- Email: [email protected]
Airborne transmission of a small round structured virus
mentioned by Remuzzi et al "steroid gastrointestinal bleeding and perforation" has been reviewed by Guslandi and Tittobellol who pointed out that the "gastrotoxic" effects of steroids are mainly due to an association with non-steroidal anti-inflammatory drugs, and that view accords with our
clinical experience. Strict metabolic control prevents the development and the progression of diabetic retinopathy so a "controlled long-term clinical trial comparing pancreas transplantation with strict glycaemic control" is no longer required because the two approaches achieve similar results in terms of metabolic control. Moreover, strict metabolic control is very difficult in patients with end-stage renal failure or who are immunosuppressed with steroids, as are diabetic renal transplant recipients. Nor does the strict metabolic control achieved with pancreas transplantation expose patients to the risk of severe hypoglycaemic episodes. Not everyone agrees that pancreas transplantation increases the risk of kidney rejection. The same rate of patient and kidney graft survival at 5 years has been reported in diabetic patients
undergoing living-related kidney transplantation (91 cases, 83% and 72%, respectively) or receiving simultaneous kidneypancreas transplantation (138 cases, 87% and 76%), indicating that a simultaneous pancreas graft does not impair survival of the transplanted kidney.2 A "formal comparison with solo kidney transplantation" has already been done. That the ideal control group to evaluate the effects of pancreas transplantation on chronic complications is diabetic patients receiving kidney transplantation alone is not in dispute.3 Improvement of peripheral neuropathy has been reported. The Stockholm study, with longer follow-up, showed that the positive effect of kidney transplantation on peripheral neuropathy last for the first year only, whereas patients receiving pancreas transplantation improve progressively up to 4 years/ These results have been confirmed in
our
institute.5
Insulin-independence after islet transplantation has been reported by several groups, not just by Warnock, and the evidence cannot be dismissed as anecdotal even though definitive figures are not yet available. Antonio Secchi, Valerio Di Carlo, Guido Pozza San Raffaele Scientific Institute, University of Milan, 20132 Milan, Italy
1
2
3
4
5
Guslandi M, Tittobello A. Steroid ulcers: a myth revisited. BMJ 1992; 304: 655-56. Susaki T, Pirsch JD, D’Alessandro AM, et al. Simultaneous kidneypancreas transplantation at University of Wisconsin-Madison Hospital. In: Terasaki PI, Cecha JM, eds. Clinical transplant 1991. Los Angeles: University of California Press, 1991: 135-39. Anon. Secondary complications and quality of life after successful kidney-pancreas allotransplantation in type I diabetes mellitus.
Diabetologia 1991; 34 (suppl 1). Solders G, Tyden G, Persson A, et al. Improvement of nerve conduction in diabetic neuropathy: a follow-up study 4 years after combined pancreatic and renal transplantation. Diabetes 1992; 41: 946-51. Comi G, Galardi G, Amadio S, et al. Neurophysiological study of the effect of combined kidney and pancreas transplantation on diabetic neuropathy: a 2 year follow-up evaluation. Diabetologia 1991; 34 (suppl 1): S103-07.
SIR-Remuzzi and colleagues’ "review" presents only selected reports that seem to fit their own verdict on pancreas transplantation. For example, they note that one major concern after pancreas transplantation is cytomegalovirus (CMV) infection, and they cite a series describing 36 patients, 18 of whom had combined kidney/pancreas transplantation, and 18 kidney transplants alone. They conclude from this small series that CMV is much more of a problem in the combined procedure. However, larger series demonstrate similar incidences of CMV infection in combined and kidney alone
recipients.1.2 While kidney/pancreas transplant recipients have a rejection rate greater than that for kidney recipients alone, it is irresponsible to state flatly that there are three times more rejection episodes in these patients. A single report does not reflect the entire literature. They go on to give an example of the negative aspects of OKT3 induction therapy by quoting a single series of heart with increase in an transplants post-transplant not seen in any single-centre disorders lymphoproliferative series before or since. Many centres use routine induction therapy even for renal transplants alone, with safe outcomes. Remuzzi et al suggest that future trials should address quality of life, but they ignored published evidence for the positive effects of kidney/pancreas transplantation on quality of life.1-4 Nor do they discuss reports of the positive impact on neuropathic changes or diabetic angiopathy. It then becomes clear in the last section of the article that Remuzzi et al feel that islet-cell transplantation is the answer to achieving normal glucose homoeostasis. They refer to several publications on success in laboratory animals, yet ignore all the clinical data notable for absence of success. The number of insulin-independent type 1 diabetics who have received successful islet-cell transplants in the past decade is less than 10, and the successes of islet-cell transplantation have been "just around the corner" for the past 25 years. The article concludes with a strong recommendation that research should concentrate on islet-cell transplantation. While I cannot disagree with this, perhaps Remuzzi et al ought to concentrate more on results with whole organ pancreas transplantation achieved in experienced centres with more hopeful outcomes than those presented in their "review". Mitchell L
