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Early hospital discharge and cross-infection
trition and death. The world’s inadequate response to the crisis in Sudan could be attributed to competition with other crises for limited resources; the news media’s difficulty of access to and lack of interest in Sudan; the impression that Sudan’s problems are chronic and unsolvable; the lack of a sustained peace; and the logistical difficulties, magnified during the rainy season, entailed in delivering aid to affected areas of this vast country. Substantially increased international support is needed for the United Nations sponsored Operation Lifeline Sudan, which is believed to have prevented widespread famine in Sudan in 1989. A high proportion of famine deaths are caused by communicable diseases such as measles and diarrhoea. Therefore, in addition to massive food aid, support for measles immunisation and oral rehydration programmes is essential. Without prompt action on a large scale, our only contribution may be to assess mortality. Barbara L Herwaldt, David C Michael J Toole
Bassett, Ray Yip, Carlos R Alonso,
Department of Health and Human Services, Centers for Disease Control and Prevention, Atlanta, Georgia 30341, USA
1 2
3 4
5
6
Centers for Disease Control. Nutrition and mortality assessment: southern Sudan, March 1993. MMWR 1993; 42: 304-08. Carlson BA, Wardlaw TM. A global, regional and country assessment of child malnutrition. UNICEF staff working paper no 7. New York: United Nations Children’s Fund, 1990. Manoncourt S, Doppler B, Enten F, et al. Public health consequences of the civil war in Somalia, April, 1992. Lancet 1992; 340: 176-77. United Nations Children’s Fund. The state of the world’s children, 1991. New York: United Nations Children’s Fund, 1992. Moore PS, Marfin AA, Quenemoen LE, et al. Mortality rates in displaced and resident populations of central Somalia during 1992 famine. Lancet 1993; 341: 935-38. Centers for Disease Control. Famine-affected, refugee, and displaced populations: recommendations for public health issues. MMWR 1992; 41: RR-13.
Early hospital discharge and cross-infection SiR-Cross-infection in hospitals is usually brought to attention by an easily-recognised marker organism (eg-methicillin resistant Staphylococcus aureus) or by an unusual illness. Early discharge policies and the increasing use of day surgery mean that infection is treated by the primary health care team, and there may be delay detecting an outbreak. This was the case when cross-infection by S aureus caused blistering rashes in otherwise healthy neonates aged between 2 and 12 days. The blisters were up to 2 cm in diameter, flaccid, and contained cloudy fluid. Attention was first drawn to 4 babies who developed blisters in hospital aged 6-8 days over a 6 week period. Inquiries from community midwives and general practitioners showed that at least another 14 babies had been managed at home with similar rashes over this period. One paediatrician had handled 17 of these 18 babies either at delivery or later. Swabs from the paediatrician’s nose, axilla, and perineum, and swabs from the characteristic lesions of 5 affected babies yielded heavy growths of the same S aureus (phage type 3A/3C, exfoliative toxin A producers). The paediatrician was suspended from duty until free from infection. The outbreak, which had lasted 2 months, ended abruptly. No environmental decontamination was done. Retrospective case-finding showed that a total of 36 babies had been affected by blisters. Nasal swabs from all staff on the same postnatal unit taken 2 months after the last case occurred revealed no one else to be carrying the epidemic strain. Exfoliative toxins of S aureus can cause a spectrum of skin disease from staphylococcal scalded skin syndrome to bullous impetigo. The babies in this outbreak were apyrexial and 120
the
showed no signs of systemic upset, although blisters alarmed the attendants. Treatment with flucloxacillin resulted in rapid resolution. This outbreak serves as a reminder that infection surveillance must not stop on discharge from hospital, and that staff should always heed advice to wash their hands between patients. We thank Dr R R Marples of the Staphycoccal Reference Laboratory for results of phage typing and toxin tests.
F G Bell Children’s
Hospital, Doncaster Royal Infirmary, Doncaster DN2 5LT, UK
P A Fenton Department of Microbiology, Doncaster Royal Infirmary
International association between Helicobacter pylori and gastric cancer SiR-The EUROGAST Study Group report (May 29, p 1359) ecological study of the association between population seroprevalence of antibody to Helicobacter pylori and record gastric cancer incidence and mortality. They state that originan
ally only 13 European (and 1 North African) populations were included, but that 1 population from the USA and 2 from Japan later added to extend the range. From looking at the regression curves showing the percentage of a random sample displaying antibody to H pylori versus cumulative gastric cancer mortality and incidence for each of the populations, one gets the impression that most of the association stems from the low figures for seroprevalence and cancer mortality in Minnesota and from the correspondingly high figures for the Japanese centres. How much of the reported association remains if only the 14 original populations are included? Is not the main finding of the study a pronounced gradient in seroprevalence and cancer mortality/incidence between USA and Japan? If this were true, the difficulties with confounding inherent to any ecological study might be even were
graver.
