Exam 1 Flashcards

1
Q

What are the 3 things Prokaryotes and Eukaryotes have in common?

A

Cell membrane, cytoplasm and DNA

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2
Q

What are the differences between Prokaryotes and Eukaryotes?

A

Prokaryotic: lack a nucleus, membrane bound organelles and tend to be smaller and more simplistic
Eukaryotic: have a nucleus, membrane bound organelles and tend to be larger and more complex

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3
Q

Spore Forming Bacteria

Main genera and species of Veterinary Interest

A
Bacillus
- B. anthracis
- B. larvae
Clostridium
- C. perfringens and C. difficile
- C. tetani
- C. botulinum
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4
Q

Examples of obligate aerobes

A

Pseudomonas aeruginosa

Mycobacterium tuberculosis

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5
Q

Examples of obligate anaerobes

A

Clostridium sp.

Bactericides sp.

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6
Q

Examples of facultative anaerobes

A

Enterobacteriaceae
Staphylococcus aureus
**Most bacteria of clinical interest!

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7
Q

Aerotolerant anaerobes

A

Arcobacter

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8
Q

Gram postive +

Aerobic Cocci

A

Staphylococcus
Streptococcus
Enterococcus

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9
Q

Gram Positive +

Aerobic Rods

A
Actinomycetes
Bacillus
Listeria
Mycobacterium
Rhodococcus
Corynebacterium/Nocardia
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10
Q

Gram Positive +

Anaerobic Rods

A

Clostridium

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11
Q

Gram Negative -

Enterobacteriaceae

A
Escherichia coli/ Shigella
Salmonella
Klebsiella/ Enterobacter
Proteus
Yersinia
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12
Q

Gram Negative -

Non-Fermentative Rods

A
Bordetella
Pseudomonas/ Burkholderia
Aeromonas/Vibro
Pasteurella/Mannheimia
Haemophiliac/ Histophilus
Brucella
Francisella
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13
Q

Gram Negative -

Anaerobic Rods

A

Clostridium

Fusobacterium

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14
Q

Curved/ Spiral bacteria

Misc.

A
Campylobacter/Helicobacter
Brachyspira
Lawsonia
Leptospira
Treponema/Borrelia
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15
Q

Obligate intracellular bacteria

Misc.

A

Ana plasma/ Ehrlichia
Chlamydia/ Chlamoydophila
Coxiella
Rickettsia

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16
Q

Bacteria without a cell wall

Misc.

A

Mycoplasma

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17
Q

Therapeutic use of antimicrobials

A

when diseased animals are treated to cure infection

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18
Q

Prophylactic use of antimicrobials

A

when heathy herds or animals are treated to prevent infection

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19
Q

Metaphylatic use of antimicrobials

A

when diseased herds are treated to cure infection in some individuals and prevent infection in others

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20
Q

Growth promotion use of antimicrobials

A

when healthy animals are treated with low (sub-therapeutic) concentrations in feed to improve growth rate and efficiency of feed utilisation and improve reproductive performance

