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187 Cards in this Set

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What are the three mechanisms of tumorigenesis?
1. Introduction of new genetic material by viruses

2. Alteration of genes by radiation or chemicals
- generates a new protein
- induces genes not normally expressed

3. Chromosomal translocations
- may become permanent when an oncogene is translocated with a promoter or enhancer => permanent activation of oncogene
How do tumors differ from normal cells?
The lack of regulation of the cell cycle leads to tumor cells -- i.e. abnormal growth of cells or tissues.

See activation of oncogenes and or inactivation of tumor suppressor genes
List 5 agents of tumorigenesis and give specific examples of each.
1. Viruses
- Papillomavirus
- EBV
- Adenovirus

2. Chemicals
"ABCD"
A - aflatoxin
B - benzene
C - chloroform
D - dichlorobenzene

3. Physical agents
- ionizing radiation

4. Genetic disposition
- absence of repair mechanisms

5. Immunodeficiency
- diminished normal immune surveillance
Tumor associated antigens vs. tumor specific antigens
* Tumor associated antigens = Ag expressed following oncogenic transformation

e.g. virus induced neoantigens are shared by all tumors induced by same virus (same specificity)

* Tumor specific antigens = chemically induced neoantigens are of different specificity
TRUE or FALSE

Tumor formation may result in the re-expression of "oncofetal antigens".
TRUE
What are the two main oncofetal antigens?
* CEA (carcinoembryogenic ag)
* AFP (alpha-fetoprotein)
Increased levels vs. cancers present

* CEA
* AFP
* ß-HCG
* PSA
* CEA levels >= 2.5 and < 10.0 ng/mL are indicative of colo-rectal cancer

* AFP levels > 20ng/mL are indicative of hepatoma, non-seminal testicular, and ovarian

* ß-HCG levels elevated in WOMEN are indicative of gestational trophoblastic neoplasia

* PSA levels elevated in MEN with prostate cancer OR benign prostatic hypertrophy
What are differentiation antigens?

What is the role of these antigens in immunodiagnosis?
Certain antigens are expressed at specific stages of cellular development and differentiation.

These antigens help ascertain in which stage of development and differentiation a certain cells has arrested in -> leading to developing the appropriate therapy for it
Which is more effective in host response to tumors, CMI or humoral?
CMI
Which cells of the CMI are found to be important in immunosurveillance of tumors?
NK cells, CTL cells (tumor specific), and macrophages
TRUE or FALSE

Tumor specific antibodies may mediate antibody dependent cellular cytotoxicity
TRUE
Which cytokines induce cellular anti-tumor activity?
IL-2
IL-12

IFN-αβγ
TNF-αβ
Some antibodies may protect rather than kill tumor cells. What are they called and how do they protect tumors?
Enhancing or blocking antibodies

May function as forming complexes with soluble tumor antigen
List 5 different immunotherapies available for attacking tumors.

Which are active and which are passive?
ACTIVE:

1. Cytokines
2. LAK (lymphokine activated killer cells) -- NK cells
3. TIL (tumor infiltrating lymphocytes) -- CD8+ & NK cells
4. MAK (macrophage activated killer cells)

-----

PASSIVE:

5. Antibody
Give details as to the hypersensitivity responses mentioned below:

Type I, II, III, IV
I: IgE mediated activation of mast cells

II: Ab mediated binding of cell or tissue bound antigens

III: Ab mediated immune complexes

IV: T cell mediated DTH
Type I hypersensitivity brings about what two disorders?
* Anaphylaxis
* Allergies
If a type I hypersensitivity is not mediated by IgE, what is it called?
Anaphylactoid
Anaphylactoid responses mimic ___________ but do not involve ___________
Anaphylaxis, IgE
TRUE or FALSE

Bee stings can mimic anaphylaxis as melitin can degranulate mast cells
TRUE
Production of IgE by B cells is under the control of which cells?
Th2
IgE binds to Ag and can produce both local and systemic reactions.

Name them.
Local: wheal and flare reaction

Systemic: serious and possibly fatal
The wheal and flare reaction can be demonstrated by this method.
Prausnitz-Kustner reaction
In which units is IgE measured?

