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especially after the development of infectious disease hospitals from the 1870s.70 Beds in these hospitals came to be dominated by scarlet fever patients by the end of the century; for example, they were the largest group in the City Fever Hospital, Edinburgh between 1888 and 1892 and again in 1904, when the 942 admissions, with a fatality rate of just below 3%, constituted 33% of all patients.71 However, the decline in mortality was mainly due to a decrease in the virulence of the organism.72 Wolverhampton guardians took measures to prevent outbreaks in the workhouse by restricting visiting when scarlet fever was prevalent in the town in the 1870s and 1880s.73 In the following decade, they arranged for cases to be admitted to Wolverhampton Borough Hospital for infectious diseases for a payment of 2s and 6d per patient per day.74 There are no further reports of patients with scarlet fever remaining in the workhouse, but 1,215 patients with scarlet fever were treated in the hospital between 1888 and 1892.75 Birmingham guardians took a different approach in 1889, allowing the town’s health committee to use a building, previously employed as a test workhouse for able-bodied men, for children convalescing after a bout of scarlet fever, as they would no longer be infectious. The move released 30 to 40 beds in the town’s isolation hospital.76 Over the years 1877-80 and 1894-1911, only one case of scarlet fever was recorded in the workhouse (on 29 June 1895), but the numbers are one-day counts on only a few days in the year and may not represent the overall prevalence for those years. In addition, the isolation hospital in Lodge Road Hardy, p.56.

Pickstone, pp.158-59; Gray, pp.65, 148-49.

J. Woodward, ‘Medicine and the city: the nineteenth century experience’, in R. Woods and J.

Woodward (eds), Urban Disease and Mortality in Nineteenth-Century England, London, 1984, p.68.

WALS, WBG, PU/WOL/A/17, 19 October 1777; PU/WOL/A/20, 26 March 1886.

WALS, WBG, PU /WOL/A/25, 13 December 1895.

BPP, 1895 (28), p.354.

BCL, WMC, GP/B/2/3/2/1, 28 May 1889.

had been admitting patients with scarlet fever from 1875, with 424 admissions that year. In 1882 they increased to 627 and, in the four years from 1888, they treated 7,206 patients, including 2,525 in 1890.77 However, these patients continued to be admitted to the workhouse infirmary; for instance, six cases in a four-month period in 1886 and five in the twelve months to 31 May 1910.78 In summary, the co-operation between the guardians in both towns and the sanitary authorities ensured that as few patients as possible with scarlet fever were admitted to the poor law institutions.

As scarlet fever waned in virulence toward the end of the century, diphtheria took its place as a major killer of young children. It had only become recognised in England as a distinct disease entity in mid-century after an epidemic of throat-disease in 1858.

Prior to that time, it had been included in mortality statistics under scarlatina.79 The disease results in inflammation and severe swelling in the upper airways, which can cause obstruction and death by respiratory failure. It is spread by droplet infection following direct contact with cases or carriers. The main form of management was strict isolation in hospital to limit spread of infection, but this had little effect on the mortality from the disease. By the middle of the 1890s, the organism could be isolated from throat swabs, aiding accurate diagnosis, and anti-toxin was available to counteract the systemic effects on the heart and nervous system.80 However, to be effective anti-toxin had to be administered within the first four days of the illness,

–  –  –

expensive and not provided free of charge by the sanitary authorities in Birmingham BPP, 1895 (28), p.402; TNA, MH/13365, ‘Health of the City’, pp.49-51.

BCL, Incident Book, GP/B (ACC2009/109), box 15; IMC, GP/B/2/4/4/5, 11 July 1910.

Creighton, p.736; Hardy, p.80. The causative organism is Corynebacterium diphtheriae, which affects the pharynx and larynx, with resultant membrane formation, and produces a toxin, causing cardiac damage and neurological lesions. There were three strains of the bacterium, namely gravis, intermedia and mitis, with case fatality being highest in the first and lowest in the last.

