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Micro > Micro Exam 4- Chapter 15 > Flashcards

Micro Exam 4- Chapter 15 Flashcards

1
Q

• Pathogenicity

A

is the ability to cause disease by overcoming host defenses

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2
Q

Virulence:

A

the degree of pathogenicity

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3
Q

Requirements for pathogenicity

A

▪ Must gain access to host
▪ Adhere to host tissues
▪ Penetrate host defenses
▪ Direct damage or through accumulation of waste products

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4
Q

How Microorganisms Enter a Host

Portals of Entry

A
  1. Mucous membranes: Lining the respiratory tract, gastrointestinal tract, genitourinary tract, and conjunctiva
  2. Skin: openings in the skin such as hair follicles and sweat gland ducts
  3. Parenteral route
    • Deposited directly into tissues when barriers are penetrated
    • Punctures, injections, bites, cuts, wounds, surgery, splitting of skin or mucous membrane can all establish parenteral route
    • HIV, Hepatitis viruses, bacteria that cause tetanus and gangrene
    • Most pathogens have a preferred portal of entry if they gain access to the body by another portal, disease might not occur
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5
Q

How Microorganisms Enter a Host

Portals of Entry

A
  1. Skin: openings in the skin such as hair follicles and sweat gland ducts
  2. Parenteral route
    • Deposited directly into tissues when barriers are penetrated
    • Punctures, injections, bites, cuts, wounds, surgery, splitting of skin or mucous membrane can all establish parenteral route
    • HIV, Hepatitis viruses, bacteria that cause tetanus and gangrene
    • Most pathogens have a preferred portal of entry if they gain access to the body by another portal, disease might not occur
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6
Q

How Microorganisms Enter a Host

Portals of Entry

A
  1. Parenteral route
    • Deposited directly into tissues when barriers are penetrated
    • Punctures, injections, bites, cuts, wounds, surgery, splitting of skin or mucous membrane can all establish parenteral route
    • HIV, Hepatitis viruses, bacteria that cause tetanus and gangrene

**Most pathogens have a preferred portal of entry if they gain access to the body by another portal, disease might not occur

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7
Q

Portals of Entry for Common Pathogens

A
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8
Q

Number of invading microbes

A

• The likelihood of disease increases as the number of pathogens increases

• Virulence of a microbe is often expressed as
ID50: Infectious dose (no of organisms) for 50% of a sample population

LD50: lethal dose for 50% of a sample population
• Measures potency of a toxin

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9
Q

Number of invading microbes

A
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10
Q

adherence (adhesion)

A

pathogens attach to host tissues in a process called

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11
Q

• Surface molecules known as Adhesins (ligands) on the pathogen bind to receptors on the host cells

A

• Adhesins can be located on pathogens glycocalyx, and other surface structures such as pili, fimbriae, flagella
EX. Glycoproteins or lipoproteins –Adhesins
Carbohydrates such as mannose- Receptors
• Microbes form biofilms (communities that share nutrients)

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12
Q

Adherence

A
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13
Q

Penetration of Host Defenses
Although some pathogens can damage on the surface of tissues, most must penetrate tissues to cause disease. Factors that contribute to the ability of bacteria to invade a host

A

Capsules
Cell Wall Components
Antigenic Variation
Penetration into the Host Cell Cytoskeleton

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14
Q

Capsules

A
  • Some bacteria make Glycocalyx around the cell wall
  • This increases virulence and resist host defenses
  • Impair phagocytosis (means body cells engulf & destroy microbes)
  • Streptococcus pneumoniae—pneumonia
  • Haemophilus influenzae—pneumonia and meningitis
  • Bacillus anthracis—anthrax
  • Yersinia pestis—plague
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15
Q

Cell Wall Components

A
  • Contain chemical substances that contribute to virulence
  • M protein found in Streptococcus pyogenes cell surface and fimbriae resists phagocytosis
  • Resistant to heat and acid
  • It mediates attachment of bacterium to epithelial cells of host
  • Opa protein allows attachment to host cells
  • Neisseria gonorrhoeae
  • Waxy lipid (mycolic acid) resists digestion
  • Mycobacterium tuberculosis
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16
Q

