Exam 3(Lect. 27-32) Flashcards
(203 cards)
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.