Neglected Generations · Post 1 of 3

The hidden burden behind a bad flu season.

COUNTED NOT COUNTED

Key message

Respiratory infections are easy to underestimate. Some are never diagnosed, and some of their consequences appear later in the records as something else.

In the week to 16 August 2026, 177 people were admitted to four Auckland hospitals with severe acute respiratory illness (SARI). It was the highest weekly SARI admission rate recorded in Tāmaki Makaurau since 2015.

Influenza was the most commonly detected virus. Emergency departments were under pressure, wards were full, and for a few weeks, respiratory illness gained prominence in the news.

What we could see was a fraction of what was there. It is a consequence of how respiratory disease is counted, and the gap turns out to be wider than most people realise.

There are several quite different ways the burden drops out of view. Sometimes the infection is never identified, because the patient does not match the definition being used, or because no test was done. Sometimes the illness is recorded perfectly well, but the infection’s contribution to it is not. And sometimes the infection has resolved by the time its consequence arrives, so the consequence is filed under an entirely different diagnosis. Influenza, RSV and pneumococcal disease each go missing in their own way. The heart attacks and lost independence that follow them go missing in another way again.

Not all of those 177 admissions were influenza. SARI stands for severe acute respiratory infection, and SARI surveillance counts people admitted with a respiratory illness of some kind. It is a smoke alarm rather than a diagnosis: quick to tell you something is burning, not designed to tell you what.

New Zealand data give some sense of the scale. A modelling study covering 1994 to 2008 estimated that influenza contributed an average of about 2,260 hospitalisations a year across all medical illness, against about 822 a year in the narrower pneumonia-and-influenza category. Both are influenza-attributable estimates, which means they come from modelling how admissions rise and fall with influenza activity rather than from counting discharge records with influenza written on them. Many of those 2,260 admissions were coded as something else. The authors concluded that influenza’s real contribution to hospital admissions was around nine times greater than routine discharge data suggested.

Why the Numbers Miss So Much

Two systems generate most of what we know about respiratory disease in hospitals, and neither was built to measure total burden.

Surveillance tracks disease occurrence and trends; its job is to tell public health teams what is circulating and whether it is going up. Hospital administrative coding does something else again. It records what happened during a clinical episode and supports billing, planning and the running of the system. Both are useful, and neither on its own tells you how much disease there actually is. The gap between the two takes a different form in each of the winter pathogens.

Why doesn’t influenza always look like influenza in an eighty-year-old?

In a healthy forty-year-old it usually does: sudden fever, cough, aches all over. In an eighty-year-old the fever may be blunted or absent altogether, and what brings them in might be confusion, a fall, breathlessness, or a chronic condition that has abruptly worsened. Look for influenza using a description written around a fit adult and you will walk past it in the people most likely to end up seriously unwell.

The CIRN Serious Outcomes Surveillance Network in Canada put a number on this, comparing standard influenza-like-illness criteria against laboratory-confirmed infection in hospitalised adults across several seasons. The measure that matters is sensitivity: of the people who genuinely had influenza, what proportion did the criteria pick up? In patients under 65 the criteria caught 51.1% of confirmed cases. In patients 65 and over, sensitivity fell to 44.6%. More than half the laboratory-confirmed influenza in older hospitalised adults did not meet the definition being used to count influenza.

Coding adds a second layer. A US modelling study asked what happens if you count influenza-associated hospitalisations only where a pneumonia diagnosis code is present. Across adults, that approach missed around 31% of influenza-associated respiratory and circulatory hospitalisations. The precise figure varies by age group and by modelling assumption. The direction does not.

