ABSTRACT
BACKGROUND: Childhood chronic illness imposes financial burdens that may affect the entire family. OBJECTIVE: The aim was to assess whether adults living with children with 2 childhood chronic illnesses-asthma and diabetes-are more likely to forego their own medical care, and experience financial strain, relative to those living with children without these illnesses. RESEARCH DESIGN: 2009-2018 National Health Interview Survey. SUBJECTS: Adult-child dyads, consisting of one randomly sampled child and adult in each family. MEASURES: The main exposure was a diagnosis of asthma or diabetes in the child. The outcomes were delayed/foregone medical care for the adult as well as family financial strain; the authors evaluated their association with the child's illness using multivariable logistic regressions adjusted for potential confounders. RESULTS: The authors identified 93,264 adult-child dyads; 8499 included a child with asthma, and 179 a child with diabetes. Families with children with either illness had more medical bill problems, food insecurity, and medical expenses. Adults living with children with each illness reported more health care access problems. For instance, relative to other adults, those living with a child with asthma were more likely to forego/delay care (14.7% vs. 10.2%, adjusted odds ratio: 1.27; 95% CI: 1.16-1.39) and were more likely to forego medications, specialist, mental health, and dental care. Adults living with a child with diabetes were also more likely to forego/delay care (adjusted odds ratio: 1.76; 95% CI: 1.18-2.64). CONCLUSIONS: Adults living with children with chronic illnesses may sacrifice their own care because of cost concerns. Reducing out-of-pocket health care costs, improving health coverage, and expanding social supports for families with children with chronic conditions might mitigate such impacts.
Subject(s)
Asthma , Diabetes Mellitus , Humans , Adult , United States , Child , Health Services Accessibility , Diabetes Mellitus/epidemiology , Diabetes Mellitus/therapy , Asthma/therapy , Chronic Disease , Surveys and QuestionnairesABSTRACT
Salmonella enterica serovar Typhimurium colonizes and invades host intestinal epithelial cells using the type three secretion system (T3SS) encoded on Salmonella pathogenicity island 1 (SPI1). The level of SPI1 T3SS gene expression is controlled by the transcriptional activator HilA, encoded on SPI1. Expression of hilA is positively regulated by three homologous transcriptional regulators, HilD, HilC, and RtsA, belonging to the AraC/XylS family. These regulators also activate the hilD, hilC, and rtsA genes by binding to the same DNA sequences upstream of these promoters, forming a complex feed-forward loop to control SPI1 expression. Despite the apparent redundancy in function, HilD has a unique role in SPI1 regulation because the majority of external regulatory inputs act exclusively through HilD. To better understand SPI1 regulation, the nature of interaction between HilD, HilC, and RtsA has been characterized using biochemical and genetic techniques. Our results showed that HilD, HilC, and RtsA can form heterodimers as well as homodimers in solution. Comparison with other AraC family members identified a putative α-helix in the N-terminal domain, which acts as the dimerization domain. Alanine substitution in this region results in reduced dimerization of HilD and HilC and also affects their ability to activate hilA expression. The dimer interactions of HilD, HilC, and RtsA add another layer of complexity to the SPI1 regulatory circuit, providing a more comprehensive understanding of SPI1 T3SS regulation and Salmonella pathogenesis.IMPORTANCE The SPI1 type three secretion system is a key virulence factor required for Salmonella to both cause gastroenteritis and initiate serious systemic disease. The system responds to numerous environmental signals in the intestine, integrating this information via a complex regulatory network. Here, we show that the primary regulatory proteins in the network function as both homodimers and heterodimers, providing information regarding both regulation of virulence in this important pathogen and general signal integration to control gene expression.
