496
like this approach because one never knows when the judicial eye is going to open. If doctors want to change the law then one approach is to directly challenge it, as Dr Bourne did in 1939.2 Not many are brave enough or convinced enough of their principles for such confrontation. The other approach is to make withdrawal of treatment, especially in the persistent vegetative state, a public issue. This may be achieved by debate in medical journals, articles in national newspapers, and public debate on television. Medicine and law are only in place to serve society. I believe that medical practice is being adapted to suit the changes demanded by society. The law must also change. Intensive Therapy Unit, Western Infirmary, Glasgow G11 6NT, UK
NICHOLAS PACE
1. Pace N, Plenderleith JL, Dougall JR. Moral support. Br J Hosp Med (m press). 2. R v Bourne. 1939. 1KB 687.
principles m withdrawing advanced life
SIR,—The Institute of Medical Ethics Working Party’s the withdrawal of life support from patients in a persistent vegetative state should have included in its argument the complications of enteral alimentation. Nasogastric tubes can cause pressure sores along the route of insertion, oesophageal bleeding, and sinus infections.1 The use of gastrostomy tubes is complicated by the need for open surgical or percutaneous placement.2 In 70 elderly patients Ciocon et al3 showed an increased frequency of aspiration with gastrostomy tubes (56%) compared with nasogastric tubes (44%). Fluid overload and congestive failure are also seen in artificial feeding. Artificial feeding therefore shares with other medical treatments the potential for harm as well as good. In a persistent vegetative state, as defmed by the Working Party, tube feeding is indeed a futile and sometimes harmful therapy. statement on
12311 Ventura Boulevard, Studio City, California 91604, USA
VICTOR L. KOVNER
1. Olins
NJ, Annas GJ. Comments on withdrawal of artificial feeding: Professor Annas responds. Am JPubl Health 1985; 75: 1347-48. 2 Ponsky JL, Gauderer MWL, Stellato TA, et al. Percutaneous approaches to enteral hyperalimentation. Am J Surg 1985; 149: 102-05. 3. Ciocon JO, Silverstone FA, Graver LM, et al. Tube feeding m elderly patients: indications, benefits, and complications. Arch Intern Med 1988; 148: 429-33.
Parvovirus B19 infection and transient fetal
hydrops SIR,-Human parvovirus (B19) infection can lead to nonhydrops and fetal death,l possibly because of anaemia secondary to infection of erythroid progenitor cells. Although there immune
have been instances of normal outcome despite serological evidence of intrauterine infection,l or after treatment with intrauterine blood transfusion/,3 there are no reports of successful pregnancies complicated by B19-induced hydrops without such intervention. However, we now describe such a case. A 33-year-old woman, who was para 3 plus 0 and blood group A rhesus positive, requested ultrasound scanning at 21 weeks’ gestation to determine fetal sex. Gross fetal ascites and a small pericardial effusion were found. Fetal blood sampling revealed mild anaemia (packed cell volume 0-26) with increased erythropoietic activity (184 reticulocytes/ 103 red blood cells). Fetal karyotype was 46XY and maternal serum alpha-fetoprotein was within the normal range (153 pgJl). Parvovirus B19 DNA was detected in fetal serum by dot-blot hybridisation and parvovirus particles were seen by immune electron microscopy.’ B19-specific IgG was present (85 RIA units),5 but specific IgM was not detected. Fetal serum was unable to infect erythroid progenitor cells in vitro, which suggests that the observed viral particles had been neutralised by specific antibody. Maternal serum taken at the same time contained no B 19 DNA, but did have B19-specific IgG (more than 100 RIA units) and IgM (11 RIA units), consistent with recent infection. The mother recalled a brief, influenza-like illness at about 10 weeks’ gestation, but denied rash or arthralgia.
