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Influenza Viruses: Clinical Spectrum and Management Methods Based on Haemagglutination-Inhibi• 'Influence' of the Planets at Times of Respira• Tion

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Influenza Viruses: Clinical Spectrum and Management Methods Based on Haemagglutination-Inhibi• 'Influence' of the Planets at Times of Respira• Tion INFLUENZA VIRUSES: CLINICAL 15 SPECTRUM AND MANAGEMENT Karl Nicholson 15.1 Introduction 15.1 INTRODUCTION 15.2 History Influenza is an acute, febrile respiratory illness 15.3 Pandemic influenza of global importance caused by influenza A or 15.3.1 Influenza pandemics - 1847 to B virus. Influenza in humans occurs in two 1977 epidemiological forms - pandemic influenza 15.4 Interpandemic influenza which results from the emergence of a new 15.4.1 Herald waves 15.4.2 Importance of children in the influenza A virus to which the population pos­ spread of influenza sesses little or no immunity, so it spreads with 15.4.3 Influenza in residential homes a high attack rate in all parts of the world; and 15.5 Transmission and pathogenesis interpandemic influenza A or B, occurring as 15.5.1 Transmission sporadic infections, a localized outbreak, or 15.5.2 Infection and replication epidemic, the latter representing an outbreak 15.6 Clinical features in a given community which usually occurs 15.6.1 Adults abruptly, peaks within 2-3 weeks, lasts 5-6 15.6.2 Infants and children weeks, and is associated with a significant drift 15.7 The complications of influenza of the surface haemagglutinin and neu­ 15.7.1 Infection in the elderly and raminidase antigens. Epidemics occur virtu­ excess deaths ally every year almost exclusively in the 15.7.2 Influenza during pregnancy 'winter' months in the northern hemisphere and the effects on the fetus and (October to April), and May to September in offspring the southern hemisphere. Explosive epi­ 15.7.3 Respiratory tract complications demics of influenza can exert an enormous toll 15.7.4 Complications in diabetics in terms of morbidity, mortality, and economic 15.7.5 Myocarditis and pericarditis and social costs. 15.7.6 Neurological complications Influenza has no pathognomonic features 15.7.7 Toxic shock syndrome so a precise picture of its impact was impossi­ 15.7.8 Myositis, myoglobinuria and ble until the first isolation of influenza A virus renal failure in 1933 [170], and influenza B virus in 1940. 15.8 Antivirals Further advances came with the recognition of 15.8.1 Adamantanes influenza virus replication in hens' eggs in 15.9 References 1936 [20], discovery of the haemagglutinating Viral and Other Infections of the Human Respiratory Tract. properties of influenza virus in 1941, and the Edited by S. Myint and D. Taylor-Robinson. Published in 1996 by Chapman & Hall.ISBN 978-94-011-7932-4 subsequent development of serological 276 Influenza viruses: clinical spectrum and management methods based on haemagglutination-inhibi­ 'influence' of the planets at times of respira­ tion. In the absence of these tools, a combina­ tory epidemics [178]. 'Influenza' was used in tion of the explosive nature of influenza, its England during the outbreak of 1743 [50], but tendency for seasonality, high attack rates, earlier references to the malady included and respiratory and systemic features allow an 'newe acquayantance', the gentle correction, overview of the disease since ancient times. epidemic catarrh, or catarrhal fever [32, 50]. 15.2 HISTORY 15.3 PANDEMIC INFLUENZA Langmuir and colleagues [111] proposed that 15.3.1 INFLUENZA PANDEMICS - 1847 TO 1977 the plague of Athens in the years 430-427 BC The influenza pandemic of 1847-1848 was caused by influenza associated with toxic shock syndrome and named the association Review of mortality statistics for 'influenza' in 'the Thucydides syndrome'. The epidemic in London since 1840 reveals a 39-fold rise in 412 BC described by Hippocrates was proba­ deaths during the fourth quarter of 1847 as bly influenza [158]. Clear historical accounts of compared with the average for the same quar­ influenza in Italy, Germany and England can ter during the 7-year period 1840-1846 [151]. be traced back to the epidemic of 1173 [89]. The increase was 11-fold for the first quarter of Hirsch [89] and Thompson [181] provide 1848 as compared with the average for the accounts of epidemics from the twelfth and same period during the eight preceding years. sixteenth centuries respectively, and Hirsch Such abrupt increases in mortality, with out­ [89] referred to 'pandemics' occurring over a breaks occurring in both eastern and western great part of the globe and noted their occur­ hemispheres, suggest the occurrence of a pan­ rence in the years 1510, 1557, 1580, 1593, demic associated with antigenic shift. London 1732-1733, 1767, 1781-1782, 1802-1803, mortality statistics and the 1847-1848 pan­ demic enabled William Farr to provide the first 1830-1833, 1836-1837, 1847-1848, 1850-1851, estimate of influenza-associated mortality. 