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179 Cards in this Set

  • Front
  • Back
An organism that lives on or in another organism and depends upon the host for nutrition
Parasite needs a host to complete life cycle
Obligate parasite
Parasite may or may not need host to complete life cycle
Facultative parasite
Host susceptibility depends on ___, _____, & __________.
nutrition, age, and genotype
CD8+ cells only recognize antigens on _______. They are essential for ______ immunity and control ___________ pathogens
-Cell mediated
CD4+ recognize antigens on ______ and are essential for _______ immunity.
-Antibody mediated (humoral)
Th1 Response involves which cytokines?
Pro or Anti inflammatory?
What type of immunity?
-IFN gamma, IL-12, IL-12
-IgG antibodies
-Cell mediated
Th2 Response involves which cytokines?
Pro or Anti inflammatory?
What type of immunity?
-IL-4, 5, 9, 10
-IgG and IgE
When Th1 cells improve ________ response release interferon gamma: _________ are activated, and expression of ______ on ____ are amplified
-Cell mediated
-MHC II cells on Antigen Presenting Cells
Th2 cells assist in improving _____ immunity and release IL-4, which stimulate ______. Th2 cells also activate _____ to defend against parasites via ___ antibodies
- Humoral immunity
-B cells
Helminth parasites do not induce synthesis of IL-12, they stimulate this __(cytokine)__ which drives _____ pathway development
If _______ is present during early helminth infection, TH2
development does not occur; reduction in ____ and ____
-IgE and eosinophils
What methods is used to kill parasites?
- Direct killing via NO by macrophages
-ADCC by macrophages and eosinophils
What mechanisms do parasites use to evade immune system?
-Antigenic variation
-Evasion from macrophages
-Resistance to complement lysis
-Immune suprression
Surface and secreted antioxidant enzymes
How do parasites evade macrophages?
-Prevent lysosome-phagosome fusion
-prevent lysosomal toxic action
-Escape into cytoplasm
How do macrophages and eosinophils kill an organism via ADCC?
IgE binds to eosinophil Fc receptor and parasite and degranulates, releasing reactive oxygen and intermediates and toxins
Parasites stimulate the innate immune system because they are detected as ______
INTRAcellular protozoan parasite
-promastigotes in macrophages transform into amastigotes which live in phagosomal vacuole
-Sand Fly vector
Three disease types of Leishmania
1. Visceral (L. donovani)
2. Cutaneous (L. major, tropica, mexicana)
3. Mucocutaneous (L. brasiliensis)
Present on the leishmania parasite surface that is recognized by toll-like receptors
LPG (lipophosphoglycan)
When toll-like receptors recognize LPG on parasite surface, how to macrophages respond?
Destroy intracellular parasite by producing nitric oxide and reactive oxygen intermediates
Leishmania recovery depends on ______.
Cell mediated Immunity
How does leishmania evade the immune system?
-Hide within macrophages
-Activate complement, where opsonization uptakes parasite into macrophages
-LPG inhibits lysosomal enzymes, MAC, and IL-12 (fewer macrophages)
Danger of Live, virulent Leishmania major vaccine
May develops ulcerating primary lesions (slow to non-healing)
Parasites responsible for African Sleeping Sickness
-Intra or Extracellular?
-Trypanosoma brucei gambiense (West Africa) - chronic infection
-Trypanosoma brucei rhodesiense (East Africa) - acute illness
-Tsetse Fly
Host immune response to African Sleeping sickness?
-Antibody and complement
-High levels of IgM/Eosinophils
-B Cell proliferation
Africa Sleeping sickness Evasion strategies
-Antigenic switching of variant surface glycoprotein coat
-Waves of fever and parasitemia
Chagas Disease
-Intra or Extracellular
-Trypanosoma cruzi
-Reduuvid (kissing bug)
Acute phase of Chagas infects _____, ____ and ______ cells.
Macrophages, muscle, and nerve cells
Chronic phase of Chagas disease affects ______ & ______ in 30 % of cases.
heart and digestive tract
Chagas parasites cross react with _____ & _______ antigens, causing immune reaction to targest host's antigens.
