Graves proceeds, with much candour, to show how mistaken had been the reasons assigned equally for the mild type of scarlatina between 1804 and 1831 and for the severe type of it previous to 1804:

From 1829 to 1833 there are numerous references to the scarlatina maligna in England and Scotland: at Plymouth[1344] in 1829, Bridlington[1345] in 1831, Baddeley Green, Brown Edge, and other places in Staffordshire[1346] in the summer of 1831, Beaconsfield, Bucks[1347], in 1832, Edinburgh[1348] in 1832-1833. It is in 1830 that scarlet fever begins to have a line to itself in the old and inadequate bills of the Parish Clerks of London, the deaths that year being 94; in the next seven years they are 143, 388, 481, 523, 445, 261 and 189. In 1835 we begin to have statistics of the deaths from it in Glasgow[1349] for five years, during which they fell much below the deaths from either measles or smallpox.

Deaths from Scarlatina in Glasgow.

The two first years of this period, which had the most scarlatina deaths, correspond to the years of the Dublin epidemic, and were also the years when it was common in Edinburgh[1350]. Probably the smaller mortality of Glasgow in 1837 and 1838 was general; for, when registration of the causes of death began in England and Wales in the latter half of 1837, it found the scarlatina mortality at a much lower figure than it reached in 1839 and continued to keep thereafter.

Scarlatina since the beginning of Registration, 1837.

The first returns of the causes of death under the new Registration Act happened to correspond with a great epidemic of typhus fever, and with an equally great epidemic of smallpox which took its victims in largest part among infants and young children. The deaths from scarlatina were also considerable during those two years and a half; but in 1840 scarlatina nearly doubled its mortality, and continued year after year for a whole generation to be the leading cause of death among the infectious maladies of childhood. The figures for England and Wales are given in a table at p. 614, in comparison with the annual deaths by smallpox, measles, and diphtheria. The enormous number of deaths from scarlatina during some thirty or forty years in the middle of the 19th century will appear in the history as one of the most remarkable things in our epidemiology. There can be no reasonable doubt that this scarlatinal period was preceded by a whole generation with moderate or small mortality from that disease, just as it is now being followed by annual death-rates which are less than a half, perhaps not more than a third, of the average during forty years before 1880.

The first great epidemic all over England was in 1840 (it had reached a maximum in London the year before), another came in 1844, a third in 1848 (in which the London death-rate was 2·12 per thousand living). In the next decennial period, 1851-60, the worst years for scarlatina were 1858-59, which were also the years of the return of diphtheria; in the period 1861-70, the great scarlatinal years were 1863-64 and 1868-70; in the period 1871-80, the year 1874 was the epidemic year. The annual average death-rates per million inhabitants in all England and Wales were as follows in four decennial periods:

In the greatest epidemic years since 1863 the death-rates per million for the whole country have been:

In those years scarlatina made from four to six and a half per cent. of the deaths from all causes.

While no county of England has been free from this infection, the bulk of the deaths have fallen upon the capital, the great Lancashire and West Riding towns, the Black Country of Staffordshire with Warwickshire, the mining districts of Durham and South Wales, and, in the earlier part of the period, upon the south-western counties.

Highest Mortalities by Scarlatina in three Epidemics.

In Lancashire and South Staffordshire there has been less fluctuation of the mortality from year to year than elsewhere. The stress of an epidemic has not fallen equally on all the principal centres in the same year or years: thus Durham has had the epidemic in advance of other centres, while South Wales has had it in arrear. The decline of the south-western counties from their leading position in 1863-64 has been remarkable. Plymouth, Devonport and Stonehouse, which had contributed most to the high scarlatinal death-rate of Devonshire in 1863-64, were found on the average of the next decennial period to have low rates from scarlatina, but death-rates from measles which were unapproached in any other region of England. In the following table four Devonshire towns are compared with certain Staffordshire registration districts in which the scarlatinal death-rate has remained high.

Annual average Death-rates per 1000 living, 1871-80.

