Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
252 Cards in this Set
- Front
- Back
|
Which type of staining should be used for Mycobacterium (they turn red)?
|
Acid Fast (Ziehl-Neelsen)
|
|
|
Which medium should Mycobacterium be grown on?
|
Lowenstein-Jensen medium (egg based). They grown very slow and could take up to 8 weeks for isolation
|
|
|
Can Mycobacterium leprae be cultured?
|
Nope.
|
|
|
What is the most common cause of infection-related mortality?
|
TB
|
|
|
What are the 2 virulence factors of Mycobacterium tuberculosis and what do they do?
|
Cording Factor (inhibits PMN granulation and induces granuloma formation) and sulfatides (glycolipids that inhibit phagocytosis)
|
|
|
Where is cording factor derived from?
|
Mycolic acid
|
|
|
What is Ghon's complex?
|
Lesions in the lungs caused by Mycobacterium tuberculosis. May calcify.
|
|
|
Name 3 types of Mycobacterium tuberculosis infections
|
Resolution, latent, progressive primary
|
|
|
A progressive primary infection of Mycobacterium tuberculosis can lead to a systemic infection referred to as...?
|
Miliary tuberculosis. Usually high mortality and occurs in compromised subjects.
|
|
|
What is hemoptysis and which bacterium is it associated with?
|
Bloody sputum, Mycobacterium tuberculosis
|
|
|
Which bacterium causes Pott's disease of the spine?
|
Mycobacterium tuberculosis
|
|
|
What is scrofula?
|
Infected, caseating lymph nodes, draining sinuses
|
|
|
What test allows you to determine the species of Mycobacterium tuberculosis?
|
Nucleic acid probe hybridization
|
|
|
What type of reaction is the PPD skin test for TB testing?
|
Delayed-type hypersensitivity reaction (Th1)
|
|
|
An induration of ____ mm or more in a TB skin test is a positive reading for anyone
|
15
|
|
|
For HCWs, an induration of ___ mm is positive for a TB skin test
|
10. Unless there is known exposure, then it is 5 mm
|
|
|
In an aim to prevent resistant strains, ______ must be treated with 2 drugs for several months.
|
Tuberculosis. Do 4 drugs for 8 weeks, then 2 (continuation phase)
|
|
|
Name 4 primary anti-TB drugs
|
Ethambutol, pyrazinamide, isoniazid, and rifampin. These have many side effects.
|
|
|
Name 2 secondary anti-TB drugs
|
Amikacin and kanamycin. Less potent, less toxic, but more expensive.
|
|
|
What drug is given to asymptomatic patients with a positive TB test?
|
Isoniazid for 9 months
|
|
|
What is XDR-TB?
|
Mycobacterium tuberculosis that is resistant to all 1st and 2nd line drugs. It is extremely difficult to treat and there were 4 cases in the US in 2008.
|
|
|
What are the 3 criteria for a patient with TB to be considered non-contagious?
|
When they have received adequate treatment for 2 weeks or longer, symptoms have improved, and they have had 3 consecutive negative sputum smears, all taken in 8-24 hour intervals
|
|
|
The vaccination for which bacteria is of species bovis and is a BCG vaccination?
|
Mycobacterium tuberculosis
|
|
|
What does MOTT stand for?
|
Mycobacterium other than tuberculosis
|
|
|
Which MOTT is most commonly isolated and what is its reservoir?
|
Mycobacterium avium-intercellulare. Birds and mammals
|
|
|
Which bacteria is usually only found in AIDS, or otherwise compromised, patients, presents as COPD, and highly resistant to drugs?
|
Mycobacterium avium-intercullulare
|
|
|
What shape and staining qualities do Mycobacterium leprae have?
|
Acid fast (red) bacillus
|
|
|
What is the incubation time of Mycobacterium leprae?
|
5 years or more
|
|
|
What are the 2 forms of leprosy and what are their characteristics?
|
Tuberculoid (Mild, good Th1 response) and lepromatous (poor response, severely disfiguring disease)
|
|
|
Up to 60% of patients with _______ exhibit oral lesions
|
Lepramatous leprosy
|
|
|
Which 4 drugs are recommended to treat Mycobacterium leprae? What new drug has been found to be very effective?
|
Rifampin, ofloxacin, minocycline, and dapsone. Moxifloxacine.
