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Nasogastric tube placement is frequently performed in various medical settings. While generally deemed safe in patients without risk factors, complications may occur due to malposition, justifying the need of systematic confirmation of position with chest radiographs. We present the case of a critically ill male adult patient for whom the tube position was initially deemed very unusual on postinsertion radiographs, prompting further workup which ultimately confirmed an oropharyngeal perforation with a left parapharyngeal, left visceral, retrotracheal, and right retrodiaphragmatic course, and resulting in a recurrent pneumothorax and empyema treated by surgical decortication., (© 2024 The Authors. Published by Elsevier Inc. on behalf of University of Washington.)

Werner syndrome (WS) is a progeroid disorder caused by mutations in a protein containing both a DNA exonuclease and DNA helicase domains. Previous studies indicated that males lacking the helicase domain of the Wrn protein orthologue exhibited hepatic transcriptomic and metabolic alterations. In this study, we used a label-free liquid chromatography-tandem mass spectrometry approach to uncover proteins abundance associated with specific biological processes that differed depending on the age (four or ten months) and/or the genotype (wild type or Wrn mutant) in the serum and liver of mice. Principal component analysis of the proteomic data from both serum and hepatic tissue revealed a sexual dimorphism regardless of the age and the genotype of the mice. Moreover, although all Wrn mutant mice exhibited fatty liver by the age of ten months, a significant age and genotype dependent enrichment of proteins involved in lipid and fatty acid metabolic processes were uncovered only in males. Also, a genotype dependent increase in serum oxidant detoxification processes was observed in the serum of Wrn mutant males. Despite these sexual differences, several aspects of the immune system were affected in both females and males. Finally, an increase of specific immunoglobulin molecules was common in the liver and serum of both older Wrn mutant females and males. Such results suggest that specific immunoglobulin variants maybe associated with fatty liver progression in WS.

The development of Metabolic Syndrome (MetS) affects a large number of people around the world and represents a major issue in the field of health. Thus, it is important to implement new strategies to reduce its prevalence, and various approaches are currently under development. Recently, an eco-friendly technology named electrodialysis with ultrafiltration membrane (EDUF) was used successfully for the first time at a semi-industrial scale to produce three fractions concentrated in bioactive peptides (BPs) from an enzymatically hydrolyzed whey protein concentrate (WPC): the initial (F1), the final (F2) and the recovery fraction (F3), and it was demonstrated in vitro that F3 exhibited interesting DPP-IV inhibitory effects. Therefore, the present study aimed to evaluate the effect of each fraction on in vivo models of obesity. A daily dose of 312.5 mg/kg was administered to High Fat/High Sucrose diet (HFHS) induced C57BL6/J mice for eight weeks. The physiological parameters of each group and alterations of their gut microbiota by the fractions were assessed. Little effect of the different fractions was demonstrated on the physiological state of the mice, probably due to the digestion process of the BP content. However, there were changes in the gut microbiota composition and functions of mice treated with F3.

Antimicrobial resistance (AMR) is continuing to grow across the world. Though often thought of as a mostly public health issue, AMR is also a major agricultural and environmental problem. As such, many researchers refer to it as the preeminent One Health issue. Aerial transport of antimicrobial-resistant bacteria via bioaerosols is still poorly understood. Recent work has highlighted the presence of antibiotic resistance genes in bioaerosols. Emissions of AMR bacteria and genes have been detected from various sources, including wastewater treatment plants, hospitals, and agricultural practices; however, their impacts on the broader environment are poorly understood. Contextualizing the roles of bioaerosols in the dissemination of AMR necessitates a multidisciplinary approach. Environmental factors, industrial and medical practices, as well as ecological principles influence the aerial dissemination of resistant bacteria. This article introduces an ongoing project assessing the presence and fate of AMR in bioaerosols across Canada. Its various sub-studies include the assessment of the emissions of antibiotic resistance genes from many agricultural practices, their long-distance transport, new integrative methods of assessment, and the creation of dissemination models over short and long distances. Results from sub-studies are beginning to be published. Consequently, this paper explains the background behind the development of the various sub-studies and highlight their shared aspects.

