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MEASLES AND RESPIRATORY SYNCYTIAL VIRUSES
1096 and the feet. She does not have a history of frequent respiratory or gastrointestinal disease. To our knowledge this is the first case of IgA absence reported in a patient with a ring-18 chromosome. Although the absence of IgA in this patient may be a fortuitous accompaniment of her chromosomal aberration, we suggest that other investigators with patients with deletion of an 18 chromosome should look for the absence of IgA. The details of the in this patient will be
clinical, cytogenetic, and laboratory findings published in the near future. SARA C. FINLEY WAYNE H. FINLEY THOMAS A. NOTO IRENE A. UCHIDA ROY F. RODDAM.
Laboratory of Medical Genetics and Departments of Pediatrics, Medicine, and Clinical Pathology, The Medical Center, University of Alabama in Birmingham, Alabama 35233.
cultures. The serological findings in cases 3 and5 indicate that in these at least the R.S.V. infections followed the measles infections. From mid-March to June, when R.s.v. was no longer epidemic, 24 patients showed clinical and serological evidence of measles infection; only 1 of these showed a rising titre to R.s.v. and the onset of illness in this child was in the middle of March. These findings suggest that there are no C.F. cross-reactions between measles and R.s.v. but that children with measles may contract infection with R.s.v. when this virus is epidemic in the
community. Regional Virus Laboratory, Department of Infectious Diseases, Ruchill Hospital, Glasgow N.W.
CONSTANCE A. C. Ross I. W. PINKERTON.
DEATH FROM HYDROGEN-SULPHIDE FUMES MEASLES AND RESPIRATORY SYNCYTIAL VIRUSES the Dr. SIR,-In Gray and her colleagues (March 2, paper by p. 446) 4 of the 31 patients reported as having respiratory syncytial virus (R.s.v.) infections showed rising complementfixing (c.F.) antibody titres to measles. Dr. Miller and Dr. Taylor (March 30, p. 697) suggest that the interpretation of serological findings in 3 of these 4 patients is puzzling. Presumably they are concerned about the possibility of an antigenic relationship between measles and R.S.v. A one-way crossreaction between measles and R.s.v. was suggested by Jensen,1 who found that children with measles usually developed a concomitant rise of antibody to both measles and R.s.v. whereas children with R.s.v. infections developed antibody to R.S.V. only and not to measles. During the period November, 1964, to June, 1965, measles was epidemic in the Glasgow area. During the first three DETAILS OF
N.T.
5 CHILDREN WITH MEASLES AND
—Not tested.
* R.s.v.
RISING TITRES TO R.S.V.
also isolated from throat swab.
months of this period (i.e., to the end of February) there was a concurrent epidemic of R.S.V. infection. This afforded us the opportunity to test C.F. antibody responses to both measles and R.S.V. in children with R.s.v. infections and in those with measles. During the concurrent epidemics 30 children were diagnosed as R.s.v. infections on the basis of clinical findings together with a fourfold or greater rise in antibody titre to R.S.V.; none showed rising or high titres ( &bgr; 128) to measles. Also during the concurrent epidemics 25 children showed clinical and serological evidence of measles infection; 5 (20%) showed rising titres to R.s.v. (see table). In only 1 of these 5 was a throat swab received for virus isolation and this yielded R.s.v. in Bristol hela-cell1.
Jensen, K. E. Conference p. 194. 1962.