Subject(s)
Bacterial Proteins/metabolism , Gene Expression Regulation, Bacterial , Genomic Islands , Salmonella typhimurium/metabolism , Transcription Factors/metabolism , Type III Secretion Systems/metabolism , Bacterial Proteins/chemistry , Bacterial Proteins/genetics , Dimerization , Protein Domains , Salmonella typhimurium/genetics , Transcription Factors/chemistry , Transcription Factors/genetics , Type III Secretion Systems/geneticsABSTRACT
Incidences of bacterial foodborne illness caused by ingestion of fresh produce are rising. Instead of this being due to incidental contamination, the animal pathogen Salmonella enterica utilizes specific molecular mechanisms to attach to and colonize plants. This work characterizes two S. enterica genes of unknown function: a putative periplasmic protein, STM0278, and a putative protein with a hydrolase in the C-terminus, STM0650. STM0278 and STM0650 are important for seedling colonization but appear to have different roles during the process of colonization. Mutants of either STM0278 or STM0650 showed reduced colonization of alfalfa seedlings at 24 h, and the STM0278 mutant also showed reduced colonization at 48 h. Both genes were expressed in planta at 4 h following inoculation of 3-day-old seedlings and at 72 h after seed inoculation. This suggests that the role of STM0650 in seedling colonization is less important later in the process or is duplicated by other mechanisms. Mutants of STM0278 and STM0650 were defective in swarming. The STM0278 mutant failed to swarm in 24 h, while swarming of the STM0650 mutant was delayed. Addition of surfactant restored swarming of the STM0278 mutant, suggesting that STM0278 is involved in surfactant or osmotic agent production or deployment. Alfalfa seed exudates as the sole nutrient source were capable of perpetuating S. enterica swarming. Sequence analysis revealed sequences homologous to STM0278 and STM0650 in plant-associated bacteria, but none in Escherichia coli. Phylogenetic analysis of STM0650 showed similar sequences from diverse classes of plant-associated bacteria. Bacteria that preferentially colonize roots, including S. enterica, may use a similar hydrolase for swarming or biofilm production on plants. Multicellular behaviours by S. enterica appear central to plant colonization. S. enterica genes involved in plant colonization and survival outside of a host are most likely among the 'function unknown' genes of this bacterium.
Subject(s)
Bacterial Proteins/genetics , Hydrolases/genetics , Periplasmic Proteins/genetics , Salmonella enterica/genetics , Seedlings/microbiology , Biofilms/growth & development , Genes, Bacterial , Medicago sativa/microbiology , Mutation , Phylogeny , Salmonella enterica/growth & developmentABSTRACT
U.S. salmonellosis outbreaks have occurred following consumption of tomato and cantaloupe but not lettuce. We report differential contamination among agricultural seedlings by Salmonella enterica via soil. Members of the family Brassicaceae had a higher incidence of outbreak than carrot, lettuce, and tomato. Once they were contaminated, phyllosphere populations were similar, except for tomato. Contamination differences exist among tomato cultivars.
Subject(s)
Bacterial Adhesion , Crops, Agricultural/microbiology , Food Microbiology , Salmonella enterica/growth & development , Soil Microbiology , Colony Count, Microbial , Disease Outbreaks , Humans , Lactuca/microbiology , Solanum lycopersicum/microbiology , Salmonella Food Poisoning/microbiologyABSTRACT
Shiga toxin-producing Escherichia coli (STEC) is a leading cause of foodborne illness worldwide. The present study developed the use of DNA microarrays with the ampliPHOX colorimetric method to rapidly detect and genotype STEC strains. A low-density 30-mer oligonucleotide DNA microarray was designed to target O-antigen gene clusters of 11 E. coli serogroups (O26, O45, O91, O103, O104, O111, O113, O121, O128, O145, and O157) that have been associated with the majority of STEC infections. In addition, the DNA microarray targeted 11 virulence genes, encoding adhesins, cytotoxins, proteases, and receptor proteins, which have been implicated in conferring increased ability to cause disease for STEC. Results from the validation experiments demonstrated that this microarray-based colorimetric method allowed for a rapid and accurate genotyping of STEC reference strains from environmental and clinical sources and from distinct geographical locations. Positive hybridization signals were detected only for probes targeting serotype and virulence genes known to be present in the STEC reference strains. Quantification analysis indicated that the mean pixel intensities of the signal for probes targeting O-antigen or virulence genes were at least three times higher when compared to the background. Furthermore, this microarray-based colorimetric method was then employed to genotype a group of E. coli isolates from watershed sediment and animal fecal samples that were collected from an important region for leafy-vegetable production in the central coast of California. The results indicated an accurate identification of O-type and virulence genes in the tested isolates and confirmed that the ampliPHOX colorimetric method with low-density DNA microarrays enabled a fast assessment of the virulence potential of STEC using low-cost reagents and instrumentation.