DOCSLIB.ORG

Don't Touch the Poison Ivy!

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Don't Touch the Poison Ivy! DON’T TOUCH THE POISON IVY! Fantastic Voyage Revisited: a conversation about the immune system, allergic hypersensitivity, and selected immunological issues OUTLINE OF ACTIVITY An overview of the immune system and vaccination stories (45 min) followed by a 15 minute break. Hypersensitivity (Bee stings and Poison Ivy), Anaphylaxis and stories (45 min) followed by a 15 minute break. Selected immune disorders [Hepatitis B, Type I Diabetes, HIV/AIDS, & one Zoonotic Example] (45 min) followed by discussion 15 minutes. *Constant questioning would be appreciated, let’s make this a conversation rather than a lecture! LET’S BEGIN THE FANTASTIC VOYAGE WHY DO WE NEED AN IMMUNE SYSTEM? BACTERIA, VIRUSES, FUNGI, PARASITES & NEOPLASTIC CELLS THINGS TO REMEMBER ON THE JOURNEY! Recognition Specificity Regulation Memory SO WHAT MAKES UP AN IMMUNE SYSTEM WHOA! ANTIGEN PRESENTATION AND T-CELL HELP & MEMORY HUMMORAL IMMUNITY B-CELL ACTIVATION ANTIBODY STRUCTURE KILLING OF MICROBES BY ANTIBODY CELLULAR IMMUNITY KILLING OF MICROBES BY CELLULAR IMMUNITY VACCINATION VACCINATION RATIONALE Vaccine Development Observations of natural immunity Identification of immunological targets Formulation and manufacturing Clinical trials, safety, efficacy Marketing Expected Outcome Elimination of clinical infection Eradication of disease All in the presence of evolving organisms, politics, opinions, legal challenges, and markets HOLD THAT THOUGHT! WE WILL BEGIN TO ITCH IN THE NEXT HALF HOUR. IGE-DEPENDENT IMMUNE RESPONSES & ALLERGIC DISEASE ACTIVATION OF TH2 CELLS AND PRODUCTION OF IGE Nature of Allergens WHAT HAPPENS UPON EXPOSURE TO ALLERGEN (ANTIGEN) MAST CELLS, BASOPHILS, & EOSINOPHILS MAST CELL & BASOPHIL MEDIATORS Biogenic amines Granule enzymes Proteoglycans Cytokines Lipid mediators Prostaglandin D2 Leukotrienes EOSINOPHIL MEDIATORS Granule proteins that are toxic to parasitic organisms and may injure normal tissue. Major basic protein Eosinophil cationic protein Eosinophil peroxidase Lipid mediators THE IMMEDIATE REACTION The wheal and flare reaction THE LATE-PHASE REACTION IGE MEDIATED ALLERGIC DISEASES Systemic Anaphylaxis ANAPHYLAXIS Vasodilation, fall in blood pressure (shock) Smooth muscle constriction of upper and lower airways, laryngeal edema, hypermotility of the gut, outpouring of mucous in the gut and respiratory tract, hives in the skin (respiratory distress) Epinephrine (adrenalin) reverses bronchoconstriction, vasodilation and increases cardiac output Antihistamines may also be beneficial OTHER IGE MEDIATED ALLERGIC DISEASES Bronchial Asthma Allergic Rhinitis Food allergies Urticaria and Eczema IMMUNOTHERAPY Desensitization (allergy shots) Shift from IgE to IgG Specific T cell tolerance Th2 to Th1 SO WHAT IS THE VALUE OF IGE & MAST CELLS? Protection against parasites Mast cells play an important protective role as part of innate immune response to bacterial infections Slower bleeding time in atopics, sudden cardiac arrest less common As a result of heightened response, protection against arthropod vectored diseases (my speculation) Just an unfortunate consequence of otherwise protective responses. The price we have to pay? Or have some organisms through evolution co-opted hypersensitivity to there own benefit (toxins)? CUTANEOUS “DELAYED” T-CELL MEDIATED HYPERSENSITIVITY Poison Ivy/Poison Oak Contact allergens Urushiol ALLERGIC DISEASE IN CATTLE: PSOROPTIC SCABIES (COWS ITCH TOO!!) YES!! ADDITIONAL IMMUNOLOGICAL TOPICS Autoimmune disease, > 30 diseases or syndromes Transplantation immunology Neuroimmunology Reproductive immunology Tumor immunology AUTOIMMUNE HEPATITIS Infection of the liver with the hepatitis B virus (HBV, serum hepatitis) 350 million people affected worldwide Little cytopathology caused by the virus Liver damage can be massive and devastating When serious damage occurs, it is the immune system that causes most, if