Introduction. – L’artérite inflammatoire mésentérique est rare au cours de la maladie de Horton, l’analyse de la littérature ne nous ayant permis ’en recenser que 31 cas. Nous en rapportons deux nouvelles observations. Observations. – Il s’agit de deux hommes, qui présentent des signes généraux (n = 2), des douleurs abdominales (n = 1), des symptômes orientant ers une maladie de Horton (n = 1). Le diagnostic de l’atteinte artérielle mésentérique est porté par angioscanner, qui objective un épaississement irconférentiel et régulier de la paroi de l’artère mésentérique supérieure. Lors du suivi, l’angioscanner montre une amélioration des lésions rtérielles mésentériques chez les deux patients. Conclusion. – Notre travail montre que l’angioscanner est un examen utile pour dépister les atteintes artérielles mésentériques de la maladie e Horton. Il suggère également l’intérêt de l’angioscanner dans le suivi des localisations mésentériques de la maladie ; de fait, cet examen, en uthentifiant l’amélioration des lésions artérielles mésentériques nous a été utile pour guider le traitement des patients. 2008 Elsevier Masson SAS. Tous droits réservés.

Introduction. - Mesenteric involvement has been rarely reported in giant cell arteritis (GCA). Our literature search using the Medline database I (1966-2008). reviewing all articles in English and French languages identified only 3 1 cases of mesenteric ischemia related to GCA. We report two additional cases.Case reports. - We report two men with GCA. At diagnosis of GCA-associated mesenteric involvement, patients exhibited: fever/fatigue (n = 2), abdominal complaints (it = 1). clinical sips of GCA (it = 1). In both patient,,, abdominal CT-scan showed Circumferential halo around the Superior mesenteric artery. At systematic follow-up. CT-scan revealed improvement of mesenteric damage in both patients.Conclusion. - Our study indicates that CT-scan is it useful technique in diagnosis of GCA-associated mesenteric involvement. Furthermore. we suggest that CT-scan may also be helpful in both the monitoring and the medical management of GCA-related mesenteric artery involvement. (c) 2008 Elsevier Masson SAS.

Le purpura traduit une extravasation des hématies au sein du derme. L'aspect du purpura est un élément d'orientation diagnostique : purpura pétéchial ou ecchymotique, purpura infiltré, purpura nécrotique. Les purpuras thrombopéniques sont fréquents et se manifestent par un purpura pétéchial ou ecchymotique. Les thrombopénies périphériques (myélogramme normal) relèvent de causes infectieuses (virales ou bactériennes), médicamenteuses, auto-immunes, ou sont idiopathiques (purpura thrombopénique idiopathique). Elles peuvent s'intégrer dans des tableaux graves de coagulation intravasculaire disséminée (CIVD) ou de purpura fulminans. Les purpuras thrombopéniques d'origine médullaire, par insuffisance de production, relèvent de diverses causes, constitutionnelles ou acquises. Les purpuras thrombopathiques sont plus rares. Une fragilité vasculaire peut entraîner un purpura ecchymotique au moindre traumatisme (purpura de Bateman de la peau sénescente, scorbut, corticothérapie au long cours). Les purpuras nécrotiques, associés généralement à un livedo inflammatoire et à des nécroses cutanées, doivent faire rechercher une pathologie thrombotique (thromboses d'origine plaquettaire, intolérance à l'héparine, syndromes myéloprolifératifs, pathologies thrombophiliques, thrombi d'origine infectieuse) ou embolique (embolies graisseuses, de cristaux de cholestérol, myxome). Les purpuras infiltrés doivent faire pratiquer une biopsie cutanée à la recherche d'une vasculite. Les purpuras pigmentés constituent des entités anatomocliniques individualisées, d'évolution bénigne mais chronique, et d'étiologie indéterminée. Certaines dermatoses peuvent comporter, dans leur expression, une composante purpurique (urticaire, toxidermies, érysipèle, parapsoriasis). Certains tableaux s'individualisent enfin par leur topographie (purpura papuleux en gants et chaussettes) ou par leur contexte (syndrome de Gardner et Diamond). Les formes de l'enfant comportent des entités individualisées : purpura fulminans néonatal (traduisant un déficit en protéine S ou en protéine C), purpura rhumatoïde, œdème aigu hémorragique du nourrisson.Purpura is the consequence of a dermal extravasation of red cells. The purpura presentation is relevant for the diagnostic orientation: petechial purpura, ecchymoses, infiltrated or necrotic purpura. Thrombocytopenia is a frequent cause of purpura and induces petechial purpura or ecchymoses. Thrombocytopenia with normal medullar analysis may be due to infection (viral or bacterial), drugs, auto-immune disease or is idiopathic (idiopathic thrombocytopenic purpura). Thrombocytopenia may be one of the elements of severe disseminated intravascular coagulation or purpura fulminans. Decreased production of platelets may be due to diverse bone marrow diseases, congenital or acquired. Abnormal platelet functions are less frequently observed. Skin aging, vitamin C deficiency, or prolonged corticoid therapy may induce ecchymotic purpura due to frail vascular walls. Necrotic purpura, generally associated with inflammatory livedo and skin necrosis, may be due to microvascular thrombosis (platelet plugs (heparin, myeloproliferative diseases with thrombocytosis), occlusion due to infective agents growing in vessels, alterations in coagulation control (protein C or S deficiency, antiphospholipids)) or embolization (fat embolization, cholesterol emboli, myxoma). Palpable (infiltrated) and inflammatory pupuras require skin biopsy seeking leukocytoclastic vasculitis. Chronic pigmented purpuras represent a group of characteristic anatomo-clinical entities, of chronic but benign evolution. Pathogenesis is unknown. Some dermatosis may be purpuric (urticaria, drug reactions, erysipelas, pityriasis lichenoides). Some purpuras are characterized by their topography (socks and gloves syndrome) or their context (Gardner-Diamond syndrome). Pediatric entities are neonatal purpura fulminans (protein S or C deficiency), Henoch-Schonlein purpura, acute hemorrhagic oedema of childhood.

