Toxoplasma gondii is an intracellular protozoan parasite with a worldwide distribution. T gondii has a complex life cycle, and members of the family, Felidae (domestic cats and their relatives), are the only definitive host. Oocysts are shed in the faeces of felids, and there are two routes of becoming infected: (1) ingestion of T gondii oocysts from contaminated food or water or (2) consumption of infected tissue (Dubey and others 2003, Dubey and Jones 2008). Oocysts from T gondii are known to survive and remain viable in seawater at 4°C (Lindsay and others 2003), and survive harsh environmental conditions, including freezing temperatures (Frenkel and Dubey 1973, Buxton and others 2007). Mortality and morbidity are potential outcomes of T gondii infection in marine mammals (Dubey and others 2003, 2007, Fayer and others 2004,). Studies have documented the presence of antibodies against T gondii in wild and captive marine mammals from Asia, Europe and America (Dubey and others 2003, 2005, 2009 Dubey 2010). Antibodies against T gondii have been detected in pinnipeds from the arctic ecosystem, including hooded (Cystophora cristata), ringed (pusa hispida), bearded (Erignathus barbatus), harbour (phoca vitulina), grey (Halichoerus grypus) and spotted (phoca largha) seals, as well as walruses (odobenus rosmarus) (Dubey and others 2003, Gajadhar and others 2004, Measures and others 2004, Prestrud and others 2007, Jensen and others 2010). Migratory birds, in which tissue cyst and asexual reproduction occurs, may also serve as intermediate hosts (Dubey 2010), and may thus be a potential source of transmission (Prestrud and others 2007). Also, a marked increase in cruise-ship traffic and human activity can potentially act as a source of introduction of T gondii. Toxoplasmosis, due to waterborne oocyst transmission, has been reported in humans (Benenson and others 1982, De Moura and others 2006). Jensen and others (2010) suggested a marine transmission pathway of T gondii into the arctic.

Background: Faltered growth has been shown to affect 161 million children worldwide and derail cognitive development from early childhood. The neural pathways by which growth faltering in early childhood affects future cognitive outcomes remain unclear, which is partially due to the scarcity of research using both neuroimaging and sensitive behavioral techniques in low-income settings. We employed EEG to examine the association between growth faltering and brain functional connectivity and whether brain functional connectivity mediates the effect of early adversity on cognitive development. Methods: We recruited participants from an urban impoverished neighborhood in Dhaka, Bangladesh. One sample consisted of 85 children whose EEG and growth measures (height for age, weight for age, and weight to height) were collected at 6 months and cognitive outcomes were assessed at 27 months. Another sample consisted of 115 children whose EEG and growth measures were collected at 36 months and IQ scores were assessed at 48 months. Path analysis was used to test the effect of growth measures on cognitive outcomes through brain functional connectivity. Findings: Faltered growth was found to be accompanied by overall increased functional connectivity in the theta and low-beta frequency bands for the 36-month-old cohort. For both cohorts, brain functional connectivity was negatively predictive of later cognitive outcomes at 27 and 48 months, respectively. Faltered growth was found to have a negative impact on children's IQ scores in the older cohort, and this effect was found to be mediated by brain functional connectivity in the low-beta band. Interpretation: The association found between growth measures and brain functional connectivity may reflect a broad deleterious effect of malnutrition on children's brain development. The mediation effect of functional connectivity on the relation between physical growth and later IQ scores provides the first experimental evidence that brain functional connectivity may mediate the effect of biological adversity on cognitive development.

Two cases of gas-forming Fournier's gangrene were recently treated in a urology department. The etiology, pathology, bacteriology and treatment of Fournier's gangrene are discussed. An aggressive attitude with respect to both surgery and antibiotic therapy is recommended as possible means of reducing the high mortality associated with the condition.