Pickstone, p.159.

until 1902.81 Nevertheless, throat swabbing and anti-toxin helped to check the spread of the disease and contributed to the rapid reduction in mortality, although a decline in virulence may also have occurred. It was the only disease in the nineteenth century that was affected by the germ theory and that preventive measures linked laboratory investigations, clinical practice and public health action in a co-ordinated way.82 The incidence of diphtheria in Birmingham had declined markedly after 1873, but a sudden increase in deaths occurred in 1895 (mortality rate, 0.33 per thousand of the population), compared with the year before (0.1 per thousand). Notified cases did not increase to the same extent (from 316 in 1894 to 640 the following year).83 However, admissions to the workhouse did not take place until five years later and continued sporadically through the 1900s (Appendix A). In addition, there was an outbreak in the female epileptic wards in 1912.84 According to F. B. Smith, Birmingham had the reputation as a ‘notoriously bad’ diphtheria town.85 However, a large increase in cases occurred also in Wolverhampton in 1895 (308, compared with 82 the year before) and they remained at that level for the following two years. By contrast, the fatality rate was lower in 1895 (27%, compared with 40% in 1894) and it fell to 8% by 1897.86 The mortality rate among children under six years old was 2% or less in the first half of the 1890s, but increased to between 6% and 11% after 1894.87 An outbreak occurred in Wolverhampton workhouse in December 1896, with the disease affecting eight boys, of whom one died, and nurses Hilton, Riley, Whittaker and Wright over the following three months. The boys were isolated in a ward away from Smith, p.151; A. Hill, ‘Reports of Medical Officers of Health’, The Lancet, ii (1902), p.178.

Pickstone, p.159.

A. Hill, ‘Remarks on the Incidence of Diphtheria in Birmingham’, Public Health, 8 (1895-96), p.342.

BCL, BBG, GP/B/2/1/81, 20 November 1912.

Smith, p.151.

TNA, MH12/11721, H. Malet, ‘Annual Report of Health of Wolverhampton for 1898’.


other children and the nurses in their rooms. The MO raised concerns over the condition of the lavatories attached to the wards where the disease had begun and requested measures to improve the drainage.88 It is surprising that the disease was being linked to sanitary issues at that time, as the bacterium had been discovered in 1883 and the toxin had been in use in Britain since 1894. However, Hardy comments that bacteria were not fully accepted as the cause of the disease in England until the mid-1890s.89 The Medical Officers of Health (hereafter MOsH) for Birmingham and Stoke Newington believed, at that time, that insanitary conditions were a predisposing cause of the disease due to the release of sewage gases.90 The Medical Officer of Health (hereafter MOH) for the County of Fife also held that sewer gases were a vehicle for the spread of diphtheria and more attention needed to be paid to improving

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enlightened approach was taken by the members of the Workhouse Visiting Committee in Wolverhampton at that time when they instructed the MO to send throat secretions to London for examination if more cases of diphtheria arose.92 He did not do so during that outbreak, but the following year he sent secretions from the throat of nurse Rogers for analysis and the charge of 5s and 9d was approved.93 At that time, laboratory testing remained concentrated in the capital and no facilities for the detection of diphtheria were available in large cities such as Birmingham.94 WALS, WBG, PU/WOL/A/26, 29 January, 5 February, 19 February, 26 February 1897; TNA, MH12/11715, 6 January, 10 February, 1 March 1897.

Hardy, p.84.

Hill, ‘Incidence of Diphtheria’, pp.342-43; H. Kenwood, Notes on the Origin of Diphtheria’, Public Health, 8 (1895-96), p.344.

T. G. Naysmith, ‘The Relation of Diphtheria to Insanitary Conditions’, Public Health, 8 (1895-96), pp.4-5.

WALS, Workhouse Visiting Committee (hereafter WVC), PU/WOL/H/2, 1 January 1897.

Ibid., 25 November 1898.

Worboys, Spreading Germs, p.262.

Table 3.1: Prevalence of Communicable Diseases in Britain in Nineteenth and Early Twentieth Centuries

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Tuberculosis Endemic; mortality declined towards end of nineteenth century Childhood infectious disease occurred in workhouse infirmaries to a variable extent, but measles and whooping cough were rarely absent, as was diphtheria from the end of the century. In the main, they were managed in the workhouse without difficulty and so are mentioned in the records infrequently. It was in the early years after the NPL that guardians were concerned that childhood infection might spread throughout the workhouse because of a lack of appropriate isolation facilities. In the majority of outbreaks, the guardians and MOs took steps to manage the situation appropriately.