This looks like a correlation between measles and scarlatina. The excessive death-rate from measles in Plymouth, Stonehouse and Devonport was due to a disastrous epidemic in the last two years of the decennium, 1879 and 1880 (338 deaths at Plymouth, 121 at Stonehouse, and 235 at Devonport). Measles remained high in Plymouth all through the next decennium, scarlatina still continuing low until the very end of it, when in 1889 there was a mortality of 270, equal to a death-rate of 3·39 per 1000 living. In like manner Stoke-on-Trent had its great epidemic of measles in 1888, causing 342 deaths, or a rate of 2·8. The high Plymouth death-rate, after nearly twenty years with extremely little scarlet fever, was surpassed in 1882 by an epidemic of 346 deaths in the colliery townships of Aberystruth and Tredegar, Monmouthshire, equal to a death-rate of 6·1 per 1000. Other high death-rates for single years were at Wakefield and Swansea in 1889 and at Neath in 1890. The highest death-rates from scarlatina on an average of ten years, 1871-80, were at Durham 1·70, Todmorden 1·64, Auckland 1·63, Gateshead 1·60, Sheffield 1·49, Leigh 1·41, Wigan 1·30, Newcastle 1·28. The purely agricultural counties have the lowest death-rates[1351].

As to age-incidence, the proportion of deaths under five has been almost exactly two-thirds steadily for the last four decennial periods (supra p. 625). The following table by Dr Ogle, the Superintendent of Statistics, shows both age and sex of the scarlatina mortality[1352]:

Mean annual Mortality from Scarlet Fever per million living at successive age-periods 1859-85. England and Wales.

From certain hospital statistics on a large scale, and some figures of cases and deaths at Christiania, it was also found that the attacks of scarlatina were much more fatal in the first years of life, the fatality decreasing rapidly after five. This was only to be expected. But it was somewhat surprising to find that more girls were attacked than boys, while the fatalities among boys were more than among an equal number of girls at all ages until womanhood, when the few females attacked by scarlatina had more fatalities among them than the somewhat fewer males of the same ages. A slight excess of fatality in the female sex over the male between the ages of ten and twenty years, is shown also for smallpox by the table at p. 618. Recent notifications of infectious diseases to medical officers of health have enabled a comparison to be made between the number of cases of scarlatina notified, with age and sex, and the number of deaths certified in the corresponding time and place to the Registrar-General; from which the above generalities as to the proportions of fatal cases in the several age-periods of either sex have been confirmed[1353].

The enormous mortalities of some years may be taken to have depended in part upon an increased prevalence of the disease, but still more upon an increased fatality among the subjects of it. Since the establishment of the Metropolitan Fever Hospitals in 1870 the percentage of deaths to cases has ranged from 15·3 in 1879 to 6·6 in 1873 and 6·7 in 1891. Among the smaller totals of the London Fever Hospital the percentage of deaths has ranged even more widely from year to year[1354]. What is thus statistically proved is also a matter of common experience; there have been whole epidemics, extending perhaps over two or three years, marked by high malignancy, and epidemics just as uniformly marked by mildness of type. The severe type has usually been made by the sloughing in the neck or throat; but there has also been a class of cases tending to a fatal issue early in the attack by a sunken pulse and with few external manifestations. The cause of these variations in the severity of scarlatina is the old problem of epidemic constitutions: sometimes the constitution is “putrid” or “pestilential” or malignant, sometimes it is mild or benign.

Graves, in the passage above cited, has sufficiently exposed the fallacy of attributing changes of type to modes of treatment. On the other hand there is reason to think that the percentage of deaths (by which the “type” is usually judged) is higher in children carried off to hospitals than in those treated at home. As the same fact has been uniformly observed in epidemics of Asiatic cholera, when the ambulances have been almost as busy as those of the Metropolitan Asylums Board during an ordinary autumnal rise of scarlatina, it is probable that the reasons which used to be given in the former case hold good also in the latter.

Scarlet Fever in London, 1890 and 1891.