not all, of the damage Both CD4 and CD8 cells are activated and a delayed-hypersensitivity reaction ensues. AUTOIMMUNITY: DIABETES (TYPE I) INSULIN DEPENDENT Age of onset 11 to 12 years Chronic autoimmune disease destroying the insulin + producing βcells in the pancreas (CD4 TH1, Cytokine TNF and IL-1, and potentially anti-insulin antibodies) No gender bias Strong genetic component (HLA-DR3, DR4) Possible onset with environmental “triggers” Viral infection, an example Serotype B Coxsackie virus Tandem repeats within the insulin promoter (genetic) T cells the major destructive agent with antigen being glutamic acid decarboxylase (GAD). Insulin itself also appears to be a target. Epidemiology data suggest that repeated infection protects from diabetes. Possible reason for increase incidence in developed countries. New Therapies: inducing immunological tolerance, generating or giving regulatory T cells to patients. A VIRAL DISEASE AFFECTING THE IMMUNE SYSTEM: HIV/AIDS First reported in 1981, opportunistic infections, Pneumocystis carinii, oral candidiasis, tuberculosis, and Kaposi’s sarcoma The human immunodeficiency virus (HIV) was identified in 1983 as a retrovirus. The coat proteins mutate at an extraordinarily high rate. Infects and causes a gradual loss of CD4 helper T cells Drug treatment is of 4 categories: nucleoside analogs, reverse transcriptase inhibitors, protease inhibitors and fusion inhibitors. HIV HIV has a surface coat protein gp 120 that specifically recognizes and binds to the CD4 molecule found on CD4 T cells Following binding the gp 120 molecule twists and reveals a second binding molecule gp 41 that binds a second coreceptor of the CD4 cell surface, called fusin. With both binding events the virus can enter the cell. Therapy Drug Cocktails – enfuvirtide blocks gp 41/fusin Vaccine is available for SIV and FIV, and observe cases of natural effective immunity. DNA based vaccine/CD8 preferential stimulation Molecular Medicine (gene therapy) antisense with target of suppression of fusin Selective expression of thymidine kinase and treatment with acyclovir ZOONOTIC IMMUNE DISORDER: CATTLE GRUB, HYPODERMA LINEATUM IMMUNE DISORDERS Human Case of Cattle Grub Infestation THE END BUT STAY TUNED .
Load more

Recommended publications
  • Urticaria Is a Skin Condition Commonly Known As Hives. It Produces an Itchy Rash That Tends to Come and Go and Can Last for a Variable Period of Time
    Hives Also known as Urticaria What is urticaria? Urticaria is a skin condition commonly known as hives. It produces an itchy rash that tends to come and go and can last for a variable period of time. The condition can be acute (lasting less than 6 weeks) or chronic (lasting longer than 6 weeks). Most cases of urticaria have no known cause. What causes urticaria? Urticaria occurs when certain substances such as histamine are released from specific cells in the skin. This process is usually triggered by various immunologic mechanisms, most commonly involving the presee of irulatig IgE atiodies, although other pathays ay also e ioled. The ause of this iuologi triggerig is uko i the ajority of ases, ut a soeties e associated with various types of infections, chronic immunologic diseases or allergy to foods or medications. The use of intravenous dyes during some radiological tests can sometimes trigger urticaria as well. Physical urticaria is a type of urticaria that may be caused by exposure of the skin to cold, heat, pressure or rubbing. What does urticaria look like? Urticaria typically looks like a raised rash that may be a normal skin colour or pinkish or red in colour. The rash may occur anywhere on the body and often starts off as small round spots that quickly enlarge and spread. The rash can be very itchy but it usually only lasts for a few hours before settling, and eventually resolving completely within 24 to 48 hours. Which other problems may occur with urticaria? A viral illness can occur before urticaria develops, especially in children.
