Aims:To review the burden of allergic and infectious diseases and the evidence for a link to microbial exposure, the human microbiome and immune system, and to assess whether we could develop lifestyles which reconnect us with exposures which could reduce the risk of allergic disease while also protecting against infectious disease.Methods:Using methodology based on the Delphi technique, six experts in infectious and allergic disease were surveyed to allow for elicitation of group judgement and consensus view on issues pertinent to the aim.Results:Key themes emerged where evidence shows that interaction with microbes that inhabit the natural environment and human microbiome plays an essential role in immune regulation. Changes in lifestyle and environmental exposure, rapid urbanisation, altered diet and antibiotic use have had profound effects on the human microbiome, leading to failure of immunotolerance and increased risk of allergic disease. Although evidence supports the concept of immune regulation driven by microbe–host interactions, the term ‘hygiene hypothesis’ is a misleading misnomer. There is no good evidence that hygiene, as the public understands, is responsible for the clinically relevant changes to microbial exposures.Conclusion:Evidence suggests a combination of strategies, including natural childbirth, breast feeding, increased social exposure through sport, other outdoor activities, less time spent indoors, diet and appropriate antibiotic use, may help restore the microbiome and perhaps reduce risks of allergic disease. Preventive efforts must focus on early life. The term ‘hygiene hypothesis’ must be abandoned. Promotion of a risk assessment approach (targeted hygiene) provides a framework for maximising protection against pathogen exposure while allowing spread of essential microbes between family members. To build on these findings, we must change public, public health and professional perceptions about the microbiome and about hygiene. We need to restore public understanding of hygiene as a means to prevent infectious disease.

Summary The ‘hygiene hypothesis’ as originally formulated by Strachan, proposes that a cause of the recent rapid rise in atopic disorders could be a lower incidence of infection in early childhood, transmitted by unhygienic contact with older siblings. Use of the term ‘hygiene hypothesis’ has led to several interpretations, some of which are not supported by a broader survey of the evidence. The increase in allergic disorders does not correlate with the decrease in infection with pathogenic organisms, nor can it be explained by changes in domestic hygiene. A consensus is beginning to develop round the view that more fundamental changes in lifestyle have led to decreased exposure to certain microbial or other species, such as helminths, that are important for the development of immunoregulatory mechanisms. Although this review concludes that the relationship of the hypothesis to hygiene practice is not proven, it lends strong support to initiatives seeking to improve hygiene practice. It would however be helpful if the hypothesis were renamed, e.g. as the ‘microbial exposure’ hypothesis, or ‘microbial deprivation’ hypothesis, as proposed for instance by Bjorksten. Avoiding the term ‘hygiene’ would help focus attention on determining the true impact of microbes on atopic diseases, while minimizing risks of discouraging good hygiene practice.

SUMMARYThis case control study investigated environmental factors in 74 confirmed cases of meningococcal disease (MD). In children aged under 5, passive smoking in the home (30 or more cigarettes daily) was associated with an odds ratio (OR) of 7 5 (95% confidence interval (CI) 1P46-38-66). ORs increased both with the numbers of cigarettes smoked and with the number of smokers in the household, suggesting a dose-response relationship. MD in this age group was also significantly associated with household overcrowding (more than 1P5 persons per room) (OR 60, 95% CI 110-32-8), with kisses on the mouth with 4 or more contacts in the previous 2 weeks (OR 2-46, 95% CI 1P09-5 56), with exposure to dust from plaster, brick or stone in the previous 2 weeks (OR 2-24, 95 % CI 107-465); and with changes in residence (OR 30, 95% CI 1P0-899), marital arguments (OR 3-0, 95 % CI 1P26-7 17) and legal disputes in the previous 6 months (OR 3-10, 95% CI 1P24-7 78). These associations were independent of social class. Public health measures to lower the prevalence of cigarette smoking by parents of young children may reduce the incidence of MD. The influence of building dust and stressful life events merits further investigation.

