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The familial incidence of rheumatic fever
I
N THE etiology of rheumatic fe\-er, t\lo funtlanltmtal mechanisms have been thought to play a role: contagion and heredity. It can hardly be doubted. in the face of actual epidemics of rheumatic fever zmciatetl \\.ith henwlytic streptococcus infection, that contagion plays a part both as an inciting factor in the development of the “initial” attack of rheumatic fever and in the esacerljation of the disease process in recurrent rheumatic fever. The fairly factual data on the infectious origin of rheumatic fever are not paralleled by similar material to support the role of heredity, although \Vilsonl has attenlpted to place the role of heredity (111 a firm stat i&cd basis. She has stated : “It should seem fair to conclude from the genetic analysis of our tlata that the susceptibilit>, for rheunlatic fever is transmitted as a single autosomal recessive gene.“““.‘” In further consideration of the hereditary mechanisnl. attention must necessaril!be placetl on the unusual age distritmtion of thedisease, particularly its sparing of children ill the early years of life. As Pau12,g.g6 has statetl, “the infant lllust gron’ up to become rheurtlatic.” Thus, if we are to accept the hereditary mechanisnl as tlominant, might x\-e 11ot believe that it is a “susceptibilit~~” of sorile obscure tl,pe that is inheritetl. according to Wilson’s genetic hypothesis, and that the “growingup” phase represents the development of some sensitizing mechanism. that is, the development of hypersensitivit) ? (‘ertain it is that most phenomena of the rheunlatic state appear to have a basic allergic nlechanism (Rich and C;regor>” and Akiawa4). Therefore, both Wilson and Paul have ernphasizetl the need for furthm- studies on the familial aspects of rheumatic fever.
The problem of familial incidence in rheumatic fever, sinlply stated, is-the problem of separating hereclitary front contact factors. Each separately, or both operating sirtlultaneousl~. nlay pIa\- a role either in favoring the initial attack From thr? Graduate Angeks, Calif. Rcceiwd for publication
Divisicm March
of
the 11,
School
of
1047.
438
Mediciru?,
Lvniversity
of
Southern
California,
Los
or in precipitating recurrent attacks. The role of heredity in rheunlatic fever has been supported by the following studies and observations. 1. The similarity in susceFtibi1ity to rheunlatic fever of identical and fraternal twins, (Wilson,’ Irvine-Jones,5 and Raufmann and Scheerer6). These analyses have been fairly uniform in shoxving that identical t\\.ins behave similarl> genetically; that is, either both do contract rheumatic fever, or both do not. HoLvever, this is not always the case, as Paui2VP. O” has pointetl out. 2. Genetic analysis of rheumatic families in relation to RIendelian precliction rates in various types of gene transmission (IlYlson and Schweitzer’). Studies such as these form the basis for Wilson’s thesis of “autosomal recesto which we have referred. From a critical analysis of sive Rene transmission” these studies, Paul has concluded that “some inherited relationship exists between parental rheumatic fever and that of the siblings.“2S *. go More indirect evidence of the operation of heredity is obtained from Paul’s consideration of the age at nhich second members of a rheumatic family acquire their initial attack. This occurs most often at an older age than that of the first member and is tlifficult, actually. almost impossible, to explain on the basis of contagion alone. It may be n:ore logically explained on the basis of a gradually developing susceptibility of poststreptococcal origin. The justification for the presentation of our data lies in the opFortunit!v to inquire into the history of a large number of young adult rheun:atic fever patientwho have been separated for a varying period of tinle front tte fawily contact. The history of the individual following the hrenk franljr;mil>f rostnc-t afforc’s an important method of separating hereditary influences from the factors of conta!:,ion. SOURCE
OF
hfATERIAL
It is the purpose of this communication to present observations on the OCCUTrence of rheumatic fever, both initial and recurrent attacks, in relation to familial and postfamilial contacts. In contrast to the observations of IVilson and of Paul, who studied children in a relatively small number of families, this study is concerned with young adults of military ape from a larg-e number of families distributed widely over the United States. As controls, a group of tuberculous patients, a group of healthy physicians, and a group of patients in a veterans’ hospital were studied. Four separate series of patients form the basis for the present study. In each group, personal interviews were conducted by one of us, and information relative to previous rheumatic fever and family history tabulated. The composition of the four groups was as follo\vs: Group 1: 3,594 patients with rheumatic fever, a-ho \\err inlerviewecl over a periocl of twenty months in 1944 and 1945, in a naval hospital devoted almost entirely to the treatment of this disease. C‘ontrol Group 2: 519 patients of nlilitary ag-e with tuberculosis \\:ho were seen in the same naval hospital. Control Group 3: 254 healthy physicians who were working in a large general civilian hospital.
