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179 Cards in this Set
- Front
- Back
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An organism that lives on or in another organism and depends upon the host for nutrition
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Parasitism
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Parasite needs a host to complete life cycle
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Obligate parasite
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Parasite may or may not need host to complete life cycle
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Facultative parasite
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Host susceptibility depends on ___, _____, & __________.
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nutrition, age, and genotype
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CD8+ cells only recognize antigens on _______. They are essential for ______ immunity and control ___________ pathogens
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-MHC I
-Cell mediated -Intracellular |
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CD4+ recognize antigens on ______ and are essential for _______ immunity.
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-MHC II
-Antibody mediated (humoral) |
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Th1 Response involves which cytokines?
Antibodies? Pro or Anti inflammatory? What type of immunity? |
-IFN gamma, IL-12, IL-12
-IgG antibodies -Pro-inflammatory -Cell mediated |
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Th2 Response involves which cytokines?
Antibodies? Pro or Anti inflammatory? What type of immunity? |
-IL-4, 5, 9, 10
-IgG and IgE -Anti-inflammatory -Humoral |
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When Th1 cells improve ________ response release interferon gamma: _________ are activated, and expression of ______ on ____ are amplified
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-Cell mediated
-Macrophages -MHC II cells on Antigen Presenting Cells |
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Th2 cells assist in improving _____ immunity and release IL-4, which stimulate ______. Th2 cells also activate _____ to defend against parasites via ___ antibodies
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- Humoral immunity
-B cells -eosinophils -IgE |
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Helminth parasites do not induce synthesis of IL-12, they stimulate this __(cytokine)__ which drives _____ pathway development
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-IL-4
-Th2 |
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If _______ is present during early helminth infection, TH2
development does not occur; reduction in ____ and ____ |
-IL-12
-IgE and eosinophils |
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What methods is used to kill parasites?
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- Direct killing via NO by macrophages
-ADCC by macrophages and eosinophils |
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What mechanisms do parasites use to evade immune system?
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-Antigenic variation
-Evasion from macrophages -Resistance to complement lysis -Immune suprression Surface and secreted antioxidant enzymes |
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How do parasites evade macrophages?
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-Prevent lysosome-phagosome fusion
-prevent lysosomal toxic action -Escape into cytoplasm |
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How do macrophages and eosinophils kill an organism via ADCC?
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IgE binds to eosinophil Fc receptor and parasite and degranulates, releasing reactive oxygen and intermediates and toxins
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Parasites stimulate the innate immune system because they are detected as ______
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PAMPs
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INTRAcellular protozoan parasite
-promastigotes in macrophages transform into amastigotes which live in phagosomal vacuole -Sand Fly vector |
Leishmania
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Three disease types of Leishmania
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1. Visceral (L. donovani)
2. Cutaneous (L. major, tropica, mexicana) 3. Mucocutaneous (L. brasiliensis) |
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Present on the leishmania parasite surface that is recognized by toll-like receptors
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LPG (lipophosphoglycan)
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When toll-like receptors recognize LPG on parasite surface, how to macrophages respond?
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Destroy intracellular parasite by producing nitric oxide and reactive oxygen intermediates
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Leishmania recovery depends on ______.
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Cell mediated Immunity
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How does leishmania evade the immune system?
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-Hide within macrophages
-Activate complement, where opsonization uptakes parasite into macrophages -LPG inhibits lysosomal enzymes, MAC, and IL-12 (fewer macrophages) |
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Danger of Live, virulent Leishmania major vaccine
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May develops ulcerating primary lesions (slow to non-healing)
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Parasites responsible for African Sleeping Sickness
Vector? -Intra or Extracellular? |
-Trypanosoma brucei gambiense (West Africa) - chronic infection
-Trypanosoma brucei rhodesiense (East Africa) - acute illness -Tsetse Fly -Extracellular |
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Host immune response to African Sleeping sickness?
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-Antibody and complement
-High levels of IgM/Eosinophils -B Cell proliferation |
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Africa Sleeping sickness Evasion strategies
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-Antigenic switching of variant surface glycoprotein coat
-Waves of fever and parasitemia |
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Chagas Disease
-Parasite -Vector -Intra or Extracellular |
-Trypanosoma cruzi
-Reduuvid (kissing bug) -Intracellular |
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Acute phase of Chagas infects _____, ____ and ______ cells.