ABSTRACT RB49 is a virulent bacteriophage that infects Escherichia coli. Its virion morphology is indistinguishable from the well-known T-even phage T4, but DNA hybridization indicated that it was phylogenetically distant from T4 and thus it was classified as a pseudo-T-even phage. To further characterize RB49, we randomly sequenced small fragments corresponding to about 20% of the ≈170-kb genome. Most of these nucleotide sequences lacked sufficient homology to T4 to be detected in an NCBI BlastN analysis. However, when translated, about 70% of them encoded proteins with homology to T4 proteins. Among these sequences were the numerous components of the virion and the phage DNA replication apparatus. Mapping the RB49 genes revealed that many of them had the same relative order found in the T4 genome. The complete nucleotide sequence was determined for the two regions of RB49 genome that contain most of the genes involved in DNA replication. This sequencing revealed that RB49 has homologues of all the essential T4 replication genes, but, as expected, their sequences diverged considerably from their T4 homologues. Many of the nonessential T4 genes are absent from RB49 and have been replaced by unknown sequences. The intergenic sequences of RB49 are less conserved than the coding sequences, and in at least some cases, RB49 has evolved alternative regulatory strategies. For example, an analysis of transcription in RB49 revealed a simpler pattern of regulation than in T4, with only two, rather than three, classes of temporally controlled promoters. These results indicate that RB49 and T4 have diverged substantially from their last common ancestor. The different T4-type phages appear to contain a set of common genes that can be exploited differently, by means of plasticity in the regulatory sequences and the precise choice of a large group of facultative genes.