This is a comparison of two parts of the same epidemic, which had a very moderate fatality in any case. The real problem of malignity or severity of type arises over such epidemics as those of 1840, 1848, 1858-59, 1868-70 and 1874, in which the doubling of the deaths, for one year, or for two or even three consecutive years, had depended less upon an increased number of seizures than upon a higher ratio of fatalities. An explanation for each occasion will have to be sought either in the condition of the patients, or in the inherent properties or external favouring circumstances of the virus. As to the former, the most fatal epidemic years of scarlet fever have not been marked in any such uniform way as the great seasons of typhus or relapsing fever; nor is scarlatina an infection that keeps mainly within the poorer classes. Among factors of the external kind, a rainfall below the average has been thought a relevant thing: thus in the three years 1862-64, the annual average rainfall at Greenwich was only 20·6 inches, the scarlatina death-rate in London for the same years reaching the high figure of 1·33 per 1000 inhabitants; in the next three years, 1865-67, the death-rate fell to ·56 (it would have fallen in any case), while the rainfall reached the very high average of 29 inches; in the three years following, 1868-70, the death-rate reached the excessive annual average of 1·5 per 1000 in London, the rainfall of the same period averaging only 22·3 inches. Thereafter for a number of years the rainfall was moderate and the scarlatina death-rate low; but in the years 1883-87, they were both low together, the scarlatina death-rate of ·26 being lower than it had ever been since registration began[1355].

Although an empirical correspondence between the great scarlatina periods and a series of dry years has not been made out without important exceptions, hitherto unexplained, yet there is a very obvious correspondence between the great rise of scarlatina deaths in London every year and the season of late autumn, which is the season when the ground-water touches its lowest level or begins to rise therefrom to the high water-mark of spring. Of all the curves of seasonal rise and fall constructed by Buchan and Mitchell from the weekly bills of mortality in London from 1845 to 1874, that of scarlatina is the most decided next to that of infantile diarrhoea, the deaths rising in October and November far above the mean line of the year, and falling farthest below the mean in spring and early summer[1356]. This was an old observation—by Sydenham for the scarlatina simplex of that age, by Willan in the end of the 18th century (one or two spring epidemics being remarked upon as exceptional). It is a very curious fact, and one that is as certain (for London at least) as it is curious. Sydenham explained it by the doctrine of his time, that the favouring things were in the human body, namely, some susceptibility of the humours owing to the heat of the preceding summer; but, according to modern views, it should bring scarlatina into the same class with the soil-poisons of enteric fever, yellow fever and cholera, which are believed to become more rife owing to the greater activity of their respective miasmatic viruses when the pores of the ground are occupied to the greatest depth with air in place of water.

It would be singular indeed if, after all, we should have to include scarlatina among the miasmatic diseases; for it is an exquisite instance of an infection which is passed from person to person, or by the agency of volatile contagion, or by fomites in clothes, bed-linen, house-furnishings and the like. The controversy which has raged so keenly in the past between contagionists and non-contagionists over the instances of plague, yellow fever and Asiatic cholera, would become still more keen over scarlatina—and be still more confused if it were not stated in more correct terms at the outset. What we all find so hard to learn is, that the one way of infection does not exclude the other. Plague was for the most part a miasmatic infection in the air of a plague-stricken town; but it could be conveyed in clothes or bales, while it was prudent to remain not too long in the company of a plague-patient. In like manner contagion from the person was, as Rush said and Blane confirmed, a “contingency” in yellow fever; and there are some authentic cases of Asiatic cholera which cannot well be explained except on the hypothesis of contact with the persons of those sick or dead of the disease. Scarlatina is more contagious than any of these, because it shows so much on the surface of the body and scatters its infective matter into the atmosphere of a room with the fine scales or dust of desquamation. Still, there are conditions for the contagiousness of scarlatina, just as there are for the rarer event of contagion from the persons of the sick in the plague, yellow fever and cholera. It is a remarkable fact that scarlet fever should ever be sporadic, or that a single case should appear in the midst of a crowded population (as I have seen in a coast town filled with strangers during the herring fishery to the extent of one-half more than its usual numbers), and no other cases follow for months after, although there had been not the smallest attempt at isolation. Every medical practitioner knows, if some laymen and legislators do not, that scarlatina is sometimes highly contagious, and sometimes hardly contagious at all; and who can say whether the mechanical routine of “stamping out” contagion, which certain persons pursue with more zeal than knowledge, may not be the means of turning a mere potency into an actuality? The tact of individuals rather than the grinding machinery of an Act of Parliament is needed in dealing with vagaries such as Willan thus describes:

There are two special forms of epidemic scarlatina which may prove to be finger-post instances for the general pathology. It happens from time to time in the surgical wards of hospitals for children, where many cases of suppurating diseases (especially of the bones or joints) are aggregated and kept together perhaps for months, that groups of the patients acquire a scarlet rash, or an erysipelatous rash, or a hybrid form of rash, along with the constitutional symptoms of scarlatina. Whether it be from the suppuration, or from the blood of operations, this disease must be reckoned a product of so-called “hospitalism.” It is not without significance that there may be an element of erysipelas in such cases. They are probably cases of “blood poisoning,” in a double meaning of the term—poisoning of the living blood by dead blood or by pus which is closely allied to blood[1358].

The other special kind of epidemic scarlatina is that which has broken out among the inmates of houses supplied with milk from a common source. There have been many such outbreaks, including one most remarkable instance in which a large number of guests at an evening party, who had partaken of cream with strawberries, were shortly thereafter attacked by scarlet fever at their widely scattered homes. There can be no question that milk, or cream, has been the vehicle of scarlatinal infection. The first hypothesis tried was that of scarlatina on the dairyman’s premises; the effluvia of a scarlatinal patient might have become mixed with the milk. In some instances, it was actually shown that there had been a case or cases of scarlet fever among the dairyman’s children; but there were other instances in which that could not be shown, and it was, of course, possible to refer the cases, where they did occur, to a common cause in the milk used at the dairy and in the milk distributed from it. As more and more outbreaks of the kind came to be investigated, it was indeed made probable that the infection had got into the milk from the cow[1359]. Someone threw out the suggestion that the cow suffered from scarlet fever, the sign of it being soreness of the paps. Without taking seriously so random a hypothesis as that, we find much agreement as to the fact that the cows, to which the contaminated milk has been traced, were affected, one or more of them, with sore paps. In some cases the disease of the teats had been admitted to be the same as cowpox; in other cases that has been denied; in a third variety, a cow has had cowpox on one teat and something else on another. It matters little what name be given to the affection of the cow’s paps. All soreness of the skin of the teats has the same effect so far as concerns the purity of the milk. Unless the milk be drawn off by a catheter (according to a German practice), the paps are necessarily made to bleed by being “stripped”; it has been admitted by milkers that the blood, pus, and scabs are apt to become mixed with the milk; and the discharges from the sore paps have actually been seen, by a scientific witness, to trickle over the fingers of the milkers into the milk-pail[1360]. The contamination of the milk which produces scarlatina in those who use it is neither more nor less specific than that. The disease is blood poisoning in the double sense of the term—poisoning of the living blood by dead blood. Blood is a peculiar fluid, and so is milk. When the two come together the result is peculiar. Both are animal fluids that curdle by some peculiar ferment-change in their constituents. Again, milk is peculiar in its property of taking up organic effluvia; thus the milk standing in shallow vessels has been known to acquire the taste and odour of tar from a tarpaulin in the adjoining farmyard. With such properties of the milk, a small quantity of blood or pus in it will go a long way.

The one thing that connects the scarlatina of surgical wards in children’s hospitals and the scarlatina of the milk-pail is putrefying blood or pus: the disease is a septic effect of blood, just as a scarlet rash is known to be a toxic effect of very various drugs in peculiarly susceptible subjects. The obviously septic varieties of scarlatina make but an insignificant part of the whole; but they may be finger-post instances. Thus, if we assume that the infection may be miasmatic from the ground as well as contagious from the person, there are certain facts, or suspicions, that will fit the hypothesis of putrefying blood. A theory of scarlatina was put forward in 1871, on the basis of observations near Croydon, that its virus came from the blood and offal of slaughter-houses collected at particular spots to be used as manure[1361]. The first death in a recent small epidemic within the writer’s knowledge was of a school-girl who lived just across the road from a slaughter-house. The septic hypothesis of scarlatina might be made to include other corrupting animal matters. Some practitioners have a suspicion that scarlet fever is bred in the atmosphere of a horse-mews. On the greater scale, others have traced a connexion between the more signal outbreaks of angina maligna and preceding murrains of cattle[1362]. The animal matters which may become toxic to man, in miasmatic or other form, are indeed many. If scarlatinal drug-eruptions are any clue to the mystery of scarlet fever, we need not be surprised to find a somewhat uniform disease-effect produced by a variety of septic agents[1363]. But, in that hypothesis, the refuse of the shambles will merit most attention. This was thought the one great nuisance of London in the sanitary ordinances of Edward III., Richard II. and Henry VII.; it was then considered a danger to health in the measure of its offensiveness to sight and smell, but there may still be dangers from it which are subtle and unperceived.

