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PubMed2025

Quantifying evidence for phenotypic specificity (PP4) for syndromic phenotypes: Large-scale integration of rare germline FH variants from diagnostic laboratory testing for HLRCC and renal cancer.

PURPOSE: Hereditary leiomyomatosis and renal cell cancer (HLRCC) is a rare cancer susceptibility syndrome exclusively attributable to pathogenic variants in FH (HGNC:3700). This article quantitatively weights the phenotypic context (PP4/PS4) of such very rare variants in FH. METHODS: We collated clinical diagnostic testing data on germline FH variants from 387 individuals with HLRCC and 1780 individuals with renal cancer and compared the frequency of "very-rare" variants in each phenotypic cohort with 562,295 population controls. We generated pan-gene very rare variant likelihood ratios (PG-VRV-LRs), domain-specific likelihood ratios for missense variants (DS-VRMV-LR) using spatial clustering analysis, and log2.08 likelihood ratios (LLRs) as applicable within the updated American College of Medical Genetics and Genomics/Association for Molecular Pathology variant classification framework. RESULTS: For HLRCC, the PG-VRV-LR was estimated to be 2669.4 (95% CI 1843.4-3881.2, LLR 10.77) for truncating variants and 214.7 (95% CI 185.0-246.9, LLR 7.33) for missense variants. For renal cancer, the PG-VRV-LR was 95.5 (95% CI 48.9-183.0, LLR 6.23) for truncating variants and 5.8 (95% CI 3.5-9.3, LLR 2.39) for missense variants. Clustering analysis in HLRCC cases revealed 3 "hotspot" regions wherein the DS-VRMV-LR increased to 1226.9. CONCLUSION: These data provide quantitative measures for very rare missense and truncating variants in FH, which reflect the differing phenotypic specificity of HLRCC and renal cancer and may be applicable in clinical variant classification.

Humans↗
PubMed2003

Fluorescent pseudomonads associated with the phyllosphere of grasses; Pseudomonas trivialis sp. nov., Pseudomonas poae sp. nov. and Pseudomonas congelans sp. nov.

Strains of fluorescent pseudomonads, isolated from the phyllosphere of grasses, were analysed by a polyphasic approach in order to clarify their interspecific position. Classification on the basis of ribotyping revealed six genotypes; four of these, which could be differentiated clearly from each other and from Pseudomonas species with validly published names on the basis of phenotypic features, were chosen for detailed phylogenetic analysis. DNA-DNA hybridization studies among representative strains of the four genotypes and closely related Pseudomonas species, determined by comparison of 16S rDNA sequences, showed that three of the studied ribotypes represented novel species. Two of them were related to mainly saprophytic fluorescent pseudomonads and could be easily distinguished by a negative arginine dihydrolase reaction. One ribotype, also characterized by a negative arginine dihydrolase reaction, was closely related to potentially plant-pathogenic fluorescent pseudomonads and differed in certain phenotypic features from its phylogenetic neighbours. As a consequence of the phenotypic and phylogenetic analyses, Pseudomonas trivialis sp. nov. (type strain: P 513/19(T)=DSM 14937(T)=LMG 21464(T)), Pseudomonas poae sp. nov. (type strain: P 527/13(T)=DSM 14936(T)=LMG 21465(T)) and Pseudomonas congelans sp. nov. (type strain: P 538/23(T)=DSM 14939(T)=LMG 21466(T)) are proposed.

DNA, Bacterial↗
PubMed1998

Mitochondria in neuromuscular disorders.

This review considers primary mitochondrial diseases affecting the respiratory chain. As diseases due to mitochondrial DNA defects defy traditional anatomical classifications, we have not limited our discussion to neuromuscular disorders, but have extended it to include mitochondrial encephalomyopathies. Primary mitochondrial diseases can be due to mutations in either the nuclear or the mitochondrial genome. Nuclear mutations can affect (i) genes encoding enzymatic or structural mitochondrial proteins; (ii) translocases; (iii) mitochondrial protein importation; and (iv) intergenomic signaling. We review briefly recent molecular data and outstanding questions regarding these mendelian disorders, with special emphasis on cytochrome c oxidase deficiency and coenzyme Q10 deficiency. Mitochondrial DNA mutations fall into three main categories: (i) sporadic rearrangements (deletions/duplications); (ii) maternally inherited rearrangements (duplications); and (iii) maternally inherited point mutations. We summarize the most common clinical presentations and discuss pathogenic mechanisms, which remain largely elusive. Uncertainties about pathogenesis extend to the process of cell death, although excitotoxicity in neurons and apoptosis in muscle seem to have important roles.