    [Show full text]
  • Four Diseases, PLAID, APLAID, FCAS3 and CVID and One Gene
    Four diseases, PLAID, APLAID, FCAS3 and CVID and one gene (PHOSPHOLIPASE C, GAMMA-2; PLCG2 ) : striking clinical phenotypic overlap and difference Necil Kutukculer1, Ezgi Yilmaz1, Afig Berdeli1, Raziye Burcu G¨uven Bilgin1, Ayca Aykut1, Asude Durmaz1, Ozgur Cogulu1, G¨uzideAksu1, and Neslihan Karaca1 1Ege University Faculty of Medicine May 15, 2020 Abstract We suggest PLAID,APLAID and FCAS3 have to be considered as same diseases,because of our long-term clinical experiences and genetic results in six patients.Small proportion of CVID patients are also PLAID/APLAID/FCAS3 patients and all these have disease-causing-mutations in PLCG2-genes,so it may be better to define all of them as “PLCG2 deficiency”. Key Clinical Message: Germline mutations in PLCG2 gene cause PLAID,APLAID,FCAS3, and CVID.Clinical experiences in patients with PLCG2 mutations led us to consider that PLAID, APLAID and FCAS3 are same diseases.It may be better to define all of them as “PLCG2 deficiency”. INTRODUCTION The PLCG2 gene which is located on the 16th chromosome (16q23.3) encodes phospholipase Cg2 (PLCG2), a transmembrane signaling enzyme that catalyzes the production of second messenger molecules utilizing calcium as a cofactor and propagates downstream signals in several hematopoietic cells (1). Recently, het- erozygous germline mutations in human PLCG2 were linked to some clinical phenotypes with some overlap- ping features|PLCg2-associated antibody deficiency and immune dysregulation syndrome (PLAID) (OMIM 614878) and autoinflammation, antibody deficiency, and immune dysregulation syndrome (APLAID) (OMIM 614878) (2-4) and familial cold autoinflammatory syndrome (FCAS3) (OMIM 614468) (5). All of them are autosomal dominant inherited diseases.
    [Show full text]
  • Open Access for Incredible Lupus Research
    Lupus: Open Access Editorial Note Lupus: Open Access for Incredible Lupus Research Yves Renaudineau* Immunotherapy Graft Oncology, Innovative Medicines initiative precisesads, Réseau épigénétique et réseau canaux ioniques du Cancéropole Grand Ouest, European University of Brittany, Brest, France EDITOR’S PICKS The 04th Volume of this esteemed journal addresses the novel research performed by authors from parts of the world. Lupus is an Incurable auto immune disorder in which body Weinmann-Menke J, et al. in their case reports discusses that immune system attacks its own tissues or organs. It affects many Since our patient is suffering from the autoimmune disease parts of the body including Skin (Subcutaneous/cutaneous lupus erythematodes and is listed for kidney transplantation due Lupus), Kidneys (Lupus Nephrites), Brain (Cerebral/CNS to end stage renal disease, it is very likely that Lupus) etc., with several symptoms of Rashes (Malar, Discoid or immunosuppressant therapy will have to be initiated again in the photosensitive), Musculoskeletal Problems, Serositis, Anemia, future [1]. Seziures and several many more. We can find several Diagnostic approaches for Lupus. Elagib EM, et al. in his research article discloses that It is important to identify the possible differences in the effectiveness There is no cure for lupus, Yet many treatment options includes of rituximab in treating patients of CAPS associated with SLE NSAIDS, Immunosuoressives, Malario therapy, Usage of and patients of primary CAPS in order to determine the possible Steroids along with life style modifications and healthy diet can prognostic factors that could affect the therapeutic decisions and reduce the risk of lupus effected patients. The statistics provided results [2].
