First health care worker fatality in New Zealand

Deaths of health care workers is something we watch closely as they are usually a healthly group that has high exposure to illnesses like pandemic influenza. Seeing an increase in death or hospitalization in health care workers might be a trigger indicator that we're seeing more severe outbreaks, changes in the virus, etc.

So, even though we have not seen any clusters of deaths in health care workers, it is important to take note of stories such as this one of the first health care worker death in New Zealand.

"The 39-year-old woman who died of swine flu in Wellington Hospital this week was a front-line health worker at Hutt Hospital, officials have confirmed.

The woman understood to have been a nurse in the children's ward is believed to be the first health worker to die from the virus in New Zealand.

Her death from a rare complication on Monday, after 11 days in intensive care, is the 13th to be officially recorded.


The woman had suffered a miscarriage within the previous two months. Pregnancy is a known risk factor for viral complications. However, it is not known whether she had the virus at the time she miscarried."

For the full story, go here:
http://www.stuff.co.nz/national/health/2705831/Swine-flu-victim-first-health-worker-to-die

ECDC posts the UK planning assumptions for pandemic flu

The European Centre for Disease Prevention and Control posted the UK planning assumptions for pandemic waves in the fall and winter.

Clinical attack rate	30%
Peak clinical attack rate	6.5% (local planning assumptions 4.5% to 8%) per week
Complication rate	15% of clinical cases
Hospitalisation rate	2% of clinical cases
Case fatality rate	0.1% to 0.2% (cannot exclude up to 0.35%) of clinical cases
Peak Absence Rate	12% of workforce

"UK parameters and their broader applicability

The UK paper is based on a model using parameter estimates from the UK and abroad on the 2009 strain and fitted using real data on UK cases over the period when the majority of cases were confirmed and reported daily.

Clinical attack rate
This is 30 % (The UK clinical attack rate is based on an assumption that half of the infected become symptomatic so this would imply a total infection attack rate of about 60 %). WHO assumptions are that two thirds become symptomatic [5]. Whether the UK or WHO is correct will be determined later when the results from serology become available. The UK assumptions imply a basic reproductive number Ro in the interval 1.4 – 1.5 which seems to be the case at present in the UK. A Ro of value 1.4 implies a total infection attack rate of about 50 % (which would imply a clinical attack rate of 25 % in the UK planning assumptions). A higher value of Ro of 2.0 implies a total infection attack rate of about 80 % (hence a clinical attack rate of 40% in the UK planning assumptions).

Peak clinical attack rate
This can depend on a number of factors such as seasonality, immunity in the population and interventions that might prolong the epidemic but also reduce the peak attack rate [6]. A particularly important point to note is that local epidemics are often shorter and sharper in a pandemic than national rates and so there is a higher value for the peak clinical attack rates for local application [1,3].

Case fatality rate
This is one of the most eagerly sought parameters but it is also amongst the hardest to determine with any accuracy. The earliest studies of this pandemic gave a high CFR of about 0.4 % [7] compared to lower rates for the 1957 and 1968 pandemics but higher rates for 1918 [8]. The UK estimates are of a CFR of 0.1-0.2 though values of up 0.35% cannot be ruled out as impossible [3]. The CFR number reported in the UK are thus as stated the reasonable worst case scenario unless the virus changes its characteristics in terms of lethality while the Norwegian figure is more based on what has been directly observed, adjusted for assumed underreporting."

For the full discussion, see: http://www.ecdc.europa.eu/en/health_content/phdev/090729_ph.aspx

Potential "mismatch" for the seasonal flu vaccine

Seasonal influenza vaccines are actually created to fight off several virus strains. Experts gather in late winter/early spring to select what they think will be the predominant strains next fall and winter. Then vaccine production begins.

Sometimes experts get it right, sometimes there's a "mismatch" and another virus strain begins to dominate.

Reporting from Helen Branswell and the ProMed network are raising the possibility that in addition to pandemic strain (novel H1N1), for which we will have limited vaccine supplies, there may be a mismatch for the seasonal flu vaccine as well.

"A component of the seasonal flu shot may not be well matched to the circulating viruses, potentially setting up what's known as a vaccine mismatch.

Some samples of the emerging new strain of H3N2 viruses show a substantially reduced response to antibodies generated by the corresponding virus in the seasonal vaccine, raising the possibility of significantly reduced protection in some cases.

Vaccine mismatches are bad at the best of times. More people get sick during flu seasons with mismatches. But a seasonal flu vaccine mismatch coinciding with a flu pandemic? That is no one's idea of a good time."

We don't know yet, however, how much of the seasonal flu we will see in the Northern Hemisphere or if it will be crowded out by H1N1. Also, worlwide we haven't be able to track the varriant of H3N2 because of the flood of pandemic virus reporting and analysis:

"The new variant has been seen on a number of continents, though it still remains a minority member of the H3N2 family, according to experts at the World Health Organization and the U.S. Centers for Disease Control in Atlanta.

With the demands the ongoing pandemic is placing on the WHO's laboratory network, researchers haven't yet had time to study whether the new variant is making up a growing percentage of H3N2 viruses, said Dr. Nancy Cox, director of the CDC's influenza division.

