Posted on 08/10/2014 12:46:23 AM PDT by Smokin' Joe
I have spent a little time compiling links to threads about the Ebola outbreak in the interest of having all the links in one thread for future reference.
Please add links to new threads and articles of interest as the situation develops.
Thank You all for you participation.
The lawyers will sort this out pronto.
Every person who comes in contact with an ebola patient, or their fluids (lab workers) will be garbed up just like the MSF workers in Africa. Perhaps even moreso with their own air supplies.
It won’t take paying for many courses of treatment and whole hospital wards isolated for just one patient for insurance companies to get in on the act as well. And insist it as part of liability coverage.
Of course, it's the HCW fault
MSF clearly cares more for their health workers than the CDC. They make sure their garb is sufficient to protect them in case of human error.
From Emergence of Zaire Ebola Virus Disease in Guinea (nejm). My ancient, old math says that is a 3% variation. How significant that is remains to be seen.
I’ll put the credit where it really belongs, imho, to the army of FReepers who have posted articles from around the world on the outbreak and related topics. It really is a group effort.
There is a good reason that the CDC is blaming the HCW.
The blame game is on in full strength in Wash DC.
Better to blame the HCW than face up to the full implications for both Health Care and immigration policy that means.
MSF has the practical expierience of dealing with Ebola, and makes sure they have optimum equipment for working in an epidemic firestorm.
The CDC is dealing with protocals that worked with past expierience; and in their arrogance, have not modified equipment to reflect current need.
MSF has already modified from (previous)N-95 to P-100 masks, goggles ,and face mask,full hood, nitrile gloves in multiple layers,rubber boots and booties.
This ain't the same critter that the CDC has dealt with in the past when the disease is spreading fully 1/3rd faster than previous outbreaks , and
the spread in not just a matter of access to better transportation, as some have presumed.
CORRECTION : :" Dallas health worker who tested positive for Ebola wore ‘full’ protective gear" as reccomended by the CDC .
It's past time to switch to MSF protocal equipment , and acknowldege the CDC equipment needs updating and improvement.
Incidently since so much is attributed to "Human Error" as the basis for HCW getting infected ,..
Does anyone have the sequence of Protective Equipment removal, after possible contamination ?
I don't recall seeing the sequence listed to minimize contamination .
Pixie at the PFIF has the text for the CDC news conference this Sunday morning —
{Pixie comments in these}
CDC press conference:
Frieden:
Confirmatory testing under way at CDC.
We don’t know what occurred in the care of the index patient, but at some point there was a breach in protocol.
The HCW developed symptoms on Friday. They were assessed Friday and tested yesterday.
Test result came in 12 hours ago.
The individual was self-monitoring and immediately upon developing symptoms contacted healthcare system. Came in and was immediately isolated.
Symptoms and test suggest level of virus she had was low.
1. Care for patient.
2. Assess her contacts. Only one contact who may have had contact with her while she may have been infectious.
3. Evaluating other HCW exposure. Possible other individuals were exposed. This individual did provide care to the index patient on multiple occasions. Had “extensive contact” with patient.
4. Will undertake complete investigation as to how this may have occurred.
Safe & effective care:
Had already begun to ramp up the education and training of HCWs at this facility. “The care of Ebola can be done safely but it’s hard to do it safely. It requires meticulous and scrupulous attention to infection control.”
{yes, blood just shot out of my eyes…}
“And even a single inadvertent innocent slip can result in contamination.”
{HCWs everywhere are now wondering why Ebola patients are not treated in highly specialized facilities by highly trained workers using the highest level of PPE….because in other words, one “slip” can be fatal.}
“We are recommending to the facility that the number of health care workers who care for anyone expected of Ebola be kept to an absolute minimum.”
We recommend that the procedures…be limited solely to essential procedures.
“We are looking at personal protective equipment. Understanding that there is a balance and putting more on ($$$) isn’t always safer and may make it harder to provide effective care.”
{Sure, that’s what the guys working in all the BSL-4 labs always sit around and say when they’re shooting the breeze over a beer, that less PPE would just be easier, and when they get back to the lab on Mondays, they suit up in full head-to-tow hazmat gear. Wink }
Recommend one person be placed in charge of infection control while Ebola patient is being cared for. {This isn’t already being done?!?}
CDC has sent additional staff to TX.
