Micro 22 Unit 4 Chapter 15

Front 1

parenteral route

Back 1

microorganisms gain access to the body when they are deposited directly into the tissues beneath the skin or onto mucuous membranes when these barriers are pentrated or injured

ie. injections, bites, cuts, wounds, surgery

Front 2

adherence

Back 2

- adhesion

- attachment of a microbe to another's plasma membrane or other surface

Front 3

adhesins (or ligans)

Back 3

- surface molecules on pathogens that bind specifically to complementary surface receptors on the cells of certain host tissues (for adherence)

Front 4

biofilms

Back 4

a microbial community that usually forms a slimy layer on a surface

- represents another method of adherence and are important because they resist disinfectants and antibiotics

- ie. dental plaque on teeth, algae in pools, shower scum

Front 5

phagocytosis

Back 5

- the ingestion of particles by eukaryotic cells

Front 6

collagenase

Back 6

an enzyme that breaks down collagen (connective tissue of muscles and organs)

- facilitates spread of gas gangrene

Front 7

hyaluronidase

Back 7

- an enzyme secreted by certain bacteria that hydrolyzes hyalyronic acid (type of polysaccharide that holds together certain cells in the body) and helps spread microorganisms from their initial site of infection

- causes blackening of infected wounds

- may be mixed with a drug to promote the spread of a drug through body tissue

Front 8

IgA proteases

Back 8

enzymes that can destroy IgA antibodies, the body's defense against adherence of pathogens

Front 9

Coagulase

Back 9

- bacterial enzyme that coagulate the fibrinogen in blood

- fibrin clot may protect bacterium from phagocytosis and isolate it from other defenses of the host

Front 10

Antigenic variation

Back 10

- pathogens altering their surface antigens to avoid destruction from antibodies

Front 11

Invasins

Back 11

surface protein produced by Salmonella typhimurtum and E. coli that rearranges nerby actin filaments in the cytoskeleton of a host cell

Front 12

siderophores

Back 12

- protein secreted by pathogens to obtain iron

- takes iron away from iron-transport proteins by binding the iron even more tightly

- one iron siderophore is formed then it is brought into the bacterium

Front 13

leukocidin

Back 13

- membrane-disrupting toxins that kill phagocytic leukocytes (white blood cells) and macrophages

-decreases host resistance

Front 14

lecithinase

Back 14

dissolves cell membranes; pathogen can digest cell contents

Front 15

hemolysin

Back 15

an enzyme that destroy red blood cells

Front 16

hemolysis (alpha vs. beta vs. gamma)

Back 16

Alpha Hemolysis: greenish zone around coloy on blood agar

Beta Hemolysis: complete hemolysis, causes clear colorless zone around colony

Gamma Hemolysis: NO hemolysis

Front 17

superantigens

Back 17

an antigen that activates many different T cells, thereby eliciting a large immune response

- stimulate T cells to release large amounts of cytokines

Front 18

genotoxins

Back 18

- toxins that damage DNA

- causes mutations, disrupts cell division, and may lead to cancer

Front 19

septic shock (vs. sepsis referring to pages 639-641 in the 12th edition too!)

Back 19

- a sudden drop in blood pressure induced by bacerial toxins

Sepsis - presence of a toxin or pathogenic organism in blood and tissue

Front 20

lysogenic conversion

Back 20

acquisition of new properties by a host cell infected by a lysogenic phage

- bacterial cell is immune to infection by the same type of phage

- some bacterial pathogensis is caused by the prophages they contain

Front 21

Identify the principal portals of entry

Back 21

1. Mucuous Membranes

a. Respiratory Tract

b. Gastrointestinal Tract

c. Genitourinary Tract

2. Skin

3. The Parenteral Route

Front 22

LD50 and ID50

Back 22

LD50 - Lethal Dose of a toxin for 50% of a sample population

ID50 - Infectious Dose for 50% of a sample population

Front 23

What is meant by infective dosage of pathogens?