Repeat ultrasound examination
at
22 weeks’
spontaneous resolution of hydrops, and further
gestation showed
25 and 31 weeks’ revealed normal fetal growth. Labour was induced at 39 weeks’ and a boy weighing 3111 g was delivered with Apgar scores of ten at both I and 5 minutes. Physical examination was normal and cord blood haemoglobin was 15-7 g/dl with 11% normoblasts. Macroscopic and histological examination of the placenta were normal. No residual B19 DNA was found either in the placenta by non-isotopic in-situ hybridisation or in cord blood serum by dot-blot hybridisation,’* and cord blood serum did not transmit infection to erythroid progenitor cells in vitro. Although B19specific IgG was detected in the cord blood (more than 100 RIA units), no specific IgM was present, confirming that cord blood IgM is not a reliable marker of intrauterine parvovirus infection.’ Postnatal course was uneventful and the infant was well at 2 months. The occurrence of hydrops in a fetus infected with human parvovirus B 19 is not necessarily a preterminal event; B 19 may be a cause of "transitory fetal ascites". The successful outcome without intervention suggests that a cautious approach to intrauterine transfusion should be adopted, especially in view of the risk of depressing natural compensatory erythropoiesis. Prolonged posttransfusion intra-amniotic bleeding secondary to B19-induced thrombocytopenia has also been noted.3Recent reports of myocarditis in B19-infected fetuses6 and young childrensuggest that hydrops may not be due to anaemia alone, and that monitoring of survivors of intrauterine B19 infection (whether transfused or not) for possible long-term myocardial damage should also be a scans at
priority. We thank Mr 1. Z. MacKenzie (Nuffield Department of Obstetncs and Gynaecology, Oxford) for permission to report details of this case, and Dr K. A. Fleming (Nuffield Department of Pathology and Bacteriology, Oxford) for technical advice and support. Nuffield Department of Pathology & John Radcliffe Hospital, Oxford OX3 9DU, UK
Bacteriology,
A. L. MOREY
Fetal Medicine Unit, Queen Charlotte’s Hospital, London
U. NICOLINI C. R. WELCH
Nuffield Department of Obstetrics & Gynaecology
D. ECONOMIDES P. F. CHAMBERLAIN
Virus Reference Laboratory, Central Public Health Laboratory, London
B. J. COHEN
1. Hall SM, Cohen BJ, Mortimer PP, et al. Prospective study of human parvovirus (B19) infection m pregnancy. Br Med J 1990; 300: 1166-70 2. Soothill P Intrauterine blood transfusion for non-immume hydrops fetalis due to parvovirus B19 infection. Lancet 1990; 336: 121-22. 3. Peters MT, Nicolaides KH Cordocentesis for the diagnosis and treatment of human fetal parvovirus infection. Obstet Gynecol 1990; 75: 501-04 4. Clewley JP, Cohen BJ, Field AM. Detection of parvovirus B19 DNA, antigen, and particles in the human fetus. J Med Virol 1987, 23: 367-76 5. Cohen BJ, Mortimer PP, Pereira MS Diagnostic assays with monoclonal antibodies for the human serum parvovirus-like virus (SPLV). J Hyg 1983; 91: 113-30 6. Porter HJ, Quantrill AM, Fleming KA. B19 parvovirus infection of myocardial cells Lancet 1988; i: 535-36. 7. Saint-Martin J, Choulot JJ, Bonnaud E, Mormet F Myocarditis caused by
parvovirus J Pediatrics 1990, 116: 1007.
Detection of pathogenic Yersinia enterocolitica by polymerase chain reaction SIR,—Dr Wren and Prof Tabaqchali (Sept 15, p 693) describe detection of pathogenic Yersinia enterocolitica by the polymerase chain reaction (PCR). Although specific amplification was achieved in isolates containing the virulence plasmid (pYV), 13-5% of the pathogenic Y enterocolitica strains tested gave a negative result. because of plasmid loss on subculture. We have developed a PCR technique that avoids such false-negative results by amplifying a segment of the pathogenic Yersinia-specific attachment invasion locus gene1. Two synthetic primers 5’-CTATTGGTTATGCGCAAAGC-3’ and 5’-TGGAAGTGGGTTGAATTGCA-3’ were used to amplify a 359 bp product from overnight broth cultures. We tested 44 yersinia isolates, including pathogenic (biotypes 2, 3, and 4) and non-pathogenic (biotype lA) strains of Yenterocolztica and other Yersinia species Y intermedia-
like this approach because one never knows when the judicial eye is going to open. If doctors want to change the law then one approach is to directly challenge it, as Dr Bourne did in 1939.2 Not many are brave enough or convinced enough of their principles for such confrontation. The other approach is to make withdrawal of treatment, especially in the persistent vegetative state, a public issue. This may be achieved by debate in medical journals, articles in national newspapers, and public debate on television. Medicine and law are only in place to serve society. I believe that medical practice is being adapted to suit the changes demanded by society. The law must also change. Intensive Therapy Unit, Western Infirmary, Glasgow G11 6NT, UK