ABSTRACT We examined a number of bacteriophages with T4-type morphology that propagate in different genera of enterobacteria, Aeromonas , Burkholderia, and Vibrio . Most of these phages had a prolate icosahedral head, a contractile tail, and a genome size that was similar to that of T4. A few of them had more elongated heads and larger genomes. All these phages are phylogenetically related, since they each had sequences homologous to the capsid gene (gene 23 ), tail sheath gene (gene 18 ), and tail tube gene (gene 19 ) of T4. On the basis of the sequence comparison of their virion genes, the T4-type phages can be classified into three subgroups with increasing divergence from T4: the T-evens, pseudoT-evens, and schizoT-evens. In general, the phages that infect closely related host species have virion genes that are phylogenetically closer to each other than those of phages that infect distantly related hosts. However, some of the phages appear to be chimeras, indicating that, at least occasionally, some genetic shuffling has occurred between the different T4-type subgroups. The compilation of a number of gene 23 sequences reveals a pattern of conserved motifs separated by sequences that differ in the T4-type subgroups. Such variable patches in the gene 23 sequences may determine the size of the virion head and consequently the viral genome length. This sequence analysis provides molecular evidence that phages related to T4 are widespread in the biosphere and diverged from a common ancestor in acquiring the ability to infect different host bacteria and to occupy new ecological niches.

Sequence analysis of a 10-kb region of the genome of the marine cyanomyovirus S-PM2 reveals a homology to coliphage T4 that extends as a contiguous block from gene (g)18 to g23. The order of the S-PM2 genes in this region is similar to that of T4, but there are insertions and deletions of small ORFs of unknown function. In T4, g18 codes for the tail sheath, g19, the tail tube, g20, the head portal protein, g21, the prohead core protein, g22, a scaffolding protein, and g23, the major capsid protein. Thus, the entire module that determines the structural components of the phage head and contractile tail is conserved between T4 and this cyanophage. The significant differences in the morphology of these phages must reflect the considerable divergence of the amino acid sequence of their homologous virion proteins, which uniformly exceeds 50%. We suggest that their enormous diversity in the sea could be a result of genetic shuffling between disparate phages mediated by such commonly shared modules. These conserved sequences could facilitate genetic exchange by providing partially homologous substrates for recombination between otherwise divergent phage genomes. Such a mechanism would thus expand the pool of phage genes accessible by recombination to all those phages that share common modules.

The adsorption specificity of the T-even phages is determined by the protein sequence near the tip of the long tail fibers. These adhesin sequences are highly variable in both their sequence and specificity for bacterial receptors. The tail fiber adhesin domains are located in different genes in closely related phages of the T-even type. In phage T4, the adhesin sequence is encoded by the C-terminal domain of the large tail fiber gene (gene 37), but in T2, the adhesin is a separate gene product (gene 38) that binds to the tip of T2 tail fibers. Analysis of phage T6 and Ac3 sequences reveals additional variant forms of this locus. The tail fiber host specificity determinants can be exchanged, although the different loci have only limited homology. Chimeric fibers can be created by crossovers either between small homologies within the structural part of the fiber gene or in conserved motifs of the adhesin domain. For example, the T2 adhesin determinants are flanked by G-rich DNA motifs and exchanges involving these sequences can replace the specificity determinants. These features of the distal tail fiber loci genetically link their different forms and can mediate acquisition of diverse host range determinants, including those that allow it to cross species boundaries and infect taxonomically distant hosts.

Polymerase chain reaction analysis of a large collection of bacteriophages with T-even morphology revealed four phages that are distantly related to all the others. The genomes of these pseudo T-even phages hybridized under stringent conditions to only a limited portion of the T4 genome that encodes virus head, head-to-tail joining and contractile tail genes. Except for this region, no extensive hybridization was detected between most pairs of the different pseudo T-even genomes. Sequencing of this conserved region of the pseudo T-even phage RB49 revealed substantial nucleotide sequence divergence from T4 (∼30% to 40%), and random genomic sequencing of this phage indicated that more than a third of its sequences had no detectable homology to T4. Among those sequences related to the T-even genes were virion structural components including the constituents of the phage base plate. Only a few sequences had homology to T4 early functions; these included ribonucleotide diphosphatase reductase, DNA ligase and the large subunit of DNA topoisomerase. The genomes of the pseudo T-even phage were digested by restriction enzymes that are unable to digest the T-even DNAs which contain glucosylated hydroxymethyl-cytosine residues. This suggests that only limited nucleotide modifications must be present in the pseudo T-even genomes. Conservation of much of the morphogenetic region of these diverse phage genomes may reflect particularly strong sequence constraints on these gene products. However, other explanations are considered, including the possibility that the various morphogenetic segments were acquired by the pseudo T-even genomes by modular evolution. These results support the notion that phage evolution may proceed within a network of both closely and distantly related genomes.

