Influenza Virus Survival At Opposite Ends Of The Humidity Spectrum

Photo Credit PHIL (Public Health Image Library)

 

 

# 6763

 

Although just about everybody knows that winter heralds the arrival of influenza season, one of the enduring mysteries about influenza is why it is predominantly a winter phenomenon – at least in temperate zones of the world.

Numerous theories abound, including;

 

• During the winter people tend to gather indoors, with less outside ventilation.
• Diminished sunlight exposure may reduced Vitamin D levels (see Study: Vitamin D And Flu-Like Illnesses)
• With schools in session, millions of children co-mingle and more efficiently share viruses

 

While these may be factors, they don’t satisfactorily explain our yearly winter flu season. Nor are they very helpful in explaining why the flu transmits pretty well in the tropics, where there is little temperature variability. 

 

In recent years, researchers have been looking at relative humidity (RH) and absolute humidity (AB)as factors in aiding influenza virus survival (IVS). 

 

In 2007, we looked at a study (see Cold And Dry Statistics) that appeared in  PLoS Pathogens  entitled  Influenza Virus Transmission Is Dependent on Relative Humidity and Temperature  by Anice C. Lowen, Samira Mubareka, John Steel,  and Peter Palese. 

 

Using a guinea pig as a model host, they showed that airborne spread of the  influenza virus was at least partially dependent upon both ambient relative humidity and temperature.

 

The link was significant, but not overwhelming.

The following year researchers Jeffrey Shaman and Melvin Kohn and found an even stronger correlation between the AH (Absolute Humidity) and the survival, and transmission of the influenza virus (see It's Not So Much The Heat, It's The Humidity).

 

Absolute humidity modulates influenza survival, transmission, and seasonality

Jeffrey Shaman, and Melvin Kohn

 

In early 2010, Jeffrey Shaman returned – joined by Virginia E. Pitzer, Cécile Viboud, Bryan T. Grenfell and Marc Lipsitch – to pen a study published in PLoS Biology called:

 

Absolute Humidity and the Seasonal Onset of Influenza in the Continental United States

(Excerpt)

Here we extend these findings to the human population level, showing that the onset of increased wintertime influenza-related mortality in the United States is associated with anomalously low absolute humidity levels during the prior weeks. We then use an epidemiological model, in which observed absolute humidity conditions temper influenza transmission rates, to successfully simulate the seasonal cycle of observed influenza-related mortality.  

 

During the summer, ambient air often contains 4 times as much water as it does on a cool dry winter's day. This, increasingly, is beginning to look as if it is a significant factor in the spread of influenza viruses.

 

As a side note, the Chinese have long boiled vinegar in their homes to ward off respiratory ailments, such as influenza.  

 

The noxious odor was supposed to `purify' the air inside the home, and newspapers still recommend this practice during their influenza season.

 

It may well be that the `active ingredient' is really the water vapor being released, raising the absolute humidity in their homes to an unfavorable level for influenza virus survival and transmission.

 

All of which is neat and tidy until you consider that flu transmits readily in the tropics, where the atmosphere is often nearly saturated with water vapor.

 

Enter researchers from Virginia Tech who have found that both extremely low and extremely high levels of humidity appear to aid and abet the viability of the flu virus – at least when it resides in mucus and respiratory fluids like those found in your nose, throat, or lungs.

 

This is an open access article, available from PloS One.

 

Relationship between Humidity and Influenza A Viability in Droplets and Implications for Influenza’s Seasonality

PLoS ONE 7(10): e46789. doi:10.1371/journal.pone.0046789

Wan Yang, Subbiah Elankumaran, Linsey C. Marr

Abstract (excerpts reparagraphed for readability)

Humidity has been associated with influenza’s seasonality, but the mechanisms underlying the relationship remain unclear. There is no consistent explanation for influenza’s transmission patterns that applies to both temperate and tropical regions.

 

This study aimed to determine the relationship between ambient humidity and viability of the influenza A virus (IAV) during transmission between hosts and to explain the mechanisms underlying it.

 

We measured the viability of IAV in droplets consisting of various model media, chosen to isolate effects of salts and proteins found in respiratory fluid, and in human mucus, at relative humidities (RH) ranging from 17% to 100%.

 

In all media and mucus, viability was highest when RH was either close to 100% or below ~50%. When RH decreased from 84% to 50%, the relationship between viability and RH depended on droplet composition: viability decreased in saline solutions, did not change significantly in solutions supplemented with proteins, and increased dramatically in mucus.

(Continue. . . . )

 

 

Essentially, these researchers inoculated droplets of simulated respiratory fluids (containing salts & proteins) with influenza viruses, and tested their survivability at different humidity levels.

 

• At low humidity (< 50%) the droplets evaporated quickly, and the virus survived well in a dry environment.
• At high humidity (near 100%), the droplets were stable, and the virus survived as well.

 

But at humidity levels in-between, the droplets slowly dried out, increasing the concentration of salts and proteins to which the viruses were exposed, decreasing their survival rate.

 

As these experiments were conducted on relatively large droplets, how these findings would relate to viruses carried by smaller, aerosolized particles (that would desiccate much faster, even at higher humidities) remains untested.

 

Still, it’s fascinating research, and it adds incrementally to our understanding of how the influenza virus survives outside of a host.

 

You may recall I featured another study by these same researchers in early 2011 (see Why Size Matters) where they analyzed the amount of influenza virus suspended in the air in several environments, including a daycare center, a healthcare waiting room,  and aboard commercial aircraft.

 

They found airborne virus particles in half of the air samples tested, and in quantities they believe sufficient to enable transmission of the virus.

 

Many of these virus particles were very small, less than 2.5 micrometers, which can remain aloft on a room’s air currents for hours. Larger droplets would settle far sooner, and theoretically present less of a threat.

 

"As a whole," the three authors concluded in the Journal of the Royal Society Interface, "our results provide quantitative support for the possibility of airborne transmission of influenza in indoor environments."

 

All of which makes the influenza virus a formidable foe, and highlights the importance of maintaining good flu hygiene (hand washing, covering coughs & sneezes & staying home when sick), and the wisdom of getting that flu shot every year.

»» Read More

When Viruses Jump Cages

 

Ebola Virus - Credit CDC

 

# 6722

 

 

With Uganda’s second outbreak of Ebola Sudan in recent months announced earlier this week, along with their ongoing outbreak of Marburg Hemorrhagic Fever, the news that researchers in Canada have documented the transmission of Ebola Zaire from pigs to monkeys – without direct contact - has captured a good deal of attention this week.

