key: cord-0763928-d9qn84ha
authors: Boughton, C. R.; Hawkes, R. A.; Lehmann, N. I.; Grohmann, G. S.
title: Hepatitis A Outbreak in a Residential School
date: 2008-03-25
journal: Aust N Z J Med
DOI: 10.1111/j.1445-5994.1980.tb03409.x
sha: d3d06df2c9146a260efb957a8b3c9fbea9cea8a7
doc_id: 763928
cord_uid: d9qn84ha

Summary: Hepatitis A outbreak in a residential school. C. R. Boughton, R. A. Hawkes, N. I. Lehmann and G. S. Grohmann, Aust. N.Z. J. Med., 1980, 10, pp. 4–6. Outbreaks of hepatitis A occurred sequentially in two wards for children in a residential institution for the mentally retarded in Sydney. Twenty‐six of 47 children were initially susceptible to hepatitis A. In the first ward affected, 77 of 13 susceptible children (85%), and in the second ward, four of 13 susceptible (31%), were infected. Of the 15 showing serological evidence of infection, five (33%) were clinically jaundiced.

The recent development of laboratory techniques for the detection of hepatitis A particles (HAV) in stools and subsequently serological tests for detection of antibodies to hepatitis A virus (anti-HAV) in serum, has enabled more precise definition of the diagnosis and epidemiology of hepatitis A. During a recent outbreak in two wards of a residential institution for the mentally retarded, appropriate specimens were obtained from inmates for liver function tests, for anti-HAV (total and specific IgM) and for HAV particles in stools.

The population studied were residcntial inmates of two wards. A and R. Ten of the total 31 patients had Down's syndrome (DS) and the rcmainder had mental deficiency duc to other causes (non-Down's, ND). These children were moderately retarded, ambulant and able to attcnd special schools. Some suffered episodes of diarrhoea and the personal hygiene of some children was unsatisfactory. The children from the two wards ate in the same dining room but at different times, played separately, attended several different schools outside the hospital, but occasionally joined an organiscd outing together.

The index case was a nine-year-old girl diagnosed on 2 February 1978, in Ward A which housed 22 patients aged from five to 14 years. The first case in Ward B was an 1 l-yearold girl diagnosed on 18 February 1978; this ward housed 19 children, aged from eight to 15 years.

Pooled human immune globulin was given by intramuscular injection to all children of Wards A and B on 3

February. Blood specimens were taken initially from those suspected of having hepatitis A, from all inmates on 15 February and again five weeks later. Those who were seronegative at the latter bleed had a further serum spccimen tested ten weeks later. Stool specimens were collected from the 34 childrcn in whom this was practicable.

Laboratory Method.s Srra: Liver function tests (serum bilirubin, serum glutamic pyruvic transaminase and serum glutamic oxalacetic transaminase) were carried out on all serum specimens. Examination for hepatitis B surface antigen (HBsAg) was carried out by radioimmunoassay (Ausria 11, Abbott Laboratories). The techniques used for the detection of anti-HAV (total and IgM specific) in sera were based on the radioimmunoassay method of Purccll et ul.' x 5 Slool , s p e c i m~w : Stool zpccirnens mere pIcpared for wlid phase ra dioiiiiiiiunoa ( S P K I A ) and immunoelectronmicroscopy (ItlZ.1) by cthod briccd on that dcscriheti by Locarnirii.' The SPIKA technique tiaed for the detection of H.4V particlcs in slool specimens was :I modification of Ilia1 of Purcell.'

Of the 22 patientr in Ward 4 nine had anti-HhV. hut ofnon-IghI type, in their seim indicating prior immuniry. Of thc I ? susceptihles. I I developed serological evidence ol' recent HA\' infection w t h the appearance of specific lgM anti-H.4V. T h e e (?:",,) of these had clinical jaunclice ( Table 1 J and ward staff suspected hepatitis in three of the non jaundiced patients because the children became listless. stools were noted to he pale and urine dark brown. These children erological cvidencc of HAL' infection. Ten of' the 1 I inrccted children showed biochemical and scrological evidence of H.4V intcction in thc first scinnii specinieri obtained on 15 February. The remaining patient did n o t 4iow IgM anli-HAV until the third specimen taken at the beginning of June.

