Tag Archives: pandemic

PLoS One: Effectiveness of HPAI H5N1 Vaccination in Poultry – Indonesia

The problem cannot be solved via vaccination – given the diversity and greed in the global market.

Poultry%2BVaccination.JPG

#13,068

With H5N6, H5N8, H5N1 and an array of lesser HPAI H5 viruses continuing to expand globally we’ve seen desperate pleas from some hard hit farmers to allow the use of poultry AI vaccines (see South Africa: DAFF Statement On Vaccines For Avian Flu and USDA Issues 2nd Request for Proposals for HPAI Vaccine)

With the exception of China, Egypt, Indonesia, Vietnam, and Hong Kong, most countries eschew the use of bird flu vaccines, and opt instead for the OIE recommended course of culling and containment.

The reasons run the gamut from fears that poultry vaccines may only mask bird flu – not prevent it – to concerns over selling vaccinated  birds to foreign markets.  Once vaccinated, antibody tests would show positive titres, whether the birds were infected or not.

Reasons why, for more than a decade, the OIE has warned that vaccination of poultry cannot be considered a long-term solution to combating avian flu. And that “Any decision to use vaccination must include an exit strategy, i.e. conditions to be met to stop vaccination. – OIE on H7N9 Poultry Vaccines.

Countries that have gone the vaccine route over the past dozen years haven’t found an easy way to that `exit strategy’ – and while vaccine use may have them spared some economic pain – avian influenza has become increasingly entrenched in their poultry industries. 

The problem is that as avian viruses evolve, poultry vaccines become increasingly less effective; often only masking the symptoms of infection.

As an example, a 2012 study (see Egypt: A Paltry Poultry Vaccine), examined the effectiveness of six commercially available H5 poultry vaccines used in Egypt; only one (based on a locally acquired H5N1 seed virus) actually appeared to offer protection.

Poor vaccine matches can allow AI viruses to spread silently among flocks, to continue to reassort and evolve, and potentially lead to the emergence new subtypes of avian flu. A few earlier blogs on that include:

Subclinical Highly Pathogenic Avian Influenza Virus Infection among Vaccinated Chickens, China).

Study: Recombinant H5N2 Avian Influenza Virus Strains In Vaccinated Chickens

EID Journal: Subclinical HPAI In Vaccinated Poultry – China

We’ve a new study, published late last week in PLoS One, that looks at the effectiveness of HPAI H5 vaccination in Indonesia, a country once known as the world’s hot spot for human H5N1 infection, but now (for reasons cloaked in mystery) has fallen off that list. 

Since Indonesia declared bird flu `endemic’ in 2006, they haven’t had to make regular OIE reports – and so like from Egypt – we get relatively little solid reporting on their bird flu struggles in recent years. 

Today’s report, however, paints a less than impressive picture of poultry vaccination effectiveness in Indonesia over the past decade. The authors cite frequent low HI titres in poultry even after three rounds of vaccines, vaccination failures, and warn of silent infections and the generation of new H5N1 antigenic variants. 

While the authors recommend steps they believe would improve Indonesia’s AI vaccine performance, the upshot is that effective poultry vaccination programs have been elusive in Indonesia even after a decade of use, and are far more complex to mount than most people believe.

I’ve only included some of the highlights from a much longer study, follow the link to read the paper in its entirety.

Field effectiveness of highly pathogenic avian influenza H5N1 vaccination in commercial layers in Indonesia 

Simson Tarigan ,Michael Haryadi Wibowo,Risa Indriani,Sumarningsih Sumarningsih, Sidna Artanto, Syafrison Idris,Peter A. Durr, Widya Asmara, Esmaeil Ebrahimie,Mark A. Stevenson,Jagoda Ignjatovic

Abstract

Although vaccination of poultry for control of highly pathogenic avian influenza virus (HPAIV) H5N1 has been practiced during the last decade in several countries, its effectiveness under field conditions remains largely unquantified. Effective HPAI vaccination is however essential in preventing incursions, silent infections and generation of new H5N1 antigenic variants. 