Enzymes

A

Virulence of some bacteria is aided by the production of extracellular enzymes and related substances. These chemicals digest materials between cells and form or digest blood clots, among other functions

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17
Q

• Coagulases:

A

coagulate fibrinogen (clot blood)

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18
Q

• Kinases

A

: digest fibrin clots (i.e., blood clots)

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19
Q

• Hyaluronidase

A

digests polysaccharides that hold cells together

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20
Q

• Collagenase

A

breaks down collagen

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21
Q

IgA proteases

A

: destroy IgA antibodies of mucus membrane

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22
Q

Applications of Microbiology

A
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23
Q

Antigenic Variation

A

Pathogens alter their surface antigens (and antibodies are rendered ineffective)

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24
Q

Penetration into the Host Cell Cytoskeleton

A
  • Microbes attach to host cells by ADHESINS
  • Invasins: Surface proteins produced by bacteria that rearrange actin filaments of the cytoskeleton [Cause membrane ruffling]
  • Use ACTIN to move from one cell to the next
  • Shigella and Listeria
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25
Q

• Upon entry into host cells microbes first encounter

A

phagocytes

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26
Q

If pathogens overcome phagocytes, then it can damage host cells in 4 basic ways

A
  1. By using the host’s nutrients
  2. By causing direct damage in the immediate vicinity of the invasion
  3. By producing toxins
  4. By inducing hypersensitivity reactions
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27
Q

Using the Host’s Nutrients: Siderophores

A
  • Iron is required for most pathogenic bacteria
  • Concentration of free Fe in human body is low
  • Siderophores are proteins secreted by pathogens that bind iron more tightly than host cells
  • Siderophore receptors on the bacterial surface takes up the Fe-siderophore complex
28
Q

Direct Damage

A
  • Disrupts host cell function
  • Uses host cell nutrients
  • Produces waste products
  • Multiplies in host cells and causes ruptures
  • By excreting enzymes or by their own motility
29
Q

Toxins:

A

poisonous substances produced by microorganisms

30
Q

• Toxigenicity:

A

ability of a microorganism to produce a toxin

31
Q

• Toxemia:

A

presence of toxin in the host’s blood

32
Q

• Intoxications: presence of toxin without microbial growth

A

presence of toxin without microbial growth

33
Q
  1. Exotoxins:
A

Produced inside some bacteria as a part of their growth and metabolism and are secreted into surrounding medium or released following lysis
• Produce fever, cardiovascular problems, diarrhea, and neurotoxins, hepatotoxins

34
Q
  1. Endotoxins
A

Part of outer portion of Gram-negative cell wall

35
Q

Exotoxins Produced and secreted by bacteria either

A

G+ve or G-ve

36
Q

Exotoxins are proteins and many are

A

enzymes that catalyze only certain biochemical reactions

Soluble in bodily fluids; destroy host cells and inhibit metabolic functions

37
Q

Exotoxins are among the most

A

lethal substances known

▪ 1 mg of botulinum toxin is enough to kill 1 million guinea pigs
▪ Diseases caused by bacteria that produce exotoxins are often caused by minute amounts of exotoxins, not by bacteria themselves
EXAMPLES: (C. botulinum, Staph intoxications)

38
Q

Exotoxin process

A
39
Q

Antitoxins:

A

antibodies against specific exotoxins

40
Q

Exotoxins when inactivated by heat, or by formaldehyde, iodine or other chemicals

A

they no longer cause the disease but can stimulate the body to produce antitoxins

41
Q

• Altered exotoxins are called

A

toxoids

42
Q

Toxoids:

A

inactivated exotoxins used in vaccines
Ex. Diphtheria and tetanus

43
Q

Types of Exotoxins

A
  1. A-B toxins
  2. Membrane-disrupting toxins
  3. Superantigens
44
Q
  1. A-B toxins
A

contain an enzyme component (A part) and a binding component (B part)
• Diphtheria toxin

45
Q
  1. Membrane-
A

disrupting toxins lyse host cells by disrupting plasma membranes

46
Q

• Leukocidins—

A

kill phagocytic leukocytes (white blood cells)