All previously published epidemiological studies of the health effects of bathing in marine waters contaminated with domestic sewage contain three major methodological weaknesses in study design: (1) failure to control for the substantial amount of temporal and spatial variation in indicator organism densities shown to occur within just a few hours at marine water bathing locations; (2) failure to relate indicator organism density directly to the individual bather; and (3) failure to rigorously control for non-water-related risk factors on previously reported associations between bathing in marine waters and illness among such bathers. We report the results of two intervention follow-up studies specifically designed to address these methodological weaknesses. We restricted study outcome to bathing-associated gastroenteritis since this is the illness most consistently reported to be associated with bathing in marine waters, and upon which both current US Marine Water Quality Criteria and other standards used worldwide are based. Our results show that faecal streptococci was the only indicator organism to predict the occurrence of gastroenteritis among bathers, and this occurred at only one of the three water quality sampling depths used in our study. The consumption of three different foods known or suspected to act as vectors in the transmission of gastroenteritis, as well as one non-food, non-water-related risk factor for gastroenteritis were found to significantly increase the risk of gastroenteritis among bathers. Multiple logistic regression modelling showed that these non-water-related risk factors confounded the relationship between exposure to marine waters of varying faecal streptococci densities and the occurrence of gastroenteritis among bathers to a moderate degree. Moreover, these analyses showed that the risk of gastroenteritis to the individual bather caused by these non-water-related risk factors, approximated the risk of gastroenteritis among bathers exposed to waters containing relatively high faecal streptococci densities. The implications of these findings with regard to the validity of present marine water quality criteria and on the need for, and design of, future epidemiological studies of bathing water associated illness are discussed.

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SUMMARYA large outbreak of Legionnaires’ disease was associated with Stafford District General Hospital. A total of 68 confirmed cases was treated in hospital and 22 of these patients died. A further 35 patients, 14 of whom were treated at home, were suspected cases of Legionnaires’ disease. All these patients had visited the hospital during April 1985. Epidemiological investigations demonstrated that there had been a high risk of acquiring the disease in the out patient department (OPD), but no risk in other parts of the hospital. The epidemic strain ofLegionella pneumophila, serogroup 1, subgroup Pontiac la was isolated from the cooling water system of one of the air conditioning plants. This plant served several departments of the hospital including the OPD. The water in the cooling tower and a chiller unit which cooled the air entering the OPD were contaminated with legionellae. Bacteriological and engineering investigations showed how the chiller unit could have been contaminated and how an aerosol containing legionellae could have been generated in the U–trap below the chiller unit. These results, together with the epidemiological evidence, suggest that the chiller unit was most likely to have been the major source of the outbreak.Nearly one third of hospital staff had legionella antibodies. These staff were likely to have worked in areas of the hospital ventilated by the contaminated air conditioning plant, but not necessarily the OPD. There was evidence that a small proportion of these staff had a mild legionellosis and that these ‘influenza–like’ illnesses had been spread over a 5–month period. A possible explanation of this finding is that small amounts of aerosol from cooling tower sources could have entered the air–intake and been distributed throughout the areas of the hospital served by this ventilation system. Legionellae, subsequently found to be of the epidemic strain, had been found in the cooling tower pond in November 1984 and thus it is possible that staff were exposed to low doses of contaminated aerosol over several months.Control measures are described, but it was later apparent that the outbreak had ended before these interventions were introduced. The investigations revealed faults in the design of the ventilation system.

THERE WERE 34 outbreaks of water-borne disease recorded in the UK between 1937 and 1986, comprising over I I 794 cases and at least six deaths.A total of 21 outbreaks were due to public water supplies, 11 of thcni contaminated at source; in eight of these 11 the water was unchlorinated or defectively chlorinated. None of the six' reported deaths was due t o contamination of public supplies at source. About 1 000 cases of gastro-intestinal illness were caused by consumption ofafoods, particularly milk and canned nicats, that had been contaminated by polluted water during processing. Shellfish harvested from pollutcd cstuarics gave rise to increasing numbers of outbreaks of viral gastroenteritis and hepatitis A. The recreational use of water was associated with about 400 serious infections and probably many minor illnesses. Sonie hospital infections may have hecn derived from the potable water supply. A total of 14 outbreaks of legionnaires' disease and eight of humidifier fever were associated with water in buildings.Thc future control of water-borne and waterassociated disease demands not only continued vigilance in the water industry but closer collaboration between public health doctors and water engineers and scientists.

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