Britain and the 1918-19 Influenza Pandemic

A Dark Epilogue

Niall Johnson

• Publisher: Routledge
• Year: 2006
• eBook ISBN: 9781134215003
• Edition: 1
• Topic: History
• Subtopic: British History
• Index: History

Between August 1918 and March 1919 a flu pandemic spread across the globe and in just under a year 40 million people had died from the virus worldwide. This is the first book to provide a total history and seriously analyze the British experiences during that time.The book provides the most up-to-date tally of the pandemic's impact, including the vast mortality, as well as questioning the apparent origins of the pandemic. A 'total' history, this book ranges from the spread of the 1918–1919 pandemic, to the basic biology of influenza, and how epidemics and pandemics are possible, to consider the demographic, social, economic and political impacts of such a massive pandemic, including the cultural dimensions of naming, blame, metaphors, memory, the media, art and literature.

An inter-disciplinary study, it stretches from history and geography through to medicine in order to convey the full magnitude of the first global medical 'disaster' of the twentieth century, and looks ahead to possible pandemics of the future.

Niall Johnson brings an impressive scholarly eye on this fascinating and highly relevant topic making this essential reading for historians and those with an interest in British and medical history.

1 Introduction to an unregarded killer

Since the earliest descriptions of influenza-like disease by Hippocrates, influenza has infected billions and killed millions of people across the globe. A highly contagious disease, it is usually limited to just a few days’ illness with a low fatality rate. However, in times of epidemic and pandemic it can become so prevalent, infecting the majority of the population, that these elevated rates give rise to massive surges in mortality as influenza strikes ‘like a flash flood’ (Stöhr 2005: 407). With pneumonia, influenza remains one of the ten leading causes of death in the United States of America (Crosby 1993: 807) and Australia (AIHW 2004: 45). These two respiratory infections are commonly tallied together and frequently interact – in 1918 it was the complications from pneumonia that killed so many, contributing to a death toll of tens of millions. In the UK the average annual influenza death toll is currently around 12,000, and in the first week of 1999 alone more than 3,000 Britons died of influenza (BBC 1999g) – an outbreak that forced one hospital to hire a refrigerated truck as a temporary mortuary (BBC 1999c) – and this was not officially regarded as an epidemic. The winter of 1989–90 saw an epidemic claim an estimated 29,000 British lives (Radford 1995). Even in non-epidemic years it can have a major impact; for example, in Britain an average of approximately three working days per patient are lost annually as a result of flu, and it may account for approximately 10 per cent of sickness absences (BBC 1999d). An average year in the USA sees approximately 36,000 flu deaths, with more than 200,000 hospitalised (CDC 2004) at a cost to the economy of US$71–167 billion (WHO 2003).

The World Health Organisation (WHO) estimates that influenza causes ‘between three to five million cases of severe illness and between 250,000 and 500,000 deaths every year around the world’ (WHO 2003). But all this may pale against the possibility of a pandemic that many now regard as inevitable, if not imminent. Indeed, in early 2005 the British government apparently recognised that an influenza pandemic was a greater risk than terrorism, particularly in terms of the number of people directly affected and the potential to disrupt society (Hall and Sample 2005).

Rosenberg suggests that ‘there is no human crisis more compelling than an epidemic’, but specifies epidemics of diseases such as yellow fever, cholera and plague. Such epidemics are of such a scale and of such a terrifying nature that ‘most physicians and historians have tended to view them as something alien, something outside of society and contending with it’ (Rosenberg 1992: 110). Influenza is something with which we are well acquainted and rarely regard as a major threat to health, and even less as a mortal threat. This work examines the 1918–19 influenza pandemic and demonstrates how it was one of the most massive disease outbreaks in human history, and how influenza remains a threat. While the British experience is the focus, this was a true pandemic, a global epidemic, and as such necessarily detailed consideration is given to the global extent of the pandemic, often to highlight the universality of the pandemic, as well as drawing comparisons between the British experience and that experienced elsewhere. Given the very real possibility of future flu pandemics, the parallels and portents that can be drawn from the 1918 experience, and how they might be played out in a future pandemic, are also discussed. Thus the consideration of flu is not parochial but encompasses the scale of the pandemic, both in time and space.

