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Block 6; Week 1-Michelle > Hunter-Innate Immunity > Flashcards

Hunter-Innate Immunity Flashcards

1
Q

What are 3 mucosal surfaces that pathogens could potentially enter?

A

airway
gut
reproductive tract

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2
Q

What are some modes of transmission via the airway mucosal surface?

A 
inhaled droplet (via sneeze)
spore
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3
Q

What are some ways that pathogens could get in via external surfaces?

A 
external surface
wounds or abrasion (punctures, infected animals)
insect bites (mosquito bites, deer tick bites)
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4
Q

Salmonella typhi in the GI could cause which disease?

A

typhoid fever

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5
Q

Rotavirus in the GI tract could cause which problem?

A

diarrhea

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6
Q

Which pathogen causes syphilis?

A

treponema pallidum

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7
Q

Which pathogen causes athlete’s foot?

A

trichophyton

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8
Q

Handling infected animals could lead to acquiring the pathogen francisella tularenis…causing which disease?

A

tularemia

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9
Q

A mosquito bite w/ flavivirus could cause which disease?

A

yellow fever

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10
Q

What are 3 potential sources of pathogens?

A

environment
humans
animals

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11
Q

If I have resistant staph in my nose….what am I considered?

A

not infected with staph

you are considered colonized by staph

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12
Q

If you have cholera are you infected?

A

No, b/c it doesn’t penetrate your tissues. You do get a disease from the exotoxins it secretes, however.

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13
Q

What are opportunistic pathogens? What is an example of when they go crazy?

A

these are pathogens that reside in or on the body but cause disease only when the host is immunosuppressed
Ex: AIDs; malnutrition

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14
Q

What are some mechanical barriers to infection of the skin?

A

epithelial cells joined by tight jcns

longitudinal flow of air

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15
Q

What is a chemical barrier to infection of the skin?

A

fatty acids
beta defensins
lamellar bodies
cathelicidin

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16
Q

What are some mechanical barriers to infection of the gut?

A

epithelial cells joined by tight jcns

longitudinal flow of fluid

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17
Q

What are some chemical barriers to infection of the gut?

A 
low pH
pepsin
alpha defensins
RegIII
cathelicidin
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18
Q

What are some mechanical barriers to infection of the lungs?

A

epithelial cells joined by tight jcns

movement of mucus by the cilia

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19
Q

What are some chemical barriers to infection of the lungs?

A

pulmonary surfactant
alpha defensins
cathelicidin

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20
Q

What are some mechanical barriers to infection of the eyes/nose/oral cavity?

A

epithelial cells joined by tight jcns
tears
nasal cilia

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21
Q

What are some chemical barriers to infection of the eyes/nose/oral cavity?

A

lysozyme in tears & saliva
histatins
beta defensins

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22
Q

How does the microbiota help defend mucosal surfaces against infection? How can you wipe this out & make a person more susceptible to infection?

A

these good bacteria keep the really bad guys from adhering to the epithelial lining
taking broad spectrum antibiotics can wipe this out & leave you vulnerable

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23
Q

What is microbial pathogenesis?

A

direct mechanism of tissue damage by pathogens

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24
Q

What is immunopathology?

A

indirect mechanisms of tissue damage by pathogens

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25
Q

What are some examples of organisms that make exotoxins?

A 
streptococcus pyogenes
staphylococcus aureus
corynebacterium diptheria
clostridium tetani
vibrio cholera
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26
Q

What are some examples of some diseases caused by exotoxins?

A 
tonsillitis
scarlet fever
toxic shock syndrome
food poisoning
diphtheria
tetanus
cholera
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27
Q

What’s the idea behind exotoxins? Are they out to get us?

A

the reason exotoxins damage us is b/c they penetrate our tissues to get to nourishment. this obviously creates a variety of diseases.

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28
Q

What is an endotoxin made of? What types of organisms make endotoxins? What do they do?

A

lipopolysaccharide
gram negative bacteria
perturb the immune system

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29
Q

E Coli, Hemophilus influenza, salmonella typhi, shigella, pseudomonas aeruginosa, yersina pestis all produce what?

A

endotoxins!

