to the home to give it in curative or in immunizing doses as you may direct.

There is no excuse at the present time for neglecting to inmunize those exposed to diphtheria. I question if you could defend yourself comfortably in a legal action if you were called upon to prove that you had used "reasonable care" when you had neglected to immunize a family, if those exposed subsequently developed the disease, and the family then proceeded against you.

There seems to be a rational method of dosage even in immunizing. I would recommend for the household 500 units for those not directly exposed, 1,000 units for those directly exposed, and 1.500 units if any sign of illness were present.

I have not yet seen a case of diphtheria develop where a patient had been immunized at the time of exposure or soon after.

In conclusion, I would remind you that in New York City (Manhattan and the Bronx), Brooklyn, Chicago, and Philadelphia, 18,121 lives have been saved through the introduction of antitoxin as a curative and prophylactic agent in the treatment of diphtheria.

The death rate in diphtheria hospitals has been greatly reduced and in many instances cut in half by the introduction of serum therapy. We would plead for a dose of antitoxin in proportion to the amount of exudate and location of the exudate. We would urge a large dose of antitoxin in nasal, nasopharyngeal, and laryngeal diphtheria. We would plead for the general use of antitoxin earlier in the disease. We would plead for more general use of antitoxin as a prophylactic measure in a dose proportionate to the amount of exposure and time of exposure.

BY R. W. MARSDEN, M.D., M.R.C.P., HON PHYSICIAN,

ANCOATS HOSPITAL, ETC.

(Continued from June No., page 370)

Macewen1 gives an account of a clerk who was apparently strong and healthy till fifteen years of age, when he had a severe attack of scarlet fever, which apparently initiated a series of symptoms culminating in marked manifestations of rickets. There is no further statement from which suggestive evidence for or against rickets in infancy can be obtained, and it may be that, from the profound change produced by the severe attack of scarlet fever, this is one of the very rare instances where the most detailed examination would fail to have revealed indications of rickets in infancy; but this point must remain inconclusive.

A consideration of the above cases is, to say the least, suggestive of the fact that in most instances of so-called late rickets there has throughout life been some interference with the normal growth of bone, and calls forth the question whether the evident arrest of development seen in several of the cases, even though unaccompanied by an epiphysial enlargement or bony deformity, may not have been of a rachitic nature. Can it be that the rachitic process is in a sense capable of becoming quiescent: ossification and growth being deficient, but the process insufficiently active to produce the characteristic morphological changes until a further factor is added, e.g., puberty, violent exercise, a severe illness, etc.? It is possible that the use of the Röntgen rays in future cases of defective development may throw some light upon this point. Late rickets being then of an essentially identical nature to infantile rickets, it is evident, as suggested by Clutton, that there may be three possible modes of origin. Thus it may be that it occurs for the first time at the later period of life in an individual previously quite healthy. Secondly, it may be that an attack of rickets in infancy does not completely subside, so that, from defective treatment or superadded cause, a relapse occurs, and the process again becomes active. Thirdly, it is possible that the attack of infantile rickets may completely be recovered from, and after a variable period of normal growth a recurrence takes place. It is evident that, in the present state of our knowl

edge, cases belonging to type (2) will seldom enter into question; and most writers would agree with Clutton, even though they did not limit, like him, the age of the patients to a definite number of years, that a continuous and clear connection with infantile rickets excludes inclusion in the late variety.

It would seem that Ollier' was the first, in 1861, to attribute many of the bony deformities of later childhood and adolescence to rickets, which had previously been considered to be due to osteomalacia. He spoke of a primary form, agreeing with Clutton's first type, and of a secondary form, identical with the latter's third type. In addition, he noted the rarity of the primary form, and pointed out the difficulty of making the diagnosis, on account of the frequent impossibility of proving the absence of rickets in infancy.

I have already dealt with this question; and though not denying the occurrence of the primary form, have suggested that it is still rarer than is usually believed, since, on account of a less limited view of the manifestations requisite for the suspicion, if not the diagnosis, of rickets, I consider it possible that even such apparently typical cases of the primary form as those reported by Clutton, Roos, and myself may in future be shown, by an extended observation through life, with the assistance of the Röntgen rays, to have exhibited previous signs of rachitic changes at the growing ends of the bones.

