This long review covers everything in the lecture lessons, inclass assignments, and the pre-lessons.  It is mostly my long notes where I discuss topics in complete sentences.   To review the text, please review the chapter summaries, to review the homework, please look over your homework reading and assignment.  Material in homeworks 3 will be on the final.  For the text and the homework, the objectives provide you with the topics to know.    Yellow highlighted stuff we may have skipped, if so, you do not need to review it.

Host defense part I

Learning goals

  1. Be able to differentiate between non-specific and specific defenses.
  2. Be able to give examples of nonspecific defenses, (both mechanical and chemical defenses).
  3. Be familiar with the various kinds of blood cells and their roles.
  4. Understand the process of inflammation and what chemicals and cells play a role in inflammation.
  5. Be able to describe interferons and their role in host defenses.
  6. Be able to list the effects of complement activation.

Nonspecific & Specific Defenses

Last time we learned about disease, what causes it, how virulence factors allow the pathogen to establish itself and grow in a host
Today, we will learn about host defenses and how they protect the host.  
The body has a number of defenses against pathogens.  These defenses fall into two types:

  1. Nonspecific defenses are defenses that protect against any pathogen, regardless of the organism.
  2. Specific defenses protect against specific pathogens. Specific defenses involve specialized cells of the immune system called lymphocytes and the production of antibodies.  We will talk more about these in our next lesson.

Similar to Table 15.5:  Nonspecific & Specific Defenses

First line of defense
2nd line of defense
3rd line of defense
(specific defenses)
intact skin phagocytic white blood cells Specialized lymphocytes:B and T cells
mucous membranes & secretions inflammation & fever antibodies
  antimicrobial substances   

Fig. 15.1: The Skin

Mucous Membranes

The Respiratory System and its Defenses:

Other Defenses and Barriers:

So the various systems of the body have mechanical and chemical barriers which serve as a first line of defense against infection.  
They are nonspecific in that they defend against many different pathogens.

The Second Line of Defense

Granulocytes are WBC with visible granules in their cytoplasm (Fig 15.5). They include:

Agranulocytes are WBC w/o visible cytoplasmic granules. They include:

Video of Phagocytosis
Phagocytosis by neutrophils, eosinophils and mono/macrophages occur in five phases ( Fig. 15.8)

  1. Attraction -the phagocyte is attracted to the microbe. This is called chemotaxis. Compounds produced by the microorganism and damaged host cells attract the phagocytes. Compliment proteins and cytokines secreted from leukocytes can also attract phagocytes to an infection site.  We'll discuss these later.
  2. Adherence -the phagocyte must then adhere to the microbe .  If a microbe is first coated by an opsonin protein, the phagocyte more readily adheres to it.  The coating of microbes with opsonin (op'-so-nin or op'-saw-nin) proteins (antibodies and certain complement proteins) is called opsonization.
  3. Ingestion -The phagocyte ingests the microbe, surrounding it by a sac called a phagosome.
  4. Digestion or killing. Phagosomes fuse with lysosomes containing lysozyme and ~30  enzymes which hydrolyze the macromolecules of the microorganism.  Lysosomes contain lactic acids (pH ~ 4), hydrogen peroxide, superoxide radicals, and hydroxyl radicals to destroy microbes. The residual body is the indigested material left from the process. 
  5. Elimination, the residual body (the digested phagosome) moves to the plamsa membrane and is discharged outside the cell by exocytosis.  
    What happens to the free radicles?  Cells have enzymes to neutralize them.  You'll study catalase in the lab 2H2O2 --> H2O + O2.



We've talked about phagocytes, inflammation and fever as secondary lines of defense.    Two other secondary lines of defense include: Interferon & complement.



The Compliment Cascade


Host Defenses II

Learning goals

  1. Be able to compare and contrast humoral and cell-mediated immunity.
  2. Be able to list the results of antibody binding.
  3. Be able to describe the structures of the various kinds of antibody molecules as well as their functions.
  4. Understand how immunity can be artificially, as well as naturally, acquired.  Differentiate between active and passive immunity.
  5. Be able to describe the types of T-cells and their functions.
  6. Know the difference between T-dependent and T-independent antigens.