Meta-analyses suggest that yogurt consumption reduces type 2 diabetes incidence in humans, but the molecular basis of these observations remains unknown. Here we show that dietary yogurt intake preserves whole-body glucose homeostasis and prevents hepatic insulin resistance and liver steatosis in a dietary mouse model of obesity-linked type 2 diabetes. Fecal microbiota transplantation studies reveal that these effects are partly linked to the gut microbiota. We further show that yogurt intake impacts the hepatic metabolome, notably maintaining the levels of branched chain hydroxy acids (BCHA) which correlate with improved metabolic parameters. These metabolites are generated upon milk fermentation and concentrated in yogurt. Remarkably, diet-induced obesity reduces plasma and tissue BCHA levels, and this is partly prevented by dietary yogurt intake. We further show that BCHA improve insulin action on glucose metabolism in liver and muscle cells, identifying BCHA as cell-autonomous metabolic regulators and potential mediators of yogurt's health effects., (© 2022. The Author(s).)

Over the past years, promising results from studies have shown that herring milt hydrolysates (HMH) can counter immune-metabolic disorders associated with obesity. However, more studies must corroborate these results. Thus, three commercial hydrolysates (HMH1, HMH2, and HMH3) as well as the fractions of two of them (HMH4 and HMH5) obtained by electrodialysis with ultrafiltration membranes (EDUF) were evaluated in vivo at higher doses compared to a previous study. To achieve this, seven groups of mice were fed for 8 weeks with either a control Chow diet or an obesogenic diet rich in fat and sucrose (HFHS) and supplemented by daily gavage with water or 312.5 mg/kg of one of the five HMH products. In summary, HMH supplements had no impact on weight gain. In the insulin tolerance test (ITT), HMH2 and its HMH5 fraction significantly reduced the blood sugar variation ( p < 0.05). However, during the glucose tolerance (OGTT), HMH2 supplement increased the hyperinsulinemia variation ( p < 0.05) induced by the HFHS diet. HMH1, HMH2, and HMH5 supplements generated potentially beneficial changes for health in the gut microbiota. These results reveal that HMH do not counteract obesity effects but may decrease certain physiological effects induced by obesity.

Background: Recent meta-analyses suggest that the consumption of fermented dairy products reduces type 2 diabetes and cardiovascular disease (CVD) risk, although the underlying mechanisms remain unclear., Objective: We evaluated whether dairy protein products modulated gut microbiota and cardiometabolic features in mouse models of diet-induced obesity and CVD., Methods: Eight-week-old C57BL/6J wild-type (WT) and LDLr-/-ApoB100/100 (LRKO) male mice were fed for 12 and 24 wk, respectively, with a high-fat/high-sucrose diet [66% kcal lipids, 22% kcal carbohydrates (100% sucrose), 12% kcal proteins]. The protein sources of the 4 diets were 100% nondairy protein (NDP), or 50% of the NDP energy replaced by milk (MP), milk fermented by Lactobacillus helveticus (FMP), or Greek-style yogurt (YP) protein. Fecal 16S rRNA gene-based amplicon sequencing, intestinal gene expression, and glucose tolerance test were conducted. Hepatic inflammation and circulating adhesion molecules were measured by multiplex assays., Results: Feeding WT mice for 12 wk led to a 74% increase in body weight, whereas after 24 wk the LRKO mice had a 101.5% increase compared with initial body weight. Compared with NDP and MP, the consumption of FMP and YP modulated the gut microbiota composition in a similar clustering pattern, upregulating the Streptococcus genus in both genotypes. In WT mice, feeding YP compared with NDP increased the expression of genes involved in jejunal (Reg3b, 7.3-fold, P = 0.049) and ileal (Ocln, 1.7-fold, P = 0.047; Il1-β,1.7-fold, P = 0.038; Nos2, 3.8-fold, P = 0.018) immunity and integrity. In LRKO mice, feeding YP compared with MP improved insulin sensitivity by 65% (P = 0.039). In LRKO mice, feeding with FMP versus NDP attenuated hepatic inflammation (monocyte chemoattractant protein 1, 2.1-fold, P ˂ 0.0001; IL1-β, 5.7-fold, P = 0.0003; INF-γ, 1.7-fold, P = 0.002) whereas both FMP [vascular adhesion molecule 1 (VCAM1), 1.3-fold, P = 0.0003] and YP (VCAM1, 1.04-fold, P = 0.013; intracellular adhesion molecule 1, 1.4-fold, P = 0.028) decreased circulating adhesion molecules., Conclusion: Both fermented dairy protein products reduce cardiometabolic risk factors in diet-induced obese mice, possibly by modulating the gut microbiota., (Copyright © The Author(s) on behalf of the American Society for Nutrition 2020.)

