Microbiology Exam 3. Ch 15 Study Guide

Front 1

What are the principal portals of entry?

Back 1

1) Mucous membranes
2) Skin
3) Direct deposition beneath the skin or membranes (the parenteral route)

Front 2

Portals of Entry: Through the Mucous Membrane

Back 2

1) bacteria and viruses penetrate the mucous membrane of the respiratory tract. The respiratory tract is the easiest and most frequently traveled portal for infectious disease.
2) The gastrointestinal tract is accessed through food and water and contaminated fingers. Most are killed by hydrochloric acid and enzymes in the stomach or bile in the small intestines.
3) Genitourinary Tract is the tract for pathogens contracted sexually. Some STIs may penetrate an unbroken mucous membrane

Front 3

Portals of Entry: Through the skin

Back 3

Unbroken skin is almost impenetrable by most microorganisms. Some microbes gain access through openings such as sweat gland ducts and follicles.
Conjunctiva is a delicate mucous membrane that lines the eyelids and covers the white of the eyeballs.

Front 4

Portals of Entry: The Parenteral Route

Back 4

Microorganisms gain access to the body when they are deposited directly into the tissues beneath the skin or into the mucous membranes when these barriers are penetrated or injured (punctures, bites, cuts, wounds, surgery, swelling, drying)

Front 5

Preferred Portal of Entry

Back 5

Pathogens have a preferred portal of entry that is key to their ability to cause disease. If they enter through a different portal, disease may not occur. (Ex. if swallowed Salmonella makes you ill, but if rubbed on skin there is no reaction)

Front 6

What is ID50?

Back 6

ID50 describes the virulence of a pathogen. Infectious Dose in 50% of the population.

Front 7

What is LD50?

Back 7

LD50 describes the potency of a pathogen. Lethal Dose for 50% of the population

Front 8

What does Adherence mean?

Back 8

The means of a of attachment that pathogens need to attach themselves to host tissues

Front 9

Adhesins

Back 9

Surface molecules on pathogen that allow for adherence

Front 10

Ligands

Back 10

Complementary surface receptors on host cells that Adhesins use to attach

Front 11

What are the principal portals of entry?

Back 11

1) Mucous membranes
2) Skin
3) Direct deposition beneath the skin or membranes (the parenteral route)

Front 12

Portals of Entry: Through the Mucous Membrane

Back 12

1) bacteria and viruses penetrate the mucous membrane of the respiratory tract. The respiratory tract is the easiest and most frequently traveled portal for infectious disease.
2) The gastrointestinal tract is accessed through food and water and contaminated fingers. Most are killed by hydrochloric acid and enzymes in the stomach or bile in the small intestines.
3) Genitourinary Tract is the tract for pathogens contracted sexually. Some STIs may penetrate an unbroken mucous membrane

Front 13

Portals of Entry: Through the skin

Back 13

Unbroken skin is almost impenetrable by most microorganisms. Some microbes gain access through openings such as sweat gland ducts and follicles.
Conjunctiva is a delicate mucous membrane that lines the eyelids and covers the white of the eyeballs.

Front 14

Portals of Entry: The Parenteral Route

Back 14

Microorganisms gain access to the body when they are deposited directly into the tissues beneath the skin or into the mucous membranes when these barriers are penetrated or injured (punctures, bites, cuts, wounds, surgery, swelling, drying)

Front 15

Preferred Portal of Entry

Back 15

Pathogens have a preferred portal of entry that is key to their ability to cause disease. If they enter through a different portal, disease may not occur. (Ex. if swallowed Salmonella makes you ill, but if rubbed on skin there is no reaction)

Front 16

What is ID50?

Back 16

ID50 describes the virulence of a pathogen. Infectious Dose in 50% of the population.

Front 17

What is LD50?

Back 17

LD50 describes the potency of a pathogen. Lethal Dose for 50% of the population

Front 18

What does Adherence mean?