Scarlet fever was a different matter, where guardians in Wolverhampton and Birmingham sought to make arrangements for admission to the local isolation hospitals. However, isolation facilities were not in place until later in the century and, until then, workhouses had to shoulder the burden of caring for sufferers from infectious disease. In Wolverhampton in 1891, the lack of an isolation hospital meant that all cases of infectious disease were treated at home, except for two patients with scarlet fever, who were admitted to the workhouse.95 Until isolation policies were introduced, children would not have been admitted to medical institutions primarily because of their illness if they could have been looked after at home. It is more likely that infection was coincidental to their admission with their parents or contracted while in the workhouse.

Diarrhoeal and Dirt Diseases Workhouses were the obvious locus of institutional care for paupers suffering from diseases associated with poverty and guardians responded to the demand by adopting varying strategies to cope with the influx or to divert it to other facilities. Typhus and typhoid fever are linked as ‘so-called’ dirt diseases since they flourish in conditions of

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transmitted to humans from body lice, is contracted by the inhalation of contaminated dust, resulting in fever, headaches and a purpuric rash, and had a case fatality rate of 20-45%.97 However, louse transmission was not demonstrated until 1909 and medical men remained in ‘total ignorance’ of the nature and origins of typhus throughout the TNA, MH12/11711, MOH’s report for 1891.

B. Luckin, ‘Evaluating the sanitary revolution: typhus and typhoid in London, 1851-1900’, in R.

Woods and J. Woodward (eds), Urban Disease and Mortality in Nineteenth-Century England, London, 1984, p.118.

Hardy, pp.192, 210. The causative organism, Rickettsia prowazekii, is excreted in the faeces of the body louse and can survive in them for many months.

nineteenth century.98 Nevertheless, by the 1860s, it was accepted as a contagious disease, associated with destitution and overcrowding.99 Consequently, typhus was endemic in urban areas, but two major epidemics, which were less dependent on domestic and working conditions, occurred in the nineteenth century in the years 1837-38 and 1846-47. The first caused the deaths of 75 individuals in Birmingham in the second half of 1837 and 45 in Wolverhampton.100 The latter one reached England from Ireland at the time of the famine and was referred to as the ‘Irish fever’. Over 17,000 people died in England and Wales from typhus in that year, following which the number declined to under 1,000 by 1878 and less than 250 by 1886. By the end of the century, it had virtually disappeared. The decline of the disease has been attributed to rising living standards, improved sanitary conditions and better personal hygiene, as well as the isolation in hospital of infected families, which allowed the opportunity of disinfecting their homes.101 It was liable to cause outbreaks in crowded institutions; hence its pseudonyms of ‘jail fever’, ‘hospital fever’ and ‘workhouse fever’, the last because of its prevalence in eighteenth-century workhouses.102 After its appearance in Birmingham workhouse in 1847, there were usually a few cases present over the following decade (Appendix B).

A few infected patients were admitted in Wolverhampton workhouse in 1842, one of which caused the lying-in ward to be closed for a month. Two years later, Ann Morris was brought to the workhouse in an open cart suffering from typhus, with Ibid.

Ibid., p.194.

Creighton, p.195.

Hardy, p.204; Luckin, p.111.

Dobson, p.36; K. Siena, ‘Contagion, Exclusion and the Unique Medical World of the EighteenthCentury Workhouse’, in J. Reinarz and L. Schwarz (eds), Medicine and the Workhouse, Rochester, 2013, p.27.

‘high state of fever and delirium’, but the MO detained her in the receiving room.103 On one day in December 1869, the only patients in the workhouse with infectious disease were 25 with typhus and they constituted 10% of all patients. By contrast, no patients in Birmingham workhouse suffered from the disease on that day and only 325 did so in all the English and Welsh workhouses.104 It is surprising that so little is recorded about infection with typhus in the workhouse, as admission of infected paupers in the 1860s usually led to severe outbreaks within workhouse infirmaries in London.105 It is possible that the practice of removing the clothes of inmates and subjecting them to bathing on admission may have limited the spread of body lice to other inmates.

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