Children’s migration and chronic illness among older parents ‘left behind’ in China

The relationship between adult children’s migration and the health of their older parents ‘left behind’ is an emerging research area and existing studies reflect mixed findings. This study aims to investigate the association between having migrant (adult) children and older parents’ chronic illness in China, using chronic stomach or other digestive diseases as a proxy. Secondary analysis of the national baseline survey of the 2011 China Health and Retirement Longitudinal Study (CHARLS) was conducted. Analyses were conducted in a total of sample of 6495 individuals aged 60 years and above from 28 out of 31 provinces in China, who had at least one child at the baseline survey. Binary logistic regression was used. The prevalence of any of the diagnosed conditions of chronic stomach or other digestive diseases was higher among older people with a migrant son than among those without (27 percent vs 21 percent, p < 0.001). More specifically, the odds ratio of reporting a disease was higher among older adults with at least one adult son living in another county or province than among those with all their sons living closer (OR = 1.29, 95% CI = 1.10–1.51). The results from this large sample of older adults support the hypothesis that migration of sons significantly increases the risk of chronic stomach and other digestive diseases among ‘left behind’ elderly parents in contemporary China

The structure of IS<i>256</i> and its extrachromosomal circular DNA in OC8.

<p>In A, the structure of IS<i>256</i> (OC8) is based on the OC8 genome sequence (GenBank accession number AP017377); the structure was very similar to previously described IS<i>256</i> structures [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0164168#pone.0164168.ref027" target="_blank">27</a>,<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0164168#pone.0164168.ref048" target="_blank">48</a>,<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0164168#pone.0164168.ref049" target="_blank">49</a>]. PCR primers to detect an IS<i>256</i> circular DNA were designed based on the OC8 genome sequence. In B, the PCR primer set (R-R1 and L-R2, shown in A) exactly detected IS<i>256</i> circular DNA for OC8 (PCR product size, approximately 200 bp), while there were no amplified bands for strain USA300-0114, which lacked IS<i>256</i>. In C (and B), the 194-bp nucleotide sequence of the estimated PCR product, perfectly matched the IR_L side and IR_R side regions of IS<i>256</i> (OC8), and contained a 6-bp stretch, marked in red; 26-bp imperfect IR sequences and 6-bp stretch sequences were underlined in C. However, the 6-bp stretch data showed a “mixed” result, with TTTTTT as the highest base content (followed by AAAAAA). Since the 6-bp stretch originates from a flanking <i>att</i> sequence [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0164168#pone.0164168.ref048" target="_blank">48</a>] and OC8 carries 19 IS<i>256</i> copies with distinct <i>att</i> sequences, the “mixed” 6-bp stretch reflects the presence of heterogeneous circular DNA (in terms of stretch sequences) in OC8. This observation is consistent with the AT-rich <i>att</i> sequences of 19 IS<i>256</i> copies on the genome.</p

Sequence comparison between OC8 and USA300 FPR3757 genomes and visualization of a large genomic inversion.

<p>Genomic sequence comparisons were performed using WebACT for the visualization of genomic inversions. The genome sequence of USA300 FPR3757 was from GenBank Accession number CP000255. The OC8 inverted region relative to USA300 FPR3757 is highlighted in blue.</p

PCR targeting the OC8-type megabase inversion (MbIN).

<p>In A and B, PCR primers targeting the junction sites of OC8 MbIN (A-C and B-D) and those targeting the corresponding region of USA300 FPR3757 (A-B and C-D) were designed based on the OC8 or USA300 FPR3757 complete genome sequence, respectively. The structures of the MbIN junction regions of OC8 and the corresponding regions of USA300 FPR3757 are from <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0164168#pone.0164168.g005" target="_blank">Fig 5</a>. In C to E, PCR products with an asterisk were sequenced, and the sequences determined were consistent with the OC8 or USA300 FPR3757 genome sequence. ST8_Kras is ST8/SCC<i>mec</i>IVc MRSA from Krasnoyarsk, Siberian Russia. The geographical location of MRSA isolated in European Russia: Mow, Moscow; St. P, St. Petersburg; Yar, Yaroslavl. Regarding Far Eastern Russia, MRSA was isolated in Vladivostok.</p

Relevant characteristics of MRSA strains^a.

<p>Relevant characteristics of MRSA strains<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0164168#t001fn001" target="_blank">^a</a>.</p

Possible mechanisms for the large genomic inversion in OC8.

