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1
(Editor), Gavin Spickett, and Ian G. Lewin (Editor), eds. Current Themes in Allergy and Immunology. Royal College of Physicians of London, 1994.
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2
Kirkham, Bruce. Immunology and cytokine pathways. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198737582.003.0007.
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Psoriatic arthritis immunopathology has become the subject of intense study. These findings show differences to other forms of inflammatory arthritis in key pathways. Increased knowledge of innate immunity and the important role of IL-17/23 biology in both psoriasis and psoriatic arthritis, have led to new theories of immunopathogenesis in both conditions. Direct environmental stimuli could trigger innate immune cells resident in skin, which may then initiate a chronic adaptive immune response. The joint has fewer resident innate immune cells, but new studies show cells producing IL-17 may play key roles in immunopathology. The new information summarized here will provide important hypotheses for investigation of pathogenic pathways. Differences in non-immune cell function may also be critical mediators of response, for example, production of IL-12 or IL-23 by dendritic cells. Keratinocytes in skin and fibroblasts in joints may be critical in mediating cytokine production and effector function.
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Dambuza, Ivy M., Jeanette Wagener, Gordon D. Brown, and Neil A. R. Gow. Immunology of fungal disease. Edited by Christopher C. Kibbler, Richard Barton, Neil A. R. Gow, Susan Howell, Donna M. MacCallum, and Rohini J. Manuel. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755388.003.0009.
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Advances in modern medicine, such as organ transplantations and the appearance of HIV (human immunodeficiency virus), have significantly increased the patient cohort at risk of developing chronic superficial and life-threatening invasive fungal infections. To tackle this major healthcare problem, there is an urgent need to understand immunity against fungal infections for the purposes of vaccine design or immune-mediated interventions. In this chapter, we give an overview of the components of the innate and adaptive immune system and how they contribute to host defence against fungi. The various cell types contributing to fungal recognition and the subsequent stimulation of phagocytosis, the activation of inflammatory and B- and T-cell responses, and fungal clearance are discussed using the major fungal pathogens as model systems.
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Keshav, Satish, and Alexandra Kent. Immunology and genetics in gastrointestinal and hepatic medicine. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0196.
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The gut has a pivotal role in immune homeostasis. It is constantly exposed to a wide array of antigens in food, and resident and consumed microorganisms. It is estimated that the number of bacterial cells in the gastrointestinal tract is tenfold greater than the number of cells in the human body. The gut needs to recognize harmful bacteria, and consequently contains the largest number of immune cells in the body. However, it must remain tolerant to commensal bacteria. Bacteria express antigens that stimulate an immunological response via the gut-associated lymphoid tissue (GALT). The GALT includes the appendix, tonsils, Peyer’s patches, and mesenteric lymph nodes. Therefore, the intestinal immune system is finely balanced between tolerance and reactivity. An example of an abnormal response that generally the individual should be tolerant to is gliadin peptides in coeliac disease. An example of excessive tolerance to an otherwise controllable infection is cryptosporidiosis, which causes diarrhoea in patients with HIV infection. The understanding of genetics in disease has progressed rapidly with the introduction of genome-wide association studies. The Welcome Trust Case Control Consortium has performed extensive research on the genetics of many illnesses, including Crohn’s disease, ulcerative colitis, Barrett’s oesophagus, oesophageal adenocarcinoma, and primary biliary cholangitis. Although these studies have increased our understanding of the molecular basis of disease, they have had little impact on clinical management. This may change as studies associate genotype and phenotype. Several gastrointestinal diseases have an etiology based on immunological or genetic aberrations, and these immunological mechanisms and genetic mutations can be utilized for diagnostic purposes. However, there is no genetic or immunological marker that is 100% specific to a disease and, consequently, the markers are used to support clinical, histological, and/or radiological findings.
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Foster, Brogan, and Paul A. Brogan. Juvenile idiopathic arthritis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198738756.003.0003.
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This chapter describes the JIA subtypes, uveitis, prognostic indicators, the spectrum of JIA in adults and updated chapters on the genetics and immunology of JIA. There are updated sections on treatment approaches, pathways (including reference to NICE and guidance from North America and Europe) and disease activity scores.
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Gavin, Spickett, Lewin Ian G, and Royal College of Physicians of London., eds. Current themes in allergy and immunology: Papers based on an Interfaces in Medicine Conference organised by the Royal College of Physicians, London. London: Royal College of Physicians of London, 1994.
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7
Giesser, Barbara S., ed. Primer on Multiple Sclerosis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199341016.001.0001.