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21
Q

BETA-LACTAMS-

Penicillins

A

Penicillin G/V
Ampicillin/amoxicyllin
Amoxicillin / clavulanic acid

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22
Q

Tetracyclines

A

Tetracycline
Oxytetracycline
Doxycycline

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23
Q

Quinolones

A

Oxolinic acid
Enrofloxacin/Marbofloxacin
Pradofloxacin/Norfloxacin

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24
Q

Sulfonamides

A

Sulfiadiazine

Sulfadiazine/Trimethoprim

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25
Phenicols
Chloramphenicol | Florfenicol
26
BETA-LACTAMS- | Cephalosporins
Cefalexin/Cephadroxil Cefpodoxime/Ceftiofur Cefovecin, Cefquinome
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Macrolides
Erythromycin | Tiamulin, Tilmicosin
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Lincosamides
Lycomycin/Clindamycin
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Aminoglycosides
Streptomycin Gentamicin/Neomycin Amikacin
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Polypeptides
Colistin/Polymixin
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Misc antimicrobials
Metronidazole
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antimicrobials Not Authorized for Veterinary Use Primarily injectable
``` CARBAPENEMS- Imipenem/meropenem Ertapenem/doripenem GLYCOPEPTIDES- Vancomycin/Teicoplanin OXAZOLIDINONES- Linezolide ```
33
Classification of antibiotics according to origin
* Natural – produced by fungi and bacteria (antibiotics) * Semi-synthetic – chemically altered natural compounds * Synthetic – chemically designed by man
34
Classification according to effect | on bacteria
``` •Bactericidal drugs- kill •Bacteriostatic drugs- inhibt growth -- Some drugs may be bactericidal or bacteriostatic depending on: --> Drug concentration --> Presence of other drugs --> Bacterial species ```
35
Spectra of activity for β-lactams- | Penicillins
* Penicillin G / V (narrow spectrum, Gram +) * Methicillin, oxacillin(antistaph penicillins) * Aminopenicillins (more active against Gram-) * Carbooxypenicillins (active against Pseudomonas and Proteus)
36
Spectra of activity for β-lactams- | Cephalosporins
* 1st generation (mainly Gram+) * 2nd generation (more active against Gram-) * 3rd generation (broader spectrum incl. Pseudomonas) * 4th generation (both Gram+ and Gram+, less susceptibile to β-lactamases)
37
Spectra of activity for β-lactams- | Carbapenems
• Imipenem, meropenem (highly resistant to β-lactamases, injectable)
38
Drugs active against Gram+ cocci Non-Penicillate producing Grampositive cocci - Enterococcus - Streptococcus
Good- •Penicilins •Aminopenicilins Bad- •Metronidazole
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Drugs active against penicillate-producing staphylococci- Penicillase-producing Staphylococcus
``` Good- •Amoxicillin/clavulanate •Cephalosporins •Sulfonamides •Aminoglycosides •Fluoroquinolones ``` Bad- •Penicilins •Aminopenicillins •Metronidazole
40
``` Drugs active against Gram- rods - Glucose-fermentative Gram-negative rods Escherichia Enterobacter Klebsiella Proteus Pasteurella ```
``` Good- •Amoxicillin/clavulanate •Cephalosporins •Fluoroquinolones •Aminoglycosides •Sulfonamides ``` ``` Bad- •Metronidazole •Penicillins •Lincosamides •Macrolides ```
41
Drugs active against anaerobes ``` Actinomyces Clostridium Peptostreptococcus Bacteroides Fusobacterium Porphyromonas Prevotella ```
``` Good- •Penicilins •Aminopenicillins •Lincosamides •Metronidazole ``` Bad- •Amino glycosides
42
Classification based on PK/PD index
--Time-dependent antibiotics (index: time over MIC) are most effective if their concentration is maintained above the MIC as long as possible (at least 50% of the dosing interval for beta-lactams). --Concentration-dependent antibiotics (index CMAX/CMI) are most effective if they reach a high concentration compared to the MIC at the site of infection, while the time that they maintain this concentration is less important. • Many antibacterial classes (e.g. macrolides, lincosamides and tetracyclines) fall into a third category, where efficacy depends both on concentration and time (index AUC/CMI).