cardiac muscle and mesenteric nerve antigens
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
Chagas Parasite evasion strategies
-Evade complement by binding C3b and C4b (express gp160)
-Escape in cytoplasm of macrophage
-Down regulate MHC II expression on APCs (turn off macrophage)
Issues with Chaga's vaccine?
Potential autoimmune. Unclear if the immune response should be stimulated to eliminate parasite or inhibited to avoid autoimmunity.
-Intra or Extracellular?
How do malaria parasites alter RBC membranes & what is its effect on the body?
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
What type of immune response is associated with malaria?
What cytokines are involved?
What proinflammatory cytokine rises in serum levels?
-IFNgamma, IL-2, IL-12
Malaria merozoite surface proteins active ____________
Toll-like receptors
After RBC rupture and release antigen Host immune involvement in 1st malaria infection?
-Merozoite surface proteins activate toll-like receptors
-Inflammatory cytokines (TNFalpha)
-NK Cells and T cells produce IFNgamma
-NO and free radical kill parasites
What is the body's immune response in a repeat infection of malaria?
-Spleen filters blood and removes antigens
-Decrease inflammation (decrease TNFalpha by IL-10)
-Th1 becomes a Th2 response (IL-10)
Cerebral malaria is a result of
Increased IFNgamma production in re-exposure to malaria, increasing macrophage activation and production of inflammatory TNF and NO (interfere with neurotransmission)
Malaria Cell Mediated Immunity Evasion Strategies
-Antigenically distinct stages in lifecyle
-Hide in RBC and liver cells
-Modulate T & B Cell responses
Why are malaria cells within RBC not recognized by CD8+ cells?
Red blood cells do not have MHC Class I antigens
How do malaria parasites modulate memory T & B cells response to evade the immune system?
-Memory Th1 cells depleted
-Deplete CD4+ specific cells
How do malaria parasites cause immunosuppression?
Prevent antigen presentation and downregulate T Cells
Malaria Antibody Mediated Immunity Evasion Strategies
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)
-Antigen needed by P. vivax merozoites to enter RBCs
-Resistant to P. vivax if without
Duffy antigen
A person is more likely to survive acute illness from P. falciparum if they have ______, where red blood cell have an abnormal shape
Inherited Sickle Cell trait
Multicellular worms that have long life spans, are usually extracellular, have life cyles with intermediate hosts, larval stages, and adults
Parasitical filarial worms that cause Lymphatic filariasis
Brugia malayi and Wuchereria bancrofti
Host immune response to microfilariae is primarily _______.
Primary cytokines include?
IL-4, 5, 10
(IgE and IgG as well)
Host immune to response to adult filarial worms living in the _______ is ______.
Lymphatic system, proinflammatory (TH1)
Lymphatic damage from filariasis can lead to thickened _____ and _____ or ______ superinfections
bacteria or fungal
Pathogenesis from filarial can be contributed to elevated levels of ______, _____, & ________
IgE, IgG, and Cell mediated immunity
Filariasis parasite evasion strategy
-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)
In Schistosomiasis, when adults _______ that secrete soluble antigens into tissues, early _____ response switches to _____
lay eggs, TH1, TH2
In Schistomiasis, these cytokines ______ promote recruitment of eosinophils, B Cells, T cells, and macrophages form ______ around eggs, leaving fibrotic plaques
IL-4, 5, 13
Human symptoms from schistosomes
hepatoslenomegaly, portal hypertension
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
Schistosome evasion strategies
-double libid bilayer tegument
-blocking abs protects new larvae
-TNFalpha increases egg production
-Proteases that vleave host Ig secreted
Extracellular tissue nematode found in the muscles
-matures in gut and migrates via blood to skeletal muscle
Trichinella spiralis
Immune system response to trichinella?
Intracellular or Extra
Extracellular - TH2 Response
-high levels of IL-4 & IL-5
-Eosinophils and IgE
Trichinlla evasion strategies?
