Scandinavian Journal of Infectious Diseases

ISSN: 0036-5548 (Print) 1651-1980 (Online) Journal homepage: http://www.tandfonline.com/loi/infd19

HBsAg Positive Adopted Children as a Cause of Intrafamilial Spread of Hepatitis B Erik Nordenfelt & Erik Dahlquist To cite this article: Erik Nordenfelt & Erik Dahlquist (1978) HBsAg Positive Adopted Children as a Cause of Intrafamilial Spread of Hepatitis B, Scandinavian Journal of Infectious Diseases, 10:3, 161-163, DOI: 10.3109/inf.1978.10.issue-3.01 To link to this article: http://dx.doi.org/10.3109/inf.1978.10.issue-3.01

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Date: 16 March 2016, At: 06:07

Scand J Infect Dis 10: 161-163. 1978

HBsAg Positive Adopted Children as a Cause of lntrafamilial Spread of Hepatitis B ERIK NORDENFELT and ERIK DAHLQUIST

Scandinavian Journal of Infectious Diseases 1978.10:161-163.

From the Depnrtments of Medicnl Microbiology nnd lnfectioits Diseases, University Hospital, Lund, Sweden

ABSTRACT. About 5 % of the children adopted to Sweden from mostly India and Korea are chronic carriers of HBsAg. Most of them are also e-antigen positive. In this investigation 12 families with such children have been studied to evaluate the infectivity risk. Out of 36 family members 5 have had clinical hepatitis, another 2 were HBsAg positive without clinical symptoms and 15 had anti-HBs. It seems clear that these children are a source of infection and all children adopted from countries with high prevalence of hepatitis B should be screened to be able to define the risk group.

INTRODUCTION

MATERIAL AND METHODS

Each year a number of children from foreign countries are adopted in Swedish families. The children come mostly from India and Korea. When they arrive in Sweden they generally have a health control and at our hospital they have also been screened with regard to hepatitis B antigen (HBsAg). During the last 6 years about 400 children have been investigated. As expected these children have a much higher carrier rate, about 5 % ( 2 ) , than the general Swedish population which has 0.1-0.5 % (3, 7). The possible infectivity risk of the HBsAg positive children is in many cases a social problem. From previous studies it seems that e-antigen is a good marker for infectivity (1, 9). We have found that most of these children are chronic carriers and e-antigen positive. There is thus a need to evaluate this risk. We have in our investigation examined 12 families with HBsAg positive adopted children with regard to serologic evidence of hepatitis B.

Childreti examined There are two groups of children. Firstly, of those found to be HBsAg positive at the health control at the Clinic of Infectious Diseases, University Hospital, Lund, we have been able to follow 9 children from 8 families who have had regular controls with regard to liver enzymes and HBsAg. At the coFtrols during 1977 all family members were asked to give blood samples to be tested for HBsAg and anti-HBsAg. The other group consists of 5 children from 4 families living in other parts of Sweden, from whom single blood samples have been sent to the Department of Medical Microbiology, for HBsAg and e-antigen tests during 1977. In connection with these tests the family members have also been tested for HBsAg and anti-HBsAg. Seven children have come from India, 6 from Korea and 1 from Thailand. At the time of this investigation the children were between 9 months and 16 years old. Laboratory methods HBsAg and anti-HBs were determined by radioimmunoassay (Ausria and Ausab from Abbott, USA). The

Table I. Summary of duta from 14 HBsAg positive children No. of children

e-antigen positive

I. Regularly followed

9

9

11. Not regularly

5

5

followed

11-781953

Clinical status

Time in Sweden

Asymptomatic. All slight raise of transferases Asymptomatic. No regular controls on liver enzymes

1.5 to 5 years 9 months to 6 years

Sctrtid J InJkr Dis 10

162

E. Nordenfelt and E. Dahlquist

Table 11. Signs ofhepatitis B infection in 38 family members Clinical disease

Scandinavian Journal of Infectious Diseases 1978.10:161-163.