    [Show full text]
  • Immune Disorder
    EDITORIAL Immune disorder Dr.Dingliang Lv* EDITORIAL vaccines and antiseptics, kids today aren’t exposed to as many germs as they were at intervals the past. The shortage of exposure might produce their Immune Disorder could also be a condition at intervals that your system system liable to react to harmless substances. mistakenly attacks your body. The system guards against germs like bacteria and viruses. Once it senses these foreign invaders, it sends out a military of The early symptoms of the many response diseases square measure terribly fighter cells to attack them. In degree illness, the system mistakes a section similar, such as: Fatigue, aching muscles, Swelling and redness, inferior of your body, like your joints or skin, as foreign. It releases proteins fever, bother concentrating, symptom and tingling within the hands and mentioned as auto antibodies that attack healthy cells. Some reaction feet, Hair loss, Skin rashes. diseases target only 1 organ. The system can tell the excellence between Individual diseases may also have their own distinctive symptoms. For foreign cells and your own cells. instance, kind one polygenic disorder causes extreme thirst, weight loss, and Immune System Attack the body because of the following reasons however fatigue. IBD causes belly pain, bloating, and looseness of the bowels. With some people square Measure plenty of probably to induce degree illness response diseases like skin condition or RA, symptoms might return and go. than others. In step with a 2014 study, girls get reaction diseases at a rate of An amount of symptoms is termed outburst. An amount once the regarding 2 to 1 compared to men-half-dozen.4 proportion of women vs.
    [Show full text]
  • Hypersensitivity in General Immune System Is Protective in Nature by Protecting Host Body from Harmful and Infectious Foreign Microorganisms
    Hypersensitivity In general immune system is protective in nature by protecting host body from harmful and infectious foreign microorganisms. But hypersensitivity is an immune disorder where immune system responds more than required and cause harmful effects in host. Hypersensitivity is defined as an exaggeration immune response that results in tissue damage in a sensitized individual on 2nd or subsequent contact with specific antigens. This condition is also called allergy. The first contact with an antigen leads to sensitization the immune system in the host for production of specific allergen produces the manifestation of hypersensitivity. This is known as shocking dose. Basing on the time required for the appearance of the hypersensitivity reactions. They are classified into two types: 1. Immediate hypersensitivity 2. Delayed hypersensitivity Peter Gell and Robert Coombs classified hypersensitivity reactions into 4 types based on the mechanism of pathogenesis: Type 1: IgE mediated hypersensitivity Type 2: Ab dependent cytotoxic hypersensitivity Type 3: Immune complex mediated hypersensitivity Type 4: Cell mediated delayed hypersensitivity The first three types of hypersensitivity reactions are mediated through the production of Antibodies and the fourth type of reaction is mediated through the production of T cells. Type 1: IgE mediated hypersensitivity It occurs in two forms anaphylaxis and atopy. i. Anaphylaxis It is an acute, fatal and systemic form of type I hypersensitivity. The allergens include antibiotics like Penicillin, antitoxin, insect venom etc. On first contact with allergen and lymphocytes are differentiated into plasma cells and produce specific Immunoglobulin IgE also called as ''Reagin antibodies'' which binds to the Fc receptors of mast cells or basophiles and sensitizes these cells that make the individual allergic to the antigen.
