979
Respiratory syncytial virus infection in special care nursery SIR,—Respiratory syncytial virus (RSV) infection in newborn babies has been reported to produce only mild disease.1 We report a small outbreak in January, 1990, in which two babies required ventilation. At the time of the outbreak there were only twelve babies in the nursery. Details of the four infected with RSV are shown in the table. Three babies were on tube feeding before the outbreak but were otherwise well, and the fourth baby was about to be discharged home. Cases 1, 2, and 3 were in the same four-bed area and case 4 in an adjoining area. The four babies were isolated and nursed separately as soon as the diagnosis was confirmed. Aerosolised ribavirin was given to cases 2 and 4 for 3 days but not to cases 1 and 3 who were already being ventilated when the diagnosis was confirmed. Two other babies in close proximity to the RSV infected ones were nursed separately and away from the confirmed cases. The remaining six babies were considered potentially infected. The unit was closed for admissions for 2 days; after that new admissions were nursed separately and kept apart from infected and potentially infected babies, putting a great strain on the unit’s nurses. The unit has only two intensivecare cots and these were occupied by two babies being ventilated before the RSV outbreak. The laboratory used an RSV antigen detection test on exfoliated epithelial cells on specimens obtained by nasopharyngeal aspiration. The result was reported the same day. The fluorescein-conjugated pool of RSV-specific monoclonal antibodies used in this test (Novo Nordisk, Cambridge, UK) is sensitive and specific.2 All potentially infected babies were screened on days 1,5,6, and 7. No further cases occurred. The four infected babies were re-tested on 7 and 8 days after the initial diagnosis, and were negative. After two consecutive RSV-negative aspirations the babies were deemed to be at very low infection risk and isolation was stopped. It was impracticable to try to identify the source of infection. Most staff and many visitors had had respiratory infections, and 3 young healthy adults may have clinically silent RSV infections. Visitors with respiratory illness, especially during the winter epidemic months, should be discouraged. During the outbreak any nurses with upper respiratory symptoms were designated to care for the four infected babies. RSV is spread in droplets and infected fomites, and thorough handwashing, the wearing of gowns, and the segregation of infected babies should help to prevent spread. In 1970 a small RSV outbreak affected eight babies in one maternity unit,l but the disease was very mild. In Hall and CLINICAL DETAILS OF FOUR CASES OF NEONATAL RSV INFECTION
colleagues’ study" mainly pre-term babies were infected. When illness began before 3 weeks of age, it tended to be milder with more non-specific signs and less lower-respiratory-tract disease and apnoea; of the four deaths (17%) three were in babies older than 3 weeks. In a French study, five babies had RSV infection in the first month of life and symptoms were more severe; four had pneumonia and two required ventilation.5 In our small outbreak three babies were premature and the disease was not mild. Three babies with lower-respiratory-tract signs had previous respiratory problems (table) and the two with respiratory failure had previously been ventilated. The variable severity of neonatal infection may be related to the differing pathogenicity of RSV subtypes.6 Early diagnosis is important so that ribavirin can be started, and infected cases should be isolated. Examination of nasopharyngeal aspirates for RSV antigens by direct immunofluorescence is a convenient and
rapid test. Stobhill General Hospital, Glasgow G21 3UW, UK
MADELEINE P. WHITE
Department of Microbiology, Royal Hospital for Sick Children, Glasgow
PETER L. K. MACKIE
1. Neligan GA, Steiner H, Gardner PS, McQuillin J. Respiratory syncytial virus infection of the newborn. Br Med J 1970; iii: 146-47. 2. Freke A, Stott EJ, Roome APSH, Caul EO. The detection of respiratory syncytial virus in nasopharyngeal aspirates. J Med Virol 1986; 18: 181-91. 3. Hall CB. The nosocomial spread of respiratory syncytial viral infections. Annu Rev Med 1983; 34: 311-19. 4. Hall CB, Kopeland MD,
Douglas GR, Geiman JM, Meagher PM. Neonatal respiratory syncytial virus infection. N Engl J Med 1979; 300: 393-96. 5. Sauvageon G, Castaing H, Dupard MC, Fournet JP, Ferre P. Les bronchiolites severes du nourisson. Poumon Coeur 1977; 33: 287-94. 6. Akerlind B, Norrby E. Occurrence of respiratory syncytial virus subtypes A and B strain in Sweden. JMed Virol 1986; 19: 241-47.
