Air-quality-related health impacts from climate change and from adaptation of cooling demand for buildings in the eastern United States: An interdisciplinary modeling study.

BACKGROUND: Climate change negatively impacts human health through heat stress and exposure to worsened air pollution, amongst other pathways. Indoor use of air conditioning can be an effective strategy to reduce heat exposure. However, increased air conditioning use increases emissions of air pollutants from power plants, in turn worsening air quality and human health impacts. We used an interdisciplinary linked model system to quantify the impacts of heat-driven adaptation through building cooling demand on air-quality-related health outcomes in a representative mid-century climate scenario. METHODS AND FINDINGS: We used a modeling system that included downscaling historical and future climate data with the Weather Research and Forecasting (WRF) model, simulating building electricity demand using the Regional Building Energy Simulation System (RBESS), simulating power sector production and emissions using MyPower, simulating ambient air quality using the Community Multiscale Air Quality (CMAQ) model, and calculating the incidence of adverse health outcomes using the Environmental Benefits Mapping and Analysis Program (BenMAP). We performed simulations for a representative present-day climate scenario and 2 representative mid-century climate scenarios, with and without exacerbated power sector emissions from adaptation in building energy use. We find that by mid-century, climate change alone can increase fine particulate matter (PM2.5) concentrations by 58.6% (2.50 µg/m3) and ozone (O3) by 14.9% (8.06 parts per billion by volume [ppbv]) for the month of July. A larger change is found when comparing the present day to the combined impact of climate change and increased building energy use, where PM2.5 increases 61.1% (2.60 µg/m3) and O3 increases 15.9% (8.64 ppbv). Therefore, 3.8% of the total increase in PM2.5 and 6.7% of the total increase in O3 is attributable to adaptive behavior (extra air conditioning use). Health impacts assessment finds that for a mid-century climate change scenario (with adaptation), annual PM2.5-related adult mortality increases by 13,547 deaths (14 concentration-response functions with mean incidence range of 1,320 to 26,481, approximately US$126 billion cost) and annual O3-related adult mortality increases by 3,514 deaths (3 functions with mean incidence range of 2,175 to 4,920, approximately US$32.5 billion cost), calculated as a 3-month summer estimate based on July modeling. Air conditioning adaptation accounts for 654 (range of 87 to 1,245) of the PM2.5-related deaths (approximately US$6 billion cost, a 4.8% increase above climate change impacts alone) and 315 (range of 198 to 438) of the O3-related deaths (approximately US$3 billion cost, an 8.7% increase above climate change impacts alone). Limitations of this study include modeling only a single month, based on 1 model-year of future climate simulations. As a result, we do not project the future, but rather describe the potential damages from interactions arising between climate, energy use, and air quality. CONCLUSIONS: This study examines the contribution of future air-pollution-related health damages that are caused by the power sector through heat-driven air conditioning adaptation in buildings. Results show that without intervention, approximately 5%-9% of exacerbated air-pollution-related mortality will be due to increases in power sector emissions from heat-driven building electricity demand. This analysis highlights the need for cleaner energy sources, energy efficiency, and energy conservation to meet our growing dependence on building cooling systems and simultaneously mitigate climate change.

Response of Power Plant Emissions to Ambient Temperature in the Eastern United States.

Past studies have established strong connections between meteorology and air quality, via chemistry, transport, and natural emissions. A less understood linkage between weather and air quality is the temperature-dependence of emissions from electricity generating units (EGUs), associated with high electricity demand to support building cooling on hot days. This study quantifies the relationship between ambient surface temperatures and EGU air emissions (CO2, SO2, and NOX) using historical data. We find that EGUs in the Eastern U.S. region from 2007 to 2012 exhibited a 3.87% ± 0.41% increase in electricity generation per °C increase during summer months. This is associated with a 3.35%/°C ± 0.50%/°C increase in SO2 emissions, a 3.60%/°C ± 0.49%/°C increase in NOX emissions, and a 3.32%/°C ± 0.36%/°C increase in CO2 emissions. Sensitivities vary by year and by pollutant, with SO2 both the highest sensitivity (5.04% in 2012) and lowest sensitivity (2.19% in 2007) in terms of a regional average. Texas displays 2007-2012 sensitivities of 2.34%/°C ± 0.28%/°C for generation, 0.91%/°C ± 0.25%/°C for SO2 emissions, 2.15%/°C ± 0.29%/°C for NOX emissions, and 1.78%/°C ± 0.22%/°C for CO2 emissions. These results suggest demand-side and supply side technological improvements and fuel choice could play an important role in cost-effective reduction of carbon emissions and air pollution.

