Microbiology Unit 3 Test Revised

Infection and Disease:

1. Colonization vs. Infection

2. Pathogenicity vs. Virulence

3. Virulence Factors

Pathogens and Disease:

4. True pathogens

5. Opportunistic pathogens

6. Normal biota (flora)

7. Endogenous infections

Infectious Dose (ID):

8. What question does it answer?

1. Colonization means that microbes are present; there is no disease. Normal microbiota is beneficial; they compete with pathogens, help digestion, and produce vitamins. Infections are not the same! In an infection, microbes invade and cause damage. Antibiotics can disrupt normal flora.

2. Pathogenicity is the ability to cause disease, while virulence is the degree of pathogenicity (how severe). A common cold is pathogenic but low virulence, and the rabies virus is highly virulent.

3. Help microbes cause disease (capsules, toxins, enzymes).

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4. True pathogens- An agent that consistently causes disease in a healthy host with a normal, intact immune system

5. Opportunistic pathogens- A microbe that is normally harmless or beneficial but is capable of causing disease when the host’s immune system is weakened, the natural microbiome is disrupted, or the microbe enters a sterile site of the body

6. Normal biota (flora)- Describes the diverse group of organisms, including bacteria, fungi, viruses, and archaea that harmlessly inhabit various surfaces and internal tracts of the healthy human body.

7. Endogenous infections- A disease or illness caused by the body’s own naturally occurring microorganisms rather than from an external source

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8. Answers the question- how many organisms are needed before diseases occurs?

• The number of organisms required to establish an infection (organisms with smaller IDs, requiring few cells, have greater virulence)

Communicability:

1. Communicable

2. Contagious

3. Non-communicable

Virulence Factors:

4. Virulence factor forms

5. Fimbriae

6. Capsules

7. Coagulase

8. Leukocidins

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Endotoxins vs. Exotoxins

9. What are toxins?

10. Exotoxins

11. Endotoxins

1. Communicable- Capable of being transmitted from one individual to another

2. Contagious- Communicable; transmissible by direct contact with infected individuals and their fresh secretions or excretions

3. Non-communicable- An infectious disease that does not arrive through transmission of an infectious agent from host to host (non-living reservoir, own microbiota)

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4. Virulence factors come in many forms- some help bacteria hide from the immune system, while others help them directly attack our defenses.

5. Fimbriae- Numerous, short, hair-like surface appendages found mainly on bacterial cells that facilitate mechanical attachment and adherence to specific target host cell surface receptors

6. Capsules- An organized polysaccharide layer that masks immunogenic surface structures and physically interferes with phagocytic recognition and engulfment

7. Coagulase- An enzyme that causes plasma to clot. This is produced by Staphylococcus aureus to help evade the immune system

8. Leukocidins- Toxins that kill white blood cells, destroying neutrophils and other immune cells.

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9. Toxins are virulence factors and refer to how microbes cause damage. Bacteria can make us sick in 2 major ways: bacteria can invade and damage tissue themselves OR they can release chemicals (toxins) that do the damage.

10. Gram (+)→ exotoxins

• An exotoxin is a protein toxin that is actively produced and released by living bacteria. An example is Tetanus, Botulinum toxin, Cholera toxin, and diphtheria toxin. Think of this as a criminal throwing grenade. The bacteria are alive and intentionally releasing harmful molecules.

11. Gram (-)→ exotoxins+endotoxins

• Endotoxins are produced by Gram-negative bacteria.

• Endotoxins, are not secreted (not made and released), they are part of the bacterial body (gram-negative outer membrane- built into cell wall). Specifically, LPS, which contains Lipid A as the toxic portion.

• Endotoxin causes issues when the bacteria break apart. When bacteria die, lyse or are destroyed by immune cells, LPS is released and stimulates inflammation.

• We care about endotoxins cause they can cause fever, inflammation, hypotension, and septic shock.