Reappearance of Diphtheria in 1856-59.

The memorable outburst of epidemic throat-disease in Britain about the years 1858-59 was part of a sudden uprising of the malady all over the globe—in Europe, America, North Africa, India, China, and the Pacific[1364]. It was only in some parts of France, and of Norway and Denmark, that “diphtheria” had been epidemic in the generation before. Of its novelty to nearly the whole British profession in 1858, familiar as they were with the angina of scarlet fever, there can be no question. Its appearance among diseases coincided with the publication of Darwin’s hypothesis of the origin of species by natural selection; and it was in the terms of that hypothesis that Farr, of the Registration Department, spoke of the phenomenon of diphtheria. New diseases, he said, “are only recognized as distinct species when they have existed for some time. Diphtheria is an example. It obtains a distinct line in the Tables of this year [1859] for the first time”—with a total of 9587 deaths. For four years before that, it had been in a “provisional table” under the names of “diphtheria” and “cynanche maligna”; but in the general table, the deaths under these names had been merged with the scarlatinal deaths. This inclusion for a time of diphtheria under scarlatina could not have been because practitioners had any difficulty in diagnosing the one from the other, but probably because scarlatina anginosa seemed the nearest affinity in the nosological system. Diphtheria in 1858 had no scarlet rash, and yet it was supposed to be the same disease that had made so much commotion in England about the middle of the 18th century: “In Fothergill’s account,” says Farr, “the symptoms are confused by the introduction of the eruption of scarlatina into his description”—as if his description had been a patchwork of his fancy, with some characters taken from “diphtheria” and some from scarlet fever. The greatest of our nosologists, Cullen, had long before that separated “cynanche maligna” from “scarlatina anginosa,” but the separation was not made on the ground of absent or present rash. Both had the rash, the cynanche having, besides a general exanthem, very distinctively the peculiar scarlet redness, with swelling and stiffness, of the fingers which Fothergill described, while the scarlatina rash was “commonly more considerable and universal.” Both also might have a discharge from the nose; but when the coryza did occur in scarlatina, “it is less acrid, and has not the foetid smell which it has in the other disease.” It was really on the ground of malignancy or fatality that Cullen separated them. In forty years he had seen scarlatina anginosa six or seven times prevailing as an epidemic in Scotland, and he had seen two or three epidemics of cynanche maligna. He had seen mild cases in the latter, as well as in the former; but whereas there would be only one or two malignant cases in a hundred of scarlatina anginosa, the malignant or putrid cases in an epidemic of cynanche were four-fifths of the whole[1365]. On the other hand Willan, writing just fifty years before the modern diphtheria made its appearance, maintained that “no British author has yet described any epidemical and contagious sore-throat except that which attends the scarlet fever,” not even Starr, whose “morbus strangulatorius” he held to be “the most virulent form of scarlatina[1366].”

The name diphtheria, which appeared for the first time among the classified causes of death in England in the report for the year 1855 (published two years after), had been given originally in 1826, with the termination itis according to the then Broussaisian fashion, by Bretonneau in his account of epidemics at Tours in 1818-21 and at La Ferrière in 1824-25[1367]. It was in January, 1855, or just before the disease became general in Europe, that he changed the termination to diphtherie[1368]. This name was taken from διφθέρα, a prepared skin or hide, suggesting in strict correctness, a certain toughness and texture which were actually found in only a small proportion of all the diphtheritic deposits or exudations or sloughing infiltrations in the first great epidemic and subsequently.

The interval between 1793-94, the date of Rumsey’s diphtheria or “croup” at Chesham, and the outbreak of diphtheria in England in 1856-59, affords several instances of the disease, some of which were contemporaneous with Bretonneau’s in France, but were still called “croup” in this country. These I shall merely enumerate in a note, passing at once to the beginnings of the great outbreak[1369].

