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PID Exam 1 > Exam 1 > Flashcards

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
Q

Phenicols

A

Chloramphenicol

Florfenicol

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26
Q

BETA-LACTAMS-

Cephalosporins

A

Cefalexin/Cephadroxil
Cefpodoxime/Ceftiofur
Cefovecin, Cefquinome

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27
Q

Macrolides

A

Erythromycin

Tiamulin, Tilmicosin

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28
Q

Lincosamides

A

Lycomycin/Clindamycin

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29
Q

Aminoglycosides

A

Streptomycin
Gentamicin/Neomycin
Amikacin

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30
Q

Polypeptides

A

Colistin/Polymixin

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31
Q

Misc antimicrobials

A

Metronidazole

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32
Q

antimicrobials
Not Authorized for Veterinary Use
Primarily injectable

A 
CARBAPENEMS-
Imipenem/meropenem
Ertapenem/doripenem
GLYCOPEPTIDES-
Vancomycin/Teicoplanin
OXAZOLIDINONES-
Linezolide
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33
Q

Classification of antibiotics according to origin

A
  • Natural – produced by fungi and bacteria (antibiotics)
  • Semi-synthetic – chemically altered natural compounds
  • Synthetic – chemically designed by man
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34
Q

Classification according to effect

on bacteria

A 
•Bactericidal drugs- kill
•Bacteriostatic drugs- inhibt growth
-- Some drugs may be bactericidal or
bacteriostatic depending on:
--> Drug concentration
--> Presence of other drugs
--> Bacterial species
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35
Q

Spectra of activity for β-lactams-

Penicillins

A
  • Penicillin G / V (narrow spectrum, Gram +)
  • Methicillin, oxacillin(antistaph penicillins)
  • Aminopenicillins (more active against Gram-)
  • Carbooxypenicillins (active against Pseudomonas and Proteus)
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36
Q

Spectra of activity for β-lactams-

Cephalosporins

A
  • 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)
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37
Q

Spectra of activity for β-lactams-

Carbapenems

A

• Imipenem, meropenem (highly resistant to β-lactamases, injectable)

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38
Q

Drugs active against Gram+ cocci
Non-Penicillate producing Grampositive cocci
- Enterococcus
- Streptococcus

A

Good-
•Penicilins
•Aminopenicilins

Bad-
•Metronidazole

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39
Q

Drugs active against penicillate-producing
staphylococci-
Penicillase-producing
Staphylococcus

A 
Good-
•Amoxicillin/clavulanate
•Cephalosporins
•Sulfonamides
•Aminoglycosides
•Fluoroquinolones

Bad-
•Penicilins
•Aminopenicillins
•Metronidazole

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40
Q 
Drugs active against Gram- rods -
Glucose-fermentative  Gram-negative rods
Escherichia
Enterobacter
Klebsiella
Proteus
Pasteurella
A 
Good-
•Amoxicillin/clavulanate
•Cephalosporins
•Fluoroquinolones
•Aminoglycosides
•Sulfonamides
Bad-
•Metronidazole
•Penicillins
•Lincosamides
•Macrolides
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41
Q

Drugs active against anaerobes

Actinomyces
Clostridium
Peptostreptococcus
Bacteroides
Fusobacterium
Porphyromonas
Prevotella
A 
Good-
•Penicilins
•Aminopenicillins
•Lincosamides
•Metronidazole

Bad-
•Amino glycosides

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42
Q

Classification based on PK/PD index

A

–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).

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43
Q

Concentration- vs time-dependent drugs

A

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
Q

Mutualism

A

both are necessary and relation is positive for both

45
Q

Commensalism

A

good for one, no problem for the other (eg. Most of the intestinal flora)

46
Q

Parasitism

A

one takes advantage of the other

47
Q

Pathogenic (types)

A 
Facultative pathogenic 
• Endogenic infection
---- E. coli
---- S. aureus
• Exogenic infection
Obligate pathogenic
48
Q

Balanced and unbalance pathogenicity

A
  • Balanced: damage with recovery

* Unbalanced: high damage/death

49
Q

Infection

A

• Invasion and multiplication of micro-organism, ev. with disease

50
Q

Disease

A 
• Structural and functional damage
• Clinical/Subclinical
    --- Subclinical ex: Mastitis (in dairy cattle, reduced milk production)
• Opportunistic
• Septicaemiae/bacteraemia
51
Q

Adhesion via Flagella

A 
• Not in all bacteria
• Motility
• H-antigens
• Composition 
• Flagellin
• Mainly in Gram-negative bacteria
Ex: Listeria monocytogenes
52
Q

Pili, fimbria & fibrillae

A

Pili = fimbriae = fibrillae
• Adhesion
• F-antigens
Ex: E. coli: ETEC, F4, F5,…

Special pili = sex pili
• Bacteria conjugation (plasmid transfer)

53
Q

Invasion of bacteria (3 ways)

A

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
Q

Invasion-

• Virulence factors involved

A
  • Capsule
  • Proteins that circumvent innate immunity
  • Iron uptake
  • Production of extracellular enzymes
    • Hyaluronidases • Collagenases • Fibrinolysins • Coagulases • Hemolysins • Leucocidins
55
Q

Capsule

A 
• Not in all bacteria
• Polysaccharides-proteins
• Virulence factor  
  ---> Colonisation
  ---> Invasion
  ---> Adhesion
  ---> Protection against :
            • phagocytosis
            • Complement
• Environmental protection
• Capsular antigens (K-antigens)
56
Q