Three ways the respiratory burden goes uncounted. Influenza: standard influenza-like-illness criteria had 44.6% sensitivity among hospitalised adults aged 65 and over. RSV: hospitalisation rate 347 per 100,000 after adjustment for testing and test sensitivity, against 157 per 100,000 unadjusted. Pneumonia and pneumococcus: 55 to 58 per cent of community-acquired pneumonia hospitalisations in adults 50 and over recorded pneumonia as other than the most responsible diagnosis.
Three Ways the Respiratory Burden Goes Uncounted. Each panel uses its own scale; the three measures are not comparable with one another. Sources: Andrew et al. 2020; Li et al. 2023; Grajales Beltrán et al. 2023.

RSV goes missing earlier, at the testing stage

With RSV the problem is not whether the patient fits a definition. It is whether anyone looked. Older adults admitted with a respiratory illness are not routinely tested for RSV, and the tests we do use are less sensitive in adults, where viral loads run lower than in infants. An infection nobody tested for cannot appear in any count.

A global systematic review and modelling study tried to correct for both problems at once, adjusting reported RSV hospitalisation rates in adults 65 and older for how often testing happens and how sensitive those tests are. The unadjusted rate was 157 per 100,000. After adjustment it was 347 per 100,000, more than double. Scaled across high-income countries, that implies roughly 787,000 RSV-associated hospitalisations in a single year.

How big that correction should be depends on the assumptions built into the model, and reasonable people argue about them. The direction is not in dispute. European analyses using entirely different national datasets arrive at the same conclusion by another route.

New Zealand has less to work with here than it should. A scoping review of Australian and New Zealand data found substantial gaps in the local literature. That is not an undercount in itself, but a disease whose local burden has never been properly characterised is an easy one to leave out of the conversation.

Pneumonia is recorded, just not where anyone looks for it

When someone is admitted, the record carries one main diagnosis, formally the most responsible diagnosis, meaning the single condition considered most responsible for the admission and the length of stay. Everything else going on at the time is recorded as secondary. Researchers estimating disease burden usually count only the admissions where their condition of interest is the main diagnosis, because it is the cleanest and most consistent thing to count. Which is a bit like working out what is in someone’s shopping trolley by looking only at the largest item.

A Canadian analysis of a decade of hospital data found that between 55% and 58% of community-acquired pneumonia hospitalisations in adults 50 and older recorded pneumonia as something other than the most responsible diagnosis. These were not trivial admissions. They had longer stays and higher in-hospital mortality than the ones where pneumonia was the headline.

Here the disease has not vanished from the record at all. Its place in the story has.

Pneumococcus then adds a layer of its own. Even when the pneumonia is properly recorded, the organism responsible is frequently never identified, because non-bacteraemic pneumococcal pneumonia is difficult to confirm with routine testing. The pneumonia is real, the admission is real, and the cause stays unattributed. We know this happens. We cannot put a reliable number on how often.

None of which means these systems are failing. They do the job they were built for. The difficulty comes afterwards, when their outputs are read as though they were measurements of how much disease exists.

When the Consequence Is Counted and the Cause Is Not

Everything so far has been about infections that were missed, or recorded without their contribution being recognised. There is a further problem.

An acute infection can set something off that arrives days later under a completely different diagnostic heading. By the time the consequence turns up (say a heart attack), the infection may be resolved, undocumented, or simply beside the point to whoever is coding the new admission. The burden is counted. The cause is not.

Did the influenza cause the heart attack, or do sick people simply get sick?

This is genuinely hard to study. People who catch influenza and people who have heart attacks differ in all sorts of ways, including age, frailty, existing heart disease and smoking, and no amount of statistical adjustment removes that problem entirely.

So the trick is to stop comparing people with each other and start comparing each person with themselves. Take patients who had both a confirmed influenza infection and a heart attack, then ask whether the heart attacks cluster in the days immediately afterwards or scatter evenly across the rest of the year. It is the epidemiological equivalent of checking whether you trip over more often when the hallway light is off, rather than comparing yourself with your neighbour. Because every patient acts as their own comparison, fixed characteristics cannot explain the result. The design is called a self-controlled case series.

