Archive for the ‘Ebola’ Category
Emerging Infectious Diseases 20-year Timeline
Sourced through Scoop.it from: wwwnc.cdc.gov
It is well worth remembering that the CDC’s EID has been in the forefront of reliable reporting on emerging viral diseases – as well as others, of course – for a quarter century now.
And I’ve been getting it that long…they used to send it out for free, AND it was available on the Web from very early on, so I used to regularly use articles from it for teaching 3rd year students.
It is a great institution, and I wish it well!
REGISTRATION IS NOW OPEN – VIROLOGY AFRICA 2015
On behalf of the Institute of Infectious Disease and Molecular Medicine of the University of Cape Town and the Poliomyelitis Research Foundation, we are pleased to invite you to Virology Africa 2015 at the Cape Town Waterfront.
VENUE AND DATES:
The conference will run from Tuesday 1st – Thursday 3rd December 2015. The conference venue is the Radisson Blu Hotel with a magnificent view of the ocean. The hotel school next door will host the cocktail party on the Monday night 30th November and in keeping with Virology Africa tradition, the dinner venue is the Two Oceans Aquarium.
Early Bird Registration closes – 30 September 2015
Abstract Submissions deadline – 30 September 2015
The ACADEMIC PROGRAMME will include plenary-type presentations from internationally recognised speakers. We wish to emphasise that this is intended as a general virology conference – which means we will welcome plant, human, animal and bacterial virology contributions. The venue will allow for parallel workshops of oral presentations. There will also be poster sessions. Senior students will be encouraged to present their research. We have sponsorship for students to attend the meeting and details will be announced later in the year.
A program outline has been added to the website
Our preliminary programme includes two workshops.
There is a hands-on workshop on “Plant cell packs for transient expression: Innovating the field of molecular biopharming”, with the contact person being Dr Inga Hitzeroth – Inga.Hitzeroth@uct.ac.za. This workshop will run at UCT one day before the conference, 30th November, and a second day, 4th December, after the conference.
The second workshop is on “”Viromics for virus discovery and viral community analysis”. The workshop at UCT will be on 4 and 5 December with the contact person being Dr Tracy Meiring – email@example.com.
Some of the workshop presenters will be integrated into the conference programme but the practical components will be run at University of Cape Town. Separate applications are necessary for each workshop.
If you are prepared to fund an internationally recognised scientist to speak at the conference or if you wish to organise a specialist workshop as part of the conference, please contact
Anna-Lise Williamson or Ed Rybicki.
For any enquiries please contact
Miss Bridget Petersen/ Email: firstname.lastname@example.org or phone: +27 21 486 9111
Ms Deborah McTeer/Email: email@example.com or +27 83 457 1975
20 years after I first posted something by Laurie Garrett – who has written two of the the most thought-provoking, informative and frightening books I have ever read (The Coming Plague, and Betrayal of Trust) – I see she has just published possibly the single best account of the recent Ebola virus disease outbreak in West Africa.
Seriously. Exhaustive, deep, analytical – and like her books, throwing some harsh light on world health care systems (or the lack thereof, in the case of the WHO), while at the same time making useful suggestions.
Like this one:
“And so it comes back to money. The world will get what it pays for—and right now, that is not very much.”
Absolutely: consider that the late and haphazard and meagre response by most governments let the epidemic peak and then start to subside – without actually, in the case of the US, managing to get more than one treatment centre functional in Liberia, before they ran out of patients. That the health systems of all three countries are in such bad shape that they can’t deal with childbirth and malaria right now.
Laurie, it’s a great piece, really it is. It’s also depressing as hell. But that’s life!
I would like to test the response to a Introduction to Virology ebook that I want to develop from my extant Web-based material, given that this is likely to disappear soon with our Web renewal project here at UCT.
Download the Virus Picture Book excerpt here. And then please tell me what you think / whether you would buy one (projected price US$15 – 20)? Ta!