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30
Q

What are some common diseases caused by endotoxins?

A 
gram negative sepsis
meningitis
pneumonia
typhoid fever
bacillary dysentery
wound infection
plague
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31
Q

What’s the deal with a direct cytopathic effect?

A

in this case the bad guy uses the cell’s own machinery to reproduce

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32
Q

What are some examples of villains that use the direct cytopathic effect?

A 
variola
varicella-zoster
Hep B virus
polio virus
measles virus
influenza virus
herpes simplex virus
HHV8
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33
Q

What are some diseases caused by villains who use the direct cytopathic effect?

A 
smallpox
chickenpox
shingles
hepatitis
poliomyelitis
measles
influenza
cold sores
kaposi's sarcoma
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34
Q

What are some things that use immune complexes to causes immunopathology?

A 
Hep B
Malaria
streptococcus pyogenes
treponema pallidum
most acute infections
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35
Q

What are some diseases caused by immune complexes?

A 
kidney disease
vascular deposits
glomerulonephritis
kidney damage in secondary syphilis
transient renal deposits
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36
Q

What are some things that use anti-host antibodies to cause disease? As in…this things recognizes bad guys but also attacks some of the good guys.

A

streptococcus pyogenes

mycoplasma pneumonia

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37
Q

What are some diseases caused by anti-host antibodies?

A

rheumatic fever

hemolytic anemia

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38
Q

What are some infectious agents that cause problems via cell-mediated immunity?

A 
mycobacterium tuberculosis
mycobacterium leprae
lymphocytic choriomeningitis virus
borrelia Burgdorferi
schistosoma mansoni
herpes simplex virus
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39
Q

What are some diseases caused by infectious agents that use cell-mediated immunity to cause immunopathology?

A 
TB
TB leprosy
aseptic meningitis
lyme arthritis
schistosomiasis
herpes stromal keratitis
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40
Q

What is the function of anti-microbial enzymes?

A

it is to eat away the cell wall of microorganisms; a defense mechanism

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41
Q

What are 3 anti-microbial enzymes?

A

lysozyme–found in tears
pepsin–gut
secretory phospholipase A2

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42
Q

What are 3 important classes of anti-microbial peptides?

A

defensins (alpha & beta)
cathelicidins
histatins

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43
Q

What are 2 important characteristics of anti-microbial peptides? What is their fcn?

A

short peptides
amphipathic
**defensins form pores in the walls of microorganisms. Mess with the osmotic gradient & destroy them.

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44
Q

Anti-microbial peptides begin as _______.

A

pro-peptides. They are cleaved into their active forms.

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45
Q

Inflammation is a part of which immune response? When is it needed?

A

early induced immune response
**it is needed when the pathogens penetrate a bunch of barriers b/c the antimicrobial enzymes & peptides were insufficient

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46
Q

What are the 4 parts of inflammation?

A

rubor, calor, tumor, dolor

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47
Q

Describe the early induced response in detail.

A

Villains make it thru the mucosal barrier (sorry antimicrobial enzymes & peptides)
Macrophages & complement system are waiting for them.
Macrophages recognize villains via TLR genome encoded receptors on their surface.
Macrophages have a meal of the villains.
But oh no–they aren’t all destroyed!!
Macrophages release cytokines & chemokines.
Chemokines get more cells from bone marrow to enter the battle.
Cytokines cause increased vascular permeability & vasodilation.
Neutrophils & macrophages are called into battle.
Kinin & coagulation pathways activated.
Hopefully, the pathogens are conquered before the adaptive immune response has to take place.

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48
Q

What do cytokines cause? What is an example of a cytokine? How does this relate to chemokines?

A

Cytokines cause increased vascular permeability & vasodilation. Ex: TNFalpha; chemokines are a type of cytokine

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49
Q

What do chemokines do?

A

they go to the bone marrow
they recruit more cells for battle
they create a gradient by which the cells can get to the battleground (like little ‘ol bread crumbs)

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50
Q

What’s the deal with the kinin pathway?

A

causes increased vascular permeability & a sensation of pain

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51
Q

What’s the purpose of the coagulation pathway?