We look at what happens before someone goes in, what happens in that space, what happens when they leave. Two areas looking at closely - kidney dialysis and respiratory intubation. Both of those procedures may spread contaminated materials and are considered high-risk procedures. They were undertaken on the index patients a desperate measure to try to save his life.
{I’m sure that during congressional hearings looking into all of this that MSF doctors, in addition to Drs. Brantley and Saco, will testify that the hospital and CDC were INSANE if they were allowing any HCW to undertake such high-risk procedures while not in head-to-toe PPE, after having trained for such eventuality and having had knowledgeable assistance with its donning and doffing.}
Two final points.
We may see additional cases of Ebola. “This is because HCWs who cared for this individual may have had a breach of the same nature of the individual who appears now to have a preliminary positive test.”
{And, right on schedule, Frieden throws the health care workers UNDER the bus!!!
I can hear the swearing from Dallas in CT, and my bet is that a couple of big screen TV’s in the Dallas metro area just got broken by incoming high velocity objects. }
Here you go.
I couldn’t believe it when I heard Duncan had been intubated. Poor resp tech, I can’t imagine intubating a level 4 viral factory. And then dialysis to boot. Sheesh.
yea it sounds like they were not trained at all (like a 10 minute presentation).. Also I don’t think they decontaminated their PPE before they took it off.
CBS: CDC chief on second Ebola case: There was a breach in protocol
"We're deeply concerned about this new development," Dr. Thomas Frieden said in an interview on CBS' "Face the Nation" Sunday. "I think the fact that we don't know of a breach in protocol is concerning because clearly there was a breach in protocol. We have the ability to prevent the spread of Ebola by caring safely for patients."
Despite the fact they cannot identify a "breach of protocol," they're going to assume a "breach of protocol" rather than consider that the CDC's assurances that Level 2 protocols are sufficient is, in fact, WRONG! Level 2 protocols are wholly inappropriate when dealing with a level 4 pathogen!
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I wonder how many times my keyboard can take the headbanging.
Let’s get OSHA involved. Compared with HHS, they do not f*** around.
If this is not a worker safety issue, I don’t know what is.
Blame the victim works as an explanation for the LIV masses. The first time or two.
If two or more caregivers come up positive that explanation gets trickier. If human error is likely with a given protection scheme, clearly that protection scheme needs updating. Because humans do make errors.
No one wants to take a chance, suicidal chance, on making a mistake with a protocol. They’ll just stop coming to work. Look at Spain. Many nurses have turned in notice there over the inadequate protection garments.
Warning: Molecular Biology lesson follows!
The significance is not so much in the pathology of the disease, but in determination of origin of the particular clade, which is significant for disease control. For example, the analysis of the gene sequences shows that there was a single introduction of Ebola into the human population--meaning that there is not some animal reservoir that is repeatedly introducing the disease, as is the case with bird flus. Because this is the case, disease control efforts are focused on interrupting the human chain of infection, rather than trying to cull the animal reservoir (which still has not been definitively identified).
Viruses, especially RNA viruses, mutate quite readily. This is because there are not RNA repair mechanisms to fix the RNA if an incorrect nucleotide is incorporated into the growing strand. So, whenever someone is infected with an RNA virus, they are not infected with millions of identical copies of the virus, but with millions of different viruses that all differ slightly from what we call the "consensus sequence"--the sequence that represents the most common letter at any given position within the sequence.
For example, you might be sequencing multiple samples and have the following result:
Observed sequences:
AGATTTCT
ACAATACT
ACATTAAT
GCATGACT
ATATTAGT
ACCTTGCT
ACATTATA
Consensus sequence:
ACATTACT - not observed experimentally
When the researchers talk about polymorphisms, they are referring to positions within the sequence where two or more letters are equally represented.
Before someone with advanced Dunning-Kruger attempts to claim that I clearly don't know what I'm talking about because I use the word "letter" instead of "nucleotide" or "base" or some other scientifically correct word, let me point out that it's easier to say "letter", because sequences can just as easily be amino acid sequences.
