Exam 3(Lect. 27-32) Flashcards
Which of the following would be characteristic of a highly evolved pathogen?
A. Incidence of infection 50%, mortality 95%
B. Incidence of infection 1 in 10,000, mortality 2%
C. Incidence of infection 100%, mortality 100%
D. Incidence of infection 1 in 10,000, mortality 90%
E. Incidence of infection 90%, mortality 1 in 1,000
Incidence of infection 90%, mortality 1 in 1,000
What are “pathogenicity islands”?
A. Clusters of virulence factor genes that can be transmitted by horizontal gene transfer
B. Groups of pathogenic bacteria bound to M cells
C. Patches of membrane receptors to which pathogenic bacteria bind
D. Plasmids on which multiple antibiotic resistance genes are located
E. Endemic disease foci with high prevalence of a particular disease
Clusters of virulence factor genes that can be transmitted by horizontal gene transfer
How do bacteria with Type III secretion systems (T3SS) typically enter host cells?
A. The T3SS pokes a hole in the host cell membrane through which the bacteria enter.
B. The T3SS kills the host cell, making it easier for the bacteria to enter.
C. The T3SS enhances binding to macrophages, which engulf the bacteria.
D. Effectors secreted through the T3SS cause the host cell to enfold the bacteria in
membrane ruffles.
E. They don’t. T3SS are for secreting exotoxins, not for entering host cells.
Effectors secreted through the T3SS cause the host cell to enfold the bacteria in
membrane ruffles.
Which of the following is a method for bacteria to evade the host immune defenses?
A. They use flagella to move from cell to cell .
B. They have capsules to avoid phagocytosis.
C. They bind the C3b protein, stealing it from the host.
D. They block transport of iron, a major oxidant.
E. They bind the Fab arms of antibodies.
They have capsules to avoid phagocytosis.
Several organisms (Staphylococcus, Pseudomonas, Enterococcus) cause disease in catheterized
patients much more frequently than in non-catheterized patients. What is the most important virulence
factor for these organisms?
A. Antiphagocytic capsule
B. Exotoxin production
C. Respiratory transmission
D. Intracellular spread via actin polymerization
E. Ability to form biofilms on the catheter
Ability to form biofilms on the catheter
A male patient ingests a dose equal to the ID50 of E. coli that expresses the type P pilus. What
would be the most likely outcome?
A. Pneumonia
B. Diarrhea
C. Urinary tract infection
D. An induced autoimmune disease
E. No infection
No infection
A pathogen that has evolved for a long time in the same environment as its host will exhibit which
of the following?
A. High prevalence and high mortality
B. High prevalence and low mortality
C. Low prevalence and high mortality
D. Low prevalence and low mortality
E. High incidence and low prevalence
High prevalence and low mortality
Elderly patients on long-term oral penicillin therapy often acquire the infectious disease
pseudomembranous colitis, caused by Clostridium difficile. How does penicillin use affect the course
of this disease?
A. Penicillin kills native flora, allowing C. difficile to colonize.
B. Penicillin creates a “super” strain of C. difficile that is more infectious.
C. Penicillin triggers a hypersensitivity response in the patient.
D. Penicillin reduces the severity of the C. difficile infection.
E. Penicillin has no effect on the course of this disease.
Penicillin kills native flora, allowing C. difficile to colonize.
Which of the mechanisms below can bacteria use to escape phagocytosis?
A. Enhanced motility to get away from phagocytes
B. Extra iron binding proteins
C. Production of lysins to lyse the phagocyte
D. Producing an IgG protease
E. Preventing cytokine secretion from T cells.
Production of lysins to lyse the phagocyte
A pathogen that has recently emerged in a particular region of the world would be expected to
have which of the following epidemiological characteristics?
A. High virulence and low prevalence
B. Low infectious dose and low mortality
C. Low prevalence and high incidence
D. Low mortality and high prevalence
E. balanced pathogenicity
High virulence and low prevalence
What is a major difference between an infection and an intoxication?
