Epidemiology and burden of rotavirus diarrhea in day care centers in Lyon, France.
This study gives, for the first time, an estimate of the incidence and the cost of rotavirus infection in day care centers in Lyon, France.
Biomedical subjects
Publications and source records attributed to Daniel Floret.
This study gives, for the first time, an estimate of the incidence and the cost of rotavirus infection in day care centers in Lyon, France.
OBJECTIVE: The aim of the study was to determine the risk factors of a severe outcome for children severely injured [killed or with an Injury Severity Score (ISS)>or=16] in a road accident. MATERIALS AND METHODS: Casualties that occurred between 1996 and 2001 which involved children under 14 years of age were assessed in a population-based study based on data included in a French road trauma Registry. A severe traumatic brain injury (TBI) was defined as a head injury with an Abbreviated Injury Scale (AIS) severity score>or=3. A multivariate logistic regression was performed to quantify the risk of a "severe outcome" defined as death or an expected serious impairment 1 year later. RESULTS: The annual incidence of an ISS of 16+ was 7.7 per 100,000 children. Among the 126 severely injured children included in this study, 40 died (including 16 immediate deaths), and a severe outcome was expected for 54 of the 86 survivors. Children with an "isolated severe TBI" and those with "multiple injuries including TBI" were more likely to have a severe outcome than those who had an "isolated severe injury without TBI" (OR: 7.91; 95%CI: 1.43-43.77 and OR: 8.37; 95%CI: 1.52-46.13, respectively). Age was inversely linked to a severe outcome. The unprotected motor vehicle occupants (MVO) had an odds ratio of 7.56 (95%CI: 1.07-53.56) compared to the protected MVO. Only 30% of children who survived a severe TBI were admitted to rehabilitation. CONCLUSION: The mechanism of the injury, an injury pattern involving the head and a young age were associated with a severe outcome following a road accident. A majority of children severely injured were not referred to inpatient rehabilitation.
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OBJECTIVES: To assess the age-specific seroprevalence of varicella in the French population and to explore age-adjusted differences according to gender and geographic region. METHODS: Data were obtained from 1257 randomly selected, frozen serum samples, from subjects 1-30 years of age, that were sent to the Pasteur-Cerba laboratory in November 2003 to January 2004 for the following clinical indications: allergies, respiratory infections, herpes virus infections excluding varicella and endocrinologic tests. IgG concentrations were tested with an indirect enzyme immunoassay. Statistical analyses included use of locally weighted, scatterplot smoothers. RESULTS: Age-specific seroprevalence of varicella increased by >6-fold between 1 and 8 years of age, ie, from 15.0% (95% confidence interval, 8.6-23.5%) for subjects 1-2 years of age to 89.0% (95% confidence interval, 81.0-94.3%) for those 7-8 years of age. The smoothed curve of age-specific seroprevalence suggested that the steepest rate of increase occurred between 1 and 8 years of age, followed by a considerable slowing in the rate of increase, reaching a prevalence of approximately 95% by age 30. Varicella seroprevalence rates were similar for the samples referred for the 4 clinical indications, as follows: allergies, 76.2%; respiratory infections, 74.0%; herpes virus infections excluding varicella, 73.3%; endocrinologic tests, 73.7% (P = 0.84). CONCLUSIONS: Most varicella-zoster virus infections occur during early childhood. Seroprevalence rates reach approximately 50% by 4 years of age and approximately 90% by 8 years. Therefore, the best strategy to reduce the prevalence of wild-type varicella-zoster virus in the French population would be to immunize children 12-18 months of age, as is currently performed in the United States.