For a nerdy geek like me, looking at those small variations in sequence and mapping them out with phylogenetic tree generation software is a fascinating activity that can keep me happily employed for days.
Anyway, the significance of the genetic variability of viruses is that a person infected with one particular variant of the virus can infect someone else with a slightly different variant. And that person infects someone else with yet another variant. And so on. Reconstructing the variability patterns leads us back to the original source of infection. By comparing that original source in Guinea to circulating strains in DRC, we can estimate how long ago the virus was introduced into Guinea (within its animal reservoir). Estimates will vary, depending on working assumptions.
One aspect of the genetic variability is that the change of genetic sequence can lead to changes in protein sequence. Many changes do not. When the virus is consistently observed to change in the RNA sequence but not the amino acid sequence at a specific position or region within the expressed proteins, we call that "conserved" or, here, they use the term "synonymous" (passage from NEJM article follows at end). Biologically, that means that any deviation from the consensus sequence at that position makes the virus non-viable. Three of the amino acid substitutions listed change the charge state and size of the amino acid side group. For instance, the glycine to glutamic acid substitution introduces a bulky side chain with a negative charge. Depending on where that substitution occurs within the protein, the protein shape could be affected, or its binding to host cell proteins could be changed, or something--the significance of such a change cannot really be determined without having structural and empirical data generated by a variety of experimental strategies. Those studies can, BTW, be conducted at BSL2, since they do not require an intact virus.
Now, the pertinent passage from NEJM. Note that of the six polymorphisms observed, three are conservative and three change the physical properties of the expressed protein at those positions. In other words, the 97% variance seen in the RNA does not translate to a 97% variance seen in the proteins--the functional parts of the virus.
The EBOV in samples obtained from three patients was completely sequenced with the use of conventional Sanger techniques (GenBank accession numbers, KJ660346, KJ660347, and KJ660348; the sequences in the preliminary report have been updated). The three sequences, each 18,959 nucleotides in length, were identical, with the exception of a few polymorphisms at positions 2124 (G→A, NP552 glycine→glutamic acid), 2185 (A→G, synonymous), 6909 (A→T, sGP291 arginine→tryptophan), 9923 (T→C, synonymous), 13856 (A→G, L759 aspartic acid→glycine), and 15660 (T→C, synonymous). The Guinean EBOV strain showed 97% identity to EBOV strains from the Democratic Republic of Congo and Gabon. Phylogenetic analysis of the full-length sequences by means of Bayesian and maximum-likelihood methods revealed a separate, basal position of the Guinean EBOV within the EBOV clade.
Lancet 5 Mar 2011: Ebola haemorrhagic fever
Ebola virus has a broad cell tropism, infecting a wide range of cell types. In-situ hybridisation and electron microscopic analyses of tissues from patients with fatal disease or from experimentally infected non-human primates show that monocytes, macrophages, dendritic cells, endothelial cells, fibroblasts, hepatocytes, adrenal cortical cells, and several types of epithelial cells all lend support to replication of these viruses.50,51,57,60—63 Temporal studies in non-human primates experimentally infected with Zaire Ebola virus suggest that monocytes, macrophages, and dendritic cells are early and preferred replication sites of these viruses (figure 2).62 These cells seem to have pivotal roles in dissemination of the virus as it spreads from the initial infection site via monocytes, macrophages, and dendritic cells to regional lymph nodes, probably through the lymphatic system, and to the liver and spleen through the blood.62, 64 Monocytes, macrophages, and dendritic cells infected with Ebola virus migrate out of the spleen and lymph nodes to other tissues, thus disseminating the infection (figure 2).Although the endothelium is thought to play an important part in the pathogenesis of Ebola virus (figure 2), studies defining the molecular mechanisms of endothelial impairment are incomplete. Researchers thought that the virus' glycoprotein is the primary determinant of vascular-cell injury and that Ebola virus infection of endothelial cells induces structural damage,65 which could contribute to the haemorrhagic diathesis. However, histological analysis of autopsy tissues from several of the early outbreaks did not identify vascular lesions,66 and no vascular lesions in any subsequent studies have been reported so far. Similarly, no evidence of substantial vascular lesions in non-human primates infected with Ebola virus exists.57,60—62 In one temporal study in cynomolgus macaques, infection of endothelial cells by Zaire Ebola virus was infrequent and was mainly restricted to the terminal stages of disease.62