A. An infection is best treated by inducing active immunity in an ill patient.
B. An intoxication is best treated by passive immunization.
C. An intoxication usually results in disorientation and neural paralysis.
D. An infection is more acute than an intoxication.
E. The consequences of an intoxication are not as serious as those of an infection.
An intoxication is best treated by passive immunization.
Many pathogenic bacteria have evolved a C5a peptidase. What is the function of this virulence
factor?
A. It reduces the host’s ability to recruit phagocytes to the site of infection.
B. It binds host antibodies and neutralizes them.
C. It prevents the use of the membrane attack complex by the complement system.
D. It allows the bacterium to survive inside macrophages.
E. It creates membrane ruffles that enhance bacterial uptake by host cells.
It reduces the host’s ability to recruit phagocytes to the site of infection.
Which of the following is the best example of balanced pathogenicity?
A. an organism that causes acute respiratory disease that is rapidly fatal
B. a foodborne organism that causes septicemia
C. both bacteria and viruses can cause pneumonia
D. a virus that causes mild diarrhea and is spread fecal-oral with an ID50 of 20 organisms
E. a bacterium that causes an equal number of respiratory and skin diseases
a virus that causes mild diarrhea and is spread fecal-oral with an ID50 of 20 organisms
The picture at right shows a bacterium (arrow) entering an epithelial cell. The elaborate structure
that surrounds the bacterium forms . . .
A. when the PAMP on the epithelial cell contacts the
TLR on the bacterium.
B. by extension of the bacterial cell envelope
C. as a defense mechanism to prevent the epithelial
cell from being infected
D. in response to a bacterial protein secreted by a
Type III secretory system
E. as the first step in the membrane fusion process.
in response to a bacterial protein secreted by a
Type III secretory system
Neisseria gonorrhoeae (Ng) can bind a host’s C3b regulatory protein. Why does Ng do that?
A. to inactivate C3b when it binds to Ng
B. to recruit more C3b to bind to Ng
C. to enhance Ng’s uptake into the host cell
D. to avoid the immune response by coating Ng with “self” antigens
E. That’s how the body recognizes that Ng is a pathogen.
to inactivate C3b when it binds to Ng
What is the function of the Staphylococcal protein A?
A. IgA protease
B. Fc receptor
C. adhesin
D. prevents phagosome / lysosome fusion
E. activates complement C5a
Fc receptor
Which of the following would you expect to be the eventual outcome of an evolutionary selection
process in a pathogenic bacterium?
A. Its ID50 will change gradually from 102
bacteria to 106
bacteria.
B. It will lose the proteins at the tips of its adhesion pili.
C. It will increase the size of its genome as it acquires a broad metabolic capacity.
D. It will change from an acute infection to a chronic one.
E. It will acquire the ability to kill its host much more quickly.
It will change from an acute infection to a chronic one.
Correctly order the following steps in the Shigella infection cycle.
A. M cell entry → macrophage entry → epithelial cell entry → actin polymerization
B. macrophage entry → actin polymerization → epithelial cell entry → bacteremia
C. M cell entry → actin polymerization → epithelial cell entry → macrophage entry
D. macrophage entry → bacteremia → toxin production → epithelial cell entry
E. epithelial cell entry → actin polymerization → macrophage entry → bacteremia
M cell entry → macrophage entry → epithelial cell entry → actin polymerization
Which of the following would typically NOT be true of an attenuated organism?
A. It lacks one or more pathogenicity islands.
B. Its ID50 is very low.
C. It lacks adhesion pili.
D. It generally causes a sub-clinical infection.
E. You develop a strong immune response against it.
Its ID50 is very low.
A microbiologist tells you that there is no model organism for the disease he is studying. What
does he mean by this?
A. The structure of the disease organism is difficult to represent with a model.
B. There is no single organism that causes the disease.
C. The disease is an intoxication rather than an infection.
D. He will have to rely on Koch’s postulates to study it.
E. The disease only affects humans.
The disease only affects humans.
Which bacterial invasion and colonization (I/C) factor is correctly matched with its role in an
infection?
