H5N1

ECDC: Influenza virus characterisation, Summary Europe, September 2018

ECDC has published Influenza virus characterisation, Summary Europe, September 2018. The summary:

This is the eighth, and final, report of the 2017–18 influenza season. 

As of week 39/2018, over 240 000 influenza detections across the WHO European Region have been reported. Forty-four percent of the detected viruses were type A, with A(H1N1)pdm09 and A(H3N2) viruses being detected in equal numbers. Type B viruses accounted for 56%; B/Yamagata viruses prevailed over B/Victoria viruses at a ratio of over 50:1.

ECDC: Seasonal influenza - Annual Epidemiological Report for 2017 - 2018

ECDC has published Seasonal influenza - Annual Epidemiological Report for 2017 - 2018. The executive summary:

Influenza activity started in week 47/2017 and returned to baseline levels in week 18/2018.  

In northern and south-western Europe (EU/EEA) , the activity started to increase between mid-December and early January, similar to the timing of the 2016–2017 season but earlier than in the previous five seasons.  

The peak in activity was in early January in south-western Europe and in mid-February 2018 in northern Europe (EU/EEA). In some countries in Eastern Europe, influenza activity did not peak until mid- to late March. 

The majority of influenza viruses detected were of type B, representing a higher level of circulation of influenza B viruses compared to recent seasons. Of all subtyped influenza B viruses detected in sentinel samples, 97% were B/Yamagata and 3% were B/Victoria viruses. Both influenza A subtypes, A(H3N2) and A(H1N1)pdm09 co-circulated in the region. Of all subtyped A viruses detected in sentinel samples, 38% were A(H3N2) viruses and 62% were A(H1N1)pdm09 viruses. 

Influenza viruses circulated at high levels between weeks 51/2017 and 13/2018. This is longer than in recent seasons and may have contributed to the high severity of the 2017/18 season. Especially influenza B activity was detected for a longer period of the season and at a greater magnitude than in the previous seasons. Severe cases were observed in hospital settings due to B virus, but also due to A(H3N2) and A(H1N1)pdm09 viruses. 

Overall, the majority of severe cases were due to influenza virus type B infection and mostly were persons 40 years of age or older. Patients in intensive care units were mostly infected by influenza type A virus.  

Overall, excess mortality from all causes was reported by the majority of 21 reporting countries during the influenza season and was mainly observed in people aged 65 years or older.

Spanish flu: The killer that still stalks us, 100 years on

Via The Guardian: Spanish flu: the killer that still stalks us, 100 years on. Excerpt:

One hundred years ago this month, just as the first world war was drawing to a fitful close, an influenza virus unlike any before or since swept across the British Isles, felling soldiers and civilians alike. One of the first casualties was the British prime minister and war leader, David Lloyd George. 

On 11 September 1918, Lloyd George, riding high on news of recent Allied successes, arrived in Manchester to be presented with the keys to the city. Female munitions workers and soldiers home on furlough cheered his passage from Piccadilly train station to Albert Square. But later that evening, he developed a sore throat and fever and collapsed. 

He spent the next 10 days confined to a sickbed in Manchester town hall, too ill to move and with a respirator to aid his breathing. Newspapers, including the Manchester Guardian, underplayed the severity of his condition for fear of presenting the Germans with a propaganda coup. But, according to his valet, it had been “touch and go”. 

Lloyd George, then aged 55, survived, but others were not so lucky. In an era before antibiotics and vaccines, the “Spanish influenza” – so-called because neutral Spain was one of the few countries in 1918 where correspondents were free to report on the outbreak – claimed the lives of nearly 250,000 Britons. Cruelly for a nation that had seen the flower of British male youth mown down by German guns, the majority were adults aged 20 to 40. The mortality was the inverse of most flu seasons, when deaths fall most heavily on the elderly and the under-fives. 

The global death toll was inconceivable: according to the most recent estimates, between 50 million and 100 million people worldwide perished in the three pandemic waves between the spring of 1918 and the winter of 1919. Adjusting for population growth, that is equivalent to between 200 million and 425 million today.  