Together with the macrophage-rich lymphoid tissues, the liver and the adrenal gland seem to be important targets for filoviruses (figure 2), and this tropism probably has an equally important role in the disease pathogenesis. Various degrees of hepatocellular necrosis have been reported in infected people and non-human primates;1, 13, 51, 57, 66 however, the hepatocellular lesions are generally not serious enough to explain the cause of death. Importantly, haemorrhagic tendencies could be related to decreased synthesis of coagulation and other plasma proteins because of severe hepatocellular necrosis. Adrenocortical infection and necrosis have also been reported in humans and non-human primates infected with Ebola virus.1, 51 The adrenal cortex plays an important part in control of blood pressure homoeostasis. Impaired secretion of enzymes that synthesise steroids leads to hypotension and sodium loss with hypovolaemia, which are important elements that have been reported in nearly all cases of Ebola haemorrhagic fever.1 Impairment of adrenocortical function by Ebola virus infection could therefore have an especially important role in the evolution of shock that typifies late stages of Ebola haemorrhagic fever (figure 2).
(snip)
Pathogenesis
Information about the pathology and pathogenesis of Ebola virus infections in man is sparse. This shortcoming is partly attributable to the inaccessibility of the geographical regions in which these natural infections arise. However, comprehensive studies have been done in animals. Rodents such as guineapigs and mice have been used to study Ebola haemorrhagic fever.42—44 Because isolates of Ebola virus obtained from primates do not typically produce severe disease in rodents on initial exposure, serial adaptation is needed to produce a uniformly lethal infection. Mice and guineapigs have served well as early screens for assessment of antiviral drugs and candidate vaccines, and genetically engineered mice are clearly useful for the dissection of specific host—pathogen interactions. However, the disease pathogenesis recorded in rodents is less accurate in representation of the human disorder than is the disease recorded in non-human primates.45, 46
Route of infection
Ebola virus seems to enter the host through mucosal surfaces, breaks, and abrasions in the skin, or by parenteral introduction. Most human infections in outbreaks seem to occur by direct contact with infected patients or cadavers.13, 14, 47, 48 Infectious virus particles or viral RNA have been detected in semen, genital secretions,40, 49 and in skin of infected patients;50 they have also been isolated from skin, body fluids, and nasal secretions of experimentally infected non-human primates.51, 52
Laboratory exposure through needlestick and blood has been reported.53—55 Reuse of contaminated needles played an important part in the 1976 outbreaks of Ebola virus in Sudan and Zaire.13, 14 Butchering of a chimpanzee for food was linked to outbreaks of Zaire Ebola virus in Gabon,56 and contact exposure was the probable route of transmission. Although proper cooking of foods should inactivate infectious Ebola virus, ingestion of contaminated food cannot wholly be ruled out as a possible route of exposure in natural infections. Notably, handling and consumption of freshly killed bats was associated with an outbreak of Zaire Ebola virus in DRC.34 Organ infectivity titres in non-human primates infected with Ebola virus are frequently in the range of 107 to 108 pfu/g;51 thus, exposure through the oral route could invariably be associated with very high infectious doses. In fact, Zaire Ebola virus is highly lethal when given orally to rhesus macaques.57 The role of aerosol transmission in outbreaks is unknown, but is thought to be rare.
In human beings, the route of infection seems to affect the disease course and outcome. The mean incubation period for cases of Zaire Ebola virus infection known to be due to injection is 6•3 days, versus 9•5 days for contact exposures.58 Moreover, the case-fatality rate in the 1976 outbreak of Zaire Ebola virus was 100% (85 of 85) in cases associated with injection compared with about 80% (119 of 149) in cases of known contact exposure.58 For non-human primates infected with Zaire Ebola virus, the disease course seems to progress faster in animals exposed by intramuscular or intraperitoneal injection than in animals exposed by aerosol droplets.59
I wish I had any confidence at all in OSHA but I fear that even they have been staffed with yes-men and idiots.
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