A

macrophages orchestrate local coagulation so that microorganisms can stay imprisoned. Don’t want inflammation to become systemic–>sepsis. Yikes!!

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52
Q

What is CXCL8?

A

aka interleukin 8

chemokine that attracts neutrophils & monocytes as a second line of defense in inflammation

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53
Q

How does the life span of macrophages & neutrophils differ?

A

macrophages come from monocytes & then chill in the tissues. They live for quite a while. Neutrophils live for like a day. They have to be actively recruited as a part of the second line of defense for inflammation.

54
Q

T/F The early induced innate response differs from the adaptive response in that it requires no new synthesis of proteins.

A

FALSE. It does require new proteins to be made.

55
Q

What are PAMPs?

A

pathogen associated molecular patterns

these are highly conserved molecular motifs found on microorganisms.

56
Q

What is an example of a PAMP?

A

Ex 1: Gram negative bacteria
lipopolysaccharide (endotoxin) can be recognized by TLR receptor on macrophage.
Ex 2: Gram positive bacteria
peptidoglycan can be recognized by TLR receptor on macrophage

57
Q

PAMPs are important for self non self discrimination. What detects these patterns? What would f-met-leu-phe indicate?

A

TLR (toll like receptors) on macrophages detect PAMPs

this indicates bacteria

58
Q

What does the PAMP of a mannose receptor indicate if detected by a TLR on a macrophage?

A

could be bacteria, fungus, virus

59
Q

If a TLR detected scavenger receptors–>which villain do they have in custody?

A

these are acetylated lipoproteins

they prob have bacteria

60
Q

What does the PAMP of a dectin-1 glucan receptor indicate?

A

fungus!

61
Q

What is CD14?

A

LPS receptor

62
Q

What does TLR4 detect?

A

gram negative bacteria

senses LPS binding protein or endotoxin

63
Q

How many common TLR genes are there in humans? What do they code for?

A

10! They code for TLR proteins-these are PAMP receptors.

64
Q

Where are TLRs found in macrophages?

A

some are on the cell surface

others are endosomal (intracellular)

65
Q

What basically happens with TLR activation?

A

this engages transcription factor NF-kappa beta

induces the production of inflammatory mediators

66
Q

What’s the deal with TLR-5?

A

this detects flaggelin–found in flagella of bacteria

67
Q

What are NOD-like proteins?

A

nucleoside oligomerization domain-like proteins
similar to TLR
detect cytoplasmic bacteria
signal inflammation

68
Q

What are RIG-like proteins?

A

Retinoic acid inducible gene-1 proteins

detect viral RNA in cytoplasm & signal inflammation

69
Q

Describe the basics of how TLR signaling induces gene transcription.

A

TLR recognizes the PAMP.
TLR dimerize on the cell surface.
They recruit IRAK-4….a lot of other stuff w/ intracellular signaling.
NFkappa beta goes into the nucleus & you get gene transcription, including cytokines that give inflammation!

70
Q

A 9-year-old girl was admitted to the hospital with septic arthritis due to Streptococcus pneumoniae. Her history was significant for previous hospitalizations for several deep-seated abscesses caused by Staphylococci or Streptococcus pyogenes. On each occasion, full blood counts were normal, including lymphocyte and neutrophil counts. Other screening tests such as functional complement, serum immunoglobulin levels, and antibody production were normal. When her peripheral blood monocytes were stimulated with a variety of Toll-like receptor ligands, they produced very low levels of the proinflammatory cytokine TNF-a. It was thought that she might have a defect in the NF-κB pathway; on sequencing of her IRAK-4 gene, this was found to be the case.
What does this patient have?

A

Interleukin 1 Receptor-Associated Kinase 4 Deficiency (IRAK4 Deficiency)
**can’t achieve inflammation–susceptible to pyogenic bacterial infections

71
Q

How is IRAK-1 deficiency inherited?

A

via aut recessive

72
Q

Give 2 diseases that are immunodeficiencies in neutrophils that are defects in intracellular killing in the form of abnormal respiratory bursts.

A

chronic granulomatous disease

Glucose-6-phosphate dehydrogenase deficiency

73
Q

Give 3 diseases that are immunodeficiencies in neutrophils that are defects in intracellular killing in the form of granule abnormalities.