Potential for Electrified Vehicles to Contribute to U.S. Petroleum and Climate Goals and Implications for Advanced Biofuels.

To examine the national fuel and emissions impacts from increasingly electrified light-duty transportation, we reconstructed the vehicle technology portfolios from two national vehicle studies. Using these vehicle portfolios, we normalized assumptions and examined sensitivity around the rates of electrified vehicle penetration, travel demand growth, and electricity decarbonization. We further examined the impact of substituting low-carbon advanced cellulosic biofuels in place of petroleum. Twenty-seven scenarios were benchmarked against a 50% petroleum-reduction target and an 80% GHG-reduction target. We found that with high rates of electrification (40% of miles traveled) the petroleum-reduction benchmark could be satisfied, even with high travel demand growth. The same highly electrified scenarios, however, could not satisfy 80% GHG-reduction targets, even assuming 80% decarbonized electricity and no growth in travel demand. Regardless of precise consumer vehicle preferences, emissions are a function of the total reliance on electricity versus liquid fuels and the corresponding greenhouse gas intensities of both. We found that at a relatively high rate of electrification (40% of miles and 26% by fuel), an 80% GHG reduction could only be achieved with significant quantities of low-carbon liquid fuel in cases with low or moderate travel demand growth.

Underutilization of Lynch syndrome screening in a multisite study of patients with colorectal cancer.

PURPOSE: The aim of this study was to examine Lynch syndrome screening of patients with metastatic colorectal cancer in integrated health-care-delivery organizations. METHODS: We determined the availability of Lynch syndrome screening criteria and actual Lynch syndrome screening in the medical records of 1,188 patients diagnosed with metastatic colorectal cancer between 2004 and 2009 at seven institutions in the Cancer Research Network. RESULTS: We found infrequent use of Lynch syndrome screening (41/1,188). Family history was available for 937 of the 1,188 patients (79%). There was sufficient information to assess Lynch syndrome risk using family history-based criteria in 719 of the 937 patients (77%) with family history documentation. In 391 individuals with a family history of a Lynch syndrome-associated cancer, 107 (27%) could not be evaluated due to missing information such as age of cancer onset. Eleven percent of patients who met the Bethesda criteria and 25% of individuals who met the Amsterdam II criteria were screened for Lynch syndrome. Recommended guidelines were adhered to during screening, but no testing method was preferred. CONCLUSION: The information required for Lynch syndrome screening decisions is routinely collected but seldom used. There is a critical gap between collection of family history and its use to guide Lynch syndrome screening, which may support a case for implementation of universal screening guidelines.

KRAS testing and epidermal growth factor receptor inhibitor treatment for colorectal cancer in community settings.

BACKGROUND: In metastatic colorectal cancer (mCRC), mutations in the KRAS gene predict poor response to EGF receptor (EGFR) inhibitors. Clinical treatment guidelines now recommend KRAS testing if EGFR inhibitors are considered. Our study investigates the clinical uptake and utilization of KRAS testing. METHODS: We included 1,188 patients with mCRCs diagnosed from 2004 to 2009, from seven integrated health care delivery systems with a combined membership of 5.5 million. We used electronic medical records and targeted manual chart review to capture the complexity and breadth of real-world clinical oncology care. RESULTS: Overall, 428 patients (36%) received KRAS testing during their clinical care, and 266 (22%) were treated with EGFR inhibitors. Age at diagnosis (P = 0.0034), comorbid conditions (P = 0.0316), and survival time from diagnosis (P < 0.0001) influence KRAS testing and EGFR inhibitor prescribing. The proportion who received KRAS testing increased from 7% to 97% for those treated in 2006 and 2010, respectively, and 83% of all treated patients had a KRAS wild-type genotype. Most patients with a KRAS mutation (86%) were not treated with EGFR inhibitors. The interval between mCRC diagnosis and receipt of KRAS testing decreased from 26 months (2006) to 10 months (2009). CONCLUSIONS: These findings show rapid uptake and incorporation of this predictive biomarker into clinical oncology care. IMPACT: In this delivery setting, KRAS testing is widely used to guide treatment decisions with EGFR inhibitors in patients with mCRCs. An important future research goal is to evaluate utilization of KRAS testing in other delivery settings in the United States.