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Macrophages, muscle, and nerve cells
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Chronic phase of Chagas disease affects ______ & ______ in 30 % of cases.
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heart and digestive tract
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Chagas parasites cross react with _____ & _______ antigens, causing immune reaction to targest host's antigens.
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cardiac muscle and mesenteric nerve antigens
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Chagas Host Immune Response
-Type of Response -Intracellular or extracellular? |
-Intracellular with short extra periods ---TH1
-Macrophages, lysosomes, reactive oxygen species, and NO -IL-12 , Increase IFN gamma, develop Th1 Response -Both CMI and Ab mediated Immunity in chronic stage |
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Chagas Parasite evasion strategies
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-Intracellular
-Evade complement by binding C3b and C4b (express gp160) -Escape in cytoplasm of macrophage -Down regulate MHC II expression on APCs (turn off macrophage) |
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Issues with Chaga's vaccine?
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Potential autoimmune. Unclear if the immune response should be stimulated to eliminate parasite or inhibited to avoid autoimmunity.
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Malaria
-Parasite -Vector -Intra or Extracellular? |
-Plasmodium
-Anopheles -Intracellular |
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How do malaria parasites alter RBC membranes & what is its effect on the body?
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RBC develop sticky knobs on surface, causing RBC to stick together and adhere to capiillaries. The result is clogging of cerebral microcirulation, hypoxia, or increased lactate production
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What type of immune response is associated with malaria?
What cytokines are involved? What proinflammatory cytokine rises in serum levels? |
-Th1
-IFNgamma, IL-2, IL-12 -TNFalpha |
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Malaria merozoite surface proteins active ____________
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Toll-like receptors
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After RBC rupture and release antigen Host immune involvement in 1st malaria infection?
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-Merozoite surface proteins activate toll-like receptors
-Inflammatory cytokines (TNFalpha) -Macrophages -NK Cells and T cells produce IFNgamma -NO and free radical kill parasites |
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What is the body's immune response in a repeat infection of malaria?
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-Spleen filters blood and removes antigens
-Decrease inflammation (decrease TNFalpha by IL-10) -Th1 becomes a Th2 response (IL-10) |
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Cerebral malaria is a result of
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Increased IFNgamma production in re-exposure to malaria, increasing macrophage activation and production of inflammatory TNF and NO (interfere with neurotransmission)
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Malaria Cell Mediated Immunity Evasion Strategies
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-Antigenically distinct stages in lifecyle
-Hide in RBC and liver cells -Immunosuppression -Modulate T & B Cell responses |
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Why are malaria cells within RBC not recognized by CD8+ cells?
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Red blood cells do not have MHC Class I antigens
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How do malaria parasites modulate memory T & B cells response to evade the immune system?
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-Memory Th1 cells depleted
-Deplete CD4+ specific cells |
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How do malaria parasites cause immunosuppression?
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Prevent antigen presentation and downregulate T Cells
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Malaria Antibody Mediated Immunity Evasion Strategies
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Alter surface molecules through "var" genes (Antigenic variation) (PfEMP1)
-Antibodies against Merozoite surface surface protein prevent invasion of region -Abs are strain specific (change in different regions) |
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-Antigen needed by P. vivax merozoites to enter RBCs
-Resistant to P. vivax if without |
Duffy antigen
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A person is more likely to survive acute illness from P. falciparum if they have ______, where red blood cell have an abnormal shape
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Inherited Sickle Cell trait
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Multicellular worms that have long life spans, are usually extracellular, have life cyles with intermediate hosts, larval stages, and adults
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Helminths
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Parasitical filarial worms that cause Lymphatic filariasis
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Brugia malayi and Wuchereria bancrofti
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Host immune response to microfilariae is primarily _______.
Primary cytokines include? |
TH2
IL-4, 5, 10 (IgE and IgG as well) |
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Host immune to response to adult filarial worms living in the _______ is ______.
