scholarly journals Identification offusB-Mediated Fusidic Acid Resistance Islands in Staphylococcus epidermidis Isolates

2011 ◽  
Vol 55 (12) ◽  
pp. 5842-5849 ◽  
Author(s):  
Hsiao-Jan Chen ◽  
Jui-Chang Tsai ◽  
Wei-Chun Hung ◽  
Sung-Pin Tseng ◽  
Po-Ren Hsueh ◽  
...  
Keyword(s):  
Fusidic Acid ◽  
Staphylococcus Epidermidis ◽  
Acid Resistance ◽  
Nucleotide Position ◽  
Type I ◽  
Type Ii ◽  
Content Type ◽  
Type Iii ◽  
High Prevalence ◽  
Flanking Regions

ABSTRACTTo understand the high prevalence offusBgenes in fusidic acid-resistantStaphylococcus epidermidis, analysis of resistance elements in 34 isolates was performed. First, sequence analysis of theaj1-LP-fusBregion indicated that at least three types were present. Type I contained full-lengthaj1, type II contained a partialaj1truncated from nucleotide position 93 to 421, and type III contained a more truncatedaj1that retained only the last 37 bp. Isolates with type I or type IIaj1displayed slightly higher levels of resistance to fusidic acid (MICs, 8 to 32 μg/ml) than did those with type IIIaj1(MICs, 4 to 16 μg/ml). Subsequent sequencing of the flanking regions offusBfrom four selected isolates carrying different types ofaj1-LP-fusBregions revealed that thefusBgenes were all located on phage-related resistance islands (RIs), referred to as SeRIfusB-2793, SeRIfusB-704, SeRIfusB-5907, and SeRIfusB-7778, respectively. Among them, three islands (SeRIfusB-2793, SeRIfusB-704, and SeRIfusB-5907) were located downstream ofgroEL(corresponding to the 44-min position based onStaphylococcus aureuswhole genomic sequences), and one (SeRIfusB-7778) was located downstream ofrpsR(corresponding to the 8-min position). All of the RIs were inserted into integrase-recognizedattsites. Among 34 isolates, the insertion sites offusBRIs were mostly (28/34, 82%) located downstream ofgroELand two were located downstream ofrpsR, but four remained unidentified. The pulsotype distribution indicated thatfusB-containingS. epidermidisisolates were heterogeneous. In conclusion, thefusBresistance determinant inS. epidermidiswas highly associated with phage-related RIs. This is the first report offusBRI inS. epidermidis.

scholarly journals Phylogenetic and Structural Comparisons of the Three Types of Methyl Coenzyme M Reductase from Methanococcales and Methanobacteriales

2017 ◽  
Vol 199 (16) ◽  
Author(s):  
Tristan Wagner ◽  
Carl-Eric Wegner ◽  
Jörg Kahnt ◽  
Ulrich Ermler ◽  
Seigo Shima
Keyword(s):  
Active Site ◽  
Phylogenetic Analyses ◽  
Methanogenic Archaea ◽  
Methane Formation ◽  
Type I ◽  
Type Ii ◽  
Coenzyme M ◽  
Content Type ◽  
Type Iii ◽  
Methyl Coenzyme M Reductase

ABSTRACT The phylogenetically diverse family of methanogenic archaea universally use methyl coenzyme M reductase (MCR) for catalyzing the final methane-forming reaction step of the methanogenic energy metabolism. Some methanogens of the orders Methanobacteriales and Methanococcales contain two isoenzymes. Comprehensive phylogenetic analyses on the basis of all three subunits grouped MCRs from Methanobacteriales and Methanococcales into three distinct types: (i) MCRs from Methanobacteriales, (ii) MCRs from Methanobacteriales and Methanococcales, and (iii) MCRs from Methanococcales. The first and second types contain MCR isoenzymes I and II from Methanothermobacter marburgensis, respectively; therefore, they were designated MCR type I and type II and accordingly; the third one was designated MCR type III. For comparison with the known MCR type I and type II structures, we determined the structure of MCR type III from Methanotorris formicicus and Methanothermococcus thermolithotrophicus. As predicted, the three MCR types revealed highly similar overall structures and virtually identical active site architectures reflecting the chemically challenging mechanism of methane formation. Pronounced differences were found at the protein surface with respect to loop geometries and electrostatic properties, which also involve the entrance of the active-site funnel. In addition, the C-terminal end of the γ-subunit is prolonged by an extra helix after helix γ8 in MCR type II and type III, which is, however, differently arranged in the two MCR types. MCR types I, II, and III share most of the posttranslational modifications which appear to fine-tune the enzymatic catalysis. Interestingly, MCR type III lacks the methyl-cysteine but possesses in subunit α of M. formicicus a 6-hydroxy-tryptophan, which thus far has been found only in the α-amanitin toxin peptide but not in proteins. IMPORTANCE Methyl coenzyme M reductase (MCR) represents a prime target for the mitigation of methane releases. Phylogenetic analyses of MCRs suggested several distinct sequence clusters; those from Methanobacteriales and Methanococcales were subdivided into three types: MCR type I from Methanobacteriales, MCR type II from Methanobacteriales and Methanococcales, and the newly designated MCR type III exclusively from Methanococcales. We determined the first X-ray structures for an MCR type III. Detailed analyses revealed substantial differences between the three types only in the peripheral region. The subtle modifications identified and electrostatic profiles suggested enhanced substrate binding for MCR type III. In addition, MCR type III from Methanotorris formicicus contains 6-hydroxy-tryptophan, a new posttranslational modification that thus far has been found only in the α-amanitin toxin.

