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Immunology > Exam 3 > Flashcards

Exam 3 Flashcards

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1
Q

Discuss how the body develops immunity to bacterial diseases?

A

The body produces the alternative pathway, phagocytes, and lysosomes via an innate response. The body will eventually produce antibodies through the adaptive response.
The problem with the antibody production is that the bacteria often have a significant amount of subgroups and little cross reactivity, so poor antibody production for subsequent infections.

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2
Q

How does the body develop immunity to rickettsia and mycoplasma diseases?

A

Antibodies, T cells, phagocytosis, Interferon, NK activation

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3
Q

List the”febrile agglutinins” (TORCH) microbes.

A

Antibodies produced in response to certain pathogenic microbes that produce a persistent fever and are difficult to grow in the lab
Examples include: Brucella abortus, Francisella antigens, Proteus OX-19, OX-2, and OX-K antigens, Salmonella antigens

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4
Q

What is streptolysin O and why is the antibody production of concern?

A

Streptolysin O is produced by Strep A bacteria. It is heat liable and it produces holes in the RBCs. Streptolysin S is not antigenic. The antibody produced against O is cross reactive with the heart and kidneys

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5
Q

Hyaluronidase

A

Is known as spreading factor produced by Group A Beta Strep and some other microbes. The body makes anti-hyaluronidase in response

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6
Q

DNase

A

degrades deoxyribose acid. The body also makes anti-DNase

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7
Q

Explain streptozyme testing principle

A

Sheep’s RBC’s are coated with streptolysin, streptokinase, hyaluronidase, DNases and NADase. Antibodies produced against any of these substances will be detected at low sensitivity and specificity.

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8
Q

What is the immune response in Strep toxic shock syndrome?

A

Superantigens activate many T cells of different specificities

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9
Q

What would be a good test to detect glomerulonephritis caused by Strep. pyogenes?

A

Anti-DNAse

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10
Q

Which antibody is the first and second class of antibodies made in the typical immune response?

A

First class: IgM

Second class: either IgG, IgA, IgE

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11
Q

What is the laboratory diagnosis of the following fungus: Histoplasmosis, Aspergillosis, Coccidiomycosis, Blastomycosis, Sporotrichosis, and Cryptococcosis?

A

The alternative complement pathway initiates but usually a very poor response by immune system
Starting molecular testing

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12
Q

Discuss how the body’s immune system responds in parasitic diseases?

A

The normal response to any kind of infection. The phagocytes attempt to engulf the foreign invader while complement is activated and inflammation, opsonization, and lysis can occur. The APCs present to Helper T cells which activate the phagocytes and B cells. Antibodies are produced.

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13
Q

How do parasites avoid immunological responses?

A

Changing of the surface antigens

Coat themselves with the protein and Fc portion of the antibody

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14
Q

What is the etiology and definitive hosts for toxoplasmosis?

A

Toxoplasmosis is a single celled organism known as Toxoplasma gondii. Definitive host is the cat and is found in the feces. Ingestion of the eggs is the cause.

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15
Q

Acquired Toxoplasmosis infection signs and symptoms

A

Mild with mono-like symptoms. Fever, chills, headache and extreme fatigue

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16
Q

Chronic Toxoplasmosis infection signs and symptoms

A

CNS malformation or prenatal mortality. Blindness or severe neurologic sequelae may occur.

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17
Q

What is the laboratory detection methods for Toxoplasmosis?

A

Serological testing: IgM and/or IgG levels (EIA or IFA)

CSF—no testing

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18
Q

What are the complications that may arise and the tests that should be done concerning toxoplasmosis in the AIDS patient?

A

Reactivation of cerebral toxoplasmosis is a concern for HIV patients

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19
Q

A titer against a parasite is IgG/:1024 and IgM/:1024, how long ago was the infection?

A

Within the last four months

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20
Q

What is the causative agent and stages of disease for syphilis.

