ETIOLOGY.--The exact nature of the measles contagium has never been

satisfactorily established, although we are in possession of numerous

researches in that direction, which, however, are to a great extent

contradictory. A brief examination of these various observations will

not prove uninteresting. Hallier found in the blood and sputa numbers

of free cocci, which fructified upon various substrata, but was

invariably the same fungus--mucor mucedo verus, Fres. In 1862,

Salisbury[3] published {558} his observations on the relation of the

straw fungus to measles. He recorded instances of inoculation with

this organism that resulted, according to him, in the production of a

modified form of rubeola, and, moreover, was protective against

further attacks of the same disease. In an exhaustive paper bearing on

this question H. C. Wood[4] quotes certain experimental inoculations

made by William Pepper, which showed conclusively that measles was not

propagated in this way, and that where any symptoms were developed

they were not those of true measles, nor did they protect the subjects

from unquestioned measles. Salisbury also claimed that measles had

occurred in camps where damp and mouldy straw had been employed for

bedding. J. J. Woodward in his work on _Camp Diseases_ points out that

camp measles prevailed almost exclusively in regiments from the rural

districts, while men enlisted in towns and cities were more or less

completely exempt. The explanation was, that those from the country

had hitherto escaped the disease, while townspeople had suffered from

it at some previous time--a condition of affairs inconsistent with the

theory of the straw fungus. Coxe and Felz found numerous bacteria in

the blood of measles patients, especially in regions where the

eruption was most pronounced. The nasal mucus also contained similar

germs. Inoculation of the blood from the subjects of measles upon

rabbits did not produce an analogous affection (Thomas). Klebs[5]

obtained micrococci from the trachea and from blood taken from the

hearts of infant cadavers. "In the latter, collected in flattened

capillary tubes, there developed balls of micrococci; in the trachea

both micrococci and bacteria were present in large quantities. Under

observation, pale, finely-granular micrococcus balls developed and

changed very quickly to bacteria, which moved about very actively.

These sought the periphery, about 1/2 mm. distant from the centre of

development, and formed a zone, comparable with a hedge or fence that

is composed of rods. From this were formed new masses of micrococci,

but further no regular process of arrangement or development could be

observed."

[Footnote 3: _Am. Jour. Med. Sci._, July and Oct., 1862.]

[Footnote 4: _Ibid._, Oct., 1868, p. 333.]

[Footnote 5: _Würzbr. Verh._, N. F., v., 1874, quoted by Forchheimer

in Supplement to _Ziemssen's Cyclopedia_, W. T., 1881, p. 102.]

Braidwood and Vacher,[6] as the result of a number of experiments,

believed that they had sufficient evidence for concluding that the

most active mode of the transmission of measles was through the

breath, and accordingly instituted a series of experiments by

carefully examining the breath of children in the acute stage of the

disease.[7] With this object in view they coated over with glycerine

the inside of several clean glass tubes of a diameter of a half to

three-quarters of an inch. As soon as the nature of the eruption was

manifest the patient was required to breathe through one or more of

the tubes, and so on each day till the eruption had faded. Upon

examination of the glycerine with an one-eighth objective every

specimen showed numerous sparkling bodies, something like those found

in vaccine, but larger. Some were spherical; others were elongated,

with sharpened ends. They were most abundant during the first and

second days of the eruption. Healthy children and patients suffering

from typhoid and scarlet fevers were made to imitate these {559}

experiments, but no such bodies were to be seen in their specimens.

They conclude from these observations that the small spherical

elements discovered in the breath are perhaps the active agents in the

propagation of measles. Upon post-mortem of patients who had died of

rubeola these germs were found in the lungs and liver, and,

particularly, close to the walls of the capillaries. They believe that

the "lungs are the favorite breeding-ground of the contagium."

[Footnote 6: _Brit. Med. Jour._, Jan. 21, 1882.]

[Footnote 7: Several years ago Ransome of Manchester obtained

particles from the breath of two persons suffering from measles

(Squire).]

