NationalLibraryOfScotland/medical-history-of-british-india huggingface dataset:
Hereditary Transmission and Predisposition.
207
neither case were any tubercles found in the fœtal organs,
though the presence of tubercle bacilli was proved by micros-
copical observation and animal experiment. The foetus was
still born in either case, and there is thus much room left for
speculation as to the ultimate fate of the child, if it had lived.
A distinction must clearly be drawn between a congenital or
hereditary disease and an infection from the parent through the
placental circulation of the child. Instances of congenital
tuberculosis have been recorded from time to time, but still are
so extremely rare and often also so uncertain as not to invalidate
the above statement.
When the influence of heredity in a disease such as
leprosy is under discussion, and it is known or proved that the
disease itself is not the thing transmitted from parent to child,
but only the predisposition to it, great care and caution must
be exercised in finding out how far in each case the congenital
predisposition has not only been inherited, but also inherited in
a legitimate manner. That is, this question must be consider-
ed, how far the leprosy of the child is due to the leprosy of its
ancestor and how far due to other morbid conditions of the
parent, which may have transmitted a congenital predisposition
to the child. It must not be forgotten that in leprosy as in
tuberculosis a predisposition is necessary for the disease to
appear at any time. This predisposition may be due to many
agents and factors, and it may therefore be quite possible that
the factors which produced the predisposition in the parent,
quite apart from the resulting leprosy, may be the cause of the
congenital predisposition transmitted to the child. This, how-
ever, would not be a legitimate inheritance. Now, where
practical questions regarding heredity are under consideration,
which may result in such measures as separation of husband
and wife or interdiction of marriages between the affected, it
is of the utmost importance to study the influence of the
disease itself in causing a specific predisposition in the offspring.
The fact, acknowledged equally for tuberculosis and
2o8
REPORT OF THE LEPROSY COMMISSION:
leprosy, that the diseases occasionally " skip a generation,"
speaks strongly in favour of a more general than specific
form of inheritance, and hence also for the possibility that a
non-tubercular or non-leprous condition of the parent may
cause the predisposition in the child necessary for the develop-
ment of tuberculosis or leprosy, as the case may be.
" With tuberculosis it is certain that in the congenital and
developmental conditions of the offspring there is nothing of a
dyscrasia. When in a tubercular family one child after another
dies of tubercular arachnitis, this proves the existence of a
specific dyscrasia as little as when in another family one mem-
ber after another becomes insane. From this it can evidently
only be argued that the brain and its membranes hereditarily
suffer fromc ertain abnormalities. Even the fact that in the
same family one child will be affected with tubercular arachnitis,
another with tubercular arthritis, and a third with laryngeal
phthisis, does in no way prove the existence of a dyscrasia
which in one case attacks the arachnoid, in another the
bones, and in a third the larynx. These facts can only prove
that the exciting causes select one or other part, and that
several areas of the body are in the same predisposed condi-
tion."
Mutatis mutandis the same applies to leprosy. And when
it is remembered that a predisposition may just as easily be
acquired, it is felt that great stress must be laid on the external
surrounding conditions. It is therefore necessary to study the
effect of a specific hereditary predisposition pure and simple,
and carefully exclude the influence of such external relations.
It is evidently not sufficient to argue from the fact that a near
relation had leprosy, that therefore the congenital predisposition
was specifically or legitimately inherited. The congenital pre-
disposition can only be said to have been thus inherited, if the
child was actually born of a leprous parent. If born of a parent
( 9 ) For these and the preceding remarks also cf. Virchow, loc. cit., pages 718 — 720.
Hereditary Transmission and Predisposition.
209
who some years, and frequently many years, after the birth of
the child becomes a leper, this child cannot possibly be supposed
to have inherited a specific leprous predisposition in a legitimate
manner. The fact that the parent eventually falls a victim to
the disease cannot make the inherited predisposition any more
specific or legitimate. This can only prove that certain con-
ditions and abnormalities of the parent, which eventually led to
the establishment of a predisposition capable of being acted
upon by the exciting causes responsible for the development of
leprosy, have been transmitted to the offspring. And even this
can only be so, if the possibility of an acquired predisposition
in either case can be excluded.