The nature of antigens: Fig. 16.1

Lymphocytes of Specific Host Defenses

T Cells

B Cells

The Results of Antibody Binding


IgG - is a monomer that is the most abundant Ig type in blood and is small enough to leave the blood and enter tissues. It enhances phagocytosis when bound to antigens, it neutralizes toxins and viruses, it protects against bacteria by triggering the complement system, it crosses the placenta and protects the fetus.  In short it can do everything against an antigen.

IgM - a pentamer of five Y's held together via a J-chain. It is especially involved in agglutination reactions (it has ten places for binding!) and in enhancing phagocytosis. It can do most things IgG can do except that it it too large to leave the blood and cross the placenta.  IgM is the first antibody produced on initial exposure to an antigen. A few days into the infection IgG is produced instead. If a second exposure takes place IgM levels rise some but the abundance of antibody that's produced is IgG.

IgA - is both a monomer and a dimer and is most common in mucus and secretions like saliva, tears and breast milk. The secretory form is a dimer, serum IgA is a monomer. Prevents attachment of pathogens to mucosal surfaces, important in resistance to respiratory infections. Its presence in colostrum helps protect infants form gastrointestinal infections.

IgE - is a monomer that attaches to mast cells and basophils (ba'-so-phils) to release histamine causing inflammation. It is involved in allergic reactions. When an antigen such as pollen attaches to the IgE on a mast cell or basophil, the cell releases histamine and other chemicals. This may be a protective response especially in the response to parasitic worms as it attracts phagocytic cells. Yet, it is a problem in allergies.

IgD is a monomer and the B cell receptor, BCR.  It is found on the surface of B cells. Each BCR is specific for only one antigenic determinant and each B cell is covered with ~500,000 identical BCRs. When Antigen binds to a BCR clonal selection occurs to that B cell.  Note, some BCR's are also IgM.  You should realize that the IgD which initially binds to an antigen later becomes the IgM which will bind to the same antigen that later becomes the IgG which binds to the same antigen.  The same B-cell makes all these antibodies types, though at different times. 

(Note: everything in red font will not be on Midterm2.   The exact cutoff point may be sooner than this and will be discussed in class.)

Immunity can be acquired naturally or artificially and can be active or passive

Natural -you get the Antigen naturally (you get the flu) Active -you get immunity yourself (you make Ab)
Artificial -you get Antigen fr/ a health care provider 
    (you get a flu shot)
Passive -you get immunity fr/ another
   (the doctor gives you antibodies)

Cell mediated immunity   

Cytotoxic T cells (TC) destroy target cells on contact. Tc cells are particularly effective against viruses and bacteria inside host cells.    Tc video.

Helper T cells (TH) produce cytokines. Upon exposure to an antigen by an Antigen Presentation Cells (mainly macrophages and their kin), they differentiate into type1 and type 2 helper T cells.

Type 1 helper T-cells   produce cytokines that activate and stimulate the proliferation of cytotoxic T cells.  Fig. 16.16.   Stimulated cytotoxic T cells proliferate and attack infected cells. Remember that cytotoxic T-cells contain multiple copies of one T-cell receptor on its surface that can bind to only one antigenic determinant so that cell mediated responses are specific.

Type 2 helper T-cells make cytokines that further expand a clone of B-cells and activate them in the production of antibodies. 

Types of Antigens

CD 4 vs CD 8


Lesson 10:  Immunization and Hypersensitivities

Learning Goals:

  1. Be able to name the different types of vaccines and list their advantages and weaknesses.
  2. Be able to relate how B and T-cells work from an earlier lesson to how vaccines work.
  3. Be able to list the 4 types of hypersensitivities, whether they are B or T-cell cell mediated, and be able to give an example.
  4. Be able to discuss how autoimmune diseases come about.
  5. Be able to discuss how which autoimmune diseases get what infections.


