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Rapid immune response to influenza vaccination
the child after birth, but none has terminated a pregnancy for this reason. We do not insist on parental testing, but recommend that it be considered before another pregnancy is conceived, and that other appropriate family members be informed of the carrier risk for CF and consider testing. test
done
on
S H Black, D P Bick, A Maddalena, J D Schulman, S L Jones, L Fallon, E Cummings, G Menapace-Drew Genetics and IVF Institute, Fairfax, VA 22031, USA; and Medical
antibody isotype detection
assay with
heparinised blood from vaccinees. We found that influenza specific IgA, IgG, and IgM secreting cells could be detected within 4-7 days postvaccination.4 Our results reported here indicate that immune responses to influenza vaccine can develop within a few days. There may be, therefore, a place for influenza vaccination within a period of influenza activity for those individuals at risk who have missed their annual vaccination.
College of Virginia,
Richmond
1 Bick D, Maddalena A, Black SH, et al. Prenatal screening for &Dgr;F508 mutation in population not selected for cystic fibrosis. Lancet 1990; 336:1324. 2 Bick DP, Maddalena A, Black SH, et al. Pilot study for the &Dgr;F508 cystic fibrosis (CF) mutation in an unselected population. Am J Hum Genet 1990; 47: A209. 3 Maddalena A, Bick D, Black SH, et al. Prenatal screening for cystic fibrosis (CF) in United States couples without a previously affected child. Am J Hum Genet 1991; 49: 329.
Mark Zuckerman, Rebecca Lars Haaheim, John Oxford
University College London Medical School, Division of Virology, London WC1 6DP, UK; Department of Academic Virology, London Hospital Medical College, London E1; and National Institute for Biological Standards and Control, South Mimms, Potters Bar, Hertfordshire
1 2
3
Rapid immune response to influenza vaccination SiR-In the light of recent reports of influenza A H3N2 activity in the USA,1 we report results of an inactivated influenza vaccination study done with 16 volunteers, aged between 20 and 80 years, where a rapid immune response was detected. 0-5 mL of inactivated trivalent subunit influenza vaccine (Influvac, Duphar BV, Weesp, Netherlands; 10 ug/mL of A/Guizhou/54/89 H3N2, A/Taiwan/l/86 H1N1, and B/ Yamagata/16/88) was given intramuscularly into the deltoid aspect of the arm after collection of a blood sample. Further blood samples were taken from each volunteer at days 2, 4, 6, and 21 post-vaccination. The sera were examined for the viral antibodies to vaccine components by haemagglutination inhibition (HI) for influenza A and single radial haemolysis (SRH) for influenza B with standard techniques.2 An HI titre of at least 40 HI units and an SRH zone of at least 25 mm2 indicate protective antibody levels.3 Although a proportion of the volunteers had protective antibodies pre-vaccination, a rapid response was seen in some individuals between 2 and 6 days post-vaccination (table). 2 vaccinees had detectable SRH antibody rises to B/Yamagata/ 16/88 virus within 2 days and 10 individuals (63%) had significant antibody responses to at least one vaccine strain by 10 days post-vaccination. Overall, 75-94% of the volunteers had protective antibody to all three vaccine virus strains within 6 days post-vaccination and 81-100% had protective antibody by 21 days. 4 of the 16 volunteers who were in an at-risk group had received influenza vaccine the previous year as recommended by the UK Department of Health. Of note, all 4 had reasonable amounts of pre-existing antibody to all three vaccine components. In a larger study, we have focused on an alternative method to look at vaccine responses by examining plasma cell antibody secretion immediately post-vaccination by use of a sensitive
Table : % volunteers with protective antibody to Inactivated Influenza vaccine
Cox, Janette Taylor, John Wood,
4
Anon. Influenza in summer 1993. Commun Dis Rep Wk 1993; 3 (39): 1. Zuckerman MA, Wood J, Chakraverty P, et al. Serological responses in volunteers to inactivated trivalent subunit influenza vaccine. J Med Virol 1991; 33: 133-37. Jennings R, Smith TL, Mellersh AR, et al. Antibody response and persistence in volunteers following immunisation with varying dosages of a trivalent surface antigen influenza virus vaccine. J Hyg 1985; 94: 87-95. Cox RJ, Haaheim LR, Zuckerman MA, Oxford JS. A rapid immune response to inactivated influenza vaccine. Presented at International Scientific Conference on Options for the Control of Influenza II, Sept 26-Oct 2, 1992, Courchevel, France.