Kwong and colleagues applied it to influenza and acute myocardial infarction. Hospitalisation for a heart attack was roughly six times more likely in the seven days after a positive influenza test than during the same patients’ control periods, and after day seven, the elevation vanished. That disappearance matters as much as the spike, because it is what you would expect from a trigger rather than from a group who were simply at higher risk all along. A later study of senior US veterans, using the same design, found much the same thing.

This is strong evidence that influenza can act as a trigger for a heart attack. It is not evidence about any particular patient, and no individual heart attack can be pinned on a preceding infection on the strength of these studies.

The seven-day risk window. Acute myocardial infarction hospitalisation was about six times more likely during days one to seven after laboratory-confirmed influenza, compared with control periods in the same patients. Relative incidence, not absolute risk.
The 7-Day Risk Window. Relative incidence compared with control periods in the same patients, not absolute risk. Source: Kwong JC et al. N Engl J Med 2018;378:345–353.

The heart attack gets coded as a heart attack. The influenza sitting upstream of it rarely gets mentioned in the same sentence, and almost never in the same statistic.

Nor are cardiac complications some rare curiosity at the edge of the data.

Key evidence

  • Cardiac events are common in people hospitalised with influenza. Among nearly 90,000 US adults hospitalised with laboratory-confirmed influenza, 11.7% had an acute cardiovascular event during that admission.
  • RSV does much the same thing. In a separate US surveillance study of adults aged 50 and older hospitalised with laboratory-confirmed RSV, 22.4% experienced an acute cardiac event.
  • Neither figure lands in a respiratory disease burden estimate. These events are recorded as cardiac admissions with cardiac diagnoses, which is clinically correct and statistically invisible.

The harm that never gets a diagnosis code

A heart attack is comparatively easy to count. It produces a diagnosis, a procedure, an admission, a code. Loss of function produces none of those things, which is why it slips out of routine statistics.

What it looks like in practice is an older person who is managing at home, goes into the hospital and comes out unable to any more. Someone who could get to the letterbox and now cannot. Someone who was living independently and is discharged into residential care. For a great many people in their eighties, that is the outcome that matters most.

In a Canadian cohort of adults 65 and older hospitalised with influenza or another acute respiratory illness, around one in five survivors still had persistent functional decline a month later, and one in ten met the threshold for catastrophic disability. Comparable patterns follow pneumonia in nursing home residents, RSV hospitalisation in older adults, and invasive pneumococcal disease.

Where that decline is recorded at all, it appears in an aged-care assessment or a discharge summary that says nothing about the respiratory infection a few weeks earlier.

Who Carries the Burden?

So far this has been one question: how much respiratory disease disappears from view? Of the burden that does stay visible, who is most impacted?

In New Zealand the answer has been consistent for a long time. Auckland surveillance running from 2012 to 2023 found the highest influenza-associated hospitalisation rates among adults aged 80 and over, among Māori and Pacific peoples, and among people living in low socioeconomic status areas. Rates climbed sharply after the pandemic across most groups, reaching 196.7 per 100,000 among Pacific adults in 2023.

That is recent data, but the pattern is not new:

  • Community-acquired pneumonia. A hospital study in Christchurch and Hamilton found the overall rate was 3.03 times higher among Māori than non-Māori, with significant differences in every 10-year age band from 45 to 74. Pneumococcal pneumonia was 3.23 times higher overall, though the age-specific comparisons there did not reach statistical significance.
  • Influenza mortality. National modelling found Māori aged 65 to 79 dying from influenza at 3.6 times the rate of European and Other New Zealanders in the same age band, and Pacific peoples at 2.4 times.
  • Deprivation, measured separately. People living in the most deprived areas died at around 1.8 times the rate of those in the least deprived. Ethnicity and deprivation overlap, but they are not the same variable and were not analysed as one.
  • Invasive pneumococcal disease. Auckland surveillance found the highest rates among Pacific peoples, at 33 per 100,000.
Who carries the burden of severe respiratory illness in New Zealand. Modelled influenza mortality rate ratios for ages 65 to 79: Māori 3.6 times, Pacific peoples 2.4 times, European or Other 1.0 as the reference group. Measured separately, most deprived areas about 1.8 times least deprived. Invasive pneumococcal disease incidence per 100,000 in the Auckland region: Pacific peoples 33, Māori 14, European 10.
Uneven From the Start. Two datasets measuring different outcomes on different scales; the direction of inequality is consistent across both. These data show unequal disease burden, not unequal surveillance. Sources: Khieu TQT et al. J Infect 2017; Eichler N et al. J Prim Health Care 2019.

