital or a remote village, most victims are infected shortly after the first case of infection is present. The quick onset of symptoms from the time the disease becomes contagious in an individual makes it easy to identify sick individuals and limits an individual’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.[25]

Virology[edit]

Main article: Ebola virus
Genus Ebolavirus: species and their EVD-causing viruses
Species name Virus name (abbreviation)
Bundibugyo ebolavirus (accepted)[26] Bundibugyo virus (BDBV; previously BEBOV)
Sudan ebolavirus Sudan virus (SUDV; previously SEBOV)
Taï Forest ebolavirus Taï Forest virus (TAFV; previously CIEBOV)
Zaire ebolavirus* Ebola virus (EBOV; previously ZEBOV)

Table legend: “*” denotes the type species and “accepted” refers to a taxon that has been accepted by the Executive Committee of the ICTV but that has yet to be ratified.

Genome[edit]

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.[27] 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.[28] 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[edit]

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.[28] 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 to be 795–828 nm), but particles as long as 14,000 nm have been detected in tissue culture.[29] Ebolavirions consist of seven structural proteins. At the center is the helical ribonucleocapsid, which consists of the genomic RNA wrapped around a polymer of nucleoproteins (NP). Associated with the ribonucleoprotein is the RNA-dependent RNA polymerase (L) with the polymerase cofactor (VP35) and a transcription activator (VP30). The ribonucleoprotein is embedded in a matrix, formed by the major (VP40) and minor (VP24) matrix proteins. These particles are surrounded by a lipid membrane derived from the host cell membrane. The membrane anchors a glycoprotein (GP1,2) that projects 7 to 10 nm spikes away from its surface. While nearly identical to marburgvirions in structure, ebolavirions are antigenically distinct.

Entry[edit]

Niemann–Pick C1 (NPC1) appears to be essential for Ebola infection. Two independent studies reported in the same issue of Nature showed that Ebola virus cell entry and replication requires the cholesterol transporter protein NPC1.[30][31] When cells from Niemann-Pick disease, type C1 patients (who have a mutated form of NPC1) were exposed to Ebola virus in the laboratory, the cells survived and appeared immune to the virus, further indicating that Ebola relies on NPC1 to enter cells. This might imply that genetic mutations in the NPC1 gene in humans could make some people resistant to one of the deadliest known viruses affecting humans. The same studies described similar results with Ebola’s cousin in the filovirus group, Marburg virus, showing that it too needs NPC1 to enter cells.[30][31] Furthermore, NPC1 was shown to be critical to filovirus entry because it mediates infection by binding directly to the viral envelope glycoprotein.[31] A later study confirmed the findings that NPC1 is a critical filovirus receptor that mediates infection by binding directly to the viral envelope glycoprotein and that the second lysosomal domain of NPC1 mediates this binding.[32]

In one of the original studies, a small molecule was shown to inhibit Ebola virus infection by preventing the virus glycoprotein from binding to NPC1.[31][33] In the other study, mice that were heterozygous for NPC1 were shown to be protected from lethal challenge with mouse adapted Ebola virus.[30] Together, these studies suggest NPC1 may be potential therapeutic target for an Ebola anti-viral drug.

Replication[edit]

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.[34]

Pathophysiology[edit]

Pathogenesis schematic

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.[35] 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.[36]

Diagnosis[edit]

EVD cannot be separated from Marburg virus disease based on symptoms. 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.[citation needed] 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 intoxication.[37][38][39][40]

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 reacting to infection with characteristic cytopathic effects.[41][42] 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.[29] 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[43][44][45][46][47][48][49] in conjunction with antigen-capture ELISA[50][51][52][53][54] 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.

Classification[edit]

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 andMarburg-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.[55]

Phylogenetic tree comparing the Ebolavirus and Marburgvirus. Numbers indicate percent confidence of branches.

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.[56] However, paleoviruses (genomic fossils) offiloviruses (Filoviridae) found in mammals indicate that the family itself is at least tens of millions of years old.[17] Fossilized viruses that are closely related to ebolaviruses have been found in the genome of the Chinese hamster.[57]

The five characterised Ebola species are:

Zaire ebolavirus (EBOV; previously ZEBOV) 
Also known simply as the Zaire virus, ZEBOV has the highest case-fatality rate of the ebolaviruses, up to 90% in some epidemics, with an average case fatality rate of approximately 83% over 27 years. There have been more outbreaks of Zaire ebolavirus than of any other species. The first outbreak occurred on 26 August 1976 in Yambuku.[58] The first recorded case was Mabalo Lokela, a 44‑year-old schoolteacher. The symptoms resembled malaria, and subsequent patients receivedquinine. Transmission has been attributed to reuse of unsterilized needles and close personal contact.
Sudan ebolavirus (SUDV; previously SEBOV) 
Like the Zaire virus, SEBOV emerged in 1976; it was at first assumed to be identical with the Zaire species.[59] SEBOV is believed to have broken out first among cotton factory workers in Nzara, Sudan (now South Sudan), with the first case reported as a worker exposed to a potential natural reservoir. The virus was not found in any of the local animals and insects that were tested in response. The carrier is still unknown. The lack of barrier nursing (or “bedside isolation”) facilitated the spread of the disease. The most recent outbreak occurred in May, 2004. Twenty confirmed cases were reported in Yambio County, Sudan (now South Sudan), with five deaths resulting. The average fatality rates for SEBOV were 54% in 1976, 68% in 1979, and 53% in 2000 and 2001.
Reston ebolavirus (RESTV; previously REBOV) 
Discovered during an outbreak of simian hemorrhagic fever virus (SHFV) in crab-eating macaques from Hazleton Laboratories (now Covance) in 1989. Since the initial outbreak in Reston, Virginia, it has since been found in non-human primates in Pennsylvania, Texas and Siena, Italy. In each case, the affected animals had been imported from a facility in the Philippines,[60] where the virus has also infected pigs.[61] Despite having a Biosafety status of Level‑4 and its apparent pathogenicity in monkeys, REBOV did not cause disease in exposed human laboratory workers.[62]
Côte d’Ivoire ebolavirus (TAFV; previously CIEBOV)
Also referred to as Taï Forest ebolavirus and by the English place name, “Ivory Coast”, it was first discovered among chimpanzees from the Taï Forest in Côte d’Ivoire, Africa, in 1994. Necropsies showed blood within the heart to be brown; no obvious marks were seen on the organs; and one necropsy showed lungs filled with blood. Studies of tissues taken from the chimpanzees showed results similar to human cases during the 1976 Ebola outbreaks in Zaire and Sudan. As more dead chimpanzees were discovered, many tested positive for Ebola using molecular techniques. The source of the virus was believed to be the meat of infected Western Red Colobus monkeys, upon which the chimpanzees preyed. One of the scientists performing the necropsies on the infected chimpanzees contracted Ebola. She developed symptoms similar to those of dengue fever approximately a week after the necropsy, and was transported to Switzerland for treatment. She was discharged from the hospital after two weeks and had fully recovered six weeks after the infection.[63]
Bundibugyo ebolavirus (BDBV; previously BEBOV)
On 24 November 2007, the Uganda Ministry of Health confirmed an outbreak of Ebolavirus in the Bundibugyo District. After confirmation of samples tested by the United States National Reference Laboratories and the CDC, the World Health Organization confirmed the presence of the new species. On 20 February 2008, the Uganda Ministry officially announced the end of the epidemic in Bundibugyo, with the last infected person discharged on 8 January 2008.[64] An epidemiological study conducted by WHO and Uganda Ministry of Health scientists determined there were 116 confirmed and probable cases of the new Ebola species, and that the outbreak had a mortality rate of 34% (39 deaths). In 2012, there was an outbreak of Bundibugyo ebolavirus in a northeastern province of the Democratic Republic of the Congo. There were 15 confirmed cases and 10 fatalities.[65]