If they were, that would suggest the variant was on its way to becoming the dominant H3N2 virus and a vaccine mismatch would be on the cards.

Further clouding the issue is the fact that labs around the world haven't been submitting as many H3N2 viruses to the WHO network. There are simply fewer of them around.

"We haven't had that many H3N2 viruses to analyze because we've had such a flood of the novel H1N1 viruses because they're predominating," Cox said."

To read the whole story, visit: http://www.google.com/hostednews/canadianpress/article/ALeqM5jPDEE_BdufsSNIxDs5NN-W0GiWoQ

or http://www.promedmail.org/pls/otn/f?p=2400:1001:2699631650126880::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,78478

Preliminary estimate of the reproduction number from New Zealand

Estimating the reproduction number, sometimes shown or referred to as "R", is very important because it tells us how well a particular influenza virus will spread. Reproduction number refers to the average number of secondary influenza cases caused by one primary case. In other words, if we have an influenza virus with a reproductive number of 3, then each person infected will likely spread the virus to three other people, on average.

Of course, the true reproduction number is difficult to know since we can't be certain of the total number of influenza cases, etc. However, scientists have pretty good methods for estimating it.

A study just out from New Zealand puts the reproduction number at 1.96. The study notes that estimates from Mexico were ranged from 1.4–1.6 and in Japan, for the current wave, 2.0–2.6.


What does this mean? Seasonal flu has a reproduction number of 1.3 - 1.5, so if estimates in New Zealand and Japan are correct, then it would mean that H1N1 is transmitting more efficiently (and will spread more quickly) than seasonal flu. However, these estimates contradict some preliminary studies of H1N1 in ferrets. We'll have to keep an eye on the evidence as it accumulates.

To read the study, visit: http://www.nzma.org.nz/journal/122-1299/3722/

Novel H1N1 vaccine trials begin today in Australia

From ABC News in Australia, pandemic vaccine trials start in Adelaide today.

"Rachel David from vaccine makers CSL says the Royal Adelaide Hospital trials will take about seven months, but there will be enough data by September for the Government to start planning distribution in October.

"I think what the chief medical officer in Canberra has been saying in terms of October is quite reasonable," she said.

There will be 240 volunteers between 18 and 64 split into two groups.

Dr David says one group of volunteers will get a single dose of the vaccine.

"The other group is going to receive a double dose," she said, adding that the company is not concerned about the risk of side effects.

"Three weeks after today, they're going to have their blood tested to see what sort of response, or immune response, they've had to that vaccine.

"Sometimes with these brand new strains that start circulating, you need a higher dose to get a decent immune response."

A trial on children aged from six months to nine years will start at Adelaide's Women's and Children's Hospital next month."

http://www.abc.net.au/news/stories/2009/07/22/2632625.htm

Religious rites adapted to prevent the spread of flu

A short but interesting article from Reuters on how religious communities in Britain are adapting rites to prevent the spread of flu.

A great learning piece from this article is that decisions are being made locally on measures that will be taken. It's important that local religious leaders, who are often leaders in their community, are able to understand flu prevention measures and make adaptations to their particular service.

http://www.reuters.com/article/swineFlu/idUSB471158?feedType=RSS&feedName=swineFlu&virtualBrandChannel=10521

New perspective article from NEJM: "The Persistant Legacy of the 1918 Influenza Virus"P

NEJM just published a great perspectives article on recent findings/thinking about the 1918 virus with an easy to understand analogy of the gene segments of the virus:

"To understand what has been happening since 1918, it is helpful to think of influenza viruses not as distinct entities but as eight-member "gene teams" that work together and must sometimes trade away one or more team members to make way for new gene "players" with unique skills. In nature, avian influenza A viruses seem to exist as transient complexes of eight genes that assemble and reassemble promiscuously, if not randomly, in an enormous global avian reservoir. Within this reservoir, avian viruses remain stably adapted to the enteric tracts of hundreds of avian species, single members of which are often simultaneously infected by multiple viruses that engage in prolific gene reassortment. Because of this continual reassortment, a seemingly endless variety of new viruses with potentially new properties are continually being engineered. Indeed, thousands of unique gene constellations making up avian influenza viruses have already been identified; as research continues, the number will undoubtedly grow."


Most interesting to me was this article seems to continue some of the thinking from this weeks PNAS article in challenging some previously held notions,

"But the long-held belief that shifts always cause severe pandemics, whereas drifts lead to more modest increases in seasonal mortality, has been called into question. The effects on mortality of new influenza viruses created by the several genetic mechanisms mentioned above are not easily characterized"

Conclusion was interesting as well:

"If there is good news, it is that successive pandemics and pandemic-like events generally appear to be decreasing in severity over time. This diminution is surely due in part to advances in medicine and public health, but it may also reflect viral evolutionary "choices" that favor optimal transmissibility with minimal pathogenicity — a virus that kills its hosts or sends them to bed is not optimally transmissible. Although we must be prepared to deal with the possibility of a new and clinically severe influenza pandemic caused by an entirely new virus, we must also understand in greater depth, and continue to explore, the determinants and dynamics of the pandemic era in which we live."

Highly recommend the quick read: http://content.nejm.org/cgi/content/full/361/3/225