Disease

Introduction

After a half century of medical and scientific progress in understanding and eradicating many diseases, it is very difficult to fully comprehend the situation in which 15% or so of children would die within their first few weeks of life and that some 30% or more would be dead by the age of 15. Today's childhood diseases would ravage a population; other diseases especially smallpox would peak and then decay only to reappear within a few years. Cholera, especially the epidemics of 1832/3 installed great fear into a population (see for example the rapid rise in Methodist membership in these years).

Major cities in Britain introduced bills of mortality from the early 17th century in which experienced 'searchers' noted the number and cause of death - these bills, essentially those for London, give the first detailed information. However as discussed later, these large urban centres would not be typical of the countryside; detailed examination of what records exist indicate that many deaths would be of the middle aged and older who moved into the city from the countryside indicating that they had not experienced certain diseases prior to this move.

Unlike England and Wales which had seen the start of compulsory registration in 1837, the first official notification of the cause of death was only required from the start of compulsory registration on the Island in 1877 - before this time the dates of various epidemics can be judged from the burial registers, although smallpox was often shown as such, it is now quite difficult to fully determine the causes of other epidemics. As Woods and Shelton show in their Atlas of Victorian Mortality the differences between the overcrowded industrial towns and cities and the countryside was quite marked for many diseases. Cholera, for example, spread quickly in towns through polluted water supply.

Many mortality statistics (e.g. Infant Mortality) are correlated with social class - in the 1960's infant mortality rates for Social Class V (e.g. unskilled labourers) was 2.5 times higher than for Social Class I (professions). Without entering into the minefield of social classes and their definition, it does indicate that for 'recognised' groups of people their life style gives their offspring a poorer expectation of life. This social gradient in the figures has been identified since the 19th century - it would appear that the lowest social class appears to lag by about a generation (30 years) in adopting the better practices (it would also appear to have held in early 19th century - see Oswald's letter of 1837 re smallpox vaccination). Increased infant mortality of the poor has been associated with overcrowding probably because infants contacted infections at a younger and more vulnerable age, as well as poorer nutrition.

Childbirth was especially risky - not for nothing was the 'churching of women' after a safe delivery a well respected custom.

Life Expectancy

Life expectancy in the mid 16th century when parish records can start to give some indication was around 30 and remained at around this figure until the mid 18th century when better nutrition (and, it is now thought, better maternal nutrition played a key role) saw a slow increase to around 45 around 1851. This was followed by a gradual rise as public health acts began to make their impact and then a faster rate post 1940 as antibiotics etc. became known, until today it is around 80.

This single figure hides much - as Woods & Shelton show for 1861 the life expectancy was considerably lower in larger towns and cities. the best fit for the figures shows that life expectancy was approximately = 100.9 - 12.5 log(x) where x = size of population. (e.g. in comparing a town of 10,000 and a city of 100,000 life expectancy in the later was 12.5 years less). For the Island this had an impact as Douglas grew quickly from the end of the 18th century; some estimate of the overcrowding can be seen in the census returns of number of dwellings compared with number of inhabitants for 1821 onwards. The new buildings that came during the start of the Island's tourist trade were not for the poor who crowded into the older building dating from the mid 18th century when Douglas boomed as the centre of the 'running trade'.

Factors

Three key factors in determining mortality from various diseases are:

With the benefit of today's scientific knowledge we can see that for a disease to become endemic it should not kill a high proportion of those it infects otherwise it starves itself to death. Those that do are likely to be cross-species infections that have just begun their escape into the human host population. Likewise it should be as infectious as possible before the sufferer shows signs of distress which could warn others to stay clear. The first principle can be seen in the gradual emergence of less virulent strains as the pathogen mutates to produce a variant better adapted to its host, which of course will also adapt by learning to produce antibodies. Measles is probably an excellent example, this viral infection, probably derived from canine distemper, can only infect primates (Man and monkeys) and has evolved over the thousands of years since Man domesticated animals. It has developed so as to infect the next host before the tell-tale red spots appear to give warning - assuming that the host survives the attack its antibody reactions are primed and will repulse any further infection. Such a 'policy' on the part of the microbe needs a large population to provide the necessary reservoir (estimated around 250,000) and thus it cannot be endemic in isolated rural communities (as was most of Europe until the 12th century when measles was first noticed). Likewise the disease will find children whose immune system has not yet been primed an obvious host population - the advent of schools etc. proving an efficient mechanism of infection. Measles was still a major killer of children in the 19th century - some 77 deaths due to measles were recorded in the first Registrar's report of 1880 for the Island (and 27 in 1909).