Prognostic significance of intracranial dissemination of glioblastoma multiforme in adults

2005 ◽  
Vol 102 (4) ◽  
pp. 622-628 ◽  
Author(s):  
Andrew T. Parsa ◽  
Scott Wachhorst ◽  
Kathleen R. Lamborn ◽  
Michael D. Prados ◽  
Michael W. McDermott ◽  
...  
Keyword(s):  
Glioblastoma Multiforme ◽  
Tumor Progression ◽  
Prognostic Significance ◽  
Type I ◽  
Type Ii ◽  
Content Type ◽  
Type Iii ◽  
Multifocal Lesions ◽  
Tumor Dissemination ◽  
Fine Print

Object. The clinical outcome and treatment of adult patients with disseminated intracranial glioblastoma multiforme (GBM) is unclear. The objective in the present study was to assess the prognostic significance of disseminated intracranial GBM in adults at presentation and at the time of tumor progression. Methods. Clinical data from 1491 patients older than 17 years and harboring a GBM that had been diagnosed between 1988 and 1998 at the University of California at San Francisco neurooncology clinic were retrospectively reviewed. Dissemination of the GBM (126 patients) was determined based on Gd-enhanced magnetic resonance images. Classification of dissemination was as follows: Type I, single lesion with subependymal or subarachnoid spread; Type II, multifocal lesions without subependymal or subarachnoid spread; and Type III, multifocal lesions with subependymal or subarachnoid spread. Subgroups of patients were compared using Kaplan—Meier curves that depicted survival probability. The median postprogression survival (PPS), defined according to neuroimaging demonstrated dissemination, was 37 weeks for Type I (23 patients), 25 weeks for Type II (50 patients), and 10 weeks for Type III spread (19 patients). Patients with dissemination at first tumor progression (52 patients) overall had a shorter PPS than those in a control group with local progression, after adjusting for age, Karnofsky Performance Scale score, and time from tumor diagnosis to its progression (311 patients). When analyzed according to tumor dissemination type, PPS was significantly shorter in patients with Type II (33 patients, p < 0.01) and Type III spread (11 patients, p < 0.01) but not in those with Type I spread (eight patients, p = 0.18). Conclusions. Apparently, the presence of intracranial tumor dissemination on initial diagnosis does not in itself preclude aggressive treatment if a patient is otherwise well. A single focus of GBM that later demonstrates Type I dissemination on progression does not have a worse prognosis than a lesion that exhibits only local recurrence.

Primary extradural meningiomas: a report on nine cases and review of the CT-era literature

2000 ◽  
Vol 93 (6) ◽  
pp. 940-950 ◽  
Author(s):  
Frederick F. Lang ◽  
O. Kenneth Macdonald ◽  
Gregory N. Fuller ◽  
Franco DeMonte
Keyword(s):  
Skull Base ◽  
Death Rate ◽  
Benign Tumors ◽  
Data Sets ◽  
Type I ◽  
Type Ii ◽  
Content Type ◽  
Type Iii ◽  
Clinical Records ◽  
Fine Print