Back 18

The means of a of attachment that pathogens need to attach themselves to host tissues

Front 19

Adhesins

Back 19

Surface molecules on pathogen that allow for adherence

Front 20

Ligands

Back 20

Complementary surface receptors on host cells that Adhesins use to attach

Front 21

Biofilms

Back 21

Masses of bacteria that cling to surfaces, and take in a share nutrients. They multiply and secrete glycocalyx that further attaches the bacteria to each other and the surface (Ex. plaque on teeth, algae)

Front 22

Capsules

Back 22

Glycocalyx material that forms a capsule around bacterial cell walls. This property increases the virulence of the species. The capsule resists the host's body defenses by impairing phagocytosis.

Front 23

Cell wall components

Back 23

Some Cell walls in bacteria contain chemical substances that contribute to virulence. (Ex. M Protein and waxy lipids that help resist phagocytosis) or )

Front 24

Enzymes: Coagulases

Back 24

Bacterial enzymes that coagulate (clot) the fibrinogen in blood. The fibrin clot may protect the bacterium from phagocytosis and isolate it from other host defenses

Front 25

Enzymes

Back 25

The virulence of bacteria is often aided by enzymes. Enzymes are chemicals that can digest materials between cells and form or digest blood clots, among other functions

Front 26

Enzymes: Bacterial Kinases

Back 26

Bacterial enzymes that break down fibrin and thus digest blood clots formed by the body to isolate infection

Front 27

Enzymes: Hyaluronidase

Back 27

A bacterial enzyme that hydrolyzes hyaluronic, a type of polysaccharide that holds together certain cells of the body. Involved in tissue blackening. Also produced by some bacteria that cause gangrene. Can be used therapeutically, by mixing with a drug to spread the drug throughout the whole body tissue

Front 28

Enzymes: Collagenase

Back 28

Facilitates the spread of gangrene by breaking down collagen, which forms the connective tissue of muscles and other organs and tissues

Front 29

Enzymes: IgA Protease

Back 29

As a defense against adherence of pathogens to mucosal surfaces, the body produces a class of antibodies called IgA antibodies. Some pathogens produce IgA Protease which can destroy these antibodies.

Front 30

Antigenic Variation

Back 30

A process by which pathogens alter surface antigens to remain undetected by antibodies

Front 31

Penetration into the host cell Cytoplasm

Back 31

After pathogens attach by adhesins, the host cell activates factors that result in the entrance of bacteria into the cell.
Actin is a major component that is used by microbes to penetrate host cells.
Invasins are surface protiens of some pathogens that rearrange actin filaments. This causes the host cell plasma membrane to resemble a splash of water, Membrane Ruffling

Front 32

Siderophores

Back 32

Proteins secreted by pathogens to obtain free iron. When Iron is needed, siderophores are released into the medium where they take the iron from the iron transporters by binding the iron even more tightly than the transporters

Front 33

4 ways that pathogens damage host cells

Back 33

1) By using the host's nutrients
2) By causing direct damage in the immediate vicinity of the invasion
3) By producing toxins, transported by blood and lymph, that damage sites far removed from the original site of invasion
4) By inducing hypersensitive reactions

Front 34

What is required for the growth of most pathogenic bacteria?

Back 34

Iron

Front 35

How do pathogens cause direct damage?

Back 35

They cause direct damage as they use the host cell for nutrients and produce waste products. Also, rupture cells, phagocytosis-like behavior, enzymes. Most damage, however, is done by toxins

Front 36

Exotoxins

Back 36

Toxins produced inside some bacteria as part of their growth and metabolism and are secreted by the bacterium into the surrounding medium or released following lysis. Exotoxins are proteins and many are enzymes that catalyze only certain biochemical reactions

Front 37

Antitoxins

Back 37

Antibodies produced by the body to provide immunity to exotoxins. Sometimes, Exotoxins no longer produce disease but still cause the body to produce antitoxins, these are called toxoids

Front 38

Exotoxins: A-B Toxins

Back 38

First toxins studied. Have two parts, A and B, which are both polypeptides. The A part is the active (enzyme) component. The B part is the binding component (Pg 435)

Front 39

Process of A-B Toxin

Back 39

1) Bacterium Produces and releases exotoxin
2) B (binding) component of exotoxin attaches to host receptor cell
3) A-B exotoxin enters host cell by endocytosis
4) A-B exotoxin enclosed in pinched-off portion of plasma membrane during pinocytosis
5) A-B components of exotoxin separate. The A component alters cell function by inhibiting protein synthesis. The B component is released from the host cell.