A. siderophore – steals iron from the eukaryotic host
B. fimbriae – injected into a host cell and damage its cytoskeleton
C. Type III effectors – prevent uptake of bacteria by host cells
D. coagulase – alters the membrane structure of eukaryotic host cells
E. IgA protease – allows a bacterium to cause bacteremia
siderophore – steals iron from the eukaryotic host
How are bacterial type III secretion system effectors involved in causing disease?
A. They rearrange the host cytoskeleton and allow the bacterium to enter host cells.
B. They allow the bacterium to compete with the host for binding iron.
C. They are leukocidins that the bacterium uses to kill phagocytes.
D. They mimic “cancel kill” signals so NK cells don’t kill infected host cells.
E. They bind to host cell receptors and are internalized like toxins.
They rearrange the host cytoskeleton and allow the bacterium to enter host cells.
What are “pathogenicity islands”?
A. Patches of membrane receptors to which pathogenic bacteria bind
B. Plasmids on which multiple antibiotic resistance genes are located
C. Clusters of virulence factor genes that can be transmitted by horizontal gene transfer
D. Groups of pathogenic bacteria bound to M cells
E. Endemic disease foci with high prevalence of a particular disease
Clusters of virulence factor genes that can be transmitted by horizontal gene transfer
At the right is a photomicrograph showing the bacterium Listeria monocytogenes (Lm) infecting a
human cell. What can you conclude about how this bacterium lives in its host?
A. Lm must have an M-protein on its surface.
B. Lm grows into long, filamentous cells once it is inside its host.
C. After it passes through MALT tissue, Lm invades the epithelial
basal membrane.
D. Lm probably has an antiphagocytic capsule.
E. Lm is able to use actin from its host to avoid humoral immunity.
Lm is able to use actin from its host to avoid humoral immunity.
In the past 130 years we have learned quite a bit about microbes. Some things we have learned
have required us to modify the system Robert Koch developed in 1880 to identify the causative agent
of a disease. Which of the following has NOT required such a modification?
A. The recognition that we can only culture about 1% of the bacteria we’ve discovered
B. The discovery of infections caused by biofilms involving several bacterial species
C. Realizing that some diseases are of an inflammatory rather than an infectious nature
D. Recognizing the concept of idiopathic cases of an infectious disease
E. The development of cell culture models to study disease processes at the cellular level
Realizing that some diseases are of an inflammatory rather than an infectious nature
What are fimbriae?
A. Special pili with adhesive proteins at their tips
B. Cells in mucous membranes that uptake bacteria
C. A type of bacterial exotoxins
D. Bacterial proteins that bind iron in host blood serum
E. Dense polysaccharide fibers present in bacterial biofilms
Special pili with adhesive proteins at their tips
The genes for which of the following would be LEAST likely to be located on a pathogenicity
island?
A. A Type III secretory system
B. A bacterial siderophore
C. A superantigen toxin
D. An I/C factor
E. LPS biosynthesis
LPS biosynthesis
Which of the following is a mechanism that bacteria use to avoid the host’s immune response?
A. Bacteria digest IgG
B. Bacteria secrete iron
C. Bacteria induce autoimmmune reactions
D. Bacteria cover themselves with antibodies
E. Bacteria cover themselves with C3b
Bacteria cover themselves with antibodies
You are testing antibiotics in a mouse model of a new bacterial disease. You have determined the
MIC for the antibiotics from an E-test, and administered each antibiotic to several mice at greater than
the MIC dose. But all the mice still die. Which of the following would be a logical conclusion from
the results of this experiment?
A. You should look for the production of a toxin by the new bacterium.
B. You shouldn’t have used an E-test to determine the MIC of the antibiotics.
C. This new disease is probably polymicrobial.
D. You should have administered the antibiotics at a dose less than the MIC, not more.
E. Animal models are not valid for study of human diseases.
You should look for the production of a toxin by the new bacterium.
All of the following are important for bacterial survival in a host EXCEPT the ability to . . .