Object. Primary meningiomas arising outside the intracranial compartment (primary extradural meningiomas [PEMs]) are rare tumors. To develop a better understanding of these tumors and to establish a comprehensive classification scheme for them, the authors analyzed a series of patients treated at the M. D. Anderson Cancer Center (MDACC) and reviewed all cases reported in the English-language literature since the inception of the use of computerized tomography (CT) scanning.Methods. Clinical records, results of radiographic studies, and histological slides were reviewed for all cases of PEM at MDACC. Demographic features, symptoms, tumor location, histological grade, and patient outcome were assessed in all cases. A comprehensive literature search identified 168 PEMs in 142 patients reported during the CT era. These reports were also analyzed for common features. Tumors for both data sets were classified as purely extracalvarial (Type I), purely calvarial (Type II), and calvarial with extracalvarial extension (Type III). Type II and Type III tumors were further categorized as convexity (C) or skull base (B) lesions.The incidence of PEMs at MDACC was 1.6%, which was consistent with the rate reported in the literature. In both data sets, the male/female ratio was nearly 1:1. The most common presenting symptom was a gradually expanding mass. The age of patients at diagnosis of PEM was bimodal, peaking during the second decade and during the fifth to seventh decades. In all MDACC cases and in 90% of those reported in the literature the PEMs were located in the head and neck. The majority of tumors originated in the skull (70%).In the MDACC series and in the literature review, the majority (67% and 89%, respectively) of tumors were histologically benign. Although fewer PEMs were malignant or atypical (33% at MDACC and 11% in the literature), their incidence was higher than that observed for primary intracranial meningiomas. Distant metastasis was not a common feature reported for patients with PEMs (6% in the literature).Outcome data were available in 96 of the cases culled from the CT-era literature. The combination of the MDACC data and the data obtained from the literature demonstrated that patients with benign Type IIB or Type IIIB lesions were more likely to experience recurrence than patients with benign Type IIC or Type IIIC tumors (26% compared with 0%, p < 0.05). The more aggressive atypical and malignant tumors were associated with a statistically significant higher death rate (29%) relative to benign tumors (4.8% death rate, p < 0.004).Conclusions. Defining a tumor as a PEM is dependent on the tumor's relation to the dura mater and the extent and direction of its growth. Classification of PEMs as calvarial or extracalvarial and as convexity or skull base lesions correlates well with clinical outcome.

scholarly journals A Novel Staphylococcal Cassette Chromosomal Element, SCCfusC, CarryingfusCandspeGin Fusidic Acid-Resistant Methicillin-Resistant Staphylococcus aureus

2013 ◽  
Vol 58 (2) ◽  
pp. 1224-1227 ◽  
Author(s):  
Yu-Tzu Lin ◽  
Jui-Chang Tsai ◽  
Hsiao-Jan Chen ◽  
Wei-Chun Hung ◽  
Po-Ren Hsueh ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Fusidic Acid ◽  
Methicillin Resistant Staphylococcus Aureus ◽  
Nucleotide Sequencing ◽  
Methicillin Resistant ◽  
Content Type ◽  
High Prevalence ◽  
Flanking Regions ◽  
Staphylococcal Cassette Chromosome

ABSTRACTA high prevalence offusC(16/46, 59%) was found in fusidic acid-resistant methicillin-resistantStaphylococcus aureusisolates collected from 2008 to 2010. Nucleotide sequencing offusCand flanking regions revealed a novel staphylococcal cassette chromosome (SCC) structure, SCCfusC, which was integrated intorlmHand located upstream from SCCmec. The SCCfusCelement containedspeG, which may contribute to the polyamine resistance.

scholarly journals New Structure of Phage-Related Islands CarryingfusBand a Virulence Gene in Fusidic Acid-Resistant Staphylococcus epidermidis

2013 ◽  
Vol 57 (11) ◽  
pp. 5737-5739 ◽  
Author(s):  
Hsiao-Jan Chen ◽  
Ya-Chun Chang ◽  
Jui-Chang Tsai ◽  
Wei-Chun Hung ◽  
Yu-Tzu Lin ◽  
...  
Keyword(s):  
Fusidic Acid ◽  
Staphylococcus Epidermidis ◽  
Virulence Gene ◽  
Leader Peptide ◽  
Nucleotide Sequencing ◽  
The Novel ◽  
Content Type ◽  
Putative Virulence Gene ◽  
Type Iv ◽  
Flanking Regions

ABSTRACTNucleotide sequencing of thefusB-flanking regions in two fusidic acid-resistantStaphylococcus epidermidisisolates with the type IVaj1-leader peptide (LP)-fusBstructure (lackingaj1) revealed that theirfusBgene was located on novel phage-related islands inserted downstream ofsmpBand are here referred to as SeRIfusB-3692and SePIfusB-857. The novel SePIfusB-857structure was followed by SeCI857, forming a composite pathogenicity island which contained a putative virulence gene,vapE. The linkage offusBandvapEmay contribute to bacterial adaption.