The 1918–19 pandemic struck a Britain undergoing quite profound change, including a reappraisal of the nation’s position in the world. From being the global superpower at the height of its imperial reach, there were already signs of the Empire breaking apart. For example, South Africa had been lost in the long, brutal South African War. This was a shock that had been compounded as Britain ground out what must have seemed a rather hollow and expensive victory in the Great War. The political and social order at home was also undergoing much change as Lloyd George’s administration started to bring about many of the changes that were to give the state a greater role in the life of individual Britons. These changes from a laissez-faire state to a more interventionist state were by no means a smooth transition. Nor was the welfare state of the later twentieth century in place by any means. The Ministry of Health, while foreshadowed, did not exist and public health was largely the preserve of the local authorities and their MOHs. The Local Government Board (LGB), the national government’s public health body, was little more than an advisory body rather than a service-delivery authority. Thus it was a very different place that influenza struck in 1918.

Influenza

Our acquaintance with influenza is centuries old and in our classifications of disease, influenza is one disease whose classification has remained essentially unchanged. This suggests a disease whose nature and symptoms we have long recognised, even if the actual causal organism, the flu virus, was not identified until 1933 (Smith et al., 1993). Influenza is universal: all ages and both sexes are susceptible to the disease. During times of epidemic, between 15 and 40 per cent of the non-immunised are stricken and this figure can climb markedly under pandemic conditions. It is ‘a disease of paradoxes’ and is widely considered to be ‘a disease of little consequence, one which is a nuisance but causes only minor illness. However, it is also a disease which kills’ (Riordan 1986: III). Influenza is transmitted person-to-person, usually as droplets. These droplets of respiratory secretions are exhaled by an infected person and inhaled by others. Droplets can range in size, with the smallest remaining suspended in the air for as long as an hour. Factors such as the amount of virus shed, proximity, crowding and ambient conditions can all influence the efficacy of transmission. Furthermore, some sufferers can be ‘supershedders’, broadcasting masses of virus-containing droplets.

Symptoms and diagnosis

The symptoms of influenza are relatively easy to determine, but also make diagnosis difficult as many of them are shared with other conditions, including the common cold. But what exactly is influenza? We all have personal knowledge – every one of us has been struck by the disease at some stage But what is the clinical description of the disease? In uncomplicated influenza, the first symptoms appear two to four days after infection. These first symptoms include headache, shivering and a dry cough accompanied by a sudden onset of fever. In adults malaise and an aching of the limb muscles and back can often occur. Nasal irritation or discharge can occur, as can a loss of sleep and dizziness. In some patients the symptoms subside rapidly after the first twenty-four hours. But the disease can have a prolonged course for some, with the temperature remaining high for up to five days, and with a residual weakness and/or a cough. Without complications, one usually recovers within ten days of the onset of illness. However, in some cases a persistent weakness or mental depression may require longer convalescence. Of the clinical features of influenza, the fever, a temperature of 38–40°C (100–104°F), is that which most typically distinguishes flu from the common cold (which is caused by a completely different type of virus) (Schild 1977: 350–1). Thus, influenza is an acute respiratory infection with an abrupt onset, and typified by high fever, sudden chills, muscular pain, dry cough and prostration that can also lead to diarrhoea, gastrointestinal pain, head cold, sore throat, nose bleeds and a fall in blood pressure.

Very young children, older people and those with weakened or damaged cardiovascular and/or respiratory systems are most prone to attack from influenza. Not only are young children the most likely to be attacked by the disease but they are also more likely to succumb. This pattern of mortality is reflected in the hospitalisation rates. While the highest incidence occurs in children and young adults, the rates of hospitalisation for ‘severe or complicated influenza are lowest, around six per 10,000, in persons five to twenty-four years old’ (Cate 1987: 16). The highest hospitalisation rates are in the extreme age groups – the youngest and the oldest – and ‘age-related deaths due to pneumonia and influenza during epidemics tend to follow a pattern similar to . . . rates of hospitalization’ (Cate 1987: 16). This age pattern, of illness and particularly mortality, is in marked contrast to that encountered in 1918–19.

Complications and sequelae

Influenza itself can pose a significant health problem. However, it is not always unaccompanied, and the complications and sequelae can be important in determining both morbidity and mortality. Significant proportions of the mortality associated with influenza may be caused by the sequelae and complications as even a ‘low frequency of complications results in measur-able increases in rates of hospitalisations, and often in mortality’ (WHO 1999d: 34). Furthermore, the impact of the 1918 pandemic will be understated as long as the scale of these complications and sequelae is ignored. These complications usually involve the lower respiratory tract (tracheobron-chitis, bronchiolitis and influenzal pneumonia or other secondary bacterial, mixed viral-bacterial, or viral infections), the cardiovascular system (often occurring through exacerbation of existing chronic conditions) and the nervous system. Our understanding of what conditions and diseases can be related to influenza has grown a great deal since the 1918–19 pandemic.