A. digest C5a
B. produce siderophores
C. bind complement regulatory protein
D. induce autoimmune antibodies
E. produce an Fc binding protein
induce autoimmune antibodies
What do the structures in these two pictures have in common?
A. They are both parts of the same bacterial cell.
B. Both involve rearrangements of the host’s cytoskeletal proteins.
C. Both occur when a bacterial capsule is produced within a host cell.
D. Both are immune responses to the presence of a bacterium.
E. Both are ways that Shigella can enter macrophages.
Both involve rearrangements of the host’s cytoskeletal proteins.
When we say that a patient has a “disseminated” bacterial infection, what can we assume?
A. It was transmitted in sexual secretions as an STI.
B. The patient has or has had bacteremia.
C. The patient is suffering from an autoimmune sequela.
D. The infection is transmitted by the airborne route.
E. It is an infection of the disseminate, an accessory part of the digestive system.
The patient has or has had bacteremia.
Throughout the 20th century, we have had to modify Koch’s postulates as we learned more
about host-pathogen interactions. All of the following observations have required modification
of Koch’s postulates, EXCEPT . . .
A. Occasionally a disease does not have an identifiable cause.
B. Bacteria eventually evolve less virulence as hosts evolve more resistance.
C. Most bacteria cannot be cultured in laboratory media.
D. Some infections are caused by several bacteria growing together in a biofilm.
E. Some bacteria that cause human disease do not cause the same disease in animals.
Bacteria eventually evolve less virulence as hosts evolve more resistance.
Shigella are intestinal bacteria that can break out of the phagosome. What strategy do they
use to infect a host?
A. Prevent opsonization with antibodies to avoid phagocytosis
B. Coat themselves with host proteins to resemble “self” cells
C. Use Type III effectors to enter the apical membrane of intestinal epithelial cells
D. Get into macrophages as quickly as possible through intestinal M-cells
E. Develop a large anti-phagocytic polysaccharide capsule
Get into macrophages as quickly as possible through intestinal M-cells
Which of the following is a method for viruses to evade the host immune defenses?
A. They use the host’s cytoskeleton to spread intercellularly.
B. They inhibit their binding to cell surface receptors.
C. They produce an antiphagocytic lipid capsule.
D. They prevent recruitment of the MAC by the complement cascade
E. They produce their own “cancel kill” signal for NK cells.
They produce their own “cancel kill” signal for NK cells.
Which of the following is true of endotoxin, but not of an exotoxin?
A. Endotoxin is a cytoplasmic protein.
B. Endotoxin has much higher toxocity.
C. Endotoxin stimulates interleukin release, which results in fever.
D. Endotoxin can be the target for a vaccine.
E. Diseases caused by endotoxin can rarely be treated with antibiotics.
Endotoxin stimulates interleukin release, which results in fever.
Most of the really dangerous pathogenic fungi can do which of the following?
A. Get inhaled as mold spores and transition to yeast in the host’s body
B. Produce spores within the host’s body
C. Escape the immune system by living inside red blood cells
D. Produce endotoxin
E. Grow as yeast in an environmental reservoir outside the host
Get inhaled as mold spores and transition to yeast in the host’s body
How does your body respond to the presence of a superantigen toxin?
A. By secreting lots of cytokines and mounting a massive inflammatory response
B. By producing many more antibodies than normal, causing hypersensitivity reactions
C. By recruiting the complement cascade to kill host cells as well as bacteria
D. By engulfing the toxin and disseminating it via the blood to the tissues
E. By destroying connective tissue, resulting in necrosis.
By secreting lots of cytokines and mounting a massive inflammatory response
What is the function of the B part of A-B toxins?
A. It binds to and inhibits B cells.
B. It enters the host cell and damages host cell metabolism.
C. It binds to surface receptors on the host cell.
D. It causes the main symptoms of anthrax.
E. It inhibits phagosome-lysosome fusion.
It binds to surface receptors on the host cell.
Which of the following is usually true of an exotoxin, but not true of endotoxin?