 

This transmission occurred in an artificial laboratory setting, with prolonged-close, but-not-direct-contact, and doesn’t necessarily represent how things happen in the `real world’.

 

Nonetheless, it is notable since the conventional wisdom of how Ebola viruses are spread has long been:

 

People can be exposed to Ebola virus from direct contact with the blood and/or secretions of an infected person. Thus, the virus is often spread through families and friends because they come in close contact with such secretions when caring for infected persons. People can also be exposed to Ebola virus through contact with objects, such as needles, that have been contaminated with infected secretions. – CDC Special Pathogens Branch

 

At this point it is important to note that there is nothing in this new research to suggest that the Ebola virus has suddenly gone `airborne’. 

 

But we’ll get to that a little later. 

 

We’ve known since 2008 that pigs can carry some Ebola viruses (see When Viruses Jump Species), usually without showing ill effects. 

 

First detection of Ebola-Reston virus in pigs

23-12-2008

FAO/OIE/WHO offer assistance to the Philippines

Manila/Roma, 23 December 2008 - Following the detection of the Ebola-Reston virus in pigs in the Philippines, FAO, the World Organization for Animal Health (OIE) and the World Health Organization (WHO) announced today that the government of the Philippines has requested the three agencies send an expert mission to work with human and animal health experts in the Philippines to further investigate the situation.

(Continue . . .)

 

Roughly a month later, we learned that several farm workers in contact with infected pigs tested positive for antibodies to the Ebola-Reston virus.  None displayed any signs of illness.

 

Ebola Reston in pigs and humans in the Philippines

3 February 2009 - On 23 January 2009, the Government of the Philippines announced that a person thought to have come in contact with sick pigs had tested positive for Ebola Reston Virus (ERV) antibodies (IgG). On 30 January 2009 the Government announced that a further four individuals had been found positive for ERV antibodies: two farm workers in Bulacan and one farm worker in Pangasinan - the two farms currently under quarantine in northern Luzon because of ERV infection was found in pigs - and one butcher from a slaughterhouse in Pangasinan. The person announced on 23 January to have tested positive for ERV antibodies is reported to be a backyard pig farmer from Valenzuela City - a neighbourhood within Metro Manila.

(Continue . . .)

Ebola-Reston is the only one of five known Ebola viruses that is not pathogenic in humans.  It can kill simians, and its ability to infect pigs is worrisome given how similar human and porcine immune systems are to each other.

 

The natural reservoir for Ebola viruses are believed to be fruit bats of the Pteropodidae family. While the route of initial transmission to a human host is often undetermined, the assumption is that it is usually linked to the consumption of infected bushmeat (probably an intermediate host).

 

Although Ebola-Reston has been documented in pigs in the Philippines, it isn’t clear what role – if any - pigs play in the ecology of Ebolaviruses virus in Africa.

 

In 2011 researchers showed that pigs were also highly susceptible to Ebola-Zaire, which can be up to 90% fatal in humans. 

 

This from the Journal of Infectious Diseases.

 

 

Replication, Pathogenicity, Shedding, and Transmission of Zaire ebolavirus in Pigs

Gary P. Kobinger, Anders Leung, James Neufeld, Jason S. Richardson, Darryl Falzarano, Greg Smith, Kevin Tierney, Ami Patel and Hana M. Weingartl

 

 

This week’s study, which appears in Scientific Reports, takes this information one step further. Researchers placed four macaques in a wire cage inside a pig pen where pigs, infected with Ebola-Zaire, were kept.

 

Although sharing common living space, they were separated by the wire cage. Yet after 2 weeks of shared confinement, all four macaques had contracted the virus.

 

 

Transmission of Ebola virus from pigs to non-human primates

Hana M. Weingartl,Carissa Embury-Hyatt,Charles Nfon,Anders Leung,Greg Smith& Gary Kobinger

Article number: 811 doi:10.1038/srep00811

 

Abstract (Excerpt)

Here we show ZEBOV transmission from pigs to cynomolgus macaques without direct contact. Interestingly, transmission between macaques in similar housing conditions was never observed. Piglets inoculated oro-nasally with ZEBOV were transferred to the room housing macaques in an open inaccessible cage system. All macaques became infected. Infectious virus was detected in oro-nasal swabs of piglets, and in blood, swabs, and tissues of macaques. This is the first report of experimental interspecies virus transmission, with the macaques also used as a human surrogate. Our finding may influence prevention and control measures during EBOV outbreaks.

 

Researchers speculate that:

 

. . .  transmission of ZEBOV could have occurred either by inhalation (of aerosol or larger droplets), and/or droplet inoculation of eyes and mucosal surfaces and/or by fomites due to droplets generated during the cleaning of the room. Infection of all four macaques in an environment, preventing direct contact between the two species and between the macaques themselves, supports the concept of airborne transmission.

While there is some degree of ambiguity here, the idea that large droplet transmission over a very short distance occurred in this setting is not unreasonable. The researchers conclude by stating (reparagraphed for readability):

The present study provides evidence that infected pigs can efficiently transmit ZEBOV to NHPs in conditions resembling farm setting.

 

Our findings support the hypothesis that airborne transmission may contribute to ZEBOV spread, specifically from pigs to primates, and may need to be considered in assessing transmission from animals to humans in general.

 

The present experimental findings would explain REBOV seropositivity of pig farmers in Philippines that were not involved in slaughtering or had no known contact with contaminated pig tissues.

 

The results of this study also raise a possibility that wild or domestic pigs may be a natural (non-reservoir) host for EBOV participating in the EBOV transmission to other species in sub-Saharan Africa.

 

According to a report by Ed Yong in The Scientist  (see Ebola from Pigs to Monkeys), these researchers are now planning a trip to Africa to do serological testing of pigs in areas that have experienced Ebola outbreaks.

»» Read More

The Flight Of The Bacterial Intruder

Credit CDC PHIL

 

 

# 6625

 

HCAIs (Health care associated Infections) or HAIs (Hospital acquired infections) constitute a major threat to life, health, and the cost of medical care in this country, and around the world. This oft quoted assessment from the CDC on the burden of Hospital Acquired Infections in the United States is from 2010.

 

A new report from CDC updates previous estimates of healthcare-associated infections. In American hospitals alone, healthcare-associated infections account for an estimated 1.7 million infections and 99,000 associated deaths each year. Of these infections:

• 32 percent of all healthcare-associated infection are urinary tract infections
• 22 percent are surgical site infections
• 15 percent are pneumonia (lung infections)
• 14 percent are bloodstream infections

 

A 2009 report The Direct Medical Costs of Healthcare-associated Infections in U.S. Hospitals and the Benefits of Prevention finds:

 

Applying two different Consumer Price Index
(CPI) adjustments to account for the rate of inflation in hospital resource prices, the overall annual direct medical costs of HAI to U.S. hospitals ranges from $28.4 to $33.8 billion (after adjusting to 2007 dollars using the CPI for all urban consumers) and $35.7 billion to $45 billion (after adjusting to 2007 dollars using the CPI for inpatient hospital services).