In Ward R six 01' the total 19 children were fouiid to be already immune; of the I 3 susceptihlcs, lour showed serological evidence of HAV infechm of whom to had clinical jaundice (Table 1) . Of the four patients infected. seroconvci-sion occurred hy 17 February in two, arid the other two had scroconvcrtcd by 7 3 .Ilarch.

The administration of pooled human imniiinc globuliri to seronegative children did not result in dctectahli: anti-HAV titres when sarnplcd 12 day> later.

No sera showed the presence of FIHs.-\g.

Stools froin four of 34 cliildren examined contained HAV. HA\' particles were not found in specimens from patients without clinical, biochemical and serological evidence of hepatitis A. Enterovirus-like particles re detected in scven paticnts. and coronavirus particles i n file. The significance of the viruses other than HAV is not known.

The outbreak in Ward A was explosive, five children developing clinical illness within tw70 days. Ten of the 11 showing evidence of HAV infection apparently acquired the virus at approximately the same time from a single source. It is probable that the latter was a 13year-old girl who had subclinical infection: serial sera from this child showed no increase in total anti-HAV but did show the presence of anti-HAV of IgM type. All other patients with infection showed both an increase in total anti-HAV and the presence of specific IgM anti-HAV. The remaining patient who did not seroconvert until June, had subclinical infection probably modified by the injection of pooled human globulin.

Ward B may have beeo infected either from the original sourcc or sequentially from another inmate of Ward A; the latter patients ei-e probably infective for two to three weeks prior to the onset of their illness. Spread among Ward B inmates was apparently sequential, in that two children had clinical hepatitis on 18 and 20 February, and two had (subclinical) hepatitis shown serologically five weeks later. The two cases with clinical hepatitis in Ward B had received globulin on 3 February, apparently too late to render the infection subclinical.

The rate of clinical expression did not differ significantly between DS and ND patients. Five of 15 patients infected (33)!,,) were clinically jaundiced: a rather higher proportion than has been considered usual in HAV infection. However a recent similar serological and epidemiological study revealed a high clinical expression rate.3

In this environment the attack rate of hepatitis A among susceptibles was high (in Ward A 1 l 8 13 (85:,;)$ Ward B 4,'13 (317"). overall 58",;;). The patients in both wards ho developed evidence of HAV infection late in the outbreak, had all received globulin and all had subclinical infection.

I 976): A microtiter solid phase radioimmunoassay for hepatitis A antigen and antibody

Seroepidemiological in!cstigauon of patients and family contacts in an epidemic of hepdtitir A. J. .%fedrcal VWOIOK) I

Coronary Artery Spasm: Use of Ergonovine in Diagnosis*

From the Hallstrom Institute of Cardiology

We would like to acknowledge the assistance of Dr. R. C. Lonie, Medical Superintendent and the ward staff of Gladesville Hospital. Dr. Steven Locarnini kindly carried out electronmicroscopy on some of the faecal samples.Aust. N.Z. J . Med. 11980L 10. DD. [6][7][8][9][10][11] 

Summary: Coronary artery spasm: Use of ergonovine in diagnosis. S. 6. Freedman, R. Coronary artery spasm may cause variant angina pectoris',' and precipitate both unstable angina3 and myocardial infarction! Although spontaneous spasm has been observed at angiography', this occurrence is so uncommon that a reliable provocative test for spasm has been sought. Ergonovine maleate, a vasoconstrictor, was first used as a test for coronary artery disease in 1949 by Stein', and recently coronary artery spasm has been provoked by ergonovine in patients with either fixed coronary arterial obstruction or normal coronary arteries6" The present study evaluated the diagnostic use of ergonovine in patients with chest pain but without significant coronary obstruction.

Sixty-nine patients (