NICHOLAS PACE
1. Pace N, Plenderleith JL, Dougall JR. Moral support. Br J Hosp Med (m press). 2. R v Bourne. 1939. 1KB 687.
principles m withdrawing advanced life
SIR,—The Institute of Medical Ethics Working Party’s the withdrawal of life support from patients in a persistent vegetative state should have included in its argument the complications of enteral alimentation. Nasogastric tubes can cause pressure sores along the route of insertion, oesophageal bleeding, and sinus infections.1 The use of gastrostomy tubes is complicated by the need for open surgical or percutaneous placement.2 In 70 elderly patients Ciocon et al3 showed an increased frequency of aspiration with gastrostomy tubes (56%) compared with nasogastric tubes (44%). Fluid overload and congestive failure are also seen in artificial feeding. Artificial feeding therefore shares with other medical treatments the potential for harm as well as good. In a persistent vegetative state, as defmed by the Working Party, tube feeding is indeed a futile and sometimes harmful therapy. statement on
12311 Ventura Boulevard, Studio City, California 91604, USA
VICTOR L. KOVNER
1. Olins
NJ, Annas GJ. Comments on withdrawal of artificial feeding: Professor Annas responds. Am JPubl Health 1985; 75: 1347-48. 2 Ponsky JL, Gauderer MWL, Stellato TA, et al. Percutaneous approaches to enteral hyperalimentation. Am J Surg 1985; 149: 102-05. 3. Ciocon JO, Silverstone FA, Graver LM, et al. Tube feeding m elderly patients: indications, benefits, and complications. Arch Intern Med 1988; 148: 429-33.
Parvovirus B19 infection and transient fetal
hydrops SIR,-Human parvovirus (B19) infection can lead to nonhydrops and fetal death,l possibly because of anaemia secondary to infection of erythroid progenitor cells. Although there immune
have been instances of normal outcome despite serological evidence of intrauterine infection,l or after treatment with intrauterine blood transfusion/,3 there are no reports of successful pregnancies complicated by B19-induced hydrops without such intervention. However, we now describe such a case. A 33-year-old woman, who was para 3 plus 0 and blood group A rhesus positive, requested ultrasound scanning at 21 weeks’ gestation to determine fetal sex. Gross fetal ascites and a small pericardial effusion were found. Fetal blood sampling revealed mild anaemia (packed cell volume 0-26) with increased erythropoietic activity (184 reticulocytes/ 103 red blood cells). Fetal karyotype was 46XY and maternal serum alpha-fetoprotein was within the normal range (153 pgJl). Parvovirus B19 DNA was detected in fetal serum by dot-blot hybridisation and parvovirus particles were seen by immune electron microscopy.’ B19-specific IgG was present (85 RIA units),5 but specific IgM was not detected. Fetal serum was unable to infect erythroid progenitor cells in vitro, which suggests that the observed viral particles had been neutralised by specific antibody. Maternal serum taken at the same time contained no B 19 DNA, but did have B19-specific IgG (more than 100 RIA units) and IgM (11 RIA units), consistent with recent infection. The mother recalled a brief, influenza-like illness at about 10 weeks’ gestation, but denied rash or arthralgia.