Prevention[edit]

A researcher working with the Ebola virus while wearing a BSL-4 positive pressure suit to avoid infection

Ebola viruses are highly infectious as well as contagious. Governments and individuals often quickly respond to quarantine the area while the lack of roads and transportation in many parts of Africa helps to contain the outbreak.[60] Airline crews are trained to spot the symptoms of Ebola in passengers flying from places where the virus is found. Crews are told to quarantine anyone who looks infected.[66]

As an outbreak of ebola progresses, bodily fluids from diarrhea, vomiting, and bleeding represent a hazard. Due to lack of proper equipment and hygienic practices, large-scale epidemics occur mostly in poor, isolated areas without modern hospitals or well-educated medical staff. Many areas where the infectious reservoir exists have just these characteristics. In such environments, all that can be done is to immediately cease all needle-sharing or use without adequate sterilization procedures, isolate patients, and observe strict barrier nursing procedures with the use of a medical-rated disposable face mask, gloves, goggles, and a gown at all times, strictly enforced for all medical personnel and visitors.[67] The aim of all of these techniques is to avoid any person’s contact with the blood or secretions of any patient, including those who are deceased.[68]

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.[69] 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,[70] opening clinical trials in humans.[71] 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.[72] Trying the vaccine on a strain of Ebola that more resembles the one that infects humans is the next step.[citation needed]

The Food and Drug Administration has approved no candidate vaccines,[73][74][75] the most promising whereof are DNA vaccines[76] or derive from adenoviruses,[69] vesicular stomatitis Indiana virus (VSIV)[77][78][79] or filovirus-like particles (VLPs)[80] because these candidates could protect nonhuman primates from ebolavirus-induced disease. DNA vaccines, adenovirus-based vaccines, and VSIV-based vaccines have entered clinical trials.[71][72][81][82]

Ebolaviruses are not transmitted by aerosol during natural EVD outbreaks. Without an approved vaccine, EVD prevention predominantly involves behavior modification, properpersonal protective equipment, and sterilization/disinfection.

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. The research is reported in Proceedings of National Academy of Sciences.[83]

Endemic zones[edit]

The natural maintenance hosts of ebolaviruses are unidentified: primary infection may not necessarily be preventable in nature. Fruit bats are thought to be the natural hosts (primary source needed, but see e.g. BBC). Thus, to avoid EVD, risk factors such as contact with bats, nonhuman primates, and bush meat should be avoided.

During outbreaks[edit]

The most straightforward prevention method during EVD outbreaks is not touching patients, their excretions, and body fluids, or possibly contaminated materials and utensils. Patients should be isolated, and medical staff should be trained and apply strict barrier nursing techniques (disposable face mask, gloves, goggles, and a gown at all times). Traditional burial rituals, especially those requiring embalming of bodies, should be discouraged or modified.[67]

In the laboratory[edit]

Ebola viruses are World Health Organization Risk Group 4 Pathogens, requiring Biosafety Level 4-equivalent containment. Laboratory researchers have to be properly trained in BSL-4 practices and wear proper personal protective equipment.

Treatment[edit]

A hospital isolation ward inGulu, Uganda, during the October 2000 outbreak

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.[84][85][86]

Experimental therapies[edit]

Hyperimmune equine immunoglobulin raised against EBOV has been used in Russia to treat a laboratory worker who accidentally infected herself with EBOV—but the person died anyway.[87][clarification needed] 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.[88][89][clarification needed] Such a recombinant post-exposure vaccine was also used to treat a German researcher who accidentally pricked herself with a possibly EBOV-contaminated needle. Treatment might have been successful as she survived. However, actual EBOV infection could never be demonstrated without a doubt.[90] Novel, very promising,[editorializing] 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.[91][92]

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.[93] Ninety percent of the mice treated with clomiphene and 50 percent of those treated with toremifene survived the tests.[94] 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.[95]However, this potential treatment is considered controversial.[59]

Prognosis[edit]

The disease has a high death rate: often between 50% and 90%.[1][2] If an infected person survives, recovery may be quick and complete, or prolonged with 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 andblindness have also been described. EBOV and SUDV may be able to persist in the sperm of some survivors, which could give rise to secondary infections and disease via sexual intercourse.[1]

Epidemiology[edit]

For more about specific outbreaks and their descriptions, see List of Ebola outbreaks.

Outbreaks of EVD have occurred mainly in Africa.

Ebola virus disease (EVD) outbreaks
Year Virus Geographic Location Human Deaths Cases CFR (case-fatality risk)
1976 SUDV Juba, Maridi, Nzara, and Tembura, Sudan 151 284 53%
1976 EBOV Yambuku, Zaire 280 318 88%
1977 EBOV Bonduni, Zaire 1 1 100%
1979 SUDV Nzara, Sudan 22 34 65%
1988 EBOV Porton Down, United Kingdom [laboratory accident] 0 1 0%
1994 TAFV Taï National Park, Côte d’Ivoire 0 1 0%
1994–1995 EBOV Woleu-Ntem and Ogooué-Ivindo Provinces, Gabon 32 52 62%
1995 EBOV Kikwit, Zaire 245 317 77%
1996 EBOV Mayibout 2, Gabon 21 31 68%
1996 EBOV Sergiyev Posad, Russia [laboratory accident] 1 1 100%
1996–1997 EBOV Ogooué-Ivindo Province, Gabon; Cuvette-Ouest Department, Republic of the Congo 46 62 74%
2000–2001 SUDV Gulu, Mbarara, and Masindi Districts, Uganda 224 425 53%
2001–2002 EBOV Ogooué-Ivindo Province, Gabon; Cuvette-Ouest Department, Republic of the Congo 97 124 78%
2002 EBOV Ogooué-Ivindo Province, Gabon; Cuvette-Ouest Department, Republic of the Congo 10 11 91%
2002–2003 EBOV Cuvette-Ouest Department, Republic of the Congo; Ogooué-Ivindo Province, Gabon 128 143 90%
2003–2004 EBOV Cuvette-Ouest Department, Republic of the Congo 29 35 83%
2004 EBOV Koltsovo, Russia [laboratory accident] 1 1 100%
2004 SUDV Yambio County, Sudan 7 17 41%
2005 EBOV Cuvette-Ouest Department, Republic of the Congo 9 11 82%
2007 EBOV Kasai Occidental Province, Democratic Republic of the Congo 186 264 71%
2007–2008 BDBV Bundibugyo District, Uganda 39 116 34%
2008–2009 EBOV Kasai Occidental Province, Democratic Republic of the Congo 15 32 47%
2011 SUDV Luweero District, Uganda 1 1 100%
2012 SUDV Kibaale District, Western Uganda 17 24 71%
2012 BDBV Orientale Province, Democratic Republic of the Congo 36 77 47%
2014 EBOV Guinea, Sierra Leone, Liberia, Nigeria[96][97] 672 1201 56%