<p>In this model, shown in A, we hypothesized ancestor strains of OC8 for a one-megabase inversion (MbIN) and simultaneously-occurring deletion events. An initial ancestor strain (OC8 ancestor 1) lacks IS<i>256</i>, but has <i>att</i> site sequences, similar to USA300 FPR3757 (GenBank accession number CP000255); the size of OC8 ancestor 1 DNA flanked by two <i>att</i> sites on the right side of the figure was estimated to be 3,356 bp. The first step (step 1) includes three IS<i>256</i> insertions at different <i>att</i> sites. As shown on the right side of the figure, a homogenous recombination (step 2) then occurs between the direct repeats of IS<i>256</i> (in OC8 ancestor 1a), deleting a small region and leaving only one copy of IS<i>256</i> (generating OC8 ancestor 2). In step 3, a homogenous recombination subsequently occurs between the inverted repeats of IS<i>256</i> (on OC8 ancestor 2), with the one-megabase region being inverted, and generating OC8. The genes of NTPase, <i>hsdS</i>, and <i>hsdM</i> (on the top right side) were located in the genomic island vSAβ (marked with a red line). In B, figures focus on a vSAβ split event, which occurred simultaneously with MbIN. OC8 ancestor 1, OC8 ancestor 2, and OC8 are the same as those described in A. In C, a hypothetical folded chromosome structure with loop domains is illustrated, based on [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0164168#pone.0164168.ref057" target="_blank">57</a>], to boost the crossover and subsequent MbIN events at the two genomic locations, which are far from each other. (The diagram is not to scale.)</p

Pulsed-field gel electrophoresis (PFGE) analysis (right and left) and plasmid carriage patterns (center) of MRSA strains isolated in Krasnoyarsk.

<p>The MRSA strains shown are those described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0128017#pone.0128017.t002" target="_blank">Table 2</a>. Group A (A1 and A2) and group B are described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0128017#pone.0128017.t003" target="_blank">Table 3</a>. The color of the strain name indicates fatal pneumonia (red), possible sepsis (brown), and carrier cases (green). Of the cases of fatal pneumonia, OC3, OC8C, OC11, OC76 were from hospital-acquired pneumonia (HAP), while OC8, OC22, OC23, and OC59 were from community-acquired pneumonia (CAP). Of the carrier cases, OC14C and OC52 were from hospital workers and OC217 was from a student.</p

Analysis of the <i>tst</i>⁺ SaPI (SaPI2R) structure and <i>tst</i> nucleotide and deduced amino acid sequences of the ST239_Kras strain OC3.

<p>In A, the integration site (<i>att</i>) and <i>att</i> sequences of SaPI2R of the ST239_Kras strain OC3 are shown. In B, the SaPI2R structure was compared with those of <i>tst</i>^- SaPI (ATCC25923) and <i>tst</i>⁺ SaPI2 (RN3984). Homologous regions between SaPI structures are shaded with color. Genes: <i>tst</i>, toxic shock syndrome toxin-1 gene; <i>eta</i>, <i>S</i>. <i>hyicus</i> exfoliatin A gene; <i>ter</i>, terminase gene (which cleaves multimeric DNA); <i>rep</i>, replication initiator gene; <i>int</i>, the integrase gene. In C, the nucleotide sequences of <i>tst</i>⁺ SaPIs and <i>tst</i>^- SaPI (ATCC25923) were analyzed for phylogenetic diversity. In D-a, the nucleotide sequences of the <i>tst</i> genes were analyzed for phylogenetic diversity. In this figure, each GenBank record year is also shown. In D-b, the deduced amino acid sequences of the <i>tst</i> gene products were analyzed for phylogenetic diversity. The origin (reported source) of each isolate is indicated by the color of the isolate name: red, Russia; yellow, United Kingdom (UK); blue, United States (USA); dark red, Korea; light blue, Argentine; purple, Japan; green, those for animal isolates. In C and D, the scale bar represents substitutions per single-nucleotide polymorphism site. In E, the representative <i>tst</i> gene sequences were compared with the reference sequences (of pRN6100). Arrows indicate the positions of the nucleotide and amino acid changes for the representative <i>tst</i> genes. At the bottom of the figure (green), different amino acids from the amino acid sequences of purified TSST-1 (MN8; GenBank accession number EFH95768) and the deduced amino acid sequence of the <i>tst</i> gene (pRN6100) are indicated in red letters.</p

Healthcare- and Community-Associated Methicillin-Resistant <i>Staphylococcus aureus</i> (MRSA) and Fatal Pneumonia with Pediatric Deaths in Krasnoyarsk, Siberian Russia: Unique MRSA's Multiple Virulence Factors, Genome, and Stepwise Evolution