Henry
Division of Surgery, Ohio State University, Columbus, Ohio 43210, USA
Cheung HS, Sutherland DER, Gillingham KJ, et al. Simultaneous pancreas-kidney transplant versus kidney transplant alone in diabetic patients. Kidney Int 1992; 41: 924-29. 2 Henry ML, Ketel BL, Ferguson RM, et al. The role of transplantation in diabetics with end-stage renal disease. Clin Transpl 1990; 22: 203-15. 3 Nathan DM, Fogel H, Norman D, et al. Long-term metabolic and quality of life results with pancreatic/renal trnaplantation in insulindependent diabetes mellitus. Transplantation 1991; 52: 85-91. 4 Bentley FR, Jung S, Garrison RN. Neuropathy and psychosocial adjustment after pancreas transplant. Tranplant Proc 1990; 22: 691-95. 1
Airborne transmission of a small round structured virus SiR-Whilst not discounting the possibility of airborne transmission of small round structured viruses (SRSV) in the outbreak as described by Chadwick and colleagues (Jan 15, I think that the evidence is inconclusive. With an organism such as SRSV, which can cause infection with a very low dose, case-to-case transmission may occur with very little contact. This is clearly exemplified by the (presumably) high attack rate in the hotel, in which even staff were affected. We are not told if the 89-year-old primary case vomited in a toilet on the coach or in a sickness bag. She would almost certainly have contaminated her hands. The 15 other members of the coach party may have had direct contact with her or with the toilet, seats, or other objects on the coach contaminated by her. Presumably similar contamination occurred in the hotel. The phrase "airborne transmission" is much used in infectious disease epidemiology but needs qualifying. This usually means that a primary case releases an organism into the air which then causes infection through the air pasages of a secondary case.’ With very low dose infections, there must be a possibility that the airborne organism settles on an object which is then touched by a secondary case and is then transferred to the mouth ("air-oral transmission"). I suspect p
171),
that if direct contact was not the cause of transmission in the coach, air-oral transmission was more likely than pure airborne transmission. Norman D Noah Department of Public Health and Epidemiology, King’s College School of Medicine and Dentistry, London SE5 9PJ, UK
1 Benenson AS, ed. Control of communicable disease in man, 15th ed. Washington, DC: American Public Health Association, 1990.
Author’s reply
-
SIR—We agree that it is not possible to be absolutely sure how transmission occurred. There was a toilet on the coach, but the
89-year-old
woman
vomited while in her seat,
producing
a
localised area of direct contamination with vomit. In view of this and because of the high attack rate we believe that airborne dissemination of viruses by vomiting probably accounted for most cases among coach passengers. Vomiting is important in the epidemiology of infection due to SRSV and transmission by one or more different mechanisms is possible. Whether transmission on the coach was "pure airborne" or "air-oral" we cannot say. Nevertheless, there is evidence to implicate airborne dissemination of SRSV, in association with vomiting, and we can supply references including a recent study of a hospital outbreak of gastroenteritis in Salford.1
for certain. Preventive measures should include disinfecting of toilets and surfaces likely to have been contaminated by aerosol droplets from stool or vomitus.3 Workplaces differ in the risk of airborne transmission among employees, but in health-care settings preventive practices should be improved because SRSV gastroenteritis in patients tends to be managed by adoption of precautions aimed at reducing enteric transmission, and these will be only partly effective if the agent is transmitted from aerosolised vomitus or by other airborne means. In our report, 25% of cases occurred among staff, and one-fourth of these were in employees not normally exposed to excreta or vomitus. Infection may have been introduced by staff who also worked in an affiliated acute care hospital, where staff cases of acute gastroenteritis had preceded those in the convalescent facility. Respiratory precautions for hospital patients with acute gastroenteritis may be warranted when a pattern of explosive onset of disease such as that caused by SRSV, is observed. Hospital infection control personnel will need to investigate outbreaks of suspected SRSV gastroenteritis to assess whether the introduction of respiratory precautions does reduce transmission.