A 
4) stages
Primary stage
-(9) days to (3) months after infection
-Hardened charncre
Secondary Stage
-(3) weeks -(6) months after infection
-skin rash, loss of hair, malaise, mild fever
-spirochete present
Latent Period
-Up to (20) years
-Antibodies present
Tertiary phase
-Organism begins multiplying
-Create lesions that affect many organs

Specific anti-treponemogenic antibodies in early or untreated early latent syphilis are mostly IgM. The IgG antibodies follow rapidly. IgG antibodies are highest in secondary syphilis

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21
Q

Nontreponemal testing (screening):

A

RPR and VDRL
VDRL: used for CSF investigation and is a flocculation test
RPR: an agglutination test with a charcoal tag. The patient serum is mixed with cardiolipin antigen, if reagin is present, agglutination occurs.

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22
Q

Treponemal testing (confirmatory):

A

FTA-ABS (fluorescent treponemal antibody absorption. Test uses killed suspension of T. pallidum on a slide.

MHA-TP (microhemagglutination for Treponema pallidum) uses treated sheep RBCs that are coated with treponemal antigens.

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23
Q

Lyme disease

A

There is an increased suppressor cell activity and decreased killer cell activity. The diagnostic evaluation includes a bull’s eyes rash (Erythema migrans) at the bite site in about 85% of the cases and eventual antibody detection
Etiological agent: tick born Borrelia burgdorferi

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24
Q

Ehrlichiosis

A

Tickborne-Ehrlichia rickettsia (ricketsiar inclusions in leukocytes seen morula or mulberry forms) Testing: PCR or antibody titer of at least 1:80