In an investigation of this nature, therefore, it is necessary
first to enquire into the number of cases and families in which
a specific hereditary predisposition may be assumed actually to
exist, that is, to enquire into the condition of the children born
of leprous parents. Then it must be seen whether such speci-
fic inherited predisposition has a greater influence on the deve-
lopment of the disease than a non-specific congenital predis-
position. On this must turn the issue of reformatory measures
such as forcible separation of husband and wife and interdiction
of marriages. If facts do not establish a greater influence for
the former, then the solution of the question cannot be sought
in such rigorous rules, but must direct itself to the amelioration
of the general external conditions.
These considerations have guided all the subsequent argu-
ments in a complex and difficult question.
I.—A case was never seen of a child leprous at the time of
birth, or so shortly afterwards, that it might fairly be considered
a congenital case. This point has so often been insisted on by
other authors and is so well known a fact that it is unnecessary
to comment any further on it. Now it is obviously fatal to the
conception of an hereditary transmission of a condition acquir-
ed by the parent, if it be established that such condition never
appears congenitally. And this fact must be kept in view
p
210
REPORT OF THE LEPROSY COMMISSION
more particularly in the investigation of a disease of bacillary
origin, for it is easy to conceive that the ovum or embryo could
be invaded by the bacillus.
Though this argument tells forcibly against the hereditary
transmission of the actual morbid condition or an infection
through the placental circulation, a belief in a transmitted
specific predisposition might still be maintained. It might be
assumed that some constitutional defect causally related to the
leprosy of the parent is set up in the embryo, which subse-
quently, under favourable conditions, gives rise to the disease.
Other facts, however, while still further disproving hereditary
transmission, cast doubt also upon the possibility of an inheri-
ted specific predisposition.
II.—Since leprosy cannot in any case be regarded as a
congenital disease, an enquiry must be made as to how often
it is possible to trace a family taint in the direct line, from
parent to offspring, and to this question the discussion in this
chapter will be wholly confined.
From collateral relationship little, if anything, can be argued,
as here so inextricable a maze of transmissions exists that it is
impossible to disentangle one factor from another. If the
facts available with regard to family taint in the direct line be
not sufficient to establish inheritance, then à fortiori, argu-
ments from collateral relationships must be altogether without
force. Dr. Vandyke Carter, 10 who collected information from
all parts of the Bombay Presidency, gives a most careful and
exhaustive table showing the number and proportion of blood
relations, and found that about 20 per cent. of lepers acknow-
ledged a family taint. In 14.5 per cent. of these, however, the
taint was in the collateral line. As cousins are included in these
14.5 per cent., it may be submitted that with so much ad-
mixture of alien blood little can be deduced from the figures.
Arguments and deductions from distant relationships, as e.g.
( 10 ) Vandyke Carter: loc. cit. page 184.
Hereditary Transmission and Predisposition.
211
from grandparent to grand-child are of still less force, and of
no real scientific value for the subject under discussion. In
fact they argue rather against a specific inherited predisposition.
It may be well here to repeat the words of Hjort, quoted by
Dr. Liveing : 11 " From time to time the relationship of many
hundred lepers to each other has been carefully investigated,
and the result has shown that many of them are more or less
akin, and hence the conclusion has been drawn that the disease
was hereditary in all those lepers who were related." It will be
plain to all that this conclusion does not rest on a sound basis,
and that a malady can only be inherited when the seeds thereof
pass in a direct line from parents to children, while those
persons who are only collaterally related cannot inherit the dis-
ease one from another. Lastly, when the term " atavism " is
used in support of the theory of heredity, and marked "as a
form of inheritance worthy of special notice on account of its
frequent occurrence," a protest must be raised against the
unwarrantable introduction into human pathology of a term
which, whatever its place may be in the province of biological
speculations, must remain meaningless to the pathologist en-
quiring into the ætiology of so markedly a general disease as
leprosy. In the study of the inheritance of embryological
deformities atavism may be of great importance, but if the term
is employed to denote the sudden appearance of a constitu-
tional disease after having " skipped one or several generations,"
it is inapplicable. Atavism can have no place in the ætiology
of leprosy.