43
Concentration- vs time-dependent drugs
Time-dependent Time>MIC --> Penicillins --> Cephalosporins AUC/MIC - -> Macrolides - -> Lincosamides - -> Tetracyclines Conc.-dependent Cmax/MIC --> Aminoglycosides --> Fluoroquinolones* *The efficacy of fluoroquinolones is also predicted by AUC/MIC > 100 for treatment of Gram-negative bacterial infections In order to maximize clinical efficacy: • High doses for concentration-dependent drugs • Regular dose intervals for time-dependent drugs
44
Mutualism
both are necessary and relation is positive for both
45
Commensalism
good for one, no problem for the other (eg. Most of the intestinal flora)
46
Parasitism
one takes advantage of the other
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Pathogenic (types)
``` Facultative pathogenic • Endogenic infection ---- E. coli ---- S. aureus • Exogenic infection Obligate pathogenic ```
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Balanced and unbalance pathogenicity
* Balanced: damage with recovery | * Unbalanced: high damage/death
49
Infection
• Invasion and multiplication of micro-organism, ev. with disease
50
Disease
``` • Structural and functional damage • Clinical/Subclinical --- Subclinical ex: Mastitis (in dairy cattle, reduced milk production) • Opportunistic • Septicaemiae/bacteraemia ```
51
Adhesion via Flagella
``` • Not in all bacteria • Motility • H-antigens • Composition • Flagellin • Mainly in Gram-negative bacteria Ex: Listeria monocytogenes ```
52
Pili, fimbria & fibrillae
Pili = fimbriae = fibrillae • Adhesion • F-antigens Ex: E. coli: ETEC, F4, F5,... Special pili = sex pili • Bacteria conjugation (plasmid transfer)
53
Invasion of bacteria (3 ways)
Extracellular • Thromboses, local use of nutrients/oxygen • Immunological reaction: oxygen radicals/enzymes by macrophages and neutrophils Facultative intracellular • Cell lysis Obligate intracellular • Cell lysis
54
Invasion- | • Virulence factors involved
- Capsule - Proteins that circumvent innate immunity - Iron uptake - Production of extracellular enzymes • Hyaluronidases • Collagenases • Fibrinolysins • Coagulases • Hemolysins • Leucocidins
55
Capsule
``` • Not in all bacteria • Polysaccharides-proteins • Virulence factor ---> Colonisation ---> Invasion ---> Adhesion ---> Protection against : • phagocytosis • Complement • Environmental protection • Capsular antigens (K-antigens) ```
56
Toxins: exotoxins
• Bacterial metabolites ---> Clostridium • Proteins with in general high molecular weight (are thus antigenic) -- Exceptions: eg. Heat stable enterotoxin (Sta, Stb) of ETEC • Types I, II, III • ‘Anatoxins’: chemically treated (eg. formalin) toxins --Toxicity:- -- Antigenicity: + (vaccination)
57
Types of Exotoxins
• Type I -Bind receptor - Disturbance of cell metabolism • Examples: • Sta of ETEC • Clostridiumperfringens • Staphylococci and Streptococci • Type II - Cell wall damage - Staphylococcus aureus: alfa-toxin (hemolysis) - Actinobacillus pleuropneumoniae: Apx Toxins (pore forming) • Type III - Intracellular toxins - A component: goes IC - B (binding) component: binds membrane • Examples: • Heat labile toxin (LT) of ETEC • Shiga toxin (ST) of VTEC, EHEC • Botulinum toxin • tetanospasmin
58
Toxins: endotoxins, Gr -
``` • Cell wall components • Damage +++ • Immune reaction + • LPS (heat stable) -- Protection against • Toxic products • Complement -- Acts as an endotoxin • Infection with a Gram-negative bacterium • Fever, general sickness • Tissue damage • Cardiovascular shock • Death ```
59
Toxins cell wall Gr+
• Lipoteichoic acid (LTA) --- Example: Staphylococcus aureus • Lipoarabinomannan (Mycobacteria) (LAM) • Peptidoglycan • Fever, general sickness • Tissue damage • Cardiovascular shock • Death