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Primer on Multiple Sclerosis, second edition is designed to be a practical guide to the basic science and clinical manifestations of multiple sclerosis. It is intended primarily for neurologists and other health care professionals who treat persons with this disease. The book starts with a review of the history of multiple sclerosis and the basic genetics, immunology, electrophysiology, and pathophysiology that are central to the disease. It then reviews the common and uncommon clinical signs and symptoms of multiple sclerosis and the management of these conditions. The latest diagnostic strategies are presented. There is extensive coverage of approved and experimental disease-modifying therapies, including algorithms to assist clincians in choosing these therapies. Complementary and alternative therapies that are popular among persons with multiple sclerosis are examined. New additions to this edition include a chapter for nursing health care professionals, and updates on therapeutics. Unique to this book are the chapters on the legal, psychosocial, and vocational issues that often present challenges for person with multiple sclerosis, topics that typically are not covered in standard texts.
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Bielekova, Bibiana, Gary Birnbaum, and Robert P. Lisak, eds. Neuroimmunology. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780190050801.001.0001.
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This book provides clinical and supporting scientific background on a diverse group of neurological disorders in an expanding field of neurology, that of neuroimmunology. It includes chapters on multiple sclerosis and related disorders in adults and children, neuromyelitis optica spectrum disorder, Guillain-Barré syndrome, chronic inflammatory deymyelinating polyradiculoneuropathy and variants, immune-mediated disorders of the neuromuscular junction, inflammatory myopathies, paraneoplastic disorders and autoimmune encephalitities, and neurologic manifestations of systemic immune-mediated diseases. In addition there is an introductory chapter dealing with basic of immunology and another on mechanisms of action of therapies used in neuroimmunologic disorders. The clinical chapters cover epidemiology, pathology, pathogenesis, and pathophysiology of the different diseases along with clinical presentation, diagnostic testing, differential diagnosis, and treatment.
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Swash, Michael. Myology. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199658602.003.0012.
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Diseases of muscle have become better understood by careful clinical observations, resulting in a clinically useful classification of the different groups of disorders e.g. inherited muscular dystrophies such as Duchenne muscular dystrophy, limb-girdle and metabolic myopathies, and myotonic disorders. A number of scientific approaches have determined the directions taken by this evolving classification. Understanding of the anatomy of the motor unit’s distribution in muscle transformed muscle pathology and muscle electrophysiology, and key to these pathological advances was the use of the histochemical technique for identifying myofibrillar ATPase in muscle fibres. This allowed studies of the distribution of fibre types in muscle in many different disorders. The inflammatory muscle diseases have been better understood since recent advances in immunology have characterized the underlying processes. The limb-girdle and childhood myopathies have proven to be heterogeneous, with many different, apparently causative, underlying genetic mutations.
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Kirk, Robert G. W., and Michael Worboys. Medicine and Species: One Medicine, One History? Edited by Mark Jackson. Oxford University Press, 2012. http://dx.doi.org/10.1093/oxfordhb/9780199546497.013.0031.
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This article surveys the present position of the animal within the history of human medicine, linking this to work in the history of veterinary medicine, and also speculates on the value of making ‘species’ a central and unifying theme of a new history of medicine. It mentions that re-conceiving medicine as a set of knowledge-practices grounded in interspecies interactions promises to reinvigorate the subject. It draws on a diverse theoretical literature ranging from ‘animal studies’ to ‘post-human’ literature in order to suggest how such an approach could allow us to re-imagine what medicine has been and still may be. This is a timely project as the medical and veterinary professions, after long debating the notion of ‘one medicine’ as ‘a common pool of knowledge in microbiology, immunology, physiology, pathology and epidemiology’, are now calling to develop the field.
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Messmer, Michelle N., Colleen S. Netherby, and Scott I. Abrams. Unique Challenges Facing Immunotherapy of Metastatic Ovarian Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0012.
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The immune system serves as an integral checkpoint to developing malignancies. However, when cancer ultimately becomes detectable, this implicates an inherent failure of effective immune control. One constant theme in cancer biology has been the ability of these “diseases,” in particular, ovarian cancer, to compromise immune-mediated mechanisms of neoplastic control. These empirical observations have subsequently laid the scientific foundation to investigate ways in which the immune system can be reengaged as a powerful therapeutic weapon, singly or in combination with other modalities. This field has been coined “cancer immunotherapy” and, importantly, strong progress has been made to date to justify its feasibility and potential merit. This chapter focuses on the fundamental immunologic principles that have guided the development of the cancer immunotherapy concept, as well as details both the successes and the limitations of cancer immunotherapy in patients with metastatic ovarian cancer.