The objective of this study was to asses the level and duration of vaccine induced immunity in commercial layers in Indonesia. Titres of H5N1 haemagglutination inhibition (HI) antibodies were followed in individual birds from sixteen flocks, age 18–68 week old (wo).

The study revealed that H5N1 vaccination had highly variable outcome, including vaccination failures, and was largely ineffective in providing long lasting protective immunity.

Flocks were vaccinated with seven different vaccines, administer at various times that could be grouped into three regimes: In regime A, flocks (n = 8) were vaccinated two or three times before 19 wo; in regime B (n = 2), two times before and once after 19 wo; and in regime C (n = 6) three to four times before and two to three times after 19 wo. HI titres in regime C birds were significantly higher during the entire observation period in comparison to titres of regime A or B birds, which also differed significantly from each other. 

The HI titres of individual birds in each flock differed significantly from birds in other flocks, indicating that the effectiveness of field vaccination was highly variable and farm related. Protective HI titres of >4log2, were present in the majority of flocks at 18 wo, declined thereafter at variable rate and only two regime C flocks had protective HI titres at 68 wo. 

Laboratory challenge with HPAIV H5N1 of birds from regime A and C flocks confirmed that protective immunity differed significantly between flocks vaccinated by these two regimes. The study revealed that effectiveness of the currently applied H5N1 vaccination could be improved and measures to achieve this are discussed.

         (SNIP)

Conclusions

HPAI vaccination, intensively applied in Sector 3 layers in Indonesia, had highly variable outcome, including vaccination failures and did not provide sufficiently long protective immunity in the majority of flocks. Indonesia adopted HPAI vaccination in 2004 with the aim of reducing the incidence of H5N1 infections in poultry, with the ultimate objective of achieving eradication of the virus.

Assessment of field effectiveness of the currently applied H5N1 vaccination was useful in demonstrating that vaccination, as practiced in Sector 3 poultry, could be improved. In particular, we have identified that the most frequently used vaccination regime, consisting of three vaccinations before 19 wo, does not provide sufficiently long lasting immunity and protection of layers with any of the commonly used HPAI vaccines.

Instead, four or five vaccinations, of which two are during the laying period at 26–28 and 40–48 wo, would ensure longer lasting protection and further reduce the risk from exogenously introduced H5N1 infections. Monitoring the level of immunity in vaccinated flocks would help to identify key factors that contribute to inadequate responses to vaccination, short duration of protective immunity and vaccination failures. The timing of re-vaccination could be adjusted according to the flock immunity, ensuring an effective response and longer lasting protective immunity.

(Continue . . . )

Aussie Flu, UK Flu – who cares? Get vaccinated.

Some thoughts from Dr Katherine Arden and myself  about where the flu viruses sweeping the UK came from.

Is it the “Aussie flu”? The short answer is simply “No”. There is an influenza type B virus dominating the UK right now, not an influenza type A virus. It was A (H3N2) viruses which dominated in Aus this past Flu season.

The longer answer (but please do go and read the entire piece!) is that it’s not easy to tell in a heavily travelled world constantly and rapidly producing and moving flu strains around it.

The 2017-18 influenza season has been large all over the world.

Influenza virus transmission: with or without symptoms, you’re dropping Flu virus

Given that we keep on shedding virus for days after we’re infected, it’s no surprise that office-workers who take just 1 or 2 days off may feel well enough to once again face the workload, but they are probably infecting their co-workers and helping to keep the Flu season alive.

Influenza viruses infect our cells, but cell entry alone does not result in influenza (the disease).

What happens after our cells get infected can depend on quite a few things. These include…

  1. our innate immune response. It recognises various generalized parts of the virus without having to have a specific memory of the viral strain from previous infection. It can then respond with a range of antiviral measures
  2. whether we have a pre-existing immune memory of the virus. These antibodies and cells can awake to fend off a foothold situation
  3. our age. Children have had fewer infections than adults so children succumb more often/easily
  4. the strain of Flu virus and whether it is more able to dodge, or even over-stimulate, our immune response; where in our body it prefers to replicate; how good it is at replicating
  5. which past Flu epidemics and pandemics we may have survived (related to No. 2, 3 and 4) because this affects how susceptible we are to the latest subtypes or strains
  6. how much virus lands on how many cells (includes how many exposures to the virus and how long each exposure is)
  7. how the virus arrives; via direct contact, droplet or aerosol (also called airborne or droplet nucleus transmission), self inoculation or a mix
  8. where the virus is introduced. Virus may enter via the cell eyes, throat, nose, lungs etc.