George A Gellert, Roger I Glass Project HOPE Health Sciences Education Center, Millwood, VA 22646, USA; and Viral Gastroenteritis Unit, Centers for Disease Control and Prevention, Atlanta, Georgia
1
Paul Chadwick Manchester Public Health
Laboratory, Withington Hospital, Manchester M20 8LR, UK 2
1 Chadwick PR, McCann R. Transmission of a small round structured virus by vomiting during a hospital outbreak of gastroenteritis. J Hosp
3
Infect (in press). 4
SiR-Chadwick and colleagues cite our report of an SRSV outbreak with evidence of airborne transmission but transmission of SRSV by this route has been suspected on epidemiological grounds in other episodes,1,2 and all three of those outbreaks happened in settings where chronically ill, debilitated, or elderly patients may reside. Transmission of SRSV by airborne droplets was also implicated in an outbreak on a cruise ship, where index patients who had vomited in their cabins were more likely to have had cabinmates who subsequently became ill than were index patients who had not vomited.3 Although further documentation of airborne SRSV transmission is needed the public health and infection control implications should be discussed. Apart from infections of the upper respiratory tract, acute gastroenteritis is probably the most common (although underreported) source of communicable disease morbidity in the industrialised countries. It causes huge losses in productivity. In 1985 acute gastroenteritis was one of the top three diagnoses in 87 181 entries on a database that contains only one-sixth of all US hospital admissions.4 From 1979 to 1987 annual deaths from diarrhoeal disease in the US averaged 3170.5 Most gastroenterological infections are assumed to involve faecal-oral transmission, and people with symptoms do not always stay off work. Increasing evidence of transmission of SRSV via the airborne or respiratory route could warrant changes in occupational health practice. Perhaps employees should respond to "stomach flu" just as they do influenza-by staying away from work during the acute illness. Those who vomit should be sent home immediately. Enforced sick leave during the symptomatic period (when viral shedding is maximal) may reduce the risk of secondary infection of work colleagues. SRSV-associated gastroenteritis commonly occurs with diarrhoea but no vomiting. Airborne transmission in the absence of aerosolised vomitus is unlikely but we do not know
5
Sawyer LA, Murphy JJ, Kaplan JE, et al. 25- to 30-nm virus particle associated with a hospital outbreak of acute gastroenteritis with evidence of airborne transmission. Am J Epidemiol 1988; 127: 1261-71. Kaplan JE, Schonberger LB, Varano G, et al. An outbreak of acute nonbacterial gastroenteritis in a nursing home. Am J Epidemiol 1982; 116: 940-48. Ho M-S, Glass RI, Monroe SS, et al. Viral gastroenteritis aboard a cruise ship. Lancet 1989; ii: 961-64. Gangarosa RE, Glass RI, Lew JF, Boring JR. Hospitalizations involving gastroenteritis in the United States, 1985: the special burden of the disease among the elderly. Am J Epidemiol 1992; 135: 281-90. Lew JF, Glass RI, Gangarosa RE, et al. Diarrheal deaths in the United States, 1979 through 1987. JAMA 1991; 265: 3280-84.
Vaccine-associated poliomyelitis SiR-lon-Nedelcu and colleagues (Jan 1, p 51) conclude that immune function should be investigated when poliomyelitis is suspected. We report a similar case that illustrates the value of both immunological and virological investigation. A 7-month-old boy was admitted to hospital with a history of ear infection for 2 weeks and irritability for 2 days. He had previously been well. His general practitioner had treated him with erythromycin and co-trimoxazole. He was febrile, posturing, and fitting, but had no focal signs. His cerebrospinal fluid (CSF) was clear and contained 84 white cells/L (85% polymorphs) and 04 g/L protein. No organisms were detected by Gram stain, culture, or latex agglutination. A computed tomographic brain scan was normal. He seemed to improve slightly when treated with intravenous cefotaxime but remained pyrexial. CSF, a throat swab, and stool sample were taken for viral culture. On the third day the child had a seizure and respiratory arrest and died. Histology of brain tissue taken at necropsy showed a patchy myelitis with a polymorph infiltrate. This was seen in the cerebrum but was predominantly in the anterior horn cells of the spinal cord and cerebellum. Poliovirus type 1 was cultured from the CSF, types 1 and 2 from the throat swab, and type 2 from the faeces. The viral isolates were confirmed as vaccinelike by polyconal intratypic neutralisation.1 Sections of spinal cord were deparaffinised with xylene and digested with proteinase K. Extracted RNA was subjected to polymerase chain reaction (PCR) using primers in the VP1 capsid gene,2 and the products were sequenced. The capsid sequences amplified were poliovirus type 1, and showed only 5 differences 609