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Lymphatic system, proinflammatory (TH1)
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Lymphatic damage from filariasis can lead to thickened _____ and _____ or ______ superinfections
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skin
bacteria or fungal |
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Pathogenesis from filarial can be contributed to elevated levels of ______, _____, & ________
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IgE, IgG, and Cell mediated immunity
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Filariasis parasite evasion strategy
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-Brugia expresses proteins during molting that induce Treg (downregulate immune response)
-Protease inhibitors block MHCII presentation -Surface glycans interrupts inflammatory response -Acquire host serum albumin on cuticle (disguise) |
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In Schistosomiasis, when adults _______ that secrete soluble antigens into tissues, early _____ response switches to _____
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lay eggs, TH1, TH2
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In Schistomiasis, these cytokines ______ promote recruitment of eosinophils, B Cells, T cells, and macrophages form ______ around eggs, leaving fibrotic plaques
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IL-4, 5, 13
granulomas |
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Human symptoms from schistosomes
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hepatoslenomegaly, portal hypertension
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This worm has a double lipid bilayer tegument that is rapidly replaced, presents few antigens, and participates in molecular mimicry to evade the immuen system
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schistosomes
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Schistosome evasion strategies
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-double libid bilayer tegument
-blocking abs protects new larvae -TNFalpha increases egg production -Proteases that vleave host Ig secreted |
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Extracellular tissue nematode found in the muscles
-matures in gut and migrates via blood to skeletal muscle |
Trichinella spiralis
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Immune system response to trichinella?
Intracellular or Extra |
Extracellular - TH2 Response
-high levels of IL-4 & IL-5 -Eosinophils and IgE -IMMEDIATE HYPERSENSITIVITY rxn |
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Trichinlla evasion strategies?
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-Lives in muscle cells
-Inhibits Macrophages -Nonspecific immunosuppression |
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-Dog tapeworm
-Zoonotic infection -Eggs can be ingested by human and infect an organ, most commonly the liver and lung -Forms hydatid cysts |
Echinococcus granulosas
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Echinococcus granulosus evasion strategies
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-Hydatid cyst development
-Antigens elicit TH2 response, not protective TH1 -Depletes complement |
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Fibrotic host capsule that shelters parasite. If ruptures it releases antigens and a person can go into anaphylactic shock
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Hydatid cyst
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Large, intestinal soil transmitted helminth that evade immune system by molecular mimicry (collagen) and lowering TH1 and TH2 responses
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Ascaris lumbricoides
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Intestinal threadowmr which can be transmitted via soil, autoinfection and breast milk. Evades immune system by autoinfection by inducing IL-10 secretion (antiinflammatory)
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Strongyloides stercoralis
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Helminth that sheds teguments and migrates around gut to avoid local inflammation
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Hookworm (Necatur americanus, Ancylstoma duodenale)
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Host immune response to soil-transmitted helminths (Ascaris, Threadworm, Hookworm)
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-TH2 response (large extracellular worms)
-Antibody + complement -Increased eosinophils and mast cells -IL-4 & IL-5 to activate macrophages /eosinophils -IL-4, 9, 13 to expel gut nematodes |
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Which cytokines are responsible for nematode gut expulsion?
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IL-4, 9, and 13
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Two basic forms of fungi
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Yeast and Molds
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Unicellular fungi that reproduced by budding
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Yeast
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Multicellular hyphae fungi that can reproduce asexually and/or sexually
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Mold
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Free living, not obligate parasites that are ubiquitous, grow in/on soil, plants and water, and produce infection due to immunodeficiency
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Fungi
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Innate Immunity against Fungi
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-Skin
-Mucuous membrane -serum -skin secretions -phagocytosis |
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3 types of Diseases caused by Fungi
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-superficial (dermatophytes - skin hair nails, candida infection of mucosal surface)
-subcutaneous (puncture wounds, abscess) -systemic |
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How does one get mycoses?
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Inhalation of spores free living pathogenic fungi
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Systemic mycoses results from inhalation of ______ of free living fungi.
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-spores
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Opprtunistic mycoses are _____ infections that compromise immune system.