I have already done a partial retrospective on having been reporting on Ebola haemorrhagic fever viruses for just over 20 years – but I totally forgot to commemorate that I have been producing Web pages for just over 21! So I’m going to go on a nostalgic ramble through the past, mainly using Ebola as the vehicle, and highlighting some of the history of virology along the way.
By the way, I HAVE to commend the Wayback Machine here: I have also previously bemoaned the fact that Web pages are NEVER preserved by their creators at regular intervals – but this is exactly what they do. From 1997 onwards in the case of the whole of the University of Cape Town’s site and mine as part of that – and how interesting it has been to go back and look at what I thought was cool then! But actually, what’s not to like? I mean, there’s hepatitis G, Congo fever, smallpox, Ebola, “equine morbillivirus” (aka Hendra virus) – and life on Mars. Or not B-)
What’s interesting, though, is that they have preserved almost all of my Ebola news pages – dating from May 1995, from right near the onset of the Kikwit Ebola epidemic. There’s all sorts of interesting stuff there – though with some holes, caused by Lost Pages – ranging from a discussion of the possibility of finding Ebola in cotton plants [not!], with my old friend Murilo Zerbini, to a thread on “Candidate for the Ebola Reservoir Organism” from the late lamented bionet.virology discussion group, to whether Ebola Reston was airborne (probably not).
Great historical stuff, right there – and thank deities it is preserved via Wayback, because our upcoming Web renewal project here at UCT will kill ALL links from our Departmental site. Get it while you can!
And while we’re at it: here’s a useful list of all Ebola-related posts on ViroBlogy since 2011. Note when the first mention of plant-made antibodies to Ebola virus was….
18 July, 2015
29 January, 2015
30 December, 2014
13 November, 2014
26 October, 2014
8 September, 2014
25 August, 2014
20 August, 2014
13 August, 2014
5 August, 2014
30 July, 2014
8 August, 2012
1 August, 2012
31 July, 2012
14 June, 2012
Current Opinion in Virology – Mass extinctions, biodiversity and mitochondrial function: are bats ‘special’ as reservoirs for emerging viruses?
5 April, 2012
14 January, 2012
19 December, 2011
6 December, 2011
In 2008–09, evidence of Reston ebolavirus (RESTV) infection was found in domestic pigs and pig workers in the Philippines. With species of bats having been shown to be the cryptic reservoir of filoviruses elsewhere, the Philippine government, in conjunction with the Food and Agriculture Organization of the United Nations, assembled a multi-disciplinary and multi-institutional team to investigate Philippine bats as the possible reservoir of RESTV.
Sourced through Scoop.it from: www.virologyj.com
I recall at the time of its discovery, thinking that the virus must have reservoir species back home in the East – and that the fact that no disease had ever been reported from there in humans, meant it was completely under the radar.
There was also the issue that the virus seemed to have been transmitted between monkeys in the Reston facility without any direct contact – and even between rooms, which would imply airborne transmission.
Which frightened the cr@p out of many people, and I am sure especially those primate centre workers who were found to be seropositive for the virus, in the absence of any symptoms – even though at teh time, unsanitary conditions and overcrowding were blamed (http://www.mcb.uct.ac.za/ebola/ebolair.html).
It is still something that needs to be looked at seriously: is Ebola Reston more transmissible than Zaire, Sudan and the rest – and if so, why?
Those interested can pick up on what happened at the time, here on the Ebola information pages I ran for a while:
I have to thank my long-time digital media guru, Alan J Cann, for reviewing our humble eBook offerings in MicrobiologyBytes. You good man! Much appreciated, and it will not have escaped our attention that this endorsement may actually result in sales. If so, a glass or three of the finest red is yours if you come to these shores, good sir B-)
The discovery of filoviruses: Marburg and Ebola
In 1967, the world was introduced to a new virus: thirty-one people in Marburg and Frankfurt in Germany, and Belgrade in the then Yugoslavia, became infected in a linked outbreak with a novel haemorrhagic fever agent. Twenty-five of them were laboratory workers associated with research centres, and were directly infected via contact with infected vervet monkeys (Chlorocebus aethiops) imported to all three centres from Uganda. Seven people died. In what what was a remarkably short period of time for that era – given that this was pre-sequencing and cloning of nucleic acids, let alone viruses – it took less than three months for scientists from Marburg and Hamburg to isolate and characterise what was being called “green monkey virus” virus. The new agent was named Marburg virus (MARV), after the city with the greatest number of cases.
