¹ Anthony Burgess, Little Wilson and Big God: being the first part of the confessions of Anthony Burgess, London, Heinemann, 1987, p. 18. I would like to thank Niall Johnson for drawing my attention to this passage.

² Geddes Smith, Plague on us, London, Oxford University Press, 1941; Fred R van Hartesveldt (ed.), The 1918–1919 pandemic of influenza: the urban impact in the western world, Lampeter, Edwin Mellen Press, 1992, p. 1.

³ David K Patterson and Gerald F Pyle, ‘The geography and mortality of the 1918 influenza pandemic’, Bull. Hist. Med., 1991, 65: 4–21, p. 19; I D Mills, ‘1918–1919 influenza pandemic: the Indian experience’, Ind. Econ. soc. Hist. Rev., 1986, 23: 1–40; Niall Johnson, ‘Aspects of the historical geography of the 1918–19 influenza pandemic in Britain’, PhD thesis, University of Cambridge, 2001, p. 158; Niall P A S Johnson and Juergen Mueller, ‘Updating the accounts: global mortality of the 1918–1920 “Spanish Influenza” pandemic’, Bull. Hist. Med., 2002, 76: 105–15.

⁴ In many countries the peak had already past by the time of the Armistice and general demobilization, but Crosby describes recrudescences of the epidemic associated with Armistice celebrations in the United States. Alfred W Crosby, America's forgotten pandemic: the influenza of 1918, Cambridge University Press, 1989, pp. 85, 105. See also Johnson, op. cit., note 3 above, p. 183.

⁵ The public perception of a full scale epidemic may have been tempered by the muted press reports in combatant nations where the full extent of the death toll was not reported. In neutral Spain, the pandemic received far greater prominence in the press, and it was reports in the London press of epidemic influenza in Spain which led to it being called “the Spanish 'flu”. Patterson and Pyle, op. cit., note 3 above, p. 7; Johnson, op. cit., note 3 above, pp. 105–9.

⁶ Sandra M Tomkins, ‘Britain and the influenza pandemic of 1918–19’, PhD thesis, University of Cambridge, 1989, ch. 3.

⁷ See Johnson, op. cit., note 3 above; Christopher Langford, ‘The age pattern of mortality in the 1918–19 influenza pandemic: an attempted explanation based on data for England and Wales’, Med. Hist., 2002, 46: 1–20; Johnson and Mueller, op. cit., note 3 above; J S Oxford, A Sefton, R Jackson, N P A S Johnson and R S Daniels, ‘Who's that lady?’, Nature Medicine, 1999, 5(12): 1351–52; Svenn-Erik Mamelund, ‘Spanish influenza mortality of ethnic minorities in Norway 1918–1919’, Eur. J. Popul., 2003, 19: 83–102.

⁸ Langford, op. cit., note 7 above, p. 11. See also G Cerasoli, ‘Italian pediatricians and the influenza pandemic of 1918–19’, Ital. J. Pediatr., 2002, 28: 163–6, p. 164.

⁹ Langford, op. cit., note 7 above, pp. 11, 15–16.

¹⁰ Irvine Loudon, Death in childbirth: an international study of maternal care and maternal mortality 1800–1950, Oxford, Clarendon Press, 1992, p. 484, quotes studies showing mortality among infants whose mothers died within one year after the confinement to be four to five and a half times higher than among infants whose mothers did not die.

¹¹ Sandra M Tomkins, ‘The failure of expertise: public health policy in Britain during the 1918–19 influenza epidemic’, Soc. Hist. Med., 1992, 5(3): 435–54, p. 453.

¹² In Britain, available evidence suggests that regular wages and food supplements may have improved infant health during the war (J M Winter, ‘The impact of the first world war on civilian health in Britain’, Econ. Hist. Rev., 1977, 30: 487–507; idem, ‘Aspects of the impact of the first world war on infant mortality in Britain’, J. Eur. Econ. Hist., 1982, 11: 713–38).

¹³ These outbreaks shared the same precise clinical and physiological descriptions as the influenza of the pandemic. Oxford, et al., op. cit., note 7 above. See also Johnson, op. cit., note 3 above, pp. 113–21.

¹⁴ Registrar-General, Supplement to the eighty-first annual report of the Registrar-General, Report on the mortality from influenza in England and Wales during the epidemic of 1918–19, London, HMSO, 1920, p. 5.

¹⁵ Fred R van Hartesveldt, ‘Manchester’, in van Hartesveldt (ed.), op. cit., note 2 above, pp. 91–103, on p. 91.

¹⁶ Oxford, et al., op. cit., note 7 above, p. 1351.