Front 40

Exotoxins: Membrane-disrupting Toxins

Back 40

Cause lysis of host cells by disrupting their plasma membranes. Membranes disrupting toxins increase virulence by killing host cells, especially phagocytes and aiding the escape of bacteria trapped within phagosomes

Front 41

Leukocidins

Back 41

Membrane disrupting toxins that kill phagocytic white blood cells

Front 42

Hemolysins

Back 42

Membrane disrupting cells that destroy erythrocytes, also by forming protein channels.
Hemolysins produced by streptococci are called Streptolysins

Front 43

Exotoxins: Superantigens

Back 43

Antigens (Bacterial proteins) that provoke a strong immune response. Specifically T cells.

Front 44

Cytokines

Back 44

Chemical proteins that regulate immune response and mediate cell to cell communication

Front 45

Representative Exotoxins: Diphtheria Toxin

Back 45

Release Exotoxin only when infected by lysogenic phage. Inhibits protein synthesis in eukaryotic cells using A-B mechanism

Front 46

Representative Exotoxins: Erythrogenic Toxins

Back 46

Streptococcus pyrogenes releases 3 cytotoxins, A, B and C. These are superantigens that damage the plasma membranes of blood capillaries under the skin and produce a red rash

Front 47

Representative Exotoxins: Botulinum Toxin

Back 47

An A-B neurotoxin. Works at the neuromuscular junction and prevents the transmission of nerve impulses from the nerve cell to muscles

Front 48

Representative Exotoxins: Tetnus Toxin

Back 48

An A-B Toxin of the central nervous system. Binds to nerve cells. The result is uncontrollable muscle contractions and convulsive symptoms. (ex. lockjaw)

Front 49

Representative Exotoxins: Vibrio Enterotoxin

Back 49

An A-B Toxin. Causes cells to secrete a large amount of fluid amd electrolytes. Normal muscular contractions are disturbed, leading to severe diarrhea that may be accompanied by vomiting

Front 50

Representative Exotoxins: Staphylococcal Enterotoxin

Back 50

A superantigen that causes toxic shock syndrome

Front 51

Endotoxins

Back 51

Part of the outer portion of the cell wall of gram-negative bacteria. Specifically, the lipid portion of the endotoxin, Lipid A. Endotoxins are released when gram-negative bacteria die and the cell wall is lysed. All endotoxins produce the same signs and symptoms. They cause macrophages to release cytokines in very high concentrations causing a variety of symptoms chills, fever, weakness, aches, shock or death. Can cause miscarriage

Front 52

What is the difference between exotoxins and endotoxins?

Back 52

Endotoxins are lipopolysaccharides
Exotoxins are proteins

Front 53

What is the pyrogenic response? (4 steps)

Back 53

The fever (pyrogenic) response occurs in 4 stages.
1) A macrophage ingests a gram-negative bacterium
2) The bacterium is degraded in a vacuole, releasing endotoxins that induce the macrophage to produce cytokines Interleukin-1 (IL1) and tumor necrosis factor alpha (TNF@)
3) The cytokines are carried via blood to the hypothalamus a temperature control center of the brain.
4) The cytokines induce the hypothalamus to release lipids called prostaglandins, which reset the thermostat in the hypothalamus at a higher temperature. The result is fever.

Front 54

Shock

Back 54

Any life threatening decrease in blood pressure

Front 55

Septic shock

Back 55

Shock caused by bacteria

Front 56

What are common viral mechanisms for invading host cells?