440
,\MEKIC.\N
Control Group 4: of a veterans’ hospital.
HEART
624 patients
JOURPiAI.
on the general, medical,
and surgical
wards
Groups 1 and 2 consisted of enlisted and officer personnel sent to the naval hospital for treatment. They were representative individuals from installations and ships of the United States Navy throughout the world. RESULTS
The results TABLE
of our observations I.
COMPARISON
-..-
OF
STUDY
are summarized
in Tables I and II
OF FAMILIAL INCIDENCE IN THE RHEUMATIC FEVER GROUP WITH CONTR,OL GROUPS __- _-. ~- .----.~ 1
PiIJMBER
._-..
1 PER CEXT
-Groufi
(4 (b) (4 (4
1
RhelAvnatic
Fever
Total patients (and therefore Total patients (initial attack Total patients positive Total patients positive Total family
Patients
Total
3,591:
with “initial” attack during military after separation from family) with “recurrent” attack during military occurred at home) with “initial” attack in service; family
history,
with
history-
attack
in service;
(a) (b) (c)
Control
Total Total Total
2
with “initial” and “recurrent” positive; (c) plus (d)
3
(a) (b)
Total Total
(c)
!?oI?rvphysicians
Control
(a) (b) (c)
with with with
family
attacks
4
general general general
78 4
775
/ /
21
?38
)
6 3 oi total 9.8 of total
j
16.4 c f tot‘rl
592
Zbtal
Patients
Physicians
Total
with
family: x1
(775);
with -I5 0
519
General patients patients patients
positive
Patients
1 1
25-I
with history of previous rheumatic who had rheumatic fever before with
6
in service,
history of previous rheumatic fever rheumatic fever before break from family positive history of rheumatic fever in farnil)
Healthy
physicians physicians
Group Total Total Total
Tuberculous
patients patients patients
Group
j
354
patients history
Group
2.819 service I
“recurrent”
Percentage of patients with “initial” attacks (2,819) history positive (238); (c) divided by (n) Percentage of patients with “recurrent” attacks family history positive (354); (d) divided by (b)
Control
I
service
history
of rheumatic
in a Veterans
Hospital
who had had Rh. F. who had Rh. F. before break with positive history of Rh.
fcvcr break
from
fever
Total
from fam$ F. in farnIl>
in
blJ
Ll 9 9
10 1 7 1 7
Group
Control
Control
C‘ontrol
1 Incidence rheumatic
of family histor! in patients with fever: that is, while still in contact Total rheumatic fever patients (“initial” Total family history. positive
“initial” attacks of with the farnil> attack at home)
Group 2 Incidence of familial history in tuberculous patients had rheumatic fever while still in contact with farnil! Total tuberculous patients with rheumatic fever Total with family history positive Group 3 Incidence of familial history in physicians who matic fever while still in contact with farnil! Total physicians with rheumatic fcvrr Total with family history positive
hacl
\rho
45 0 755 354
had 21 0
had
rheu
Group 4 Inciclcnce of familial history in general patients in a veteran:, hospital who had had rheumatic fever while still in contact with farnil\ ’ Total vetcrans’ hospital patients \vith rheumatic fever Total with familv history positive Average familial ~incidencc for all groups
53 .i I
15 8
40 15
Comment: (1) In Group 1, Table I, 16.4 per cent of all patients with rheumatic fever had a Fositive family background; 45.6 per cent of rheunratic fever patients with “recurrent” attacks had a positive family background. In the three control groups, patients with tuberculosis, healthy physicians, and patients in a general veterans hospital, the incidence of a positive family history of rheumatic fever was 1.7 per cent, 3.5 per cent, and 2.4 per cent, respectively. These figures are not, to our knowledge, unlike those in previously published reports, and call attention again to the definite importance of the family in the etiology of rheumatic fever. (2) Of the rheumatic fever patients who developed an “initial” attack after separation from the family, 8.4 per cent had a positive family backgrouncl, while 91.6 per cent of these patients had no knowledge of any occurrence of the disease within the family. It would appear that the actual attack rate, as esemplified in this large group of military personnel separated from familial contact, was determined by external factors, such as environment and infection, rather than by hereditary or familial factors. (3) Table II illustrates the familial incidence in those patients who had had rheumatic fever while still in contact with family. In these groups, the incidence of a positive family history (44.7 per cent, average) is considerably higher than the incidence (16.4 per cent, average) in the rheumatic patients of Group 1. This high incidence shows the importance of a factor or factors which increase the tendency to develop rheumatic fever while in the home. It should be noted
