chapter 48: infectious diseases & immune system 48-1 nonspecific defenses 48-2 specific...

Chapter 48: Infectious Diseases & Immune System

48-1 Nonspecific Defenses

48-2 Specific Defenses: The Immune System48-3 AIDS

I. Disease Transmission (Genetic, Environmental, Infectious)• INFECTIOUS disease RESULTS from pathogenic INVASION of body.

48-1 Nonspecific Defenses

(1) Robert Koch (Nobel Prize Recipient, 1905 for “Koch’s Postulates”)• German physicist REVEALED process for DETERMINING the CAUSE (etiology) of a disease.

• Postulate ONE

Suspected pathogen MUST be present in DISEASED animal’s tissues and NOT in a healthy animal.

• Postulate TWO

Suspected pathogen should be ISOLATED and CULTURED in a laboratory.• Postulate THREE

A HEALTHY animal inoculated with THIS culture should develop the SAME disease.

• Postulate FOUR

Pathogen from NEWLY infected animal should be IDENTICAL to ORIGINAL infected animal when examined.

(1) In many cases, NOT all of Koch’s postulates can be applied to determine the cause of a HUMAN disease. Why might this be?

Critical Thinking

II. Skin and Mucous Membranes• FIRST lines of MECHNICAL defense (a tough keratinized shield).

(1)Mucous Membranes (cell linings SECRETE mucus)• Epithelial tissues PROTECT interiors of body (e.g., LININGS of digestive, respiratory, and excretory tracts).

(2) Mucus• Thick, STICKY secretion TRAPS and DISSOLVES pathogens.

III. The Inflammatory Response• Initiated when DAMAGED cells release CHEMICAL messengers, including HISTAMINE. (e.g., Results in Swelling, Redness, Warmth, and Pain)

(1) Histamine (released by DAMAGED cells)• Increase BLOOD FLOW to injury and PERMEABILITY of nearby capillaries.

(2) Neutrophils (MOST common phagocytes DRAWN close by histamines)• Circulate through BLOOD and SQUEEZE through a capillary to reach a marked INFECTION site.

(3) Macrophage (class of phagocytes)• Consume pathogens, worn out cells, and cellular debris.

(4) Natural Killer Cell (NON-specific leukocyte)• Patrol body looking for any “foreign” cells AND will puncture membrane, causing LYSIS (e.g., viral-infected cells, cancer cells).

IV. Other Nonspecific Defenses• INTERFERON and FEVER; work with skin, mucous membranes, and inflammatory response to rid NON-SPECIFIC pathogens.

(2) Many people take FEVER-REDUCING drugs as soon as their temperature exceeds 99 degrees F. Why might it NOT be a good idea to immediately reduce a fever with drugs? On the other hand, what may be the BENEFITS of taking fever-reducing drugs?

Critical Thinking

(1) Interferon (protein/CYTOKINE produced by INFECTED body cells)• WARNING SIGNAL that alerts nearby cells to make and release ENZYMES to INHIBIT viral production.

(2) Fever (chemically-induced by macrophage “smoke signals”)• Brain told to ELEVATE metabolism results in HIGH body temperature.

GOAL: To stimulate the immunoresponse (WBC activity) and/or SUPPRESS the growth of some BACTERIAL/VIRAL infections.

I. The Immune System (leukocytes, lymphocytes, and antibodies)• Includes bone marrow, THYMUS gland, lymphatic system, and SPLEEN.

48-2 Specific Defenses: The Immune System

(1) Thymus (GLAND located above heart)• T cells made in bone marrow BUT develop and mature in thymus gland.

(2) Spleen• Stocked with LEUKOCYTES to FILTER pathogens in bloodstream.

(3) B cells (lymphocyte; produced AND mature in bone marrow)• Can be activated by ANTIGENS to make and release ANTIBODIES.

(4) T cells (lymphocyte; MADE in bone marrow BUT matures in THYMUS) 3 types

(1) Helper T Cell (2) Cytotoxic T Cell (3) Suppressor T cells

II. Recognizing Pathogens (SPECIFIC DEFENSE)• Lymphocytes respond WHEN antigen is recognized as FOREIGN (non-self).

(4) Virologists have created an effective vaccine for smallpox, BUT have not been able to do so for HIV. What does this suggest about the rate of evolution of the smallpox virus?

Critical Thinking

(1) Immune Response (TWO methods of DEFENSE)• A 2-way assault on a PATHOGEN:

(1) Cell-mediated

(2) Humoral

(2) Antigen (a protein OR glycoprotein, often on CELL SURFACE)• Includes pathogen, PARTS of pathogen, toxins, insect venom, & POLLEN.