The first public notice of the reappearance of a fatal throat epidemic in England appears to have been in the Registrar-General’s third quarterly report of the year 1857, when attention was drawn to the remarks by various local registrars (Thame, Billericay, Maldon, Liskeard, Truro and Chesterfield) as to fatalities from “inflammation of the throat,” “putrid sore throat,” “malignant sore throat,” “disease in the throat,” and “throat-fever.” About this time it was also called the “Boulogne sore throat.” There had been an epidemic at Launceston from 30 September, 1855, which had come to a height in August, 1856; several deaths had occurred near Spalding, in Lincolnshire, in July, 1856, and the disease had been seen at Ash, in Kent, in November, 1856. When the registered causes of death during the year 1855 were classified (in 1857), “diphtheria” was credited with 186 deaths, in the Supplementary Table then first introduced, “cynanche maligna” having 199 deaths. The following shows the progress of the epidemic during the four first years, and the mode of entry:

In 1857 and 1858 the deaths from croup were above the average, and probably included some of the new disease.

Accounts of the epidemic began to come into the medical journals[1370] from various localities in the course of 1858,—from Lincolnshire, Essex, Kent, Sussex, etc. A systematic inquiry, conducted by Greenhow and Sanderson for the Medical Department, under the direction of Simon, gave an exact picture of the several degrees of throat-distemper that constituted the epidemic in the year 1858, in certain of the more severely visited centres of Lincolnshire, South Staffordshire, Cornwall, Kent, and other counties[1371]. The numerous cases of throat disease occurred often in the midst of scarlatina, but sometimes also where there was no scarlatina. One of the worst centres was in and around Spalding, a market town situated in a flat grazing country within the fen district of Lincolnshire. A thousand cases were counted in and near Spalding, many of them mild, a small ratio of them gangrenous and mortal; one practitioner had 200 cases with 5 deaths, another 200 cases with 2 deaths, another 160 cases with 17 deaths (of 65 tabulated with 9 deaths, which occurred in 35 houses, the first four all died from gangrene in June, 1858). The doctor at Pinchbeck, in the same district, had some 500 cases of which 300 occurred in the space of about six weeks; most of the 19 deaths in his extensive series happened in the first cases (this was observed also in the New Hampshire epidemic of 1735). At Launceston, in Cornwall, there were about a thousand cases known, the height of the epidemic having been in the summer and autumn of 1856; among 126 taken as they came in 98 families, 18 died. The mildest and the most severe cases were equally parts of the epidemic constitution, and occurred side by side in the same households; many of them were quinsies, ulcerated sore-throats, or the like, others were gangrenous. In this great variety, only a part could be reckoned “true diphtheria.” From the first, the remarkable sequel of paralysis, not only of deglutition but of the motor powers generally, was remarked here and there. Sometimes an eruption of the skin was seen, but desquamation did not occur[1372]. Albumen in the urine was somewhat constant. It is noteworthy, the more so that the coincidence was not remarked at the time, that the true diphtheritic pellicle,—tough, leathery, elastic,—was found most distinctively, if not exclusively, where it was found in 1748, namely in Cornwall[1373].

Although the epidemic was not confined to low and damp situations, yet there was no mistaking the severity of it in Lincolnshire; and although it fell upon both clean and filthy houses, yet it is probable that the cases with most pronounced gangrene or foetor happened amidst the most unwholesome surroundings. The disease was very general in England in 1858. When the deaths from it in 1859 (9587) were tabulated for the first time according to counties, it was found that they came from every part of England and Wales. The highest death-rate was in Lincolnshire, 1·2 per 1000 on the annual average of 1859 and 1860 (995 deaths in the two years). Sussex, Kent, Essex and Norfolk had also high death-rates, the agricultural counties in general having somewhat more than their usual share of an infective mortality as compared with the industrial centres. But it would be erroneous to suppose that diphtheria was at all specially a country disease. The mining districts of Staffordshire, Durham and South Wales had considerable mortalities, and so had Lancashire and the West Riding. But the North Riding and East Riding had their full share or even more than their share; whereas, if it had been scarlatina or enteric fever, they would have been far behind the great industrial division of Yorkshire in ratio of their populations. In the more recent prevalence of diphtheria the country districts have lost their preeminence, according to the following table of death-rates per million living in registration districts classified roughly as sparse, dense and medium[1374]:

Diphtheria Death-rates per million, according to density of population.