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-Secondary
-Canida, aspergillus, cryptococcus, pneumocystosis |
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Systemic mycoses featuring chronic pulmonary disease that mimics TB
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Histoplasma capsulatum
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Systemic mycoses features acute pulmonary disease affecting lungs, skin, or GI
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Blastomyces dermatitidis
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Systemic mycoses featureing pulomary or disseminate to the meninges, bones, joints, and cutaneous tissue
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Coccidoides immitis
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Opportunistic mycoses
-Normal commensal -Infects any body surface or organ -Immunodeficient at risk |
Candida albicans
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-Allergic pulomary and invasive Opportunistic mycoses
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Aspergillus
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-Opportunitic mycoses acquired in childhood from pigeon droppings
-Can reactive in AIDS patients |
Cryptococcus neoformans
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-Opportunistic mycoses
-Infect by age 3-4 with pneumonia -#1 cause of death among immunocompromised |
-Pneumocyst jiroveci
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Innate immune response to Fungi
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-Skin, flora, complement
-Neutrophils (phagocytosis) to site by chemotactic factors or complement activation -Alveolar macrophages -NK Cells |
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Issues with Neutorphils in yeast immune response?
How bout those alveolar macrophages? What is wrong with them? |
Yeast inhibits neutrophil function because capsule prevents receptor binding
Alveolar Macs inhaled from spores need to activated |
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Acquired host immune response to fungi?
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- Dependent on pathogenic specific TH1 cells
-Neutrophils produce IL-12 -> TH1 --> macrophages -TH2 / IL-4 reduce TH1 cells |
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Dermatophytes can be controlled by a strong ________ response. _____-type hypersensitivity (th1) can clear infection. ______-type hypersensitivity response (th2) leads to chronic infection
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-Inflammatory
-Delayed-type -Weak or immediate |
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Aspergillus
-Opportunistic or System mycoses? -Evasion strategy? |
-Opportunistic
-Inhibit complement |
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Candida
-Opportunistic or Systemic mycoses? -Evasion Strategy? |
-Opportunistic
-Degrade C3 with protease and hydrolytic enzymes invade host cells |
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Cryptococcus
-Opportunistic or Systemic? -Evasion strategies? |
-Opportunistic
-Sheds capsular coat and bind complement receptors, suppress C5a, secrete enzymes |
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Pneumocytis
-Opportunistic or Systemic? -Evasion strategies? |
-Opportunistic
-MSG antigen variation, similar to VSG in trypanosomes |
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Coccidoides
-Opportunistic or Systemic? -Evasion strategies? |
-Systemic
-Forms tissue cysts, no inflammation |
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Histoplasma
-Opportunistic or Systemic? -Evasion strategies? |
-Systemic
-proliferates intracellularly in alveolar macrophages |
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Blastomyces
-Opportunistic or Systemic? -Evasion strategies? |
-Systemic
-BAD1 antigen uses complement receptor to bind to other host cells and tissues & change surface antigens |
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Gram + cell wall made up of _______. Gram - cell wall made up of ________.
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-Peptidoglycan
-Lipopolysaccharide |
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Gram + peptidoglycan cell wall is broken down by ____ and ____
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lysosomal enzymes and phagocytosis
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Gram - lipopolysaccharide wall is broken down by _____ and _____
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complement & cytotoxic cells
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Mycobateria cell wall is made up of ____ * ____
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glycolipids and mycolic acid
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Spirochaetes cell wall is made up of ____ & _____
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lipoprotein and outer envelope
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Primary Defense against bacteria is mainly by the ________ & _______
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skin and pH changes
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Secondary-non antibody mediated defense against bacteria
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-complement activation (alternative pathway, C3a and C5a, histamine, increased vascular permeability, activate macs and neutrophils, opsonization)
-chemotaxis attract phagocytes -macrophages and NK cells (cytokines released) -Lipopolysaccharide neutralized by LPS binding protein (TLR 4 --> macrophage activation) -IL-1 resets hypothalamus to higher temp |
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Cytokines released during secondary-non antibody mediated defense against bacteria
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-TNFalpha & IL-12: stimulated NK, TH1