60
Membrane vesicles | Structure and Roles
``` Spheric structures • Lipid membrane (part of outer membrane) • Contain • Enzymes • exotoxins • DNA(Transformation) • Signalmolecules ``` ``` Roles • Pathogenesis • Signaling (quorum sensing) • Excretion of toxic products • Killing of competitors • Immunomodulation • Excretion of bacterial toxic products • Transformation ```
61
Biofilms
``` •Hard to treat • Bacteria in sessile form included • Composition: -- Polysaccharides -- Proteins -- Nucleic acids (DNA) • Bacterial persistence (endocarditis) • Reduction of host immunity • Local damage • Reduced susceptibility to antibiotics • Different surfaces: Catheters, pipelines (drinking water farms),... ```
62
Outer membrane proteins
* (Lipo)proteins-porins * Role: * Pathogenesis * Adhesion * Iron uptake * Physiological role
63
Iron uptake
- By the cell wall proteins - In first line defense (innate defense) • No free iron in the body • Intracellular: • Epithelial cells: ferritin • Erythrocytes; hemoglobin • Muscular cells: myoglobin • Serum: transferrin • mucosae: lactoferrin • Infection: neutrophils ---> lactoferrin • Pathogenic bacteria can circumvent iron restriction • Alternative for iron • E.g. manganese in Borrelia burgdorferi • Expression of iron uptake system under iron restrictive conditions • Siderophorereceptor (neonatal E.colisepticaemiae) • Transferrine / lactoferrine receptor ** • Hemoglobinereceptor** (**Actinobacillus; pleuropneumoniae)
64
Virulence factors and innate immunity
No complement activation • Sialic acid (E. coli) on the surface • Enzymes that degrade the complement system No lysis of bacterium • LPS • Capsule Inhibition of the complement mediated inflammation • Membrane vesicles • Expel of complement factors • Intracellular multiplication
65
Cellular mechanism of innate immunity
Phagocytes • Macrophages • Neutrophils NK cells
66
Virulence factors against phagocytes
* Extracellular bacteria * Capsule * Metabolites-exotoxins * Biofilm * Facultative intracellular
67
Kinds of vaccines
- Vaccines with living organisms (attenuated) - Vaccines without living organisms • DNA vaccines • Vaccines based on antigen ---> Toxoid: inactivated exotoxin • Isolated from bacterium or recombinant ---> Bacterins:inactivatedcompletebacterium ---> Subunit vaccines • Fimbriae, surface antigens • Isolated fro; bacterium or recombinant
68
Vaccines with living organisms (attenuated) | --- What is attenuated?
``` Attenuation • Serial passages in Vitro (Pasteur & rabies) • Genetic manipulation - Culture + mutagen - Deletion mutants - Vector vaccines - Not so frequent against bacteria • BCG vaccine (TB) • Bordetellabronchiseptica • E. coli (APEC, ETEC swine) - Both cellular and humoral immunity - One vaccination • Care: no antibiotic treatment!! - Fast induction of protection - Vector vaccines • use of eg. attenuated Salmonella • Expression of immunogen epitope ```
69
Vaccines based on antigen Classification 3 Main types
* In general a lot of antigen present * Frequently an adjuvant added * 2 administrations with 3-4 w interval * Safe * Mainly production of antibodies *3 Main Types - Toxoid • Exotoxin + formol • Recombinant - Bacterins • Complete bacterium • Note: autovaccine ---> Bacterium isolated from diseased animal & inactivation (formol) ---> Care: side effects - Subunit • Fimbriae (ETEC) • Iron capture systems; transferrin binding proteins (APP)
70
Vaccines- Combinations
• Bacterin + toxoid • Subunit + toxoid ---> ETEC: Fimbriae and LT
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What is the role of a veterinarian | in regards to Parasitology?
``` To equip you with information on parasites you will need as a veterinarian in North America: • which cause disease • clinically relevant • which are zoonoses • diagnostic tools • minimize impact on production • treatments used daily in practice • sustainable interventions to manage ```
72
What are 3 main classes of parasites that can cause disease in humans?