on
Newer
Respiratory Disease Viruses,
SIR,-Hydrogen sulphide (H2S) rarely causes death in modern industrial settings. The unpleasant and irritating properties of the gas provide its own built-in safety factor. The odour is detectable in concentrations as low as 0-025 p.p.m., is distinct at 0-3 p.p.m., is offensive and moderately intense at 3 to 5 p.p.m., and is strong but not intolerable at 20 to 30 p.p.m.1 At higher concentrations the odour seems less intense, and the olfactory sense fatigues rapidly. A recent industrial death from exposure to hydrogen-sulphide fumes prompts this report. A Caucasian man, fifty-five years of age, was received at the Coroner’s office. He had been working in a tank, 15 ft. (4-57 m.) high and 5 ft. (1-52 m.) in diameter, at 9.15 A.M. Five minutes later he was found unconscious by a fellow worker. He was pronounced dead at 10.00 A.M. The tank in which he had been working was used for storage of coal-tar resins, although it was empty at the time except for small deposits at the bottom. Necropsy revealed the following: acute bilateral pulmonary oedema, chronic passive congestion of the lungs, chronic bronchitis, chronic passive congestion of both the liver and spleen, and slight atherosclerosis of the coronary arteries and aorta; cut sections of the lungs showed extremely wet frothy congested surfaces with a diffuse red to red-brown and purple appearance; the tracheobronchial tree was lined with a tenacious pale grayish-yellow to grayish-red material, containing a great amount of mucus which extended deep into the bronchiolar system; the brain was somewhat oedematous. This man had no history of disease. His last physical examination in 1967, had showed no significant abnormal findings. Air-samples taken from the tank at 2 ft. (61 cm.) from the top and midway from the top gave levels of 1900 and 6100 p.p.m., respectively, of hydrogen sulphide. Toxicological analyses of body tissues taken at necropsy revealed the following levels of hydrogen sulphide, in {g. per 100 g.: blood 92; brain 106; kidney 34; liver 38. Part of the hydrogen sulphide had probably been dissipated by the vigorous treatment, including artificial respiration and resuscitation. Analyses for other toxicants were negative. Inhaled hydrogen sulphide is converted in the human body inactive compounds such as thiosulphate or sulphate, but with high concentrations this oxidation offers no protection. At high concentrations, death results from respiratory paralysis or asphyxiation. The maximum allowable concentration for hydrogen sulphide is given as 20 p.p.m.,2 and the threshold limit value as lOp.p.m. Avalueof400to700p.p.m.isconsidered dangerous after an exposure of half to one hour.2 Concentrations higher than 1000 p.p.m. are instantly fatal.3 CHARLES L. WINEK Department of Toxicology and Pathology, WELLON D. COLLOM Coroner’s Allegheny County Office, CYRIL H. WECHT. Pittsburgh, Pennsylvania 15219. to
1.
Patty, F. A., Industrial Hygiene and Toxicology; Vol. II, p. 896. New York.
Conference of Governmental Industrial Hygienists; Threshold Limit Values for 1966; p. 10. Cincinnati, Ohio, 1966. 3. Sax, N. I. Dangerous Properties of Industrial Materials; p. 888. New York, 1963.
2. American
clinical, cytogenetic, and laboratory findings published in the near future. SARA C. FINLEY WAYNE H. FINLEY THOMAS A. NOTO IRENE A. UCHIDA ROY F. RODDAM.
Laboratory of Medical Genetics and Departments of Pediatrics, Medicine, and Clinical Pathology, The Medical Center, University of Alabama in Birmingham, Alabama 35233.
cultures. The serological findings in cases 3 and5 indicate that in these at least the R.S.V. infections followed the measles infections. From mid-March to June, when R.s.v. was no longer epidemic, 24 patients showed clinical and serological evidence of measles infection; only 1 of these showed a rising titre to R.s.v. and the onset of illness in this child was in the middle of March. These findings suggest that there are no C.F. cross-reactions between measles and R.s.v. but that children with measles may contract infection with R.s.v. when this virus is epidemic in the
community. Regional Virus Laboratory, Department of Infectious Diseases, Ruchill Hospital, Glasgow N.W.
CONSTANCE A. C. Ross I. W. PINKERTON.
DEATH FROM HYDROGEN-SULPHIDE FUMES MEASLES AND RESPIRATORY SYNCYTIAL VIRUSES the Dr. SIR,-In Gray and her colleagues (March 2, paper by p. 446) 4 of the 31 patients reported as having respiratory syncytial virus (R.s.v.) infections showed rising complementfixing (c.F.) antibody titres to measles. Dr. Miller and Dr. Taylor (March 30, p. 697) suggest that the interpretation of serological findings in 3 of these 4 patients is puzzling. Presumably they are concerned about the possibility of an antigenic relationship between measles and R.S.v. A one-way crossreaction between measles and R.s.v. was suggested by Jensen,1 who found that children with measles usually developed a concomitant rise of antibody to both measles and R.s.v. whereas children with R.s.v. infections developed antibody to R.S.V. only and not to measles. During the period November, 1964, to June, 1965, measles was epidemic in the Glasgow area. During the first three DETAILS OF
N.T.