clinical experience. Strict metabolic control prevents the development and the progression of diabetic retinopathy so a "controlled long-term clinical trial comparing pancreas transplantation with strict glycaemic control" is no longer required because the two approaches achieve similar results in terms of metabolic control. Moreover, strict metabolic control is very difficult in patients with end-stage renal failure or who are immunosuppressed with steroids, as are diabetic renal transplant recipients. Nor does the strict metabolic control achieved with pancreas transplantation expose patients to the risk of severe hypoglycaemic episodes. Not everyone agrees that pancreas transplantation increases the risk of kidney rejection. The same rate of patient and kidney graft survival at 5 years has been reported in diabetic patients
undergoing living-related kidney transplantation (91 cases, 83% and 72%, respectively) or receiving simultaneous kidneypancreas transplantation (138 cases, 87% and 76%), indicating that a simultaneous pancreas graft does not impair survival of the transplanted kidney.2 A "formal comparison with solo kidney transplantation" has already been done. That the ideal control group to evaluate the effects of pancreas transplantation on chronic complications is diabetic patients receiving kidney transplantation alone is not in dispute.3 Improvement of peripheral neuropathy has been reported. The Stockholm study, with longer follow-up, showed that the positive effect of kidney transplantation on peripheral neuropathy last for the first year only, whereas patients receiving pancreas transplantation improve progressively up to 4 years/ These results have been confirmed in
our
institute.5
Insulin-independence after islet transplantation has been reported by several groups, not just by Warnock, and the evidence cannot be dismissed as anecdotal even though definitive figures are not yet available. Antonio Secchi, Valerio Di Carlo, Guido Pozza San Raffaele Scientific Institute, University of Milan, 20132 Milan, Italy
1
2
3
4
5
Guslandi M, Tittobello A. Steroid ulcers: a myth revisited. BMJ 1992; 304: 655-56. Susaki T, Pirsch JD, D’Alessandro AM, et al. Simultaneous kidneypancreas transplantation at University of Wisconsin-Madison Hospital. In: Terasaki PI, Cecha JM, eds. Clinical transplant 1991. Los Angeles: University of California Press, 1991: 135-39. Anon. Secondary complications and quality of life after successful kidney-pancreas allotransplantation in type I diabetes mellitus.
Diabetologia 1991; 34 (suppl 1). Solders G, Tyden G, Persson A, et al. Improvement of nerve conduction in diabetic neuropathy: a follow-up study 4 years after combined pancreatic and renal transplantation. Diabetes 1992; 41: 946-51. Comi G, Galardi G, Amadio S, et al. Neurophysiological study of the effect of combined kidney and pancreas transplantation on diabetic neuropathy: a 2 year follow-up evaluation. Diabetologia 1991; 34 (suppl 1): S103-07.
SIR-Remuzzi and colleagues’ "review" presents only selected reports that seem to fit their own verdict on pancreas transplantation. For example, they note that one major concern after pancreas transplantation is cytomegalovirus (CMV) infection, and they cite a series describing 36 patients, 18 of whom had combined kidney/pancreas transplantation, and 18 kidney transplants alone. They conclude from this small series that CMV is much more of a problem in the combined procedure. However, larger series demonstrate similar incidences of CMV infection in combined and kidney alone
recipients.1.2 While kidney/pancreas transplant recipients have a rejection rate greater than that for kidney recipients alone, it is irresponsible to state flatly that there are three times more rejection episodes in these patients. A single report does not reflect the entire literature. They go on to give an example of the negative aspects of OKT3 induction therapy by quoting a single series of heart with increase in an transplants post-transplant not seen in any single-centre disorders lymphoproliferative series before or since. Many centres use routine induction therapy even for renal transplants alone, with safe outcomes. Remuzzi et al suggest that future trials should address quality of life, but they ignored published evidence for the positive effects of kidney/pancreas transplantation on quality of life.1-4 Nor do they discuss reports of the positive impact on neuropathic changes or diabetic angiopathy. It then becomes clear in the last section of the article that Remuzzi et al feel that islet-cell transplantation is the answer to achieving normal glucose homoeostasis. They refer to several publications on success in laboratory animals, yet ignore all the clinical data notable for absence of success. The number of insulin-independent type 1 diabetics who have received successful islet-cell transplants in the past decade is less than 10, and the successes of islet-cell transplantation have been "just around the corner" for the past 25 years. The article concludes with a strong recommendation that research should concentrate on islet-cell transplantation. While I cannot disagree with this, perhaps Remuzzi et al ought to concentrate more on results with whole organ pancreas transplantation achieved in experienced centres with more hopeful outcomes than those presented in their "review". Mitchell L