III. Immune Response (HOW one is ELICITED)• Pathogen Macrophage APC—Interleukin-1 Helper T Cell —IL-2 Cytotoxic & Suppressor T Cells [interleukins = cytokines]

(1) Cell-Mediated Immunoresponse (CMI, NO antibodies YET)• 1st arm of DEFENSE Cytotoxic T-cell attack on a PATHOGEN.

(5) Cytotoxic T cells attack and destroy some kinds of CANCER cells. What can you conclude about the surface proteins of these cancer cells?

Critical Thinking

(2) Humoral Immunoresponse (HMI)• 2nd arm of DEFENSE B cells and ANTIBODIES.

(3) Helper T Cell (activates BOTH cytotoxic T cells AND B cells)• Coordinates BOTH methods of immunoresponse against an antigen.

(A) Cell-Mediated Immunoresponse (1st Arm)• IL-2 (Helper T Cell) stimulates Cytotoxic T cells and Suppressor T cells to rapidly divide.

(1) Cytotoxic T Cell (antigen-SPECIFIC lymphocyte)• Programmed to destroy ONLY cells with antigens that MATCH its receptors (i.e., only specifically INFECTED cells)

(2) Suppressor T Cell (signals to B cells to STOP making antibodies)•SHUTS DOWN immunoresponse ONCE pathogen is CLEARED from body.

(B) Humoral Immunoresponse (2nd Arm)• IL-2 and APC stimulates B cell to DIVIDE into ANTIBODY-making “PLASMA CELLS.”

(1) Plasma Cells• Activated B cells release ANTIGEN-SPECIFIC antibodies into blood.

(2) Antibodies (30,000 released per SECOND, immobilizers)• Tiny, Y-shaped sticky PROTEINS attach to antigens ~ immobilization.

(C) Primary and Secondary Immune Response• AFTER infection, immuneresponse is SHUT DOWN and MOST cells die.

(6) A friend tells you that because he has JUST recovered from a cold, he now cannot get the flu. Is your friend right? Explain.

Critical Thinking

(1) Memory Cells (how you ACQUIRE immunity)• Long-term B and T cells patrol body for YEARS; if pathogen ENTERS, they quickly divide and wipe it out BEFORE symptoms appear.

(2) Primary Immune Response• 1st time body encounters an antigen (SLOWER than a secondary response, antigen is NEW).

(3) Secondary Immune Response• A 2nd infection caused by SAME pathogen, MUCH FASTER and MORE POWERFUL immunoresponse. (LOTS of antibodies made quickly)

IV. Immunity (passive & active) and Vaccination• A VACCINE prepares immune system to RECOGNIZE a pathogen should it REAPPEAR in its disease-causing (virulent) form.

(1) Immunity (i.e., resistance to pathogens)• Immunity is ACQUIRED through exposure (to a pathogen) through sickness OR vaccination. (GOAL: To produce those Memory B and T cells)

V. Allergies (e.g., ALLERGENS can be pollen, food, mold spores, venom)• WBCs attack a HARMLESS antigen, symptoms associated with release of HISTAMINE (i.e., watery eyes, sneezing, wheezing))

VI. Autoimmune Disease (e.g., MS, Lupus, Type 1 diabetes, Arthritis)• WBCs mistakenly recognize SELF tissue as FOREIGN, and attack healthy body tissues AS IF they WERE pathogenic.

I. HIV and AIDS

• HIV (a retrovirus) may invade several types of WBCs, BUT targets Helper T Cells via a CD-4 receptor.

48-3 AIDS

(6) The Center for Disease Control (CDC) is reviewing TWO proposals for HIV research, BUT it can fund only ONE. Suppose you are asked to provide input. Which proposal would you recommend the CDC fund? (NOTE: considering effectiveness and potential adverse side effects)

Proposal One: Develop a drug that interferes with protein synthesis.

Proposal Two: Develop a drug that binds to CD4 receptors on helper T cells.

Critical Thinking

(A) Course of the Disease• As helper T cells falls, immunity weakens, opening up for opportunistic infections.

(1)Opportunistic Infections (when T cell count drops below 200/mL)• Include cancers, pneumonia, influenza, and usually strike people

with a compromised immune system (normal T cell count ~ 600-700/mL blood)

(B) Transmission (intercourse, non-sterilized syringes)• Body fluids containing HIV or HIV-infected cells.

(C) Treatment and Vaccines• HIV genes mutate frequently; NO current cure for HIV although experimental vaccines AND antiviral drugs are being explored.