That inoculation of morbillous blood may convey the disease was first

demonstrated by Home in 1757, which experiments were verified by

Speranza in 1822 and by Katona in 1842. The inoculations of the latter

are especially noteworthy, as they numbered more than a thousand. No

person inoculated by him died, and only 7 per cent. of the

inoculations failed. On the other hand, inoculations made by Mayr gave

negative results. It is stated that Monro and Locke communicated

measles by inoculating with the tears and saliva. Attempts of the same

kind were fruitlessly made in Philadelphia in 1801, although the

blood, the tears, the nasal and bronchial mucus, and the exfoliated

lamellæ of the epidermis were successively employed in the trials.[8]

[Footnote 8: Rayer, _Diseases of the Skin_, Phila., 1845.]

Mayr has shown that the nasal mucus is capable upon inoculation of

propagating the disease. He performed the experiment upon two healthy

children living at a distance from each other, at a time when the

disease had ceased to be epidemic. Some nasal mucus taken from the

patient during the stadium flavitionis, and kept fluid in a glass

tube, was the same day placed upon the mucous membrane of each of

these children. In one of them the first symptom of sneezing occurred

after eight days, in the other at the expiration of nine days. Febrile

symptoms set in two days later. In each child the rash appeared on the

thirteenth day after infection. The inoculated disease was mild and

regular in its course.

While it is perhaps true that the contagion of measles is not so

tenacious as that of small-pox and scarlatina, it is a matter of

observation that susceptible persons are liable to contract the

disease, even if not directly exposed to its influence. There is

incontestable evidence that it is conveyed by fomites--a fact well

worth bearing in mind.

It is but just to say that so excellent an observer as Mayr taught

that measles could not be conveyed by clothes, linen, etc. unless

transferred immediately from one individual to another. Panum,

however, showed that contagion could be carried many miles by an

unaffected third person without losing its activity. Aitken[9] has

also pointed out the fact that children's clothes sent home in boxes

from schools where the disease has raged communicated the disease, and

that susceptible children who had slept in the same beds, in the same

rooms, after they had been occupied by persons suffering from measles,

have taken the malady. Squire observes that the contagium of measles,

except in the catarrhal stage, is not far diffusible in the air, but

clings to surfaces, and may be thus carried from place to place; on

the other hand, children have been brought, while in full eruption,

into a house among others, and nursed in a room apart, without any

extension of the disease to the most susceptible.

[Footnote 9: _Science and Pract. of Med._, Phila., 1868.]

{560} Various circumstances render it probable that measles is most

readily propagated during the stage of efflorescence; but that it is

also highly infectious during the prodromal period is now universally

acknowledged.

According to Niemeyer, the probability of infection during the

prodromal stage is supported by the wonderful spread of measles

through schools; for, while the strictest surveillance is established

over children with any suspicious eruptions, and those known to have

had the disease are not allowed to return till long past the stage of

desquamation, no heed is paid to those exhibiting the premonitory

cough and coryza. There is no reason for believing that measles can be

propagated during the period of incubation; on the other hand, there

is no satisfactory argument for the denial of its infectiousness in

the desquamative stage. Although Panum is inclined to doubt its

contagiousness at this time--and his observations are worthy of the

greatest confidence--other good authorities differ from him

materially, and extend the stage of personal infection to a period of

from three weeks (Squire) to forty days (Hillairet).

Reasoning from analogy, we would naturally expect that the period of

incubation in measles suffered a certain amount of variation; the

result of numerous observations confirms this expectation. It is

manifestly a difficult matter in densely populated communities to

establish with accuracy the date of a given infection, but from a

study of more or less carefully noted cases it will be found that the

period of incubation may vary from three to thirty days. For the vast

majority of cases the average time between the reception of the

measles poison and the appearance of the characteristic eruption will

be about from thirteen to fourteen days. Panum, under exceptionally

favorable surroundings, found it more frequently fourteen than

thirteen days. Therefore, deducting the three or four days occupied by

the invasion stage, we shall find that the real incubation period is

from nine to ten days from the date of exposure. Mayr's two cases of

inoculation with nasal mucus showed no departure from this rule, but

in the inoculations made by Katona with blood the prodromic symptoms

made their appearance in seven days, the cutaneous lesions developing

two, and at the most three, days afterward.