Suboptimal intake of dietary vitamin C (ascorbate) increases the risk of several chronic diseases but the exact metabolic pathways affected are still unknown. In this study, we examined the metabolic profile of mice lacking the enzyme gulonolactone oxidase (Gulo) required for the biosynthesis of ascorbate. Gulo-/- mice were supplemented with 0%, 0.01%, and 0.4% ascorbate (w/v) in drinking water and serum was collected for metabolite measurements by targeted mass spectrometry. We also quantified 42 serum cytokines and examined the levels of different stress markers in liver. The metabolic profiles of Gulo-/- mice treated with ascorbate were different from untreated Gulo-/- and normal wild type mice. The cytokine profiles of Gulo-/-mice, in return, overlapped the profile of wild type animals upon 0.01% or 0.4% vitamin C supplementation. The life span of Gulo-/- mice increased with the amount of ascorbate in drinking water. It also correlated significantly with the ratios of serum arginine/lysine, tyrosine/phenylalanine, and the ratio of specific species of saturated/unsaturated phosphatidylcholines. Finally, levels of hepatic phosphorylated endoplasmic reticulum associated stress markers IRE1α and eIF2α correlated inversely with serum ascorbate and life span suggesting that vitamin C modulates endoplasmic reticulum stress response and longevity in Gulo-/- mice.

Werner syndrome (WS) is a premature aging disorder caused by mutations in a RecQ-family DNA helicase, WRN. Mice lacking part of the helicase domain of the WRN orthologue exhibit many phenotypic features of WS, including metabolic abnormalities and a shorter mean life span. In contrast, mice lacking the entire Wrn protein (i.e. Wrn null mice) do not exhibit a premature aging phenotype. In this study, we used a targeted mass spectrometry-based metabolomic approach to identify serum metabolites that are differentially altered in young Wrn helicase mutant and Wrn null mice. An antibody-based quantification of 43 serum cytokines and markers of cardiovascular disease risk complemented this study. We found that Wrn helicase mutants exhibited elevated and decreased levels, respectively, of the anti-inflammatory cytokine IL-10 and the pro-inflammatory cytokine IL-18. Wrn helicase mutants also exhibited an increase in serum hydroxyproline and plasminogen activator inhibitor-1, markers of extracellular matrix remodeling of the vascular system and inflammation in aging. We also observed an abnormal increase in the ratio of very long chain to short chain lysophosphatidylcholines in the Wrn helicase mutants underlying a peroxisome perturbation in these mice. Remarkably, the Wrn mutant helicase protein was mislocalized to the endoplasmic reticulum and the peroxisomal fractions in liver tissues. Additional analyses with mouse embryonic fibroblasts indicated a severe defect of the autophagy flux in cells derived from Wrn helicase mutants compared to wild type and Wrn null animals. These results indicate that the deleterious effects of the helicase-deficient Wrn protein are mediated by the dysfunction of several cellular organelles.

