Medical Simulation as a Vital Adjunct to Identifying Clinical Life-Threatening Gaps in Austere Environments

Background

Maternal mortality and morbidity are major causes of death in low-resource countries, especially those in Sub-Saharan Africa. Healthcare workforce scarcities present in these locations result in poor perioperative care access and quality. These scarcities also limit the capacity for progressive development and enhancement of workforce training, and skills through continuing medical education. Newly available low-cost, in-situ simulation systems make it possible for a small cadre of trainers to use simulation to identify areas needing improvement and to rehearse best practice approaches, relevant to the context of target environments.

Nasopharyngeal carriage of penicillin-resistant Streptococcus pneumoniae in healthy children

Streptococcus pneumoniae carriage is a risk factor for the development of respiratory system infections and the spread of penicillin-resistant strains. The aim of this study was to investigate nasopharyngeal carriage of S. pneumoniae in healthy children and resistance to penicillin and other antimicrobials and to assess related risk factors. Nasopharyngeal specimens collected from healthy children less than six years of age, visiting a Mother and Child Health Center for health control, were investigated microbiologically between February-March 2004. Carriage rate was 37.2% (n=112/301); 33.9% intermediate and 5.4% high penicillin resistance were detected. According to multivariate analysis, carriage rate was inversely related to number of rooms (OR:0.574) and child age (OR:0.978), while penicillin resistance was correlated well with antibiotic use in the last two months (OR:2.193). Decreased sensitivity plus resistance to other antimicrobials were: trimethoprim-sulfamethoxazole (TMP-SMX) 45.6%; erythromycin 16.1%, tetracycline 16.1%; clindamycin 9.8%, and ofloxacin 3.6% in pneumococcal isolates, which increased significantly (p<0.05) to 72.7%, 31.8%, 27.3%, 20.5%, and 6.8%, respectively, in penicillin non-sensitive S. pneumoniae (PNSSP) except for ofloxacin. Overall multidrug resistance was 17.9%, while PNSSP exhibited a resistance rate of 38.6%. In conclusion, S. pneumoniae carriage rates determined in healthy children were high and PNSSP strains also showed increased resistance to other antimicrobials.     

Inhibition of suicidal erythrocyte death by nitric oxide

Nitric oxide (NO) is known to counteract apoptosis by S-nitrosylation of protein thiol groups. NO is generated and stored in erythrocytes, which may undergo eryptosis, a suicidal cell death similar to apoptosis of nucleated cells. Eryptosis is triggered by increased cytosolic Ca²⁺ activity and/or ceramide and characterized by cell shrinkage and phosphatidylserine exposure at the cell surface. The present study explored whether nitric oxide could interfere with the machinery underlying eryptosis. To this end, erythrocyte phosphatidylserine exposure (annexin V-binding) and cell volume (forward scatter) were determined by flow cytometry. The Ca²⁺ ionophore ionomycin (0.1 μM) increased cytosolic Ca²⁺ activity, triggered annexin binding, and decreased forward scatter. The annexin binding and decrease of forward scatter but not the increase of cytosolic Ca²⁺ activity were reversed by the NO-donor nitroprusside (1 μM) and papanonoate (100 μM). Higher concentrations of nitroprusside (0.1 and 1 mM) stimulated eryptosis. Glucose depletion, exposure to C₆-ceramide (3 μM), hypertonic (addition of 550 mM sucrose), and isotonic (replacement of Cl⁻ with gluconate) cell shrinkage all triggered annexin V binding, effects all reversed by nitroprusside (1 μM). Dibutyryl–cGMP (1 mM) blunted the ionomycin- but not the ceramide-induced annexin V binding. Ionomycin decreased protein nitrosylation and thioredoxin activity, effects reversed by the NO-donor papanonoate. Clearance of erythrocytes from circulating blood was significantly faster in eNOS knockout mice than in their wild-type littermates. In conclusion, nitric oxide participates in the regulation of erythrocyte survival, an effect partially mimicked by cGMP and paralleled by alterations of protein nitrosylation and thioredoxin activity. This study is dedicated to the memory of Rudi Busse, a unique scientist with outstanding sharp mind, strength, and dedication.