<div><p>Methicillin-resistant <i>Staphylococcus aureus</i> (MRSA) is a common multidrug-resistant (MDR) pathogen. We herein discussed MRSA and its infections in Krasnoyarsk, Siberian Russia between 2007 and 2011. The incidence of MRSA in 3,662 subjects was 22.0% and 2.9% for healthcare- and community-associated MRSA (HA- and CA-MRSA), respectively. The 15-day mortality rates for MRSA hospital- and community-acquired pneumonia (HAP and CAP) were 6.5% and 50%, respectively. MRSA CAP cases included pediatric deaths; of the MRSA pneumonia episodes available, ≥27.3% were associated with bacteremia. Most cases of HA-MRSA examined exhibited ST239/<i>spa</i>3(t037)/SCC<i>mec</i>III.1.1.2 (designated as ST239_Kras), while all CA-MRSA cases examined were ST8/<i>spa</i>1(t008)/SCC<i>mec</i>IV.3.1.1(IVc) (designated as ST8_Kras). ST239_Kras and ST8_Kras strongly expressed cytolytic peptide (phenol-soluble modulin α, PSMα; and δ-hemolysin, Hld) genes, similar to CA-MRSA. ST239_Kras pneumonia may have been attributed to a unique set of multiple virulence factors (MVFs): toxic shock syndrome toxin-1 (TSST-1), elevated PSMα/Hld expression, α-hemolysin, the staphylococcal enterotoxin SEK/SEQ, the immune evasion factor SCIN/SAK, and collagen adhesin. Regarding ST8_Kras, SEA was included in MVFs, some of which were common to ST239_Kras. The ST239_Kras (strain OC3) genome contained: a completely unique phage, φSa7-like (W), with no <i>att</i> repetition; <i>S</i>. <i>aureus</i> pathogenicity island SaPI2R, the first TSST-1 gene-positive (<i>tst</i>⁺) SaPI in the ST239 lineage; and a super copy of IS<i>256</i> (≥22 copies/genome). ST239_Kras carried the Brazilian SCC<i>mec</i>III.1.1.2 and United Kingdom-type <i>tst</i>. ST239_Kras and ST8_Kras were MDR, with the same levofloxacin resistance mutations; small, but transmissible chloramphenicol resistance plasmids spread widely enough to not be ignored. These results suggest that novel MDR and MVF⁺ HA- and CA-MRSA (ST239_Kras and ST8_Kras) emerged in Siberian Russia (Krasnoyarsk) associated with fatal pneumonia, and also with ST239_Kras, a new (Siberian Russian) clade of the ST239 lineage, which was created through stepwise evolution during its potential transmission route of Brazil-Europe-Russia/Krasnoyarsk, thereby selective advantages from unique MVFs and the MDR.</p></div

Genome information for the ST239_Kras strain OC3, in comparison with the ST239 MRSA strain TW20.

<p>The ST239_Kras OC3 genome contigs (including filled contigs and complete structures; total 2.91-Mb) were mapped on the 3,043,210-bp TW20 genome (GenBank accession number FN433596); in the figure, the two genome structures were drawn as two circles on a common genome map, outside OC3 and inside TW20. Genome information included staphylococcal cassette chromosome <i>mec</i> (SCC<i>mec</i>), other drug resistance structures (such as a transposon, Tn, plasmid-related structure, and gene mutations), characteristic virulence genes, phages, <i>S</i>. <i>aureus</i> pathogenicity islands (SaPIs), genomic islands (νSa), and characteristic insertion sequences (ISs). SCC<i>mec</i>: SCC<i>mec</i>IIIA (in OC3), SCC<i>mec</i>III.1.1.2; SCC<i>mec</i>III (in TW20), SCC<i>mec</i>III.1.1.1 connected to SCC<i>Hg</i>. Drug resistance (gene mutations): Lvx^r, levofloxacin resistance; Rif^r, rifampicin resistance; Su^r, sulfamethoxazole resistance. Virulence genes (region): <i>tst</i>, toxic shock syndrome toxin-1 gene; <i>hld</i>, δ-hemolysin gene; <i>cna</i>, collagen adhesin gene; <i>spa</i>, protein A gene; <i>psmα</i>, phenol-soluble modulin (PSM) gene; <i>hla</i>, α-hemolysin (α-toxin) gene; IEC, immune evasion cluster. The CC30 and CC8 genome sections are from Holden <i>et al</i>. [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0128017#pone.0128017.ref019" target="_blank">19</a>], and the genetic element IEC<i>6013</i> is from [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0128017#pone.0128017.ref060" target="_blank">60</a>]. The plasmid pOC3 (2,908 bp; contig 75) of strain OC3 is not shown in the figure. The location of pSK41-related structure (with two IS<i>431</i> repeats at both ends) currently remains uncertain.</p