The first electron micrograph of the virus clearly exhibits the filamentous nature of the particles, complete with the now-famous “shepherd’s crook”.
The virus disappeared until 1975, when an Australian hitchhiker who had travelled through what is now Zimbabwe was hospitalised in Johannesburg, South Africa, with symptoms reminiscent of Marburg disease. He died, and his female companion and then a nurse also became infected with what was suspected to be yellow fever or Lassa viruses. In an example for later outbreaks, this led to rapid implementation of strict barrier nursing and isolation of the patients and their contacts, which resulted in quick containment of the outbreak – with recovery of the two secondary cases. MARV was later identified in all three patients.
Ebola viruses burst from obscurity in 1976, with two spectacular outbreaks of severe haemorrhagic fever in people – both in Africa. In the better-known outbreak for which the viruses were later named, Ebola virus (EBOV) was first associated with an outbreak that eventually totalled 318 cases, starting in September 1976. This was in the Bumba Zone of the Equateur Region in the north of what was then Zaire, and is now the Democratic Republic of the Congo (DRC). The index case in the outbreak, as well as many of those subsequently infected, was treated in the Yambuku Mission Hospital. He was injected with chloroquine to treat his presumptive malaria: within a few days fever symptoms developed again; within a week, several others who had received injections around the same time also developed fevers which in several cases had haemorrhagic complications.
Interestingly, women 15-29 years of age were most affected by the disease: this was strongly correlated with their attending antenatal clinics at the hospital, where they regularly received injections.
Apparently the hospital had only five old-style syringes and needles, and these were reused without proper sterilisation. Nearly all cases in this outbreak either received injections at the hospital, or had close contact with those who had.
Most people were infected within the first four weeks of the outbreak, after which the hospital was closed because 11 of 17 staff had died. Another 269 people died, for a total estimated case-fatality rate of 88%.
The incubation period for needle- transmitted Ebola virus was 5 to 7 days and that for person to person transmitted disease was 6 to 12 days.
Interestingly, in post-epidemic serosurveys in DRC, antibody prevalence to the “Zaire Ebola virus” has been 3 to 7%: this indicates that subclinical infections with the disease agent may well be reasonably common.
The team that discovered the virus at the Antwerp Institute of Tropical Medicine in Belgium, did so after receiving blood samples in September 1976 from a sick Belgian nun with haemorrhagic symptoms who had been evacuated from Yambuku to Kinshasa in the DRC, for them to investigate a possible diagnosis of yellow fever. Following her death, liver biopsy samples were also shipped to Antwerp – where the team had already ruled out yellow fever and Lassa fever. Because of the severe nature of the disease, and its apparently novel agent, the World Health Organisation (WHO) arranged that samples be sent to other reference centres for haemorrhagic viruses, including the Centres for Disease Control (CDC) in Atlanta, USA.
The Belgian team were the first to image the virus derived from cell cultures on an electron microscope – when it was obvious that the only thing it resembled was Marburg virus.
The CDC quickly confirmed that it was Marburg-like, with possibly the most famous virus image in the world, but that it was a distinct and new virus.
This meant it needed a name – and it was given one derived from the Ebola River that was supposed to be near the town of Yambuku.
Another, minor outbreak of the virus occurred in June 1997 in Tandala in north-western DRC: one young child died, and virus was recovered from her – and subsequent investigations showed that “two previous clinical infections with Ebola virus had occurred in 1972 and that about 7% of the residents had immunofluorescent antibodies to the virus”. This further reinforced the idea that subclinical infections were possible.
In June 1976 – before the Yambuku epidemic in DRC – an outbreak of a haemorrhagic fever began in the southern Sudanese town of Nzara. The presumed index case was a storekeeper in a cotton factory, who was hospitalised on June 30th, and died within a week.