Minor epidemics of measles are said to occur every three to five

years, more extensive and severe ones every seven or eight years. In

the centres of population measles may be said to be endemic; in

isolated regions the visitations of the disease may be widely

separated. Measles is a less severe disease in warm than in cold

climates, and, as a rule, we also find the affection more common and

more intense in the fall, winter, and spring than in the summer

months.[10] Epidemics of measles are usually short, and it is thought

that there is a definite relation between the severity of their onset

and their duration, this being in general short in proportion as the

given epidemic was at first severe (Mayr). Intestinal complications

are more frequent in summer, and involvements of the respiratory

organs more common in winter. The varying aspects of different {561}

epidemics--sthenic, asthenic, etc.--depend on changes in the weather,

season of the year, the presence of complications, and other agencies

not very clearly understood. Epidemics of whooping cough may precede,

accompany, or follow in the wake of measles, and it has therefore been

suggested that it stands in some peculiarly close connection with the

latter; but, aside from this often-observed coincidence, we are not

justified in our present state of knowledge in assuming any definite

relation of cause and effect between the two diseases.

[Footnote 10: Aitken (_op. cit._, p. 295) declares that the mortality

returns from England and Wales show that the influence of season is

most trifling. Occasionally it has been found that the deaths in

summer exceeded those in winter, but we believe that the statement

made above is, in the main, correct. For instance, Parson's figures

for Berlin for the years 1863-67, inclusive, are: spring, 11.9 per

cent.; summer, 13.3; autumn, 33.4; winter, 41.4. Voit's statistics in

an average of thirty years at the Children's Clinic at Würzburg

establish the same general principles (Thomas).]

There would seem to be neither geographical nor racial bar to the

propagation of measles, for it has been observed in all countries and

among all peoples. As in the case of other zymotic diseases, a

tolerance is established for measles in countries where the disease is

more or less constantly prevalent; but where the affection becomes

epidemic for the first time, or reappears after many years, it rages

with terrific violence. This fact was particularly exemplified in the

epidemic in the Faroe Islands, and more especially in the recent

(1877) visitation of the Fiji Islands, where one-fourth of the

population succumbed in a comparatively short time.

It is quite probable, as asserted by Mayr, that children affected with

scrofulous complaints, as well as those who are the subjects of

diseases of the respiratory organs--pertussis, bronchitis, or

tuberculosis--are eminently susceptible of measles; but his statement

that sufferers from epilepsy, chorea, and paralysis exhibit an unusual

power of resistance cannot be accepted without reservation. Acute

diseases often appear to delay the outbreak of measles, so that the

latter does not appear till convalescence from the former (Thomas).

The development of vaccinia is occasionally interfered with by an

attack of rubeola; on the other hand, the two diseases may be seen

running their courses together.[11] The emphatic statement made by

Hebra, that measles is never seen to occupy a patient simultaneously

with another acute exanthem, has not been confirmed by other

observers. My own experience furnishes several examples. Measles may

also occur during the course of other acute or chronic maladies. From

a study of the literature of measles complicating pregnancy and

parturition Underhill[12] finds it to be quite uncommon, due probably

to the fact that most adults are insusceptible of further attacks; but

when it does occur in pregnancy he regards it as a very serious and

frequently fatal complication. Underhill believes measles to be most

fatal when it supervenes soon after delivery, while those who are

confined during the course of the malady stand a better chance of

recovering from it. That puerperal women are not always unfavorably

affected by measles is well shown in two remarkable cases reported by

Nelson[13] of St. Louis and Chantier[14] of Geneva, in which the

mothers were safely delivered, though suffering from measles

contracted at the end of their pregnancies.

[Footnote 11: Hardaway, _Essentials of Vaccination_, p. 60.]

[Footnote 12: _Obstet. Jour. Great Britain and Ireland_, July, 1880.]

[Footnote 13: _St. Louis Courier of Med._, Sept., 1879.]

[Footnote 14: _Annales de Gynécologie_, May, 1879.]

