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Buruli ulcer (BU) is a subcutaneous necrotic infection of the skin caused by Mycobacterium ulcerans. It is the third most common human mycobacterial disease after tuberculosis (TB) and leprosy. The available methods for detection of the bacilli in lesions are microscopic detection, isolation and cultivation of the bacterium, histopathology, and polymerase chain reaction (PCR). These methods, although approved by the World Health Organization (WHO), have infrastructural and resource challenges in medical centres and cell-mediated immunity (CMI) and/or serology-based tests have been suggested as easier and more appropriate for accurate assessment of the disease, especially in remote or underdeveloped areas. This study systematically reviewed and conducted a meta-analysis for all research aimed at developing cell-mediated immunity (CMI) and/or serology-based tests for M. ulcerans disease. Information for this review was searched through PubMed and Web of Science databases and identified up to June 2019. References from relevant articles and reports from the WHO Annual Meeting of the Global Buruli Ulcer Initiative were also used. Twelve studies beginning in 1952, that attempted to develop CMI and/or serology-based tests for the disease were identified. These studies addressed issues of specificity and sensitivity in context of antigen composition as well as study heterogeneity and bias. The two main types of antigenic preparations considered were pathogen-derived and recombinant protein preparations. There was slight difference in test performance when M. ulcerans recombinant proteins [positivity: 67.5%; 32.5%] or pathogen-derived [positivity: 76.0%; 24.0%] preparations were used as test antigens among BU patients. However, pathogen-derived preparations were better at differentiating between patients and control groups [odds ratio (OR) of 27.92, 95%CI: 5.05–154.28]. This was followed by tests with the recombinant proteins [OR = 1.23, 95%CI: 0.27–5.62]. Overall, study heterogeneity index, I2 was 92.4% (p = 0.000). It is apparent from this review that standardisation is needed in any future CMI and/or serology-based tests used for M. ulcerans disease. Author summary: Buruli ulcer (BU) is a debilitating skin infection caused by M. ulcerans. It is the third most common mycobacterial disease after tuberculosis and leprosy. BU is mainly restricted to the tropical and subtropical countries of the world, though temperate regions report sporadic cases. Polymerase chain reaction targeting IS2404 is the gold standard for M. ulcerans disease diagnosis and other methods such as histopathology, acid fast staining and microscopy are used for validity checks. The currently approved diagnostic tools lack sensitivity and specificity and there are many resource challenges in underdeveloped regions. Isolation and culture of the bacillus from tissue biopsies is the only method that detects viable cells. However, the long incubation period of the pathogen makes it not ideal and rapid enough for point-of-care diagnosis. Cell-mediated immunity and serology-based methods have been suggested as appropriate tools for accurate and rapid testing for the disease within "at-risk-communities". This study systematically reviewed and conducted a meta-analysis on all research aimed at developing cell-mediated immunity and/or serology-based tests for M. ulcerans disease. [ABSTRACT FROM AUTHOR]

Mycobacterium ulcerans disease is a necrotising disease of the skin and subcutaneous tissue and is effectively treated with eight-weeks antibiotic therapy. Significant toxicities, however, are experienced under this prolonged regimen. Here, we investigated the length of antibiotic duration required to achieve negative cultures of M. ulcerans disease lesions and evaluated the influence of patient characteristics on this outcome. M. ulcerans cases from an observational cohort that underwent antibiotic treatment prior to surgery and had post-excision culture assessment at Barwon Health, Victoria, from May 25 1998 to June 30 2019, were included. Antibiotic duration before surgery was grouped as <2 weeks, ≥2-<4 weeks, ≥4-<6 weeks, ≥6-<8 weeks, ≥8-<10 weeks and ≥10–20 weeks. Cox regression analyses were performed to assess the association between variables and culture positive results. Ninety-two patients fitted the inclusion criteria. The median age was 60 years (IQR 28–74.5) and 51 (55.4%) were male. Rifampicin-based regimens were predominantly used in combination with clarithromycin (47.8%) and ciprofloxacin (46.7%), and the median duration of antibiotic treatment before surgery was 23 days (IQR, 8.0–45.5). There were no culture positive results after 19 days of antibiotic treatment and there was a significant association between antibiotic duration before surgery and a culture positive outcome (p<0.001). The World Health Organisation category of the lesion and the antibiotic regimen used had no association with the culture outcome. Antibiotics appear to be effective at achieving negative cultures of M. ulcerans disease lesions in less than the currently recommended eight-week duration. [ABSTRACT FROM AUTHOR]