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25
Babesiosis
Tick borne-microscopic parasite Babesiosis. Inclusions seen in RBCs Testing in PCR
26
Lyme disease stages
Primary: Slowly expanding skin lesions, erythema migrans (bullseye rash) Secondary: Target systems and organs which may include nervous system, heart, eyes, (follow a variable latent period) Tertiary: Arthritis, late neurologic complications (weeks to years after infection)
27
Syphilis Stages
Primary Stage • Chancre: Painless lesion 10‐90 days. Caused by Treponema pallidum. Treat with penicillin Secondary Stage • 1‐2 months after primary chancre disappears • Systemic Dissemination, Rash, Lymphadenopathy Latent • Lack of clinical symptoms • Congenital Syphilis Tertiary • 10‐30 years after secondary stage (if untreated) Gummas, Cardiovascular Complications, Neurosyphilis ‐
28
What are the methods for laboratory detection of human herpesvirus I and II, variceilla zoster, and human herpesvirus 6?
Herpes I and II—CPE, shell vial Variceilla zoster—shell culture, ELISA Human herpesvirus 6—immunofluorescence, PCR, and ELISA
29
What are the characteristics of cytomegalovirus and the clinical picture of the infection?
CMV alters T cell subsets. It increases CD8s and decreases CD4s. There is linkage to carcinomas
30
How can you differentiate an early primary infection of CMV from immunity status?
The primary infection will initiate the production of IgM antibodies for several months If there is only IgG antibodies an immunity status is appearing
31
What type of testing is used to diagnose a cytomegalovirus infection?
Shell vial-slow CMV antigen assay PCR
32
Explain the immunologic manifestations of infectious mononucleosis, including heterophil antibodies. Discuss the principle of the Paul-Bunnell and Davidson differential test
Guinea pig kidney absorbs out forssman and serum sickness (other heterophil) antibodies and leaves the mono antibodies to react by themselves, if present, to horse RBC's
33
Explain specific serological investigation including: anti-VCA, IgM and IgG, anti-EA-D, anti-EA-R, and anti-EBNA-IgG and the stage of the infection:
a. Anti-VCA IgM—viral capsid antigen—low amount, appears early during incubation period and disappear in 2-4 months b. Anti-VCA IgG—seen in 4-7 days after symptoms start and may persist for life c. EA-D—early antigen-n-diffuse—found in infected B-cell nucleus and cytoplasm-IgG = acute infection, disappears in about 3 months (increase in titer in reactivation). Not good indicator of disease d. EA-R-early IgG antigen-restricted—usually found only in the cytoplasmin young infections, not a good indicator of disease e. Anti-EBNA (IgG) does not appear until convalescent period f. Reactivation—IgM and IgG VCA antibodies alone with anti-EBNA IgG
34
What mono antigens are expressed on the surface of infected lymphocytes?
``` Viral capsid antigens (VCA) Early Antigen (EA) Nuclear antigen (NA) ```
35
Hepatitis A
Etiology and transmission: RNA virus with fecal oral route transmission Incubation: 2 to 6 weeks Symptoms: Often subclinical with elevated liver enzymes and bilirubin. Jaundice may appear later Diagnostic evaluation: Finding Anti-HAV. Early IgM followed by IgG
36
Hepatitis B
Etiology DNA virus (hepadna virus group), transmission by sex and body fluids Incubation: 8 - 26 weeks Symptoms: acute to fatal fulminating hepatitis Diagnostic evaluation: The virus has a double shelled outer surface and inside is a double stranded DNA. HBsAg-antigen on surface, HBcAg-antigen within shell
37
Hepatitis C
Etiology and Transmission: RNA virus, blood and body fluid transmission Incubation: 2 - 15 weeks Symptoms: Mild-severe Diagnostic evaluation: Anti-HCV (IgM or IgG)
38
Hepatitis D
Etiology and transmission RNA virus, blood and body fluid transmission Incubation: 30-50 days Symptoms: Must have Hep B (acute or carrier stage) Diagnostic evaluation: HDV antibodies (IgM, IgG)
39
Hepatitis E
Etiology and transmission RNA virus, waterborne transmission Incubation: 2-9 weeks Symptoms: Acute infections are self limited Serious if pregnant with 10-20% mortality rate Diagnostic evaluation: anti-HEV (IgG or IgM)
40
When do the following agents appear in the course of Hepatitis B testing?
* HBsAg incubation and prodrome early acute phase | * HBeAg Appears early in convalescence
41
When do the following antibodies appear in the course of Hepatitis B testing? Anti-HBc Anti - HBe Anti - Hbs
HBc - Prodrome and acute disease and remains elevated but physiologically doesn't do much. HBe - Appears early in convalescence through late convalescence. HBs - Convalescence and vaccination. Helps with immunity.
42
``` Discuss the antigens/antibodies present in the following stages of Hepatitis B incubation: Prodrome/Acute: Convalescence: Early Late ```
``` incubation: HBsAg Prodrome/Acute: HBsAg and anti-HBs and Anti- HBc Convalescence: Early anti-HBc Late anti-HBs and anti-HBc ```
43
Compare and contrast acute vs. chronic HBV infections:
Chronic HBV individuals actually have the viral DNA incorporated into their liver cell's DNA, which may lead to hepatic carcinoma Acute HBV have good T cell responses and chronic patient don't
