immunity to bacteria and related organisms in animal
DESCRIPTION
Immune responses to infection in animalTRANSCRIPT
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Acquired Immunity to Bacteria and Related Organisms
Pakawadee Kumpolngam D.V.M.
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• Acquired immunity– Immunity to Toxigenic Bacteria– Immunity to Invasive Bacteria– Immunity to Intracellular Bacteria– Modification of bacterial disease by immune responses
• Evasion of the immune response– Prevention of recognition– Resistance to effector mechanisms
• Adverse consequences of the immune responses• Serology of bacterial infections• Immunity to fungal infections
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Acquired-immune responses to bacterial infection
There are 5 basic mechanisms• Neutralization : toxins or enzymes by
antibody• Killing bacteria : antibodies and complement• Opsonization : by antibodies and
complement, resulting phagocytosis and destruction
• Intracellular destruction : by activated macrophages
• Direct killing : by cytotoxic T cells and NK cells
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Acquired immunity
The mechanisms by which the immune responses can protect the body against bacterial invasion.
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Acquired immunity
• Immunity to Toxigenic Bacteria– Toxigenic bacteria such as B. anthracis– Immune response eliminate bacteria and
neutralize their exotoxins– Neutralization : Antibody prevents Toxin from
binding to its receptors on a target cell.– Once the toxin has combined with receptors,
antibodies ineffective in reversing this combination.
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Immunity to Invasive Bacteria• Alternative or lectin pathways : innate defense mechanisms
-> MAC -> Lysis• Antibody and Complement activate Classical pathway to
destroy bacteria -> MAC -> Lysis• Antibodies or C3b against surface antigens of Bacteria :
capsular (K) antigen or cell wall (O) antigen– Antibodies or C3b act as opsonins
• Opsonization : antibodies and complement against bacteria resulting phagocytosis by neutrophils and macrophages
• Bacteria are either opsonized or lysed
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Immunity to Intracellular Bacteria• Bacteria can evade intracellular destruction
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Immunity to Intracellular Bacteria
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Evasion of the immune response
1. Avioding antibody- Change protein surface- Produce protease destroy Ab.
2. Avoiding phagocytosis- Capsule protect macrophage - Produce protein interfere macrophage function
3. Avoiding complement4. Inhibit the expression of MHC I and II on DC surface
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Immunity to Intracellular Bacteria
The type of immune response stimulated by bacteria depends on whether the bacteria are live or dead and whether they grow inside or outside cells.
IFN-γ
IL-2
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Acquired immunity :Johne’s disease
• Modification of bacterial disease by immune responses
A.Lepromatous form-poor cell-mediated response -very high antibody levels-lesion contain so many bacteriaB.Tuberculoid form-intense cell-mediated response -minimal antibody response-lesion contain very few bacteria
(Mycobacterium paratuberculosis)
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Modification of bacterial disease by immune responses
Immune response can swing between Th1 and Th2 response, perhaps several times, this variation appears to be a common feature of chronic infection such as tuberculosis.
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Adverse consequences of the immune responses
• The adverse consequences of the immune responses correspond in their mechanism to the Hypersensitivity types described in next chapter.For example– a local Type I hypersensitivity– Type II cytotoxic reaction– Type III immune complex reaction
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Serology of bacterial infections
• Detecting the specific antibodies– Bacterial agglutination tests
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Immunity to fungal infections
• Innate immunity– Phagocytosis by
neutrophils and macrophages
– γδ T cells at epithelium – NK cells
• Adaptive immunity– Th1 response– Opsonization : antibody
induce phagocytosis
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Acquired Immunity to Viruses
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Acquired Immunity to Viruses
• Virus structure and antigens• Pathogenesis of virus infections• Immunity to virus• Evasion of the immune response by virus• Adverse consequences of immunity to viruses• Serology of viral diseases
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Virus structure and antigens
• Viral antigensNucleic acid coreCapsid protein Envelope– Lipoprotein – Glycoprotein
• Cannot grow or reproduce without host cell
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Innate immunity to Viruses• Interferons
The sequential production of interferon and antibody following intranasal vaccination of calves with infectious bovine rhinotracheitis vaccine. (From data kindly provided by Dr. M savan.)
