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Acquired Immunity to Bacteria 
and Related Organisms 
Pakawadee Kumpolngam D.V.M.
• 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
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
Acquired immunity 
The mechanisms by which the immune responses can protect the body against 
bacterial invasion.
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.
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
Immunity to Intracellular Bacteria 
• Bacteria can evade intracellular destruction
Immunity to Intracellular Bacteria
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 complement 
4. Inhibit the expression of MHC I and II on DC surface
Immunity to Intracellular Bacteria 
IFN-γ 
IL-2 
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.
Acquired immunity : 
Johne’s disease 
(Mycobacterium paratuberculosis) 
• Modification of bacterial disease 
by immune responses 
A.Lepromatous form 
-poor cell-mediated response 
-very high antibody levels 
-lesion contain so many bacteria 
B.Tuberculoid form 
-intense cell-mediated response 
-minimal antibody response 
-lesion contain very few bacteria
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.
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
Serology of bacterial infections 
• Detecting the specific antibodies 
– Bacterial agglutination tests
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
Acquired Immunity to Viruses
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
Virus structure and antigens 
• Viral antigens 
Nucleic acid core 
Capsid protein 
Envelope 
– Lipoprotein 
– Glycoprotein 
• Cannot grow or 
reproduce without host 
cell
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.)
Innate immunity to Viruses 
1. 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
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
Immunity to virus 
 Antibody-Mediated Immunity 
 Cell-mediated Immunity 
 Interferons 
 NK cells
Immunity to virus
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
Inhibition of Humoral immunity
Adverse consequences of immunity to 
viruses 
• Infectious canine hepatitis 
– Canine adenovirus 1 
• Feline Infectious Peritonitis (FIP) 
– Coronavirus
Adverse consequences of immunity to 
viruses 
 Infectious canine hepatitis
Adverse consequences of immunity to 
viruses 
 Feline Infectious 
Peritonitis (FIP) 
 Immune-complexes 
deposite in serosal 
blood vessel causing 
 Pleuritis 
 Peritonitis 
 Glomerulonephritis
Serology of viral diseases 
• Test to detect and identify Viruses and 
Antibodies 
– Immunofluorescence 
– ELISA 
– HA, HI 
– Gel precipitation 
– Western blotting 
– Complement fixation 
– Virus neutralization
Immunity to Parasites 
http://www.huldaclarkzappers.com/php2/therapies.php
Immunity to Parasites 
• Immunity to Protozoa 
– Innate immunity 
– Acquired immunity 
– Evasion of the immune response 
– Adverse consequences 
– Vaccination
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
Immunity to Protozoa 
Acquired 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.
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.
Immunity to Protozoa 
• Acquired immunity 
The points in the life cycle of 
Toxoplasma gondii at which 
the immune system can exert 
a controlling influence.
Immunity to Protozoa 
• Evasion of the immune response 
1. 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
Immunity to Protozoa 
• Adverse consequences 
Hypersensitivity types 
– Type I hypersensitivity 
– Type II cytotoxic reaction 
– Type III immune complex reaction 
– Type IV hypersensitivity reaction
Immunity to Protozoa 
• Vaccination 
Successful vaccination against protozoan 
infections of domestic animals is currently 
limited to coccidiosis, babesiosis, giardiasis 
and theileriosis
Acquired Immunity to Parasites 
• Immunity to Helminths 
– Humoral immunity 
– Eosinophils and Parasite destruction 
– Cell-mediated immunity 
– Evasion of the immune response 
– Vaccination
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.
Immunity to Helminths 
• Humoral immunity 
The mechanisms involved in the self-cure reaction against intestinal helminths.
Immunity to Helminths 
• Horse skin allergy by 
migrating parasitic 
helminth larvae. 
• Eosinophils presence 
• Type I hypersensitivity
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
Immunity to Helminths 
• Eosinophils and Parasite destruction 
Some of the molecules released from eosinophils that 
cause damage to parasitic helminths.
Immunity to Helminths 
• Eosinophils and Parasite destruction 
Some effects of the immune responses on the stages of helminth development.
Immunity to Helminths 
• Cell-mediated immunity
Immunity to Helminths 
• Evasion of the immune response
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
Antibody function and immune response to organisms
Acquired Immunity to Parasites 
• Immunity to Arthropods 
– Demodectic Mange 
– Flea-Bite dermatitis 
– Tick infestation 
– Hypodermal infestation
Immunity to Arthropods 
Demodectic Mange 
• T cell response 
• Infiltrating lymphocytes 
• Granuloma formation 
• Type I,IV hypersensitivity 
reaction
• Flea-Bite dermatitis 
© 2013 Campus Veterinary Clinic
Immunity to Arthropods 
• Tick infestation 
www.parasiticpests.com
Immunity to Arthropods 
• Hypodermal infestation 
• Hypodermin A, the 
protease secreted by 
larvae 
• inhibit immune 
responses and reduce 
IL-2
Reference 
• Tizard, I. R., 2009. Veterinary Immunology an 
introduction. 8th. Elsevier Saunders. 
เสริมความเข้าใจเพิ่มเติม 
• ภูมิคุ้มกันหรรษา!" ตอนที่ 3: การจู่โจมของแบคทีเรีย 
http://topicstock.pantip.com/wahkor/topicstock/2011/06/ 
X10643274/X10643274.html 
• ตอนที่ 2: เมื่อไวรัสมาเยือน 
https://www.facebook.com/media/set/?set=a.4859982 
41472908.1073741829.484858994920166&type=3

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Immunity to bacteria and related organisms in animal

  • 1. Acquired Immunity to Bacteria and Related Organisms Pakawadee Kumpolngam D.V.M.