-IL-1 reset hypothalamus to higher temp |
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Antibody mediated defense against Bacteria
-Neutralize _____ and ______ -Prevent binding to ______ -Block ______ and _______ -More efficient targeting of _______, including direct _________ of bacterial cells and enhanced binding & uptake by phagocytes, which is part of the ______ pathway. |
-toxins and enzymes
-epithelial surface (IgA) -transport mechanism and receptors -complement, opsonization, Classical Pathway |
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When antibody mediated complement targets gram positive bacteria, No _______ forms
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MAC Complex
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Antibody mediated mechanisms for combating infection by extracellular bacteria
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-Opsonization via macrophage Fc receptors
-Complement via Classical Pathway (No MAC for G+) -ADCC (neutrophil) |
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Antibody mediated mechanisms for combating infection by intracellular bacteria
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- Antigen presented to CD8 for MHC I and CD4 for MHCII
- Antibodies bind bacterial antigens present on host surface (ADCC) -TH1 cells activate macrophages -> protease & ROI ->infected cell death |
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Most bacteria is killed by _____
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Phagocytosis
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Phagocytes are attracted to (4 things). They attach to an organism via (3 things)
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-Complement, cytokines, chemokines, chemotaxis
-Lectins, Complement, Fc receptors on phagocyte linking Antibody |
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Microbicidal activity during phagocytosis includes:
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-reactive oxygen intermediates
-reactive nitrogen intermediates -catonic proteins -acidification lysozyme -lactoferrin |
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Bacteria's main defense is to _______
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avoid complement mediated damage
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How do bacteria avoid complement (x6)
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-capsule blocks attachment
-fimbrae/flagella block attachment -surface structure divert attachment of lytic complex -surface bound enzyme degrades/releases bound complement -Decoy proteins (secrete inhibitors of complement) -lytic complex cannot penetrate cell wall |
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Intracellular defense BY bacteria
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-Secrete toxins and block actiation of cells by INF
-Avoid death by phagocytosis -Infected cells do not act as APC -Lysis of infected cell releases many infectious bacteria |
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-Secreted by bacteria, it can cause illness without invading tissue
-Attach to epithelial surface -Can invade tissue, causing illness from immunopathologic reaction or occupy space |
Exotoxin
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Exotoxins that increase cyclic AMP,GMP leading to fluid secretion an diarrhea
-Example Vibrio cholera |
Enterotoxin
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Exotoxin that increases ulceration (S. aureus) and increases invasivenes (Shigella)
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Cytotoxins
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-Lipopolysaccharide (LPS) is a componenent of the cell wall of gram negative bacteria & is released when lysed
-Exess triggeres massive release of cytokines and causes endothelial cells to produce cell adhesion molecules and thromboplastin --> intravascular coagulation, fluid moves into tissues |
Endotoxin
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Species specific outermost segment of Endotoxin that has antigenic variability
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O Antigen
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Genus specific middle segment of endotoxin that contains unique sugars and phosphate groups that confer stability within the cell wall
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Core polysaccharide
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Inner segment of the endotoxin structure that has very limited variability and variable amounts of toxicity
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Lipid A
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Exotoxins v. Endotoxins
-Comes from? -Heat? -Toxicity? -Toxoidable (denatures to remove toxicity and retain antigenicity) -G+ or G-? |
- Secreted from active bacteria / part of structure
- Labile / Stable - Very toxic / variable - Yes / No - Both / G- |
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Three types of anthrax
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-Cutaenous, Gastrointestinal, Inahlation
|
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Anthrax
-Gram + or -? |
-spore forming Gram +
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-Spore forming gram postivie, non-motile bacillus
-Spores grow in macrophage and is transported to lymph nodes and spread through lymph and cicrulatory system Cutaneous form forms e schar |
Anthrax
|
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Three toxins coded by large plasmids in bacterium = # of plasmid copies influences virulence
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-Protective Antigen (PA)
-Lethal Factor (LF) -Edema Factor (EF) |
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-Anthrax toxins require how many separate proteins for activity?
