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Disease Syndrome (disease + syndrome)
Selected AbstractsShell disease in crustaceans , just chitin recycling gone wrong?ENVIRONMENTAL MICROBIOLOGY, Issue 4 2008Claire L. Vogan Summary The exoskeletons of aquatic crustaceans and other arthropods contain chitin, a biopolymer of ,-(1,4)-linked N -acetylglucosamine together with associated proteins. Despite the vast amounts of chitin within such animals little is found in sediments and open water because microorganisms rapidly degrade this following its loss after moulting or upon the animals' death. Shell disease syndrome is a worldwide disease condition that affects a wide range of crustaceans. It comes about as a result of bacterial degradation of the exoskeleton leading to unsightly lesions and even death if the underlying tissues become infected. There are at least two potential forms of the disease; one that appears to centre around chitin degradation and an additional form termed ,epizootic' shell disease, in which chitin degradation is of less significance. This account reviews our current understanding of the causative agents of this syndrome, assesses the potential economic consequences of the disease, and critically examines whether it is associated with anthropogenic disturbances including pollution. Overall, despite extensive studies during the last few decades, the potential links between faecal, heavy metal and insecticide pollution and shell disease are still unclear. [source] Transmission of Ehrlichia risticii, the agent of Potomac horse fever, using naturally infected aquatic insects and helminth vectors: preliminary reportEQUINE VETERINARY JOURNAL, Issue 4 2000J. E. Madigan Summary Ehrlichia risticii, the agent of Potomac horse fever (PHF), has been recently detected in trematode stages found in snail secretions and in aquatic insects. Based on these findings, horses could conceivably be exposed to E. risticii by skin penetration with infected cercariae, by ingestion of infected cercariae in water or via metacercariae in a second intermediate host, such as an aquatic insect. In order to test this hypothesis, horses were challenged with infectious snail secretions and aquatic insects collected from a PHFendemic region in northern California. Two horses stood with their front feet in waterharbouring E. risticii -infected cercariae, 2 horses drank water harbouring E. risticii -infected cercariae, and 6 horses were fed pools of different aquatic insects harbouring E. risticii -infected metacercariae. In this preliminary study, only the one horse infected orally with mature caddisflies (Dicosmoecus gilvipes) developed the clinical and haematological disease syndrome of PHF. The agent was isolated from the blood of the infected horse in a continuous cell line and identified as E. risticii by characterisation of the 16S rRNA gene. Therefore, E. risticii is maintained in nature in a complex aquatic ecosystem and transmission to horses can occur through accidental ingestion of insects such as caddisflies containing infected metacercariae. At present, the small number of horses used in this study does not exclude other insects and free trematode stages as potential sources of infection. [source] Screening for the BRCA1-ins6kbEx13 mutation: potential for misdiagnosis,,HUMAN MUTATION, Issue 5 2007Susan J Ramus Abstract Misdiagnosis of a germline mutation associated with an inherited disease syndrome can have serious implications for the clinical management of patients. A false negative diagnosis (mutation missed by genetic screening) limits decision making about intervention strategies within families. More serious is the consequence of a false positive diagnosis (genetic test suggesting a mutation is present when it is not). This could lead to an individual, falsely diagnosed as a mutation carrier, undergoing unnecessary clinical intervention, possibly involving risk-reducing surgery. As part of screening 283 ovarian cancer families for BRCA1 mutations, we used two different methods (mutation specific PCR and multiplex ligation-dependant probe amplification) to screen for a known rearrangement mutation L78833.1:g.44369_50449dup (ins6kbEx13). We found false positive and false negative results in several families. We then tested 61 known carriers or non-carriers from an epidemiological study of BRCA1 and BRCA2 mutation carriers (the EMBRACE study). These data highlight the need for caution when interpreting analyses of the ins6kbEx13 mutation and similar mutations, where characterising the exact sequence alteration for a deleterious mutation is not a part of the routine genetic test. © 2007 Wiley-Liss, Inc. [source] Fas ligand-induced murine pulmonary inflammation is reduced by a stable decoy receptor 3 analogueIMMUNOLOGY, Issue 2 2003Mark A. Wortinger Summary Fas ligand (FasL)-induced lung inflammation has recently been suggested to play an important role in the pathogenesis of acute respiratory disease syndrome (ARDS). In order to further explore this connection, we established a FasL-induced murine model of pulmonary inflammation. Instillation of recombinant FasL (rFasL) into the lung induced neutrophil infiltration and increased pulmonary permeability, as evidenced by increased total protein in the airspace; both occur in patients with ARDS. These effects were accompanied with a rapid induction of proinflammatory mediators: cytokine granulocyte,macrophage colony-stimulating factor (GM-CSF) and the chemokines macrophage inflammatory protein-2 (MIP-2) and KC. Pretreatment with a FasL antagonist, a decoy receptor 3 analogue (DcR3 analogue), reduced neutrophil infiltration into the airspace and resulted in a highly significant reduction in the levels of GM-CSF, MIP-2 and KC in bronchoalveolar lavage (BAL) fluid. We postulate that rFasL may be responsible for induction of proinflammatory chemokines and cytokines in the lung, which in turn attract neutrophil infiltration into the airspace. This proinflammatory process and the associated pulmonary permeability may, in part, explain the association of FasL with severe pulmonary inflammation, such as ARDS, and shed new light on FasL and its role in lung injury. [source] Pneumocystis jiroveci thyroiditis: report of 15 cases in the literatureMYCOSES, Issue 6 2007Alexandre P. Zavascki Summary The authors review the epidemiology, clinical manifestations, diagnosis