Collateral and distant relationships may consequently be
disregarded, and the present enquiry is confined to the number
of instances in which a family taint could be ascertained to
exist in direct lines of descent. This will best be given in a
tabular form. The first column of the following table specifies
the name of the asylum or locality where the lepers were ex-
( 11 ) R. Liveing : loc. cit., page 85.
p 2
212
REPORT OF THE LEPROSY COMMISSION:
amined. The figures are arranged in two columns, (a) number
of instances of family taint, regardless of the fact whether the
parent or parents were leprous at the time the child was born,
(b) number of instances of lepers actually born of leprous
parent or parents, after the exclusion of all those cases, where
the parent or parents became lepers sometime after the birth
of the child,
TABLE I.
Family Taint in the Direct Line.
NAME OF ASYLUM
OR LOCALITY.
Agra
Aligarh
Almora .
Bangalore
Belgaum
Benares .
Bombay .
Burdwan
Calcutta .
Calicut .
Cawnpore
Conjeeveram
Darjeeling
Dehra Dun
Delhi
Dharmsala
Fyzabad .
Gwalior .
Gya
Hyderabad
Jubbulpore
Jummoo .
No. of
cases seen.
54
10
108
55
23
32
259
21
89
26
10
18
3
88
11
12
17
13
42
21
15
2
No. of cases
in which a
family taint
vas confessed.
3
1
17
4
1
1
34
...
5
..
5
...
15
...
3
1
1
6
...
3
1
No. of cases in
which parent
or parents were
lepers at time of
birth of
offspring.
1
1
4
2
1
1
8
...
3
...
...
3
...
6
3
1
1
6
...
2
1
REMARKS.
This case is very doubtful.
No statement made as to
condition of parent at time
of birth.
In 1 no statement.
In 2 no statement.
In 1 no statement.
No statement.
In 6 no statement.
1 very doubtful.
In both no statement.
No statement.
Hereditary Transmission and Predisposition.
213
Table I—continued.
Family Taint in the Direct Line.
NAME OF ASYLUM
OK LOCALITY.
Kapurthalla
Lahore .
Lucknow
Madras .
Madura .
Mandalay
Meerut .
Moulmein
Nagpur .
Naini and Alla-
habad.
Naini Tal
Patiala .
Peshawar
Poona
Prome
Purulia .
Rangoon
Rawalpindi
Sialkot .
Subathu .
Tanjore
Tarn Taran
Thayelmyo
Trichinopoly
Umballa
Yerrowda Priso
TOTAL
No. of
ases seen.
10
2
13
184
177
9
25
174
66
2
9
2
45
30
99
62
47
40
46
16
146
62
16
32
15
2,371
No. of cases
in which a
family taint
as confessed.
3
...
...
28
16
5
...
2
7
1
...
1
...
5
1
18
5
11
4
8
4
28
8
3
5
...
264
= 11.1 per
cent.
No. of cases in
which parent
r parents were
lepers at time of
birth of
offspring.
3
...
...
22
7
3
1
6
1
...
1
...
4
...
9
3
5
2
1
3
9
4
1
1
...
130
= 5.48 per
cent.
REMARKS.
In all no statement.
n 18 no statement and
3 cases doubtful.
n 4 no statement.
n all no statement.
n all no statement.
In 1 no statement.
No statement.
In one case father, grand-
father, and brother lepers.
In 5 no statement.
In 3 no statement.
In 3 no statement.
In 1 no statement.
In 3 no statement.
In 1 no statement.
In 2 no statement.