that these silnilarl>; high percentages xvere obtainetl by random sampling of \vitlrl! separated ant1 dissimilar control groqs. It ih of great ini[:ortance to notch that 110ne of the patients in (‘ontrol (;roul:s 2 anti .3 who hat1 rhrunlatic fr\w AI honor tlevclopctl later attacks. It IIMJ. 1)~ assunletl that tht> big-h Ixrcrnta~c of familial incitlenw in those Ixtients \vho tlevelopetl the rheuniatic state Lvhilt* in c-olltac‘t with thy famil) n.as tlue to contact i1: the IIO~IIC, in the sanw \~a\- that the high percetltagc of patients \vho tlevelopecl rheunlatic fcvel- \vithout a famil!~ histor! \\xb tlur to contact with an inciting agent in the cro\+xlecl quarters of the IJarrat-ks;. It k crrtailli!~ not within the scopt’ of this JLlJWl 10 enJargr uJ:o~i the tl;tturt or modus operantli of the infyctious agent or to rlal;orate ul on the J ossil!ilit>of a sensitization n:cchanisln. \\-e I)elic\~r, ho~~vt~r. I hat attent ioll hhoultl IF calle:l to the clisJ:arit>. lxtwren the low familial incidence iII “initial” at tack5 (Taljle I, Group 1) occurring after separation front the fan-iI\. (6.3 Jxr- crilt ) an(l the high familial incidence in those groups (Table II J u.110 tle~do~:~l the “initial” attack Lvhilc in contact with the family (44.7 per cent, a~rage for the four groups). In the Iililitar). service the vast majority of cases of rheun:atic ftlxw- cleveloped in the training c-amI:s, \\-herr cro\vcling in IJar-racks prrmit trtl epitltwic-s of hemolytic streptococcus infection lo otxwr. I~iitloul~tt~clly such epi(lemitx Is it ~ossiblc that those patients tvho clr~&~petl rheuoccur-red frolli contact. nlatic fever prior to nlilitary service nlight ha\-e tlone so from conta(? \\,itli the streptococcus in the home. 2 ()ne may, therrfore, raise the question \\-het her the fanlily carries a significantly larger place in the t+olog\, of rhrunlatic ft,\.t*r than a snuI-ce of cOIltact. Is the fanlil>, different froul the barracks or a tl-aining center as a locus for contact with the inciting infectious agent? The further St WI>- of 1 who tleveloped rheumat it: feL-er after the 78.4 per cent of patients in (;~CJUIseparation front the fanlily \vill help to ans\!-car- the probltw of heretlitar!. susceptil)ility versus poststreptococcal sensitivity. ah tht, cause of recurrent at tacks.
1. Four groups of young adults have been interviewed. One group of rheumatic fever patients (3,504) and three groups of nonrheumatic individuals (I,397), serving as controls, formed the basis of the >tucly. 2. Group 1 shows that approsimately 78 per cent of the patients \vith “initial” rheunlatic fever developed the disease after separation front the family. \d,-e raise the question \\-hether this indicates some agynt outside of the family as the chief factor qerative in the etiology of rheumatic fever. 3. The tuberculous patients and health!’ ph>-sicians \vho had “initial” attacks of rheunlatic fever Mhile at home tlicl not develop secondary attacks after separation from the family. 4. It is notetl in Groups 2, 3, and 4, the controls, that the individuals who tleveloI:etl rheumatic fever prior to seJ-aration from the family, &on-et1 a similar family incidence, and that this incidence tloes not diHer greatly from that found in the rheunlatic I:atients studied. 5. The high familial incidence of rheumatic fever, averaging 44.7 per cent in those \\-ho developed the disease while still at home, seems to indicate that
GRIFFITH
ET
:\I,.:
FAMILIAL
INCIDENCE
OF
RHEUMATIC
there is some factor within the family. Is this factor or contact with the inciting agent in the home? 6. The great need for further data on the subject nlent is evident.
