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Arch Dis Child. 2007 May; 92(5): 470.
PMCID: PMC2083722

Lucina

In the last two decades the prevalence of myopia in early adolescence has increased, reaching 10‐25% in Europe and North America and 60‐80% in East Asia. Data from the 1958 British birth cohort have been used to assess the predictive value of uncorrected distance visual acuity (DVA) measured at age 16 years (BJO, published Online First 4 October 2006; 10.1136/bjo.2006.102277). A total of 1867 people had DVA assessed at 16 years and autorefraction at 45 years. As adults 35% of this group were myopic and 24% of these myopic adults had had reduced DVA as teenagers. The sensitivity of reduced teenage DVA for the prediction of adult myopia was 16% overall and 69% for high myopia. The lifetime probability of primary myopia among people with a reduced uncorrected DVA at age 16 was 91%. Measuring uncorrected DVA in adolescence is not a useful way of identifying the majority of people who will be myopic as adults but it does identify refractive error (myopia or hypermetropia) present at the time of testing.

Annual influenza vaccination of children in school may protect household members, both children and adults. In the autumn of 2004 in four US states children aged 5‐14 years in 11 schools were offered intranasal live attenuated influenza vaccine and children in 17 schools acted as controls (New England Journal of Medicine 2006;355:2523–32; see also editorial, ibid: 2586–7). Forty seven per cent of children in intervention schools received the vaccine. Household surveys were performed during the predicted week of peak influenza activity in early 2005. During the survey week intervention‐school households had significantly lower rates of influenza‐like symptoms in both adults and children compared with control‐school households. These households also received less treatment and had lower rates of absence from school or work.

In theory childhood immunisation might increase the risk of atopy by reducing early childhood infections or by directly stimulating allergic responses. Studies have given conflicting results for pertussis, diphtheria, tetanus, and poliomyelitis vaccines but no studies of measles, BCG, or smallpox vaccination have shown an association with increased risk of atopy. Now a study in Tasmania (Thorax, published Online First 7 November 2006; doi: 10.1136/thx.2006.062547) has shown little effect of childhood immunisation on the risk of later atopy. All children born in Tasmania in 1961 were assessed by questionnaires at ages 7 (99% response) and 13 years (87% response) and a random sample of 1763 individuals were assessed at the age of 30 years. There were weak associations between diphtheria immunisation and increased risk of asthma by age 7 and between immunisations against diphtheria, tetanus, pertussis, and poliomyelitis and the risks of eczema or food allergies by age 7. None of the immunisations was associated with increased risk of hay fever, and atopy becoming symptomatic between the ages of 7 and 30 years was not related to immunisation history. These researchers conclude that the fear of atopic disease should not deter parents from immunising their children, especially when weighed against the benefits.

Salmonella infections have been associated with the handling of reptiles, amphibians, chickens, ducklings, kittens and hedgehogs. Now a widespread outbreak associated with pet rodents has been reported from the USA (New England Journal of Medicine 2007;356:21–8). In August 2004 eight hamsters from a Minnesota pet distributor were found to be infected with an uncommon strain (by pulsed‐field gel electrophoresis) of Salmonellaenterica serotype Typhimurium, a strain isolated from only 0.1% of human salmonella Typhimurium isolates. This strain had been isolated during the summer of 2004 from a 4‐year‐old boy in South Carolina and a 5‐year old boy in Minnesota. One of these children had recently had a pet hamster and the other a pet mouse; both animals had been ill. A national database search for more cases revealed 28 people from whom the same strain of salmonella had been isolated during 2004. Twenty‐two of these were contacted and 13 had been in contact with pet rodents. Another two had been in contact with a patient who had acquired the disease from a pet rodent. The 15 patients with direct or indirect exposure to pet rodents lived in 10 states. Their median age was 16 years (range 0–43 years) and seven were less than 8 years old. Of the 13 patients with primary exposure four had been exposed to pet mice or rats, two to pet hamsters and seven to mice or rats kept to be fed to snakes. Each of the thirteen patients had bought their rodents from a different pet store in the ten states. All of the isolates were resistant to ampicillin, chloramphenicol, streptomycin, sulfisoxazole, and tetracycline.

Congenital toxoplasmosis occurs only when the mother is infected during pregnancy, and even then in only about a third of infected mothers. Only 4% or fewer of congenitally infected infants suffer from permanent neurological or severe visual damage. The effectiveness of prenatal screening and treatment is uncertain. Systematic reviews of observational data published in 1996 and 1999 did not resolve the problem and there have been no randomised controlled trials. Now another systematic review of 26 cohort studies (Lancet 2007;369:115–22) has led to the conclusion that what is needed is a large randomised controlled trial. There was weak evidence that maternal treatment within 3 weeks of seroconversion was more effective in preventing mother‐to‐child transmission than treatment begun after 8 weeks or more. Greater gestational age at seroconversion was associated with increased risk of transmission but reduced risk of intracranial lesions in the child; it did not affect the ocular risk. There was no evidence that prenatal treatment significantly affected the risk of clinically manifest disease among liveborn infected infants detected by prenatal or neonatal screening. The authors of this paper believe that more observational studies would not be helpful.

Until recently 12 people had been identified as having congenital leptin deficiency due to mutation in the leptin gene and three people in one family had been shown to have a mutation in the leptin receptor gene (LEPR). Now a study of 300 people with severe, early‐onset (<1 year) obesity (New England Journal of Medicine 2007;356:237–47) has led to the detection of nine more LEPR mutations in another eight people. There were five nonsense and four missense mutations (seven homozygotes and one compound heterozygote). The characteristic clinical features were hyperphagia, severe obesity, immune dysfunction, and delayed puberty due to hypogonadotropic hypogonadism. Circulating leptin concentrations had been very high in the first reported case but were normal for body weight in these eight subjects. Their clinical features were less severe than those of people with congenital leptin deficiency.


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