All ages are susceptible to the measles poison, and the apparent

exemption enjoyed by adults is due to the fact that most grown-up

people have already suffered the disease in childhood; but in Panum's

epidemic, mentioned above, it was discovered that nearly all who had

not had measles {562} elsewhere, or were not old enough to have been

exposed at the last visitation, sixty-five years before, acquired the

affection regardless of age. It is quite probable, however, that the

law of decrease of susceptibility with age holds good for measles as

well as for variola, etc., but to a less degree. It will therefore be

seen that measles is not essentially a disease of childhood. Although

there is no special limit to the susceptibility of rubeola at one

extreme of life, it would seem to be quite well established that it is

much modified at the other--namely, that infants under six months are

rarely attacked. This latter fact is conceded by individual

experience, by the records of epidemics, and by the testimony of most

observers.[15]

[Footnote 15: On the other hand, as quoted by Forchheimer (_loc.

cit._), H. C. Fox publishes some tables which show that for England

and London a much larger number of young children are attacked by

measles than other statistics would lead us to believe.]

+-------------+-------------+

| England. | London. |

+------+------+------+------+

| | Fem- | | Fem- |

|Males.| ales.|Males.| ales.|

---------------------------------------+------+------+------+------+

Under one year | 3022 | 2530 | 3571 | 2987 |

One and under two years | 6086 | 5825 | 8630 | 8050 |

Two " " three " | 3178 | 3255 | 4683 | 4757 |

Three " " four " | 1730 | 1851 | 2594 | 2620 |

Four " " five " | 980 | 1028 | 1358 | 1466 |

|------+------+------+------|

|------+------+------+------|

Five and under ten years | 255 | 278 | 301 | 316 |

Ten " " fifteen " | 29 | 38 | 24 | 32 |

Fifteen " " twenty " | 9 | 13 | 9 | 11 |

Twenty " " twenty-five " | 7 | 9 | 5 | 7 |

Twenty-five " " thirty-five " | 5 | 8 | 5 | 7 |

Thirty-five " " forty-five " | 3 | 5 | 2 | 3 |

---------------------------------------+------+------+------+------+

Even sucklings do not enjoy a complete immunity from measles.

Steiner[16] states that he has met with it in children only four or

five weeks old. Monti has recorded ten cases of rubeola in children

under two months of age. A case is reported by Kunze where a mother in

the stage of efflorescence gave birth to a child, which contracted the

disease five days afterward. Quite a number of cases of congenital

measles have been put on record from time to time; but Thomas, after a

careful investigation, says that he has been able to discover but six

authentic accounts of such occurrences.[17] That children born to

mothers suffering at the time of parturition from measles may yet

escape it themselves is proven by the cases of Nelson and Gautier

mentioned above. Whether a pregnant woman attacked by measles

transmits the disease to the foetus in utero, thereby securing

immunity from it in after life, is a question difficult of decision,

especially as we have not yet been able to decide this same inquiry,

with infinitely better opportunities, for vaccinia.[18]

[Footnote 16: _Compendium of Children's Diseases_, N.Y., 1875, p.

396.]

[Footnote 17: I believe that, under certain circumstances, the

erythema papulatum of the new-born is often mistaken for measles.]

[Footnote 18: See experiments of Burckhardt, Rickett, Gart, and

others, quoted in Hardaway's _Essentials of Vaccination_, p. 38.]

There is no good reason to believe that sex is of much importance in

establishing a predisposition to measles, although the statement has

been repeatedly made that males are more frequently attacked than

females. {563} Fox's statistics show a slight preponderance in favor

of the male sex; but a careful examination of accessible statistics

proves, as would be expected, that this degree of susceptibility

varies at different times in obedience to circumstances not readily

understood.

