Ch 4: Host Pathogen Relationships Flashcards

(63 cards)

1
Q

Pathology is the study of ____

A

Disease

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2
Q

Etiology is the study of _____

A

Cause of disease

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3
Q

What is Pathogenesis?

A

Disease process

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4
Q

What is infection?

A

Colonization by microbe

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5
Q

______ is the degree of pathogenicity

A

Virulence

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6
Q

What is bacteremia?

A

Presence of bacteria in the blood

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7
Q

______ is generalized inflammatory response to an infection

A

Sepsis

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8
Q

Difference between infection vs disease?

A

Infection is invasion by parasitic microbes (can occur without causing disease)
Disease is changes in health, damage to host.

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9
Q

Name the phases of disease

A

Incubation: time between introduction of organism to onset of symptoms
Illness: individual experiences signs and symptoms of disease
Convalescence: period of recuperation and recovery, infections diseases may still spread

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10
Q

Who provided the first scientific definition of sepsis: “sepsis is a state caused by microbial invasion from a local infectious source into the bloodstream which leads to signs of systemic illness in remote organs”

A

Hugo Schottmuller

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11
Q

ToF: Commensalism is when one benefits and the other neither benefits or is harmed

A

T

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12
Q

ToF: Mutualism is when both organisms benefit

A

T

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13
Q

What type of host pathogen relationship is when one organism benefits and the other is harmed?

A

Parasitism

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14
Q

ToF: Opportunistic pathogens normally cause disease

A

F: Do not normally cause disease, but may under some circumstances (Normal flora in wrong environment, compromised immune system, disruption of homeostasis)

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15
Q

Name four portals of entry of pathogenic microorganisms

A

Mucous membranes, skin, parenteral, placenta

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16
Q

ToF: Mucous membranes of the respiratory tract are the easiest and most frequent portal of entry

A

T

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17
Q

How is the mucous membranes of the respiratory tract a portal of entry for pathogens?

A

Microbes are inhaled into mouth or nose in droplets of moisture or dust particles

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18
Q

How is mucous membranes of the GIT a portal of entry?

A

Microbes gain entrance through contaminated food and water or fingers and hands

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19
Q

Most microbes that enter the GIT are destroyed by ____ and ______

A

Hydrochloric acid and enzymes of the stomach and small intestine

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20
Q

Which diseases commonly enter through mucous membranes of the genitourinary tract?

A

Sexually transmitted diseases
Ex. Gonorreah, Syphilis, Chlamydiasis, HIV

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21
Q

How do microbes enter through mucous membranes of the conjunctiva?

A

Mucous membranes that cover the eyeball and lines the eyelid

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22
Q

ToF: Herpes ocularis commonly enters the body through mucous membranes of the conjunctiva

A

T

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23
Q

Name two common diseases contracted via the skin?

A

Staphylococcus infections and Mycosis

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24
Q

ToF: The skin is not an effective barrier for microorganisms to enter

A

F: When unbroken it is an effective barrier
Some microbes can gain entrance through openings in the skin (hair follicles and sweat glands)