No statement.
No statement in 74 cases.
214
REPORT OF THE LEPROSY COMMISSION:
It will thus be seen that what might be regarded as an
hereditary taint in the direct line could be traced in only 130
cases out of 2,371, or in 5.48 per cent. Now, in 74 cases out
of the 130 either no statement was made as to the condition of
the parent or parents at the time of the child's birth or some
doubt was expressed as to diagnosis, and allowing for this, it
would perhaps be nearer the mark to say that a true family taint
in the direct line could be established in about 4 per cent. of
the cases seen.
Family taint in the direct line is, therefore, established in
only a few cases, and, consequently, as far as these figures go,
one is forced to look for other and more potent causes for the
origin of the disease. If the results of Höegh and Bidenkap, 13
who traced the disease in the direct line in 25 per cent., and
further those of Van Sommeren, 13 who amongst 31 cases found
only two hereditary ones, prompted Virchow to the remark that
heredity cannot explain the spread of the disease, how much
less do the above figures justify the belief in the high import-
ance of an hereditary influence ?
Table I has been constructed from the cases actually seen
and examined by the Commissioners. As, however, many
patients confessed to having leprous children or parents, either
deceased or absent, it is necessary to construct another table
including all these cases. This is done in Table II which is
arranged on the same plan as the previous one.
( 12 ) Höegh and Bidenkap: Norsk Magazin for Lagevidenskaben, 1860,
Vol. XIV.
( 13 ) Van Sommeren: A brief Historical Sketch of the Madras Leper Hospital.
Hereditary Transmission and Predisposition.
215
TABLE II.
Family Taint in the Direct Line.
NAME OF ASYLUM
OR LOCALITY.
Agra
Aligarh
Almora .
Bangalore
Belgaum
Benares . . .
Bombay .
Burdwan
Calcutta .
Calicut .
Cawnpore
Conjeeveram .
Darjeeling
Dehra Dun
Delhi
Dharmsala
Fyzabad .
Gwalior »
Gya
Hyderabad
Jubbulpore
Jummoo .
Kapurthalla
Lahore .
.
Lucknow
Madras .
Madura ,
No. of
ases seen.
55
10
113
56
23
3 2
260
21
89
26
10
19
3
89
11
12
17
13
43
21
16
2
10
2
13
194
115
No. of cases
in which a
family taint
was con-
fessed.
4
1
21
5
1
1
35
5
...
...
6
...
T6
...
3
1
1
7
4
1
3
...
35
23
No. of cases in
which parent or
parents were
lepers at time of
birth of
offspring.
I
I
5
2
1
1
8
...
3
...
...
4
...
6
...
3
1
1
7
...
3
1
3
...
...
24
10
REMARKS.
This case is very doubtful.
In 1 no statement.
In 1 no statement.
ln 2 no statement.
In 1 no statement.
In 1 no statement.
In 1 doubtful diagnosis;
6 no statement.
In 3 no statement.
In 1 no statement.
In 3 no statement.
In 3 doubtful diagnosis.
18 no statement.
In 5 no statement.
216
REPORT OF THE LEPROSY COMMISSION;
Table II—continued.
Family Taint in the Direct Line,
NAME OF ASYLUM
OK LOCALITY.
Mandalay
Meerut .
Moulmein
Nagpur .
Naini and Allah-
abad .
Naini Tal
Patiala .
Peshawar
Poona
Prome
Purulia .
Rangoon
Rawalpindi
Sialkot .
Subathu .
Tanjore .
Tarn Taran
Thayetmyo
Trichinopoly .
Umballa
Yerrowda Prison
TOTAL
No. of
cases seen.
179
9
25
176
66
2
9
2
45
31
105
62
51
40
48
16
154
63
17
32
16
2,423
No. of cases
in which a
family taint
was con-
fessed.
5
...
2
9
1
...
1
...
5
2
25
5
15
4
10
4
36
9
4
5
1
316
= 13.0
per cent.