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 USAMRIIDdiscovered filoviruses similar in appearance to Ebola in tissue samples taken from crab-eating macaque imported from the Philippines to Hazleton Laboratories Reston, Virginia.[98]

Blood samples were taken from 178 animal handlers during the incident.[99] Of those, six animal handlers eventually seroconverted. When the handlers failed to become ill, the CDC concluded that the virus had a very low pathogenicity to humans.[100]

Because of the virus’s high mortality, it is a potential agent for biological warfare.[101]

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 aCategory A bioterrorism agent by the Centers for Disease Control and Prevention. It has the potential to be weaponized for use in biological warfare.[102] The BBC reports in a study that frequent outbreaks of Ebola may have resulted in the deaths of 5,000 gorillas.[103]

2007 to 2011[edit]

As of 30 August 2007, 103 people (100 adults and three children) were infected by a suspected hemorrhagic fever outbreak in the village ofKampungu, 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 are the result ofEbolavirus.[104][105] 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.[106]

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 is now tentatively named Bundibugyo.[107] 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.[108] The virus appeared in southern Kasai Occidental on 27 November 2008,[109] and blood and stool samples were sent to laboratories in Gabon and South Africa for identification.

On 25 December 2008, a mysterious disease that had killed 11 and infected 21 people in southern Democratic Republic of Congo was identified as the Ebola virus.[110] Doctors Without Borders reported 11 deaths as of 29 December 2008 in the Western Kasai province of the Democratic Republic of Congo, stating that a further 24 cases were being treated. In January 2009, Angola closed down part of its border with DRC to prevent the spread of the outbreak.[111]

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 has passed as of 2 April 2009, she has been declared healthy and safe. It remains unclear whether or not she was ever actually infected with the virus.[112]

In May 2011, a 12-year-old girl in Uganda died from Ebola (Sudan subspecies). No further cases were recorded.[113]

2012 outbreaks[edit]

In July 2012, the Ugandan Health Ministry confirmed 13 deaths due to an outbreak of the Ebola-Sudan variant[114] in the Kibaale District.[115] As of 28 July 2012, 14 out of 20 (70% mortality rate) had died in Kibaale.[116] On July 30, Stephen Byaruhanga, a health official in Kibaale District, said the Ebola outbreak has spread from one remote village to several villages.[117]

The World Health Organization‘s 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 have been no confirmed cases outside of Kibaale District except for a patient who was medically evacuated to Kampala District and has since died. WHO and CDC support is on the ground in Uganda supporting the government response. There have been no confirmed cases outside of Uganda.[118] Included among the populations confirmed to be affected are prisoners in Kabbale prison. One of the inmates suspected of infection escaped from medical isolation on the same day.[119]Dr. Joaquim Saweka, the WHO representative to Uganda, also reported that the outbreak was then under control and that everyone known to have had contact with a known Ebola patient is now in isolation.[120]

On 8 August 2012, the Ugandan Ministry of Health has 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 are being followed up during the incubation period of 21 days.[121]

On 17 August 2012, the Ministry of Health of the Democratic Republic of the Congo reported an outbreak of the Ebola-Bundibugyo variant[122] in the eastern region.[123] By August 21, the WHO reported a total of 15 cases and 10 fatalities.[124] No evidence suggests that this outbreak connects to the Ugandan outbreak.[125] By 13 September 2012, the World Health Organisation 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.[126]

2014 outbreak[edit]

In 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 have been reported in Guinea, 22 suspected cases in Liberia including 14 deaths, 8 suspected cases in Sierra Leone including 6 deaths, and 1 suspected case inMali.[127][128] Investigations on these are under way.[129][130][131] By late June 2014 the death toll had reached 390 with over 600 cases reported.[132] By July 2014, the World Health Organization had reported 844 cases including 518 deaths since the epidemic began in March.[133]

History[edit]

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[134] and Sudan.[135] The strain of Ebola that broke out in Zaire has one of the highest case fatality rates of any human virus, roughly 90%.[136]

The name of the disease originated from one of those first recorded outbreaks in 1976 in Yambuku, Democratic Republic of the Congo (then Zaire) which lies on the Ebola River.[134]

The Philippines and the United States had no previous cases of infection, and upon further isolation it was concluded to be another strain of Ebola or a new filovirus of Asian origin, and 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.[137]

Other animals[edit]

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.[138] 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.[139]

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.[139] 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.[140]

Domestic animals[edit]

Ebola virus can be transmitted to dogs and pigs.[141] While dogs may be asymptomatic, pigs tend to develop clinical disease.

#ESPN’S STEPHEN A SMITH SAID WHAT?

ESPN’s Stephen A. Smith Says Women Should Be Careful Not to Provoke Domestic Violence, Then Mansplains How Women Missed His Point

YUP

THAT IS WHAT THIS BLACK BOY SAID ON  AIR

HE’S A CREEP

HE’S SAID OTHER THINGS ON AIR IN THE PAST

AND WAS FORCED TO APOLOGIZE FOR IT

IF IT WASN’T SO SAD IT WOULD BE HILARIOUS!

======================================

OF course black women are quick to forgive his ‘WORD SALAD” – not my invention but I love it just the same – it describes so much in two words – but I don’t and other women do not.

Woman are asking for his firing; men are still listening to his “sports analysis” on ESPN-2 and the rest of us are wondering what would happen if SMITH were a white man?

Yeah he would have been sacked already.

Black men in the news skate like Gold Medalists.

White guys go to jail

But then why are 4 out of 5 black men of all ages in jails in America?

Because they hit  their women and abuse their kids

And afterwards – these women forgive them and go back to them for a most certain violent future

And these kids grow up only to be housed like Daddy in the BIG HOUSE.

PLEASE

IF YOU’RE GOING TO RANT AT ME

THAT I’M WRONG

SAVE IT FOR SOMEONE WHO GIVES A SHIT WHAT YOU THINK ABOUT.

THAT PERSON

AIN’T ME

NEXT STOP

PERHAPS MINORITY MEN SHOULD GO TO JAIL FIRST  – LET US CALL ‘JAIL’ THEIR PREP SCHOOL – WE KICK THE SHIT OUT OF THEM, THEY LEARN ABOUT LIFE AND WE RELEASE THEM TO BECOME MODEL CITIZENS OF THE WORLD EVENTUALLY

IF NOT

NO 2ND CHANCES

AS FOR STEPHEN A SMITH

FIRE HIS BLACK ASS.

HE DOESN’T DESERVE TO BE IN A JOB.