-Which one is always required? -EF & LF inhibit ______ production. -EF is activated by ______ |
-2 (Binary toxin)
-PA -cytokine -calmodulin |
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-Bacilli that has a complex cell wall with unique fatty acid components, and infection leads to a cell mediated (delayed type) hypersensitivity reaction
-Acid fast stain |
Mycobacteria
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Mycobacteria infection leads cell mediate ________ type hypersensitivity reaction (tuberculosis!)
|
Delayed type
|
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Stain used when mycobacterium bacilli have concentration of high molecular weight lipids in cell wall that makes organism resistant to aqueous bacteriocidal agents
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Acid fast stain (bacilli)
|
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Mycobacterium tuberculosis
Gram + or - |
Gram +
|
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Site of primary infection for inhaled TB
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Alveoli of lung where macrophages ingest
|
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After TB bacilli multiply in the macrophages they are transported to the __________, Bacilli can survive within a macrophage because they inhibit _________ and resist _________
|
-Lymph nodes
-Lysosome-phagosome fusion -Lysosomal enzymes-cell wall components |
|
How do granulomas form around tuberculosis bacilli??
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Active Th1 cells secrete cytokines that recruit macrophages. Specific T cells surround an interior of macrophages, which can cause tissue damage
|
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A tuberculosis granuloma has healed if ________ occurs
|
Collagenization and calcification of granuloma
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Secondary tuberculosis is a dormant infection the granulomata which can develop into _______, areas with central caseous necrosis. The infection causes extensive tissue necrosis and may erode into the _____ and drain infectious material.
|
tubercles
bronchi |
|
Tuberculin skin test (PPD) is a ________ mediated response, that depends on a _______________ reaction. Can it distinguish between primary and past infection or immunization?
|
-T- Cell
-Delayed Type IV hypersensitivity -Cannot distinguish between present and past infection |
|
Immediate hypersensitivity involves the antigen cross linking of _______ on the surface of ______ cells.
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IgE
mast cells |
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________ hypersensitivity involves IgG immune complex formation and cell damage through complement activation and either NK cells (type II) or neutrophils (type III)
|
Intermediate
|
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Delayed type hypersensitivity has two phases, the first is a sensitization stage where TH cells differentiate and proliferate into _______. The second phase is the _____ phase, where these cells contact same antigen and secrete cytokines to attract macrophages
|
Tdth cells
Effector phase |
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Absence of PPD reactivity in persons infected with TB is known as ________. Those who are this may be immunocompromised or newly infected.
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anergy
|
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Blood screening assay for latent and disease TB that uses an ELISA assay for IFNgamma release
|
QuaniFERON Gold (wheeerre da gold at)
|
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TB treatment success involves _______ for at least ___ months. Symptoms typically improve after __ weeks an sputum cultures negative after _______
|
Combination therapy - 6 months
-4 weeks -3 months |
|
Combination therapy drugs for TB:
|
(RIPE)
Rifambin Isoniazid Pyrazinamide Ethambutol |
|
______ prevents the development of active TB after exposure (INH with Vitamin B6)
|
Prophylaxis
|
|
TB Vaccine is a ______ strain produced from _______.
PPD + or negative after vaccine given? |
BCG (Bacille Calmette Guerin)
M. Bovis PPD + |
|
Of the 30% people who are infected with TB ___% will end up with disease ( if HIV+ _____%). Of those that are infected without disease __% will become reactivated with the disease (if HIV+ ____% per year)
|
-5% normal
-40% HIV -5% -2-10% HIV per year |
|
The only animal known to carry LEPROSY is the
|
armadillo
|
|
Obligate INTRACELLULAR Mycobacterium disease transmitted by person to person via aerosolized nasal secretions
-Can cause disabling peripheral neuropathy -Affects cool temperatured body parts such as the skin, peripheral nerves, mucose of URT, and eyes |
Leprosy - Hansen's Disease
|
|
Leprosy infects which cells?
What happens to your nerves? -M.leprae attacks the ______ cell of the peripheral nervous system |
-Macrophages
-thickening of nerves -Schwann cells |
|
Leprosy is diagnosed when the presence of bacilli in smears from _______ or ________ mucosa. ______ is the measure of bacterial load. If negative smears at all sites, known as _____, if positive smears known as _______.
|
-nasal or skin mucosa
-Bacterial index -paucibacillary -multibacillary |
|
-Multibacillary form of leprosy that lacks effective cell-mediated immune response to M. leprae.