A

Myeloperoxidase deficiency
Specific granule deficiency
Chédiak-Higashi syndrome

74
Q

Give 2 diseases that are immunodeficiencies in neutrophils that are adhesion defects, specifically leukocyte adhesion deficiency.

A

Type 1, integrin deficiency

Type 2, E-selectin ligand deficiency

75
Q

What is the Most Important Means of Defense Against Extracellular Bacteria, Fungi, and Protozoan Parasites?

A

phagocytosis & intracellular killing, mainly via macrophages & neutrophils

76
Q

Phagocytosis happens via______ & _______.

A

endocytosis & micropinocytosis

77
Q

What is the difference b/w a phagosome & a phagolysosome?

A

phagosome: invagination of the cell membrane
phagolysosome: is when the phagosome fuses with the lysosome & stuff can start to be destroyed

78
Q

Where is NADPH Oxidase found? What is its function?

A

found in the phagolysosome
fcn is to make this area a hostile environment with a low pH for proper degradation of the bad guys via respiratory burst & proton gradient

79
Q

What prompts the formation of the multi-unit NADPH oxidase?

A

happens with microbe phagocytosis by a macrophage or neutrophil
signaling via g protein receptors (C5a)

80
Q

What are some of the subunits of the NADPH oxidase?

A

p21
gp91
p47
p67

81
Q

Which things are released by the NADPH oxidase in the respiratory burst?

A

antimicrobial superoxide
hydrogen peroxide
ROS

82
Q

Why is it that a phagolysosome burst won’t totally kill the host?

A

b/c the enzymes contained in them are only active at a total low pH

83
Q

Once again, what types of things are found in a phagolysosome?

A 
ROS
nitric oxide
antimicrobial peptides
enzymes
competitors (lactoferrin)
84
Q

At the age of 4 weeks, a male infant develops a staphylococcal abscess of the chest wall requiring surgical incision and a course of dicloxacillin. He had a leukocytosis with 90% neutrophils. At the age of 3 months, he was readmitted to the hospital with a large abscess on his face that grew Serratia marcescens. By the age of 2 years, he had been hospitalized five times with bacterial abscesses. Family history revealed that three older brothers had died of infections at ages ranging from 7 months to 3 years, but his parents and two sisters were healthy. On examination, he had bilateral axillary and inguinal lymphadenopathy with marked hepatosplenomegaly. A dihydrorhodamine test showed that his neutrophils failed to reduce the dye and that his mother had two populations of neutrophils, one normal and one also unable to reduce dihydrorhodamine.
What does this pt have?

A

chronic granulomatous disease

85
Q

What causes chronic granulomatous disease?

A

failure of NADPH oxidase to form in phagolysosomes

86
Q

How can chronic granulomatous disease be inherited?

A

X linked recessive (gp91)

autosomal recessive

87
Q

What causes the granulomatous lesions of CGD?

A

pyogenic bacteria & fungi

88
Q

What test helps reveal CGD?

A

dihydrorhodamine test; it uses flow cytometry–>shows a defective respiratory burst b/c of a messed up NADPH oxidase

89
Q

What are some of the treatments for CGD?

A

long term antibacterial & anti fungal agents
IFN-gamma
bone marrow transplant

90
Q

T/F Granulomas can be seen on chest X-ray.

A

True.

91
Q

A 10-month-old infant presents with severe pyoderma over much of his body. His history is significant for other infections including pneumonia and for bruising easily. Both parents are healthy with no significant medical history. Physical exam reveals an ill infant with large areas of hypopigmentation of the skin, silvery hair, and very pale eyes. Gingival inflammation and bleeding of the gums and generalized lymphadenopathy are noted. A WBC count reveals moderate leukopenia and thrombocytopenia. Definitive diagnosis is made by examination of a peripheral blood smear which showed unusually large granules within neutrophils and eosinophils.
What does this patient have?

A

Chediak-Higashi Syndrome

92
Q

What is Chediak-Higashi Syndrome? How is it inherited?

A

defect in microtubule polymerization involving actin–decreases phagolysosome formation
aut recessive

93
Q

What is the presentation of Chediak-Higashi Syndrome?