What is the normal range?
3-150 ng/ml, usually < 100
What is the normal range for IgG?
5.4 - 16.1 mg/ml, usually ~10 mg/ml
Very high levels of IgE are seen in which atopic disease?
Eczema
Allergens and IgE levels can be determined by which tests?
* Skin prick test = semi-quantitative and specific

* RAST = quantitative and specific
How is a skin prick test administered?
1. Place small drop of allergen solution on the patient's skin

2. Insert into intra-epidermis using hypodermic needle

3. Wheal and flare response = positive (+) result
What two chemicals act as positive and negative controls?
+ = histamine

- = saline
Which blocker should be discontinued prior to testing?

Which diseases preclude the test from being carried out?
H1 blockers

Eczema and other similar conditions
Name the advantages and disadvantages of the skin prick test.
Advantages:
- cheap
- results available immediately
- sensitive to Ag
- results visible to patient

Disadvantages:
- must know the procedure for these tests
How is a RAST test administered?
1. Insoluble Ag incubated in test serum to react with Ag-specific Ab

2. Then incubated in radiolabeled anti-human IgE => binds radiolabel in a specific and quantifiable way
Does RAST require knowledge of skin testing technique?

Does it require availability of allergen extracts?
No to both
Does RAST pose a risk of systemic reaction?

Can it be used with current skin conditions such as eczema, dermatitis, psoriasis?
No

Yes
Compared to the skin prick test, what are the advantages and disadvantages of RAST?
advantages: can be used on patients using antihistamines and antidepressants

disadvantages: expensive and time consuming
What is the significance of results with allergy testing?
1. results may not correlate with a clinical condition

2. one needs to have an idea what the allergen is prior to testing

3. positive result DOES NOT correlate with improvement in condition
Transmission of atopicity is ____________ and ____________
multigenic and autosomal
Which antigens elicit strong IgE responses?
penicillin

certain pollens
What determines a protein to be an allergen?
It's shape and surface features
TRUE or FALSE

Repeated exposure is necessary for an allergy to develop.
TRUE
List some of the common allergens.

* Airborne
* Food
AIRBORNE
- grass, tree pollen
- mold spores
- animal dander
- house-dust mite

FOOD
- fish/shellfish
- eggs
- peanuts
- milk
- gluten
This type of mast cells occurs in the skin, intestinal submucosa, breast, and axillary lymph nodes
MC-TC
This type of mast cells occur in the lung and intestinal mucosa.
MC-T
Mast cells contain these type of proteinases
* tryptase
* chymase
This humoral cell type is associated with an inflammatory response to helminth parasites.

Name the two major proteins it contains.
Eosinophils

Major basic protein (MBP)
Major cationic protein (MCP)
Regulation of eosinophils appear to be controlled by ________ and ________
IL-5
Eotaxin
IgE attaches to eosinophills through this receptor.
Fc-RII (CD23)
The cross-linking of this molecule on the surface of mast cells and basophils results in mediators and cytokines.
Fc-RI
Basophils and mast cells release two types of mediators. Name them.
* preformed mediators (incl. biogenic amines)

* newly synthesized mediators
Name a preformed mediator (biogenic amine).
Histamine
Histamine binds to which target cell receptors?
H1, H2, H3, H4
What are the effects of histamine?
1. smooth muscle contraction resulting in increased peristalsis of gut & bronchospasms in lung

2. vasodilation: large vessels constricted & small ones dilated -> "blushing effect"
List some of the newly formed mast cell mediators.
* PGD2 = vasodilation, smooth muscle contraction

* LTC4/LTD4/LTE4 = vasodilation, smooth muscle contraction

* PAF = vasoconstriction, increased permeability
These mediators have similar effects to histamine but over a much longer period of time

AND

are responsible for much of the late phase response to anaphylaxis

LIPOXYGENASE PATHWAY
Leukotrienes

LTC4, LTD4, LTE4
This group of mediators causes contraction of cardiac and smooth muscle

AND

it can activate many leukocytes inclduing platelets and mast cells
PAF
This group of mediators causes contractions of smooth muscle

AND

acts as a vasoldilator and bronchoconstrictor

AND

will stimulate pain and stimulate the hypothamalus to induce fever

CYCLOOXYGENASE PATHWAY
Prostaglandin D2
What is the treatment for anaphylactic shock?

