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Microbiology LECTURE > Chapter 15 > Flashcards

Chapter 15 Flashcards

Microbial Mechanisms of Pathogenecity

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1
Q

Portals of entry

A
  1. Mucous membrane
  2. Skin
  3. The parenteral route
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2
Q

Mucous membrane

A

Respiratory tract, gastrointestinal tract, genitourinary tract, conjunctiva

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3
Q

Which is the easiest and most frequently traveled portal entry for infectious micro organisms

A

Respiratory tract

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4
Q

How do micro organisms gain access to the GI tract

A

Food water and via contaminated objects

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5
Q

How do pathogens access the genitourinary tract

A

They penetrate through unbroken mucous membrane or broken membranes as a result of sexual contact

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6
Q

If broken skin is impenetrable by most microorganisms then how do some microbes gain access to the body

A

They gain access through openings in the skin such as hair follicles and sweat gland ducts

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7
Q

What organisms can bore through the skin

A

Larvae of hookworms

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8
Q

What organisms can grow on the skin

A

Fungi can infect the keratin in skin or infect the skin itself

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9
Q

The parenteral route

A

Access gained to the body when microorganisms are deposited directly into the tissues beneath the skin and into mucous membrane when these barriers are penetrated or injured.

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10
Q

What are the different ways the skin and mucous membranes penetrated

A

Punctured, injections, bites cuts, wounds, surgery and splitting of the skin or mucous membrane due to swelling or drying

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11
Q

To micro organisms caused disease after they have entered the body

A

No, not necessarily. A pathogen has a preferred portal of entry that it must go through before it is able to cause disease.

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12
Q

What is ID50

A

The virulence of a microbe expressed like this means infectious dose for 50% of a sample population
In other words the # of microorganisms required to infect 50% of the population

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13
Q

What is LD50

A

The potency of a toxin is expressed as this meaning the lethal dose for 50% of a sample population
In other words, the # of microorganisms required to kill 50% of the population

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14
Q

Adherence (in pathogenic microbes)

A

A means of pathigens attaching themselves to host tissues at their portal of entry

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15
Q

How do pathogens attach to a host

A

This is accomplished by means of surface molecules on the pathogen called adhesind or ligands that bind specifically to complimentary surface receptors on the cells of certain host’s tissues.

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16
Q

Where are microbe adhesins located

A

On the glycocalyx, pili, fimbriae, or flagella

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17
Q

Biofilms

A

Communities of microbes that mass together and cling to surfaces with their extra cellular products that can attach to living and non living surfaces, and share available nutrients

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18
Q

What are factors that contribute to the ability of bacteria to invade a host

A

Bacterial capsules, Specific cell wall components, Extracellular enzymes, Antigenic variation, Production of proteins called invasins

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19
Q

Capsules

A

Made up of glycocalyx material that forms capsules around the cell walls. This increases the virulence of the species and resists the host offenses by impairing phagocytosis.

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20
Q

Can a host cell produce antibodies against a bacterial capsule

A

Yes, the human body can produce antibodies against the capsule and when these antibodies are present on the capsule surface, the encapsulated bacteria are easily destroyed by phagocytosis.

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21
Q

What are cell wall components that contribute to bacterial virulence

A

M protein, fimbriae, Opa, and waxy outer wall lipid layer

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22
Q

M protein

A

Heat resistant and acid resistant protein found on both the cell surface and fimbriae of certain bacteria. It mediate attachment of the bacterium to epithelial cells of the host and helps the bacterium resist phagocytosis by white blood cells.

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23
Q

What bacteria carry the M protein

A

Streptococcus pyogenes

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24
Q

Opa

A

An outer membrane protein that attaches to host cells, with Opa and fimbriae attached to host cell, the host cell takes in the bacteria

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25
Q

Waxy lipid

A

Mycolic acid that makes up the cell wall of Mycobacterium tuberculosis, also increases virulence by resisting digestion by phagocytes and can even multiply inside phagocytes

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26
Q

Coagulases

A

A bacterial enzyme that coagulate the fibrinogen in blood forming a blood clot. The clot may protect the bacterium from phagocytosis and isolate it from other defenses of the host

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27
Q

Bacterial kinases

A

Bacterial enzyme that breaks down fibrin and thus digest clots formed by the body to isolate the infection

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28
Q

How is bacterial kinase used in a medical setting

A

To break down clots in a coronary artery bl♡ckage

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29
Q

Hyaluronidase

A

Enzyme secreted by certain bacteria such as streptococci. It hydrolyzes hyaluronic acid, a type of polysaccharide that holds together certain cells of the body, particularly cells in connective tissue.

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30
Q

What are some of the effects of hyaluronidase

A

The digesting action is thought to be involved in the tissue blackening of infected wounds and to help the microorganism spread from its initial site of infection it can also produce gas gangrene in some with certain bacteria.

