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Microbiology > Chapter 19 Micro > Flashcards

Chapter 19 Micro Flashcards

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1
Q

What is hypersensitivity?

A

overreaction; response to antigens (allergens) leading to damage

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2
Q

Autoimmune diseases can be described as…

A

reactions against self

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3
Q

HLA issues

A

transplantation, human vs. human

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4
Q

Cancer in relation to immune disorders…

A

immune surveillance

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5
Q

What are the 4 types of hypersensitivity reactions and what are the times after exposure for clinical symptoms?

A 
Type 1 (anaphylactic): occurs in less than 30 mins 
Type II (cytotoxic): occurs in 5-12 hours 
Type III (immune complex): 3-8 hours 
Type IV (delayed, cell medicated or delayed hypersensitivity): 24-48 hours
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6
Q

Hypersensitivity requires ____ a ____ _____

A

SENSITIZATION, prior exposure

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7
Q

Describe type 1 (anaphylactic) reactions

A
  • Prophylaxis is protection
  • Localized or systemic
  • IgE must trigger mast cells and basophils
  • Mast cells and basophils must degranulate to release 3 mediators
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8
Q

What are the three mediators released during a type I reaction?

A
  • Histamine: pre existing: edema, erythema, mucus
  • Leukotrienes
  • Prostaglandin
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9
Q

What is a mast cell?

A
  • Monocyte
  • filled w granules
  • derives from myeloid lineage
  • found in connective tissue
  • helps with healing, angiogenesis, immune tolerance
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10
Q

What is the key takeaway about mechanism of anaphylaxis?

A

allergen bridges or crosslinks adjacent IgE molecules

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11
Q

What is localized anaphylaxis?

A

Causes hives/hay fever and asthma

  • Mast cells are in the mucous membranes of upper respiratory tracts
  • responsive to antihistamine drugs
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12
Q

What are some food allergies many people have?

What are the most common side effects/reactions?

A 
Eggs
Peanuts
Tree nuts
Milk
Soy 
Fish
Wheat 
Peas

Hives and GI upset, systemic anaphylaxis and death is possible

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13
Q

What is systemic anaphylaxis?

A
  • injected or ingested
  • bee stings, jellyfish stings
  • can result in circulatory collapse and death
  • treatment is EPI PEN
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14
Q

Skin testing is used to….

A
  • determine allergens more precisely

- Allergen in the epidermis w/ pos results gives raised reaction

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15
Q

How can anaphylaxis be prevented?

A
  • Desensitization injection of Ag
  • doses of antigen are gradually increased under the skin
  • results in IgG instead of IgE
  • IgG intercepts antigen when re-exposed
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16
Q

What are type II (cytotoxic reactions)?

A
  • IgG or IgM antibodies and complement
  • Antibodies react well cell surface antigens
  • Complement activation leads to cell lysis
  • Macrophages are damaged after they are recruited over several hours
  • Include transfusion reactions like ABO, Rh blood and drug induced
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17
Q

What are the antibodies of AB blood group?

A

Neither A or anti-B antibodies

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18
Q

What are the antibodies of B blood group?

A

Anti A

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19
Q

What are the antibodies of the A blood group?

A

Anti B

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20
Q

What are the antibodies for O blood group?

A

Anti A and Anti B

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21
Q

Individuals with type O blood are more susceptible to what disease?

A

Cholera

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22
Q

Populations with low A and AB blood types may be more susceptible in what?

A

Smallpox epidemics

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23
Q

Which blood type is less severely affected by malaria?

A

Type O

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24
Q

How do antibodies against A and B blood group antigens arise?

A

Presumably in response to microorganisms in ingested foods that have antigenic determinants similar to blood group antigens

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25
Q

What is the Rh blood group system?

A
  • either Rh+ or Rh-
  • different from blood types in antibodies that react with Rh antigen do not occur naturally in serum of Rh-
  • Rh- exposure to Rh+ makes sensitivity
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26
Q

What is hemolytic disease of the newborn?

A
  • prevented by artificially acquired passive immunization
  • RhoGAM is antibodies to the Rh antigen
  • RhoGAM is given to pregnant women to bind fetal red blood cells and keep them from mounting immune response
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27
Q

Drug induced cytotoxic reactions…

A
  • drug or other small molecule stimulates immune system as hapten
  • second exposure the drug binds to platelets leading to thrombocytopenic purpura , granulocytes causing agranulocytosis and to RBC causing hemolytic anemia
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28
Q

What happens in drug induced thrombocytopenic purpura?

A
  1. Drug binds to platelet, forming hapten platelet complex
  2. Complex induces formation of antibodies against hapten
  3. Action of antibodies and complement causes platlet destruction
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29
Q

What is a type II (immune complex) reactions?

A
  • IgG antibodies and antigens form immune complexes that lodge in basement membrane
  • Complexes form at certain Ag/Ab ratio
  • Complexes passes between vessel endothelial cells and attract neutrophils to release enzymes to cause damage
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30
Q

What are type IV (cell mediated) reactions?