What helps to alleviate the late phase response?
Epinephrine

Corticosteroids
This drug acts as a mast cell stabilizer for asthma and other respiratory conditions.
Sodium cromoglycate
Name four ways that type II hypersensitivity causes damage.

Give examples of each.
1. activate complement leading to cell damage == immune thrombocytopenic purpura (ITP), intravascular autoimmune hemolytic anemia

2. activate ADCC for cytotoxic cell attack == autoimmune thyroiditis

3. antibodies induce phagocytosis of target cells. This occurs when M cells destroy red cells in the spleen and liver == extravascular autoimmune hemolytic anemia

4. Bind to receptors to either:

activate the function of a cell or organ == hyperthyroidism

OR

switch off the function of a cell or organ == hypothyroidism
Name the different immunological conditions that bring about type III hypersensitivity.
1. large amount of Ag and Ab accumulate creating a lattice

2. Ab-Ag complexes do not activate the classical complement cascade == complement deficiency

3. Ab-Ag complexes evade activation of the classical complement pathway
TRUE or FALSE

Immune complexes circulate throughout the body and are deposited in various sites, most notably: kidneys, joints, skin
TRUE
Immune complexes activate and recruit what?
activate complement (through IgM, IgG3,1,2) and directly or indirectly recruit a number of inflammatory cells (neutrophils, M)
How does the immune system protect against immune complexes?
* The complement cascade and M cells act to remove IC.

* Erythrocytes carry away IC using CR1 to the liver and spleen

* M cells attach to the IC using FcR and carry out phagocytosis
What are the basic clinical and immunological characteristics of Lupus?
It affects the vasculature, kidneys, skin, joints, CNS, serous tissue

It's incidence approaches 1:2500 in the general population

Higher in females between menarche and menopause

*** Numerous ANAs will be found in Lupus
What is the difference between Serum sickness and Arthus reaction?
Arthus reaction (LOCAL):
local tissue bound type III reaction that occurs after IM injection of antigens

= pain and necrosis

Serum sickness (SYSTEMIC):
problem occurs when equine antiserum for bacterial toxins is administered.

after subsequent administration, arthritis, myalgia, malaise, fever occur

= IC may activate complement, release anaphylatoxins and cause mast cell degranulation
Differentiate between glomerulonephritis due to Goodpasture's syndrome and that due to the Lupus
GOODPASTURE'S SYNDROME
Ab cross-reacts with the glomerular basement membrane and the alveolar basement membrane (type II)

linear deposition of IgG along the glomerular basement membrane

LUPUS
clumps of immune complex deposited on the glomerular basement membrane that have a "lumpy-bumpy" appearance
What is the mechanism operating in type IV hypersensitivity?
Immune response mediated by CD4+ T cells -- archetypal Th1 response

In some situations CD8+ T cells are also recruited. As expected from Th1 cells, the "effector cells" are largely M.
DTH is a major immune response against tissues or organs that the body detects as dangerous. Name them.

What are some of the common conditions in which type IV takes place?
DTH acts against solid organ transplants (heart, liver, kidney) and solid tumors.

Acute:
- poison ivy
- hair dye
- nickel
- cement
- cosmetics
- latex
The substances that induce contact hypersensitivity are usually ____________
haptens
What is the function of type I hypersensitivity?
As an anaphylactic reaction, it rids the body of parasites and tapeworms
An individual who has an allergy is _____________
Atopic
TRUE or FALSE

Diseases can occur in isolation but they can also present with a mixture of hypersensitivity responses.
TRUE
Name a anaphylactoid responses.
Bee stings can mimic anaphylaxis!
IgE binds to which receptor on mast cells and basophils?
FcER
What is worrying about type I hypersensitivity?
It can sometimes have a late phase reaction that occurs about 2 hours later and peaks at about 24 hours.
TRUE or FALSE

The presence of staph aureus in the skin can exacerbate eczema in 50% of the cases
TRUE
TRUE or FALSE

Children of atopic parents show greater likelihood of also being atopic
TRUE
These cytokines induce the production of IgE
IL-4, IL-13
Name two important allergens that cause a reaction in people.
Penicillin
Pollen antigen
What are the four fungi cell types?
1. Yeasts (single celled)
2. Molds (filamentous)
3. Dimorphic (filamentous -> yeast)
4. mushroom, puffballs (filamentous cells organized into visible fruiting bodies)
Describe the general cell structure of the fungi.