Quick facts about Flu virus incubation 

We incubate Flu virus for about 2 days after infection.

Virus usually reaches peak levels within 3 days after infection, reaching slightly higher levels in children than adults, and stopping after about a week.[1]

Shedding of Flu virus can last as long as 3 weeks, but more commonly stops within a week after signs and symptoms start.[1,23] Shedding can last longer in very sick infants.[1]

The next person we infect in the transmission chain can begin to show symptoms at around 2 to 4 days. For the SARS coronavirus, this range was 8 to 10 days.[1]

So we quickly reach peak virus levels and become infectious. These numbers all come as part of a range – higher or lower, longer or shorter all being possible. In those with mild or no symptoms, peak Flu virus levels are generally lower than in those who have clear signs and symptoms.[1]

Flu: from me to you

Flu viruses transmit via propelled droplets (≥5μm), aerosols [7] or after contact with infected people or contaminated surfaces and objects onto which virus-laden droplets have settled.[1]

It may amaze some to learn that 1 of every 3 adults have been observed to nose-pick or eye-rub each hour.[21] AN not just once per hour. Another study found that people touched surfaces and their mouth/nose 3 to 4 times per hour![24] That’s how those surfaces come into play; our fingertips become contaminated and then we inoculate ourselves with Flu virus.

Hand washing is really important but that’s a lot of touches. Holding off on touching our faces until after we can wash our hands is a good habit to develop.

As well as the virus itself, environmental conditions impact on how long Flu virus can remain infectious on surfaces and in these droplets and droplet nuclei.[12,13] Flu viruses can also remain infectious on nonporous surfaces for some time in general. We come into contact with these kinds of materials many times each day.[2,3] Unless we live on an island near a Jedi temple.

Infection without illness

Occasionally influenza infects without us showing any signs or feeling any symptoms of having become a virus taxi.

Among these outcomes – called subclinical or asymptomatic – if we looked hard enough we might  sometimes find a small temperature rise, or a bit of a sniffle or tickly throat that we shuck off as nothing. But we seldom think about that. We can also get mild common cold-like illness from a Flu virus infection. We certainly wouldn’t go to a Doctor for these but we would go to school, work, parties and shopping.

Mild or asymptomatic outcomes from Flu infection can occur in as many as 50-77% of infected people.[1,22]

Studies using ferrets – a small animal model that can be infected using human Flu viruses and show relevant illness – identified that the amount of virus in the nose correlated with transmission of Flu virus from infected to uninfected ferrets.[20] Obvious signs of ferret sickness were not necessary. Droplets from symptomatic ferrets late in the disease course did not result in infection of sentinel uninfected ferrets but direct contact usually did (as it did in the early stages too).

Flu viruses may also transmit during the “presymptomatic” period. This is the time between when we’ve been infected and virus is replicating in our airways but the we’re not yet showing signs of the illness to come. Presymptomatic ferrets could produce infectious droplets (and aerosols?).[20] And direct contact (which is pretty direct among ferrets) was a transmission risk before and during symptoms. Another reminder to wash those hands (or paws, if you’re a ferret)!

One study found that neither contact tracing nor isolation of infected people would likely prevent an epidemic. Asymptomatic/presymptomatic spread of infection is a good reason for this.[4]

But hang on a tick. How can Flu virus be transmitted from a person or an animal if they are infected but not coughing or sneezing out droplets and aerosols and contaminating surfaces?

No coughing or sneezing but we all do some breathing

Good question. One way might be through breathing and talking – yes, it might be that easy.[5,6,8,9]

Studies have used different methods to collect breath from virus-infected humans and found virus genetic material. Commonly this is RNA from viruses that have RNA genomes like Flu viruses, respiratory syncytial viruses, rhinoviruses, coronaviruses and parainfluenzaviruses.[7,8,18]

Viruses were not able to be grown in culture, or culture was not used in these studies and this is a limitation because we can’t say with certainty that viruses were breathed out during such studies could infect a susceptible person; we don’t know if the positive results mean  infectious virus was present.

