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Mechanisms of Microbial Disease > Chapter 7 > Flashcards

Chapter 7 Flashcards

1
Q

Why can’t mosquitoes transmit HIV?

A

Because mosquitoes don’t possess the host cells that can accept HIV
Possible, but there is no evidence

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2
Q

What is direct pathology?

A

When the microbe directly harms cells by its own means

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3
Q

What are some examples of direct pathology from a microbe?

A

Multiply within the host to cause rupture

Dormants can bud out of the cell without killing

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4
Q

What is indirect pathology?

A

When the pathogen uses the host’s immune system to evoke a response that damage the host

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5
Q

What are exotoxins?

A

Proteins that are secreted by parasites to cause serious damage
Can be encoded on plasmids/phages
Cause local infection

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6
Q

What are toxoids?

A

A toxin inactivated by formaldehyde used in vaccinations
Diptheria
Toxins are well conserved (streptococcal erythrotoxin causin scarlet fever)

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7
Q

What is good about toxins being well conserved?

A

Their structure is very similar between species of bacteria so you are able to have one vaccine for multiple bacteria

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8
Q

How do exotoxins use hemolysis?

A

They lyse not only red blood cells but many other cells
Using enzymes like phospholipase C produced by clostridium perfringenes
Using alpha toxin produced by staphylococcus aureus to form pores (works like complement system)

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9
Q

What does clostridium perfringenes cause?

A

Gas gangrene

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10
Q

How do exotoxins alter metabolic machinery?

A

There are two subunits of the AB toxin.
A subunit (active) goes in to the cell and does the work
B subunit (binding) provides specificity to the toxin and is responsible for attachment to the host cell
Can be lots of variation in numbers of subunits
Cholera toxin has 5 B subunits and 1 A subunit

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11
Q

What are some examples of exotoxins that alter metabolic machinery?

A

The diptheria toxin inhibits protein synthesis so the cell will die, creating a mass of dead cells at the site of infection.
The cholera toxin causes ions to leak from the cell into the lumen, water follows.

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12
Q

How do exotoxins interfere with nerve-muscle transmission?

A

The B subunit of AB toxins bind to ganglioside receptors on nerve cells.
Botulinum and tetanus

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13
Q

How does tetanus interfere with nerve-muscle transmission?

A

Tetanus binds to nerve cell receptor and the A subunit is carried to the CNS and inhibits synthesis of the neurotransmitter that allows for relaxation of muscles so they are continuously stimulated, causing spastic paralysis.

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14
Q

How does botulinum interfere with nerve-muscle transmission?

A

Botulinum toxin binds to peripheral nerve endings at the neuromuscular junction and blocks acetylcholine release, blocking contraction of muscles causing flaccid paralysis.

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15
Q

What is diarrhea?

A

The invariable result of intestinal infections that allows the host to get rid of the infecting organism and allows the parasite to spread to fresh hosts

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16
Q

Why may antidiarrheal drugs not be good?

A

Ex: Immodium desensitizes the epithelial cells to stop diarrhea. This allows bacteria to continue replicating and producing more toxin.

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17
Q

What is the immune system very good at and not very good at?

A

Very good at distinguishing itself from foreign things

Bad at giving an appropriate response (overactivation resulting in host tissue damage)

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18
Q

What are endotoxins?

A

Lipopolysaccharides (LPS) which are found in the cell wall that are released when cells die.
Cause systemic infection

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19
Q

What are LPS composed of?

A

Lipid A, core oligosaccharide and an O-polysaccharide (variable)

20
Q

What types of cells produce LPS?

A

Gram negative organisms

E. coli, pseudonomas, neisseria meningtidis

21
Q

How are fever and shock caused?

A

Fever is caused by release of cytokines by macrophages

The effect of IL-1 and TNF on the hypothalamus

22
Q

What other microbial molecules stimulate cytokines?

A

T-cells of TSST-1

Toxic shock syndrome

23
Q

What can LPS activate?

A

Both the alternative (from polysaccharide) and classical (from lipid A) complement pathways

24
Q

What happens when the complement system is activated by LPS?

A

Chemotactic factors C3a and C5a are produced

Polymorphonuclear leukocytes adhere to vessel walls and realease toxic molecules that damage host cells

25
Q

What is a type I allergic response?

A

An immediate reaction to an antigen (allergen) in the environment
Most common
Symptoms can vary greatly. Will be at location of the effector cells but may be unrelated to the actual point of entry of the allergen

26
Q

What happens with people who have multiple allergies or severe allergies?