helminths, ectoparasites (Arthropods) and protozoa.
73
Diagnostic methods of parasitology
SIS!!!! • Host Species • Site of Infection • Size of parasite
74
Treatment and prevention | in parasitology
* Parasiticides * Sustainable management of the host * Management of the environment * Life cycle is used to determine treatment and prevention
75
Parasites of veterinary importance
``` Phylum Nemathelminthes (Roundworms) Class Nematoda (Roundworms) Phylum Platyhelminthes (Flatworms) Class Cestoda (Tapeworms) Class Trematoda (Flukes) Phylum Arthropoda Class Insecta Class Arachnida Subkingdom Protozoa Phylum Mastigophora Phylum Apicomplexa - Five orders (Helminths) Phylum Nemathelminthes (Roundworms) Class Nematoda (Roundworms) Phylum Platyhelminthes (Flatworms) Class Cestoda (Tapeworms) Class Trematoda (Flukes) ```
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Nematodes (roundworms)
``` Helminths Phylum Nemathelminthes (Roundworms) Class Nematoda (Roundworms) ex: Ascaris suum • Free-living or parasitic • Elongate/cylindrical • Alimentary canal present • Sexes usually separate • Life cycle direct or indirect ```
77
Cestodes (tapeworms)
``` Helminths Phylum Platyhelminthes (Flatworms) Class Cestoda (Tapeworms) ex: Dipylidium caninum • Flat body and no alimentary canal • Scolex (holdfast organ) • Strobila (body) with proglottids • Each proglottid- hermaphroditic • Indirect life cycle • Types of characteristic larval stages ```
78
Trematodes (flukes)
``` Helminths Phylum Platyhelminthes (Flatworms) Class Trematoda ex: Fasciola hepatica • Dorso-ventrally flattened • Leaf-like • Oral and ventral suckers • Indirect life cycle- molluscan IH • Usually genitally independent ```
79
Arthropods
``` Phylum Arthropoda Class Insecta & Class Arachnida Insects • Flies(Diptera) • Fleas(Siphonaptera) • Lice(Phthiraptera) • Hemiptera --> Identification • Adults: 3 pairs of legs • Head, thorax, abdomen • Antenna ``` ``` Arachnids -- Acari • Ticks • Mites --> Identification • Nymphs and adults: 4 pairs of legs • Larvae: 3 pairs of legs • Body: cephalo-thorax and abdomen • No antennae, but palps ```
80
Protozoa
``` Subkingdom Protozoa Phylum Mastigophora Phylum Apicomplexa - Five orders ex: Giardia • Unicellular, eukaryotic animals • Classified based on their mode of locomotion • Locomotion is accomplished by: Pseudopodia Flagella Gliding movements Cilia ```
81
Common routes of parasite entry
Ingestion: • Giardia, Balantidium coli, Toxoplasma gondii, Cryptosporidium, Cestodes, some Nematodes, some Trematodes Skin or mucosal penetration: • Hookworm, Strongyloides stercoralis; schistosomes Transplacental (prenatal) • Toxoplasma gondii, Toxocara canis, Strongyloides stercoralis Transmammary (milk) • Toxocara canis, T. cati, Ancylosotma caninum Arthropod bite (vector): • Babesia, heartworm, Leishmania, Trypanosomes Sexual contact • Tritrichomonas foetus
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Attachment of parasites
``` • Mechanical or biting mouthparts  • Oral cavity (capsule) • Attachment organs • Suction disk • Biting mouthparts • Direct penetration • Molecular interaction ```
83
Molecular interactions of attachment in parasites
Parasites Target Receptor Trypanosome cruzi Fibroblast Fibronectin & its receptor Leishmania mexicana macrophage Major surface protease (MSP or GP63) & CR2 Babesia spp. Red blood cells C3b receptor Giardia duodenalis Duodenal & jejunal Lectin and epithelium mannose-6- phosphate adherence molecule 1 on disk
84
Cell and Tissue Damage: | Mechanical Tissue damage
``` • Blockage of internal organs: Ascaris, tapeworms, schistosomes, filarial worm • Pressure atrophy: Echinococcus, Cysticerci • Migration through tissues: Helminthic larvae ```
85
Cell and Tissue Damage: | Toxic Parasite Products
``` • Destructive enzymes: Anasakiasis, schistosome cercariae, hookworms • Endotoxins: African trypanosomes, malaria • Toxic secretions: Tickparalysis ```
86
Loss of nutrients via parasites | and examples