A

early childhood recurrent infections of staph & strep, including gingival infections
partial albinism
large lysosomal vesicles (just can’t fuse) in neutrophils & eosinophils
see large granules on slide

94
Q

What is the treatment for Chediak-Higashi Syndrome?

A

long term antibiotics

bone marrow transplant

95
Q

What is pyoderma?

A

infection in the skin

96
Q

What is the most common defect in granulocyte-mediated host defenses?

A

neutropenia: decreased absolutely neutrophil count

can be drug-induced, autoimmune, hereditary

97
Q

What is considered a neutrophil level consistent with neutropenia? What does this leave the patient susceptible to?

A

1500-2000 cells/mm3 blood

pt susceptible to pyogenic bacteria-staph, gram negative bacteria, encapsulated bacteria, fungi

98
Q

What are 3 types of hereditary neutropenia?

A

Familial (benign, ethnic) neutropenia
Infantile genetic agranulocytosis (severe congenital neutropenia)*
Cyclic neutropenia

99
Q

What types of drugs could cause acquired neutropenia?

A

cytotoxic drugs used in cancer

100
Q

A 72-year-old man with chronic lymphocytic leukemia (CLL) presented to the cancer care clinic for a follow-up appointment 10 days after his first cycle of chemotherapy with fludarabine, cyclophosphamide, and rituximab. He complained of mild chills and a moderate fever of 100.7°F. He did not seek medical attention before his appointment because he attributed the fever to CLL. His vital signs were normal. He was found to be neutropenic with an absolute neutrophil count of 120 cells/mm3. He was treated for neutropenic sepsis with broad-spectrum antibiotics. Blood cultures showed Candida albicans
What does this patient have?

A

drug-induced neutropenia
**cancer therapy caused it.
usu get the sepsis from a catheter

101
Q

What causes the neutropenic sepsis?

A

pyogenic bacteria & fungi

102
Q

What causes 15% of sepsis?

A

candida albicans

103
Q

What is the usual treatment for drug-induced neutropenia?

A

broad-spectrum antibiotics
hrG-CSF (human recombinant granulocyte stimulating factor)
subsequent chemotherapy if pt has cancer.

104
Q

A 3-week-old lethargic male infant was brought to the ER with a skin infection. His temperature was 40.2°C , respirations 180, and blood pressure 60/35 mmHg. He was placed on fluids and broad-spectrum antibiotics. Staphylococcus aureus was cultured from both skin and blood. His absolute neutrophil count (ANC) was 174/ml. After 2 weeks in the hospital, he was improved but his neutrophils numbers were still low. A bone marrow aspirate showed a severe block in neutrophil differentiation at the promyelocyte state.
What does this patient have?

A

Severe Congenital Neutropenia (Kostmann Disease)

105
Q

How do patients with severe congenital neutropenia usu present?

A

w/ recurrent infections of skin, soft tissues, lungs and deep organs. sepsis is common.
neutrophils below 200
maturation arrent at the promyelocyte or myelocyte stage

106
Q

What is the treatment for severe congenital neutropenia?

A

rhG-CSF

bone marrow transplants

107
Q

What is there a risk of with patients with severe congenital neutropenia?

A

myelodysplasia

acute myeloid leukemia

108
Q

Once again, what are the steps to neutrophils getting to the site of injury?

A

rolling adhesion
tight binding
diapedesis
migration

109
Q

What are the 4 types of adhesion molecules?

A 
vascular addressin (CD34)
selectin
integrin
ICAM-1
110
Q

What is CD18 a component of?

A

a component of ICAM-1.

If this is messed up–>neutrophils can’t get to proper sites well

111
Q

A 2-week-old female newborn delivered at term is brought to the physician by her mother because of an increasingly severe diaper rash since birth. No congenital anomalies were noted after delivery. There are ulcerations of the skin but no purulent exudate in the area of the diaper. A culture of one of the ulcers grows Staphylococcus aureus. Physical examination shows a red and swollen umbilical remnant that has not separated. Despite antibiotic therapy, 1 month later she develops a perirectal fissure, culture of which grows Escherichia coli but a smear of which shows scarce segmented neutrophils.
What does this patient have?