Animals↗
PubMed2006

Histological classification and molecular genetics of meningiomas.

Meningiomas account for up to 30% of all primary intracranial tumours. They are histologically classified according to the World Health Organization (WHO) classification of tumours of the nervous system. Most meningiomas are benign lesions of WHO grade I, whereas some meningioma variants correspond with WHO grades II and III and are associated with a higher risk of recurrence and shorter survival times. Mutations in the NF2 gene and loss of chromosome 22q are the most common genetic alterations associated with the initiation of meningiomas. With increase in tumour grade, additional progression-associated molecular aberrations can be found; however, most of the relevant genes are yet to be identified. High-throughput techniques of global genome and transcriptome analyses and new meningioma models provide increasing insight into meningioma biology and will help to identify common pathogenic pathways that may be targeted by new therapeutic approaches.

Histological Techniques↗
PubMed1990

Virulence attributes of the liposaccharides of the HAP group organisms.

The pathogenic potential of purified gram-negative bacterial endotoxin is well documented. However, the role of endotoxin in the disease producing ability of pathogenic organisms, including those of the HAP group, remains in doubt. Endotoxin is not a classic virulence factor, but likely contributes to the pathogenic potential of gram-negative bacteria by activation of host defensive systems which ultimately results in the clinical signs and tissue damage that we recognize as disease. On the other hand, the proinflammatory nature of endotoxin, as well as liposaccharide antigens, play a critical role in the successful elimination of the infecting organism. How the induction of host defensive systems by endotoxin might benefit the infecting organism is difficult to reconcile. In this regard, host response to endotoxin often appears to be in excess of that necessary to clear the infection. Regardless of the role endotoxin might play in the pathogenesis of an infection, liposaccharide antigens are important in the serologically based classification of bacterial strains, are known to contribute to protective immunity, and are useful in the serological diagnosis of infection.

Animals↗
PubMed2001

Classification and genetic features of neonatal haemochromatosis: a study of 27 affected pedigrees and molecular analysis of genes implicated in iron metabolism.

Neonatal haemochromatosis (NH) is a severe and newly recognised syndrome of uncertain aetiology, characterised by congenital cirrhosis or fulminant hepatitis and widespread tissue iron deposition. NH occurs in the context of maternal disease including viral infection, as a complication of metabolic disease in the fetus, and sporadically or recurrently, without overt cause, in sibs. Although an underlying genetic basis for NH has been suspected, no test is available for predictive analysis in at risk pregnancies. As a first step towards an understanding of the putative genetic basis for neonatal haemochromatosis, we have conducted a systematic study of the mode of transmission of this disorder in a total of 40 infants born to 27 families. We have moreover carried out a molecular analysis of candidate genes (beta(2)-microglobulin, HFE, and haem oxygenases 1 and 2) implicated in iron metabolism. No pathogenic mutations in these genes were identified that segregate consistently with the disease phenotype in multiplex pedigrees. However, excluding four pedigrees with clear evidence of maternal infection associated with NH, a pedigree showing transmission of maternal antinuclear factor and ribonucleoprotein antibodies to the affected infants, and two families with possible matrilineal inheritance of disease in maternal half sibs, a large subgroup of the affected pedigrees point to the inheritance of an autosomal recessive trait. This included 14 pedigrees with affected and unaffected infants and a single pedigree where all four affected infants were the sole offspring of consanguineous but otherwise healthy parents. We thus report three distinct patterns of disease transmission in neonatal haemochromatosis. In the differentiation of a large subgroup showing transmission of disease in a manner suggesting autosomal recessive inheritance, we also provide the basis for further genome wide studies to define chromosomal determinants of iron storage disease in the newborn.

Adolescent↗
PubMed2000

Distinguishing species of the Burkholderia cepacia complex and Burkholderia gladioli by automated ribotyping.