Johan Giesecke Department of Epidemiology, London School of London WC1E 7HT, UK
Hygiene and Tropical Medicine,
Authors’reply SIR—When we extended the EUROGAST study to include additional centres, it was before any H pylori seroprevalence results were available. A priori, we wanted to include centres that were representative of the world-wide range in cancer rates, not merely the range that existed in Europe; this was possible by including populations from Japan and the USA. Giesecke asks how much of the association between rates of gastric cancer and H pylori seroprevalence remains after omitting Japanese and US centres. After removal, the regression coefficient for gastric cancer mortality changed from 1 ’79 (p = 0-002) to 0-62 (p = 03). Removal oflhe 2 Japanese centres alone changed the regression coefficient to 1 23 (p 0-055), and removal of the American centre alone changed the coefficient to 1-36 (p=0-012). Hence, there were significant associations between the remaining centres after omitting centres from either country, but not both. Inspection of the plots in our report shows that the Greek centre, Crete, is an obvious outlier. Removal of this centre, as well as those from Japan and the USA changed the regression coefficient to 1.88 (p 0-002), resulting in an effect as strong as that seen with all the data. It would be clearly inappropriate to exclude centres from a geographic comparison because they do not fit in with the hypothesis under test-as it would be to exclude the Japanese and American centres because they do fit. =
=
Bassett, Ray Yip, Carlos R Alonso,
Department of Health and Human Services, Centers for Disease Control and Prevention, Atlanta, Georgia 30341, USA
1 2
3 4
5
6
Centers for Disease Control. Nutrition and mortality assessment: southern Sudan, March 1993. MMWR 1993; 42: 304-08. Carlson BA, Wardlaw TM. A global, regional and country assessment of child malnutrition. UNICEF staff working paper no 7. New York: United Nations Children’s Fund, 1990. Manoncourt S, Doppler B, Enten F, et al. Public health consequences of the civil war in Somalia, April, 1992. Lancet 1992; 340: 176-77. United Nations Children’s Fund. The state of the world’s children, 1991. New York: United Nations Children’s Fund, 1992. Moore PS, Marfin AA, Quenemoen LE, et al. Mortality rates in displaced and resident populations of central Somalia during 1992 famine. Lancet 1993; 341: 935-38. Centers for Disease Control. Famine-affected, refugee, and displaced populations: recommendations for public health issues. MMWR 1992; 41: RR-13.
Early hospital discharge and cross-infection SiR-Cross-infection in hospitals is usually brought to attention by an easily-recognised marker organism (eg-methicillin resistant Staphylococcus aureus) or by an unusual illness. Early discharge policies and the increasing use of day surgery mean that infection is treated by the primary health care team, and there may be delay detecting an outbreak. This was the case when cross-infection by S aureus caused blistering rashes in otherwise healthy neonates aged between 2 and 12 days. The blisters were up to 2 cm in diameter, flaccid, and contained cloudy fluid. Attention was first drawn to 4 babies who developed blisters in hospital aged 6-8 days over a 6 week period. Inquiries from community midwives and general practitioners showed that at least another 14 babies had been managed at home with similar rashes over this period. One paediatrician had handled 17 of these 18 babies either at delivery or later. Swabs from the paediatrician’s nose, axilla, and perineum, and swabs from the characteristic lesions of 5 affected babies yielded heavy growths of the same S aureus (phage type 3A/3C, exfoliative toxin A producers). The paediatrician was suspended from duty until free from infection. The outbreak, which had lasted 2 months, ended abruptly. No environmental decontamination was done. Retrospective case-finding showed that a total of 36 babies had been affected by blisters. Nasal swabs from all staff on the same postnatal unit taken 2 months after the last case occurred revealed no one else to be carrying the epidemic strain. Exfoliative toxins of S aureus can cause a spectrum of skin disease from staphylococcal scalded skin syndrome to bullous impetigo. The babies in this outbreak were apyrexial and 120
the
showed no signs of systemic upset, although blisters alarmed the attendants. Treatment with flucloxacillin resulted in rapid resolution. This outbreak serves as a reminder that infection surveillance must not stop on discharge from hospital, and that staff should always heed advice to wash their hands between patients. We thank Dr R R Marples of the Staphycoccal Reference Laboratory for results of phage typing and toxin tests.
F G Bell Children’s
Hospital, Doncaster Royal Infirmary, Doncaster DN2 5LT, UK
P A Fenton Department of Microbiology, Doncaster Royal Infirmary
International association between Helicobacter pylori and gastric cancer SiR-The EUROGAST Study Group report (May 29, p 1359) ecological study of the association between population seroprevalence of antibody to Helicobacter pylori and record gastric cancer incidence and mortality. They state that originan
ally only 13 European (and 1 North African) populations were included, but that 1 population from the USA and 2 from Japan later added to extend the range. From looking at the regression curves showing the percentage of a random sample displaying antibody to H pylori versus cumulative gastric cancer mortality and incidence for each of the populations, one gets the impression that most of the association stems from the low figures for seroprevalence and cancer mortality in Minnesota and from the correspondingly high figures for the Japanese centres. How much of the reported association remains if only the 14 original populations are included? Is not the main finding of the study a pronounced gradient in seroprevalence and cancer mortality/incidence between USA and Japan? If this were true, the difficulties with confounding inherent to any ecological study might be even were
graver.
Johan Giesecke Department of Epidemiology, London School of London WC1E 7HT, UK
Hygiene and Tropical Medicine,
Authors’reply SIR—When we extended the EUROGAST study to include additional centres, it was before any H pylori seroprevalence results were available. A priori, we wanted to include centres that were representative of the world-wide range in cancer rates, not merely the range that existed in Europe; this was possible by including populations from Japan and the USA. Giesecke asks how much of the association between rates of gastric cancer and H pylori seroprevalence remains after omitting Japanese and US centres. After removal, the regression coefficient for gastric cancer mortality changed from 1 ’79 (p = 0-002) to 0-62 (p = 03). Removal oflhe 2 Japanese centres alone changed the regression coefficient to 1 23 (p 0-055), and removal of the American centre alone changed the coefficient to 1-36 (p=0-012). Hence, there were significant associations between the remaining centres after omitting centres from either country, but not both. Inspection of the plots in our report shows that the Greek centre, Crete, is an obvious outlier. Removal of this centre, as well as those from Japan and the USA changed the regression coefficient to 1.88 (p 0-002), resulting in an effect as strong as that seen with all the data. It would be clearly inappropriate to exclude centres from a geographic comparison because they do not fit in with the hypothesis under test-as it would be to exclude the Japanese and American centres because they do fit. =
=