ASIDE: PCR methods are used to detect viral RNA. These may be too sensitive to define the period during which a person is infectious, as was found in a study that used ferrets.[10]

Flu virus RNA, parainfluenza virus-3 RNA or rhinovirus RNA has been detected from infected ill subjects breathing only through their noses or their mouths, and/or while talking or coughing.[8,9]  Rhinovirus RNA was also collected from the breath of 3 talking or just breathing infected but asymptomatic subjects.[9]

In a study of 2 ill subjects, infectious rhinovirus was produced as shown by virus replicating in laboratory cell cultures from samples of exhaled nasal breath and coughing breath.[8] Flu isn’t the only respiratory virus that may spread via hot air.

So how big is the risk of transmitting virus by breathing?

Despite Flu RNA being detected in 81% of infected people with coughs in a different study, infectious Flu virus was only identified from 2 of 21 people’s cough aerosols.[11] Another study found RNA in a lot, but recovered infectious Flu virus from only 2 naturally infected volunteers; those with the highest levels of Flu virus RNA in their breath.[5] Intriguingly, the authors also reported more Flu virus RNA in the smaller droplet nuclei than in larger droplets.[5,13]

These findings confirm that infectious virus can be produced from breathing alone, but that only a fraction of those infected seem to do this.

But let’s not sideline this route too much. The most infectious 20% of children and adults in one study, were responsible for 80% of infectiousness (infectious = amount of Flu virus RNA being shed).[23] Even when only a few infected asymptomatic people shed infectious Flu virus, each of those few may infect several or more others.

ASIDE: All of this work is heavily impacted upon by biological variability. These results apply using these particular methods, those scientists, that subject group, their experimental conditions and those Flu virus strains. Interesting hybrid detection methods can help address the RNA vs. virus detection issue, improving the sensitivity of detecting infectious virus.[17] Such techniques can be useful to smooth out some of the differences between studies and to improve upon past studies that only detected RNA.[17]

The range of an aerosol

A final topic on Flu virus transmission; distance. Flu virus RNA has been detected in air collected 1.828m (6 feet) away from ill patients.[18] The authors proposed that there may have been enough infectious virus in that air to cause an infection.

Research from 2014 showed bacteria-laden cough aerosols could travel 4m (13 feet!) and retain bacterial infectivity.[19] Also, aerosols can hang around (literally) until they impact with something. I’d wager that viruses could manage a similar feat.

Air management including of humidity, filtration, flow rate and pressure differences are important protections against spread of infection within healthcare settings. Appropriate personal protective equipment is also important to reduce exhaled or expelled droplets and protect from those expelled by other infected people.[5] This is known.

Droplets and droplet nuclei add to what is clearly a complex Flu equation.

So What? Being infected but looking healthy is nothing to sneeze at

Aerosols play an important part in the transmission of Flu viruses. Virus can be recovered from asymptomatic folks and breathing and talking are the likely ways transmission occurs before anyone around us knows we are sick.

Given that we keep on shedding virus for days after we’re infected, it’s no surprise that office-workers who take just 1 or 2 days off may feel well enough to once again face the workload, but they are probably infecting their co-workers and helping to keep the Flu season alive.

Flu viruses and the Flu thank you for your tireless efforts.

They thank you less if you got a vaccine which may have reduced the likelihood that a virus gains a foothold in your system or if it does, perhaps reduced the amount of virus you shed, the length of time you shed it or how sick you get at all.