Several species belonging to the genus Burkholderia are clinically relevant, opportunistic pathogens that inhabit major environmental reservoirs. Consequently, the availability of means for adequate identification and epidemiological characterization of individual environmental or clinical isolates is mandatory. In the present communication we describe the use of the Riboprinter microbial characterization system (Qualicon, Warwick, United Kingdom) for automated ribotyping of 104 strains of Burkholderia species from diverse sources, including several publicly accessible collections. The main outcome of this analysis was that all strains were typeable and that strains of Burkholderia gladioli and of each species of the B. cepacia complex, including B. multivorans, B. stabilis, and B. vietnamiensis, were effectively discriminated. Furthermore, different ribotypes were discerned within each species. Ribotyping results were in general agreement with strain classification based on restriction fragment analysis of 16S ribosomal amplicons, but the resolution of ribotyping was much higher. This enabled automated molecular typing below the species level. Cluster analysis of the patterns obtained by ribotyping (riboprints) showed that within B. gladioli, B. multivorans, and B. cepacia genomovar VI, the different riboprints identified always clustered together. Riboprints of B. cepacia genomovars I and III, B. stabilis, and B. vietnamiensis did not show distinct clustering but rather exhibited the formation of loose assemblages within which several smaller, genomovar-specific clusters were delineated. Therefore, ribotyping proved useful for genomovar identification. Analysis of serial isolates from individual patients demonstrated that infection with a single ribotype had occurred, despite minor genetic differences that were detected by pulsed-field gel electrophoresis of DNA macrorestriction fragments. The automated approach allows very rapid and reliable identification and epidemiological characterization of strains and generates an easily manageable database suited for expansion with information on additional bacterial isolates.

Automation↗
PubMedDate not supplied

[Disorders of pulmonary gas diffusion in liver cirrhosis].

UNLABELLED: There is no consensus on the pathogenesis and incidence of diffusion disorder in chronic liver diseases. It is supposed that the pathogenic mechanisms responsible for the reduction of diffusion capacity in liver diseases are multifactorial, including: ventilation-perfusion mismatching, diffuse interstitial pulmonary diseases and reduced transitory time in hyperperfused lung areas [1]. The increase of diffusion of oxygen molecules within dilated blood vessels during the inspiration of 100% O2 in patients with liver cirrhosis is called "diffusion-perfusion defect" or "alveolar-capillary oxygen disequilibrium" [3]. AIM OF THE STUDY: The aim of the study was to determine how the inadequate pulmonary perfusion and intrapulmonary vascular dilatation affect the diffusion disorder in liver cirrhosis. One of the aims was to establish the correlative relations between diffusion disorder and cirrhosis grade according to Child classification. METHOD: The study was performed over the period 1997-2000, including 50 patients with liver cirrhosis. They were diagnosed and treated at the Department of Hepatology and Gastroenterology, Clinical Centre of Serbia, Belgrade. Functional and morphological studies were based on the laboratory tests of liver function and histopathologic findings. The grade of liver insufficiency (A, B or C) was determined according to Child-Pugh score. The alveolar-arterial gradient was calculated from the gas analysis in the arterial blood, in supine and sitting position, in conditions of room air breathing and 100% oxygen. Diffusion parameters were measured by method of single inspiration of carbon monoxide. Spirometry and body pletismography were used for determination of ventilatory disorders. RESULTS: The reduced transfer factor (TLco) was recorded in 27 (54%) patients, while reduced transfer coefficient (Kco) was found in 33 (66%) patients. The mean TLco value was 7.27 (73%) in Child group A (n = 16); 6.98 (73%) in Child B group (n = 20); 6.65 (71%) in Child C group (n = 14). The comparison of these values in Child A, B and C groups by t-test showed no statistically significant difference (p > 0.05). The mean value of TLco was 7.24 (73%) in patients with spider naevi (n = 19), and 6.86 (72%) in patients without spiders (n = 31), without statistically significant difference among these mean values (t-test, p = 0.52). The restrictive ventilation disorders were present in 14 (28%) patients, while the reduced transfer factor was found in 27 (54%) patients. The incidences of restrictive ventilatory disorders and reduced transfer factor were compared (x2-test). The incidence of TLco, decrease was more significant than the incidence of restrictive disorders (p = 0.0082). The elevated alveolar-arterial gradient was present in 29 (58%) patients. No significant difference was found between alveolar-arterial gradient and diffusion disorders (x2-test, p = 0.62). DISCUSSION: There is no consensus on the incidence of diffusion disorder in chronic liver diseases. Robin et al. 1982 reported that only 20% of patients with liver cirrhosis had pathological diffusion, presuming that it was induced by reduction of transit time in hyperperfused lung regions [8]. Hourani et al. 1991 reported that the most frequent functional disorder was TLco decrease (52%) in the group of 116 patients planned for liver transplantation [1]. Krowka et al. 1992 found the lowest values of diffusion capacity in patients with Child C grade of liver cirrhosis [11]. Our results confirm the high incidence (54%) of diffusion disorder in liver cirrhosis, but the grade of liver insufficiency (Child score) does not correlate with the reduction of diffusion capacity. Several studies have reported various degrees of restrictive ventilatory disorders, with disproportionately higher reduction of TLco [1, 14, 15]. Our results confirm the higher incidence of diffusion disorder compared to restrictive disorders. Recent studies report that the isolated reduction of TLco is caused mainly by the intrapulmonary vascular dilatation, but the other factors also play the role (diffuse interstitial lung diseases without restrictive disorders in early stages, the passage through nonventilated alveoli, i.e. ventilatory perfusion mismatching and/or the other pulmonary vascular diseases) [16]. CONCLUSION: The impairment of diffusion capacity is a very common functional disorder in patients with liver cirrhosis and portal hypertension. Disproportionately, higher reduction of the transfer factor compared to restrictive ventilatory disorder, suggests that diffusion disorder is primarily induced by inadequate pulmonary perfusion. The isolated reduction of the transfer factor cannot be only explained in each case by intrapulmonary vascular dilatation.