============================================

 

black women have to STOP allowing Black MEN to beat up on them and their kids.

Stand strong against Abusers – it is NOT YOUR FAULT YOUR MAN IS AN ASSHOLE

By

Photo: Jamie McCarthy/Getty Images

For knocking his then-fiancée unconscious at an Atlantic City casino and then dragging her limp body from the elevator, all of it caught on surveillance video, Baltimore Ravens running back Ray Rice was suspended just two games by the NFL. If that alone doesn’t blur your eyes with rage, try the reaction of ESPN analyst Stephen A. Smith, who on First Take this morning said to the women of the world, “let’s make sure we don’t do anything to provoke wrong actions … I think that just talking about what guys shouldn’t do, we got to also make sure that you can do your part to do whatever you can do to make, to try to make sure it doesn’t happen.”

And if that sounds like victim-blaming, Stephen A. Smith would like you to know, ladies, that you just don’t understand him. “Enough is enough,” he wrote after a few hours of internet backlash against his comments. “I simply asked: now what about the other side … what about addressing women on how they can help prevent the obvious wrong being done upon them?”

Here’s the rest of the monologue, via Deadspin, including the part about the “elements of provocation” (emphasis ours):

It’s not about him, then. It’s about you, and here’s what I mean by that. We keep talking about the guys. We know you have no business putting your hands on a woman. I don’t know how many times I got to reiterate that. […] But what I’ve tried to employ the female members of my family, some of who you all met and talked to and what have you, is that again, and this what, I’ve done this all my life, let’s make sure we don’t do anything to provoke wrong actions, because if I come, or somebody else come, whether it’s law enforcement officials, your brother or the fellas that you know, if we come after somebody has put their hands on you, it doesn’t negate the fact that they already put their hands on you. So let’s try to make sure that we can do our part in making sure that that doesn’t happen. Now you got some dudes that are just horrible and they’re going to do it anyway, and there’s never an excuse to put your hands on a woman. But domestic violence or whatever the case may be, with men putting their hands on women, is obviously a very real, real issue in our society. And I think that just talking about what guys shouldn’t do, we got to also make sure that you can do your part to do whatever you can do to make, to try to make sure it doesn’t happen. We know they’re wrong. We know they’re criminals. We know they probably deserve to be in jail. In Ray Rice’s case, he probably deserves more than a 2-game suspension which we both acknowledged. But at the same time, we also have to make sure that we learn as much as we can about elements of provocation. Not that there’s real provocation, but the elements of provocation, you got to make sure that you address them, because we’ve got to do is do what we can to try to prevent the situation from happening in any way. And I don’t think that’s broached enough, is all I’m saying. No point of blame.

“No point of blame,” he says in closing, after offering the opposite. Smith’s ESPN colleague Michelle Beadle, of SportsNation, responded eloquently on Twitter:

So I was just forced to watch this morning’s First Take. A) I’ll never feel clean again B) I’m now aware that I can provoke my own beating.

I’m thinking about wearing a miniskirt this weekend…I’d hate to think what I’d be asking for by doing so @stephenasmith.

I was in an abusive relationship once. I’m aware that men & women can both be the abuser. To spread a message that we not ‘provoke’ is wrong

In a week in which LGBT & domestic abuse issues have been primarily discussed in one-sided formats, I stand by my words.

Which only led Smith to dig himself deeper in a string of tweets that provided no clarification:

Upon hearing what I had to say, although admitting I could’ve been more articulate on the matter, let me be clear: I don’t understand how on earth someone could interpret that I somehow was saying women are to blame for domestic violence. And when I saw ‪@MichelleDBeadle — a colleague I have profound respect for — tweet what she tweeted, enough is enough. Something needs to be said right now. REPEATEDLY i said: There is absolutely no excuse to put your hands on a women. REPEATEDLY, I said dudes who do that need to be dealt with. REPEATEDLY, I echoed when confronted by it in the past — when someone was stupid enough to touch a loved one of this man, raised by 4 older sisters, a mom and numerous female relatives and loved ones, that man was dealt with. From that point, I simply asked: now what about the other side. If a man is pathetic and stupid enough to put his hands on a woman — which I have NEVER DONE, btw — of course he needs to pay the price. Who on earth is denying that? But what about addressing women on how they can help prevent the obvious wrong being done upon them? In no way was I accusing a women of being wrong. I was simply saying what that preventive measures always need to be addressed because there’s only but so much that can be done after the fact….once the damage is already done. Nothing more.My apologies to ‪@MichelleDBeadle And any woman out there who misconstrued what I said. I have always — and will always — find violence against a women every bit as horrific as women, themselves, find it. Always have. Always will, which my personal behavior exemplifies. I’ll strive to be more articulate in the future. But be clear, I wasn’t BLAMING women for anything. I was simply saying to take all things into consideration for preventative purposes. Period.

(In a second statement, Smith added, “I do NOT believe a woman provokes the horrible domestic abuses that are sadly such a major problem in our society. I wasn’t trying to say that or even imply it when I was discussing my own personal upbringing and the important role the women in my family have played in my life. I understand why my comments could be taken another way.” The rest is here.)

.@stephenasmith No one misconstruing your words;”how can women prevent” is WRONG conversation. Try again. Hint: Start with “How can men…”

Of course the problem goes far beyond Smith and ESPN, which has not commented on the segment or said whether Smith will face any disciplinary action. But for NFL fans at least, Smith’s ignorance, stated so forcefully, makes him a prime (and at least somewhat deserving) target of all of the frustration that has been building with regard to the terrible handling of the ugly Rice incident on all sides, not to mention the hideous ways society at large treats abused women. When Rice appeared at a press conference with his victim, who is now his wife, he apologized to his team, but never to her. “Sometimes in life, you will get knocked down,” he said. She apologized as well, a fact the official Ravens Twitter account was sure to note:

Janay Rice says she deeply regrets the role that she played the night of the incident.

Smith, in other words, did not come to these ideas on his own.

 

================================================================

Leave it to Stephen A. Smith, who NBC Dallas aptly points out is best known for shouting at people on television, to make the Cowboys look more sympathetic. He had this to say in January 2012:

“This dude [Romo) didn’t get it done. So when I sit here and listen to somebody like Brett Favre opening his mouth talking about Tony Romo like he’s a victim, what are you talking about? He had DeMarco Murray, he had Dez Bryant, he had Miles Austin even though he got hurt, you always had Jason Witten. … You’re playing in a billion-dollar playpen and you’re talking about this dude as a victim?”

The fact that all of the players he mentioned, aside from Jason Witten, missed significant time with injury that season are the kind of insignificant details Stephen A. has never been fond of. He continued:

“I’m saying [Favre] has a lot of nerve and a lot of gall saying what he said. The victim in Dallas is Mr. Jerry Jones, an owner that puts his money where his mouth is and has given Tony Romo the weapons to produce, and he hasn’t gotten there.”

