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Cholera is a diarrhoeal disease caused by Vibrio cholerae (V. cholerae) bacterium, with strains belonging to serogroups 01 and 0139 causing a huge proportion of the disease. V. cholerae can contaminate drinking water sources and food through poor sanitation and hygiene. This study aimed to identify environmental routes of exposure to V. cholerae within Mukuru informal settlement in Nairobi. We collected nine types of environmental samples (drinking water, flood water, open drains, surface water, shaved ice, raw produce, street food, soil, and public latrine swabs) over 12 months. All samples were analysed for V. cholerae by culture and qPCR, then qPCR-positive samples were quantified using a V. cholerae DNA standard. Data about the frequency of contact with the environment was collected using behavioural surveys. Of the 803 samples collected, 28.5% were positive for V. cholerae by qPCR. However, none were positive for V. cholerae by culture. V. cholerae genes were detected in majority of the environmental water samples (79.3%), including open drains, flood water, and surface water, but were only detected in small proportions of other sample types. Vibrio-positive environmental water samples had higher mean V. cholerae concentrations [2490-3469 genome copies (gc) per millilitre (mL)] compared to drinking water samples (25.6 gc/mL). Combined with the behavioural data, exposure assessment showed that contact with surface water had the highest contribution to the total V. cholerae exposure among children while ingestion of municipal drinking water and street food and contact with surface water made substantial contributions to the total V. cholerae exposure for adults. Detection of V. cholerae in street food and drinking water indicates possible risk of exposure to toxigenic V. cholerae in this community. Exposure to V. cholerae through multiple pathways highlights the need to improve water and sanitation infrastructure, strengthen food hygiene practices, and roll out cholera vaccination., Competing Interests: The authors have declared that no competing interests exist., (Copyright: © 2024 Kering et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

The causative agent of typhoid fever, Salmonella enterica serovar Typhi, is a human restricted pathogen. Human carriers, 90% of whom have gallstones in their gallbladder, continue to shed the pathogen after treatment. The genetic mechanisms involved in establishing the carrier state are poorly understood, but S . Typhi is thought to undergo specific genetic changes within the gallbladder as an adaptive mechanism. In the current study, we aimed to identify biofilm forming ability and the genetic differences in longitudinal clinical S . Typhi isolates from asymptomatic carriers with gallstones in Nairobi, Kenya. Whole genome sequences were analyzed from 22 S . Typhi isolates, 20 from stool and 2 from blood samples, all genotype 4.3.1 (H58). Nineteen strains were from four patients also diagnosed with gallstones, of whom, three had typhoid symptoms and continued to shed S . Typhi after treatment. All isolates had point mutations in the quinolone resistance determining region (QRDR) and only sub-lineage 4.3.1.2EA3 encoded multidrug resistance genes. There was no variation in antimicrobial resistance patterns among strains from the same patient/household. Non-multidrug resistant (MDR), isolates formed significantly stronger biofilms in vitro than the MDR isolates, p < 0.001 . A point mutation within the treB gene ( treB A383T) was observed in strains isolated after clinical resolution from patients living in 75% of the households. Missense mutations in Vi capsular polysaccharide genes, tviE P263S was also observed in 18% of the isolates. This study provides insights into the role of typhoid carriage, biofilm formation, AMR genes and genetic variations in S. Typhi from asymptomatic carriers., Competing Interests: Conflict of Interest The authors declare that they have no competing interests.

Background: Children who have been discharged from hospital in sub-Saharan Africa remain at substantial risk of mortality in the post-discharge period. Antimicrobial resistance (AMR) may be an important factor. We sought to determine the prevalence and risk factors associated with AMR in commensal Escherichia coli (E. coli) from Kenyan children at the time of discharge., Methodology/principle Findings: Fecal samples were collected from 406 children aged 1-59 months in western Kenya at the time of discharge from hospital and cultured for E. coli. Susceptibility to ampicillin, ceftriaxone, cefotaxime, ceftazidime, cefoxitin, imipenem, ciprofloxacin, gentamicin, combined amoxicillin/clavulanic acid, trimethoprim-sulfamethoxazole, azithromycin, and chloramphenicol was determined by disc diffusion according to guidelines from the Clinical and Laboratory Standards Institute (CLSI). Poisson regression was used to determine associations between participant characteristics and the presence of extended-spectrum beta-lactamases (ESBL) producing E. coli. Non-susceptibility to ampicillin (95%), gentamicin (44%), ceftriaxone (46%), and the presence of ESBL (44%) was high. Receipt of antibiotics during the hospitalization was associated with the presence of ESBL (aPR = 2.23; 95% CI: 1.29-3.83) as was being hospitalized within the prior year (aPR = 1.32 [1.07-1.69]). Open defecation (aPR = 2.02; 95% CI: 1.39-2.94), having a toilet shared with other households (aPR = 1.49; 95% CI: 1.17-1.89), and being female (aPR = 1.42; 95% CI: 1.15-1.76) were associated with carriage of ESBL E. coli., Conclusions/significance: AMR is common among isolates of E. coli from children at hospital discharge in Kenya, including nearly half having detectable ESBL., Competing Interests: The authors have declared that no competing interests exist.