These findings describe unequal outcomes, not unequal surveillance. Nothing here suggests case-finding works less well for some populations than others. That would be a different claim needing a different study design.

What the datasets do show, consistently across incidence, mortality and invasive disease over roughly two decades, is that Māori, Pacific peoples and people living in the most deprived areas carry a disproportionate share of severe respiratory disease.

Before We Talk About Value

When a health problem turns out to be bigger than the headline numbers suggest, the reflex is to jump to the economics. Is prevention worth what it costs? I will discuss this topic in Part 2, but ‘is it worth it’ cannot be easily answered because the answer depends entirely on what you count as the thing being prevented.

On the evidence above, that includes influenza infections that never met the case definition used to record them, RSV admissions where no test was done, and pneumonia sitting behind another main diagnosis. It also includes heart attacks arriving in the week after an infection that goes unmentioned in the cardiac record, and the loss of independence that follows a bad chest infection and is never traced back to it. And of course, none of it falls evenly across the population.

A cost-effectiveness model that counts only laboratory-confirmed influenza admissions is answering a much smaller question than the one we are actually asking.

Part 2 takes up the economics directly. When we say a vaccine “pays for itself”, what exactly is being counted, and what falls outside the model?

Read Part 2 →

Primary sources

  1. Andrew MK et al. Influenza surveillance case definitions miss a substantial proportion of older adults hospitalized with laboratory-confirmed influenza: A report from CIRN SOS. Infect Control Hosp Epidemiol. 2020;41(5):499–504. doi:10.1017/ice.2020.22
  2. Ortiz JR et al. Influenza Pneumonia Surveillance among Hospitalized Adults May Underestimate the Burden of Severe Influenza Disease. PLoS ONE. 2014;9(11):e113903. doi:10.1371/journal.pone.0113903
  3. Li Y et al. Adjusting for Case Under-Ascertainment in Estimating RSV Hospitalisation Burden of Older Adults in High-Income Countries: a Systematic Review and Modelling Study. Infect Dis Ther. 2023;12(4):1137–1149. doi:10.1007/s40121-023-00792-3
  4. Zhang T et al. Estimating the respiratory syncytial virus-associated hospitalisation burden in older adults in European countries. BMC Medicine. 2025. doi:10.1186/s12916-025-04249-x
  5. Farquharson K et al. Burden of respiratory syncytial virus disease across the lifespan in Australia and New Zealand: a scoping review. Public Health. 2024;226:8–16. doi:10.1016/j.puhe.2023.10.031
  6. Grajales Beltrán AG et al. Burden of Acute-Care Hospitalization for Community-Acquired Pneumonia in Canadian Adults Aged 50 Years or Older. Vaccines. 2023;11(4):748. doi:10.3390/vaccines11040748
  7. Elias C, Nunes MC, Saadatian-Elahi M. Epidemiology of community-acquired pneumonia caused by Streptococcus pneumoniae in older adults: a narrative review. Curr Opin Infect Dis. 2024. doi:10.1097/QCO.0000000000001005
  8. Kwong JC et al. Acute Myocardial Infarction after Laboratory-Confirmed Influenza Infection. N Engl J Med. 2018;378:345–353. doi:10.1056/NEJMoa1702090