The protein tyrosine phosphatase (PTPase) Src-homology 2-domain-containing phosphatase (SHP)-1 was recently reported to be a novel regulator of insulin's metabolic action. In order to examine the role of this PTPase in skeletal muscle, we used adenovirus (AdV)-mediated gene transfer to express an interfering mutant of SHP-1 [dominant negative (DN)SHP-1; mutation C453S] in L6 myocytes. Expression of DNSHP-1 increased insulin-induced Akt serine-threonine kinase phosphorylation and augmented glucose uptake and glycogen synthesis. Pharmacological inhibition of glucose transporter type 4 (GLUT4) activity using indinavir and GLUT4 translocation assays revealed an important role for this transporter in the increased insulin-induced glucose uptake in DNSHP-1-expressing myocytes. Both GLUT4 mRNA and protein expression were also found to be increased by DNSHP-1 expression. Furthermore, AdV-mediated delivery of DNSHP-1 in skeletal muscle of transgenic mice overexpressing Coxsackie and AdV receptor also enhanced GLUT4 protein expression. Together, these findings confirm that SHP-1 regulates muscle insulin action in a cell-autonomous manner and further suggest that the PTPase negatively modulates insulin action through down-regulation of both insulin signaling to Akt and GLUT4 translocation, as well as GLUT4 expression.

Background: Heterogeneity in microvascular perfusion is associated with impaired tissue oxygenation. We hypothesized that cardiac surgery with or without cardiopulmonary bypass (CPB) could induce microvascular alterations., Methods: We used an orthogonal polarization spectral imaging technique to evaluate the sublingual microcirculation in patients undergoing cardiac surgery with (n = 9) or without (n = 6) CPB. We also included, as a control group, 7 patients undergoing thyroidectomy with the same anesthetic procedure. Hemodynamic and microcirculatory variables were obtained the day before surgery, after induction of anesthesia, during CPB, on admission to the intensive care unit or the recovery room, and 6 and 24 hours after the end of the surgical procedure. Data are presented as median (25th to 75th percentile)., Results: No differences in hemodynamic variables were observed between the two cardiac surgery groups. The proportion of perfused vessels was similar in all three groups at baseline (89% [87% to 90%]), and decreased similarly after induction of anesthesia to 71% (69% to 74%). It decreased further during CPB to 53% (50% to 56%). On admission to the intensive care unit or recovery room, alterations were more severe in CPB than in off-pump patients (60% [59% to 62%] versus 64% [61% to 65%]; p = 0.03), whereas they had already normalized in thyroidectomy patients (89% [86% to 90%]; p = 0.0005 versus cardiac surgery). In both cardiac surgery groups these microcirculatory alterations decreased with time, but persisted at 24 hours. The severity of microvascular alterations correlated with peak lactate levels after cardiac surgery (y = 11.5 - 0.15x; r(2) = 0.65; p < 0.05)., Conclusions: Microcirculatory alterations are observed in cardiac surgery patients whether or not CPB is used. Anesthesia contributes to these alterations, but its effects are transient.