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Wohl, David A., and Jeffrey T. Kirchner. Cardiovascular Disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0041.
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There is a growing body of evidence that HIV-infected persons are at increased risk for cardiovascular disease (CVD) and associated complications, including myocardial infarction and stroke. Autopsy studies have noted premature atherosclerosis in HIV-infected adults, and epidemiological studies demonstrate higher rates of CVD among HIV-infected compared to HIV-uninfected patients. These findings are in part due to chronic inflammation and immune activation associated with HIV infection. Traditional CVD risk factors, including hypertension, hyperlipidemia, and cigarette smoking, also play keys roles. There is additional evidence from observational cohort studies that some antiretroviral drugs, including protease inhibitors and nucleoside reverse transcriptase inhibitors, may increase the risk of myocardial infarction. Treatment interventions to reduce the risk of CVD include diet, exercise, smoking cessation, lipid-lowering agents, and antihypertensive medications. For select patients, changing antiretroviral therapy to improve lipid profiles may be appropriate but should not compromise virologic or immunologic control.
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Elewaut, Dirk, Heleen Cypers, Matthew L. Stoll, and Charles O. Elson. Extra-articular manifestations: inflammatory bowel disease. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198734444.003.0017.
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A significant overlap exists between spondyloarthritis (SpA) and inflammatory bowel disease (IBD), particularly in the IL-23/IL-17 pathway. Shared immunologic mechanisms include aberrant innate immune responses, an excess of Th1/Th17-mediated immunity, and inadequate immune regulation. Many genetic factors associated with IBD are involved in host–pathogen interactions and intestinal barrier function, and the intestinal microbiota do appear to play an important role in disease development. Hence the current hypothesis for IBD pathogenesis is that it stems from a dysregulated immune response to intestinal microbiota in a genetically susceptible host. In SpA, evidence for a role of intestinal microbiota is less abundant, but given the overlap with IBD, it is plausible that gut microbiota are important players in SpA pathogenesis as well. However, there are significant genetic differences between these two conditions, as well as differing responses to biologic therapy.
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Mease, Philip. Biologic treatments for psoriatic arthritis apart from TNF inhibition. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198737582.003.0030.
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Psoriatic arthritis (PsA) is an immunologically mediated inflammatory disease characterized by arthritis, enthesitis, dactylitis, spondylitis, and psoriasis. Prior to the introduction of targeted biologic medications, such as TNF inhibitors, the ability to control disease activity was limited, with only modest effects noted with traditional oral medications such as methotrexate and sulfasalazine. The introduction of TNF inhibitors substantially changed the outlook of PsA patients, yielding significant response in all relevant clinical domains and demonstrating the ability to inhibit progressive structural damage of joints. However, not all patients responded to these agents and many patients displayed initial response which waned over time, partly due to immunogenicity (development of antibodies which blocked full therapeutic effect of the biologic protein), or because of tolerability and side effect issues. Thus, it has been important to develop new medicines which target other key cytokines and immunologic pathways. Several medicines with a different mechanism of action have been approved or are in development for the treatment of PsA. Ustekinumab inhibits both IL12 and IL23 and thus is felt to work in both the TH1 and TH7 pathways of inflammation. The oral medicine apremilast inhibits phosphodiesterase 4, thus modulating the cyclic AMP pathway in immunologic cells, yielding an anti-inflammatory effect. Both of these medicines have been approved for the treatment of PsA as well as psoriasis. An emerging group of therapies, the IL17 inhibitors, has demonstrated significant effectiveness in psoriasis and PsA and one of these, Secukinumab, has been approved for psoriasis, PsA, and AS. Other medicines in development include the co-stimulatory blockade agent, abatacept, oral Janus Kinase (JAK) inhibitors, and an emerging group of therapies which inhibit IL23. As modulators of immune cell function, these agents have the potential to increase risk for infection, as well as other side effects. These must be discussed with the patient and considered when determining overall risk benefit analysis regarding their use. The emergence of medicines with a different mechanism of action than TNF inhibition has broadened and strengthened our ability to effectively treat PsA.
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Oldstone, Michael B. A. Viruses, Plagues, and History. Oxford University Press, 2020. http://dx.doi.org/10.1093/oso/9780190056780.001.0001.