Summary: Background: Eczema is a chronic inflammatory skin disease. Domestic water with high mineral content (hard water) is a risk factor for eczema in children, but this association has not been assessed in adults. Objectives: To examine the association between domestic hard water supply and eczema prevalence and incidence in adults aged 40–69 years and the contextual effect in eczema outcomes by postcode in adults in the UK. Methods: We used data from the UK Biobank study collected in 2006–10 (baseline) and 2013–14 (follow‐up). Eczema prevalence at baseline (2006–10) and at follow‐up (2013–14) and incidence (new onset between baseline and follow‐up) were determined from the touchscreen questionnaires and nurse‐led interviews. Domestic hard water information was obtained in 2005 and 2013 from the local water supply companies in England, Wales and Scotland as CaCO3 concentrations. We fitted multilevel logistic regression models with random intercepts for postcode areas to examine the effect of domestic hard water on eczema outcomes, and we measured components of variance. Results: In total, 306 531 participants with a mean age of 57 years nested across 7642 postcodes were included in the baseline analysis, and 31 036 participants nested across 3695 postcodes were included in the follow‐up analysis. We observed an increase in the odds of eczema at baseline [odds ratio (OR) 1·02, 95% confidence interval (CI) 1·01–1·04] per 50 mg L−1 of CaCO3 increase. Furthermore, exposure to domestic hard water (> 200 mg L−1 of CaCO3) was associated with increased odds of prevalent eczema at baseline (OR 1·12, 95% CI 1·04–1·22). Moreover, there was a significant linear trend (P < 0·001) in which increasing levels of hard water increased eczema prevalence risk. No association was observed with incident eczema or eczema at follow‐up. The intraclass correlation coefficient for postcode was 1·6% (95% CI 0·7–3·4), which remained unexplained by area‐level socioeconomic measures. Conclusions: Increasing levels of domestic hard water, as measured by CaCO3 concentrations, were associated with an increased prevalence of eczema in adults but not increased incidence. Ongoing efforts to reduce hard water exposure may have a beneficial effect in reducing the burden of eczema in adults. Further research is needed to explore area‐level factors that may lead to eczema. What is already known about this topic?Hard water is formed when minerals are dissolved in water from filtration through sedimentary rocks.Several studies have reported a higher prevalence of eczema in areas with hard water.However, all studies on this topic have assessed this in infants and school‐aged children, while this association has not been explored in adults. What does this study add?Our findings suggest that exposure to higher concentrations of domestic hard water is associated with an increase in eczema prevalence in adults aged 40–69 years.Ongoing efforts to reduce hard water exposure may have a beneficial effect in reducing eczema prevalence in adults. [ABSTRACT FROM AUTHOR]

Reports suggest that unintended food allergen presence in processed foods caused by allergen cross-contact (i.e. food comes into contact with another food) may be the leading cause of contamination resulting in adverse reactions. The aim of this study was to examine factors which contribute to undeclared allergens being present in processed foods in Australia, by examining food recalls. There is a need for improved packaging practices to minimise foods with undeclared allergens and increase food safety for food allergic consumers. [Extracted from the article]

To examine protective and risk factors for Buruli ulcer (BU), we conducted a case–control study of 245 adult BU cases and 481 postcode-matched controls across BU-endemic areas of Victoria, Australia. We calculated age- and sex-adjusted odds ratios for socio-environmental, host, and behavioral factors associated with BU by using conditional logistic regression. Odds of BU were >2-fold for persons with diabetes mellitus and persons working outdoors who had soil contact in BUendemic areas (compared with indoor work) but were lower among persons who had bacillus Calmette– Guérin vaccinations. BU was associated with increasing numbers of possums and with ponds and bore water use at residences. Using insect repellent, covering arms and legs outdoors, and immediately washing wounds were protective; undertaking multiple protective behaviors was associated with the lowest odds of BU. Skin hygiene/protection behaviors and previous bacillus Calmette–Guérin vaccination might provide protection against BU in BU-endemic areas. [ABSTRACT FROM AUTHOR]