Henry
Division of Surgery, Ohio State University, Columbus, Ohio 43210, USA
Cheung HS, Sutherland DER, Gillingham KJ, et al. Simultaneous pancreas-kidney transplant versus kidney transplant alone in diabetic patients. Kidney Int 1992; 41: 924-29. 2 Henry ML, Ketel BL, Ferguson RM, et al. The role of transplantation in diabetics with end-stage renal disease. Clin Transpl 1990; 22: 203-15. 3 Nathan DM, Fogel H, Norman D, et al. Long-term metabolic and quality of life results with pancreatic/renal trnaplantation in insulindependent diabetes mellitus. Transplantation 1991; 52: 85-91. 4 Bentley FR, Jung S, Garrison RN. Neuropathy and psychosocial adjustment after pancreas transplant. Tranplant Proc 1990; 22: 691-95. 1
Airborne transmission of a small round structured virus SiR-Whilst not discounting the possibility of airborne transmission of small round structured viruses (SRSV) in the outbreak as described by Chadwick and colleagues (Jan 15, I think that the evidence is inconclusive. With an organism such as SRSV, which can cause infection with a very low dose, case-to-case transmission may occur with very little contact. This is clearly exemplified by the (presumably) high attack rate in the hotel, in which even staff were affected. We are not told if the 89-year-old primary case vomited in a toilet on the coach or in a sickness bag. She would almost certainly have contaminated her hands. The 15 other members of the coach party may have had direct contact with her or with the toilet, seats, or other objects on the coach contaminated by her. Presumably similar contamination occurred in the hotel. The phrase "airborne transmission" is much used in infectious disease epidemiology but needs qualifying. This usually means that a primary case releases an organism into the air which then causes infection through the air pasages of a secondary case.’ With very low dose infections, there must be a possibility that the airborne organism settles on an object which is then touched by a secondary case and is then transferred to the mouth ("air-oral transmission"). I suspect p
171),
that if direct contact was not the cause of transmission in the coach, air-oral transmission was more likely than pure airborne transmission. Norman D Noah Department of Public Health and Epidemiology, King’s College School of Medicine and Dentistry, London SE5 9PJ, UK
1 Benenson AS, ed. Control of communicable disease in man, 15th ed. Washington, DC: American Public Health Association, 1990.
Author’s reply
-
SIR—We agree that it is not possible to be absolutely sure how transmission occurred. There was a toilet on the coach, but the
89-year-old
woman
vomited while in her seat,
producing
a
localised area of direct contamination with vomit. In view of this and because of the high attack rate we believe that airborne dissemination of viruses by vomiting probably accounted for most cases among coach passengers. Vomiting is important in the epidemiology of infection due to SRSV and transmission by one or more different mechanisms is possible. Whether transmission on the coach was "pure airborne" or "air-oral" we cannot say. Nevertheless, there is evidence to implicate airborne dissemination of SRSV, in association with vomiting, and we can supply references including a recent study of a hospital outbreak of gastroenteritis in Salford.1
for certain. Preventive measures should include disinfecting of toilets and surfaces likely to have been contaminated by aerosol droplets from stool or vomitus.3 Workplaces differ in the risk of airborne transmission among employees, but in health-care settings preventive practices should be improved because SRSV gastroenteritis in patients tends to be managed by adoption of precautions aimed at reducing enteric transmission, and these will be only partly effective if the agent is transmitted from aerosolised vomitus or by other airborne means. In our report, 25% of cases occurred among staff, and one-fourth of these were in employees not normally exposed to excreta or vomitus. Infection may have been introduced by staff who also worked in an affiliated acute care hospital, where staff cases of acute gastroenteritis had preceded those in the convalescent facility. Respiratory precautions for hospital patients with acute gastroenteritis may be warranted when a pattern of explosive onset of disease such as that caused by SRSV, is observed. Hospital infection control personnel will need to investigate outbreaks of suspected SRSV gastroenteritis to assess whether the introduction of respiratory precautions does reduce transmission.