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25
What is the parenteral portal of entry?
Microorganisms deposited into the tissues below the skin or mucous membranes through: punctures, injections, bites, scratches, surgery, etc.
26
Name three common diseases contracted vis parenteral
Cytomegalovirus, Hepatitis, HIV
27
What does LD50 mean?
Number of microbes in a dose that kills 50% of the organisms infected in a sample
28
ToF: ID50 is the number of microbes in a dose that kill 50% of the organisms infected in a sample
F: ID50 is the number of microbes in a dose that causes disease in 50% of the organisms infected
29
Name and describe the three steps of pathogens invading an organism
1. Adherence: pathogens have attachment structures (ex. Pili) 2. Invasion/Colonization: multiply (need food, water, space) and protect from host defenses (must compete with normal flora, immunity, etc.) 3. Cause damage: tissue destruction (ex. Toxic byproducts and degradation enzymes), production of toxins, escape of host defenses
30
What is immunopathogenesis?
Excessive innate, immune and inflammatory responses triggered by the infection (superantigens; immune complexes precipitation)
31
What is a virulence factor?
A pathogen-produced substance that promotes the establishment and maintenance of disease
32
What are the types of virulence factors?
Adhesion factors, evading immune response, degradative enzymes, and toxins
33
What are some adhesion factors?
Pili: short, rigid and numerous Adhesions: molecules that bind to specific receptors on tissues
34
A _______ prevents phagocytosis by macrophages or neutrophils by not being ‘seen’ by these cells
Capsule
35
__________is when antigenic similarity occurs between molecules found on some disease-causing microorganisms and specific previously healthy body cells/tissues
Antigenic mimicry
36
What is antigenic shift?
Genetic alteration occurring in an infectious agent that causes change in antigen protein. This stimulates the production of antibodies by the host immune systems
37
ToF: Antigenic shift had been studied in influenza type A viruses
T: they experience this change once every 10 years
38
Describe how the inhibition of phagolysosome fusion that allows pathogens to avoid immune response
Bacteria is enclosed in phagosome and lysosome needs to fuse to destroy it. They stop this fusion and bacteria stays alive in the phagosome
39
______ attack certain types of white blood cells, preventing phagocytosis. They release and rupture lysosomes
Leukocidins
40
What do hemolysins do?
Cause the lysis of red blood cells. Ex. Streptococci
41
What do coagulase do?
cause blood to coagulate, blood clots protect bacteria from phagocytosis from white blood cells Ex. Staphylococci (causes boils and abscesses)
42
ToF: Kinases dissolve blood clots
T
43
ToF: Kinases do not help the spread of bacteria (bacteremia)
F
44
What is the mechanism of Hyaluronidase?
Breaks down hyaluronic acid (found in connective tissues) and is a spreading factor. It also allows bacteria to use hyaluronan as a carbon source
45
Which of the following is produced by Streptococci, Staphylococci and Clostridium? A) Kinases B) Collagenase C) Hemolysis D) Hyaluronidase
D) Hyaluronidase
46
ToF: Collagenase breaks down collagen
T
47
ToF: Colstridium perfringens uses kinases to spread through muscle tissue
F: uses collagenase to spread through muscle tissue
48
What is a necrotizing factor?
Causes death (necrosis) to tissue cells Caused by Streptococcus class A (flesh eating bacteria)
49
What are toxins?
Poisonous substances produces by microorganisms (can be exotoxins or endotoxins)
50
What is it called when toxins are in the bloodstream?
Toxemia
51
ToF: Exotoxins are released intracellular
F: released extracellularly
52
How do Leukotoxins function?
Invoke a very strong immune response, affect T cells which release a lot of cytokines that cause severe symptoms
53
How do cytotoxins damage tissues?
Disrupt host plasma membrane by targeting protein channels and phospholipid disruption
54
What pathogen is responsible for causing symptoms of botulism, prevention transmission of signal from nerve cell to muscle cell?
Clostridium botulinum
55
What pathogen is responsible for the symptoms of tetanus?
Clostridium tetani
56
ToF: Clostridium botulinum and Clostridium tetani are examples of neurotoxins
T
57
ToF: Endotoxins are present in Gram positive bacteria
F: Gram negative bacteria
58
ToF: Endotoxins are part of the outer portion of the cell wall
T: the lipid A portion of
59
ToF: Endotoxins are not very stable and can be destroyed easily
F: they are very stable and cannot be destroyed easily
60
Macrophages release _____ when they attack some gram negative cells. This binds to many tissues of host and may cause to blood capillaries and the blood brain barrier.
Tumor necrosis factor (TNF)
61
What is the main symptom of endotoxins?
Pyrogenic response: Macrophages ingests gram negative bacteria Release interleukin-1 in bloodstream IL-1 travels to hypothalamus and produces prostaglandins and it reset the body’s thermostat
62
Name factors effecting susceptibility to resistance of host
Age, stress, diet, pre-existing disease, gender, behaviour, weather and the first line of defense
63
What type of toxin causes leukopenia followed by leukocytosis, activation of complement, thrombocytopenia, disseminated intravascular clotting, loss of eater and decrease in blood pressure, and eventually death?
Endotoxin