Toxins: exotoxins

A

• 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
Q

Types of Exotoxins

A

• 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
Q

Toxins: endotoxins, Gr -

A 
• 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
Q

Toxins cell wall Gr+

A

• Lipoteichoic acid (LTA)
— Example: Staphylococcus aureus
• Lipoarabinomannan (Mycobacteria) (LAM) • Peptidoglycan
• Fever, general sickness • Tissue damage
• Cardiovascular shock
• Death

60
Q

Membrane vesicles

Structure and Roles

A 
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
Q

Biofilms

A 
•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
Q

Outer membrane proteins

A
  • (Lipo)proteins-porins
    • Role:
      * Pathogenesis
      * Adhesion
      * Iron uptake
    • Physiological role
63
Q

Iron uptake

A
  • 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
Q

Virulence factors and innate immunity

A

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
Q

Cellular mechanism of innate immunity

A

Phagocytes
• Macrophages
• Neutrophils
NK cells

66
Q

Virulence factors against phagocytes

A
  • Extracellular bacteria
    * Capsule
    * Metabolites-exotoxins
  • Biofilm
  • Facultative intracellular
67
Q

Kinds of vaccines

A
  • 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
Q

Vaccines with living organisms (attenuated)

— What is attenuated?

A 
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
Q

Vaccines based on antigen
Classification
3 Main types

A
  • 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
Q

Vaccines- Combinations

A

• Bacterin + toxoid
• Subunit + toxoid
—> ETEC: Fimbriae and LT

71
Q

What is the role of a veterinarian

in regards to Parasitology?

A 
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
Q

What are 3 main classes of parasites that can cause disease in humans?

A

helminths, ectoparasites (Arthropods) and protozoa.

73
Q

Diagnostic methods of parasitology

A

SIS!!!!
• Host Species
• Site of Infection
• Size of parasite

74
Q

Treatment and prevention

in parasitology

A
  • Parasiticides
  • Sustainable management of the host
  • Management of the environment
  • Life cycle is used to determine treatment and prevention
75
Q

Parasites of veterinary importance

A 
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)
76
Q

Nematodes (roundworms)

A 
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
Q

Cestodes (tapeworms)

A 
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
Q

Trematodes (flukes)

A 
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
Q

Arthropods

A 
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
Q

Protozoa

A 
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
Q

Common routes of parasite entry

A

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

82
Q

Attachment of parasites

A 
• Mechanical or biting mouthparts 
• Oral cavity (capsule)
• Attachment organs 
• Suction disk
• Biting mouthparts 
• Direct penetration
• Molecular interaction
83
Q

Molecular interactions of attachment in parasites

A

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
Q

Cell and Tissue Damage:

Mechanical Tissue damage

A 
• Blockage of internal organs:  
        Ascaris, tapeworms, schistosomes, filarial worm
• Pressure atrophy: 
        Echinococcus, Cysticerci
• Migration through tissues: 
        Helminthic larvae
85
Q

Cell and Tissue Damage:

Toxic Parasite Products

A 
• Destructive enzymes: 
          Anasakiasis, schistosome cercariae, hookworms
• Endotoxins: 
          African trypanosomes, malaria 
• Toxic secretions:
          Tickparalysis
86
Q

Loss of nutrients via parasites

and examples

A

• Competition with hosts for nutrients –
Diphyllobothrium latum (fish tapeworm)
• Interference with nutrient absorption –
Giardia duodenalis & Strongylodies stercoralis
• Nutrient loss –
hookworm, iron loss;

87
Q

Disruption, evasion, and inactivation of host defenses

A

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
Q

Innate immunity

- Complement pathways

A

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
Q

Adaptive immunity components

A
  • 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
Q

Summarize the Classical pathway

A

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
Q

Summarize the Lectin pathway

A

Activator – mannan binding lectin (MBL), MBL‐associated
serine protease‐2 (MASP‐2)
Initial complement component – C4, C2 C3
convertase – C4bC2b
C5 convertase – C4bC2bC3b

92
Q

Innate Immune Defenses

A

Functions in normal host without prior expose to invading microbes

Includes:
•  Constitutional factors
•  Natural barriers & normal flora  Cytokines/Interferons
•  Phagocytosis
•  Complement
93
Q

Immune Defenses - Adaptive Response

A

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
Q

Constitutional factors of

Innate Immune Defenses

A

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
Q

Major Functions of Type I Interferons (IFN)

of Innate Immune Defenses

A

–> 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
Q

Innate Immune Defenses

Cell types involved in the defence
against microbes

A 
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
Q

Innate Immune Defences

Phagocytosis

A

Engulfment & digestion of infectious agents or other
foreign bodies by phagocytic cells
Phagocytic cells – phagocytes- major 2: macrophages & neutrophils

98
Q

Distinguishing Infected‐Self from Uninfected Self

A

• 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
Q

Describe the Multi-phasic act of Phagocytosis

A

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
Q

Neutrophils

Describe primary function and process

A

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
Q

Macrophages

what do they do and how do they do it?

A

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
Q

Eosinophils

A

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
Q

Natural Killer Cells

A

• 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
Q

NK Cell Recognition of Infected Cells:

Detection of Altered Self

A

• 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
Q

Summarize Alternative Pathway

A

Activator – contact of microbial cell wall with C3
Initial complement component – C3, Factor B, Factor D, & properdin
C3 convertase – C3bBb
C5 convertase – C3bBbC3b

106
Q

What are paratopes?

A

• 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)

PID Exam 1 (1 decks)

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