George A Gellert, Roger I Glass Project HOPE Health Sciences Education Center, Millwood, VA 22646, USA; and Viral Gastroenteritis Unit, Centers for Disease Control and Prevention, Atlanta, Georgia
1
Paul Chadwick Manchester Public Health
Laboratory, Withington Hospital, Manchester M20 8LR, UK 2
1 Chadwick PR, McCann R. Transmission of a small round structured virus by vomiting during a hospital outbreak of gastroenteritis. J Hosp
3
Infect (in press). 4
SiR-Chadwick and colleagues cite our report of an SRSV outbreak with evidence of airborne transmission but transmission of SRSV by this route has been suspected on epidemiological grounds in other episodes,1,2 and all three of those outbreaks happened in settings where chronically ill, debilitated, or elderly patients may reside. Transmission of SRSV by airborne droplets was also implicated in an outbreak on a cruise ship, where index patients who had vomited in their cabins were more likely to have had cabinmates who subsequently became ill than were index patients who had not vomited.3 Although further documentation of airborne SRSV transmission is needed the public health and infection control implications should be discussed. Apart from infections of the upper respiratory tract, acute gastroenteritis is probably the most common (although underreported) source of communicable disease morbidity in the industrialised countries. It causes huge losses in productivity. In 1985 acute gastroenteritis was one of the top three diagnoses in 87 181 entries on a database that contains only one-sixth of all US hospital admissions.4 From 1979 to 1987 annual deaths from diarrhoeal disease in the US averaged 3170.5 Most gastroenterological infections are assumed to involve faecal-oral transmission, and people with symptoms do not always stay off work. Increasing evidence of transmission of SRSV via the airborne or respiratory route could warrant changes in occupational health practice. Perhaps employees should respond to "stomach flu" just as they do influenza-by staying away from work during the acute illness. Those who vomit should be sent home immediately. Enforced sick leave during the symptomatic period (when viral shedding is maximal) may reduce the risk of secondary infection of work colleagues. SRSV-associated gastroenteritis commonly occurs with diarrhoea but no vomiting. Airborne transmission in the absence of aerosolised vomitus is unlikely but we do not know
5
Sawyer LA, Murphy JJ, Kaplan JE, et al. 25- to 30-nm virus particle associated with a hospital outbreak of acute gastroenteritis with evidence of airborne transmission. Am J Epidemiol 1988; 127: 1261-71. Kaplan JE, Schonberger LB, Varano G, et al. An outbreak of acute nonbacterial gastroenteritis in a nursing home. Am J Epidemiol 1982; 116: 940-48. Ho M-S, Glass RI, Monroe SS, et al. Viral gastroenteritis aboard a cruise ship. Lancet 1989; ii: 961-64. Gangarosa RE, Glass RI, Lew JF, Boring JR. Hospitalizations involving gastroenteritis in the United States, 1985: the special burden of the disease among the elderly. Am J Epidemiol 1992; 135: 281-90. Lew JF, Glass RI, Gangarosa RE, et al. Diarrheal deaths in the United States, 1979 through 1987. JAMA 1991; 265: 3280-84.
Vaccine-associated poliomyelitis SiR-lon-Nedelcu and colleagues (Jan 1, p 51) conclude that immune function should be investigated when poliomyelitis is suspected. We report a similar case that illustrates the value of both immunological and virological investigation. A 7-month-old boy was admitted to hospital with a history of ear infection for 2 weeks and irritability for 2 days. He had previously been well. His general practitioner had treated him with erythromycin and co-trimoxazole. He was febrile, posturing, and fitting, but had no focal signs. His cerebrospinal fluid (CSF) was clear and contained 84 white cells/L (85% polymorphs) and 04 g/L protein. No organisms were detected by Gram stain, culture, or latex agglutination. A computed tomographic brain scan was normal. He seemed to improve slightly when treated with intravenous cefotaxime but remained pyrexial. CSF, a throat swab, and stool sample were taken for viral culture. On the third day the child had a seizure and respiratory arrest and died. Histology of brain tissue taken at necropsy showed a patchy myelitis with a polymorph infiltrate. This was seen in the cerebrum but was predominantly in the anterior horn cells of the spinal cord and cerebellum. Poliovirus type 1 was cultured from the CSF, types 1 and 2 from the throat swab, and type 2 from the faeces. The viral isolates were confirmed as vaccinelike by polyconal intratypic neutralisation.1 Sections of spinal cord were deparaffinised with xylene and digested with proteinase K. Extracted RNA was subjected to polymerase chain reaction (PCR) using primers in the VP1 capsid gene,2 and the products were sequenced. The capsid sequences amplified were poliovirus type 1, and showed only 5 differences 609