Prematurity and severity are associated with Toxoplasma gondii alleles (NCCCTS, 1981-2009).

BACKGROUND: Congenital toxoplasmosis is a severe, life-altering disease in the United States. A recently developed enzyme-linked immunosorbent assay (ELISA) distinguishes Toxoplasma gondii parasite types (II and not exclusively II [NE-II]) by detecting antibodies in human sera that recognize allelic peptide motifs of distinct parasite types. METHODS: ELISA determined parasite serotype for 193 congenitally infected infants and their mothers in the National Collaborative Chicago-based Congenital Toxoplasmosis Study (NCCCTS), 1981-2009. Associations of parasite serotype with demographics, manifestations at birth, and effects of treatment were determined. RESULTS: Serotypes II and NE-II occurred in the United States with similar proportions during 3 decades. For persons diagnosed before or at birth and treated in infancy, and persons diagnosed after 1 year of age who missed treatment in infancy, proportions were similar (P = .91). NE-II serotype was more common in hot, humid regions (P = .02) but was also present in other regions. NE-II serotype was associated with rural residence (P < .01), lower socioeconomic status (P < .001), and Hispanic ethnicity (P < .001). Prematurity (P = .03) and severe disease at birth (P < .01) were associated with NE-II serotype. Treatment with lower and higher doses of pyrimethamine with sulfadizine improved outcomes relative to those outcomes of persons in the literature who did not receive such treatment. CONCLUSIONS: Type II and NE-II parasites cause congenital toxoplasmosis in North America. NE-II serotype was more prevalent in certain demographics and associated with prematurity and severe disease at birth. Both type II and NE-II infections improved with treatment. CLINICAL TRIALS REGISTRATION: NCT00004317.

Unrecognized ingestion of Toxoplasma gondii oocysts leads to congenital toxoplasmosis and causes epidemics in North America.

BACKGROUND: Congenital toxoplasmosis presents as severe, life-altering disease in North America. If mothers of infants with congenital toxoplasmosis could be identified by risks, it would provide strong support for educating pregnant women about risks, to eliminate this disease. Conversely, if not all risks are identifiable, undetectable risks are suggested. A new test detecting antibodies to sporozoites demonstrated that oocysts were the predominant source of Toxoplasma gondii infection in 4 North American epidemics and in mothers of children in the National Collaborative Chicago-based Congenital Toxoplasmosis Study (NCCCTS). This novel test offered the opportunity to determine whether risk factors or demographic characteristics could identify mothers infected with oocysts. METHODS: Acutely infected mothers and their congenitally infected infants were evaluated, including in-person interviews concerning risks and evaluation of perinatal maternal serum samples. RESULTS: Fifty-nine (78%) of 76 mothers of congenitally infected infants in NCCCTS had primary infection with oocysts. Only 49% of these mothers identified significant risk factors for sporozoite acquisition. Socioeconomic status, hometown size, maternal clinical presentations, and ethnicity were not reliable predictors. CONCLUSIONS: Undetected contamination of food and water by oocysts frequently causes human infections in North America. Risks are often unrecognized by those infected. Demographic characteristics did not identify oocyst infections. Thus, although education programs describing hygienic measures may be beneficial, they will not suffice to prevent the suffering and economic consequences associated with congenital toxoplasmosis. Only a vaccine or implementation of systematic serologic testing of pregnant women and newborns, followed by treatment, will prevent most congenital toxoplasmosis in North America.

Lesões coriorretinianas em mães de crianças com toxoplasmose congênita no national collaborative Chicago-based, toxoplasmosis study / Chorioretinal lesions in mothers of children with congenital toxoplasmosis in the national collaborative Chicago-based, congenital toxoplasmosis study

Aims: To determine whether mothers of children with congenital toxoplasmosis have chorioretinal lesions consistent with toxoplasmosis. Methods: Prospective cohort study. Ophthalmologists in our study have examined 173 children with congenital toxoplasmosis in a hospital outpatient setting. These children were referred to us by their primary care physicians. One hundred and thirty mothers of these children had retina examinations of both eyes at least once. Main outcome measure was lesion(s) consistent with ocular toxoplasmosis. Results: Of 130 mothers examined between 1991-2005, 10 (7.7%, 95% Confidence Interval 3.8%, 13.7%) had chorioretinal lesions which likely represent resolved toxoplasmic chorioretinitis. Most of these were small peripheral chorioretinal lesions. None reactivated between 1991-2005. Conclusions: Chorioretinal lesions consistent with quiescent ocular toxoplasmosis occur in mothers of children with congenital toxoplasmosis in the United States.