¹⁷ Tomkins, op. cit., note 6 above, pp. 26, 30.

¹⁸ Registrar-General, op. cit., note 14 above, p. 7.

¹⁹Lancet, 18 Oct. 1919, ii, p. 699, quoted in Johnson, op. cit., note 3 above, p. 265.

²⁰ A W Bourne, ‘Influenza: pregnancy, labour, the puerperium, and diseases of women’, in F G Crookshank (ed.), Influenza: essays by several authors, London, Heinemann, 1922, pp. 433–43, on pp. 439–40. This difference is probably understated as pregnancy was not always noted on the death certificate and it is probable that many of the other women in the child-bearing ages who died were also pregnant.

²¹ John W Harris, ‘Influenza occurring in pregnant women, a statistical study of thirteen hundred and fifty cases’, J. Am. med. Assoc., 1919, 72 (3 April): 978–80, p. 798. See also Paul A Buelow, ‘Chicago’, in van Hartesveldt, op. cit., note 2 above, 119–45, on p. 131, who states that 46 per cent of all hospitalized pregnant women died from 'flu and pneumonia in Chicago.

²² See Sir Charles H Stuart-Harris, Geoffrey C Schild and John S Oxford, Influenza: the viruses and the disease, 2nd ed., London, Edward Arnold, 1985, p. 105; Edwin D Kilbourne, Influenza, New York, Plenum Medical, 1987, p. 163.

²³ Kathleen Maletic Neuzil, George W Reed, Edward F Mitchel, Lone Simonsen and Marie R Griffin, ‘Impact of influenza on acute cardiopulmonary hospitalizations in pregnant women’, Am. J. Epidemiol., 1998, 148: 1094–102.

²⁴ Kilbourne, op. cit., note 22 above, p. 163.

²⁵ Neuzil, et al., op. cit., note 23 above, p. 1101.

²⁶ E Weinberg, ‘Pregnancy and resistance to infectious disease’, Rev. Infect. Dis., 1984, 6: 814–31. Not to be confused with PAIDS referring to paediatric acquired immunodeficiency syndrome (see Arthur A Ammann, Diane W Wara and Mort J Cowan, ‘Pediatric acquired immunodeficiency syndrome’, Ann. N. Y. Acad. Sci., 1984, 437: 340–9).

²⁷ Bourne, op. cit., note 20 above, p. 437.

²⁸ Harris, op. cit., note 21 above, p. 979. See also Johnson, op. cit., note 3 above, p. 265, for similar statistics for Paris and Sydney.

²⁹ G Wynne Griffith, A M Adelstein, P M Lambert, J A C Weatherall, ‘Influenza and infant mortality’, Br. med. J., 1972, iii: 553–6.

³⁰ See J S MacKenzie and M Houghton, ‘Influenza infections during pregnancy: association with congenital malformations and with subsequent neoplasms in children, and potential hazards of live virus vaccines’, Bacteriol. Rev., 1974, 38: 356–70.

³¹ Victoria P Coffey and W T E Jessop, ‘Maternal influenza and congenital deformities: a prospective study’, Lancet, 1959, ii: 935–7.

³² MacKenzie and Houghton, op. cit., note 30 above, p. 364.

³³ The birth registers are temporarily housed in the Cambridge Group for the History of Population and Social Structure, on loan from the MRC Unit in Southampton. The data set is described in more detail elsewhere. See Alice Reid, ‘Infant and child health and mortality in Derbyshire from the Great War to the mid-1920s’, PhD thesis, University of Cambridge, 1999; idem, ‘Neonatal mortality and stillbirths in early twentieth century Derbyshire, England’, Popul. Stud., 2001, 55(3): 213–32; idem, ‘Infant feeding and post neonatal mortality in Derbyshire, England, in the early twentieth century’, Popul. Stud., 2002, 56(2):151–66.

³⁴ These were Derby CB, Chesterfield MB, Glossop MB, and Ilkeston MB. None of these towns, nor Buxton MB, contributed to the data set.

³⁵ The data on which this graph was based were kindly provided by Niall Johnson.

³⁶ See Johnson, op. cit., note 3, pp. 320–6.

³⁷ The rest of the North Midlands includes Lincolnshire, Nottinghamshire, Rutland, and Leicestershire (and it would normally include Derbyshire, which is here shown separately). The West Midlands consists of Gloucestershire, Herefordshire, Worcestershire, Warwickshire, Shropshire, and Staffordshire. Cities and large towns include county boroughs, London boroughs, and metropolitan boroughs and large urban areas with populations greater than 20,000. These data are derived from the data set SN4350 ‘1918–1919 influenza pandemic mortality in England and Wales’ in the UK data archive, created by Niall Johnson. The original published source was the Registrar-General, op. cit., note 14 above, pp. 48–80.