Carcinoembryonic antigen-related cell adhesion molecule 1 (CC1) is a cell adhesion molecule within the Ig superfamily. The Tyr-phosphorylated isoform of CC1 (CC1-L) plays an important metabolic role in the regulation of hepatic insulin clearance. In this report, we show that CC1-deficient (Cc1(-/-)) mice are prone to hepatic steatosis, as revealed by significantly elevated hepatic triglyceride and both total and esterified cholesterol levels compared with age-matched wild-type controls. Cc1(-/-) mice were also predisposed to lipid-induced hepatic steatosis and dysfunction as indicated by their greater susceptibility to store lipids and express elevated levels of enzymatic markers of liver damage after chronic feeding of a high-fat diet. Hepatic steatosis in the Cc1(-/-) mice was linked to a significant increase in the expression of key lipogenic (fatty acid synthase, acetyl CoA carboxylase) and cholesterol synthetic (3-hydroxy-3-methylglutaryl-coenzyme A reductase) enzymes under the control of sterol regulatory element binding proteins-1c and -2 transcription factors. Cc1(-/-) mice also exhibited impaired insulin clearance, glucose intolerance, liver insulin resistance, and elevated hepatic expression of the key gluconeogenic transcriptional activators peroxisome proliferator-activated receptor-gamma coactivator-1 and Forkhead box O1. Lack of CC1 also exacerbated both glucose intolerance and hepatic insulin resistance induced by high-fat feeding, but insulin clearance was not further deteriorated in the high-fat-fed Cc1(-/-) mice. In conclusion, our data indicate that CC1 is a key regulator of hepatic lipogenesis and that Cc1(-/-) mice are predisposed to liver steatosis, leading to hepatic insulin resistance and liver damage, particularly when chronically exposed to dietary fat.

Background: Percutaneous catheterization is a frequently-used technique to gain access to the central venous circulation. Inadvertent arterial puncture is often without consequence, but can lead to devastating complications if it goes unrecognized and a large-bore dilator or catheter is inserted. The present study reviews our experience with these complications and the literature to determine the safest way to manage catheter-related cervicothoracic arterial injury (CRCAI)., Methods: We retrospectively identified all cases of iatrogenic carotid or subclavian injury following central venous catheterization at three large institutions in Montreal. We reviewed the French and English literature published from 1980 to 2006, in PubMed, and selected studies with the following criteria: arterial misplacement of a large-caliber cannula (>/=7F), adult patients (>18 years old), description of the method for managing arterial trauma, reference population (denominator) to estimate the success rate of the therapeutic option chosen. A consensus panel of vascular surgeons, anesthetists and intensivists reviewed this information and proposed a treatment algorithm., Results: Thirteen patients were treated for CRCAI in participating institutions. Five of them underwent immediate catheter removal and compression, and all had severe complications resulting in major stroke and death in one patient, with the other four undergoing further intervention for a false aneurysm or massive bleeding. The remaining eight patients were treated by immediate open repair (six) or through an endovascular approach (two) for subclavian artery trauma without complications. Five articles met all our inclusion criteria, for a total of 30 patients with iatrogenic arterial cannulation: 17 were treated by immediate catheter removal and direct external pressure; eight (47%) had major complications requiring further interventions; and two died. The remaining 13 patients submitted to immediate surgical exploration, catheter removal and artery repair under direct vision, without any complications (47% vs 0%, P = .004)., Conclusion: During central venous placement, prevention of arterial puncture and cannulation is essential to minimize serious sequelae. If arterial trauma with a large-caliber catheter occurs, prompt surgical or endovascular treatment seems to be the safest approach. The pull/pressure technique is associated with a significant risk of hematoma, airway obstruction, stroke, and false aneurysm. Endovascular treatment appears to be safe for the management of arterial injuries that are difficult to expose surgically, such as those below or behind the clavicle. After arterial repair, prompt neurological evaluation should be performed, even if it requires postponing elective intervention. Imaging is suggested to exclude arterial complications, especially if arterial trauma site was not examined and repaired.

The protein tyrosine phosphatase SHP-1 is a well-known inhibitor of activation-promoting signaling cascades in hematopoietic cells but its potential role in insulin target tissues is unknown. Here we show that Ptpn6(me-v/me-v) (also known as viable motheaten) mice bearing a functionally deficient SHP-1 protein are markedly glucose tolerant and insulin sensitive as compared to wild-type littermates, as a result of enhanced insulin receptor signaling to IRS-PI3K-Akt in liver and muscle. Downregulation of SHP-1 activity in liver of normal mice by adenoviral expression of a catalytically inert mutant of SHP-1, or after small hairpin RNA-mediated SHP-1 silencing, further confirmed this phenotype. Tyrosine phosphorylation of CEACAM1, a modulator of hepatic insulin clearance, and clearance of serum [125I]-insulin were markedly increased in SHP-1-deficient mice or SHP-1-deficient hepatic cells in vitro. These findings show a novel role for SHP-1 in the regulation of glucose homeostasis through modulation of insulin signaling in liver and muscle as well as hepatic insulin clearance.