    [Show full text]
  • Hypersensitivity Adverse Event Reporting in Clinical Cancer Trials: Barriers and Potential Solutions to Studying Severe Events on a Population Level
    University of Wisconsin Milwaukee UWM Digital Commons Theses and Dissertations May 2020 Hypersensitivity Adverse Event Reporting in Clinical Cancer Trials: Barriers and Potential Solutions to Studying Severe Events on a Population Level Christina E. Eldredge University of Wisconsin-Milwaukee Follow this and additional works at: https://dc.uwm.edu/etd Part of the Library and Information Science Commons, and the Medicine and Health Sciences Commons Recommended Citation Eldredge, Christina E., "Hypersensitivity Adverse Event Reporting in Clinical Cancer Trials: Barriers and Potential Solutions to Studying Severe Events on a Population Level" (2020). Theses and Dissertations. 2371. https://dc.uwm.edu/etd/2371 This Dissertation is brought to you for free and open access by UWM Digital Commons. It has been accepted for inclusion in Theses and Dissertations by an authorized administrator of UWM Digital Commons. For more information, please contact [email protected]. HYPERSENSITIVITY ADVERSE EVENT REPORTING IN CLINICAL CANCER TRIALS: BARRIERS AND POTENTIAL SOLUTIONS TO STUDYING SEVERE EVENTS ON A POPULATION LEVEL by Christina Eldredge A Dissertation Submitted in Partial Fulfillment of the Requirements for the Degree of Doctor in Philosophy in Biomedical and Health Informatics at The University of Wisconsin-Milwaukee May 2020 ABSTRACT HYPERSENSITIVITY ADVERSE EVENT REPORTING IN CLINICAL CANCER TRIALS: BARRIERS AND POTENTIAL SOLUTIONS TO STUDYING ALLERGIC EVENTS ON A POPULATION LEVEL by Christina Eldredge The University of Wisconsin-Milwaukee, 2020 Under the Supervision of Professor Timothy Patrick Clinical cancer trial interventions are associated with hypersensitivity events (HEs) which are recorded in the national clinical trial registry, ClinicalTrials.gov and publicly available. This data could potentially be leveraged to study predictors for HEs to identify at risk patients who may benefit from desensitization therapies to prevent these potentially life-threatening reactions.
    [Show full text]
  • Poison Ivy (Toxicodendron Radicans) DESCRIPTION
    Weed Identification and Control Sheet: www.goodoak.com/weeds Poison Ivy (Toxicodendron radicans) DESCRIPTION: Poison ivy is a native woody vine and member of the sumac family. It can be found in shady and sunny sites rambling along the ground, forming a small shrub, or climbing up trees. The vines attach to surfaces by means of thin aerial roots which grow along the length of the stem. The plant always has three leaflets which are often serrated. Usually these leaflets have one dominant lobe, giving the outer two leaves the appearance of mittens with the central leaf resembling a mitten with two thumbs. Young leaves are often dark green or maroonish, and the attractive fall foliage can range from brick to fire- engine red. Poison ivy is generally not considered a threat to native plant communities, in fact, the white berries provide winter food for birds and deer relish the foliage. Though harmless to most animals, many humans are allergic to the urushiol (yoo-roo-shee-ol) oil produced by the plant which results in itching, inflammation and blisters. This oil is found in all parts of the plant during all times of the year. This oil can also be spread by contact with clothing, shoes, pets or equipment that have touched poison ivy weeks or months after initial contact. It can even be transmitted in the air when poison ivy is burned, which presents a severe risk if inhaled and has been known to result in hospitalization and death. Though some people are not alleargic to the oil, its important to wear pants, long sleeves and gloves when working around poison ivy since the allergy can develop af- ter repeated exposures to urushiol.
    [Show full text]
  • Understanding Allergies Feel Better
    Understanding Allergies Feel Better. Breathe Better. Live Better. Special Edition of Who We Are Allergy & Asthma Network is the leading nonprofit patient outreach, education, advocacy and research organization for people with asthma, allergies and related 8229 Boone Blvd. conditions. Suite 260 Vienna, VA 22182 Our patient-centered network 800.878.4403 unites individuals, families, AllergyAsthmaNetwork.org healthcare professionals, industry [email protected] leaders and government decision- makers to improve health and Understanding Allergies – Allergy quality of life for the millions of & Asthma Today Special Edition people affected by asthma and is published by Allergy & Asthma allergies. Network, Copyright 2020. All rights reserved. An innovator in encouraging family participation in treatment Call 800.878.4403 to order FREE plans, Allergy & Asthma Network copies; shipping and handling specializes in making accurate charges apply. medical information relevant and understandable to all while promoting standards of care that are proven to work. We believe that integrating prevention with treatment helps reduce emergency healthcare visits, keeps children in school and adults at work, and allows participation in sports and other activities of daily life. Our Mission PUBLISHER To end needless death and suffering Allergy & Asthma Network due to asthma, allergies and related conditions through outreach, PRESIDENT AND CEO education, advocacy and research. Tonya Winders Allergy & Asthma Network is a MANAGING EDITOR 501(c)(3) organization.