Background: The heterogeneity of development and progression of eczema suggests multiple underlying subclasses for which aetiology and prognosis may vary. A better understanding may provide a comprehensive overview of eczema development and progression in childhood. Thus, we aimed to determine longitudinal eczema subclasses based on assessments and identify their associations with risk factors and allergic outcomes. Methods: A total of 619 participants with a family history of allergic disease were assessed at 24 time‐points from birth to 12 years. At each time, eczema was defined as the report of current rash treated with topical steroid‐based preparations. Longitudinal latent class analysis was used to determine eczema subclasses. Subsequent analyses using regression models assessed the associations between eczema subclasses and potential risk factors and allergic outcomes at 18‐ and 25‐year follow‐ups (eczema, allergic rhinitis, asthma and allergic sensitization). Results: We identified five eczema subclasses 'early‐onset persistent', 'early‐onset resolving', 'mid‐onset persistent', 'mid‐onset resolving' and 'minimal eczema'. Filaggrin null mutations were associated with the early‐onset persistent (OR = 2.58 [1.09–6.08]) and mid‐onset persistent class (OR = 2.58 [1.32–5.06]). Compared with 'minimal eczema', participants from early‐onset persistent class had higher odds of eczema (OR = 11.8 [5.20–26.6]) and allergic rhinitis (OR = 3.13 [1.43–6.85]) at 18 and at 25 years eczema (OR = 9.37 [3.17–27.65]), allergic rhinitis (OR = 3.26 [1.07–9.93]) and asthma (OR = 2.91 [1.14–7.43]). Likewise, mid‐onset persistent class had higher odds of eczema (OR = 2.59 [1.31–5.14]), allergic rhinitis (OR = 1.70 [1.00–2.89]) and asthma (OR = 2.00 [1.10–3.63]) at 18 and at 25 years eczema (OR = 6.75 [3.11–14–65]), allergic rhinitis (OR = 2.74 [1.28–5.88]) and asthma (OR = 2.50 [1.25–5.00]). Allergic and food sensitization in early life was more common in those in the persistent eczema subclasses. Conclusion: We identified five distinct eczema subclasses. These classes were differentially associated with risk factors, suggesting differences in aetiology, and also with the development of allergic outcomes, highlighting their potential to identify high‐risk groups for close monitoring and intervention. [ABSTRACT FROM AUTHOR]

Context It has been hypothesized that a mother's diet during pregnancy may modulate her offspring's immune system development and lead to development of allergic diseases among offspring. However, the evidence for this is unclear and inconclusive. Objective This systematic review was undertaken to examine the weight of evidence for causality from cohort studies on the association between maternal free sugar intake during pregnancy and development of allergies in offspring. Data Sources Using a systematic search strategy, PubMed, SCOPUS, and Web of Science databases were searched from inception to May 2020. Data Extraction For the reporting of this systematic review, the PRISMA guideline was followed. Studies examining maternal sugar consumption during pregnancy (using self-reported data) and the development of allergic diseases among offspring (infancy to 5 years) were included. Data Analysis The Newcastle–Ottawa Scale quality assessment tool was used to assess the study quality. Meta-analysis was conducted using a random-effects model to synthesize the findings. Of 159 publications identified from the search, 5 articles with 4 unique cohort studies were included in this systematic review. The limited meta-analysis showed that a mother's increased free sugar intake during pregnancy was associated with an increased risk of developing asthma in offspring (odds ratio 1.07 [95% CI, 1.00 to 1.14; I2 = 0%]). High free sugar intake by the mother during pregnancy was also associated with increased odds of offspring (to age 7.7 years) developing other common allergies, including allergic rhinitis, atopy and eczema, wheeze, and food allergies. Conclusion From the limited evidence, this review suggests that high free sugar consumption during pregnancy may be associated with the development of allergies in offspring. Clinical guidelines and public health policy recommendations for maternal diet in pregnancy should include advice about reducing free sugar intake due to a possible association with allergies in offspring. However, recommendations should be made with caution considering other maternal and fetal risk factors. [ABSTRACT FROM AUTHOR]

Despite the growing body of evidence on lung function trajectories over the life course and their risk factors, the literature has not been systematically synthesized. Publications related to lung function trajectories were identified from PubMed, EMBASE and CINAHL databases. Two authors independently identified publications for inclusion according to predefined selection criteria. Studies that modelled lung function trajectories and reported associated exposures were included. Meta-analyses could not be conducted due to heterogeneity in the exposures and methods used to model lung function trajectories. Nine publications were eligible for inclusion of which four used group-based trajectory modelling to model lung function trajectories, while five used latent profile analysis. Studies with repeated lung function measurements over the life course identified more trajectories than others. Only one study spanning from childhood to middle age reported catch-up trajectory. The following childhood risk factors for subnormal lung function trajectories were observed in at least across two studies: low birth weight, early wheezing, asthma, allergic sensitization, eczema, allergic rhinitis, lower respiratory tract infections, family history of asthma and second-hand smoke exposure. Adult active asthma and personal cigarette smoking were observed to be associated with accelerated decline lung trajectories. Our review identified 10 risk factors associated with the growth, catch-up, reduced plateau and decline trajectories of lung function. Intervention directed at childhood asthma and infections, and tobacco smoke exposure at all ages would help promote lung health and prevent subnormal lung function trajectories. [ABSTRACT FROM AUTHOR]