|
|
|
Are spirochetes Gm- or Gm+?
|
Gm-, but not visualized with gram stain. Silver stain used instead.
|
|
|
Which spiral, anaerobic bacteria cannot be cultured on a medium and has been implicated in periodontal disease?
|
Treponema pallidum (syphilis)
|
|
|
What are the 5 clinical stages of syphilis?
|
Primary, secondary, latent, tertiary, congenital
|
|
|
What is a primary syphilis lesion called?
|
A chancre. They are usually painless and highly infectious
|
|
|
What are the symptoms, timeline, and characteristics of secondary syphilis infections?
|
Occurs in 1/4 of infected 2-10 weeks after primary infection, still infectious. Symptoms include a skin rash (EVEN ON PALMS AND SOLES), mucous patches, fever, and warts called condylomata lata
|
|
|
What percentage of patients with untreated secondary syphilis develop latent syphilis?
|
15%. There are no symptoms and it's infectious for 4 years.
|
|
|
What is a gumma?
|
A painless lesion from a tertiary syphilis infection. They are highly destructive. It's very hard to visualize spirochetes in them.
|
|
|
What is a perforated pallet, Charcot's joints, and an aortic aneurysm characteristic of?
|
Tertiary syphilis
|
|
|
What is general paresis?
|
A form of late tertiary neurosyphilis resulting in brain cortex degeneration
|
|
|
What is Tabes dorsalis?
|
A form of tertiary neurosyphilis resulting in damage to the dorsal root ganglia, ataxia, and loss of sensation
|
|
|
How can congenital syphilis be prevented?
|
Antibiotic treatment of the mother
|
|
|
Which 5 craniofacial abnormalities are associated with congenital syphilis?
|
Hutchinson's teeth, Mulberry (Moon's) molars, mucous patches, perforated palate, and saddle nose
|
|
|
What are the characteristics of Hutchinson's teeth?
|
Permanent incisors end up being wider mesiodistally at the cervical aspect than the incisal and having a crescent shaped notch on the incisal edge.
|
|
|
Which teeth are affected by Mulberry Molar and which disease causes it?
|
Permanent first molars and congenital syphilis.
|
|
|
What is DOC for Treponema pallidum?
|
Penicillin
|
|
|
What bacteria is associated with a Jarisch-Herxheimer reaction and what causes it?
|
Treponema pallidum. Too many spirochetes are killed at once, compromising cell walls
|
|
|
How can a patient be declared cured from syphilis?
|
Non-treponemal titers decline, treponemal titers remain positive
|
|
|
What is Yaws?
|
An African skin disease caused by Treponema pallidum subspecies pertenue.
|
|
|
What is Pinta?
|
A South American skin disease caused by Treponema pallidum subspecies carateum
|
|
|
Name a Treponema that is normal oral flora, but linked to periodontal disease
|
Treponema denticola
|
|
|
Which bacteria causes endemic relapsing fever in the western US, has a rodent and tick vector? What is DOC?
|
Borrelia hermsii. DOC is tetracycline
|
|
|
Which bacteria causes epidemic relapsing fever in Africa and has body louse vector?
|
Borrelia recurrentis. DOC is tetracycline
|
|
|
Which bacteria causes Lyme disease?
|
Borrelia burgdorferi
|
|
|
What is erythema migrans and which disease/bacteria is it associated with?
|
It is a concentric circle skin rash associated with Borrelia burgdorferi (Lyme disease)
|
|
|
Which 3 complications can untreated (late) Lyme disease cause?
|
Meningitis, arthritis, acute arthritis
|
|
|
Diagnosis of Lyme disease...?
|
Serology, silver stain
|
|
|
DOC for early stage Lyme disease?
|
Tetracycline
|
|
|
DOC for late stage Lyme disease?
|
Ceftriaxone
|
|
|
What are the 4 basic principles of antimicrobial therapy? The agent should...
|
1. Show selective toxicity 2. Reach the site of infection 3. Penetrate and bind target 4. Have low propensity for resistance against
|
|
|
Name 4 routes of administration
|
Local or topical, parenteral, systemic, direct
|
|
|
Name 3 drugs metabolized by liver
|
Chloramphenicol, tetracycline, erythromycin
|
|
|
True or false: Most antibiotics are excreted in the urine in inactive form
|
False. They are usually excreted in active form.