Does
antiarrhythmic magnesium therapy
enhance malarial infection? SiR-Several reports in The Lancet have shown that antimalarial drugs such as quinine, quinidine, and halofantrine induce QT-lengthening and arrhythmogenic effects (Karbwang and colleagues, Aug 21, p 501 and refs 1,2). Hypomagnesaemia can prolong repolarisation and may contribute to the predisposition of acquired long QT syndrome (LQTS) and ventricular tachycardia. High-dose intravenous magnesium is recommended for the initial treatment of acquired LQTS and accompanying torsades de pointes.3 However, magnesium deficiency was reported to have some protective effect in Plasmodium chabaudi and P vinckei but not in P berghei infections in mice. Mg2+ supplements in magnesium-deficient individuals were postulated to lead to a rapid multiplication of existing parasites and to the development of clinical malaria.4 Thus the use of magnesium for treatment of drug-induced arrhythmias should not enhance
plasmodial growth. We therefore investigated the influence of high magnesium concentrations on P falciparum in cultures and on the course of P berghei infection in 20 NMRI mice. Plasma magnesium concentrations were measured on days 0, 5, and 10 after inoculation of 21 x 106 parasitised erythrocytes. Mean values were 1 62 mmol/L in the group fed magnesium aspartate hydrochloride (10 000 parts per million [ppm]) compared with 1-01 mmol/L in controls (500 ppm). The infections evolved similarly in both groups. Mean latent periods in magnesiumfed and control mice, respectively, were 3-3(2-7) and 2-3(1-3) days, mean survival time 139 (9-22) and 10-6 (7-22) days, and mean peak parasitaemias 53 2 (17-73) and 511% (35-84). Our results suggest that there are no adverse effects of increased plasma magnesium on the course of P berghei infection and confirmed our in-vitro results with P falciparum.S We conclude that for treatment of LQTS and ventricular tachycardia induced by antimalarial drugs magnesium should be considered. Since magnesium deficiency is common, especially in developing countries because of malnutrition, frequent pregnancies, and lack of magnesium salts in tropical
1113
done
on
S H Black, D P Bick, A Maddalena, J D Schulman, S L Jones, L Fallon, E Cummings, G Menapace-Drew Genetics and IVF Institute, Fairfax, VA 22031, USA; and Medical
antibody isotype detection
assay with
heparinised blood from vaccinees. We found that influenza specific IgA, IgG, and IgM secreting cells could be detected within 4-7 days postvaccination.4 Our results reported here indicate that immune responses to influenza vaccine can develop within a few days. There may be, therefore, a place for influenza vaccination within a period of influenza activity for those individuals at risk who have missed their annual vaccination.
College of Virginia,
Richmond
1 Bick D, Maddalena A, Black SH, et al. Prenatal screening for &Dgr;F508 mutation in population not selected for cystic fibrosis. Lancet 1990; 336:1324. 2 Bick DP, Maddalena A, Black SH, et al. Pilot study for the &Dgr;F508 cystic fibrosis (CF) mutation in an unselected population. Am J Hum Genet 1990; 47: A209. 3 Maddalena A, Bick D, Black SH, et al. Prenatal screening for cystic fibrosis (CF) in United States couples without a previously affected child. Am J Hum Genet 1991; 49: 329.