In Scotland, also, the incidence was the same: e.g. in 1862, of 997 deaths, 360 were in the towns, 617 in the mainland rural and 20 in the insular districts[1375].

The law of incidence of diphtheria upon town and country respectively has become a good deal confused by the extraordinary severity with which diphtheria has fallen in the last two or three years upon most parts of London and upon the adjoining municipal boroughs of Croydon and West Ham. The following table compares the annual death-rates per million in all England and Wales and in London from the year of the first recognition of diphtheria to the present time.

Death-rates from Diphtheria per million, in all England and in London.

The deaths in London in 1893 were 3196, having been 1962 the year before, but never more than half the latter total in any year previous to 1888. Besides Croydon and West Ham, Cardiff is the great town which has come nearest the London rate, having had O·68 deaths from diphtheria per 1000 living in 1892, while Swansea had only 0·05, Wolverhampton (including Bilston and Willenhall) only 0·06, Huddersfield 0·03 and Blackburn 0·02. In London the very high death-rate of 1893 was distributed not unequally over all the divisions, the highest mortality corresponding to the highest fecundity.

Diphtheria in London in 1893.

Diphtheria shows no such decided preference for the late autumnal or early winter season as scarlatina, but the winter is on the whole its most fatal season, according to the following annual averages of the quarters of the year for twenty years from 1870 to 1889 (total of 67,676 deaths in England and Wales).

Annual average of Diphtheria deaths in the quarters of the year.

According to some recent returns under the Notification Act, which are of doubtful value owing to the laxity of diagnosis (greater perhaps in throat-disorders than in any other class of diseases), the second and third quarters of the year have also the lowest mortality in proportion to the number of attacks[1376]. As to the ages at which diphtheria proves fatal, they are somewhat similar to those of fatal scarlatina, but slightly higher all over; thus, while two-thirds of the deaths from scarlatina are of infants and children under five years, only one-half of the deaths from diphtheria are under that age. In the first epidemic period, 1855-61, Farr reckoned that 1553 adults had died of diphtheria above the age of twenty-five, while the deaths under that age had been 28,216. In its age-incidence diphtheria is very different from croup, which attacks chiefly children of one, two, and three years of age, the boys dying in greater numbers than the girls[1377]. But in all comparisons between diphtheria and croup, as regards sex and age, it should be kept in mind that many cases of angina of the throat, which end in death by extension to the larynx and trachea, are registered as croup, even in epidemics. Diphtheria is the only epidemic disease besides whooping-cough which is more fatal to female children than to males in proportion to the numbers of each sex living. The following annual average death-rates per million for the period 1855-80 show the higher death-rates of females at certain age periods[1378]:

It is not until the third year that female children begin to die of diphtheria in excess of males; which means that the usually greater risk to male infants holds good also in this disease for the two first years, while some difference between the sexes becomes thereafter so marked as to turn the balance of fatality to the side of the females. Something of the same kind happens in whooping-cough; and it is probable that in both maladies the cause lies in the earlier acquisition by the male of secondary sexual characters in the throat and larynx, as suggested in the chapter on whooping-cough.

Conditions Favouring Diphtheria.

The circumstances of the great and sudden explosion of diphtheria in 1858 and 1859 are as likely as any to throw light on the causes or determining conditions of the disease. Those two years were remarkable for the Thames running so low in summer as to give out a stench, which was thought to forebode much fever[1379]. The expected epidemic of fever did not come; on the contrary the fever deaths in London were much lower than usual in 1858 and 1859, and, to judge from the few admissions of each kind to the London Fever Hospital, enteric fever declined as well as typhus[1380]. It was diphtheria that came. The lowness of the rivers was due to a succession of years with rainfall below the average:

The low state of the rivers was an index of a low level of the ground-water. If diphtheria is to be included among the infections that have the habitat of their virus in the soil, it will probably be found to be affected by irregularities in the movements of the subsoil water. A series of observations have been made which seem to favour that hypothesis.