  • 2. • 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
  • 3. 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
  • 4. Acquired immunity The mechanisms by which the immune responses can protect the body against bacterial invasion.
  • 5. 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.
  • 6. 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
  • 7. Immunity to Intracellular Bacteria • Bacteria can evade intracellular destruction
  • 9. 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 complement 4. Inhibit the expression of MHC I and II on DC surface
  • 10. Immunity to Intracellular Bacteria IFN-γ IL-2 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.
  • 11. Acquired immunity : Johne’s disease (Mycobacterium paratuberculosis) • Modification of bacterial disease by immune responses A.Lepromatous form -poor cell-mediated response -very high antibody levels -lesion contain so many bacteria B.Tuberculoid form -intense cell-mediated response -minimal antibody response -lesion contain very few bacteria
  • 12. 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.
  • 13. 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
  • 14. Serology of bacterial infections • Detecting the specific antibodies – Bacterial agglutination tests
  • 15. 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
  • 17. 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
  • 18. Virus structure and antigens • Viral antigens Nucleic acid core Capsid protein Envelope – Lipoprotein – Glycoprotein • Cannot grow or reproduce without host cell
  • 19. 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.)
  • 20. Innate immunity to Viruses 1. 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
  • 21. 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
  • 22. Immunity to virus  Antibody-Mediated Immunity  Cell-mediated Immunity  Interferons  NK cells
  • 24. 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
  • 26. Adverse consequences of immunity to viruses • Infectious canine hepatitis – Canine adenovirus 1 • Feline Infectious Peritonitis (FIP) – Coronavirus
  • 27. Adverse consequences of immunity to viruses  Infectious canine hepatitis
  • 28. Adverse consequences of immunity to viruses  Feline Infectious Peritonitis (FIP)  Immune-complexes deposite in serosal blood vessel causing  Pleuritis  Peritonitis  Glomerulonephritis
  • 29. Serology of viral diseases • Test to detect and identify Viruses and Antibodies – Immunofluorescence – ELISA – HA, HI – Gel precipitation – Western blotting – Complement fixation – Virus neutralization
  • 30. Immunity to Parasites http://www.huldaclarkzappers.com/php2/therapies.php
  • 31. Immunity to Parasites • Immunity to Protozoa – Innate immunity – Acquired immunity – Evasion of the immune response – Adverse consequences – Vaccination
  • 32. 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
  • 33. Immunity to Protozoa Acquired 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.
  • 34. 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.
  • 35. Immunity to Protozoa • Acquired immunity The points in the life cycle of Toxoplasma gondii at which the immune system can exert a controlling influence.
  • 36. Immunity to Protozoa • Evasion of the immune response 1. 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
  • 37. Immunity to Protozoa • Adverse consequences Hypersensitivity types – Type I hypersensitivity – Type II cytotoxic reaction – Type III immune complex reaction – Type IV hypersensitivity reaction
  • 38. Immunity to Protozoa • Vaccination Successful vaccination against protozoan infections of domestic animals is currently limited to coccidiosis, babesiosis, giardiasis and theileriosis
  • 39. Acquired Immunity to Parasites • Immunity to Helminths – Humoral immunity – Eosinophils and Parasite destruction – Cell-mediated immunity – Evasion of the immune response – Vaccination
  • 40. 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.
  • 41. Immunity to Helminths • Humoral immunity The mechanisms involved in the self-cure reaction against intestinal helminths.
  • 42. Immunity to Helminths • Horse skin allergy by migrating parasitic helminth larvae. • Eosinophils presence • Type I hypersensitivity
  • 43. 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
  • 44. Immunity to Helminths • Eosinophils and Parasite destruction Some of the molecules released from eosinophils that cause damage to parasitic helminths.
  • 45. Immunity to Helminths • Eosinophils and Parasite destruction Some effects of the immune responses on the stages of helminth development.
  • 46. Immunity to Helminths • Cell-mediated immunity
  • 47. Immunity to Helminths • Evasion of the immune response
  • 48. 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
  • 49. Antibody function and immune response to organisms
  • 50. Acquired Immunity to Parasites • Immunity to Arthropods – Demodectic Mange – Flea-Bite dermatitis – Tick infestation – Hypodermal infestation
  • 51. Immunity to Arthropods Demodectic Mange • T cell response • Infiltrating lymphocytes • Granuloma formation • Type I,IV hypersensitivity reaction
  • 52. • Flea-Bite dermatitis © 2013 Campus Veterinary Clinic
  • 53. Immunity to Arthropods • Tick infestation www.parasiticpests.com
  • 54. Immunity to Arthropods • Hypodermal infestation • Hypodermin A, the protease secreted by larvae • inhibit immune responses and reduce IL-2
  • 55. Reference • Tizard, I. R., 2009. Veterinary Immunology an introduction. 8th. Elsevier Saunders. เสริมความเข้าใจเพิ่มเติม • ภูมิคุ้มกันหรรษา!" ตอนที่ 3: การจู่โจมของแบคทีเรีย http://topicstock.pantip.com/wahkor/topicstock/2011/06/ X10643274/X10643274.html • ตอนที่ 2: เมื่อไวรัสมาเยือน https://www.facebook.com/media/set/?set=a.4859982 41472908.1073741829.484858994920166&type=3