Back 56

1) Viruses can penetrate and grow inside host cells where immune system components can't reach them. They gain access through attachment sites
2) Mimic substances useful to cells to gain access.
3) Hide attachments from immunity cells and attack immunity cells (HIV)

Front 57

Cytopathic Effects (CPE)

Back 57

The visual effects of viral infection

Front 58

Cytocidal effects

Back 58

The cytopathic effects that result in cell death

Front 59

Noncytocidal effects

Back 59

The cytopathic effects that result in damage to cells but NOT death

Front 60

What are the 9 Cytopathic effects of viral infections?

Back 60

1) Cytocidal viruses cause the macromolecular synthesis (mitosis) within a host cell to stop. (ex herpes)
2) Cause the cells lysosomes to release their enzymes, resulting in destruction of the intracellular contents and host death
3) Inclusion bodies are found in infected cells (sometimes viral parts). They are used to help identify the virus causing infection.
4) Several adjacent cells merge to form a very large multinucleated cell called a Syncytium
5) Some result in changes to host cell's function, w/ no visible changes to infected cells
6) Some virus infected cells produce interferons. These protect neighboring cells from infection by sending a warning
7) Many viral infections induce antigenic changes on the surface of infected cells. These changes illicit a host response against the cell
8) Some induce chromosomal changes in the host cell
9) Many infected cells lose contact inhibition

Front 61

Examples of viral Cytopathic Effects

Back 61

Poliovirus - Cytocidal
Papovavirus - Acidophilic inclusion bodies in nucleus
Adenovirus - Basophilic inclusion bodies in nucleus
Rhabdovirus - Acidophilic inclusion bodies in nucleus
Measles - Cell fusion
Polymavirus - transformation
HIV - Destruction of T cells

Front 62

Pathogenic Properties: Fungi

Back 62

Fungi do not have a well defined set of virulence factors. Some have metabolic processes that are toxic. Chronic fungal infections.
Some cause skin infection
Some inhibit protein synthesis

Front 63

Fungal Toxins: Ergot

Back 63

The hallucinogenic toxin. Natural LSD

Front 64

Fungal Toxins: Aflatoxin

Back 64

Carcinogenic toxin

Front 65

Fungal Toxins: Mycotoxin

Back 65

Mushroom toxin Ex. phalloidin and amanitin, known as deathcap. Potent toxins that result in death

Front 66

Pathogenic Properties: Protozoa

Back 66

The presence of Protozoa and their waste products often produces disease symptoms

Front 67

Protozoa toxins: Giardia

Back 67

Attaches to host cell by a sucking disc and digests the host cells and fluids. Causes diarrhea.

Front 68

Protozoa Toxins: Trypanosoma

Back 68

Causes african sleeping sickness. Changes it's antigen to fool body defenses

Front 69

Pathogenic Properties: Helminths

Back 69

Use host tissue for their own parasitic growth and produce large parasitic masses

Front 70

Helminth Toxins: Wuchereria bancrofti

Back 70

Causative agent of elephantiasis. The parasite blocks lymphatic circulation and causes accumulation and massive swelling in legs.

Front 71

Algae Toxins: Alexandrium

Back 71

Important because they produce Saxitoxin. In shellfish/mollusks. Shell fish poisoning similar to Butulism

Front 72

Portal of Entry

Back 72

Microbes enter the body through a preferred portal of entry to cause ideal pathogenicity

Front 73

Portals of Exit

Back 73

Pathogens leave the body through secretions, excretions, discharges, or shed tissues. Most common are the respiratory and gastrointestinal tracts.

Front 74

Portals of Exit: Respiratory Tract

Back 74

One of the most common portals of exit. Pathogens are often dislodged through coughing or sneezing

Front 75

Portals of Exit: Gastrointestinal Tract

Back 75

Urine and feces

Front 76

Portals of Exit Chart 15.9 pg. 445

Back 76

Portals of Exit chart 15.9 pg. 445