Humans↗
PubMed2001

Pneumonia in patients with severe burns : a classification according to the concept of the carrier state.

OBJECTIVE: To establish baseline values of pneumonia incidence and mortality and to distinguish primary endogenous from secondary endogenous and exogenous pneumonias in a homogeneous patient population with severe burns. DESIGN: Cohort study. SETTING: A six-bed burn ICU. PATIENTS: All patients of > or = 14 years admitted to the ICU between January 1995 and June 1996 with a total body surface area burn of > or = 20%. INTERVENTION: Collection of data on surveillance samples from throat and rectum on admission and twice weekly afterward, and pneumonias during the ICU stay. MEASUREMENTS AND RESULTS: Fifty-six patients fulfilled the criteria of the study. Mean age was 43 +/- 19.8 years; total body surface area burn, 41 +/- 18.2%; the area of full-thickness burn was 24 +/- 17.7%. Forty-one patients required mechanical ventilation. Twenty-seven patients (48%) experienced 37 episodes of pneumonia. Twenty-one pneumonias were of primary endogenous development, ie, caused by potential pathogens carried in the admission flora. There were 14 secondary endogenous and 2 exogenous infections caused by microorganisms acquired on the burn unit. Inhalation injury was identified in 26 patients. The pneumonia rate was two times higher in the subset of patients with inhalation injury compared with the group of patients without inhalation injury (p < 0.001). Overall mortality was 25%. CONCLUSIONS: This study shows that pneumonia in burn patients is mainly an endogenous problem. Interventions that prevent the development of endogenous infections deserve prospective evaluation in patients with severe burns.

Adolescent↗
PubMed2006

Unify QSAR approach to antimicrobials. Part 1: predicting antifungal activity against different species.