Propafenone SIR,-In your Dec 23 editorial (p 1490) on the recently introduced antiarrhythmic drug propafenone, you advise caution in its use in severe chronic obstructive airways disease because of its weak beta adrenergic blocking action. An investigation of the drug given orally in doses of up to 300 mg 8 hourly to subjects with mild asthma showed no significant fall in 1-s forced expiratory volume (FEV.) and no increase in asthmatic symptoms, although there was an increase in sensitivity to inhaled methacholine.1 We wish to point out that the danger of exacerbation of asthma by this drug is not confined to individuals with severe chronic obstructive airways disease. We have seen a woman aged 50 years in whom troublesome cough and wheezing developed one week after starting propafenone 150 mg three times daily. Asthma had not been diagnosed previously although when seen initially she had admitted to wheezing on exertion. She had been treated earlier with metoprolol and atenolol without any respiratory side-effects. She had clear evidence of asthma with reversible airflow obstruction with a large response to salbutamol and further improvement with the introduction of inhaled beclomethasone. So that we could elucidate the role of propafenone the patient stopped the drug for three days, and was then admitted. The drug was then reintroduced with regular monitoring of ventilatory function. Within five days the symptoms recurred and early morning values of peak flow fell from 340 1/min before reintroduction of the drug to 180 1/min. She retained a good response to inhaled beta stimulants. Propafenone was discontinued and flecainide introduced, whereupon the wheezing resolved and function improved. We suggest that doctors should seek past indications of asthma before prescribing propafenone and monitor airway function in patients with previous or new symptoms suggestive of asthma. Regional Cardiothoracic Centre, Freeman Hospital, High Heaton, Newcastle upon Tyne NE7 7DN, UK
RDS = respiratory
distress syndrome; I PPV = ontermlttent ven2laLOn; CPAP= continuous positive airways pressure
positive-pressure
D. VEALE J. M. MCCOMB G. J. GIBSON
1. Hill MR, Gotz VP, Harmen B, McLeod I, Hendeles L. Evaluation of the asthmogenicity of propafenone, a new anti-arrhythmic drug. Chest 1986; 90: 698-702.
Respiratory syncytial virus infection in special care nursery SIR,—Respiratory syncytial virus (RSV) infection in newborn babies has been reported to produce only mild disease.1 We report a small outbreak in January, 1990, in which two babies required ventilation. At the time of the outbreak there were only twelve babies in the nursery. Details of the four infected with RSV are shown in the table. Three babies were on tube feeding before the outbreak but were otherwise well, and the fourth baby was about to be discharged home. Cases 1, 2, and 3 were in the same four-bed area and case 4 in an adjoining area. The four babies were isolated and nursed separately as soon as the diagnosis was confirmed. Aerosolised ribavirin was given to cases 2 and 4 for 3 days but not to cases 1 and 3 who were already being ventilated when the diagnosis was confirmed. Two other babies in close proximity to the RSV infected ones were nursed separately and away from the confirmed cases. The remaining six babies were considered potentially infected. The unit was closed for admissions for 2 days; after that new admissions were nursed separately and kept apart from infected and potentially infected babies, putting a great strain on the unit’s nurses. The unit has only two intensivecare cots and these were occupied by two babies being ventilated before the RSV outbreak. The laboratory used an RSV antigen detection test on exfoliated epithelial cells on specimens obtained by nasopharyngeal aspiration. The result was reported the same day. The fluorescein-conjugated pool of RSV-specific monoclonal antibodies used in this test (Novo Nordisk, Cambridge, UK) is sensitive and specific.2 All potentially infected babies were screened on days 1,5,6, and 7. No further cases occurred. The four infected babies were re-tested on 7 and 8 days after the initial diagnosis, and were negative. After two consecutive RSV-negative aspirations the babies were deemed to be at very low infection risk and isolation was stopped. It was impracticable to try to identify the source of infection. Most staff and many visitors had had respiratory infections, and 3 young healthy adults may have clinically silent RSV infections. Visitors with respiratory illness, especially during the winter epidemic months, should be discouraged. During the outbreak any nurses with upper respiratory symptoms were designated to care for the four infected babies. RSV is spread in droplets and infected fomites, and thorough handwashing, the wearing of gowns, and the segregation of infected babies should help to prevent spread. In 1970 a small RSV outbreak affected eight babies in one maternity unit,l but the disease was very mild. In Hall and CLINICAL DETAILS OF FOUR CASES OF NEONATAL RSV INFECTION