Chorioretinal lesions in mothers of children with congenital toxoplasmosis in the National Collaborative Chicago-based, Congenital Toxoplasmosis Study.

AIMS: To determine whether mothers of children with congenital toxoplasmosis have chorioretinal lesions consistent with toxoplasmosis. METHODS: Prospective cohort study. Ophthalmologists in our study have examined 173 children with congenital toxoplasmosis in a hospital outpatient setting. These children were referred to us by their primary care physicians. One hundred and thirty mothers of these children had retina examinations of both eyes at least once. Main outcome measure was lesion(s) consistent with ocular toxoplasmosis. RESULTS: Of 130 mothers examined between 1991-2005, 10 (7.7%, 95% Confidence Interval 3.8%, 13.7%) had chorioretinal lesions which likely represent resolved toxoplasmic chorioretinitis. Most of these were small peripheral chorioretinal lesions. None reactivated between 1991-2005. CONCLUSIONS: Chorioretinal lesions consistent with quiescent ocular toxoplasmosis occur in mothers of children with congenital toxoplasmosis in the United States.

Longitudinal study of new eye lesions in children with toxoplasmosis who were not treated during the first year of life.

PURPOSE: To determine the incidence of new chorioretinal lesions in children with toxoplasmosis diagnosed after, and therefore not treated during, their first year. DESIGN: Prospective longitudinal cohort study. METHODS: Thirty-eight children were evaluated in Chicago between 1981 and 2005 for new chorioretinal lesions. Thirty-eight children and mothers had serum IgG antibody to Toxoplasma gondii. RESULTS: Twenty-eight of 38 children had one of the following: diagnosis with serum antibody to T. gondii indicative of chronic infection at age 24 months, central nervous system calcifications, hydrocephalus, illness compatible with congenital toxoplasmosis perinatally but not diagnosed at that time. Twenty-five returned for follow-up during 1981 to 2005. Their mean (range) age at last exam was 10.9 +/- 5.7 (range, 3.5 to 27.2) years and mean follow-up was 5.7 +/- 2.9 years. Eighteen (72%) children developed at least one new lesion. Thirteen (52%) had new central lesions, 11 (44%) had new peripheral lesions, and six (24%) had both. Thirteen (52%) had new lesions diagnosed at age > or =10 years. New lesions were found at more than one visit in four (22%), and bilateral new lesions developed in seven (39%) of 18 children who developed new lesions. Of 10 additional children with eye findings and serologic tests indicative of chronic infection, six returned for follow-up, four (67%) developing new lesions at > or =10 years of age. CONCLUSIONS: More than 70% developed new chorioretinal lesions. New lesions were commonly diagnosed after the first decade of life.

Genetic and epigenetic factors at COL2A1 and ABCA4 influence clinical outcome in congenital toxoplasmosis.

BACKGROUND: Primary Toxoplasma gondii infection during pregnancy can be transmitted to the fetus. At birth, infected infants may have intracranial calcification, hydrocephalus, and retinochoroiditis, and new ocular lesions can occur at any age after birth. Not all children who acquire infection in utero develop these clinical signs of disease. Whilst severity of disease is influenced by trimester in which infection is acquired by the mother, other factors including genetic predisposition may contribute. METHODS AND FINDINGS: In 457 mother-child pairs from Europe, and 149 child/parent trios from North America, we show that ocular and brain disease in congenital toxoplasmosis associate with polymorphisms in ABCA4 encoding ATP-binding cassette transporter, subfamily A, member 4. Polymorphisms at COL2A1 encoding type II collagen associate only with ocular disease. Both loci showed unusual inheritance patterns for the disease allele when comparing outcomes in heterozygous affected children with outcomes in affected children of heterozygous mothers. Modeling suggested either an effect of mother's genotype, or parent-of-origin effects. Experimental studies showed that both ABCA4 and COL2A1 show isoform-specific epigenetic modifications consistent with imprinting. CONCLUSIONS: These associations between clinical outcomes of congenital toxoplasmosis and polymorphisms at ABCA4 and COL2A1 provide novel insight into the molecular pathways that can be affected by congenital infection with this parasite.

