The study of several Escherichia coli intestinal commensal isolates per individual in 265 healthy human subjects belonging to seven populations distributed worldwide showed that the E. coli population is highly structured, with major differences between the tropical and temperate populations.Escherichia coli is a commensal inhabitant of the intestinal tracts of healthy humans and many animal species, but it can also cause a wide range of diseases, ranging from diarrhea to extraintestinal infections (8). As it has been proposed that pathogenic E. coli strains are derived from commensal strains by the acquisition of chromosomal or extrachromosomal virulence operons (19), identifying the factors that shape the genetic structure of commensal strains might help us understand the emergence of virulence. E. coli can be considered to have a clonal genetic structure with a low level of recombination (7, 10). Four main phylogenetic groups, A, B1, B2, and D, constitute the bulk of the species (15). A few authors have examined commensal strains from humans (3-5, 13) using population genetics molecular tools (for a pioneer review, see reference 14). A significant locale-specific distribution among groups A, B1, B2, and D has been observed in human commensal strains in three geographically distinct human populations (French, Croatian, and Malian) (9).To gain insight into the composition of the E. coli human commensal microbiota, we characterized the relative abundance of E. coli phylogenetic groups in a large collection of 1,740 isolates from 265 subjects belonging to seven populations spread over three continents and compared the results to those of previous studies using the same approach.Bacterial isolates. Isolates were collected between 1999 and 2001 from seven human populations composed of healthy adult subjects of both sexes from 15 to 65 years of age, except when otherwise stated. The populations were the following: (i) 27 subjects living in the Paris area (mainland France, Europe), (ii) 21 university students living in Brest (Brittany, mainland France), (iii) 25 bank and insurance workers (BIW) living in seven distinct areas of Brittany (mainland France), (iv) 25 pig farmers (PF) living in the same seven areas as the BIW, (v) 93 ethnically homogeneous Wayampi Amerindians living in three villages of southern French Guyana (South America) with no modern sanitary or hygienic facilities, (vi) 46 women living in Cotonou (Benin, Africa), and (vii) 28 subjects living in Bogotá (Colombia, South America). The individuals in the BIW and PF populations in Brittany were matched for county of residence, age (20 to 60 years), and sex (13 men and 12 women). A subset of 25 Amerindians was also matched for age and sex with the BIW and PF populations. These matched populations had neither been hospitalized nor had taken antibiotics for at least 1 month before stool sampling. In all, 1,740 E. coli isolates were obtained after plating fresh fecal samples on Drigalski agar, with 5 or 10 randomly chosen E. coli isolates per individual.The...

The host mechanisms responsible for protection against malaria remain poorly understood, with only a few protective genetic effects mapped in humans. Here, we characterize a host-specific genome-wide signature in whole-blood transcriptomes of Plasmodium falciparum-infected West African children and report a demonstration of genotype-by-infection interactions in vivo. Several associations involve transcripts sensitive to infection and implicate complement system, antigen processing and presentation, and T-cell activation (i.e., SLC39A8, C3AR1, FCGR3B, RAD21, RETN, LRRC25, SLC3A2, and TAPBP), including one association that validated a genome-wide association candidate gene (SCO1), implicating binding variation within a noncoding regulatory element. Gene expression profiles in mice infected with Plasmodium chabaudi revealed and validated similar responses and highlighted specific pathways and genes that are likely important responders in both hosts. These results suggest that host variation and its interplay with infection affect children's ability to cope with infection and suggest a polygenic model mounted at the transcriptional level for susceptibility.host response | parasite load | eQTL | eSNP | genotype-by-environment interactions

The results demonstrate that this specifically tailored strategy is relevant to this setting, given the unique conditions of this African country.

No abstract

Sickle cell disease (SCD) is associated with an increased risk of medical complications during pregnancy. In sub-Saharan Africa, fetal and maternal mortality rates are particularly high. This study evaluated the effect of an active prenatal management program on pregnancy outcome in patients with SCD in an African setting. Pregnant women with SCD attending the National Teaching Hospital in Cotonou (The Republic of Benin, West Africa) were recruited before the 28th week of gestation. Management was based on providing information and education about SCD and improving nutritional status, malaria prevention, early detection of bacterial infections, and restricted use of blood transfusion. Maternal and fetal mortality rates and SCD-related morbidity were the principal variables assessed. One hundred and eight patients (42 SS and 66 SC) with 111 fetuses were included in the study. Thirteen fetal deaths (from 9 SS and 4 SC mothers) were recorded and 2 deaths of SC mothers. The maternal mortality rate of 1.8% was comparable with the overall maternal mortality rate for this maternity unit (1.2%). Few SCD-related events were recorded. Plasmodium falciparum malaria infection was the major cause of morbidity. Sixty-three patients (19 SS and 44 SC) successfully completed their pregnancy (58.3%) without requiring transfusion. Providing pregnant SCD patients with relevant medical care based on simple cost-effective approaches can have a positive impact on SCD-associated morbidity and mortality in an otherwise difficult setting in Africa.