Unlike now, when reports of new bird flu outbreaks in south-east Asia are closely monitored by the World Health Organisation, there was no early warning system. Consequently, when it was reported in May 1918 that King Alfonso XIII was ill in Madrid, most people dismissed the Spanish flu as a joke. The main advice was to gargle with salt water and to isolate yourself until the fever had passed. However, these rules did not apply to munitions workers who were urged to “carry on” for the sake of the war effort.  

As in other 20th-century epidemics and pandemics, such as HIV/Aids, Africans and Asians suffered proportionately more than Europeans and north Americans. Thus, while the average case mortality in the developed world was about 2%, in India, where 18.5 million perished, it was 6%, and in Egypt, where 138,000 died, it was 10%. In isolated regions with “virgin” populations with no immunity to flu, the impact was truly astonishing – in Western Samoa, for example, a quarter of the population was wiped out. By contrast, American Samoa recorded no casualties. 

The severity of the pandemic and the peculiar death pattern puzzle scientists to this day. Few epidemiologists believe the pandemic began in Spain, pointing instead to pre-pandemic waves in Copenhagen and other northern European cities in the summer of 1918. Where the virus first leapt from birds to humans or some other mammal is even more perplexing, with some scientists favouring a Kansas point of origin and others northern France or China.

ECDC: Influenza virus characterisation

ECDC has published a surveillance report: Influenza virus characterisation. Click or tap through to download the report. The summary:

This is the seventh report of the 2017–18 influenza season.  

As of week 30/2018, over 239 000 influenza detections across the WHO European Region have been reported. Forty-four percent of the detected viruses were type A, with A(H1N1)pdm09 and A(H3N2) viruses being detected in equal numbers. Type B viruses accounted for 56%; B/Yamagata viruses prevailed over B/Victoria viruses at a ratio of over 50:1. 

Swine flu claims eighth human victim in Vietnam in 2018

Thanks to FluTrackers for posting about this story. Via VnExpress International: Swine flu claims eighth human victim in Vietnam in 2018.

A 60-year-old man from Tra Vinh Province has become the eighth person to die of swine flu in Vietnam this year. 

Nguyen Thanh Hong, who tested positive for the A/H1N1 influenza virus, was pronounced dead on Monday at the Cho Ray Hospital in Ho Chi Minh City, the Vietnam News Agency reported on Thursday. 

Hong had been hospitalized at a local medical center in Tra Vinh, three-hour drive to the northeast of Saigon, with symptoms of high blood pressure and respiratory failure.  

A day later, he was transferred to Cho Ray where doctors found him infected with the flu. After five days of treatment, he passed away. 

The city has reported three swine flu casualties so far this year. Four other deaths were recorded in the southern provinces of Dong Thap, Ben Tre, Vinh Long and Ca Mau.  

On June 1, 16 people in HCMC's Tu Du Hospital, the biggest obstetrics facility in the south, also tested positive for the virus after an infected woman was admitted for gynecological procedure. 

Pregnant women and infants and young children under two are among the groups identified by the World Health Organization as being at increased risk for complications arising from swine flu. 

The H1N1 virus broke out worldwide in 2009 and was responsible for more than 17,000 deaths.  

Some strains of the virus are endemic in humans and cause a small fraction of all seasonal flu while others are endemic in pigs and birds, better known as swine flu and avian flu.  

Vietnam has recorded more than 11,000 human infections so far. No swine flu casualties were reported in the country between 2015 and 2017.

Anti-vaccine activists have taken vaccine science hostage

Via The New York Times, a very important op-ed by Melinda Wenner Moyer with a British Columbia angle: Anti-Vaccine Activists Have Taken Vaccine Science Hostage. Excerpt and then a comment:

Americans who don’t want to vaccinate are increasingly getting their way: A June study found that, over the past decade, the number of philosophical vaccine exemptions rose in two-thirds of the states that allow them. 

What drives these wrongheaded decisions is fear — fear that vaccines are somehow dangerous, even though research shows the opposite. And these choices have consequences. The 2015 Disneyland measles outbreak sickened at least 125 people, many of them unvaccinated. 