scholarly journals Characterization of a Novel Arginine Catabolic Mobile Element (ACME) and Staphylococcal Chromosomal CassettemecComposite Island with Significant Homology to Staphylococcus epidermidis ACME Type II in Methicillin-Resistant Staphylococcus aureus Genotype ST22-MRSA-IV

2011 ◽  
Vol 55 (5) ◽  
pp. 1896-1905 ◽  
Author(s):  
Anna C. Shore ◽  
Angela S. Rossney ◽  
Orla M. Brennan ◽  
Peter M. Kinnevey ◽  
Hilary Humphreys ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Staphylococcus Epidermidis ◽  
Mobile Element ◽  
Type I ◽  
Type Ii ◽  
Coagulase Negative Staphylococci ◽  
Methicillin Resistant ◽  
Content Type ◽  
Arginine Catabolic Mobile Element

ABSTRACTThe arginine catabolic mobile element (ACME) is prevalent among methicillin-resistantStaphylococcus aureus(MRSA) isolates of sequence type 8 (ST8) and staphylococcal chromosomal cassettemec(SCCmec) type IVa (USA300) (ST8-MRSA-IVa isolates), and evidence suggests that ACME enhances the ability of ST8-MRSA-IVa to grow and survive on its host. ACME has been identified in a small number of isolates belonging to other MRSA clones but is widespread among coagulase-negative staphylococci (CoNS). This study reports the first description of ACME in two distinct strains of the pandemic ST22-MRSA-IV clone. A total of 238 MRSA isolates recovered in Ireland between 1971 and 2008 were investigated for ACME using a DNA microarray. Twenty-three isolates (9.7%) were ACME positive, and all were either MRSA genotype ST8-MRSA-IVa (7/23, 30%) or MRSA genotype ST22-MRSA-IV (16/23, 70%). Whole-genome sequencing and comprehensive molecular characterization revealed the presence of a novel 46-kb ACME and staphylococcal chromosomal cassettemec(SCCmec) composite island (ACME/SCCmec-CI) in ST22-MRSA-IVh isolates (n= 15). This ACME/SCCmec-CI consists of a 12-kb DNA region previously identified in ACME type II inS. epidermidisATCC 12228, a truncated copy of the J1 region of SCCmectype I, and a complete SCCmectype IVh element. The composite island has a novel genetic organization, with ACME located withinorfXand SCCmeclocated downstream of ACME. One PVL locus-positive ST22-MRSA-IVa isolate carried ACME located downstream of SCCmectype IVa, as previously described in ST8-MRSA-IVa. These results suggest that ACME has been acquired by ST22-MRSA-IV on two independent occasions. At least one of these instances may have involved horizontal transfer and recombination events between MRSA and CoNS. The presence of ACME may enhance dissemination of ST22-MRSA-IV, an already successful MRSA clone.

scholarly journals Regulation of Coenzyme A Biosynthesis in the Hyperthermophilic Bacterium Thermotoga maritima

2016 ◽  
Vol 198 (14) ◽  
pp. 1993-2000 ◽  
Author(s):  
Takahiro Shimosaka ◽  
Hiroya Tomita ◽  
Haruyuki Atomi
Keyword(s):  
Coenzyme A ◽  
Feedback Inhibition ◽  
Thermotoga Maritima ◽  
Single Type ◽  
Type I ◽  
Type Ii ◽  
Pantothenate Kinase ◽  
Content Type ◽  
Type Iii ◽  
Hyperthermophilic Bacterium