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“Viruses, Plagues, & History” focuses on the effects of viral diseases on human history. Written by an eminent internationally respected virologist, it couples the fabric of history with major concepts developed in virology, immunology, vaccination, and accounts by people who first had, saw and acted at the times these events occurred. Much of the preventive and therapeutic progress (vaccines, antiviral drugs) has been made in the last 60 years. Many of those who played commanding roles in the fight to understand, control and eradicate viruses and viral diseases are (were) personally known to the author and several episodes described in this book reflect their input. The book records the amazing accomplishments that led to the control of lethal and disabling viral diseases caused by Smallpox, Yellow Fever, Measles, Polio, Hepatitis A, B and C, and HIV. These six success stories are contrasted with viral infections currently out of control—COVID-19, Ebola virus, Lassa Fever virus, Hantavirus, West Nile virus, and Zika. Influenza, under reasonable containment at present, but with the potential to revert to a world-wide pandemic similar to 1918–1919 where over 50 million people were killed. The new platforms to develop inhibitory and prophylactic vaccines to limit these and other viral diseases is contrasted to the anti-vaccine movement and the false prophets of autism.
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Colbert, Robert A., and Paul Bowness. Immune mechanisms: HLA-B27. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198734444.003.0006.
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HLA-B27 is present in the majority of patients with ankylosing spondylitis (AS). Although we have learned a considerable amount about the natural immunologic function of HLA class I proteins, this has not provided a definitive mechanism of AS pathogenesis. While HLA-B27 is adept at presenting antigenic peptides to CD8+ T cells, ‘arthritogenic’ peptides targeted by a cross-reactive T or natural killer cell response have not been described, nor have autoreactive T cells been found. Newer concepts have evolved based on the propensity of HLA-B27 to ‘misbehave’, both inside cells and on the cell surface. Misfolded HLA-B27 molecules may stimulate an endoplasmic reticulum stress response, promoting production of IL-23 and then IL-17 and related cytokines. Aberrant cell-surface HLA-B27 molecules are ligands for natural killer and related immunoreceptors, and recognition can lead to IL-17 proinflammatory responses. There is growing evidence to suggest that these aberrant behaviours contribute to AS pathogenesis.
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Rohani, Pejman, and Samuel Scarpino, eds. Pertussis. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198811879.001.0001.
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Pertussis, or whooping cough, is a respiratory disease caused primarily by infection with the bacterium Bordetella pertussis. It remains one of the leading causes of death among vaccine-preventable diseases worldwide and recent years have seen its alarming re-emergence in many regions (including the United States and much of Europe), despite sustained high levels of vaccine coverage. The causes of the resurgence remain contentious, in part due to inherent complexities of the pathogen’s biology, in part due to pronounced variation in the treatment and prevention strategies between different countries and regions, and in part due to long-standing disagreement among scientific researchers studying pertussis. This edited volume brings together expert knowledge from disparate fields with the overall aim of synthesizing the current understanding of this critically important, global pathogen. Pertussis: Epidemiology, Immunology, and Evolution is an advanced text suitable for graduate-level students taking courses in evolutionary epidemiology, disease ecology, and evolutionary biology, as well as academics, public health officials, and researchers in these fields. It also offers a very useful introduction to a wider audience of public health practitioners, microbiologists, epidemiologists, medical professionals, and vaccine biologists
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Sklar, Larry A., ed. Flow Cytometry for Biotechnology. Oxford University Press, 2005. http://dx.doi.org/10.1093/oso/9780195183146.001.0001.
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Flow cytometry is a sensitive and quantitative platform for the measurement of particle fluorescence. In flow cytometry, the particles in a sample flow in single file through a focused laser beam at rates of hundreds to thousands of particles per second. During the time each particle is in the laser beam, on the order of ten microseconds, one or more fluorescent dyes associated with that particle are excited. The fluorescence emitted from each particle is collected through a microscope objective, spectrally filtered, and detected with photomultiplier tubes. Flow cytometry is uniquely capable of the precise and quantitative molecular analysis of genomic sequence information, interactions between purified biomolecules and cellular function. Combined with automated sample handling for increased sample throughput, these features make flow cytometry a versatile platform with applications at many stages of drug discovery. Traditionally, the particles studied are cells, especially blood cells; flow cytometry is used extensively in immunology. This volume shows how flow cytometry is integrated into modern biotechnology, dealing with issues of throughput, content, sensitivity, and high throughput informatics with applications in genomics, proteomics and protein-protein interactions, drug discovery, vaccine development, plant and reproductive biology, pharmacology and toxicology, cell-cell interactions and protein engineering.