  9. Young-Xu Y et al. Laboratory-confirmed influenza infection and acute myocardial infarction among United States senior Veterans. PLoS ONE. 2020;15(12):e0243248. doi:10.1371/journal.pone.0243248
  10. Chow EJ et al. Acute Cardiovascular Events Associated With Influenza in Hospitalized Adults: A Cross-sectional Study. Ann Intern Med. 2020;173(8):605–613. doi:10.7326/M20-1509
  11. Woodruff RC et al. Acute Cardiac Events in Hospitalized Older Adults With Respiratory Syncytial Virus Infection. JAMA Intern Med. 2024;184(6):602–611. doi:10.1001/jamainternmed.2024.0212
  12. Verschoor CP et al. Respiratory Syncytial Virus (RSV)-Related Hospitalization and Increased Rate of Cardiovascular Events in Older Adults. J Am Geriatr Soc. 2025. doi:10.1111/jgs.19591
  13. Hoogendijk EO et al. Adverse effects of pneumonia on physical functioning in nursing home residents: Results from the INCUR study. Arch Gerontol Geriatr. 2016;65:116–121. doi:10.1016/j.archger.2016.03.011
  14. Griffith MF et al. Nursing Home Residents Face Severe Functional Limitation or Death After Hospitalization for Pneumonia. J Am Med Dir Assoc. 2020. doi:10.1016/j.jamda.2020.09.010
  15. Branche AR et al. Change in functional status associated with respiratory syncytial virus infection in hospitalized older adults. Influenza Other Respir Viruses. 2022;16(6):1151–1160. doi:10.1111/irv.13043
  16. Maruyama T, Fujisawa T, Suga S. Risk factors for mortality and severe functional decline in adults with invasive pneumococcal disease. Int J Infect Dis. 2026. doi:10.1016/j.ijid.2026.108691
  17. Andrew MK et al. Persistent Functional Decline Following Hospitalization with Influenza or Acute Respiratory Illness. J Am Geriatr Soc. 2021;69(3):696–703. doi:10.1111/jgs.16950
  18. Khieu TQT et al. Estimating the contribution of influenza to hospitalisations in New Zealand from 1994 to 2008. Vaccine. 2015;33(33):4087–4092. doi:10.1016/j.vaccine.2015.06.080
  19. Khieu TQT, Pierse N, Telfar-Barnard L, Zhang J, Huang QS. Modelled seasonal influenza mortality shows marked differences in risk by age, sex, ethnicity and socioeconomic position in New Zealand. J Infect. 2017;75(3):225–233. doi:10.1016/j.jinf.2017.05.017
  20. Aminisani N et al. The Burden of HMPV- and Influenza-Associated Hospitalizations in Adults in New Zealand Before and After the COVID-19 Pandemic, 2012–2023. J Infect Dis. 2025;232(Suppl 1):S47–S57. doi:10.1093/infdis/jiaf150
  21. Chambers ST et al. Māori have a much higher incidence of community-acquired pneumonia and pneumococcal pneumonia than non-Māori: findings from two New Zealand hospitals. N Z Med J. 2006;119(1234):U1978. PubMed
  22. Eichler N et al. Invasive pneumococcal disease and serotype emergence in the Auckland region during the vaccine era 2009-16. J Prim Health Care. 2019;11(1):24–31. doi:10.1071/HC17080

Current-season figures: PHF Science severe acute respiratory illness surveillance, Auckland, week ending 16 August 2026, as reported 20 August 2026 (RNZ).

About this series

Neglected Generations examines why adult immunisation in New Zealand, and in comparable health systems abroad, has been assembled one vaccine at a time rather than designed as a coherent programme.

  • Post 1 · The hidden burden — what standard surveillance and coding miss, and who carries it
  • Post 2 · The vaccine math we’re getting wrong — what “pays for itself” leaves out
  • Post 3 · We have the vaccines. Where is the programme? — the policy case, using New Zealand as the example