Grandparents Mothers Fathers Brothers/ sisters Total

1

2 I

AntiHBsAg HBs

I I

1

5

2

No sign

Not tested

I 4 5

1

5

4

1

15

14

2

1

5 4

specificity of the reactions was determined by either immunodiffusion (ID) (8) or by neutralisation test, i.e. inhibition of the reaction by adding known anti-HBs or HBsAg to the sample prior to the determination in the assay. e-antigen was determined by ID as earlier described (6). In the gel was now also included 2.5% polyethylenglycol (PEG) which has been shown to enhance precipitation (4). We have found this true also for the e-antigen system. With PEG 2 distinct e-antigen lines are regularly detected, sometimes even three (10). Core associated DNA polymerase was determined as previously described (9).

RESULTS The first group of children investigated in Lund have been followed between 1.5 to 5 years. During this time at least 5 and up to 10 controls on each child have been done. In the controls they have been both HBsAg and e-antigen positive. In 5 of 7 children tested, also core associated DNA polymerase has been detected. Liver transferases have in most instances shown slightly raised values. Some children have had, in single controls, normal liver transferases. All 9 children have seemed completely healthy during the whole observation period and have had a normal development (Table I). The other 5 children have been in Sweden between 9 months and 6 years. In the samples tested they have all been e-antigen positive. They have had a normal development and been clinically healthy. At the time for their investigation 1 of 2 children had slightly raised transferases. In 3 children no biochemical tests have been performed (Table I ) . The 14 children belong to 12 families who have 38 members consisting of parents, brothers and sisters. In one family also the grandparents were included as they regularly took care of the children. Blood samples have been obtained from 36 family members.

Five cases of clinical hepatitis have been diagnosed among the family members since the arrival of the children. The diagnoses have been hepatitis B in 4 cases based on positive tests for HBsAg. The 5th case now has anti-HBs. The children had been in the families from 6 to 41 months (mean 15 months) at the time of clinical disease. I5 persons were found to have anti-HBs and 2 had HBsAg without clinical symptoms of hepatitis. The results are summarised in Table 11. It appears that out of 36 investigated persons 22 showed signs of infection with hepatitis B (61 %). Only in one of these 12 families none of the members had any signs of infection. That family consists of 4 members and the child was adopted 4 years ago. This child was e-antigen positive but DNA polymerase negative. No real control group has been included in this study. During 1977 we have, however, studied the frequency of anti-HBs in some selected groups in our region. The results are presented in Table 111. The prevalence of anti-HBs in these groups could be used for comparison; it varies from 2 % among blood donors up to 23 % in a clinic for renal dialysis where a hepatit B epidemic took place some years ago. Among addicts the prevalence of anti-HBs was 55 %. DISCUSSION Other possible sources for hepatitis B infection can of course not be excluded by this investigation. For example in one family both parents are physicians and in another the mother is a nurse. However, in all the other families the parents' professions do not indicate any special risk for hepatitis B. No hospital Table 111. Anti-HBs in some selected groups Total no. investigated Blood donors Staff in Dentist Dracticeu Surgery'department Infectious disease department Dialysis department Addicts

Anti-HBs positive

No.

%

423

I

2

401 69

21 I

10

90 91 140

16

21 I1

5

18 23 55

Figures are part of ongoing investigation of hepatitis spread in dentist practice in collaboration with Prof. Bertil Hoorn and Ass. Prof. Goran Kock, Central Hospital, Jonkoping.

Scandinavian Journal of Infectious Diseases 1978.10:161-163.

Intrafumiliul spread of hepatitis B

treatment with transfusion is known. Thus the occurrence of both clinical cases and high prevalence of anti-HBs among the family members strongly indicate these children as the source of infection. In agreement with this is an investigation reporting evidence of transmission of both hepatitis A and B from Vietnamese orphans adopted in American families (12). By information and simple rules for avoiding blood contact we have good experience in preventing spread of hepatitis B in hospitals and institutions (5). To prevent intrafamilial spread especially from children is much more difficult. In spite of the information to the family members about certain precautions to avoid infection we have found this considerable spread. It would for obvious reasons be very unlucky if these children should be isolated from normal social upbringing. We have until now no information about cases with clinical hepatitis B as a result of extrafamilial spread of the infection from these children. With simple rules for avoiding blood contact in schools and other institutions the risk for any spread ought to be small. It should be pointed out that the clinical cases in this study have been mild and that most infected family members have had a subclinical infection. We think therefore that the findings of intrafamilial spread of hepatitis B should not implicate any isolation measures of the children from the society. As vaccine against hepatitis B is foreseeable such intrafamilial spread could probably be prevented in the near future. Before the vaccine is available perhaps passive immunisation could be considered. Preventive treatment with hyperimmunoglobulin is however very expensive and there are limited supplies available. Ordinary gamma globulin has a certain amount of anti-HBs and has given a passiveactive immunity which suggests that such treatment could be tried (1 1). We think that all children adopted from countries with high prevalence of hepatitis B should be tested to be able to define the risk group which is relatively small as about 95 % of the children are HBsAg negative. Furthermore, all parents who are planning to adopt children should be informed about the risk.