|
|
|
Name the 4 types of anti-bacterial agents
|
Bacterial cell wall synthesis inhibitors, protein synthesis inhibitors, nucleic acid synthesis inhibitors, and antimetabolites
|
|
|
List bacterial cell wall synthesis inhibitors
|
Beta lactam antibiotics (ie penicillin, cephalosporins), vancomycin, bacitracin, cycloserine, and isoniazid (affects mycolic acid synthesis)
|
|
|
Which enzymes do beta lactam antibiotics bind to and inhibit? What is their function?
|
Penicillin binding proteins (PBP). They cross-link bacterial cell wall proteins. Transpepotidase links NAM and NAG
|
|
|
Penicillin has the highest incidence of drug allergy. What percentage of those sensitive to penicillin are also sensitive to cephalosporins?
|
10%.
|
|
|
Name 1 beta-lactamase resistant penicillin
|
Methicillin
|
|
|
What is Augmentin?
|
A drug that inhibits beta-lactamase. Commonly given with amoxicillin (in animals too, fun fact. It's called Clavamox)
|
|
|
What kind of bacteria do penicillins work on?
|
Gram positive cocci
|
|
|
What kind of bacteria do 1st gen. cephalosporins work on?
|
Gm+ cocci, some Gm-
|
|
|
What kind of bacteria do 2nd gen. cephalosporins work on?
|
Gm+ cocci, extended Gm-
|
|
|
What kind of bacteria do 1st gen. cephalosporins work on?
|
Gm- bacilli
|
|
|
Which generation(s) of cephalosporins are beta-lactamase resistant?
|
2nd and 3rd (Ceftriaxone is a 3rd)
|
|
|
Mechanism of vancomycin?
|
Binds D-ala D-ala residues to shut down cell wall synthesis. Works on many Gm+ cocci, bacilli
|
|
|
Mechanism of cycloserine?
|
Inhibits addition of D-ala D-ala into NAM
|
|
|
What is Red Man Syndrome?
|
Vancomycin toxicity. Stimulates histamine release from mast cells and mimics anaphylaxis
|
|
|
Which protein synthesis inhibitors interact with the 30S ribosome?
|
Aminoglycosides, tetracyclines, and spectinomycin
|
|
|
Which protein synthesis inhibitors interact with the 50S ribosome?
|
Macrolides, chloramphenicol, fusidic acid, and linezolid
|
|
|
Name some aminoglycosides
|
Gentamycin, amikacin, tobramycin, neomycin, streptomycin
|
|
|
What are the 2 main areas of the body that aminoglycosides are toxic to?
|
Ear and kidneys
|
|
|
T of F: Tetracyclines are bacteriostatic
|
True
|
|
|
Name 1 long and 1 short acting tetracycline
|
Short- tetracycline
Long-Doxycycline |
|
|
What's the difference between the mechanisms of aminoglycosides and tetracyclines?
|
Aminoglycosides bind IRreversibly to to 30S subunit, tetracyclins bind reversibly
|
|
|
What is the mechanism by which tetracycline stains teeth?
|
Chelates calcium
|
|
|
Name 3 macrolides
|
Erythromycin, azithromycin, clarithromycin. They're bacteriostatic.
|
|
|
Which class of drugs are the first choice for patients allergic to penicillins?
|
Macrolides
|
|
|
What is the mechanism of macrolides?
|
Bind reversibly to the 50S ribosome subunit. So does chloramphenicol.
|
|
|
What is the only disease that chloramphenicol is DOC for?
|
Typhoid
|
|
|
Name 2 side effects of chloramphenicol
|
Aplastic anemia and gray baby syndrome
|
|
|
Which drugs are DNA gyrase inhibitors? Name one of them.
|
Quinolones, Ciprofloxacin. They inhibit the supercoiling of bacterial DNA/
|
|
|
Which bacteriostatic, 50S binding drug is used in MRSA?
|
Linezolid
|
|
|
Name 4 nucleic acid inhibitors
|
Cipro, metronidazole, rifampin, and daptomycin
|
|
|
Sulfonamides and Trimethoprim inhibit the synthesis of...?
|
Folic acid
|
|
|
Which drugs are the 2nd most common cause of antibiotic allergy?