Most of up-to-date reported molecular descriptors encode only information about the molecular structure. In previous papers, we have extended stochastic descriptors to encode additional information such as target site, partition system, or biological species [Bioorg. Med. Chem. Lett.2005, 15, 551; Bioorg. Med. Chem. 2005, 13, 1119]. This work develops an unify Markov model to describe with a single linear equation the biological activity of 74 drugs tested in the literature against some of the fungi species selected from a list of 87 species (491 cases in total). The data were processed by linear discriminant analysis (LDA) classifying drugs as active or non-active against the different tested fungi species. The model correctly classifies 338 out of 368 active compounds (91.85%) and 89 out of 123 non-active compounds (72.36%). Overall training predictability was 86.97% (427 out of 491 compounds). Validation of the model was carried out by means of leave-species-out (LSO) procedure. After elimination step-by-step of all drugs tested against one specific species, we record the percentage of good classification of leave-out compounds (LSO-predictability). In addition, robustness of the model to the elimination of the compounds (LSO-robustness) was considered. This aspect was considered as the variation of the percentage of good classification of the modified model (Delta) in LSO with respect to the original one. Average LSO-predictability was 86.41+/-0.95% (average+/-SD) and Delta = -0.55%, being 6 the average number of drugs tested against each fungi species. Results for some of the 87 studied species were Candida albicans: 43 tested compounds, 100% of LSO-predictability, Delta = -3.49%; Candida parapsilosis 23, 100%, Delta = -0.86%; Aspergillus fumigatus 21, 95.20%, Delta = 0.05%; Microsporum canis 12, 91.60%, Delta = -2.84%; Trichophyton mentagrophytes 11, 100%, Delta = -0.51%; Cryptococcus neoformans 10, 90%, Delta = -0.90%. The present one is the first reported unify model that allows one predicting antifungal activity of any organic compound against a very large diversity of fungi pathogens.

Antifungal Agents↗
PubMed2005

Gene expression profiling of sporadic Parkinson's disease substantia nigra pars compacta reveals impairment of ubiquitin-proteasome subunits, SKP1A, aldehyde dehydrogenase, and chaperone HSC-70.

Sporadic Parkinson's disease (PD) constitutes 99% of the disorder, while the remaining 1% of the cases is of familial (genetic) origin. The mutations reported to be associated with familial PD indicate impairment in protein processing and misfolding, as is handled by the ubiquitin-proteasome system (UPS), and in mitochondrial function. For these reasons, we have recently applied, for the first time, Affymetrix oligonucleotide microarray technique in the substantia nigra pars compacta of sporadic parkinsonian patients for studying global gene expression analysis and comparison to the alterations identified in inherited PD. This study identified decreased expression of 68 genes and elevation of 69 genes. Classification into functional groups revealed that the downregulated genes are related to signal transduction, protein degradation (e.g., ubiquitin-proteasome subunits), dopaminergic transmission/metabolism, iron transport, protein modification/phosphorylation, and energy pathways/glycolysis functional classes. A major finding is the decreased expressions of 5 subunits of the UPS, SKP1A, a member of the SCF (E3) ubiquitin ligase complex, and chaperone HSC-70, which can lead to a wide impairment in the function of an entire repertoire of proteins. The upregulated genes are clustered in cell adhesion/cytoskeleton, extracellular matrix components, cell cycle, protein modification/phosphorylation, protein metabolism and transcription, and inflammation/hypoxia (e.g., key iron and oxygen sensor EGLN1) classes. The study shows, for the first time, a convergence in the pathogenic processes that are observed in hereditary (familial) and sporadic PD, where abnormal iron metabolism, oxidative stress, and aggregation of proteins occur. An additional breakthrough in this research is the identification of a number of previously unsuspected crucial gene players that are also involved in the process of neurodegeneration, which can serve as specific biomarkers for PD and novel drug development.

Aldehyde Dehydrogenase↗
PubMed1964

PORCINE CONTAGIOUS PLEUROPNEUMONIA. I. EXPERIMENTAL TRANSMISSION, ETIOLOGY, AND PATHOLOGY.

An acute frequently rapidly fatal respiratory illness occurring as an epidemic disease in Argentine swine has been shown to have a bacterium of the genus Hemophilus as its causative agent. This organism, for which the name Hemophilus pleuropneumoniae is suggested, causes a singular, fulminating pleuropneumonia in experimental swine. The very marked effectiveness of H. pleuropneumoniae as a respiratory pathogen contrasts strikingly with the relatively mild pathogenicity of the well known swine Hemophilus, H. influenzae suis, which, in concert with a virus, causes a less highly fatal respiratory ailment, swine influenza. Porcine contagious pleuropneumonia (PCP) is contagious under experimental conditions. In the pathogenesis of the disease, histopathological studies of early cases suggest that the lymphatics of the lung and pleura may be primarily involved and that the pneumonia and pleuritis then proceed from these initial sites of reaction.