    [Show full text]
  • Bronchial Mucosal Manifestations of Atopy: a Comparison of Markers of Inflammation Between Atopic Asthmatics, Atopic Nonasthmatics and Healthy Controls
    Eur Resplr J 1992, 5, 538-544 Bronchial mucosal manifestations of atopy: a comparison of markers of inflammation between atopic asthmatics, atopic nonasthmatics and healthy controls R. Djukanovi6*, C.K.W. Lai**, J.W. Wilson*, K.M. Britten*, S.J. Wilson*, W.R. Roche***, P.H. Howarth*, S.T. Holgate* Bronchial mucosal manifestations of atopy: a comparison of markers of infiamma· • Immunopharmacology Group, Medi· tion between atopic asthmatics, atopic nonasthmatics and healthy controls. cine 1, Southampton University General R. Djukanovic, C.K. W. Lai, J. W. Wilson, K.M. Britten, S.J. Wilson, W.R. Roche, Hospital, Southampton, UK. P.H. Howarth, S.T. Holgate. • • Presently at Dept of Medicine, Prince ABSTRACT: We studied the role of atopy, as defined by positive skin tests to of Wales Hospital, Shatin, Hong Kong. common Inhalant allergens, In allergic bronchial inflammation. ••• Pathology, Southampton University Endobronc.hlal biopsies were taken via the fibreoptic bronchoscope ln 13 General Hospital, Southampton, UK. symptomatic atopic asthmatics, 10 atopic nonasthmatlcs, and 7 normals. Correspondence: R. Djukanovic, The numbers of mast cells, Identified In the submucosa by Immunohisto­ Immunopharmacology Group, Medicine chemistry using the AA1 monoclonal a.ntibody against tryptase, were no dif­ 1, Southampton University General ferent between the three groups, but electron microscopy showed that mast cell Hospital, Southampton S09 4XY, UK. degranulation, although less marked In atopic nonastbmatlcs, was a feature of Keywords: Allergic rhinitis; asthma; atopy In general. The numbers or eoslnophlls, ldentlfled by Immunohisto­ collagen; eosinophils; mast cells; chemical staining using the monoclonal anti-eosinophil cationic protein antibody, mucous membrane. EG2, were greatest In the asthmatics, low or absent in the normals and inter· mediate In the atopic nonasthmatlcs.
    [Show full text]
  • Rheumatoid Arthritis
    Straub Arthritis Research & Therapy 2014, 16(Suppl 2):I1 http://arthritis-research.com/content/16/S2/I1 INTRODUCTION Rheumatoid arthritis – a neuroendocrine immune disorder: glucocorticoid resistance, relative glucocorticoid defi ciency, low-dose glucocorticoid therapy, and insulin resistance Rainer H Straub* Neuroendocrine immunology owes much to the fore- can exist for a long time beyond acute infl ammation sighted work of Philip S Hench, who together with control (that is, imprinting). In such a situation, long- Edward C Kendall and Tadeus Reichstein introduced term therapy with low-dose GC must be recognized as a glucocorticoids (GCs) into clinical medicine. Since the supplementary therapy for the adrenal glands. 1990s, more than 40 years after adding GC to the thera- Indeed, between 1990 and today the outstanding role peutic armamentarium, important work has been carried of low-dose GC (approximately 5 mg/day) was discovered out to understand GC action. Th ere were three major in rheumatoid arthritis (RA) patients using placebo- pathways of discoveries between 1990 and today. controlled randomized clinical trials, as summarized in Firstly, the groups of George Chrousos and of Steven this supplement by Marlies van der Goes and colleagues. Lamberts defi ned hereditary GC resistance due to abnor- In an unstressed individual, the usual daily production of malities of the GC receptor (fi rst reviewed in [1,2]). endogenous cortisol mounts to 5.7 mg/m2 (depending on While genetically determined alterations of the GC body surface, ≈10 to 14 mg/day) [5], which equals 2.5 to receptor were rare in the population, infl ammation- 3.5 mg prednisolone/day.