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Olson-Chen, Courtney. Neurologic Infections in Pregnancy. Edited by Emma Ciafaloni, Cheryl Bushnell, and Loralei L. Thornburg. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190667351.003.0011.
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Despite advances in prevention, diagnosis, and treatment, infectious diseases continue to be a major cause of maternal, fetal, and neonatal morbidity and mortality. Immunologic changes in pregnancy can increase both susceptibility to certain infections and the severity of infection. Infectious diseases in pregnancy contribute to the development of congenital fetal syndromes in addition to adverse outcomes including preterm birth, stillbirth, and intrauterine growth restriction. While infections of the maternal central nervous system, or CNS, are rare during pregnancy, the potential impact can be critical.1 This chapter will cover both the types of infections within the CNS and the potential organisms that cause these infections. The chapter will also provide general management recommendations for pregnancy in order to both prevent and maintain awareness about CNS infections.
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Muñoz, George E., and Isabella Leoni Garcia. Functional Medicine Approach to Addiction. Edited by Shahla J. Modir and George E. Muñoz. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190275334.003.0018.
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The functional medicine protocol complements and enhances the traditional approach to recovery. Seen from a functional medicine perspective, the path to substance/and or food addiction recovery involves a multimodal approach. It shifts the focus from the imbalances in the brain and neurotransmitters to treat the whole person. It does so by considering the metabolic, hormonal, psychologic, immunologic, and neurologic functions that have been disturbed by addiction and that further perpetuate the inflammatory state of active addiction and during recovery phases. The gut-brain axis is reviewed from all aspects. Specific microbiome interventions, micronutrient, and vitamin deficiency support is reviewed. These interventions can be addressed through lifestyle modifications (including stress-reduction techniques), nutrition, supplementation, and in-depth case protocols, which will be further reviewed in the chapter.
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Morris, Peter J., and Jeremy R. Chapman. The evolution of kidney transplantation. Edited by Jeremy R. Chapman. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0275.
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The history of kidney transplantation starts in 1902 with Ullman transplanting kidneys between dogs, and Carrel’s development of vascular anastomotic techniques. The developments in the 1950s in Boston, Paris, and the laboratories of Medawar and others demonstrated both proof of the principle and some of the barriers to clinical kidney transplantation. The 1960s laid the groundwork for organ preservation, immunosuppression, and histocompatibility leading to the creation of transplant units in many countries. In the 1970s, there was steady progress in understanding the immunology of allograft rejection and its suppression. The advent of azathioprine used with steroids in the early 1960s resulted in 1-year graft survival rates of around 60% and patient survival of 90% in good units. However, with the introduction of ciclosporin in the early 1980s, renal transplantation became an even more reliable renal replacement option as there was a dramatic reduction in the incidence of irreversible acute rejection. The 1990s saw the introduction of both better immunosuppression and better infection prophylaxis, which further improved patient outcomes. The first decade of the twenty-first century has been characterized by the promise of new technologies in many areas, only some of which have delivered clinical benefit. Molecular human leucocyte antigen (HLA) typing and detection of antibodies to HLA antigens, standardized immunosuppression and anti-infective prophylaxis, surveillance biopsy, and developing systems for increasing donation rates are delivering major benefits. Gene biomarkers, stem cell therapy, and tolerance protocols have yet to make an impact. This chapter describes the historical development of transplantation and how it has yielded the results delivered in clinical practice today.
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Nass, MD, Ruth, and Yitzchak Frank, MD, eds. Cognitive and Behavioral Abnormalities of Pediatric Diseases. Oxford University Press, 2010. http://dx.doi.org/10.1093/oso/9780195342680.001.0001.
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This book provides a detailed account of intellectual, other neuropsychological and behavioral manifestations of general pediatric diseases. The conditions discussed include the whole range of pediatric diseases - genetic syndromes, other congenital conditions, metabolic, endocrine, gastrointestinal, infectious, immunologic, toxic, trauma, and neoplastic, as well as sensory disabilities including deafness and blindness. Although the book is not intended to discuss cognitive and behavioral manifestations of conditions usually considered to be primary neurological disease, some of those, including cerebral palsy, muscular dystrophy, myotonic dystrophy and epilepsy, are included. Where possible, a "translational" approach is used, linking the behavioral and cognitive manifestations of these conditions, to the underlying structural, chemical or genetic abnormalities and their effect on the brain, and, in turn, on behavior and cognition. At the same time, included are significant psychosocial factors. Together, those factors have a major effect on patients' performance, including school performance, and on their families. This book is unique in its extensive coverage of the major pediatric conditions and of the detailed neurological, neuropsychological and behavioral aspects of each condition.