Symptoms vs. Signs

1. What are they?

2. Symptoms

3. Signs

Mutualism, Commensalism, Parasitism:

4. Mutualism

5. Commensalism

6. Parasitism

Normal Microbiota:

7. What is it^?

8. Microbial antagonism

1. Evidence that a pathogen established an infection.

2. Subjective experiences; experiences that the patient can describe (pain, nausea, fatigue)

3. Objective findings; can be measured or observed (usually by healthcare providers) (fever, rash, elevated WBC count, positive culture)

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4. Mutualism- Describes a relationship where organisms live in an obligatory but mutually beneficial relationship

5. Commensalism- An unequal relationship where one species derives benefit without harming the other

6. Parasitism- A relationship between two organisms where the host is harmed in some way, and the colonizer benefits

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7. As humans we are not sterile: colonization starts during and right after birth as we encounter microbes from our mother and environment.

• Occupy skin, GI tract, res. tract, and genitourinary tract

• Often protect us from pathogens

8. The normal flora that is present in/on the body that prevents pathogens from becoming established in the body. ← normal biota is beneficial or at worst commensal to host in good health

• Normal flora occupies the limited number of attachment sites in the host, so they are unlikely to be displaced

• The normal flora competes for available nutrients, competes for available attachment sites, and some species produce inhibitory substances with antimicrobial properties

Sequelae:

1. What is it?

Disease Frequency Terms:

2. Endemic

3. Epidemic

4. Pandemic

5. Sporadic

Nosocomial (Hospital-Acquired) Infections:

6. What are they? Give examples

7. Where are they common?

8. Cause and Prevention

Reservoirs and Transmission:

9. Reservoir

10. Direct transmission

11. Indirect transmission

12. Vertical transmission

13. Vector

14. Endogenous transfer

1. Long-term effects that remain after the original infection has been resolved (pathogen has been eliminated) ← Rheumatic fever after Strep throat

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2. Endemic- Disease that is consistently present in a population like the common cold or in some regions, malaria. Endemic = expected.

3. Epidemic- More cases than expected in a specific area. Example= measles outbreak.

4. Pandemic- An epidemic that spreads across countries or continents. Example-SARS-CoV-2.

5. Sporadic- Cases occur occasionally and irregularly (randomly). Example: Tetanus.

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6. Healthcare-associated infections; CAUTI (catheter associated UTI), CLABSI (central line associated blood stream infections, and SSI (surgical site infections)

7. Common in urinary tracts, wounds, or surgical sites

8. Caused by weakened immunity or exposure in healthcare setting; prevention by infection control officer (implements proper practices and procedures, tracks potential outbreaks, and trains workers in aseptic techniques) and universal precautions

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9. Reservoir- The natural host or habitat of a pathogen (human, animal, soil, water, plants)

10. Direct transmission- Involves very close proximity or physical contact between 2 hosts. Touching, kissing, droplet contact

11. Indirect transmission- Infectious agent must pass from an infected host to an intermediate vehicle to another host. Fomite (inanimate object harboring pathogen)

12. Vertical transmission- Transmission from parent to offspring via the ovum, sperm, placenta, or milk

13. Vector- arthropods that harbor infectious agent and transfer it to humans (2 types: mechanical- insect carries microbes to host on its body parts and biological- insect injects microbes into host)

14. Endogenous transfer- An infection caused by microbes that already exist naturally in the body, rather than being acquired from an outside source (when native microbes spread to previously sterile tissue)

Innate (Non-Specific) Immunity

First Line of Defense (Always Active):

1. First Line of Defense

2. Physical Barriers

3. Chemical Barriers

Inflammation

4. What is it?

5. 4 classical signs

Inflammation Process (order):

1. Initial reaction/changes

2. Vascular changes

3. Edema/pus formation

4. Resolution/healing

1. Consists of barriers that prevent microorganisms from entering the body in the 1st place. These defenses are always active and do not wait until you are infected.

2. Physically block microorganisms from entering tissues.

• Skin, mucous membranes, cilia, tears washing the eyes, urine flushing the urinary tract

• When a patient has suffered from a burn, they are at increased risk of infection because the skin barrier has been damaged.