44
Describe the etiology and epidemiology of rubella infection.
Rubella is an RNA virus in the toga virus group. It is transmitted though respiratory secretions. The greatest risk of fetal abnormalities occurs when the mother has a rubella infection is the first trimester Acquired disease cause life long immunity where the congenital levels of antibodies drops away and the individual is susceptible again The diagnostic evaluation includes the EIA method of detecting either IgM or IgG antibodies
45
How do you know if a person is probably immune to rubella:
IgG antibody present
46
How can you tell in a newborn if the baby had rubella as a fetus?
IgM antibodies
47
What is the criteria that must be met before a person can be infected with Hepatitis D?
Hepatitis D requires Hepatitis B genome to complete its' genome, therefore the patient must be infected by Hep B.
48
How are blood donor units screened to detect presence of hepatitis in order to eliminate transmission in blood products?
HbsAg, HCV, ALT
49
``` Disease Hepatitis A DNA or RNA Incubation Period Mode of Transmission Vaccine/Immunglobulin Ag's and Ab's included in diagnostic panel ```
RNA Incubation Period: 2-6 weeks Mode of Transmission: Fecal-oral Vaccine/Immunglobulin: yes/yes Ag's and Ab's included in diagnostic panel: finding Anti-HAV, IgM: early IgG: later
50
``` Disease Hepatitis B DNA or RNA Incubation Period Mode of Transmission Vaccine/Immunglobulin Ag's and Ab's included in diagnostic panel ```
DNA Incubation Period 8-26 weeks Mode of Transmission: Sexual, body fluids Vaccine/Immunglobulin: yes/Yes Ag's and Ab's included in diagnostic panel: HBcAg-present in acute infection HBs Ag-1st marker = infectivity Anti-HBs indicates immunity HBeAg correlates with infectivity, predicts severe course, chronic liver disease Anti-HBe = low infectivity
51
``` Disease Hepatitis C RNA or DNA Incubation Period: Mode of Transmission: Vaccine/Immunglobulin: Ag's and Ab's included in diagnostic panel: ```
RNA Incubation Period: 2-15 wks Mode of Transmission: Blood/body fluid Vaccine/Immunglobulin: no/no Ag's and Ab's included in diagnostic panel: Anti-HCV =infectivity or carrier state PCR
52
``` Disease Hepatitis D DNA or RNA Mode of Transmission Vaccine/Immunglobulin Ag's and Ab's included in diagnostic panel ```
RNA Mode of Transmission: body fluid/blood transmission Vaccine/Immunglobulin: yes/yes with Hep B vac and Ig Ag's and Ab's included in diagnostic panel:Anti-HDV, IgM or IgG HDVag with HBsAg
53
``` Disease Hepatitis E DNA or RNA Incubation Period Mode of Transmission Vaccine/Immunglobulin Ag's and Ab's included in diagnostic panel ```
RNA Incubation Period: 2-9 wks Mode of Transmission: Water born transmission Vaccine/Immunglobulin: no Ag's and Ab's included in diagnostic panel: Anti-HEV
54
What infectious disease transmission are we worried about in blood product transfusions for immunosuppressed individuals (newborns included) in addition to the typical screening tests?
Cytomegalovirus (CMV)
55
ELISA testing would have what type of indicator tag to reflect quantitation of an unknown. Give examples:
An enzyme would be the indicator tag | Enzymes could include: horseradish peroxidase, G6PD, alkaline phosphatase, Beta-D-galactidase
56
The most common cause of congenital infections in the United States is by what infectious agent?
Cytomegalovirus
57
Give the facts on variceilla zoster virus
Chickenpox, or varicella, is a very contagious disease caused by the varicella-zoster virus (VZV). It causes a blister-like rash, itching, tiredness, and fever. Chickenpox can be serious, especially in babies, adults, and people with weakened immune systems.
58
Explain the etiology, viral characteristics, and the epidemiology including modes of transmission of (HIV-1). Describe the immunologic manifestations and cellular abnormalities of HIV-1 infections. Include the antigen and antibody testing (screen and confirmatory) available and the specific component we are looking for in each case:
Etiology: RNA retrovirus • -Primary infection of cells in blood, mucosa • Infection established in lymphoid tissues • Spread of infection throughout the body • Immune response Viral Characteristics: A virus composed of lipid membrane structural proteins and glycoproteins that protrude from the surface Transmission: Blood and body fluids Immunologic manifestations: CD4 decreases Testing: Screen: EIA methodology for the detection of HIV 1,2 antigen and antibody • Antibody confirmation is western blot, IFA, and PCR • Antigen confirmation—neutralization test
59
What are the proteins of serologic importance in HIV testing?
p24, gp120/160, gp41
60
What T cell ratio occurs during the course of an HIV infection?
Early: CD4:CD8 (2:1) | Late CD4: CD8 (1:2)
61
In HIV western Blot testing what HIV proteins are detected to be considered a positive confirmatory test after a positive EIA test?
Gp41, Gp120/160 and/or p24

Immunology (4 decks)

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