ACKNOWLEDGEMENTS

163

Bertil Hoorn, Central Hospital, Jonkoping and Dr 0. Paulsen, Central Hospital, Boden for all help in collecting the material. We also thank Miss Lena Eriksson, Mrs Britt-Marie Karlsson and Mrs Eva Miller for excellent technical assistance. This investigation was supported by the Swedish Medical Research Council (project B77-36X-2865-01).

REFERENCES 1. Alter, H. J., Seeff, L. B., Kaplan, P. M., McAuliffe,

V. J., Wright, E. C., Gerin, J. L., Purcell, R. H., Helland, P. V. & Zimmerman, H. J.: Type B hepatitis: The infectivity of blood positive for e-antigen and DNA polymerase after accidental needle-stick exposure. N Engl J Med 295: 909, 1976. 2. EdCn, T., Nordenfelt, E. & Ursing, B.: Adoptivbarn och halsokontroll. Lakartidningen 10: 944, 1975. 3. Hansson, B. G., Sundstrom, G. & Johansson, T.: Occurrence of hepatitis B surface antigen (HBsAg) in blood donors and patients suffering from transfusion hepatitis. Acta Pathol Microbiol Scand [C] 83: 112, 1975. 4. Harrington, J. C., Fenton, J. W. & Pert, J. H.: Polymer-induced precipitation of antigen-antibody complexes: “Preciplex” reactions. Immunochemistry 8:413, 1971. 5. Iwarson, S., Magnius, L., Lindholm, A., Nordenfelt, E. & Ringertz, 0.: Medicinska, vardtekniska och sociala aspekter pB barare av hepatit B (Au) antigen. Lakartidningen 71: 5171, 1974. 6. Lofgren, B., Myhre, E. & Nordenfelt, E.: e-antigen in patients with transient and chronic carriership of hepatitis B antigen. Scand J Infect Dis 8: 225, 1976. 7. Nordenfelt, E.: Australien-antigen och hepatit. Thesis. Studentlitteratur 1971. 8. Nordenfelt, E. & LeBouvier, G.: The distribution of subtypes in various Swedish populations positive for hepatitis B antigen. Scand J Infect Dis 5: 279, 1973. 9. Nordenfelt, E. & KjellCn, L.: Dane particles, DNA polymerase and e-antigen in two different categories of hepatitis B antigen carriers. Intervirology 5: 225, 1975. 10 Nordenfelt, E.: Unpublished observations. 11. .US Public Health service Advisory Committee on Immunization Practices: Immune globulins for protection against viral hepatitis: CDC MMWR 26: 425, 1977. 12. Vernon, T. M., Wright, R. A., Kohler, P. F. & Merrill, D. A.: Hepatitis A and B in the family unit. Nonparental transmission of asymptomatic children. JAMA 235: 2829, 1976.

Address f o r reprints:

E. Nordenfelt, M .D., Inst. Med. Microbiology, Solvegatan 23, S-22362 Lund, Sweden

We thank Drs Birgitta Borulf, Central Hospital, Halmstad, and I. Frolov, Central Hospital, Kristianstad, Professor Sctitrd J Inject Di.v 10

HBsAg positive adopted children as a cause of intrafamilial spread of hepatitis B.

Scandinavian Journal of Infectious Diseases ISSN: 0036-5548 (Print) 1651-1980 (Online) Journal homepage: http://www.tandfonline.com/loi/infd19 HBsAg...
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