References…

  1. Nonpharmaceutical Interventions for Pandemic Influenza, International Measures
    http://ift.tt/2DcboFB
  2. Survival of Influenza Viruses on Environmental Surfaces
    http://ift.tt/2iyxODh
  3. Influenza Virus Contamination of Common Household Surfaces during the 2009 Influenza A (H1N1) Pandemic in Bangkok, Thailand: Implications for Contact Transmission
    http://ift.tt/2DcH8KR
  4. Factors that make an infectious disease outbreak controllable
    http://ift.tt/2AYhkMd
  5. Influenza Virus Aerosols in Human Exhaled Breath: Particle Size, Culturability, and Effect of Surgical Masks
    http://ift.tt/2h2C9Mv
  6. Influenza Virus in Human Exhaled Breath: An Observational Study
    http://ift.tt/2AYhljf
  7. Aerosol transmission of influenza A virus: a review of new studies
    http://ift.tt/2DayCf9
  8. A New Method for Sampling and Detection of Exhaled Respiratory Virus Aerosols
    http://ift.tt/2AZvsFa
  9. Exhalation of respiratory viruses by breathing, coughing, and talking
    http://ift.tt/2DdNOIw
  10. Correlation Between the Interval of Influenza Virus Infectivity and Results of Diagnostic Assays in a Ferret Model
    http://ift.tt/2AZvtcc
  11. Measurements of Airborne Influenza Virus in Aerosol Particles from Human Coughs
    http://ift.tt/2Dc81OY
  12. Influenza Virus Aerosols in the Air and Their Infectiousness
    http://ift.tt/2AYhmUl
  13. Ebola virus may be spread by droplets, but not by an airborne route: what that means
    http://ift.tt/2DdNPMA
  14. Comparison of the Levels of Infectious Virus in Respirable Aerosols Exhaled by Ferrets Infected with Influenza Viruses Exhibiting Diverse Transmissibility Phenotypes
    http://ift.tt/2AZvuNi
  15. Influenza Virus Respiratory Infection and Transmission Following Ocular Inoculation in Ferrets
    http://ift.tt/2DdNQA8
  16. Ocular Tropism of Influenza A Viruses: Identification of H7 Subtype-Specific Host Responses in Human Respiratory and Ocular Cells
    http://ift.tt/2AZvvRm
  17. Enhanced detection of infectious airborne influenza virus
    http://ift.tt/2D9KAWt
  18. Exposure to Influenza Virus Aerosols During Routine Patient Care
    http://ift.tt/2Dt4EyO
  19. Viability of Pseudomonas aeruginosa in cough aerosols generated by persons with cystic fibrosis
    http://ift.tt/2DdNREc
  20. Transmission of a 2009 H1N1 Pandemic Influenza Virus Occurs before Fever Is Detected, in the Ferret Model
    http://ift.tt/2AYhp2t
  21. Transmission of rhinovirus colds by self-inoculation
    http://ift.tt/2DdNSbe
  22. Comparative community burden and severity of seasonal and pandemic infl uenza: results of the Flu Watch cohort study
    http://ift.tt/2AZvwoo
  23. Heterogeneity in Viral Shedding Among Individuals With Medically Attended Influenza A Virus Infection
    http://ift.tt/2D7HfqK
  24. Facing Ubiquitous Viruses: When Hand Washing Is Not Enough
    http://ift.tt/2AYhq6x

Landscape and rodent community composition are associated with risk of hemorrhagic fever with renal syndrome in two cities in China, 2006–2013

Supply rodents with more food than normal – and you get more rodents and more become diseased and pass disease to humans planting more food – duh? Hemorrhagic fever with renal syndrome (HFRS) is a rodent-borne disease caused by hantaviruses. Landscape can influence the risk of hantavirus infection for humans, mainly through its effect on rodent community…

CDC FluView Week 52: Influenza `Increased Sharply’ Across The Nation

wash hands, doors, handles, phones, keyboards, touch screens…

http://ift.tt/2i6mLj8

#13,034

For the second week in a row the CDC’s FluView report shows influenza activity has increased sharply across the nation, with the number of patient visits for ILI (Influenza-like Illness) so far matching the 2014-15 season, but on a pace that seems likely to exceed anything we’ve seen in recent years.

http://ift.tt/2i6mLj8

As always, the FluView report is a snapshot of flu activity more than a week ago, and so the numbers being racked up today are likely higher. 

Add in reporting delays over the holidays, and ongoing data collection problems with the P&I Mortality rate (which runs 2 weeks behind the rest of the data) and today’s report probably doesn’t do this year’s flu season justice. 