The microbe theory of disease began to be accepted towards the end of the 19th century - with it came insight into which techniques (medical, public health ...) would reduce mortality. Activities which today would appear obvious to us, would prior to this time be hotly contested on grounds of efficacy, cost or undue interference with personal freedom. The first outbreak of Cholera in 1832/3 can be taken as a watershed in ideas of disease and its causes. It must be remembered that at this time most people believed in the literal interpretation of Scripture (a view today only adopted by some right-wing American fundamentalists) which was only just starting to be challenged by scientific geology which indicated that Genesis could not be true in any literal sense and that life on earth stretched back somewhat further than 4004 BC! Darwin's theory of evolution still lay some 30 years in the future, thus it was difficult to conceive that a 'loving God' could deliberately create disease unless he wished in some sense to punish sections of Mankind. This moral aspect can be seen in the reaction of many evangelicals towards the Cholera outbreak, a topic well covered by R.J. Moore and neatly summed up by the Wesleyans in 1832:

..if not a sparrow falls to the ground without our Heavenly Father; an event so important as death can in no instance befall intelligent, redeemed and immortal man, but under Divine direction. "The pestilence walketh in darkness, and the arrow flieth by day", but every victim is selected by infinite wisdom, acting under the direction of mercy or of justice, according to the character of the person whose days are numbered.

[Wesleyan Methodist Mag 12 3rd series p21 - quoted by Moore]

Characteristics that would help such selection naturally included addiction to alcohol, aversion to chapel etc. In many respects this attitude was merely harking back to the days of the plague when, in the absence of any other understanding, population turned to prayer and mortification in an ineffectual attempt to procure divine intervention.

Such a fatalistic approach was not taken by all; the connection between the arrival of a sick person and the subsequent spread of the illness within a population had been observed for centuries. Mechanisms to prevent such movements could be seen in the the bells that lepers had to carry to warn of their arrival and the concept of quarantine brought in from the 14th century to help prevent the introduction of the plague. However whilst control over the movement of beggars was acceptable, though difficult, mechanisms should not unduly hamper trade otherwise they would be circumvented.

Scientific medicine effectively started in some Scottish universities towards the end of the 18th century - whilst such trained doctors had few, if any, effective cures, they were trained to be observant. The paradigm of such observations was that of Dr Snow in London who connected the transfer of cholera with polluted water supply. His observations had little effect in the 1830's but during the 1854 outbreak he demonstrated conclusively that cholera was waterborne and by the removal of a pump handle the epidemic was halted. However even then it took another outbreak in 1866 to fully convince the authorities, after which public health measures were applied to all water supplies. It was not until Koch's work in the 1880's that the actual pathogen was found.

Individual Diseases

 I do not intend in this section to give a complete aetiology and epidemiology of the various diseases which have afflicted the Island, in many respects it would be little different than its much larger, and better recorded, neighbours. What I hope to do is to bring out any local implications that would not be noticed in a wider study of the British Isles. Until the development of Douglas in the late 18th century most Manx lived in small isolated communities with easy access to clean water (though as Lamplugh noted often from shallow sources that could be easily poluted) and with an adequate (though poor) diet. Feltham, and others, visiting at the end of the 18th century commented on the longevity of the Manx as compared with nearby England.

Bubonic Plague (or the Black Death)

So called from its distinctive signs of buboes, blotches and boils that suddenly appear at different places on the body (plague derives from the Latin plaga - wounding blow). Other signs were the distinctive swellings of regional lymph nodes in the groin or armpit which would swell to the size of apples.