The adsorption specificity of T4 is determined by the tip of the gene 37 tail fibers which bind to receptors on the bacterial surface. T4 infects only Escherichia coli and closely related Shigella species, but rare host range mutants can be isolated that infect Yersinia pseudotuberculosis I, an evolutionally distant bacterium. Some of these mutations result in amino acid residue substitutions in the C-terminal portion of gene 37, but others involve unequal exchanges between a series of sequence motifs (His boxes) in the same region. The duplication or mutational alteration of this segment apparently suffices for phage adsorption to a Yersinia receptor. It is suggested that recombination between the His box sequences can generate diversity in phage host range by shuffling receptor recognition domains.

We have compared the genomes of 49 bacteriophages related to T4. PCR analysis of six chromosomal regions reveals two types of local sequence variation. In four loci, we found only two alternative configurations in all the genomes that could be analyzed. In contrast, two highly polymorphic loci exhibit variations in the number, the order and the identity of the sequences present. In phage T4, both highly polymorphic loci encode internal proteins (IPs) that are encapsidated in the phage particle and injected with the viral DNA. Among the various T4‐related phages, 10 different ORFs have been identified in the IP loci; their amino acid sequences have the characteristics of internal proteins. At the beginning of each of these coding sequences is a highly conserved 11 amino acid leader motif. In addition, both 5′ and 3′ to most of these ORFs, there is a approximately 70 bp sequence that contains a T4 early promoter sequence with an overlapping inversely repeated sequence. The homologies within these flanking sequences may mediate the recombinational shuffling of the IP sequences within the locus. A role for the new IP‐like sequences in determining the phage host range is proposed since such a role has been previously demonstrated for the IP1 gene of T4.

The cell-cycle parameters of an Escherichia coli strain expressing essential division gene ftsZ at one-fifth of its normal level, because of antisense regulation by DicF RNA, have been analysed. Inhibition of FtsZ expression affects neither the generation time nor the replication initiation mass, the C period, or the constriction period, but it does dramatically retard the initiation of constriction relative to replication termination. Separation of the nucleoids is equally postponed, indicating that division is not coupled to termination of replication, but to partitioning. The severe inhibition of nucleoid separation by DicF RNA, and its suppression by overproduction of FtsZ, suggest a role for FtsZ in the control of separation, and consequently in the coupling of separation and division. We suggest that the normal pattern of nucleoid separation previously found in cells deficient in ftsZ function was a consequence of the loss of a negative effect exerted by FtsZ on separation. In agreement with this view, we find that nucleoid separation is temporarily inhibited after arrest of FtsZ synthesis, but is later resumed as FtsZ is further diluted into the elongating filaments.

We show that the 53-nucleotide RNA molecule encoded by gene dicF blocks cell division in Escherichia coli by inhibiting the translation of ftsZ mRNA. Such a role for dicF had been predicted on the basis of the complementarity of DicF RNA with the ribosome-binding region of the ftsZ mRNA. An analysis of ftsZ expression at its chromosomal locus, and of an ftsZ-lacZ translational fusion controlled by promoters ftsZ1p and ftsZ2p only, indicates that ftsZ is not autoregulated. Partial inhibition of FtsZ synthesis leads to increased cell size. However, the number of FtsZ molecules per cell can be reduced threefold without affecting the division rate significantly. Our results suggest that septation is not triggered by a fixed number of newly synthesized FtsZ molecules per cell.

Proper positioning of division sites in Escherichia coli requires balanced expression of minC, minD, and minE gene products. Previous genetic analysis has shown that either MinD or an apparently unrelated protein, DicB, cooperates with MinC to inhibit division. We have isolated and sequenced minC mutations that suppress division inhibition caused by overproduction of either DicB or MinD proteins. Most missense mutations were located in the amino acid 160 to 200 region of MinC (231 amino acids). Some mutations exhibited preferential resistance to one or the other coinhibitor, suggesting that two distinct proteins, possibly MinD and DicB themselves, interact in slightly different manners with the same region of MinC to promote division inhibition.