Bio 321 Exam 12
Due 10/10/01
Name ________________________
_____ Which enzyme is proposed to play a role in both Cholera toxin binding to intestinal mucosa cells and P.
aeruginosa binding to epithelial cells by modifying receptor molecules?
A. Neuraminidase
B. Peptidase
C. Phospholipase
D. Cytolysin
E. Hemolysin
_____ Diphtheria toxin production is controlled by the DtxR protein in response to ___.
A. temperature
B. iron levels
C. calcium levels
D. nitrogen levels
E. oxygen levels
_____ Cholera toxin results in disease by causing constitutive activation of ___ resulting in ___.
A. elongation factor-2 … inactivation of ribosomes
B. adenylate cyclase … release of excess calcium
C. phospholipase C … disruption of the host cell wall
D. neurotransmitters … paralysis
E. elastase … loss of integrity of epidermal layer
_____ Diphtheria toxin targets a special histidine derivative called ___ a component of ___.
A. histamine … ribosomes
B. histamine … EF-2
C. diphthamide … ribosomes
D. diphthamide … EF-2
E. heparin … EF-2
_____ Cholera toxin binds to ____ on the surface of host mucosal cells.
A. GS
B. GM1
C. Galpha
D. GTP
E. ARF
_____ Test used to identify toxigenic strains of C. diphtheria.
A. Elek plate
B. ELISA
C. Polymerase Chain Reaction
D. Ligase Chain Reaction
E. Rocket electrophoresis
_____ Which of the following is an example of post-transcriptional regulation?
A. The use of an alternative sigma factor.
B. DNA Supercoiling.
C. DNA rearrangement.
D. Different ribosome binding sites upstream of each gene within an operon.
_____ Bordetella pertussis preferentially binds to ____.
A. the intestinal mucosa
B. ciliated cells
C. M cells
D. goblet cells
_____ Pertussis toxin ___.
A. is identical to cholera toxin in structure and target.
B. is identical to cholera toxin in target but a different structure
C. is identical to cholera toxin in structure but a different target
D. is similar to cholera toxin but different in structure and target
_____ Cholera toxin is a popular choice as a conjugate for vaccine development because ___.
A. it directs the antigen to the intestinal mucosa where it illicits the appropriate immune response.
B. it avoids the host defense systems
C. it causes the release of fluids which helps spread the antigen around
D. it provides resistance to both cholera and to the conjugated antigen
_____ Theh toxic effects of invasive adenylate cyclase is specific for eukaryotic cells because ___.
A. it can only bind to host cells
B. it requires calmodulin for activity
C. it only interacts with eukaryotic AMP
D. it requires a host G protein for activity
Cholera toxin production is controlled by several environmental factors and there are as many as 20 other
Vibrio cholera genes regulated in a similar manner. It has recently been discovered that the toxin genes are
located on a temperate bacteriophage that inserts into the V. cholera genome, however, the regulatory genes
toxR, toxS and toxT are located elsewhere on the chromosome. Discuss the significance of these observations
with respect to the evolution of toxin regulation.
Discuss the similarities and differences between the food borne diseases caused by Clostridium botulinum and
Staphylococcus aureus. Be sure to address possible treatment strategies such as antibiotics and vaccines.
The symptoms of Toxic shock syndrome are caused by the Toxic shock syndrome toxin-1 (TSST-1). There
are a number of similarities between the symptoms of toxic shock syndrome and the septic shock associated
with LPS - mainly due to the release of excess cytokines. Describe the different pathways of TSST-1 and LPS
interaction with the host that lead to cytokine release.
Describe three types of mutations that eukaryotic cells might acquire that would make them resistant to
diphtheria toxin. Explain the significance of each mutation with respect to toxin structure or function.
Clostridium botulinum is capable of causes three very different types of disease. Describe the three disease
syndromes caused by this organism and address the different treatment or prevention strategies for each.
A microbiologist has used transposon mutagenesis to isolate a strain of Salmonella typhi that can no longer enter tissue
culture cells. She would next like to identify factors that control expression of this newly identified locus. Starting with
her mutant strain, how should she proceed to study the regulation of her gene?
Bordetella pertussis virulence genes are controlled by the BvgA/BvgS proteins. These two regulatory proteins
constitute a fairly typical two-component regulatory system. Describe how the BvgA/BvgS two-component
regulatory system controls expression of vir-activated genes (vag).
List the desirable properties of a vaccine against a bacterial disease and explain why those properties are
important.
Toxic Shock Syndrome (TSS) and Toxic Shock-Like Syndrome (TSLS) are distinct illnesses resulting in
similar pathologies but TSLS has a significantly high mortality rate than TSS. Why?
The crystal structure of diphtheria toxin reveals three domains corresponding to the three functions associated
with the toxin. What are those three functions?
Botulinal toxin and Tetanus toxin have very different pathologies yet they are very closely related structurally
and functionally. How can to very similar toxins have such different pathologies.
Why should infants not be given honey?
The amount of a virulence factor produced by a bacterial pathogen can be controlled by a variety of
mechanisms. List five of the possible mechanisms discussed in class and give a brief description of each.
Toxigenic strains of Corynebacterium diphtheriae are lysogenized with one of a related group of
bacteriophages. Identification of these phages and their encoded toxin gene differed significantly from the
identification of the phage that encodes the toxin coregulated pilus of Vibrio cholera. How were each of these
phages identified?
Describe the structure and function of cholera toxin. The functional description should include a model for
how the toxin is able to exert its effect on various enzymes within the cell.
Bordetella pertussis produces a number of toxins. Two of these toxins lead to increased levels of cAMP.
Describe both toxins and mechanism by which each toxin leads to overproduction of cAMP.