Evolution of antimicrobial resistance and serotype distribution of Streptococcus pneumoniae isolated from children with invasive and noninvasive pneumococcal diseases in Algeria from 2005 to 2012.

Pneumococcal infections are a major cause of morbidity and mortality in developing countries. The introduction of pneumococcal conjugate vaccines (PCVs) has dramatically reduced the incidence of pneumococcal diseases. PCVs are not currently being used in Algeria. We conducted a prospective study from 2005 to 2012 in Algeria to determine antimicrobial drug resistance and serotype distribution of Streptococcus pneumoniae from children with pneumococcal disease. Among 270 isolated strains from children, 97 (36%) were invasive disease; of these, 48% were not susceptible to penicillin and 53% not susceptible to erythromycin. A high rate of antimicrobial nonsusceptibility was observed in strains isolated from children with meningitis. The serotype distribution from pneumococci isolated from children with invasive infections was (by order of prevalence): 14, 1, 19F, 19A, 6B, 5, 3, 6A and 23F. Multidrug resistance was observed in serotypes 14, 19F, 19A and 6B. The vaccine coverage of serotypes isolated from children aged <5 years was 55.3% for PCV7, 71.1% for PCV10 and 86.8% for PCV13. Our results highlight the burden of pneumococcal disease in Algeria and the increasing S. pneumoniae antibiotic resistance. The current pneumococcal vaccines cover a high percentage of the circulating strains. Therefore, vaccination would reduce the incidence of pneumococcal disease in Algeria.

A Comparison between the hp-version of Finite Element Method with EIDORS for Electrical Impedance Tomography.

In this study, a hp-version of Finite Element Method (FEM) was applied for forward modeling in image reconstruction of Electrical Impedance Tomography (EIT). The EIT forward solver is normally based on the conventional Finite Element Method (h-FEM). In h-FEM, the polynomial order (p) of the element shape functions is constant and the element size (h) is decreasing. To have an accurate simulation with the h-FEM, a mesh with large number of nodes and elements is usually needed. In order to overcome this problem, the high order finite element method (p-FEM) was proposed. In the p-version, the polynomial order is increasing and the mesh size is constant. Combining the advantages of two previously mentioned methods, the element size (h) was decreased and the polynomial order (p) was increased, simultaneously, which is called the hp-version of Finite Element Method (hp-FEM). The hp-FEM needs a smaller number of nodes and consequently, less computational time and less memory to achieve the same or even better accuracy than h-FEM. The SNR value is 42db for hp-FEM and is 9db for h-FEM. The numerical results are presented and verified that the performance of the hp-version is better than of the h-version in image reconstruction of EIT.

Quantitative analysis of left ventricular performance from sequences of cardiac magnetic resonance imaging using active mesh model.

In this study, the local and global left ventricular function are estimated by fitting three-dimensional active mesh model (3D-AMM) to the initial sparse displacement which is measured from an establishing point correspondence procedure. To evaluate the performance of the algorithm, eight image sequences were used and the results were compared with those reported by other researchers. The findings were consistent with previously published values and the clinical evidence as well. The results demonstrated the superiority of the novel strategy with respect to formerly presented algorithm reported by author et al. Furthermore, the results are comparable to the current state-of-the-art methods.

RP1 protein truncating mutations predominate at the RP1 adRP locus.