³⁸ The data set excludes the County Borough of Derby, the Municipal Boroughs of Ilkeston, Glossop, Buxton, and Chesterfield, and the rural and small town area around Chesterfield, as these were administered separately.

³⁹ For more information on life table techniques and hazard modelling, see David W Hosmer and Stanley Lemenshow, Applied survival analysis: regression modeling of time to event data, New York and Chichester, John Wiley, 1999.

⁴⁰ Reid, ‘Infant and child health’, op. cit., note 33 above, p. 215. For the 1–5 figure, a life table measure was generated by the data set and subsequently transformed into an age-specific death rate.

⁴¹ Naomi Williams, ‘The reporting and classification of causes of death in mid-nineteenth-century England: the example of Sheffield’, Hist. Methods, 1996, 29(2): 58–71.

⁴² Wynne Griffith, op. cit., note 29 above.

⁴³ Independent variables significantly increasing the risk of stillbirth were multiple birth, male sex, parity one then increasing linearly with parity after parity two, having a doctor present at the birth (as opposed to just a midwife), father being manual social class, mother having been employed during pregnancy, and being born in winter months (October to April). Those significantly increasing the risk of neonatal mortality were multiple birth, male sex, parities four and above, having a doctor present at birth, being born in winter months, living in a more densely populated district, and living in a district where over half the population had a privy midden as opposed to more sanitary toilet facility (see Reid, ‘Neonatal mortality’, op. cit., note 33 above, pp. 216–21). Independent variables significantly increasing the risk of post-neonatal mortality were multiple birth, male sex, illegitimacy, higher parities, having been artificially fed by the end of the first month, living in a mining district, having fewer than four rooms in the house, and living at higher altitude (see Reid, ‘Infant feeding’, op. cit., note 33 above, pp. 155–7).

⁴⁴ Thus the risk of dying from a particular group of causes, such as congenital malformation, is assessed against the risk of not dying from that group of causes. In such analyses, infants dying from causes other than that being examined are treated as censored (i.e. gone out of observation) on their death.

⁴⁵ Williams, op. cit., note 41 above, p. 68.

⁴⁶ Stillbirth registration was introduced in 1927 in England and Wales, and although from 1915 stillbirths were supposed to be notified under the Notification of Births (Extension) Act, it has been estimated that around a fifth to a quarter of stillbirths were not notified. It appears that the health visitor data set conforms to this pattern. See Registrar-General, The Registrar-General's statistical review 1927, London, HMSO, 1929, text p. 128; E A Wrigley, ‘Explaining the rise in marital fertility in England in the “long” eighteenth century’, Econ. Hist. Rev., 1998, 51: 435–64, pp. 441–2; Graham Mooney, ‘Stillbirths and the measurement of urban infant mortality rates’, Local Popul. Stud., 1994, 53: 42–52.

⁴⁷ There is only one documented case of transplacental transmission of the disease although the passage of other viruses is well accepted. David H Yawn, Joella C Pyeatte, Stephan L Eichler, Rafael Garcia-Bunuel, ‘Transplacental transfer of influenza virus’, J. Am. med. Assoc., 1971, 216: 1022–23.

⁴⁸ Johnson, op. cit., note 3 above, pp. 113–22.

⁴⁹ Nadia Badawi, Jennifer J Kurinczuk, John M Keogh, Louisa M Alessandri, Fiona O'Sullivan, Paul R Burton, Patrick J Pemberton and Fiona J Stanley, ‘Antepartum risk factors for newborn encephalopoathy: the western Australian case-control study’, Br. med. J., 1998, 317: 1549–53.

⁵⁰ See Coffey and Jessop, op. cit., note 31 above, pp. 935–7, and MacKenzie and Houghton, op. cit., note 30 above, pp. 356–64.

⁵¹ See Wynne Griffith, et al. op. cit., note 29 above.

⁵² Where more than one cause of death (such as “pneumonia following influenza”) was recorded in the ledgers, the antecedent cause (in this case influenza) was recorded as the primary cause.

⁵³ This includes infants who were receiving both breast and artificial food. A similar graph can be drawn for those receiving only breast milk which shows the same effect.

⁵⁴ Charles Graves, Invasion by virus: can it happen again? London, Icon Books, 1969. Other help was in the form of coal, milk and food expenses.

⁵⁵ Burgess, op. cit., note 1 above, p. 18.