As a science journalist, I’ve written several articles to quell vaccine angst and encourage immunization. But lately, I’ve noticed that the cloud of fear surrounding vaccines is having another nefarious effect: It is eroding the integrity of vaccine science. 

In February I was awarded a fellowship by the nonpartisan Alicia Patterson Foundation to report on vaccines. Soon after, I found myself hitting a wall. When I tried to report on unexpected or controversial aspects of vaccine efficacy or safety, scientists often didn’t want to talk with me. When I did get them on the phone, a worrying theme emerged: Scientists are so terrified of the public’s vaccine hesitancy that they are censoring themselves, playing down undesirable findings and perhaps even avoiding undertaking studies that could show unwanted effects. Those who break these unwritten rules are criticized. 

The goal is to protect the public — to ensure that more people embrace vaccines — but in the long-term, the approach will backfire. Our arsenal of vaccines is exceptional, but it could always be better. Progress requires scientific candor and a willingness to ask inconvenient questions. 

Here’s a case that typifies this problem and illustrates how beneficial it can be when critical findings get published. In 2005, Lone Simonsen, who was then with the National Institute of Allergy and Infectious Diseases, and her colleagues published a study in JAMA Internal Medicine showing that the flu vaccine prevented fewer deaths than expected in people over 65.  

“I had interesting conversations with vaccine people. They said, ‘What are you doing, Lone? You are ruining everything,’” recalls Dr. Simonsen, who is now a global public health researcher at George Washington University. Her work helped lead to the development of a more effective flu vaccine for older people, yet she felt ostracized. “I felt it personally, because I wasn’t really invited to meetings,” she says. “It took a good decade before it was no longer controversial.” 

It’s understandable for scientists to be nervous. The internet has made it easy for anti-vaccine activists to mislead. Dr. Simonsen’s study, for instance, inspired a story with the ridiculous headline “Flu Vaccines Are Killing Senior Citizens, Study Warns.”

...

In 2009, Danuta Skowronski, the lead epidemiologist in the division of Influenza and Emerging Respiratory Pathogens at the British Columbia Center for Disease Control, and her colleagues stumbled across unexpected data that suggested a link between seasonal flu shots and an increased risk for pandemic flu. The findings could not prove a causal link — perhaps people who get seasonal flu shots differ from those who don’t in ways that make them more susceptible to pandemic strains. 

But one possible interpretation is that seasonal flu shots inhibit immunity to those strains. Dr. Skowronski’s team replicated the findings in five different studies and then shared the data with trusted colleagues.

“There was tremendous pushback,” Dr. Skowronski recalls, and some questioned whether “the findings were appropriate for publication.”

“I believed I had no right to not publish those findings,” Dr. Skowronski says. “They were too important.” The findings were submitted to three journals and underwent at least eight lengthy reviews before the final study was published in PLoS Medicine.

First, if vaccines are killing seniors, I can report that Heaven is remarkably like Vancouver, British Columbia, right down to the availability of the internet and flu vaccination. So far, however, I have been unable to find my own death certificate, so I can't tell which of my routine annual vaccinations did me in.

Second, even if I were indeed safely in Heaven I would not quarrel with Dr. Danuta Skowronski about influenza, vaccination, or anything else. I may be dead, but I'm not stupid.

Third, medical scientists who don't understand that they're in politics—evidence-based politics—need a quiet word from some of their colleagues.

The 1918 influenza pandemic: One hundred years of progress, but where now?

Via The Lancet Respiratory Medicine: The 1918 Influenza Pandemic: one hundred years of progress, but where now? The concluding paragraphs:

As in every influenza outbreak, the very young and very old were badly affected by the Spanish influenza pandemic, but in 1918 an exceptional number of influenza-related deaths occurred in relatively young healthy adults between 15–30 years of age, giving rise to the so-called W-shaped mortality curve. Just as in 2009, and in the H1N1 mini-pandemic of 1977, people older than a certain age who had been infected in early life with a virus of similar antigenicity were likely to have either maintained sufficiently high levels of antibody or retained immunological memory that was quickly activated to protect them from infection or disease. An influenza virus of the same H1 subtype as 1918 that might have circulated before 1889 might explain the relative protection of individuals older than 30 years compared with those in their 20s in 1918.  