There were a total of 284 cases in this outbreak: there were 67 in Nzara, where it is presumed to have originated, and where infection spread from factory workers to their familes. There were also 213 in Maridi, a few hours drive away – where, as in Yambuku, the outbreak was amplified by “nosocomial” or hospital-acquired transmission in a large hospital. In this case, transmission seems to have been associated with nursing of patients. The incubation period in this outbreak was 7 – 14 days, with a case mortality rate of 53%.
Two viral isolates were made from sera from Maridi hospital patients in November 1976. Antibodies to the now-identified “Ebola virus” from DRC were detected in 42 of 48 patients clinically-diagnosed patients from Maridi – but in only 6 of 31 patients from Nzara. However, it was subsequently shown that the Sudan and DRC Ebola viruses were different enough from one another to be separate viral species (see later), which undoubtedly affected the results.
Interestingly, 19% of the Maridi case contacts had antibodies to the virus – with very few of them with any history of illness. This strongly indicates that the Sudan virus can cause mild or even subclinical infections.
An indication of the possible origin of the epidemic is the fact that 37% of the workers in the Nzara cotton factory appeared to have been infected, with 6 independently-acquired infections – and that this was concentrated in the cloth room, where there were numerous rats as well as thousands of insectivorous bats in the roof. However, subsequent study of antibodies in the bats failed to detect evidence of infection, and no virus was isolated from bat tissue.
There was another outbreak of the same type of Ebola haemorrhagic fever in the area of Nzara in July – October 1979: this resulted in 34 cases, 22 of them fatal, with the index patient working at the cotton factory and all others being infected via the hospital he was admitted to. It is interesting that antibodies to the Sudan virus were detected in 18% of adults not associated with the outbreak, leading the report’s authors to speculate that the virus was endemic in this region.
It was thought that the Sudan and DRC outbreaks were linked: the original WHO Bulletin report on the Sudan outbreak even speculates that extensive truck-borne commercial goods traffic between Bumba in DRC and Nzara in what is now South Sudan could have caused the DRC outbreak. However, comparisons between the viruses isolated from the two epidemics later showed that they were distinct, both in terms of virulence, and antigenicity – meaning the Sudan virus got its own name.
Epidemics and outbreaks have resulted from person to person transmission, nosocomial or in-hospital spread, or laboratory infections. The mode of primary infection and the natural ecology of these viruses are unknown. Association with bats has been implicated directly in at least 2 episodes when individuals entered the same bat-filled cave in Eastern Kenya. Ebola infections in Sudan in 1976 and 1979 occurred in workers of a cotton factory containing thousands of bats in the roof. However, in all early instances, study of antibody in bats failed to detect evidence of infection, and no virus was isolated form bat tissue.
Scientists at the Institut Pasteur in France who are tracking the Ebola outbreak in Guinea say the virus has mutated.
I would be surprised it there weren’t evidence by now of adaptation to humans: never in any previous outbreak of EHD [Ebola haemorrhagic disease] has the person-person chain of transmission been sustained for so long, meaning never before has there been the opportunity for human-specific adaptations to become established.
The article points out that on consequence of mutation may be that the virus becomes less virulent, leading to a greater incidence of asymptomatic infection – of which there is already evidence from previous outbreaks, and which has been implicated in the lessening incidence of transmission because of increasing herd immunity.
However, this same property might lead to increased transmission to the non-exposed, because of a lack of signs that contacts with the infected person(s) should be avoided – and for a disease as lethal as EHD, even a reduced mortality rate still means you should avoid it at all costs.
The idea of developing a modified live measles virus vaccine as an Ebola virus vaccine vector, which is what the Institut Pasteur is apparently doing, seems to be a very good one. Measles is still a major potential problem in that part of the world, necessitating regular infant immunisations, and coupling anti-measles with an anti-Ebola vaccine in those countries is probably very good use of both a proven vaccine and existing EPI infrastructure.