There are two major types of complication or sequelae for influenza. These are the cardio-pulmonary conditions, including other respiratory diseases, e.g. bronchitis, pneumonia and tuberculosis, and the neurological conditions, e.g. schizophrenia, encephalitis lethargica and Parkinsonism. The cardio-pulmonary conditions are often implicated in exacerbating the severity of influenza, whereas the neurological conditions tend to be sequelae to influenza. The dangers of both should not be overlooked, as the ‘risk of serious and fatal disease is much higher . . . in patients with certain well-defined pre-existing underlying conditions. These conditions . . . predispose not to the risk of acquiring influenza virus infection but to the risk of suffering severe disease once infection is established’ (Kilbourne 1987: 159).

Underlying cardiovascular disease can contribute to serious pulmonary manifestations of influenza. This can be particularly dire if the patient develops pneumonia, as studies have shown high mortality rates in such cases. The extra strain on an already damaged heart appears to lead to cardiac failure (Kilbourne 1987: 162–3). Changes in electro-cardiograph (ECG) reading seen in people with existing cardiac conditions during acute influenza have been ascribed to ‘exacerbation of the underlying cardiac disease rather than direct involvement of the myocardium [heart] with influenza virus’ (WHO 1999d: 35–6). Forms of carditis, such as myocarditis and pericarditis, are thought to occur as complications on occasion, and may also contribute to death. The Registrar-General noted in 1920 that in Britain an increase in certain types of ‘heart disease’ were linked to the pandemic and indeed that excess deaths in one form (‘organic heart disease (No. 79)’) were attributed to the pandemic (Registrar-General 1920: 3).

A range of pulmonary or respiratory conditions can cause complications and raise the risk of death. These can include infectious and non-infectious complications or conditions such as croup, pneumonia and any exacerbation of any of the chronic obstructive pulmonary diseases (e.g. asthma, chronic bronchitis and cystic fibrosis), with pneumonia being the greatest threat. Of the different forms of pneumonia, three types have been described in relation to influenza: bacterial pneumonia, combined viral and bacterial pneumonia, and pure viral pneumonia (WHO 1999d: 34–5). The prominent virologist Ed Kilbourne states that existing ‘chronic bronchopulmonary disease is equal to pre-existing cardiac disease as a factor leading to severe or complicated influenza’, and notes further conditions that can lead to pulmonary insufficiency or obstruction, including ‘chronic bronchitis, bronchiectasis, pulmonary fibrosis, asthma, emphysema, or bronchopulmonary neoplastic disease.’ For children, asthma is a particular concern, being recognised as a high-risk factor associated with increased hospitalisation (Kilbourne 1987: 164). All of these pulmonary or respiratory conditions can contribute to increased severity of an influenzal episode.

Pneumonic complications were widely described in the fatal cases of the 1918–19 pandemic. The dreaded diagnostic feature of the ‘heliotrope cyanosis’ indicated, almost invariably, terminal pneumonic complications (Abrahams et al. 1917, 1919; Cummins 1919; Frost 1919; Hammond et al. 1917; Levinthal et al. 1921; Lister and Taylor 1919; MacPherson et al. 1920; Ministry of Health 1920c; Opie et al. 1921; Royal Society of Medicine 1918, including 67–70). Pneumonic complications contributed a substan-tial proportion of the pandemic’s total mortality. Burnet and Clark reported that 80 per cent of patients in the autumn wave of the pandemic still endured ‘typical three- to five-day influenza without complication. . . . The only feature noted as unusual was the frequent occurrence of epistaxis [nose bleeds] as an initial symptom.’ However, of the other 20 per cent of patients who ‘developed pneumonic complications with a mortality of 40–50%’, the pneumonic symptoms, other than the cyanosis, did not indicate the severity of illness, as the ‘physical signs were irregular and usually slight in relation to the sickness of the patient’ with the most obvious features of the severe cases being ‘the rapidity of the respirations and the characteristic heliotrope cyanosis. There was little subjective distress and though some showed delirium and coma a majority were fully conscious to within an hour of death’ (Burnet and Clark 1942: 88, citing Ministry of Health 1920c).