    [Show full text]
  • Intriguing World of Weeds Iiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiii
    Intriguing World of Weeds iiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiii Poison-Ivy/Poison-Oak/Poison-Sumac-The Virulent Weeds 1 LARRY W. MITICH2 I I; INTRODUCTION I, ii The word poison entered the English language in 1387 as 'poysoun" (18), and in Memoirs ofAmerican Academy of Arts and Sciences, v. 1, 1785, the word poison-ivy was used for the first time: "Poison ivy ... produces the same kind of inflammation and eruptions . as poison wood tree" (18). · The first known reference to poison-ivy, Toxicodendron radicans (L.) Ktze., dates from the 7th century in China and the 10th century in Japan. Since Toxicodendron species do not grow in Europe, the plants re­ mained unknown to Western civiliza­ tion until explorers visited the New World seven centuries later (7). Capt. John Smith (1579-1631) wrote the first description of poison-ivy and origi­ nated its common name; he noted a similarity in the climbing habit of They used that name for a shrub of the Southern States, North American poison-ivy to English with crenately-lobed, very pubescent leaflets (1). ivy (Hedera helix L.) (7). Toxicodendron, a pre-Linnaean name, was not accepted Joseph Pitton de Tournefort (1656-1708) established at the generic level by Linnaeus. Tournefort limited the the genus for poison-ivy in lnstitutiones rei herbariae, v. genus to ternate-leaved plants, thus omitting such close 1, p. 610, 1700 (7). The name is from the Latin for poison­ relatives of poison-ivy as poison-sumac and the oriental ous tree (9). lacquer tree (7). The lacquer tree has been known for In 1635 Jacques Philippe Cornut ( 1601-1651) wrote the first book on Canadian botany (Canadensium Plantarum thousands of years, and descriptions of the inflammations aliarumque nondum editarum historia, Parisiis [Paris]).
    [Show full text]
  • Diseases of the Immune System 813
    Chapter 19 | Diseases of the Immune System 813 Chapter 19 Diseases of the Immune System Figure 19.1 Bee stings and other allergens can cause life-threatening, systemic allergic reactions. Sensitive individuals may need to carry an epinephrine auto-injector (e.g., EpiPen) in case of a sting. A bee-sting allergy is an example of an immune response that is harmful to the host rather than protective; epinephrine counteracts the severe drop in blood pressure that can result from the immune response. (credit right: modification of work by Carol Bleistine) Chapter Outline 19.1 Hypersensitivities 19.2 Autoimmune Disorders 19.3 Organ Transplantation and Rejection 19.4 Immunodeficiency 19.5 Cancer Immunobiology and Immunotherapy Introduction An allergic reaction is an immune response to a type of antigen called an allergen. Allergens can be found in many different items, from peanuts and insect stings to latex and some drugs. Unlike other kinds of antigens, allergens are not necessarily associated with pathogenic microbes, and many allergens provoke no immune response at all in most people. Allergic responses vary in severity. Some are mild and localized, like hay fever or hives, but others can result in systemic, life-threatening reactions. Anaphylaxis, for example, is a rapidly developing allergic reaction that can cause a dangerous drop in blood pressure and severe swelling of the throat that may close off the airway. Allergies are just one example of how the immune system—the system normally responsible for preventing disease—can actually cause or mediate disease symptoms. In this chapter, we will further explore allergies and other disorders of the immune system, including hypersensitivity reactions, autoimmune diseases, transplant rejection, and diseases associated with immunodeficiency.
    [Show full text]