Antibody responses to recombinant, yeast-derived hepatitis B vaccine in teenage New Zealand children.

Three groups of healthy teenage New Zealand children were given 2.5 micrograms, 5 micrograms and 10 micrograms, which is the currently recommended dose, of Merck Sharp and Dohme recombinant yeast-derived hepatitis B vaccine at time 0, 1 and 6 months and tested for antibody responses to vaccine and for other hepatitis B virus markers. Seroconversion rates exceeded 98% in all three groups. Geometric mean titres (GMT) of the anti-HBs increased with higher doses. There was no significant differences in GMT between the sexes. Under the conditions of this study, 2.5 micrograms doses of this vaccine induced an excellent antibody response in children 12-14 years of age.

Immunogenicity of low doses of hepatitis B vaccine in children: a study in 650 New Zealand children.

Six hundred and fifty New Zealand children from 2-12 years of age were vaccinated three times with 2 mcg intramuscular (IM) doses of Merck Sharp and Dohme plasma-derived hepatitis B vaccine (H-B-Vax), at 0, 1, and 6 months, and tested 2-3 months later for antibody to hepatitis B surface antigen (anti-HBs) by radioimmunoassay (RIA). Overall, 96.5% of the children seroconverted for anti-HBs by RIA, having levels greater than 2.1 RIA S/N units, with 91.2% having values greater than 10 S/N units. Anti-HBs levels were also determined by enzyme immunoassay (EIA), by which method a significantly better response was demonstrated in 2-4-year-olds than in older children. This study demonstrated that a satisfactory anti-HBs response was obtained using one-fifth of the recommended doses of hepatitis B vaccine.

Low-dose vaccination against hepatitis B in children: one-year follow-up.

Six hundred forty-three children, negative for markers of hepatitis B virus (HBV) infections, were given three X 2-micrograms doses of Merck, Sharp and Dohme (MSD) plasma derived hepatitis B vaccine (H-B-Vax) at monthly intervals. Twelve months after the first dose of vaccine, antibody to hepatitis B surface antigen (anti-HBs) was detected in 89% of children by radioimmunoassay (RIA) and in 83% by enzyme immunoassay (EIA). Seroconversion rates and anti-HBs titres were significantly greater in 1-4-year-olds than in older children (p less than 0.01). Eighteen children with no anti-HBs or other markers of HBV at this time were given 10 micrograms of vaccine and tested one month later. Seventeen developed anti-HBs, 12 at levels consistent with an anamnestic response. Forty-nine HBV-marker-negative children seroconverted for antibody to hepatitis B core antigen (anti-HBc) in the 8-month period before or the 12-month period following vaccination. Forty-six of these children were positive for anti-HBs, and one has been confirmed as a chronic carrier of hepatitis B surface antigen (HBsAg). Three cases of clinical hepatitis B in children have been seen in the community since the vaccination programme began. Two of these were amongst the estimated 5% of children who were not vaccinated. The third was in a vaccinee and occurred 4 1/2 months after the last dose of vaccine.(ABSTRACT TRUNCATED AT 250 WORDS)

A seroepidemiological study of the prevalence of hepatitis B infections in a hyperendemic New Zealand community.

The prevalence of hepatitis B surface antigen (HBsAg) and its antibody (anti-HBs) were studied in 93% of the population of the New Zealand township of Kawerau. Sera were collected from 7901 subjects over six months old, and 3318 (42%) had markers of hepatitis B virus (HBV) infections. Five hundred and nineteen (6.6%) were positive for HBsAg and 485 (96.4%) of 503 retested were confirmed as chronic carriers. HBsAg prevalence was 5.4% in the 0-4 years age group but only 1 of 66 children under one year old was positive suggesting that later cross infection, rather than perinatal transmission was the major factor responsible for the high pre-school carrier rate. Total HBV marker prevalence increased dramatically in early school years and peak marker prevalence was 67.7% in the 15-19 year age group. Prevalence of HBsAg was more than four times higher in non-europeans than in Europeans (Caucasians). Other factors significantly associated with hepatitis B virus marker prevalence in children were: number of years spent in Kawerau, which was associated with anti-HBs prevalence; and size of household, which was associated with HBsAg prevalence. Number of siblings was not a significant risk factor over and above the effect of size of household. Factors associated with marker prevalence in adults were: number of years spent in Kawerau, which was associated with anti-HBs; birth in the Northern half of the North Island, which was associated with both HBsAg and anti-HBs; size of household, which was more strongly associated with HBsAg prevalence; and amateur tattoos, which were associated with anti-HBs prevalence but not with HBsAg prevalence.

Low dose hepatitis B vaccination in children.

