Respiratory viruses and sudden infant death.

Viruses were shown to be present in the respiratory tract in 200 of 763 cases of the sudden infant death syndrome studied in the nine years 1974-82. Epidemiological and pathological evidence suggested that the distribution of viruses in the sudden infant death syndrome differs between infants aged 3 months or less and those aged over 3 months: the incidence of detection of virus was 14% in the younger group compared with 39% in the older group. The distribution of the viruses in these two groups was compared with that in 1341 live infants with respiratory virus infections. Adenovirus, influenza virus, parainfluenza virus, and rhinovirus had similar distribution among the victims of the sudden infant death syndrome and live controls. The incidence of detection of respiratory syncytial virus was increased in the older infants dying of the sudden infant death syndrome (90% of the cases detected) compared with the older group of live infants (53%). Antibody studies, detection of virus, and epidemiological data suggest that respiratory syncytial virus may be a precipitating factor of sudden death in older infants.     

Bereavement counselling after sudden infant death.

Of 14 families who suffered a sudden infant death, eight were followed up intensively over several months and offered individual counselling, parents'' group meetings, and interviews with doctors as a way of helping them come to terms with their feelings of loss. Five couples accepted short term support from their health visitor, and one refused help. Many families experienced considerable stress including marital conflict, difficulties with surviving children, and anxiety about future children becoming victims of the sudden infant death syndrome. It was concluded that medical social workers, health visitors, hospital paediatricians, general practitioners, and parent self help groups are in key positions to help. The success of such help is likely to depend on the confidence that each helper has that his or her contribution will be valued by the bereaved family.     

Thermal environment and sudden infant death syndrome: case-control study.

OBJECTIVE--To compare the thermal environment of infants who died of the sudden infant death syndrome with that of age matched control infants. DESIGN--Case-control study. Infants who died were matched with two controls, one for age and one for age and birth weight. Thermal measurements were conducted at the death scene for cases and at the scene of last sleep for control infants, who were visited unexpectedly within four weeks of the index infant''s death on a day of similar climatic conditions. A follow up questionnaire was administered to parents of cases and controls. SETTING--The geographical area served by the professional Tasmanian state ambulance service, which includes 94% of the Tasmanian population. SUBJECTS--41 infants died of the sudden infant death syndrome at home; thermal observations at death scene were available for 28 (68%), parental questionnaire data were available for 40 (96%). 38 controls matched for age and 41 matched for age and birth weight. RESULTS--Cases had more excess thermal insulation for their given room temperature (2.3 togs) than matched controls (0.6 togs) (p = 0.009). For every excess thermal insulation unit (tog) the relative risk of the sudden infant death syndrome was 1.26 (95% confidence interval 1.05 to 1.52). The average thermal bedding value calculated from parental recall was similar to that observed by attendant ambulance officers (mean difference = 0.4 tog, p = 0.39). Cases were more likely to have been found prone (odds ratio 4.58; 1.48 to 14.11). Prone sleeping position was not a confounder or effect modifier of the relation between excess thermal insulation and the syndrome. CONCLUSIONS--Overheating and the prone sleeping position are independently associated with an increased risk of the sudden infant death syndrome. Further work on infant thermal balance and sudden infant death is required and guidelines for appropriate infant thermal care need to be developed.     

Bottle feeding and the sudden infant death syndrome.

OBJECTIVE--To determine whether the risk of the sudden infant death syndrome is increased in bottle fed babies. DESIGN--Population based case-control study matching for age and time. SUBJECTS--All babies aged 1 week to 1 year dying of sudden infant death syndrome during November 1987 to April 1989 or February 1990 to June 1991 and two live controls. SETTING--Avon and north Somerset. MAIN OUTCOME MEASURES--Breast or bottle feeding, sleeping position, maternal smoking, parental employment, and length of gestation. RESULTS--Compared with being fully breast fed, the crude odds ratio for sudden infant death in fully bottle fed babies was 3.1 and for mixed breast and bottle fed babies 1.5. These odds ratios fell to 1.8 (95% confidence interval 0.7 to 4.8) and 1.2 (0.5 to 2.7) respectively after maternal smoking, parental employment, preterm gestation, and sleeping position had been adjusted for. Sleeping position partly masked the effect of being bottle fed on sudden infant death as breast fed babies were more likely to have slept prone than bottle fed babies. CONCLUSIONS--Bottle feeding is not a significant independent risk factor for the sudden infant death syndrome. Patterns of maternal smoking, preterm gestation, and parental employment status account for most of the apparent association with bottle feeding.     