A

Can be related to a genetic disorder in which there is an overproduction of IL-4. This selects for IgE production over IgG, increased IL-4 receptors on B cells or even certain types of MHC-II

27
Q

What happens during initial exposure in a type I allergic response?

A

IgE formation following the primary Ab-mediated immune response. IgE binds via the Fc portion of basophils (in blood) and mast cells (in tissue). Both contain histamine

28
Q

What happens during the second and subsequent exposures in a type I allergic response?

A

The allergen binds to the V region of the Fab and crosslinks two adjacent IgEs on the mast cell/basophil surface. The crosslinking triggers degranulation and release of histamine and other mediators which causes an immediate response. minutes after exposure.

29
Q

What are the symptoms of a type I allergic response?

A

Hay fever or allergic rhinitis (watery eyes, runny nose from vascular permeability, edema)
Swelling and itchiness (nasal congestion, hives, edema)
Anaphylaxis (bronchoconstriction, shock, edema)
Asthma (smooth muscle constriction)

30
Q

What is histamine?

A

Preformed molecules in granules that bind to receptors on target cells (lungs, skin, blood vessels) and cause vasodilation, capillary permeability and smooth muscle contraction.
Key mediator of type I allergic response.

31
Q

How are chronic allergies treated?

A

Using antihistamines to block histamine receptors

Corticosteroids to block degranulation of mast cells

32
Q

What is the slow reacting substance of anaphylaxis (SRS-A)?

A 
A bronchoconstrictor (asthma) produced after exposure to allergen (not preformed) with slow release and lag time
Key mediator of type I allergic responses.
33
Q

How are acute allergies (anaphylactic shock) treated?

A

Using epinephrine, which works immediately for a short period of time (20 minutes).
Injected directly to increase cAMP levels, which decreases mediator release. Results in an increase in blood pressure that prevents shock.
Followed by intravenous antihistimines

34
Q

What is hyposensitization?

A

When the patient is exposed to the allergen in small doses over time so that the reaction will lessen or be completely gone

35
Q

What is Type II cytotoxic hypersensitivity?

A

An antibody-mediated response is made for non-self cells/autoantibodies (recognizes entire cell, not just antigen)

36
Q

What happens during a type II hypersensitivity reaction?

A

IgG is produced and binds to the non-self cell surface and activates the classical complement pathway (MAC attack) so the cell is lysed

37
Q

What are some examples of type II hypersensitivity reactions?

A

ABO blood transfusion reactions
Rh incompatibility in 2nd pregnancy
Blood stage malaria (parasite Ag picked up by red blood cells)
Antimyocardial antibody of GAS infection (cross reacting carbohydrate antigen)

38
Q

What is type III immune complex hypersensitivity?

A

An antigen-antibody complex forms and precipitates because it is insoluble due to cross-linking that causes activation of complement, attraction of phagocytes and general tissue damage

39
Q

Where do type III hypersensitivity reactions sediment?

A

In a spot in the body where there is high flow such as lungs, kidney and joints
Arthus reaction, farmer’s lung, serum sickness

40
Q

What is serum sickness?

A

Follows repeated injections of foreign proteins (passive immunizations) that creates circulating complexes that deposits in kidneys, skin and joints (glomerulonephritis, rheumatoid arthritis)

41
Q

What is type IV delayed or cell-mediated hypersensitivity?

A

No antibody involvement
Helper T cell and Cytotoxic T cell mediated causes tissue damage
Delayed-can start hours/days after contact and can last for days

42
Q

What is an example of type IV hypersensitivity?

A

Tuberculosis skin test (occurs if patient has been exposed to TB or has been vaccinated against TB)

43
Q

What is the hygiene hypothesis?

A

Since everything is so clean now, people are not exposed to as many microbes as they used to which is why allergies and inflammatory bowel disease (clean water) are more prevalent

44
Q

What are some lifestyle factors that could affect the amount of allergies a person has?

A

C-section rather than vaginal birth gives more allergies

Grow up on a farm, having pets gives less allergies

45
Q

What viruses can cause cancer?

A

Hepatitis B and C viruses can cause liver cancer.

HPV can cause cervical or skin cancer

46
Q

What bacteria can cause cancer?

A

Helicobacter pylori because it allows acid to repeatedly damage the stomach cells. These cells must continually reproduce and replace the damaged ones, this process could go out of control (cancer).

Mechanisms of Microbial Disease (17 decks)

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