No. of cases in
which parent or
parents were
lepers at time of
birth of
offspring.
3
...
1
7
1
...
1
...
4
...
10
3
7
2
1
3
12
4
1
1
...
146
= 6.0
per cent.
REMARKS.
In 3 no statement.
In 7 no statement.
In 1 no statement,
In 1 no statement.
In 5 doubtful diagnosis.
In 4 no statement.
In 3 no statement.
In 3 no statement.
In 1 no statement.
In 3 no statement.
In 2 no statement.
In 2 no statement.
In 1 no statement.
In S3 insufficient statement.
Hereditary Transmission and Predisposition.
217
Thus according to this enlarged table it is seen that a
family taint in the direct line existed in 6 per cent., a higher
percentage than the corresponding ratio of the former table.
But, on the other hand, the number of cases noted as doubtful
or as wanting in the detailed statement is greater, and as the
additional 52 lepers could not be seen, the suspicion of a wrong
diagnosis also is not excluded. Making allowance for all these
factors it may be said that this second table fairly represents a
percentage of 4.5 of a possible heredity, so that the conclusions
derived from a comparison of these two tables are more or less
in harmony, and as far as such figures go, establish only to a
slight degree the existence of a family taint, and 4 per cent.
might, therefore, fairly be accepted as representing the ratio of
a specific family taint in the direct line.
These figures tend to confirm Hansen's disbelief in an
inherited specific predisposition.
In constitutional diseases
such as leprosy the greatest caution must be exercised in
accepting any theory of inheritance. As the importance of
inheritance as an ætiological factor vanishes, so that of exter-
nal conditions must rise into prominence. And parent and
child being subjected usually to exactly similar surrounding
conditions and circumstances, it is well within the bounds of
probability that the disease has started de novo in both. One
might otherwise with equal reason classify rickets amongst the
hereditary diseases. Now that the pathology of fœtal rickets
has been elucidated, it is well known that rickets is a disease
of bad nutrition and is never congenital or hereditary ; yet it
would not be difficult in London to find a family taint in 4 per
cent. of rickety patients. Unless the influence of external
causes can be excluded, and an inheritance proved in a
majority of cases and on sound evidence, the hereditary trans-
mission of, or specific predisposition to a disease cannot be
said to be established. A protest must be raised when such
cases as quoted by M. de Valencé are considered convincing
218
REPORT OF THE LEPROSY COMMISSION:
proofs of an hereditary transmission. 14 For one of his exam-
ples of inherited leprosy rests on the "confession of a patient,
that he vaguely remembered having heard that his maternal
grandmother had had leprosy." 15 His parents apparently
were healthy and he himself was certainly untainted when his
three children were born. Two of the latter became leprous
and died before the patient himself was affected. The details
in the history of inheritance of the other case are too insuffi-
cient. Of four sisters and two brothers of apparently healthy
descent, the two latter became diseased. One of them died
without issue, while the other had a leprous son. " The sisters
had children affected with leprosy, and it is possible at the
present day to trace easily the descendants of these four
sisters and enumerate the members of the family who died
from the disease." 16 Thus as the case stands, a transmission
by inheritance can at best only be established from one of the
brothers to his son. Yet this evidence, in a leading article of
the Lancet, 17 has been described as convincing on the ques-
tion of hereditary transmission. It is on this account only,
that notice had to be taken of M. de Valencé's paper.
The great importance of external conditions in the aetio-
logy of leprosy must be admitted, and the figures therefore
tend to reduce the importance of inheritance so greatly, that
practically it may be altogether disregarded.
Again, if heredity have an appreciable influence on the
spread or origin of the disease, it should be possible to trace
leprosy through several generations in a sufficiently large num-
ber of cases. In each instance, therefore, when a family taint
in the direct line was acknowledged, careful enquiries were
made as to the condition of the grand-parents. Only eighteen
( 14 ) Lancet, 1890, Vol. I, page 1077.