A

Leukocyte Adhesion Deficiency (Type 1)

112
Q

What is Leukocyte Adhesion Deficiency (Type 1)? How is it inherited?

A

aut recessive
recurrent bacterial infections (problems with neutrophil adhesion)
omphalitis, pneumonia, gingivitis, and peritonitis may happen
CD18 is messed up.

113
Q

How do you diagnose leukocyte adhesion deficiency type 1 & how do you treat it?

A

Diagnosed by finding low CD18 on neutrophils by flow cytometry
Treatment involves bone marrow transplantation

114
Q

T/F Leukocyte adhesion deficiency type 1 shows neutropenia.

A

False. Neutrophilia. Too many neutrophils in the blood. The problem isn’t their production, but their adhesion.

115
Q

In the acute phase response…acute phase proteins are made where? What are some examples of these proteins?

A 
made in the liver
Ex:
Sp-A, Sp-D (surfactants)
mannose-binding lectin
fibrinogen (clotting)
C-reactive protein (promotes phagocytosis)
serum amyloid protein
116
Q

What prompts the liver to make acute phase proteins?

A

IL-6 released from macrophages

117
Q

C-reactive protein (CRP) is an _______, and is used to identify patients with active _____________.

A

opsonin

active inflammatory processes

118
Q

What does ferritin do?

A

binds iron to inhibit microbial growth

119
Q

How does fibrinogen indicate inflammatory levels?

A

b/c it correlates with erythrocyte sedimentation rate

120
Q

What happens to the production of albumin during the acute phase response?

A

it is down regulated

121
Q

What exactly does C-reactive protein do?

A

it binds phosphocholine on bacterial surfaces
acts as an opsonin
activates complement

122
Q

What is an opsonin?

A

a molecule that enhances phagocytosis by marking an antigen for an immune response

123
Q

What exactly does mannose-binding lectin do?

A

binds mannose residues on bacterial surfaces
opsonin!
activates complement

124
Q

Viral RNA induces expression of what?

A

inteferon alpha beta expression

125
Q

In the 2 mechanisms shown…describe the one that begins in the cytosol & ends in interferon alpha beta expression.

A

It involves MDA-5 (mazda)
RIG-1 (big rig)
CARDIF
Of course, it involves IRF3 & IRF7.

126
Q

In the 2 mechanisms shown….describe the one that begins in an endosome & ends in interferon alpha beta expression.

A

TLR-3 in the endosome w/ viral RNA
TRIF binds in cytosol
IRF3 & IRF7 involved somehow.

127
Q

Interferons are activated in virally-infected cells. What do these interferons do?

A
  • *induce resistance to viral replication
  • *increase expression of ligands for receptors on NK cells
  • *activate NK cells to kill viral-infected cells
  • *activates RNAse to kill viral & host mRNA & prompt apoptosis
  • *increases the expression of MHCI molecules on nucleated cells
128
Q

After a viral infection has begun…what is the defense @ day 1, day 3, day 8?

A

Day 1: Production of IFN-alpha, IFN-beta, IFN-gamma, TNF-alpha, IL-2
Day 3: NK-cell mediated killing of viral-infected cells
Day 8: T-cell mediated killing of infected cells

129
Q

NK cells are derived from _______ progenitor. They produce large amounts of ______. What is their fcn?

A

lymphoid progenitor
large amounts of IFN-gamma
fcn: Kill virus-infected cells, cells with intracellular pathogens, and tumors using cytotoxic granules (perforin and granzymes); Kill infected cells and tumors that express stress molecules and kill antibody-coated pathogens (antibody dependent cell-mediated cytotoxicity or ADCC

130
Q

T/F NK cells kill normal MHC Class I labeled cells.

A

False. They do kill molecules with abnormal MHC Class I labels, as in those that are infected.

131
Q

What do NK deficiencies cause?

A

Natural killer (NK) cell deficiencies increase susceptibility to severe and/or recurrent infection with herpes viruses, including varicella zoster virus, Herpes simplex viruses 1 and 2, Epstein Barr virus and cytomegalovirus

Block 6; Week 1-Michelle (6 decks)

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