A. There is a serum binding protein that binds to it.
B. It is an integral part of the cell envelope
C. It is easily detected by the Limulus amoebocyte assay
D. It usually causes a fever
E. The genes encoding it can be passed among cells on a pathogenicity island.
The genes encoding it can be passed among cells on a pathogenicity island.
How does a phospholipase toxin kill cells?
A. By preventing phospholipid synthesis
B. By removing the head groups, thus destroying the amphipathic nature of the
phospholipid
C. By adding ADP + ribose to stop protein synthesis
D. By preventing uptake via membrane fusion
E. By digesting fatty acids, causing the lipids to not pack together as well
By removing the head groups, thus destroying the amphipathic nature of the
phospholipid
How does a superantigen toxin function?
A. It is a very strong antigen that provokes a massive antibody response.
B. It crosslinks the TCR of TH cells to MHC2 that is not presenting an antigen.
C. It crosslinks TH cells to B cells, thereby producing lots of antibodies.
D. It dissolves the material that holds cells together in tissues.
E. It adds ADP-ribose to a protein, thereby inactivating it and killing cells.
It crosslinks the TCR of TH cells to MHC2 that is not presenting an antigen.
The bacterium Listeria monocytogenes can live in phagocytes by breaking down the phagolysosome
membrane. Which of the following toxins could help L. monocytogenes do this?
A. A hyaluronidase
B. A superantigen
C. Endotoxin
D. An AB toxin
E. A phospholipase
A phospholipase
How is LPS toxic to humans?
A. It agglutinates a type of red blood cell, causing DIC.
B. It activates B cells even without antigen binding, causing massive antibody release.
C. It binds to cells in the hypothalamus, damaging them and causing fever.
D. It increases cAMP concentration, causing edema and cell death.
E. It binds strongly to macrophages, causing a response that can lead to hypovolemia.
It binds strongly to macrophages, causing a response that can lead to hypovolemia.
What is the function of the A part of an AB toxin?
A. It binds to surface receptors on the host cell
B. It hydrolyzes the head group of phospholipids
C. It facilitates bacterial spread through a tissue and into the bloodstream
D. It activates large numbers of TH cells
E. It enters the cytoplasm and kills the host cell, often by altering cell metabolism
It enters the cytoplasm and kills the host cell, often by altering cell metabolism
For which bacterial toxins have we found a pharmaceutical use to make anesthetics more readily
able to penetrate through skin and other tissues?
A. ADP-ribosylating A-B toxins
B. hemolysins
C. hyaluronidases
D. endotoxins
E. superantigen toxins
hyaluronidases
One reason why a vaccine against malaria has proven difficult to design is that the malaria parasite
. . .
A. has no surface proteins
B. has a virus-like protective coating that prevents antibody binding
C. covers itself with host antigens
D. lives in red blood cells, where it can avoid both cellular and humoral immunity
E. can swim through a tissue, avoiding humoral immunity
lives in red blood cells, where it can avoid both cellular and humoral immunity
How does production of phospholipase enhance bacterial survival inside macrophages?
A. It binds the Fc end of IgG, thereby disguising the bacterium as a “self” cell.
B. It oxidizes macrophage proteins and kills the macrophage.
C. It prevents C3b from binding to the bacterial surface and activating complement.
D. It digests the antibody that most commonly attacks bacteria inside macrophages.
E. It disrupts the phagosome membrane, allowing the bacterium to escape.
It disrupts the phagosome membrane, allowing the bacterium to escape.
Diphtheria toxin is an AB toxin. What does this mean?
A. It can be detected by the limulus amoebocyte assay.
B. There can be no vaccine made against it.
C. There is a receptor for it on a host cell membrane.
D. Diphtheria is mainly an intracellular pathogen.
E. It binds to and alters the structure of antibodies.
There is a receptor for it on a host cell membrane.
How do bacteria with Type III secretion systems (T3SS) typically enter host cells?