( 15 ) Lancet, 1890, Vol. I, page 1065.
( 16 ) Lancet, 1890, Vol. I, page 1077.
( 17 ) Lancet, 1890, Vol. I, page 1065.
Hereditary Transmission and Predisposition.
219
cases could be obtained where the disease could be traced
from the grandfather or grandmother downwards. Now in
five cases the statements were insufficient or the diagnosis
of leprosy doubtful (Nos. 3, 4, 5, 8, 9), and in further six cases
the children were in each instance born of healthy parents, so
that the conditions are such as to exclude an inherited specific
predisposition (Nos. 1, 11, 12, 13, 14, 15). These cases will
now be given in an analysed form.
TABLE 11a.
Analysis of Cases where a Family Taint in the Direct Line could
be traced through more than One Generation.
(a) Bombay:
(i) Mother = Leper (HER FAMILY HISTORY WAS QUITE CLEAR).
!
Two sons = both healthy. Daughter=Leper (BECAME A LEPER BEFORE HER
MOTHER).
Daughter = Leper.
Son == Leper.
Both these children were born when their mother was healthy, and they became
affected about the same time as their grandmother, three to five years after their
mother. The whole family was seen and examined.
(¿0 Dehra Dun : (2) Maternal grandfather = Leper.
Mother
= Leper.
Daughter
= Leper (This patient was seen and exa-
mined).
Two children who died as healthy infants.
In each instance the parent was a leper before the birth of the child.
(c)
Gya:
(3) Father
= Leper (His FAMILY HISTORY WAS QUITE CLEAR).
Only son = Leper
(These two were seen and examined).
Only child = Leper
In each instance the parent was a leper before the birth of the child.
(d) Kapurthall \ill\ : (4) Grandmother = Leper (No STATEMENT MADE, WHETHER PATER-
|
NAL OR MATERNAL).
Father
= Leper.
Son
= Leper (This patient was seen and examined).
No statements were made whether the parent in each instance was
a leper before or after the birth of the offspring, nor as to the
number of children each parent had.
220
REPORT OF THE LEPROSY COMMISSION :
Table 11a—continued.
Analysis of Cases where a Family Taint in the Direct Line could
be traced through more than One Generation.
(e) Madras:
(5) Grandfather = Leper (No STATEMENT MADE, WHETHER PATERNAL
OR MATERNAL).
Mother
= Leper.
Son
= Leper (This patient was seen and questioned).
Three children (one of them said to be a leper, but diagnosis extremely
doubtful).
(6) Father and Mother
= Lepers.
Two daughters
= Lepers (These two and the child were seen
and examined).
One of these has a child = Leper (BUT DIAGNOSIS IS EXTREMELY
DOUBTFUL).
(7) Maternal grandfather
= Leper.
Mother
=
Leper (This patient and her leprous child
were seen).
Two children and one of them = Leper (the other is healthy, married and
has several healthy grown up
children).
(8) Maternal grandfather = Leper.
Mother
= Leper.
Daughter
= Leper (This patient was seen and examined).
(f) Madura : (9) Father
= Leper (His FAMILY HISTORY QUITE
CLEAR).
Only child
= Leper.
Two children and one of them = Leper (BUT DIAGNOSIS WAS EXTREME-
LY DOUBTFUL,).
(g) Poona: (10) Grandfather=Leper.
Father and Mother=Lepers.
Two sons = Lepers (These two were seen and questioned).
(h) Purulia: (11) Grandparents on one side=Lepers.
Parents = Lepers.
Two out of five children=Lepers (These two were seen : all adults).
(12)
Mother=Leper (HER OWN FAMILY HISTORY CLEAR).
Son=Leper.
Daughter= Leper (BOTH SON AND DAUGHTER BORN
LONG BEFORE MOTHER
BECAME A LEPER).
Two sons=Lepers (BOTH BORN BEFORE MANIFESTA-
TION OF DISEASE IN THEIR
MOTHER).
The whole family was seen and questioned.