Indeed, the concept that previous immunological experience of influenza shapes the outcome of subsequent infections is increasingly being used to explain observations about influenza in modern times; the first influenza infection an individual experiences appears to establish the response to subsequent infections. This concept has been termed original antigenic sin. It is now thought that the ‘sin’ extends to viruses with HAs that lie in the same phylogenetic group. People who have previously been infected with H1 subtype viruses are less likely to be zoonotically affected by H5 avian influenza viruses, whereas if the first influenza was H3, then a level of protection against H7 infection is observed.  

Conversely, a strong immunological imprint can render certain age groups more vulnerable to a related but drifted virus: in the 2013–14 influenza season, people in their 50s were particularly vulnerable to an antigenically drifted version of the H1N1 pandemic virus because their imprinted immune system preferred to respond to the original 2009 strain that was antigenically similar to an H1 virus they had experienced as children.  

The left-sided dip of the W is more difficult to account for. Why were children aged 5–15 less likely than 25-year-olds to succumb to infection in 1918? An attractive hypothesis is that a different quality of the maturing paediatric immune response was less likely to trigger the immunopathological pathways that paved the way for viral damage and subsequent bacterial descent to the lung. One study of childhood response to influenza infection found a qualitative difference related to age, but further studies are required to thoroughly understand this so-called honeymoon period. 

Understanding the exceptional impact of the 1918 influenza pandemic, including the immunological explanations for the atypical age-related sensitivity to virus infection, might have important implications for dealing with future influenza pandemics: at a time when the world is calling for new approaches to influenza vaccination, we are embarking on novel vaccination strategies that induce quite different arms of the immune response to those engaged by traditional vaccines or natural immune responses. It is important that we consider the possible immunological ramifications of these innovations on the outcome of infection by contemporary and future influenza viruses.

Unanswered questions about the 1918 influenza pandemic: origin, pathology, and the virus itself

Via The Lancet Infectious Diseases, a review by John Oxford and Douglas Gill: Unanswered questions about the 1918 influenza pandemic: origin, pathology, and the virus itself. The article is behind a paywall; here is the abstract:

The influenza epidemic of 1918 represented the greatest failure of medical science in the 20th century. Fortunately, research throughout subsequent years has been making amends. Some studies have applied RT-PCR to the tissue samples from that time, whereas others have reconstructed the pathogen in its virulent state. 

But the resurrection of the 1918 influenza virus leaves questions unanswered: although more virulent than contemporary H1N1 epidemic viruses in animal models, this increased virulence of the 1918 influenza virus is not sufficient to have been the sole cause of the high mortality rates recorded in humans during the epidemic. 

Thus, other hypotheses have been investigated. The immune history of the different age groups exposed at the time to the pandemic virus could be a factor, and the notion of original antigenic sin provides an explanation for the unusual pattern of deaths. The presence, or absence, of a cytokine storm in the lungs of young adults might also be involved. The time and location that the 1918 influenza pandemic first emerged from its avian reservoir is contentious, with arguments for China, Europe, and the USA, at various dates. Novel vaccines were tested during 1918, which are the precursors of the universal influenza vaccines that might offer protection in a future pandemic.

Whatever happened to H5N1?

For old times' sake I just visited WHO's tally of human H5N1 cases from 2003 to May 28, 2018. It confirmed my impression that H5N1, the original subject of this blog, seems to have vanished as a threat to humans.

As recently as 2015, H5N1 was diagnosed in 145 cases, 42 of them fatal (136 of the cases and 39 of the deaths were in Egypt). In 2016, just 10 cases and three deaths, all in Egypt. Indonesia had one fatal case in 2017; Egypt had three, with one death. No human H5N1 case has been reported at all so far this year.

This is quite a contrast from the early years. After its suppression in Hong Kong in 1997, H5N1 seemed to vanish until it returned in 2003 with one case in China and three in Vietnam, all fatal. The next year saw 46 cases and 32 deaths, and the disease had turned up in Thailand (17 cases, 12 deaths). By 2006, H5N1 was suddenly everywhere: Azerbaijan, Cambodia, China, Djibouti, Egypt, Indonesia, Iraq, and Turkey.