A. The T3SS pokes a hole in the host cell membrane through which the bacteria enter.
B. The T3SS kills the host cell, making it easier for the bacteria to enter.
C. The T3SS enhances binding to macrophages, which engulf the bacteria.
D. Effectors secreted through the T3SS cause the host cell to enfold the bacteria in
membrane ruffles.
E. They don’t. T3SS are for secreting exotoxins, not for entering host cells.
Effectors secreted through the T3SS cause the host cell to enfold the bacteria in
membrane ruffles.
What is this diagram depicting?
A. The typical activation of a TH cell by a macrophage
B. The function of a superantigen toxin
C. The function of an AB toxin
D. The attachment of a bacterium to a T cell
E. The activity of Staphylococcal protein A
The function of a superantigen toxin
Why do some viruses produce an analog of MHC1?
A. To stop NK cells from killing cells infected by the virus
B. So the viruses can bind to the MHC1 and be internalized more readily
C. To be able to present viral proteins more easily on the surface of the host cell
D. It is a viral toxin that initiates an autoimmune reaction in the host
E. To reduce the efficiency of interferon binding to neighboring cells
To stop NK cells from killing cells infected by the virus
Which of the following statements is accurate when comparing Anthrax toxin to LPS?
A. LPS is more likely to be inactivated by heat or formalin.
B. LPS is probably more toxic per microgram than Anthrax toxin.
C. The genes for Anthrax toxin are more likely to be located on a plasmid.
D. LPS contains more protein components than Anthrax toxin.
E. Anthrax toxin is more likely to remain attached to the bacterial cell membrane.
The genes for Anthrax toxin are more likely to be located on a plasmid.
The bacterium that causes necrotizing fasciitis produces a hyaluronidase toxin. This toxin gives an
advantage to the bacterium because it allows the bacterium to . . .
A. spread more rapidly between the cells in a tissue
B. avoid the humoral immune response
C. induce a huge cytokine response in the host
D. be internalized more quickly by host macrophages
E. break out of the phagolysosome
spread more rapidly between the cells in a tissue
Some viruses like Papillomavirus encode an inhibitor of the eukaryotic protein p53. Why?
A. so that they can coat themselves with a “self” protein
B. so that they can prevent infected cells from undergoing apoptosis
C. to cancel the “kill” signal that NK cells recognize
D. to allow them to invade deep tissues beyond the skin
E. so that they can escape from the phagosome before it fuses with the lysosome
so that they can prevent infected cells from undergoing apoptosis
During some viral infections, infected cells fuse to form___________because_____________.
A. giant cells ; these cells are easier for the immune system to recognize
B. granulomas ; infected macrophages continue to secrete cytokines
C. granulomas ; these “activated” cells have a more potent oxidative burst
D. syncytia ; it allows the virus to avoid serum antibodies
E. syncytia ; these fused cells cannot produce interferon
syncytia ; it allows the virus to avoid serum antibodies
Why can’t we produce a successful vaccine against endotoxin?
A. Our immune response against it is too weak.
B. It can’t be inactivated because it isn’t a protein.
C. It resembles human host proteins too closely.
D. It enters host cells so quickly that antibodies never encounter it.
E. It is found on a plasmid, and can spread too rapidly through a bacterial population.
It can’t be inactivated because it isn’t a protein.
For which type of bacterial toxin is there a medical use - to make anesthetics more readily able to
penetrate through skin and other tissues?
A. cAMP-producing A-B toxins
B. phospholipases
C. IgA proteases
D. hyaluronidases
E. superantigen toxins
hyaluronidases
The malaria parasite has a particularly effective method of avoiding both humoral and cellular host
immune defenses. Which of the following is correct about this parasite?
A. It lives in red blood cells
B. It produces keratinase
C. It grows within and travels between host epithelial cells
D. It coats itself with host proteins so that it resembles “self”
E. It causes host cells to fuse into syncytia
It lives in red blood cells
What would be the most effective way to protect a patient against bacterial endotoxin?