* general
* membrane
* cell wall
GENERAL
eukaryotic cells with all of the organelles intact

MEMBRANE
made up of "ERGOSTEROL", a major sterol membrane

CELL WALL
complex carbohydrate composed of "chitin with glucan" and mannose-proteins
Which parts of the fungi cell are targets of anti-fungal drugs?
ergosterol membrane
cell wall glucan
Define the following terms:

Saprobes/saprophytes
Symbionts
Commensals
Parasites
* Saprobes/saprophytes
fungus living on dead organic material == breakdown wide range of organic materials including CELLULOSE

* Symbionts
benefit each other (lichens = combination of fungus with algae)

* Commensals
2 organisms living together where one benefits; other not harmed

* Parasites
2 organisms living together; one not benefiting and in cases harmed
Name the two routes that most fungi infect us by?
1. airborne spores
2. traumatic implantation
Define the following:

* yeast, hyphae, pseudohyphae
yeast: single celled fungi

hyphae: septate or aseptate filament of a fungus

pseudohyphae: chains of cells formed by budding that, when elongated, resemble true hyphae; they differ from true hyphae by being constricted at the septa, forming branches that begin with a septation, and having terminal cells smaller than the other cells.
Define.

* dimorphic fungi
Alternate between hyphal and yeast forms depending on environmental conditions

yeast @ 37C on enriched media
hyphae @ 30C or lower on most media == "if it's cold, it's mold"
Define.

* septate and aseptate
filamentous fungi have one of these two types of hyphae

ASEPTATE
- lack regular cross walls
- width is irregular
- RAPID GROWTH
- serious opportunists -> fatal overnight
- phylum: zygomycota

SEPTATE
- has cross walls
- UNIFORM WIDTH
- most of the filamentous fungi fall under this heading
Define.

* dematiaceous and hyaline
There are 2 basic colors for hyphase

dematiaceous = dark
hyaline = colorless
Which type of hyphae is known for its rapid growth?

Which one is known for its uniform width?
aseptate = rapid growth
septate = uniform width
In order to see the basic colors of hyphae, what must one do to the microscope?
Lower it light output
Name the four major dimorphic pathogenic genera found in the US general population
"Blasted Cocci Spread Histo"

Blastomyces
Coccidioides
Sporothrix
Histoplasma
Describe Candida albicans.

* yeast?
* does it have hyphae and/or pseudohyphae?
* part of normal flora?
* opportunistic?
* major cause of nosocomial bloodstream infections?
* drug resistance a problem?
* yeast
* both hyphae and pseudohyphae
* normal flora
* opportunistic
* causes nosocomial infections
* drug resistance seen in several Candida species
Define.

blastoconidia and conidia
Both are spores

* blastoconidia = blastospores = buds (asexual spores)

* conidia = spore bearing stalks
- microconidia (small) or macroconidia (large)
Which of the following is used for ID of fungal cultures?

blastoconidia or conidia
conidia
Name the four ways that fungi cause disease.

Give examples for each.
1. infections
- mycoses
- adherence and invasion of tissue

2. allergy
- airborne spores

3. mycotoxicosis
- alfatoxin in stored peanuts

4. poisonings
- poisonous mushroom ingestion
- fermentation of carbs -> alcoholism
How do we acquire fungal infections?
* Immune system plays important role in whether we get sick or not from our exposures

* Cell-mediated immunity is most important
How do we diagnose fungal infections?
1. Direct detection with special fungal stains

2. Fungal cultures and antifungal susceptibilities

3. Serology: pt. Ab to fungus for system

4. Genetic probes

5. Skin testing: exposure or anergy?
Name the fungal stains used for detection and the color of the fungi as a result.
Gomori silver stain - black
Periodic Acid Schiff - pink
Calcofluor - white
Immunofluorescents - ?
What is the classical treatment for Goodpasture's syndrome?
Removal of the antibody through plasmapheresis can be of great value

plasmapheresis == rotating the blood quickly allowing the plasma to rise to the top and removing it automatically

e.g. see cows and milk
Name a disease associated with type III hypersensitivity and the build-up of immune complexe lattice.
Henoch-Schonlein Purpura