 

 

As you can imagine, hospitals are engaged in a perpetual battle against the spread of infection - and while progress is being made - many pathogens continue to slip past the infection control safeguards.

 

A study from the University of Leeds recently published in the Journal Building and Environment may provide a clue as to why the infection control measures being used today have failed to curb the spread of bacteria in the hospital setting.

 

 

Bioaerosol Deposition in Single and Two-Bed Hospital Rooms: A Numerical and Experimental Study

M.F. King, C.J. Noakes, P.A. Sleigh, M.A. Camargo-Valero

 

You’ll find the abstract, along with figures and tables from this article, at the link above. But the full paper is behind a pay wall. The University of Leeds website, however, has a synopsis of this research project, which is excerpted below:.

 

 

Superbugs ride air currents around hospital wards

Published Thursday 11th October 12

Hospital superbugs can float on air currents and contaminate surfaces far from infected patients’ beds, according to University of Leeds researchers.

 

The results of the study, which was funded by the Engineering and Physical Sciences Research Council (EPSRC), may explain why, despite strict cleaning regimes and hygiene controls, some hospitals still struggle to prevent bacteria moving from patient to patient.

 

It is already recognised that hospital superbugs, such as MRSA and C-difficile, can be spread through contact. Patients, visitors or even hospital staff can inadvertently touch surfaces contaminated with bacteria and then pass the infection on to others, resulting in a great stress in hospitals on keeping hands and surfaces clean.

 

But the University of Leeds research showed that coughing, sneezing or simply shaking the bedclothes can send superbugs into flight, allowing them to contaminate recently-cleaned surfaces.

 

PhD student Marco-Felipe King used a biological aerosol chamber, one of a handful in the world, to replicate conditions in one- and two-bedded hospital rooms. He released tiny aerosol droplets containing Staphyloccus aureus, a bacteria related to MRSA, from a heated mannequin simulating the heat emitted by a human body. He placed open Petri dishes where other patients’ beds, bedside tables, chairs and washbasins might be and then checked where the bacteria landed and grew.

 

The results confirmed that contamination can spread to surfaces across a ward. “The level of contamination immediately around the patient’s bed was high but you would expect that. Hospitals keep beds clean and disinfect the tables and surfaces next to beds,” said Dr Cath Noakes, from the University’s School of Civil Engineering, who supervised the work. “However, we also captured significant quantities of bacteria right across the room, up to 3.5 metres away and especially along the route of the airflows in the room.”

 

“We now need to find out whether this airborne dispersion is an important route of spreading infection,” added co-supervisor Dr Andy Sleigh.

(Continue . . .)

 

 

While we often think first of viruses when it comes to airborne transmission of illness, some types of bacteria (e.g. Legionella, Mycoplasma pneumonia, Tuberculosis) are easily aerosolized and transmitted.

 

This study is not the first to identify the airborne spread of Staphylococcus aureus, but they have developed an ingenious way to quantify it.

 

Regarding MRSA and C. Difficile the Journal of The Royal Society published a review in 2009 called:

 

Airborne transmission of disease in hospitals

I. Eames, J. W. Tang,Y. Li and P. Wilson

(EXCERPT)

MRSA can survive on surfaces or skin scales for up to 80 days and spores of Clostridium difficile may last even longer. MRSA can be transmitted in aerosol from the respiratory tract but commonly attaches to skin scales of various sizes. The distance of travel depends on the size of the scale, the larger falling to the floor within 1–2 m, the smaller travelling the entire length of the ward.

<SNIP>

Clostridium difficile spores are thought to spread in the air and can be found near a patient carrying the organism (Roberts et al. 2008). However, unlike MRSA, they are rarely isolated from air samples.

 

 

Not surprisingly, in 2010, we saw a study published in the AJIC: American Journal of Infection Control that found that the more roommates you have during a hospital stay, the greater chance you will have of contracting an HAI like MRSA or C. Diff.

 

Exposure to hospital roommates as a risk factor for health care–associated infection

Meghan Hamel, MSc, Dick Zoutman, MD, FRCPC, Chris O'Callaghan, DVM, MSc, PhD

 

The authors used this study to promote the idea  of making private (or at least, semi-private) rooms the norm in Canadian hospitals. While acknowledging that it would involve considerable up-front costs, they believe the long-term savings would be considerable.

 

All of this highlights the great challenges involved in substantially reducing the incidence of HAIs in our health care facilities.

 

Solutions must not only include stringent hand hygiene and improved cleaning methods, but engineering solutions as well.

 

For more on the prevention of Hospital Acquired Infections you may wish to visit the CDC’s HAI PAGE.

 

 

Or revisit some of these earlier blogs on hospital acquired infections.

 

HPA: Healthcare-Associated Infection (HCAI) Survey

A Barrier To Good Hand Hygiene

Study: Hospital Uniforms And Bacteria

Study: HAIs, Universal Surveillance, & MRSA

 

And finally, the subject of HAIs is often addressed by Maryn McKenna on her excellent Superbug Blog, and was a major focus of her book SUPERBUG: The Fatal Menace Of MRSA.

 

Both are highly recommended.

»» Read More

Pathogens At the Gate

Thermal Scanner – Credit Wikipedia

 

# 6593

 

While there are no indications that the coronavirus detected recently in the Middle East has spread beyond the first two cases, some places around the world are taking this threat very seriously.

 

For example, local media is reporting that thermal scanners have been deployed at the Ninoy Aquino International Airport in the Philippines in an attempt to screen arrivals from the Middle East for possible infection.

 

Whenever a novel virus appears, people’s thoughts understandably turn to a pandemic scenario, even though experience has shown that most emerging viruses don’t have the `legs’ to spark a global epidemic (see Novel Viruses & Chekhov’s Gun).

 

Nevertheless, history tells us that pandemics come along several times each century, and another pandemic is all but inevitable.

 

And so the world’s attention this week has quite naturally focused on the novel coronavirus that killed one man in Saudi Arabia last July and has a Qatari man currently hospitalized in London.

 

Memories of the SARS outbreak in 2002 and 2003 remain vivid, particularly in Asia, where the virus hit hardest.