The first of several epidemics to hit Western Europe was in 1348 coming from Asia both along the Northern trade route across the steppes and the southern trade route into the Mediterranean. A subsequent epidemic struck in the 1360's and recurred approximately every generation until its unexplained disappearance after the 17th century. The pathogen is a bacterium that infects rodents and their parasitic fleas - the flea however is quite willing to transfer its affections to a human host if its rodent host dies. The bacterium can apparently survive outside of its host for some time thus providing a reservoir of infection. It is thought that the vector was the black rat (Rattus rattus) widespread in Europe and easily infected, usually fatally. Fleas from dying rats would then feed off nearby humans and transfer the bacilli in the process. The bacilli spread very quickly, first killing off cells in the region of the bite producing a blackening blister and then, as the lymphatic system transfers the bacilli to the lymph nodes in an ineffectual attempt to produce antibodies quickly enough, the lymph nodes swell enormously and the bacilli spread throughout the body causing fever, excruciating headache and delirium. All this occurs within about 4-6 days - within 10 days about 60% of those infected will be dead. Although the main transmission is via fleas, it is possible to transfer the bacilli by airborne infection by coughing - this form of infection is generally fatal. It is estimated that in this first outbreak some 20% of the Eurasian population died - in some regions mortality was as high as 40-50%. The sudden and very high number of deaths within a short period caused many social conventions to break under the strain - normal care of others would be impossible, food production ceases and pollution would encourage other diseases. The black house rat is a non-migratory creature that generally cannot survive away from human habitation where it used to live in the thatch roof and clay wall of the houses of the poor - it is also the common ship rat thus infections tend to follow trade routes.

Bubonic plague is a warm weather disease - the flea's eggs do not hatch below 55° F and are killed below 45° F though adult fleas can tolerate colder temperatures. Cases thus tend to appear in late spring or early summer, peaking late summer/early autumn and ceasing from start of December. The pneumonic form of the disease requires close (and repeated) contact between people - it thus tends to be a winter disease in overcrowded towns, an unlikely scenario for the Island. The 1348 black death appears to have been a sequence of bubonic and pneumonic plague though some have argued that Anthrax was also involved.

The 1348 epidemic in England has been widely studied for its effects on the political and social structure - it is not clear however if it spread to the Island. Plague is very much an urban disease and at that time the Manx would live in isolated hamlets. Possibly the Papal dispensation of 1349 to ordain 8 men of illegitimate birth was in response to a high death toll of priests who would naturally come in close contact with the dying and the dead. However the Chronicle of Man makes no mention of the plague - merely stating that 1348 saw the election of the first Manxman to the Bishopric and that he then went to Avignon to be confirmed in office by the Pope (though that itself may be a sign of abnormal times as Furness would normally be expected to provide the Bishop) .

The plague re-occurred each generation from then on, though the disease could be just as virulent (however it would appear many outbreaks were less so) it no longer caused the social upheaval of the first. The last serious outbreak in Britain was in Scotland in 1645-9 when possibly some 20% of the urban population died. Houston comments that the effect on the overall (English) population may have been overestimated by the contemporary alarm from city dwellers who, though highly visible in the records, formed but a small fraction of the total population; even so he estimates that between 1580 and 1650 it accounted for just 15% of the deaths in London (my italics).

There was possibly a major outbreak of plague in North West England in 1623 though Appleby argues that the peak in death rate was due to localised famine - a significant peak can be seen in the burial rate in the few Manx burial registers of the period.

The last outbreak in London in 1665 prior to the great fire, which in popular legend at least was responsible for the disappearance of the disease by killing off the rat population, had some effect on the Island as it encouraged some merchants to move from London to exploit the tax-haven status of the Island effectively founding the running trade.