ABSTRACTRegulation of coenzyme A (CoA) biosynthesis in bacteria and eukaryotes occurs through feedback inhibition targeting type I and type II pantothenate kinase (PanK), respectively. In contrast, the activity of type III PanK is not affected by CoA. As the hyperthermophilic bacteriumThermotoga maritimaharbors only a single type III PanK (Tm-PanK), here we examined the mechanisms that regulate CoA biosynthesis in this organism. We first examined the enzyme responsible for the ketopantoate reductase (KPR) reaction, which is the target of feedback inhibition in archaea. A classical KPR homolog was not present on theT. maritimagenome, but we found a homolog (TM0550) of the ketol-acid reductoisomerase (KARI) fromCorynebacterium glutamicum, which exhibits KPR activity. The purified TM0550 protein displayed both KPR and KARI activities and was designatedTm-KPR/KARI. WhenT. maritimacell extract was subjected to anion-exchange chromatography, the fractions containing high levels of KPR activity also displayed positive signals in a Western blot analysis using polyclonal anti-TM0550 protein antisera, strongly suggesting thatTm-KPR/KARI was the major source of KPR activity in the organism. The KPR activity ofTm-KPR/KARI was not inhibited in the presence of CoA. We thus examined the properties ofTm-PanK and the pantothenate synthetase (Tm-PS) of this organism.Tm-PS was not affected by CoA. Surprisingly however,Tm-PanK was inhibited by CoA, with almost complete inhibition in the presence of 400 μM CoA. Our results suggest that CoA biosynthesis inT. maritimais regulated by feedback inhibition targeting PanK, althoughTm-PanK is a type III enzyme.IMPORTANCEBacteria and eukaryotes regulate the biosynthesis of coenzyme A (CoA) by feedback inhibition targeting type I or type II pantothenate kinase (PanK). The hyperthermophilic bacteriumThermotoga maritimaharbors a single type III PanK (Tm-PanK), previously considered to be unaffected by CoA. By examining the properties of three enzymes involved in CoA biosynthesis in this organism, we found thatTm-PanK, although a type III enzyme, is inhibited by CoA. The results provide a feasible explanation of how CoA biosynthesis is regulated inT. maritima, which may also apply for other bacteria that harbor only type III PanK enzymes.

scholarly journals Type II Toxoplasma gondii Induction of CD40 on Infected Macrophages Enhances Interleukin-12 Responses

2014 ◽  
Vol 82 (10) ◽  
pp. 4047-4055 ◽  
Author(s):  
Pedro Morgado ◽  
Dattanand M. Sudarshana ◽  
Lanny Gov ◽  
Katherine S. Harker ◽  
Tonika Lam ◽  
...  
Keyword(s):  
Toxoplasma Gondii ◽  
Transcript Level ◽  
Forward Genetics ◽  
Interleukin 12 ◽  
Type I ◽  
Dependent Manner ◽  
Type Ii ◽  
Content Type ◽  
Type Iii ◽  
Infected Cells

ABSTRACTToxoplasma gondiiis an obligate intracellular parasite that can cause severe neurological disease in infected humans. CD40 is a receptor on macrophages that plays a critical role in controllingT. gondiiinfection. We examined the regulation of CD40 on the surface ofT. gondii-infected bone marrow-derived macrophages (BMdMs).T. gondiiinduced CD40 expression both at the transcript level and on the cell surface, and interestingly, the effect was parasite strain specific: CD40 levels were dramatically increased in type IIT. gondii-infected BMdMs compared to type I- or type III-infected cells. Type II induction of CD40 was specific to cells harboring intracellular parasites and detectable as early as 6 h postinfection (hpi) at the transcript level. CD40 protein expression peaked at 18 hpi. Using forward genetics with progeny from a type II × type III cross, we found that CD40 induction mapped to a region of chromosome X that included the gene encoding the dense granule protein 15 (GRA15). Using type I parasites stably expressing the type II allele ofGRA15(GRA15II), we found that type I GRA15IIparasites induced the expression of CD40 on infected cells in an NF-κB-dependent manner. In addition, stable expression of hemagglutinin-tagged GRA15IIin THP-1 cells resulted in CD40 upregulation in the absence of infection. Since CD40 signaling contributes to interleukin-12 (IL-12) production, we examined IL-12 from infected macrophages and found that CD40L engagement of CD40 amplified the IL-12 response in type II-infected cells. These data indicate that GRA15IIinduction of CD40 promotes parasite immunity through the production of IL-12.

scholarly journals Differential Gene Expression in Mice Infected with Distinct Toxoplasma Strains

2011 ◽  
Vol 80 (3) ◽  
pp. 968-974 ◽  
Author(s):  
Rachel D. Hill ◽  
Julia S. Gouffon ◽  
Arnold M. Saxton ◽  
Chunlei Su
Keyword(s):  
Gene Expression ◽  
Parasite Burden ◽  
Type I ◽  
Type Ii ◽  
Gene Expression Response ◽  
Content Type ◽  
Type Iii ◽  
Clonal Type ◽  
Expression Response ◽  
Macrophage Populations