3. Substances that inhibit or destroy microorganisms

• Stomach acid, lysozymes in tears, sebum, vaginal acidity, and antimicrobial substances in saliva

^ The 2nd line of defense responds after a microbe has entered the body and made it past the barriers. ← 1 of the earliest responses is inflammation

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4. Natural nonspecific response to tissue injury that protects the host from further damage- stimulates immune reactivity and blocks the spread of pathogen.

5. Rubor (redness- increased circulation and vasodilation in the injured tissue), calor (heat given off by increased blood flow), tumor (swelling caused by increased fluid escaping into the tissues), and dolor (pain caused by stimulation of nerve endings).

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1. Initial reaction/changes- this is where tissue damage occurs, and tissues are damaged or invaded by microorganisms. Damaged cells release chemical signals that alert the immune system.

2. Vascular changes- In response to these signals, the nearby blood vessels dilate, increasing blood flow. This causes rubor (redness) and calor (heat). The increased permeability allows the immune cells and proteins to leave the bloodstream

3. Edema/pus formation- As the blood vessels become more permeable, fluid leaks out into the surrounding tissues, causing edema. Chemical signals released at the site of infection attract WBC through chemotaxis (movement of immune cells toward an area of infection). To reach tissues, the cells use diapedesis (squeeze between the walls of blood vessels). As neutrophils accumulate and die fighting the infection, along with dead microbes and tissue debris, pus may form.

4. Resolution/healing- In this stage, the pathogen is removed, and the tissue is gradually repaired (to healthy tissue or scar tissue). Inflammation stops.

Key Terms:

1. Edema

2. Chemotaxis

3. Diapedesis

Fever:

4. What is it?^

5. Caused by…

Phagocytosis Steps

What is it?^

1. Chemotaxis

2. Engulfment

3. Phagolysosome formation

4. Destruction

1. Edema- swelling; accumulation of excess fluids in cells, tissues, or cavities

2. Chemotaxis- movement of immune cells toward chemical signals

3. Diapedesis- the migration of intact blood cells between endothelial cells of a blood vessel

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4. 1 of the most common systemic responses (inflammation occurs locally, and fever is a systemic component of inflammation). The goal is to create an environment that is less favorable for microbial growth (elevated body temp. controlled by the hypothalamus).

5. Pyrogens, which come from bacteria, viruses, and cytokines released by our immune cells. They reset the hypothalamic thermostat to a higher setting (and decrease heat loss through vasoconstriction).

• Fever helps slow microbial growth and enhances the immune system function. It is part of the body’s defense strategy.

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Phagocytosis is a specialized process by which immune cells engulf and destroy microorganisms or foreign material.

• 1 of the major goals of inflammation is to bring phagocytic cells to the site of infection. This occurs in the following steps. The cell 1st moves towards the microbe using chemotaxis→ surrounds and engulfs it into a vesicle (phagosome)→ fuses the phagosome with a lysosome (phagolysosome)→ destroys the microbe using digestive enzymes (myeloperoxidase) and toxic chemicals

• 3 main cells: neutrophils, macrophages, dendritic cells

1. Chemotaxis- The tendency of organisms to move in response to a chemical gradient (toward an attractant)

2. Engulfment- microbe enclosed in phagosome

3. Phagolysosome formation- lysosome fuses with phagosome (granules with antimicrobial chemicals released here to dismantle ingested material)

4. Destruction- microbe killed and digested

Key Cells:

1. Neutrophils

2. Macrophages

3. Leukocytes

Proteins and Molecules:

4. What do they do?^

5. Interferons

6. Complement System

7. Antimicrobial peptides

8. Cytokines

9. PAMPs

Induced vs. Non-Specific:

10. Non-specific

11. Induced

1. Neutrophils- First responders, most abundant WBC. Highly effective but have a short lifespan (component of pus). Macrophages arrive later and survive longer to continue both defense and “clean up” activities.

2. Macrophages- Derived from monocytes; Long-lived tissue phagocytes. Part of the clean-up after an immune response, and important in nonspecific phagocytosis. Histocytes are tissue-resident macrophages.