 

Fortunately, while there is still much we don’t know about this emerging pathogen, there are no immediate signs that this virus poses a pandemic threat.

 

While we may not know when - or which virus - will spark the next global health crisis, we have pretty good idea how it will arrive in most countries.

 

Scheduled airline traffic around the world, circa June 2009 – Credit Wikipedia

 

The world’s airlines carry 2.6 billion passengers each year, on more than 17 million flights.  And as the map above indicates, millions of them are international flights.

 

With most viral diseases having an incubation period of several days or longer, someone who is newly infected with a virus could change planes and continents several times before showing their first signs of illness.

 

Last July, in MIT: Contagion Dynamics Of International Air Travel we looked at a study appearing in PloS One, that simulated the early spread of a pandemic virus via air travel and ranked U.S. airports based on how much they contributed to the spread of the illness.

 

An excerpt from a report that appeared in MIT News.

 

New model of disease contagion ranks U.S. airports in terms of their spreading influence

Airports in New York, Los Angeles and Honolulu are judged likeliest to play a significant role in the growth of a pandemic.

Kennedy Airport is ranked first by the model, followed by airports in Los Angeles, Honolulu, San Francisco, Newark, Chicago (O'Hare) and Washington (Dulles). Atlanta's Hartsfield-Jackson International Airport, which is first in number of flights, ranks eighth in contagion influence. Boston's Logan International Airport ranks 15th.

 

 

All of which begs the question, can we really screen, identify, and isolate infectious airline passengers before they can spread a pandemic virus?

 

 

Sadly, the evidence to date has not been very encouraging.

 

Last April, in EID Journal: Airport Screening For Pandemic Flu In New Zealand, we examined a study that found the screening methods used at New Zealand’s airport were inadequate to slow the entry of the 2009 pandemic flu into their country, detecting less than 6% of those infected.

 

New Zealand did not employ thermal scanners, although countries that did, didn’t fare much better.

  

Proving that `there’s no place like home’ during a global crisis, in Vietnam Discovers Passengers Beating Thermal Scanners, we saw evidence of passengers taking fever-reducers to beat the airport scanners in a desperate attempt to get home.

 

In December of 2009, in Travel-Associated H1N1 Influenza in Singapore, I blogged on a NEJM Journal Watch article on of a new study that has been published, ahead of print, in the CDC’s  EID Journal  entitled:

 

Epidemiology of travel-associated pandemic (H1N1) 2009 infection in 116 patients, Singapore. Emerg Infect Dis 2010 Jan; [e-pub ahead of print]. Mukherjee P et al

Travel-Associated H1N1 Influenza in Singapore

Airport thermal scanners detected only 12% of travel-associated flu cases; many travelers boarded flights despite symptoms.

 

 

In June of 2010  CIDRAP carried this piece on a study of thermal scanners in New Zealand in 2008 (before the pandemic) presented at 2010’s ICEID.

 

Thermal scanners are poor flu predictors

Thermal scanners for screening travelers do moderately well at detecting fever, but do a poor job at flagging influenza, according to researchers from New Zealand who presented their findings today at the International Conference on Emerging Infectious Diseases (ICEID) in Atlanta.

 

And in early 2009, Helen Branswell penned an article for the Canadian Press, that stated:

 

Studies show little merit in airport temperature screening for disease

Monday, 16 February 2009 - 11:58am.

By Helen Branswell

TORONTO — Using temperature scanners in airports to try to identify and block entry of sick travellers during a disease outbreak is unlikely to achieve the desired goal, a report by French public health officials suggests.

(Continue. . .)

 

 

The evidence is pretty clear.

 

With the technology of today, coupled with likelihood of having many pre-symptomatic and asymptomatic carriers, there isn’t much hope to identify more than a fraction of infected travelers.

 

As far as the risk of catching a pandemic flu virus while a passenger on an airliner, in May of 2010 we saw a study that appeared in the BMJ that looked at that very topic (see BMJ: Flu Transmission Risks On Airplanes)

 

BMJ 2010;340:c2424

Research

Transmission of pandemic A/H1N1 2009 influenza on passenger aircraft: retrospective cohort study

Conclusions

A low but measurable risk of transmission of pandemic A/H1N1 exists during modern commercial air travel. This risk is concentrated close to infected passengers with symptoms. Follow-up and screening of exposed passengers is slow and difficult once they have left the airport.

 

Another study, conducted by researchers at UCLA and published in BMC Medicine in late 2009:

 

Calculating the potential for within-flight transmission of influenza A (H1N1)

Bradley G Wagner, Brian J Coburn and Sally Blower^*

Results

The risk of catching H1N1 will essentially be confined to passengers travelling in the same cabin as the source case. Not surprisingly, we find that the longer the flight the greater the number of infections that can be expected. We calculate that H1N1, even during long flights, poses a low to moderate within-flight transmission risk if the source case travels First Class.

(Continue . . .)

 

 

While there will likely be intense public clamor to try to block the entry of a pandemic virus into this, or any other country, the truth is – it is highly unlikely that it will work.

Areas that receive a very small number of arrivals might be able to institute a quarantine system (see Can Island Nations Effectively Quarantine Against Pandemic Flu? ), but even then the ability to identify and isolate infected travelers won’t be 100%.

 

Still, even if the success rate is likely to be low, there may be some value in trying to limit the number of infected persons arriving into a country, particularly during the opening days and weeks of an outbreak.

 

The more introductions of a virus into a population, the more points it will have from which to spread.

 

Since it takes months to produce and deploy a vaccine, and time to prepare a society to deal with a pandemic, any delaying action that can reduce the speed and spread of the virus has value.

 

The takeaway from all of this is that we ignore global healthcare and infectious disease outbreaks – even in the remotest areas of the world – at our own peril.

 

Vast oceans and extended travel times no longer offer us protection, and there is no technological shield that we can erect that would keep an emerging pandemic virus out.

 

The place to try to stop the next pandemic is not at the gate, but in the places around the world where they are likely to emerge.

 

Which makes the funding and support of international public health initiatives, animal health initiatives, and disease surveillance ever so important, no matter where on this globe you happen to live.

»» Read More

EID Journal: Guinea Pigs As Reservoirs For Influenza

 

 

# 6369

 

 

From the CDC’s EID Journal we’ve a new study that looks at influenza infections in farm-raised guinea pigs in Ecuador, that provides several surprising results.

 

Ferrets and mice are often used in influenza research, but neither is truly ideal.

 

So in recent years a number of researchers have looked at guinea pigs as possible model mammalian host for influenza virus studies (see PNAS The guinea pig as a transmission model for human influenza viruses by Peter Palese et al. 2006).