Animals↗
PubMed2003

[Mucosal damage caused by nonsteroidal anti-inflammatory agents in H. pylori infection].

BACKGROUND: The pathogenic role of Helicobacter pylori (H. pylori) infection in the setting of NSAID use is still controversial. Aim of the study is to prove increased incidence of gastric mucosa damage in H. pylori positive NSAID users compared to H. pylori negative patients. METHODS: Patients with dyspeptic symptoms (n = 160, average age 62.13 +/- 6.24, ranged from 51 to 77 years) were divided in two groups: 80 patients (45 male, 35 female) with positive history of using NSAID and same group with negative history for NSAID. All patients underwent endoscopy, examined to H. pylori presence by rapid unease test. Patients with ulcer or erosions (> 5) were evaluated and grade of gastric mucosa damage were done according to Forrest classification of gastrointestinal bleeding. RESULTS: In first group 69/80 of examined patients were H. pylori positive, in second group 56/80 were H. pylori positive (X2 = 5.266; p = 0.022). In gastric mucosa bleeding, caused with NSAIDs, H. pylori was not diagnosed more often compared to other group (p > 0.05). CONCLUSION: Patients with NSAID induced gastric injury were significantly greater incidence of H. pylori infection compared to patients without history of NSAIDs abuse. H. pylori was not significantly present in complication of ulcer disease (bleeding) caused by NSAID.

Aged↗
PubMed1994

Specific genomic fingerprints of phytopathogenic Xanthomonas and Pseudomonas pathovars and strains generated with repetitive sequences and PCR.

DNA primers corresponding to conserved motifs in bacterial repetitive (REP, ERIC, and BOX) elements and PCR were used to show that REP-, ERIC-, and BOX-like DNA sequences are widely distributed in phytopathogenic Xanthomonas and Pseudomonas strains. REP-, ERIC, and BOX-PCR (collectively known as rep-PCR) were used to generate genomic fingerprints of a variety of Xanthomonas and Pseudomonas isolates and to identify pathovars and strains that were previously not distinguishable by other classification methods. Analogous rep-PCR-derived genomic fingerprints were generated from purified genomic DNA, colonies on agar plates, liquid cultures, and directly from lesions on infected plants. REP, ERIC, and BOX-PCR-generated fingerprints of specific Xanthomonas and Pseudomonas strains were found to yield similar conclusions wtih regard to the identity of and relationship between these strains. This suggests that the distribution of REP-, ERIC, and BOX-like sequences in these strains is a reflection of their genomic structure. Thus, the rep-PCR technique appears to be a rapid, simple, and reproducible method to identify and classify Xanthomonas and Pseudomonas strains, and it may be a useful diagnostic tool for these important plant pathogens.

Base Sequence↗
PubMed2006

Neuropsychiatric manifestations of systemic lupus erythematosus.

Central nervous system (CNS) involvement in systemic lupus erythematosus (SLE) can produce a broad range of disease-specific neuropsychiatric manifestations that must be differentiated from infections, metabolic complications, and drug-induced toxicity. Despite the development of classification criteria by the American College of Rheumatology, the prevalence of neuropsychiatric systemic lupus erythematosus (NPSLE) varies widely across studies. Some of the neuropsychiatric manifestations are extremely rare, indicating a need for multicenter studies. Mechanisms that can lead to neuropsychiatric manifestations include intracranial vascular lesions (vasculitis and thrombosis); production of autoantibodies to neuronal antigens, ribosomes, and phospholipids; and inflammation related to local cytokine production. As a rule, no reference standard is available for establishing the diagnosis of NPSLE. Several investigations can be used to assist in the clinical diagnosis and to evaluate severity. Treatment remains largely empirical, given the absence of controlled studies. Variable combinations of corticosteroids, immunosuppressants, and symptomatic drugs are used according to the presumptive main pathogenic mechanism.

Humans↗
PubMed2004

The usefulness of molecular techniques to assess the presence of Aeromonas spp. harboring virulence markers in foods.