• Competition with hosts for nutrients – Diphyllobothrium latum (fish tapeworm) • Interference with nutrient absorption – Giardia duodenalis & Strongylodies stercoralis • Nutrient loss – hookworm, iron loss;
87
Disruption, evasion, and inactivation of host defenses
Host immunity • Natural or innate immunity – A defense mechanism that does not depend upon prior exposure to the invader. -- Cytokines and cytokine receptors -- Antimicrobial molecules and pattern recognition receptors -- Cellular defense, phagocytosis • Acquired immunity – conferred by a host’s specific immunity response developed as a result of a previous parasitic infection. • Premunition: resistance to superinfection by presence of parasites in check by host immunity-malaria, toxoplasmosis • Concomitant immunity: a parasite elicits a protection against reinfection, but the parasite itself remains in the host, unaffected by the immune response- schistosomiasis
88
Innate immunity | - Complement pathways
3 Pathways There are three pathways of complement activation, two initiated by microorganisms without the require- ment for antibody, called the alternative and lectin pathways, and a third initiated by immune complexes, called the classical pathway * all end up with the production of C3b, which is part of C5 convertase which will activate C5 in the downstream chain reaction - end effects = Cell lysis; inflammation; opsonization; clearance of immune complexes • activation factors, C3 and C5 convertase, terminal pathway and MAC, results of complement activation
89
Adaptive immunity components
* Humeral immunity * Primary and secondary humeral immune response * Antibody (type & structure) Two Distinct types of adaptive immune responses: ---> Humeoral immunity is mediated by antibodies secreted by antigen- activated B cells and their progeny plasma cells. ---> Cell mediated immunity is mediated by antigen- activated T cells and the cytokines they secrete. • CD8+Tcellsfunctionas cytotoxic T lymphocytes (CTL • CD4+TH1cellsandactivated macrophages function in DTH (delayed type hypersensitivity) responses.
90
Summarize the Classical pathway
Activator – binding of Ab to Ag; C1 reactive protein binding Initial complement component – C1q, C1r, C1s, C4, C2 C3 convertase – C4bC2b C5 convertase – C4bC2bC3b *** explained well on pages 30 + 31 in book
91
Summarize the Lectin pathway
Activator – mannan binding lectin (MBL), MBL‐associated serine protease‐2 (MASP‐2) Initial complement component – C4, C2 C3 convertase – C4bC2b C5 convertase – C4bC2bC3b
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Innate Immune Defenses
Functions in normal host without prior expose to invading microbes ``` Includes: • Constitutional factors • Natural barriers & normal flora  Cytokines/Interferons •  Phagocytosis •  Complement ```
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Immune Defenses - Adaptive Response
Adaptive, specific immune responses are induced by exposure to an antigen(s), the response is specific for the inducing antigen(s), and immunologic memory is generated. --Consists of antibody response (humoral) and lymphocyte‐ mediated response (cell‐mediated) response – tailored to particular microbial infection and characterised by memory
94
Constitutional factors of | Innate Immune Defenses
Making one species innately susceptible and another resistant to certain infections:  Genetic – between species  Age – the young more susceptible  Metabolic factors – hypoadrenal & hypothyroid states  Neuroendocrine factors  Environment – malnutrition, poor living conditions, overcrowding
95
Major Functions of Type I Interferons (IFN) | of Innate Immune Defenses
--> Induce resistance to viral replication in all cells --> Increase MHC Class 1 expression and antigen presentation in all cells --> Activate NK cells to kill virus-infected cells IFN System ‐ Crucial for Antiviral Defense • Demonstrated in animal models – treatment with anti‐IFN Ab – gene knockout mice • Defective IFN response – reduced ability to contain infection – increased illness and death • Abrogation of IFN‐α/β – global increase in susceptibility – IFN‐γ – modest effect