- IgA forms IC
- demonstrated in respiratory infection where IC builds up in skin, gut, kidney
- leads to PURPURA
This fungal culture is a gold standard used through labs
Sabouraud's
TRUE or FALSE

Enriched media with antibiotics and cycloheximide is used as a fungal culture
TRUE
For disease to occur the autoantibody titer is usually ___________ and it must be the ___________ type.
high, correct
___________ is associated with disease or can actually be involved in pathology
antibodies
Name three diseases in which T cells are involved in the pathogenesis.
1. Insulin dependent diabetes mellitus (type 1 IDDM)

2. Hashimoto's thyroiditis

3. Multiple sclerosis
TRUE OR FALSE

If a patient has one organ specific autoimmune disease, they have a higher than normal chance of having another autoimmune disease at another site.
TRUE
Which autoantibodies is usually present in autoimmune diseases?
IgG
Type IV hypersensitivity is mediated by ________ (CD4+/CD8+) T cells of the _______ (Th1/Th2) type
CD4+, Th1
What are the factors behind autoimmunity?
1. Exposure to pathogen or stimulus

2. Genetics

3. Gender, age, hormones
There is evidence that the following disease are linked to previous viral or bacterial exposures:
1. Type 1 IDDM
2. Multiple sclerosis
3. DeQuervain's thyroiditis
4. Guillain-Barre syndrome
Describe MS.
- episodes of neurological defects, separated in time, attributable to demyelinating white matter lesions that are separated in space.

- alternating relapses, remissions
- cell immunity directed against myelin proteins (MBP)
- more common at higher latitudes but migration to lower latitudes before age 15 decreases risk = some benefit from vitamin D

- presence of oligoclonal bands in CSF = found in tertiary syphilis, SSPE, and rubeola infections
Describe deQuervain's thyroiditis.
Mimics symptoms of autoimmune thyroiditis due to a known viral infection
Describe Guillain-Barre syndrome.
- acute inflammatory demyelinating polyneuropathy
- ascending paralysis

+ associated with CMV, EBV, and C. Jejuni
Why do infections initiate autoimmunity?
1. Molecular mimicry = cross reacts with self Ag leading to an autoimmune disease

2. Disruption of cell or tissue barrier = if organism can break down immunoprivileged site, then autoimmune response can occur against the sequestered self-ag
What is an example of disruption of cell or tissue barrier?
Mumps or orchitis leading to male sterility
Name two 'reactive arthritides' diseases.

What are the commonly associated with?

What are negatively associated with?
Ankylosing spondylitis, Reiter's syndrome

Associated with HLA-B27

Negatively associated for RF (seronegative arthritides)
Describe ankylosing spondylitis.
Chronic inflammatory disease affecting the vertebrae and sacroiliac joints
What are the triad of symptoms associated with Reiter's syndrome?
"Can't see, can't pee, can't climb a tree"

- Arthritis
- Non-gonococcal urethritis
- Conjunctivitis
Which bacterial infections is associated with AR and which with RS?
AR = Klebsiella spp.
RS = Chlamydia Trachomatis
What is the association between Type 1 IDDM and HLA?
HLA-DR3, HLA-DR4
These two disease are linked to gender instead of genetics for their autoimmunity manifestations.
- Lupus
- Pemphigus vulgaris
This autoimmune disease is always associated with pregnancy.
Herpes Gestationis
Define primary and secondary immunodeficiencies.
Primary: idiopathic; as not being secondary to an infection, malignancy, or drugs

Secondary: acquired during life and are subsequents to other disease, condition, or therapy
What is the DiGeorge Syndrome?

What are some of the physical manifestations?
Congenital thymic hypoplasia due to incomplete development of 3/4 pharyngeal pouches

- abnormal facies, hypoparathyroidism, CHD
What is the Wiskott-Aldrich syndrome?
- x-linked disease

- WASp (protein) functions as a bridge between signaling and movement of actin filament in the cytoskeleton

- limited to hematopoietic lineages
What is WAS characterized by?
- Thrombocytopenia
- Eczema
- Immunodeficiency (increased bacterial or viral infections)
What is CVI (common variable immunodeficiency)?

When does it occur in life?

What are the complications of this condition?
low total IgG, IgA levels

3rd, 4th decade of life

infections and lymphoma (bacterial infections)
What is the most common primary immunodeficiency disease?

Are there IgE levels high or low?