Smallpox

So called from the size of the pustules (or pox) - the Great Pox (or commonly just Pox) was Syphilis which had reached Europe by the end of the fifteenth century. It is a viral infection (and thus not amenable to antibiotics) which exists in two main strains variola major with a death rate of around 25-30% and the much milder variola minor with a death rate of around 1%. The sole host of the virus is Man though related viral strains infect, for example, cattle. Infection is either by contact with the pus or scabs, or by inhaling the virus by close contact with an infected person. The infection period of some 12 days allows an infected person to spread the disease before displaying obvious signs. It is likely that like many other diseases it evolved with the early domestication of animals in the Middle East - it is thought that some Egyptian mummies show signs of childhood smallpox. It was certainly endemic by the 10th century in a wide band stretching from Portugal through to China - it is possible that this was a mild variant as it was considered as an inevitable childhood disease. On previously unexposed populations it was deadly - the Spaniards took it with them to the Americas in 1519 (probably via the children of settlers) where it had a major impact on the Amerindian population and was almost certainly the key factor by which Spain conquered its empire. Studies from the better recorded 20th century smallpox epidemics indicate that death rate is highest among older children and young adults - those that recover from such infections are generally immune for the remainder of their life (though it is possible that genetic mutations in the smallpox varus may remove some of this immunity). It is possible that a more virulent strain developed during the early days of the African slave trade which recrossed the Atlantic sometime in the 17th century (an epidemic in Iceland in 1707 killed 25%). Smallpox became epidemically important in England after 1600 and in the North from c. 1650. Certainly by the 1670's this strain, which was a major killer of children, was endemic in lowland Scotland and parts of England (in the 18th century it was endemic in London though possibly not across all of England). Once endemic, a transplacental antibody, which appears to be short-lived, provides strong immunity for the first month after birth and partial immunity for the first four to six months after birth thus deaths tend to be concentrated on young children born since the last epidemic. It is possible that some of these earlier epidemics outbreaks were caused by variola minor strains (with mortality rates of 0.1 - 2 %) thus possibly not being significant enough to observe in any burial register whereas the variola major strains (with mortality rates of 5-40%) would provoke an immediately noticeable number of entries in the register. From personal transcriptions of the Kirk German registers there are seen the occasional isolated smallpox death.

Feltham writing in 1798 re Lezayre states that "Jane Corlet, (F.S.) 1685, was the first person who died in the island of the small pox. It was brought into the Isle by Wm. Killey from abroad, and it was called in Manks, 'Brack Willy Killy' from thence, on the information of an old inhabitant."

Many parish registers indicate Smallpox as a cause of death - Kirk Michael parish registers indicate that severe epidemics of smallpox were recorded in 1684, 1704, 1725, 1732, 1764, 1772 . There were earlier high death rates in 1623, 1629 and 1639 though no special note was made of the cause.

After the incubation period, which could evince few symptoms, victims would suffer a high fever and severe pains in the head and major muscles, sometimes dying at this point from internal haemorrhages. Most would live a further few days to see the characteristic rash of pimples develop into pustules. The fewer the pustules the higher the chance of survival - however once the scabs dropped off the pustules would leave deep disfiguring pock marks. Survivors would however be immune to further infections.

Smallpox acquired by inhalation would kill around 25% of its victims - however it was found that infection from the pus from a victim killed only about 2% of those infected and left fewer pockmarks. This form of deliberate introduction (called variolation), in which the pus was entered into a slight cut in the skin was practised from 1720 onwards. Note that this variolation still gives the deliberately infected person smallpox (which could infect others) but the chance of survival are some 10 times better! One child that did not survive was the daughter of Henry and Jody Corrin's whose epitaph was recorded by Feltham

" Asleep in bed I laid,
Where none I did offend;
From thence against my will convey'd,
To a plaguey pox by men.
Dear parents, cease to weep,
I innocently forgive;
Rather remember me to meet,
Where love doth ever live."

The Kirk German burial register for 1772 and 1794 note deaths from innoculation - in 1794 it would appear that such deliberate innoculation was the source of a major outbreak.

It was Jenner's observation that those who had previously suffered from cowpox did not go onto to develop smallpox after such variolation, that led to the idea of deliberately infecting people with the much milder cowpox rather than smallpox. He published his ideas of vaccination (from vaccina Latin for cow) in 1798 and it was rapidly taken up, bringing the number of deaths by smallpox down to almost zero by the end of the 19th century - however there was an outbreak at Laxey in the 1870's. By 1801 the Manx press was noting that cow-pox had been introduced and a number of children innoculated. Smallpox has now been been completely eradicated by a global vaccination campaign to remove any new hosts for the disease.

There was however considerable opposition to such vaccination on the Island. Train gives the following account (Tear was a famous folk doctor of the time)

Another singular instance of the influence of the empirics of the order of seer Tear, over the minds of the people, occurred in 1837. The small pox made great havoc in Douglas, and yet the majority of the inhabitants rejected with scorns the " genuine variola," even when gratuitously offered by all the humane practitioners in medicine.