A total of 78 raw and 123 processed and ready-to-eat retail food samples were used to assess the presence of motile Aeromonas spp. harboring virulence genes (cytotoxic enterotoxin and hemolysin genes) using a recently described PCR method in comparison with the conventional cultivation method based on the use of Ampicillin-Dextrin Agar (ADA) medium. With the ADA-based method, 65/201 (32.3%) samples showed presumptive Aeromonas spp. colonies whereas the PCR method revealed the presence of Aeromonas spp. harboring the targeted virulence genes in 51/201 (25.4%) of the tested samples. The rate of contaminated samples and the presence of pathogenic Aeromonas were significantly lower with both methods for processed than in case of raw samples. A polyphasic identification approach including biochemical and molecular techniques was applied to a selection of 34 PCR-positive presumptive Aeromonas isolates. Following fatty acid methyl ester (FAME) analysis and amplified fragment length polymorphism (AFLP) fingerprinting, a total of 33 isolates (97%) could be identified to the DNA hybridization group (HG) level. The majority of these isolates belonged to the species Aeromonas hydrophila HG3 (50%) and Aeromonas veronii biovar sobria (HG8/10) (38%). Molecular characterization of PCR amplicons obtained from these strains by PCR-Restriction Fragment Length Polymorphism (PCR-RFLP) fingerprinting and PCR-Amplicon Sequence Analysis (PCR-ASA) allowed classification of all strains in a known PCR-RFLP and PCR-ASA type. In conclusion, the current findings demonstrate that the combined use of PCR-based virulence marker detection, PCR-RFLP and PCR-ASA offers a rapid, sensitive, and specific system to assess the presence and prevalence of Aeromonas spp. harboring virulence markers in food samples.

Aeromonas↗
PubMed2005

Distribution of Ixodes ricinus in the British Isles: investigation of historical records.

Ixodes ricinus Linnaeus (Acari: Ixodidae) is the most abundant and widely distributed tick in the British Isles, and is a vector for a number of bacterial, viral and protozoal pathogens of both medical and veterinary importance. This report provides an update to the historical distribution data of I. ricinus, published by the Biological Records Centre (BRC), Monks Wood in The Provisional Atlas of the Ticks (Ixodidae) of the British Isles by K. P. Martyn (1988), and is supplemented with additional BRC records since 1988, additional data from published scientific literature and unpublished field studies, and enhanced with spatial and temporal information on tick stages collected and their host associations. Records have been mapped at 10 km resolution and enhanced to 5 km, 1 km and 0.1 km. Differentiation between records representing one-off collections from those representing populations of I. ricinus has been achieved through the classification of the records into either reported or established populations. Detailed seasonality and host associations of records are investigated, highlighting the value in obtaining additional detailed contemporary data to aid risk assessments and research within this field.

Animals↗
PubMed2002

Analysis of phylogenetic relationship of Cylindrocarpon lichenicola and Acremonium falciforme to the Fusarium solani species complex and a review of similarities in the spectrum of opportunistic infections caused by these fungi.

An emerging pattern of similarity in medical case reports led to a project to compare the phylogenetic affinities of two well-known tropical fungal opportunistic pathogens, Cylindrocarpon lichenicola and Acremonium falciforme, to members of the Fusarium solani species complex. C. lichenicola and A. falciforme, despite their deviating conidial morphologies, were shown via sequencing of the ribosomal large subunit to be well instituted within a clade mainly consisting of typical F. solani strains and other species until recently considered variants of F. solani. The original name Fusarium lichenicola C. B. Massalongo is reestablished, and the new combination F. falciforme is made. Recognition of these species as fusaria is necessary for correct interpretation of current and future molecular diagnostic tests. Reevaluation of species morphology in light of the molecular findings showed that certain features, especially elongate filiform conidiophores with integrated terminal phialides, facilitate correct microscopic classification of these atypical Fusarium species. There is a strong and underrecognized overlap in the spectra of cases caused by members of the F. solani clade, particularly ocular infections, mycetomas, and, in the neutropenic host, disseminated and other serious systemic infections. A novel synthesis of case reports shows that patients from areas with warm climates may develop a distinctive fusarial intertrigo caused by F. solani, Fusarium lichenicola, or Fusarium oxysporum.

Acremonium↗