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About 90% of cases of hemorrhagic uremic syndrome (HUS) occur in early childhood and most frequently are preceded by bloody diarrhea due to shiga-like toxin (SLT) producing Escherichia coli. We report a case of a newborn girl presenting with bloody diarrhea on her 7th day of life. Acute renal failure, severe arterial hypertension and hemolytic anemia were detected and prompt peritoneal dialysis and antihypertensive therapy were required. The girl had several episodes of seizures, necessitating intravenous phenobarbital. Transfontanel ultrasonography 48 h after disease onset was normal, whereas, MRI investigation 10 days later revealed severe ischemic lesions with beginning cystic encephalopathy. Renal function recovered and only very moderate tubular dysfunction remained. Serum analysis of factor H, von Willebrand factor protease, homocystinemia, proteins C and S, and antithrombin III were all normal. Mutation analysis of factor V Leiden, factor II, and methyltetrahydrofolate-reductase were normal. E. coli 0157:H7 and SLT 2 were detected in the stool. SLT 2 was also found in the mother's stool. This is the first report of mother-to-child transmission of SLT-producing E. coli.
Chronic granulomatous disease is an inherited disorder in which phagocytes lack a functional NADPH oxidase and so cannot generate superoxide anions (O(2) (-)). The most common form is caused by mutations in CYBB encoding gp91 phox, the heavy chain of flavocytochrome b(558) (XCGD). We investigated 11 male patients and their families suspected of suffering from X-linked CGD. These XCGD patients were classified as having different variants (X91(0), X91(-) or X91(+)) according to their cytochrome b(558) expression and NADPH oxidase activity. Nine patients had X91(0) CGD, one had X91(-) CGD and one had X91(+) CGD. Six mutations in CYBB were novel. Of the four new X91(0) CGD cases, three were point mutations: G65A in exon 2, G387T in exon 5 and G970T in exon 9, leading to premature stop codons at positions Try18, Try125 and Glu320, respectively, in gp91 phox. One case of X91(0) CGD originated from a new 1005G deletion detected in exon 9. Surprisingly, four nonsense mutations in exon 5 led to the generation of two mRNAs, one with a normal size containing the mutation and the other in which exon 5 had been spliced. A novel X91(-) CGD case with low gp91 phox expression was diagnosed. It was caused by an 11-bp deletion in the linking region between exon 12 and intron 12, activating a new cryptic site. Finally, a new X91(+) CGD case was detected, characterized by a missense mutation Leu505Arg in the potential NADPH-binding site of gp91 phox. No clear correlation between the severity of the clinical symptoms and the sub-type of XCGD could be established.
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BACKGROUND: The aim of this study was to determine the burden of influenza-related diseases in children 0 to 11 months of age during the peak of the 2001 to 2002 influenza epidemic. METHODS: This was a prospective study at the Pediatric Emergency Department of Edouard Herriot tertiary teaching hospital in Lyon, France. The study included 304 infants 0 to 11 months of age. Consecutive patients were systematically enrolled during the 4 weeks of the influenza epidemic peak (Weeks 3 to 6, 2002). Influenza viruses were detected by antigen detection and virus culture from nasal swabs. Structured telephone interviews were conducted on Days 8 and 15 after virus detection. There was also a 6-month survey into the medicoadministrative database to detect late complications that required delayed hospitalization of influenza-positive children. RESULTS: Influenza virus was detected in 99 (33%) of 304 patients (A/H3N2 in 30% and B in 3%). Nonrespiratory symptoms were the dominant clinical manifestations in 30% of influenza-positive children. One child with influenza presented with febrile seizures. Twenty (20%) children with influenza were hospitalized. Parents reported recovery from the illness in 63 and 94% of children on Days 8 and 15, respectively. The median length of an influenza episode was 8 days. CONCLUSIONS: Our results confirm the high prevalence of influenza-related morbidity in infants during the epidemic peak. One child in three consulting to the pediatric emergency room had a virologically confirmed influenza infection regardless of the body temperature. Every fifth child with influenza was admitted to hospital, which corresponds to an admission rate of 237 per 100 000 children 0 to 11 months of age.