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31
Q

Collagenase

A

An enzyme produced by several species of Clostridium. It facilitates the spread of gas gangrene and breaks down the protein collagen which forms the connective tissue of muscles and other body organs and tissues.

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32
Q

As a defense against adherence of pathogens to mucosal surfaces, what class of antibodies does the body produce

A

IgA antibodies

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33
Q

What do some pathogens produce that destroy IgA antibodies

A

IgA proteases

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34
Q

Antigenic variation

A

The ability for some pathogens to alter their surface antigens and thus preventing an immune response against the pathogen that is unaffected by the antibodies the host produces.

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35
Q

How does activating alternative genes help with antigenic variation

A

They result in antigenic changes, such as N. gonorrhea has several copies of Opa-encoding gene, resulting in cells with different antigens and in cells that express different antigens over time.

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36
Q

What is adaptive immunity

A

A specific defense response of the body to an infection or to antigens. The body produces antibodies which bind to the antigens and inactivate or destroy them.

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37
Q

What component of the cytoskeleton of a eukaryotic cell does a bacterial cell hija6for its own purpose

A

The protein actin which is used by some microbes to penetrate host cells and by others to move through and between host cells.

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38
Q

What protein do microbes use to rearrange nearby actin filaments of the cytoskeleton

A

Invasins

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39
Q

How do invasins penetration the host cell

A

Invasins of a microbe cause the appearance of the host cell plasma membrane to resemble the splash of a drop of a liquid hitting a solid surface, disrupting the cytoskeleton, sinking in and becoming engulfed by the host cell

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40
Q

Membrane ruffling

A

The effect caused by the Invasin hitting the plasma membrane

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41
Q

How is actin used to penetrate the host cell

A

Actin is used to propel themselves through the host cell cytoplasm and from one host cell l to another

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42
Q

What are the 4 basic ways a microorganism can damage host cells

A
  1. Using the host’s nutrients
  2. Causing direct damage in the immediate vicinity of the invasion
  3. Producing toxins transported by blood and lymph that damage sites far removed from the original site of invasion
  4. Inducing hypersensitivity reactions
43
Q

What nutrient is required for the growth of most pathogenic bacteria

A

Iron

44
Q

Why do bacteria have trouble getting iron from the human body

A

Free iron is fairly low because most of it is tightly bound to iron transport proteins such as a lactoferrin, transferrin, ferritin, and hemoglobin

45
Q

How do pathogens obtain free iron from their host

A

They secrete proteins called siderophores

46
Q

How do siderophores work

A

When a pathogen needs iron, siderophores are released into the medium where they take iron away from iron transport proteins by binding that iron even more tightly

47
Q

Hiw do siderophores get the iron into the bacterial cell

A

Once the iron-siderophore complex is formed, receptors on bacterial surface allow it in or the iron is released before it is kept in

48
Q

What is an alternative to iron acquisition by siderophores

A

Pathogens have receptor that binds directly to iron transport proteins and hemoglobin

49
Q

What happens when the host has low iron levels, How does bacteria get its iron

A

Some bacteria produce toxins when iron levels are low. The toxins kill host cells releasing their iron and thereby making it available to the bacteria.

50
Q

Most damage by bacteria is done by

A

Toxins

51
Q

How do pathogens cause direct damage to host cells

A
  1. By using host cell for nutrients and producing waste products
  2. As pathogens metabolize and multiply in cells, the cells usually rupture.
  3. When they rupture they can spread to other tissues and even greater numbers
  4. They can enter other cells through a reverse phagocytosis process
  5. Penetration into host cell
  6. Toxins
52
Q

Toxins

A

Poisonous substance that are produced by certain micro organisms

53
Q

Toxigenicity

A

Capacity of microorganisms to produce toxins

54
Q

What is the primary factor contributing to pathogenic properties of microbes

A

Toxins

55
Q

When can toxins cause serious and sometimes fatal effects

A

When they are transported by blood or lymph

56
Q

What are some of the toxic effects of toxins

A

Produce fever, Cardiovascular disturbances, Diarrhea, Shock, inhibit protein synthesis, Destroy blood cells, Destroy blood vessels, Disrupt nervous system by causing spasms

57
Q

Toxemia

A

Presence of toxins in the blood

58
Q

2 general types of toxins

A

Exotoxins and endotoxins

59
Q

Exotoxins

A

Proteins or enzymes 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

60
Q

Which bacteria produce exotoxins

A

Gram positive or gram negative

61
Q

Where are exotoxins carried on microbes

A

Genes carried on bacterial plasmids or phages

62
Q

Why are exoroxins easily diffusible into blood and transported throughout the body

A

Because they are solub6in body fluids

63
Q

How do exotoxins work

A

By destroying particular parts of the host’s cells or by inhibiting certain metabolic functions.