-Lives in muscle cells
-Inhibits Macrophages
-Nonspecific immunosuppression
-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
Echinococcus granulosus evasion strategies
-Hydatid cyst development
-Antigens elicit TH2 response, not protective TH1
-Depletes complement
Fibrotic host capsule that shelters parasite. If ruptures it releases antigens and a person can go into anaphylactic shock
Hydatid cyst
Large, intestinal soil transmitted helminth that evade immune system by molecular mimicry (collagen) and lowering TH1 and TH2 responses
Ascaris lumbricoides
Intestinal threadowmr which can be transmitted via soil, autoinfection and breast milk. Evades immune system by autoinfection by inducing IL-10 secretion (antiinflammatory)
Strongyloides stercoralis
Helminth that sheds teguments and migrates around gut to avoid local inflammation
Hookworm (Necatur americanus, Ancylstoma duodenale)
Host immune response to soil-transmitted helminths (Ascaris, Threadworm, Hookworm)
-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
Which cytokines are responsible for nematode gut expulsion?
IL-4, 9, and 13
Two basic forms of fungi
Yeast and Molds
Unicellular fungi that reproduced by budding
Multicellular hyphae fungi that can reproduce asexually and/or sexually
Free living, not obligate parasites that are ubiquitous, grow in/on soil, plants and water, and produce infection due to immunodeficiency
Innate Immunity against Fungi
-Mucuous membrane
-skin secretions
3 types of Diseases caused by Fungi
-superficial (dermatophytes - skin hair nails, candida infection of mucosal surface)
-subcutaneous (puncture wounds, abscess)
How does one get mycoses?
Inhalation of spores free living pathogenic fungi
Systemic mycoses results from inhalation of ______ of free living fungi.
Opprtunistic mycoses are _____ infections that compromise immune system.
-Canida, aspergillus, cryptococcus, pneumocystosis
Systemic mycoses featuring chronic pulmonary disease that mimics TB
Histoplasma capsulatum
Systemic mycoses features acute pulmonary disease affecting lungs, skin, or GI
Blastomyces dermatitidis
Systemic mycoses featureing pulomary or disseminate to the meninges, bones, joints, and cutaneous tissue
Coccidoides immitis
Opportunistic mycoses
-Normal commensal
-Infects any body surface or organ
-Immunodeficient at risk
Candida albicans
-Allergic pulomary and invasive Opportunistic mycoses
-Opportunitic mycoses acquired in childhood from pigeon droppings
-Can reactive in AIDS patients
Cryptococcus neoformans
-Opportunistic mycoses
-Infect by age 3-4 with pneumonia
-#1 cause of death among immunocompromised
-Pneumocyst jiroveci
Innate immune response to Fungi
-Skin, flora, complement
-Neutrophils (phagocytosis) to site by chemotactic factors or complement activation
-Alveolar macrophages
-NK Cells
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
Acquired host immune response to fungi?
- Dependent on pathogenic specific TH1 cells
-Neutrophils produce IL-12 -> TH1 --> macrophages
-TH2 / IL-4 reduce TH1 cells
Dermatophytes can be controlled by a strong ________ response. _____-type hypersensitivity (th1) can clear infection. ______-type hypersensitivity response (th2) leads to chronic infection
-Weak or immediate
-Opportunistic or System mycoses?
-Evasion strategy?
-Inhibit complement
-Opportunistic or Systemic mycoses?
-Evasion Strategy?
-Degrade C3 with protease and hydrolytic enzymes invade host cells
-Opportunistic or Systemic?
-Evasion strategies?
-Sheds capsular coat and bind complement receptors, suppress C5a, secrete enzymes
-Opportunistic or Systemic?
-Evasion strategies?
-MSG antigen variation, similar to VSG in trypanosomes
-Opportunistic or Systemic?
-Evasion strategies?
-Forms tissue cysts, no inflammation
-Opportunistic or Systemic?
-Evasion strategies?
-proliferates intracellularly in alveolar macrophages
-Opportunistic or Systemic?
-Evasion strategies?
-BAD1 antigen uses complement receptor to bind to other host cells and tissues & change surface antigens
Gram + cell wall made up of _______. Gram - cell wall made up of ________.