Longitudinal study of new eye lesions in treated congenital toxoplasmosis.

OBJECTIVE: To determine the incidence of new chorioretinal lesions in patients with congenital toxoplasmosis who were treated throughout their first year of life. DESIGN: Prospective longitudinal observation of a cohort. PARTICIPANTS: One hundred thirty-two children were studied as part of the longitudinal observation. METHODS: One hundred thirty-two children were treated during their first year of life with pyrimethamine, sulfadiazine, and leucovorin. They had eye examinations at prespecified intervals. MAIN OUTCOME MEASURES: New chorioretinal lesions on fundus examination and fundus photographs. RESULTS: The mean age (+/- standard deviation) is 10.8+/-5.1 years (range, 0.2-23). One hundred eight children have been evaluated for new chorioretinal lesions. Thirty-four (31%; 95% confidence interval, 23%-41%) of 108 children developed at least one chorioretinal lesion that was previously undetected. These occurred at varying times during their follow-up course. Fifteen children (14%) developed new central lesions, and 27 (25%) had newly detected lesions peripherally. Ten (9%) had more than one occurrence of new lesions developing, and 13 (12%) had new lesions in both eyes. Of those who developed new lesions, 14 children (41%) did so at age 10 or later. CONCLUSION: New central chorioretinal lesions are uncommon in children with congenital toxoplasmosis who are treated during their first year of life. This finding contrasts markedly with earlier reports in the literature for untreated children or those treated for only 1 month near birth, in whom new lesions were much more prevalent (>/=82%). Our observation that 14 (41%) of the 34 children with new chorioretinal lesions had occurrences when they were 10 years or older indicates that long-term follow-up into the second decade of life is important in assessing the efficacy of treating toxoplasmosis during infancy.

Impact of visual impairment on measures of cognitive function for children with congenital toxoplasmosis: implications for compensatory intervention strategies.