So in one breath he’s mockingly referring to the cost of Cowboys Stadium and in the next he’s bemoaning poor victimized billionaire Jerry Jones. So Brett Favre has no business expressing his opinion publicly about quarterbacks in the NFL and GM Jerry Jones, who has said himself he’s responsible for everything the Cowboys do, is the victim.

Okay. Gotcha.

=================================================================

In February 2012, the NY Daily News reported on an interesting couple of segments on Stephen A. Smith’s New York radio show on ESPN. Screamed the loud one:

“I report stuff weeks in advance and get vilified for it. But when it comes to fruition, no one remembers they vilified me…I won’t tell you anything. I have nothing to prove. If you don’t like it, don’t watch me [on ESPN]. I don’t have to do it [break stories]. I have a radio show, a TV show and a column. I don’t need to do that.”

Talk radio in any form isn’t generally known as a bastion of sanity and respect, but reacting to a caller chiding him about one of the manyNBA rumors he has reported that turned out to be wrong, by exploding into a psychotic fit of rage—a little ridiculous, to say the least.

He basically threatened his audience and told them not to listen to his show. Lovely. Surely the network executives all loved that.

Later in the show his sidekick Ryan Ruocco mentioned comedian Jay Pharoah’s impression of Stephen A. on Saturday Night Live and here’s how he responded:

“As long as it’s funny, I’m honored. You know what annoys me is when guys take themselves too seriously.”

Hmm. Something tells me irony is lost on Stephen A.

=============================================================

As was widely reported in the sports media, Stephen A. Smith lost his marbles when he mistook a fictional article about him on The Onion as non-fiction in September 2012. The article was entitled “Stephen A. Smith Thinking Son Is Finally Ready For The Sex Argument,” and he responded (hilariously) via Twitter:

“I thought I’d heard enough despicable lies about myself. Now there’s some article out that I have a 9-yr-old son and I’m going to have a … Conversation with him about Sex. Mind you, I neither have a son nor a 9-Year-old. Some ppl are beyond despicable. No end! Sad what extent … People will go to. Amazing how folks try to tear cats down, primarily due to perceived power of the spoken word. Damn Shame, but too bad. … Because I don’t intend on going anywhere. Really, Really sad, though!”

The capitalization impaired response spanned four painful tweets, all of which were later deleted when Stephen A. pretended to be a good sport about the fact that he didn’t get the satire. He added, “Peeps got jokes, It’s cool!” Peeps got jokes indeed.

Next time Stephen A. should try reading something before getting so bent out of shape about it. If he did more reading and less screaming, perhaps he’d start to grasp the grammatical fundamentals of the written word.

=====================================================================

In February 2013, Stephen A. Smith was invited to address the Greater Travelers Rest Baptist Church. Because it’s what Jesus would have wanted, naturally he boasted about it on Twitter:

For those interested in hearing the Sermon — yes Sermon — I gave last Sunday in Decatur, Ga, here’s a way to get it: … And Btw…the ONLY reason I called it a sermond is b/c that’s what folks in attendance called it. I have a loooonnnggg way to go in my faith … There is no hypocrite in me. Would never pretend to be something I’m not……especially in God’s House. Please know this!

Listen, you guys—Stephen A. wasn’t calling it a sermon! He’s no hypocrite. He’s still working on his faith. He would never boast about himself in the house of the Lord!

He was only repeating what he heard from the hundreds of adoring parishioners were screaming from the pews. Can’t you tell the difference, stupid?

======================================================================

As much of a blowhard as Stephen A. Smith is, he routinely finds himself out of his league squaring off with Skip Bayless on First Take. He’s quick to admit that he knows absolutely nothing when it comes to anything outside the NBA.

He tweeted the following about Texas A&M quarterback Johnny Manziel, the obvious Heisman frontrunner, in early December 2012:

“I’m an honorable man, so I must admit @realskipbayless is right-on with that. He IS the one who told me about Manziel. … I’m an honorable man so I have to admit:@RealSkipBayless is telling the truth. Didn’t know a damn thing about Manziel until Skip told me.”

There’s no question that the Heisman race was a complete tossup through much of the college football year, but he Manziel had definitely solidified himself as the front-runner by December.

The fact that Stephen A., whose idiocy ESPN airs at least 20 hours of per week, had no idea who Johnny Manziel was (until he was educated by Skip Bayless) until the end of the college football season is beyond inexcusable.

=========================================================================

Stephen A. Smith has found himself in hot water for using the n-word more than once on First Take. The first time he said it was in December 2011, referring to LeBron James as “this n—a.”

He faced relatively little fallout stemming from this incident, despite the fact that it was said in a much more serious tone than the more recent incident.

The more recent incident in question came in October 2012. Smith was asked if he believed Kobe Bryant would miss the start of the Lakers’ season due to an injury. He replied quickly and audibly:

“He’ll be just fine. Opening night, Kobe Bryant is going to miss it because [his] foot is sprained? Are y’all crazy? N—a please.”

His comments blew up into national news story when the video of his comment began circulating on the web. Naturally, he handled it in a way that only Stephen A. could…or would…

Instead of issuing a simple innocuous apology for saying the thing we all heard him say, he completely denied saying the thing we all heard him say. Or he could have just said, “I said it, I’m not sorry.”

Arguing against the one thing everyone knows for sure—that you said it—is just too Stephen A. Smith for words.

=======================================================================

One of the most irritating things about Stephen A. Smith, besides the screaming, is the excessive hyperbole he employs in lieu of anything substantive. His way with words can only be described as Donald Trump-esque, with the limited depth and vocabulary he possesses.

In August 2012, the unhinged yellers at First Take took on the much debated issue of the Nationals preseason decision to shut down pitching ace Stephen Strasburg, who was coming off of Tommy John surgery, after 160 innings. Said he:

“I still think it’s disgraceful. The fact of the matter is that this is a young stud. Somebody’s got to figure something out. … I just don’t know what’s happened to the sport. I’m not in a position to argue about it. I just don’t understand how these guys are so coddled, and the need to protect these guys. I know he’s less than two years removed from Tommy John surgery. I understand that. I truly do. But I’m thinking about those paying customers.”

So doing something they said they were going to do before the season began in an effort to protect the long-term health of Strasburg, not to mention their own investment, is disgraceful? Agree or disagree with the Nats’ decision, but labeling it disgraceful is just ignorant.

And if Stephen A. concedes right off the bat that he is in no position to argue the point, why exactly does he continue to do so with such gusto? He truly understands the medical issues but is just worried about the fans? Don’t worry Stephen A.—Natties fans don’t need an incompetent, baseball-deficient boob championing them.

======================================================================

n October 2012, Stephen A. Smith had this to say about longtime respected Washington Post columnist Michael Wilbon, one of his colleagues at ESPN, for expressing support for Redskins quarterback Robert Griffin III for the 2012 MVP:

“I think Mike Wilbon is insane. …I love him dearly. We’re very good friends. I love him, but he’s crazy. … He’s a little bit biased. Mike gets a little bit excited there. I mean, Mike’s willing to come off the golf course for those two cities [DC and Chicago] … But I’m not letting those Washington homers [Wilbon and Tony Kornheiser], those D.C. homers, get away with this one. No no no no no no.”