One hundred and sixty-nine children negative for hepatitis B surface antigen (HBsAg) and antibody (anti-HBs), were given three doses of hepatitis B vaccine at monthly intervals. Doses were two micrograms or four micrograms given intradermally (ID) or intramuscularly (IM). All children were tested for HBsAg, anti-HBs and antibody to hepatitis B core antigen (anti-HBc) one month after the second dose of vaccine. Overall, 74% of children on two micrograms doses and 71% of children on four micrograms doses responded to two doses of vaccine by the production of anti-HBs. At this point, mass immunisation of other susceptible children was commenced. Four of 92 (4%) three to five year old subjects and 20 of 77 (26%) nine to 12 year olds were found to be anti-HBc positive alone, indicating prior infection. All 77 older children were further tested two months after the third dose of vaccine. All 20 who were anti-HBc positive, sero-converted for anti-HBs. Of the remaining 57, 52 (91%) produced anti-HBs at acceptable geometric mean titres (GMT). Three doses of two micrograms of H-B-VAX, given at monthly intervals were chosen for mass vaccination of high risk susceptible children in this mobile community, providing over 90% sero-conversion at low cost with a minimum of side effects.

Prevalence of hepatitis B infections in a multiracial New Zealand community.

Plans to control hepatitis B virus (HBV) infections in a high risk mixed race community, included the need for prevalence studies of HBV markers. Accordingly 7901 subjects, 93% of the population of Kawerau, where European and non-European children are present in almost equal numbers, were tested for hepatitis B surface antigen (HBsAg) and antibody to HBsAg (anti-HBs). Positive HBsAg sera were titred and tested for hepatitis B e antigen (HBeAg). Highest rates for HBsAg and anti-HBs combined, were found in the 15-19 year old age groups; 61.6% in Europeans and 74.5% in non-Europeans. HBsAg prevalence was 4.2% and 18.2% respectively in the same groups. Ninety-six point four percent of 503 HBsAg positives followed up were confirmed as carriers. Infectivity as shown by HBeAg prevalence and HBsAg titre was highest in 0-10 year olds and declined with age. Prevalences were low in children aged less than one year old, suggesting that perinatal transmission was not a major factor in childhood carriage. Therefore attempts to control acquisition of carriage by vaccinating only those children of HBeAg positive mothers are unlikely to be successful.

Lymphocyte-mediated cytotoxicity against gliomas.

The effects of peripheral blood lymphocytes from patients with glioma on glioma cells grown in culture was studied using an in vitro microcytotoxicity test. Lymphocytes from 12 of the 20 patients studied showed significant cytotoxic activity against their own tumour cells. Four of them reacted against heterologous glioma cells and 4 also showed some reactivity against foetal brain cells. An attempt to correlate in vitro cytotoxicity with the degree of lymphocytic infiltration of the tumour suggested an association, but the number of cases examined was too small to achieve statistical significance.

The migratory behavior of T blasts to contact sensitivity reactions in activelyand passively sensitized mice.

The arrival of cells from lymph nodes immunized with the contact sensitizing agents oxazolone and picryl chloride at ears challenged with these antigens was studied inmice using the technique of labelling with -51Cr. An apparent specificity of arrival was seen because the immune cells transfered contact sensitivity passively, giving rise to an inflammatory response in the ear, to which a subpopulation of cells (T blasts) was non-specifically attracted. It was also shown that there are at least two distinct populations of cells with the ability to move to inflammatory sites: the first, found in immunized lymph nodes, moves to contact sensitivity reactions in both actively and passively sensitized mice; the second, found in bone marrow and oil-induced peritoneal exudates, moves to contact sensitivity reactions in actively sensitized mice, whereas in passively sensitized mice, the arrival of these cells at contact sensitivity reaction is poor. It is suggested that the ability of T blasts to move to sites of inflammation my be useful as an assay technique for contact sensitivity reactions.

Torulopsis glabrata endocarditis complicating aortic homograft valve treated with 5-fluorocytosine: case report with discussion of antifungal chemotherapy.

A case of Torulopsis glabrata endocarditis occurring in a patient 14 months after aortic homograft valve replacement is reported. The infection was not controlled by amphotericin B which led to progressive renal impairment. Re-operation was delayed by the development of multiple infarctions due to coronary emboli. The infection was subsequently eradicated by oral treatment with the newer antifungal agent, 5-fluorocytosine, but death of the patient eventually occurred from an arrhythmia related to the persisting myocardial failure consequent upon episodes of transmural infarction. Current evidence favours the use of early re-operation in all cases of endocarditis in addition to aggressive chemotherapy with a combined regime of amphotericin B and 5-fluorocytosine. Clinical pharmacology of 5-fluorocytosine is briefly discussed.