|
Sulfonamides. They're used for UTIs
|
|
|
Septra is a drug that combines the actions of which 2 drugs that inhibit sequential steps of folic acid synthesis?
|
Trimethoprim and sulfonamides. Used on E. Coli UTIs
|
|
|
Name 3 types of bacterial resistance
|
Primary, acquired, and cross-resistance
|
|
|
Which mechanism of resistance: Target enzyme is altered, still kind of fxnal
|
Altered target
|
|
|
Which mechanism of resistance: decreases permeability of cell, won't let drug in
|
Altered uptake
|
|
|
Which mechanism of resistance: pumping drug out of cell
|
Rapid ejection
|
|
|
Which mechanism of resistance: destroy or modify the antibacterial agent
|
Drug inactivation
|
|
|
What does NDM-1 stand for?
|
New Delhi metallo-beta-lactamase
|
|
|
NBM-1 superbugs are found mostly in what type of infections?
|
UTIs
|
|
|
Which drugs are NDM-1 superbugs resistant to?
|
Could be ALL OF THEM!@!@$!@#$@#$
|
|
|
The amount, in pounds, of antibiotics prescribed to animals in 2000 was __ times higher than the amount prescribed to humans
|
8. 24 mill in animals, 3 mill in humans
|
|
|
Which 2 classes of bacteria infect humans? How do they reproduce?
|
Deuteromycetes (not sexual) and zygomycetes (sexual). Most pathogenic species are deuteromycetes
|
|
|
Yeasts are unicellular, how do they reproduce?
|
Budding
|
|
|
What are the 3 types of asexual fungi reproduction?
|
Spores, conidia formed at tips of hyphae, and fragmentation
|
|
|
What are sexual spores for on hyphae called?
|
zygospores
|
|
|
Name 2 media that fungi are usually grown on
|
Sabouraud agar and Pagano-Levin agar
|
|
|
Which media is best for distinguishing types of candida?
|
Pagano-Levin agar
|
|
|
Which fungal media usually contains antibacterial agents and works well for slow growing fungi?
|
Sabouraud agar
|
|
|
What is DOC for systemic fungal infections?
|
Amphotericin B
|
|
|
What is the mechanism of Amphotericin B and what are its side effects?
|
Binds to ergosterol to disrupt cell membranes. It's nephrotoxic and suppresses bone marrow.
|
|
|
What are echinocandins (Micafungin) used to treat?
|
Severe candida infections
|
|
|
What drugs would you used to treat a fungal nail infection?
|
Griseofulvin (oral for up to 1 year) or Naftifine (oral and topical)
|
|
|
What are the 4 clinical classes of fungi?
|
Superficial cutaneous, subcutaneous, opportunistic, and systemic
|
|
|
Which fungus is the most common cause of athletes foot?
|
Trichophyton rubrum
|
|
|
What is tinea capitis and what causes it?
|
A fungal infection resulting in bald spots on the scalp, caused by trichophyton tonsurans
|
|
|
What is DOC for tinea (ringworm)?
|
Miconazole, griseofulvin, naftitine
|
|
|
What is Malassezia furfur and what is DOC?
|
A fungus that causes tinea versicolor and DOC is ketoconazole
|
|
|
Sulfur granules... what causes them?
|
A fungus called Pseudallescheria boydii
|
|
|
What is the most common factor predisposing someone to infection with opportunistic fungi?
|
Broad-spectrum antibiotics
|
|
|
Which fungi are budding yeasts with pseudohyphae and chlamydospores?
|
Candida
|
|
|
Which type of oral candidiasis causes 60% of denture stomatitis in elderly?
|
Chronic atrophic
|
|
|
Where is Cryptococcus neoformans found?
|
Found as spore in chicken and pigeon poop
|
|
|
Does Cryptococcus neoformans have a capsule?
|
Yes
|
|
|
What are the 2 most common infections associated with Cryptococcus neoformans?
|
Pulmonary and meningitis (especially in AIDS patients)
|
|
|
How is Cryptococcus neoformans diagnosed?
|
India ink or cryptococcal latex agglutination test
|
|
|
What is DOC for Cryptococcus neoformans?
|
Amphotericin B
|
|
|
DOC for Aspergillus fumigatus?