See the letter by Dr Oswald re popular opposition in 1837. It would appear that variolation was still being practiced - this dangerous scheme ran the severe risk of re-introducing smallpox into the population. Variolation (or innoculation) was made illegal in 1876 (see Moore's History p706)

Further opposition developed later in the century (and into the 20th) especially after vaccination was made compulsory in 1878 - free churchmen (such as Rev Carr) seemed particularly opposed to such avoidance of Divine retribution.

Cholera

Morris gives an excellent account of the four Cholera epidemics which spread across Europe in the 19th century. Originally confined to the Bengal region of India (and thus known as Asiatic cholera) where it periodically ravaged the region; it somehow, in 1817, underwent a change. Morris attributes this to two factors - more overseas trade which encouraged its spread across to Persia (Iran) and thence on to Europe and the British Army's regular rotation of troops which allowed it to escape out of its confined region. The disease was thus familiar to Army doctors and to troops (it is estimated that it killed some 3000 of Hastings' 10,000 strong army). By 1823 it had reached Russian Astrakhan and for a period stopped. In 1826 it re-occurred at a great religious pilgrimage at Hurdwar and was carried back by pilgrims along trade routes. Unfortunately it reached Russian Nijni-Novogorod in time to infect the autumn trade fair - again trade routes saw it spread quickly to Moscow in 1830 and from then on it was merely a matter of time before it spread to all of Europe. In September 1831 it had reached Hamburg which had many trade links with Britain - the first British death occurred in October at Sunderland.

The arrival of the Cholera was long heralded in the Manx Press which from 1831 tracked its progress across Europe; on 25th May 1832 it reported Cholera in Liverpool and the first case in Douglas (Thomas Woods) was reported 17 July 1832 (see also account by George Head). This outbreak lasted until September 1832, a second outbreak occurred in August-September 1833. Some of the social attitudes have already been mentioned above.

Without treatment Cholera kills around 40-60% of those infected. The disease causes constant vomiting and purging of the bowels - often as much as several pints in a few minutes. Descriptions abound of sodden bedclothes (highly infectious) and floors awash - such dehydration causes cramps, the body shrivels so much so that the sufferer is said to look like a monkey and the blood becomes too thick to be easily circulated thus turning the extremities black or blue. However this acute stage only lasts some 24 hours, at the end of which the victim is either dead or on their way to a slow recovery. As mentioned in the introduction, infection is by polluted water in which the excreta of an infected person enter into drinking water. The microbe is however killed by heat or by acid, some people can drink polluted water and avoid infection due to their stomach acid. Nurses would use vinegar to remove the smell of vomit from their hands, by doing so they would also kill the microbe.

Douglas and Castletown bore the brunt of the outbreak - special graves were opened in Kirk Braddan and St. George's. It is possible that there was a similar arrangement at Kirk Malew (for Castletown) but if so no marker has survived.

Kathleen Forrest, writing some 60 years later but possibly based on other's personal observation, though I suspect also based on desciptions of London burials (Douglas was small and the crowded section is in easy reach of St George's and the number of deaths limited), writes:

In 1832 a dreadful epidemic of cholera visited the island. People. were literally swept away by the hand of death. All day long the dead-cart seemed to be going its rounds from house to house, and the cry heard, "Bring out your dead-bring out your dead! " It was during this time that Charles, Captain Jones' servant, mentioned previously, one day that he had occasion to go from Douglas to Peel, said to his mistress on starting that he had a presentiment that he should die before night. That evening he returned, sickened, and died of cholera.

In Douglas was the greatest mortality; and at night in St. George's churchyard the burial of the dead, as described by eyewitnesses, was a mournful and appalling sight never to be forgotten. There, by dim lanterns held in the hand, or suspended from the trees, the graves were dug, and in many cases the uncoffined bodies heaped in one after the other, and no stone ever to record more than one word-CHOLERA, close to the south-west entrance of St. George's Church, a large memorial stone, railed round, is erected to commemorate the dreadful time. Engraven upon it is a lengthy record of the event, surrounded by a sculptured relieve, illustrating the horrors of pestilence.

St. George's

Some 34 burials are reported for St. George's in 1832 and another 86 for 1833.

This memorial tablet was erected in 1841 to commemorate Matthias Kelly (a soap manufacturer and brother of William Kelly) who died from Cholera in 1833. The stone, cut by Charles Swinnerton records the description of the Cholera Outbreak.