64
Q

Which toxin is the most lethal and why

A

Exotoxins. Because they are highly specific in their effects on body tissues. They are often caused by minute amounts that produce specific signs and, and are disease specific

65
Q

How does the human body try to prevent exotoxins from causing harm

A

By producing antibodies called anti toxins that provide immunity

66
Q

Toxoids

A

The alteration of to exotoxins to which they are inactivated to where they no longer cause disease but still stimulate the body to produce antitoxins

67
Q

How are exotoxins inactivated

A

By heat or by formaldehyde, iodine, or other chemicals

68
Q

Example of a toxoid

A

When toxoids are injected into the bodies as a vaccine, they stimulate antitoxin production so that immunity is produced. Such as with a Tetanus and diphtheria vaccine

69
Q

How are exotoxins name

A

Their name based on the type of a host cell they attack, Or the disease in which they are associated with, Or based on the specific bacteria that produce them

70
Q

Types of exotoxins

A
  1. A-B toxins
  2. Membrane disrupting toxins
  3. Superantigens
71
Q

Leukocidins

A

Membrane disrupting toxins that kill phagocytic leukocytes

72
Q

Hemolysins

A

Membrane disrupting toxins that destroy erythrocytes also by forming protein channels

73
Q

Streptolysins

A

Hemolysins produced by Streptococci

74
Q

Superantigens

A

Antigens that provoke a very intense immune response. They are bacterial proteins.

75
Q

Endotoxins

A

Are part of the outer portion of the cell wall of gram negative bacteria

76
Q

Where are endotoxins found on gram negative bacteria

A

On the outer membrane and they are called lipid A

77
Q

When our endotoxins released

A

When gram negative bacteria die and their cell walls undergo lyses, this liberates the Endotoxin. They can also be released during bacterial multiplication.

78
Q

How do endotoxins work

A

They exert their effects by stimulating macrophages to release cytokines in very high concentrations, these are toxic. They also activate blood clotting proteins.

79
Q

What effect does the release of cytokines have on the human body

A

The hypothalamus to release lipids called prostaglandins which reset that thermostat at a higher temperature resulting in a fever

80
Q

What effect or consequences to blood clot formations cause

A

They obstruct capillaries and result in decreased but blood supply which induces death of tissues; known as Disseminated intravascular coagulation

81
Q

Shock

A

Any life threatening decrease in blood pressure

82
Q

Septic shock

A

Shock caused by bacteria

83
Q

What causes endotoxic shock

A

Gram negative bacteria

84
Q

Plasmids

A

Small circular DNA molecules that are not connected to the main bacterial chromosome and are capable of independent replication

85
Q

R factors

A

A group of plasmid’s with resistant factors that are responsible for the resistance of some micro organisms to antibiotics

86
Q

Lysogenic conversion

A

A change in the characteristics of a microbe due to a prophage

87
Q

What is lysogeny

A

Some bacterial fages can incorporate their DNA into the bacterial chromosome becoming a prophage and thus remain latent

88
Q

How do viruses gain access to host cells

A

Viruses gain access to cells because they have attachments sites for receptors on their target cells. When an attachment site is brought together with an appropriate receptor the virus can bind to and penetrate the cell. Some viruses can gain access because their attachment sites mimic substance as useful to those cells.

89
Q

Cytopathic effects

A

The visible effects of viral infection

90
Q

What are the different cytopathic effects

A

Stopping mitosis, lysis, formation of inclusion bodies, cell fusion, antigenic changes, chromosomal changes, and transformation

91
Q

Cytocidal effects

A

Cell death as a result of a cytopathic effect

92
Q

How do viruses avoid the hosts immune response

A

By growing inside cells. Some can remain latent in a host cell for prolonged periods

93
Q

What is a cytopathic effect that results in cell damage

A

Noncytocidal effect

94
Q

What are CPEs used for

A

To diagnose many viral infections, such as inclusions

95
Q

Inclusion bodies

A

Granules found in the cytoplasm or nucleus of some infected cells. They are sometimes viral parts such as nucleic acids or proteins in the process of being assembled into virions.

96
Q

What causes symptoms of fungal infections

A

Capsules, toxins, and allergic responses

97
Q

Symptoms of protozoan and helminthic disease can be caused by what

A

Damage to host tissue or by the metabolic waste products of the parasite

98
Q

Some protozoa change their surface antigens while growing in a host, what does this avoid?

A

Destruction by the host’s antibodies

99
Q

What do some algae produce that is caused after ingestion

A

They produce neuro toxins that cause paralysis when ingested by humans

100
Q

How do microbes leave the body

A

Via specific routes called portals of exits in secretions, excretions, discharges, or tissue that has been shed

101
Q

Does a microbe use the same portal for entry and exit

A

Yes

102
Q

What are the most common portals of exit

A

Respiratory and gastrointestinal tracts

103
Q

What are the portals of exit

A

Mucous membranes
Skin
Parenteral route

104
Q

Do pathogenic fungi have specific virulence factors

A

No. Capsules, metabolic products, toxins, and allergic responses contribute to the virulence of pathogenic fungi.

Microbiology LECTURE (13 decks)

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