Valacyclovir was administered to 28 immunocompromised children (ages 5-12 years) to obtain preliminary pharmacokinetic and safety information. Patients were randomized to valacyclovir regimens of 250 mg (9.4-13.3 mg/kg) or 500 mg (13.9-27.0 mg/kg) twice daily or 500 mg (13.2-21.7 mg/kg) 3 times a day. Acyclovir pharmacokinetics were evaluated at steady state. Valacyclovir was rapidly absorbed and converted to acyclovir. Mean (+/-SD) acyclovir peak concentrations from 250 mg and 500 mg valacyclovir were 4.11+/-1.41 and 5.19+/-1.96 microg/mL, respectively. Corresponding single dose area-under-curve values were 12.14+/-6.60 and 14.49+/-4.69h microg/mL. By using historical data for intravenous acyclovir as reference, the overall estimate of acyclovir bioavailability from valacyclovir was 48%, 2- to 4-fold greater than for oral acyclovir. In general, adverse events were not attributable to valacyclovir and were consistent with disease-related expectations and concomitant therapies. Dosage options for using valacyclovir in children are discussed.
To characterize the clinical and bacteriologic characteristics of community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) infections, we reviewed 14 cases that were diagnosed in previously healthy patients during an 18-month period in France. Eleven patients had skin or soft-tissue infections. Two patients died of CA-MRSA necrotizing pneumonia. A case of pleurisy occurred in a child who acquired CA-MRSA from his mother, who had a breast abscess. The Panton-Valentine leukocidin genes and the lukE-lukD leukocidin genes were detected in all 14 isolates. The clonal origin of all of the isolates was demonstrated on the basis of their pulsotypes and antibiotic resistance profiles. All isolates had an agr3 allele. The combination of the Panton-Valentine leukocidin determinant (which encodes a virulence factor for primary skin infection and pneumonia) with the mecA gene (which confers antibiotic resistance and epidemicity) appears to have created a superadapted S. aureus strain that is spreading in the community.
BACKGROUND: Between 1986 and 1998, eight cases of community-acquired pneumonia due to Staphylococcus aureus strains carrying the gene for the Panton-Valentine leukocidin (PVL) were recorded in France, six of which were fatal. We aimed to assess the clinical features of these eight cases, and those of other cases identified prospectively, and to compare them with the characteristics of patients with pneumonia caused by PVL-negative strains. METHODS: We compared eight retrospective and eight prospective cases of PVL-positive S aureus pneumonia with 36 cases of PVL-negative S aureus pneumonia. For all patients, we recorded age, length of hospital stay, risk factors for infection, signs and symptoms, laboratory findings, antibiotic treatment, and serial radiological findings. FINDINGS: Median age was 14.8 years (IQR 5.4-24.0) for the PVL-positive patients and 70.1 years (59.2-81.4) for the others (p=0.001). Influenza-like illness had occurred during the 2 days before admission in 12 of the 16 PVL-positive patients, but in only three of 33 PVL-negative patients (p<0.001). PVL-positive infections were more often marked by: temperature greater than 39 degrees C (p=0.01), heart rate above 140 beats per min (p=0.02), haemoptysis (p=0.005), onset of pleural effusion during hospital stay (p=0.004), and leucopenia (p=0.001). The survival rate 48 h after admission was 63% for the PVL-positive patients and 94% for PVL-negative individuals (p=0.007). Histopathological examination of lungs at necropsy from three cases of necrotising pneumonia associated with PVL-positive S aureus showed extensive necrotic ulcerations of the tracheal and bronchial mucosa and massive haemorrhagic necrosis of interalveolar septa. INTERPRETATION: PVL-producing S aureus strains cause rapidly progressive, haemorrhagic, necrotising pneumonia, mainly in otherwise healthy children and young adults. The pneumonia is often preceded by influenza-like symptoms and has a high lethality rate.
Two vaccines against varicella are now being licensed in France, both deriving from the Oka strain. Seroconversion has been obtained in almost 100% of the cases after one dose in toddlers and children, and two doses in adolescents and adults. Efficacy has been mainly established from the US experience, where a universal immunisation programme of children aged > 12 months with a catch-up for susceptible adolescents and adults was begun in 1995. The incidence of varicella has decreased by about 85% over all age groups. The safety of the vaccine is good, and most adverse events are represented by fever, reactions at the injection site and varicella-like rashes. For the time being, France has adopted restrictive recommendations for the use of this vaccine because of uncertainties with respect to the duration of protection, a shift of the disease towards older age and the potential increase of the incidence of herpes-zoster.