In any event, the numbers we have are plenty bad enough.  A brief summary shows:

2017-2018 Influenza Season Week 52 ending December 30, 2017

All data are preliminary and may change as more reports are received.
Synopsis:

During week 52 (December 24-30, 2017), influenza activity increased sharply in the United States.

Viral Surveillance: The most frequently identified influenza virus subtype reported by public health laboratories during week 52 was influenza A(H3). The percentage of respiratory specimens testing positive for influenza in clinical laboratories increased.
Pneumonia and Influenza Mortality: The proportion of deaths attributed to pneumonia and influenza (P&I) was below the system-specific epidemic threshold in the National Center for Health Statistics (NCHS) Mortality Surveillance System.
Influenza-associated Pediatric Deaths: One influenza-associated pediatric death was reported.
Influenza-associated Hospitalizations: A cumulative rate of 13.7 laboratory-confirmed influenza-associated hospitalizations per 100,000 population was reported.
Outpatient Illness Surveillance:The proportion of outpatient visits for influenza-like illness (ILI) was 5.8%, which is above the national baseline of 2.2%. All 10 regions reported ILI at or above region-specific baseline levels. New York City and 26 states experienced high ILI activity; Puerto Rico and nine states experienced moderate ILI activity; the District of Columbia and six states experienced low ILI activity; and nine states experienced minimal ILI activity.
Geographic Spread of Influenza:The geographic spread of influenza in 46 states was reported as widespread; four states reported regional activity; the District of Columbia reported local activity; and Guam, Puerto Rico, and the U.S. Virgin Islands did not report.
(Continue . ..  )

If you haven’t gotten the flu vaccine, it isn’t too late.  While it may not protect as well as we’d like against H3N2, influenza B and H1N1 are part of this year’s mix, and the vaccine is expected to do much better against those strains.

If you aren’t practicing heavy duty flu hygiene (covering coughs, washing hands, staying home when sick, etc.) and somehow you haven’t gotten sick yet, you need to start.

And as we discussed last week, in Yes, We Have No Pandemic . . . But Line Up A Flu Buddy Anyway, now is a good time to form alliances with friends, relatives, and neighbors to help you (and them) get through this flu season.

While it may be too soon to call this year’s flu season `epic’, the early numbers are very impressive.  And not in a good way.

Keep%2Bcalm%2BSanitizer%2Bcup%2Bnew.jpg



 

CDC Update: Candida Auris – December 2017

Yikes – no explanation for the spread by state…

Candida%2Bauris%2Bus%2Bmap.JPG
Credit CDC

#12,973

In June of last year the CDC issued a Clinical Alert to U.S. Health care facilities about the Global Emergence of Invasive Infections Caused by the Multidrug-Resistant Yeast Candida auris.

C. auris is an emerging fungal pathogen that was first isolated in Japan in 2009. It was initially found in the discharge from a patient’s external ear (hence the name `auris’).  Retrospective analysis has traced this fungal infection back over 20 years.

Since then the CDC and public health entities have been monitoring an increasing number of cases (and hospital clusters) in the United States and abroad, generally involving bloodstream infections, wound infections or otitis (see November Update).

Adding to the concern:

  1. C. auris infections have a high fatality rate
  2. The strain appears to be resistant to multiple classes of anti-fungals  
  3. This strain is unusually persistent on fomites in healthcare environments.
  4. And it can be difficult for labs to differentiate it from other Candida strains

The CDC has updated their C. Auris surveillance page, where they show – as of November 30th – 174 confirmed cases and 29 probable cases, across 10 states.

The number of colonized asymptomatic cases detected by targeted screening in four states has risen to 257  (see FAQ for Patients and Family Members).

Candida%2BCDC%2Bupdate.JPG

Last August the CDC promoted the first ever Fungal Disease Awareness Week, and presented a COCA call webinar called Tackling an Invasive, Emerging, Multi-drug Resistant Yeast: Candida auris — What Healthcare Providers Need to Know, which is now archived and available online.