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Innate immunity to Viruses1. Interferons • Type I IFN : IFN α, β, τ and δ• Type II IFN : IFN γ (gamma)• IFN α/ß are released from virus-
infected cells or plasmacytoid DCs – stimulate autocrine and
paracrine into antiviral stages• IFN γ released from NK cells and
Th1 cells – stimulate cytotoxic T cells and
Macrophages
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Innate immunity to Viruses
2. NK cells• NK cells cytotoxicity is stimulated by IFN α• NK cells produce IFN γ -> antiviral effect• NK cells reduce severity of viral infection before the
development of acquired immunity
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Immunity to virus
Antibody-Mediated Immunity
Cell-mediated Immunity
Interferons
NK cells
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Immunity to virus
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Evasion of the immune response by viruses
• Inhibition of Humoral immunity– They undergo mutation, selection and change the
structure of their hemagglutinins and neuraminidases : H16 N9 (2011)
– Antigenic drift / Antigenic shift (Antigenic variation)
• Interference with Interferons and Antibody• Inhibition of Apoptosis– Virus can replicate in infected cells
• Inhibition of Cytotoxic T cells and NK Cells– Inhibit mature DCs and induce DCs dead
• Latency : HIV
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Inhibition of Humoral immunity
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Adverse consequences of immunity to viruses
• Infectious canine hepatitis – Canine adenovirus 1
• Feline Infectious Peritonitis (FIP)– Coronavirus
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Adverse consequences of immunity to viruses
Infectious canine hepatitis
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Adverse consequences of immunity to viruses
Feline Infectious Peritonitis (FIP)
Immune-complexes deposite in serosal blood vessel causing
Pleuritis Peritonitis Glomerulonephritis
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Serology of viral diseases
• Test to detect and identify Viruses and Antibodies– Immunofluorescence – ELISA– HA, HI– Gel precipitation– Western blotting– Complement fixation– Virus neutralization
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Immunity to Parasites
http://www.huldaclarkzappers.com/php2/therapies.php
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Immunity to Parasites
• Immunity to Protozoa– Innate immunity– Acquired immunity– Evasion of the immune response– Adverse consequences– Vaccination
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Immunity to Protozoa
Innate immunity• In vertebrates, extracellular protozoa are eliminated
by phagocytosis and complement activation. • T cell responses.
- Extracellular protozoa - Th2 cytokines released for antibody production.
- Intracellular protozoa - Cytotoxic lymphocytes (CTL’s) kill infected cells. Th1 cytokines produced to activate macrophages
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Immunity to ProtozoaAcquired immunity• Antibody responses.
- Extracellular protozoa are eliminated by opsonization, complement activation and ADCC. - Intracellular protozoa are prevented from entering the host cells by a process of neutralisation e.g. neutralising antibody against malaria sporozoites, blocks cell receptor for entry into liver cells.
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Immunity to Protozoa
• Acquired immunity• Th1 response for
intracellular parasite• T. gondii tachizoites
grow within cells, the infected cell rupture and tachizoites are released to invade other cells.
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Immunity to Protozoa
• Acquired immunity
The points in the life cycle of Toxoplasma gondii at which the immune system can exert a controlling influence.
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Immunity to Protozoa
• Evasion of the immune response1. Avoid antibody
- Trypanosomes with a new surface glycoprotein antigen
2. Avoid neutrophil attachment and phagocytosis- T. gondii inhibit lysosome-phagosome fusion
3. Many protozoa are immunosuppressive- Plasmodium suppress DCs to process antigen
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Immunity to Protozoa
• Adverse consequencesHypersensitivity types – Type I hypersensitivity– Type II cytotoxic reaction– Type III immune complex reaction– Type IV hypersensitivity reaction
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Immunity to Protozoa
• VaccinationSuccessful vaccination against protozoan
infections of domestic animals is currently limited to coccidiosis, babesiosis, giardiasis and theileriosis
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Acquired Immunity to Parasites
• Immunity to Helminths– Humoral immunity– Eosinophils and Parasite destruction– Cell-mediated immunity– Evasion of the immune response– Vaccination
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Immunity to Helminths
• Most helminths extracellular & too large for phagocytosis.
• For the larger worms, e.g. some gastrointestinal nematodes host develops inflammation and hypersensitivity.
• Eosinophils & IgE activated to initiate inflammatory response
• Mast cells release histamine elicited reactions are similar to allergic reactions.
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Immunity to Helminths• Humoral immunity
The mechanisms involved in the self-cure reaction against intestinal helminths.
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Immunity to Helminths
• Horse skin allergy by migrating parasitic helminth larvae.
• Eosinophils presence• Type I hypersensitivity
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Immunity to Helminths
• The factors involved in the activation of eosinophils– Granulocyte-macrophage
colony-stimulating factor (GM-CSF)
– EAF ; Eosinophil Activating Factor
– PAF ; Platelet-Activation Factor
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Immunity to Helminths
• Eosinophils and Parasite destruction
Some of the molecules released from eosinophils that cause damage to parasitic helminths.
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Immunity to Helminths• Eosinophils and Parasite destruction
Some effects of the immune responses on the stages of helminth development.
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Immunity to Helminths• Cell-mediated immunity
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Immunity to Helminths• Evasion of the immune response
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Immunity to Helminths• Vaccination– Traditional vaccines little use– Recombinant T. ovis vaccine can induce protective
immunity in seep• Prevention – Control or prevent an infestation of helminths– Treat by drug
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Antibody function and immune response to organisms
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Acquired Immunity to Parasites
• Immunity to Arthropods– Demodectic Mange– Flea-Bite dermatitis– Tick infestation– Hypodermal infestation
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Immunity to Arthropods
Demodectic Mange• T cell response• Infiltrating lymphocytes• Granuloma formation• Type I,IV hypersensitivity
reaction
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• Flea-Bite dermatitis
© 2013 Campus Veterinary Clinic
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Immunity to Arthropods
• Tick infestation
www.parasiticpests.com
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Immunity to Arthropods
• Hypodermal infestation
• Hypodermin A, the protease secreted by larvae
• inhibit immune responses and reduce IL-2
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Reference
• Tizard, I. R., 2009. Veterinary Immunology an introduction. 8th. Elsevier Saunders.
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