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Howard, Colin R. Arenaviruses. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0032.
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There are few groups of viral zoonoses that have attracted such widespread publicity as the arenaviruses, particularly during the 1960’s and 1970’s when Lassa emerged as a major cause of haemorrhagic disease in West Africa. More than any other zoonoses, members of the family are used extensively for the study of virus-host relationships. Thus the study of this unique group of enveloped, single-stranded RNA viruses has been pursued for two quite separate reasons. First, lymphocytic choriomeningitis virus (LCM) has been used as a model of persistent virus infections for over half a century; its study has contributed, and continues to contribute, a number of cardinal concepts to our present understanding of immunology. LCM virus remains the prototype of the Arenaviridae and is a common infection of laboratory mice, rats and hamsters. Once thought rare in humans there is now increasing evidence of LCM virus being implicated in renal disease and as a complication in organ transplantation. Second, certain arenaviruses cause severe haemorrhagic diseases in man, notably Lassa fever in Africa, Argentine and Bolivian haemorrhagic fevers in South America, Guaranito infection in Venezuela and Chaparé virus in Bolivia. The latter is a prime example for the need of ever-continuing vigilance for the emergence of new viral diseases; over the past few years several new arenaviruses have been reported as implicated with severe human disease and indeed the number of new arenaviruses discovered since the last edition of this book have increased the size of this virus family significantly.In common with LCM, the natural reservoir of these infections is a limited number of rodent species (Howard, 1986). Although the initial isolates from South America were at first erroneously designated as newly defined arboviruses, there is no evidence to implicate arthropod transmission for any arenavirus. However, similar methods of isolation and the necessity of trapping small animals have meant that the majority of arenaviruses have been isolated by workers in the arbovirus field. A good example of this is Guaranito virus that emerged during investigation of a dengue virus outbreak in Venezuela (Salas et al. 1991).There is an interesting spectrum of pathological processes among these viruses. All the evidence so far available suggests that the morbidity of Lassa fever and South American haemorrhagic fevers due to arenavirus infection results from the direct cytopathic action of these agents. This is in sharp contrast to the immunopathological basis of ‘classic’ lymphocytic choriomeningitis disease seen in adult mice infected with LCM virus and the use of this system for elucidating the phenomenon of H2-restriction of the host cytotoxic T cell response (Zinkernagel and Doherty 1979). Despite the utility of this experimental model for dissecting the nature of the immune response to virus infection and the growing interest in arenaviruses of rodents, there remains much to be done to elucidate the pathogenesis of these infections in humans.
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Vogelnest, Larry, and Timothy Portas, eds. Current Therapy in Medicine of Australian Mammals. CSIRO Publishing, 2019. http://dx.doi.org/10.1071/9781486307524.
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Current Therapy in Medicine of Australian Mammals provides an update on Australian mammal medicine. Although much of the companion volume, Medicine of Australian Mammals, is still relevant and current, there have been significant advances in Australian mammal medicine and surgery since its publication in 2008. The two texts together remain the most comprehensive source of information available in this field.
This volume is divided into two sections. The first includes comprehensive chapters on general topics and topics relevant to multiple taxa. Several new topics are presented including: wildlife health in Australia and the important role veterinarians play in Australia’s biosecurity systems; medical aspects of native mammal reintroductions and translocations; disease risk analysis; wildlife rehabilitation practices in Australia with an emphasis on welfare of animals undergoing rehabilitation; management of overabundant populations; immunology; and stress physiology. The second section provides updates on current knowledge relevant to specific taxa. Several appendices provide useful reference data and information on clinical reference ranges, recommended venipuncture sites, chemical restraint agent doses and regimens, a drug formulary and dental charts.
Written by Australian experts, Current Therapy in Medicine of Australian Mammals is clinically oriented, with emphasis on practical content with easy-to-use reference material. It is a must-have for veterinarians, students, biologists, zoologists and wildlife carers and other wildlife professionals. This volume also complements, updates and utilises the resources of other books such as Radiology of Australian Mammals (Vogelnest and Allan 2015), Pathology of Australian Native Wildlife (Ladds 2009), Haematology of Australian Mammals (Clark 2004) and Australian Mammals: Biology and Captive Management (Jackson 2003), all CSIRO Publishing publications.