Objective: To determine whether hypoalbuminemia is an independent risk factor for poor outcome in the acutely ill, and to assess the potential of exogenous albumin administration for improving outcomes in hypoalbuminemic patients., Summary Background Data: Hypoalbuminemia is associated with poor outcomes in acutely ill patients, but whether this association is causal has remained unclear. Trials investigating albumin therapy to correct hypoalbuminemia have proven inconclusive., Methods: A meta-analysis was conducted of 90 cohort studies with 291,433 total patients evaluating hypoalbuminemia as an outcome predictor by multivariate analysis and, separately, of nine prospective controlled trials with 535 total patients on correcting hypoalbuminemia., Results: Hypoalbuminemia was a potent, dose-dependent independent predictor of poor outcome. Each 10-g/L decline in serum albumin concentration significantly raised the odds of mortality by 137%, morbidity by 89%, prolonged intensive care unit and hospital stay respectively by 28% and 71%, and increased resource utilization by 66%. The association between hypoalbuminemia and poor outcome appeared to be independent of both nutritional status and inflammation. Analysis of dose-dependency in controlled trials of albumin therapy suggested that complication rates may be reduced when the serum albumin level attained during albumin administration exceeds 30 g/L., Conclusions: Hypoalbuminemia is strongly associated with poor clinical outcomes. Further well-designed trials are needed to characterize the effects of albumin therapy in hypoalbuminemic patients. In the interim, there is no compelling basis to withhold albumin therapy if it is judged clinically appropriate.

Microvascular blood flow alterations are frequent in animal models of sepsis and may impair tissue oxygenation. We hypothesized that alterations of the microcirculation are present in patients with sepsis. We used an orthogonal polarization spectral imaging technique to investigate the sublingual microcirculation in 10 healthy volunteers, 16 patients before cardiac surgery, 10 acutely ill patients without sepsis (intensive care unit control subjects), and 50 patients with severe sepsis. The effects of topical application of acetylcholine (10(-2) M) were tested in 11 patients with sepsis. In each subject, five to seven sublingual areas were recorded and analyzed semiquantitatively. Data were analyzed with nonparametric tests and are presented as medians (25th-75th percentiles). No significant difference in microvascular blood flow was observed between healthy volunteers and patients before cardiac surgery or intensive care unit control subjects. The density of all vessels was significantly reduced in patients with severe sepsis (4.5 [4.2-5.2] versus 5.4 [5.4-6.3]/mm in volunteers, p < 0.01). The proportion of perfused small (< 20 microm) vessels was reduced in patients with sepsis (48 [33-61] versus 90 [89-92]% in volunteers, p < 0.001). These alterations were more severe in nonsurvivors. The topical application of acetylcholine totally reversed these alterations. In conclusion, microvascular blood flow alterations are frequent in patients with sepsis and are more severe in patients with a worse outcome.

Delirium in the intensive care unit is a serious problem that has recently attracted much attention. User-friendly and reliable tools, such as the Confusion Assessment Method for the Intensive Care Unit (CAM-ICU), offer the clinician the opportunity to identify delirium in patients better. Diagnosis of delirium in a critical care population is often a difficult task because classical psychiatric evaluation is impossible for a number of reasons. The CAM-ICU makes use of nonverbal assessments to evaluate the cardinal features of delirium (i.e. acute or fluctuating onset, inattention, disorganized thinking and altered level of consciousness). Its development for use in the critical care setting represents a significant advance that could lead to better care for such patients.