and treatment of Pneumocystis jiroveci thyroiditis of 15 cases reported in the medical literature. Patients with acquired immunodeficiency disease syndrome were particularly at risk. P. jiroveci thyroiditis was diagnosed at autopsy as a part of disseminated infection in a substantial number of patients without clinical manifestations and laboratory evidence of thyroid dysfunction. Local signs and symptoms of infection were indistinguishable from other infectious thyroiditis and included neck enlargement with or without cervical pain, sometimes associated with dysphagia and dysphonia, and clinical and laboratory features of hypothyroidism. Antemortem diagnosis of fungal thyroiditis was made by direct microscopy and culture of a fine-needle aspirate in most cases. As most patients with P. jiroveci thyroiditis had disseminated Pneumocystis infection with a delay in diagnosis and treatment, the overall mortality was high. Pneumocystis jiroveci thyroiditis is rare but should be suspected in HIV-infected patients with CD4 count lower than 200 cells ,,1 on prophylatic inhalatory pentamidine who present with neck enlargement with or without pain, and clinical and laboratory evidence of hypothyroidism. [source] Clinicopathological findings associated with feline infectious peritonitis in Sydney, Australia: 42 cases (1990,2002)AUSTRALIAN VETERINARY JOURNAL, Issue 11 2005JM NORRIS Objectives To review the clinicopathological findings in naturally-occurring, histopathologically confirmed cases of feline infectious peritonitis in client-owned cats in Sydney, Australia, with the purpose of identifying factors assisting in the diagnosis of this complex disease syndrome and to characterise the disease as it occurs in this region. Design Retrospective clinical study: the clinical records of all cats with histopathologically confirmed feline infectious peritonitis at the University Veterinary Centre Sydney and a private cat hospital in Sydney between 1990 and 2002 were reviewed for signalment, history, physical findings, diagnostic test results and the distribution of histological lesions throughout the body at necropsy. Results Forty-two cats met the inclusion criteria. Significant features of this study that unique to the contemporary literature are i) the over-representation of certain breeds (Burmese, Australian Mist, British Shorthaired, and Cornish Rex) and the under-representation of other breeds (Domestic Shorthaired, Persian); ii) the overrepresentation of males; iii) the tendency for effusive disease in Australian Mist cats and non-effusive disease in Burmese; iv) the even age distribution of disease seen in cats older than 2 years-of-age; and v) the presence of fulminant immune-mediated haemolytic anaemia in two cats in this study. Conclusion The study highlights the diverse range of clinical manifestations and the complexities experienced by clinicians in diagnosing this fatal disease. Some aspects of the epidemiology and clinical manifestations of feline infectious peritonitis appear different to the disease encountered in Europe and North America, most notably the over-representation of specific breeds and the presence of immune-mediated haemolytic anaemia. [source] The cutaneous pathology of lupus erythematosus: a reviewJOURNAL OF CUTANEOUS PATHOLOGY, Issue 1 2001A. Neil Crowson The presentation of lupus erythematosus (LE) ranges from a skin rash unaccompanied by extracutaneous stigmata to a rapidly progressive lethal multiorgan disease. The diagnosis and subclassification is traditionally based on the correlation of serological and clinical findings. The latter include a photoinduced skin rash, arthralgia, arthritis, fever, Raynaud's phenomenon, anemia, leukopenia, serositis, nephritis and central nervous sysdtem disease. The conventional classification scheme includes systemic, subacute cutaneous and discoid LE. Recent advances in our understanding of the cutaneous histopathology which correlates with the traditional forms of LE, along with certain novel LE subtypes, are the focus of this review. In addition to the main subtypes of LE, we will discuss associated vasculopathic lesions and the contribution of immunofluorescence microscopy to the diagnosis of LE and related connective tissue disease syndromes. Consideration will be given to unusual variants of LE such as anti-Ro/SSA-positive systemic lupus erythematosus (SLE), bullous SLE, lymphomatoid LE, lupus erythematosus profundus, drug induced LE, linear cutaneous LE, chiblains LE and parvovirus B19-associated LE. [source] Non-atopic intrinsic asthma and the ,family tree' of chronic respiratory disease syndromesCLINICAL & EXPERIMENTAL ALLERGY, Issue 6 2009P. G. Holt Summary We present a scheme below in which the most common forms of inflammatory diseases of the respiratory tract, notably atopic and non-atopic asthma and COPD, are depicted as separate offshoots from a common ,at-risk' pathway underpinned by genotypes related to aberrations in control of host defence and tissue repair mechanisms. We propose that entrance into this pathway is initially programmed by environmental experience during infancy and early childhood, in particular by severe lower respiratory tract infection, and that further progression towards expression of specific disease phenotype(s) is determined by the nature, timing and frequency of additional environmental insults subsequently encountered. At the one extreme, early sensitization of at-risk subjects to aeroallergens can potentially drive rapid progression towards expression of the atopic asthmatic phenotype under the dual onslaught of inflammatory responses to allergens/pathogens. At the opposite end of the spectrum the drip-feed effects of occasional infections on respiratory function(s) are amplified over a longer time frame by inflammation resulting from exposure to tobacco smoke and/or related chemical pollutants. Non-atopic asthma is envisaged to fit between these two extremes, being driven essentially by the downstream effects of respiratory infections alone in at-risk subjects. An important common factor in all three disease phenotypes is that acute exacerbations are typically driven by infections, the host responses to which display a characteristic T-helper type 2-like footprint, which in our view points to underlying genotype(s) which result in unbalanced host responses to respiratory pathogens. [source] | |||||||||||||