A month later Stephen A. tweeted this:

“I simply cannot believe that the Knicks picked the night they’re facing Jeremy Lin to stink up the joint. I’m so ashamed of them right now!”

So speaking out in favor of RG3 being named the MVP, an opinion that gained traction far outside the Washington beltway, that’s being a homer.

But taking a personal investment (also known as a grudge) in how the Knicks perform against someone Stephen A. feverishly hated before he left New York to sign with the Rockets—that’s just good journalism?

=====================================================================

Nobody on ESPN hides their ignorance about hockey—when it’s a topic broached on Around The Horn, the participants generally begin their argument with “Well, I’m not Mr. Hockey…but.” God forbid they learn about it.

Stephen A. Smith doesn’t hide his ignorance of anything, he prefers to flaunt it, and there’s nothing dislikes more and knows less about than the NHL. When “discussing” the Blackhawks’ record winning streak in March 2013, he had this to say:

“Excuse me … it wasn’t 21 games. It was really an 8-game streak. There are three ties. I’m sorry, that doesn’t count. … I’m not into the tie business. This isn’t soccer. OK? … And and and and and and the hockey stuff, I’m sorry, I’m not buying it. … Not only that: If you go to the overtime you get a point. If you win the game, you get a couple of points. I’m sorry, you want a cookie? Last time I checked, when you take to the ice, it’s to actually win. It’s not to tie. So I don’t get all of this stuff. Hockey’s clearly all about points, because if you go to overtime 20 times you get 20 points. I don’t understand that. You either win or you lose in sports. … When the Stanley Cup champion is crowned, is it because of a tie? No, it’s because of a win.”

You aren’t into hockey, Stephen A.? Well you don’t say! Could’ve fooled us.

Suppose it doesn’t matter that hockey hasn’t had ties since 2004 and that all games are settled via a shootout if the tie isn’t broken during five minutes of overtime. And that ties have never existed in the playoffs, but rather sudden-death periods of overtime that function the same as additional full periods of hockey.

So maybe the last time he “checked” was 2004? But that’s being generous because it’s more than abundantly clear that Stephen A. has never and will never know anything about anything aside from the NBA. He doesn’t even try to hide his ignorance on the subject, or any subject, and seems quite content with yelling nonsense.

==================================================================

 

 

AMERICAN DOCTORS IN AFRICA ARE INFECTED WITH EBOLA & THEN THIS HAPPENED?

DOCTOR KENT BRANTLY was in Liberia tending to African’s afflicted with the Ebola virus. 607 people have died from it this year and one was a highly influential and top Liberian doctor who died this weekend.

Meanwhile This doctor was seen unprotected in several pictures:

 

 

american doctor ebola virus_Naijapals[dot]com

this is the doctor who was such a dumb ass he brought his young family to live with him in Africa:

072714+Brantly+family

1 week before Doctor Brantly took ill – this mother and her two young kids returned home to the US – FORT WORTH TEXAS. THEY WERE WITH HIM IN THIS AREA SINCE OCTOBER OF 2013.

THEY WERE ALLOWED TO RETURN HOME ON PLANE WHICH – I FEAR – THEY HAVE INFECTED ALL THOSE PEOPLE. I THINK THIS MOTHER AND HER TWO KIDS ARE ALSO INFECTED WITH EBOLA

OF WHICH

THERE IS

NO CURE!

=============================================================

IS HE A HERO FOR TAKING CARE OF THESE SICK AFRICANS?

NO

HE’S A DUMB ASS FOR NOT WEARING A HAZMAT SUIT

AND FOR TAKING HIS YOUNG FAMILY AND PUTTING THEM AT RISK

AND FOR THAT MATTER

THE REST OF US!

EBOLA IS THE MOST DEADLY DISEASE ON THE PLANET

IT IS

THE EQUIVALENT TO

ZOMBIE CURSE OF THE WALKING DEAD

THIS DISEASE COULD VERY WELL WIPE OUT THE ENTIRE PLANET

I ONLY HOPE THE REPUBLICANS, TEA TARDS AND COLLECTIVE CHRISTIAN BIBLE HUMPING WACKADOOS

ALL GO FIRST.

================================================================

Ebola Takes Heavy Toll on Health Workers

VIDEO: American Doctor Undergoing Treatment After Testing Positive for Ebola

I can talk about this shit until I’m blue in the face (which I don’t want) but if Americans and the world citizens don’t take this shit seriously – we are totally fucked. 

The Ebola virus continues its grim march across west Africa as the first two Americans were reported to be infected and a top Liberian doctor died this weekend.

Officials are also concerned after an infected man managed to board a plane from Liberia to Nigeria, potentially spreading the deadly virus to a fourth country.

The World Health Organization has reported that 1,093 people were infected with the virus as of July 20 in Guinea, Sierra Leone and Liberia, and of those infected 660 have died.

This weekend an American relief organization reported that both Dr. Kent Brantly and aid worker Nancy Writebol were sickened with the virus. They were helping the joint SIM/Samaritan’s Purse team treating Ebola patients at the Case Management Center in Monrovia.

The country’s medical team also suffered a serious blow when top Ebola doctor Dr. Samuel Brisbane died from an Ebola infection on Saturday.

Health officials are particularly vulnerable to contracting the virus, which is spread through blood and other secretions. The WHO reported that at least 100 health workers have been infected with the disease and 50 percent of them have died.

Last week Dr. Sheik Humarr Khan, the doctor in charge of battling Sierra Leone’s outbreak, was infected with the disease.

Dr. Steve Monroe, deputy director in Infectious Diseases at the U.S. Centers for Disease Control and Prevention, told ABC News that the outbreak has been going on for a long time and that usually health workers are infected at the beginning of an outbreak before the disease has been identified.

When a health worker is infected, officials will look for lapses in the use of the heavy safety gear designed to protect health workers, ABC News chief medical correspondent Dr. Richard Besser said.

“I’ve worn that gear and after about 15 minutes you are so hot in that gear you either have to get out of there or you’re going to be dehydrated,” Besser said. “Or there can be lapses. They’re going to look and see if there was some break in that procedure.”

Although the outbreak has been going on for months, there is no sign it will end soon.

The second American to be infected was identified as Nancy Writebol, who is employed by SIM in Liberia and was helping the joint SIM/Samaritan’s Purse team that is treating Ebola patients at the Case Management Center in Monrovia.

SIM manages ELWA Hospital in Morovia, and the two organizations have been working closely to combat Ebola since the current outbreak began in Liberia in March.

Writebol,who is married with two children, had been working as a hygienist who decontaminated those entering and leaving the Ebola care area at the hospital, Ken Isaacs, a vice president of Samaritan’s Purse, told The Associated Press.

“She is showing full symptoms of the disease,” Isaacs said.

Dr. Kent Brantly, 33-year-old American doctor who was treating Ebola patients, also tested positive for the deadly disease. He was reported to be sitting up in his isolated hospital bed and working on his computer after he contracted the deadly virus this week.