OBJECTIVES: The purpose of this work was to determine whether visual impairment caused by toxoplasmic chorioretinitis is associated with impaired performance of specific tasks on standardized tests of cognitive function. If so, then we worked to determine whether there are patterns in these difficulties that provide a logical basis for development of measures of cognitive function independent of visual impairment and compensatory intervention strategies to facilitate learning for such children. METHODS: Sixty-four children with congenital toxoplasmosis with intelligence quotient scores > or = 50 and visual acuity sufficient to cooperate with all of the intelligence quotient subscales had assessments of their vision, appearance of their retinas, and cognitive testing performed between 3.5 and 5 years of age. These evaluations took place between 1981 and 1998 as part of a longitudinal study to determine outcome of congenital toxoplasmosis. Children were evaluated at 3.5 or 5 (37 children) or both 3.5 and 5 (27 children) years of age. Cognitive function was measured using the Wechsler Preschool and Primary Scale of Intelligence-Revised. Wechsler Preschool and Primary Scale of Intelligence-Revised scale scores were compared for children grouped as those children who had normal visual acuity in their best eye (group 1), and those who had impaired vision in their best eye (acuity < 20/40) because of macular disease (group 2). Demographic characteristics were compared for children in the 2 groups. Test scores were compared between groups using all of the 3.5-year-old visits, all of the 5-year-old visits, and using each child's "last" visit (ie, using the 5-year-old test results when a child was tested at both 3.5 and 5 years of age or only at 5 years, otherwise using the 3.5-year-old test results). The results were similar and, therefore, only the results from the last analysis are reported here. RESULTS: There were 48 children with normal visual acuity in their best eye (group 1) and 16 children with impaired vision because of macular involvement in their best eye (group 2). Ethnicity and socioeconomic scores were similar. There was a significantly greater proportion of males in group 2 compared with group 1 (81% vs 46%). There was no significant diminution in Wechsler Preschool and Primary Scale of Intelligence-Revised test scores between 3.5 and 5 years of age for the 27 children tested at both of these ages. Verbal intelligence quotient, performance intelligence quotient, full-scale intelligence quotient scores, and all of the scaled scores except arithmetic and block design were significantly lower for children in group 2 compared with group 1. The majority of the differences remained statistically significant or borderline significant after adjusting for gender. However, the difference in overall verbal scores does not remain statistically significant. Mean +/- SD verbal (98 +/- 20) and performance (95 +/- 17) intelligence quotients were not significantly different for children in group 1. However, verbal (88 +/- 13) and performance intelligence quotients (78 +/- 17) were significantly different for children in group 2. For children in group 2, their lowest scale scores were in object assembly, geometric design, mazes, and picture completion, all timed tests that involved visual discrimination of linear forms with small intersecting lines. In the 2 scales scored that did not differ between groups 1 and 2, arithmetic and block design, timing and vision but not linear forms were components of the tasks. Children with monocular and binocular normal visual acuity did not differ in verbal, performance, or full-scale intelligence quotients or any of the subscale tests. Difficulty with sight or concomitant neurologic involvement also seemed to impact the ability to acquire information, comprehension skills, and vocabulary and performance in similarities testing. After controlling for gender, however, these differences were diminished, and there were no longer differences in overall verbal scores. As noted above, results were generally similar when all of the tests for 3.5-year-olds or 5-year-olds were analyzed separately. At the 3.5-year visit there were fewer significant differences between the 2 groups for the verbal components than at the 5-year visit. CONCLUSIONS: In children with congenital toxoplasmosis and bilateral macular disease (group 2) because of toxoplasmic chorioretinitis, scaled scores were lowest on timed tests that require discrimination of fine intersecting lines. Although the severity of ocular and neurologic involvement is often congruent in children with congenital toxoplasmosis, ophthalmologic involvement seems to account for certain specific limitations on tests of cognitive function. Children with such visual impairment compensate with higher verbal skills, but their verbal scores are still less than those of children with normal vision, and in some cases significantly so, indicating that vision impairment might affect other aspects of cognitive testing. Patterns of difficulties noted in the subscales indicate that certain compensatory intervention strategies to facilitate learning and performance may be particularly helpful for children with these impairments. These patterns also provide a basis for the development of measures of cognitive function independent of visual impairment.

Outcome of treatment for congenital toxoplasmosis, 1981-2004: the National Collaborative Chicago-Based, Congenital Toxoplasmosis Study.

BACKGROUND: Without treatment, congenital toxoplasmosis has recurrent, recrudescent, adverse outcomes. Long-term follow-up of infants with congenital toxoplasmosis treated throughout their first year of life with pyrimethamine and sulfadiazine has not been reported. METHODS: Between 1981 and 2004, one hundred twenty infants (current mean age +/- standard deviation, 10.5 +/- 4.8 years) with congenital toxoplasmosis were treated with 1 of 2 doses of pyrimethamine plus sulfadiazine; therapy was initiated shortly after birth and continued for 12 months. Children who received treatment were evaluated at birth and at predetermined intervals; the focus of the evaluations was on prespecified end points: motor abnormalities, cognitive outcome, vision impairment, formation of new eye lesions, and hearing loss. RESULTS: Treatment of infants without substantial neurologic disease at birth with pyrimethamine and sulfadiazine for 1 year resulted in normal cognitive, neurologic, and auditory outcomes for all patients. Treatment of infants who had moderate or severe neurologic disease (as defined in this article in the Treatments subsection of Methods) at birth resulted in normal neurologic and/or cognitive outcomes for >72% of the patients, and none had sensorineural hearing loss. Ninety-one percent of children without substantial neurologic disease and 64% of those with moderate or severe neurologic disease at birth did not develop new eye lesions. Almost all of these outcomes are markedly better than outcomes reported for children who were untreated or treated for 1 month in earlier decades (P<.01 to P<.001). Sex and severity of disease were comparable in our 2 treatment groups, and no significant differences in efficacy or toxicity were noted between the 2 treatment groups (P > .05). CONCLUSIONS: Although not all children did well with treatment, the favorable outcomes we noted indicate the importance of diagnosis and treatment of infants with congenital toxoplasmosis.

Risk factors for Toxoplasma gondii infection in mothers of infants with congenital toxoplasmosis: Implications for prenatal management and screening.