Toxoplasma gondiiis the causative agent of toxoplasmosis in human and animals. In a mouse model,T. gondiistrains can be divided into three groups, including the virulent, intermediately virulent, and nonvirulent. The clonal type I, II, and IIIT. gondiistrains belong to these three groups, respectively. To better understand the basis of virulence phenotypes, we investigated mouse gene expression responses to the infection of differentT. gondiistrains at day 5 after intraperitoneal inoculation with 500 tachyzoites. The transcriptomes of mouse peritoneal cells showed that 1,927, 1,573, and 1,009 transcripts were altered more than 2-fold by type I, II, and III infections, respectively, and that the majority of altered transcripts were shared. Overall transcription patterns were similar in type I and type II infections, and both had greater changes than infection with type III. Quantification of parasite burden in mouse spleens showed that the burden with type I infection was 1,000 times higher than that of type II and that the type II burden was 20 times higher than that of type III. Fluorescence-activated cell sorting revealed that type I and II infections had comparable macrophage populations, and both were higher than the population with type III infection. In addition, type I infection had a higher percentage of neutrophils than type II and III infections. Taken together, these results suggested that there is a common gene expression response toT. gondiiinfection in mice. This response is further modified by parasite strain-specific factors that determine their distinct virulence phenotypes.

The validity of classification for the clinical presentation of intracranial dural arteriovenous fistulas

1996 ◽  
Vol 85 (5) ◽  
pp. 830-837 ◽  
Author(s):  
Mark A. Davies ◽  
Karel TerBrugge ◽  
Robert Willinsky ◽  
Terry Coyne ◽  
Jamshid Saleh ◽  
...  
Keyword(s):  
Neurological Deficit ◽  
Clinical Presentation ◽  
Type I ◽  
Type Ii ◽  
Content Type ◽  
Type Iii ◽  
Arteriovenous Fistulas ◽  
Type Iv ◽  
Type V ◽  
Fine Print

✓ A number of classification schemes for intracranial dural arteriovenous fistulas (AVFs) have been published that claim to predict which lesions will present in a benign or aggressive fashion based on radiological anatomy. We have tested the validity of two proposed classification schemes for the first time in a large single-institution study. A series of 102 intracranial dural AVFs in 98 patients assessed at a single institution was analyzed. All patients were classified according to two grading scales: the more descriptive schema of Cognard, et al. (Cognard) and that recently proposed by Borden, et al. (Borden). According to the Borden classification, 55 patients were Type I, 18 Type II, and 29 Type III. Using the Cognard classification, 40 patients were Type I, 15 Type IIA, eight Type IIB, 10 Type IIA+B, 13 Type III, 12 Type IV, and four Type V. Intracranial hemorrhage (ICH) or nonhemorrhagic neurological deficit was considered an aggressive presenting clinical feature. A total of 16 (16%) of 102 intracranial dural AVFs presented with hemorrhage. Eleven of these hemorrhages (69%) occurred in either anterior cranial fossa or tentorial lesions. When analyzed according to the Borden classification, none (0%) of 55 Type I intracranial dural AVFs, two (11%) of 18 Type II, and 14 (48%) of 29 Type III intracranial dural AVFs presented with hemorrhage (p < 0.0001). After exclusion of visual or cranial nerve deficits that were clearly related to cavernous sinus intracranial dural AVFs, nonhemorrhagic neurological deficits were a feature of presentation in one (2%) of 55 Type I, five (28%) of 18 Type II, and nine (31%) of 29 Type III patients (p < 0.0001). When combined, an aggressive clinical presentation (ICH or nonhemorrhagic neurological deficit) was seen most commonly in intracranial dural AVFs located in the tentorium (11 (79%) of 14) and the anterior cranial fossa (three (75%) of four), but this simply reflected the number of higher grade lesions in these locations. Aggressive clinical presentation strongly correlated with Borden types: one (2%) of 55 Type I, seven (39%) of 18 Type II, and 23 (79%) of 29 Type III patients (p < 0.0001). A similar correlation with aggressive presentation was seen with the Cognard classification: none (0%) of 40 Type I, one (7%) of 15 Type IIA, three (38%) of eight Type IIB, four (40%) of 10 Type IIA+B, nine (69%) of 13 Type III, 10 (83%) of 12 Type IV, and four (100%) of four Type V (p < 0.0001). No location is immune from harboring lesions capable of an aggressive presentation. Location itself only raises the index of suspicion for dangerous venous anatomy in some intracranial dural AVFs. The configuration of venous anatomy as reflected by both the Cognard and Borden classifications strongly predicts intracranial dural AVFs that will present with ICH or nonhemorrhagic neurological deficit.

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