The burial pit itself is unmarked - being just a large plot of bare grass.

Memorial stone St Geoerge's

Kirk Braddan

Memorial Stone Kirk Braddan

Some 83 victims were buried in Old Kirk Braddan yard between July and September 1832. Pantin suggests that an 1837 outbreak saw the highest number of deaths - possibly as high as 120. It is possible however that these deaths were due to typhus.

According to Sir George Head's account these small stones were of individual graves

Train's account (History Chap XXIII), written in 1837, makes interesting reading

Such is the blind reliance placed on those impostors called " fairy doctors," and female empirics, that when the cholera broke out in 1832, some of the people who were affected with that malady refused all medical aid or interference on the part of the regular medical practitioners, although frequently offered gratuitously by some of those gentlemen in the most handsome manner. Having more faith in charms,and the mysterious virtue ascribed to certain plants, than in the skill of the most experienced physician or pharmacopolist. Fairy doctors and certain old women were brought from the most remote parts of the Island to Castletown and Douglas, to administer to those unfortunate persons who were suffering under the dreadful epidemic; while all those of the school of Esculapius remained, not only unemployed, but were obliged to keep out of the way, their lives being endangered by popular prejudice. An absurd report was spread abroad, and believed by a greater proportion of the community, that the springs of the Island were poisoned by the doctors, in order to receive a premium of ten pounds from government, to be paid them for every individual that fell a victim to cholera.

This belief in the poisoning of wells and springs may explain the strange hostility that George Head encounted near Polvaish. The main source of infection was however the water carriers of Douglas who in that dry year drew water from the river rather than from their normal springs which had dried up.

Other outbreaks were

1849 Cregneash and Port St. Mary
1866 Peel (small outbreak brought over from Ireland by fishing boat Annie)

A very full account is given by the late Mary McHardy - Journal IoM Family History Special Issue. For a list of reported deaths and some newspaper extracts see my Cholera page.

Typhoid

Caused by a member of the Salmonella family of bacteria (others of this family are well known for causing food poisoning), its symptoms include high fever, prolonged diarrhea, abdominal pain etc. which can last for weeks in the absence of antibiotics, with sometimes rosy red patches on the abdomen. It will kill around 10 to 20% of those infected - often from complications induced by the illness. Like cholera, infection is via the excreta of an infected person entering into the mouth (by contact), food (possibly by fly borne contact with outdoor privies), or more commonly, into the drinking water of the next victim; it is thus easily transmitted in overcrowded or unhygienic situations and is usually associated with the poor. Some individuals (around 3% of those infected) can continue to harbour the bacilli but not suffer any further consequences - they then act as a walking reservoir ready to infect others.

It was the death of Prince Albert, in 1861, supposedly from typhoid (though now thought to be a stomach ailment) that was the driving force to improve sewage systems in major cities in Britain and a much improved public health education ('wash your hands...'). Modern western systems of hygiene have virtually eradicated the disease though it is endemic in less hygiene conscious communities.

During the 19th century it was a major problem, especially in the overcrowded sections of Douglas that had no sewage system apart from open gutters and easily infected water supplies until the provison of piped water.

Sometimes confused with typhus as both share common symptom of a high fever -also sometimes went under the name 'English Cholera'.

Typhus

Typically associated with war or famine when men are crowded together in unhygienic situations (for this reason often known as 'camp fever', 'jail fever' , 'ship fever' or just 'fever' etc. though these terms can apply to other diseases). Caused by a microbe midway between a virus and a bacterium which is transmitted via the human body louse (though rats and their fleas can also play a part). Its symptoms are a high fever and a body rash that lasts one or two weeks. Easily confused with typhoid - prior to c.1880 both names were sometimes used for the same disease. Like typhoid, the pathogen can survive in those who have recovered from the disease thus providing the mechanism for transfer to new hosts. Again, like typhoid, seen as a disease of the poor, especially in cooler climates where layers of unwashed clothes provide the perfect breeding ground for the louse. Fatalities are between 10 to 40% and was a major cause of death for those nursing the sick - A M. Hardy considers that it was typhus that killed Dr and Mrs. Railton in Peel in 1863.