Deydier18, a pupil of Ollier, subdivides the latter's classification into a general form, which is rare, and into a local form, in which only one, or a few, regions of the bony skeleton are affected. The local form, he says, is much commoner, and includes the cases of so-called idiopathic genu valgum and varum, as well as scoliosis, which develop in adolescence.

Deydier made the above classification in 1895. Clutton, writing nine years previously, excluded from the heading of late rickets those cases of bending of the bones about puberty or later, which occur without epiphysial enlargement. Such cases he considers to be "due to a want of proper consolidation of the bones in proportion to the increasing weight of the body." He would admit cases, such as the five described by Lucas1o, where, in youths from twelve to seventeen years of age, scoliosis, or genu valgum, was in each instance accompanied by enlargement at the epiphysial ends of one or more of the

long bones of the limbs. I have previously stated that, in my opinion, epiphysial enlargement, though of the greatest importance, is not a sufficiently reliable test of the presence or absence of rickets; and this view is strongly supported, if not verified, by the evidence which we possess on the point under consideration.

Mikulicz20, in 1879, after an extended observation conducted on the lower end of the femur in normal and abnormal cases, found that the whole breadth of the epiphysial cartilage in the frontal section of a normal femur during the period of growth is 1 to 2 mm. On the other hand, in a youth with slight genu valgum, he found that there was a considerable broadening of the epiphysial cartilage. The enlargement especially affected the columnar layer of growing cells, which had a breadth of 2 to 3 mm., whereas in the normal condition it was only onehalf mm. Moreover, he states that "the macroscopical and microscopical findings agree so remarkably with the changes which one recognizes as characteristic of rickets, that here. we can rightly say there is present a rachitic broadening of the epiphysial cartilage."

Thiersch

also reports the case of a girl sixteen years of age of rachitic build, with genu valgum, who died with evidence of advanced contracted kidneys, whilst "the epiphysial cartilage showed the irregular growth which is characteristic (zukommen) of rickets."

Others writers, in addition to genu valgum, have included cases of scoliosis and flat foot. Tripier22 having stated that rickets appears more especially at the times when the normal growth of the skeleton is most rapid, finds that genu valgum is most likely to arise at various ages at which the "height of the conjugating cartilage of the lower extremity of the femur is increased," which he considers, I think erroneously, tantamount to saying that growth in height is more active. He is fully aware "that some writer will object that this greater height of the conjugal cartilage is a rachitic lesion," but he considers that Broca has shown that more than an increase in height is necessary to characterize a rachitic alteration. I have been unable to find this communication by Broca.

Without entering any further into the bibliography of this subject, I think we may accept Macewen's 23 conclusions that

osseous deformities of the lower extremities (knock-knees, bow-legs; and various femoral and tibial curves) originate in rickets, since

(1) Their etiology is identical-some cause of severe and prolonged debility. (2) Rickets and these osseous deformities abound in the same individual. (3) The period of life during which these deformities occur is limited and is identical with the period during which rickets attacks the body-the period of growth. (4) Deformities which are physically identical with those above mentioned arise from rickets, and in the few cases examined the histological characters are the same.

Accepting Ollier's basis, then, for the classification of cases of late rickets, and supplementing Deydier's addition, we may recognize the following types:-(A) A general affection, which may be (1) primary or (2) secondary. (B) A local affection, which may be (1) primary or (2) secondary.

Late rickets being a rare disease, but of an essentially similar or identical nature to the common infantile form, it is natural to inquire whether its supervention throws any light upon the much disputed pathology of the rachitic process.

I think it may be safely asserted that rickets is a disease sui generis; that is to say, that it is a distinct entity, even though it exhibits, like other diseases, multifarious manifestations. On this account, therefore, it is only natural to expect that either it will always be caused by the same etiological factor, or, if many factors are concerned, that they will show a very close connection, to explain their similarity of action. A moment's reflection will show that the second suggestion offers the readiest solution of the difficulty, since by such means only can we hope to combine the numerous influences which have been proved to be concerned in the causation of rickets.

At the present time it is generally recognized that rickets is not simply a disease of the bones, but a general affection, of which the enlarged epiphysial ends, and bending of the shafts, etc., constitute the local, but more or less disseminated, indications.

Though, as stated by Sir William Jenner24, "we see all degrees of enlargement of the ends of the ribs, and of the other long bones, from that where one might maintain the enlargement was only that proper to the child, to that in which