FEVER.
a hereditary of heredity
443
I
susceptibility versus
environ-
REFERENCES
I. 2. 3.
1. 5. 6. 7. 8.
Wilson,
May G.: Rheumatic Fever, New York, 1940, The Commonwealth Fund, Division of Publications. I’aul, John R.: The Epidemiology of Rheumatic Fever and Some of Its Public Health Aspects, New York, 1943, Metropolitan Life Insurance Company. Rich, A. R., and Gregory, J. E.: Further Experimental Cardiac Lesions of the Rheumatic Types Produced by Anaphylactic Hypersensitivity, Bull. Johns Hopkins Hosp. 7.5: 115, 1941. Akiawa, J. K.: Hypersensitivity and Rheumatic Fever, Part II! Ann. Int. Med. 23:969, 1946. Irvine-Jones, E.: Acute Rheumatism as a Familial Disease, Am. J. I>is. Child. 45:118-1-, 1933. Kaufmann, O., and Scheerer, E.: Heredity of Acute Articular Rheumatism: Studies on 72 Sets of Twins, Ztschr. f. menschl. \:ererb.-u. Konstitutionslehre 21:687, 1938. Wilson, M. G., and Schweitzer, H. D.: Rheumatic Fever as a Familial Disease, J. Clin. Investigation 16:X5, 1937. Faulkner, J. M., and White, P. I).: The Incidence of Rheumatic Fever, Chorea and Rheumatic Heart Disease With Especial Reference to Their Occurrence in Families, J. A. M. A. 83:425, 1924.
N THE etiology of rheumatic fe\-er, t\lo funtlanltmtal mechanisms have been thought to play a role: contagion and heredity. It can hardly be doubted. in the face of actual epidemics of rheumatic fever zmciatetl \\.ith henwlytic streptococcus infection, that contagion plays a part both as an inciting factor in the development of the “initial” attack of rheumatic fever and in the esacerljation of the disease process in recurrent rheumatic fever. The fairly factual data on the infectious origin of rheumatic fever are not paralleled by similar material to support the role of heredity, although \Vilsonl has attenlpted to place the role of heredity (111 a firm stat i&cd basis. She has stated : “It should seem fair to conclude from the genetic analysis of our tlata that the susceptibilit>, for rheunlatic fever is transmitted as a single autosomal recessive gene.“““.‘” In further consideration of the hereditary mechanisnl. attention must necessaril!be placetl on the unusual age distritmtion of thedisease, particularly its sparing of children ill the early years of life. As Pau12,g.g6 has statetl, “the infant lllust gron’ up to become rheurtlatic.” Thus, if we are to accept the hereditary mechanisnl as tlominant, might x\-e 11ot believe that it is a “susceptibilit~~” of sorile obscure tl,pe that is inheritetl. according to Wilson’s genetic hypothesis, and that the “growingup” phase represents the development of some sensitizing mechanism. that is, the development of hypersensitivit) ? (‘ertain it is that most phenomena of the rheunlatic state appear to have a basic allergic nlechanism (Rich and C;regor>” and Akiawa4). Therefore, both Wilson and Paul have ernphasizetl the need for furthm- studies on the familial aspects of rheumatic fever.
The problem of familial incidence in rheumatic fever, sinlply stated, is-the problem of separating hereclitary front contact factors. Each separately, or both operating sirtlultaneousl~. nlay pIa\- a role either in favoring the initial attack From thr? Graduate Angeks, Calif. Rcceiwd for publication
Divisicm March
of
the 11,
School
of
1047.