PURPOSE: Recent reports have shown that the autosomal dominant retinitis pigmentosa (adRP) phenotype linked to the pericentric region of chromosome 8 is associated with mutations in a gene designated RP1. Screening of the whole gene in a large cohort of patients has not been undertaken to date. To assess the involvement and character of RP1 mutations in adRP, the gene was screened in a panel of 266 unrelated patients of British origin and a Pakistani family linked to this locus. METHODS: Patients exhibiting the adRP phenotype were screened for mutations in the four exons of the RP1 gene by heteroduplex analysis and direct sequencing. Linkage of the Pakistani family was achieved using microsatellite markers. Polymerase chain reaction (PCR) products were separated by nondenaturing polyacrylamide gel electrophoresis. Alleles were assigned to individuals, which allowed calculation of LOD scores. Microsatellite marker haplotyping was used to determine ancestry of patients carrying the same mutation. RESULTS: In the 266 British patients and 1 Pakistani family analyzed, 21 loss-of-function mutations and 7 amino acid substitutions were identified, some of which may also be disease-causing. The mutations, many of which were deletion or insertion events, were clustered in the 5' end of exon 4. Most mutations resulted in a premature termination codon in the mRNA. Haplotype analysis of nine patients carrying an R677X mutation suggested that these patients are not ancestrally related. CONCLUSIONS: RP1 mutations account for 8% to 10% of the mutations in our cohort of British patients. The most common disease-causing mechanism is deduced to be one involving the presence of a truncated protein. Mutations in RP1 have now been described in adRP patients of four ethnically diverse populations. The different disease haplotype seen in the nine patients carrying the same mutation suggests that this mutation has arisen independently many times, possibly due to a mutation hot spot in this part of the gene.

[An epidemiological study of health care seeking behavior of children under 5 years of age in Algeria: what lessons for improving the health care system?]. / Etude épidémiologique du recours aux soins curatifs des enfants de moins de 5 ans en Algérie: quelles leçons pour le système de santé?

In many developing countries, dissatisfaction with primary health care has been accompanied by inappropriate use of university teaching hospitals, frequently for benign health problems. This situation is often attributed to the user population who supposedly misunderstands the functioning of health systems. This article describes the health seeking process and outcome of consultations for under-five children in two geographic zones in Algeria (very different in their care networks, and in the socioeconomic and educational characteristics of their populations), using a representative sample of users of public and private health services. During 4 one-week periods in 1991, a cross-sectional study was carried out among families of children and the health personnel they consulted, in all the health structures in the 2 zones. A Franco-Algerian supervisory team prepared consensual definitions of both the seriousness and the urgency of the pathology, as well as of the appropriateness of the health care structure chosen for that condition. The analysis of 1560 consultations shows dysfunctions in the health seeking process: numerous "self-referrals" (94%); unjustified recourse to university hospitals in 29% of cases; important delays before consulting (> or = 1 week in 14% of cases); absence of the mother during the consultation; differences in the mode of recourse according to the child's sex (for equivalent seriousness and urgency, recourse is more frequent to the emergency room and university hospital for boys, but girls are more often hospitalized). Nonetheless, the Algerian supervisors of the research consider that the choice of the health care facility is appropriate in 91% of cases. At the service level, dysfunctions are equally frequent, especially the absence of the transfer of information on the child between different health care professionals. The primary preoccupation of parents is with accessibility (distance, cost), which leads to recommending the revitalizing of small first-line facilities, especially in rural areas, the more so because they are used and appreciated by families.

Refined genetic and physical positioning of the gene for Doyne honeycomb retinal dystrophy (DHRD).

Doyne honeycomb retinal dystrophy (DHRD) is a late-onset autosomal dominant disorder that causes degeneration of the retina and can lead to blindness. We have previously assigned DHRD to a 5-cM region of chromosome 2p16 between marker loci D2S2739 and D2S378. Using sequence-tagged sites (STSs), expressed sequence tags (ESTs) and polymorphic markers within the DHRD region, we have identified 18 yeast artificial chromosomes (YACs) encompassing the DHRD locus, spanning approximately 3 Mb. The YAC contig was constructed by STS content mapping of these YACs and incorporates 13 STSs, including four genes and six polymorphic marker loci. We also report the genetic mapping of two families with a dominant drusen phenotype to the DHRD locus, and genetic refinement of the disease locus to a critical interval flanked by microsatellite marker loci D2S2352 and D2S2251, a distance of approximately 700 kb. These studies exclude a number of candidate genes and provide a resource for construction of a transcriptional map of the region, as a prerequisite to identification of the DHRD disease-causing gene and genes for other diseases mapping in the region, such as Malattia leventinese and Carney complex.