The civil war in England saw a major outbreak in 1643 at the siege of Reading (it impartially ravaged both parties) and again in 1650; a major epidemic occurred in Ireland between 1816-19 which spread to England (and possibly the Island ?). The recognition of the key role played by the human louse led to the use of de-lousing stations in the western front in WW1 and no typhus outbreak occurred there - whereas on the eastern front over 150,000 died in Serbia alone.

Known outbreaks in 1837, 1853 and 1866. It is typically a disease of the winter when the cold discourages bathing and changing clothes - it tends to disaapear in the spring; it also kills adults rather than children (who however sicken but usually survive).


Childbirth

Obviously not a disease but considered here as a factor in mortality! Statistics of maternal mortality (i.e. death during or within a short period after, giving birth), are available for England and Wales only from mid 19th century (and for the Island from some years later in the century). However as improved obstetrics (and later antibiotics) only came in from the 1920's, the earlier figures can be used as a lower bound on (and reasonable approximation to) the figures for earlier centuries. English figures for the end of the 19th century were around 5 maternal deaths per 1000 births, Manx figures for period 1913 to 1926 were consistent at 5.2 per 1000 births. It is likely that earlier figures would be somewhat higher, e.g. in the 1930's the Maternal Mortality Rate in the United States was 64 per 10,000 births. Currently the figure is less than 2 per 10,000 - the chance of dying during childbirth at the end of the 20th century has declined to approximately 1/50th of its figure mid century.

These statistics are averaged across all births, as for many diseases it is likely that unsanitary towns (on the Island this would be just Douglas) would have higher figures than the countryside. It is likely, though I have not seen detailed statistics, that the mortality of first births was considerably higher than the average over all births. Houston estimates that maternal mortality accounted for a maximum of 20% of all deaths of women in age group 25-34 and some 11-14% for those 20-24 or 35-44. However it would appear a relatively distant experience as a population of 1000 of whom 25% would be women of childbearing age would expect 1 maternal death every 3 years.

Stillbirths (i.e. children dead before or dying during birth) have also seen a great reduction over the last 50 years. In the 1930's the Manx statistic was 52 per 1000 live births - with much improved antenatal care today's figure is around 5 per 1000. Previous centuries would have seen higher figures as maternal health and nutrition is an important contributory factor e.g. rickets in childhood leads to poor pelvic development and thus difficulty giving birth.

References

General

K.F. Tiple (ed) Plague, Pox & Pestilence: Disease in Society London: Wiedenfield and Nicholson 1997 (ISBN 0-297-82254-3) - collection of short chapters giving expert coverage of the many diseases that have afflicted populations.

W.H. McNeil Plagues and People Oxford:Blackwell 1977 (ISBN 0-631-17880-5) - wide coverage both geographic and in time - excellent overview.

R.A. Houston The Population History of Britain and Ireland 1500-1750 Studies in Economic and Social History London:Macmillan 1992 (ISBN 0-333-56564-9)

R. Woods & N. Shelton An Atlas of Victorian Mortality Liverpool University Press 1997 (ISBN 0-85323-542-2) - covers England and Wales drawing on the numerous statistical returns post 1840.

R.J. Morris Cholera 1832 New York: Holmes & Meier 1976 (ISBN 0-8419-0288-7) - besides the medical and public health aspects gives considerable coverage to how various religious and social groupings reacted.

Manx references

Chief-Registrars Annual Report and Statistical Review of the Births, Marriages and Deaths on the Isle of Man - series started 1880 , copies in Manx Museum (1909 on-line).

Manx National Heritage Cholera and Nineteenth Century Health Issues Manx Museum Bibliography No. 6 (free fact sheet from Manx Museum) - gives bibliographic reference of many sources held by MNH.

G. Pantin Labours of Love Douglas:St Bridget's Hospice 1988 (ISBN 1-871801-00-1) - the commentary on this reprint of the story of Nellie Braddan gives an excellent account of the arrival of Cholera on the Island.

G. Pantin The Story of the Jane Crookall Maternity Home Douglas:St Bridget's Hospice 1992 (ISBN 1-871801-03-6) - gives an excellent history of 20th century progress on the Island as well as a history of the 'Jane'.

 


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Any comments, errors or omissions gratefully received The Editor
© F.Coakley , 2001