Background: There is limited information on risk factors for eczema in adults. Recent evidence suggests that air pollution may be associated with increased incidence of eczema in adults. We aimed to assess this possible association. Methods: Ambient air pollution exposures (distance from a major road, nitrogen dioxide [NO2], fine particulate matter with an aerodynamic diameter ≤2.5 µm [PM2.5]) were assessed for the residential address of Tasmanian Longitudinal Health Study participants at ages 43 and 53 years. Eczema incidence (onset after age 43 years), prevalence (at 53 years), and persistence were assessed from surveys, while IgE sensitization was assessed using skin prick tests. The presence or absence of eczema and sensitization was classified into four groups: no atopy or eczema, atopy alone, non‐atopic eczema, and atopic eczema. Adjusted logistic and multinomial regression models were fitted to estimate associations between ambient air pollution and eczema, and interaction by sex was assessed. Results: Of 3153 participants in both follow‐ups, 2369 had valid skin prick tests. For males, a 2.3 ppb increase in baselineNO2was associated with increased odds of prevalent eczema (OR = 1.15 [95% CI 0.98–1.36]) and prevalent atopic eczema (OR = 1.26 [1.00–1.59]). These associations were not seen in females (p for interaction = 0.08, <0.01). For both sexes, a 1.6 µg/m3 increase in PM2.5 exposure at follow‐up was associated with increased odds of aeroallergen sensitization (OR = 1.15 [1.03–1.30]). Conclusion: Increased exposure to residential ambient air pollutants was associated with an increased odds of eczema, only in males, and aeroallergen sensitization in both genders. [ABSTRACT FROM AUTHOR]

Background: The association between grass pollen exposure and early markers of asthma exacerbations such as lung function changes and increase in airway inflammation is limited. We investigated the associations between short‐term grass pollen exposure and lung function and airway inflammation in a community‐based sample, and whether any such associations were modified by current asthma, current hay fever, pollen sensitization, age, and other environmental factors. Methods: Cross‐sectional and short‐term analyses of data from the Melbourne Atopy Cohort Study (MACS) participants (n = 936). Lung function was assessed using spirometry. Airway inflammation was assessed by fractional exhaled nitric oxide (FeNO) and exhaled breath condensate pH and nitrogen oxides (NOx). Daily pollen counts were collected using a volumetric spore trap. The associations were examined by linear regression. Results: Higher ambient levels of grass pollen 2 days before (lag 2) were associated with lower mid‐forced expiratory flow (FEF25%‐75%) and FEV1/FVC ratio (Coef. [95% CI] = −119 [−226, −11] mL/s and −1.0 [−3.0, −0.03] %, respectively) and also 3 days before (lag 3). Increased levels of grass pollen a day before (lag 1) were associated with increased FeNO (4.35 [−0.1, 8.7] ppb) and also at lag 2. Adverse associations between pollen and multiple outcomes were greater in adults with current asthma, hay fever, and pollen sensitization. Conclusion: Grass pollen exposure was associated with eosinophilic airway inflammation 1‐2 days after exposure and airway obstruction 2‐3 days after exposure. Adults and individuals with asthma, hay fever, and pollen sensitization may be at higher risk. [ABSTRACT FROM AUTHOR]

Background: Glutathione S-transferase (GST) genes are involved in the management of oxidative stress in the lungs. We aimed to determine whether they modify the associations between early life smoke exposure and adverse lung health outcomes.Methods: The Melbourne Atopy Cohort study (a high-risk birth cohort) enrolled 620 children and followed them prospectively from birth. We recorded perinatal tobacco smoke exposure, asthma, and lung function at 12 (59%) and 18 years (66%) and genotyped for GSTM1, GSTT1, and GSTP1 (69%).Results: GST genotypes were found to interact with tobacco smoke exposure on lung function outcomes (P interaction ≤ .05). Only among children with GSTT1 null genotypes was exposure to mother's, father's, or parental tobacco smoke in early life associated with an increased risk of reductions in prebronchodilator (BD) FEV1 and FVC at both 12 and 18 years. These associations were not seen in children with GSTT1 present. Similarly, only among children with GSTM1 null genotypes was exposure to father's or parental smoking associated with reductions in pre- and post-BD FEV1 and FVC at 18 years. Only among children with Ile/Ile genotypes of GSTP1 was exposure to mother's smoking associated with increased risk of reduced FEV1 at 18 years, but this was not the case among children with Val/Val or Ile/Val genotypes.Conclusions: Our study provides evidence of interaction between early tobacco smoke exposure and GST genotypes on lung function. Carriers of GST null mutations and GSTP1 Ile/Ile alleles may be more susceptible when exposed to tobacco smoke in early life. These findings support stronger recommendations to protect all infants from tobacco smoke exposure.Trial Registry: Australian and New Zealand Clinical Trials Registry; No.: ACTRN12609000734268; URL: http://www.anzctr.org.au/. [ABSTRACT FROM AUTHOR]