Assessment of the phenotypic range seen in Doyne honeycomb retinal dystrophy.

OBJECTIVE: Using molecular genetics as the basis for diagnosis, to assess the phenotype in the family originally described as having dominantly inherited Doyne honeycomb retinal dystrophy (DHRD) linked to chromosome 2p16. DESIGN: Clinical examination including fluorescein angiography was undertaken in 107 family members. Nine affected patients underwent electroretinography, perimetry, dark adaptometry, color-contrast sensitivity measurement, and autofluorescent fundus imaging. PATIENTS: The disease-associated haplotype used to allocate disease status was based on our further refinement of the DHRD locus to between loci D2S2739 and D2S378. The study identified 50 affected patients. In addition, previously published information on a further 8 individuals was used. The study population represented 6 generations of a 9-generation pedigree. RESULTS: Three types of deposits were seen: large, soft drusen at the macula and abutting the optic nerve head; small, hard deposits that in some patients radiated from the macula; and autofluorescent deposits. Most younger affected individuals exhibited small hard drusen only at the macula and had normal visual function. Information on 2 patients suggested that DHRD can be a cause of childhood-onset blindness. Advanced disease was associated with severe visual loss and posterior pole atrophy without signs of drusen. Advanced age was not invariably associated with severe visual loss. CONCLUSIONS: Previously identified characteristics of DHRD were confirmed and new features identified. Contrary to previous reports, the constancy and severity of radial (basal laminar) drusen seen clinically are the only features that can be used to differentiate between DHRD and malattia leventinese. The highly variable phenotype suggests that the influence of the DHRD-mutant gene may be modulated by other genetic and/or environmental factors.

The gene responsible for autosomal dominant Doyne's honeycomb retinal dystrophy (DHRD) maps to chromosome 2p16.

Degeneration in the macula region of the retina is a feature of a heterogeneous group of inherited, progressive disorders, causing blinding visual impairment. Autosomal dominant Doyne's honeycomb retinal dystrophy (DHRD) is characterised by the presence of drusen deposits at the level of Bruch's membrane in the macula and around the edge of the optic nerve head. We have studied 63 members of a large, nine-generation British pedigree by linkage analysis. Two-point analysis showed significant linkage to nine markers on the short arm of chromosome 2, a region overlapping that recently reported to be linked to Malattia leventinese. A maximum lod score (Zmax) of 7.29 (theta = 0.0) was obtained at marker locus D2S2251. Haplotype analysis of recombination events localised the disease to a 5 cM region between marker loci D2S2316 and D2S378. Striking clinical similarities between DHRD and the more common condition age-related macular degeneration (ARMD) suggest that the disease gene at this locus could be considered as the most likely candidate in future studies on ARMD.

[Acute respiratory infections of viral origin in the children of Algiers, Algeria based on a seroepidemiological study]. / Les infections respiratoires aiguës d'origine virale chez les enfants à Alger--Algérie, à travers une étude séro-épidémiologique.

401 double serum samples from 0 to 14 year old children with acute respiratory diseases (ARD) were analysed in view to establish the viral etiology. 198 (49.4%) out of the 401 were positive. The syncytial respiratory virus (SRV) was the most frequent (29.8%) among the positives, followed by the parainfluenzae virus type 3 (24.7), the influenza A virus (23.7%), the parainfluenzae type 1 (8.5%), the influenza B (7%) and the parainfluenza type 2 (2%). Seven samples out of 109 were positive for adenovirus. The SRV infections were very frequent before one year of age and after six. The parainfluenza virus type 3 was found mostly during the second year of life and was different in this from the types 1 and 2 prevalent after the age of six. The SRV is responsible for subglottic ARD (73%), as well as the parainfluenza virus type 3 (68.5%), the influenza virus types A (69%) and B (61.5%). On the contrary, the parainfluenza viruses types 1 (70%) and 2 (67%) attacked especially the upper respiratory tract. Studies were also worked out on the effects of season, sex, antibiotherapy, as well as on the viruses most incriminated in hospitalization.