438
Mediciru?,
Lvniversity
of
Southern
California,
Los
or in precipitating recurrent attacks. The role of heredity in rheunlatic fever has been supported by the following studies and observations. 1. The similarity in susceFtibi1ity to rheunlatic fever of identical and fraternal twins, (Wilson,’ Irvine-Jones,5 and Raufmann and Scheerer6). These analyses have been fairly uniform in shoxving that identical t\\.ins behave similarl> genetically; that is, either both do contract rheumatic fever, or both do not. HoLvever, this is not always the case, as Paui2VP. O” has pointetl out. 2. Genetic analysis of rheumatic families in relation to RIendelian precliction rates in various types of gene transmission (IlYlson and Schweitzer’). Studies such as these form the basis for Wilson’s thesis of “autosomal recesto which we have referred. From a critical analysis of sive Rene transmission” these studies, Paul has concluded that “some inherited relationship exists between parental rheumatic fever and that of the siblings.“2S *. go More indirect evidence of the operation of heredity is obtained from Paul’s consideration of the age at nhich second members of a rheumatic family acquire their initial attack. This occurs most often at an older age than that of the first member and is tlifficult, actually. almost impossible, to explain on the basis of contagion alone. It may be n:ore logically explained on the basis of a gradually developing susceptibility of poststreptococcal origin. The justification for the presentation of our data lies in the opFortunit!v to inquire into the history of a large number of young adult rheun:atic fever patientwho have been separated for a varying period of tinle front tte fawily contact. The history of the individual following the hrenk franljr;mil>f rostnc-t afforc’s an important method of separating hereditary influences from the factors of conta!:,ion. SOURCE
OF
hfATERIAL
It is the purpose of this communication to present observations on the OCCUTrence of rheumatic fever, both initial and recurrent attacks, in relation to familial and postfamilial contacts. In contrast to the observations of IVilson and of Paul, who studied children in a relatively small number of families, this study is concerned with young adults of military ape from a larg-e number of families distributed widely over the United States. As controls, a group of tuberculous patients, a group of healthy physicians, and a group of patients in a veterans’ hospital were studied. Four separate series of patients form the basis for the present study. In each group, personal interviews were conducted by one of us, and information relative to previous rheumatic fever and family history tabulated. The composition of the four groups was as follo\vs: Group 1: 3,594 patients with rheumatic fever, a-ho \\err inlerviewecl over a periocl of twenty months in 1944 and 1945, in a naval hospital devoted almost entirely to the treatment of this disease. C‘ontrol Group 2: 519 patients of nlilitary ag-e with tuberculosis \\:ho were seen in the same naval hospital. Control Group 3: 254 healthy physicians who were working in a large general civilian hospital.
440
,\MEKIC.\N
Control Group 4: of a veterans’ hospital.
HEART
624 patients
JOURPiAI.
on the general, medical,
and surgical
wards
Groups 1 and 2 consisted of enlisted and officer personnel sent to the naval hospital for treatment. They were representative individuals from installations and ships of the United States Navy throughout the world. RESULTS
The results TABLE
of our observations I.
COMPARISON
-..-
OF
STUDY
are summarized
in Tables I and II
OF FAMILIAL INCIDENCE IN THE RHEUMATIC FEVER GROUP WITH CONTR,OL GROUPS __- _-. ~- .----.~ 1
PiIJMBER
._-..
1 PER CEXT
-Groufi
(4 (b) (4 (4
1
RhelAvnatic
Fever
Total patients (and therefore Total patients (initial attack Total patients positive Total patients positive Total family
Patients
Total
3,591:
with “initial” attack during military after separation from family) with “recurrent” attack during military occurred at home) with “initial” attack in service; family
history,
with
history-
attack
in service;
(a) (b) (c)
Control
Total Total Total
2
with “initial” and “recurrent” positive; (c) plus (d)
3
(a) (b)
Total Total
(c)
!?oI?rvphysicians
Control
(a) (b) (c)
with with with
family
attacks
4
general general general
78 4
775
/ /
21
?38
)
6 3 oi total 9.8 of total
j
16.4 c f tot‘rl
592
Zbtal
Patients
Physicians
Total
with
family: x1
(775);
with -I5 0
519
General patients patients patients
positive
Patients
1 1
25-I
with history of previous rheumatic who had rheumatic fever before with
6
in service,
history of previous rheumatic fever rheumatic fever before break from family positive history of rheumatic fever in farnil)
Healthy
physicians physicians
Group Total Total Total
Tuberculous
patients patients patients
Group
j
354
patients history
Group
2.819 service I
“recurrent”
Percentage of patients with “initial” attacks (2,819) history positive (238); (c) divided by (n) Percentage of patients with “recurrent” attacks family history positive (354); (d) divided by (b)
Control
I
service
history
of rheumatic
in a Veterans
Hospital
who had had Rh. F. who had Rh. F. before break with positive history of Rh.