colleagues’ study" mainly pre-term babies were infected. When illness began before 3 weeks of age, it tended to be milder with more non-specific signs and less lower-respiratory-tract disease and apnoea; of the four deaths (17%) three were in babies older than 3 weeks. In a French study, five babies had RSV infection in the first month of life and symptoms were more severe; four had pneumonia and two required ventilation.5 In our small outbreak three babies were premature and the disease was not mild. Three babies with lower-respiratory-tract signs had previous respiratory problems (table) and the two with respiratory failure had previously been ventilated. The variable severity of neonatal infection may be related to the differing pathogenicity of RSV subtypes.6 Early diagnosis is important so that ribavirin can be started, and infected cases should be isolated. Examination of nasopharyngeal aspirates for RSV antigens by direct immunofluorescence is a convenient and
rapid test. Stobhill General Hospital, Glasgow G21 3UW, UK
MADELEINE P. WHITE
Department of Microbiology, Royal Hospital for Sick Children, Glasgow
PETER L. K. MACKIE
1. Neligan GA, Steiner H, Gardner PS, McQuillin J. Respiratory syncytial virus infection of the newborn. Br Med J 1970; iii: 146-47. 2. Freke A, Stott EJ, Roome APSH, Caul EO. The detection of respiratory syncytial virus in nasopharyngeal aspirates. J Med Virol 1986; 18: 181-91. 3. Hall CB. The nosocomial spread of respiratory syncytial viral infections. Annu Rev Med 1983; 34: 311-19. 4. Hall CB, Kopeland MD,
Douglas GR, Geiman JM, Meagher PM. Neonatal respiratory syncytial virus infection. N Engl J Med 1979; 300: 393-96. 5. Sauvageon G, Castaing H, Dupard MC, Fournet JP, Ferre P. Les bronchiolites severes du nourisson. Poumon Coeur 1977; 33: 287-94. 6. Akerlind B, Norrby E. Occurrence of respiratory syncytial virus subtypes A and B strain in Sweden. JMed Virol 1986; 19: 241-47.
Propafenone SIR,-In your Dec 23 editorial (p 1490) on the recently introduced antiarrhythmic drug propafenone, you advise caution in its use in severe chronic obstructive airways disease because of its weak beta adrenergic blocking action. An investigation of the drug given orally in doses of up to 300 mg 8 hourly to subjects with mild asthma showed no significant fall in 1-s forced expiratory volume (FEV.) and no increase in asthmatic symptoms, although there was an increase in sensitivity to inhaled methacholine.1 We wish to point out that the danger of exacerbation of asthma by this drug is not confined to individuals with severe chronic obstructive airways disease. We have seen a woman aged 50 years in whom troublesome cough and wheezing developed one week after starting propafenone 150 mg three times daily. Asthma had not been diagnosed previously although when seen initially she had admitted to wheezing on exertion. She had been treated earlier with metoprolol and atenolol without any respiratory side-effects. She had clear evidence of asthma with reversible airflow obstruction with a large response to salbutamol and further improvement with the introduction of inhaled beclomethasone. So that we could elucidate the role of propafenone the patient stopped the drug for three days, and was then admitted. The drug was then reintroduced with regular monitoring of ventilatory function. Within five days the symptoms recurred and early morning values of peak flow fell from 340 1/min before reintroduction of the drug to 180 1/min. She retained a good response to inhaled beta stimulants. Propafenone was discontinued and flecainide introduced, whereupon the wheezing resolved and function improved. We suggest that doctors should seek past indications of asthma before prescribing propafenone and monitor airway function in patients with previous or new symptoms suggestive of asthma. Regional Cardiothoracic Centre, Freeman Hospital, High Heaton, Newcastle upon Tyne NE7 7DN, UK
RDS = respiratory
distress syndrome; I PPV = ontermlttent ven2laLOn; CPAP= continuous positive airways pressure
positive-pressure
D. VEALE J. M. MCCOMB G. J. GIBSON
1. Hill MR, Gotz VP, Harmen B, McLeod I, Hendeles L. Evaluation of the asthmogenicity of propafenone, a new anti-arrhythmic drug. Chest 1986; 90: 698-702.