|
Amphotericin B or surgery
|
|
|
Which fungus produces aflatoxin and where is it usually found?
|
Aspergillus flavus, often found in peanuts. Exposure causes liver problems, including hepatoma
|
|
|
Which fungus is the cause of zygomycosis (mucormycosis)?
|
Rhizopus arrhizus. It is one of the few zygomycetes to infect humans. Lid pushers.
|
|
|
What is DOC for Rhizopus arrhizus?
|
Amphotericin B, surgery, treat underlying condition
|
|
|
Which fungus causes rhinocerebral/rhinofacial zygomycosis and in whom does it typically occur?
|
Rhizopus arrhizus. Diabetics. Spores get into soft palate, sinuses, cribriform plate and then into brain and behind eyes.
|
|
|
Name a fungus that lacks ergosterol. How does it usually present?
|
Pneumocystis jirovecii. Presents as penumonia
|
|
|
What is DOC for Pneumocystis jirovecii?
|
Trimethoprim-sulfamethoxazole
|
|
|
Which fungus can get on contact lenses and infect the eyes? How do you treat it?
|
Fusarium, topical natamycin
|
|
|
What is the natural form of dimorphic fungi?
|
Mold, infectious, grows at 25 C
|
|
|
What is the tissue form of dimorphic fungi?
|
Yeast. Parasitic, grows at 37 C
|
|
|
What is the most common dissemination of Histoplasma capsulatum and what is DOC?
|
Pulmonary infection resembling TB. DOC is amphotericin B
|
|
|
What is the most common dissemination of Blastomyces dermatitidis and what is DOC?
|
Pulmonary, also skin and bone. DOC is amphotericin B
|
|
|
Which fungus causes Valley Fever?
|
Coccidioides immitis
|
|
|
What is tissue form of Coccidioides immitis? What is DOC?
|
Spherules, NOT YEAST. A spherule is a thick walled sphere containing endospores. Amphotericin B is DOC.
|
|
|
Where are Sporothrix schenkii spores found? What is DOC?
|
Rose thorns, railroad ties, and sphagnum moss. If cutaneous, KI solution by mouth. If disseminated, amphotericin B
|
|
|
Which chromosome is the blood group gene on?
|
9
|
|
|
What does the "A" gene code for?
|
Alpha 1,3 N-Acetylgalactosaminyltransferase
|
|
|
What does the "B" gene code for?
|
Alpha 1,3 galactosyltransferase
|
|
|
What is missing in Bombay antigen that is present in O antigen?
|
Fucose
|
|
|
Isoagglutinins are serum antibodies. Which class are they in and at what age do they appear?
|
IgM, 2 months
|
|
|
What is agglutination used to determine?
|
Blood type
|
|
|
What is the most common type of immune-mediated blood transfusion reaction?
|
Donor RBC destroyed by recipients's antibodies. Other donor blood cells are also destroyed recipient antibodies.
|
|
|
Name 3 types of non-immune mediated blood transfusion reactions
|
Circulation overload, red cell damage, and bacterial/viral contamination
|
|
|
What are the 3 antigens in the Rhesus system?
|
Cc, D, Ee. Rh+ or Rh- refers to the D antigen
|
|
|
Name the genes that code for Rhesus antigens. Where are they located?
|
RhD codes for the D antigen. RhCE encodes Cc and Ee. They homologous, closely linked, and on chromosome 1
|
|
|
What causes the most serious type of hemolytic disease of the newborn?
|
Rhesus incompatibility between mother and fetus.
|
|
|
Does Rh incompatibility cause problems with the first pregnancy?
|
No. During the first delivery, some of the child's Rh+ blood gets into the mother's system and causes a primary IgM response. During subsequent pregnancies, a small amount of fetus blood crosses into the mother's system, stimulating a secondary antibody response
|
|
|
Name all immunoglobulins that are transferred from mother to fetus through the placenta and their mode of transfer
|
IgG. Active transport via IgG Fc receptors on placenta.
|
|
|
Describe the process of a direct Coomb's test
|
RBCs are washed and incubated with Coomb's reagent, which is rabbit anti-human Ig. The Ig will bind to antibodies on the RBCs, if present, and cause agglutination.