A
  • delayed type hypersensitivities due to T cells
  • takes time for T cells and macrophages to migrate to the site of stimulating antigen
  • cytokines attract macrophages and Tc cells, leading to tissue damage
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31
Q

Allergic contact dermatitis

A
  • primary contact makes the T cells sensitized and causes immune response in 7-10 days
  • secondary contact causes many active T cells which leads to dermatitis
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32
Q

What are autoimmune diseases?

A
  • Clonal deletion of T cells during fetal development in thymus
  • Autoimmunity is lack of self tolerance
  • Anti self antibodies arise in response to infectious agents like hep C
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33
Q

Cytotoxic auto immune diseases

A

Antibodies react with cell surface antigens

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34
Q

Immune complex auto immune diseases

A

IgM, IgG, complement immune complexes deposit in tissues

35
Q

Cell mediated autoimmune diseases

A

mediated by T cells

36
Q

How are immune reactions measured?

A

Quantitatively

37
Q

What is the issue with autoantibodies?

A

Difficult to define

-Antibody binding does not define unique molecular signature, antibody can bind to diff. epitopes

38
Q

Why are autoantibodies that cause disease are rare?

A

Only certain diseases of the immune system generate significant amounts of autoantibodies

39
Q

What type of disease is lupus and rheumatoid arthritis?

A

Immune complex autoimmune disease

  • Lupus causes IC deposits in kidney
  • RA causes IC deposits in joints
40
Q

What type of disease is multiple sclerosis and insulin dependent diabetes mellitus?

A

Cell mediated autoimmune disease

  • MS causes immune cells to attack myelin
  • Diabetes Mellitus causes cells to attack pancreas
41
Q

Histocompatibility antigens are…

A

self antigens on cell surfaces

42
Q

What is the major histocompatibility complex?

A

Genes encoding histocompatibility antigens

  • MHC class I on all cells
  • MHC class II on immune system cells
43
Q

What is the human leukocyte antigen complex?

A

MHC genes in humans

HLA typing or tissue typing for tissue transplants

44
Q

What is HLA typing?

A
  1. anti hla antibodies attach to HLAs on lymphocyte
  2. complement and trypan blue are added
  3. Cell damaged by complement takes up dye
45
Q

What are some diseases related to specific HLAs?

A
  • MS
  • Rheumatic fever
  • Addisons disease
  • Graves disease
  • Hodgkins disease
46
Q

What are some reactions to transplantation?

A
  • Transplants make be attacked by T cells, macrophages and complement fixing antibodies
  • Transplants to privileged sites do not cause immune response (cornea, brain, heart valve, fetus)
47
Q

How can transplantation be improved?

A

Stem cells

  • ES cells are pluripotent
  • Adult stem cells can be found in many tissues
  • iPS cells
48
Q

How are pluripotent stem cells made?

A
  1. Embryo from discarded in vitro fertilized egg
  2. Embryo divides repeatedly and makes hollow ball of cells
  3. ES stem cells from embryoblast are grown on feeder cells in culture medium
49
Q

An autograft is…

A

Use of one’s own tissue

50
Q

What is an isograft?

A

use of identical twins tissue

51
Q

Allograft can be described as

A

use of tissue from another person

52
Q

Xenotransplantation

A

Use of nonhuman tissue

53
Q

Graft vs. host disease

A

can result from transplanted bone marrow that contains immunocompetent cells

54
Q

What is immunosupression?

A
  • Prevents an immune response to transplanted tissues
  • Cyclosporine and Tacrolimus suppress IL-2
  • Mycophenolate mofetil (MMF) inhibits T cell and B cell reproduction
  • Sirolimus blocks IL-2
  • Basiliximab and daclizumab block IL-2
  • (IL-2, Interleukin-2, is a cytokine that is the major growth factor for T cells)
55
Q

What is immune surveillance?

A

the recognition and removal of abnormal cells by the immune system

56
Q

What to CTL cells do?

A

Lyse cancer cells

57
Q

What did Willam Coley notice?

A

that if cancer patients contracted typhoid fever, their cancers often diminished noticably

58
Q

What is Coley’s toxin?

A

endotoxins gram-negative bacteria
stimulates TNF-production by
macrophages

59
Q

Name some immunotherapies for cancer.

A

-Coley’s toxin - therapeutic
-Vaccines - prophylactic
Human Papilloma Virus (HPV) - cervical cancer
Hepatitis B Virus (HBV) - liver cancer
Feline leukemia (FLV)
-Monoclonal antibodies
Herceptin (Trastuzumab)
a monoclonal antibody that interferes with the Her2/Neu protein, a receptor for FGF signals

60
Q

Tumor necrosis factor, IL-2 and interferons may…

A

kill cancer cells

61
Q

What do immunotoxins do?

A

link poisons with a monoclonal antibody directed at a tumor antigen

62
Q

What is congenital immunodeficiency?