The cardiometabolic syndrome (CMS) is associated with cardiovascular disease (CVD) and includes a constellation of risk factors such as central obesity, hypertension, insulin resistance, dyslipidemia, microalbuminuria, and hypercoagulability. Collectively, these risk factors increase CVD endpoints such as stroke, congestive heart failure, chronic kidney disease (CKD), and overall mortality. The CMS is associated with endothelial dysfunction, inflammation, abnormal thrombolysis, and increased oxidative stress that accentuate progression of CVD. We will review how the varying components of the CMS relate to an increased CVD and renal disease risk.

Insulin resistance is invariably present in patients with the cardiometabolic syndrome and is thought to play a key role in its pathogenesis. It represents a complex interaction of maladaptive characteristics related to impaired insulin action at target organs and external factors such as genetics and environment. It is likely that the molecular factors that underlie insulin resistance and resultant hyperinsulinemia contribute to many of the clinical components of the cardiometabolic syndrome, although the precise associations remain poorly understood. Abnormalities of various adipocytokines (particularly reduced circulating levels of adiponectin and leptin) resistance may also play a role in the genesis of insulin resistance. Genetic factors are an important determinant of insulin sensitivity. Effective management of the cardiometabolic syndrome will ultimately depend on our understanding of the underlying molecular mechanisms of key components of this disorder, such as insulin resistance.

Hypertension in pregnancy contributes significantly to both maternal and neonatal morbidity and mortality. Among different forms of pregnancy-associated hypertension, preeclampsia-eclampsia has the highest impact on morbidity and mortality. Chronic hypertension may result in preterm and small for gestational age infants, even when it is mild-to-moderate. Chronic hypertension is a risk factor for superimposed preeclampsia and results in higher rates of adverse outcome. Preeclampsia is a multisystemic disease that is thought to be initiated by abnormalities in placental perfusion and endothelial dysfunction, ultimately resulting in multiorgan failure. Preeclampsia is more common in women of minority ethnicity who are socioeconomically disadvantaged. Pharmacologic therapy for hypertensive disorders in pregnancy is limited by concerns regarding the safety of both mother and fetus. Although treatment of severe hypertension is not debated, there is no consensus on the rationale for pharmacologic therapy of mild-to-moderate hypertension in pregnancy.

This article reprises four presentations on Gerontology Education in Kenya, a seminar at the 2004 Annual Meeting of the Association of Gerontology in Higher Education. It describes the process by which the Gerontology Institute of Georgia State University established a 3-year gerontology education and research partnership with Kenyatta University in Nairobi, Kenya, and the field experiences of two scholars who have conducted aging research in Kenya. We provide four key elements of cultural competence and recommendations for American gerontologists wishing to establish international linkages.

Many of the studies evaluating implications of the metabolic syndrome have not looked specifically at varied ethnic groups to compare and contrast the effects of ethnicity on the metabolic syndrome. Most of the data regarding ethnicity comes from cross sectional studies of national data bases such as NHANES. Other studies seem to have lower numbers of ethnic groups other than Caucasians. For clinical practice, most of the data may be extrapolated until data from randomized prospective trials are available. Certainly it would appear that many of the cardiovascular implications persist when adjusted for race. Lifestyle changes such as diet and physical activity may be universally recommended for all persons at risk, regardless of ethnicity and, where necessary, pharmacological interventions may be used.

We developed a simple and versatile new technique (Multi-Track) for percutaneous mitral valvotomy using two two separate balloon catheters positioned on a single guidewire. The first catheter, with only a distal guidewire lumen and a proximal balloon, is introduced over the guidewire into the vein and then advanced into the mitral valve orifice. Subsequently, a normal balloon catheter running on the same guidewire is inserted and lined up with the first catheter so the two are positioned side by side. The balloons are then inflated simultaneously. The technique was applied in 12 patients between 10 and 44 years of age (mean, 27.1) and weighing 24-80 kg (mean, 50.3). Valve area increased from 0.66 cm2 (range, 0.3-0.9 cm2) to 1.97 cm2 (range, 1.3-3.1 cm2) and mean left atrial pressure dropped from 31 mmHg (range, 18-52 mmHg) to 12 mmHg (range, 5-22 mmHg). Mitral dilatation with the Multi-Track system gives results comparable to those with previously described techniques and uses simpler and less costly catheters.