A. Vaccinate the patient with an endotoxoid vaccine.
B. Test to see if intravenous fluids given to the patient coagulate Limulus blood cells.
C. Autoclave all intravenous fluids that might be given to the patient.
D. Use a Western Blot to screen any intravenous fluids given to the patient.
E. Passively immunize the patient against bacterial endotoxin.
Test to see if intravenous fluids given to the patient coagulate Limulus blood cells.
All of the following are characteristic of bacterial A-B toxins EXCEPT . . .
A. The A part can cause increased production of cAMP
B. Multiple B parts can bind to multiple receptors
C. The B part can be used to produce a toxoid vaccine
D. An “attenuated” bacterium might have a mutation in the A part
E. They hydrolyze the A part of phospholipids away from the B part
They hydrolyze the A part of phospholipids away from the B part
Why is there not yet a vaccine directed against bacterial endotoxin?
A. There is no market for one, so no one has tried hard enough to produce it.
B. There are too many different varieties of endotoxin.
C. Endotoxin is also a self-antigen in humans.
D. Endotoxin does not produce a strong enough immune response.
E. Endotoxin cannot be inactivated to produce a toxoid.
Endotoxin cannot be inactivated to produce a toxoid.
How does a bacterial A-B toxin work?
A. It digests the host’s cell membrane phospholipids.
B. The B part blocks protein synthesis; the A part activates cAMP production.
C. The B part binds to receptors; the A part enters the host cell.
D. The A part activates the B part, which then binds to host cells and kills them.
E. The B part protects the A part from attack by the host’s immune system.
The B part binds to receptors; the A part enters the host cell.
How could you tell if a particular pathogen produced a superantigen toxin when it infected a
patient?
A. Look for complete clearing when the pathogen is grown on a Blood Agar plate.
B. Look for tissue damage in a patient. Only superantigen toxins can do that.
C. Look for the release of cytokines from TH cells that do not recognize the pathogen.
D. Look for a larger than normal antibody titer against the pathogen.
E. Look for symptoms of DIC. Any pathogen that causes DIC probably produces a
superantigen toxin.
Look for the release of cytokines from TH cells that do not recognize the pathogen.
Viruses use all of the following strategies to avoid the immune system EXCEPT . . .
A. production of an IgA protease
B. production of an interferon repressor
C. formation of syncytia
D. inhibition of the tumor suppressor p53
E. reversing the MHC-I antigen presentation pathway
production of an IgA protease
Can the structure shown at the right be toxic? If so, how? If not, why not?
A. Yes, the part labeled ‘A’ can combine with antibodies to create a
hypersensitivity reaction
B. Yes, the part labeled ‘B’ can bind to a protein that induces a
strong cytokine response from macrophages.
C. Yes, the whole structure can bridge the interaction between naive
TH cells and APCs
D. No, the structure as shown lacks the toxic portion, and can only
bind to receptors.
E. No, the structure is not bacterial and has nothing to do with a toxin.
Yes, the part labeled ‘B’ can bind to a protein that induces a
strong cytokine response from macrophages.
Which of the following statements about AB toxins is accurate?
A. The B-part of the toxin can inhibit the function of B cells.
B. The A-part of the toxin can hydrolyze phospholipid head groups.
C. The B-part of the toxin can be used as a vaccine antigen.
D. They have a medical use to allow anesthetics to penetrate tissue better.
E. They are only produced by Gram positive bacteria.
The B-part of the toxin can be used as a vaccine antigen.
. A naked virus, HPV, produces a protein called E6. Recalling what infection HPV causes,
how does the E6 protein contribute to the infection?
A. It prevents the action of the p53 tumor suppressor gene in the host.
B. It blocks the MHC-I antigen presentation pathway in the host.
C. It allows the virus to form syncytia between infected host cells.
D. It prevents activation of TH cells by acting like an analog of MHC-II.
E. It stimulates the action of NK cells, which cause the HPV skin lesions.
It prevents the action of the p53 tumor suppressor gene in the host.
The malaria parasite spends most of the human part of its life cycle in red blood cells
(RBCs). What does this imply about the body’s response to the presence of this parasite?