Gram + peptidoglycan cell wall is broken down by ____ and ____
lysosomal enzymes and phagocytosis
Gram - lipopolysaccharide wall is broken down by _____ and _____
complement & cytotoxic cells
Mycobateria cell wall is made up of ____ * ____
glycolipids and mycolic acid
Spirochaetes cell wall is made up of ____ & _____
lipoprotein and outer envelope
Primary Defense against bacteria is mainly by the ________ & _______
skin and pH changes
Secondary-non antibody mediated defense against bacteria
-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
Cytokines released during secondary-non antibody mediated defense against bacteria
-TNFalpha & IL-12: stimulated NK, TH1
-IL-1 reset hypothalamus to higher temp
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
When antibody mediated complement targets gram positive bacteria, No _______ forms
MAC Complex
Antibody mediated mechanisms for combating infection by extracellular bacteria
-Opsonization via macrophage Fc receptors
-Complement via Classical Pathway (No MAC for G+)
-ADCC (neutrophil)
Antibody mediated mechanisms for combating infection by intracellular bacteria
- 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
Most bacteria is killed by _____
Phagocytes are attracted to (4 things). They attach to an organism via (3 things)
-Complement, cytokines, chemokines, chemotaxis

-Lectins, Complement, Fc receptors on phagocyte linking Antibody
Microbicidal activity during phagocytosis includes:
-reactive oxygen intermediates
-reactive nitrogen intermediates
-catonic proteins
Bacteria's main defense is to _______
avoid complement mediated damage
How do bacteria avoid complement (x6)
-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
Intracellular defense BY bacteria
-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
-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
Exotoxins that increase cyclic AMP,GMP leading to fluid secretion an diarrhea
-Example Vibrio cholera
Exotoxin that increases ulceration (S. aureus) and increases invasivenes (Shigella)
-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
Species specific outermost segment of Endotoxin that has antigenic variability
O Antigen
Genus specific middle segment of endotoxin that contains unique sugars and phosphate groups that confer stability within the cell wall
Core polysaccharide
Inner segment of the endotoxin structure that has very limited variability and variable amounts of toxicity
Lipid A
Exotoxins v. Endotoxins
-Comes from?
-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-
Three types of anthrax
-Cutaenous, Gastrointestinal, Inahlation
-Gram + or -?
-spore forming Gram +
-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
Three toxins coded by large plasmids in bacterium = # of plasmid copies influences virulence
-Protective Antigen (PA)
-Lethal Factor (LF)
-Edema Factor (EF)
-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)

-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 infection leads cell mediate ________ type hypersensitivity reaction (tuberculosis!)
Delayed type
Stain used when mycobacterium bacilli have concentration of high molecular weight lipids in cell wall that makes organism resistant to aqueous bacteriocidal agents
Acid fast stain (bacilli)
Mycobacterium tuberculosis
Gram + or -
Gram +
Site of primary infection for inhaled TB
Alveoli of lung where macrophages ingest
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??
Active Th1 cells secrete cytokines that recruit macrophages. Specific T cells surround an interior of macrophages, which can cause tissue damage
A tuberculosis granuloma has healed if ________ occurs
Collagenization and calcification of granuloma
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.

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.
mast cells
________ hypersensitivity involves IgG immune complex formation and cell damage through complement activation and either NK cells (type II) or neutrophils (type III)
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
Absence of PPD reactivity in persons infected with TB is known as ________. Those who are this may be immunocompromised or newly infected.
Blood screening assay for latent and disease TB that uses an ELISA assay for IFNgamma release
QuaniFERON Gold (wheeerre da gold at)
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:
______ prevents the development of active TB after exposure (INH with Vitamin B6)
TB Vaccine is a ______ strain produced from _______.

PPD + or negative after vaccine given?
BCG (Bacille Calmette Guerin)
M. Bovis

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

-2-10% HIV per year
The only animal known to carry LEPROSY is the
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
-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
-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!)
Syphilis can only be distinguished by nature of lesion and clinical course of disease, not ___________
serological assay
Patients with syphilis develop antibodies against extract of _________. Treponeme cell wall contains ______.
Normal tissue (Cardiolipin)
Primary syphilis shows the development of a _____ at inoculation site 21 days post infection. ________ thickening occurs, as well as aggregation of ______, ______, and ______
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
Tertiary syphilis
Non treponemal assays, which include _____ & ____, measure IgG & IgM antibody to ______.
Reagin (cardiolipin)
Treponemal assays measure ____ to treponemal antigen, and include _____, ____, and _____
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 ________
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
Assays used for diagnosis of Leptospirosis
-No effective test to cover all serotypes
-Latex Agglutination
-Indirect hemagglutination assay****
Assay that uses human type O erthrocytes coated with genus specific leptospiral antigens
-When incubated, positive serum will cause agglutination
Indirect Hemagglutination Assay
Problem with the diagnostic tests for leptospirosis
-Antibodies develop very late
-tests are not very sensitive, resulting in many false positives
What is unique about lyme disease genetically?
Genes encodeing outer membrane are on a linear plasmid and can be exchanged between organism
Symbolic symptom of acute Lyme disease
Bulls-eye rash
Desseminated Lyme disease symptoms
-Secondary rashes
- Neurological, Musculoskeletal, and cardiac issues
Initial immune response of Lyme Disease is a ______ .
-T cell suppression of antibody (TH1)
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)
If a person is seropositive for Lyme disease, is this a mark for active disease? Do those with antibodies indicate protective immunity?
-NO, could be from an undetermined time in the past
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
Lonestar tickborne disease similar to Lyme Disease that has no chronc illness, is unculturable, and is not cross reactive with B burgdorferi
STARI (Southern Tick Associated Rash Illness)