By the older writers (Willan, Rosenstein, Fuchs) it was very

dogmatically asserted that one attack of measles completely

extinguished all future susceptibility to the disease. Of late years

this dogma has met with much opposition, and numerous observations

have been recorded which, if entirely trustworthy, would lead us to

believe that rubeola may occur not only twice, but several times, in

the same individual. While from analogy and actual experience we are

quite sure that the recurrence of measles is not so uncommon an event

as it was once held to be, a closer examination of the question in all

its bearings clearly confirms us in the belief that subsequent attacks

are much more infrequent than is now thought to be the case by many,

and that other diseases, more or less resembling true measles, are

largely responsible for errors of diagnosis in this regard. Panum

found that all the old people who had measles during the epidemic on

the Faroe Islands in 1781 escaped it in 1846. Both Rosenstein and

Willan declared that they had never witnessed an instance of the true

recurrence of measles. Among other facts, it may be stated in this

connection that Woodward (_loc. cit._) has shown that during our late

war, while members of regiments recruited from the rural districts,

who had never before had measles, largely took it when exposed to its

influence, regiments from the cities, who had presumably acquired the

disease in childhood, remained almost entirely exempt.[19] Other

arguments of a similar sort could be readily adduced. There is no

question that mistakes in diagnosis have occurred from confounding

rötheln, roseola, etc., which closely simulate measles, with that

disease. Those particularly engaged in the treatment of cutaneous

affections could multiply instances of such errors. It is quite

significant that for certain analogous infectious diseases--_e.g._

variola and scarlatina--the same frequency of recurrence is not

claimed, although as a matter of fact they do occur. The explanation

would seem to lie in the fact that neither small-pox nor scarlet fever

is so closely counterfeited by other skin affections, notably by

rötheln, as is measles. But it would be entirely contrary to analogy

and indubitable experience to go to the extreme of the older writers

and absolutely deny the possibility of second, and even third, attacks

of rubeola. The frequency of such cases is, however, as Henoch[20]

truly states, much overestimated.

[Footnote 19: These observations of Woodward were made without any

reference to the question at issue.]

[Footnote 20: _Lectures on Diseases of Children_, N.Y., 1882, p. 282.]

Occupying quite a different position from the measles induced by

reinfection from without are the so-called relapses of rubeola. These

relapses, which may occur in from two to four weeks after the original

invasion, are analogous to the similar occurrences in scarlatina and

typhoid fever. I am cognizant of but a single case of this sort, but

Steiner and other accurate observers record a number of such

instances.

SYMPTOMS AND COURSE.--It is generally stated that the stage of

incubation exhibits no symptoms whatever; but it is undoubtedly true

that the patient will sometimes appear dull and listless, and, on

occasion, even give evidence of some slight and ephemeral elevations

of temperature. {564} As a rule, however, this period is devoid of any

marked indication of the presence of the measles poison in the

system.[21]

[Footnote 21: Some writers describe a much more marked train of

symptoms as prevailing at this time than seems warranted by general

experience, and Rehn has gone so far as to declare that the prodromal

period, as usually understood, properly commences in the stage of

incubation. Bohn is inclined to a similar view. The prodromic stage of

authors is, then, to be looked upon as the "period of the mucous

membrane exanthem."]

The prodromal stage is usually ushered in by symptoms of general

malaise, fretfulness, more or less frontal headache, shiverings,

nausea, loss of appetite, excited sleep, and sometimes delirium.

Vomiting is not so common in measles as in scarlatina, and may occur

at any time previous to the appearance of the rash. The tongue is apt

to be coated, although it may remain clean; the taste is bad, and

pressure over the stomach and bowels occasionally elicits considerable

pain; an aching pain over the sternum is also noted. As a general

thing, at this time patients are drowsy and inclined to sleep much.

Meigs and Pepper found this a very constant symptom, which they state

is in no way alarming unless associated with other more serious

symptoms of local or general disturbance. Constipation is present in

some cases, or the bowels may be relaxed or remain in their natural

state.

The prodromal fever of measles follows a peculiar course. It is

remarkably remittent in character, and is rarely of such intensity as

to threaten life, as is often the case in scarlet fever. The

temperature will rise on the first day to 102°-104° F., and the height

of the fever at this time will measurably foreshadow the character of

the subsequent course. On the second day of the prodromal stage the

fever suffers a marked remission, or may even entirely disappear, to

again rise in the evening. Smith has observed two exacerbations in the

day. Again, in some instances, after the high initiatory fever, the

temperature may remain normal till just before the rash comes out

(Bohn). It is this peculiar behavior of the fever, together with the

fact that the child may regain its usual vivacity in the fever-free

intervals, which so often misleads the physician into the diagnosis of

malarial poisoning.

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