1855, 1857-1858 and 1874-1875. Interestingly, Farr noted that 'the epidemic was most fatal to several of these pandemics, such as the ones in adults and the aged' ... 'the mortality in child­ 1781-1782, 1801 (1802-1803), 1830-1833 and hood was raised 83%, in manhood 104%, in 1847-1848, seem to have spread to Europe old age 247%' ... 'from the age 4 to 25, however, across Russia from the Far East and Hirsch the mortality was comparatively not much commented upon the 'regular progress of the increased' . disease from east to west'. Modern influenza surveillance has shown that the virus affects much of the globe in most years; 'pandemics' The influenza pandemic of 1889-1890 with high attack rates are associated with anti­ The number of influenza deaths in London genic 'shift' of the virus rather than antigenic gradually decreased from 1739 during the 'drift', and such pandemics occur infrequently winter of 1847-1848 to less than 10 during each with two of the most recent (' Asian' and 'Hong winter from 1884 to 1889 [151]. Some 558 Kong') originating in the Far East. The short 'influenza' deaths were recorded during the intervals between several 'pandemics' in first quarter of 1890, and outbreaks of respira­ Hirsch's review question whether they were tory disease with high attack rates were noted associated with antigenic shift. throughout the United Kingdom [151]. The The origin of the term 'influenza' is uncer­ first cases were described in May 1889 in tain, although the chronicles of a Florentine North America and in Bokhara, and the family used it in reference to the possible Russian doctors at that time called the disease Pandemkinfiuenza 277 'Chinese' influenza. The outbreak reached 1890, beyond that during the three previous Western Europe via Central Asia and years, amounted to at least 5500 cases, but only European Russia and reached London by 213 of all deaths were attributed by the certify­ November 1889. High attack rates throughout ing medical attendants to influenza [151]. Europe were associated with excess deaths as Table 15.1 shows the relative increase in compared with those in previous years. deaths from chronic conditions including dia­ Seroprevalence studies carried out during betes, 'wasting', alcoholism, heart disease, the emergence of 'Asian' influenza in tuberculosis, and chronic bronchitis during 1957-1958 revealed the presence of pre-exist­ the epidemic as compared with the average ing antibody in people aged ~ 71 years of age during the three previous years. These and [139]. This suggested that the viruses responsi­ more recent observations identify 'risk factors' ble for both the 1889-1890 and 1957-1958 pan­ and provide the basis for current vaccine rec­ demics contained an H2 haem agglutinin and ommendations. A further interesting observa­ led to the proposal that influenza virus might tion, which has been noted in more recent recycle. However, during the Asian influenza pandemics, was the increase in influenza mor­ pandemic (1957-1958) there was no evident tality during the second and third waves in reduction in pneumonia and influenza death 1891 and 1892 as compared with the first. This rates with increasing age, implying that the may reflect an increasing awareness of elderly had little or no protection following influenza among attendant physicians at the prior exposure to related H2 viruses [166]. time or an increase in virulence of the virus. The 1889-1890 pandemic is the first pan­ demic for which there are good public health Possible H3 pandemic during the late records. Data collected during this period con­ nineteenth century firmed and extended those obtained during The number of 'influenza' deaths in England 1847-1848, notably that during periods of and Wales fell after 1892 to about 100 per mil­ influenza activity, certified influenza deaths lion of the population in 1896 but exceeded represent only a small proportion of the 400 per million in 1900 [178]. Some historians excess. In Paris, the excess mortality between suspect the emergence of an H3 strain at the 15th December 1889 and the end of January turn of the century based on the finding by Table 15.1 Increase in deaths during the 1889-90 epidemic in Paris. (Data abstracted from [151]) Cause of death Ratio, 1889-1990 (Dec 1S-Jan 31) to average number in the same period during 3 previous years * Pneumonia 3.19 Paralysis 2.50 Pleurisy 1.99 'Wasting' 1.94 ,Alcoholism' 1.86 Heart disease 1.78 Acute bronchitis 1.67 Tuberculosis 1.58 Chronic bronchitis 1.44 • Period 15th December to 31st January 278 Influenza viruses: clinical spectrum and management independent investigators in Asia, Europe and garglings from patients with influenza in 1933 North America that a large number of elderly [170]. The subsequent recognition that persons, principally those over 75 years of age influenza virus would replicate in hens' eggs, in 1968, had high levels of antibody to the and the development of serologic techniques A;Hong Kong (H3) strain of influenza before provided the means to monitor the spread and the pandemic in 1968 [35,55,118,122].
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