3. Leukocytes- General term for WBC

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4. The body relies on a variety of proteins and chemical messengers/signaling molecules to help coordinate defenses and directly combat pathogens.

5. Interferons- Proteins produced by virus-infected cells that warn neighboring cells of the infection (inhibit viral replication and used against viral infections+cancer)

6. Complement System- A group of plasma proteins that circulate in an inactive state and become activated during infection (antigen-antibody complex). These proteins help attract immune cells, enhance phagocytosis, and can directly lyse microorganisms.

7. Antimicrobial peptides- Natural antibiotics produced by the body that can disrupt the cell membranes and inhibit microbial growth (can form pores-defensins)

8. Cytokines- chemical messengers; allows communication between immune cells

9. PAMPs- Pathogen-associated molecular patterns; unique microbial structures recognized by the immune system. They are present on microbes and allow the immune system to recognize that something foreign has entered the body.

• Recognition of PAMPs by host PRR (pattern recognition receptors) is the first step for immune response (innate)

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10. Non-specific- Innate. Respond the same way every time, regardless of the pathogen. Responds quick but lacks memory. Include skin, fever, inflammation, and phagocytosis

11. Induced- activated after exposure and triggered when needed. Includes inflammation, fever, complement activation

Adaptive (Specific) Immunity:

Adaptive Immunity

B cells vs. T cells:

1. B cells (Humoral Immunity)

2. T cells (Cell-Mediated Immunity)

MHC Markers

3. Importance to T cells

4. MHC I

5. MHC II

Antigen-Presenting Cells (APCs):

6. Used by…

7. Include…

8. Display…

Slower to develop but highly specific and capable of remembering previous infections.

1. B cells (Humoral Immunity)- Fight extracellular threats and produce antibodies (attach to antigens-inactivate, neutralize, mark for destruction). They differentiate into plasma cells and memory B cells.

• Require helper T cells to fully activate

2. T cells (Cell-Mediated Immunity)- Attack infected or abnormal cells and coordinate immune responses. Do not produce antibodies, they attack.

• Require antigen/MHC complex on APC to activate

^ Both are types of lymphocytes and recognize specific antigens, BUT defend the body in different ways.

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3. For T cells to respond, they need a way to identify what is foreign and what is not.

• Found on all cells except RBC

3. MHC I- Is found on almost all nucleated cells (marks them as self-molecules). It displays internal antigens and is recognized by cytotoxic T cells (CD8)

4. MHC II- Found on APCs only. Displays foreign antigens and is recognized by Helper T cells (CD4)

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5. Used by… T cells must be shown antigens by APCs

6. Include… macrophages, dendritic (most potent), and B cells

7. Display engulfed microbes, which they degrade to smaller peptides/pieces.

• APCs process the antigen→ move it to APC membrane→display antigen on MHC II→activate Helper T cells

Cells and Functions:

1. Helper T cells

2. Cytotoxic T cells

3. Memory T cells

4. Plasma cells

5. Natural Killer cells

Antibodies (Immunoglobulins):

1. IgM

2. IgG

3. IgA

4. IgE

5. IgD

1. Helper T cells- CD4; coordinate immune response, activate macrophages, activate B cells, activate cytotoxic T cells, and release cytokines. Most important cell in adaptive immunity.

• Responsible for delayed hypersensitivity

2. Cytotoxic T cells- CD8; kill infected cells and recognize MHC I

3. Memory T cells- Provide faster future response and long-term immunity

4. Plasma cells- Activated B cells that secrete antibodies

5. Natural Killer cells- Technically part of innate immunity (respond quickly and act less specifically); they kill abnormal cells (virus-infected cells and cancer cells) but do not require antigen presentation.

• Release large quantities of cytokines, causing cell death

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1. IgM- 1st antibody produced in response to an antigen. Fixes complement and can serve as B cell receptor.

2. IgG- Provides long-term immunity (binds to phagocytes), crosses the placenta to provide passive immunity to the fetus. Neutralizes toxins, opsonizes, and fixes complement. Most abundant.