 

The success in using guinea pigs in lab studies has led some scientists to wonder just how guinea pigs might fit into the hosting and spread of flu viruses outside of the laboratory.

 

Which brings us to a dispatch (again from Peter Palese et al.) that was published yesterday in the EID journal called:

 

Dispatch

Influenza Virus Infection in Guinea Pigs Raised as Livestock, Ecuador

Victor H. Leyva-Grado, Samira Mubareka, Florian Krammer, Washington B. Cárdenas, and Peter Palese

Abstract

To determine whether guinea pigs are infected with influenza virus in nature, we conducted a serologic study in domestic guinea pigs in Ecuador. Detection of antibodies against influenza A and B raises the question about the role of guinea pigs in the ecology and epidemiology of influenza virus in the region.

 

 

Guinea pigs are raised and used as food in parts of South America (Peruvians reportedly consume more than 65 million of them each year, and they may also be found on the menu in Bolivia, Ecuador, and Columbia).

 

While the consumption of guinea pigs may seem an unusual culinary choice to many of us, it is so entrenched in the Andean culture that in 1753 - when Marcos Zapata painted his version of `The Last Supper’ for Peru (which now hangs in The Cathedral Of Cusco ) - he depicted Christ and the Apostles dining on a platter of cuy, or guinea pig.

Photo Source – Wikipedia.

 

But I digress . . .

 

Most of these animals are raised on small farms, and often in close contact with other livestock as well as humans.

 

Given these conditions, and their propensity for hosting and spreading influenza in laboratory studies, a seroprevalence study was undertaken to see how widespread influenza infection among guinea pigs might be outside of the laboratory.

 

This study examined blood samples from 40 guinea pigs taken from 3 locations across Ecuador, and subsequently found evidence of previous Influenza A infections in a unusually large number of them.

 

The surprises (of which there were several) included:

 

• The high percentage of positive influenza A samples (50% H1, 45% H3)
• The detection of several (n=14)animals carrying antibodies to an H5 virus
• And perhaps the biggest surprise of all – finding evidence of influenza B infections (previously only thought to infect humans) in 27 of the 40 samples tested.

 

 

An earlier seroprevalence study of influenza A among humans in Ecuador showed a seroprevalence of H1 (5.1%) and H3 (5.5%) -  about 1/10th that found in these guinea pigs.

 

The authors suggest that the way these animals are raised (caged together and in close quarters) may facilitate the spread of influenza. 

 

The discovery of H5 antibodies is intriguing, but since this study only tested only for seroreactivity to parts of the H5 virus, further study will be required to identify and quantify the prevalence of avian influenza viruses in this population.

 

And the last finding - that of Influenza B in roughly 2/3rds of the samples – support the idea that this type of influenza can be readily transmitted from humans to other hosts.

 

The authors write:

 

Further studies are needed to isolate and characterize the type B influenza virus present in the population of guinea pigs to determine if there has been an adaptation to the new host or if the guinea pig is only a transient reservoir for the human virus.

 

The authors conclude this dispatch by stating:

 

We did not determine whether guinea pigs are an incidental host for influenza virus infection or, if instead, the virus has been adapted to these animals or if guinea pigs are a natural reservoir for some influenza viruses. To this end, virus isolation and characterization would be necessary to determine the virus strains circulating in this population. In the laboratory, guinea pigs are infected and efficiently transmit influenza viruses to naive hosts without showing any overt clinical signs of disease (1). Therefore, further studies are needed to address the specific role of guinea pigs raised as livestock in the ecology and epidemiology of influenza viruses in the region.

 

 

For more details on the methods used, the full text is available online at this link.

 

While this research might seem a bit obscure to all but the most ardent infectious disease geeks, it serves to show just how little we still know about influenza viruses and their host range,  and that there are still plenty of surprises waiting out there yet to be uncovered.

»» Read More

Route Of Shenzhen Bird Flu Infection Unclear

 

    # 6046

 

 

 

The means by which a 39-year-old bus driver from the city of Shenzhen in Guangdong Province, China came to contract a fatal H5N1 infection remain unclear according to a report in today’s China Daily.

 

The victim, named Chen, was reported yesterday to have died after spending nearly a week in a coma at a local hospital (see Shenzhen Bird Flu Suspect Dies).

 

Early reports indicate he neither had contact with poultry, or had traveled outside of the city, in the past 30 days. First an excerpt from the Xinhua news report, then I’ll return with more.

 

Cause of bird flu death in S China still unclear

Updated: 2012-01-01 21:06

(Xinhua)

GUANGZHOU - Health authorities in south Guangdong province have yet to find the cause of the highly pathogenic H5N1 virus, commonly known as bird flu, that led to the death of a bus driver, a local disease control official said Sunday.

 

The 39-year-old man surnamed Chen in Bao'an district of Shenzhen was hospitalized for fever on December 21 and tested positive for the H5N1 avian influenza virus. He died of multiple organ failure Saturday afternoon, the Guangdong Health Department said in a statement.

 

The department also said that during the previous month prior to his fever, he had no direct contact with poultry and hadn't traveled out of the city.

 

Chen's wife said he had a habit of doing morning exercises every day near a wetland park and an artificial lake not far from his home, but "no proof has been found that his infection is connected with the migratory birds there," He Jianfeng, director of the Epidemics Studies Institute of the Guangdong Disease Control Center, said Sunday.

 

"We also don't know whether he had eaten poultry before he fell ill," He said.

(Continue . . .)

 

 

Determining the likely route of infection in a specific bird flu patient has always been tricky, and often the `official’ determination is based on circumstantial evidence.  

 

Direct contact with sick or dead birds has been the most common mode cited over the years, even in some cases where the aforementioned birds were not identified or confirmed to be infected with the virus.

 

And often, that was probably a reasonable enough assumption.  Occam's razor being – the simplest explanation is most likely the correct one.

 

Without specific regard to today’s case, it is worth noting that we’ve also seen serological evidence of subclinical, or asymptomatic infection with the H5N1 virus in China and in Thailand, and even among some people who were unlikely to have acquired it directly from poultry.

 

Last December, in Study: Subclinical H5 & H9 Infections In Humans, we saw a report out of China on the detection of antibodies to both H9 and H5 avian influenza viruses among a small number of villagers in and around Beijing, China.