96
Innate Immune Defenses Cell types involved in the defence against microbes
``` Phagocytic cells • Polymorphonulcear neutrophils • Mononuclear phagocytes (monocytes in blood, macrophage in tissue) • Eosinophils ``` Lymphocytes B cells- Ab producing plasma cells T cells- Cell mediated immune response Help B cells in Ab production Large granular lymphocytes (null cells or NK cells)- Kill other rogue cells in a nonspecific manner against microbes
97
Innate Immune Defences Phagocytosis
Engulfment & digestion of infectious agents or other foreign bodies by phagocytic cells Phagocytic cells – phagocytes- major 2: macrophages & neutrophils
98
Distinguishing Infected‐Self from Uninfected Self
• Innate immune system – Pattern recognition receptors (PRRs) • Toll‐likereceptors(TLRs) • Rig‐likereceptors(RLR) • complement – Missing/altered self receptors (NK cells) • Adaptive immune system – Antigen presentation (MHC) – Antibodies – T cell receptors
99
Describe the Multi-phasic act of Phagocytosis
1) Bacterium becomes attached to membrane evaginations called pseudopodia 2) Bacterium is ingested, forming phagosome 3) Phagosome fuses with lysosome 4) Lysosomal enzymes digest captured material 5) Digestion products are released from cell **Just because a foreign body undergoes phagocytosis, doesn't necessarily mean it is automatically being destroyed or killed. Most are killed, but some pathogens have evolved methods to evade attachment, etc.
100
Neutrophils | Describe primary function and process
Type of phagocyte; Innate immunity - Primarily function to phagocytise and kill extracellular bacterial and yeasts pathogens in acute inflammation. - Live only ~ 1 day in tissues!! - Dead neutrophils are cleaned up by macrophages. Process- --> Neutrophils express receptors for many bacterial and fungal constituents --> Neutrophils bind bacteria, engulf then and destroy them with the toxic content of the neutrophil granules
101
Macrophages | what do they do and how do they do it?
Type of phagocyte; Innate immunity Process- --> The macrophage expresses several receptors specific for bacterial constituents --> Bacteria bind to macrophage receptors --> Macrophage engulfs and digests bound bacteria
102
Eosinophils
Type of phagocyte; Innate immunity - Eosinophils are an important defense against helminths. - Eosinophils are 1-3% WBC but #’s increase in parasite infections and patients with type I hypersensitivities
103
Natural Killer Cells
• Abundant lymphocytes – 2% of circulating • Large, granular lymphocytes – lack antigen‐ specific receptors found on T and B cells • Number increases rapidly after viral infection ‐ stimulated to divide by IFN produced by infected cells and dendritic cells • On binding release mix of cytokines (IFN γ and TNFα) • Kill cells by releasing perforins and granzymes – perforate membranes and trigger caspase ‐ mediated cell death
104
NK Cell Recognition of Infected Cells: | Detection of Altered Self
• Recognize “altered self” • Two receptor‐binding interactions required for discrimination – one to activate and one to block if cell is not infected • Virus infection‐associated ligand – activating • MHC I molecule – blocking • Virus‐infected cells are prime targets (fewer MHC I on surface) *** good table for visualization on slide 27 of Host Defense 1 ppt
105
Summarize Alternative Pathway
Activator – contact of microbial cell wall with C3 Initial complement component – C3, Factor B, Factor D, & properdin C3 convertase – C3bBb C5 convertase – C3bBbC3b
106
What are paratopes?
• the part of an antibody which recognizes an antigen, the antigen-binding site of an antibody • a small region (of 15–22 amino acids) of the antibody's Fab region ** know the type & structure of the antibodies (last ~9 slides of Host 2 ppt)