Brantly, from Fort Worth, Texas, has been living and working in Monrovia, Liberia since last October, when he moved there with his wife and two young children as part of a post-residency program set up by Samaritan’s Purse, a nondenominational evangelical Christian organization that aims to provide international aid.

The Associated Press contributed to this report.

 

OBAMA HAS STOPPED ILLEGAL KIDS DEPORTATION-WANTS TO USE EXECUTIVE ORDER TO KEEP THEM HERE?

WHICH I AM AGAINST

I DO NOT AGREE THAT THESE CHILDREN SHOULD BE ALLOWED TO STAY IN AMERICA

IT’S UNAMERICAN

AND WE HAVE OUR OWN KIDS WHO ARE STARVING AND HOMELESS

IF OBAMA USES EXECUTIVE ORDER

HE SHOULD BE STOPPED DEAD COLD BY CONGRESS

AND HE CANNOT BE ALLOWED TO DO THIS

IF HISPANIC LEADERS WANT TO ADOPT ALL OF THESE KIDS

OKAY – BUT IF NOT AND THESE KIDS GET ADDED TO OUR MEDICAID WITHOUT PAYING TAXES

WITHOUT COMING HERE LEGALLY

THIS IS OUTRAGEOUS

GIVE THE STATUE OF LIBERTY BACK TO THE FRENCH

AND CLOSE THE DOORS

THROW OUT THE SIGN

AMERICA IS CLOSED.

=====================================================

Maybe these HISPANIC LEADERS should be deported as well.

Hispanic Lawmakers to Obama: Take ‘Executive Action’ to Stop All Deportations

July 10, 2014 – 4:02 PM
Luis Gutierrez

Rep. Luis Gutierrez (D-Ill.) spoke at a press conference on July 10, 2014 in Washington, D.C., calling on President Barack Obama to stop deportations of illegal aliens in the United States using executive orders. (CNSNews.com/Penny Starr)

WRITE TO THESE TWO REPS ON TWITTER – DEMAND THEY PUT THEIR MONEY WHERE THEIR BIG MOUTH IS: ADOPT THESE ILLEGAL KIDS OR DEPORT THEM. 

Reps. Luis Guiterrez (D-Ill.) – not on twitter but the other guy is:

Raul M. Grijalva

@RepRaulGrijalva

(CNSNews.com) –Reps. Luis Guiterrez (D-Ill.) and Raul Grijalva (D-Ariz.) joined immigration activists Thursday in calling on President Barack Obama to stop deportations and allow illegal aliens to have work permits. It’s the latest effort to compel the president to make sweeping changes to immigration law through executive orders.The Democrats also want Obama’s Deferred Action on Childhood Arrivals (DACA) policy to apply to parents of so-called Dreamers and others, putting them on a path to citizenship as spelled out in the immigration bill (S.744) as passed by the Senate in June 2013. The House has not taken up that bill.

“I believe the president of the United States can take the kind of broad, executive action that can help millions of people stop their deportation and be in deportation proceedings, No. 1, or possibly ever be deported, and give them a work permit,” said Guiterrez, who with Grijalva is also a member of the Congressional Hispanic Caucus (CHC).

“Now it is the authority of the president to provide that security, that comfort to millions and millions of families,” Grijalva said.

In December 2013, Grijalva and 17 other lawmakers sent a letter to Obama asking him to halt all deportations until Congress had passed legislation on “comprehensive immigration reform.”

The letter also called for expanding those eligible for DACA to include “family and neighbors” of children brought here illegally by their parents.

“We cannot continue to witness potential citizens in our districts go through the anguish of deportation when legalization could be just around the corner for them,” the letter states. “We look to you to firmly contribute to advancing inclusion for immigrants by suspending deportations and expanding DACA.”

In April, the CHC sent a 6-page memorandum to Homeland Security Secretary Jeh Johnson seeking “administrative relief and more humane enforcement practices” from and of immigration laws.

The list of recommendations basically would protect all illegal aliens except those with disqualifying crimes from being detained or deported and also calls for an end to the Secure Communities program, a highly successful program, according to DHS’s Immigration and Custom’s Enforcement.

“Under Secure Communities, the FBI automatically sends the fingerprints to DHS to check against its immigration databases,” the ICE website said about the program.

“If these checks reveal that an individual is unlawfully present in the United States or otherwise removable due to a criminal conviction, ICE takes enforcement action – prioritizing the removal of individuals who present the most significant threats to public safety as determined by the severity of their crime, their criminal history, and other factors – as well as those who have repeatedly violated immigration laws,” it added.

Both Gutierrez and Grijalva said that the immigration crisis on the border involving a recent surge of illegal aliens crossing the U.S. border with Mexico, including more than 50,000 unaccompanied children, should not stop immigration reforms but encourage it.

“I also want to be sure that we do not allow the humanitarian crisis on our border to impact or somehow deteriorate the momentum of our movement or our petition for the president,” Gutierrez said at the press conference. “If anything, that humanitarian crisis on the border should urge the president to do more and more quickly and to be broader.”

“The fact of the matter is these kids are here now, and by law and by value, this country has an obligation – both a moral imperative and a legal obligation – to provide custodial care and process these kids correctly,” Grijalva said.Raul Grijalva

 

TALIBAN IS STILL INSIDE AFGHANISTAN

AND THIS IS NO SHOCK FOR ME

THEY WERE THERE BEFORE AND WILL BE THERE AFTER

TALIBAN ARE TERRORISTS

MUCH LIKE AMERICAN TEA PARTY

AMERICAN GOP

AMERICAN CONSERVATIVE CHRISTIANS

THESE ARE AMERICAN TALIBAN

========================================================

Photo

Afghan police recruits trained in Kabul on Tuesday. Security forces have been under increasing fire in areas around the capital. CreditDiego Ibarra Sanchez for The New York Times

MAHMUD RAQI, Afghanistan — Talibanfighters are scoring early gains in several strategic areas near the capital this summer, inflicting heavy casualties and casting new doubt on the ability of Afghan forces to contain the insurgency as the United States moves to complete its withdrawal of combat troops, according to Afghan officials and local elders.

The Taliban have found success beyond their traditional strongholds in the rural south and are now dominating territory near crucial highways and cities that surround Kabul, the capital, in strategic provinces like Kapisa and Nangarhar.

Their advance has gone unreported because most American forces have left the field and officials in Kabul have largely refused to talk about it. The Afghan ministries have not released casualty statistics since an alarming rise in army and police deaths last year.

At a time when an election crisis is threatening the stability of the government, the Taliban’s increasingly aggressive campaign is threatening another crucial facet of the American withdrawal plan, full security by Afghan forces this year.

“They are running a series of tests right now at the military level, seeing how people respond,” one Western official said, describing a Taliban effort to gauge how quickly they could advance. “They are trying to figure out: Can they do it now, or will it have to wait” until after the American withdrawal, the official added, speaking on the condition of anonymity because the coalition has officially ceded security control.

Interviews with local officials and residents in several strategic areas around the country suggest that, given the success of their attacks, the Taliban are growing bolder just two months into the fighting season, at great cost to Afghan military and police forces.