 

The study was titled:

 

Infection With Multiple Avian Influenza Viruses in a Man Without Poultry-Handling Practices Suggesting an Increased Probability of Emergent Pandemic Influenza Virus in General Population

Peng Yang, Weixian Shi, Shujuan Cui, Yi Zhang, Xiujun Liu, and Quanyi Wang

 

 

In September of last year we saw a study that reported the results of this kind of serological testing conducted in a rural village in Thailand in 2008 (see Bangladesh To Share H9N2 Bird Flu Virus). 

 

Out of 800 villagers tested, the authors found 4.7% were seropositive for the Hong Kong H9N2 avian strain, 5.6% had antibodies to A/Thailand/676/2005 H5N1 bird flu, and 3.5% were shown to be seropositive to A/Thailand/384/2006 H5N1.

 

The implications of these studies are that human infection with these avian viruses – while still rare – is probably more common that current surveillance and reporting suggests.

 

And that opens the possibility, at least, that asymptomatic H5N1 infections could (in rare cases) provide a silent route of transmission of the virus.

 

Again, the evidence here is both scant, and primarily circumstantial. And there is no evidence to suggest sustained or efficient transmission.

 

For now, the H5N1 virus appears poorly adapted to human physiology. And while the concern is that, over time, that could change, it is also possible that this virus will never adapt fully to humans.

 

But with the recent laboratory successes in turning the H5N1 virus into a more easily transmissible pathogen (see The H5N1 Research Debate Goes On), there are renewed concerns in the scientific community that this avian virus may one day evolve enough to pose a serious pandemic threat to mankind.

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The Birth Of The Flus

 

 

# 5963

 

 

Southeast Asia has long been considered `the cradle of influenza’, an area of the world where influenza viruses circulate year round, more than a billion people live in close proximity, and where humans and farm animals often come into close contact with one another.

 

An ideal breeding ground, and launching pad, for flu pandemics. 

 

During the 20th century, 2 of the 3 influenza pandemics (1957 Asian Flu, 1968 Hong Kong Flu) originated from this region.

 

But new research on the the spread of influenza A, published yesterday in PNAS, indicates that Southeast Asia isn’t the only birthplace of the flu.

 

The dauntingly titled open access study can be found at:

 

 

Temporally structured metapopulation dynamics and persistence of influenza A H3N2 virus in humans

Published online before print November 14, 2011, doi: 10.1073/pnas.1109314108 PNAS November 14, 2011

Justin Bahl, Martha I. Nelson, Kwok H. Chan, Rubing Chen, Dhanasekaran Vijaykrishna, Rebecca A. Halpin, Timothy B. Stockwell, Xudong Lin, David E. Wentworth, Elodie Ghedin, Yi Guan, J. S. Malik Peiris, Steven Riley, Andrew Rambaut, Edward C. Holmes, and Gavin J. D. Smith

 

(EXCERPT)

Although the virus population that migrated between Southeast Asia and Hong Kong persisted through time, this was dependent on virus input from temperate regions and these tropical regions did not maintain a source for annual H3N2 influenza epidemics.

 

We further show that multiple lineages may seed annual influenza epidemics, and that each region may function as a potential source population. We therefore propose that the global persistence of H3N2 influenza A virus is the result of a migrating metapopulation in which multiple different localities may seed seasonal epidemics in temperate regions in a given year.

 

Such complex global migration dynamics may confound control efforts and contribute to the emergence and spread of antigenic variants and drug-resistant viruses.

 

 

The entire study is available online, but for those of us who find the finer details of Bayesian phylogeographic analysis of viral migration above our pay grade, we’ve a press release from Duke University Medical Center that helps summarize this paper.

 

Study finds tropical areas aren't the only source of seasonal flu

DURHAM, N.C. and SINGAPORE – A commonly held theory says that flu virus originates every year in Southeast and Eastern Asia, making this region the source of seasonal flu epidemics in other parts of the world.

 

However, researchers at Duke-NUS Graduate Medical School in Singapore have found that influenza virus in tropical areas isn't the only global source of flu epidemics. The international team of scientists involved in the work found that any one of the urban centers they studied could act as a source for a flu epidemic in any other locality.

 

"We found that these regions are just one node in a network of urban centers connected by air travel, through which flu virus circulates and causes a series of local epidemics that overlap in time," said Gavin Smith, PhD, senior author and Associate Professor in the Program in Emerging Infectious Diseases at Duke-NUS.

 

The study was published the week of Nov. 14 in the online Early Edition of the Proceedings of the National Academy of Sciences.

 

The research team chose to study influenza A because it is much more prevalent than both influenza B and C. Influenza is a significant cause of human illness and death worldwide – the World Health Organization estimates that 250,000 to 500,000 influenza A related deaths occur per year worldwide, and about 49,000 deaths occur in the United States.

 

The team obtained RNA sequences of virus samples from 2003 to 2006 in Australia, Europe, Japan, New York, New Zealand and Southeast Asia, as well as some more recently sequenced viruses from Hong Kong. The virus populations from tropical Southeast Asia and Hong Kong showed relatively low levels of genetic diversity and no seasonal fluctuations in comparison with annual temperate-area epidemics.

 

The analysis used time and space parameters to reveal high rates of viral migration among the urban centers tested. Although the virus population that migrated between Southeast Asia and Hong Kong persisted through time, the pattern of infections also depended on virus input from temperate regions that have distinct seasons. None of the temperate and tropical regions they examined was the source of all of the new flu strains in a given year.

 

The scientists showed that multiple lineages of a virus could seed annual flu epidemics, and that each region could function as a potential source population.

(Continue . . . )

 

 

Six weeks before the 2009 H1N1 pandemic virus emerged in Mexico, I wrote  blog called:

 

Sunday, March 08, 2009

How The Next Pandemic Will Arrive

# 2876

There is a lot we don't currently know about the next pandemic.  We don't know when it will arrive.  We don't know what virus will cause it.  And we don't know how bad it will be.

 

But there is one thing almost certain.

 

It will arrive in most countries by airplane.

The video above, which as been making the rounds for several months, was made by ZHAW (Zürcher Hochschule für Angewandte Wissenschaften) or The Zurich University of Applied Sciences.

(Continue . . .)

 

 

Before the advent and explosion in international air travel, the tropical regions of Southeast Asia probably played a much bigger role in the the creation, incubation, and spread of influenza viruses. 

 

With man’s help, influenza today has become an accomplished world traveler. No longer are we protected by vast oceans and long transit times.

 

New strains and viral reassortments that a few decades ago might have sputtered and died out unnoticed in some remote region of the world, or have been detected and quarantined aboard slow moving ships, can now hop a plane and find new hosts in a matter of hours.

 

Something we saw as recently as the 2009 H1N1 pandemic, which began not in Asia, but in the Americas.