Immunity and Vaccines

  1. Attenuated live vaccines
  2. Inactivated (killed) vaccines
  3. Toxoid vaccines

Attenuated live vaccines 

Inactivated (killed) vaccines 

Toxoid vaccines 


Types of hypersensitivitis:

Type I:  Anaphalactic (an-a-fill-ac-tic) Response

  1. First exposure to antigen sensitizes your system to the antigen (Sensitization)
  2. Second Exposure of Antigen 
  3. Response

Type II:  Cytotoxic Hypersensitivity Response

Type III: Immune Complex Hypersensitivity

Type IV: Cell-Mediated Hypersensitivity

Review of Types of Hypersensitivity


Time before signs



Type I (anaphylactic)

< 30 min.

IgE binds to mast cells or basophiles causing release of histamine

anaphylactic shock from drug or insect bite, hay fever, asthma

Type II (cytotoxic)

5-12 hrs

IgG & IgM bind to target cell, complement is activated, cell destroyed

blood transfusion reactions,

Rh incompatibility

Type III (immune complex)

3-8 hrs

IgG & antigen  form complexes that cause inflammation

hypersensitivity pneumonitis

Type IV  
(cell mediated)

24-72 hrs.

Tc kill target cells

rejected transplants, 
poison ivy

AutoImmune Diseases

There are many autoimmune disease of two types:

  1. Single Tissue diseases
  2. Systemic Autoimmune Diseases

Congenital Immunodeficiency Diseases

Lesson 11:  Viruses

Learning Goals:


Viral Structure:
Viruses have different components to their structure, including

Viral Classification

  1. So, viruses vary quite a bit in their size, shape, whether they are enveloped or not, if they have spikes, if their genome is DNA or RNA, and if the genome is single or double stranded.
  2. Much of this variation is used to classify viruses including their:
  1. Viruses are referred to by their common English names instead of using Latin genus and species names.
  2. They also are not classified into superkingdoms, kingdoms, phylums, and classes, though a few have orders.
  3. They are generally only grouped into families, genera, species, and strains.
  4. They are classified by the kingdom they infect, for example animal and bacterial viruses.


Lytic Life Cycle

Viral Life Cycles

Bacteriophage Lysogeny 

Bacteriophages and Human Health

Animal Virus Budding and Persistent Infections 

Animal Virus Latency

Animal Viruses




Personal Reviews


Lesson 12:  Pathogenic Viruses

Learning Goals:

Viruses and Disease:

AntiViral Therapies:

DNA Viruses:


Other Pox Viruses

Herpes Family of Viruses:

New Name Common Name Disease and notes
Human herpesvirus 1 herpes simplex virus-1 cold sores, whitlow (wit'-lō), ocular herpes
Human herpesvirus 2 herpes simplex virus-2 genital lesions, whitlow, neonatal herpes
Human herpesvirus 3 Varicella-Zoster chickenpox and shingles (was ~90%)
Human herpesvirus 4 Epstein-Barr Virus, EBV most asymptomatic, mono, Burkitt's lymphoma, etc. (~90%)
Human herpesvirus 5 Cytomegalovirus, CMV most asymptomatic but may be severe in fetuses, newborns and immunocompromised (US ~50, some 90%)
Human herpesvirus 6 Roseolavirus (rō-zē'-ō-la) causes illness and a skin rash in children, may play role in MS, ~100%
Human herpesvirus 7 also Roseolavirus causes illness and a skin rash in children usually a short time later than HHV 6.
Human herpesvirus 8   --- causes Kaposi's sarcoma, a blood vessel cancer seen in the skin (very low %)

The Family Papillomavirus

Adenovirus Family

RNA Viruses

Family Picornaviridae

Families Togaviridae and Flaviviridae (Togaviruses and Flaviviruses)


-Hepatitis C

Family Coronavirus

Family Paramyxoviridae

Family Orthomyxoviridae


Lesson 13:  Pathogenic Gram+ Bacteria

Learning Goals:

Bacterial Pathogens


Recall that the cell walls of this bacillus have lots of mycolic (mī-kol’ic) acid, a long lipid chain of 60-90 carbons, giving Mycobacterium these properties:


Mycobacterium tuberculosis

  1. Infection can start anywhere, but most start in the lungs as a respiratory infection.
  2. Mycobacterium attracts macrophages which engulf the bacteria in phagosomes, but the bacteria prevent fusion of the lysosome and phagosome.
  3. When the bacilli grow inside the phagosomes, they eventually kill the macrophage, releasing bacteria and attracting more macrophages to the area.  The cycle repeats as the released bacteria are phagocytized by other macrophages.  
  4. The large numbers of infiltrating macrophages begin to form a tubercle at the site of infection.  
  5. Other cells encase the tubercle in collagen.  After a few weeks many of the macrophages in the tubercle die releasing bacilli and forming a caseous center.  You are looking at a caseous substance here.
  6. The disease may remain dormant at this stage for decades.

Host/Bacterial Stalemate

Diagnosis and Treatment

Incidence and Risk Factors

Why Does Evolution Matter Video

Staphyloccoccal Infections

  1. Staphyloccocus aureus
  2. Staphyloccocus epidermidis

Staphyloccocus aureus

  1. structures to evade phagocytosis
  2. enzymes
  3. toxins

Structures to Evade Phagocytosis

Enzymes that Increase Virulence

Toxins of S. aureus

Staphyloccoccal Enterotoxicosis

Cutaneous Disease

Scalded skin syndrome  

Impetigo (im-pe-tī’-gō) 

Folliculitis, Boils and Carbuncles

Systemic Diseases of S. aureus

Bacteremia (bak-tēr-rēm'-mē-a)

Toxic Shock Syndrome


Gram- Bacteria from ch 20

Enterics (family Enterobacteriaceae en'ter-ō-bak-tēr-ē-ā-sē-ē)

enteric antigens
  1. a core polysaccharide that all have, so its called the common antigen
  2. the "O polysaccharide" that varies by species
  3. lipid A (which can cause serious disease)
  4. some species also have K and H antigens
  1. coliforms
  2. noncoliforms
  3. true pathogens



True Enteric Pathogens

  • Yersinia enterocolitica and pseudotuberculosis follow the fecal to oral route of transmission.
  • Yersinia pestis is transmitted either by flea bites or by respiration of aerosols.
  • Yersinia pestis has two forms of the disease:
    1. bubonic plague
    2. pneumonic plague

  1. bubonic plague
    • when spread by starving fleas (infection blocks their esophagus, so they jump around and bite a lot), the infection causes painful swelling in the lymph nodes called buboes (bū'-bōs), giving it its name.
    • if it gets in the blood, it becomes disseminated and may grow widely.
    • If it grows subcutaneously, it kills tissue inviting secondary infection by Clostridium causing gangrene.  The dark color of the dead skin gives it its second name, the "Black Death."
  2. pneumonic plague
    • When it grows in the lungs, either from dissemination of the blood or by respiratory infection it is called pneumonic plague.
    • This form develops rapidly, it starts with a fever, malaise and pulmonary distress follow w/i a day.  It is fatal if not treated rapidly.
    • Pneumonic plague can spread from person to person, but is unlikely because it grows deep in the lungs.  The most likely culprit is this guy!

Bartonella Family

Pseudomonas Family

Pseudomonas, Cystic Fibrosis and Biofilms

Biofilms have a number of properties that aid bacterial survival.

  • The Center for Disease Control (CDC) estimates that biofilms account for about two-thirds of all bacterial infections in man.

 Other Gram- Bacteria from ch 20

  • Assigned reading, but not covering much of the chapter
  • Know things like the families of bacteria and the diseases they cause as in the chapter summary.
  • Understand the Case Studies done in class (or Homework)  Similar will be on final.

Lesson 15: Other Bacteria from ch 21


Mycoplasma pneumoniae (my-koh-plaz˘-mah  new-moan˘-ee-ee)


Rickettsia (rik-kett˘-see-ah)


Treponema pallidum pallidum (trep-ō-nē'ma  pal'li-dum ...)

Untreated, Syphilis has 4 stages:

Other Treponema pallidums