|
|
|
Describe the process of an indirect Coomb's test
|
Test RBCs are incubated with the testing patient's serum. Cells are then washed and incubated with Coomb's reagent (rabbit, anti-human Ig) and checked for agglutination. This test is used to see if a patient has antibodies to the antigens present on the test cell. If they do, they antibodies in the serum will bind the antigen on the test cells, then will agglutinate when the reagent is added.
|
|
|
True or false: ABO incompatibility will protect against Rh compatibility and prevent sensitization to D
|
True
|
|
|
Name the 2 kinds of viruses that are carcinogenic and give an example of each
|
DNA tumor viruses- HPV
RNA Viruses (retroviruses)- T-cell leukemias, breast and prostate cancer |
|
|
Name 3 types of carcinogenic gene abnormalities and give an example of each
|
Proto-oncogenes- Ras (normal cells that mutate and grow out of control)
Tumor suppressor genes- p53, Rb Chromosomal abnormalities- Burkitt's lymphoma |
|
|
Is a colorectal carcinoma a result of deletion or translocation?
|
Deletion
|
|
|
What does the immune surveillance theory state?
|
We all get cancer all the time, but our bodies take care of it like they would a regular cold. When our immune system fails to eliminate a cancer, it flourishes into was we usually consider "cancer"
|
|
|
What are the 4 conditions of the immune surveillance theory?
|
The tumor antigens must be immunogenic to the tumor-bearing host, the host must be immunocompetent, the immune response to the tumor cells must be cytotoxic or cytostatic, and the response must not result in tolerance or enhancement of tumor growth.
|
|
|
Name 5 antigenic changes in tumor cells
|
Oncofetal antigens, loss of MHC, TATA, unique neoatnigens, and overexpression of a normal cell antigen
|
|
|
Name 3 oncofetal antigens
|
Carcinoembryonic antigen (CEA) (predictive value), Glypican-3, and alpha-fetoprotein (diagnostic and predictive values)
|
|
|
Name the 2 types of evidence for tumor immunity and give examples of each
|
Circumstantial- spontaneous regression, lymphocyte proliferation in draining lymph nodes, increased tumor incidence in immunosuppressed patients, and increased tumor incidence with aging
Experimental- Anti-tumor antibodies found in cancer patients, animals models rejecting tumors, and activation of lymphocytes by tumor antigens |
|
|
Name 5 antitumor effector mechanisms
|
Cytotoxic T cells, NK cells, macrophages, induction of ADCC, and complement activation
|
|
|
What is the first line of defense against malignant cells and cells infected with viruses?
|
NK cells
|
|
|
What are the 3 ways for a tumor cell to evade recognition by T cells?
|
Antigen-loss by tumor cell, loss of class 1 MHC by tumor cell, and possession of immunosuppressive cytokines by the tumor cell
|
|
|
True of false: In children with a primary immune deficiency, there is an increased risk of common tumors, especially lymphoreticular neoplasms
|
False. There is no increased risk of common tumors.
|
|
|
Do adults with secondary immune deficiency have an increased risk of breast and colon cancer?
|
No
|
|
|
Name the 4 types of cancer immunotherapy
|
Active specific immunotherapy, monoclonal antibodies, biological response modifiers (IFN, IL-2, LAK, and LACTL), and adjuvants (BCG)
|
|
|
Name a specific immunosuppressive cytokine produced and utilized by tumor cells
|
TGF-Beta
|
|
|
Which type of hypersensitivity is IgE mediated?
|
Type I (Immediate hypersensitivity, allergy, atopy, and anaphylxis)
|
|
|
Which type of hypersensitivity is both IgG and IgM mediated?
|
Type II (cytotoxic reaction)
|
|
|
Which type of hypersensitivity is only IgG mediated?
|
Type III (immune complex diseases)
|
|
|
Which type of hypersensitivity is T-lymphocyte mediated?
|
Type IV (delayed type hypersensitivity)
|
|
|
What percentage of circulating WBCs are basophils?
|
0.5-1.0%
|
|
|
What percentage of serum Igs are IgE?
|
Less than .001%
|
|
|
Which type of immune response do IgEs provoke?
|
Th2
|
|
|
Which disease has the highest IgE levels?
|
Atopic eczema. Then asthma, hay fever, and rhinitis
|
|
|
Which type of immune response do T lymphocytes provoke in a type IV reaction?