 

Further proof that as the world evolves and become more complex, so does the threat from emerging infectious diseases.

»» Read More

EID Journal: Pre-Symptomatic Influenza Transmission

 

 

 

# 5780

 

Remarkably, our understanding of exactly how – and under what conditions – influenza is transmitted from one person to another is still limited. 

 

We know that large droplets expelled by coughing and sneezing, along with smaller aerosolized virus particles that may remain airborne longer,  plus contaminated surfaces (fomites) all play a role . . . but exactly how much each contributes has not been determined.

 

Similarly, it is believed that asymptomatic carriers of the virus may be able to transmit the virus to others despite not showing symptoms themselves, as well as those who are incubating the virus but are still presymptomatic.

 

But scientific evidence remains scant.

 

All of this is terribly important – particularly during an influenza pandemic – because if true, calls to isolate those showing symptoms wouldn’t stop its transmission.

 

Today, in the CDC’s EID Journal we have a dispatch that examines early transmission of the 2009 H1N1 virus in Japan, and finds evidence suggesting transmission of the virus during a carrier’s presymptomatic phase.

 

Pandemic (H1N1) 2009 Transmission during Presymptomatic Phase, Japan

Yoshiaki Gu,  Nobuhiro Komiya, Hajime Kamiya, Yoshinori Yasui, Kiyosu Taniguchi, and Nobuhiko Okabe

Author affiliation: National Institute of Infectious Diseases, Tokyo, Japan

Abstract
During an epidemiologic investigation of pandemic influenza (H1N1) 2009 virus infection in May 2009 in Osaka, Japan, we found 3 clusters in which virus transmission occurred during the presymptomatic phase. This finding has public health implications because it indicates that viral transmission in communities cannot be prevented solely by isolating symptomatic case-patients.

 

 

Three clusters of pandemic (H1N1) 2009 presymptomatic transmission in May 2009 in Osaka, Japan. All cases were confirmed as pandemic (H1N1) 2009 virus infection by real-time reverse transcription PCR. Squares indicate male case-patients, and circles indicate female case-patients. Colors of the squares and circles denote the similar or different schools the students attended.

(Continue . . . )

 

During the 2009 H1N1 pandemic Japan, India, and China were among the nations that attempted to identify, interdict, and isolate those who might be carrying the H1N1 virus when they entered their country.  

 

While their efforts may have slowed the introduction of the virus, they certainly didn’t stop it.  Earlier blogs on these attempts include:

 

Japan: Quarantine At Ports Ineffective Against Pandemic Flu

Experts: Extreme Measures Won’t Stop The Flu

 

Their failure was likely due to the large number of presymptomatic, and asymptomatic carriers of the virus that arrived without showing signs of illness.

 

It has been suggested that areas that receive a small number of arrivals might be able to institute a quarantine system (see Can Island Nations Effectively Quarantine Against Pandemic Flu? ), but even then their ability to interdict infected travelers wouldn’t be 100%.

 

The authors of today’s study conclude by writing:

 

Our epidemiologic results provide useful clues for understanding the transmission of pandemic (H1N1) 2009 virus. This finding of presymptomatic transmission has critical implications for public health because it indicates that viral transmission in communities cannot be completely prevented solely by isolating symptomatic case-patients.

 

Further proof, that with influenza, there are no easy answers.

»» Read More

Why Size Matters

 

 

 

# 5279

 

 

Determining the modes by which the influenza virus can be transmitted is more than just an academic exercise for researchers, as the answers will help determine how we protect front line health care workers, patients, and the general public during a pandemic.

 

The `classic’ answer is that influenza is spread primarily by `large droplets' expressed by infected individuals when they cough or sneeze.  These heavy viral laden droplets are assumed to travel only a few feet, and to settle to the ground (or other surfaces) in a matter of seconds.

 

Photo Credit PHIL (Public Health Image Library)

 

A secondary route of infection, via fomites (inanimate objects that have viral contamination) is also assumed, although how much fomites contribute to influenza transmission is unknown.

 

But the third possibility, aerosolized particles that can remain suspended in the air for minutes or even hours, and potentially travel much longer distances, remains controversial.  

 

Last November in Study: Aerosolized Transmission Of Influenza, we saw a report of an influenza patient receiving a ventilation treatment in an open ward next to another air current producing device that lead to the apparent aerosolized spread of the virus.

 

Last September in Ferreting Out The Transmissibility Of Aerosolized H5N1 we saw a study on the transmission of aerosolize bird flu among ferrets.

 

And in August of last year, in Another Mask Study To Ponder, we looked at research on the relative effectiveness of N95 respirators and surgical masks in blocking aerosolized particles. 

 

Today, a press release on study to be published today in the Journal of the Royal Society Interface that looked at the amount of influenza virus suspended in the air in several environments, including a daycare center, a healthcare waiting room,  and aboard commercial aircraft. 

 

They found airborne virus particles in half of the air samples tested, and in quantities they believe sufficient to enable transmission of the virus.

 

Many of these virus particles were very small, less than 2.5 micrometers, which can remain aloft on a room’s air currents for hours. Larger droplets would settle far sooner, and theoretically present less of a threat.

 

So size, in this case, really matters.

 

 

 

Size of airborne flu virus impacts risk, Virginia Tech researchers say

A parent's wise advice to never go to a hospital unless you want to get sick may be gaining support from scientific studies on a specific airborne virus.

 

The results of a Virginia Tech study by environmental engineers and a virologist on the risk of airborne infection in public places from concentrations of influenza A viruses is appearing today in the on-line, Feb. 2 issue of the United Kingdom's Journal of the Royal Society Interface.

 

Linsey Marr, associate professor of civil and environmental engineering at Virginia Tech, http://www.cee.vt.edu/people/lmarr.html and her colleagues, Wan Yang, of Blacksburg, Va., one of her graduate students, and Elankumaran Subbiah, a virologist in the biomedical sciences and pathobiology department of the Virginia-Maryland Regional College of Veterinary Medicine, http://www.vetmed.vt.edu/org/dbsp/faculty/subbiah.asp conducted their research in a health center, a daycare facility, and onboard airplanes.

 

"The relative importance of the airborne route in influenza transmission—in which tiny respiratory droplets from infected individuals are inhaled by others—is not known," Marr, who received a National Science Foundation CAREER Award to pinpoint sources of unhealthy air pollutants, said.

 

<SNIP>

To conduct their studies, the Virginia Tech researchers collected samples from a waiting room of a health care center, two toddlers' rooms and one babies' area of a daycare center, as well as three cross-country flights between Roanoke, Va., and San Francisco, Ca. They collected 16 samples between Dec. 10, 2009 and Apr. 22, 2010.

