Intro to Immunology

Question 1

How the healthy animal defend itself against pathogens at diff stages

Answer 1

1. The infection can be prevented entirely
2. If infection does occur the defenses may stop the process before disease is apparent
3. The defenses that are necessary to defeat a parasite may not be effective until infectious disease is well into progress

Question 2

What 2 host defense mechanism

Answer 2

1.Non- specific defense (constitutive/ innate / natural)
2. Inducible defense - ( acquired immune response )

Question 3

What is non- specific defense

Answer 3

1. Non – specific defenses (constitutive/ innate/ natural) - Is part of the normal constitution of the body
   - Provide general protection against invasion
   normal flora or pathogens
   - Do not need prior contact with a particular microbe
   - Immediately ready to come into play

Question 4

What is inducible defenses

Answer 4

2. Inducible defenses –(acquired immune responses)
   - Host defenses that must be induced or turned on by host exposure to a pathogen (as during an infection)

• Not immediately ready to come into play until after the host is exposed to the particular microbe
• Involve the immune responses to a pathogen causing an infection

Question 5

Innate defenses

Answer 5

 Differences in susceptibility to certain pathogens  Anatomical defenses
 Microbial antagonism
 Tissue bactericides, including complement
 Inflammation (ability to under go inflammatory response)
 Phagocytosis

Question 6

What is species resistance

Answer 6

Certain pathogens infect only humans, not lower animals (syphilis, gonorrhea, measles, poliomyelitis) –why?
1. Absence of specific tissue or cellular receptors for attachment (colonization) by pathogen
2. Lack of exact nutritional requirements to support the growth of the pathogen
3. Lack of a target site for a microbial toxin

Question 7

What example of Individual resistance

Answer 7

-Age: relates to the development and status of immune system – the very young and elderly most susceptible
 Sex :linked to development of the sex organs and also effect of sex hormones mastitis, orchitis
 Diet ,malnutrition
 Undercurrent disease or trauma
 Therapy against other diseases

Question 8

Example of Anatomical Defenses

Answer 8

Eye- blink, tears,lyzm
Skin- sweat, lactic acid, lyszm
Urogenital Tract- lyszm
Respiratory Tract- mucus, phagocycte, lyszm
Gi Tract- stomach acidity , peristalsis, antimicrobial

Question 9

What is microbial antagonism

Answer 9

There are three main ways that the normal flora protect the surfaces where they are colonized

1. Competition with non – indigenous species for binding (colonization) sites.
2. Specific antagonism against non-indigenous species – production bacteriocins
3. Nonspecific antagonism against non- indigenous species.

Question 10

What is complement

Answer 10

-Complement is an enzymatic system of serum proteins made up of 9 major components (C1-C9)
 Sequentially activated in many Ag-Ab reactions resulting in disruption of membranes – bacterial lysis
 Complement in the classical pathway – is activated some immunoglobulins
(IgG and IgM) can fix complement. This initiates a cascading reaction resulting on the surface of the microbe the principal effects of which are:-

Question 11

What is alternative pathway of complement activation

Answer 11

 Complement activation occurs independent of immunuglobulins.
 Bacterial polysaccharides, LPS , peptidoglycan and teichoic acids can trigger the alternate pathway or “properdin pathway”
 Important in initial (pre-antibody) defense against invading microbe

Question 12

What is the complement system

Answer 12

 Aim is to cleave C3 & C5 and activate membrane attack complex
 Classical pathway
 Alternative or properdin pathway
 Lectin pathway – MBP MASP act on C4 C2 like C3 convertase
 Recognition unit
 C3 convertase
 C5 convertase

Question 13

What are the result of complement activation

Answer 13

1. Generation of inflammatory factors, C3a and C5a - focus on antimicrobial serum factors and leucocytes into the site of infection
2. Attraction of phagocytes. Chemotactic factors C3a and C5a attract phagocytes to the site
3. Enhancement of phagocytic engulfment-C3b
4. Lysis of bacterial cells (lysozme- mediated) or virus – infected cells – C8 & C9

Question 14

Inflammation n cardinal signs

Answer 14

 Inflammation is a tissue reaction to injury or infection
 Characteristic symptoms – cardinal signs
1.redness - increased blood flow to area
2.swelling - increase extra-vascular fluid, phagocyte
infiltration to area
3.heat - increase blood flow and action of pyogens
4.pain - local tissue damage & irritation of sensory nerve receptors

Question 15

What phagocytosis

Answer 15

 Phagocytosis - “the eating of cells” is the process by which neutrophils and tissue macrophages derived from monocytes engulf and kill microbes
 Neutrophils particularly, engulf extracellular bacteria – (oxygen dependent killing)
 Macrophages most active against intracellular bacteria, protozoa and viruses
 Eosinophils are involved in metazoan parasitic infections – (Oxygen independent )

Question 16

Non- specific defenses summary

Answer 16

 The 1st line of defense are skin and mucous membrane
 2nd line defense are provided by integrated phagocytosis and complement (alternative pathway) with some additional chemical factors
 Phagocytosis is principally by neutrophils for most bacterial infections and by macrophages for intracellular bacteria, protozoa & viruses
 Complement acts by assisting phagocytosis, by increasing vascular permeability and supply of neutrophils to infected tissues, and by lysing bacteria
 Additional chemical factors include lysozyme and acute phase proteins such as C –reactive protein

Question 17

Immunodeficiency

Answer 17

1) Disorders of specific immunity
a) Humoral immunodeficiency
b) Cell mediated immunodeficiency c) Combined immunodeficiency
2) Disorders of Complement 3) Disorders of Phagocytosis

Question 18

Autoimmunity

Answer 18

1. Loss of tolerance to self antigens due to cross reactivity to bacterial antigens, polyclonal activation of lymphocytes or genetic predisposition (HLA-B27 – juvenile RA)
2. Auto-antibodies