A

Due to defective or missing genes
Example: DiGeorge Syndrome
aka 22q11.2 deletion syndrome
patients lack thymus

63
Q

What is acquired immunodeficiency?

A

Develop during an individual’s life

Due to drugs, cancers, and infections

64
Q

What is the origin of AIDS?

A

-HIV evolved from viruses that harmlessly infected monkeys and chimps in Africa, probably during the handling of bushmeat
-Crossed the species barrier into humans in the 1930s
-Patient who died in 1959 in Congo is the oldest
known case
-Spread in Africa as a result of urbanization
-Spread worldwide through modern transportation and unsafe sexual practices
-Norwegian sailor who died in 1976 is the first known case in Western world

65
Q

AIDS in the 80’s

A

1981: In United States, cluster of Pneumocystis and Kaposi’s sarcoma discovered in homosexual men in Los Angeles
The men showed loss of immune function, they were immunosuppressed
1983: Discovery of virus causing loss of immune function

66
Q

What is HIV?

A

primarily infects CD4+ T-cells
it is often spread by dendritic cells
memory T-cells serve as reservoirs for decades
reservoirs exist throughout the body

67
Q

Describe HIV attachement

A

the viral protein gp120
binds
CD4
as a receptor

with CCR5 or CXCR4
as a co-receptor

68
Q

Active HIV in CD4 T cells

A

provirus,
integrated into
chromosomal
DNA

69
Q

Active HIV in macrophages

A 
macrophages
actively
infected,
producing
HIV viruses
70
Q

Latent HIV infection in CD4 T cells

A

memory T-cells carrying
HIV proviruses are reservoirs inaccessible to treatment
located in
brain, lymphoid tissue, bone marrow, and the genital tract

71
Q

What is phase 1 of HIV infection?

A

Asymptomatic or chronic lymphadenopathy
millions of viruses in blood in first week
billions of infected cells in first few weeks
symptoms may be just swollen lymph nodes
lasts 3 years

72
Q

What is phase 2 of HIV infection?

A

Symptomatic; early indications of immune failure
virus replicates at a low level
T-cell decline steadily
some persistent infections

73
Q

What is phase 3 of HIV Infection?

A

AIDS indicator conditions

T-cell counts become extremely low, officially AIDS

74
Q

What are the two diagnostic methods for HIV?

A

-seroconversion takes up to 3 months
HIV antibodies detected by ELISA
HIV antigens detected by Western blotting
-Plasma viral load (PVL) is determined by PCR or nucleic acid hybridization

75
Q

Survival with HIV infection details what?

A
  • anti retroviral chemotherapy
  • some may be exposed but not infected (due to mutation in co-receptor CCR5)
  • long term nonprogressors
  • bone marrow transplants may help cure some
76
Q

Describe HIV transmission

A

HIV survives 6 hours outside a cell
HIV survives less than 1.5 days inside a cell
Infected body fluids transmit HIV via

77
Q

What are the body fluids that can transmit HIV?

A 
Sexual contact
Breast milk
Transplacental infection of fetus
Blood-contaminated needles
Organ transplants
Artificial insemination
Blood transfusion
78
Q

Why is there no HIV vaccine if it is a virus?

A

Not for the lack of trying
Mutation rate of virus in replication
Genetic diversity
Virus exposure to antibodies is brief or nonexistent
Antibody-binding sites hidden by glycosylation
Infected cells not susceptible to CTLs
Latency/Proviruses
Reservoirs in gut, bone marrow (and other places?)

79
Q

mRNA based HIV vaccine

A

-Using the same mRNA technology used for COVID-19 vaccines, Moderna developed two vaccines for HIV (still in phase 1)

80
Q

HIV chemotherapy

A

Nucleoside reverse transcriptase inhibitors
Non-nucleoside reverse transcriptase inhibitors
Protease inhibitors
Fusion inhibitors

81
Q

What is HAART?

A

Highly active antiretroviral therapy

82
Q

How does HAART work?

A

Combinations of nucleoside reverse transcriptase inhibitors plus
Non-nucleoside reverse transcriptase inhibitor or
Protease inhibitor

83
Q

A cure for HIV/AIDS?

A
  • One adult in Berlin was cured by a combination of antiviral therapy and bone marrow transplant from a person who is naturally HIV resistant (due to a mutant CCR5 co-receptor gene).
  • A baby in Mississippi was infected at birth, received a three-drug treatment within hours and was believed to be cured.
84
Q

What is the problem of HIV reservoirs in the body?

A

The ‘Mississippi baby’ was born to an HIV-positive mother who had not received any treatment during pregnancy. Doctors began treating the child by the time she was 30 hours old, but the family stopped antiretroviral therapy at 18 months. She remained off the drugs for the next 27 months with no signs of the virus in her blood.
Two months shy of her fourth birthday, her pediatricians found her HIV infection had rebounded. The young patient will now face years, if not a lifetime, of antiretroviral therapy. And researchers are now scrambling to determine how this will affect clinical trials aiming to repeat the child’s apparent cure.

Microbiology (7 decks)

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