|
Th1
|
|
|
Which cytokines induce a Th1 response?
|
IL-2, IFN-gamma, TNF-alpha, TNF-beta,
|
|
|
Which type of hypersensitivity is IgE mediated?
|
Type I (Immediate hypersensitivity, allergy, atopy, and anaphylxis)
|
|
|
Which type of hypersensitivity is both IgG and IgM mediated?
|
Type II (cytotoxic reaction)
|
|
|
Which type of hypersensitivity is only IgG mediated?
|
Type III (immune complex diseases)
|
|
|
Which type of hypersensitivity is T-lymphocyte mediated?
|
Type IV (delayed type hypersensitivity)
|
|
|
What percentage of circulating WBCs are basophils?
|
0.5-1.0%
|
|
|
What percentage of serum Igs are IgE?
|
Less than .001%
|
|
|
Which type of immune response do IgEs provoke?
|
Th2
|
|
|
Which disease has the highest IgE levels?
|
Atopic eczema. Then asthma, hay fever, and rhinitis
|
|
|
Which type of immune response do T lymphocytes provoke in a type IV reaction?
|
Th1
|
|
|
Which cytokines induce a Th1 response?
|
IL-2, IFN-gamma, TNF-alpha, TNF-beta, IL-3, and GM-CSF
|
|
|
Which cytokines induce a Th2 response?
|
IL-4, IL-5, IL-6, IL-10, TGF-beta, IL-3, and GM-CSF
|
|
|
Which histamine receptor mediates: contraction of bronchial and gut smooth muscle, systemic vasodilation, increased venule permeability?
|
H1
|
|
|
Which histamine receptor stimulates gastric acid secretion?
|
H2
|
|
|
Which histamine receptor modulates neurotransmitter release?
|
H3
|
|
|
Which histamine receptor mediates mast cell chemotaxis?
|
H4
|
|
|
Name 2 secondary mediators of type 1 hypersensitivity reactions
|
Eicosanoids and newly-formed cytokines
|
|
|
What percentage of the population is affected by type 1 hypersensitivity?
|
20%
|
|
|
In allergic subjects, what is the dominant T cell response to an allergen?
|
Th2 response
|
|
|
What do you call a massive degranulation of basophils?
|
Anaphylaxis
|
|
|
Name 2 benefits of hyposensitization
|
Downregulation of IgE synthesis, and increased synthesis of IgG-blocking antibodies.
|
|
|
(S. pneumonia picture) in an immunocompetent adult, the most common serious manifestation of infection by this organism is:
|
Pneumonia
|
|
|
Which of the following organisms are most likely to be involved in subacute bacterial endocarditis?
|
Viridans streptococci
|
|
|
For most Streptococci, the antigenic component on which the Lancefield grouping is based is a:
|
Cell wall polysaccharide
|
|
|
Which Streptococcus pyogenes antigen is responsible for the induction of protective antibody?
|
M-protein
|
|
|
Currently, Staphylococcal Toxic Shock Syndrome is most commonly associated with:
|
Wound infection
|
|
|
A close contact of a person who develops neisserial meningitis should be prophylactically treated with:
|
Ciprofloxacin
|
|
|
The most reliable means of diagnosing typhoid fever is:
|
Bone marrow culture
|
|
|
The drug of choice for severe antimicrobial-associated enterocolitis is:
|
Vancomycin
|
|
|
The major virulence factor of Clostridium perfringens is a:
|
Lecithinase
|
|
|
Which of the following cells can be capable of both phagocytosis and antigen presentation to T-cells?
|
Monocytes
|
|
|
Patients with sickle cell anemia are at greatly increased risk of infection with certain organisms, particular those which possess:
|
Capsules
|
|
|
What does cromolyn sodium do?
|
Blocks Ca influx into mast cells and stabilizes the membranes so they won't degranulate
|
|
|
Which class of type 1 hypersensitivity treatment is successful with asthma and rhinitis?
|
Leukotriene inhibitors (ie Singulair)
|
|
|
How do IgEs kill helminths?