5 CHILDREN WITH MEASLES AND
—Not tested.
* R.s.v.
RISING TITRES TO R.S.V.
also isolated from throat swab.
months of this period (i.e., to the end of February) there was a concurrent epidemic of R.S.V. infection. This afforded us the opportunity to test C.F. antibody responses to both measles and R.S.V. in children with R.s.v. infections and in those with measles. During the concurrent epidemics 30 children were diagnosed as R.s.v. infections on the basis of clinical findings together with a fourfold or greater rise in antibody titre to R.S.V.; none showed rising or high titres ( &bgr; 128) to measles. Also during the concurrent epidemics 25 children showed clinical and serological evidence of measles infection; 5 (20%) showed rising titres to R.s.v. (see table). In only 1 of these 5 was a throat swab received for virus isolation and this yielded R.s.v. in Bristol hela-cell1.
Jensen, K. E. Conference p. 194. 1962.
on
Newer
Respiratory Disease Viruses,
SIR,-Hydrogen sulphide (H2S) rarely causes death in modern industrial settings. The unpleasant and irritating properties of the gas provide its own built-in safety factor. The odour is detectable in concentrations as low as 0-025 p.p.m., is distinct at 0-3 p.p.m., is offensive and moderately intense at 3 to 5 p.p.m., and is strong but not intolerable at 20 to 30 p.p.m.1 At higher concentrations the odour seems less intense, and the olfactory sense fatigues rapidly. A recent industrial death from exposure to hydrogen-sulphide fumes prompts this report. A Caucasian man, fifty-five years of age, was received at the Coroner’s office. He had been working in a tank, 15 ft. (4-57 m.) high and 5 ft. (1-52 m.) in diameter, at 9.15 A.M. Five minutes later he was found unconscious by a fellow worker. He was pronounced dead at 10.00 A.M. The tank in which he had been working was used for storage of coal-tar resins, although it was empty at the time except for small deposits at the bottom. Necropsy revealed the following: acute bilateral pulmonary oedema, chronic passive congestion of the lungs, chronic bronchitis, chronic passive congestion of both the liver and spleen, and slight atherosclerosis of the coronary arteries and aorta; cut sections of the lungs showed extremely wet frothy congested surfaces with a diffuse red to red-brown and purple appearance; the tracheobronchial tree was lined with a tenacious pale grayish-yellow to grayish-red material, containing a great amount of mucus which extended deep into the bronchiolar system; the brain was somewhat oedematous. This man had no history of disease. His last physical examination in 1967, had showed no significant abnormal findings. Air-samples taken from the tank at 2 ft. (61 cm.) from the top and midway from the top gave levels of 1900 and 6100 p.p.m., respectively, of hydrogen sulphide. Toxicological analyses of body tissues taken at necropsy revealed the following levels of hydrogen sulphide, in {g. per 100 g.: blood 92; brain 106; kidney 34; liver 38. Part of the hydrogen sulphide had probably been dissipated by the vigorous treatment, including artificial respiration and resuscitation. Analyses for other toxicants were negative. Inhaled hydrogen sulphide is converted in the human body inactive compounds such as thiosulphate or sulphate, but with high concentrations this oxidation offers no protection. At high concentrations, death results from respiratory paralysis or asphyxiation. The maximum allowable concentration for hydrogen sulphide is given as 20 p.p.m.,2 and the threshold limit value as lOp.p.m. Avalueof400to700p.p.m.isconsidered dangerous after an exposure of half to one hour.2 Concentrations higher than 1000 p.p.m. are instantly fatal.3 CHARLES L. WINEK Department of Toxicology and Pathology, WELLON D. COLLOM Coroner’s Allegheny County Office, CYRIL H. WECHT. Pittsburgh, Pennsylvania 15219. to
1.
Patty, F. A., Industrial Hygiene and Toxicology; Vol. II, p. 896. New York.
Conference of Governmental Industrial Hygienists; Threshold Limit Values for 1966; p. 10. Cincinnati, Ohio, 1966. 3. Sax, N. I. Dangerous Properties of Industrial Materials; p. 888. New York, 1963.
2. American