A. Antibodies can’t bind to the parasite, but TC cells can still kill infected RBCs.
B. Infected RBCs can only be killed by NK cells.
C. The parasite can be neutralized by antibodies once the antibodies bind to RBCs.
D. The parasite is exposed to neither humoral nor cellular immune responses.
E. The parasite’s surface proteins resemble those of the host.
The parasite is exposed to neither humoral nor cellular immune responses.
For a chronic disease that is transmitted poorly between hosts (e.g. HIV) . . .
A. prevalence would be only slightly higher than incidence
B. incidence would be only slightly higher than prevalence
C. prevalence would be MUCH higher than incidence
D. incidence would be MUCH higher than prevalence
E. incidence would always be very low in a population
prevalence would be MUCH higher than incidence
Which of the following is an important difference between droplet transmission and aerosol
transmission of a disease?
A. Aerosol transmission is limited to hosts who come into direct contact.
B. Only aerosol transmission results in an epidemic disease.
C. Droplet transmission almost always occurs via fomites.
D. Droplet transmission rarely results in a common-source outbreak.
E. Aerosol transmission is almost exclusively for digestive system diseases.
Droplet transmission rarely results in a common-source outbreak.
The most effective way to reduce the incidence of nosocomially spread infections is to . . .
A. Disinfect operating rooms better between surgeries
B. Use more antibiotics in hospitals
C. Fit HEPA filters in all patient rooms
D. Separate patients into wards, grouped by the disease they have.
E. Have health care workers wash their hands between each patient they touch.
Have health care workers wash their hands between each patient they touch.
A newborn with a case of trachoma is an example of . . .
A. Vertical disease transmission
B. Horizontal disease transmission
C. An immunodeficiency disease
D. Seasonal disease incidence
E. An endemic disease focus
Vertical disease transmission
A person has a Staphylococcal skin infection. Another person acquires the same infection by
sleeping on the same sheet as the first person. The sheet in this scenario serves as . . .
A. A vector
B. A reservoir
C. A fomite
D. A portal of entry
E. A host
A fomite
An example of an emerging or re-emerging disease is . . .
A. Cholera in India
B. Coccidioidomycosis in New Mexico
C. the annual Influenza epidemic
D. Tuberculosis in Europe
E. Gonorrhea in the United States
Tuberculosis in Europe
Which of the following requires the strictest isolation between an infected patient and a healthcare
worker?
A. Standard precautions
B. Airborne precautions
C. Droplet precautions
D. Contact precautions
E. Blood and body fluid precautions
Airborne precautions
Who or what is a fomite?
A. A dried sputum droplet that can become aerosolized
B. An exotoxin secreted by Streptococcus
C. The first person to become ill during an epidemic
D. An inanimate object that spreads infection via indirect contact
E. An air-filled vacuole within macrophages where bacteria are stored before digestion
An inanimate object that spreads infection via indirect contact
The most common nosocomial infections are . . .
A. respiratory infections due to Staphylococcus transmitted in aerosols
B. surgical site infections from improper skin disinfection before surgery
C. urinary tract infections from improperly disinfected catheters
D. bacteremias caused by extremely drug resistant bacterial strains
E. ear, nose and throat infections like sinusitis or otitis media
respiratory infections due to Staphylococcus transmitted in aerosols
Which of the following isolation procedures commonly used in hospitals is the least rigorous (i.e.
requires the minimum use of additional protective barriers between patient and healthcare worker)?
A. Body substance precautions
B. Droplet precautions
C. Airborne precautions
D. Contact precautions
E. Sterile precautions
Body substance precautions
In a recent mumps outbreak the case incidence rate over
time is recorded as shown (x-axis is in weeks). This is an
example of . . .
A. A common-source epidemic
B. Fecal-oral transmission
C. Delayed hypersensitivity
D. A person-to-person epidemic
E. An endemic disease
A person-to-person epidemic
Which of the following is a major portal of entry, but not a major portal of exit?
A. Upper Respiratory Tract
B. Digestive Tract
C. Wounds
D. Vaginal Epithelial Cells
E. Unbroken Skin
Wounds