OBJECTIVE: The purpose of this study was to determine whether demographic characteristics, history of exposure to recognized transmission vehicles, or illness that was compatible with acute toxoplasmosis during gestation identified most mothers of infants with congenital toxoplasmosis. STUDY DESIGN: Mothers of 131 infants and children who were referred to a national study of treatment for congenital toxoplasmosis were characterized demographically and questioned concerning exposure to recognized risk factors or illness. RESULTS: No broad demographic features identified populations that were at risk. Only 48% of mothers recognized epidemiologic risk factors (direct or indirect exposure to raw/undercooked meat or to cat excrement) or gestational illnesses that were compatible with acute acquired toxoplasmosis during pregnancy. CONCLUSION: Maternal risk factors or compatible illnesses were recognized in retrospect by fewer than one half of North American mothers of infants with toxoplasmosis. Educational programs might have prevented acquisition of Toxoplasma gondii by those mothers who had clear exposure risks. However, only systematic serologic screening of all pregnant women at prenatal visits or of all newborn infants at birth would prevent or detect a higher proportion of these congenital infections.

Microangiopathic anemia without thrombocytopenia and kidney disease in a child with diarrhea caused by Shiga toxin-producing Escherichia coli.

A child with a history of diarrhea presented with transient anemia, reticolucytosis, and red blood cell fragmentation. Blood pressure and levels of blood platelets, creatinine, and urea were normal, as were results of urinalysis. Escherichia coli harboring genes for Shiga toxin were detected in stool specimens. It is concluded that extraintestinal diseases caused by Shiga toxin-producing bacteria sometimes present without any renal involvement.

Prevention of iron deficiency anemia in adolescent and adult pregnancies.

OBJECTIVE: Worldwide attention over iron deficiency anemia (IDA) in pregnancy has shifted recently from providing supplements during pregnancy to attempting to ensure that women, especially adolescents, have adequate iron stores prior to conception. We sought to determine whether adolescent and/or adult women still need supplements during pregnancy to avoid IDA, even if iron stores are adequate, and whether the IDA translates into maternal and/or infant morbidity and mortality. DESIGN: Randomized, double-blind clinical trial with placebo control. SETTING: Multicenter clinic setting in central Wisconsin. PARTICIPANTS: Adolescent women 18 years or less in their first pregnancy, and adult women 19 years or older, who were found to be healthy and iron sufficient at their first prenatal visit. METHODS: Participants were randomized to receive iron supplementation (60 mg/day elemental iron) or placebo. Serum ferritin of 12 ng/mL or less with simultaneous hemoglobin of 11 g/dL or less defined IDA. When IDA occurred at the second trimester, a therapeutic supplement of 180 mg of elemental iron per day was initiated. RESULTS: Forty-seven percent of all placebo-supplemented and 16% of all iron-supplemented patients exhibited IDA (p<0.001); 59% of adolescent placebo-supplemented and 20% of adolescent iron-supplemented patients exhibited IDA (p=0.021). Nausea, vomiting, diarrhea, and constipation were not significantly different in the iron supplemented group compared to the placebo group, and no significant differences were seen in maternal or neonatal health, but the number of women studied was limiting for analysis of these adverse events. CONCLUSION: IDA is common in healthy, iron-sufficient adolescent pregnant women during the second trimester, and body stores of iron decline in both adolescent and adult pregnancies. The incidence of IDA during adolescent and adult pregnancies is substantially reduced with 60 mg of elemental iron per day. However, there remains no clear evidence that maternal or neonatal health will benefit from correcting these deficits.

Leptotrichia amnionii sp. nov., a novel bacterium isolated from the amniotic fluid of a woman after intrauterine fetal demise.

A novel bacterium was isolated and characterized from the amniotic fluid of a woman who experienced intrauterine fetal demise in the second trimester of pregnancy. The bacterium was a slow-growing, gram-negative anaerobic coccobacillus belonging to the genus LEPTOTRICHIA: Unlike Leptotrichia sanguinegens, the isolate did not grow in chopped-meat glucose broth or on sheep blood agar upon subculturing. The isolate was characterized by sequencing and analyzing its 16S rRNA gene. The 1,493-bp 16S ribosomal DNA sequence had only 96% homology with L. sanguinegens. Several phylogenetic analyses indicated that L. amnionii is a distinct species and most closely related to L. sanguiegens.