|
They bind to worm, FcERI mast cells interact with the IgE and degranulate. This releases Eosinophil chemotactic factors, which bind to the worm through their FcER. Then the eosinophils produce major basic protein and eosinophilic cationic protein, which is toxic to helminths
|
|
|
Give an example of type II hypersensitivity
|
Blood transfusion reactions, hemolytic disease of the newborn, drug-induced hemolytic anemia
|
|
|
Give an example of type III hypersensitivity
|
Glomerulonephritis. Immune complexes build up, especially in areas of tricky blood flow
|
|
|
If cheap earrings make your ears turn red and sore, what type of hypersensitivity are you experiencing?
|
Type IV
|
|
|
In type IV hypersensitivity, which type of cells present the antigen to T cells?
|
Langerhans cells
|
|
|
What type of hypersensitivity is a latex reaction?
|
Can be type I or type IV
|
|
|
In skin tests, how long does a reaction take for type I, type III, and type IV reactions?
|
Type I- minutes
Type III- 4-12 hours Type IV- 48-72 hours |
|
|
Who created the live smallpox vaccine and what year was it?
|
Edward Jenner in 1796
|
|
|
Who created the rabies attenuated vaccine and what year was it?
|
Louis Pasteur in 1885
|
|
|
What are the 2 ways to get your own long lasting antibodies?
|
Natural- exposure to infectious agent or artificial- immunization
|
|
|
What are the 2 ways to get temporary, passive immunity?
|
Natural- maternal antibodies or artificial- antibodies from other sources
|
|
|
At what point in an infant's life do their own IgG antibodies outnumber the mother's?
|
40 weeks
|
|
|
Which cellular immune components are present in breast milk?
|
T and B lymphocytes, neutrophils, and macrophages.
|
|
|
Which non-cellular components are present in breast milk?
|
IgA, lysozyme, lactoferrin
|
|
|
Artificial passive immunization uses preformed human antibodies to confer temporary immunity. Name some diseases that are immunized in this way
|
Tetanus, diptheria antitoxin, hepatitis A and B, Agammaglobulinemia, monoclonal antibodies like RSV
|
|
|
True or false: Childhood vaccinations cause autism
|
FALSE!! If you put true, she will kill you.
|
|
|
What are the 2 classifications of vaccines?
|
Live/live attenuated and inactivated (whole cell or fractional)
|
|
|
The smallpox vaccine consists of live virus, name 3 adverse reactions to the vaccine
|
Bacterial superinfection and eczema vaccinatum, vaccinia
|
|
|
Name some commonly used live attenuated vaccines
|
MMR, yellow fever, chickenpox, flu, rotavirus, TB, oral typhoid
|
|
|
Name disadvantages of killed/inactivated vaccines
|
Takes a lot of boosters, larger doses, may not elicit local IgA response, poorly immunogenic compared to live
|
|
|
Name some commonly used killed/inactivated vaccines
|
Rabies, Hep A, Polio (Salk)
|
|
|
Name some commonly used fraction subunit vaccines
|
Hep B, flu, pertussis, HPV, anthrax
|
|
|
Name some commonly used fraction toxoid vaccines
|
Diptheria and tetanus
|
|
|
Characteristics of trivalent inactivated flu vaccine?
|
Given IM to people over 6 months old, healthy or with chronic medical conditions.
|
|
|
Characteristics of live attenuated flu vaccine?
|
Healthy people ages 2-49 who are not pregnant. Intranasal.
|
|
|
Describe the pertussis vaccine
|
It is acellular, containing pertussis toxin and one or several components, including adhesion factor
|
|
|
The HPV vaccine contains antigens from which 4 papilloma viruses?
|
6, 11, 16, 18
|
|
|
What are the disadvantages of pure polysaccharide vaccines?
|
Poorly immunogenic in children under 2, short lived responses, memory is minimal, only IgM
|
|
|
Are polysaccharide-toxoid conjugate vaccines effective?
|
Yes, very. They confer long lasting immunity, good memory, and IgG
|
|
|
Are DNA vaccines effective?
|
Not really
|
|
|
Vaccination against which disease may cause encephalopathy, an indication that that vaccine should never be given again?
|
Pertussis
|
|
|
True or false: Vaccinating someone with an acute illness could cause serious side effects
|
False. There is no evidence that this will do anything bad.
|
|
|
Should vaccines be given to pregnant women?
|
Killed/inactivated and toxoid are usually safe, but wait until 2nd or 3rd trimester. Live attenuated should not be given to pregnant women.
|