CIDRAP’s Antimicrobial Stewardship Project (ASP) also held an hour long webinar (see below), which is now available on the CIDRAPASP Youtube channel.

https://www.youtube.com/watch?v=gCO7kWdnbkY

 (Note: you’ll find more than a dozen other on-topic videos available on this channel as well).

For more on this emerging fungal pathogen, you may wish peruse the CDC’s dedicated web page:

And for some older blogs on the topic, you may wish to revisit:

Conference tweets: what’s your aim here?

There are many lists detailing what you need to consider when you use Twitter and Tweet stuff during a conference. Mine is below. But before we get to that, ask yourself this: what am I aiming to do here? It’s a pretty simple question but one that you may not have asked yourself before you decided to share your thoughts with the the world.

I’m assuming that you understand that when you Tweet, you’re not emailing friends or talking on the phone or just to a select few sciency mates; this is worldwide communication. 

But before that list, here’s a short pre-list checklist of things…

  • Why do I want to Tweet?
    Gonna stick to 20-year old in-jokes and name drops for your hardcore science krew or try to breakdown complexity, explain the science, descrrbe the talk, engage the public and advertise your expertise?
  • Who am I tweeting for?
    Think about your intended audience(s). It may be that you could just talk to those people at drinks or lunch?
  • Have I checked with the organizers that tweeting is okay and made sure there are no “don’t tweet this” signs on the slides? 
    Some people like to show their unsubmitted-data-for-future-publication to a room full of competitors but not to the internet. Or something.
  • Have I looked for Twitter handles beforehand
    Help out a presenter – use their handle and get them some more love (or maybe a collaboration or two)!
  • Make sure your Twitter account has a good photo (whether a headshot, lab photo or a graphic-it’s going to be your brand for a while) and a relevant bio
    Mention your role(s), passions and home city at least. 
  • Do I have the time to do this usefully and the skills to do it professionally?
    If you’re tweeting because “shiny new social media thing” or “My University says I have to communicate” but you don’t really know what that means then perhaps sit this one out. A lot of people aren’t that good at communicating clearly, quickly or outside their nerd herd. Perhaps just sit back and observe what’s going on around you in the conference twittersphere. Join in later maybe. Or maybe it’s just not for you.

Tweetings from meetings…

  1. Use the conference hashtag in every tweet
  2. Apart from live-tweeting the presentations, Tweet info about the host city, restaurants, public transport, good coffee spots, cheap eats etc.
    Be helpful and useful. Maybe even call for company for morning coffee or shout out to form a group around a topic and have dinner together
  3. Identify the speaker (always give credit) – name, Twitter handle (see above), talk subject in first Tweet
    After that just refer to last name or leave it out entirely if you are confident you can thread the tweets about each talk
  4. Add some detail about the talk in a follow-up tweet…or 2…or 3
    “Bob talking about Protein-X “….WHAT about Protein-X? What’s Bob saying? Has Bob made a good point? Is there some info to share? 
  5. If you want your Tweet to get noticed and to spread around, make sure it has context – why is work/research cool and what will it lead to? 
    Why should I care about your tweet or Bob’s work or Bob or you? These are mini-stories-don’t just flash up the cover, overview the book. This applies if tweeting just for you peers or for the wider world 
  6. Take and share slide photos – but good quality ones, not blurry or unzoomable nightmares 
    Presenters have put time and effort into conveying their data to their audience – you are now expanding their audience to dozens or thousands of extra seats, so do them justice
  7. Check the hashtag during the meeting – retweet other Tweets, comment on their comments
    Engage, follow, laugh, enjoy, expand and curate on your networks; it is social media after all
  8. Try and work in some humour
    Who doesn’t like a laugh? Be interesting and engaging.
  9. Try and find some data to quantify the reach and impact of your tweeting
    For the Masters. Symplur’s free monitoring of healthcare conference hashtags is a good start to see who is doing well. But look at the numbers of your retweets and engagements via Twitter analytics too. Talk about it. It’s an output and its quantifiable

Remember you are tweeting to the world as well as to scientists. This is a great opportunity to test out your communication skills and to inform those who will ultimately benefit from (and often fund) your contribution to the history of science – the public.

Having a Twitter account is one thing. Using it to science is entirely another.