Repeat ultrasound examination
at
22 weeks’
spontaneous resolution of hydrops, and further
gestation showed
25 and 31 weeks’ revealed normal fetal growth. Labour was induced at 39 weeks’ and a boy weighing 3111 g was delivered with Apgar scores of ten at both I and 5 minutes. Physical examination was normal and cord blood haemoglobin was 15-7 g/dl with 11% normoblasts. Macroscopic and histological examination of the placenta were normal. No residual B19 DNA was found either in the placenta by non-isotopic in-situ hybridisation or in cord blood serum by dot-blot hybridisation,’* and cord blood serum did not transmit infection to erythroid progenitor cells in vitro. Although B19specific IgG was detected in the cord blood (more than 100 RIA units), no specific IgM was present, confirming that cord blood IgM is not a reliable marker of intrauterine parvovirus infection.’ Postnatal course was uneventful and the infant was well at 2 months. The occurrence of hydrops in a fetus infected with human parvovirus B 19 is not necessarily a preterminal event; B 19 may be a cause of "transitory fetal ascites". The successful outcome without intervention suggests that a cautious approach to intrauterine transfusion should be adopted, especially in view of the risk of depressing natural compensatory erythropoiesis. Prolonged posttransfusion intra-amniotic bleeding secondary to B19-induced thrombocytopenia has also been noted.3Recent reports of myocarditis in B19-infected fetuses6 and young childrensuggest that hydrops may not be due to anaemia alone, and that monitoring of survivors of intrauterine B19 infection (whether transfused or not) for possible long-term myocardial damage should also be a scans at
priority. We thank Mr 1. Z. MacKenzie (Nuffield Department of Obstetncs and Gynaecology, Oxford) for permission to report details of this case, and Dr K. A. Fleming (Nuffield Department of Pathology and Bacteriology, Oxford) for technical advice and support. Nuffield Department of Pathology & John Radcliffe Hospital, Oxford OX3 9DU, UK
Bacteriology,
A. L. MOREY
Fetal Medicine Unit, Queen Charlotte’s Hospital, London
U. NICOLINI C. R. WELCH
Nuffield Department of Obstetrics & Gynaecology
D. ECONOMIDES P. F. CHAMBERLAIN
Virus Reference Laboratory, Central Public Health Laboratory, London
B. J. COHEN
1. Hall SM, Cohen BJ, Mortimer PP, et al. Prospective study of human parvovirus (B19) infection m pregnancy. Br Med J 1990; 300: 1166-70 2. Soothill P Intrauterine blood transfusion for non-immume hydrops fetalis due to parvovirus B19 infection. Lancet 1990; 336: 121-22. 3. Peters MT, Nicolaides KH Cordocentesis for the diagnosis and treatment of human fetal parvovirus infection. Obstet Gynecol 1990; 75: 501-04 4. Clewley JP, Cohen BJ, Field AM. Detection of parvovirus B19 DNA, antigen, and particles in the human fetus. J Med Virol 1987, 23: 367-76 5. Cohen BJ, Mortimer PP, Pereira MS Diagnostic assays with monoclonal antibodies for the human serum parvovirus-like virus (SPLV). J Hyg 1983; 91: 113-30 6. Porter HJ, Quantrill AM, Fleming KA. B19 parvovirus infection of myocardial cells Lancet 1988; i: 535-36. 7. Saint-Martin J, Choulot JJ, Bonnaud E, Mormet F Myocarditis caused by
parvovirus J Pediatrics 1990, 116: 1007.
Detection of pathogenic Yersinia enterocolitica by polymerase chain reaction SIR,—Dr Wren and Prof Tabaqchali (Sept 15, p 693) describe detection of pathogenic Yersinia enterocolitica by the polymerase chain reaction (PCR). Although specific amplification was achieved in isolates containing the virulence plasmid (pYV), 13-5% of the pathogenic Y enterocolitica strains tested gave a negative result. because of plasmid loss on subculture. We have developed a PCR technique that avoids such false-negative results by amplifying a segment of the pathogenic Yersinia-specific attachment invasion locus gene1. Two synthetic primers 5’-CTATTGGTTATGCGCAAAGC-3’ and 5’-TGGAAGTGGGTTGAATTGCA-3’ were used to amplify a 359 bp product from overnight broth cultures. We tested 44 yersinia isolates, including pathogenic (biotypes 2, 3, and 4) and non-pathogenic (biotype lA) strains of Yenterocolztica and other Yersinia species Y intermedia-
