Elevate the Flu baseline

Summer has technically ended in Australia (sure – go look at a temperature prediction!) and Flu spent all of it being abnormally active.

Laboratory-confirmed Flu (“notifications”) cases in Australia ranged from 3-times above the previous highest ever recorded December in 2018 to 2-times the previous total for January and for February 2019.[1]

The 2018 Flu season peaked in September but generated just 10-20% of the number of laboratory-confirmed cases seen in the huge 2017 season. Those two facts are probably related. We undoubtedly had a lot of people coming out of 2017’s winter with immunity to one or more of the multiple Flu strains that circulated. Immunity = protection from illness, for however long that protection lasts. While protection is probably strongest to those strains that infected the person, there may also be cross-protection that wards of illness from related but still distinct Flu strains.

Could a big 2018/19 summer be due to overseas travel from? Yes and no

The unusual summer Flu activity was partly ascribed to travel into Australia from the northern hemisphere’s winter Flu season. The theory being that infected travellers were bringing new Flu strains into Australia.

‘The high number of cases is thought to be in part due to travellers returning from the northern hemisphere,’

Dr Mark Morgan, Chair of the RACGP Expert Committee – Quality Care [2]

Yes, that happens. But it surely happens every year. Why was this summer such a big one?

A Flu here is a Flu everywhere.

For this to drive our summer situation, there are two options. We’ve either experienced more travel than in previous years or we’ve been gifted a more new and different virus strain via infected travellers than we usually see. Remember, something has to be different about this summer compared to previous summers. So did we experience a lot more visitors? To find answers, I went to the Australian Bureau of Statistics (ABS) site and found some cool travel data.[3]

As the ABS graph below shows, there is no summer 2018/19 spike that could explain the coinciding 2-3 times higher than normal number of Flu cases this summer based on short-term overseas visitor arrivals.

Short-term visitor arrivals to Australia.
Source: Australian Bureau of Statistics.[3,4]

There is the usual year-on-year growth of arrivals – a steady and constant upward trend. There’s also a year-on-year growth of our population.

Travel is a still a prime culprit; in substance not in volume

This steadiness doesn’t exclude the cause being due to Flu-infected travellers. But we need to re-frame that idea. We’d be talking more about travellers bringing in a new Flu virus strain from somewhere else. The idea that there have been increased numbers of infected travellers is busted because we can say there’s been no unusual increase. But it might be a bit more different than normal to change the pattern this much.

It was also interesting to note that December/January is Australia’s peak period for visitors. So if there was a virus strain emerging somewhere else, this would sure be a good time to have it quickly delivered here via human postpak!

What else can travel data tell us?

In the next ABS graph, we look at Australian residents returning home after a short-term jaunt overseas. Same basic trend. Also interestingly, Australians come back home most often just as tourists are arriving to make the most of our summer.

Short-term resident returns to Australia.
Source: Australian Bureau of Statistics.[3,4]

Lastly, I wondered where most of the short-term travellers were coming to Australia from. As we can see below, China is on top and has contributed a very steeply increasing number of visitors to Australia from 2010 onwards.


Country of residence of short-term visitor arrivals to Australia.
Source: Australian Bureau of Statistics.[3,4]

How could summer be virus-related?

Let’s talk about viruses and immunity then.

If there are more infections this summer, then there must have been fewer immune people coming into the season. When we’re immune, a virus can still infect us but it usually doesn’t go on to drive full-blown disease. We can get immunity from infection or from vaccination.

A drop in defences

These summer cases could be due to a drop in pre-existing immunity. We hear about Flu vaccine-induced immunity waning over the year between vaccines so this is possible. Also, an asymptomatic or mild infection that results in a low level of illness might produce weak or short-lived immunity.

Coloured up influenza virion.
Source: Flickr, Sanofi Pasteur [5]

A new strain on the block

We might instead have a strain of FluA/H1N1, the predominant virus this season, or FluA/H3N2 which tried hard to supplant FluA/H1N1 over summer, that looks slightly different to our immune response because of changes via mutation (see the graphs below; see what I mean about low numbers being characterised?).