Back 23

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Front 24

Using examples, explain how microbes adhere to host cells

Back 24

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Front 25

Explain how biofilms, capsules and cell wall components contribute to pathogenicity

Back 25

Biofilms: another way of adherence, usually resistant to disinfectant and antibiotics

Capsules: increases virulence by resisting phagocytosis, but vulnerable to antibodies

Cell Wall Components: contain chemical substances that contribute to virulence

1. Fimbriae: used to attach to host cells

2. Opa: outer membrane protein

3. Waxy Lipid (Mycolic Acid): resists digestion by phagocytes/allows for multiplication in phagocytres

ie. M protein (heat-resistant and acid-resistance protein)

Front 26

Compare the effects of the bacterial enzymes of virulence outlined in class/your textbook

(Read the Applications of Microbiology: Streptococcus: Harmful or Helpful? pg. 422)

Back 26

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Front 27

Define and give an example of antigenic variation

Back 27

- changes in surgace antigens that occur in a microbial population

ie. N. gonorrhoeae has several copies of the Opa-encoding gene, resulting in cells with diff antigens

ie. influenza virus

Front 28

Describe how bacteria use the host cell's cytoskeleton to enter the cell

Back 28

1. Make contact with host cell plasma membrane

2. Dramatic changes in membrane at contact area

3. Invasins produce to rearrange nerby actin filaments of cytoskeleton

4. Bacteria use actin to propel themselves through host cell cytoplasm and from one cell to another

Front 29

Nature and Effects of Exotoxins (Figure 15.4, 15.5, 15.3) (proteins)

Back 29

Proteins produced inside pathogenic bacteria, most commonly gram +, as part of their growth and metabolism. Secreted into surrounding medium during log phase.

- destory particular parts of the host's cells or inhibiting certain metabolic functions, among most lethal

- body produces antibodies called antitoxins for immunity against exotoxins

- toxoids: altered exotoxins that stimulate antitoxin production

Front 30

Nature and Effects of Endotoxins (Figure 15.4, 15.5, 15.3) (lipopolysaccharides)

Back 30

Lipid portions of lipopolysacharides (LPS) that are part of the outer membrane of the cell wall or gram - bacteria. The endotoxins are liberated when the bacteria die and the cell wall lyses.

- Lipid A, lipid portion of LPS that is the endotoxin

Front 31

What is the proposed mechanisms by which endotoxins cause fever (see page 428 + fig. 15.6)

Back 31

1. A microphage ingests a gram - bacterium

2. Bacterium is degraded in a vacuole, releasing endotoxins that induce the macrophage to produce cytokines, interleukin, and tumor necrosis

3. Cytokines released into blood stream --> travels to hypothalamus (temperature control of the brain)

4. Cytokines induce hypothalamus to produce prostaglandins, which reset the body's "thermostat" to a higher temperature, producing fever.

Front 32

Signs and Symptoms of Sepsis

Back 32

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Front 33

Important of Infections that develop into Septic Shock

Back 33

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Front 34

Gram-Negative Sepsis

Back 34

- Endotoxic shock

- 750,000 cases/yr in US; at least 2250,000 are fatal (textbook)

Front 35

Gram-Positive Sepsis

Back 35

-

Front 36

Puerperal Sepsis

Back 36

- Childbirth fever

- Nosocomial infection or HAI

Front 37

Cytopathic Effects (CPE)

Back 37

visible effects of viral infection

Front 38

List 5 Cytopathic effects of Viral Infections

Back 38

1. Macromolecular synthesis within host cell stops. (ie. stopping mitosis)

2. Host cell lysosomes are made to release their enzymes, resulting in destruction of intracellular contents and host cell death.

3. Inclusion bodies are found in the cytoplasm or nucleus of some infected cells.

4. Synctium, a large multinucleate cell is formed.

5. Changes in host cell's functions.

6. Antigenic changes on surgace of infected cells.

7. Chromosomal changes

8. Cancer

9. produce alpha and beta inerferons

Front 39

What are 3 common portals of exit?

Back 39

- most microbes tend to use the same portal for entry and exit

1. Respiratory Tract

- discharges through mouth or nose

2. Gastrointestinal Tract

- feces and saliva

3. Genitourinary Tract

- secretions from penis and vagina

Front 40

Draw out Table 15.3 Exotoxins and Endotoxins

Back 40

do it bruh

Front 41

kinases

Back 41

dissolve clots (ie. streptokinase)

Front 42

Toxin

Back 42

Substances that contribute to pathogenicty

Front 43

Toxigenicty

Back 43

Ability to produce a toxin

Front 44

Toxemia

Back 44

Prescence of toxin in host's blood

Front 45

Antitoxin

Back 45

Antibodies our body produces against a specific toxin

Front 46

Toxoid

Back 46

Inactivated toxin used in a vaccine

- when toxoids are injected as a vaccine, thye stimulate antitoxin production so taht immunity is produced (ie. Diptheria and tetanus toxoid)

Front 47

Damage to Host Cells

Back 47

1. By using the host's nutrients

- Siderophores: proteins pathogens produce to get the iron they need from the host

2. By causing direct damage in the immediate vicinity of the invasion

3. By producing toxins