Cardiac conduction disorders in six infants with "near-miss" sudden infant deaths.

Cardiac conduction disorders caused sudden serious illnesses in six infants that might have been fatal if diagnosis and treatment had been delayed. These cases provide circumstantial evidence to support a link between cardiac conduction disorders and some sudden infant deaths. A further potential long-term effect of these disorders is illustrated in one child in whom psychomotor retardation seemed to develop after an episode of cerebral hypoxia that was probably by an arrhythmia associated with the Wolff-Parkinson-White syndrome. Cardiac conduction disorders may be detected by routine neonatal ECG screening, and it may therefore be appropriate to start prophylactic antiarrhythmic treatment in certain children before clinical signs develop.     

Interleukin-10 and sudden infant death syndrome

Uncontrolled pro-inflammatory responses to infections or bacterial toxins have been suggested to play a role in triggering the physiological events leading to sudden infant death syndrome (SIDS). We tested the hypothesis that these uncontrolled responses might be due to interactions between the gene polymorphisms inducing low levels of IL-10 and exposure to cigarette smoke. In vitro, the IL-10 (G-1082A) polymorphism was associated with low IL-10 levels and the -1082G allele was associated with high levels. The first objective was to assess the distribution of this polymorphism among SIDS infants, parents of SIDS infants and controls, and two ethnic groups: Aboriginal Australians who have a high incidence of SIDS; and Bangladeshis who in Britain have a low incidence of SIDS compared with Europeans. The second objective was to assess effects of human recombinant IL-10 on interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-alpha) responses of human leukocytes to staphylococcal toxins implicated in SIDS. The third objective was to assess IL-10 responses to endotoxin and toxic shock syndrome toxin (TSST) from leukocytes of smokers and non-smokers in relation to the IL-10 (G-1082A) polymorphism. There were major differences in the distributions of these polymorphisms between Europeans and Bangladeshis (p=0.00) and between Europeans and Aboriginal Australians (p=0.00); however, they were similar for the Bangladeshi and Aboriginal Australian subjects. There were no significant differences in the distribution of these polymorphisms among SIDS infants or parents of SIDS infants compared to control groups. IL-10 significantly reduced IL-6 and TNF-alpha responses to TSST and staphylococcal enterotoxins A and C. At 50 ng ml(-1), IL-10 significantly increased TNF-alpha but not IL-6 responses to TSST and enterotoxin A. Although IL-10 responses to endotoxin were lower from leukocytes of smokers who were homozygous for the G allele, the differences were not significant; however, significantly lower IL-10 responses were found for smokers who were homozygous for the A allele (p=0.01) and heterozygotes (p=0.04). The pooled data found smokers had significantly lower levels of IL-10 responses to TSST, but there were no significant differences for smokers compared with non-smokers for the three genotypes. The high incidence of SIDS and serious respiratory infections among Aboriginal Australian infants and the low incidence of these conditions among Bangladeshi infants might be explained in part by our findings of differences in IL-10 responses between smokers and non-smokers. The lowest levels of IL-10 responses were observed among smokers who were homozygous for the A allele which is most prevalent among the Aboriginal Australians (83%) and Bangladeshis (84%). The major difference between the risk factors for SIDS in these two groups is the level of exposure of infants to cigarette smoke associated with maternal smoking.     

Lung immunoglobulins in the sudden infant death syndrome.

The incidence of the sudden infant death syndrome parallels that of respiratory tract infections in the paediatric community. On the basis that the aetiology of the sudden infant death syndrome may lie in an unusual response to a trivial intercurrent respiratory infection a necropsy study was carried out investigating pulmonary immunoglobulins in 16 victims of the syndrome and a series of infants (controls) who had died of non-pulmonary causes. Compared with the controls victims of the sudden infant death syndrome had grossly raised concentrations of IgG, IgM, and to a less extent IgA in lung lavage samples. In addition, pulmonary interstitial and terminal airway cells expressing these immunoglobulins were identified far more often in victims than controls. The study failed to determine whether the increased immunoglobulin concentrations were a consequence of an unusual response to a trivial infection or an expression of otherwise altered immunological control in the respiratory tract. Epidemiological evidence and the findings of this study suggest that the respiratory tract is the prime target organ in the sudden infant death syndrome.