Are they susceptible to allergies?

What might they develop if given blood products containing IgA?
Selective IgA deficiency

High IgE

Susceptible to allergies

Develop anaphylaxis if given IgA with blood products
What is Bruton's Disease?
- mutation in gene coding for Bruton tyrosine kinase (BTK)

- BTK is critical to the maturation of pre-B cells to mature B cells

- These pts have NO PLASMA CELLS and NO SERUM ANTIBODIES
What bacterial infections do Bruton's Disease pts suffer from?

To which therapy do patients respond to?
Encapsulated bacteria
- S. pneumoniae
- H. Influenzae

Gamma-globulin therapy
What is the marker for SCID?

What is the only hope for these patients?
Low T cell count

Bone marrow transplant or enzyme replacement
Lack of C1 inhibitor causes what disease?

What is the most feared complication of HAE?
Hereditary angioedema (HAE): an acute swelling of subcutaneous or submucosal tissue

Laryngeal edema
C1 inhibitor inhibits the components of what pathways?
Fibrinolytic, clotting, and kinin pathways
A deficiency of C5, C6, C7, C8 is associated with which infection?
Neisseria infection = gram negative (-)
Name a primary phagocyte deficiency.

What is it deficient in?

What infections take advantage of this?

How can it be detected?
CGD (chronic granulomatous disease)

It lacks the ability to carry out a oxidative burst

Gram negative (-) = S. aureus, Enterobacteriaceae

By NBT (nitro-blue tetrazolium) = goes from yellow to blue
Name two opportunistic infections.
PCP (pneumocystis jiroveci)

M. avium complex (MAC)
Give the definitions for the following:

Allograft
Isograft
Autologous
Homograft
Xenograft
Allograft: genetically distinct individuals of the same species

Isograft: genetically identical individuals (twins) of the same species

Autologous: transplants within one individual

Homograft: graft from same species

Xenograft: graft from another species
Rejectin is an immunological process with both _________ and ___________
memory, specificity
For optimal graft outcome, compatibility at 3 HLA loci is needed. What are they?
HLA-A, HLA-B, HLA-C
For related donors, what technique is used to confirm a match?
Mixed lymphocyte reaction (MLR)
Name the typing carried out on elective transplant.

Name the typing carried out on cadaver transplants.
HLA typing

ABO tpying
What is the mixed lymphocyte reaction (MLR)?
Donor and recipient cells cultured together.

- if compatible, nothing happens otherwise cells will proliferate

- measured by uptake of H3-thymidine
Why is mixed lymphocyte reaction important for bone marrow transfer?

What test is carried out to assure not alloreactivity occurs?
Because we could have a graft versus host disease (GVHD) come up.

one way MLC = irradiation of both donor and recipient cells, if no proliferation, then a match
Name a minor histocompatibility gene influencing graft rejection.
HY proteins on encoded on the Y chromosome can become a problem if the donor is male and recipient female

LEADS TO REJECTION
What are the immunological steps in graft rejection?
1. CD4+ of Th1 type initiate DTH (type IV)

2. CD8+ and NK cells kill donor cells

3. Ab give rise to complement activation and ADCC
What type of hypersensitivity is witnessed by:

xenografts
allografts
xenografts = type III

allografts = type II
In a bone marrow transplant, GVHD can occur.

What does GVHD attack in the recipient?
- skin (blister)
- gut (slough)
- liver (hepatitis)
What is the difference between:

Acute GVH
Chronic GVH
Acute GVH = difficult to treat once established

Chronic GVH = attack similar sites to acute GVHD; symptoms similar to autoimmune diseases
TRUE OR FALSE

Skin is a major barrier against infection
TRUE
How does skin defend against infection?
- fatty acids inhibit microbial growth

- bacterial commensals on the surface as part of the normal flora
What are three expulsion mechanisms for getting rid of pathogens?
1. cough and sneeze reflex
2. vomiting and diarrhea
3. urinary flow
Eczema is exacerbated by the presence of ______________ on the skin
S. aureus
High body temperature inhibits the growth of ______________
M. leprae
Poliovirus resides in the gut without causing disease but only when it reaches the __________ does paralysis occur
CNS
What is the virulent version of E. coli
O157:H7
What is vertical transmission?