fcvcr break
from
fever
Total
from fam$ F. in farnIl>
in
blJ
Ll 9 9
10 1 7 1 7
Group
Control
Control
C‘ontrol
1 Incidence rheumatic
of family histor! in patients with fever: that is, while still in contact Total rheumatic fever patients (“initial” Total family history. positive
“initial” attacks of with the farnil> attack at home)
Group 2 Incidence of familial history in tuberculous patients had rheumatic fever while still in contact with farnil! Total tuberculous patients with rheumatic fever Total with family history positive Group 3 Incidence of familial history in physicians who matic fever while still in contact with farnil! Total physicians with rheumatic fcvrr Total with family history positive
hacl
\rho
45 0 755 354
had 21 0
had
rheu
Group 4 Inciclcnce of familial history in general patients in a veteran:, hospital who had had rheumatic fever while still in contact with farnil\ ’ Total vetcrans’ hospital patients \vith rheumatic fever Total with familv history positive Average familial ~incidencc for all groups
53 .i I
15 8
40 15
Comment: (1) In Group 1, Table I, 16.4 per cent of all patients with rheumatic fever had a Fositive family background; 45.6 per cent of rheunratic fever patients with “recurrent” attacks had a positive family background. In the three control groups, patients with tuberculosis, healthy physicians, and patients in a general veterans hospital, the incidence of a positive family history of rheumatic fever was 1.7 per cent, 3.5 per cent, and 2.4 per cent, respectively. These figures are not, to our knowledge, unlike those in previously published reports, and call attention again to the definite importance of the family in the etiology of rheumatic fever. (2) Of the rheumatic fever patients who developed an “initial” attack after separation from the family, 8.4 per cent had a positive family backgrouncl, while 91.6 per cent of these patients had no knowledge of any occurrence of the disease within the family. It would appear that the actual attack rate, as esemplified in this large group of military personnel separated from familial contact, was determined by external factors, such as environment and infection, rather than by hereditary or familial factors. (3) Table II illustrates the familial incidence in those patients who had had rheumatic fever while still in contact with family. In these groups, the incidence of a positive family history (44.7 per cent, average) is considerably higher than the incidence (16.4 per cent, average) in the rheumatic patients of Group 1. This high incidence shows the importance of a factor or factors which increase the tendency to develop rheumatic fever while in the home. It should be noted
that these silnilarl>; high percentages xvere obtainetl by random sampling of \vitlrl! separated ant1 dissimilar control groqs. It ih of great ini[:ortance to notch that 110ne of the patients in (‘ontrol (;roul:s 2 anti .3 who hat1 rhrunlatic fr\w AI honor tlevclopctl later attacks. It IIMJ. 1)~ assunletl that tht> big-h Ixrcrnta~c of familial incitlenw in those Ixtients \vho tlevelopetl the rheuniatic state Lvhilt* in c-olltac‘t with thy famil) n.as tlue to contact i1: the IIO~IIC, in the sanw \~a\- that the high percetltagc of patients \vho tlevelopecl rheunlatic fcvel- \vithout a famil!~ histor! \\xb tlur to contact with an inciting agent in the cro\+xlecl quarters of the IJarrat-ks;. It k crrtailli!