Is domestic tap water a risk for infections in neutropenic patients?

BACKGROUND: Home care has become popular in the management of hemato-oncologic patients. Therefore, we conducted a prospective study to assess whether tap water from the domestic environment of neutropenic patients poses a risk for infections from the waterborne pathogens nontuberculous mycobacteria (NTM), Legionella spp., and Pseudomonas aeruginosa. MATERIALS AND METHODS: Tap water samples were taken in the homes of 65 hemato-oncologic patients who were discharged from the hospital whilst neutropenic and had a suspected period of neutropenia of a minimum of 10 days. Selective culture for Legionella, P. aeruginosa, and NTM was performed. Patients who required hospital readmission were monitored for infection with the aforementioned pathogens over the following 3 months. RESULTS: NTM were cultured in 62 (95.4%) households in concentrations from 1 to 1,000 CFU/500 ml. The facultative pathogenic species Mycobacterium chelonae (58.5% of taps) and M. mucogenicum (38.5% of taps) were most frequently detected. Legionella spp. was cultured from six households (9.2%), including five households with L. pneumophila in concentrations from 25 to 2,500 CFU/500 ml. P. aeruginosa was found in seven households (10.8%) in concentrations from 5 to 2,500 CFU/500 ml. While clinical infection with Legionella spp. was not detected in any patients, infection with M. chelonae and P. aeruginosa occurred in one and seven patients, respectively. However, transmission from household water could not be confirmed. CONCLUSION: Although the risk of infection from household water-borne pathogens appears low, preventive measures may be considered on an individual basis in patients with long-term immunosuppression as well as in patients with long-term central-vascular catheterization.

[Chronic exposure to environmental lead in Chilean infants. II: Effects on the psychomotor development]. / Exposición crónica a plomo ambiental en lactantes chilenos. II: Efectos en el desarrollo psicomotor.

BACKGROUND: Lactating children are specially susceptible to lead toxicity due to their underdeveloped nervous system, lower body mass, higher intestinal absorption and lower elimination rates. AIM: To determine the effects of lead exposure, comparing Chilean lactating children residing in rural areas with low lead exposure, and in urban areas with high lead exposure. MATERIAL AND METHODS: Newborns from public maternity hospitals of the rural locality of San Felipe and from Metropolitan Santiago, were recruited for the study. On admission to the study, umbilical cord and maternal blood samples were obtained and an inquiry about perinatal, sociohereditary and lead exposure history was done. Children were followed every 6 months until 24 months of age, measuring blood parameters and neurobehavioral development using Bayley scales. RESULTS: Three hundred twelve children from Santiago and 113 from San Felipe were studied. Maternal and children blood lead levels were higher in Santiago, but lower than those reported in other international studies. At 24 months of age, 4.5% of children from Santiago and 0.7% of children from San Felipe had levels over 10 micrograms/dl. No differences in neurobehavioral development were observed between children of both cities. At 24 months, scores of MDI scales were 91 in Santiago and 97 in San Felipe. The figures for PDI scale were 93 in Santiago and 93 in San Felipe. Main risk factors for a retarded neurobehavioral development were socieconomic level with a mean Odds ratio of 3.5 (0.99-12.4), made sex with an Odds ratio of 2.3 (1.09-5.07) and stimulation at home with an Odds ratio of 0.7 (0.53-0.82). CONCLUSIONS: In this cohort of children, no effect of lead levels on neurobehavioral development was found.

[Chronic exposure to environmental lead in Chilean infants]. / Exposición crónica a plomo ambiental en lactantes chilenos.

BACKGROUND: In Chile, there are several sources of environmental lead exposure. However, the few studies about lead levels in Chilean infants, do not allow to establish the prevalence of high lead levels in this population. AIM: To measure blood lead levels in nursing infants, living in rural and urban areas, from birth until two years of age. SUBJECTS AND METHODS: Newborns from public maternity hospitals in Santiago and a rural area were selected for the study. An umbilical cord blood sample was obtained at birth and venous blood samples thereafter, every 6 months until the age of 24 months. Lead levels were measured by atomic absorption spectrophotometry. Atmospheric lead was measured simultaneously every week in Santiago and the rural area. RESULTS: Three hundred twelve children from Santiago and 113 from the rural area completed the 24 months follow-up. The mean lead exposure for infants living in Santiago and in the rural area was 1.23 +/- 0.66 and 0.19 +/- 0.15 micrograms/m3 respectively (p < 0.001). Mean blood levels were always higher in infants from Santiago, compared to those from the rural area. At 24 months, 4.5% of children from Santiago and 0.7% of children from the rural area had blood lead levels over 10 micrograms/dl. Significant risk factors for high lead levels were recent painting of the house where the infant lives, eating soil, biting banisters and familiar labor exposure to lead. CONCLUSIONS: Infants living in an urban area and exposed to increased atmospheric lead levels have higher blood lead levels than infants living in a rural area.

Veratridine-induced release of endogenous glutamate from rat brain cortex slices: a reappraisal of the role of calcium.

The efflux of endogenous glutamate from thin slices of rat brain cortex superfused in vitro with artificial cerebrospinal fluid (ACSF) was studied. Initially, glutamate efflux was very high (2.5 nmol/mg protein/min), possibly because of the cutting procedure, but declined sharply, and at 30 min of superfusion was 25 pmol/mg protein/min. In ACSF without added calcium, spontaneous glutamate efflux was always higher than that in calcium-containing medium, e.g. at 30 min it was 75 pmol/mg protein/min. Addition of 10 microM veratridine for 2 min, between 30 and 32 min of superfusion, led, in ACSF with calcium, to an increase in glutamate efflux of 288%, when the maximum efflux following veratridine is compared to the glutamate efflux that immediately preceded the application of this drug (from 25 to 97 pmol/mg protein/min), while in ACSF without added calcium, veratridine induced an increase of only 117% (from 75 to 163 pmol/mg protein/min). These results are interpreted as due to the dual effect of veratridine. In calcium-containing ACSF, veratridine increases sodium influx which depolarizes the neurons and opens voltage-sensitive calcium channels. The increased intraneuronal calcium induces glutamate release from synaptic vesicles, while increased intracellular sodium enhances the release of soluble cytoplasmic glutamate by the reverse operation of the plasma membrane, sodium-dependent glutamate carrier. In ACSF without calcium, the release of vesicular glutamate is suppressed, while the sodium-dependent mechanism remains. This appears as if veratridine-induced glutamate efflux were only partially calcium-dependent.