Sepsis remains one of the leading causes of mortality in critically ill patients. Increased insight into the complexities of this disease process has resulted in the targeting of various aspects of the inflammatory response as offering potential therapeutic benefits. There have been encouraging results in the past few years. Some of the tested agents have been shown to improve mortality rates in large randomized controlled trials involving patients with severe sepsis. In this article, we discuss the positive and negative results of trials in this field; some of the possible reasons for the negative results are examined, and directions for the future are suggested.

Objectives: To determine the aetiology of urethritis in Bangui, Central African Republic., Methods: 410 men presenting with urethral discharge and 100 asymptomatic controls were enrolled. Urethral swabs were obtained and processed by gonococcal culture and polymerase chain reaction for the detection of Neisseria gonorrhoeae, Chlamydia trachomatis, Mycoplasma genitalium, Trichomonas vaginalis, and Ureaplasma urealyticum., Results: In multivariate analyses, M genitalium and C trachomatis were significantly associated with urethral discharge when comparing cases of non-gonococcal urethritis (NGU) with controls. T vaginalis was also more common in cases than in controls, but this reached statistical significance only among cases in whom N gonorrhoeae was also detected. U urealyticum was not associated with urethritis. The gonococcus was found in 69% of cases of urethral discharge. M genitalium was the predominant pathogen in patients with NGU, being found in 42% (53/127) of such patients while C trachomatis was found in only 17% (22/127). T vaginalis was found in 18% (23/127) of patients with NGU, but also in 15% (43/283) of patients with gonococcal urethritis, and two thirds of patients with T vaginalis also had the gonococcus. Multiple infections were common. M genitalium caused a syndrome similar to chlamydial urethritis, with a less severe inflammation than in gonococcal infection. No behavioural or clinical characteristic could discriminate between the various aetiological agents., Conclusions: M genitalium is more prevalent than C trachomatis and is the most common cause of NGU in BANGUI: It causes a syndrome similar to chlamydial urethritis. T vaginalis is weakly associated with urethritis, and is often found along with other pathogens.

Background: Interventions for upgrading sexually transmitted disease (STD) management in sub-Saharan Africa have focused on the public sector, and to a much lower extent on private medical practitioners and pharmacies. However, in most African cities there is a large informal sector that provides care to many patients with STD symptoms., Goal: To compare the quality of treatments offered to patients with major STD syndromes in the public sector, pharmacies, and the informal sector of the same city., Study Design: Healthcare providers in health centers, pharmacies, private laboratories, and market drug peddlers in Bangui, Central African Republic, were asked to complete a short form for every patient consulting them with genital complaints. The treatments they ordered were evaluated for their potential efficacy against the major etiologic agents of the syndrome for which the patient consulted., Results: The majority of male patients with STDs preferred to seek care in pharmacies and in the informal sector. The STD treatments offered to patients with urethral discharge or genital ulcers in pharmacies and in the informal sector tended to focus on a single etiologic agent. The quality of STD treatments offered by drug peddlers and private laboratories was poor, apart from adequate coverage of syphilis in patients with genital ulcers and of candidiasis in women with vaginal discharge. For instance, 41% and 34% of patients with urethral discharge managed by drug peddlers and private laboratories did not receive a drug active against either Neisseria gonorrhoeae or Chlamydia trachomatis, whereas this proportion was 22% in pharmacies and 14% in health centers. For patients with genital ulcers, the proportion offered a drug active against Haemophilus ducreyi was 2% if seen by drug peddlers, 0% in laboratories, 10% in pharmacies, and 25% in health centers. For each syndrome and each category of provider, between one fourth and two thirds of patients had already received another ineffective treatment elsewhere., Conclusion: National STD and HIV control programs will have to improve STD management in pharmacies and in the informal sector if they are to have any impact on the dynamics of HIV infection in urban centers.