Mark Zuckerman, Rebecca Lars Haaheim, John Oxford
University College London Medical School, Division of Virology, London WC1 6DP, UK; Department of Academic Virology, London Hospital Medical College, London E1; and National Institute for Biological Standards and Control, South Mimms, Potters Bar, Hertfordshire
1 2
3
Rapid immune response to influenza vaccination SiR-In the light of recent reports of influenza A H3N2 activity in the USA,1 we report results of an inactivated influenza vaccination study done with 16 volunteers, aged between 20 and 80 years, where a rapid immune response was detected. 0-5 mL of inactivated trivalent subunit influenza vaccine (Influvac, Duphar BV, Weesp, Netherlands; 10 ug/mL of A/Guizhou/54/89 H3N2, A/Taiwan/l/86 H1N1, and B/ Yamagata/16/88) was given intramuscularly into the deltoid aspect of the arm after collection of a blood sample. Further blood samples were taken from each volunteer at days 2, 4, 6, and 21 post-vaccination. The sera were examined for the viral antibodies to vaccine components by haemagglutination inhibition (HI) for influenza A and single radial haemolysis (SRH) for influenza B with standard techniques.2 An HI titre of at least 40 HI units and an SRH zone of at least 25 mm2 indicate protective antibody levels.3 Although a proportion of the volunteers had protective antibodies pre-vaccination, a rapid response was seen in some individuals between 2 and 6 days post-vaccination (table). 2 vaccinees had detectable SRH antibody rises to B/Yamagata/ 16/88 virus within 2 days and 10 individuals (63%) had significant antibody responses to at least one vaccine strain by 10 days post-vaccination. Overall, 75-94% of the volunteers had protective antibody to all three vaccine virus strains within 6 days post-vaccination and 81-100% had protective antibody by 21 days. 4 of the 16 volunteers who were in an at-risk group had received influenza vaccine the previous year as recommended by the UK Department of Health. Of note, all 4 had reasonable amounts of pre-existing antibody to all three vaccine components. In a larger study, we have focused on an alternative method to look at vaccine responses by examining plasma cell antibody secretion immediately post-vaccination by use of a sensitive
Table : % volunteers with protective antibody to Inactivated Influenza vaccine
Cox, Janette Taylor, John Wood,
4
Anon. Influenza in summer 1993. Commun Dis Rep Wk 1993; 3 (39): 1. Zuckerman MA, Wood J, Chakraverty P, et al. Serological responses in volunteers to inactivated trivalent subunit influenza vaccine. J Med Virol 1991; 33: 133-37. Jennings R, Smith TL, Mellersh AR, et al. Antibody response and persistence in volunteers following immunisation with varying dosages of a trivalent surface antigen influenza virus vaccine. J Hyg 1985; 94: 87-95. Cox RJ, Haaheim LR, Zuckerman MA, Oxford JS. A rapid immune response to inactivated influenza vaccine. Presented at International Scientific Conference on Options for the Control of Influenza II, Sept 26-Oct 2, 1992, Courchevel, France.
Does
antiarrhythmic magnesium therapy
enhance malarial infection? SiR-Several reports in The Lancet have shown that antimalarial drugs such as quinine, quinidine, and halofantrine induce QT-lengthening and arrhythmogenic effects (Karbwang and colleagues, Aug 21, p 501 and refs 1,2). Hypomagnesaemia can prolong repolarisation and may contribute to the predisposition of acquired long QT syndrome (LQTS) and ventricular tachycardia. High-dose intravenous magnesium is recommended for the initial treatment of acquired LQTS and accompanying torsades de pointes.3 However, magnesium deficiency was reported to have some protective effect in Plasmodium chabaudi and P vinckei but not in P berghei infections in mice. Mg2+ supplements in magnesium-deficient individuals were postulated to lead to a rapid multiplication of existing parasites and to the development of clinical malaria.4 Thus the use of magnesium for treatment of drug-induced arrhythmias should not enhance
plasmodial growth. We therefore investigated the influence of high magnesium concentrations on P falciparum in cultures and on the course of P berghei infection in 20 NMRI mice. Plasma magnesium concentrations were measured on days 0, 5, and 10 after inoculation of 21 x 106 parasitised erythrocytes. Mean values were 1 62 mmol/L in the group fed magnesium aspartate hydrochloride (10 000 parts per million [ppm]) compared with 1-01 mmol/L in controls (500 ppm). The infections evolved similarly in both groups. Mean latent periods in magnesiumfed and control mice, respectively, were 3-3(2-7) and 2-3(1-3) days, mean survival time 139 (9-22) and 10-6 (7-22) days, and mean peak parasitaemias 53 2 (17-73) and 511% (35-84). Our results suggest that there are no adverse effects of increased plasma magnesium on the course of P berghei infection and confirmed our in-vitro results with P falciparum.S We conclude that for treatment of LQTS and ventricular tachycardia induced by antimalarial drugs magnesium should be considered. Since magnesium deficiency is common, especially in developing countries because of malnutrition, frequent pregnancies, and lack of magnesium salts in tropical
1113