Whereas the cardiovascular and pulmonary conditions tend to be complications of influenza, making the disease episode more serious, the neurological conditions that have been associated with influenza tend to be sequelae, conditions that follow influenza infection with the assumption being that the influenza infection facilitates the later condition. It appears that many neurological conditions or maladies of the central nervous system (CNS) may be exacerbated, facilitated or otherwise associated with influenza, including asthenia, depression, mania, transverse myelitis, encephalitis lethargica, Parkinsonism, senile dementia and schizophrenia (Kilbourne 1987: 171–7; Ravenholt 1993; WHO 1999d: 36). These associations have been noticed for some time, even if the mechanisms have not been fully understood. One observer, who on detecting such sequelae in 1918–19, ‘recalled that influenza worsened existing neuroses and created “nerve invalids” who sometimes lost “their moral bearings” in theft and drunkenness. “Post-influenzal depression”, “lassitude”, “lethargy”, “ grippe catalepsy”, “hysterical coma”, “psychosis”, “melancholy”, “nona” (somnolence and absent-mindedness), “despondency”, “neuritis”, “neurasthenia”, “shattered nerves”, and “loss of grip” all became popular ascriptions of sequelae in the 1890s’ (Smith 1995: 71). Similar observations were made elsewhere. For example, Phillips found these cases of

Post-’flu debility and lassitude were by no means unusual. Recovery was often slow and uneven . . . ‘impaired vitality’, ‘breathless’, ‘suffered palpitations’, ‘temporarily forgetful, deaf, blind or bald’, ‘anaemia’, ‘post-influenza melancholia’ and ‘several cases of suicide were attributed to this post-’flu melancholia’ with others ‘left with their health permanently impaired by, for example, deafness, weak lungs, heart trouble and a susceptibility to other diseases such as phthisis, tuberculosis, parkin-sonism, nephritis, meningitis and encephalitis lethargica’.

(Phillips 1990a: 189–91)

One set of neurological conditions that have been linked to influenza are those that fall under the term schizophrenia. Viral, behavioural, epidemiological and neuropathological evidence suggests that influenza, particularly in epidemics, can be ‘neurovirulent’ and can induce clinical schizophrenia in addition to ‘manias’, epidemic encephalitis, affective psychoses and Parkinson’s disease (Maurizi 1984, 1985; Menninger 1994).

Charles Maurizi gave a first-hand account of influenza-related neurological disturbance. A serious influenza B infection induced a viral encephalopa-thy during which he ‘could not complete abstract thought, had difficulty judging time, and had periods of intense anxiety’. Some two weeks following the initial onset of fever, his thinking and behaviour resumed a normal state and he began to feel better. Though much better (in fact he felt wonderful), this in itself was not good as he had ‘a manic psychosis with elation, hyperactivity, poor judgement, grandiose delusions and decreased need for sleep’. Four months of treatment with lithium carbonate seemed to restore him to health. However, four weeks after stopping the treatment, the mania recurred before abating upon the resumption of the lithium (Maurizi 1984: 163). Maurizi drew parallels between his condition (and treatment) and that of an Australian soldier serving in Europe who was diagnosed in 1917 as suffering from ‘cerebro-spinal fever’. Cerebro-spinal fever was certainly discussed in relation to the influenza at the time of the pandemic with little conclusive evidence (e.g. Hamer 1918: 2; Ministry of Health 1920c; Royal Society of Medicine 1918: 6–7 and PRO MH 55 57). Apparently this soldier was the first patient to be treated with lithium following mild cerebro-spinal fever and after ‘this encephalitis he was mentally disturbed’. Maurizi wonders if he had been infected by a ‘neurotropic influenza virus’ and considers it quite possible, if not probable. The soldier reportedly endured bouts of ‘mania’ for more than thirty years, including chronic mania for five years prior to the lithium treatment. It appears that the lithium treatment helped him, as it had Maurizi, at least to a point – he ‘later died of lithium intoxication’ (Maurizi 1984: 166).

Disruptions of the central nervous system caused by influenza do not have to be limited to those already born. There is some suggestion that influenza could have been the cause of some congenital deformities in the children of women who contracted influenza during their pregnancy. The influenza virus has been implicated as a cause of both maternal morbidity and congenital anomalies, particularly of the central nervous system (MacKenzie and Houghton 1974; Mattock et al. 1988). Graham attempted to determine if the pattern of schizophrenics tending to be born in late winter or early spring could be related to mothers being exposed to influenza, particularly during the second trimester of the pregnancy, and if this may lead to transmission of the virus or viral antibodies to the developing foetus ‘leading to subtle brain damage which later manifests itself as schizophrenia’ (Graham 1996: Abstract). The results of the study were somewhat contradictory.

Another CNS complication that, although rare, can be extremely serious, is Reye’s syn...

Table of contents

• Cover Page
• Title Page
• Copyright Page
• Plates
• Figures
• Tables
• Preface
• Acknowledgements
• Abbreviations
• 1 Introduction to an unregarded killer
• 2 The history of influenza
• 3 Pandemic geographies
• 4 The human cost
• 5 Impacts and responses
• 6 Cultural dimensions
• 7 Repercussions
• 8 Possible futures
• Notes
• Bibliography
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