Nothing seemed to stop it, and circumstances seemed to encourage it: poultry smuggling is routine in many parts of Asia, public health systems are feeble, and countless families keep backyard flocks with minimal care. Those of us watching H5N1 in those days expected it to turn up in the Americas and Europe courtesy of modern air travel, whereupon we'd be in a full-blown, zombies-in-the-streets pandemic.

Instead, we were blindsided by H1N1 in 2009. It turned up almost simultaneously in Mexico and the US and then behaved just as we'd expected H5N1 to: a group of British schoolgirls went on holiday to Mexico and brought it back to the UK. (Having experienced Heathrow's swarming crowds, I can well imagine how it happened.) It was indeed a pandemic, but everyone complained about the absence of zombies.

Then H7N9 turned up, confirming avian influenza's ability to distract us with one threat while socking us with another.

By then I realized that no single disease could really be tracked alone; each is just another expression of a very complicated biosphere on which we pretend to impose various political systems. Some of those political systems regard outbreaks more as embarrassments than as existential threats, and many governments prefer to suppress news about them. I would not be surprised to learn that H7N9 has infected more people in China than Beijing has reported, or MERS infected more Saudis than Riyadh has admitted. Egypt went from 136 H5N1 cases in 2015 to ten in 2016, three in 2017, and zero so far this year. But I would not be surprised to know that it's still simmering away in the villages of the Nile delta.

And I would not be surprised if the next pandemic turned out to be a refurbished H5N1, or H7N9, or some other forgotten virus.

Venezuela: Infant with H1N1 flu dies in J.M. de los Rios Hospital

Efecto Cocoyu is a dissident website in Venezuela, and its health page is a litany of sorrow in a collapsed healthcare system. Here's a new report: Muere niño con influenza AH1N1 hospitalizado en el J. M. de los Ríos.[Boy with H1N1 influenza dies hospitalized in J.M. de los Rios] Excerpt, with my translation:

La noche del miércoles 25 de abril, se confirmó la muerte de un bebé por influenza AH1N1 en el hospital de niños José Manuel de los Ríos. El pequeño de nueve meses de nacido fue ingresado hace dos semanas en la Unidad de Terapia Intensiva Pediátrica (Utip) luego de ser referido del Hospital Elías Toro, en Catia.  

On the night of Wednesday, April 25, the death was confirmed of a baby from H1N1 influenza in the José Manuel de los Ríos pediatric hospital. The nine-month-old had been admitted two weeks earlier in the Pediatric Intensive Care Unit after being referred from Elías Toro Hospital in Catia.

El niño residía en Antímano e ingresó al J. M. de los Ríos con complicaciones respiratorias. El pasado 16 de abril, médicos del hospital confirmaron por una prueba de cultivo que se trataba de un caso de influenza AH1N1.  

The little boy lived in Antímano and entered J.M de los Ríos with respiratory complications. On April 16, hospital doctors confirmed his case was H1N1 influenza.

Efecto Cocuyo pudo conocer que otro dos casos de influenza fueron confirmados en el hospital el pasado miércoles. Los dos niños son atendidos en un área de aislamiento y los galenos activaron un plan estratégico de contención para prevenir el contagio. 

Efecto Cocuyo learned that two other flu cases were confirmed in the hospital last Wednesday. The two children are in isolation and doctors have launched a strategic plan to prevent contagion.

Otro caso sospechoso fue descartado luego de que se realizaran las pruebas correspondientes.  

Another suspected case was discarded after testing.

Vietnan Vera, médico intensivista de la Utip, indicó a Efecto Cocuyo que la unidad no cuenta con los medicamentos necesarios para tratar a los pacientes con el virus de la influenza. El niño que falleció fue tratado con el Oseltamivir disponible en el hospital, con fechas de vencimiento de 2011 y 2015.

Vietnan Vera, ICU physician, told Efecto Cocuyo that the unit lacks medications for treating influenza. The little boy who died was treated with Oseltamivir available in the hospital, with expiry dates of 2011 and 2015.