Were the same strains that dominated 2017, the ones circulating in winter 2018? Certainly, some proportion will have been and many people will have become immune to those because they got infected. Especially if Flu infection-induced immunity lasts longer than Flu vaccine-induced immunity; a topic for another day.

Unfortunately I don’t have data on what proportion of those strains are still around. That’s because of the quirks of Flu testing. And budgetary constraints. That last one’s pretty self-explanatory.

A sample sliver of a season

Flu viruses are sampled from the pool of all infected people’s biospecimens for further detailed characterisation. The sample isn’t very big (see that last pair of graphs above). It’s assumed that we pick enough examples for our sample to represent the main viral players of the Flu season. And we probably do. But we only display the main players in our results. We don’t sample enough to tell us the proportion of each minor strain circulating. By strain, I mean the virus identified after a more detailed analysis of the subtype.

I don’t think we know enough about how many different, distinct Flu viruses are co-circulating in a given season. Certainly not at the genetic level. We don’t have a reliable denominator. And I think this may affect our understanding of why Flu vaccines don’t always work as we’d expect. What proportion of all people had this strain or that strain of FluA/H3N2? Ill defined. We only know what proportion from that sample.

Checking out the cultures.
Photo by Jaron Nix on Unsplash

Is this unusual summer because of the unusual summer?

The weather. It’s been really hot in all parts of Australia. ANd really wet in some parts as well. While the heat itself probably doesn’t help Flu viruses remain infectious for longer after they’ve been coughed and sneezed onto surfaces, maybe the weather has driven more people into indoor air-conditioning; cool-seeking patterns of behaviour. From there, perhaps the closer contact is giving Flu transmission an upward nudge.

New molecular diagnostic kits are good

What has become clear in the last few years is that very fast and very sensitive testing of viral genetic material is here. It isn’t cheap, but it’s available. It’s the next big shift in high-throughput laboratory diagnostics for those labs that rely on kits and not in-house (read: home-made) molecular tests (read: PCR-based technologies). But it’s also seeing uptake in hospital emergency departments (EDs). Here, rapid testing helps move patients from a waiting room to somewhere less likely to infect all those around them as they sit around coughing out Flu virus for a while.

How much use is hard to judge. It’s certainly popular in labs and EDs along the east coast of Australia. I’m not talking about dipstick technologies. Yuck. I mean PCR-based and rapid turnaround. The good kush of the detection tech. 🤓

The best tool though would be some sort of rapid turnaround, sample-in virus-strain-out, whole-genome sequencing platform. It’s on my Christmas list.

Final thought

Whether this summer has seen elevated Flu numbers because of an immunity/vaccination evasive virus strain that’s emerged or been delivered, at an unusual time of year, or whether it’s increased testing of sick people for Flu, has yet to be resolved.

In my opinion, it’s probably a bit of everything with slightly more of the virus stuff than the testing stuff.

References

  1. Notifications of a selected disease by month and year, 1991 to present
    https://www9.health.gov.au/cda/source/rpt_3_sel.cfm
  2. Record number of influenza cases to start 2019
    https://www1.racgp.org.au/newsgp/clinical/record-number-of-influenza-cases-to-start-2019
  3. 3401.0 – Overseas Arrivals and Departures, Australia, Dec 2018, Australian Bureau of Statistics
    http://www.abs.gov.au/ausstats/abs@.nsf/products/961B6B53B87C130ACA2574030010BD05
  4. http://www.abs.gov.au/websitedbs/D3310114.nsf/Home/%C2%A9+Copyright?opendocument
  5. An influenza virus (orthomyxoviridae) seen through an electronic microscope. Photographer: Alain Grillet, Copyright Sanofi Pasteur
    https://flic.kr/p/93Bu23
  6. World Health Organization Collaborating Centre for Reference and Research on Influenza
    http://www.influenzacentre.org/surveillance_subtypes.htm

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