3. IgA- Found in secretions like tears, breastmilk, and saliva (dimer). Small quantities in the blood (monomer).

4. IgE- Produced in response to allergies, parasites (binds to basophils and mast cells).

5. IgD- Receptor on B cells and a triggering molecule for B cell activation

Key Reactions:

1. Neutralization

2. Opsonization

3. Agglutination

4. Complement Fixation

Primary vs. Secondary Response:

5. Primary

6. Secondary

7. Titer

1. Neutralization- Blocks attachment; antibodies fill surface receptors (virus) or active site (microbial enzyme)

2. Opsonization- Enhances phagocytosis; opsonins make microbes more readily recognized by phagocytes

3. Agglutination- Clumps pathogens together; renders microbes immobile and enhances phagocytosis

4. Complement Fixation- Activates complement (IgG, IgM)

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5. Primary- The first exposure to an antigen, producing a slow response. IgM predominates initially, but memory cells are formed.

6. Secondary- Occurs at second and subsequent exposures (memory cells). It is faster, stronger, and mostly IgG antibody. Peak titer is increased over primary response.

7. Concentration of antibodies

Immunity and Vaccines

Types of Immunity:

1. Active Natural

2. Active Artificial

3. Passive Natural

4. Passive Artificial

Vaccines:

5. Attenuated

6. Inactivated

Therapeutic Concepts:

7. Selective toxicity

8. Prophylaxis

9. Clonal deletion

1. Active Natural- Body makes its own antibodies; recovering from chickenpox (Varicella) ←exposed to pathogen through infection with disease

2. Active Artificial- Body makes its own antibodies; vaccination

3. Passive Natural- Receiving antibodies from another source; maternal IgG crossing placenta, IgA in breastmilk ← prenatal and postnatal mother-child relationships

4. Passive Artificial- Receiving antibodies from another source; Rabies immune globulin, antivenom ← passive immunotherapy = pre-made antibodies from another person, animal, or lab source (injection, transfusion)

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5. Attenuated- Live but weakened organism (virulence is eliminated or reduced). Ex- MMR, Varicella ← microbes can multiply

6. Inactivated- Killed organism (can be by heat/chemicals). Ex- injectable flu vaccine, Hepatitis A ←microbes cannot multiply

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7. Selective toxicity- the ability of treatment to harm a pathogen without harming the host. Ex- antibiotics targeting bacterial cell walls.

8. Prophylaxis- treatment given to prevent disease like vaccines, malaria prophylaxis, and preoperative antibiotics

9. Clonal deletion- removal of self-reactive lymphocytes during development to help prevent autoimmunity- leads to tolerance of self (immune tolerance)

• These lymphocytes may arise b/c they form specificity before antigens are present (random recombination of gene segments)

Written Response:

1. Explain why self-reactive lymphocytes must be removed.

2. Identify the safest vaccine type for immunocompromised people and why.

1. They can lead to severe damage if the immune system actually perceives self-molecules as foreign and mounts a harmful response against the host tissues. This can cause autoimmune diseases such as lupus.

2. Killed cell or inactivated virus vaccines. These vaccines have non-living microbes, which are unable to multiply and are incapable of causing the disease they are meant to prevent.

• These vaccines teach their immune system to recognize and respond to a specific pathogen to act as a shield against secondary infections. CRUCIAL because they have weakened immune system.

• Vaccines that deliver antigenic component of the microbe are also an option (vaccines with DNA/mRNA that code for microbial surface components, isolated surface structures, etc)

Written Responses continued…

3. Describe the difference between attenuated and inactivated vaccines.

4. Know which antibody appears first and which appears later in an infection.

3. Attenuated vaccines use live microbial cells or viruses (often weakened versions of a living pathogen where virulence is eliminated or reduced) that can multiply, but generally don’t cause illness. Inactivated vaccines use killed cells or inactivated/destroyed viruses (heat or chemicals may be used) that can’t multiply.

4. IgM is the first antibody the body produces when fighting a new infection. Later the class of antibodies (but not their specificity) is switched to IgG or some other class (IgA, IgE). IgG appears later but remains for long-term protection (long-term memory- levels stay elevated for a long time).