What is horizontal transmission?
vertical transmission is from mother to offspring

horizontal transmission is human to human via:

- respiratory
- oral/fecal
- sexual
- direct contact (not common)
Name the cell surface CD that the following viruses attach to:

HIV
Rhinovirus
Measles
HIV - CD4
Rhinovirus - CD54 (ICAM-1)
Measles - CD46
Define Obligate intracellular pathogens.

What are some viruses or parasites that belong to this group?
Must invade and replicate only inside cells

VIRUSES, RICKETTSIAS, CHLAMYDIAE are examples
Contrast bacteremia and septicemia.
Bacteremia: presence of viable bacteria circulating in bloodstream

Septicemia: systemic disease associated w/ presence and persistence of pathogenic microorganism or their toxins in the bloodstream
S. aureus releases this toxin and it is associated with this condition.

Is the toxin a superantigen?
SEB, food poisoning

Yes, it is a superantigen
Superantigens are mostly produced by gram __________ bacteria.

They stimulate ___________ to become activated and produce _________ and _________

Superantigens have local effects as in ______ but have systemic effects as in ____________
positive

IFN-gamma, TNF-alpha

local = SEB
systemic = toxic shock syndrome
What are intrinsic virulence factors?

Name one produced by E. coli O157:H7. What does it cause?
They are encoded on genes carried on the chromosome of a bacteriophage

Shiga-like toxin, HUS (hemolytic uremic syndrome) in children
Activation of MAC is effective against gram ___________ bacteria
negative and less so against gram (+)
Neutrophils secrete which cytokine?

What is it useful for?
IL-12, producing Th1 response (and type IV hs)
Opsonization by complement will utilize which complement receptors?
CR3, CR4
This cytokine recruits neutrophils to sites of inection.
IL-8
These cytokines can cause inflammation and initiate acute phase response
IL1, IL-6, TNF
During septicemia ___________ numbers soar and are causes for the production of pus during pyogenic infection
neutrophils
_____________ binds to the C protein of penumococci and activates the classical complement pathway.

Is this a useful marker in suspected bacterial infections
C reactive protein (CRP)

Yes, definitely!
Superantigens stimulate host T cells only if they have the correct TCR type, what is it?
TCR Vβ
Name two superantigens causing a response
SEB = s. aureus, food poisoning

TSST-1 = toxic shock syndrome
Associate the theory with the immunity:

Innate, acquired
stranger theory, danger theory
Innate = stranger

Acquired = danger
Innate immune system is activated by these macromolecules on microbes
PRRs
TLR4 binds to what?
Gram (-) LPS
TLR2 binds to what?
Gram (+) cell walls
_________ from damaged cells can activate the immune system
Uric acid
Which Igs can activate complement and which can acts as opsonins?
Opsonins = IgG 1,3,4 and IgA

Activate complement = IgG 3,1,2, IgM
Humans produce twice as much ________ (Ig) as all other Ab combined.
IgA
This type of hypersensitivity reaction is geared towards protozoa, tuberculosis.
Type IV (DTH)
This type of hypersensitivity reaction is geared towards intestinal parasites.
Type I
M. leprae has to extreme forms, name them and which T cell helper is associated with each?
Lepromatous leprosy (LL) = IgG, poor cellular response, Th2

Tuberculoid leprosy (TT) = macrophage, strong cellular response, Th1
Effective resistance to many fungi is a _________ (Th1/Th2) response
Th1
What is a Th2 response associated with (w/ respect to fungi)?

Can it cause pathology?

It can result in the production of ____________.
Susceptibility to fungal infection

Yes

IgE
If an immunodeficient individual is unable to produce the required Th1 response to fungal infection, what occurs?
Some will produce a Th2 response allowing the infection to spread and induce IgE to the fungus

ABPA (allergic bronchopulmonary aspergillosis) occurs!
Which MHC classes do each of the IFNs upregulate?
IFN-αβ = MHC I

IFN-γ = MHC II
IgA can enhance virus infectivity in some situations.

Which viruses take advantage of this opportunity?
- Dengue
- RSV
EBV (HHV-4) infecs B cells via this CD marker.
CD21 / CR2
How does EBV work?
1. Attacking T cells become activates -> begin looking like monocytes

2. CD8+ cells kill B cells

3. Continue killing of B cells results in their proliferation and ultimately B cell lymphoma