-Macrophages are not activated (_______ type immune response) -facial skin thickening, nodules on ears and nose - |
Lepromatous Leprosy
TH2 Response |
|
Paucibacillary form of leprosy who symptoms are are due to combination of bacterial proliferation and host immune response (_____ type response with _____ hypersensitivity)
-Localized skin lesions (organized in granulomas) -Nerve thickening from granulomas |
Tuberculoid Leprosy
-TH1 response, delayed type hypersensitivity |
|
Lepromatous Leprosy v Tuberculoid
-Cell mediated immunity? -Specific activated T Cells? -Bacteria in lesion? -Antibody present to M leprae? |
-- no / yes
-- no / yes -- yes / no - yes (TH2) / little to none |
|
Syphillis, Lyme Disease, and Leptospirosis are all spiral shaped, flaggelated gram ___ bacteria known as _______
|
- negative (LPS coat!)
-spirochaetes |
|
Syphilis can only be distinguished by nature of lesion and clinical course of disease, not ___________
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serological assay
|
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Patients with syphilis develop antibodies against extract of _________. Treponeme cell wall contains ______.
|
Normal tissue (Cardiolipin)
Lipids |
|
Primary syphilis shows the development of a _____ at inoculation site 21 days post infection. ________ thickening occurs, as well as aggregation of ______, ______, and ______
|
Chancre
Endothelial Lymphocytes, macrophages, and plasma cells |
|
If untreated, ___% of primarily syphilis proceed to ________ 4-10 weeks after initial chancre
|
25, Secondary syphilis
|
|
Latent syphilis occurs early and late and is noninfectious except that,
|
mother can transmit to fetus
|
|
30% of untreated cases of syphilis reach this stage, where granulomas form in the skin, eye, mucous membrane, cardiovascular system
-Neurosyphilis |
Tertiary syphilis
|
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Non treponemal assays, which include _____ & ____, measure IgG & IgM antibody to ______.
|
VDRL & RPR
Reagin (cardiolipin) |
|
Treponemal assays measure ____ to treponemal antigen, and include _____, ____, and _____
|
IgG
TPI, FTA, ELISA |
|
Why are non treponemal (VDRL, RPR) assays problematic for those who have previously been treated for syphilis?
|
Those with latent syphilis will test negative for the cardiolipin antibodies
|
|
In an RPR test for syphilis, excess antibody that does not allow Ab crosslinking with charcoal and the test becomes nonreactive. This is known as ________
|
prozone
|
|
Re-emerging disease with no universal antigen due to 200 known pathogenic serolical variants
-50% of cases in Hawaii -ingestion or contact with the mucus membranes of H2O contaminated by urine of infected animals |
Leptospirosis
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Assays used for diagnosis of Leptospirosis
-No effective test to cover all serotypes |
-Microagglutination
-ELISA -Dipstick -IFA -Latex Agglutination -Indirect hemagglutination assay**** |
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Assay that uses human type O erthrocytes coated with genus specific leptospiral antigens
-When incubated, positive serum will cause agglutination |
Indirect Hemagglutination Assay
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Problem with the diagnostic tests for leptospirosis
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-Antibodies develop very late
-tests are not very sensitive, resulting in many false positives |
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What is unique about lyme disease genetically?
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Genes encodeing outer membrane are on a linear plasmid and can be exchanged between organism
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Symbolic symptom of acute Lyme disease
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Bulls-eye rash
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Desseminated Lyme disease symptoms
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-Secondary rashes
- Neurological, Musculoskeletal, and cardiac issues |
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Initial immune response of Lyme Disease is a ______ .
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-T cell suppression of antibody (TH1)
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During what phase do antibodies peak in Lyme's disease? Are the antibodies protective?
If treated early, what happens to antibody response? Why is this a problem? |
-Arthritis stage
-Not protective -Reduction or prevention of Ab response (inability to confirm infection and protect against 2nd infection) |
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If a person is seropositive for Lyme disease, is this a mark for active disease? Do those with antibodies indicate protective immunity?
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-NO, could be from an undetermined time in the past
-No |
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Lyme Disease Screening
IgM Western Blot + if bands are positive in ___ out of 3 locations. IgG western blot positive if a band is present at ____ of 10 locations |
-2 IgM
-5 IgG |
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Lonestar tickborne disease similar to Lyme Disease that has no chronc illness, is unculturable, and is not cross reactive with B burgdorferi
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STARI (Southern Tick Associated Rash Illness)
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