 

"Half of the samples were confirmed to contain aerosolized influenza A viruses," Marr said. "In the others, it is possible that no infected individuals were present."

 

Marr added, "The average concentration was 16,000 viruses per cubic meter of air, and the majority of the viruses were associated with fine particles, less than 2.5 micrometers, which can remain suspended for hours. Given these concentrations, the amount of viruses a person would inhale over one hour would be adequate to induce infection."

(Continue . . . )

 

 

Although the article has not yet shown  up in the journal, you should be able to access the abstract later today HERE.

 

While there remain questions on the viability of these viral particles, and of the viral load required to produce infection, the authors found:

 

"As a whole," the three authors concluded in the Journal of the Royal Society Interface, "our results provide quantitative support for the possibility of airborne transmission of influenza in indoor environments."

 

No definitive answers here, of course.

 

But more data to be taken into account when making policy decisions regarding the proper kinds of PPEs (Personal Protective Equipment) and social distancing recommendations during a pandemic.

»» Read More

Something To Sneeze At

 

 

# 5221

 

 

One of the recurring themes of this blog is how much we still have to learn about the influenza virus, and how it is spread.   Amazingly, even in 2011, many of the basic questions about influenza are still unanswered.

 

How long do flu viruses remain airborne?

How far can a flu virus travel in the air?

Do surgical masks or N95 protect the wearer?

What are the relative values of hand washing, mask wearing, and social distancing during a pandemic?

We’ve seen a number of studies over the years that have provided partial – and sometimes conflicting – answers.   But solid scientific data on which to base recommendations remains scant.

 

From NTDTV, we get a report today on one Singapore research study’s attempt to quantify how far viruses may travel via coughs and sneezes. 

 

This brief report includes an English Language 2min 30sec minute video with interviews with virologist Dr. Julian Tang and slo-mo film clips of sneezes. 

 

Probably best to wait until you’ve finished breakfast to watch it.

 

As this study is planned to run until mid-2012, results won’t be going viral anytime soon.

 

 

Scientists Study Sneezes for Clues to Flu Transmission

2011-01-11 07:27

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Referral: CIDRAP On Airborne Influenza Transmission

 

 

# 5112

 

 

Although I’d entertained thoughts of blogging on this particular study, it is highly unlikely that I could produce anything half as good as has already been written by Lisa Schnirring on CIDRAP News.

 

So I’m just going to step out of the way and recommend you direct your browser to:

 

Study: Airborne particles from coughs can carry flu viruses

Lisa Schnirring Staff Writer

»» Read More

BMJ: Flu Transmission Risks On Airplanes

 

 

 

# 4586

 

 

Two years ago I flew to Washington D.C. - during flu season - to attend an HHS sponsored pandemic exercise.  

 

I changed planes in Atlanta coming and going (if you die anywhere in the southeast, no matter what your final destination, you apparently have to go through Atlanta), and spent nearly 10 hours wedged into economy class seating.  

 

All around me, people were coughing and sneezing. And you guessed it, 48 hours after my return, I was down with a nasty flu-like illness.  

Whether I picked up my virus in the confines of the plane, or at the flu conference (irony being what it is), or simply waiting in the airport terminal is something I’ll never know.  

 

But I have my suspicions.

 

Which brings us to a study which appears in the BMJ today, entitled:

 

BMJ 2010;340:c2424

Research

Transmission of pandemic A/H1N1 2009 influenza on passenger aircraft: retrospective cohort study

Michael G Baker, associate professor¹, Craig N Thornley, medical officer of health², Clair Mills, senior lecturer³, Sally Roberts, microbiologist⁴, Shanika Perera, medical officer of health², Julia Peters, medical officer of health², Anne Kelso, director⁵, Ian Barr, deputy director⁵, Nick Wilson, associate professor¹

I’ve reproduced portions of the abstract below.  The entire study is available online at the BMJ.

Objectives To assess the risk of transmission of pandemic A/H1N1 2009 influenza (pandemic A/H1N1) from an infected high school group to other passengers on an airline flight and the effectiveness of screening and follow-up of exposed passengers.

 

Design Retrospective cohort investigation using a questionnaire administered to passengers and laboratory investigation of those with symptoms.

 

Setting Auckland, New Zealand, with national and international follow-up of passengers.

Participants Passengers seated in the rear section of a Boeing 747-400 long haul flight that arrived on 25 April 2009, including a group of 24 students and teachers and 97 (out of 102) other passengers in the same section of the plane who agreed to be interviewed.

 
Main outcome measures Laboratory confirmed pandemic A/H1N1 infection in susceptible passengers within 3.2 days of arrival; sensitivity and specificity of influenza symptoms for confirmed infection; and completeness and timeliness of contact tracing.

 
Results Nine members of the school group were laboratory confirmed cases of pandemic A/H1N1 infection and had symptoms during the flight.

Two other passengers developed confirmed pandemic A/H1N1 infection, 12 and 48 hours after the flight. They reported no other potential sources of infection. Their seating was within two rows of infected passengers, implying a risk of infection of about 3.5% for the 57 passengers in those rows.

All but one of the confirmed pandemic A/H1N1 infected travellers reported cough, but more complex definitions of influenza cases had relatively low sensitivity. Rigorous follow-up by public health workers located 93% of passengers, but only 52% were contacted within 72 hours of arrival.

 
Conclusions A low but measurable risk of transmission of pandemic A/H1N1 exists during modern commercial air travel. This risk is concentrated close to infected passengers with symptoms. Follow-up and screening of exposed passengers is slow and difficult once they have left the airport.

 

 

No real surprises here, of course, except perhaps that fewer people were infected during this flight than one might have expected.  Of course, the usual caveats apply;  this is one study, of one flight, and is specific to the novel H1N1 virus.  

 

The report summarizes what this research adds to what we know this way:

 

What is already known on this topic

Respiratory agents may be transmitted during airline travel, although the level of risk is poorly defined for most agents, including influenza

 

Screening for influenza is difficult because symptoms are variable and may be mild or absent

 

Very little evidence exists on the best way to follow up arriving travellers who might have been exposed to influenza during a flight

What this study adds

A low but measurable risk of contracting influenza from infected travellers with symptoms exists during a long haul flight and is concentrated within two rows of infected travellers

 

Screening for people infected with influenza is likely to be more sensitive if it uses the presence of single symptoms such as cough, rather than more complex case definitions

 

Identification and management of passengers exposed to infections during a flight should be started before passengers leave the airport or board other flights

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