47
Q

• Hemolysins—

A

kill erythrocytes (red blood cells) by forming protein channels

48
Q

• Streptolysins—

A

hemolysins produced by streptococci

49
Q
  1. Superantigens cause an intense immune response due to release of cytokines from host cells (T cells)
    • Cause symptoms of
A

fever, nausea, vomiting, diarrhea, shock, and death

50
Q

Genotoxins damage

A

DNA (causing mutations, disrupting cell division, and leading to cancer)

51
Q

Diseases Caused By Exotoxins

A
52
Q

Endotoxins, • Endo means “within”

A
  • Endotoxins-located within the bacterial cells
  • They are part of outer cell wall of Gram-negative bacteria [Lipid A portion of lipopolysaccharides (LPS)]
  • Released during bacterial multiplication and when gram-negative bacteria die, and their cell wall undergo lysis
  • Stimulate macrophages to release cytokines
  • Cause disseminated intravascular coagulation (DIC) –activation of blood clotting proteins
53
Q

Mechanisms of Exotoxins and Endotoxins

A
54
Q

Endotoxins and the pyrogenic response.

A
55
Q

• Limulus amebocyte lysate (LAL) assay is used to test for

A

endotoxins

  • Blood of horseshoe crabs contains amebocytes
  • Amebocytes lyse in the presence of endotoxin, producing a clot
56
Q

Exotoxin & Endotoxin Table

A
57
Q

Plasmids, Lysogeny, and Pathogenicity

A
  • Plasmids may carry genes for toxins, production of antibiotics, and enzymes
  • Lysogenic conversion changes characteristics of a microbe due to incorporation of a prophage
58
Q

Viral mechanisms of evading host defenses

A
  • Gaining access to the host
  • Evading host defenses
  • Causing damage or death of host cell while reproducing themselves
59
Q

Variety of mechanisms

A

▪ Penetrate and grow inside host cells
▪ Attachment sites mimic substances useful to host cells

60
Q

Pathogenic Properties of Viruses

A

• Cytopathic effects (CPE) are visible effects of viral infection on a cell
• Stopping cell synthesis
• Causing cell lysosomes to release enzymes
• Creating inclusion bodies in the cell cytoplasm
• Fusing cells to create a syncytium
• Changing host cell function or inducing chromosomal changes
• Inducing antigenic changes on the cell surface
• Loss of contact inhibition in the cell, leading to cancer
• Producing interferons to protect uninfected

61
Q

Fungi

A
  • Toxic metabolic products
  • Provoke an allergic response
  • Trichothecene toxins inhibit protein synthesis
  • Proteases modify host cell membranes
  • Capsules prevent phagocytosis
  • Ergot are alkaloid toxins that cause hallucinations
  • Aflatoxin is a carcinogenic toxin produced by Aspergillus
  • Mycotoxins are produced by mushrooms and are neurotoxic
  • Phalloidin and amanitin
62
Q

Algae

A
  • Some produce a neurotoxin called saxitoxin
  • Paralytic shellfish poisoning
63
Q

Protozoa

A
  • Presence of protozoa and their waste products causes symptoms
  • Avoid host defenses by:
  • Digesting cells and tissue fluids
  • Growing in phagocytes
  • Antigenic variation
64
Q

Helminths

A
  • Use host tissue for growth
  • Produce large masses; cause cellular damage
  • Produce waste products
  • Produce waste products that cause symptoms
65
Q

Portals of Entry

A
  • Respiratory tract
  • Coughing and sneezing
  • Gastrointestinal tract
  • Feces and saliva
  • Genitourinary tract
  • Urine; secretions from the penis and vagina
  • Parenteral route, examples wounds, injections bites

**cannot penetrate intact skin, they can penetrate hair follicles and sweat ducts

66
Q

Portals of Exit

A

Pathogens leave the host by portal exists.

  • respiratory tract via coughing
  • GI tract, Saliva, feces or vagina or penis
  • Arthropods and syringes portal of exit microbes in blood
67
Q

Microbial Mechanisms of Pathogenicity.

A

Micro (7 decks)

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