In Kapisa, a verdant province just north of Kabul that includes a vital highway to northern Afghanistan, insurgents are openly challenging and even driving away the security forces in several districts. Security forces in Tagab District take fire daily from the Taliban, who control everything but the district center. Insurgents in Alasay District, northeast of Kabul, recently laid siege to an entire valley for more than a week, forcing hundreds of residents and 45 police officers to flee. At least some of the local police in a neighboring district have cut deals with the Taliban to save themselves.

In the past month, a once-safe district beside the major city of Jalalabad, east of Kabul, has fallen under Taliban control, and a district along a crucial highway nearby is under constant threat from the Taliban. South of Kabul, police forces in significant parts of Logar and Wardak provinces have been under frequent attack, to deadly effect.

But there are only anecdotal reports to help gauge just how deadly the offensive has been. The Afghan defense and interior ministries stopped releasing casualty data after a shocking surge of military and police deaths in 2013 began raising questions about the country’s ability to sustain the losses. By September, with more than 100 soldiers and police officers dying every week, even the commander of the International Security Assistance Force suggested the losses could not be sustained.

Asked for figures on the latest security force casualties this year, both ministries refused to provide data or confirm accounts from local officials. But there are signs that the casualty rate is already likely to be at least as bad as it was last year.

In one important indicator, the United Nations reported a 24 percent rise in civilian casualties for the first half of this year compared with a similar period from 2013, hitting a new peak since the United Nations Assistance Mission in Afghanistan began tracking the data in 2009. More significantly, for the first time, the highest number of those casualties came from ground fighting between the Afghan forces and insurgents rather than from roadside bombs.

The United Nations found that more fighting was taking place near populous areas, closer to the district centers that serve as the government seats. Ground violence also seemed to increase in areas where coalition bases had been closed, as the Taliban felt more emboldened to launch attacks without fear of reprisal.

One important effect of those gains, particularly where police forces are being driven away, is that the Taliban are establishing larger sections of lawless territory where they can intimidate local populations. They become safe havens, and staging grounds for more ambitious attacks against Kabul and other major cities, like the militant assault on Kabul’s airport on July 17.

In the immediate vicinity of the country’s main cities, the Afghan military was still holding up well, according to American and Afghan commanders. But as more marginal districts have come under unexpectedly heavy attack, the military planners’ expectations have been tested.

One widely accepted prediction was that soon after 2014, the Taliban would gain in rural areas and traditional strongholds, as the government made tough decisions about what to fight for and what to let go. Places of no strategic value in remote areas of the south and east, some officials said, could afford to be forgotten.

But heavy attacks, and some territorial losses, are already happening in those places, earlier than predicted.

On July 9, the Taliban overran a district center in Ghor Province, a rugged and violent area close to the center of the country, which left Afghan forces scrambling to reclaim it and smarting from the embarrassment. On Saturday, militants stormed Registan District in Kandahar, killing five police officers, including the district police chief, in a battle that continued into the evening.

Photo

A crowd gathered near the body of a militant fighter after an attack on the Kabul airport on July 17. Ground violence apparently has increased in areas where coalition bases have closed.CreditDiego Ibarra Sanchez for The New York Times

The heavy fighting earlier this summer in northern Helmand Province, long a Taliban stronghold and a center of opium poppy production, was mostly expected. But the breadth of the Taliban assault, which is now said by locals to extend to four districts, has surprised many, and foreshadowed a more ambitious reach for the insurgents.

The efforts of this fighting season have not been solely in the countryside, or traditional strongholds like those in Helmand. The Taliban have made strides in Nangarhar Province, home to one of the most economically vibrant cities in the country and a strategically important region. Surkh Rod, a district that borders the provincial capital Jalalabad and was safe to visit just three months ago, has become dangerous to enter.

“The difference is that five months ago there were more government forces here; now it is the Taliban,” said Nawab, a resident of Shamshapor village.

Bati Kot District, too, has become more dangerous. Outside the district center, residents say, the Taliban dominate a crucial swath of territory that straddles the main highway leading from Kabul to the eastern border with Pakistan. Villagers living in the district say the Taliban force them to feed and house insurgents, and threaten to kill them if they refuse.

Much like Nangarhar, Kapisa is connected directly to Kabul, presenting a troubling threat for the government as it struggles to safeguard the security corridor around the capital. Trouble in three districts has been the focus of a concerted American Special Forces campaign to ferret out the insurgents, who many say appear more trained and disciplined than the average Taliban.

“The command and control is incredible,” said one American Special Forces officer who has fought with his men in insurgent-controlled valleys in Kapisa. “They have found an awesome safe haven.”

The biggest fear for the province stems from Tagab and Alasay districts. Though there is an entire battalion of Afghan soldiers in the area, the vast majority of the fighting and dying are done by the police forces.

Two weeks ago, in the Askin Valley area of Alasay, insurgents surrounded a village where the local and national police had only recently taken root. Tribal and interpersonal rivalries fueled the animosity toward the police, but the consequence was clear: The government was not welcome.

An estimated 60 insurgents surrounded Askin Valley and engaged in a gunfight with about 35 local and 10 national police officers in the area, according to police officials. The two sides fought for more than a week, with coalition aircraft entering the area to offer support for the beleaguered security forces. Eventually, the police were forced to retreat, along with hundreds of villagers.

Two police officials in the area, who spoke on the condition of anonymity, relayed the account. One, a local police officer, said the Taliban’s reach permeated the entire district, and the security forces were consigned to their bases, trying to stay alive.

“The Afghan security forces are controlling the bazaar for one in every 24 hours,” the commander said. “From 9 a.m. to 10 a.m., the police, army and local police come out of their outposts and buy what they need, then they go back to their bases.”

MASTERCHEF AUSTRALIA 2014 – BRENT, AMELIA, LAURA – BRENT IS IN THE FINALS?

I BELIEVE MASTERCHEF JUDGES HAVE FIXED IT FOR BRENT

I DON’T LIKE THE GUY

IT’S TRUE

BUT HE SKATED BY ALL THESE CHALLENGES AND WHEN HE DID STUFF THAT WAS SO OBVIOUSLY WRONG

THEY ALLOWED HIM TO SKATE BY

I HAVE A FEELING

THESE JUDGES – ALL MALE – ARE ROOTING FOR THE BOY

IS THAT TOO GAY OF ME TO SAY?

PERHAPS

BRENT IS NOT FINALIST MATERIAL -

HE FAILED TOO MUCH TO BE IN THIS POSITION.

HIS GOALS ARE RIDICULOUS

“HE WANTS TO TRAVEL THE WORLD IN HIS OWN FOOD SHOW”

ANTHONY BORDAINE HAS ALREADY DONE THIS

AND SO MANY OTHERS HAVE ALSO DONE THIS

BRENT’S GOALS ARE NOT LOFTY

THEY ARE COMPLETELY SELFISH

AND I FOR ONE DON’T UNDERSTAND MEN LIKE HIM

====================================================

FINALS ARE BETWEEN BRENT & LAURA

I AGREE WITH LAURA

I SINCERELY HOPE BRENT FAILS

 

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