~ not within the scopt’ of this JLlJWl 10 enJargr uJ:o~i the tl;tturt or modus operantli of the infyctious agent or to rlal;orate ul on the J ossil!ilit>of a sensitization n:cchanisln. \\-e I)elic\~r, ho~~vt~r. I hat attent ioll hhoultl IF calle:l to the clisJ:arit>. lxtwren the low familial incidence iII “initial” at tack5 (Taljle I, Group 1) occurring after separation front the fan-iI\. (6.3 Jxr- crilt ) an(l the high familial incidence in those groups (Table II J u.110 tle~do~:~l the “initial” attack Lvhilc in contact with the family (44.7 per cent, a~rage for the four groups). In the Iililitar). service the vast majority of cases of rheun:atic ftlxw- cleveloped in the training c-amI:s, \\-herr cro\vcling in IJar-racks prrmit trtl epitltwic-s of hemolytic streptococcus infection lo otxwr. I~iitloul~tt~clly such epi(lemitx Is it ~ossiblc that those patients tvho clr~&~petl rheuoccur-red frolli contact. nlatic fever prior to nlilitary service nlight ha\-e tlone so from conta(? \\,itli the streptococcus in the home. 2 ()ne may, therrfore, raise the question \\-het her the fanlily carries a significantly larger place in the t+olog\, of rhrunlatic ft,\.t*r than a snuI-ce of cOIltact. Is the fanlil>, different froul the barracks or a tl-aining center as a locus for contact with the inciting infectious agent? The further St WI>- of 1 who tleveloped rheumat it: feL-er after the 78.4 per cent of patients in (;~CJUIseparation front the fanlily \vill help to ans\!-car- the probltw of heretlitar!. susceptil)ility versus poststreptococcal sensitivity. ah tht, cause of recurrent at tacks.
1. Four groups of young adults have been interviewed. One group of rheumatic fever patients (3,504) and three groups of nonrheumatic individuals (I,397), serving as controls, formed the basis of the >tucly. 2. Group 1 shows that approsimately 78 per cent of the patients \vith “initial” rheunlatic fever developed the disease after separation front the family. \d,-e raise the question \\-hether this indicates some agynt outside of the family as the chief factor qerative in the etiology of rheumatic fever. 3. The tuberculous patients and health!’ ph>-sicians \vho had “initial” attacks of rheunlatic fever Mhile at home tlicl not develop secondary attacks after separation from the family. 4. It is notetl in Groups 2, 3, and 4, the controls, that the individuals who tleveloI:etl rheumatic fever prior to seJ-aration from the family, &on-et1 a similar family incidence, and that this incidence tloes not diHer greatly from that found in the rheunlatic I:atients studied. 5. The high familial incidence of rheumatic fever, averaging 44.7 per cent in those \\-ho developed the disease while still at home, seems to indicate that
GRIFFITH
ET
:\I,.:
FAMILIAL
INCIDENCE
OF
RHEUMATIC
there is some factor within the family. Is this factor or contact with the inciting agent in the home? 6. The great need for further data on the subject nlent is evident.
FEVER.
a hereditary of heredity
443
I
susceptibility versus
environ-
REFERENCES
I. 2. 3.
1. 5. 6. 7. 8.
Wilson,
May G.: Rheumatic Fever, New York, 1940, The Commonwealth Fund, Division of Publications. I’aul, John R.: The Epidemiology of Rheumatic Fever and Some of Its Public Health Aspects, New York, 1943, Metropolitan Life Insurance Company. Rich, A. R., and Gregory, J. E.: Further Experimental Cardiac Lesions of the Rheumatic Types Produced by Anaphylactic Hypersensitivity, Bull. Johns Hopkins Hosp. 7.5: 115, 1941. Akiawa, J. K.: Hypersensitivity and Rheumatic Fever, Part II! Ann. Int. Med. 23:969, 1946. Irvine-Jones, E.: Acute Rheumatism as a Familial Disease, Am. J. I>is. Child. 45:118-1-, 1933. Kaufmann, O., and Scheerer, E.: Heredity of Acute Articular Rheumatism: Studies on 72 Sets of Twins, Ztschr. f. menschl. \:ererb.-u. Konstitutionslehre 21:687, 1938. Wilson, M. G., and Schweitzer, H. D.: Rheumatic Fever as a Familial Disease, J. Clin. Investigation 16:X5, 1937. Faulkner, J. M., and White, P. I).: The Incidence of Rheumatic Fever, Chorea and Rheumatic Heart Disease With Especial Reference to Their Occurrence in Families, J. A. M. A. 83:425, 1924.